A Carcinoid heart disease

The clue is a cluster of symptoms suggestive of Systemic disease with a predominant heart Complication (because it is a cardiology Question and we are told that the patient has Prominent precordial pulsations Suggesting right heart disease)Carcinoid heart disease occurs if there is accumulation of fibrous tissue in the heart. especially to the under surface of the tricuspid valve.
Carcinoid heart disease can hold the tricuspid valve in a semi-Closed position. SO tricuspid stenosis and regurgitation can occur
Pulmonary regurgitation / Sten0SiS Occurs if carcinoid heart disease affects the pulmonary valve
Right-sided heart valves are implicated because. in most cases, the primary carcinoid turnout is in the bowel and with liver metastases The latter release serotonin and kallikrein that travel through liver sinusoids and empty into the Central vein of each lobule The central veins coalesce into hepatic veins, which leave the liver and drain into the inferior versa cava and right side of the heart
Increased levels of serotorun and kallikrein create systemic symptoms such as bronchospasm. diarrhoea and flushing, which are part Of the carcinosd syndrome

B Congenital tricuspid regurgitation
Congenital tricuspid regurgitation is incorrect because this problem is not a chronic congenital issue. The patient has no significant history and this is clearly a new problem

C HIV-associated heart disease
HIV-assOCiated heart disease is incorrect because there are no clear indications that this man has HIV infection He is married and has two children HIV infection can cause cardiomyopathy. pericardial diseases. myocarditis and heart failure but the periodic attacks of wheezing and loose motions do not fit this diagnosis.

D Rheumatic heart disease
Rheumatic heart disease is incorrect because there is no history of rheumatic fever

E Traumatic heart disease
Traumatic heart disease is incorrect because the periodic attacks of wheezing and loose motions do not fit this diagnosis Traumatic tricuspid regurgitation can occur owing to ruptured chordae tendinae. but there is no wheezing or diarrhoea

D ASD with pulmonary hypertension

Here, one must consider the most common pathology in the light of clinical findings. It is unlikely that this man has an ASD and also has left-sided heart failure, otherwise his symptoms would reflect this scenario. His prominent left precordium suggests that the right ventricle is dilated and that he has increased right-sided pressures with increased turbulent flow through the pulmonary valve.

He is young, so we think immediately about congenital diseases and their complications. It is important to know that haemodynamically significant ASDs can lead to pulmonary hypertension over time.

A Atrial septal defect (ASD) with aortic regurgitation

Atrial septal defect (ASD) with aortic regurgitation is incorrect. The murmur associated with aortic regurgitation is diastolic, and this would be an abnormal association with an ASD.

B ASD with aortic stenosis

ASD with aortic stenosis is incorrect. Remember, aortic stenosis would be located in the second intercostal space on the right upper sternal edge.

C ASD with mitral stenosis

ASD with mitral stenosis is incorrect. Ostium secundum ASD in combination with rheumatic mitral stenosis (Lutembacher syndrome) can cause the same picture in advanced cases if there is pulmonary hypertension, but this is far less common.

E Uncomplicated ASD

Uncomplicated ASD is incorrect because clearly this man has a haemodynamically significant ASD with complications resulting in progressive right-sided heart failure.

D Supravalvular aortic stenosis

In supravalvular aortic stenosis, the jet is directed up the innominate artery preferentially. Other findings might include a difference in carotid pulsation or the murmur of aortic stenosis.

The symptoms will often appear similar to those of coarctation of the aorta, in which the narrowing is usually found just beyond the origin of the left subclavian artery. Also, hypertension in the arms and weak femoral pulses are the classic features of coarctation.

A Arterial occlusive disease

Arterial occlusive disease is incorrect. The term ‘Arterial occlusive disease’ is slightly unusual. There is no suggestion of coronary artery disease (no signs of angina, or significant history). In addition, coronary atherosclerosis would not account for the dichotomous readings of blood pressure.

B Artefact due to lack of simultaneous recording

Artefact due to lack of simultaneous recording is incorrect. A difference of 30 mmHg is large, clinically significant, and must be investigated. There is no suggestion that the recordings may be inaccurate.

C Subclavian steal syndrome

Subclavian steal syndrome is incorrect. In health, blood flows from the aorta into the subclavian artery, and then some of that blood leaves via the vertebral artery to supply the brain. In subclavian steal syndrome, a reduced quantity of blood flows through the proximal subclavian artery. As a result, blood travels up one of the other blood vessels to the brain (the other vertebral or carotids), reaches the basilar artery or goes around the cerebral arterial circle and descends via the (contralateral) vertebral artery to the subclavian (with the proximal blockage) and feeds blood to the distal subclavian artery (which supplies the upper limb and shoulder). This scenario can result in reduced blood pressure in one arm, but you would also expect a significant history of presyncope (sensation that one is about to faint), syncope (fainting), neurologic deficits, or severe memory problems, which are not the case here.

E Takayasu’s arteritis

Takayasu’s arteritis is incorrect. A difference in blood pressure may exist, but you would expect the patient to be anaemic and have an increased level of C-reactive protein.

E Isosorbide mononitrate

The patient has recurrent coronary artery vasospasm, the symptoms of which comprise.

*   angina-like chest pain during at rest, particularly in the early hours of the morning

*   characteristic electrocardiographic changes during exercise testing

*   normal coronary arteries on cardiac catheterisation

*   inducible coronary artery spasm during the catheterisation,

Nitrates are often effective in patients with this set of symptoms, as are a range of calcium antagonists (e.g. dihydropyridine, non-dihydropyridine agents).

A Aspirin

Aspirin is incorrect. As described above, the syndrome is not related to blockage of coronary arteries or predilection to formation of blood clots, so anti-platelet agents are not helpful for management of this condition.

B Bisoprolol

Bisoprolol is incorrect. Beta blockers can be helpful but this question asks for the agent that will best manage angina symptoms. Thus, a vasodilator is a preferable option over a beta blocker (which will not necessarily improve symptoms, but may improve long-term outcomes). In addition, beta-blockers can theoretically worsen the spasm.

C Diazepam

Diazepam is incorrect. Benzodiazepines would not be helpful in this case.

D Atenolol

Atenolol is incorrect. The fact that the answers available are two very similar beta blockers (with largely similar profiles of action) should indicate that beta blockers are not the correct choice.

E Sotalol

The patient has ventricular tachycardia. Among all the anti-arrhythmic agents tested, sotalol has shown the highest efficacy in clinical trials so far. It is, therefore, recommended as the first-choice drug to prevent recurrence of non-sustained ventricular tachycardia. Note that you have been asked to give the best ‘first-line treatment’. Immediately you must be cautious about implantable cardioverter defibrillator (ICD), radiofrequency catheter ablation and rate-responsive, dual-chamber pacemaker because each of these would not be first-line treatment.

A Flecainide

Flecainide is incorrect. Flecainide is used in the treatment of several types of supraventricular tachycardias, including atrioventricular nodal re-entrant tachycardia and Wolff-Parkinson-White syndrome. Flecainide has limited use in the treatment of ventricular tachycardia and is not first-line

treatment. In certain cases, (notably the Cardiac Arrhythmia Suppression Trial), flecainide has been shown to increase mortality if used to suppress ventricular extra systoles in the setting of acute myocardial infarction.

B Implantable cardioverter defibrillator (ICD)

ICD is incorrect because this is not first-line treatment. The decision to site an ICD would need to be considered carefully because there are risks and benefits. ICD therapy might reduce mortality in patients with aborted sudden cardiac death and in high-risk patients with ventricular tachycardia

and compromised right and left ventricular function. However, there are problems with using an ICD in right ventricular cardiomyopathy (in which the mass of right ventricular muscle might be too thin), such as low R-wave amplitude, high thresholds or lead perforation.

C Radiofrequency catheter ablation

Radiofrequency catheter ablation is incorrect. Radiofrequency catheter ablation is indicated for medically refractory ventricular tachycardia in selected patients only. Information regarding its efficacy in preventing sudden cardiac death is lacking. It is not possible to jump from the scenario provided to radiofrequency catheter ablation. The mechanism for ventricular tachycardia arrest does not sound

related to accessory or pre-excitatory pathways. It is more likely to be related to a diseased right ventricle.

D Rate-responsive, dual-chamber pacemaker

Rate-responsive, dual-chamber pacemaker is incorrect. A rate-responsive, dual-chamber pacemaker would be indicated for cardiac failure with left and right ventricular dyssynchrony, not for right ventricular failure and ventricular tachycardia arrest.

A Implantable cardioverter defibrillator (ICD)

For secondary prevention of sudden cardiac death (SCD) in patients with HOCM, there is evidence and general agreement that an ICD is the most useful option.

B Amiodarone

Amiodarone is incorrect. That said, in the primary prevention of SCD in HOCM, amiodarone may have a role in some patients. However, the general consensus is that primary prevention via an ICD is the preferred option.

C Beta Blockers

Beta blockers is incorrect. Beta blockers aid HOCM management because they can slow down the heart rate and reduce the likelihood of ectopic beats. However, this strategy should be followed after the patient has been treated correctly with an ICD in the acute setting.

D Verapamil

Verapamil is incorrect. Verapamil aids HOCM management because it can slow down the heart rate and reduce the likelihood of ectopic beats. That said, for patients who cannot tolerate beta blockers or do not have good control of symptoms with beta blockers, non-dihydropyridine calcium-channel blockers such as verapamil can be used. However, non-dihydropyridine calcium-channel blockers are potentially harmful in patients in a setting of systemic hypotension or severe dyspnoea at rest. These medications also reduce the heart rate, though their use in patients with severe outflow obstruction, elevated pulmonary artery wedge pressure, and low blood pressures should be followed with expert guidance.

E Rate-responsive, dual-chamber pacemaker

Rate-responsive, dual-chamber pacemaker is incorrect. Biventricular pacing will not help reduce the risk of cardiac arrest and will not have a useful impact in cardiac arrest because this type of device does not have a defibrillator function.

C Type III hyperlipoproteinaemia

Tuboeruptive xanthomas occur in type-III hyperlipoproteinaemia, which is due to high numbers of chylomicrons and high levels of intermediate-density lipoprotein. The most common cause for this form is the apolipoprotein E2/E2 genotype. Type-III hyperlipoproteinaemia is due to cholesterol-rich, very-low-density lipoprotein (VLDL). Its incidence has been estimated to be =l per 10,000 individuals. It is associated with hypercholesterolaemia (typically 8-12 mmol/l). hypertriglyceridaemia (typically 5-20 mmol/l), a normal concentration of apolipoprotein B, and two types of skin signs (palmar xanthomata or orange discolouration of skin creases: tuberoeruptive xanthomata on elbows and knees). It is characterised by the early onset of cardiovascular disease and peripheral vascular disease.

A Type I hyperlipoproteinaemia

Type-l hyperlipoproteinaemia is incorrect. Type-I hyperlipoproteinaemia (‘hyperchylomicronaemia”) is

associated with eruptive xanthomas. Complications include occlusion of the retinal vein, acute pancreatitis, steatosis, organomegaly and lipaemia retinalis.

B Type II hyperlipoproteinaemia

Type-II hyperlipoproteinaemia is incorrect. Type-II hyperlipoproteinaemia is associated with xanthoma

tendinosum (nodular swellings of tendons). Type-II hyperlipoproteinemia (by far the most common form) is classified further into types Ila and lib depending mainly on whether the increases in triglyceride levels occur in addition to those of low-density lipoprotein-cholesterol.

D Type IV hyperlipoproteinaemia

Type-IV hyperlipoproteinaemia is incorrect. Type-IV hyperlipoproteinaemia is associated with eruptive xanthomas.

E Type V hyperlipoproteinaemia

Type-V hyperlipoproteinaemia is incorrect. Type-V hyperlipoproteinaemia (mixed hyperlipoproteinaemia familial or mixed hyperlipidaemia) is very similar to type-l, but with high levels of VLDL in addition to many chylomicrons. It is also associated with glucose intolerance and hyperuricaemia.

E  Mitral stenosis

This is a relatively difficult question and requires familiarity with cardiac catherisation or understanding the relevance of abnormal values. The diastolic pressure in the left atrium is increased at rest and upon exercise, suggesting reduced flow through the mitral valve (as you might expect in mitral stenosis).

The haemodynamic pattern is typical of mitral stenosis and may also be seen in cor triatriatum, in which there is a left atrial membrane.

A Congenital heart disease

Congenital heart disease is incorrect. In congenital heart disease, there will be an increase in oxygen saturation in the right heart and reduction in the left heart.

B Left ventricular diastolic dysfunction

Left ventricular diastolic dysfunction is incorrect. In left ventricular diastolic dysfunction, the left ventricular end-diastolic pressure is > 15 mmHg. This is because of relative stiffness of the left ventricular wall, which is characteristic of diastolic dysfunction.

C Major occlusion of pulmonary arteries

Major occlusion of pulmonary arteries is incorrect. Major occlusion of pulmonary arteries by a clot or tumour is associated with a focal pressure gradient in a lobar or larger pulmonary artery, intravascular filling defect, or narrowing.

D Mitral regurgitation

Mitral regurgitation is incorrect. A large systolic pressure wave in wedge tracing can be seen in patients with mitral regurgitation. In addition, regurgitation of contrast to the left atrium can be seen from a left ventricular angiogram.

C Hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy is usually due to a mutation in one of nine sarcomeric genes, which results in a mutated protein in the sarcomere (the primary component of the myocyte). These are predominantly single-point missense mutations in the genes for b-myosin heavy chain, myosin-binding protein C, cardiac troponin T, or tropomyosin. These mutations cause structural abnormalities and possible deficiencies in force generation in myofibrils and myocytes. Hypertrophic cardiomyopathy appears in all ethnic groups, and its prevalence in the general population is =0.2-0.5%.

A Aortic stenosis

Aortic stenosis is incorrect. The patient is young and otherwise healthy. It is incredibly unlikely that this patient would have calcific aortic stenosis. He could have a bicuspid valve that has deteriorated rapidly, but the mid-to-late systolic impulse in the precordial motion (‘triple ripple’) is specific for hypertrophic cardiomyopathy.

B Atrial septal defect

Atrial septal defect is incorrect. An atrial septal defect would present with a prominent left precordium with an ejection murmur in the second left intercostal space. There would also be a fixed splitting of the second heart sounds.

D Mitral valve prolapse

Mitral valve prolapse is incorrect. Mitral valve prolapse is characterised by a mid-systolic click, followed by a late systolic murmur heard best at the apex.

E Mixed aortic valve disease

Mixed aortic valve disease is incorrect. Mixed aortic valve disease would present with murmurs associated with aortic stenosis (systolic, crescendo-decrescendo murmur is heard loudest at the upper right sternal border, at the second right intercostal space and radiates to the carotid arteries bilaterally) and aortic regurgitation (early diastolic and decrescendo, which is best heard in the third left intercostal space and may radiate along the left sternal border). Either of these murmurs can predominate.

C Mitral stenosis with mobile leaflets

There is a loud first heart sound and, if an opening ‘snap’ is heard, this indicates that the mitral valve is mobile (‘mobile leaflets’). The snap occurs if the superior systolic bowing of the anterior mitral valve leaflet is reversed rapidly towards the left ventricle in early diastole, owing to the high left atrial pressure.

A Mitral stenosis with a fourth heart sound

Mitral stenosis with a fourth heart sound is incorrect. There is no mention of a fourth heart sound. The latter is often associated with filling of a stiff left ventricle (this can be seen in left ventricular hypertrophy, amyloid, hypertrophic cardiomyopathy, or scarred/fibrosed left ventricle due to ischaemia). The fourth heart sound is classically late diastolic or presystolic. It occurs if augmented atrial contraction causes presystolic ventricular distension so that the ventricle contracts with greater force.

B Mitral stenosis with atrial fibrillation

Mitral stenosis with atrial fibrillation is incorrect. There is mention of an irregularly irregular pulse (atrial fibrillation). Atrial fibrillation often is associated with a variable first heart sound.

D Mitral stenosis with pulmonary hypertension

Mitral stenosis with pulmonary hypertension is incorrect. Pulmonary hypertension is associated with an accentuated pulmonary component of the second heart sound, a right ventricular third heart sound, and parasternal heave indicating a hypertrophied left atrium.

E Mitral valve prolapse

Mitral valve prolapse is incorrect. Mitral valve prolapse is associated with a mid-systolic click followed by a late systolic murmur heard best at the apex.

Important associations to be aware of:

*   ‘Soft first heart sound (S1)’: immobile mitral stenosis,

hypodynamic state, mitral regurgitation, long PR interval

*   ‘Split S1′: right bundle branch block, left bundle branch

block, ventricular tachycardia, Ebstein’s anomaly

*   “Variable S1′: atrial fibrillation, complete heart block

*   “Loud S2’: hypertension, tachycardia, atrial septal defect

*   Soft/absent S2: severe aortic stenosis

*   Fixed splitting S2: atrial septal defect

*   Wide split S2: right bundle branch block, pulmonary

stenosis, mitral regurgitation

*   ‘Single S2’: severe pulmonary stenosis, aortic stenosis,

hypertension, ventricular septal defect, tetralogy of Fallot,

Eisenmenger’s syndrome

*   ‘Reversed split S2’: left bundle branch block, right

ventricular pacing, patent ductus arteriosus, aortic

stenosis

*   ‘S3’: rapid left ventricular filling (mitral regurgitation,

ventricular septal defect), can be normal in children

*   ‘S4’: filling of stiff left ventricle (left ventricular

hypertrophy, amyloid, hypertrophic cardiomyopathy,

ischaemia).

C Haemolysis on bypass

An increase in levels of direct and indirect bilirubin, with no other changes in liver-function tests, indicates haemolysis on cardiopulmonary bypass. This can be confirmed by demonstration of increased levels of free haemoglobin in plasma. There is no specific treatment for haemolysis on cardiopulmonary bypass.

A ‘Shock liver’ syndrome

‘Shock liver’ syndrome is incorrect. Shock liver syndrome is also known as ‘ischaemic hepatitis’, and is due to acute hypoperfusion leading to diffuse heaptic injury. Markedly increased levels of enzymes are seen. This patient had no change in levels of aminotransferases, so this diagnosis is unlikely. Treatment is aimed at maximising cardiac output and oxygenation.

B Anaesthetic-induced

Anaesthetic-induced is incorrect. In a patient with no underlying liver disease (which we have no evidence of), anaesthesia is unlikely to cause an increase in bilirubin levels alone.

D Narcotic-induced

Narcotic-induced is incorrect. Narcotics are unlikely to increase bilirubin levels with no other change in liver-function tests.

E Right heart failure

Right heart failure is incorrect. Right heart failure is a possible cause of hyperbilirubinaemia in the immediate period after cardiopulmonary bypass. However, in this case, there was no increase in the level of alkaline phosphatase, which you would also expect.

D Second-degree block at the distal conduction system

In asymptomatic patients, a PPM is indicated in a second-degree type-II AV block or third (complete) heart block. A second-degree type-II AV block indicates disease at the distal conduction system rather than the AV node (which gives a second-degree heart type-1 (Wenckebach) block).

A First-degree block at the AV node

First-degree block at the atrioventricular (AV) node is incorrect. A PPM is not indicated in a first-degree block at the AV node.

B First-degree block in the distal conduction system with an HV interval < 100 ms

First-degree block in the distal conduction system with an HV interval < 100 ms is incorrect. A PPM is indicated only for cases of first-degree AV block in the distal conduction system, in which a HV interval > 100 ms is associated with symptoms.

C Second-degree block at the AV node

Second degree block at the AV node is incorrect. A second- degree type I AV block indicates disease at the AV node (Wenckebach). In patients with a second-degree type-I AV block, pacing should be considered if the patient is symptomatic, or if the pathology is located intra or infra to the bundle of His after electrophysiologic studies. These are not routinely done, however.

E Right bundle-branch block

Right bundle-branch block is incorrect. A PPM is not indicated for bundle branch block if asymptomatic because only 1-2% of patients will develop an AV block and cardiac pacing has not been shown to reduce mortality.

D Stopping smoking

All of these interventions are effective at reducing the risk of future ischaemic events, but stopping smoking is the single most effective, non-pharmacological intervention. Several studies have shown that smoking cessation is as effective as having a coronary artery bypass graft. Smoking cessation is vital for reducing the risk of worsening coronary artery disease.

A Alcohol reduction

Alcohol reduction is incorrect. There is no mention of excessive consumption of alcohol in this case. Excessive consumption of alcohol can result in worsening cardiovascular health, but it is not linked directly to cardiovascular disease (CVD) risk.

B Diet control

Diet control is incorrect. There is no mention of obesity in this case (though it may be assumed based on the apparent metabolic syndrome). Control of diet and weight is important for the management and risk reduction of CVD, but are only two of many factors to consider, and are less important then smoking cessation.

C Regular exercise

Regular exercise is incorrect. Body mass index/body weight are considered to be CVD risk factors, but the relative weighting of these factors is far less than that of smoking, so smoking cessation must be prioritised.

E Weight reduction

Weight reduction is incorrect. Body mass index/body weight are considered to be CVD risk factors, but the relative. weighting of these factors is far less than that of smoking, so smoking cessation must be prioritised.

B Automatic implantable cardioverter defibrillator

All patients who have survived a sudden cardiac arrest, regardless of the type of underlying structural heart disease, are suitable for an AICD because it reduces the risk of sudden death and total mortality compared with therapy using anti- arrhythmic drugs.

HOCM is the most common cause of cardiac arrest in those aged < 40 years. Overall, ≈1% of patients with HOCM die each year. AICDs have been shown to be effective at terminating ventricular arrhythmias in those with HOCM.

A Amiodarone

Amiodarone is incorrect. AICDs have been shown to have survival benefits compared with empirical amiodarone therapy.

C Dual-chamber pacemaker

Dual-chamber pacemaker is incorrect. A pacemaker is not beneficial in the context of cardiac arrest. The implanted device requires a defibrillator function to provide DC cardioversion in the event of cardiac arrest.

D Sotalol

Sotalol is incorrect. Sotalol is useful as medical therapy for symptom control, but the definitive long-term intervention in this case is an AICD.

E Verapamil

Verapamil is incorrect. Verapamil can be used if beta blockers are contra-indicated or ineffective, but the definitive intervention is an AICD.

C Bisoprolol

This woman has chronic heart failure (CHF) with compatible symptoms and objective evidence of left ventricular dysfunction at rest, as shown by reduced ejection fraction. There is overwhelming evidence for the long-term prognostic and symptomatic benefit of an ACEI in patients with CHF. In addition, clinical trials support the prognostic and symptomatic benefit of certain beta blockers in CHF patients, so this is the next appropriate therapy to start.

In the UK, bisoprolol and carvedilol are the two agents licensed for use in this condition. Trials of bisoprolol and carvedilol suggest a reduction of =30% in mortality. particularly in patients with severe cardiac failure.

A Amiodarone

Amiodarone is incorrect. Addition of amiodarone would have no effect on the symptoms or prognosis in this patient. In addition, amiodarone treatment is associated with a significant side-effect profile. Common side effects include feeling tired, tremors, nausea, and constipation. Amiodarone can have serious side effects (interstitial pneumonitis, liver problems, heart arrhythmias, vision problems, thyroid problems, death), so is recommended only for significant ventricular arrhythmias. If taken during pregnancy or breastfeeding, amiodarone can cause problems in the baby. Also, amiodarone is metabolised extensively in the liver by cytochrome P450 3A4, and can affect the metabolism of numerous other drugs. It interacts with digoxin, warfarin, phenytoin, and others.

B Amlodipine

Amlodipine is incorrect. These agents are safe to use in patients with CHF for symptomatic treatment of angina or associated hypertension, but there is no evidence that they influence outcome.

D Isosorbide mononitrate

Isosorbide mononitrate is incorrect. These agents are safe to use in patients with CHF for symptomatic treatment of angina or associated hypertension, but there is no evidence that they influence outcome.

E Losartan

Losartan is incorrect. ACEI plus an angiotensin receptor blocker can provide additional benefit over ACEI therapy alone. However, the combination is more likely to result in hyperkalaemia, so the risk-benefit equation for this strategy is lacking.

A Implantable cardioverter defibrillator (ICD)

For secondary prevention of sudden cardiac death (SCD) in patients with HOCM, there is evidence and general agreement that an ICD is the most useful option.

B Amiodarone

Amiodarone is incorrect. That said, in the primary prevention of SCD in HOCM, amiodarone may have a role in some patients. However, the general consensus is that primary prevention via an ICD is the preferred option.

C Beta Blockers

Beta blockers is incorrect. Beta blockers aid HOCM management because they can slow down the heart rate and reduce the likelihood of ectopic beats. However, this strategy should be followed after the patient has been treated correctly with an ICD in the acute setting.

D Verapamil

Verapamil is incorrect. Verapamil aids HOCM management because it can slow down the heart rate and reduce the likelihood of ectopic beats. That said, for patients who cannot tolerate beta blockers or do not have good control of symptoms with beta blockers, non-dihydropyridine calcium-channel blockers such as verapamil can be used. However, non-dihydropyridine calcium-channel blockers are potentially harmful in patients in a setting of systemic hypotension or severe dyspnoea at rest. These medications also reduce the heart rate, though their use in patients with severe outflow obstruction, elevated pulmonary artery wedge pressure, and low blood pressures should be followed with expert guidance.

E Rate-responsive, dual-chamber pacemaker

Rate-responsive, dual-chamber pacemaker is incorrect. Biventricular pacing will not help reduce the risk of cardiac arrest and will not have a useful impact in cardiac arrest because this type of device does not have a defibrillator function.

B Bisoprolol

She is in permanent atrial fibrillation at 150 bpm despite digoxin therapy, so better rate control is required. Digoxin on its own may not control catecholamine-driven tachycardia (e.g. during exertion).

A Amiodarone

Amiodarone is incorrect. Amiodarone may be effective, but it would not be the first choice for this young patient working outdoors due to its side-effect profile. Common side effects include feeling tired, tremors, nausea, and constipation. Amiodarone can have serious side effects (interstitial pneumonitis, liver problems, heart arrhythmias, vision problems, thyroid problems, death), so is recommended only

for significant ventricular arrhythmias. If taken during pregnancy or breastfeeding, amiodarone can cause problems in the baby. Also, amiodarone is metabolised extensively in the liver by cytochrome P450 3A4, and can affect the metabolism of numerous other drugs. It interacts with digoxin, warfarin, phenytoin, and others.

C DC shock

DC shock is incorrect. She is in permanent atrial fibrillation and, as such, by definition, sinus rhythm cannot be restored (as opposed to persistent or paroxysmal atrial fibrillation).

D Mitral valve replacement

Mitral valve replacement is incorrect. This woman has moderate, mixed mitral valve disease, so surgery is not indicated currently. It may, however, be required later if features of left heart failure progress. Even if the mitral stenosis were to be severe, heavy calcification of the valve

and concomitant mitral regurgitation would preclude percutaneous valvotomy.

E Percutaneous mitral valvotomy

Percutaneous mitral valvotomy is incorrect. This woman has moderate, mixed mitral valve disease, so surgery is not indicated currently. It may, however, be required later if features of left heart failure progress. Even if the mitral stenosis were to be severe, heavy calcification of the valve and concomitant mitral regurgitation would preclude percutaneous valvotomy.

E  Spironolactone (25 mg, once daily)

This man has decompensated congestive heart failure (CHF) with symptoms at rest (New York Heart Association class IV). Examination has revealed significant fluid retention. The initial management plan of changing to frusemide (iv) is sensible because coexistent gut-wall oedema is likely to impinge oral

absorption, and increasing the dose of ramipril (a vasodilator) is also sensible. The aldosterone antagonist spironolactone has been shown to improve the prevalence of mortality. symptoms, and hospitalisation in patients with severe CHF already on conventional treatment. Benefits are in addition to its diuretic effect because aldosterone itself has adverse effects on the structure and function of the myocardium. Careful monitoring of renal function and biochemistry is important in these patients.

A Amiloride (5 mg, once daily)

Amiloride (5 mg, once daily) is incorrect. Amiloride is contraindicated in patients with Addison’s disease,

hyperkalaemia, anuria and, in this case, hyponatraemia.

B Bendrofluazide (2.5 mg, once daily)

Bendrofluazide (2.5 mg, once daily) is incorrect. Addition of a thiazide (inhibiting sodium reabsorption in distal tubules) may work in synergy with a loop diuretic but, in combination, there is an increased risk of worsening hyponatraemia.

C Bumetanide (2 mg, twice daily)

Bumetanide (2 mg, twice daily) is incorrect. The patient is already taking a loop diuretic. Bumetanide may be used instead of furosemide, but would not be required in addition to it. It may be absorbed better by the gut, so would be an alternative to furosemide (iv) initially.

D Metolazone (5 mg, once daily)

Metolazone (5 mg, once daily) is incorrect. As above, the same is true for metolazone.

B Coronary artery disease

Coronary artery disease is the most likely underlying aetiology. Chronic heart failure is not an absolute diagnosis, and a cause must be found. In the UK, the most common aetiology is underlying ischaemic heart disease (IHD), at ≈50- 66% of cases. This patient has several risk factors for IHD, which adds weight to the likelihood of this being the diagnosis. *Left bundle branch block* is also likely to be ischaemic in origin.

A Alcohol

Alcohol is incorrect. This patient has a significant intake of alcohol, but the overall clinical picture indicates cardiac dysfunction as opposed to decompensated liver disease (in isolation). It is also a little late in life to develop alcoholic cardiomyopathy, which is usually seen in individuals aged 30- 50 years.

C Hypertension

Hypertension is incorrect. This patient is hypertensive, but this in isolation is highly unlikely to be responsible for his overall clinical condition. If hypertension was accountable in isolation, we would expect to see abnormal renal function.

D Valvular heart disease

Valvular heart disease is incorrect. The mitral regurgitation in this patient is most likely to be secondary to left ventricular dilatation and subsequent annular dilatation of the mitral valve ring. This will contribute to the development of pulmonary hypertension.

E Viral myocarditis

Viral myocarditis is incorrect. Viral myocarditis is more likely to occur in younger patients. He is not complaining of chest discomfort or systemic symptoms and there is no evidence of these features from the electrocardiogram or echocardiogram.

E Perindopril

Most clinicians now recommend addition of angiotensin- converting enzyme inhibitors (ACEIs) for patients with vascular disease irrespective of left ventricular function. This is based on evidence from large trials such as PROGRESS (perindopril) and HOPE (ramipril). Benefits of ACEIs are not related only to a reduction in blood pressure: there are also beneficial local vascular and myocardial effects. Furthermore, blood pressure is not yet optimised in this patient, and an ACEI should bring this to the desired level (< 140/85 mmHg).

A Bendroflumethiazide

Bendroflumethiazide is incorrect. Bendroflumethiazide may be used in this scenario to reduce his blood pressure, but an ACEI would be recommended rather than a diuretic due to the reasons stated above.

B Diltiazem

Diltiazem is incorrect. The patient already has excellent control of angina with a beta blocker and a long-acting nitrate, so he does not require additional anti-angina agents. Also, there is an increased risk of bradycardia and atrioventricular block if diltiazem is combined with a beta blocker, so this regimen should be avoided.

C Doxazosin

Doxazosin is incorrect. Several drugs are used before this (e.g. ACEIs, thiazide diuretics).

D Nicorandil

Nicorandil is incorrect. Nicorandil may be used as an anti-angina agent if other drugs are contraindicated or not tolerated, or as a third-line drug. This patient has well-controlled angina on his current medication, so this addition is not required.

C Radiofrequency ablation of the accessory pathway
This young man has Wolff-Parkinson-White (WPW) syndrome. The most common arrhythmia in this condition is an atrioventricular re-entry tachycardia. This is a narrow complex with anterograde conduction through the AV node and retrograde conduction via the accessory pathway. If patients with WPW syndrome develop atrial fibrillation, they are at risk of rapid anterograde conduction to the ventricles via the accessory pathway, and this may degenerate to ventricular fibrillation subsequently. The extremely rapid conduction with broad QRS duration is typical of this complication. Radiofrequency ablation of the
accessory pathway is recommended in this setting and is potentially curative.

A Atrial defibrillator implantation
Atrial defibrillator implantation is incorrect because it is not indicated.

B Intravenous and then oral loading with amiodarone

Intravenous and then oral loading with amiodarone is incorrect. Medications are used in patients in which only ablation or surgery are not options.

D Radiofrequency ablation of the atrioventricular (AV) node

Radiofrequency ablation of the AV node is incorrect. In WPW syndrome, there is an accessory pathway that connects the atria and ventricles, in addition to the AV node. This accessory pathway needs to be ablated, rather than the AV node.

E Surgical ablation of the accessory pathway
Surgical ablation of the accessory pathway is incorrect. Surgical ablation is very effective and complications rates are low, but it is more invasive than radiofrequency ablation and, therefore, is not used commonly.

D Ventricular tachycardia (VT)
The prescription suggests underlying cardiac disease with probable cardiac dysfunction. In this context, and in a patient of this age, a broad-complex tachycardia should be assumed to be VT until proved otherwise. This patient is haemodynamically compromised as a consequence of the arrhythmia.

A Atrial fibrillation (AF)
AF is incorrect. AF must conduct through the atrioventricular node. At this stage, it is subject to a refractory pause of 0.1 s, and so is rate-limited. AF is rarely > 150 bpm. He is not taking warfarin, and his ECG shows a broad complex tachycardia (as opposed to an irregularly irregular waveform).

B Atrial flutter with a 2:1 block

Atrial flutter with a 2:1 block is incorrect. For many of the reasons supplied above, atrial flutter is often rate-limited at 150 bpm and, with a 2:1 conduction, would create a heart rate of =75 bpm. The ECG waveform should have a classical ‘sawtooth’ appearance.

C Supraventricular tachycardia (SVT) with aberrant conduction

SVT with aberrant conduction is incorrect. Many ECG criteria exist to aid the differentiation of VT and SVT with aberrancy, and include: A-V dissociation, capture beats, fusion beats, extreme QRS axis, and concordance across ventricular leads. In addition, a previous ECG can be exceedingly helpful. Other clues include subtle clinical signs (e.g. intermittent cannon waves in the jugular venous pressure) and a variable first heart sound may be present in patients with A-V dissociation.

E Wolff-Parkinson-White syndrome
Wolff-Parkinson-White syndrome is incorrect. In individuals with this syndrome, electrical activity that is initiated in the sinoatrial node travels through the accessory pathway, as well as through the atrioventricular node, to activate the ventricles via both pathways. The accessory pathway does not have the impulse-slowing properties of the atrioventricular node, so the electrical impulse first activates the ventricles via the accessory pathway, and immediately afterwards via the atrioventricular node. This gives the short PR interval and slurred upstroke of the QRS complex known as the ‘delta wave’.

C Intravenous magnesium
Torsades de pointes (polymorphic VT with QRS complexes of different amplitude twisting around the isoelectric line) occurs in patients with a prolonged QT interval. Any cause of QT prolongation can predispose to the arrhythmia. Causes include congenital (Jervell-Lange-Nielsen or Romano-Ward
syndromes), QRS complexes of different amplitude, metabolic (hypocalcaemia, hypomagnesaemia or
hypokalaemia), drugs (e.g. amiodarone, tricyclic antidepressants, phenothiazines), ischaemic heart disease and mitral valve prolapse. The arrhythmia often occurs in the context of bradycardia. Intravenous magnesium (even if the serum concentration of magnesium is normal) is first-line therapy.

A DC cardioversion
DC cardioversion is incorrect. DC shock would not be helpful because episodes are non-sustained.

B Intravenous amiodarone
Intravenous amiodarone is incorrect. Amiodarone prolongs the action potential, it doesn’t actually cause torsades, but it doesn’t drive any benefit for patients.

D Oral metoprolol
Oral metoprolol is incorrect. Temporary pacing at higher rates, with or without beta blockers, would be the next line of therapy, but the initial treatment would be intravenous magnesium.

E Temporary pacing
Temporary pacing is incorrect. As stated above, initial management is intravenous magnesium.

D Glyceryl trinitrate (iv)
This patient has severe pulmonary oedema. Initial treatment includes sitting the patient up and administering high-flow oxygen. High catecholamine levels and activation of the renin-angiotensin aldosterone system drive peripheral vasoconstriction, which increases myocardial oxygen demand. Conventionally, treatment has been with diuretics, but the benefits of these probably relate to their vasodilatatory actions. Early use of more powerful vasodilators represents a more attractive strategy and includes diamorphine (iv) and glyceryl trinitrate (iv; short half-life). Early administration of an oral angiotensin- converting enzyme inhibitor would also be recommended.

A Atenolol (iv)
Atenolol (iv) is incorrect. Beta blockers are not indicated in acute heart failure. If a patient is already taking a beta blocker, however, this should be continued unless the patient is in cardiogenic shock.

B Dobutamine (iv)
Dobutamine (iv) is incorrect. Dobutamine is a sympathomimetic drug used in the treatment of heart failure and cardiogenic shock. Short term intravenous inotropic agents may be used in patients with a systolic blood pressure < 90 and/or signs and symptoms of hypoperfusion, which is not the case here, so dobutamine is not recommended.

C Dopamine (iv)
Dopamine (iv) is incorrect. At low doses, dopamine acts through the sympathetic nervous system to increase the contraction force in heart muscle and the heart rate, thereby increasing cardiac output and blood pressure. Higher doses also cause vasoconstriction that increases blood pressure
further.

E Milrinone (iv)
Milrinone (iv) is incorrect. Milrinone is a phosphodiesterase-3 inhibitor that increases cardiac contractility and reduces pulmonary vascular resistance. In critically ill patients with evidence of cardiac dysfunction, there is limited good-quality evidence to recommend its use.

D Temporary transvenous pacing
This woman has complete heart block with an unstable escape rhythm. The latter is exemplified by three syncopal episodes. Her QRS duration is prolonged (normal up to 120 ms), and this is generally more unstable than an escape rhythm of normal duration (i.e. < 120 ms) because this originates from around the bundle of His. Her blood pressure is low, particularly in light of her background of hypertension. Cardiac output will be influenced by the heart rate. In the elderly, cerebral vascular dysregulation may compound this effect, thereby contributing to cerebral hypoperfusion. Ideally
she should receive a transvenous temporary pacemaker. If further acute problems occur while waiting for a transvenous temporary pacemaker (e.g. awaiting transfer to a room with fluoroscopy) then external pacing can be instituted in the short term with appropriate sedation.

A Dobutamine
Dobutamine is incorrect. Dobutamine is not indicated in this situation. Dobutamine acts on bl receptors to increase the contractility of cardiac muscle. It is used for inotropic support in infarction, cardiomyopathies and cardiogenic shock.

B Isoprenaline
Isoprenaline is incorrect. Isoprenaline is used for bradycardia (slow heart rate), heart block and, rarely, for asthma. In humans, it is a non-selective ẞ-adrenoreceptor agonist and trace amine-associated receptor-1 agonist that is structurally similar to epinephrine. It can be used effectively in an intensive care unit because it induces positive chronotropic, dromotropic, and inotropic effects. However, in this case, it is not the optimum initial management.

C Intravenous calcium chloride
Intravenous calcium chloride is not correct. Intravenous calcium chloride has a role in the management of magnesium intoxication. It can help to protect the myocardium from dangerously high levels of serum potassium in hyperkalaemia, but has no role in bradycardia management.

E Withhold medication and observe
Withhold medication and observe is incorrect. The patient has a complete heart block with an unstable escape rhythm and low blood pressure. She requires urgent treatment.

D Percutaneous coronary intervention
This relatively young man has presented early with an anterior ST elevation myocardial infarction (MI). The key therapeutic aim is early reperfusion to save the myocardium. This can be delivered by primary percutaneous coronary intervention (PCI) or fibrinolysis. Primary PCI should be offered to patients who present < 12 hours of symptom onset and if primary PCI can be undertaken < 120 minutes of the
time when fibrinolysis could have been given. This should be the norm in most of the UK.

A Clopidogrel (75 mg)
Clopidogrel (75 mg) is incorrect. Dual antiplatelet therapy with aspirin and a second anti-platelet drug, such as clopidogrel or ticagrelor, should be commenced and continued for ≤12 months in patients with an acute MI. However, this is not definitive treatment, so is not the correct answer. Also, the dose of clopidogrel in this answer is incorrect: it should be 300 mg, not 75 mg.

B Enoxaparin
Enoxaparin is incorrect. Patients undergoing PCI should receive unfractionated heparin or low-molecular-weight heparin (e.g. enoxaparin). In addition, patients who do not receive reperfusion therapy should be treated with fondaparinux, enoxaparin, or unfractionated heparin. Enoxaparin is not definitive treatment.

C Glycoprotein llb/lla blocker
Glycoprotein Ilb/lla blocker is incorrect. A glycoprotein IIb/Illa inhibitor (e.g. tirofiban) may be used to reduce the risk of immediate vascular occlusion in intermediate- and high-risk patients undergoing PCI, but is not definitive treatment. It has a role in bridging patients pre-PCI, or if they have to have repeated PCI and need to have anticoagulation between stages, but this is not the definitive option.

E Tissue plasminogen activator
Tissue plasminogen activator is incorrect. Fibrinolysis, such as with tissue plasminogen activator, should be given only if primary PCI cannot be delivered < 120 minutes of the time fibrinolysis can be given.

D Refer for coronary angiography
The purpose of the exercise test post-myocardial infarction is risk stratification and patient self-confidence. That said, it is becoming used less frequently because of newer imaging methods (e.g. such as cardiac computed tomography, cardiac magnetic resonance imaging). Patients who cannot undergo two stages of the Bruce protocol (< 6 minutes) are at a higher risk of adverse cardiovascular events. This youngish man has an early positive exercise test, as exemplified by symptoms and associated electrocardiographic changes. He should be referred for coronary angiography to accurately
ascertain if he has prognostic disease warranting coronary artery bypass grafting (e.g. left main stem disease, proximal three-vessel disease or proximal two-vessel disease including the left anterior descending artery). Percutaneous intervention can also be considered if he has ongoing symptoms (likely in view of his symptoms upon exercise
testing).

A Add diltiazem and review in clinic
Add diltiazem and review in clinic is incorrect. He has been identified as high risk from his exercise test result, so he requires further investigation. This patient is already taking a beta blocker, so he should not also be commenced on diltiazem due to the increased risk of bradycardia and atrioventricular block.

B Arrange a stress echocardiogram
Arrange a stress echocardiogram is incorrect. It may be used as an alternative to the exercise stress test if the patient already has ECG changes or cannot exercise adequately. This patient has already been identified as high risk from his exercise test result so now requires more invasive testing to
ascertain if he requires revascularisation.

C Increase atenolol (50 mg, once daily) and repeat the exercise test
Increase atenolol (50 mg, once daily) and repeat the exercise test is incorrect. He has been identified as high risk from his exercise test result, so he requires further investigation. Increasing his atenolol dose would be a sensible amendment to his current medical therapy but further investigation of coronary arteries is needed.

E Refer for a myocardial perfusion scan
Refer for a myocardial perfusion scan is incorrect. It may be used as an alternative to the exercise stress test if the patient already has ECG changes or cannot exercise adequately. This patient has already been identified as high risk from his exercise test result so now requires more invasive testing to ascertain if he requires revascularisation.

A Amiodarone
Current recommendations for advanced life support in the UK are provided by the European Resuscitation Council and Resuscitation Council UK. In patients with refractory ventricular fibrillation or pulseless ventricular tachycardia (i.e. after three initial shocks), intravenous amiodarone should be
considered. The standard dose used is a 300-mg bolus; if central access is available, then this is the desired route. If this is not the case, then large-bore peripheral access can be used.

B Bretylium
Bretylium is incorrect. Bretylium is an anti-arrhythmic drug that was used previously for ventricular fibrillation, but has been superseded by therapies such as defibrillation and amiodarone. It is now virtually unavailable anywhere in the world.

C Calcium chloride
Calcium chloride is incorrect. Calcium chloride is indicated during cardiopulmonary resuscitation if hyperkalaemia, hypocalcaemia or calcium channel block toxicity is present.

D Lidocaine
Lidocaine is incorrect. However, lidocaine may be used if amiodarone is unavailable.

E Sodium bicarbonate
Sodium bicarbonate is incorrect. Sodium bicarbonate should not be given routinely during cardiopulmonary resuscitation, so it would not be appropriate in this situation.

B A 10 mmHg drop in diastolic blood pressure during the second trimester
Despite an expansion of the plasma volume and cardiac output of 50%, mean and diastolic blood pressures fall by -15% owing to a reduction in peripheral vascular resistance. There is little change in systolic blood pressure, but diastolic pressure is reduced (5-10 mmHg) from =12-16 weeks. Diastolic pressure usually increases thereafter to pre- pregnancy levels by =36 weeks.

A A 20% reduction in blood volume and cardiac output
A 20% reduction in blood volume and cardiac output is incorrect. There is an increase in these parameters during pregnancy.

C Bradycardia with a radial pulse rate between 45 and 55 beats per minute
Bradycardia with a radial pulse of 45-55 bpm is incorrect. Tachycardia rather than bradycardia is a recognised physiological change during pregnancy as a consequence of reduced peripheral vascular resistance and fall in blood pressure.

D Grade 2/6 diastolic murmur at the mitral area
Grade 2/6 diastolic murmur at the mitral area is incorrect. Diastolic murmurs are generally pathologic and at the mitral area may signify mitral stenosis. A pulmonary systolic murmur from high blood flow is common and there may be a physiologic third heart sound.

E Pulsus alternans
Pulsus alternans is incorrect. Pulsus alternans usually signifies advanced heart failure.

A Cholesterol embolism
It is due to cholesterol emboli lodged in peripheral arteries, commonly as a result of angiographic or other surgical vascular procedures. The most common clinical findings in atheroembolic disease are cutaneous features, kidney disease and worsening hypertension. Foot pulses with gangrenous toes should suggest cholesterol embolisation. The retina provides a unique opportunity to visualise cholesterol emboli. Kidney disease may manifest as gradual deterioration of renal function after angiography or may be acute (this may mimic acute dissection of the renal artery during renal angiography). Eosinophilia, eosinophiluria, an increased erythrocyte sedimentation rate and hypocomplementinaemia have been found in atheroembolic disease.

B Polyarteritis nodosa
Polyarteritis nodosa is a vasculitis affecting small- and medium-sized arteries. Patients often present with vague constitutional symptoms, such as fever, myalgia and weight loss. It can affect any organ, but spares the pulmonary and glomerular arteries. Peripheral nerves and skin are usually affected, with lesions including purpura, livedoid and necrotic ulcers. Gastrointestinal symptoms are common. This patient does not show symptoms suggestive of polyarteritis nodosa.

C Buerger’s disease
Inflammation and thrombosis of small- and medium-sized arteries and veins occurs in Buerger’s disease. Patients tend to present with claudication of the extremities. This patient has gangrene, which does occur in Buerger’s disease. However, the history suggests embolic disease, and he has additional disease in his retinal arteries.

D Arterial thromboembolism
Arterial thromboembolism is related to distal embolisation of a proximal, pre-existing atheroma.

E Disseminated intravascular coagulopathy
Disseminated intravascular coagulopathy occurs due to inappropriate activation of the coagulation pathway in a diffuse manner. There is subacute thrombosis and haemorrhage due to exhaustion of clotting factors. It occurs after another disorder, such as infection, malignancy, major trauma or the complications of pregnancy. We have no evidence of a precipitating factor in this patient, who appears
well systemically. Also, there are no signs of haemorrhage or organ failure.

B Kussmaul’s sign
An inspiratory increase in venous pressure (Kussmaul’s sign) and a steep y descent in the jugular pulse are features of constrictive pericarditis. Pericardial knock in early diastole is often seen in constrictive pericarditis. Causes of constrictive pericarditis are:

• Tuberculosis
• Incomplete drainage of purulent pericarditis
• Fungal and parasitic infections
• Chronic pericarditis
• Post-viral pericarditis
• Postoperative
• Post-myocardial infarction
• In association with pulmonary asbestosis.

A Pulsus paradoxus
Pulsus paradoxus is incorrect. A paradoxical pulse and prominent x trough in the jugular pulse are more common in tamponade than in constrictive pericarditis.

C Prominent x trough
Prominent x trough is incorrect. A paradoxical pulse and prominent x trough in the jugular pulse are more common in tamponade than in constrictive pericarditis.

D 4-chamber diastolic equilibrium
Four-chamber diastolic equilibrium is incorrect. A range of conditions cause failure of either side of the heart and the diastolic pressure in all cardiac chambers are equal. This doesn’t rule out or rule in pericarditis versus other conditions such as tamponade or alcoholic cardiomyopathy.

E Hypotension
Hypotension is incorrect. Hypotension is common across a range of causes of cardiac failure.

Further information:
patient.info/doctor/chronic-pericarditis

A Atrial septal defect
The causes of fixed splitting of the second heart sound include an atrial septal defect, right heart failure, and pulmonary hypertension. This patient has no signs of right heart failure (normal JVP) or of pulmonary hypertension (no breathlessness, normal JVP, and there is no loud P2). The most likely diagnosis in a young, asymptomatic patient is an atrial septal defect.

B Aortic stenosis
Aortic stenosis in incorrect. Clearly this patient is too young to have senile calcification (even on a bicuspid valve) leading to adult aortic stenosis; however, if she had congenital aortic stenosis she could present with symptoms in her twenties. Aortic stenosis causes a reversal of the physiological splitting
of the second heart sound. Usually A2 occurs before P2, but in severe aortic stenosis the closure of the aortic valve is delayed, and P2 occurs before A2 (this can be difficult to appreciate clinically). The A2 component of the second heart sound also becomes softer in severe aortic stenosis. However,
although aortic stenosis may cause wide splitting of the second heart sound, it does not cause a fixed splitting. There will still be natural variation in the splitting with the patient’s respiration. Furthermore, the typical presenting symptoms of aortic stenosis would be breathlessness, angina, or syncope,
not palpitations. You would expect the ECG to demonstrate left ventricular hypertrophy, but it is normal here.

C Coarctation
Coarctation is incorrect. This patient has normal blood pressure in both arms and no radiofemoral delay; there are no physical signs of coarctation. It is possible for mild coarctation to be asymptomatic until later life, therefore the patient’s late presentation does not rule out coarctation as a diagnosis. However, coarctation does not cause a fixed, widely split second heart sound without associated atrial
septal defect. You would expect to see left ventricular hypertrophy on the ECG as the left atrium must generate high pressures to overcome the resistance of the coarctation.

D Left bundle branch block
Left bundle branch block is incorrect. This patient has a normal ECG, therefore she does not have left bundle branch block. Furthermore, left bundle branch block does not cause a fixed, widely split second heart sound as seen in this patient. It does cause paradoxical splitting of the second heart sound: usually the second heart sound consists of A2 then P2, but left bundle branch block causes a delay in the depolarisation of the ventricle (as the impulse is spread via cell-to-cell contact rather than through the branches of the bundle of His). This leads to a delay in the contraction of the left ventricle, and consequently a delay in the closure of the aortic valve after systole, therefore the splitting of the second
heart sound is reversed to P2, then A2 (leading to paradoxical splitting, because the split is lost with inspiration where it would normally be enhanced with inspiration).

E Primary pulmonary hypertension
Primary pulmonary hypertension is incorrect. Pulmonary hypertension does cause a fixed split second heart sound as seen in this patient. The most notable sign of pulmonary hypertension is a loud P2, which is not seen here. However, were this clinical sign present, you would expect the patient
to complain of breathlessness. You also might expect signs of right heart overload on the ECG; for example, an R wave in V1. This patient is asymptomatic, with a normal ECG, and with a fixed widely split second heart sound which would be more consistent with an atrial septal defect. The second heart sound consists of the closure of the aortic valve (A2) followed by the closure of the pulmonary valve
(P2). Usually the second heart sound varies with respiration, becoming split with inspiration: inspiration causes negative intrathoracic pressure, increasing return of blood from the body into the right atrium and ventricle. This slightly prolongs systole in the right ventricle and therefore delays closure of the pulmonary valve, causing an appreciably split second heart sound. This physiological split can become narrower, wider, reversed, or fixed. If the split is reversed (i.e. P2 before A2) then there will be paradoxical splitting: the split will be lost with inspiration and enhanced by expiration. An atrial septal defect allows continuous blood flow from the left side of the heart to the right side of the heart. This means that there is a greater volume of blood in the right atrium, which in turn overloads the right ventricle, leading to a delayed closure of the pulmonary valve. As the flow of blood from the left to the right is relatively unaffected by respiration, it results in a fixed, widely split second heart sound.

E Hypomagnesaemia
The mechanism by which hypomagnesaemia causes prolonged QT interval is not well understood, but may be related to calcium shifts. However, intravenous magnesium has well-documented benefits in the treatment of torsades de points.

A Beta blocker therapy
Beta blocker therapy is incorrect. In fact, beta blockers are used in the treatment of long QT syndrome. The aim of therapy is to prevent the development of torsade de points; beta blockers reduce the positively chronotropic effect of sympathetic stimulation, and consequently reduce the risk of
developing tachyarrhythmia. Causes of prolonged QT interval include electrolyte disturbances such as severe hypomagnesaemia.

B Digoxin therapy
Digoxin therapy is incorrect. Digoxin does not cause a prolonged QT interval; in fact, digoxin shortens the QT interval. Digoxin inhibits the myocardial Na/K ATPase and this leads to cardiac irritability and a shortening of the refractory period of the atria and ventricles, manifesting as a short QT interval on the ECG. Causes of prolonged QT interval include electrolyte disturbances such as severe hypomagnesaemia.

C Hypercalcaemia
Hypercalcaemia is incorrect. Hypercalcaemia causes a shortened QT interval; the increased cellular calcium affects the resting membrane potential of the cardiac myocytes, and this leads to irritability and a shortened refractory period of the atria and ventricles: this is reflected as a short QT on the ECG. Consequently it would be hypocalcaemia that would cause a long QT interval. Deficiencies in other electrolytes such as hypokalaemia or hypomagnesaemia will cause a long QT interval.

D Hyperkalaemia
Hyperkalaemia is incorrect. Hyperkalaemia causes typical ECG changes including a broadened, flattened P wave, prolonged PR interval, broad QRS complexes, slurring into the ST segment, and tall tented T waves. Hypokalaemia can cause a prolonged QT interval, as potassium shifts are responsible for repolarisation in the cardiac myocytes. In hypokalaemia, this repolarisation (seen as the T wave on the ECG) is delayed, resulting in a prolonged QT interval. Other electrolyte disturbances causing a prolonged QT interval include hypocalcaemia and hypomagnesemia.

A Coagulase negative Staphylococcus
This patient has symptoms, signs and investigations consistent with subacute endocarditis. He had a prosthetic valve replacement recently; the most common causative organism in early prosthetic valve endocarditis is coagulase negative Staphylococcus.

B Pseudomonas aeruginosa
Pseudomonas aeruginosa is incorrect. Pseudomonas can cause endocarditis, but it is usually acute, whereas this presentation is subacute. Most patients with Pseudomonas endocarditis are intravenous drug users, though patients with recent cardiac instrumentation are also at risk. Coagulase negative Staphylococcus is the most likely causative organism in this case; it is the most common cause of early
prosthetic valve endocarditis.

C Staphylococcus aureus
Staphylococcus aureus is incorrect. S aureus is the most common cause of endocarditis, particularly of acute endocarditis. However, this patient has recently had a prosthetic valve replacement, and the most common cause of early prosthetic valve endocarditis is coagulase negative Staphylococcus, hence that is the most likely causative organism here.

D Streptococcus bovis
Streptococcus bovis is incorrect. Strep bovis usually resides in the gut, but can translocate into the bloodstream, especially in the context of bowel cancer. It can then cause endocarditis, usually subacute as in this patient’s case. Any patient diagnosed with Strep bovis endocarditis should have
a colonoscopy to investigate for colon cancer. However, this patient does not have any bowel symptoms, and he has recently had a prosthetic valve replacement. The most common cause of early prosthetic valve endocarditis is coagulase negative Staphylococcus, hence that is the most
likely causative organism here.

E Streptococcus viridans
Streptococcus viridans is incorrect. Strep viridans is the most common cause of subacute endocarditis (as seen in this patient), accounting for 50-60% of cases. However, the most common causative organism in early prosthetic valve endocarditis is coagulase negative Staphylococcus. This patient has had a recent aortic valve replacement, hence coagulase negative Staph is the most likely causative
organism here.

C Staphylococcus aureus
Staphylococcus aureus is the most common cause of endocarditis, and is the most common cause of acute endocarditis and endocarditis associated with intravenous drug abuse. This patient is an intravenous drug user and presents with acute endocarditis; a blood culture has isolated Gram positive cocci: all of which are consistent with Staphylococcus aureus endocarditis. Therefore the most likely
causative organism is Staphylococcus aureus.

A Haemophilus parainfluenzae
Haemophilus parainfluenza is incorrect. H. parainfluenzae is a Gram negative coccobacillus that is part of the upper respiratory tract flora, but importantly, it is one of the HACEK organisms that cause culture negative endocarditis. Therefore you would not expect a positive blood culture if this patient had Haemophilus endocarditis. Furthermore, Haemophilus usually causes a subacute endocarditis; this patient is clearly presenting with acute endocarditis. Combined with the fact that Haemophilus is a very rare cause of bacterial endocarditis, this patient’s condition is more likely to be caused by Staphylococcus aureus.

B Pseudomonas aeruginosa
Pseudomonas aeruginosa is incorrect. Pseudomonas is a Gram negative, rod shaped bacteria in contrast to the Gram positive cocci seen in this patient’s blood cultures. Pseudomonas does cause an acute endocarditis as seen in this patient (as opposed to a subacute endocarditis). It is a
rare cause of endocarditis, though most infections are seen in intravenous drug users. This patient’s endocarditis is much more likely to be caused by Staphylococcus aureus.

D Streptococcus bovis
Streptococcus bovis is incorrect. Streptococcus bovis is a Group D Streptococcus and is a Gram positive coccus, as seen in this patient’s blood cultures. Usually the endocarditis associated with these bacteria is subacute (this patient is clearly presenting with acute endocarditis). Strep. bovis is found within the gut, and consequently patients that develop Strep. bovis endocarditis should be investigated for colorectal cancer with a colonoscopy (as a tumour can allow bacteria to translocate from the gut and reach the bloodstream). This patient is quite young for colorectal cancer. Combined with the fact that Strep. bovis is an uncommon cause of bacterial endocarditis, and usually causes subacute endocarditis, this patient is unlikely to have Streptococcus bovis endocarditis; it is more likely that Staphylococcus aureus is the causative organism.

E Streptococcus viridans
Streptococcus viridans is incorrect. Streptococcus viridans is a Gram positive coccus, and is a common cause of subacute bacterial endocarditis. However, this patient has presented with acute endocarditis, not subacute. The most common cause of acute endocarditis, and especially in an intravenous
drug user, is Staphylococcus aureus, therefore this is the correct answer as it is the most likely causative organism.

D Peripheral vascular disease
Patients with a blood pressure difference of >15mmHg between arms are twice as likely to have peripheral artery disease. Indeed, this patient describes leg claudication which would be explained by peripheral artery disease. Diagnosis and treatment of this patient’s hypertension should be based
on the readings from the arm with the highest mean blood pressure.

A Aortic dissection
Aortic dissection is incorrect. You would expect the patient to present acutely, complaining of pain (chest, back, or abdominal) if this were an aortic dissection. The pain may have resolved by the time the patient presents, but there will be an acute history of pain. The patient would appear unwell,
and would need urgent surgical or endovascular management. Although an aortic aneurysm can cause
difference in blood pressure between the arms (as observed here), it would not explain the history of claudication in this patient (chronic intermittent leg pain, exacerbated by exercise and relieved by rest). It is much more likely that this patient’s signs are caused by peripheral vascular disease.

B Coarctation
Coarctation is incorrect. Coarctation (a congenital disorder causing short section stenosis of the aorta) can present in later life, and can cause a difference in blood pressure between the two arms (if the coarctation involves the left subclavian artery origin). More commonly, it causes upper limb hypertension and low or normal blood pressure in the lower limbs. However, you would expect to find radio-radial or radio-femoral delay if this were coarctation: neither were present in this patient. Furthermore, if this patient had a coarctation, it would have to involve the origin of the left subclavian in order to explain the differential blood pressure. But if the coarctation involved the left subclavian, it could not explain this patient’s lower limb claudication. Therefore the patient’s symptoms and signs are consistent with a more widespread process, best explained by peripheral vascular disease.

C Normal variant
Normal variant is incorrect. Although it is common for patients to have up to 10 mmHg difference in blood pressure between arms, a difference of greater than 10 mmHg is not physiological. In fact, research suggests that a diference of >15mmHg is a good marker of peripheral vascular disease.
This patient describes leg claudication and is hypertensive; his symptoms and signs are most likely explained by peripheral vascular disease.

E Subclavian steal syndrome
Subclavian steal syndrome is incorrect. This condition could certainly explain the difference in blood pressure between this patient’s arms. However, you would expect the patient to complain of arm claudication, intermittent vertigo, ataxia or diplopia, or facial sensory symptoms. Leg claudication, as this patient complains of, is not consistent with subclavian steal syndrome. The best explanation for this patient’s symptoms and signs is a widespread process, such as atherosclerosis in peripheral vascular disease.

D Shortness of breath a few hours after falling asleep
The onset of shortness of breath 2-3 h after the onset of sleep is characteristic of paroxysmal nocturnal dyspnoea from increased left atrial pressure.

A Shortness of breath improving during exercise
Shortness of breath improving during exercise is incorrect. This implies a non-organic cause for shortness of breath.

B No problems climbing a flight of stairs
It’s very clear that patients with reduced ejection fraction have significant difficulty with stair climbing.

C Shortness of breath worsening during the day and improving on going to sleep
Shortness of breath worsening during the day and improving on going to sleep is incorrect. This pattern of symptoms might imply exposure to an agent causing hypersensitivity or a psychosomatic cause for shortness of breath.

E Shortness of breath occurring a few minutes after cessation of exercise
Shortness of breath occurring a few minutes after cessation of exercise is incorrect. This implies exercise induced bronchospasm.

B Automatic implantable cardioverter defibrillator
Patients who have survived a sudden cardiac arrest, regardless of the type of underlying structural heart disease, are suitable for an AICD. This reduces sudden death and total mortality compared with therapy using anti-arrhythmic drugs. HOCM is the most common cause of cardiac arrest in those
under 40 years of age. Overall, 1% of HOCM patients with HOCM die each year. AICDS have been shown to be effective in those with HOCM at terminating ventricular arrhythmias.

A Amiodarone
Amiodarone is incorrect. An AICD has been shown to have survival benefits compared with empirical amiodarone therapy.

C Dual-chamber pacemaker
Dual-chamber pacemaker is incorrect. A pacemaker is not beneficial in the context of cardiac arrest. The implanted device requires a defibrillator function to provide DC cardioversion in the event of cardiac arrest.

D Sotalol
Sotalol is incorrect. Sotalol is useful as medical therapy for symptom control, but the best definitive long-term intervention in this case is an ICD.

E Verapamil
Verapamil is incorrect. Verapamil can be used if beta blockers are contra-indicated or ineffective, but the definitive intervention here is an ICD.

B Increased levels of low-density lipoprotein-cholesterol (LDL-C)
LDL particles are the main carriers of cholesterol. These particles can deposit lipid into the walls of the peripheral vasculature. There is a strong association between total- and LDL-C concentration and risk of coronary heart disease. There is a relatively weak independent link between increased concentrations of (triglyceride-rich) very low-density lipoprotein particles and cardiovascular risk.

A Increased triglyceride levels
Increased levels of triglyceride is incorrect. Very highly increased triglyceride levels (> 6 mmol/1) cause a greatly increased risk of acute pancreatitis and thrombosis of retinal veins.

C Increased levels of high-density lipoprotein cholesterol (HDL-C)
Increased levels of high-density lipoprotein cholesterol (HDL-C) is incorrect. Higher concentrations of HDL protect against cardiovascular disease. HDL also has effects on the function of platelets and the haemostatic cascade: these properties may influence thrombogenesis favourably.

D Increased numbers of chylomicrons
Increased numbers of chylomicrons is incorrect. Excess chylomicrons do not confer an excess cardiovascular risk but do increase the total concentration of triglyceride in plasma.

E Increased levels of intermediate-density lipoprotein- cholesterol (IDL-C)
Increased levels of intermediate-density lipoprotein- cholesterol (IDL-C) is incorrect. IDL-C levels are not measured routinely as part of the serum lipid profile.

C Cardiac-specific troponin T
Troponin T and troponin I are regulatory proteins released into the circulation upon damage to cardiac muscle. High- sensitivity assays have been developed and are now recommended by the National Institute for Health and Clinical Excellence. These allow detection of lower levels of troponin compared with older assays, and so can be used to detect increases in troponin levels earlier. With older assays,
troponin was repeated 10-12 hours after symptom onset. High-sensitivity assays allow earlier (< 4 hours) exclusion of myocardial infarction (MI), leading to a shorter inpatient stay for those found not to have increased levels of troponin, as well as earlier treatment for those diagnosed with MI.

A Creatine kinase
Creatine kinase can be an indicator of cardiac damage, but it can also reflect muscle breakdown and acute kidney disease.

B Creatine kinase MB
Creatine kinase MB is a cardiac-specific isoform of creatine kinase which allows greater diagnostic accuracy than creatine kinase, but is still less sensitive then troponin T.

D Aspartate aminotransferase
Aspartate aminotransferase is a non-specific enzyme that is used rarely nowadays for MI diagnosis.

E Lactate dehydrogenase
Levels of lactate dehydrogenase peak at 3-4 days and remain high for ≤ 10 days after a cardiac event. Thus, they can be useful for confirmation of MI in patients presenting several days after an episode of chest pain.

B Tricuspid incompetence
The auscultatory findings are suggestive of tricuspid incompetence. This patient most probably has carcinoid syndrome, which can occur in 5% of patients with carcinoid tumours if there are liver metastases. Cardiac abnormalities are found in 50% of patients, and consist of pulmonary stenosis or tricuspid incompetence.

A Mitral regurgitation
Mitral regurgitation is incorrect. In mitral regurgitation, a pan- systolic murmur is heard loudest at the apex and radiates widely over the precordium and into the axilla. A prominent third heart sound may be present. Mitral regurgitation does not usually occur due to carcinoid syndrome.

C Tricuspid stenosis
Tricuspid stenosis is incorrect. A rumbling mid-diastolic murmur is characteristic of tricuspid stenosis along with a prominent jugular venous a wave.

D Pulmonary stenosis
Pulmonary stenosis is incorrect. In pulmonary stenosis, the characteristic auscultatory finding is a harsh mid-systolic ejection murmur best heard on inspiration to the left of the sternum in the second intercostal space. A right ventricular fourth sound and a prominent jugular venous a wave is present if the stenosis is moderately severe.

E Prolapsing mitral valve
Prolapsing mitral valve is incorrect. A prolapsing (‘floppy’) mitral valve is commonly seen in young women and has a familial incidence. It may be associated with rheumatic or ischaemic heart disease, Marfan syndrome or thyrotoxicosis. The most common sign is a mid-systolic click followed by a late systolic murmur due to some regurgitation.

C Direct current (DC) cardioversion
This patient has an unstable blood pressure and symptoms associated with it. As such moving to DC cardioversion is the appropriate option, rather than waiting for options for chemical cardioversion to take effect.

A Digoxin
Digoxin is incorrect. This patient probably has atrial fibrillation (AF) superimposed on WPW syndrome. The aim of treatment is to suppress the conduction of the abnormal pathway. This is achieved using class I and III anti-arrhythmic drugs but not by verapamil or digoxin, which may allow faster conduction over the abnormal pathway and precipitate ventricular fibrillation (VF).

B Verapamil
Verapamil is incorrect. Verapamil will enhance the conduction over the abnormal pathway and therefore should not be used to treat atrial fibrillation (AF) associated with WPW syndrome as ventricular fibrillation (VF) may be precipitated.

D Metoprolol
Metoprolol is incorrect. Metoprolol would cause bradycardia and further hypotension, which would make this patient’s condition more unstable.

E Procainamide
Procainamide is incorrect. DC cardioversion is the default option, with procainamide only considered if there are medical reasons for why it cannot take place.

A Sustained ventricular tachycardia
The features described in the question are highly suggestive of sustained ventricular tachycardia. The diagnosis is by ECG which shows a tachycardia of 120 bpm or greater with three or more consecutive wide QRS complexes. A sustained ventricular tachycardia will last over 30 seconds, while an
unsustained ventricular tachycardia will last less than 30 seconds and resolve spontaneously. Sustained ventricular tachycardia is almost always symptomatic.

B Ventricular fibrillation
Ventricular Fibrillation is incorrect. In ventricular fibrillation, there is very rapid and irregular ventricular activation, with no mechanical effect. The patient is pulseless and rapidly becomes unconscious. The ECG shows rapid, shapeless oscillations with no hint of organised complexes.

C Torsades de pointes
Torsades de pointes is incorrect. In torsades de pointes, ventricular repolarisation is greatly prolonged (long QT syndrome). The ECG is characterised by rapid, irregular, sharp complexes that continuously change from an upright to an inverted position. Prolonged QT intervals are also seen between spells of tachycardia or immediately before the onset of tachycardia.

D Ventricular premature beats
Ventricular premature beats is incorrect. Broad QRS complexes may be seen in ventricular premature beats, but, following a premature beat, there is usually a compensatory pause. This condition is usually asymptomatic.

E Atrial tachycardia
Atrial tachycardia is incorrect. In atrial tachycardia, the P waves are abnormally shaped and occur in front of the QRS complexes.

D Temporary alleviation by carotid sinus massage
VT does not involve the AV node and therefore is not be affected by adenosine or carotid sinus massage, which temporarily blocks the AV node. Therefore, if carotid sinus massage is performed and there is slowing of heart rate, this would suggest a diagnosis of SVT with aberrancy and help
exclude VT.

A Capture beats on the electrocardiogram (ECG)
Capture beats on the electrocardiogram (ECG) is incorrect. VT may be distinguished from SVT by ECG features that indicate atrioventricular (AV) dissociation (i.e. the atria and ventricles are no longer linked in rate and rhythm). The three characteristic features of AV dissociation are irregular notching of the QRS complex, capture beats and fusion beats. Capture beats alone do not suggest SVT with
aberrancy, therefore is incorrect.

B Past history of ischaemic heart disease
A past history of ischaemic heart disease is incorrect. A past history of ischaemic heart disease is associated with a > 95% chance that broad complex tachycardia is VT.

C Right bundle-branch block morphology with left axis deviation on the ECG
Right bundle-branch block morphology with left axis deviation on the ECG is incorrect. Right bundle-branch block morphology with left axis deviation on the ECG has emerged as a distinct entity of VT characterised by its typical QRS configuration and responsiveness to verapamil. It is encountered mostly in patients with undetected structural heart disease and usually carries a good prognosis. Debate still centers on the electrophysiological mechanism involved.

E Variable intensity of the first heart sound
Variable intensity of the first heart sound is incorrect. A variable intensity of the first heart sound in a regular tachycardia suggests AV dissociation causing variable filling of the ventricles from the atria. Atrial fibrillation is the most frequent cause of variable intensity of the first heart sound.

A Direct current (DC) cardioversion
Wolff-Parkinson-White (WPW) syndrome presents with atrioventricular re-entrant tachycardia caused by an aberrant re-entry circuit via the atrium, atrioventricular (AV) node and ventricle. Orthodromic tachycardia occurs most commonly and is associated with narrow complex SVT; this occurs when
conduction goes via the AV node to the ventricles and then back via the accessory pathway. Antidromic tachycardia due to conduction from the atria directly to the ventricle via the accessory pathway is associated with broad complex tachycardia. DC cardioversion is recommended for antidromic tachycardias.

B Intravenous adenosine
Intravenous adenosine is incorrect. Treatment of orthodromic tachycardia aims to block the AV node and cut the re-entry circuit, thereby restoring sinus rhythm. The drug of choice in orthodromic tachycardia is therefore adenosine. In this case, with antidromic tachycardia, DC cardioversion is preferred.

C Intravenous amiodarone
Intravenous amiodarone is incorrect. Amiodarone can be used in narrow complex orthodromic AV reciprocating tachycardia if carotid sinus massage has failed, but not in antidromic AV reciprocating tachycardia.

D Intravenous flecainide
Intravenous flecainide is incorrect. Flecainide is the drug of choice for atrial fibrillation in WPW syndrome. Cardioversion is only required when drug therapy fails or the patient’s condition is compromised.

E Intravenous verapamil
Intravenous verapamil is incorrect. Intravenous verapamil contraindicated in antidromic AV reciprocating tachycardia. It may be used, however, in narrow complex orthodromic AV reciprocating tachycardia if carotid sinus massage has failed.

E Transthoracic echocardiography
Imaging of the left ventricular apexis best imaged by conventional two-dimensional echocardiography. Therefore, this is the correct answer.

A Cardiac magnetic resonance imaging (MRI)
Cardiac magnetic resonance imaging (MRI) is incorrect. Cardiac MRI is effective in detecting mural thrombus but may not be readily available.

B Left ventriculography
Left ventriculography is incorrect. Atypical thrombus may be apparent on contrast left ventriculography but this technique carries a risk of dislodging and embolising intraventricular thrombus.

C Multiple uptake gated acquisition scanning
Multiple uptake gated acquisition scanning is incorrect. Multiple uptake gated acquisition scanning involves the use of a radioactive isotope and a radionuclide detector to trace the absorption of the radioactive isotope. It is not a common method for visualising thrombi. More frequently, this is used
to assess coronary perfusion in patients with coronary artery disease or congestive heart failure and in patients undergoing chemotherapy.

D Transoesophageal echocardiography
Transoesophageal echocardiography is incorrect. Although an excellent technique for imaging the posterior cardiac structures (atria, left atrial appendage, valves and pulmonary veins), transoesophageal echo is less useful for imaging the structure and function of the ventricles.

E Renal artery stenosis
The differential diagnosis of acute pulmonary oedema includes:

• severe left ventricular dysfunction
• paroxysmal arrhythmias
• three-vessel or left mainstem coronary disease.

In the context of hypertension, the differential diagnosis also includes renal artery stenosis and phaeochromocytoma. Renal artery stenosis is more common than phaeochromocytoma in a 30-year-old and is therefore the correct answer in this scenario.

A Dilated cardiomyopathyDilated cardiomyopathy is incorrect. This patient has
continued in his role as a postman, implying relatively good exercise tolerance. This means that significant dilated cardiomyopathy is very unlikely as a cause of his symptoms and would be associated with long-standing, progressive deterioration in his health.

B Myocarditis
Myocarditis is incorrect. Myocarditis is associated with evidence of left ventricular dysfunction, rather than hypertrophy, and a prodromal illness would be expected before the development of the condition.

C Ischaemic heart disease
Ischaemic heart disease is incorrect. There are no risk factors noted to suggest ischaemic heart disease, such as smoking, diabetes mellitus or dyslipidaemia.

D Phaeochromocytoma
Phaeochromocytoma is incorrect. Phaeochromocytoma may have been suggested by other symptoms such as abdominal pain, chest pain, dizziness, elevated blood sugar, facial flushing, hypertension and increased respiratory rate.

A Constrictive pericarditis
The history of recent cardiac surgery points us more towards a diagnosis of constrictive pericarditis, where fibrosis is seen around the areas of bypass grafting. Constructive pericarditis can also follow infective pericarditis, tuberculosis and kidney disease.

B Dilated cardiomyopathy
Dilated cardiomyopathy may present with congestive cardiac failure; however, it would not produce prominent x and y descents.

C Pericardial effusion
A prominent x descent in the JVP may occur in constrictive pericarditis or pericardial effusion; however, pericardial effusion is more likely to present in the initial period after cardiac surgery.

D Restrictive cardiomyopathy
Restrictive cardiomyopathy may produce clinical features similar to constriction but is less common; therefore, constrictive pericarditis is more likely to be the diagnosis in this scenario.

E Severe mitral regurgitation
Severe mitral regurgitation does not produce the JVP findings seen in this case. It may present with a normal first heart sound; the second heart sound is widely split, and may be followed by a third sound gallop. There is an associated pansystolic murmur. In this case, there is no mention of a murmur, and severe mitral regurgitation would not produce the JVP findings described.

A Aortic regurgitation
Marfan syndrome is characteristically associated with progressive aortic root dilatation, leading to aortic
regurgitation and an increased risk of dissection. Other skeletal manifestations include:

• tall stature
• scoliosis
• chest wall malformations
• high arched palate
• lens dislocation.

Mitral valve prolapse is also common but there is no association with other congenital malformations or
cardiomyopathy.

B Atrial septal defect
Atrial septal defect is incorrect. Atrial septal defect is a congenital heart defect in which the blood flows between the atria via an opening in the interatrial septum. This is not associated with Marfan syndrome.

C Dilated cardiomyopathy
Dilated cardiomyopathy is incorrect. Dilated cardiomyopathy may cause problems with cardiac contraction, and patients can present with symptoms of cardiac failure. This is not associated with Marfan syndrome.

D Pulmonary regurgitation
Pulmonary regurgitation is incorrect. Pulmonary regurgitation in which there is a leaky pulmonary valve, may present with an increased jugular venous pressure and an inaudible pulmonic component of the second heart sound. A low- pressure regurgitant flow exists across the pulmonic valve when the pulmonary artery pressure is normal. This is heard as a decrescendo early diastolic murmur at the upper left sternal edge. Aortic rather than pulmonary regurgitation is associated with Marfan syndrome.

E Persistent ductus arteriosus
Persistent ductus arteriosus is incorrect. Persistent ductus arteriosus – a persistent communication between the descending thoracic aorta and the pulmonary artery – results from failure of the normal physiological closure of the fetal ductus. It is not associated with Marfan syndrome.

B Digoxin
Digoxin reduces the risk of death due to heart failure but overall cardiovascular mortality is similar to that on placebo, probably reflecting a small increase in the risk of arrhythmic death with digoxin therapy.

A Bisoprolol
Bisoprolol is incorrect. Bisoprolol has been shown to improve mortality in the CIBIS II trial. This was a multicentre double- blind randomised placebo-controlled trial involving 2647 symptomatic patients in New York Heart Association class III or IV, with left-ventricular ejection fraction of 35% or less and
who were receiving standard therapy with diuretics and angiotensin-converting enzyme inhibitors. Patients were assigned to bisoprolol 1.25 mg (n=1327) or placebo (n=1320) daily. After a mean follow-up of 1.3 years, beta-blocker therapy had benefits for survival in patients with stable heart failure.

C Enalapril
Enalapril is incorrect. Enalapril was shown in the CONSENSUS trial to provide a survival benefit in patients with heart failure. In this double-blind study, 253 patients were randomised to receive either placebo (n=126) or enalapril (n=127). After a follow-up averaging 188 days, patients who were taking
enalapril had a longer survival.

D Nitrates and hydralazine
Nitrates and hydralazine is incorrect. Nitrates and hydralazine have been demonstrated in the V-HEFT study to provide survival benefit in patients with heart failure. This trial demonstrated that treating patients with congestive heart failure with hydralazine-isosorbide dinitrate significantly reduced mortality when compared with placebo for the initial 3-year period.

E Spironolactone
Spironolactone is incorrect. Spironolactone has been shown in the RALES trial to improve mortality in patients with chronic heart failure. A total of 1663 patients were randomised to treatment (ie standard therapy and 25-50 mg spironolactone once daily) or placebo (ie standard therapy and placebo). After about 3 years spironolactone was associated with a survival benefit.

E Low HDL/elevated triglycerides
Asian patients do not have classic LDL-related risk for ischaemic heart disease. Their profile includes low HDL and elevated triglycerides, meaning that measurement of LDL alone may underestimate their cardiovascular risk.

A Elevated high-density lipoprotein (HDL)
Elevated HDL is incorrect. Elevated high-density lipoprotein (HDL) is protective against ischaemic heart disease. HDL levels are likely to be low in patients with diabetes.

B Elevated low-density lipoprotein (LDL)
LDL may be elevated is incorrect. LDL may be elevated in diabetes but may also be normal, so the measurement of LDL alone may underestimate the cardiovascular risk.

C Elevated LDL/elevated triglycerides
Elevated LDL/elevated triglycerides is incorrect. Elevated LDL/elevated triglycerides not typical in Asian patients with diabetes. If both LDL and triglycerides are raised, then this would confer a high cardiovascular risk group.

D Low HDL/elevated LDL
Low HDL/elevated LDL is incorrect. These are not typical LDL-related risk for ischaemic heart disease in Asian patients. A low HDL would mean reduced protective lipids for cardiovascular disease and an elevated LDL means a high amount of lipids increasing cardiac risk. A low HDL/elevated LDL is a high risk phenotype for ischaemic heart disease.

B Aspirin + heparin and repeat ECG in 15 min
The criteria for thrombolysis are 1 mm ST elevation in two or more limb leads or 2 mm ST elevation in adjacent chest leads, so thrombolysis is not indicated here. However, in the context of a good history of cardiac pain and borderline ECG, an acute coronary event should be strongly suspected and
aspirin and heparin given prophylactically, with a repeat ECG in 15 min. Therefore, Option B is the correct answer.

A Activated tissue plasminogen activator (tPA) + aspirin
Activated tissue plasminogen activator (tPA) + aspirin is incorrect. The patient does not fulfil the criteria for thrombolysis.

C Heparin only
Heparin only is incorrect. Heparin only may be given in venous thrombotic events.

D No treatment and repeat ECG in 15 min
No treatment; repeat ECG in 15 minutes is incorrect. There is a good history of cardiac chest pain and an acute coronary event is highly likely.

E Streptokinase + aspirin
Streptokinase + aspirin is incorrect. The criteria for thrombolysis are not met. Streptokinase is associated with hypotension, infrequent allergic reactions and, rarely, anaphylaxis. Patients treated with streptokinase develop anti- streptococcal antibodies, which can inactivate the drug if subsequent treatment is needed. Consequently, in current UK practice, patients are usually treated with streptokinase only once.

C v wave
Tricuspid regurgitation characteristically causes loss of the x descent in the JVP waveform, causing fusion of the c and v waves to produce ‘giant’ v waves, also known as cv or s waves.

A a wave
a wave is incorrect. The a wave is absent in cases of atrial fibrillation where there is uncoordinated atrial contraction.

B c wave
c wave is incorrect. The c wave is merged with the v waves in tricuspid regurgitation.

D x descent
x descent is incorrect. the x descent is lost in tricuspid regurgitation. There is a prominent x descent in constrictive pericarditis.

E y descent
y descent is incorrect. The y descent corresponds to the rapid emptying of the atrium into the ventricle following opening of the tricuspid valve. There may be a prominent and deep y descent intricuspid regurgitation. There is a slow y descent in tricuspid stenosis and cardiac tamponade.

E Resting blood pressure 220/130 mmHg
A proven (i.e. by computed tomography) intracranial haemorrhage (ICH) is an absolute contraindication to thrombolysis. A fully recovered previous transient ischaemic attack is not an absolute contraindication. However, some debate remains about the risk of ICH in the context of a previous stroke. In the American College of Cardiology guidelines (2004), a history of ischaemic stroke within 3
months is given as an absolute contraindication, as is any history of ICH.
Contraindications consistent with the NICE guidelines (2007) are detailed below:

• normal ECG, or ECG not available
• unconsciousness without known cause
• cerebrovascular accident within the last 6 months
• possible aortic dissection
• known intracranial pathology
• active pulmonary disease with cavitation
• severe hypertension with blood pressure above 180/110 mmHg
• coagulation defects, bleeding diatheses or anticoagulants
• surgery (including dental extraction), major trauma, dental extraction or haemorrhage (including heavy vaginal bleeding) within the last 2 weeks
• acute gastrointestinal bleeding, recent peptic ulcer, acute pancreatitis, oesophageal varices or severe liver disease
• laser therapy for retinopathy within the last week
• infective endocarditis, pericarditis
• pregnancy or up to 18 weeks postnatal
• prolonged or traumatic cardiopulmonary resuscitation
• in the case of streptokinase, previous allergic reactions to either streptokinase or anistreplase (no longer available)
• prolonged persistence of antibodies to streptokinase may reduce the effectiveness of subsequent treatment; therefore, streptokinase should not be used if used 5 days to 12 months previously.

A Background diabetic retinopathy
Background diabetic retinopathy is incorrect. Background diabetic retinopathy is an incorrect choice because there is only an increase risk of bleeding if there had been laser therapy treatment in the last week. Otherwise stable diabetic retinopathy is unlikely to bleed.

B Past history of a minor stroke 5 years ago with full recovery and no evidence of underlying cerebrovascular lesion
Past history of a minor stroke 5 years ago with full recovery and no evidence of underlying cerebrovascular lesion is incorrect. There is unlikely to be active bleeding lesion. So only cerebrovascular accident within the last 6 months is at high risk of bleeding.

C Menstruation
Menstruation is incorrect. No significant bleeds would result from anti-coagulation in general. The only exception is when there is very heavy active vaginal bleeding.

D Dyspeptic symptoms
Dyspeptic symptoms is incorrect. Dyspeptic symptoms is not a contraindication per se. It may be a symptom of peptic ulcers which is a contraindication. The symptom of dyspepsia on its own is not a contraindication.

B Raised jugular venous pressure (JVP)
In pulmonary hypertension, there is right atrial dilatation and increased pressure therefore the jugular venous pressure (JVP) is raised. This sign would most indicate the presence of pulmonary hypertension from the options given.

A Loud systolic murmur
Loud systolic murmur is incorrect. A loud systolic murmur may occur in other conditions such as aortic stenosis.

C Single loud second heart sound
Single loud second heart sound is incorrect. Single loud second heart sound is characteristically associated with Fallot tetralogy where pulmonary stenosis protects from developing pulmonary hypertension.

D Systolic thrill
Systolic thrill is incorrect. Once Eisenmenger complex has developed the thrill of the ventricular septal defect is absent.

E Displaced apex beat
Displaced apex beat is incorrect. Once Eisenmenger complex occurs, there are only signs of pulmonary hypertension and cyanosis. Cardiomegaly may occur with Eisenmenger complex because of right ventricular enlargement, but the left ventricle is not usually significantly enlarged and the apex
beat is not typically displaced.

D Reassure and discharge
J-point depression is a physiological response to an increase in heart rate; ST segments should therefore be measured 80 ms post-J. J-point depression produces upward-sloping ST depression, which has little predictive value for coronary artery disease. Horizontal and downward-sloping segments are more predictive than upward-sloping ones. In a young man with atypical chest pain, this exercise test would be reassuring and there would be no indication for further investigation or treatment.

A Coronary angiography
Coronary angiography is incorrect. Coronary angiography would be useful only if true coronary artery disease with stenosis is suspected.

B Dobutamine stress echocardiography
Dobutamine stress echocardiography is incorrect. Dobutamine stress echocardiography highlights perfusion defects. However, the findings are likely to be normal in this patient.

C Radionuclide myocardial perfusion scanning
Radionuclide myocardial perfusion scanning is incorrect. Radionuclide myocardial perfusion scanning would be helpful in identifying perfusion abnormalities but in this scenario would be normal.

E Repeat ECG exercise testing on anti-anginal medication
Repeat ECG exercise testing on anti-anginal medication is incorrect. Repeat ECG exercise testing on anti-anginal medication would not be helpful as it would yield similar results.

D Mobitz II atrioventricular (AV) block complicating anterior MI with blood pressure 110/70 mmHg
Second- or third-degree heart block complicating acute anterior MI requires pacing because of the expected size of the infarct that has led to the heart block.

A Asymptomatic 2.8 s sinus pauses
Asymptomatic 2.8 s sinus pauses is incorrect. Asymptomatic sinus node disease, even with prolonged pauses, carries a low risk of sudden death and can usually be managed without a temporary wire.

B A short period of complete heart block complicating inferior myocardial infarction (MI) (pre-thrombolysis) with blood pressure 110/70 mmHg
A short period of complete heart block complicating inferior myocardial infarction (MI) (pre-thrombolysis) with blood pressure 110/70 mmHg is incorrect. AV block complicating MI
should be managed conservatively if asymptomatic, for a short period and causing no haemodynamic compromise.

C Chronic asymptomatic complete heart block with broad complex ventricular complexes at 35 bpm
Chronic asymptomatic complete heart block with broad complex ventricular complexes at 35 bpm is incorrect. Chronic complete heart block has a higher risk but, if asymptomatic and with a stable escape rhythm, can also be managed in most cases without a temporary wire.

E Bifascicular block prior to aortic aneurysm repair
Bifascicular block prior to aortic aneurysm repair is incorrect. Bifascicular block carries a slightly higher risk of high-grade AV block but, in asymptomatic patients, this risk is sufficiently low to obviate the need for perioperative pacing.

E Broad ẞ disease
Palmar crease xanthomas are pathognomonic of type III hyperlipidaemia – also known as broad ẞ disease.

A Familial hypercholesterolaemia
Familial hypercholesterolaemia (type lla hyperlipidaemia) is incorrect. This is associated with high total cholesterol and low-density lipoprotein (LDL) levels due to impaired LDL receptor activity. It is associated with:

• severe atherosclerosis and premature coronary heart disease
• xanthomas
• xanthelasmata
• corneal arcus.

B Familial mixed hypercholesterolaemia
Familial mixed hypercholesterolaemia is incorrect. This is a common form of hypercholesterolemia characterised by increased LDL and triglyceride levels, often accompanied by decreased HDL.

C Hyperchylomicronaemia
Hyperchylomicronaemia is incorrect. Hyperchylomicronaemia is type I hyperlipidaemia due to lipoprotein lipase enzyme deficiency.

D Familial hypertriglyceridaemia
Familial hypertriglyceridaemia is incorrect. Familial hypertriglyceridaemia is a form of type IV hyperlipidaemia. It is an autosomal dominant condition occurring in approximately 1% of the population. Triglyceride levels, but not cholesterol, are elevated as a result of excess hepatic production of very low density lipoprotein (VLDL) or heterozygous lipoprotein lipase (LPL) deficiency. The condition is associated with premature coronary disease, though treatment sometimes differs from that for hypercholesterolemia. Patients are also at risk of pancreatitis, especially when triglyceride levels exceed 1000 mg/dL.

A 62-year-old man with two previous myocardial infarctions and a history of left ventricular failure controlled with ramipril and furosemide presents to his GP with palpitations. On examination, his BP is 100/72 mmHg, pulse 95 bpm atrial fibrillation (AF), with bibasal crackles consistent with heart
failure.
Clinical results are given in the table below:

D Digoxin
This patient presents with AF, rapid ventricular response and left ventricular failure. The history of previous MI and dilated left atrium fits with chronic atrial fibrillation. Successful cardioversion is therefore unlikely and rate control with digoxin is a more reasonable aim.

A Diltiazem
This is a cardioselective calcium channel antagonist, is significantly negatively inotropic and therefore likely to worsen cardiac failure.

B Sotalol
Although beta blockers are used in rate control of AF, bisoprolol is the usual preferred agent.

C Amiodarone
Amiodarone is more usually considered as an agent for chemical cardioversion of acute atrial fibrillation.

E Verapamil
Like diltiazem, verapamil is a cardioselective calcium antagonist. It runs the risk of significantly worsening cardiac failure in this situation.

A 30-year-old man is being investigated for hypertension. A combination of BPs estimated by colour flow Doppler and measured values are listed in the table below:

A Coarctation of aorta
The clinical scenario is of a young man (30 years old) with hypertension. He has differential blood pressure in the right arm and leg (lower blood pressure in the leg). Normally the blood pressure in the lower limbs is 10-20 mmHg greater than that in the upper limbs. The findings of reduced systolic
blood pressure in the lower extremities compared with upper extremities would be typical for a diagnosis of coarctation of the aorta. It also leads to a delay between the radial and femoral pulses (radio-femoral delay). In this clinical scenario, cardiac catheterisation + MRI scanning is the next most appropriate next step in further characterising the pressure gradient across the coarctation.

B Left subclavian artery stenosis
Left subclavian artery stenosis is incorrect. The left subclavian artery supplies blood to the left upper limb. Left subclavian artery stenosis would result in diminished pulse and blood pressure in the left upper limb only with normal blood pressure in the right upper limb and both lower limbs. Isolated left subclavian artery stenosis would also not cause hypertension. In this case hypertension with a high blood pressure in the right upper limb and low blood pressure in the right femoral artery goes against the diagnosis of left subclavian artery stenosis.

C Aortic regurgitation
Aortic regurgitation is incorrect. In aortic regurgitation, systolic blood pressure is markedly greater in the lower limbs than in the upper limbs. In this question, the blood pressure in the upper limbs is higher than the lower limbs, which goes against this diagnosis. Normal arterial systolic pressure in the legs is 10-20 mm Hg greater than the arms. In aortic regurgitation the systolic pressure in the legs is 60-100 mmHg greater than the arms. (Hill’s sign).

D Aortic stenosis
Aortic stenosis is incorrect. In aortic stenosis, the blood pressure is usually lower than normal and has a direct relation with the severity of the stenosis – the more severe the stenosis, the lower is the blood pressure. There is no difference in the blood pressure in all the four limbs and it is diminished throughout. In the question, there is hypertension and differential blood pressure between the upper and lower limbs. Both these features go against the diagnosis of aortic stenosis.

E Hypertrophic obstructive cardiomyopathy (HOCM)
Hypertrophic obstructive cardiomyopathy (HOCM) is incorrect. HOCM usually presents similar to aortic stenosis (due to systolic anterior motion (SAM) of the mitral valve leaflet) with an abnormal blood pressure response during exercise (flattening of blood pressure or fall in blood pressure with exercise). Normally blood pressure rises with exercise. During rest blood pressure may be high, normal or low. There is no difference in the blood pressure in all four limbs as indicated in the question. Coarctation of the aorta is a narrowing of the descending aorta, which is typically located at the insertion of the ductus
arteriosus just distal to the left subclavian artery (post-ductal coarctation). It may also be pre-ductal coarctation (located before the insertion of the ductus arteriosus proximal to the left subclavian artery). This defect generally results in hypertension (usually in a young person) with left ventricular
pressure overload. The site of origin of the left subclavian artery and the severity of the coarctation determine the pattern of pulse and blood pressure findings:
1. In most cases, the origin of the left subclavian artery is proximal to the coarctation (post-ductal coarctation), resulting in hypertension in both arms and lower blood pressure in both lower limbs (as indicated in the question).
2. Less often, the origin of the left subclavian artery is just distal to the coarctation (pre-ductal coarctation), so the left brachial pulse is diminished and is equal to the femoral pulse. As a result, in this setting, comparing the blood pressure from the left arm and legs can be misleading, as the coarctation is proximal to the origin of the left subclavian artery.
3. In approximately 3-4% of cases, both the right and left subclavian arteries originate below the area of coarctation, resulting in the blood pressures and pulses that are equally decreased in all four extremities.
4. In mild coarctation of the aorta, all the pulses may be easily palpable, but there may be a delay in the femoral pulse compared with the brachial pulse.
5. If the origin of the right subclavian artery is anomalously located distal to the coarctation, comparing blood pressure measurements between the right arm and leg may be misleading as they will be diminished to a similar degree. In this clinical scenario, cardiac catheterisation + MRI scanning is the next most appropriate next step in further characterising the pressure gradient across the coarctation.

A 53-year-old woman who has had chemotherapy for metastatic breast cancer six months earlier comes to the clinic complaining of shortness of breath on exertion. Her BP is 125/78 mmHg, her pulse is 94 bpm and her apex beat is displaced to the anterior axillary line. Clinical results are given in the table below:

A Doxorubicin
The clinical scenario is of a 53 years old woman who had chemotherapy for metastatic breast cancer 6 months earlier. She now presents with shortness of breath, cardiomegaly (on CXR and displaced apex) and pulmonary oedema consistent with left ventricular failure. Cancer patients who are undergoing chemotherapy have an increased risk of developing cardiovascular complications. Anthracyclines and
related compounds (e.g. doxorubicin, daunorubicin, idarubicin and mitoxantrone) are the most frequently implicated agents. Doxorubicin can be associated with heart failure, myocardial necrosis causing a dilated cardiomyopathy (reduced left ventricular ejection fraction) and tachyarrhythmias;
Other common side effects are nausea, vomiting, diarrhoea, loss of appetite, myelosuppression, alopecia, missed menstrual periods, darkening of skin or nails, weakness, tiredness, eye redness, puffy eyelids, reddish colour to urine, tears, and sweat that may last for several days. Hypersensitivity reactions are also seen.

B Docetaxel
Docetaxel is incorrect. Taxanes (e.g. paclitaxel and docetaxel) are the most commonly used chemotherapeutic agents. Docetaxel may be associated with arrhythmias and cardiac failure, although the likelihood is less than with doxorubicin. Other common side effects of docetaxel are anaemia, severe neutropenia, thrombocytopenia, leukopenia, infection, skin rash, alopecia, nausea, vomiting, diarrhoea, fever, weakness, pain, increased liver enzymes (bilirubin, AST, ALT, ALP), oedema, stomatitis, weight gain, myalgia, arthralgia, burning sensation, paresthesia, dysesthesia, nail depigmentation, nail hyperpigmentation, and thinning of nails. Taxane induced pneumonitis and hypersensitivity reactions are also seen.

C Cisplatin
Cisplatin is incorrect. Platinum-based chemotherapies are usually associated with nerve damage (peripheral neuropathy). They are not associated with heart failure or cardiomyopathy. Other common side effects of cisplatin are nausea, vomiting, diarrhoea, nephrotoxicity, ototoxicity, bone marrow depression and transient increase in liver enzymes. Hypersensitivity reactions are also seen.

D Bleomycin
Bleomycin is incorrect. The most important side effect of bleomycin is interstitial pneumonitis. Bleomycin does not cause heart failure and cardiomyopathy.

E Carbiplatin
Carboplatin is incorrect. Carboplatin, like cisplatin is most likely to be associated with peripheral neuropathy.

A 24-year-old man from a travelling family who has shunned regular medical follow-up comes to the clinic complaining of shortness of breath and chest pain. On examination, his BP is 145/82 mmHg, he is cyanosed and short of breath at rest. You review his catheterisation results, given in the table below:

B Persistent hypoxia despite maximal oxygen therapy
Persistent hypoxia despite maximal oxygen therapy Cardiac catherterisation is an invasive procedure in which catheters are inserted into the various chambers and vessels of the heart for diagnostic or therapeutic purposes. They can measure pressure and oxygen concentrations in the various
chambers and vessels and help us to diagnose complex cardiac conditions. Routine hemodynamic measurements are obtained from the aorta (Ao), left ventricle (LV), right ventricle (RV), right atrium (RA), pulmonary artery (PA), and the pulmonary artery wedge position (for pulmonary capillary
wedge pressure or PCWP). The last is usually equivalent to the left atrial (LA) pressure.
The normal values for these are as follows:

The clinical scenario is of a young man (24 years old) with shortness of breath and chest pain and no regular follow-up. He is cyanosed and is short of breath at rest. The right ventricular pressure is greater than the left ventricle and the LV oxygen saturation is <95%. All these indicate that this man has a right to left shunt. There is clear mixing of deoxygenated and oxygenated blood within the left ventricle,
as evidenced by the left ventricular oxygen saturation of 88%. The most likely diagnosis is a long-standing ventricular septal defect (VSD) with reversal of the shunt (Eisenmenger Syndrome). This would also explain the clinical features of chest pain, shortness of breath and cyanosis. In right-to-left
shunts, the arterial saturations do not change with inspired high-concentration oxygen and there is persistent hypoxia despite maximal oxygen therapy as there is persistent mixing of oxygenated and deoxygenated blood.

A A diastolic murmur
A diastolic murmur is incorrect. The typical murmur seen in VSD is a holosystolic murmur and not a diastolic murmur. Common causes of a diastolic murmur include aortic or pulmonary regurgitation. Mid-diastolic murmurs are due to turbulent flow across the atrioventricular (mitral & tricuspid) valves from mitral or tricuspid stenosis. None of these conditions would cause a drop in the oxygen saturation in the
left ventricle. This is only possible in a right to left shunt. Aortic/pulmonary regurgitation is diagnosed by a wide pulse pressure in the aortic/pulmonary pressure. When the PCWP exceeds the LVEDP, the diagnosis of mitral stenosis should be considered and when the RA pressure exceeds the RVEDP,
the diagnosis of tricuspid stenosis should be considered.

C Tapping apex beat
Tapping apex beat is incorrect. In VSD, the apex beat is usually displaced and there may be a parasternal heave. A tapping apex beat is seen is mitral stenosis which is not the
diagnosis here (as mentioned above).

D Broad P waves on ECG
Broad P waves on ECG is incorrect. In VSD, the P waves are tall on the ECG (P-pulmonale), a sign typical of that seen with right atrial overload due to pulmonary hypertension. Broad P- waves on ECG (P-mitrale) are typically seen due to left atrial overload in mitral stenosis. This is not the diagnosis in this case

E Decreased pulmonary vasculature on CXR
Decreased pulmonary vasculature on CXR is incorrect. In VSD, because of pulmonary hypertension, increased pulmonary vasculature markings are normally seen on the chest X-ray (CXR). Decreased pulmonary vasculature on CXR is seen in pulmonary stenosis. There is no information given in
the question that would indicate that the patient has pulmonary stenosis along with VSD.

B Verapamil
Verapamil leads to a reduction in the risk of torsades de pointes by reducing left ventricular transmural dispersion of repolarization and suppressing after depolarizations.

A Sotalol
Sotalol is incorrect. Sotalol is a beta blocker and therefore leads to QT prolongation, increasing the risk of torsades de pointes.

C Flecainide
Flecainide is incorrect. Flecainide is a sodium channel blocker which leads to prolongation of the action potential and therefore risks torsades de pointes.

D Digoxin
Digoxin is incorrect. Digoxin, particularly when levels approach toxicity, is associated with increased risk of torsades de pointes.

E Risperidone
Risperidone is incorrect. Risperidone is recognised to be associated with torsades de pointes, particularly where there is pre-existing cardiovascular disease. Drug-induced Torsades de Pointes
Drugs are a common cause of acquired LQTS and TdP. Many drugs have been implicated including:

• Antiarrhythmic drugs (e.g. sotalol, quinidine, disopyramide, procainamide, flecainide) Certain non-sedating antihistamines (e.g. terfenadine and astemizole)
• Antibiotics – Erythromycin, clarithromycin, azithromycin, levofloxacin, moxifloxacin, gatifloxacin, trimethoprim- sulfamethoxazole, clindamycin, pentamidine, chloroquine
• Antifungals – Ketoconazole, itraconazole
• Certain psychotropic medications (e.g. risperidone,
• haloperidol, phenothiazines, thioridazine, trifluoperazine, sertindole, zimeldine, ziprasidone) Tricyclic and tetracyclic antidepressants
• Certain gastric motility agents (e.g. cisapride)
• Lithium.

A 42-year-old patient who has a history of paroxysmal atrial fibrillation (AF) has been treated with warfarin. The AF has now resolved after successful DC cardioversion. Clinical results are given in the table below:

A 4 weeks
The clinical scenario is of a young 42 years old patient with a history of paroxysmal atrial fibrillation (treated with warfarin) that has resolved after successful DC cardioversion. Blood investigations are normal; TSH is normal (normal range = 0.4 – 4.0 U.L) and ECHO shows normal sized left atrium and no
significant valvular disease. Duration of the atrial fibrillation is not mentioned in this question. In this patient there is an increased risk of embolic events in the immediate post-cardioversion period, hence he should be continued on warfarin for 4 weeks after cardioversion.

B 6 months
6 months is incorrect. Anti-coagulation for 6 months risks significant bleeding with no added benefit with respect to reducing risk of stroke.

C 1 year
1 year is incorrect. 1 year of anticoagulation, like 6 months, risk significant bleeding with no added benefit.

D 3 years
3 years is incorrect. 3 years is inconsistent with guidance both for anti-coagulation after cardioversion and for anti- coagulation after a venous thromboembolism.

E Stop with immediate effect
Stop with immediate effect is incorrect. In this case the risk of embolic disease would be markedly increased.

A 32-year-old man presents to the clinic with shortness of breath, which is particularly bad when he goes jogging. He has recently increased his exercise to try and reduce his weight. On a couple of occasions, he has also noticed some chest discomfort which has caused him to stop exercising.
On examination, his BP is 150/88 mmHg, and he has a double apical impulse. On auscultation, there is a harsh midsystolic murmur, which is loudest between the apex and the left sternal border.
Clinical results are given in the table below:

C Degree of septal hypertrophy
The investigations are normal and ECG shows LVH and widespread Q-waves. The clinical symptoms along with the examination findings and ECG point towards a diagnosis of hypertrophic obstructive cardiomyopathy (HOCM). These patients are at increased risk of sudden cardiac death.

A Increased left ventricular outflow tract gradient
Increased left ventricular outflow tract gradient is incorrect. This is also associated with risk of sudden death but the association is less strong versus the degree of septal hypertrophy. LVOT gradient is associated with angina and syncope risk.

B Presence of mitral regurgitation
Presence of mitral regurgitation is incorrect. Mitral regurgitation is usually seen as a function of cardiac failure, and isn’t associated with increased risk of sudden death.

D Presence of atrial fibrillation
Presence of atrial fibrillation is incorrect. AF is associated with increased risk of stroke, but the risk of sudden death is less than that associated with septal hypertrophy.

E Systolic anterior motion
Systolic anterior motion of the mitral valve is incorrect. This can worsen symptoms of LVOT obstruction, but isn’t as strongly associated with sudden death as septal hypertrophy.

A The pattern of pain described
The clinical scenario of an elderly man (70 years old) with severe tearing back and chest pain that came on suddenly is characteristic of dissecting aortic aneurysm. He has a history of hypertension (on medications) and he is a smoker. Both of these are risk factors for aortic dissection. On examination,
his B.P is high (155/85 mmHg); he has bilateral upgoing plantars, weakness of left ankle dorsiflexion (4/5) and a pericardial rub. The pattern of pain described – acute onset of severe tearing back and chest pain – is classical of aortic dissection. The symptoms and signs of aortic dissection depend upon
the extent of dissection and the affected cardiovascular structures. the most common symptom is pain (occurring in 90% patients). The typical pattern is an acute onset of severe, sharp knife-like/tearing pain in the chest or/and the back that causes the patient to seek medical help within minutes to hours. The pain is described as unlike any pain experienced before. The location of the pain is typically described as anterior chest in ascending aorta (type A) dissection and back for descending aorta (type B) dissection, although this distinction isn’t invariable. Painless aortic dissection only occurs in around 10% of patients, and is more common in patients with diabetes, connective tissue disorders such as Marfan syndrome, older age and prior cardiovascular surgery.

B Hypertension
Hypertension is the most important predisposing factor for aortic dissection, however these are multiple possible causes for hypertension (e.g. genetic, family history, idiopathic, renal disease etc.) and it is a risk factor for multiple conditions (e.g. stroke, MI, aortic dissection etc.); hence it’s presence is not an
indicator for aortic dissection or any other condition. Hypertension is more common in Type B dissection (70%) as compared to Type A dissection (36%). Patients with aortic dissection can also present with hypotension, Hypotension and syncope are more common is patients with Type A
(ascending aorta) dissections, whereas hypertension is more common in patients with Type B (descending aorta) dissection. Hypotension/shock may be due to cardiac tamponade (from rupture), acute aortic regurgitation, acute MI or hemothorax.

C Bilateral upgoing plantars
Bilateral upgoing plantars is incorrect. Although this may suggest lower limb iscahaemia, of course it doesn’t necessarily imply a mechanistic link to aortic dissection.

D Left lower limb signs
Left lower limb signs is incorrect. Again focal neurological deficits are possible in aortic dissection due to distal propogation of the tear and consequent ischaemia, although they don’t necessarily imply dissection as the cause.

E Pericardial rub
Pericardial rub is incorrect. Pericardial rub is seen in patients with pericarditis. It may occur in those with aortic dissection Type A due to rupture into the pericardium causing pericarditis or inflammatory pericarditis but is rare and not a characteristic feature. Patients with dissection may also develop a new diastolic murmur (due to acute aortic regurgitation) because of proximal extension of a Type A (ascending aorta) dissection.

A 72-year-old man was admitted with an acute anterior myocardial infarction. He has chronic renal impairment, with a recent creatinine recorded at 148 μmol/litre. Medication included ramipril, atorvastatin and indapamide for the treatment of hypertension. He was taken straight to the angiography suite where he received stenting of a left main-stem stenosis. You are asked to see him after about 30 hours as the nurses feel he is deteriorating. On examination his BP is 149/84 mmHg, his pulse is 75 bpm and regular. His legs look dusky in colour, particularly his right big toe which looks blue
in colour. He has splinter haemorrhages affecting toenails on both feet. There is a loud left femoral bruit. The table below contains the investigation results.

D Cholesterol embolism
The clinical scenario is of a 72 years old man admitted with myocardial infarction. He has a past history of chronic renal impairement (baseline creatinine is 148 μmol/litre) and hypertension (on ramipril and indapamide). He has various skin changes including:

• Dusky colour of his legs – this indicates that the patient either has cyanosis (reduced blood flow) or livedo reticularis (reticulated mottled, bluish or erythematous skin due to blood flow compromise and oxygen desaturation through an affected area)
• His right big toe is blue in colour – this indicates cyanosis due to compromised blood flow. Acrocyanosis is a recognised sign of cholesterol embolism. Splinter haemorrhages affecting the toenails of both the feet-splinter haemorrhages are tiny blood clots that tend to run vertically under the nails. They are not specific to any particular condition and are associated with subacute infective endocarditis, SLE, scleroderma, psoriatic arthritis. Out of the given options, they are a cutaneous manifestation of cholesterol embolism.

The patient also has a loud left femoral bruit – this indicatespossible occlusion at the level of the femoral artery. Investigations show normal complete blood count with a high serum creatinine, hyperkalemia as well as blood and protein in urine indicative of acute kidney injury. Taking all these
features into account suggests that cholesterol embolism is the most likely cause of the clinical picture seen here.

A Renal vein thrombosis
Renal vein thrombosis is incorrect. Renal vein thrombosis is most often seen in patients with a hypercoagulable state (most commonly nephrotic syndrome, malignancy, renal cancer, antiphospholipid antibody syndrome etc). Patients usually present with other clinical features pointing towards the underlying cause (e.g. weight loss in malignancy, edema in nephrotic syndrome). Patients can also present with acute onset of flank pain and visible haematuria. Atherosclerosis and skin changes usually do not occur and there is no relation with cardiac vascular surgery. The clinical features given in the picture do not support a diagnosis of renal vein thrombosis.

B Acute tubular necrosis
Acute tubular necrosis is incorrect. Acute tubular necrosis is the most common cause of acute kidney injury. It is usually related to ischaemic or toxic insult to the renal tubules (e.g. from hypovolemia, sepsis, drugs, contrast etc.). Patients usually present with clinical features of the underlying cause
(e.g. fever from sepsis or drug history) and acute kidney injury. It does not cause embolic occlusion of blood vessels or atherosclerosis; hence the clinical scenario given does not fit with a diagnosis of acute tubular necrosis.

C Renal artery stenosis
Renal artery stenosis is incorrect. Renal artery stenosis is one of the common causes of renovascular hypertension and can be associated with atherosclerosis in other major arteries (e.g. coronary arteries, femoral artery). It usually presents as gradually progressive chronic renal insufficiency (as given in
the question); however the acute deterioration seen here is much more likely to be related to cholesterol embolism.

E Femoral artery embolism
Femoral artery embolism is incorrect. Femoral artery embolism would present as an acute onset of pain and pallor/cyanosis in the lower limb. If the obstruction was partial, it could give rise to femoral bruit and skin changes mentioned in the question; however it would be very unlikely to be bilateral (as mentioned in the question both legs look dusky). It would also not explain the acute kidney injury and
hence cholesterol embolism is still the more likely cause.

A 21-year-old woman presents to the clinic with symptoms of increased shortness of breath and decreased exercise tolerance. She used to be a keen hockey player when at school but is now virtually unable to even walk to the bus stop without becoming short of breath. On examination she
looks tired and slightly short of breath at rest. Her BP is elevated at 145/92 mmHg. Echocardiogram showed increased right atrial size and elevated right atrial pressure by Doppler. Cardiac catheterization results were as follows:

• O2 saturation SVC = 74%
• O2 saturation RA = 82%
• O2 saturation RV = 82%
• O2 saturation LA = 95%
• O2 saturation LV = 95%.

B Secundum atrial septal defect
Cardiac catheterization is an invasive procedure in which catheters are inserted into the various chambers and vessels of the heart for diagnostic or therapeutic purposes. They can measure pressure and oxygen concentrations in the various chambers and vessels and help us to diagnose complex
cardiac conditions. Routine hemodynamic measurements are obtained from the aorta (Ao), left ventricle (LV), right ventricle (RV), right atrium (RA), pulmonary artery (PA), and the pulmonary artery
wedge position (for pulmonary capillary wedge pressure or PCWP). The last is usually equivalent to the left atrial (LA) pressure. The normal values for these are as follows:

The clinical scenario is of a young woman (21 years old) with progressive breathlessness and decreased exercise tolerance (now Grade IV-V MRC – patient is having breathlessness walking to the bus stop and is breathless at rest on examination). She has hypertension, (145/92 mm Hg) and
ECHO and Doppler show increased right atrial size and pressures. 90% of ASD are ostium secundum type. Secundum atrial septal defect is associated with a shunt only between the left and right atrium and the adjoining valves and ventricular septum are intact. It is associated with an increase in oxygen
saturation in the RA and RV compared with the SVC as well as the increased size and pressure of RA. Secundum defects are often diagnosed in patients entering early adulthood. Patients with secundum defects tend to be slim and to not suffer from cyanosis. All the features in the question point
towards a diagnosis of ostium secundum asd; hence this is the correct answer. Therapy of choice is via delivery of a catheter device to close the defect or surgical closure if the defect is particularly large.

A Ostium primum atrial septal defect
Ostium primum atrial septal defect is incorrect. Ostium primum ASD is a complicated defect associated with abnormalities of the two adjoining heart valves (mitral and tricuspid valves) as well as a ventricular septal defect; hence the hemodynamics as well as oxygen saturation between the RA and RV in ostium primum ASD would vary which is not the case in this question. Here the RA and RV oxygen saturation are the same. Also, most patients with an ostium primum defect present in early childhood have signs and symptoms of congestive heart failure.

C Patent ductus arteriosus
Patent ductus arteriosus is incorrect. If the left to right shunt was between the aorta and pulmonary artery, then oxygenated blood would flow from the aorta to the pulmonary artery; hence the oxygen saturation in the SVC, RA and RV would be equal and <75% wherease in the pulmonary artery it would be >75%. Oxygen saturation in the left side of the heart (LA, LV) would be normal.

D Pulmonary stenosis
Pulmonary stenosis is incorrect. This is a valvular defect, and occurring in isolation would not be associated with abnormalities of O2 saturation.

E Tricuspid regurgitation
Tricuspid regurgitation is incorrect. In case of tricuspid regurgitation, right atrial pressure and right ventricular end- diastolic pressure are elevated. A rise or no change in right atrial pressure on deep inspiration is characteristic of tricuspid regurgitation. Mixing of blood leading to abnormalities in O2 saturation would not be expected.

B Aortic valve closure
The cardiac cycle refers to a complete heartbeat from its generation to the beginning of the next beat, and so includes the diastole (relaxation phase), the systole (contraction phase), and the intervening pause. The graph of aortic pressure throughout the cardiac cycle displays a small dip (the “incisure” or “dicrotic notch”), which coincides with the aortic valve closure. The dip in the graph is immediately followed by a brief rise (the “dicrotic wave”) then gradual decline. Just as the ventricles enter into diastole, the brief reversal of flow from the aorta back toward the left ventricle causes the aortic valves to shut. This results in the slight increase in aortic pressure caused by the elastic recoil of the semilunar valves and aorta. The aortic valve closure also coincides with the aortic component of the second heart
sound (A2) and is followed by the phase of isovolemic ventricular relaxation. Mechanism of intra-aortic balloon pump and timing with dicrotic notch – Intra-aortic balloon pumps deflate during systole, which then increases forward blood flow because of the reduction in afterload. The pump then re-inflates during diastole, increasing the blood flow to coronary arteries.

A Aortic valve opening
Aortic valve opening is incorrect. Aortic valve opening is preceeded by the isovolemic ventricular contraction phase that occurs after the first heart sound (S1). Aortic valve opening is followed by the second heart sound/dicrotic notch (S2) and does not coincide with it.

C Mitral valve opening
Mitral valve opening is incorrect. Mitral valve opening occurs after the second heart sound (S2) and dicrotic notch. Blood fills in the left ventricles from the left atrium after opening of the mitral valve.

D Mitral valve closure
Mitral valve closure is incorrect. The mitral valve closure coincides with the first heart sound (S1) and occurs in the initial part of the cardiac cycle much before the dicrotic notch. The mitral valve closure is followed by isovolemic ventricular contraction.

E Pulmonary valve closure
Pulmonary valve closure is incorrect. The pulmonary valve closure coincides with the pulmonary component of the second heart sound (P2). Normally the pulmonary component of the second heart sound occurs a few milliseconds after the aortic valve closure/aortic component of the second heart
sound (A2)/dicrotic notch; hence the pulmonary valve closure does not coincide with the dicrotic notch but occurs a few milliseconds afterwards.

A 72-year-old woman is admitted for assessment after two episodes of collapse over the past few months. She has been managed by her GP for many years for hypertension and is currently treated with indapamide and amlodipine. On examination she looks a little thin. Her BP is 175/125 mmHg.
Auscultation of the chest reveals an ejection systolic murmur. She has minor crackles at both lung bases. The table below contains the investigation results.

C Presence of symptoms
The answer is Presence of symptoms (Option C). The clinical scenario is of an old woman (72 years old) with 2 episodes of collapse. She has a past history of hypertension (on medication – indapamide, amlodipine). Her current blood pressure is also raised (175/125 mmHg). She has an ejection systolic murmur and a gradient of 50 mmHg across the aortic valve. The symptoms and clinical findings point towards a diagnosis of aortic stenosis (AS). She has minor crackles at the lung bases this could indicate mild heart failure. Based on her age, the most likely cause of aortic stenosis in this case would be degenerative calcific AS. This question tests your knowledge about the indications for
valve replacement in a case of aortic stenosis.

• Indications for aortic valve replacement (AVR):
• Patients with severe high-gradient AS who have symptoms by history or on exercise testing.
• For asymptomatic patients with severe AS and left ventricular ejection fraction (LVEF) <50%
• For patients with severe AS when undergoing other cardiac surgery
• For asymptomatic patients with very severe AS and low surgical risk
• For asymptomatic patients with severe AS and decreased exercise tolerance or fall in systemic blood pressure with exercise.
• For symptomatic patients with low-flow/low-gradient severe AS with reduced LVEF with a low-dose dobutamine stress study that shows an aortic velocity ≥4.0 m/s (or mean pressure gradient 250 mmHg) with a valve area s1.0 cm2 at any dobutamine dose.
• For symptomatic normotensive patients with low- flow/low-gradient severe AS with LVEF 250 percent, if clinical, hemodynamic, and anatomic data support valve obstruction as the most likely cause of symptoms.

Criteria for severe aortic stenosis:

• Aortic jet velocity >4.0 m/s
• Mean gradient across the aortic valve >50 mmHg (European Society of Cardiology Guidelines)
• Aortic valve area <1cm2
• Indexed aortic valve area <0.6 cm2/m2
• Velocity ratio <0.25.

The only definitive treatment for aortic stenosis is aortic valve replacement. Out of all the indications given, the presence of symptoms is the clearest indication for aortic valve replacement (AVR); hence Option C is the correct answer. Exertional dyspnea, presyncope/syncope, and angina are the primary symptoms in patients with severe AS. Natural history studies have shown that the average survival after the onset of these symptoms is only 2-3 years. There is a high risk of sudden death in symptomatic patients who are followed conservatively and corrective surgery in this setting is followed by symptomatic improvement and a substantial increase in survival. In most adults with symptomatic, severe aortic stenosis, aortic valve replacement is the surgical treatment of choice. If concomitant coronary disease is present, aortic valve replacement and coronary artery bypass graft (CABG) should be performed simultaneously. For patients who are not candidates for aortic replacement, percutaneous aortic balloon valvuloplasty may provide some symptom relief. Medical treatment (such as diuretic therapy) in aortic stenosis may provide temporary symptom relief but is generally not effective long term.

A Gradient of 50 mmHg

Gradient of 50 mmHg (Option A) is incorrect. A gradient of >40 mmHg (according to the American Heart Association Guidelines) and >50 mmHg (according to the European Society of Cardiology Guidelines) is considered as severe aortic stenosis and can be considered for aortic valve replacement in the presence of symptoms. In this clinical scenario, the patient is at the cusp of the severe category
(gradient of 50 mmHg) and elective valve replacement would not be recommended in the absence of symptoms; hence symptoms would play the major role to decide for valvular replacement.

B Presence of left ventricular hypertrophy
Presence of left ventricular hypertrophy (Option B) is incorrect. Presence of left ventricular hypertrophy is not an absolute indication for AVR. Severe LV hypertrophy (wall thickness >15mm) is a relative indication for AVR.

D Presence or absence of valvular calcification
Presence or absence of valvular calcification (Option D) is incorrect. Presence or absence of valvular calcification does not form an indication for AVR. It only determines whether the patient is eligible for valvotomy/valvuloplasty or will undergo valve replacement. Patients with valvular calcification should undergo valve replacement rather than valvotomy.

E Her relatively young age
Her relatively young age (Option E) is incorrect. Age is not considered as an indication for aortic valve replacement but rather is a predictor of outcome following surgery. The age of this patient (72 years old) puts her in the low risk of age category and we can expect a good outcome following surgery.

B Rate modulated
The choice of pacemaker in a patient depends on the specific abnormality present. Once it has been established that bradycardia or a conduction disorder warrants permanent pacing, the most appropriate mode of pacing must be selected. To facilitate the use and understanding of pacemakers, a standardized classification code/nomenclature has been developed. Nomenclature for Pacemakers
Five Position Code – A three-letter code describing the basic function of the various pacing systems was first proposed in 1974 but has now been updated to the five-position code. This code is designated The NBG Code for Pacing Nomenclature.
The code is generic and does not describe specific or unique functional characteristics for each device. When a code includes only three or four characters, it can be assumed that the positions not mentioned are “O” or absent. Position I – The first position reflects the chamber(s) paced. “A” indicates the atrium, “V” indicates the ventricle, and “D” means dual chamber (i.e., both the atrium and the ventricle). Position II – The second position refers to the chamber(s) sensed. “A” for atrium, “V” for ventricle, “D” for dual. An additional option “O” indicates an absence of sensing. Programmed in this mode, a device will pace automatically at a specified rate, ignoring any intrinsic rhythm. Position III – The third position refers to how the pacemaker responds to a sensed event: “I” indicates that a sensed event inhibits the output pulse and causes the pacemaker to recycle for one or more timing cycles. “T” indicates that an output pulse is triggered in response to a sensed event.

“D” indicates that there are dual modes of response. This designation is restricted to dual chamber systems. An event sensed in the atrium inhibits the atrial output but triggers a ventricular output. There is a programmable delay between the sensed atrial event and the triggered ventricular output to mimic the normal PR interval. If the ventricular lead senses a native ventricular signal during the programmed delay, it will inhibit the ventricular output.
“O” indicates no response to sensed input; it is most commonly used in conjunction with an “O” in the second position.
Position IV – The fourth position reflects rate modulation, also referred to as rate responsive or rate adaptive pacing:
“R” in the fourth position indicates that the pacemaker has rate modulation and incorporates a sensor to adjust its programmed paced heart rate in response to patient activity. From a practical standpoint, “R” is the only indicator commonly used in the fourth position.
“O” indicates that rate modulation is either unavailable or disabled. “O” is often omitted from the fourth position (i.e., DDD is the same as DDDO).
Position V – The rarely used fifth position specifies only the location or absence of multisite pacing, defined as stimulation sites in both atria, both ventricles, more than one stimulation
site in any single chamber, or a combination of these. The fifth position of the code is rarely used:

• “O” means no multisite pacing
• “A” indicates multisite pacing in the atrium or atria
• “V” indicates multisite pacing in the ventricle or ventricles
• “D” indicates dual multisite pacing in both atrium and ventricle

The most common application of multisite pacing is biventricular pacing for the management of heart failure (Cardiac resynchronization therapy). Based on the above nomenclature, ‘R’ in DDDR stands for
rate modulated; hence this is the correct option. Rate responsiveness also referred to as “rate modulation or rate adaptation”, refers to the ability of a pacemaker to adjust its programmed paced rate based upon patient activity. A variety of sensors have been designed to determine when a patient is physically active (e.g., vibration, minute ventilation, change in right ventricular impedance). The range of heart rates, the pace of acceleration and deceleration, and the degree of activity required to initiate this response are all programmable in rate-adaptive pacing modes.

A Rate limiting
Rate limiting is incorrect. Overdrive pacing is usually considered for patients with resistant ventricular tachycardia.

C Repolarising
Repolarising is incorrect. The action of a pacemaker is via depolarisaiton rather than repolarization.

D Rate enhancing
Rate enhancing is incorrect. In effect all pacemakers for long term use are rate enhancing in patients with symptomatic bradycardia.

E Rate reducing
Rate reducing is incorrect. Rate reducing is incorrect nomenclature, attempts at rate reduction would obviously be an aim of overdrive pacing.

A 54-year-old man with a history of smoking and hypertension presents to the Emergency Department with central crushing chest pain, nausea and sweating. On examination his BP is 104/70 mmHg, his pulse 85 bpm and regular, and he looks pale, grey and sweaty. There are no murmurs on auscultation but he has crackles at both lung bases consistent with heart failure.
Investigations reveal:

C Total occlusion of left anterior descending artery
The clinical scenario is of a 54 years old man who presents with central crushing chest pain, nausea, sweating (autonomic features). He looks pale grey and sweaty. His pulse is normal (P = 85 bpm, regular) and his BP is on the lower side of normal (B.P = 104/70 mmHg). There are no murmurs on auscultation but he has crackles at both lung bases (consistent with heart failure). His blood investigations are normal and ECG shows ST elevation in V1-V4 with reciprocal ST depression II, III and aVL. The diagnosis is Acute Anterior Wall St Elevation Myocardial Infarction (STEMI). He
also has risk factors for MI (history of smoking and hypertension). The area of the heart and vessels involved in myocardial infarction can be assessed based on the ECG findings as follows:

According to this table, this patient (with ST elevation in V1- V4) has an anterior wall myocardial infarction and the vessel involved is the left anterior descending artery. Myocardial infarction occurs when there is complete absence of blood flow to a region of the heart because of total occlusion of a coronary artery. In this case, the patient has an acute anterior wall MI and hence would have total occlusion of the left anterior descending artery.

A Total occlusion of right coronary artery
Total occlusion of right coronary artery is incorrect. This would lead to an inferior wall myocardial infarction with ST elevation in leads II, III and aVF with reciprocal ST depression in the anterior leads V1, V2, V3, V4; this does not match the clinical scenario given.

B 70% stenosis of left anterior descending artery
70% stenosis of left anterior descending artery is incorrect. This would produce angina on exertion because of compromised demand-supply of blood and oxygen during activity (ischaemia of the anterior area of the heart), however, it would not cause a myocardial infarction.

D 70% stenosis of left circumflex artery
70% stenosis of left circumflex artery is incorrect. This would produce angina on exertion because of compromised demand-supply of blood and oxygen during activity (ischaemia of the lateral area of the heart), however, it would not cause a myocardial infarction.

E Total occlusion of left circumflex artery
Total occlusion of left circumflex artery is incorrect. This would lead to a lateral wall myocardial infarction with ST elevation in leads I, aVL, V5 and V6 with reciprocal ST depression in inferior leads II, III and aVF; this does not match the clinical scenario given. ST Elevation Anterior Myocardial Infarction
The management of choice is primary percutaneous coronary intervention (PCI), as early as possible after the onset of chest pain. Studies have confirmed that primary PCI is superior to thrombolysis with rates of arterial patency in more than 90% of procedures, and lower rates of bleeding complications.

C Transthoracic ECHO
Patients with HOCM are at an increased risk of sudden cardiac death. The most common cause is ventricular arrhythmia. It usually occurs in young and asymptomatic patients and has been linked with physical exertion. HOCM is an autosomal dominant condition and most mutations have a high degree of penetrance, hence first- degree family members of an affected individual should be screened for the disease. Family screening should include history, physical examination, ECG and ECHO. Routine genetic testing is not recommended for screening of first-degree relatives unless a definite HOCM-causing mutation has been identified in the index case. The clinical diagnosis of HOCM is made with cardiac imaging- most commonly 2D ECHO or with cardiac MR. Transthoracic ECHO (TTE) is the investigation of choice for diagnosis and screening of HOCM. Transoesophageal ECHO (TEE) can also be used and provides better images but because it is invasive it is avoided unless the diagnosis is
suspected, views are poor, and enhanced assessment is needed. The diagnosis is based on the presence a hypertrophied and nondilated left ventricle in the absence of any other cardiac or systemic disease capable of producing the degree of hypertrophy (usually >=15mm in adults).

A Exercise ECG
Exercise ECG is incorrect. Treadmill exercise testing is used to determine functional capacity and response to therapy in patients with HOCM and not for the diagnosis. Exercise testing with monitoring of ECG and blood pressure is helpful in risk assessment of patients with HOCM, because abnormal
blood pressure response to exercise (defined as either a failure to increase by at least 20 mmHg or a drop of at least 20 mmHg during effort) has been demonstrated as one of the factors associated with risk of sudden cardiac death.

B Electrocardiography studies
Electrocardiographic studies is incorrect. Electrocardiographic studies includes investigations involving
the ECG including resting 12-lead ECG, exercise ECG, ambulatory ECG/Holter monitoring and so on. As mentioned above, these are not used for diagnosis but for functional capacity and baseline investigations. Ambulatory ECG monitoring/Holter monitoring is used for detection of ventricular tachyarrhythmias. This plays an important role in risk stratification of asymptomatic or symptomatic patients with HOCM because episodes of non-sustained ventricular tachycardia are a risk factor for sudden cardiac death. It is recommended to do 2 yearly holters in HOCM patients without baseline arrhythmias.

D Radionucleotide scanning
Radionucleotide scanning is incorrect. Radionucleotide scanning may show reversible perfusion defects, but these are not diagnostic of HOCM and not used for diagnosis.

E Resting 12 lead ECG
A resting 12-lead ECG is useful largely for raising the suspicion of HOCM in family members and in identifying patterns such as Wolff-Parkinson-White syndrome, which may suggest certain phenotypes of HOCM. It cannot be used for diagnosis, which is by 2D ECHO. The ECG is abnormal in 75%-95% of patients with HOCM but does not correlate with the severity or pattern of hypertrophy as determined by
ECHO.

A 60-year-old man with a history of type 2 diabetes, postural hypotension and left ventricular hypertrophy presents to the clinic. He is currently taking metformin and pioglitazone for
his glucose control. He is hypertensive, with a blood pressure of 160/95 mmHg, but his GP reports that he has suffered various side-effects of antihypertensives, including a dry, irritating cough, swollen ankles, gum hypertrophy, lethargy and urinary frequency. Investigations show:

D Irbesartan
This is an angiotensin-receptor blocker (ARB) and would be the most appropriate choice for this patient. It is beneficial in patients with established micro-albuminuria or proteinuria, as seen in this case. Irbesartan has a linear dose response and can be titrated up from a starting dose of 75 mg to a
maximum dose of 300 mg in accordance with tolerability.

A Indapamide
Indapamide is incorrect. Indamide is a thiazide diuretic and is therefore associated with increased risk of urinary frequency.

B Atenolol
Atenolol is incorrect. Atenolol is a beta blocker and is associated with erectile dysfunction and can cause lethargy.

C Amlodipine
Amlodipine is incorrect. Amlodipine is a calcium antagonist, and so it can be associated with gum hypertrophy and swollen ankles and headaches caused by vasodilation.

E Doxazocin
Doxazocin is incorrect. Doxazocin is a selective alpha-1 adrenergic receptor antagonist. It is associated with postural hypotension and should be avoided in patients with a history of postural hypotension.

A 54-year-old patient was admitted with central crushing chest pain and had a troponin rise to 3.2 μg/litre with anterior ST depression. He has a past history of hypertension for which he takes ramipril 10 mg, and smokes 20 cigarettes per day. He was recovering on the cardiology ward after
angiography and stenting when he started suffering further central chest pain 3 days later. Again his ECG showed anterior ST depression.

Investigations reveal:

C CKMB
The clinical scenario is of a 54 year old man with central crushing chest pain, massively raised troponin levels (Troponin = 3.2 µg/litre; Normal value is <0.01 µg/litre) and ST depression in the anterior leads. The diagnosis is Acute Anterior Wall Non-St Elevation Myocardial Infarction. Three days post-stenting, he again develops chest pain and ST depression in the anterior leads. At this point we have to
differentiate between non-cardiac post-operative chest pain and another acute myocardial infarction (most likely due to stent blockage). The ST depression could represent new changes of acute ischaemia or persistent ECG changes from the previous episode that have failed to resolve after stenting; hence we need the help of cardiac biomarkers to determine the exact cause of the chest pain.
The best cardiac biomarker in this scenario is CK-MB because it first appears 4-6 hours after symptom onset, peaks at 24 hours, and returns to normal in 48-72 hours; hence it can be used to diagnose reinfarction if levels rise after initially declining following acute myocardial infarction. The remaining biomarkers in the question remain elevated at 72 hours (3 days) following acute myocardial infarction and hence cannot be used to determine whether the rise at 72 hours is due to a new infarction or the previous one.

A Troponin T
Troponin T is incorrect. Troponin T begins to rise in about 2-4 hours, peaks in around 12-16 hours and returns back to normal in 7-10 days; hence 3 days after MI troponin levels would still be high and hence it would not be possible to differentiate whether the rise is due to the new infarction or previous one.

B Troponin I
Troponin I is incorrect. Like troponin T, troponin I may remain elevated for up to 7-10 days.

D LDH
Lactate dehydrogenase (LDH) is incorrect. LDH usually begins to rise within 2-4 hours, reaches a peak in 72 hours and returns back to normal in 10-14 days; hence 3 days after MI LDH levels would still be high and hence it would not be possible to differentiate whether the rise is due to the new infarction or previous one.

E AST
Aspartate transaminase (AST) is incorrect. AST is usually measured as a marker of liver disease. It is also raised in MI but is not specific for MI and is not a commonly used biomarker. It normally rises after about 12 hours, peaks in 1-2 days and returns back to normal in 3-5 days. Although it can be used to diagnose reinfarction if levels rise after initially declining following acute myocardial infarction, it is not a
commonly used biomarker as compared to CK-MB and CK-MB would be a better answer here.
Cardiac Biomarkers During Myocardial Infarction
1. Troponins (Tn):

• Cardiac troponins are the cardiac markers of choice in patients with acute coronary syndrome
• It is the most sensitive and specific test for myocardial damage. Because of its increased specificity as compared with CK-MB, troponin is a superior marker for myocardial injury.
• They are regulatory proteins found in skeletal and cardiac muscle. Troponin T (TnT) and Troponin I (Tnl) are the ones most commonly used in acute coronary syndrome
• Normal value is <0.01 μg/litre
• It begins to rise in about 2-4 hours, peaks in around 12-16 hours and returns back to normal in 7-10 days.

2. Creatinine Kinase – MB Fraction (CK-MB):

• Before the cardiac troponins, it was the biochemical marker of choice for diagnosis of acute MI
• The CK-MB isoform of creatinine kinase resides in high concentrations in the cardiac muscle
• It first appears 4-6 hours after symptom onset, peaks at 24 hours, and returns to normal in 48-72 hours
• It can be used to diagnose reinfarction if levels rise after initially declining following acute myocardial infarction The normal value for CK-MB is 5-25 IU/L
• For diagnosis of MI, the criteria used is 2 serial elevations
• above the diagnostic cut-off level or a single result more than twice the upper limit of normal
• False positive elevations occur in skeletal muscle trauma, heavy exertion and myopathy (as CK-MB also exists in lower concentrations in skeletal muscles).

3. Lactate Dehydrogenase (LDH):

• LDH-1 isoenzyme is found in cardiac muscle and LDH-2 is predominantly found in blood serum A high LDH-1: LDH-2 level suggests MI
• It usually begins to rise within 2-4 hours, reaches a peak in 72 hours and returns back to normal in 10-14 days
• LDH is not as specific as troponin and false positives are seen in patients with cancer, meningitis, encephalitis or HIV.

4. Aspartate Transaminases (AST):

• It is usually measured as a marker of liver disease but is also raised in MI and hence is not specific for MI
• Normal value is 10- 40 U/L
• It normally rises after about 12 hours, peaks in 1-2 days and returns back to normal in 3-5 days.

5. Myoglobin:

• Myoglobin is the primary oxygen-carrying pigment of skeletal and cardiac muscle tissues
• It is used less than other biomarkers for MI because it lacks specificity (it is high in any type of muscle damage). It has attracted interest because it rises and falls very rapidly (earlier than CK-MB or troponin)
• It typically rises 2-4 hours after MI, peaks at 6-12 hours
  and returns back to normal in 24-36 hours
• It has been used in assessing reperfusion after thrombolysis.

An increase in white cell count (WCC) and erythrocyte sedimentation rate (ESR) is also seen after myocardial infarction. ESR may remain elevated for a number of days after infarction.

A 67-year-old woman presents with syncope. She has suffered two or three episodes of collapse during the past 6 months, the most recent while attending church on a Sunday morning. She has a history of hypertension which is currently managed with ramipril and bendroflumethiazide and dyslipidaemia treated with simvastatin. On examination her pulse is 34 bpm and BP is 100/50 mmHg. Her chest is clear and heart sounds are normal. You notice irregular cannon waves on examination of the JVP.
Investigations reveal:

A Complete heart block
The presentation of bradycardia, relative hypotension and syncope lead to the correct diagnosis. Cannon waves occur when the right atrium contracts against a closed tricuspid valve, and these occur irregularly in complete heart block (and also in conjunction with ventricular tachycardia). Management in this case would be an ECG to confirm the diagnosis and then likely referral for insertion of permanent pacemaker.

B Mobitz type 2 heart block
Mobitz type 2 heart block is incorrect. Mobitz type 2 heart block is defined as intermitted non-conducted p-waves without progressive prolongation of the PR interval i.e. constant PR interval. Mobitz 2 is usually due to failure of conduction conduction at the level of His-Purkinje system (i.e. below AV node).

C Sinus bradycardia
Sinus bradycardia is incorrect. Whilst a possibility sinus bradycardia is unlikely to give such a presentation alone. The presence of cannon waves on examination of the JVP together with a heart rate of 40bpm suggest Complete heart block.

D Junctional rhythm
Junctional rhythm is incorrect. A junctional rhythm arises from a focus in the area of the atrioventricular node. Usually it produces an accelerated junctional rhythm (>60bpm), however a junctional escape rhythm between 40-60bpm can arise. The QRS complexes are typically narrow (<120ms) with
no relationship between the QRS complexes and any preceding atrial activity (i.e. p-waves). This rhythm does not typically produce irregular cannon waves on examination of the JVP, unlike complete heart block.

E Ventricular bigeminy
Ventricular bigeminy is incorrect. In ventricular bigeminy, a sinus beat is followed shortly by a premature ventricular contraction (PVC). A compensatory pause then occurs followed by another normal beat. PVCs are a normal electrophysiological phenomenon, not requirng investigation
of treatment, however, if patients have frequent PVCs, palpitations or a ‘skipped heart beat’ may be experienced. A PVC may trigger a re-entrant tachyarrhythmia in certain groups of patients (e.g. ischaemic heart disease, WPW). Ventricular bigemeny is unlikely to give the presentation of relative hypotension and bradycardia as in this example.

A 46-year-old man is admitted with a tachycardia. He has no previous medical history of note, but admits to excessive use of alcohol and caffeine associated with a particularly stressful period at work during his job as a bond trader. On examination his BP is 122/80 mmHg, his pulse is 180 bpm. His
chest is clear and there are no signs of cardiac failure. The table below shows the investigation results:

He has tried swallowing of crushed ice to no effect, 6 and 12 mg of adenosine iv with no effect.

A iv 12 mg adenosine
Following 6mg and 12mg of adenosine, a further 12mg of adenosine can be administered before proceeding to the next stage of the ALS algorithm. According to the Resuscitation Council (UK) guidelines the management of narrow complex tachycardia should commence with a full ABCDE assessment of the patient. If there is an absence of ‘adverse features’ i.e. shock, syncope, myocardial ischaemia or heart failure, then proceeding down the algorithm for narrow complex tachycardia is the next course of action. For management of narrow complex regular tachycardia, vagal manoeuvres are
attempted first. If these are unsuccessful, 6mg adenosine is administered via rapid IV bolus with continuous ECG monitoring. If unsuccessful, repeat IV adenosine at a higher dose of 12mg, and again at 12mg. If the patient continues to have a narrow complex tachycardia, then reassessment of the
rhythm followed by appropriate expert advice.

B iv amiodarone loading
IV amiodarone loading is incorrect. A further dose of adenosine 12mg is used for management of narrow complex (QRS duration <0.12s) tachycardias. For a broad complex (QRS > 0.12s) regular tachycardia, IV amiodarone loading would be appropriate management as the rhythm is likely to
be VT.

C iv atenolol
IV atenolol is incorrect. IV beta blockers could be considered for rate control if a further 12mg adenosine dose is unsuccessful as the rhythm could be atrial flutter, however expert help should be sought first.

D iv verapamil
IV Verapamil is incorrect. IV Adenosine 12mg would be the next line of medical management for this rhythm. If unsuccessful, verapamil or short acting beta blockers, such as esmolol, are both appropriate alternative agents for achieving sinus rhythm.

E iv flecainide
IV flecainide is incorrect. IV Adenosine 12mg would be considered next line if 6mg and initial 12mg doses were unsuccessful. Flecainide is a class 1C anti-arrhythmic acting by blocking the sodium channels in the heart reducing its excitability. Whilst flecainide is useful for chemical cardioversion for the management of supraventricular tachycardias, the Cardiac Arrhythmia Suppression Trial (CAST) demonstrated that patients with structural heart disease (e.g. Left ventricular dysfunction, previous MI) and ventricular arrhythmias sustained a higher arrhythmia-related mortality rate. Therefore, this should only be used in the presence of expert advice.

A 45-year-old man with previously diagnosed type 2 diabetes presents to the Emergency Department with severe central chest pain, nausea and sweating. He was riding his bike in an attempt to lose weight when the chest pain began 25 minutes ago. He also smokes 15 cigarettes per day and is
hypertensive, managed with ramipril and amlodipine. On examination, his BP is 155/95 mmHg, he is pale, sweaty and anxious. He has been given 300 mg of aspirin by a passer-by.
Investigations reveal:

D Percutaneous coronary intervention
Studies have shown that in patients with acute STEMI, percutaneous coronary intervention (PCI) is superior to thrombolysis. Therefore, PCI is recommended here above both streptokinase and alteplase.
Percutaneous coronary intervention should be offered as the preferred coronary reperfusion strategy for people with acute STEMI if presentation is within 12 hours of onset of symptoms and primary PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given.

A Low molecular-weight heparin
Low molecular-weight heparin is incorrect. Unfractionated or low molecular weight heparin is offered to people with acute STEMI who are undergoing percutaneous transluminal coronary angioplasty and have been treated with prasugrel or ticagrelor. However, in this question the most appropriate and definitive treatment is early percutaneous transluminal coronary angioplasty.

B Alteplase
Alteplase is incorrect. First line treatment for patients presenting with evidence of acute STEMI should be managed percutaneous transluminal coronary angioplasty (PTCA), with patients presenting with a history cocaine abuse treated in the same way. Recombinant tissue plaminogen activators (rtPA) for example Alteplase is offered to patients with acute STEMI presenting within 12 hours of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given.

C Streptokinase
Streptokinase is incorrect. Streptokinase is a fibrinolytic used for the treatment of acute STEMI if percutaneous transluminal coronary angioplasty cannot be delivered within 120 minutes of the time when fibrinolysis could have been given. Therefore, percutaneous transluminal coronary angioplasty is
the most appropriate way of managing this patient in this scenario.

E Abciximab
Abciximab is incorrect. Abciximab is a glycoprotein IIb/Illa inhibitor and guidelines indicated it should not be offered before arrival to the catheter laboratory to people with acute STEMI for whom percutaneous transluminal coronary angioplasty is planned. The American Heart Association
guidelines endorse their use in a clinically appropriate situation despite the fact that no randomised controlled trial evidence exists (circ.ahajournals.org).

A 67-year-old man is referred to the cardiology clinic with angina, progressive heart failure and two episodes of syncope. He has a history of hypertension managed with ramipril and indapamide, and suffered an inferior myocardial infarction some 4 years ago. On examination his BP is 125/105
mmHg, and he has a soft ejection systolic murmur loudest at the right second intercostal space. He has evidence of LVH and there are bilateral inspiratory crackles on auscultation of the chest consistent with LVF. The table below shows the investigation results.

C Aortic stenosis
The triad of angina, left ventricular failure and syncope is classical with respect to aortic stenosis. Two confounders exist, firstly in the elderly the more high frequency components of aortic stenosis may be heard best at the apex, the so called Gallavardin phenomenon, and also the components of the murmur may be softened in situations where cardiac output is reduced. Given this man has evidence
of coronary artery disease he may well have co-existent reduced cardiac output. Hence he requires assessment of both aortic valve and coronary artery status, with combined valve replacement and coronary artery bypass graft surgery likely to be the most appropriate way to manage him.

A Coronary artery disease
Coronary artery disease is incorrect. Whilst the patient may have coronary artery disease given his angina symptoms, previous myocardial infarction and evidence of reduced cardiac output, the presence of syncope and an ejection systolic murmur is most likely due to aortic stenosis. The
presence of LVH and bilateral inspiratory crackles indicate the presence of left ventricular failure likely due to the valvular stenosis.

B Mitral regurgitation
Mitral regurgitation is incorrect. Whilst mitral regurgitation produces a systolic murmur and may produce symptoms/signs of left ventricular failure as a consequence, a mitral regurgitation murmur usually has the characteristic pan-systolic mumur loudest at the cardiac apex. In addition to the soft ejection systolic murmur loudest at the right second intercostal space, the presence of syncope and angina is more closely associated with aortic stenosis. Two confounders exist in the elderly the more high frequency components of aortic stenosis may be heard best at the apex, the so called Gallavardin phenomenon and the components of the murmur may be softened in situations where cardiac output is reduced. An echocardiogram may be sought to differentiate these two diagnoses.

D Cardiac arrhythmias
Cardiac arrhythmias is incorrect. Cardiac arrhythmias can be the aetiology of syncope however given the presence of angina, left ventricular failure and an ejection systolic murmur, the diagnosis of aortic stenosis is most likely.

E Chronic kidney disease
Chronic kidney disease is incorrect. The patient has an elevated serum Creatinine (185 μmol/litre) however the triad of angina, left ventricular failure and syncope is classical with respect to aortic stenosis.

A 62-year-old man presents to the clinic with increasing shortness of breath. He has a history of smoking 10 cigarettes per day and hypertension for which he takes ramipril 10 mg daily. On examination his BP is 152/87 mmHg, his pulse is 75 bpm and there is reversed splitting of the second heart sound. There are no signs of cardiac failure. The table below contains the investigation results.

B Left bundle-branch block
Reversed splitting of the second heart sound occurs when the sound from the closure of the pulmonary valve occurs prior to that from the closure of the aortic valve. Causes include: aortic stenosis, left bundle-branch block and hypertrophic obstructive cardiomyopathy. Of these options, left bundle-
branch block is the correct choice.

A Atrial septal defect
Atrial septal defect is incorrect. Fixed splitting of the second heart sound where aortic valve closure occurs before the pulmonary, and which doesn’t vary with inspiration, occurs with an atrial or ventricular septal defect. The presenting case details reversed splitting of the second heart sound and of the options available left bundle-branch block is the most likely diagnosis.

C Mitral regurgitation
Mitral regurgitation is incorrect. Mitral regurgitation would give rise to a pan-systolic murmur loudest at the cardiac apex rather than splitting of the heart sounds. Patients may present with shortness of breath or left ventricular failure in severe cases.

D Right bundle-branch block
Right bundle-branch block is incorrect. A reversed splitting of the second heart sound may be associated with left bundle- branch block rather than right. Right bundle-branch block (delayed electrical activation of the right ventricle) may cause delayed pulmonary valve close and cause a subsequent wide physiological splitting of the second heart sound.

E Ventricular septal defect
Ventricular septal defect is incorrect. A ventricular septal defect can result in the aortic valve closure occurs before the pulmonary, therefore causing fixed splitting of the second heart sound which doesn’t vary with inspiration.

E Left bundle-branch block
Reversed splitting of the second heart sound occurs when closure of the pulmonary valve occurs before the aortic valve. Conditions associated with reversed splitting of the second heart sound include left bundle-branch block, hypertrophic obstructive cardiomyopathy and aortic stenosis. Of the options, left bundle-branch block is the most appropriate. The ECG would show a broad QRS complex (>120ms), tall R waves in the lateral leads (I, V5-6) and deep S waves in the right precordial leads (V1-3) and usually leads to left axis deviation. A fixed splitting of the second heart sound is associated with an atrial septal or ventricular septal defect.

A Right bundle-branch block
Right bundle-branch block is incorrect. A reversed splitting of the second heart sound may be associated with left bundle- branch block rather than right. Right bundle-branch block (delayed electrical activation of the right ventricle) may cause delayed pulmonary valve close and cause a subsequent wide physiological splitting of the second heart sound.

B QT prolongation
QT prolongation is incorrect. QT prolongation is a measure of delayed ventricular repolarisation and can predispose the myocardium to early after-depolarisations and subsequent re-entrant tachycardias. It does not typically produced any cardiac murmurs.

C P mitrale
P mitrale is incorrect. P mitrale is the presence of broad notched (bifid) P waves in lead II and is a sign of left atrial enlargement, most associated with mitral stenosis. A mitral stenosis murmur would have the characteristics of an opening snap present after the second heart sound followed by a low pitched rumbling murmur lasting from early to mid diastole.

D P pulmonale
P pulmonale is incorrect. P pulmonale is the presence of peaked P waves respresenting right atrial enlargement. The principle cause is pulmonary hypertension due to chronic lung disease, tricuspid regurgitation, congenital heart disease (pulmonary stenosis, Tetralogy of Fallot), primary pulmonary
hypertension. Conditions associated with reversed splitting of the second heart sound include left bundle-branch block, hypertrophic obstructive cardiomyopathy and aortic stenosis.

A 74-year-old man presents with acute-onset palpitations to the emergency department. His electrocardiogram (ECG) shows regular tachycardia with a ventricular rate of 150. He has a history of hypertension treated with ramipril and amlodipine, but has no other significant history. He smokes
five cigars per day. On examination, his blood pressure is 110/70 mmHg; his pulse is very rapid (≥ 130 bpm). The table below contains investigation results:

B Atrial flutter
The saw-tooth pattern that is particularly well characterised in leads II, III and aVF is typical of atrial flutter with 2:1 block. It is the second most common tachyarrhythmia after atrial fibrillation, with prevalence in those aged 65-90 years being =0.5-1%. Electrical cardioversion may be attempted;
otherwise amiodarone is the drug of choice for chemical cardioversion. If cardioversion is unsuccessful, ventricular rate may be controlled with non-dihydropyridine calcium-channel blockers (e.g. verapamil, diltiazem) or cardioselective beta blockers (e.g. metoprolol).

A Idioventricular tachycardia with dissociated AV response
Idioventricular tachycardia with a dissociated AV response is incorrect. Idioventricular tachycardia with a dissociated AV response is a ventricular rhythm with a rate of 40-120 beats per minute. ‘Idioventricular’ means relating to or affecting the ventricle alone, and refers to any ectopic ventricular
arrhythmia. Idioventricular tachycardia appears similar to ventricular tachycardia with wide QRS complexes (> 0.12 s) and a regular rhythm. It can be distinguished most easily from VT in that the rate is < 120 (and usually < 100 bpm). There may or may not be AV dissociation depending on whether it
is due to ventricular escape or AV block.

C Atrial fibrillation
Atrial fibrillation is incorrect. Atrial fibrillation is the most common serious abnormal heart rhythm worldwide, affecting =2-3% of the population. There is an absence of P waves on the ECG with disorganised electrical activity and irregular R-R intervals due to irregular impulses to ventricles.

D AV nodal re-entrant tachycardia
AV nodal re-entrant tachycardia is incorrect. AV nodal re- entrant tachycardia is caused by a reentry circuit in or around the AV node. The circuit is formed by the creation of two (slow and fast) pathways to form the re-entrant circuit. The ECG will show hidden P waves (often embedded in the QRS
complexes). A pseudo r’wave may be seen in V1, and pseudo S waves may be seen in leads II, III or aVF.

E Atrioventricular (AV) re-entrant tachycardia
AV re-entrant tachycardia is incorrect. AV re-entrant tachycardia is a type of supraventricular tachycardia originating from the bundle of His. It is the most common regular supraventricular tachycardia. It is more common in women (75% of cases) than in men.

A 55-year-old man has infective endocarditis. He has refused dental work for several years and presented with night sweats and lethargy to his general practitioner. Subsequent blood cultures demonstrated bacteraemia due to infection by Streptococcus viridans. On examination he is pyrexial (37.8°C), his blood pressure is 110/70 mmHg, and pulse is 95 bpm. Finger examination reveals splinter haemorrhages. Auscultation reveals a murmur consistent with mitral regurgitation. His chest is clear. The table below contains investigation results:

A Increasing PR interval
An Increase in the PR interval suggests extension of endocarditic infection into the myocardium. This also raises the possibility of abscess formation, particularly given the duration of antibiotic treatment so far. As such, urgent surgical referral is indicated. Rupture into the pericardium is an indication for same-day surgical intervention. You may wish to refer to: Delahaye et al., Heart 2004; 90: 618-620. Other indications for urgent surgical intervention include:

• mitral regurgitation or aortic regurgitation with heart failure
• septal perforation
• valvular obstruction.

Particularly large vegetations (> 15 mm) are also an indication for surgical assessment (though not necessarily for urgent intervention).

B Systolic murmur after 10 days of antibiotics
Systolic murmur after 10 days of antibiotics is incorrect. Systolic murmur being present after antibiotic therapy may indicate vegetation or valve damage. However, urgent surgery may not be indicated.

C Persistent fever 48hrs after starting treatment
This is incorrect. Fever is a common presentation in endocarditis and generally has no bearing on the severity of the condition. The European Society of Cardiology guidelines are reference by NICE and suggest considering early surgery in patients with persistent bacteraemia or fever after seven days of appropriate treatment (assuming other sources of persistent infection excluded). This is, however, less of a clear indication than an increasing PR interval.

D Raised erythrocyte sedimentation rate ESR
Raised erythrocyte sedimentation rate ESR is incorrect. The ESR is increased in inflammatory and infective conditions, but has little value for assessment of the need for surgery.

E Mobile vegetation > 15mm in size
Mobile vegetation > 15mm in size is incorrect. The size of the vegetation does not determine surgical necessity.

C ST elevation
This man has a classical history for acute pericarditis. As such, the most likely change during this acute phase is widespread saddle-shaped ST elevation. There may be ST depression in aVR or V1. Later changes include ST segments returning to baseline and T-wave flattening, with T-wave inversion
appearing finally. Increased levels of troponins are seen in around one-third of patients with pericarditis, though this is not thought to be associated with a poor prognosis. Non-steroidal anti-inflammatory agents are the mainstay of management, and in most cases the condition is self-limiting.

A T wave inversion
T-wave inversion is incorrect. T-wave inversion may be attributed to acute right ventricular strain and seen occasionally in patients with a massive pulmonary embolism -generally observed in the right-to-mid-precordial leads V1 to V4. This finding is the most specific ECG finding seen in a patient with a pulmonary embolism.

B ST depression
ST depression is incorrect. ST depression would be present in coronary ischaemia or due to digoxin use.

D T wave flattening
T-wave flattening is incorrect. T-wave flattening may be caused by ischaemia, emphysema, pericardial effusion, cardiomyopathy or myocarditis.

E Long QT interval
Long QT interval is incorrect. A Long QT interval may be a result of medications such as hydroxychloroquine, macrolides, quinine or erythromycin. Alternatively, it may be a congenital, inherited or acquired heart condition with delayed repolarisation of the heart after a heartbeat. The risk of torsades de pointes is increased.

C Hypertrophic obstructive cardiomyopathy (HOCM)
HOCM may follow an autosomal dominant inheritance pattern, and the symptoms described in his father are suggestive of obstruction of the left ventricular outflow tract leading to the development of angina. Also, the syncope may have been due to ventricular arrhythmias in the months preceding his death. Echocardiographic screening for HOCM should be considered for other surviving relatives.

A Congenital long QT syndrome
Congenital long QT syndrome is incorrect. Congenital long QT syndrome is a rare congenital and inherited or acquired heart condition in which delayed repolarisation of the heart after a heartbeat increases the risk of episodes of torsades de pointes.

B Brugada syndrome
Brugada syndrome is incorrect. Brugada syndrome is identified by sudden death associated with one of several electrocardiogram (ECG) patterns characterised by incomplete right bundle-branch block and ST-segment elevations in anterior precordial leads.

D Accelerated atherosclerosis
Accelerated atherosclerosis is incorrect. There is no reason to suspect a diagnosis of accelerated atherosclerosis. Given this patient’s age, (24), lack of a history of smoking, cocaine abuse or congenital dyslipidaemia, accelerated atherosclerosis is extremely unlikely.

E Wolff-Parkinson-White syndrome (WPW)
Wolff-Parkinson-White syndrome (WPW) is incorrect. WPW is caused by an abnormal accessory electrical conduction pathway between atria and ventricles. Electrical signals traveling down this abnormal pathway (known as the ‘bundle of Kent’) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an ‘atrioventricular re-entrant
tachycardia.

A 17-year-old boy is screened for hypertrophic obstructive cardiomyopathy (HOCM) in a cardiology clinic. His father died suddenly after suffering a cardiac arrest playing football 3 months earlier. The post mortem suggested a diagnosis of HOCM. On examination, his blood pressure is 142/84 mmHg and his pulse is 72 bpm. He is not in cardiac failure, and you suspect there is a double apex beat.
Investigations reveal:

B Septal wall thickness greater than 3 cm
Studies have shown that a septal wall thickness greater than 3 cm is associated with a poorer prognosis and increased risk of sudden death in HOCM.

A Double apex beat
Double apex beat is incorrect. A double apex beat is found in HOCM due to cardiomyopathy. It is not related to the prognosis.

C Aortic valve gradient of 40 mmHg
Aortic valve gradient of 40 mmHg is incorrect. An increased aortic valve gradient is associated more with a risk of angina and syncope.

D Short periods of atrial fibrillation (AF) on a 72-hour Holter monitor
Short periods of atrial fibrillation (AF) on a 72-hour Holter monitor is incorrect. A thick septal wall may be related to an increased risk of ventricular arrhythmias in HOCM. However, arrhythmias such as short periods of AF are not associated with a worse prognosis.

E Short runs of supraventricular tachycardia (SVT) on a 72-hour Holter monitor
Short runs of supraventricular tachycardia (SVT) on a 72-hour Holter monitor is incorrect. A thick septal wall may be related to an increased risk of ventricular arrhythmias in HOCM. However, arrhythmias such as short periods of SVT are not associated with a worse prognosis.

A 31-year-old woman presents to a clinic with increasing shortness of breath on exercise =6 months after the birth of her first child. She feels tired continually and even came close to passing out when she ran for a bus recently. She has no history of note, and her only medication is the combined oral
contraceptive pill. On examination, her blood pressure is 148/81 mmHg, and her pulse is 82 bpm and regular. There is a systolic murmur on auscultation of the heart, but the chest is clear. Her body mass index is 23 kg/m3.
The table below contains investigation results:

B Doppler echocardiography
This woman has a history that is entirely consistent with primary pulmonary hypertension, which is known to be more common in young women, and the first presentation often occurs after birth of an infant. She is of normal weight and previously fit and well, and we are given no history of deep
venous thrombosis that might point to chronic pulmonary emboli. Management involves confirmation of the diagnosis. Doppler echocardiography is the initial investigation of choice as long as the jet associated with tricuspid regurgitation can be visualised adequately.

A Trial of salbutamol
Trial of salbutamol is incorrect. Trial of salbutamol would be used in cases of bronchospasm, but would not be useful in pulmonary hypertension. Medical and surgical options for patients with primary pulmonary hypertension are anticoagulation, vasodilators and transplantation. Calcium-channel antagonists are the oral drugs of choice for the treatment of patients with New York Heart Association Class Il disease. These agents (in particular, dihydropyridine compounds) have beneficial effects on haemodynamics and right ventricular function, and possibly increase the chance of survival. Epoprostenol is administered by intravenous infusion, and studies have demonstrated short- and long-term improvements in symptoms, haemodynamics and survival.

C Computed tomography (CT) pulmonary angiogram
CT pulmonary angiogram is incorrect. CT pulmonary angiogram may be useful if chronic/multiple pulmonary emboli are suspected.

D Right heart catheterisation
Right heart catheterisation is incorrect. If echocardiography is technically difficult, such as in the obese or those with a history of chronic obstructive pulmonary disease, then right heart catheterisation may be the best way to measure
pulmonary arterial pressure.

E Bilateral venogram
Bilateral venogram is incorrect. Bilateral venogram of the lower limbs to show evidence of deep-vein thrombosis may suggest pulmonary embolism. This investigation, however, is unhelpful in pulmonary hypertension.

A Collapsing
Symptoms suggest that he is suffering from significant pulmonary hypertension. Preferential blood flow through the low-resistance pulmonary circulation via a patent ductus arteriosus (PDA) is leading to a collapsing peripheral pulse. He is likely to be at an increased risk of pulmonary haemorrhage, periods of severe hypoxia, and respiratory tract infection. Once pulmonary hypertension is established, it is
thought that surgical repair will be ineffective. If intraoperative occlusion does not reduce pulmonary
pressures and increase aortic diastolic pressure in particular, then the PDA should not be closed.

B Jerky
Jerky is incorrect. A Jerky (‘bisferiens’) pulse refers to a collapse of the pulse followed by a secondary rise. A jerky pulse may be present in hypertrophic cardiomyopathy.

C Slow rising
Slow rising is incorrect. A Slow rising pulse is also known as pulsus tardus et parvus. It is a sign in which, upon palpation, the pulse is weak/small and late relative to its expected characteristics. It is seen in aortic valve stenosis.

D Dicrotic
Dicrotic is incorrect. A Dicrotic pulse is characterised by a percussion wave in systole and a prominent dicrotic wave in diastole. Conditions associated with low cardiac output and high systemic vascular resistance can produce a dicrotic pulse. Moreover, conditions associated with low systemic
vascular resistance and a compliant aorta (e.g. sepsis) can also produce a dicrotic pulse, though the mechanism is understood incompletely.

E Thready
Thready is incorrect. A Thready pulse is difficult to feel or is obliterated readily with slight pressure. This may be found in cases of cardiogenic shock and indicates a life-threatening condition.

A 46-year-old man presents to the emergency department =2 hours after the onset of very rapid palpitations that have caused him to feel very faint and lightheaded. He has no history of note, though he admits to having consumed a substantial quantity of alcohol at a friend’s wedding the previous evening. On examination, his blood pressure is 105/60 mmHg and his pulse is 130 bpm (which suggests atrial fibrillation (AF)). He has no heart murmurs and his chest is clear. He is given an injection of low molecular-weight heparin.
The table below contains investigation results:

E Flecainide
In a structurally normal heart, where there is no indication of acute ischaemia, flecainide can be used to achieve chemical cardioversion. Alternative agents include propafenone and sotalol.

A Digoxin
Digoxin is incorrect. Digoxin rarely stops AF. You may wish to refer to the article by Falk et al., Ann Intern Med. 1987; 106: 503-506.

B Esmolol
Esmolol is incorrect. Esmolol, similar to digoxin, rarely stops AF

C Amiodarone
Amiodarone is incorrect. In patients with significant left ventricular hypertrophy, amiodarone is the first choice usually. We are given no indication, (especially given the normal ECHO), that LVH is present here. In patients with significant ischaemic heart disease, sotalol is the first-line agent usually. If he was subject to significant deterioration of ventricular rate or blood pressure, then progress to electrical
cardioversion would be appropriate.

D Adenosine
Adenosine is incorrect. Adenosine will slow down the heart rate in supraventricular rhythms to allow identification of fast AF. However, it will not revert rhythm to sinus rhythm, and is short-acting.

A 54-year-old man suffers an anterior myocardial infarction and is stented. He initially recovers, but on day 3 he suffers a further episode of chest pain and his blood pressure and urine output drop. On examination his BP is 100/60 mmHg, with a pulse of 90 bpm. He does not appear to be in left
ventricular failure. He is transferred to the high dependency unit where a Swann Ganz catheter is inserted. The table below contains the investigation results:

B Right ventricular failure
Typically, high right atrial pressure and low left atrial pressure are seen with a right ventricular infarct. This may be a new area of infarction, or the original area of infarct may have been the right ventricle, with misinterpretation of V1-V4 as an anteroseptal infarct rather than a right ventricular infarct.
Careful monitoring of fluids is the key to management of right ventricular infarction. Inadequate fluid replacement can exacerbate hypotension and renal impairment; excess fluid can exacerbate poor right ventricular function.

A Acute left ventricular failure
Acute left ventricular failure is incorrect. Acute left ventricular failure would be associated with high left atrial pressure.

C Cardiac tamponade
Cardiac tamponade is incorrect. Cardiac tamponade would be associated with raised right and left atrial pressure. This may result from bleeding into the pericardium.

D Pericarditis
Pericarditis is incorrect. Pericarditis would be associated with high right and left atrial pressures if it is constrictive.

E Mitral valve rupture
Mitral valve rupture is incorrect. With a mitral valve rupture, high left atrial pressure would be expected.

A 62-year-old man is assessed in a cardiovascular unit for angina symptoms. He has been suffering increasing chest pain over the past 3 months. Currently, he can walk only =35- 45 metres on the flat before he starts to suffer pain. On examination, he has a blood pressure of 144/82 mmHg and a
pulse of 74 bpm. There are no murmurs and his chest is clear.

Investigations reveal:

A Aspirin
Calcium antagonists, nitrates and potassium-channel activators have not been shown to affect the risk of future cardiovascular events. However, aspirin has been shown to reduce the risk of events across the spectrum of major adverse cardiac events (stroke, myocardial infarction and sudden cardiac death). Several studies have shown relative risk reductions of <50% for aspirin versus placebo. The CURE
trial added clopidogrel to aspirin and demonstrated a further reduction in the risk of ischaemic cardiovascular events at the expense of an increased risk of bleeding events.

B Diltiazem
Diltiazem is a non-dihydropyridine calcium-channel blocker. This subclass presents more negative chronotropic and inotropic effects than the dihydropyridine subclass. Also, diltiazem induces a significant reduction of atrioventricular conduction rate. Therefore, it is useful for acute and chronic
treatment as well as for the prevention of atrial arrhythmias. Diltiazem is also an effective and safe antihypertensive agent. It also reduces the frequency of angina episodes and increases exercise tolerance. The extended-release formulation of diltiazem allows once-daily administration,
thereby optimising antihypertensive and antianginal therapies.

C GTN
GTN is effective for rapid relief of angina symptoms by vasodilatation.

D Isosorbide mononitrate
Isosorbide mononitrate is a nitrate and relieves anginal symptoms by coronary vasodilatation.

E Nicorandil
Nicorandil is a potassium-channel activator. It induces dilatation of coronary arteries in patients with ischaemic heart disease.

E P2Y12 inhibitor
P2Y12 is an adenosine diphosphate chemoreceptor on platelet surfaces that is inhibited irreversibly by clopidogrel.

A Cyclo-oxygenase (COX) inhibitor
Cyclo-oxygenase (COX) inhibitor is incorrect. Aspirin is a COX inhibitor. COX (also known as prostaglandin endoperoxide synthase) is an enzyme responsible for prostanoid formation, including thromboxane and prostaglandins (e.g. prostacyclin). COX inhibition can provide relief from the symptoms of inflammation and pain.

B 2b3a inhibitor
2b3a inhibitors is incorrect. Agents such as tirofiban are 2b3a inhibitors used in angioplasty. They work by preventing platelet aggregation and thrombus formation.

C Phosphodiesterase inhibitor
Phosphodiesterase inhibitor is incorrect. Phosphodiesterase-5 inhibitors are used in the treatment of erectile dysfunction, having been a target for angina treatment originally. Another member of this class, ticlopidine, is associated with a significant risk of neutropaenia. The latter occurs with significantly lower incidence (=1 in 2000) in patients taking clopidogrel.

D Potassium channel activator
Potassium channel activator is incorrect. Nicorandil is a potassium-channel activator. It induces dilatation of coronary arteries in patients with ischaemic heart disease, so is used commonly to treat angina. Other potassium-channel activators include diazoxide, minoxidil and retigabine.

A ST-segment elevation in leads II, III and aVF with Q waves and T wave inversion in these leads
Usually right ventricular myocardial infarction occurs in association with an inferior-wall, left ventricular infarction, as revealed by an ECG.

B Occlusion of the left coronary artery
Occlusion of the left coronary artery is incorrect. There is a right coronary occlusion in this scenario. Therefore, occlusion of the left coronary artery is incorrect. Left main coronary artery occlusion will produce ECG findings of widespread horizontal ST depression, most prominent in leads I, II and
V4-6; ST elevation in aVR ≥ 1 mm and ST elevation in aVR >V1.

C Marked pulmonary vascular congestion
Marked pulmonary vascular congestion is incorrect. Characteristic clinical features include low cardiac-output syndrome with jugular venous distension, but no pulmonary vascular congestion. Therefore, marked pulmonary vascular congestion is incorrect.

D A rise in systolic blood pressure
A rise in systolic blood pressure is incorrect. As there is a low cardiac-output state; the systolic blood pressure will be low. Therefore, a rise in systolic blood pressure is incorrect.

E Absent Kussmaul’s sign
Absent Kussmaul’s sign is incorrect. Kussmaul’s sign (increased jugular venous distension with inspiration) may be evident. Therefore, absent Kussmaul’s sign is incorrect.

D Reassurance
The clinical scenario is of a young women (29 years old) who is 23 weeks pregnant with her first child and is complaining of palpitations that are self-terminating usually after 20-30 minutes but are occurring frequently 2-3 times/week. She has a history of SVT (diagnosed 10 years ago); hence the most likely cause is further episodes of SVT. Episodes of supraventricular tachycardias are not uncommon in pregnancy. Patients with a history of SVT may be more likely to experience episodes in pregnancy, and this may be related to increases in the resting heart rate, or a tendency to increased ectopic beats. For the vast majority of patients chronic therapy should be avoided, and patients are encouraged to use conservative measures (such as the Valsalva manoeuvre) to terminate their palpitations.

A 72 h holter monitor
72-hr. holter monitor is incorrect. Holter monitoring may help to capture an episode of SVT when it occurs but would not add anything to the management of this patient given the previous history of SVT and the fact that conservative management is the default option.

B Electrophysiological testing
Electrophysiological testing is incorrect. These are pre-cursor to radiofrequency ablation (RFA) of the abnormal focus of activity. During pregnancy, RFA would be considered for resistant arrhythmias not responsive to appropriate drug therapy.

C Thyroid function testing
Thyroid function testing is incorrect. Given the past medical history and other signs of thyrotoxicosis apart from tachycardia being absent, thyrotoxicosis is very unlikely.

E Start her on metoprolol
Start her on metoprolol is incorrect. Metoprolol is only considered in the event that events of PSVT become more frequent, symptomatic, and don’t respond to non-drug based interventions.

A 70-year-old man presents via ambulance after collapsing in the local shopping centre. On examination in the Emergency Department, he is drowsy. His BP is recorded at 105/60 mmHg, he has a broad complex tachycardia on the monitor consistent with ventricular tachycardia (VT) at a rate of > 200 bpm. He has a history of heart failure. There is pulmonary oedema on auscultation of the chest. ECG confirmed VT. The table below contains the results of blood gas analyses:

You elect to give him an antiarrhythmic.

E Verapamil
The relative hypoxia suggests that this patient has ischaemic VT and he has a history of heart failure. As such verapamil is contraindicated because it may have further negative impact on left ventricular function and drive circulatory collapse.

A Adenosine
Adenosine is incorrect. Adenosine is ineffective in VT but does have a role in cardioverting SVT with abberant conduction, hence it can be used as a way to differentiate between the two.

B Amiodarone
Amiodarone is incorrect. Amiodarone is the drug of choice for the treatment of haemodynamically stable VT.

C Bisoprolol
Bisoprolol is incorrect. While it would be of limited value in this scenario and likely to exacerbate symptoms it would not be contraindicated.

D Metoprolol
Metoprolol is incorrect. Metoprolol is also relatively contraindicated versus the amiodarone, but doesn’t carry the absolute contraindication for verapamil. It is used as long- term prophylaxis against VT associated with increased sympathetic outflow.

E Ventriculoatrial dissociation in any of the 12 leads
The clinical scenario is of an elderly gentleman (61 years old) with central crushing chest pain radiating to the left arm for the past 30 minutes. This history is typical for a cardiac event and the most likely diagnosis is myocardial infarction. The chest pain is associated with very rapid palpitations and a
feeling of light-headedness. On examination the B.P is low = 90/60 mmHg and pulse is rapid (>150 bpm). This indicates likely VT secondary to the myocardial infarction (arrhythmias are a common complication of MI and can be the presenting feature in some patients). The finding on ECG that would be most consistent with a diagnosis of ventricular tachycardia (VT) would be ventriculoatrial dissociation in any of the 12 leads.

A Heart rate > 180 bpm
Heart rate > 180 bpm is incorrect. This falls into the range consistent with VT but is not specific for VT. It can be seen in other tachyarrhythmias as well as PSVT (paroxysmal supraventricular tachycardia) and others.

B Left bundle-branch block
Left bundle-branch block is incorrect. This may be long standing, and not necessarily indicative of ventricular tachycardia (there is still potential for it to be PSVT with aberrant conduction).

C Right bundle-branch block
Right bundle-branch block is incorrect. RBBB may also be long standing and not necessarily indicative of underlying ventricular tachycardia. A supraventricular tachycardia with bundle-branch block also presents as a broad complex tachycardia on ECG and at times may be difficult to differentiate from VT. Also, RBBB may be seen in a proportion of normal patients with no cardiac symptoms of problems.
LBBB however is always pathological and a new onset LBBB in a symptomatic patient should be considered and managed as an acute MI.

D RS duration > 80 milliseconds in any precordial lead
RS duration >80 milliseconds in any precordial lead is incorrect. RS duration >100 ms is consistent with a diagnosis of ventricular tachycardia.
According To Brugada Et Al: VT is predicted by:
1. The absence of RS complexes in the precordial leads
2. RS duration >100 ms in any precordial leads
3. Ventriculoatrial dissociation in any of 12 leads
4. Certain QRS morphologies, such as QR or QS in V6.
According To Vereckei Et Al: VT is predicted by:
1. Presence of an initial R wave in aVR
2. Width of an initial r or q wave > 40 ms in aVR
3. Notching on the initial downstroke of a predominantly
negative QRS complex in aVR
4. Ventricular activation-velocity ratio (Vi/Vt) less than or
equal to 1.

A Systolic blood pressure 80 mmHg
The clinical scenario is of a woman with a massive pulmonary embolism, and persistent hypotension despite fluid bolus suggests significantly reduced ventricular filling pressure and is an indication for thrombolysis. Where the patient is in a cardiothoracic surgical centre, embolectomy could also be
considered.

B Pulse 95 beats per minute
Pulse 95 beats per minute is incorrect. This is not an indication of thrombolysis in cases of pulmonary embolism. Tachycardia (pulse >100 bpm) is a common sign found in patients with PE and does not determine therapy unless associated with haemodynamic instability.

C O2 saturation 93% on 10 litres 02
02 saturation 93% on 10 liters O2 is incorrect. This indicates hypoxia due to ventilation perfusion mismatch in case of PE. Hypoxia is commonly seen in patients with PE and is managed with oxygen. It is not an indication for thrombolysis.

D Underlying malignancy
Underlying malignancy is incorrect. This predisposes this patient for DVT/PE but does not have any influence on the decision for thrombolytic therapy; Presence of malignancy does of course impact on the duration of anti-coagulation.

E S1 Q3 T3 on ECG
S1 Q3 T3 on ECG is incorrect. This indicates a deep S-wave in lead I, Q-wave in lead III along with T-wave inversion in lead III. This pattern indicated right ventricular strain and may be seen in patients with PE. This ECG finding does not form an indication for thrombolysis unless it is accompanied by severe
right-sided heart failure and blood pressure does not respond
to fluid loading.

A Amiodarone
The clinical scenario is of a 34-years old man with resistant hypertension (on multiple antihypertensive medications – ramipril, indapamide and amlodipine).The patient says that his G.P arranged a USG scan which shows a mass above the left kidney. This is most likely a Pheochromocytoma. It’s most
likely that the VT is related to severe hypertensive heart disease as a result of the pheochromocytoma.
Amiodarone is the most effective antiarrhythmic agent for suppressing VT, an effect that has clearly been demonstrated in multiple clinical trials. Amiodarone is also used to treat VT in postmyocardial infarction and congestive heart failure patients. While amiodarone has never been shown to reduce
overall mortality, its use is not associated with an increase in mortality due to proarrhythmia (as is the case with class IC antiarrhythmic drugs).

B Metoprolol
Metoprolol is incorrect. Beta blockers (e.g. metoprolol 50- 200mg daily, carvedilol 12.5-50mg daily) and CCB’s (e.g. verapamil) are used as the first line agents in the management of VT to prevent recurrence. Beta blockers are used based on the evidence of reducing ventricular ectopy and tachyarrhythmias in cardiac conditions. These drugs are attractive since their side effect profiles are mild in comparison to antiarrhythmic agents; however beta blockade alone should be avoided in pheochromocytoma because of the risk of exacerbating hypertension (due to unopposed alpha adrenergic activity).

C Phenoxybenzamine
Phenoxybenzamine is incorrect. This is an irreversible alpha blocker and is used as the first line agent for treatment of pheochromocytoma; however, alpha blockers are not used in the treatment of VT and would not be helpful in this situation.

D Sotalol
Sotalol is incorrect. This is a class III antiarrhythmic agent (beta blockers) and is one of the agents that can be used for treatment of VT (along with amiodarone and mexiletine); however sotalol is a beta blocker and beta blockade alone should be avoided in pheochromocytoma because of the risk of exacerbating hypertension (due to unopposed alpha adrenergic activity).

E Verapamil
Verapamil is incorrect. Although idiopathic VT often responds to verapamil, it can be lethal when given to treat VT in a patient with left ventricular dysfunction, leading to profound loss of blood pressure, circulatory arrest and death. Therefore, verapamil or any other calcium channel blockers (CCB) is contraindicated in any patient with wide-complex tachycardia of uncertain etiology.

A 62-year-old man with a history of previous rheumatic fever is beginning week 2 of his treatment for infective endocarditis. This was diagnosed on blood culture and vegetations were confirmed on the mitral valve. On examination he is pyrexial at 37.8°C, and he has a murmur consistent with mitral regurgitation. There are no signs of left ventricular failure, although there is mild ankle swelling. His
blood pressure is 134/82 mmHg; his pulse is 50 beats per minute and regular.
Investigations:

E PR prolongation
This patient has endocarditis, and PR prolongation on ECG in a patient with IE suggests the presence of paravalvular extension of the infection (paravalvular abscess/myocardial abscess), which is an indication of surgery in case of infective endocarditis; Early surgery (i.e. during initial hospitalization and before completion of a full course of antibiotics) is indicated in patients with left-sided native valve IE and one or more of the following features:
1. IE-associated valve dysfunction (usually aortic or mitral regurgitation) causing symptoms or signs of heart failure
2. Paravalvular extension of infection with development of annular or aortic abscess, destructive penetrating lesion, and/or heart block
3. Infection due to a difficult-to-treat pathogen such as fungal or other highly resistant organisms (e.g. Vancomycin-resistant Enterococcus (VRE), Brucella endocarditis or multidrug-resistant Gram-negative bacilli)
4. Persistent infection (manifested as persistent bacteremia or fever lasting >10 days and provided other sites of infection and causes of fever have been excluded) after the start of appropriate antibiotic therapy
5. Persistent unexplained fever (>10 days) in culture-negative native valve endocarditis
6. Patients presenting with recurrent emboli and persistent or enlarging vegetations despite appropriate antibiotic therapy
7. Patients with severe valve regurgitation and mobile vegetations >10 mm, we suggest early surgery.
8. The presence of mobile vegetations >10 mm, particularly when involving the anterior mitral leaflet of the mitral valve and associated with other relative indications for surgery

• Partially dehisced unstable prosthetic valve
• Staphylococcus aureus prosthetic valve endocarditis with an intracardiac complication (e.g. paravalvular/myocardial abscess)
• Relapse of prosthetic valve endocarditis after optimal antimicrobial therapy
• Poorly responsive Staph aureus endocarditis involving the aortic or mitral valve