Cardiac conditions are very commonly encountered in the long case setting. Given that cardiac disease is the most common morbidity in the world’s adult population, a cardiac condition could be encountered as the main pathology or an associated condition in the long case setting. Common cardiology long cases the candidate should be well versed in are: heart failure, ischaemic heart disease, arrhythmias and hypertension. Also important are valve disease and associated clinical decision-making processes, including timing of surgery if indicated in the patient with a cardiac valvular pathology.
HYPERTENSION
Case vignette
A 57-year-old man is admitted to hospital with severe chest pain. The pain is of sudden onset, tearing in character and radiating to the back. He is diaphoretic and anxious. On examination his pulse is regular at 110 bpm. His heart sounds are normal and the chest is clear. His blood pressure in the right arm is 190/100 mmHg and in the left arm 170/70 mmHg.
Approach to the patient
Hypertension is a common finding in patients seen in the examination (see box over leaf for causes of hypertension), but rarely is it the major problem in management. Nevertheless, some thorough and accessible knowledge of hypertension can impress the examiners. Hypertension is practically defined as blood pressure readings above 140/90 mmHg on three separate occasions a week apart. However, the lowest blood pressure within the limits of tolerance is desirable. In the diabetic patient, the optimal blood pressure is 125/75 mmHg. Patients with hypertension should be investigated for other cardiovascular risk factors, because the identification and management of the full continuum of cardiovascular risk is of paramount importance.
Causes of hypertension
• Primary/idiopathic (95% of cases)
• Obesity
• Obstructive sleep apnoea
• Alcoholism
• Renal artery stenosis
• Parenchymal renal disease
• Renal tumours
• Gestational
• Pre-eclampsia
• Congenital adrenal hyperplasia
• Hypothyroidism
• Hyperthyroidism
• Acromegaly
• Conn’s syndrome (primary hyperaldosteronism)
• Cushing’s syndrome
• Phaeochromocytoma
• Polycythaemia vera
• Acute intermittent porphyria
• Raised intracranial pressure
• Medication-induced (oral contraceptives, corticosteroids, cyclosporin)
History
Ask:
Bi-occipital headache is the classic symptom of severe hypertension. Nocturia is an early symptom of the malignant phase.
Examination
Check the blood pressure and look for a postural drop. If the blood pressure is very high, check the other arm and repeat the measurement at the end of the physical examination for confirmation.
Examine the optic fundus for features of hypertensive retinopathy (see Fig 3.1 and box) and, if present, describe your findings according to the Keith-Wagener-Barker classification (see box overleaf). An apical heave and a loud aortic component of the second heart sound are signs that suggest left ventricular hypertrophy due to long-standing high blood pressure. Examine for a renal bruit, adrenal masses, polycystic kidneys, bitemporal hemianopia or acromegalic body habitus and cushingoid body habitus to exclude a secondary cause for the hypertension (see box overleaf).
Features of hypertensive retinopathy
• None—no detectable abnormality
• Mild—focal and generalised arteriolar narrowing; copper and silver wiring of arterioles; arteriovenous (AV) nipping
• Moderate—blot, dot or flame-shaped haemorrhages, cottonwool spots, microaneurysm, yellow and white exudates
• Severe—papilloedema (in addition to haemorrhages and exudates)
Keith-Wagener-Barker classification of hypertensive retinopathy
• Grade 1—Mild/focal constriction and sclerosis of the arterioles
• Grade 2—Moderate to severe constriction and sclerosis of arterioles with enhanced reflexivity and AV nipping
• Grade 3—Above changes together with retinal haemorrhages/cottonwool exudates
• Grade 4—Above changes together with papilloedema
Clinical issues of significance in a patient with high blood pressure are:
1. Is the blood pressure actually high? This raises the question of measurement error and, more particularly, ‘white coat’ hypertension (persistent ‘white coat’ hypertension has also been described as a sentinel marker of possible constant hypertension and therefore should not be ignored). In patients with poorly controlled hypertension (or in whom the diagnosis is uncertain), consider the need for 24-hour ambulatory blood pressure monitoring. Blood pressure monitored overnight should show a drop during the first half of the night. Blunting or absence of this ‘nocturnal dip’ is associated with enhanced cardiovascular risk.
2. How much target organ damage is present and how does this influence the prognosis?
3. Is there an underlying renal or endocrine cause amenable to treatment other than lowering blood pressure?
4. What other cardiovascular risk factors are present?
Investigations
Investigations that should be requested in a patient with hypertension are:
1. Electrolyte profile and renal function indices—looking for evidence of renal failure. Abnormal renal function indices should prompt further investigations to rule out parenchymal renal disease.
3. Chest X-ray—to exclude cardiomegaly, left ventricular hypertrophy and congestive cardiac failure (X-ray is capable of detecting only quite gross and irreversible left ventricular damage)
4. Echocardiogram—to assess left ventricular wall thickness and chamber size and any evidence of diastolic dysfunction (especially if there is clinical evidence of left ventricular hypertrophy or heart failure) (Fig 3.2)
5. Urine analysis—looking for proteinuria. A positive urine analysis for proteinuria should be followed up with a 24-hour urine collection to quantify the proteinuria and to assess creatinine clearance. Proteinuria of more than 2 g per day is much more likely to reflect primary renal disease and usually indicates a need for renal biopsy. Calculate the albumin-to-creatinine ratio (ACR), which is an important cardiovascular risk marker.
6. Fasting blood sugar levels and lipid profile—to assess the presence of other significant cardiovascular risk factors.
Creatinine clearance needs to be checked to clarify renal function but does not really help to distinguish between primary renal disease causing high blood pressure and renal impairment secondary to hypertensive nephrosclerosis. If there is no significant proteinuria or renal failure, a trial of effective blood pressure lowering for 6 months can be given. Deterioration of renal function at any stage is an indication for investigation. The additional investigations in this setting include a renal ultrasound (looking for renal shrinkage suggesting chronic renal failure or renovascular disease, or enlarged kidneys suggesting conditions such as polycystic kidney disease), a DTPA scan (to assess renal perfusion) and a renal arterial Doppler study (to exclude renal artery stenosis). If clinical evidence indicates renal artery stenosis, further study with computed tomography (CT) or magnetic resonance (MR) angiography is indicated.
The major endocrine investigation is the aldosterone/renin ratio, to detect primary hyperaldosteronism. This is now believed to account for 10–15% of people presenting with essential hypertension, but this does not mean that they all need adrenalectomy. Other endocrine investigations include: serum renin index (to exclude renin hypersecretion) and 24-hour urinary cortisol (to screen for Cushing’s syndrome).
If there is suspicion (tachycardia, palpitations, sweating, anxiety, postural hypotension) of phaeochromocytoma, perform serum catecholamine level, urinary metanephrines and urinary vanillylmandelic acid level.
Management
It is not wise to commence treatment at the first diagnosis itself unless there is malignant hypertension, end-organ damage (see box) or significant other vascular risk factors, or comorbidity. (Treat with antihypertensive agents if the diastolic pressure is > 100 mmHg, or systolic > 200 mmHg, or systolic pressure > 160 mmHg together with end-organ damage. The presence of other cardiovascular risk factors would be another indication for treatment.) Observation for 3–6 months with recommendation of non-pharmacological methods such as progressive muscle relaxation, weight reduction (if relevant), reduction of alcohol consumption, salt restriction and regular physical exercise would suffice initially. It is important to advise the patient against smoking. If present, hyperlipidaemia and diabetes should be treated. If the blood pressure remains elevated (>140/90 mmHg) despite adequate lifestyle modification (or due to failure of lifestyle modification), pharmacotherapy should be initiated.
Selection of the appropriate antihypertensive agent should be guided by several factors, including: the patient’s comorbidities, age, sex, ethnic background and drug allergies. Initially an attempt should be directed at monotherapy, and the commonly used agents are thiazide diuretics, beta-blockers, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blocker (ARB). If monotherapy is inadequate, combination therapy can be considered. An ACE inhibitor with a diuretic, or a beta-blocker with a diuretic, are two such combinations. There are combination pills containing an ACE inhibitor or an ARB together with a thiazide diuretic that can be prescribed. Hypertension that is not well controlled with conventional agents even with up titration and combination warrants further investigation and the addition of potent, less commonly used agents such alpha receptor blockers, centrally acting agents or arterial vasodilators.
Comorbidities that can influence the choice of therapy
• Diabetes mellitus—ACE inhibitors are the most suitable agents. Where ACE inhibitors are not tolerated, the other options to consider include ARBs and calcium channel blockers. Beta-adrenergic receptor blockers and thiazide diuretics can interfere with glycaemic control. ACE inhibitors and ARBs have significant and useful synergy in severe high blood pressure and diabetic nephropathy.
• Gout—beta-blockers, ACE inhibitors, calcium channel blockers and alpha-blockers are suitable. Thiazide diuretics can exacerbate gout.
• Dyslipidaemia—ACE inhibitors, calcium channel blockers and alpha-blockers are recommended. Beta-blockers may be less desirable due to their adverse effects on the lipid profile.
• Ischaemic heart disease—diuretics, beta-blockers, calcium channel blockers, ACE inhibitors and ARBs are suitable because of their protective properties in coronary vascular disease.
• Congestive cardiac failure—ideal agents include beta-blockers, ACE inhibitors, ARBs and diuretics, which also have proven value in the management of cardiac failure.
• Peripheral vascular disease—calcium channel blockers, alpha-adrenergic receptor blockers and diuretics are desirable agents. Beta-blockers are contraindicated.
• Pregnancy—for mild hypertension in pregnant patients, methyldopa and the alpha- and beta-adrenergic receptor blocking agent labetolol are good choices. In preeclampsia, nifedipine is a suitable agent; however, urgent delivery of the baby is an absolute requirement. Severe hypertension in the pregnant patient can be managed with intravenous (IV) hydralazine.
Adverse effects of some antihypertensive agents
It is important to have a commanding knowledge of the properties and adverse effects of the commonly used antihypertensive agents. Below is a list of adverse effects seen with different classes of antihypertensive agents, together with some important properties of selected agents.
• Thiazide diuretics—hypercholesterolaemia, hyperglycaemia, thrombocytopenia and gout
• Beta-blockers—bradycardia, postural hypotension, depression and cold peripheries. Agents with intrinsic sympathomimetic activity, such as pindolol, rarely cause bradycardia. The cardioselective agent atenolol is less lipid-soluble, and therefore has minimal central nervous system side effects.
• ACE inhibitors—angio-oedema, cough, postural hypotension, hyperkalaemia, progression of renal failure and first-dose hypotension. First-dose hypotension is a rarity but is seen particularly in patients on low-sodium diets and high-dose diuretics.
• Angiotensin II receptor blockers—similar to ACE inhibitors but cough is less common
• Calcium channel blockers—headaches, sweating, palpitations and ankle oedema
• Alpha-blockers—first-dose hypotension. Long-acting alpha-blockers such as doxazocin have less first-dose hypotension effect.
• Vasodilators—minoxidil is an agent used in resistant hypertension. It is one of the most potent antihypertensive drugs available. Minoxidil can cause sodium and water retention, leading to ankle oedema and, in the rare case, pericardial effusion. Another undesirable side effect of minoxidil is hypertrichosis. Hydralazine has its use in pregnancy and sometimes in cardiac failure. Hydralazine can cause drug-induced lupus. Nitroprusside is another vasodilator agent that is used in hypertensive crises and dissection of the aorta.
ISCHAEMIC HEART DISEASE AND ACUTE MYOCARDIAL INFARCTION
Sometimes examiners like to test candidates’ knowledge of the management of common acute medical conditions. No condition is more common than acute myocardial infarction in the physician trainee’s case repertoire, and the candidate is expected to be thoroughly familiar with the management of this condition.
Case vignette
A 45-year-old man presents with retrosternal chest tightness of 3 hours’ duration. The pain is dull in nature, 7/10 in severity and radiating along the left arm. The onset was at rest. He also complains of progressive dyspnoea and associated nausea. He denies any cardiovascular risk factors apart from a strong family history. On examination his pulse rate is 100 bpm, low in volume and regular. His blood pressure is 90/60 mmHg. There are fine crepitations bibasally in the lung fields. The ECG shows deep T wave inversions in leads I, III and aVF.
Upon stabilisation the patient is admitted to the coronary care unit (CCU). His Killip class is 2 (see box). He is managed on aspirin, metoprolol 12.5 mg twice daily and IV heparin. While in CCU his blood pressure drops to 70/40 mmHg and pulse rate to 40 bpm. His pain is progressive and the ECG shows further deepening of the T wave inversions and new ST depression in the said leads, and also in leads aVR, V1 and V2.
He is commenced on an IV glycoprotein IIb/IIIa inhibitor and referred for early catheterisation. Catheterisation reveals occlusion of the posterior descending branch of the right coronary artery, which is successfully reopened by balloon angioplasty and stenting. On day 2 he develops fever and pleuritic chest pains.
On day 3 he develops acute pulmonary oedema and cardiogenic shock. Auscultation reveals a new harsh pansystolic murmur audible all over the precordium.
(Adapted from Killip T, Kimball J T 1967 Treatment of myocardial infarction in coronary care unit. A two-year experience with 250 patients. American Journal of Cardiology 20:457)
(Adapted from Killip T, Kimball J T 1967 Treatment of myocardial infarction in coronary care unit. A two-year experience with 250 patients. American Journal of Cardiology 20:457)
Approach to the patient
History
Ask about:
• the onset of symptoms and associated symptoms
• the relationship between the pain and trigger factors such as physical exertion and emotional stress
• details of the pain—severity, exact location, radiation, factors that exacerbate or relieve the pain
• descriptive characteristics of the pain—such as sharp, dull or heavy feeling
• whether there is a pleuritic nature to the pain
• coronary risk factors
• the patient’s past history, especially cardiovascular history
• whether the patient has experienced similar pain in the past.
Examination
First and foremost, check the vital signs and establish haemodynamic stability. If the patient is having an acute episode of coronary ischaemia (or other emergency such as pneumothorax, pulmonary embolus) they may become rapidly unstable, with haemodynamic compromise or cardiopulmonary arrest.
Once the patient is stable, perform a detailed cardiovascular examination. Look in the fundus for hypertensive or diabetic changes. Listen to the heart for additional sounds such as the third and fourth heart sounds. Listen to the lung bases for crepitation of congestion.
Management
In any acute myocardial infarction the first priority is to assess the patient’s clinical stability and assess the requirement for, and urgency associated with, coronary revascularisation. Remember: patients presenting with an infarction could present with acute pulmonary oedema, cardiogenic shock, malignant ventricular tachyarrhythmias or severe bradycardia. Once the patient’s haemodynamic stability and cardiac rhythm stability are established, perform an urgent ECG to confirm the diagnosis and identify the nature of the infarction—whether it is an ST segment elevation infarction (STEMI) or a non-ST segment elevation infarction (non-STEMI).
STEMI
If the infarction is a STEMI, urgent reperfusion therapy is needed. Acute reperfusion therapy could be primary percutaneous transluminal coronary angioplasty (primary PTCA) with insertion of a stent or thrombolysis. If the centre offers a primary angioplasty service and the patient fulfils the criteria (see box), urgent transfer to the cardiac catheterisation laboratory should take place. Patients presenting in the first 4–6 hours of onset of chest pain are considered suitable for primary PTCA. Previous coronary artery bypass grafts, peripheral vascular disease, untreatable terminal illness and dementia are exclusion criteria for this procedure.
If primary PTCA is not an option, the patient should be thrombolysed with the relevant thrombolytic agent. If the patient presents within the first hour after the onset of chest pain, thrombolysis would be a preferred option (the ‘golden hour’ phenomenon). Usually a recombinant tissue plasminogen activator (rTPA) or an analogue is given to the patient immediately. Streptokinase is an alternative for patients over the age of 65 or those with evidence of an inferior myocardial infarction presenting after 4 hours of the onset of chest pain. Those who have been treated with streptokinase previously should not be given streptokinase again, due to the heightened risk of an allergic reaction.
The ECG criteria for primary PTCA and thrombolysis are similar (see box), but thrombolysis may be useful up to 12 hours or even 24 hours after the onset of chest pain.
If the decision is made to administer thrombolytics, the patient should not have any contraindications (e.g. risk of haemorrhage or allergy) to such therapy. If thrombolytic therapy has not been effective and the patient is a strong candidate for reperfusion therapy, attempts should be made to organise urgent rescue angioplasty.
Figure 3.3 Coronary angiogram of occluded artery (A) before primary PTCA (B) during primary PTCA (C) after primary PTCA; (D) ECG showing ST segment elevation in the antroseptal and lateral leads, indicating complete occlusion of the LAD artery
Non-STEMI
If a non-STEMI, the patient should be managed initially with anticoagulation and antiplatelet therapy. The patient should subsequently be referred for early coronary catheterisation.
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