The Cardiology Block

Cases 9–18 · 13,852 words · Download this chapter as PDF

This block covers the cardiology teaching of both internal medicine courses. The first course supplies cases 9 and 14; the second course supplies cases 15 and 18, which extend the block into valvular, pericardial and myocardial disease.

Hypertensive urgency and emergency is deliberately held back for the seminar case in Part II, so that Case 14 can concentrate on assessment of the newly diagnosed patient. Pulmonary thromboembolism is Seminar 11, and the four pillars of heart failure therapy are set out in Case 12 — both are cross-referenced from the second-course cases rather than duplicated.

System Opener · The Cardiovascular History and Examination

The history

The five cardinal symptoms

Risk and background

• Smoking, diabetes mellitus, hypertension, dyslipidaemia, obesity, physical inactivity, chronic kidney disease, and premature cardiovascular disease in a first-degree relative — before 55 in men and 65 in women.

• Rheumatic history: recurrent sore throats in childhood, a murmur heard at school or before marriage, previous rheumatic fever, and whether monthly penicillin injections were ever given and for how long.

• Family history of sudden death, cardiomyopathy or inherited arrhythmia, and consanguinity where relevant.

• Full drug history including over-the-counter and herbal preparations, and previous procedures — angiography, stents, bypass grafting, valve surgery, pacemakers.

The examination

General and peripheral

• Breathlessness at rest, cachexia, malar flush, marfanoid habitus, central cyanosis, and the observation chart.

• Hands: clubbing (cyanotic congenital heart disease, infective endocarditis), splinter haemorrhages, Osler nodes, Janeway lesions, tendon xanthomata, tar staining, peripheral cyanosis.

• Pulse: rate, rhythm and character. A slow-rising pulse indicates aortic stenosis; a collapsing pulse aortic regurgitation; pulsus alternans severe left ventricular dysfunction. Check for radio-radial and radio-femoral delay — the latter is the sign of coarctation, and it is missed by not looking for it.

• Blood pressure in both arms, with a postural reading. A wide pulse pressure suggests aortic regurgitation, a narrow one severe aortic stenosis.

The jugular venous pressure

Students lose more marks here than anywhere else in the cardiovascular examination. Position the patient at 45 degrees, turn the head slightly away, and look across rather than at the neck.

The praecordium

• Inspect for a midline sternotomy scar, a left lateral thoracotomy scar (the old closed mitral valvotomy), a pacemaker or defibrillator box, and visible pulsation.

• Palpate the apex beat — its position, and then its character. A tapping apex is a palpable first heart sound and means mitral stenosis. A heaving, sustained apex is pressure loading: aortic stenosis or hypertension. A thrusting, displaced apex is volume loading: mitral or aortic regurgitation. Feel for thrills and for a left parasternal heave of right ventricular hypertrophy.

• Auscultate all four areas with diaphragm and bell. Identify the first and second sounds by timing against the carotid pulse before attempting to describe anything else. Listen for added sounds — a third sound, a fourth sound, an opening snap, an ejection click, a metallic prosthetic click, a pericardial rub.

• Finish at the lung bases, the liver (pulsatile in tricuspid regurgitation), for ascites, at the sacrum and ankles, at all peripheral pulses, and with the fundi and a urine dipstick where endocarditis is possible.

Murmurs — the table to know

The rule that saves you in an examination: right-sided murmurs are louder on inspiration, left-sided murmurs on expiration. And a murmur you cannot classify should still be described accurately — timing, site, radiation and what it does with respiration — because an accurate description scores more than a confident wrong label.

Case 9 · Acute Rheumatic Fever

1. Focused History

• The preceding infection. A sore throat two to four weeks earlier — this latent period is what makes the connection easy to miss, because the throat has long recovered. Ask whether antibiotics were given and completed.

• Characterise the arthritis. Rheumatic arthritis is migratory, affects large joints asymmetrically, is exquisitely painful relative to the swelling, and settles in each joint within days. It responds dramatically to anti-inflammatory drugs — so dramatically that failure to respond should make you question the diagnosis.

• Symptoms of carditis: breathlessness, orthopnoea, reduced exercise tolerance, chest pain, palpitations.

• Symptoms of chorea: clumsiness, dropping objects, deteriorating handwriting, emotional lability and behavioural change. Chorea may appear months after the infection, long after everything else has settled, and parents often report it as naughtiness.

• Previous episodes and prophylaxis. A previous attack is the strongest risk factor for another, and each recurrence damages the valves further. Ask specifically whether monthly injections were given and when they stopped.

• Household crowding, access to healthcare, and other affected family members.

2. Physical Examination

• Fever and a tachycardia out of proportion to the fever, persisting during sleep.

• Arthritis — hot, swollen, extremely tender large joints, asymmetric and migratory. Document which joints and when, because the migration itself is diagnostic.

• Carditis — the feature that determines the patient’s future. Listen for a new or changed murmur: mitral regurgitation is the commonest, then aortic regurgitation. Listen for a pericardial rub and a third sound, and look for signs of heart failure. A resting tachycardia may be the only sign.

• Erythema marginatum — pink macules with a clear centre and a serpiginous margin, on the trunk and proximal limbs, sparing the face, evanescent and changing position over hours. Easily missed on darker skin, so look in good light.

• Subcutaneous nodules — firm, painless, mobile, over extensor surfaces and the occiput. Uncommon but strongly associated with severe carditis.

• Sydenham chorea — purposeless jerky movements, hypotonia, the milkmaid grip (irregular squeezing of the examiner’s fingers) and the darting tongue that cannot be held protruded.

3. Diagnosis: The Revised Jones Criteria

• Two exceptions: chorea alone, and indolent carditis, are sufficient without evidence of preceding streptococcal infection, because both appear so long after the throat infection that serology may already have fallen.

• A recurrence in a patient with established rheumatic heart disease may be diagnosed on three minor criteria with evidence of streptococcal infection.

4. Differential Diagnosis

5. Investigations

• Evidence of streptococcal infection: throat swab culture and rapid antigen test — often negative by now — and antistreptolysin O and anti-DNase B titres, ideally paired two weeks apart to demonstrate a rise. A single raised titre is weaker evidence than a rising one.

• Inflammatory markers: erythrocyte sedimentation rate and C-reactive protein, used both for diagnosis and to follow the course.

• Electrocardiogram — a prolonged PR interval is a minor criterion. Higher grades of block can occur and are usually transient.

• Echocardiography in every suspected case, even when no murmur is audible. Subclinical carditis is a major criterion and changes both the diagnosis and the duration of prophylaxis. This is the single most important investigation.

• Blood cultures to exclude endocarditis, complete blood count, and joint aspiration if a single joint is involved.

• Chest radiograph if there is any suspicion of cardiac failure.

6. Management

Treat the streptococcus

• Benzathine benzylpenicillin as a single intramuscular dose, or oral penicillin V for ten days. Give it even when the throat swab is negative — you are eradicating carriage, not treating pharyngitis. Use a macrolide if penicillin-allergic.

Treat the inflammation

• Aspirin in anti-inflammatory doses, or naproxen, for the arthritis. The response is usually rapid and complete.

• Corticosteroids are used for severe carditis with heart failure, although the evidence that they alter long-term valve outcome is weak. Treat the heart failure itself on its merits.

• Chorea is usually self-limiting over weeks to months. Reassure the family that it is not behavioural. Carbamazepine or sodium valproate for severe or disabling movements.

• Rest during the acute illness, with gradual return to activity guided by the carditis.

7. Teaching Points and Viva Questions

• The arthritis moves; the carditis stays. The joints cause the symptoms, the heart causes the disease.

• Echocardiography in every suspected case — subclinical carditis is invisible at the bedside and alters the prophylaxis by decades.

• An unexplained resting tachycardia during sleep is carditis until proved otherwise.

• Aspirate any single hot joint. Septic arthritis destroys a joint in days and does not wait for serology.

• The most valuable thing you can do for this boy is not what you prescribe today, but ensuring he receives an injection every four weeks for the next ten years.

Questions you should be able to answer:

• State the Jones criteria and explain why they differ between populations.

• Why can chorea be diagnosed without evidence of streptococcal infection?

• What are the two most useful investigations here, and why?

• How long will this boy need prophylaxis, and on what does that depend?

• His antistreptolysin O titre is normal. Does that exclude the diagnosis?

Case 10 · Rheumatic Mitral Stenosis

1. Focused History

• Functional class — quantify in stairs or metres, and establish over what period it changed. Deterioration over weeks usually means a new arrhythmia rather than progression of the valve lesion.

• Orthopnoea, paroxysmal nocturnal dyspnoea and haemoptysis. Haemoptysis in mitral stenosis arises from raised pulmonary venous pressure and rupture of dilated bronchial veins.

• Palpitations and their relation to the deterioration. Atrial fibrillation is the event that unmasks mitral stenosis, because losing atrial contraction and shortening diastole together collapse left ventricular filling.

• Embolic events — transient neurological symptoms, stroke, a cold painful limb, flank pain. The large fibrillating left atrium is an excellent source of thrombus.

• Compression symptoms from a dilated left atrium: hoarseness from recurrent laryngeal nerve compression, and dysphagia.

• Pregnancy plans. This is not a social question here — it is central to management, and the answer changes the timing of intervention.

• Rheumatic fever history and, specifically, when prophylaxis stopped.

2. Physical Examination

The classical signs, and what produces each

3. Differential Diagnosis

4. Investigations

• Electrocardiogram: P mitrale — a broad bifid P wave — while sinus rhythm persists, then atrial fibrillation. Right axis deviation and right ventricular hypertrophy indicate pulmonary hypertension.

• Chest radiograph — reading the film: a straightened left heart border from the enlarged left atrial appendage, a double density behind the right heart border, splaying of the carina, upper lobe blood diversion, Kerley B lines, and sometimes valve calcification. The heart is often not enlarged overall, which surprises students.

• Echocardiography is the diagnostic and grading test. It gives the valve area, the mean transmitral gradient, the pulmonary artery pressure, the left atrial size, and the presence of associated regurgitation.

• Transoesophageal echocardiography before any intervention, to exclude left atrial appendage thrombus, and to score valve morphology for suitability for balloon valvuloplasty.

• Complete blood count, thyroid function (atrial fibrillation), renal function, and natriuretic peptide where the cause of breathlessness is uncertain.

5. Management

Medical

• Rate control with a beta blocker, or digoxin in atrial fibrillation. Slowing the heart lengthens diastole and improves filling — the opposite of the instinct to treat breathlessness by increasing output.

• Anticoagulation with a vitamin K antagonist. In atrial fibrillation with rheumatic mitral stenosis, direct oral anticoagulants are contraindicated and warfarin must be used. This is one of the few remaining absolute indications for warfarin and is a favourite examination question.

• Diuretics and salt restriction for pulmonary congestion.

• Continue or restart secondary penicillin prophylaxis, and maintain dental hygiene.

Intervention

• Percutaneous balloon mitral valvuloplasty is the treatment of choice for a pliable, non-calcified valve with little regurgitation and no left atrial thrombus. It is highly effective and avoids surgery — particularly valuable in a young woman planning pregnancy.

• Surgical commissurotomy or valve replacement when the valve is calcified, when there is significant mitral regurgitation, or when thrombus is present.

• Indications: symptomatic severe stenosis; and asymptomatic severe stenosis with pulmonary hypertension, new atrial fibrillation, or a planned pregnancy.

6. Teaching Points and Viva Questions

• Mitral stenosis is a disease of diastole. Anything that shortens diastole — tachycardia, atrial fibrillation, fever, pregnancy, exercise — decompensates it.

• The interval from the second sound to the opening snap gauges severity; the loudness of the murmur does not.

• You will not hear the murmur with the diaphragm, or with the patient lying flat. Bell, left lateral, expiration.

• Warfarin, not a direct oral anticoagulant, when atrial fibrillation accompanies rheumatic mitral stenosis.

• An undisplaced apex in a breathless patient with a raised venous pressure should turn your attention to the mitral valve and the right heart.

Questions you should be able to answer:

• Explain each of the classical signs in terms of the underlying haemodynamics.

• Why does atrial fibrillation cause such abrupt deterioration in this condition?

• Why is warfarin required rather than a direct oral anticoagulant?

• Which patients are suitable for balloon valvuloplasty, and what must be excluded first?

• She becomes pregnant before any intervention. What are the risks and how would you manage her?

Case 11 · ST-Elevation Myocardial Infarction

1. Focused History — Taken While Treatment Proceeds

• The time of symptom onset. This is the single most important number in the history, because it determines the reperfusion strategy and the expected benefit. Establish it precisely, and record it.

• Characterise the pain, and ask specifically about features that suggest an alternative: tearing pain radiating to the back with maximal intensity at onset (aortic dissection), pleuritic or positional pain relieved by sitting forward (pericarditis), pain after vomiting (oesophageal rupture).

• Previous angina, infarction, angiography, stents or bypass grafting — and whether this pain is the same as before but worse.

• Whether aspirin has already been given, by the patient or by the ambulance crew.

• Cocaine or amphetamine use, particularly in a younger patient, which changes management.

• Bleeding risk and contraindications to fibrinolysis, in case primary angioplasty is not available within the time window: previous intracranial bleed, recent stroke, surgery, trauma or gastrointestinal bleeding, and anticoagulant use.

2. Physical Examination

Brief and targeted. It should not delay the electrocardiogram or reperfusion.

• Blood pressure in both arms and all peripheral pulses — a significant difference raises aortic dissection, which would make antiplatelet and anticoagulant therapy catastrophic.

• Jugular venous pressure — raised with clear lung fields in right ventricular infarction.

• Auscultation for a new murmur (mitral regurgitation from papillary muscle dysfunction, or a ventricular septal defect), a third or fourth heart sound, and a pericardial rub.

• Lung bases, to assign the Killip class, which predicts mortality directly.

3. Investigations

Localise the infarct

• Bloods: troponin (for later confirmation and infarct size), complete blood count, urea and electrolytes, glucose and glycated haemoglobin, lipid profile, coagulation screen.

• Portable chest radiograph — but never allow it to delay reperfusion. It is looking for pulmonary oedema and for a widened mediastinum.

• Echocardiography — regional wall motion abnormalities, ejection fraction, and mechanical complications. Urgently if the diagnosis is uncertain or the patient is shocked.

4. Differential Diagnosis

5. Management

Immediate, at the bedside

• Aspirin 300 mg chewed, plus a second antiplatelet agent — ticagrelor, prasugrel or clopidogrel — according to the reperfusion pathway.

• Anticoagulation as specified by the local pathway.

• Oxygen only if the saturation is below 90%. Routine oxygen in the non-hypoxic patient confers no benefit and may cause harm.

• Nitrate sublingually or by infusion for pain — withheld if the patient is hypotensive, has a right ventricular infarct, or has taken a phosphodiesterase inhibitor within 48 hours.

• Morphine with an antiemetic for pain not relieved by nitrate.

• Continuous cardiac monitoring beside a defibrillator. Ventricular fibrillation is the commonest cause of death in the first hour and is entirely treatable if witnessed and monitored.

Reperfusion — the decision that determines outcome

• Absolute contraindications to fibrinolysis: any previous intracranial haemorrhage; ischaemic stroke within 6 months; cerebral vascular malformation or tumour; major trauma, surgery or head injury within 3 weeks; gastrointestinal bleeding within a month; known bleeding disorder; suspected aortic dissection; non-compressible puncture within 24 hours.

• Right ventricular infarction — the patient is preload-dependent. Give fluid, and avoid nitrates, diuretics and opioids, all of which can precipitate profound hypotension.

Complications to anticipate

Secondary prevention — started before discharge, not at follow-up

• Dual antiplatelet therapy for 12 months, then aspirin indefinitely.

• High-intensity statin, regardless of the baseline cholesterol.

• Beta blocker and angiotensin-converting enzyme inhibitor, both started early and titrated.

• Mineralocorticoid receptor antagonist if the ejection fraction is 40% or less with heart failure or diabetes.

• Cardiac rehabilitation — as effective as several of the drugs and referred to far less often. Smoking cessation with pharmacological support. Glycaemic and blood pressure control.

• Echocardiography before discharge; reassessment of the ejection fraction at 6–12 weeks for consideration of an implantable defibrillator if it remains at 35% or less.

• Practical advice the patient will actually ask about: driving restrictions, return to work, and resumption of sexual activity.

6. Teaching Points and Viva Questions

• Electrocardiogram within ten minutes. Time is myocardium, and the clock starts at symptom onset, not at arrival.

• Reciprocal ST depression supports a true infarction and helps distinguish it from pericarditis.

• Every inferior infarct gets right-sided leads before anyone gives a nitrate.

• A new murmur three days after infarction is a mechanical complication until proved otherwise, and needs a surgeon, not a diuretic.

• Check both arms once, at the start. Thrombolysing a dissection is among the worst errors in medicine.

Questions you should be able to answer:

• Localise this infarct and name the artery.

• Primary angioplasty is 3 hours away. What do you do and why?

• The blood pressure falls to 80/50 after a nitrate in an inferior infarct. Explain what happened.

• Distinguish the electrocardiogram of pericarditis from that of infarction.

• Name the four drugs he should leave hospital taking, and the indication for each.

Case 12 · Acute Decompensated Heart Failure

1. Focused History

• Quantify the change: pillow count, distance walked, and the weight gain — which is the most sensitive marker of fluid retention and the easiest for the patient to measure at home.

• Then find the precipitant. Decompensation always has a cause, and treating the congestion without finding the cause simply returns the patient to hospital.

2. Physical Examination

• The jugular venous pressure is the single most reliable bedside sign of congestion and the one most often not attempted. Measure it, record it in centimetres, and repeat it daily.

• Displaced, thrusting apex; a third heart sound — the most specific auscultatory sign of decompensation; a functional pansystolic murmur of mitral regurgitation from ventricular dilatation.

• Bibasal crackles that do not clear with coughing, and dullness at the bases from pleural effusions.

• Tender pulsatile hepatomegaly, ascites, and pitting oedema — ankles in the ambulant patient, sacrum in the bedbound patient, which is why you must roll them.

• Assess perfusion as well as congestion: cool peripheries, narrow pulse pressure, pulsus alternans, confusion and oliguria all indicate low output.

Classify the patient in one of four boxes. It takes seconds and directs treatment better than any score.

3. Differential Diagnosis

4. Investigations

• Natriuretic peptide. Its greatest value is a negative result: a normal level in an untreated breathless patient essentially excludes heart failure as the cause.

• Electrocardiogram — atrial fibrillation, ischaemia, prior infarction, left ventricular hypertrophy, and QRS duration for later resynchronisation decisions. A completely normal tracing makes heart failure unlikely.

• Chest radiograph — reading the film: cardiomegaly with a cardiothoracic ratio above 0.5, upper lobe blood diversion, Kerley B lines, perihilar alveolar shadowing in a bat’s-wing distribution, pleural effusions, and fluid tracking into the horizontal fissure.

• Bloods: complete blood count (anaemia both causes and results from heart failure), urea, electrolytes and creatinine before and during diuresis, liver function (congestive hepatopathy), thyroid function, glucose, troponin, and iron studies — iron deficiency is common, symptomatic and treatable even without anaemia.

• Echocardiography — essential in every new case, and in decompensation of unclear cause. It gives the ejection fraction, which divides management into two entirely different pathways, and identifies valve disease and regional wall motion abnormality.

5. Management

The first hour

• Sit the patient upright. Oxygen only if hypoxic, targeting 94–98%.

• Intravenous loop diuretic — furosemide 40–80 mg, or one to two and a half times the usual home dose in a patient already taking it. Give it intravenously; gut absorption is unreliable in a congested patient.

• Nitrate infusion if the patient is hypertensive with pulmonary oedema — it reduces preload and afterload rapidly and is often more immediately effective than the diuretic.

• Continuous positive airway pressure for severe pulmonary oedema with persisting hypoxia or exhaustion. It reduces the need for intubation.

• Inotropes and vasopressors only for hypoperfusion, in a monitored setting with senior involvement. They are not a treatment for breathlessness.

• Treat the precipitant: rate control the atrial fibrillation, stop the non-steroidal anti-inflammatory drug, treat infection or ischaemia.

Monitoring

• Daily weight before breakfast is the best single measure of response — aim for 0.5–1 kg loss per day. Strict fluid balance, daily electrolytes and creatinine, and a repeated jugular venous pressure.

• Expect the creatinine to rise modestly during effective decongestion. A small rise is not a reason to stop diuresis in a patient who is still congested.

Before discharge

• Euvolaemic, on oral diuretic for at least 24 hours, with a written daily weight chart and an action plan telling her what to do if she gains 2 kg in three days.

• A titration plan for the four pillars, a documented medication review, and an explicit instruction to avoid non-steroidal anti-inflammatory drugs — with an alternative offered for her knee.

• Follow-up within seven days, which measurably reduces readmission. Vaccination, cardiac rehabilitation, and consideration of devices at reassessment.

6. Teaching Points and Viva Questions

• The jugular venous pressure and the daily weight will tell you more about this patient than any blood test.

• A normal natriuretic peptide in an untreated breathless patient sends you looking for another diagnosis.

• Always name the precipitant. "Heart failure" is not a complete diagnosis.

• Diuretics treat symptoms; the four pillars treat the disease.

• Oedema with a normal venous pressure is not heart failure — look at the liver, the kidneys and the albumin.

Questions you should be able to answer:

• Name the two precipitants in this history and explain the mechanism of each.

• Why give the diuretic intravenously rather than orally?

• Her creatinine rises from 90 to 120 during diuresis. What do you do?

• Which of her drugs prolong life and which only relieve symptoms?

• How does management differ if the ejection fraction is 55% rather than 30%?

Case 13 · Infective Endocarditis

1. Focused History

• Duration and tempo. A subacute course over weeks with sweats and weight loss suggests a viridans streptococcus on a damaged valve; a fulminant course over days suggests Staphylococcus aureus on a normal one.

• The predisposing lesion: rheumatic valve disease, prosthetic valve, previous endocarditis, congenital heart disease, degenerative valve disease, hypertrophic cardiomyopathy.

• The portal of entry: dental work and dental hygiene, skin infection, intravenous drug use, indwelling vascular catheters, haemodialysis, recent urological or gastrointestinal procedures, colorectal disease (which is associated with *Streptococcus gallolyticus* and warrants colonoscopy).

• Regionally important exposures: unpasteurised milk and dairy, and contact with sheep, goats or camels — Brucella and Coxiella burnetii are important causes of culture-negative endocarditis here and will be missed unless specifically requested.

• Recent antibiotics — the commonest reason blood cultures are sterile, and the reason this man has had five weeks of illness without a diagnosis.

• Embolic symptoms: transient neurological events, sudden limb pain, flank or left upper quadrant pain, sudden visual loss, and back pain suggesting spondylodiscitis.

2. Physical Examination

• Fever and a murmur together is endocarditis until proved otherwise. A new or changed murmur is the finding that matters; a longstanding unchanged murmur is much weaker evidence.

• Peripheral stigmata — uncommon now but classical: splinter haemorrhages; Osler nodes, which are painful and on the finger pulps; Janeway lesions, which are painless and on palms and soles; Roth spots on the retina; conjunctival and palatal petechiae; clubbing in longstanding disease.

• Splenomegaly, signs of heart failure, and a full neurological examination for embolic deficits.

• Examine the teeth and gums, injection sites, and any indwelling line.

• Dipstick the urine — microscopic haematuria from immune complex glomerulonephritis or renal infarction is a minor criterion and takes thirty seconds.

3. Investigations

• Serology for culture-negative causes: Brucella, Coxiella burnetii, Bartonella, Legionella, and fungal cultures. Request these early in this region rather than as a last resort.

• Echocardiography. Transthoracic first; transoesophageal if that is negative and suspicion persists, if there is a prosthetic valve, or if a complication is suspected. Look for vegetations, abscess, new valve regurgitation and prosthetic dehiscence. A negative study does not exclude the diagnosis — repeat it in 5–7 days if suspicion remains.

• Electrocardiogram, repeated daily. A new atrioventricular block means an aortic root abscess and is an indication for urgent surgical assessment. This is the single most important electrocardiographic finding in the disease.

• Complete blood count (normocytic anaemia, neutrophilia), C-reactive protein and erythrocyte sedimentation rate for trend, urea and electrolytes, liver function, urinalysis and microscopy, rheumatoid factor and complement.

• Imaging for emboli where clinically indicated: brain, abdomen, and spine. Computed tomography and nuclear imaging have a defined role in prosthetic valve disease.

The modified Duke criteria

Definite endocarditis: two major, or one major and three minor, or five minor criteria.

4. Management

• Treatment is by a team — cardiology, microbiology or infectious diseases, and cardiac surgery involved from the outset, not after complications appear.

• Empirical therapy after cultures are taken, guided by whether the valve is native or prosthetic and by local resistance patterns; then narrowed to the organism. Intravenous therapy for four to six weeks in most cases.

• Monitor for response: daily examination for a new murmur or heart failure, daily electrocardiogram for conduction change, repeat cultures to confirm clearance, and monitoring of renal function and antibiotic levels.

Prevention

• Dental hygiene and regular dental review in every patient with a predisposing lesion — of far greater value than antibiotic prophylaxis.

• Antibiotic prophylaxis before dental procedures involving gingival manipulation is now restricted to the highest-risk group: prosthetic valves, previous endocarditis, and certain congenital heart disease.

5. Teaching Points and Viva Questions

• Fever plus a murmur means blood cultures before antibiotics. The single commonest reason this diagnosis is delayed is a well-meant prescription.

• A new atrioventricular block is an aortic root abscess until proved otherwise — do a daily electrocardiogram.

• A normal transthoracic echocardiogram does not exclude endocarditis.

• In this region, culture-negative endocarditis should prompt Brucella and Q fever serology early rather than late.

• Half of the peripheral stigmata are named after people; none of them is as useful as three sets of blood cultures.

Questions you should be able to answer:

• He has already had antibiotics. How does that change your approach to the cultures?

• Apply the Duke criteria to this patient and state your level of certainty.

• The PR interval lengthens on day four. What has happened and what do you do?

• List the three broad indications for surgery.

• Which patients still receive antibiotic prophylaxis before dental work, and why was the guidance narrowed?

Case 14 · Newly Diagnosed Hypertension

1. Focused History

Establish that it is real, and how long it has been present

• Previous readings — at dental visits, pre-employment checks, pharmacies, or during a previous illness. Patients often have years of unrecognised readings.

• Any home readings, and how the device was used.

Screen for end-organ damage

• Chest pain, exertional breathlessness, orthopnoea, palpitations, transient neurological symptoms, visual disturbance, claudication, and frothy urine or nocturia.

Screen for a secondary cause

Quantify total cardiovascular risk

• Smoking, diabetes, lipids, family history of premature vascular disease, alcohol, salt intake, physical activity, and body weight. You are treating the total risk, not the number.

2. Physical Examination

• Body mass index and waist circumference; features of Cushing syndrome; radio-femoral delay; renal, carotid and femoral bruits; palpable kidneys.

• Apex beat character — a sustained, heaving apex suggests left ventricular hypertrophy. Listen for a fourth heart sound.

• Fundoscopy. Grade the retinopathy: arteriolar narrowing, arteriovenous nipping, then haemorrhages and exudates, and finally papilloedema — which changes the diagnosis to a hypertensive emergency and the timescale from months to hours.

• Peripheral pulses and a full neurological examination for evidence of previous events.

3. Investigations

• Confirm the diagnosis out of the office with ambulatory monitoring, or home readings twice daily for a week. This detects white-coat hypertension, which would otherwise commit a well man to lifelong drugs, and masked hypertension, which would otherwise be missed entirely. Out-of-office thresholds are lower than clinic thresholds.

• End-organ assessment: urinalysis and urine albumin-to-creatinine ratio, urea, electrolytes, creatinine and estimated glomerular filtration rate, and an electrocardiogram for left ventricular hypertrophy. Echocardiography if the tracing is abnormal or heart failure is suspected.

• Cardiovascular risk profile: fasting glucose or glycated haemoglobin, and a lipid profile.

• Investigate for a secondary cause if the patient is under 40, has resistant or abruptly worsening hypertension, has unprovoked hypokalaemia, or has suggestive features. Start with the aldosterone-to-renin ratio, plasma or urinary metanephrines, renal imaging, and — in this patient — a sleep study.

Be aware that guidelines differ: some define hypertension from 130/80 mmHg while others retain 140/90 mmHg. Know which your institution follows and say so when asked — the examiner is testing whether you know that a threshold is a convention, not a fact of nature.

4. Management

Lifestyle — offered to everyone, and worth more than students assume

• Weight reduction; salt below 5 g per day; a diet rich in fruit, vegetables and low-fat dairy; regular aerobic activity of at least 150 minutes weekly; alcohol reduction; and smoking cessation — which does not lower blood pressure but reduces cardiovascular risk more than most drugs.

• Treating the obstructive sleep apnoea in this man may improve his blood pressure and will certainly improve his daytime function.

Drug treatment

• When to start: immediately in grade 2 and grade 3; in grade 1 when there is established cardiovascular disease, end-organ damage, diabetes, chronic kidney disease, or high estimated risk. This patient has grade 2 hypertension with retinopathy and starts today.

• Start with two drugs, ideally in a single combination tablet. Combination therapy from the outset achieves control faster than sequential single agents and improves adherence.

• First-line combinations: an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, plus either a calcium channel blocker or a thiazide-like diuretic.

• In patients of Black African or Caribbean origin, begin with a calcium channel blocker or thiazide-like diuretic rather than a renin–angiotensin blocker.

• Beta blockers are not first line for uncomplicated hypertension; reserve them for angina, previous infarction, heart failure, rate control, or pregnancy.

• In pregnancy: labetalol, nifedipine or methyldopa. Renin–angiotensin system blockers are absolutely contraindicated.

Targets and follow-up

• Aim below 140/90 mmHg for everyone, and below 130/80 mmHg if tolerated, particularly with diabetes, chronic kidney disease or established vascular disease. Be less aggressive in the frail elderly, and check for postural drop before intensifying.

• Recheck urea, electrolytes and creatinine one to two weeks after starting a renin–angiotensin blocker or diuretic. A creatinine rise beyond about 30% or a falling potassium prompts review.

• Review monthly until controlled, then at least annually with reassessment of risk and end-organ damage.

5. Teaching Points and Viva Questions

• Do not diagnose lifelong hypertension on clinic readings alone. Confirm it outside the clinic.

• Measure it properly. Wrong cuff, unsupported arm and no rest period produce a wrong number, and everything that follows is built on it.

• Both arms once, at the first visit. Thereafter, the higher arm.

• Unprovoked hypokalaemia in a hypertensive patient means primary aldosteronism until proved otherwise.

• Snoring with daytime somnolence is not a lifestyle detail — it is a diagnosis with a treatment.

• You are treating total cardiovascular risk. Stopping the cigarettes will help this man more than any milligram adjustment.

Questions you should be able to answer:

• How would you confirm the diagnosis before committing him to treatment?

• Which secondary cause does this history point to, and how would you test for it?

• What would you start him on today, and why two drugs rather than one?

• His potassium is 3.1 mmol/L and he takes no diuretic. What now?

• At review his pressure is 158/96 on three drugs. Work through your approach.

Case 15 · Aortic Stenosis

1. Focused History

• Characterise the triad, and quantify the exercise tolerance in metres or flights of stairs against the patient’s own baseline.

• Syncope: establish that it was exertional, sudden, without warning, and with rapid complete recovery — the pattern of cardiac syncope.

• Heart failure symptoms: orthopnoea, paroxysmal nocturnal dyspnoea, oedema.

• Gastrointestinal bleeding — the association of aortic stenosis with colonic angiodysplasia and acquired von Willebrand abnormality (Heyde syndrome) is real and worth asking about in an anaemic patient with a murmur.

• Establish the aetiology: age and calcific degeneration in the elderly; a bicuspid valve in a younger patient, which may be familial and is associated with aortic root dilatation and coarctation; and previous rheumatic fever, which usually affects the mitral valve too.

• Comorbidity, frailty and function — because the whole management decision is which intervention, not whether to intervene, and that depends on the patient rather than the valve.

2. Physical Examination

3. Differential Diagnosis

4. Investigations

• Electrocardiogram: left ventricular hypertrophy with strain, left bundle branch block, and atrial fibrillation in late disease.

• Chest radiograph: often unremarkable. Look for a calcified valve, post-stenotic dilatation of the ascending aorta, and cardiomegaly only when the ventricle has failed.

• Echocardiography is the diagnostic and grading investigation.

• The trap of low-flow, low-gradient stenosis: a failing ventricle cannot generate a high gradient across even a very tight valve, so the gradient understates the severity. Where the valve area is small but the gradient low and the ejection fraction reduced, dobutamine stress echocardiography distinguishes true severe stenosis from pseudo-severe disease.

• Before intervention: coronary angiography or computed tomographic coronary imaging; computed tomography for transcatheter planning — annulus size, valve calcification, coronary heights and vascular access; natriuretic peptide; dental assessment; and a formal frailty assessment.

5. Management

Indications for intervention

• Severe stenosis with any symptom — this patient qualifies on all three counts.

• Asymptomatic severe stenosis with: an ejection fraction below 50%; an abnormal exercise test with symptoms or a fall in blood pressure; very severe stenosis with a velocity above 5 m/s; rapid progression; or a markedly raised natriuretic peptide.

• Severe stenosis in a patient undergoing cardiac surgery for another indication.

Which intervention

• Surgical aortic valve replacement or transcatheter aortic valve implantation — the decision belongs to a multidisciplinary heart team, weighing age, surgical risk, anatomy, frailty, comorbidity and life expectancy. Transcatheter implantation is now used across a wide spectrum of surgical risk, not only in inoperable patients.

• Balloon valvuloplasty has no lasting role in calcific adult disease; it is a bridge in extremis, or a treatment for non-calcific congenital stenosis in the young.

• A mechanical prosthesis requires lifelong warfarin — not a direct oral anticoagulant, which is contraindicated. A bioprosthesis does not require long-term anticoagulation but degenerates over time, which is the central trade-off to explain to a patient choosing between them.

Surveillance and prevention

• Echocardiographic follow-up at intervals determined by severity — annually in severe asymptomatic disease, less often in mild.

• Dental hygiene and regular dental review; antibiotic prophylaxis for the highest-risk group only, as in Case 13.

• Educate the patient to report the first symptom immediately, and record that you have done so.

6. Teaching Points and Viva Questions

• Exertional syncope in an older patient is aortic stenosis until proved otherwise.

• A soft second heart sound means severe disease; a loud murmur means nothing.

• Symptoms are the trigger for surgery, and untreated symptomatic severe stenosis kills half of patients within two years.

• Vasodilators in fixed obstruction cause syncope.

• A low gradient with a small valve area and a poor ventricle needs a stress study, not reassurance.

• Mechanical valves need warfarin, never a direct oral anticoagulant.

Questions you should be able to answer:

• Explain each of this man’s physical signs in terms of the underlying haemodynamics.

• How would you distinguish this murmur from that of hypertrophic cardiomyopathy at the bedside?

• His valve area is 0.8 cm² but the mean gradient is only 25 mmHg and his ejection fraction is 35%. What is going on and what do you do?

• A colleague starts ramipril for his blood pressure of 150/95. What is your concern?

• He is asymptomatic with a velocity of 4.2 m/s and normal function. What do you do?

Case 16 · Chronic Regurgitant Valve Disease

1. Acute or Chronic? — Ask This First

The quiet murmur with a normal-sized heart in a shocked patient is the dangerous one. Students expect severe valve disease to be loud, and acute severe regurgitation is therefore missed.

2. Focused History

• Exertional breathlessness, orthopnoea, and awareness of the heartbeat, which reflects the large stroke volume of chronic aortic regurgitation.

• Angina can occur in aortic regurgitation without coronary disease, because a low diastolic pressure reduces coronary perfusion.

• Aetiology: bicuspid valve and its family history; rheumatic fever; connective tissue disease — Marfan and Ehlers–Danlos syndromes, with a family history of aortic dissection or sudden death; ankylosing spondylitis; hypertension; previous endocarditis; and recent dental or invasive procedures.

• For mitral regurgitation: previous rheumatic fever, mitral valve prolapse, previous myocardial infarction, and features of a dilated ventricle causing secondary regurgitation.

3. Physical Examination

Aortic regurgitation — and the eponyms, each with a mechanism

All of these arise from one thing: a very large stroke volume ejected into a low-resistance circulation, giving a wide pulse pressure. Learn the mechanism and the list becomes trivial.

Mitral regurgitation

• Pansystolic murmur at the apex radiating to the axilla, loudest in expiration in the left lateral position; a soft first heart sound; a third heart sound; a displaced thrusting apex; atrial fibrillation; and, in advanced disease, the signs of pulmonary hypertension and right heart failure.

• Mitral valve prolapse gives a mid-systolic click with a late systolic murmur, and the timing of the click moves with manoeuvres that alter ventricular volume.

4. Investigations

• Electrocardiogram: left ventricular hypertrophy; atrial fibrillation in mitral disease.

• Chest radiograph: cardiomegaly, and dilatation of the aortic root and ascending aorta in aortic regurgitation.

• Echocardiography, performed serially, with the numbers recorded and compared. Severity of regurgitation, left ventricular end-diastolic and end-systolic dimensions, and ejection fraction — these are the values on which the surgical decision rests. Transoesophageal study to define the mechanism of mitral regurgitation and the feasibility of repair.

• Cardiac magnetic resonance imaging for accurate ventricular volumes and regurgitant fraction where echocardiography is equivocal.

• Computed tomographic or magnetic resonance imaging of the aorta whenever the root is dilated, with surveillance thereafter.

• Exercise testing to unmask symptoms in a patient who claims to be asymptomatic; natriuretic peptide.

5. Management

Medical

• Vasodilators help here, in contrast to aortic stenosis. Treat hypertension with an angiotensin-converting enzyme inhibitor or receptor blocker or a dihydropyridine calcium channel blocker; reducing afterload reduces the regurgitant fraction.

• Use beta blockers cautiously in aortic regurgitation — slowing the heart lengthens diastole and therefore increases the time available for regurgitation. They are, however, indicated for aortopathy in Marfan syndrome, alongside an angiotensin receptor blocker and root surveillance.

• Treat heart failure and atrial fibrillation conventionally. Medical therapy does not substitute for surgery in severe disease — it manages symptoms while the decision is made.

Indications for surgery — learn these numbers

• In degenerative mitral disease, repair is strongly preferred to replacement — it preserves ventricular function, avoids a prosthesis and anticoagulation, and has better long-term outcomes. Refer to a centre with a high repair rate.

• Transcatheter edge-to-edge repair is an option in selected patients with secondary mitral regurgitation and heart failure, or where surgical risk is prohibitive.

• Endocarditis prevention and dental care; secondary penicillin prophylaxis where the disease is rheumatic (Case 9).

6. Teaching Points and Viva Questions

• In regurgitation the ventricle tells you when to operate, not the patient.

• Every eponymous sign of aortic regurgitation comes from a wide pulse pressure.

• You will not hear the murmur unless the patient sits forward and holds the breath out.

• The Austin Flint murmur is not mitral stenosis.

• Acute severe regurgitation is quiet, has a normal-sized heart, and is a surgical emergency.

• Vasodilators help in regurgitation and harm in stenosis.

• Repair the mitral valve rather than replace it wherever possible.

Questions you should be able to answer:

• Explain his blood pressure of 160/48 and list four signs that follow from it.

• Why does he have a mid-diastolic murmur at the apex, and how do you know it is not mitral stenosis?

• He says he feels well enough. Give three findings that would still make you refer him for surgery.

• A patient with endocarditis becomes acutely breathless with a barely audible murmur and a normal chest radiograph. What has happened?

• Why is a beta blocker a mixed blessing in aortic regurgitation?

Case 17 · Pericardial Disease

1. Four Syndromes, One Pericardium

• Acute pericarditis — inflammation, with pain and a rub.

• Pericardial effusion — fluid, which may be silent.

• Cardiac tamponade — fluid under enough pressure to impair filling. A haemodynamic diagnosis, not a volume one.

• Constrictive pericarditis — a thickened, scarred pericardium restricting filling chronically.

2. Acute Pericarditis

The electrocardiogram — how it differs from infarction

Causes

• Viral and idiopathic — the great majority in young patients.

• Tuberculous pericarditis — a leading cause worldwide and an important one in this region. Subacute onset, fever, weight loss, a large effusion, and a high risk of progression to constriction. Consider it in every patient who is not straightforwardly viral.

• Bacterial and purulent; uraemic; after myocardial infarction — early, or late as Dressler syndrome; after cardiac surgery or a percutaneous procedure; malignant infiltration; autoimmune disease including lupus and rheumatoid arthritis; radiotherapy; drugs; hypothyroidism; trauma.

Investigation

• Electrocardiogram, C-reactive protein and erythrocyte sedimentation rate, troponin, complete blood count, renal function, thyroid function, chest radiograph.

• Echocardiography in every patient — for effusion, for tamponade physiology, and for ventricular function.

• A raised troponin indicates myopericarditis. If ventricular function is also impaired, the diagnosis is perimyocarditis, and the patient should be admitted and monitored.

• Tuberculosis workup where the picture is subacute or the effusion large: interferon-gamma release assay, chest imaging, and pericardial fluid for adenosine deaminase, acid-fast staining and culture if drained. Autoimmune screen; blood cultures if febrile; cross-sectional imaging in complicated cases.

Treatment

• Admit if there is fever above 38 °C, a subacute onset, a large effusion or tamponade, myopericarditis, immunosuppression, trauma, anticoagulation, or failure to respond to a week of treatment.

• Treat the specific cause: antituberculous therapy for tuberculous disease (with corticosteroids in selected cases to reduce constriction); drainage and antibiotics for purulent pericarditis; intensified dialysis for uraemic disease.

• Recurrent pericarditis: colchicine for longer, then corticosteroids, then interleukin-1 antagonists, which are highly effective in colchicine-resistant disease.

3. Cardiac Tamponade

4. Constrictive Pericarditis

• Presents as right heart failure with preserved ventricular systolic function — progressive oedema, ascites often out of proportion to peripheral oedema, hepatomegaly, fatigue and breathlessness.

• Tuberculosis is a leading cause worldwide, along with previous cardiac surgery, radiotherapy, and any cause of chronic pericarditis.

• Signs: raised venous pressure with a prominent y descent, Kussmaul sign (venous pressure rises on inspiration), a pericardial knock, atrial fibrillation, ascites and hepatomegaly.

• Distinguishing constriction from restrictive cardiomyopathy is the hard part, and it matters because one is surgically curable: look for pericardial thickening or calcification on computed tomography, septal bounce and respirophasic variation in filling on echocardiography, and characteristic changes on cardiac magnetic resonance imaging. Natriuretic peptide is typically lower in constriction than in restrictive cardiomyopathy.

• Treatment is pericardiectomy, with diuretics for symptomatic relief in the interim and antituberculous therapy where relevant.

5. Teaching Points and Viva Questions

• Pain relieved by sitting forward and radiating to the trapezius ridge is pericardial.

• Widespread saddle ST elevation with PR depression and no reciprocal change is not an infarct.

• Colchicine for three months, for everybody. Steroids make recurrence more likely.

• A raised troponin means the myocardium is involved and changes the disposition.

• Tamponade is diagnosed at the bedside; give fluid, not furosemide.

• Absent y descent means tamponade; prominent y descent and Kussmaul sign mean constriction.

• Think of tuberculosis in any pericardial disease here that is not clearly viral.

Questions you should be able to answer:

• Give four ways this electrocardiogram differs from that of an anterior infarction.

• What will you prescribe, for how long, and what will you deliberately not prescribe?

• His troponin is raised. Does that change your management?

• Two days later his blood pressure is 84/60 with a raised venous pressure and quiet heart sounds. What is happening and what do you do?

• How would you distinguish constrictive pericarditis from restrictive cardiomyopathy?

Case 18 · The Cardiomyopathies

1. Three Phenotypes

2. Hypertrophic Cardiomyopathy

Focused history

• Exertional syncope or presyncope — the red flag, and the reason this patient was referred.

• Exertional breathlessness, chest pain, palpitations.

• A detailed family history across three generations: sudden death, unexplained drowning or road death in a young relative, cardiomyopathy, defibrillators, and consanguinity. This is a family disease, and the consultation concerns everybody in it.

• Competitive and recreational sport, and the intensity of it.

Examination

• Jerky pulse with a rapid upstroke and mid-systolic decline; double apical impulse; fourth heart sound; ejection systolic murmur at the left sternal edge that does not radiate to the carotids, with the dynamic behaviour above; and often a pansystolic murmur of mitral regurgitation from systolic anterior motion of the valve.

Investigations

• Electrocardiogram — abnormal in over 90%: left ventricular hypertrophy, deep lateral T wave inversion, pathological Q waves, and giant negative T waves in the apical variant. A completely normal tracing makes the diagnosis unlikely.

• Echocardiography: asymmetric hypertrophy of 15 mm or more, or 13 mm with a family history; systolic anterior motion of the mitral valve; and the outflow tract gradient measured at rest and with provocation, since obstruction is dynamic and may be absent at rest.

• Cardiac magnetic resonance imaging for apical and unusual variants and to quantify myocardial fibrosis, which contributes to arrhythmic risk.

• Ambulatory electrocardiographic monitoring for non-sustained ventricular tachycardia, and exercise testing with blood pressure response.

• Genetic testing, and cascade screening of first-degree relatives.

Management

• Avoid dehydration, vasodilators, nitrates and excessive diuresis — all reduce preload and worsen obstruction. Avoid digoxin and inotropes, which increase contractility and therefore obstruction.

• Beta blocker first line; verapamil or disopyramide as alternatives or additions. Cardiac myosin inhibitors such as mavacamten are a targeted treatment for obstructive disease.

• Septal reduction therapy — surgical myectomy or alcohol septal ablation — for symptoms refractory to drugs.

• Risk stratification for sudden death and consideration of an implantable defibrillator, using a validated risk score. The features that raise risk: family history of sudden death, unexplained syncope, massive hypertrophy, non-sustained ventricular tachycardia, apical aneurysm, extensive fibrosis on imaging, and an abnormal blood pressure response to exercise. This patient has two of them.

• Exercise advice, individualised rather than blanket prohibition, though high-intensity competitive sport is generally discouraged in higher-risk patients.

3. Dilated Cardiomyopathy

• Management is the management of heart failure with reduced ejection fraction — the four pillars set out in Case 12, with device therapy and, ultimately, transplantation.

• But look for the reversible causes, because several are entirely correctable: alcohol (abstinence can restore function), iron overload from transfusion — relevant in thalassaemia, where chelation and T2* monitoring are the treatment, thyroid disease, sustained tachyarrhythmia, thiamine deficiency, and cardiotoxic chemotherapy.

• Peripartum cardiomyopathy presents in late pregnancy or the early puerperium; function often recovers, and a subsequent pregnancy carries significant risk if it does not. Specialist joint care is required.

4. Restrictive Cardiomyopathy — and the Diagnosis Not to Miss

5. Teaching Points and Viva Questions

• Stand the patient up. The murmur that gets louder is hypertrophic cardiomyopathy; the one that gets quieter is aortic stenosis.

• Exertional syncope in a young person with a family history of sudden death is an emergency referral, not a routine one.

• The electrocardiogram is abnormal in almost every case of hypertrophic cardiomyopathy.

• Avoid vasodilators, nitrates, digoxin and dehydration.

• Screen the family — that is where the lives are saved.

• Alcohol and iron are reversible causes of a dilated cardiomyopathy.

• A low-voltage electrocardiogram with thick walls and a history of carpal tunnel syndrome is amyloidosis.

Questions you should be able to answer:

• Which single bedside manoeuvre separates this from aortic stenosis, and what happens to the murmur?

• Name four features that increase his risk of sudden death, and say which he has.

• What do you do about his parents, his sister and his cousins?

• A colleague prescribes glyceryl trinitrate for his chest pain. What is your concern?

• A 68-year-old has heart failure with a normal ejection fraction, thick ventricular walls and a low-voltage electrocardiogram. What is your diagnosis and how do you confirm it?