CARDIOLOGY
Heart failure
A. Low output cardiac failure
i. Dominant systolic heart failure
• Ischaemic myocardial disease, coronary artery disease
• Cardiomyopathy (alcoholic, diabetic, drug-induced, idiopathic)
• Myocarditis
• Valvular heart disease
• Terminal VSD or ASD
ii. Dominant diastolic heart failure
• Hypertension
• Severe aortic stenosis
• Hypertrophic cardiomyopathy
• Restrictive cardiomyopathy
• Ischemic myocardial disease, coronary artery disease.
iii. Acute heart failure
• Acute mitral or aortic regurgitation
• Rupture of valve leaflets or supporting structures.
• Infective endocarditis with acute valve incompetence
• Myocardial infarction (MI)
B. High output cardiac failure – failure due to extra demands on the heart which cannot be met.
• Paget’s disease, thyrotoxicosis, fever, Gram negative septicaemia, pregnancy,
anaemia.
C. Right vs Left-sided heart failure
Right heart failure Left heart failure
- Commonest cause is left-sided heart - Commonest cause is ischaemic
failure heart disease, followed by
- Other cause: hypertension, mitral/aortic valve
• Chronic lung disease (cor disease and cardiomyopathy
pulmonale)
• Pulmonary embolism
• Pulmonary hypertension
• Tricuspid/pulmonary valve
disease
• Left to right shunts (ASD,
VSD)
- Heart sounds in heart failure
▪ S3: Due to rapid ventricular filling. Normal in children & young adult. In others, it signifies
heart failure or vol. overload (e.g. mitral or aortic regurgitation)
▪ S4: Due to reduced ventricular compliance. Common in ventricular hypertrophy. Can be
normal at older ages.
- Chest X-ray: ABCDE – Alveolar/pulmonary oedema, ‘Bat’s wing’ appearance [hilar oedema],
Kerley B-lines, Cardiomegaly, Upper Lobe Venous Diversion, Effusions
- Treatment: mainly to reduce pre-load and after-load.
• Reduce pre-load: Diuretics & venous vasodilators (e.g. nitrates)
• Reduce after-load: Arterial vasodilators (e.g. hydralazine)
• Reduce both pre- and after-load: ACE inhibitors & ARBs.
,- Common diuretics used:
a) Thiazide diuretics – Decrease active reabsorption of Na+ & Cl- in the distal convoluted tubule.
Excretion of uric acid & Ca2+ is decreased, whereas magnesium is increased.
b) Loop diuretics (e.g. furosemide) – Inhibit transport of NaCl out of the lumen of the thick
segment of the ascending limb of the loop of Henle. Excretion of uric acid is decreased,
whereas calcium and magnesium is increased.
c) Potassium sparing diuretics – Aldosterone antagonist, inhibits Na+ retention and decreases K+
excretion.
Hypertensions
Secondary causes
1. Renal causes
• Renovascular – Renal artery stenosis
• Renoparenchymal – Chronic glomerulonephritis, Chronic pyelonephritis, Diabetic
nephropathy, Adult polycystic kidney disease, Chronic tubulointerstitial nephritis.
2. Endocrine causes
• Conn’s syndrome (mineralocorticoid excess)
• Cushing’s syndrome (glucocorticoid excess)
• Acromegaly (growth hormone excess)
• Adrenal hyperplasia (congenital)
• Phaechromocytoma
• Hyperthyroidism
• Hypothyroidism
• Hyperparathyroidism
3. Cardiovascular causes: Coarctation of aorta
4. Pharmacological causes: OCP, corticosteroids, monoamine oxidase inhibitors, cocaine,
amphetamines, vasopressin, etc.
- When to suspect a secondary cause for hypertension?
• Young patient
• Accelerated hypertension
• Refractory hypertension
• Target organ damage at presentation – e.g. renal impairment (proteinuria,
haematuria), grade III or IV retinopathy
• Hypokalaemia – Due to adrenal conditions stated above.
• Abnormal examination – e.g. coarctation bruit, renal artery bruit, enlarged kidney,
etc.
Malignant hypertension
- Grades 3 and 4 hypertensive retinopathy using Keith-Wagener classification is diagnostic of
malignant HTN but only in the presence of a diastolic BP > 140 mmHg.
Myocardial infarction (MI)
- ‘Silent infarcts’ especially in elderly, diabetics may present as:
1. Dyspnoea (due to acute pulmonary oedema)
2. Syncope/coma (due to dysrhythmias)
3. Acute confusional states
4. Diabetic hypoglycaemic crisis.
, 5. Hypotension or shock
- ECG progression for acute MI : ST elevation → T inversion → Pathological Q waves only if is
transmural infarction (broad > 1mm, deep > 2 mm)
• II, III, aVF: Inferior MI; Culprit is right coronary
• I, aVL, V5, V6: Lateral MI; Culprit is left circumflex artery (LCX)
• V1 – V4: Anteroseptal MI; Culprit is left anterior descending (LAD) artery
- Pathological Q waves: Hallmark of transmural infarct and almost always permanent.
- Physiological Q waves may be seen in lead aVR, I & III.
- Management of acute MI
i. Morphine/diamorphine + anti-emetic
ii. Oxygen
iii. Aspirin 300 mg + Clopidogrel/Ticagrelor (usually is dual anti-platelet if is confirm case of
acute MI). Alternatively, Glycoprotein IIb/IIIa receptor antagonists (e.g. eptifibatide,
tirofiban may also be given)
iv. Nitrate – sublingual or IV GTN
v. LMWH – enoxaparin, dalteparin
vi. B-blockers (IV)
vii. ACE-inhibitors
- If is STEMI, then consider thrombolysis or primary PCI after completing the above steps.
- Thrombolysis is maximally effective if given within 12 hr of onset of cardiac chest pain. May still
be given between 12 – 24 hr after the onset of chest pain, but only if patient has continuing pain
or clinical deterioration.
Indications for thrombolysis:
• Typical cardiac chest pain for > 30 min
• < 12 hr since onset of pain
• ST elevation in 2 or more contiguous leads (> 1 mm in inferior leads; > 2 mm in
anterior or lateral leads) or new LBBB on ECG
Contraindications to thrombolysis:
• CPR for > 10 min
• Significant haemorrhage or surgery within the last month
• Stroke or TIA within the last 6 months
• Head injury within the last 6 months
• Any intracranial haemorrhage ever
• Bleeding diathesis (INR > 3)
• Hypertension (> 200/110)
• Proliferative diabetic retinopathy
• Pregnancy
• Possibility of aortic dissection (rule in/out with CXR)
- Complications of MI under 5 main headings:
1. Further chest pain
• Pericarditis – first 1 -3 days post mi. Audible rub. ECG shows ‘saddle shaped’ ST-
segment elevation in all leads. Treat with high dose Aspirin and rest. IV steroids if
persistent symptoms. Pericardiocentesis if cardiac compromise due to tamponade.
• Infarct extension – Further ST elevation
• Post-infarction angina – Usually within 10 days of acute MI. Treat with standard
medical therapy.
• Musculoskeletal pain if attempted CPR or DC cardioversion.
2. Fever
• Dressler’s syndrome – occurs weeks or even months after MI. Triad: Fever,
Pericarditis, Pericardial effusion. May need anti-inflammatories.
• Myocardial necrosis – fever peaks in 3 – 4 days post-MI
, • Other common causes – Infection, thrombophlebitis, venous thrombosis, drug
reaction, etc.
3. New systolic murmur
• Ventricular septal defect (VSD) – 5 – 10 days post MI. May present as sudden collapse,
pulmonary oedema, and hypotension
• Acute mitral regurgitation – 2 – 10 days post MI due to infarction & rupture of
papillary muscles.
• Others: Pericardial friction rub, Long-standing murmur missed initially.
4. Post-MI arrhythmias
• Sinus bradycardia – especially with infection MI. Treat with atropine first & then
electrical pacing.
• AV blockade – especially with inferior MI
• Ventricular ectopics
• Ventricular tachycardia.
5. Hypotension and shock post-MI
6. Others: Heart failure, Death, Left ventricular aneurysm (persistent ST elevation),
thromboembolism secondary to prolong inactivity or cardiac mural thrombus
Unstable Angina, NSTEMI
Definition
Unstable Angina: ACS in the absence of biochemical evidence of myocardial damage (normal Trop T.
CKMB). Can be defined by:
i) Angina at rest (> 20 minutes)
ii) New-onset Angina (Canadian Cardiovascular Society [CCS] class 3 – marked limitations of
ordinary physical activity)
iii) Increasing angina: More frequent, longer duration, lower threshold
iv) Post-MI angina (develops within 2 weeks of an acute MI)
History
1. Assess for Cardiovascular Risk Factors: Age, DM, HTN, Dyslipidaemia, Smoking, peripheral
vascular disease, previous or pre-existing heart disease, CKD, family h/o premature CAD
2. Symptoms:
• Anginal symptoms – retrosternal pressure/heaviness → radiates to jaw, arm, or neck,
may be intermittent or persistent, relieved or improved by nitrates.
• Definition as above (resting angina, post-MI angina, etc.)
• Associated symptoms – nausea, diaphoresis, dyspnoea
• Atypical (women, older people, people with DM or renal failure) – epigastric pain,
recent-indigestion, stabbing/pleuritic chest pain, syncope/pre-syncope, SOB w/o chest
pain, unexplained sweating, nausea & vomiting
Physical examination (mainly TRO other diagnoses, to identify possible cause, precipitating cause &
consequences of UA/NSTEMI)
1. Aortic dissection – unequal pulses, murmur of aortic regurgitation
2. Acute pericarditis – pericardial friction rub
3. Cardiac tamponade – pulsus paradoxus (Beck’s triad)
4. Pneumothorax – tracheal deviation, hyper-resonance, unilateral reduced air entry
5. Large pulmonary embolism – tachycardia, hypotension with raised JVP
6. Identifying precipitating factors: Thyrotoxicosis, Anaemia, Malignant HTN
7. 4th heart sound (S4) – indicated reduced myocardial relaxation d/t ischaemia.
Heart failure
A. Low output cardiac failure
i. Dominant systolic heart failure
• Ischaemic myocardial disease, coronary artery disease
• Cardiomyopathy (alcoholic, diabetic, drug-induced, idiopathic)
• Myocarditis
• Valvular heart disease
• Terminal VSD or ASD
ii. Dominant diastolic heart failure
• Hypertension
• Severe aortic stenosis
• Hypertrophic cardiomyopathy
• Restrictive cardiomyopathy
• Ischemic myocardial disease, coronary artery disease.
iii. Acute heart failure
• Acute mitral or aortic regurgitation
• Rupture of valve leaflets or supporting structures.
• Infective endocarditis with acute valve incompetence
• Myocardial infarction (MI)
B. High output cardiac failure – failure due to extra demands on the heart which cannot be met.
• Paget’s disease, thyrotoxicosis, fever, Gram negative septicaemia, pregnancy,
anaemia.
C. Right vs Left-sided heart failure
Right heart failure Left heart failure
- Commonest cause is left-sided heart - Commonest cause is ischaemic
failure heart disease, followed by
- Other cause: hypertension, mitral/aortic valve
• Chronic lung disease (cor disease and cardiomyopathy
pulmonale)
• Pulmonary embolism
• Pulmonary hypertension
• Tricuspid/pulmonary valve
disease
• Left to right shunts (ASD,
VSD)
- Heart sounds in heart failure
▪ S3: Due to rapid ventricular filling. Normal in children & young adult. In others, it signifies
heart failure or vol. overload (e.g. mitral or aortic regurgitation)
▪ S4: Due to reduced ventricular compliance. Common in ventricular hypertrophy. Can be
normal at older ages.
- Chest X-ray: ABCDE – Alveolar/pulmonary oedema, ‘Bat’s wing’ appearance [hilar oedema],
Kerley B-lines, Cardiomegaly, Upper Lobe Venous Diversion, Effusions
- Treatment: mainly to reduce pre-load and after-load.
• Reduce pre-load: Diuretics & venous vasodilators (e.g. nitrates)
• Reduce after-load: Arterial vasodilators (e.g. hydralazine)
• Reduce both pre- and after-load: ACE inhibitors & ARBs.
,- Common diuretics used:
a) Thiazide diuretics – Decrease active reabsorption of Na+ & Cl- in the distal convoluted tubule.
Excretion of uric acid & Ca2+ is decreased, whereas magnesium is increased.
b) Loop diuretics (e.g. furosemide) – Inhibit transport of NaCl out of the lumen of the thick
segment of the ascending limb of the loop of Henle. Excretion of uric acid is decreased,
whereas calcium and magnesium is increased.
c) Potassium sparing diuretics – Aldosterone antagonist, inhibits Na+ retention and decreases K+
excretion.
Hypertensions
Secondary causes
1. Renal causes
• Renovascular – Renal artery stenosis
• Renoparenchymal – Chronic glomerulonephritis, Chronic pyelonephritis, Diabetic
nephropathy, Adult polycystic kidney disease, Chronic tubulointerstitial nephritis.
2. Endocrine causes
• Conn’s syndrome (mineralocorticoid excess)
• Cushing’s syndrome (glucocorticoid excess)
• Acromegaly (growth hormone excess)
• Adrenal hyperplasia (congenital)
• Phaechromocytoma
• Hyperthyroidism
• Hypothyroidism
• Hyperparathyroidism
3. Cardiovascular causes: Coarctation of aorta
4. Pharmacological causes: OCP, corticosteroids, monoamine oxidase inhibitors, cocaine,
amphetamines, vasopressin, etc.
- When to suspect a secondary cause for hypertension?
• Young patient
• Accelerated hypertension
• Refractory hypertension
• Target organ damage at presentation – e.g. renal impairment (proteinuria,
haematuria), grade III or IV retinopathy
• Hypokalaemia – Due to adrenal conditions stated above.
• Abnormal examination – e.g. coarctation bruit, renal artery bruit, enlarged kidney,
etc.
Malignant hypertension
- Grades 3 and 4 hypertensive retinopathy using Keith-Wagener classification is diagnostic of
malignant HTN but only in the presence of a diastolic BP > 140 mmHg.
Myocardial infarction (MI)
- ‘Silent infarcts’ especially in elderly, diabetics may present as:
1. Dyspnoea (due to acute pulmonary oedema)
2. Syncope/coma (due to dysrhythmias)
3. Acute confusional states
4. Diabetic hypoglycaemic crisis.
, 5. Hypotension or shock
- ECG progression for acute MI : ST elevation → T inversion → Pathological Q waves only if is
transmural infarction (broad > 1mm, deep > 2 mm)
• II, III, aVF: Inferior MI; Culprit is right coronary
• I, aVL, V5, V6: Lateral MI; Culprit is left circumflex artery (LCX)
• V1 – V4: Anteroseptal MI; Culprit is left anterior descending (LAD) artery
- Pathological Q waves: Hallmark of transmural infarct and almost always permanent.
- Physiological Q waves may be seen in lead aVR, I & III.
- Management of acute MI
i. Morphine/diamorphine + anti-emetic
ii. Oxygen
iii. Aspirin 300 mg + Clopidogrel/Ticagrelor (usually is dual anti-platelet if is confirm case of
acute MI). Alternatively, Glycoprotein IIb/IIIa receptor antagonists (e.g. eptifibatide,
tirofiban may also be given)
iv. Nitrate – sublingual or IV GTN
v. LMWH – enoxaparin, dalteparin
vi. B-blockers (IV)
vii. ACE-inhibitors
- If is STEMI, then consider thrombolysis or primary PCI after completing the above steps.
- Thrombolysis is maximally effective if given within 12 hr of onset of cardiac chest pain. May still
be given between 12 – 24 hr after the onset of chest pain, but only if patient has continuing pain
or clinical deterioration.
Indications for thrombolysis:
• Typical cardiac chest pain for > 30 min
• < 12 hr since onset of pain
• ST elevation in 2 or more contiguous leads (> 1 mm in inferior leads; > 2 mm in
anterior or lateral leads) or new LBBB on ECG
Contraindications to thrombolysis:
• CPR for > 10 min
• Significant haemorrhage or surgery within the last month
• Stroke or TIA within the last 6 months
• Head injury within the last 6 months
• Any intracranial haemorrhage ever
• Bleeding diathesis (INR > 3)
• Hypertension (> 200/110)
• Proliferative diabetic retinopathy
• Pregnancy
• Possibility of aortic dissection (rule in/out with CXR)
- Complications of MI under 5 main headings:
1. Further chest pain
• Pericarditis – first 1 -3 days post mi. Audible rub. ECG shows ‘saddle shaped’ ST-
segment elevation in all leads. Treat with high dose Aspirin and rest. IV steroids if
persistent symptoms. Pericardiocentesis if cardiac compromise due to tamponade.
• Infarct extension – Further ST elevation
• Post-infarction angina – Usually within 10 days of acute MI. Treat with standard
medical therapy.
• Musculoskeletal pain if attempted CPR or DC cardioversion.
2. Fever
• Dressler’s syndrome – occurs weeks or even months after MI. Triad: Fever,
Pericarditis, Pericardial effusion. May need anti-inflammatories.
• Myocardial necrosis – fever peaks in 3 – 4 days post-MI
, • Other common causes – Infection, thrombophlebitis, venous thrombosis, drug
reaction, etc.
3. New systolic murmur
• Ventricular septal defect (VSD) – 5 – 10 days post MI. May present as sudden collapse,
pulmonary oedema, and hypotension
• Acute mitral regurgitation – 2 – 10 days post MI due to infarction & rupture of
papillary muscles.
• Others: Pericardial friction rub, Long-standing murmur missed initially.
4. Post-MI arrhythmias
• Sinus bradycardia – especially with infection MI. Treat with atropine first & then
electrical pacing.
• AV blockade – especially with inferior MI
• Ventricular ectopics
• Ventricular tachycardia.
5. Hypotension and shock post-MI
6. Others: Heart failure, Death, Left ventricular aneurysm (persistent ST elevation),
thromboembolism secondary to prolong inactivity or cardiac mural thrombus
Unstable Angina, NSTEMI
Definition
Unstable Angina: ACS in the absence of biochemical evidence of myocardial damage (normal Trop T.
CKMB). Can be defined by:
i) Angina at rest (> 20 minutes)
ii) New-onset Angina (Canadian Cardiovascular Society [CCS] class 3 – marked limitations of
ordinary physical activity)
iii) Increasing angina: More frequent, longer duration, lower threshold
iv) Post-MI angina (develops within 2 weeks of an acute MI)
History
1. Assess for Cardiovascular Risk Factors: Age, DM, HTN, Dyslipidaemia, Smoking, peripheral
vascular disease, previous or pre-existing heart disease, CKD, family h/o premature CAD
2. Symptoms:
• Anginal symptoms – retrosternal pressure/heaviness → radiates to jaw, arm, or neck,
may be intermittent or persistent, relieved or improved by nitrates.
• Definition as above (resting angina, post-MI angina, etc.)
• Associated symptoms – nausea, diaphoresis, dyspnoea
• Atypical (women, older people, people with DM or renal failure) – epigastric pain,
recent-indigestion, stabbing/pleuritic chest pain, syncope/pre-syncope, SOB w/o chest
pain, unexplained sweating, nausea & vomiting
Physical examination (mainly TRO other diagnoses, to identify possible cause, precipitating cause &
consequences of UA/NSTEMI)
1. Aortic dissection – unequal pulses, murmur of aortic regurgitation
2. Acute pericarditis – pericardial friction rub
3. Cardiac tamponade – pulsus paradoxus (Beck’s triad)
4. Pneumothorax – tracheal deviation, hyper-resonance, unilateral reduced air entry
5. Large pulmonary embolism – tachycardia, hypotension with raised JVP
6. Identifying precipitating factors: Thyrotoxicosis, Anaemia, Malignant HTN
7. 4th heart sound (S4) – indicated reduced myocardial relaxation d/t ischaemia.
