General Medicine
Final Professional MBBS — General Medicine. Long Questions (10 marks) and Short Notes (5 marks) across 15 systems, exam-formatted with clinical pearls, drug doses and mnemonics.
DEFINITION
Infective endocarditis is a microbial infection of the endocardial surface of the heart, most commonly involving the heart valves (native or prosthetic), producing vegetations — irregular, friable masses of platelets, fibrin, microorganisms, and inflammatory cells.
CAUSES & RISK FACTORS
Organism Setting / Key Association *S. viridans* (#1 native valve) Dental procedures; most common overall in community-acquired IE *S. aureus* (#1 acute IE) IV drug users ; prosthetic valves; IV catheters; most virulent — destroys valves rapidly *S. bovis* (S. gallolyticus) Colorectal cancer — always colonoscopy when S. bovis bacteraemia found *Enterococcus* GU tract procedures; elderly males; nosocomial IE HACEK group *Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella* — culture-negative IE; fastidious organisms Candida / Aspergillus IV drug users; prosthetic valves; immunocompromised; large vegetations Risk factors for IE:
- Valvular heart disease — rheumatic (MR > AR > MS), congenital (VSD #1; bicuspid AV), MVP with regurgitation
- IV drug use — right-sided IE (tricuspid valve); *S. aureus* most common; presents with septic pulmonary emboli
- Prosthetic heart valves — early (< 2 months): *S. epidermidis*, *S. aureus*; late (> 2 months): *S. viridans*
- Intracardiac devices (pacemakers, ICDs); haemodialysis; poor dentition; diabetes
CLINICAL FEATURES
Symptoms:
- Prolonged fever (> 1–2 weeks) + malaise + night sweats + weight loss — cardinal features
- New or changing murmur — hallmark; regurgitant murmur due to valve destruction
- Symptoms of embolic events — stroke, haematuria, flank pain, cold limb
Peripheral (embolic/immunological) signs — the classic exam findings:
Sign Description Mechanism Osler's nodes Painful, tender, red-purple nodules on finger/toe pulps Immune complex deposition (painful) Janeway lesions Painless, flat, haemorrhagic macules on palms and soles Septic emboli (painless) Splinter haemorrhages Linear, dark-red streaks under fingernails (mid-nail region) Microemboli in nail bed capillaries Roth spots Pale-centred retinal haemorrhages on fundoscopy Immune complex vasculitis Clubbing In subacute IE > 6 weeks Periosteal proliferation (VEGF) Splenomegaly Tender splenomegaly in ~50% Repeated seeding + immune hyperplasia ◆ Peripheral signs mnemonic — FROM JANE ▸ F = Finger clubbing ▸ R = Roth spots (retina) ▸ O = Osler's nodes (painful, finger pulps) ▸ M = Murmur (new/changing) ▸ J = Janeway lesions (painless, palms/soles) ▸ A = Anaemia (normocytic normochromic) ▸ N = Nail splinter haemorrhages ▸ E = Emboli (spleen, brain, kidney, lung in IVDU) DIAGNOSIS — MODIFIED DUKE CRITERIA
DEFINITE IE = 2 major + 1 major & 3 minor + 5 minor criteria
MAJOR Criteria Details 1. Positive blood cultures ≥ 2 separate cultures with typical IE organism
(*S. viridans, S. bovis, HACEK, S. aureus, Enterococcus*)
OR persistently +ve cultures ≥ 12 hrs apart2. Echo evidence Vegetation / Abscess / New dehiscence of prosthetic valve
OR new valvular regurgitationMINOR Criteria Details Predisposing heart disease or IV drug use Known risk factor Fever > 38°C Temperature criterion Vascular phenomena Major emboli, Janeway lesions, septic infarcts Immunological phenomena Osler's nodes, Roth spots, +ve RF, GN Microbiological +ve culture not meeting major criteria 💡CLINICAL PEARL: Blood cultures before antibiotics — 3 sets from different sites over 24 hours. Echo: TOE (Transoesophageal Echo) is more sensitive than TTE for vegetations, abscesses, prosthetic valves.MANAGEMENT
Empirical antibiotic therapy (before cultures):
▶ Native valve, community-acquired: Ampicillin 2 g IV 4-hourly + Cloxacillin 2 g IV 4-hourly + Gentamicin 1 mg/kg IV 8-hourly
▶ Prosthetic valve / MRSA risk: Vancomycin 15–20 mg/kg IV 12-hourly + Rifampicin 300 mg oral TDS + Gentamicin 1 mg/kg IV 8-hourly
Definitive therapy (organism-guided):
▶ S. viridans (penicillin-sensitive): Benzylpenicillin 1.2 g IV 4-hourly × 4 weeks ± Gentamicin × 2 weeks
▶ S. aureus (MSSA): Flucloxacillin 2 g IV 4-hourly × 4–6 weeks (native valve) / × 6 weeks (prosthetic)
▶ S. aureus (MRSA): Vancomycin 15–20 mg/kg IV 12-hourly × 6 weeks + Rifampicin 300 mg TDS
▶ Enterococcus: Ampicillin 2 g IV 4-hourly + Ceftriaxone 2 g IV 12-hourly × 6 weeks
Indications for surgery :
- Heart failure refractory to medical therapy — #1 indication (valve destruction → severe regurgitation)
- Uncontrolled infection — abscess, fistula, paravalvular extension, persistent bacteraemia > 5–7 days
- Prevention of embolism — large vegetation > 10 mm, prior embolic event, high-risk organisms (*S. aureus*, fungi)
- Prosthetic valve endocarditis with dehiscence or dysfunction
PROPHYLAXIS
Indicated ONLY for high-risk patients undergoing dental procedures involving gingival manipulation or mucosa perforation:
- High-risk: Prosthetic valve, previous IE , cyanotic CHD (unrepaired), cardiac transplant with valvulopathy
▶ Amoxicillin 2 g oral / IV 30–60 min before dental procedure
If allergy: Clindamycin 600 mg oral OR Azithromycin 500 mg oralNot ALL valvular disease requires prophylaxis — only prosthetic valves, previous IE, unrepaired cyanotic CHD, and cardiac transplant valvulopathy. Mitral stenosis alone does NOT require prophylaxis (AHA 2021). DEFINITION & CLASSIFICATION
Acute Coronary Syndrome (ACS) = a spectrum of conditions caused by acute reduction in coronary blood flow due to plaque rupture and thrombus formation.
Type ECG Troponin Pathology STEMI ST elevation ≥ 1 mm in ≥ 2 contiguous leads (≥ 2 mm in V1–V3) Elevated Total occlusion of coronary artery → full-thickness infarction NSTEMI ST depression / T-wave inversion / normal Elevated Partial occlusion → subendocardial infarction Unstable Angina ST depression / T-wave inversion / normal Normal Partial occlusion; severe ischaemia without necrosis ETIOPATHOGENESIS
- Plaque development: Chronic endothelial injury (hypertension, smoking, dyslipidaemia, DM) → LDL oxidation → foam cell formation → fibrous plaque (atheroma)
- Plaque rupture/erosion : Vulnerable plaque (thin fibrous cap + large lipid core + macrophage infiltration) ruptures → subendothelial collagen and lipid core exposed
- Thrombosis: Platelet activation → GP IIb/IIIa receptor expression → platelet aggregation → primary platelet plug → coagulation cascade → fibrin thrombus → coronary occlusion
- Ischaemia → Necrosis: O2 demand > supply → reversible ischaemia → irreversible necrosis after 20–40 min of sustained occlusion → troponin release
CLINICAL FEATURES
- Severe crushing/squeezing chest pain — central, retrosternal; lasting > 20 min (unlike angina which is < 15 min)
- Radiation — left arm, left shoulder, jaw, neck, epigastrium (may mimic indigestion)
- Not relieved by nitrates (unlike stable angina)
- Associated: profuse sweating, nausea/vomiting, breathlessness, sense of impending doom (angor animi)
- Diabetics — may present with silent MI (painless); elderly may present with dyspnoea or syncope only
Signs:
- Tachycardia; hypotension (shock if large MI or RV infarct); S3/S4 gallop; MR murmur (papillary muscle dysfunction)
- Signs of LVF — basal crackles, raised JVP, pulmonary oedema
INVESTIGATIONS
1. ECG — most important immediate investigation:
- Hyperacute T-waves (earliest, minutes) → ST elevation (minutes–hours) → Q waves (hours–days — permanent if transmural) → T-wave inversion
- Territory localisation : V1–V4 = anterior (LAD); II, III, aVF = inferior (RCA); I, aVL = lateral (LCx); V4R = right ventricular
2. Cardiac biomarkers :
Biomarker Rise Peak Return to Normal Notes Troponin I/T (gold standard) 3–6 hrs 12–24 hrs 7–14 days Highest sensitivity + specificity; detect up to 2 weeks CK-MB 4–6 hrs 12–24 hrs 48–72 hrs Best for reinfarction (normalises faster than troponin) Myoglobin 1–3 hrs (earliest) 4–12 hrs 24 hrs Earliest marker but not cardiac-specific LDH 12–24 hrs 48–72 hrs 7–14 days Old marker; isoforms LDH1 > LDH2 = cardiac flip 3. Echo — wall motion abnormalities; LV function; complications
4. Coronary angiography — gold standard for diagnosis and guides PCI/CABG
MANAGEMENT OF STEMI
Immediate (first 10 minutes — 'MONA' + DAPT):
◆ MONA — Immediate STEMI Management ▸ M = Morphine 2–5 mg IV (pain/anxiety; now used selectively) ▸ O = Oxygen (ONLY if SpO2 < 90% — routine O2 not recommended ) ▸ N = Nitrates (GTN 0.5 mg sublingual × 3 — if SBP > 90 mmHg) ▸ A = Aspirin 300 mg oral loading (then 75 mg OD lifelong) ▶ Aspirin 300 mg loading + Ticagrelor 180 mg loading (or Clopidogrel 600 mg) → DAPT (dual antiplatelet therapy)
▶ Anticoagulation: UFH 60 IU/kg IV bolus (max 4000 IU) then infusion OR Enoxaparin 30 mg IV bolus + 1 mg/kg SC 12-hourly
Reperfusion — Time is muscle :
Reperfusion Strategy Criteria Target Time Primary PCI (1st choice) PCI-capable centre available Door-to-balloon ≤ 90 min Thrombolysis PCI not available within 120 min Door-to-needle ≤ 30 min Rescue PCI Thrombolysis failed (< 50% ST resolution at 60–90 min) As soon as possible ▶ Thrombolytics : Streptokinase 1.5 million IU IV over 60 min (cheaper; antigenic) OR Alteplase (tPA) 15 mg bolus + 0.75 mg/kg over 30 min + 0.5 mg/kg over 60 min (fibrin-specific, preferred)
Contraindications to thrombolysis :
- Absolute: Prior intracranial haemorrhage; ischaemic stroke within 3 months; active internal bleeding; aortic dissection; intracranial neoplasm
- Relative: BP > 180/110; recent surgery > 3 weeks; CPR > 10 min; warfarin with INR > 2; pregnancy
Long-term therapy (post-MI — 4 pillars):
- Aspirin 75 mg OD lifelong + P2Y12 inhibitor (ticagrelor/clopidogrel) × 12 months (DAPT)
- Beta-blocker (bisoprolol 2.5–10 mg OD / metoprolol 25–100 mg BD) — reduces mortality; start within 24 hrs if haemodynamically stable
- ACE inhibitor (ramipril 2.5–10 mg OD) — reduces remodelling; start within 24 hrs; especially if EF < 40%
- Statin (atorvastatin 40–80 mg OD) — plaque stabilisation; start immediately regardless of baseline LDL
COMPLICATIONS OF ACUTE MI
Timing Complication Key Feature Immediate
(hours)Arrhythmias
(#1 cause of early death)VF — defibrillate immediately!
VT, AF, bradyarrhythmias, AV blocksEarly
(1–3 days)Cardiogenic shock SBP < 90 mmHg + ↓ CO + ↑ PCWP → 40–50% mortality; > 40% LV destroyed Days 3–7 Free wall rupture
VSD
Papillary muscle ruptureSudden shock + haemopericardium → tamponade
New harsh PSM + step-up O2 sat RV
Acute severe MR — new murmurWeeks Dressler's syndrome Fever + pleurisy + pericarditis 2–6 weeks post-MI; immune-mediated; treat with NSAIDs/colchicine Late
(months)LV aneurysm
Mural thrombusPersistent ST elevation ; paradoxical wall motion; anticoagulation for thrombus DEFINITION
Heart failure (HF) = the inability of the heart to pump sufficient blood to meet the metabolic demands of the body, OR to do so only at the cost of elevated filling pressures. Classified by EF: HFrEF (EF < 40%) | HFmrEF (EF 40–49%) | HFpEF (EF ≥ 50%).
CAUSES
Type Key Causes Left Heart Failure IHD/MI (#1 worldwide), Hypertension (#2), Dilated cardiomyopathy, Valvular disease (AS, AR, MR), Myocarditis Right Heart Failure LHF (most common cause of RHF) , Cor pulmonale (COPD, pulmonary HTN), MS, Pulmonary embolism Precipitants of acute decompensation FAILURE mnemonic : Forgot medication, AF, Infection (pneumonia), Ischaemia/MI, Low output (anaemia), Upregulation (pregnancy, thyrotoxicosis), Renal failure, Embolism PATHOPHYSIOLOGY
- Reduced CO: Failing LV → ↓ cardiac output → ↓ BP → baroreceptor activation → sympathetic activation (tachycardia, vasoconstriction, ↑ contractility)
- Neurohormonal activation: ↓ renal perfusion → RAAS activation → AngII + aldosterone → Na/water retention → ↑ preload → further LV dilation (vicious cycle)
- ADH release: Hyponatraemia risk; further fluid retention
- BNP/ANP : Released from ventricles in response to wall stress → natriuresis + vasodilation (compensatory but overwhelmed)
- Cardiac remodelling : Chronic pressure/volume overload → myocyte hypertrophy + fibrosis → eccentric/concentric hypertrophy → progressive dysfunction
CLINICAL FEATURES
Feature Left HF Right HF Primary symptom Dyspnoea (exertional → orthopnoea → PND → rest) Peripheral oedema (pitting, ankle → legs → ascites) Other symptoms Cough (pink frothy — pulmonary oedema ); fatigue; wheeze (cardiac asthma ) Abdominal distension; anorexia; RUQ pain (liver congestion) Signs Displaced apex; S3 (gallop); basal crepitations; ↑ JVP in decompensated ↑ JVP ; pitting oedema; hepatomegaly; ascites; TR murmur Key CXR findings Cardiomegaly; upper lobe diversion ; Kerley B lines ; bat-wing oedema; pleural effusions Cardiomegaly; right heart dilatation NYHA Functional Classification :
NYHA Class Symptoms 6-min Walk I No symptoms with ordinary activity ≥ 426 m II Slight limitation — dyspnoea on moderate exertion 300–425 m III Marked limitation — dyspnoea on minimal activity 150–299 m IV Symptoms at rest < 150 m MANAGEMENT — FOUR PILLARS OF HF
◆ Four Pillars of HFrEF (ARNI) — All proven to reduce mortality ▸ A = ACE inhibitor / ARB / ARNI (Sacubitril-Valsartan ) ▸ B = Beta-blocker (Bisoprolol / Carvedilol / Metoprolol succinate) ▸ A = Aldosterone antagonist / MRA (Spironolactone / Eplerenone) ▸ S = SGLT2 inhibitor (Dapagliflozin / Empagliflozin) — newest pillar ▶ ACE inhibitor : Ramipril 2.5–10 mg OD; Enalapril 2.5–20 mg BD. Reduces mortality 20–25%. If ACE-I cough → switch to ARB (Candesartan/Losartan).
▶ ARNI — Sacubitril-valsartan (Entresto): 49/51 mg BD → 97/103 mg BD. Inhibits neprilysin (↑ ANP/BNP) + blocks AT1. Reduces mortality 20% vs enalapril (PARADIGM-HF trial). Replace ACE-I, not add-on.
▶ Beta-blocker : Bisoprolol 1.25–10 mg OD; Carvedilol 3.125–25 mg BD; Metoprolol succinate 12.5–200 mg OD. Reduces mortality 34%. Start LOW, go SLOW. Avoid in acute decompensation.
▶ MRA/Aldosterone antagonist : Spironolactone 25–50 mg OD OR Eplerenone 25–50 mg OD. Reduces mortality 30% (RALES trial). Monitor K⁺ and renal function.
▶ SGLT2 inhibitor : Dapagliflozin 10 mg OD OR Empagliflozin 10 mg OD. Reduces HF hospitalisation + CV death (DAPA-HF, EMPEROR-Reduced). Works in both HFrEF and HFpEF.
Additional therapy:
▶ Diuretics (symptom relief) : Furosemide 20–80 mg IV/oral — reduces congestion rapidly. NOT proven to reduce mortality but essential for symptom control.
▶ Digoxin: 0.125–0.25 mg OD — reduces HF hospitalisation; useful in AF + HF. Narrow therapeutic window (0.5–0.9 ng/mL).
▶ Ivabradine: If HR ≥ 77 bpm despite max beta-blocker; reduces HF hospitalisation.
Device therapy:
- ICD — EF ≤ 35% on optimal medical therapy > 3 months; prevents sudden cardiac death (SCD)
- CRT (Cardiac Resynchronisation Therapy) — EF ≤ 35% + QRS ≥ 130 ms + LBBB + NYHA III–IV; improves symptoms + mortality
ACUTE PULMONARY OEDEMA MANAGEMENT
- Sit patient up (feet dangling) → reduces venous return + improves lung expansion
- High-flow O2 (SpO2 > 94%); if failing → CPAP/NIV
- IV Furosemide 40–80 mg stat → reduces preload by immediate venodilatation (before diuresis) then diuresis
- IV Diamorphine/Morphine 2.5–5 mg → anxiolysis + venodilatation (use cautiously)
- GTN infusion (if SBP > 100 mmHg) → powerful venodilatation → ↓ preload
- IV Digoxin if AF with fast ventricular rate
- Treat precipitant — AF, MI, hypertensive crisis, infection
DEFINITION
Acute Rheumatic Fever (ARF) is a delayed non-suppurative immunological complication of Group A beta-haemolytic Streptococcal (GAS) pharyngitis , occurring 2–4 weeks after throat infection. The heart, joints, skin, and CNS are primarily affected.
PATHOGENESIS — Molecular Mimicry
- GAS pharyngitis — *Streptococcus pyogenes* infects the throat (NOT skin infection — important )
- M-protein of GAS shares structural homology with cardiac myosin, tropomyosin, laminin, and valve matrix proteins
- Molecular mimicry : Antibodies produced against M-protein cross-react with cardiac tissue → autoimmune inflammation of the heart valves, myocardium, and pericardium (pancarditis)
- Aschoff bodies — pathognomonic histological finding: perivascular granulomas with giant cells (Anitschkow cells) in myocardium
- Repeated episodes → progressive valve damage → Rheumatic Heart Disease (RHD)
CLINICAL FEATURES — JONES CRITERIA
Diagnosis = Evidence of preceding GAS infection + 2 Major OR 1 Major + 2 Minor criteria
◆ JONES Criteria — Major Criteria (JONES mnemonic) ▸ J = Joints (Migratory polyarthritis — #1 most common feature; large joints; migratory; exquisitely tender) ▸ O = cOrditis (Carditis — most serious; pancarditis; new murmur; CCF; 40–60% of cases) ▸ N = Nodules (Subcutaneous nodules — painless, firm, over bony prominences; 5–7% of cases) ▸ E = Erythema marginatum (pink rings on trunk; characteristic; 5%) ▸ S = Sydenham's chorea (involuntary purposeless movements; emotional lability; 'St Vitus Dance') Minor Criteria:
- Clinical: Fever (38.5°C), Arthralgia (only if arthritis NOT counted as major), Previous RHD/ARF
- Lab: ↑ ESR (> 60 mm/hr), ↑ CRP, Prolonged PR interval on ECG
Evidence of preceding GAS infection (mandatory):
- Positive throat swab OR Rapid antigen test OR ↑ ASO titre (> 200 IU/mL) OR anti-DNase B titre
Carditis — the most important feature :
- Mitral regurgitation (#1 valve affected) — apical pansystolic murmur; most common valvular lesion in ARF
- Aortic regurgitation (2nd most common); MS is a sequela of repeated attacks (not acute ARF)
- Pancarditis: endocarditis + myocarditis (↓ EF, cardiac failure) + pericarditis (rub, chest pain)
TREATMENT
1. Eradicate GAS:
▶ Benzathine Penicillin G 1.2 million IU IM single dose — treatment of choice (eliminates residual streptococci)
▶ If allergy: Amoxicillin 500 mg TDS × 10 days OR Erythromycin 500 mg QDS × 10 days
2. Anti-inflammatory therapy:
▶ Arthritis only: Aspirin 100 mg/kg/day (max 4–8 g/day) × 4–6 weeks — dramatic response confirms ARF
▶ Carditis (moderate/severe): Prednisolone 1–2 mg/kg/day × 2–4 weeks then taper
3. Treat cardiac complications:
▶ Heart failure: Diuretics + ACE inhibitor + bed rest
4. Sydenham's chorea:
▶ Sodium valproate 15 mg/kg/day OR Carbamazepine — reduces chorea; haloperidol as alternative
SECONDARY PROPHYLAXIS — MOST IMPORTANT
Category Duration Drug ARF without carditis 5 years or until age 21 (whichever longer) Benzathine Penicillin G
1.2 million IU IM every 3–4 weeksARF with carditis (no residual HD) 10 years or until age 21 Same as above ARF with carditis + residual HD 10 years or until age 40
(whichever longer)Same as above Severe residual HD Lifelong Same as above ✍️EXAM TIP: Secondary prophylaxis is MORE IMPORTANT than primary prevention. Even ONE recurrence of GAS pharyngitis can cause another attack of ARF and worsen valvular damage. BPG IM every 3–4 weeks .OVERVIEW
Modern HFrEF management is built on four evidence-based pharmacological pillars — each proven independently to reduce mortality and hospitalisation. They work on complementary neurohormonal pathways and should ALL be up-titrated in every eligible patient.
THE FOUR PILLARS
Pillar Drug Class Mechanism Key Trial Mortality ↓ Pillar 1 ARNI / ACE-I / ARB
(Sacubitril-Valsartan
or Ramipril)Block RAAS
ARNI also ↑ natriuretic peptidesPARADIGM-HF
SAVE / CHARM~20–25% Pillar 2 Beta-blocker
(Bisoprolol / Carvedilol
/ Metoprolol succinate)↓ sympathetic activation
↓ heart rate
AntiremodellingMERIT-HF
COPERNICUS
CIBIS-II~34% Pillar 3 MRA / Aldosterone antagonist
(Spironolactone
Eplerenone)Block aldosterone
↓ fibrosis
K⁺-sparingRALES
EPHESUS~30% Pillar 4 (newest) SGLT2 inhibitor
(Dapagliflozin 10 mg
Empagliflozin 10 mg)Glycosuric
Osmotic diuresis
CardioprotectiveDAPA-HF
EMPEROR-Reduced~25% NEPRILYSIN INHIBITOR — ARNI SACUBITRIL-VALSARTAN
Sacubitril-Valsartan (Entresto) = ARNi (Angiotensin Receptor–Neprilysin Inhibitor) — the most significant advance in HF pharmacotherapy in decades.
Mechanism of sacubitril-valsartan:
- Sacubitril (prodrug → LBQ657) — inhibits neprilysin , the enzyme that degrades natriuretic peptides (BNP, ANP, CNP) and bradykinin
- Neprilysin inhibition → ↑ BNP + ANP → natriuresis + diuresis + vasodilation + antifibrotic + anti-remodelling effects
- Valsartan (ARB component) — blocks AT1 receptor → ↓ RAAS effects (AngII-mediated vasoconstriction, aldosterone, fibrosis)
- Combined effect: dual blockade of two harmful neurohormonal pathways + amplification of protective natriuretic peptide system
PARADIGM-HF Trial Key Findings → Sacubitril-valsartan vs enalapril in EF < 40% (NYHA II–IV) → 20% relative reduction in CV death or HF hospitalisation → Trial stopped early due to overwhelming benefit at 27 months → NNT = 21 (absolute reduction: 4.7%) — highly clinically significant ▶ Dosing: Start 49/51 mg BD (or 24/26 mg BD if ACE-I-naive); titrate every 2–4 weeks to target 97/103 mg BD
Critical prescribing rules :
- Washout period : Must stop ACE inhibitor for ≥ 36 hours BEFORE starting sacubitril-valsartan — risk of angioedema (both increase bradykinin)
- NEVER combine with ACE inhibitor — dangerous angioedema risk
- Contraindications: History of angioedema, GFR < 30, pregnancy, bilateral RAS, severe hepatic impairment
Indications (ESC 2021 guidelines) :
- HFrEF (EF ≤ 35%); NYHA Class II–IV; on optimal medical therapy → replace ACE-I/ARB with sacubitril-valsartan
- Reduces need for ICD/CRT — reversal of remodelling in many patients
BETA-BLOCKER IN HF — DETAILED
- Only 3 evidence-based : Bisoprolol, Carvedilol, Metoprolol succinate (NOT all beta-blockers)
- Start ONLY in compensated HF — avoid in acute decompensation (↓ contractility worsens acute failure)
- Start at lowest dose, titrate every 2 weeks to maximum tolerated dose
- Mechanism: ↓ sympathetic activation + antiarrhythmic + antiremodelling + ↑ EF over time
SGLT2 INHIBITORS — THE FOURTH PILLAR
- Dapagliflozin 10 mg OD or Empagliflozin 10 mg OD — regardless of diabetic status
- Mechanism: Block SGLT2 in renal tubule → ↑ glycosuria + osmotic diuresis → reduced preload + cardiac decongestive effects; also reduce inflammation and cardiac fibrosis
- Works in both HFrEF AND HFpEF (unique among the four pillars — others mainly HFrEF)
- Avoid if eGFR < 20 mL/min/1.73 m²
DEFINITION & CLASSIFICATION
Category SBP DBP Management Normal < 120 > 80 Lifestyle Elevated (prehypertension) 120–129 < 80 Lifestyle × 3 months Stage 1 HTN 130–139 80–89 Lifestyle ± drug (if risk factors) Stage 2 HTN ≥ 140 ≥ 90 Drug therapy + lifestyle Hypertensive Urgency > 180 > 120 No acute organ damage; oral therapy Hypertensive Emergency > 180 > 120 Acute organ damage; IV therapy HYPERTENSIVE EMERGENCY
Definition: Severe hypertension (usually SBP > 180 / DBP > 120 mmHg) with acute target organ damage (TOD) .
Target organs and their presentations:
- Brain: Hypertensive encephalopathy (headache + confusion + papilloedema); Haemorrhagic stroke; Ischaemic stroke
- Heart: Acute MI; Acute LVF + pulmonary oedema; Aortic dissection
- Kidney: Acute nephrosclerosis → haematuria + proteinuria + rising creatinine
- Eye: Grade III/IV hypertensive retinopathy — flame haemorrhages + soft exudates + papilloedema
Target for BP reduction :
- First hour: Reduce MAP by no more than 25% in 1 hour — rapid reduction risks watershed infarction (brain/heart used to high BP — autoregulation lost)
- Next 2–6 hrs: Reduce to 160/100 mmHg
- Exception — Aortic dissection : Target SBP < 120 mmHg rapidly (within minutes)
▶ Sodium nitroprusside IV: 0.3–10 μg/kg/min infusion — vasodilates arterial + venous; immediate onset; needs ICU/arterial line. Risk: cyanide toxicity in renal failure.
▶ Labetalol IV: 20 mg IV bolus then 0.5–2 mg/min infusion — alpha + beta blocker; preferred in pregnancy, aortic dissection (with nitroprusside).
▶ Hydralazine IV: 5–10 mg IV slowly — preferred in pregnancy (eclampsia).
▶ GTN (nitroglycerin) IV: 5–200 μg/min — preferred when LVF/pulmonary oedema is the target organ involvement.
▶ Nicardipine IV: 5–15 mg/hr — calcium channel blocker; useful in post-operative hypertension.
HYPERTENSIVE URGENCY
Severely elevated BP WITHOUT acute organ damage. Can be managed with oral therapy, reduce BP over 24–48 hours .
▶ Amlodipine 5–10 mg oral OR Nifedipine retard 20 mg oral (NOT short-acting sublingual nifedipine — risk of precipitous fall) OR Captopril 12.5–25 mg oral OR Labetalol 100–200 mg oral
ANTIHYPERTENSIVE MANAGEMENT — JNC 8 / ACC-AHA 2017
Target BP: < 130/80 mmHg (ACC/AHA 2017) for most patients; < 140/90 for elderly or certain groups.
◆ First-line antihypertensives — A, B, C, D ▸ A = ACE inhibitors / ARBs (Ramipril, Losartan) — 1st line in DM, CKD, post-MI ▸ B = Beta-blockers (Bisoprolol, Atenolol) — 1st line in angina, post-MI, HF, tachyarrhythmias ▸ C = Calcium channel blockers (Amlodipine) — 1st line in elderly, isolated systolic HTN, black patients ▸ D = Diuretics (Indapamide, Hydrochlorothiazide) — 1st line in elderly, isolated systolic, black patients Compelling Indication Drug of Choice Post-MI / IHD Beta-blocker + ACE-I + statin Heart failure (HFrEF) ACE-I + Beta-blocker + MRA + SGLT2i + ARNI Diabetes (proteinuria) ACE-I / ARB — nephroprotective CKD (proteinuria) ACE-I / ARB — reduces proteinuria Pregnancy Methyldopa (first-line); Labetalol; Nifedipine. Avoid ACE-I/ARBs (teratogenic) Isolated systolic HTN (elderly) CCB (Amlodipine) or Thiazide Benign Prostate Hypertrophy Alpha-blocker (Prazosin, Doxazosin) DEFINITION
Cyanosis = bluish discolouration of skin and mucous membranes due to absolute concentration of deoxygenated haemoglobin (deoxyHb) ≥ 5 g/dL in capillary blood. Appears earlier in polycythaemia, later in anaemia.
Feature Central Cyanosis Peripheral Cyanosis Site Warm areas: tongue , lips, mucous membranes Cold extremities: fingers, toes, earlobes Mechanism Arterial desaturation — blood leaving LV is desaturated Normal SaO2; ↑ O2 extraction by peripheral tissues Cause Cardiac shunt (R→L) , COPD, Pulmonary oedema, PE Vasoconstriction (cold, shock), CCF, Raynaud's, DVT Response to O2 Improves (lung disease) ; FIXED if cardiac shunt Does NOT improve with O2 Differential Cyanosis — classic exam topic:
Type Pattern Cause Differential cyanosis Lower limbs cyanosed + clubbed
Upper limbs normal/pinkEisenmenger's syndrome with PDA (patent ductus arteriosus)
Deoxygenated blood from RV enters aorta BELOW subclavian via PDA → lower bodyReverse differential Upper limbs cyanosed
Lower limbs normalTGA + PDA — rare; oxygenated blood enters descending aorta 🔑Key Point — Differential cyanosis = Eisenmenger's + PDA . Lower limbs blue + clubbed; upper limbs normal. The most commonly asked type in exams.- Methaemoglobinaemia: Cyanosis when MetHb > 1.5 g/dL; skin appears grey-blue; SaO2 falsely reads 85%; does NOT respond to O2; treat with methylene blue 1–2 mg/kg IV
OVERVIEW
CPR is an emergency life-saving procedure combining chest compressions and rescue breaths to maintain perfusion of vital organs during cardiac arrest. Follow the AHA 2020 BLS Algorithm .
◆ BLS Sequence — D-R-S-A-B-C-D ▸ D = Danger — ensure scene safety for rescuer and patient ▸ R = Response — check consciousness (tap shoulders, shout: 'Are you OK?') ▸ S = Shout for help — call 108/emergency services; ask someone to get AED ▸ A = Airway — head tilt-chin lift (or jaw thrust if trauma suspected) ▸ B = Breathing — look, listen, feel for normal breathing × 10 seconds ▸ C = Compressions — start CPR: 30 compressions: 2 breaths ▸ D = Defibrillation — attach AED as soon as available; shock if advised Chest Compressions — Key Parameters :
- Rate: 100–120 per minute ('push fast')
- Depth: 5–6 cm in adults ('push hard'); allow full chest recoil
- Position: Heel of both hands on lower half of sternum; arms straight
- Ratio: 30:2 (compressions:breaths) with 2 rescuers; 30:2 with 1 rescuer
- Minimise interruptions — < 10 sec pause for rhythm check
Defibrillation:
- VF/Pulseless VT — shockable rhythms; defib immediately: 200 J biphasic → resume CPR × 2 min → recheck
- PEA / Asystole — non-shockable; CPR + identify 4H/4T causes
◆ Reversible causes of cardiac arrest — 4H's + 4T's ▸ 4H: Hypoxia | Hypovolaemia | Hypo/Hyperkalaemia | Hypothermia ▸ 4T: Tension PTX | Tamponade | Thrombosis (MI/PE) | Toxins ACLS — Advanced Cardiac Life Support:
▶ Adrenaline (Epinephrine) 1 mg IV every 3–5 min — for all cardiac arrests; causes vasoconstriction → ↑ coronary perfusion pressure
▶ Amiodarone 300 mg IV bolus — for refractory VF/pulseless VT (after 3rd shock)
DEFINITION & AETIOLOGY
Mitral stenosis (MS) = narrowing of the mitral valve orifice (normal area 4–6 cm²) impeding blood flow from LA to LV during diastole, causing elevated left atrial pressure and downstream pulmonary congestion.
- Rheumatic fever (#1 cause, >90%) — commissural fusion + leaflet thickening + chordal shortening
- Other: Mitral annular calcification (elderly); Congenital MS; Carcinoid; SLE; RA
MVA (Mitral Valve Area) Severity Gradient Symptoms > 1.5 cm² Mild < 5 mmHg None or on heavy exertion 1.0–1.5 cm² Moderate 5–10 mmHg On moderate exertion < 1.0 cm² Severe > 10 mmHg At rest ; pulmonary HTN PHYSICAL SIGNS
- Malar flush (mitral facies) — plum-coloured flush over malar eminences; due to peripheral vasoconstriction + CO
- Tapping apex (palpable S1) — not displaced (small LV in MS)
- Loud S1 — leaflets shut forcefully; first sign to disappear with calcification (soft S1 = severe calcification)
- Opening snap (OS) — high-pitched sound in early diastole; earlier OS = more severe MS (↑ LA pressure opens valve sooner); A2-OS interval < 70 ms = severe
- Low-pitched, rumbling mid-diastolic murmur — at apex; best heard in left lateral position with bell; presystolic accentuation (in SR)
- Signs of complications: Irregular pulse (AF ); ↑ JVP (pulmonary HTN + RHF); RV heave; loud P2
🔑Key Point — Classic MS murmur: Loud S1 → A2 → OS → MDM . Mnemonic: LOOM (Loud S1, Opening snap, Obstructed flow, Mid-diastolic murmur).MANAGEMENT
- Medical: Diuretics (symptom relief); Beta-blockers/rate-limiting CCB (slow HR → ↑ diastolic filling time); anticoagulation if AF
▶ Warfarin INR 2–3 — for AF + MS (high thromboembolic risk; DOACs NOT recommended in rheumatic AF )
- Interventional (for MVA < 1.5 cm²):
- PTMC (Percutaneous Transvenous Mitral Commissurotomy / Balloon Valvotomy) — 1st line if pliable, non-calcified, no MR, no LA thrombus; Wilkins score ≤ 8
- Mitral valve replacement (MVR) — calcified/deformed valve; MR; LA thrombus; failed PTMC
DEFINITION
AF = rapid, irregular, chaotic atrial electrical activity (350–600 impulses/min) → irregularly irregular ventricular response → loss of atrial contraction → stasis → thromboembolism risk.
Causes of AF :
- Cardiac: Hypertension (#1), IHD, valvular disease (MS ), cardiomyopathy, post-cardiac surgery, pericarditis
- Non-cardiac: Thyrotoxicosis , pulmonary causes (PE, pneumonia, COPD), alcohol ('holiday heart' ), electrolyte disorders, sepsis
CHA₂DS₂-VASc SCORE
Risk Factor Points C = Congestive heart failure / LV dysfunction 1 H = Hypertension 1 A₂ = Age ≥ 75 years 2 D = Diabetes mellitus 1 S₂ = Stroke/TIA/thromboembolism (previous) 2 V = Vascular disease (MI, PAD, aortic plaque) 1 A = Age 65–74 years 1 Sc = Sex category — Female sex 1 Score 0 (male) / 1 (female): No anticoagulation needed
Score ≥ 1 (male) / ≥ 2 (female): AnticoagulationMax = 9 MANAGEMENT OF NON-VALVULAR AF
Step 1 — Rate control (most patients; rhythm control reserved for symptomatic/young):
▶ Beta-blocker (bisoprolol 2.5–10 mg OD / metoprolol) — 1st line for rate control; target resting HR < 110 bpm
▶ Rate-limiting CCB (diltiazem 60 mg TDS / verapamil) — if beta-blocker contraindicated
▶ Digoxin 0.125–0.25 mg OD — for sedentary/elderly or if CCF present; vagotonic
Step 2 — Rhythm control (cardioversion):
- If AF > 48 hrs or unknown duration : Anticoagulate × 3 weeks before cardioversion (or TOE to exclude LA thrombus) → then cardiovert → anticoagulate × 4 weeks after
- If AF < 48 hrs : Can cardiovert directly (low thrombus risk)
▶ DC cardioversion : 120–200 J biphasic (preferred); or chemical: Flecainide / Amiodarone IV
Step 3 — Anticoagulation (stroke prevention):
▶ DOAC (preferred for non-valvular AF): Apixaban 5 mg BD / Rivaroxaban 20 mg OD / Dabigatran 150 mg BD
▶ Warfarin (INR 2–3) — for valvular AF (rheumatic MS, mechanical prosthetic valve) — DOACs NOT appropriate
Disease Aetiology Key Murmur Key Signs Management MS Rheumatic fever (#1) MDM at apex
Loud S1, OSMalar flush
Tapping apexPTMC or MVR
Warfarin (if AF)MR Rheumatic, MVP , IE, DCM, Papillary rupture PSM at apex
radiates to axillaDisplaced apex (LV enlargement)
Soft S1, S3ACE-I, vasodilators
MVR if EF < 60%AS Bicuspid AV (young)
Calcific degenerative (old > 70)
RheumaticESM at aortic area
radiates to carotids
*Slow rising pulse*Classic triad :
Angina + Syncope + CCF
(survival 5, 3, 2 yrs)TAVR / AVR
if AVA < 1 cm²AR Rheumatic, IE, Marfan's , Aortic dissection EDM at LLSE
Austin Flint murmur (MDM)Collapsing/water hammer pulse
Wide pulse pressure
Duroziez / de Musset / Quincke / TraubeACE-I/vasodilators
AVR if EF < 50%◆ Murmur types at a glance ▸ PSM (Pansystolic murmur) = MR, VSD, TR — fills all of systole ▸ ESM (Ejection Systolic) = AS, PS, ASD, Innocent — crescendo-decrescendo ▸ MDM (Mid-Diastolic) = MS, TS — stenosis of inlet valves ▸ EDM (Early Diastolic) = AR, PR — regurgitation of outlet valves DEFINITION
DCM = dilation of both ventricles (predominantly LV) with impaired systolic function (↓ EF) in the absence of abnormal loading conditions (HTN, valvular disease) or IHD sufficient to cause global dysfunction.
CAUSES
- Idiopathic (#1, ~50%) — possibly post-viral or immune-mediated
- Genetic — familial DCM; mutations in titin (TTN — most common gene), lamin A/C, MYH7
- Viral myocarditis — Coxsackievirus B (most common), adenovirus, CMV, HIV
- Alcohol — >80 g/day for > 5 years; reversible if abstinence early
- Peripartum CM — last month of pregnancy or within 5 months of delivery; EF < 45%
- Drugs : Doxorubicin (anthracyclines), cyclophosphamide, trastuzumab (herceptin)
- Autoimmune (SLE, sarcoidosis); thyroid disease (hypothyroidism, thyrotoxicosis); tachycardia-induced CM
INVESTIGATIONS
- Echo (diagnostic) — dilated LV (LVEDD > 5.5 cm); ↓ EF (< 40%); global hypokinesia; functional MR; ± LV thrombus
- CXR — cardiomegaly (cardiothoracic ratio > 0.5); pulmonary oedema pattern
- ECG — LBBB ; sinus tachycardia; non-specific ST-T changes; AF; LV hypertrophy
- BNP/NT-proBNP — markedly elevated; guides treatment and prognosis
- Cardiac MRI — gold standard for myocardial tissue characterisation; identifies fibrosis (gadolinium LGE)
- Endomyocardial biopsy — rarely needed; for suspected giant cell myocarditis or specific diagnoses
MANAGEMENT
- Four pillars of HFrEF : ACE-I/ARNI + Beta-blocker + MRA + SGLT2i (same as heart failure management)
- Anticoagulation : If EF < 35% + LBBB OR AF + DCM → warfarin/DOAC (mural thrombus risk)
- ICD : EF ≤ 35% after 3 months optimal therapy → prevents SCD
- CRT : EF ≤ 35% + QRS ≥ 130 ms + LBBB
- Cardiac transplantation — refractory end-stage DCM; EF < 25%; NYHA IV despite optimal therapy
- Stop the cause: Alcohol abstinence; stop cardiotoxic drugs; treat underlying infection/autoimmune
DEFINITION & GENETICS
HOCM (also called HCM) = asymmetric septal hypertrophy causing dynamic LVOTO (LV outflow tract obstruction) + diastolic dysfunction. Autosomal dominant ; most common genetic cardiovascular disease (1:500). Most common cause of sudden cardiac death (SCD) in young athletes .
- Most common gene mutations: β-myosin heavy chain (MYH7) and myosin-binding protein C (MYBPC3) (most common overall)
CLINICAL FEATURES
- Classic triad : Exertional syncope + Exertional chest pain + Palpitations in a young athlete
- SCD — often first presentation; VF/VT during exercise; classic 'athlete collapse on field'
- Dyspnoea (diastolic dysfunction); family history of sudden death
Physical signs:
- Harsh ESM at LLSE (not aortic area!); radiation to axilla; does NOT radiate to carotids (unlike AS)
- Murmur INCREASES with Valsalva manoeuvre, standing, exercise (↓ preload → more obstruction)
- Murmur DECREASES with squatting, lying down, handgrip (↑ preload → less obstruction)
- Bifid pulse / bisferiens pulse (double-peaked arterial waveform); S4 gallop; double apical impulse
MANAGEMENT
- Avoid: Exercise , dehydration, vasodilators (nitrates), digoxin, diuretics (all reduce preload → worsen obstruction)
▶ Beta-blockers (bisoprolol/metoprolol) — 1st line; slow HR → ↑ filling time → ↓ obstruction; reduce symptoms
▶ Disopyramide — if beta-blocker insufficient; negative inotrope; ↓ LVOTO gradient
▶ Verapamil — if beta-blocker contraindicated; improves diastolic function
- ICD : Any major risk factor for SCD (prior SCA, sustained VT, massive hypertrophy > 30 mm, family history of SCD, unexplained syncope, NSVT)
- Septal reduction therapy : Gradient > 50 mmHg + refractory symptoms: Septal myectomy (surgical, gold standard ) OR Alcohol septal ablation (catheter-based)
▶ Mavacamten (EXPLORER-HCM 2020) — cardiac myosin inhibitor; reduces LVOTO gradient; approved for obstructive HCM with EF ≥ 55%
ACUTE PERICARDITIS
Definition: Inflammation of the pericardium (fibroserous sac surrounding the heart). Causes: Viral (#1 — Coxsackievirus B, adenovirus), TB (exudative), uraemia (fibrinous), post-MI (Dressler's) , malignancy, autoimmune (SLE, RA).
Clinical features — diagnostic triad :
- Sharp, pleuritic chest pain — worsened lying flat, relieved sitting forward ('mosque sign' )
- Pericardial friction rub — scratchy, leathery sound; best heard at LLSE with patient leaning forward; 3-component (systolic + early diastolic + presystolic)
- ECG: Diffuse saddle-shaped ST elevation in all leads (not territory-specific) + PR depression (early finding)
▶ 1st line : Aspirin 750 mg–1 g TDS × 1–2 weeks + Colchicine 0.5 mg BD × 3 months (reduces recurrence by 50% — COPE trial)
▶ Avoid NSAIDs if post-MI (worsen healing). Restrict exercise until symptom-free. Corticosteroids only if contraindication to NSAIDs.
CHRONIC CONSTRICTIVE PERICARDITIS
Definition: Chronic fibrous thickening and calcification of pericardium → constricts cardiac filling → all chambers equally pressured → pressure equalization.
- Causes: TB (#1 worldwide), viral, post-radiation, post-cardiac surgery
- Kussmaul's sign — paradoxical RISE in JVP on inspiration (normally JVP falls on inspiration)
- Pericardial knock — early diastolic sound (like S3 but earlier); abrupt cessation of ventricular filling
- CXR: Pericardial calcification ('eggshell' calcification); right heart enlargement; no pulmonary oedema
- Echo: Respiratory variation in mitral inflow > 25% ; pericardial thickening; septal bounce
- Treatment : Pericardiectomy (surgical stripping) — definitive; anti-TB therapy if TB cause
DEFINITION
Cardiac tamponade = compression of the heart by fluid accumulating in the pericardial space → ↑ intrapericardial pressure → impairs cardiac filling → ↓ CO → haemodynamic collapse. As little as 100–200 mL can cause tamponade if rapid.
- Causes: Penetrating trauma , malignancy (#1 medical cause), TB , uraemia, post-cardiac surgery, PE, aortic dissection, post-MI (free wall rupture)
CLINICAL FEATURES — BECK'S TRIAD
Beck's Triad of Cardiac Tamponade → 1. Hypotension (↓ BP) — ↓ CO from impaired filling → 2. Raised JVP (↑ venous pressure) — impaired right heart filling → 3. Muffled heart sounds — fluid insulates heart sounds - Pulsus paradoxus — fall in SBP > 10 mmHg on inspiration (normally < 10 mmHg); due to inspiratory ↑ RV filling compressing LV (interdependence in tamponade)
- Tachycardia (earliest sign); dyspnoea; oliguria; restlessness → shock
- Kussmaul's sign ABSENT in tamponade (present in constrictive pericarditis) — key differentiator
Investigations:
- Echo (bedside POCUS — most important): RA collapse in systole (earliest); RV collapse in diastole ; plethoric IVC (no collapse); > 25% respiratory variation in mitral inflow
- CXR: Cardiomegaly (globular, flask-shaped heart ) — if > 200 mL accumulated slowly
- ECG: Electrical alternans (alternating QRS height due to swinging heart); sinus tachycardia; low voltage
TREATMENT
- Pericardiocentesis (needle drainage) — emergency treatment; drain pericardial fluid; immediate haemodynamic improvement
- Surgical pericardial window — for recurrent tamponade or malignant cause
🔑Key Point — Electrical alternans = pathognomonic of large pericardial effusion / tamponade on ECG. QRS axis alternates every beat due to pendulous heart swinging in fluid.DEFINITION
RCM = impaired diastolic filling of ventricles (stiff, non-compliant) with preserved systolic function (EF normal) , due to infiltration or fibrosis of myocardium. Heart size normal or mildly enlarged.
CAUSES
- Amyloidosis (#1 in developed countries) — AL amyloid (myeloma) or ATTR amyloid (senile, familial); 'sparkling' myocardium on echo
- Haemochromatosis — iron deposition; causes DCM + RCM; treat with venesection/deferasirox
- Sarcoidosis — non-caseating granulomas; AV block + VT + RCM; treat with steroids
- Löffler's endocarditis — eosinophilic infiltration → endomyocardial fibrosis → RCM
- Post-radiation fibrosis; glycogen storage diseases (Fabry's disease — X-linked, alpha-galactosidase deficiency)
CLINICAL FEATURES — Differentiate from Constrictive Pericarditis
Feature RCM Constrictive Pericarditis Kussmaul's sign Present Present (both have it) Pericardial knock Absent Present Pericardial calcification Absent Present on CXR (TB aetiology) Echo Sparkling (amyloid) ; thick walls; biatrial enlargement Thick pericardium; septal bounce BNP/NT-proBNP Markedly ↑ Modestly elevated Cardiac MRI LGE (late gadolinium) in amyloid Pericardial enhancement Biopsy Definitive (amyloid = apple-green birefringence ) Pericardial thickening on MRI - Treatment: Treat underlying cause (venesection for haemochromatosis; steroids for sarcoidosis; cardiac transplant for amyloid)
- Avoid digoxin in amyloid (accumulates in amyloid fibrils → toxicity)
- Hypertensive urgency: SBP > 180 / DBP > 120 without organ damage → oral therapy → reduce over 24–48 hrs
- Hypertensive emergency : Same BP + acute target organ damage (brain, heart, kidney, eye) → IV therapy → reduce MAP by max 25% in 1st hour
▶ Hypertensive emergency: Sodium nitroprusside IV / Labetalol IV / Hydralazine IV (pregnancy) / GTN IV (LVF)
- Exception — Aortic dissection : Reduce SBP < 120 mmHg rapidly with IV labetalol + nitroprusside
- First-line antihypertensives (ABCD): A=ACE-I/ARB | B=Beta-blocker | C=CCB (Amlodipine) | D=Diuretic (thiazide)
- Pregnancy : Methyldopa (#1) / Labetalol / Nifedipine. Avoid ACE-I/ARBs (teratogenic)
RISK FACTORS FOR CAD
- Non-modifiable : Age (M > 45; F > 55), Male sex, Family history (1st-degree relative < 55M / < 65F), Genetic dyslipidaemia
- Modifiable (traditional) : Hypertension (#1 modifiable), Dyslipidaemia, Smoking , DM, Obesity, Physical inactivity
- Emerging : hsCRP, Lp(a), homocysteine, microalbuminuria, CIMT (carotid intima-media thickness)
INVESTIGATIONS
- Resting ECG — ST changes, T-wave inversions, Q waves, LBBB
- Exercise Stress Test (EST/TMT) — most useful non-invasive test; 1 mm horizontal/downsloping ST depression at heart rate (220 - age) × 85% = positive
- Stress echocardiography — wall motion abnormalities with exercise/dobutamine; better sensitivity than EST
- Myocardial perfusion scan (SPECT/MPS) — technetium-99m sestamibi; reversible defect = ischaemia; fixed defect = scar
- CT coronary angiography (CTCA) — non-invasive; calcium score; plaque morphology; rules out CAD (high NPV)
- Coronary angiography — GOLD standard; invasive; anatomy of stenosis; FFR > 0.80 = not haemodynamically significant
LIPID FRACTIONS
Lipid Fraction Normal Key Facts LDL cholesterol < 100 mg/dL (< 70 in very high risk) Primary target of therapy; most atherogenic; calculated by Friedewald equation HDL cholesterol M: > 40; F: > 50 mg/dL 'Good cholesterol' — reverse cholesterol transport; ↑ HDL = protective; ↑ by exercise, niacin, alcohol Triglycerides < 150 mg/dL ↑ TG = VLDL excess; pancreatitis risk if > 500; niacin + fibrates most effective Total Cholesterol < 200 mg/dL Screening tool; includes all fractions VLDL < 30 mg/dL Carries TG; calculated as TG/5; converted to LDL in circulation Lp(a) < 30 mg/dL Independent risk factor; not reduced by statins; reduced by PCSK9 inhibitors Friedewald equation : LDL = Total Cholesterol − HDL − (TG/5)
💡CLINICAL PEARL: Statin therapy : Atorvastatin 40–80 mg OD (high-intensity). All ACS/STEMI/post-MI patients get high-intensity statin regardless of baseline LDL. Reduces CV events by 25–35%.Feature Stable Angina Unstable Angina Prinzmetal Angina Pathology Fixed atherosclerotic stenosis > 70% Plaque rupture + partial thrombosis Coronary vasospasm (no fixed stenosis) Trigger Exertion ; cold; emotion Rest ; minor exertion; accelerating Rest ; early morning ; cyclical Duration < 15 min; GTN relieves in 5 min > 15 min; GTN unreliable Variable; may be prolonged ECG Normal or ST-depression (during episode) ST depression/T inversion; or normal Transient ST elevation (during spasm) Troponin Normal Normal (elevated = NSTEMI) Normal Treatment BB + CCB + nitrates + aspirin + statin Hospitalise; DAPT + anticoagulation + revascularisation CCB (nifedipine/diltiazem); nitrates; avoid beta-blockers ⚠️DANGER / REMEMBER: Prinzmetal/Vasospastic angina : CCB is the treatment of choice. Beta-blockers are CONTRAINDICATED (may worsen spasm by unopposed alpha-activity). Drug of choice = Nifedipine or Diltiazem.Test Method Sensitivity Key Points EST / TMT Treadmill; Bruce protocol; target 85% max HR 60–70% 1 mm horiz/down ST depression = +ve; stop if: chest pain, ST > 2 mm, BP drop > 10 mmHg, arrhythmia, fatigue Stress Echo 2D echo during exercise or dobutamine stress 80–85% New RWMA (regional wall motion abnormality) = ischaemia; better than EST in LBBB, pacemaker, uninterpretable ECG Myocardial Perfusion Scan (SPECT) 99mTc-sestamibi or Tl-201; rest vs stress images 85–90% Reversible defect = ischaemia ; Fixed defect = infarct/scar ; PET scan = gold standard for viability CT Coronary Angiography (CTCA) 64-slice/320-slice CT; calcium scoring + lumen 98% NPV Calcium score 0 = very low risk; high NPV for ruling out CAD; not useful if calcium score > 400 Cardiac MRI (CMR) Adenosine/regadenoson stress > 90% Best for viability (LGE = scar); identifies hibernating myocardium; tissue characterisation TMT/EST contraindications : Acute MI (< 2 days), Unstable angina, Severe AS, Uncontrolled HF, Severe HTN (> 200/110), Acute myocarditis/pericarditis, Severe arrhythmias. VAUGHAN WILLIAMS CLASSIFICATION
Class Mechanism Drugs Main Use Class I Sodium channel blockers
(↓ Phase 0 depolarisation)Ia: Quinidine, Procainamide, Disopyramide
Ib: Lidocaine (VT in MI), Mexiletine
Ic: Flecainide (AF), PropafenoneVT; AF (Ic); VF (Ib) Class II Beta-blockers
(↑ AV node refractory period)Metoprolol, Bisoprolol, Atenolol, Propranolol, Carvedilol SVT; rate control in AF/flutter; post-MI VT prevention Class III K⁺ channel blockers
(↑ action potential duration)Amiodarone , Sotalol, Dronedarone AF/flutter cardioversion; refractory VT/VF; amiodarone most broad-spectrum Class IV CCB (non-DHP)
(↓ AV node conduction)Verapamil , Diltiazem SVT termination; rate control in AF Other Cardiac glycoside; adenosine Digoxin; Adenosine (6/12/18 mg rapid IV push) Rate control in AF; PSVT termination (adenosine — drug of choice) ✍️EXAM TIP: Amiodarone — most effective antiarrhythmic; Class III but has all 4 class properties. Side effects: Pulmonary toxicity , Thyroid (hypo/hyper) , Liver toxicity, Corneal deposits, Photosensitivity, Blue-grey discolouration (check TFT, LFT, CXR, PFT annually).ATRIAL FLUTTER
- Macro-reentry circuit in right atrium around tricuspid annulus (cavotricuspid isthmus)
- Atrial rate 250–350 bpm ; AV conduction usually 2:1 → ventricular rate ~150 bpm
- ECG: Sawtooth flutter waves best seen in II, III, aVF; regular R-R interval (if fixed block); no isoelectric baseline
- Treatment: Rate control (beta-blocker/CCB/digoxin); DC cardioversion 50–100 J (highly responsive); Catheter ablation of CTI — curative, >95% success rate
PSVT — DEFINITION
Paroxysmal Supraventricular Tachycardia (PSVT) = sudden onset, regular, narrow-complex tachycardia (HR 150–250 bpm) most commonly due to AV nodal re-entry (AVNRT — #1, 60%) or AV re-entry via accessory pathway (AVRT — 30%) as in WPW syndrome.
- C/F: Sudden onset palpitations ; may have neck pulsations (cannon a-waves); dizziness; polyuria (after termination); may terminate spontaneously or with Valsalva
- ECG: Regular narrow QRS at 150–250 bpm; P waves buried in or just after QRS (AVNRT) or retrograde P after QRS (AVRT)
TREATMENT — LADDER APPROACH
- Vagal manoeuvres (first-line): Valsalva manoeuvre (strain against closed glottis) → carotid sinus massage (one side only; listen for bruit first); eyeball pressure (avoid — risk of retinal detachment)
- Adenosine (drug of choice): 6 mg rapid IV push → flush; if no response → 12 mg → 18 mg. Half-life 10 sec; blocks AV node transiently → terminates AV-dependent tachycardia. Side effects: chest tightness, flushing, transient asystole (brief), bronchospasm (caution in asthma )
▶ Adenosine 6 mg IV rapid bolus (if no response → 12 mg → 18 mg)
- If adenosine fails / contraindicated: Verapamil 5 mg IV over 2 min; or Diltiazem IV; or Metoprolol IV
- If haemodynamically unstable: Synchronised DC cardioversion (50–100 J)
- Long-term prevention: Catheter ablation of accessory pathway / slow AV nodal pathway — curative (> 95% success)
ELECTRICAL CARDIOVERSION
Cardioversion = delivery of a synchronised DC electric shock (timed to QRS) to terminate arrhythmia. 'Synchronised' avoids shock on T-wave (which would cause VF).
- AF: 120–200 J biphasic; anterior-posterior or anterior-lateral paddle position
- Atrial flutter: 50–100 J (highly responsive; lowest energy needed)
- PSVT / SVT: 50–100 J if haemodynamically unstable
- VT (with pulse): 100–200 J synchronised
- VF / Pulseless VT : 200 J UNSYNCHRONISED (defibrillation) → not synchronised as no organised QRS to synchronise to
AV BLOCK CLASSIFICATION
Block Degree ECG Features Action 1st degree Prolonged PR interval (> 0.20 sec)
All P waves conductObserve; usually benign; no treatment needed 2nd degree — Mobitz I (Wenckebach) Progressive PR lengthening then dropped QRS
Block at AV node; usually benignObserve if asymptomatic; may need pacing if symptomatic 2nd degree — Mobitz II Fixed PR interval; sudden dropped QRS
Block below AV node (His-Purkinje)High risk of CHB — pace! (permanent pacemaker) Complete (3rd degree) CHB P and QRS completely dissociated
Escaperate depends on site:
40–60 bpm (junctional); < 30 bpm (ventricular)Emergency pacing CAUSES OF COMPLETE HEART BLOCK
- IHD / Acute MI — inferior MI (RCA) → conduction system ischaemia; most common cause
- Idiopathic fibrosis (Lenegre's / Lev's disease) — progressive degeneration of conduction system; elderly
- Drugs — beta-blockers, digoxin toxicity, calcium channel blockers, amiodarone, lithium
- Infections: Lyme disease (Borrelia — consider in endemic areas), rheumatic fever, infective endocarditis, Chagas disease
- Infiltrative: Sarcoidosis , amyloidosis, haemochromatosis
- Congenital CHB — associated with maternal anti-Ro/La antibodies (SLE); neonatal lupus
TREATMENT
- Acute/Emergency: IV Atropine 0.6–1.2 mg (if rate < 40 bpm; transient) → Temporary transvenous pacing
- Isoprenaline infusion (2–10 μg/min) — beta-1 agonist → ↑ escape rhythm rate; bridge to pacing
- Permanent pacemaker — definitive treatment for symptomatic CHB or Mobitz II; VVI or DDD pacemaker
- DDD pacemaker (dual-chamber) — senses both atria/ventricles and paces both; maintains AV synchrony → preferred if SA node intact
JVP — JUGULAR VENOUS PRESSURE
JVP reflects right atrial pressure. Measured at 45° with patient semi-recumbent; use internal jugular vein (better reflects RA pressure). Normal JVP ≤ 4 cm above sternal angle (≤ 9 cmH2O).
Normal JVP waveform :
Wave Origin Timing 'a' wave RA contraction (presystole) Just before S1 'c' wave Tricuspid valve closure / carotid pulsation artifact After S1 'x' descent RA relaxation + tricuspid descent during systole Systole 'v' wave Passive venous filling of RA (tricuspid closed) Late systole 'y' descent Tricuspid opening → RV filling Early diastole Abnormal JVP waveforms :
- Cannon a-waves — large 'a' waves when RA contracts against closed tricuspid valve: CHB (regular cannon a-waves) or VT (irregular cannon a-waves)
- Absent 'a' wave — AF (no atrial contraction)
- Large 'v' waves — TR (regurgitant wave into RA during systole); VSD
- Steep 'y' descent — constrictive pericarditis (Friedreich's sign); TR
- Elevated + fixed JVP + Kussmaul's — constrictive pericarditis
HAEMODYNAMIC MONITORING
Parameter Normal Value Clinical Significance CVP (Central Venous Pressure) 0–8 mmHg Right heart preload; ↑ in RHF, tamponade; ↓ in hypovolaemia PCWP (Pulmonary Capillary Wedge Pressure — Swan-Ganz) 6–12 mmHg LV preload/LAP surrogate; ↑ in LHF/pulmonary oedema; ↓ in hypovolaemia CO (Cardiac Output) 4–8 L/min Thermodilution or Fick principle; ↓ in cardiogenic shock SVR 800–1200 dyn·sec·cm⁻⁵ Afterload; ↑ in cardiogenic shock; ↓ in septic shock SvO₂ 60–75% Mixed venous O2; ↓ = ↑ extraction (↓ CO or ↑ demand) - DVT diagnosis: Compression USS (non-compressible vein = diagnostic); D-dimer to exclude if Wells DVT score low
- PE diagnosis: Wells score → if ≤ 4: D-dimer → if > 4: CTPA (gold standard)
- PE C/F: Sudden dyspnoea (80%) + tachycardia (90%) + pleuritic chest pain; normal CXR
- ECG in PE: Sinus tachycardia (#1) + S1Q3T3 (20%) + RBBB + T inversion V1–V4
- Massive PE: Alteplase 100 mg IV over 2 hrs (thrombolysis)
- Low-risk PE: DOAC (rivaroxaban / apixaban) → anticoagulate 3–6 months (provoked) or longer (unprovoked)
💡CLINICAL PEARL: STF (Systemic Thrombolytic Therapy) = Alteplase 100 mg IV over 2 hrs. Indicated in massive PE with haemodynamic compromise (SBP < 90 mmHg). Reduce door-to-drug time.BUDD-CHIARI SYNDROME
Budd-Chiari syndrome = obstruction to hepatic venous outflow (hepatic veins or IVC) → hepatic venous hypertension → congestive hepatopathy → portal hypertension + ascites .
- Causes : Hypercoagulable states (#1) — Polycythaemia vera , PNH , Antiphospholipid syndrome, JAK2 V617F mutation ; OCP; pregnancy; tumour invasion (HCC); Behçet's disease
- Classic triad : RUQ pain + Tender hepatomegaly + Ascites (SADHE — Sudden Ascites, Distended Hepatic veins, Hepatomegaly, Elevated liver enzymes)
- Imaging : Doppler USS — hepatic vein not visualised / reversed flow; caudate lobe hypertrophy (caudate drains directly into IVC — preserved while other lobes congested)
▶ Anticoagulation (LMWH → warfarin) — all patients. TIPS (transjugular intrahepatic portosystemic shunt) — for refractory ascites. Liver transplant — severe/refractory. Treat underlying thrombophilia (hydroxyurea for PV).
ANGIOEDEMA
Angioedema = non-pitting, non-inflammatory deep subcutaneous/submucosal swelling of face, lips, tongue, throat, hands, genitalia. Potentially life-threatening if laryngeal.
- Allergic/IgE-mediated : Allergens (foods, insect stings, latex); ± urticaria + anaphylaxis; histamine-mediated → treat with adrenaline + antihistamine + steroids
- ACE inhibitor-induced : Bradykinin accumulation (ACE normally degrades bradykinin) → 1–3% of ACE-I users; onset weeks-years after starting; NO urticaria ; treat with FFP or Icatibant (bradykinin receptor antagonist ); switch to ARB
- Hereditary angioedema (HAE) : C1-esterase inhibitor (C1-INH) deficiency; autosomal dominant; recurrent non-itchy swelling without urticaria; abdominal pain (visceral oedema); treat acute: C1-INH concentrate or Icatibant; prophylaxis: Tranexamic acid / Danazol
DEFINITION & TYPES
Raynaud's phenomenon = episodic vasospasm of digital arteries and arterioles triggered by cold or emotional stress, causing triphasic colour change of fingers (and toes).
Feature Primary Raynaud's Secondary Raynaud's (Raynaud's Phenomenon) Aetiology Idiopathic; no underlying disease Associated with connective tissue disease : Systemic sclerosis (#1), SLE, RA, dermatomyositis Age/Sex Young women; onset 15–30 yrs Middle-aged; more severe Severity Mild; no tissue damage Digital ulcers , gangrene, ↑ risk of tissue loss ANA/specific antibodies Negative Positive (ANA, anti-Scl70 in scleroderma ) Nailfold capillaroscopy Normal Abnormal — dilated, tortuous capillaries + dropout Classic triphasic colour change :
- White (pallor) — vasospasm → ischaemia → white/pallid digits
- Blue (cyanosis) — hypoxia → deoxygenation → blue digits
- Red (erythema) — reperfusion → reactive hyperaemia → red/warm digits with pain/tingling
MANAGEMENT
- Non-pharmacological: Keep hands warm (gloves); avoid cold; stop smoking; avoid beta-blockers and vasoconstrictors
▶ Nifedipine (slow-release) 5–20 mg TDS — 1st line; CCB; most effective; reduces frequency and severity of attacks
▶ Amlodipine 5–10 mg OD — alternative CCB
▶ Sildenafil 25–100 mg TDS (PDE5 inhibitor) — for severe/refractory; reduces pulmonary and digital vascular tone
▶ Iloprost IV infusion — for digital ulcers; prostacyclin analogue; powerful vasodilator
- Treat underlying disease in secondary Raynaud's (immunosuppressives for scleroderma/SLE)
Cardiac arrest = sudden cessation of cardiac mechanical activity with loss of consciousness and absence of spontaneous breathing and pulse. Immediate BLS then ACLS.
SHOCKABLE vs NON-SHOCKABLE RHYTHMS
Category Rhythms Treatment Shockable VF (Ventricular Fibrillation)
Pulseless VTImmediate defibrillation 200 J biphasic → CPR × 2 min → recheck rhythm
+ Adrenaline 1 mg IV after 3rd shock
+ Amiodarone 300 mg IV after 3rd shockNon-shockable PEA (Pulseless Electrical Activity)
AsystoleCPR × 2 min + Adrenaline 1 mg IV every 3–5 min
+ Identify and treat reversible causes (4H/4T)◆ Reversible causes — 4H's + 4T's ▸ 4H: Hypoxia | Hypovolaemia | Hypo/Hyperkalaemia (electrolytes) | Hypothermia ▸ 4T: Tension pneumothorax | Tamponade (cardiac) | Thrombosis (MI / PE) | Toxins (drugs/poisons) ▶ Adrenaline (Epinephrine) 1 mg IV every 3–5 min — alpha-vasoconstriction → ↑ coronary + cerebral perfusion pressure; used in ALL rhythms
▶ Amiodarone 300 mg IV bolus — after 3rd shock in refractory VF/pVT; then 150 mg if recurs; maintenance 900 mg over 24 hrs
- Post-ROSC care : O2 (SpO2 94–98%); treat BP; targeted temperature management (TTM) 32–36°C × 24 hrs (comatose survivors); coronary angiography if cardiac cause
AORTIC REGURGITATION (AR) — Water Hammer Pulse
AR peripheral signs arise from wide pulse pressure (high SBP due to ↑ stroke volume + low DBP due to regurgitation):
Sign Test What You Find Corrigan's (water hammer) pulse Palpate radial artery with wrist raised Rapid rise + rapid collapse; bounding quality de Musset's sign Inspect patient's head Head nodding with each heartbeat Quincke's sign Press on nail bed to show capillary Visible capillary pulsation (nail bed flush + pallor) Duroziez's sign Partial compression of femoral artery with stethoscope Systolic + diastolic bruit Traube's sign Auscultate over femoral artery 'Pistol shot' sound — systolic + diastolic Mueller's sign Inspect uvula Pulsating uvula Austin Flint murmur : Mid-diastolic murmur at apex in severe AR — regurgitant jet flutters anterior MV leaflet → functional MS; no opening snap (leaflets not thickened).
EISENMENGER'S SYNDROME
Eisenmenger's syndrome = reversal of intracardiac shunt from L→R to R→L due to irreversible pulmonary arterial hypertension (PAH) from longstanding left-to-right shunt causing progressive pulmonary vascular obliteration.
- Most common underlying defects: VSD → PDA → ASD (VSD causes Eisenmenger's fastest)
- Central cyanosis + Clubbing (particularly of lower limbs if PDA — differential cyanosis )
- Not operable — surgical correction contraindicated once Eisenmenger's established
▶ Treatment: Bosentan (endothelin receptor antagonist — ERA) / Sildenafil / Macitentan — reduce PAH; lung-heart transplantation in selected cases
PULSUS PARADOXUS
Pulsus paradoxus = fall in SBP > 10 mmHg on normal inspiration (normally < 10 mmHg fall). Detected with sphygmomanometer — first Korotkoff sounds first audible only in expiration; then audible in both phases.
- Causes : Cardiac tamponade (#1), constrictive pericarditis (mild), severe asthma (exaggerated pulsus paradoxus), COPD, tension PTX
- Mechanism: Inspiratory ↑ RV filling due to ↑ venous return → interventricular interdependence → septum shifts L → compresses LV → ↓ LV filling → ↓ SBP on inspiration
CLASSIFICATION
Category Causes Key Features Atherosclerosis (#1) DM , HTN , Smoking , Dyslipidaemia, Age Gradual; Claudication (leg pain on walking, relieved by rest); ABPI < 0.9 Thromboangiitis Obliterans (TAO/Buerger's) Heavy smoker (young male < 45) Segmental thrombosis; superficial migratory thrombophlebitis ; starts distally; rest pain + gangrene ; ABI < 0.5 Acute limb ischaemia Embolism (AF #1 source), Thrombosis 6 P's : Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishingly cold Takayasu's arteritis Young Asian women; large vessel vasculitis 'Pulseless disease ' — absent radial pulses; arm claudication; ↑ ESR; treat with steroids Raynaud's See SN21 Digital vasospasm; triphasic colour change Fontaine Classification of Peripheral Arterial Disease (PAD) :
- Stage I: Asymptomatic; ABPI 0.7–0.9
- Stage II: Intermittent claudication; ABPI 0.5–0.7 (IIa: > 200 m walking; IIb: < 200 m)
- Stage III: Rest pain ; ABPI < 0.5; critical limb ischaemia threshold
- Stage IV: Tissue loss — ulcers or gangrene ; ABPI < 0.3
Management of PAD: Smoking cessation (most important); antiplatelet (aspirin/clopidogrel); statin; supervised exercise; consider revascularisation (angioplasty/bypass) for critical limb ischaemia.
DEFINITION
Rheumatic Heart Disease (RHD) = chronic, progressive valvular damage resulting from repeated episodes of acute rheumatic fever (ARF) . Each recurrence causes further valve scarring. The heart is the only organ that suffers permanent damage from ARF.
VALVE INVOLVEMENT — ORDER
Rank Valve Lesion Key Features #1 Mitral valve MS > MR (stenosis dominates with recurrence) Classic MS = commissural fusion; MDM; OS; loud S1 #2 Aortic valve AR > AS EDM; wide pulse pressure; Corrigan's pulse #3 Tricuspid valve TR > TS ↑ JVP; large v-waves; peripheral oedema Rare Pulmonary valve PR Usually uninvolved Combined MS + MR + AR + TS Multivalvular Most common combined: MS + AR CLINICAL FEATURES
- History of ARF / sore throat in childhood; often from low-income, overcrowded background
- Dyspnoea (progressive — MSex → orthopnoea → PND → rest) — due to MS + LVF
- Haemoptysis — rupture of bronchopulmonary veins (pulmonary venous hypertension in MS)
- Palpitations — AF develops in ~40% (from LA dilation); risk of stroke
- Systemic emboli — stroke, limb ischaemia from LA/LV thrombi in AF context
- Malar flush (mitral facies) — plum-coloured cheek flush
MANAGEMENT
- Medical: Diuretics; beta-blockers (slow HR); warfarin if AF (DOACs NOT appropriate in rheumatic AF )
- Antibiotic prophylaxis : Benzathine Penicillin G 1.2 MIU IM every 3–4 weeks (prevent streptococcal reinfection → further ARF → valve damage)
- Valve intervention:
- PTMC (Percutaneous Transvenous Mitral Commissurotomy) — for pliable MS; Wilkins score ≤ 8; no MR or LA thrombus
- Mitral Valve Replacement (MVR) — calcified, immobile valve; moderate MR; failed PTMC
- AVR for significant AR or AS; combined MVR + AVR for multivalvular disease
🔑Key Point — RHD prevention is the most important intervention . ARF can be prevented 100% by prompt treatment of GAS throat infection with penicillin. Once RHD established, secondary prophylaxis (BPG) prevents further valve damage.