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Cardiology Study Index and Classifications

Written by Betra Youhanna, a medical student and not a doctor — check every detail against your own teaching.

ICC-1 finals revision · 62 diseases + 55 criteria · Compiled from TheStudyFix deck

C/P
Inves
Mng
Special — pathognomonic

Ischaemic Heart Disease / ACS

5 entries
1

Stable Angina (Chronic Coronary Syndrome)

C/P
  • Predictable exertional chest pain, relieved by rest/GTN within minutes
  • Radiation to arms / jaw, ± sweating
  • Normal resting exam + normal resting ECG
  • Angina equivalents may replace chest pain — dyspnoea, fatigue, faintness
Inves
  • Stress ECG, stress echo, CT coronary angiography
  • Lipids, glucose, U&E, LFT
  • Resting ECG (rule out resting ischaemia)
  • Myocardial perfusion (thallium) scan — stress with exercise, or dobutamine if unable to exercise; reversible defect on stress only = inducible ischaemia, fixed defect on stress + rest = infarct
Mng
  • Aspirin + β-blocker + statin + sublingual GTN PRN
  • Add CCB or long-acting nitrate / nicorandil / ranolazine / ivabradine if uncontrolled
  • ACEi if echo abnormal; smoking cessation
  • PCI/CABG only if medical Rx fails or anatomy demands
Special
  • "Demand-induced" ischaemia — no resting ECG change between attacks
  • ST depression on stress (downsloping/horizontal) but baseline normal
physiology · background · low-yield
Mechanism
  • Fixed 80–90% stenosis; the ~10% residual lumen is adequate at rest — ischaemia occurs only when HR/demand rises, relieved when HR normalises
Other
  • Beta-blockers must not be stopped abruptly — rebound may precipitate dangerous arrhythmias, worsening angina or MI
  • Short-acting nifedipine can aggravate myocardial ischaemia (reflex tachycardia); verapamil is the CCB for re-entrant tachycardia
Epidemiology/Risk
  • CAD/IHD is the single leading cause of death worldwide (~29% of male, ~28% of female deaths); modifiable RFs = smoking, diabetes, hypertension, dyslipidaemia; non-modifiable = age, sex, family history, ethnicity
Exam technique
  • Levine's sign — clenched fist held over the sternum when describing ischaemic chest pain
2

Unstable Angina

C/P
  • New-onset, rest, or crescendo angina — pain >15 min, sweating
  • Normal troponin (distinguishes from NSTEMI)
Inves
  • 12-lead ECG: ST depression / T inversion / normal
  • Serial troponin (negative)
  • Echo
Mng
  • MONA-B (Morphine, O₂ if SpO₂ <94%, Nitrate, Aspirin 300 mg, β-blocker)
  • Clopidogrel/ticagrelor + LMWH/fondaparinux
  • Risk-stratify → invasive angiography per ACS pathway
Special
  • Troponin-negative ACS — only feature separating it from NSTEMI
3

NSTEMI

C/P
  • Chest pain >15 min at rest, sweating, may be atypical (elderly/diabetic)
  • Hemodynamic compromise / arrhythmia in high-risk
Inves
  • ECG: ST depression ± T inversion (no persistent ST elevation)
  • Rising/falling troponin above 99th percentile
  • Echo, lipid profile, glucose, U&E
Mng
  • MONA-B + dual antiplatelet (aspirin + ticagrelor/clopidogrel) + anticoagulant
  • NO thrombolytics (contraindicated)
  • Risk-stratify: Very high → angio <2 h; High → <24 h; Intermediate → <72 h; Low → non-invasive testing
  • Post-MI: SAAB (Statin, Aspirin, ACEi, β-blocker) + 2nd antiplatelet
Special
  • Posterior STEMI masquerades as NSTEMI — ST depression V1–V3 with tall R waves; always check posterior leads
  • Subendocardial (non-transmural) infarct — usually >1 artery severely stenosed with diffuse subendocardial ischaemia (no single territory), unlike single-vessel transmural STEMI
physiology · background · low-yield
Mechanism
  • Subendocardium is most vulnerable — coronaries are a diastolic circulation, perforators are compressed in systole, and it lies furthest from the coronaries (least supply)
4

STEMI

C/P
  • Severe crushing/heavy chest pain, sweating, nausea, radiation to arm/jaw, >20 min
  • ± Pulmonary oedema, cardiogenic shock, arrhythmia
  • Inferior MI may present with hypotension, bradycardia (vagal)
Inves
  • ECG: ST elevation in ≥2 contiguous leads
    • Anteroseptal V1–V4 (LAD)
    • Anterolateral V3–V6 + I + aVL (LAD diagonal / LCx)
    • Extensive anterior I + aVL + V1–V6 (proximal LAD — most dangerous)
    • Inferior II, III, aVF (RCA ± LCx) — reciprocal in I, aVL
    • Posterior tall R + ST depression V1–V3 (LCx / RCA)
    • RV V3R, V4R (RCA — suspect with inferior STEMI)
  • Hyperacute T (earliest), then ST elevation → Q waves at 8–12 h → T inversion → ST normalises (Q persists)
  • Troponin (rising/falling), CBC, U&E, glucose, coag, lipids
  • CK-MB vs troponin kinetics: CK-MB peaks ~24 h, normalises in 2–3 days → marker for suspected re-infarction; troponin stays elevated ~7–10 days → marker for late / missed presentation
Mng
  • MONA-B + dual antiplatelet + anticoagulant (heparin)
  • Time to PCI ≤120 min → primary PCI (wire crossing <90 min)
  • Time to PCI >120 min → fibrinolysis <10 min → transfer for PCI
  • RV infarct: NO nitrates (severe hypotension) — give fluids
  • Post-MI: SAAB long-term
  • Complications: LV failure, papillary muscle rupture (acute MR), VSD, free wall rupture (tamponade), mural thrombus, arrhythmia, LV aneurysm (persistent ST elevation >3 weeks), Dressler's (2–10 weeks)
Special
  • Persistent ST elevation >3 weeks + no enzyme rise = LV aneurysm
  • Dressler's = fever + pleuritic pain + friction rub 2–10 weeks post-MI → NSAIDs/colchicine ± steroids
  • New LBBB with chest pain = treat as STEMI (LBBB masks ischaemia)
physiology · background · low-yield
Other
  • ST-elevation voltage criteria: new elevation at the J-point ≥0.1 mV in 2 contiguous leads; in V2–V3 → men ≥40 y ≥0.2 mV, men <40 y ≥0.25 mV, women ≥0.15 mV
Mechanism
  • RCA supplies the SA node (~65%) and AV node (~90%) → inferior/RCA STEMI classically causes bradycardia / AV block (± vagal reflex)
Epidemiology/Risk
  • ~23% die before reaching hospital, ~13% die during admission, ~75% develop some complication
Background
  • Mechanical rupture (free wall / papillary muscle / septum) occurs most frequently 2–4 days post-MI, when necrotic myocardium is softest (first week)
5

Prinzmetal (Vasospastic) Angina

C/P
  • Rest pain (often nocturnal/early morning) waking from sleep
  • Episodes 5–15 min, spontaneous resolution
  • No exertional trigger; smokers, young/middle-aged
Inves
  • ECG during attack: ST elevation that resolves with pain
  • Echo, stress ECG (usually normal), CT coronary angiography (normal/non-obstructive)
  • Provocation test (ergonovine, acetylcholine)
Mng
  • Calcium channel blockers (mainstay) + GTN + statin
  • Smoking cessation
  • Avoid non-selective β-blockers (unopposed α → worse spasm)
Special
  • Transient ST elevation that disappears with pain — only ACS subtype with ST elevation in absence of fixed lesion
  • Coronary spasm, not plaque rupture
physiology · background · low-yield
Background
  • Physiological triggers in young patients: cold weather, dehydration

Aortic Disease

1 entry
6

Aortic Dissection

C/P
  • Sudden severe tearing/ripping chest pain, maximal at onset
  • Type A: anterior/retrosternal · Type B: interscapular/posterior
  • Pain may migrate as dissection propagates
  • BP/pulse asymmetry between arms, radio-radial delay
  • New early diastolic murmur (acute AR from root dilation)
  • Simultaneous chest pain + stroke (carotid extension) or + limb ischaemia (iliac extension) = red flag
  • Complications: haemopericardium ± tamponade, MI (RCA territory), acute HF, syncope; mesenteric ischaemia, renal infarction / acute renal failure, ischaemic stroke / paraplegia, GI haemorrhage, pleural effusion / aorto-pulmonary fistula, limb ischaemia
Inves
  • CT aortic angiogram = definitive
  • TOE 98%/95%; Spiral CT 100%/98% (most sensitive + specific); MRI 98%/98%
  • CXR: mediastinal widening (sensitivity only 39% — normal CXR does NOT rule out)
  • D-dimer <500 ng/mL → NPV 96% (rule-out in low-risk only)
  • ECG: 20% of Type A show ischaemia (RCA shear → inferior STEMI pattern)
  • Dissection flap on CT aortography = the confirmatory finding (intimal flap separating true/false lumen)
Mng
  • ICU + arterial line + urinary catheter + IV morphine
  • BP target SBP 100–120 mmHg via IV β-blocker + CCB + nitroprusside (reduce dP/dt)
  • Type A → emergency open surgery (graft replacement); mortality ↑1–2 %/hr without surgery
  • Type B → medical (BP control + serial imaging); surgery/stenting if complicated, expanding, Marfan, ongoing extension
  • Antiplatelet, anticoagulant & thrombolytic therapy are ABSOLUTELY contraindicated — if a dissection is misdiagnosed as MI and given these, it is catastrophic (rupture); always check BP + pulse on both sides first
Special
  • Stanford A = ascending aorta (DeBakey I/II) · Stanford B = descending only (DeBakey III)
  • "Cobweb" sign on TOE = 100% specific for false lumen
  • Cystic medial necrosis = pathological substrate
  • Type A without surgery: 40% mortality at 24 h; with surgery: 96% 1-yr survival
  • Type B on medical therapy: 85% 1-yr survival; overall in-hospital mortality 27.4%
physiology · background · low-yield
Epidemiology/Risk
  • Epidemiology: UK incidence 3–4 per 100,000/yr; peak 5th–6th decade (peak age 63); M:F 2:1; mortality as high as 1%/hr if untreated
  • Risk factors: hypertension (72%), cocaine, trauma / coronary intervention, deceleration injury, weight-lifting, coarctation; connective-tissue — Marfan, Ehlers-Danlos, Turner, bicuspid aortic valve; vasculitides — giant cell / Takayasu arteritis, RA, syphilitic aortitis; pregnancy, PKD, aortic-wall infection
Mechanism
  • Pathophysiology: cystic medial necrosis (smooth muscle + elastic fibre necrosis in tunica media) → intimal tear in ~90% → high-pressure blood cleaves the media forming a false lumen that tracks anterograde; rupture through the adventitia is often fatal
Other
  • True vs false lumen: true = round/oval, strong systolic Doppler, thrombus rare; false = crescentic, sluggish/no flow, thrombus common, cobweb sign
  • Surgical mortality: Type A operative mortality 7–36% depending on centre; surgery = excision of intimal tear + obliteration of false-lumen entry + synthetic graft reconstruction

Valvular Heart Disease

6 entries
7

Aortic Stenosis

C/P
  • SAD triad: Syncope (exertional), Angina, Dyspnoea — symptomatic = 2–3 yr survival without surgery
  • Pulsus parvus et tardus (small-volume, slow-rising carotid)
  • Apex undisplaced, sustained/heaving; ± palpable S4 ("double impulse")
  • Systolic thrill aortic area
  • ESM crescendo-decrescendo, harsh, right 2nd ICS → carotids
  • Late-peaking murmur = severe; soft/absent S2 = calcified valve
  • Reversed splitting of S2; S4 (absent in MS coexistence)
  • Causes: senile calcific aortic sclerosis, congenital bicuspid valve (can cause both stenosis & regurgitation), rheumatic heart disease
Inves
  • ECG: LVH (Sokolow-Lyon), strain pattern (ST depression + T inversion V5–V6)
  • CXR: small heart + post-stenotic dilated ascending aorta; calcified valve
  • Echo: thickened/calcified/immobile cusps + LVH; AVA, peak velocity, gradient → severity
  • Coronary angiography pre-op
Mng
  • Endocarditis + rheumatic fever prophylaxis
  • AVR for all symptomatic severe AS
  • Asymptomatic surgery: EF <50%, peak velocity >5.5 m/s, PA pressure >60 mmHg, velocity ↑ >0.3 m/s/yr, exercise symptoms/hypotension
  • TAVI if unfit for surgery
  • Balloon valvuloplasty: bridge / paeds critical AS
Special
  • Pulsus parvus et tardus — disease-specific
  • "Late-peaking" murmur duration ∝ severity (not intensity)
  • Bicuspid valve > ascending aorta 50 mm or expanding >5 mm/yr → surgery
physiology · background · low-yield
Background
  • Non-valvular LVOT obstruction: supravalvular fibrous diaphragm (Williams syndrome — learning difficulties, hypercalcaemia, 'hourglass' ascending aorta) or subvalvular fibrous ridge / HCM septal hypertrophy
  • TAVI: balloon-expandable stent valve, ~86% success, ~2% procedural / 12% 30-day mortality
Exam technique
  • Symptoms begin once orifice reduced to ~one-third normal; triad mimics HCM; murmur may be soft/inaudible in severe AS (reduced cardiac output) and the ejection click disappears once the valve is calcified/immobile
8

Aortic Regurgitation

C/P
  • Dyspnoea (late, after LV failure)
  • Hyperdynamic circulation signs:
    • Water-hammer / collapsing pulse
    • Wide pulse pressure
  • Apex displaced down-and-out, forceful
  • Soft early diastolic murmur, LSE, leaning forward + breath held in expiration
  • Austin Flint mid-diastolic rumble at apex (regurgitant jet hits anterior MV leaflet)
  • Functional ESM (volume overload)
  • Causes — acute: rheumatic fever, infective endocarditis, aortic dissection, ruptured sinus of Valsalva aneurysm, prosthetic valve failure. Chronic: rheumatic HD, syphilis, seronegative arthritides (ankylosing spondylitis, reactive arthritis, RA), severe hypertension, bicuspid valve, Marfan's, osteogenesis imperfecta
Inves
  • ECG: LVH (volume overload — tall R + deep T inversion left leads, deep S right leads); sinus rhythm
  • CXR: LV enlargement + ascending aorta dilation; calcification (syphilis = aortic wall; valvular disease = valve)
  • Echo + colour Doppler (regurgitant jet); TOE for valve/root detail
  • CMR quantifies regurgitant volume
Mng
  • Endocarditis + rheumatic fever prophylaxis
  • ACEi if LV dysfunction; β-blocker if Marfan (slows aortic dilation)
  • Acute AR (endocarditis/dissection): vasodilators + inotropes → urgent surgery
  • Surgical valve replacement: symptomatic severe AR, EF ≤50%, end-diastolic >70 mm, end-systolic >50 mm
Special
  • Eponymous peripheral signs (6): Water hammer pulse (bounding/collapsing)
  • Quincke's (nail-bed capillary pulsation)
  • De Musset's (head nodding)
  • Duroziez's (femoral to-and-fro murmur — severe AR)
  • Pistol shot femorals
  • Corrigan's (dancing carotid)
  • Three murmurs possible: AR + functional ESM (AS-like) + Austin Flint (MS-like)
physiology · background · low-yield
Background
  • Angina pectoris may occur; arrhythmias relatively uncommon
  • Prosthetic valve choice: tissue valves preferred in elderly / where anticoagulation must be avoided; contraindicated in children/young adults (rapid calcification & degeneration)
9

Mitral Stenosis

C/P
  • Progressive exertional dyspnoea, orthopnoea, frothy/blood-tinged sputum, haemoptysis
  • AF (large LA), palpitations, systemic emboli (stroke #1 site)
  • Mitral facies / malar flush
  • Small-volume pulse, irregularly irregular if AF
  • Tapping apex (palpable S1), undisplaced
  • Left parasternal heave (RVH)
  • Prominent JVP "a" wave (if SR), elevated JVP
Inves
  • ECG: P mitrale (bifid P in II, broad >3mm), AF, RVH/RAD as disease progresses, tall R in V1
  • CXR: straight left heart border, "double shadow" (LAE), pulmonary congestion, calcified valve
  • Echo (TTE): LA size, leaflet thickening/calcification/mobility, commissural fusion, MVA defines severity; PA pressure estimate
  • TOE: mandatory pre-BMV (exclude LA thrombus)
Mng
  • Endocarditis + rheumatic fever prophylaxis
  • Diuretics (low dose); β-blockers / DC cardioversion for AF rate
  • Anticoagulation (warfarin if AF or MS area ≤2 cm² — DOACs contraindicated)
  • BMV if MVA ≤1.5 cm² + symptoms/PHTN + pliable valve + no LA thrombus + no significant MR
  • Open valvotomy / MVR for calcified or regurgitant valves
Special
  • Loud S1 + opening snap + low-pitched mid-diastolic rumble at apex (bell, left lateral, expiration)
  • Pre-systolic accentuation if SR
  • Graham Steell murmur (early diastolic at pulmonary area — secondary PR from PHTN)
  • Carey-Coombs (transient mid-diastolic of acute rheumatic mitral valvulitis)
  • Almost always rheumatic origin
  • MS is the only valvulopathy that mandates warfarin for AF (DOAC contraindicated)
  • Wilkins score — echocardiographic mitral valve assessment (thickening, calcification) determining suitability for percutaneous mitral valvuloplasty
  • Echo morphology: 'hockey stick' / 'hooked' anterior mitral leaflet on long-axis, 'fish mouth' orifice on short-axis
physiology · background · low-yield
Background
  • Closed valvotomy (mobile non-calcified non-regurgitant valve, no bypass) vs open valvotomy (bypass required, often preferred); severe MS presents decades post-attack in Europe but at 10–20 yr in developing countries
10

Mitral Regurgitation

C/P
  • Asymptomatic for years (LA/LV accommodate)
  • Dyspnoea, orthopnoea, fatigue, cardiac cachexia (late)
  • Apex displaced down-and-out, hyperdynamic
  • Systolic thrill at apex (severe)
  • Pansystolic murmur at apex → axilla
  • Soft S1, S3 gallop (late, volume overload)
  • AF common (less dramatic deterioration than MS)
  • Mid-systolic click + late systolic murmur if MVP
  • Causes — functional: LV / mitral valve ring dilation (CAD, cardiomyopathy). Organic: mitral valve prolapse, rheumatic HD, endocarditis, papillary muscle ischaemia/infarction, MI
Inves
  • ECG: P mitrale, LAE, LVH, AF
  • CXR: LA + LV enlargement, ↑ cardiothoracic ratio, valve calcification
  • Echo: dilated LA + LV, regurgitant jet; aetiology + severity
  • TOE pre-op for structural assessment
Mng
  • Mild/moderate: serial echo, endocarditis + rheumatic fever prophylaxis
  • Symptomatic: diuretics, ACEi
  • Surgery (repair > replacement) if: symptomatic severe MR, end-systolic >40 mm, EF <60%, AF or PHTN even if asymptomatic
  • Torrential MR (papillary/chordal rupture, IE) → emergency MVR
  • MitraClip for non-surgical candidates
Special
  • Stricter EF/dimension thresholds than aortic valve (because LV unloads into LA — EF is artificially preserved)
  • Acute severe MR after MI = papillary rupture (posteromedial, single RCA/PDA supply) → flash pulmonary oedema
physiology · background · low-yield
Background
  • Vs mitral stenosis: thromboembolism less common but subacute infective endocarditis much more common
11

Tricuspid Stenosis

C/P
  • Right heart failure picture: abdominal pain (hepatomegaly), ascites, peripheral oedema
  • Prominent jugular venous "a" wave (SR preserved — unusual feature)
  • Pre-systolic pulsation over liver
  • Hepatomegaly, ascites, dependent oedema
Inves
  • ECG: peaked tall P in lead II (>3 mm) — P pulmonale
  • CXR: prominent right atrial bulge
  • Echo: thickened immobile TV (less visible than MV)
Mng
  • Diuretics + salt restriction
  • TV valvotomy or replacement (rarely isolated → done with other valve surgery)
Special
  • Rumbling mid-diastolic murmur LLSE, louder on inspiration (Carvallo's sign)
  • Tricuspid opening snap occasionally
  • Causes: rheumatic + carcinoid syndrome
  • May be missed behind coexisting MS murmur
physiology · background · low-yield
Epidemiology/Risk
  • Uncommon lesion, much more frequent in women than men; symptoms largely driven by coexisting left-sided rheumatic valve disease
12

Tricuspid Regurgitation

C/P
  • RHF: pulsatile tender hepatomegaly, ascites, lower limb oedema, fatigue
  • Large jugular venous "cv" wave (systolic expansion of neck veins)
  • Liver pulsates in systole
  • Left parasternal heave (RV enlargement)
  • AF common
  • Lancisi sign — the eponymous sign of TR: a giant/prominent JVP v wave (systolic retrograde flow causes exaggerated atrial filling, and the prominent v wave encroaches on the X descent)
Inves
  • Echo: RV dilation + thickened valve
Mng
  • Functional TR: diuretics — usually resolves with HF treatment
  • Severe organic: annuloplasty / annulo-plication
  • TV replacement rarely (e.g. IE) — sometimes valve removal in IV drug users
Special
  • Blowing pansystolic murmur LLSE, louder on inspiration (Carvallo's)
  • Causes include carcinoid syndrome + Ebstein's anomaly + functional (RV dilation from cor pulmonale, MI, PHTN)

Infective Endocarditis

1 entry
13

Infective Endocarditis

C/P
  • Fever (low-grade in subacute), constitutional symptoms (fatigue, weight loss, night sweats, myalgia)
  • New / changing murmur
  • Palpable splenomegaly
  • Peripheral stigmata:
    • Splinter haemorrhages (linear dark red streaks under nails)
    • Osler's nodes (painful raised lesions on finger/toe pads)
    • Janeway lesions (painless flat lesions on palms/soles)
    • Roth spots (red retinal spots with pale centre)
    • Conjunctival haemorrhage
  • Systemic embolisation (stroke, mesenteric, renal, splenic, limb)
  • Right-sided IE (IVDU) → septic pulmonary emboli
  • IVDA IE → tricuspid valve (affected in ~50%)
Inves
  • Blood cultures: 3 sets from different sites over 1 h before antibiotics
  • Echo: TTE first; TOE if left-sided / prosthetic valve / inconclusive TTE (no acoustic shadow)
  • CBC, ESR, CRP, U&E, urinalysis (RBC casts → immune complex GN)
  • Rheumatoid factor, complement, CT brain (emboli)
  • Modified Duke / 2023 ESC criteria (major: + blood culture typical organism, echo vegetation/abscess/dehiscence; minor: predisposing condition, fever >38°C, vascular phenomena, immunologic phenomena, microbiologic evidence)
Mng
  • IV antibiotics 2–8 weeks (left-sided = 6 weeks)
  • Empiric: vancomycin (native); vanc + gentamicin + cefepime/imipenem (prosthetic)
  • Source control: remove infected catheters, dental evaluation
  • V-HEART surgery: Vegetation (>10 mm), Heart failure, Extension (perivalvular abscess/fistula), AV block, Resistant organism, Treatment failure (persistent bacteraemia ~10 days)
  • IVDU right-sided: medical preferred; if surgery, repair > replacement
  • Prophylaxis (high-risk only): pre-dental procedures
  • Prophylaxis regimen: amoxicillin 2 g PO (or ampicillin 2 g IV/IM) single dose 30–60 min before a high-risk dental procedure; penicillin-allergic → cephalexin 2 g / azithromycin or clarithromycin 500 mg / doxycycline 100 mg PO
  • Prophylaxis reserved for highest-risk patients: previous IE, prosthetic valve / prosthetic repair material, any cyanotic CHD, first 6 months after prosthetic CHD repair — for dental work involving gingival / periapical / oral-mucosa manipulation
  • Empiric (lecture/UK regimen): native valve = amoxicillin + gentamicin; prosthetic valve = vancomycin + gentamicin (high-dose IV, started after cultures)
  • Stabilised patients (from day 10): step down to OPAT or oral antibiotics — perform TOE before switching (Class I); oral switch after ≥10 days IV is non-inferior and shortens hospital stay (complicated cases stay inpatient IV)
Special
  • Fever + bradycardia → aortic root abscess (needs drainage)
  • Fever + murmur + systemic embolisation → IE until proven otherwise
  • Strep viridans + Staph aureus = 80–90% (Staph aureus #1 in IVDU)
  • HACEK + Bartonella/Brucella/Coxiella/Legionella/Aspergillus = culture-negative IE
  • Biofilm (polysaccharide) shields organisms → need prolonged IV bactericidal therapy
  • Acute IE: attacks normal valves, rapidly destructive, usually S. aureus, metastatic complications — vs subacute IE: damaged valves, indolent, less virulent organism (viridans strep)
  • Most common cause of culture-negative IE = previous antibiotic therapy (clears the bloodstream but organisms survive in the vegetation); diagnose with prolonged/fungal cultures + serology (paired sera)
  • Prosthetic-valve IE organisms: early (<6 mo) = S. aureus + coagulase-negative staph (S. epidermidis), healthcare-associated; late (>6 mo) = same as native valve (viridans strep)
  • Hectic (swinging) fever pattern → indicates an abscess
physiology · background · low-yield
Epidemiology/Risk
  • Predisposing valve substrate: congenital HD, previous rheumatic HD, bicuspid/calcific aortic valve, severe MVP, HCM, prosthetic valve, prior IE (IE can also seed a previously normal valve, esp. S. aureus)
  • Prosthetic-valve IE = ~5% of all IE; highest risk in first 2 months post-op; emergency > elective surgery; mostly healthcare-associated
Mechanism
  • Pathogenesis cascade: turbulent-flow endocardial damage → sterile platelet-fibrin clot → transient bacteraemia → bacterial adherence → multiplication into vegetation → embolisation → immune-complex formation
  • Anaemia: normocytic (chronic disease)/MAHA in native valve, haemolytic (mechanical shearing) in prosthetic valve; low C3 from immune-complex consumption
  • Local complications: myocardial/valve-ring abscess (→ conduction abnormalities), aortitis, valve dehiscence, mycotic aneurysm; systemic: emboli to kidney/spleen/CNS, immune-complex glomerulonephritis
Microbiology
  • Portals of bacterial entry: dental, genitourinary, cutaneous, pulmonary infections; also IVDU injection sites and IV/central catheters
  • Overall strep + staph = 80–90%
Background
  • Non-valvular sites of IE: VSD/septal defect, PDA, aortic coarctation, AV shunt, mural endocardium/thrombi, intracardiac devices (pacemakers)
Other
  • Differential diagnosis: vasculitis, other causes of septicaemia
  • Additional workup: ASO titres, LFTs, blood film, throat swab, urine microscopy (RBC casts); ECG (watch for AV block); CXR
  • Response/follow-up: strep improve in 3–7 days (staph slower); relapse usually <4 weeks; recrudescence >6 weeks = new infection; sterile emboli/valve rupture possible up to 1 year; follow vegetation with serial echo
  • Further peripheral signs: petechiae; digital infarcts (black necrotic fingertips/toes)
Exam technique
  • ESR >100 mm/hr → also screen for malignancy, TB, autoimmune disease
  • Rule of thumb: every 1 °C rise adds ~10 bpm to HR (except myocarditis, which raises it more)
  • Fever in >95% of cases; absent fever → totally immunocompromised, more dangerous; acute IE is often dominated by heart failure

Arrhythmias

17 entries
14

Sinus Tachycardia

C/P
  • Often asymptomatic / palpitations
  • Driven by underlying cause
Inves
  • ECG: rate >100, P wave upright II, biphasic V1, negative aVR (sinus origin), 1:1 P:QRS
  • Rate usually ≤150 bpm — a rate >150 should raise suspicion for another SVT (e.g. AVNRT)
Mng
  • Treat the cause
  • Causes — physiological (APE: Anxiety, Pain, Pregnancy, Exercise); pathological (FADI: Fever, Anaemia, Dehydration, Thyrotoxicosis); drugs (adrenaline, β2-agonist, caffeine, theophylline)
Special
  • HR rises ~10 bpm per 1 °C fever — except myocarditis (rises more)
15

Sinus Bradycardia

C/P
  • Often asymptomatic; dizziness, syncope if severe
Inves
  • ECG: rate <60, normal sinus P
Mng
  • Treat cause; atropine / pacing if symptomatic
  • Causes — physiological (athletes, sleep); pathological (degenerative, ischaemia, electrolyte, hypothyroidism); drugs (β-blocker, CCB, digitalis)
Special
  • —
16

Atrial Fibrillation

C/P
  • Palpitations, dyspnoea, chest pain, dizziness (APCDE: Asymptomatic, Palpitations, Chest pain, Dyspnoea, Embolisation)
  • 30% asymptomatic
  • Stroke = most serious complication (LA appendage thrombus)
  • Irregularly irregular pulse
  • Rapid AF can precipitate acute HF
Inves
  • ECG: absent P waves, fibrillatory baseline, narrow QRS, irregularly irregular
  • Echo (LA size, LAA thrombus on TOE before cardioversion)
  • TSH, FT3/T4, CBC, electrolytes (Na, K, Ca, Mg)
Mng
  • Unstable (SBP <90): synchronised DC cardioversion + 5000 IU UFH
  • Stable: rate OR rhythm control + oral anticoagulation
  • Rate (1st-line): β-blocker → digitalis if HF / CCB (verapamil, diltiazem) if no HF (avoid CCB if EF <40%)
  • Rhythm: amiodarone (structural heart disease); flecainide/propafenone (structurally normal)
  • Pre-cardioversion: TOE OR 3 wk anticoag; post-cardioversion: 4 wk anticoag (atrial stunning)
  • Long-term: CHA₂DS₂-VA ≥2 → OAC recommended; =1 → consider; =0 → no OAC
  • Warfarin (NOT DOAC) if metallic valve, rheumatic MS, MVA ≤2 cm², amyloid, HCM
  • HAS-BLED: assess bleeding risk, modify factors (BP, alcohol) — not a contraindication
  • Ablation (pulmonary vein isolation) if rhythm control failed
  • Rate control is first-line for most patients; choose rhythm control if reversible cause, new-onset AF, symptomatic despite rate control, or rate-control failure
  • If anticoagulation contraindicated → percutaneous left atrial appendage occlusion (LAAO); antiplatelets must NOT be used as an alternative for stroke prevention
Special
  • AF prevalence: ~2% general, 15% over 75
  • Hypertension = most important cause
  • AF + mitral stenosis = warfarin only
  • AF + cardiac amyloidosis or HCM → anticoagulate regardless of CHA₂DS₂-VA score, DOACs preferred (the warfarin-only rule applies to metallic valve / rheumatic MS / MVA ≤2 cm² — not amyloid/HCM)
  • Digoxin toxicity — nausea/vomiting, confusion, xanthopsia (yellow-green vision, haloes) and arrhythmias (e.g. paroxysmal atrial tachycardia with block, bidirectional VT); precipitated by hypokalaemia / hypomagnesaemia / renal impairment → withhold digoxin, correct K⁺/Mg²⁺, digoxin-specific antibody (Digibind) if severe
  • Amiodarone toxicity — thyroid dysfunction (hypo- or hyper-), pulmonary fibrosis, hepatotoxicity, corneal microdeposits, slate-grey photosensitive skin, peripheral neuropathy; baseline + periodic TFT/LFT/CXR monitoring; potent CYP450 & P-gp inhibitor (raises warfarin & digoxin levels)
physiology · background · low-yield
Other
  • DOAC classes: dabigatran = direct thrombin inhibitor; rivaroxaban/apixaban/edoxaban = factor Xa inhibitors; warfarin target INR 2.0–3.0
Mechanism
  • Ectopic foci arise predominantly in the pulmonary veins, discharging at 300–600/min → no coordinated atrial contraction
Epidemiology/Risk
  • Most important causes (5): hypertension, heart failure, hyperthyroidism, valvular heart disease, cardiac surgery (post-op AF)
17

Atrial Flutter

C/P
  • Palpitations, ± dyspnoea; often regular
Inves
  • ECG: sawtooth flutter (F) waves, atrial rate ~300, ventricular response usually 150 (2:1 block), regular or irregular if variable block
Mng
  • Same as AF (rate / rhythm / anticoagulation)
  • Cavotricuspid isthmus ablation = high cure rate
Special
  • Sawtooth pattern best seen in inferior leads
  • 2:1 conduction with HR 150 = classic flutter clue
18

SVT

C/P
  • Sudden-onset palpitations, ± dizziness, chest pain
  • Often young, structurally normal heart
Inves
  • ECG: regular narrow QRS, HR 150–250, no visible P waves (hidden in T)
Mng
  • Unstable → synchronised DC cardioversion
  • Stable → ABC: Adenosine 6 mg → 12 mg, β-blockers, CCB (verapamil/diltiazem)
  • Long-term: oral β-blocker / CCB; ablation
Special
  • Vagal manoeuvres (Valsalva, carotid sinus massage) first-line for termination
  • AVNRT (AV nodal reentrant tachycardia) = most common type/mechanism of SVT
19

VT

C/P
  • Palpitations, syncope, chest pain, cardiac arrest
  • Hemodynamic compromise common
Inves
  • ECG: wide QRS ≥120 ms, regular, HR >100
  • AV dissociation (no constant P-QRS relation)
  • T wave opposite direction to QRS
Mng
  • Unstable → synchronised DC cardioversion
  • Stable → IV amiodarone
  • Long-term: oral amiodarone + ICD
Special
  • AV dissociation + capture/fusion beats = VT (until proven otherwise)
  • Any wide-complex tachycardia in a patient with structural heart disease (e.g. IHD / prior MI or CABG) should be treated as VT until proven otherwise
20

Torsades de Pointes

C/P
  • Recurrent syncope, palpitations, sudden cardiac death
  • Often in setting of prolonged QT (drugs, electrolytes, congenital LQTS)
Inves
  • ECG: polymorphic VT with QRS "twisting" around baseline (sinusoidal axis change)
  • Baseline ECG: long QTc >500 ms
  • Electrolytes: K⁺, Mg²⁺, Ca²⁺
Mng
  • IV magnesium sulphate (first-line, even if normal Mg)
  • Correct K⁺ (>4.0) and Mg²⁺
  • Stop offending drug
  • Overdrive pacing or isoprenaline (↑ rate, ↓ QT)
  • Unstable → defibrillation
Special
  • Polymorphic VT with QT prolongation = TdP (different from monomorphic VT)
  • Causes of long QT: hypoK / hypoMg / hypoCa, drugs (Class Ia/III antiarrhythmics, macrolides, antipsychotics), congenital LQTS
  • Usually terminates spontaneously but frequently recurs; may degenerate into VF
21

VF

C/P
  • Cardiac arrest, unresponsive, no pulse, no breathing
Inves
  • ECG: chaotic irregular deflections, no identifiable P/QRS/T, varying amplitude
  • Rate 150–500/min; amplitude decreases with duration (coarse VF → fine VF) as myocardial energy depletes
Mng
  • Unsynchronised defibrillation (CPR + ACLS)
  • Post-arrest: IV amiodarone + therapeutic hypothermia
  • Long-term: ICD
Special
  • VF = cardiac arrest = immediate defibrillation, not synchronised cardioversion
22

Premature Beats (PACs / PVCs / Bigeminy / Trigeminy)

C/P
  • Palpitations ("missed beat"), often asymptomatic
  • Usually benign unless frequent or structural disease
Inves
  • ECG: early beat with abnormal morphology
  • PAC: early narrow QRS with abnormal P
  • PVC: early wide QRS, no preceding P, T discordant
  • Bigeminy = PVC every 2nd beat; Trigeminy = every 3rd
  • PVC → full compensatory pause (premature cycle + pause = 2 sinus cycles; spans exactly 2 normal R-R); PAC → incomplete (non-compensatory) pause
Mng
  • Reassurance if benign
  • Treat trigger (caffeine, alcohol, electrolyte)
  • β-blocker if symptomatic
  • Ablation if frequent + symptomatic + LV dysfunction
Special
  • Couplets (2 consecutive PVCs), interpolated PVCs (squeezed between normal beats)
  • >10% PVC burden can cause tachycardia-induced CM
23

WPW Syndrome

C/P
  • Asymptomatic OR palpitations / SVT / syncope / sudden death
  • Pre-excited AF = very rapid, life-threatening
Inves
  • ECG: short PR <120 ms + delta wave (slurred QRS upstroke) + wide QRS >120 ms
  • ST-T changes opposite direction to QRS
  • Type A: dominant R in V1 (left-sided pathway, mimics RBBB)
  • Type B: dominant S in V1 (right-sided pathway)
  • Pre-excited AF: irregular, wide QRS, very fast (~300 bpm), T inversion
Mng
  • Stable SVT: vagal → adenosine
  • Pre-excited AF: synchronised cardioversion + IV heparin
  • CONTRAINDICATED: AV nodal blockers (digoxin, β-blockers, CCBs, adenosine) in pre-excited AF — block AV node → bypass tract conducts AF unopposed → VF
  • Definitive: accessory pathway ablation
Special
  • Delta wave + short PR + wide QRS = WPW triad
  • AF rate ~300 in WPW vs ~150 in normal AF
  • Electrical alternans favours pre-excitation
  • Differentiating AF+WPW vs AF+LBBB: check old ECG, rate clue, empiric DC cardioversion + heparin (safe for both)
24

1st-degree AV Block

C/P
  • Asymptomatic
Inves
  • ECG: PR uniformly prolonged >200 ms (>5 small squares); every P conducted; regular
Mng
  • None usually; observe
  • Stop AV-nodal drugs if symptomatic
Special
  • "If the R is far from P / Then it must be a First Degree"
25

2nd-degree Mobitz I (Wenckebach)

C/P
  • Usually asymptomatic; occasional dizziness
Inves
  • ECG: progressive PR lengthening → dropped QRS → cycle resets; irregular rhythm
  • Block at AV node
  • Grouped beating — QRS complexes cluster in groups separated by non-conducted P waves; P:QRS ratio varies (e.g. 5:4 to 6:5)
Mng
  • Observation usually sufficient
  • Atropine if symptomatic
Special
  • "If PR gets longer then a QRS drop / Then it must be a Type I Wenckebach"
  • Often benign; lower risk than Mobitz II
26

2nd-degree Mobitz II

C/P
  • May be asymptomatic, or dizziness/syncope
  • Higher risk of progression to complete heart block
Inves
  • ECG: dropped QRS without progressive PR prolongation; PR uniform; wide QRS (infranodal block); 2:1, 3:1, 4:1 ratios
Mng
  • Permanent pacemaker (usually indicated)
Special
  • "If PR stays normal and QRS quits / Then it must be a Type II Mobitz"
  • Block at His bundle (infranodal) → unstable, unreliable escape
  • Almost always needs pacing
27

3rd-degree (Complete) AV Block

C/P
  • Severe bradycardia, dizziness, syncope, Stokes-Adams attacks, sudden death
Inves
  • ECG: AV dissociation (P and QRS independent); P:QRS no constant relation; regular ventricular rhythm
  • Narrow-complex escape (His bundle, 50–60 bpm) — proximal block, reliable
  • Broad-complex escape (His-Purkinje, 15–40 bpm) — distal block, unreliable
Mng
  • Transient/recent-onset: IV atropine + temporary pacing standby
  • Chronic / symptomatic / broad escape → permanent dual-chamber pacemaker
Special
  • "If P and QRS beat independently / Then it must be a complete Third Degree"
  • Stokes-Adams syncope = hallmark of broad-complex CHB
  • Pacemaker significantly reduces mortality
28

LBBB

C/P
  • Usually asymptomatic; syncope if intermittent CHB
Inves
  • ECG: QRS ≥120 ms; QS or rS in V1, V2; monophasic (± notched) R in V5, V6, I; secondary T inversion V5–V6
  • Almost always pathological (AS, HTN, MI, severe CAD)
Mng
  • Treat underlying cause
  • Symptomatic + EF reduced → CRT
  • New LBBB + chest pain = treat as STEMI
Special
  • LBBB masks MI, ischaemia, ventricular enlargement, hemiblock
29

RBBB

C/P
  • Usually asymptomatic
Inves
  • ECG: QRS ≥120 ms; rsR' "rabbit ears" in V1, V2; wide slurred S in I, V5, V6; secondary T inversion V1–V3
  • 5% normal variant; pathological causes: ASD, PE, PHTN
Mng
  • Treat underlying cause
Special
  • RBBB masks ischaemia and ventricular enlargement ONLY (MI still diagnosable, unlike LBBB)
30

Fascicular Blocks / Hemiblocks

C/P
  • Asymptomatic
Inves
  • LAHB: pathology in left anterior fascicle → left axis deviation, deep S in II, III, aVF
  • LPHB: pathology in left posterior fascicle → right axis deviation, deep S in I, aVL
  • Bifascicular = RBBB + LAHB or RBBB + LPHB
  • Trifascicular = bifascicular + 1st-degree AV block
Mng
  • Observe; pacing if symptomatic or trifascicular
Special
  • LAHB: most common cause of LAD
  • LPHB: rare in isolation
physiology · background · low-yield
Other
  • Intraventricular conduction delay (IVCD) = wide QRS >120 ms whose pattern fits neither LBBB nor RBBB (e.g. hyperkalaemia, TCA toxicity, severe fibrosis)

Heart Failure

4 entries
31

Chronic HF (HFrEF / HFmrEF / HFpEF)

C/P
  • Dyspnoea (exertional, orthopnoea, PND), fatigue, ↓ exercise tolerance
  • Left HF: pulmonary congestion (crackles, wheeze)
  • Right HF: raised JVP, peripheral oedema, hepatomegaly, ascites
  • Displaced apex (cardiomegaly)
  • S3 gallop (volume overload) / S4
  • Right HF congestion also: anorexia / GI distress, hepatosplenomegaly (tender), RUQ pain, ± jaundice / raised bilirubin (hepatic congestion), nausea/vomiting
Inves
  • BNP / NT-proBNP (rule-out + prognosis)
  • ECG (rarely normal): ischaemia, BBB, LVH, AF
  • Echo (TTE): LVEF classification — HFrEF ≤40%, HFmrEF 41–49%, HFpEF ≥50%
  • CXR: cardiomegaly, Kerley B lines, upper-lobe diversion, pleural effusion
  • Cardiac MRI for aetiology
  • U&E, FBC, TFTs, ferritin (iron deficiency — even without anaemia)
Mng
  • Lifestyle: salt restriction, fluid restriction, weight monitoring
  • 4 Pillars of HFrEF: β-blocker + ACEi/ARB/ARNI + MRA + SGLT2i
  • Diuretic (loop) for congestion
  • Sacubitril/valsartan (ARNI) replaces ACEi
  • Device: CRT (LBBB + EF ≤35% + NYHA II–IV); ICD (EF ≤35% + NYHA II–III)
  • LVAD / transplant if end-stage
  • NYHA I → IV severity classification
Special
  • ACC/AHA stage A (risk factors) → B (structural) → C (symptomatic) → D (refractory)
  • ARNI contraindicated within 36 h of ACEi (angioedema risk)
  • Acute decompensation = "48-h biological penalty" → long-term organ damage
physiology · background · low-yield
Exam technique
  • S3 = volume overload (heard just after S2; MR, AR, VSD, PDA; can be normal in children, pregnant women, athletes) vs S4 = pressure overload (heard just before S1; hypertension, CAD)
  • PND is more specific for HF than orthopnoea — nocturnal fluid redistribution from lower limbs overwhelms the failing LV, causing sudden pulmonary congestion
Background
  • High-output HF causes: anaemia, thyrotoxicosis, Paget's disease, arteriovenous fistula, sepsis
Other
  • Diuretics improve symptoms but do NOT reduce mortality — the mortality benefit comes from the 4 pillars
Background
  • Evidence-based NP cut-offs (normal GFR): NT-proBNP HF unlikely <300; HF likely >450 (age 21–50), >900 (50–75), >1800 pg/mL (>75). BNP: <100 unlikely / >500 likely (thresholds shift with age = ↑baseline NP, and with GFR <60 = ↓clearance)
32

Acute HF / Pulmonary Oedema

C/P
  • Sudden severe dyspnoea, pink frothy sputum, orthopnoea
  • Crackles (basal → diffuse), wheeze ("cardiac asthma")
  • Tachycardia, hypertension or hypotension, sweating, distressed
  • ↑ JVP if biventricular
Inves
  • BNP/NT-proBNP (acutely elevated)
  • ABG (hypoxaemia, ± hypercapnia, respiratory alkalosis early)
  • CXR: bat-wing pattern, Kerley B, pleural effusion, cardiomegaly
  • ECG, troponin (precipitant — MI, arrhythmia)
  • Bedside echo
Mng
  • Sit upright + O₂ + monitor
  • Loop diuretic IV + IV nitrates (if SBP >110) + morphine (cautious)
  • CPAP / NIPPV for refractory hypoxaemia
  • Inotropes (dobutamine) if low output / cardiogenic shock
  • Treat precipitant (MI, AF, infection, non-compliance)
  • Ultrafiltration if diuretic resistant
Special
  • Pink frothy sputum = transudative alveolar oedema
  • NIPPV: ↑ intrathoracic pressure → ↓ preload, ↓ afterload, ↑ oxygenation
  • Cardiogenic (↑ hydrostatic pressure, intact capillaries) vs non-cardiogenic (↑ capillary permeability, damaged capillaries) pulmonary oedema; non-cardiogenic types = high-altitude, neurogenic, re-expansion (rapid aspiration of effusion/pneumothorax), post-cardiopulmonary bypass
physiology · background · low-yield
Other
  • Severe hypertensive APE (afterload problem) → add an arteriolar vasodilator (sodium nitroprusside or hydralazine) to reduce afterload
33

Cardiogenic Shock

C/P
  • Hypotension (SBP <90) + signs of poor perfusion (cool extremities, oliguria, confusion, mottling, lactate)
  • Pulmonary oedema (left-sided cause)
  • Raised JVP
  • Often post-MI (extensive anterior), mechanical complication, severe HF
Inves
  • ECG, troponin, echo (LV function, MR, VSD, tamponade)
  • ABG, lactate, U&E
  • Right heart catheter (low CI, high wedge)
Mng
  • ICU + arterial + central line
  • Inotropes: dobutamine, dopamine; vasopressor: noradrenaline if hypotensive
  • Mechanical support: LVAD
  • Treat cause (urgent revascularisation if MI; valve surgery if mechanical complication)
  • Contraindicated in shock: beta-blockers, ACEi/ARB, nitrates (worsen hypotension) — use positive inotropes (dobutamine) + vasopressor (noradrenaline) until perfusion restored
  • Ventilation: intubate + mechanical ventilation — NIPPV / CPAP is CONTRAINDICATED (it drops preload further in an already hypotensive patient, worsening perfusion) — unlike 'WET' pulmonary oedema where NIPPV helps
  • Contraindicated list also includes IV diuretics (drop preload) and MRAs (too slow + hyperkalaemia risk) — classic MCQ: in a hypotensive, oliguric (no urine output) patient, diuretics / ACEi / β-blockers / MRA are ALL wrong; give inotrope + pressor first, then neurohormonal blockade once stable
Special
  • Mortality high; reverse cause + mechanical support
34

Cor Pulmonale (Right HF from lung disease)

C/P
  • Underlying chronic lung disease (COPD, ILD, PHTN)
  • Dyspnoea, fatigue
  • Raised JVP, hepatomegaly, peripheral oedema, ascites
  • Loud P2 (PHTN); right parasternal heave (RVH)
Inves
  • ECG: RVH (tall R V1), RAD, P pulmonale
  • CXR: enlarged pulmonary arteries
  • Echo: RV dilation/hypertrophy, ↑ PA pressure
  • ABG, spirometry
Mng
  • Treat underlying lung disease
  • Long-term O₂ if chronic hypoxaemia
  • Diuretics for oedema (cautious)
  • Specific PAH therapy if indicated
Special
  • RV failure secondary to lung disease specifically (not from left HF)
physiology · background · low-yield
Background
  • Left-sided HF is the single most common cause of right HF overall; cor pulmonale specifically = right HF from primary lung disease (e.g. COPD → pulmonary hypertension → ↑ RV afterload)

Cardiomyopathies

10 entries
35

HCM (Hypertrophic Cardiomyopathy)

C/P
  • Often asymptomatic — detected by family screening / ECG
  • Chest pain, dyspnoea, syncope or pre-syncope (especially exertional)
  • Arrhythmia, sudden cardiac death (most common cause in <35 yo)
  • Triad mimics AS: angina + syncope + dyspnoea
  • Double apical pulsation (palpable S4)
  • Jerky carotid pulse (rapid up then obstruction)
  • ESM at 3rd LICS — ↑ with Valsalva / standing (↓ afterload); ↓ with squatting (↑ afterload)
  • Pansystolic murmur if SAM-related MR
  • S4 (if SR)
Inves
  • ECG: LVH (often massive), ST/T changes, abnormal Q waves inferolateral leads
  • Echo: asymmetric septal hypertrophy (ASH), systolic anterior motion (SAM) of anterior MV leaflet, vigorous LV contraction, normal EF, small LV cavity
  • CMR: hypertrophy + abnormal myocardial fibrosis
  • Genetic testing (MYH7, MYBPC3)
  • Holter for non-sustained VT
Mng
  • β-blockers + verapamil (1st line for symptoms)
  • Disopyramide if LVOT obstruction
  • AVOID: nitrates, vasodilators (worsen obstruction)
  • Alcohol septal ablation / surgical myectomy
  • ICD if ≥2 risk factors: LVH >30 mm, FHx SCD <50 yr, NSVT, unexplained syncope, abnormal BP response to exercise
  • AF deteriorates rapidly → oral anticoagulation regardless of CHA₂DS₂-VA
  • Dual-chamber pacing if LVOT obstruction + symptoms
  • Avoid vigorous / competitive exercise — intense exertion worsens outflow obstruction → myocardial ischaemia → fatal ventricular arrhythmia
  • Alcohol septal ablation carries two specific risks: complete heart block + myocardial infarction
Special
  • Autosomal dominant; 1 in 500
  • Murmur ↑ with Valsalva differentiates from AS (which ↓)
  • Sudden death up to 6%/yr in adolescents
  • HOCM = HCM with LVOT obstruction (25%)
  • Associated syndromes / phenocopies: Noonan's, LEOPARD, Friedreich's ataxia; glycogen storage diseases (Danon, Pompe, Fabry) — may be echo-indistinguishable from inherited HCM; infants of diabetic mothers
physiology · background · low-yield
Mechanism
  • Full sarcomeric gene panel: β-myosin heavy chain (commonest), myosin-binding protein C, troponin T, troponin I, α-tropomyosin, myosin light chains — top 3 = 70–80% of cases
  • Histology: haphazard myocyte disarray, whorling of myocytes around central collagen, sub-aortic fibrosis, interstitial fibrosis; gross banana-shaped LV cavity
Background
  • Diagnosis requires absence of an alternative cause (e.g. aortic stenosis, hypertension); hypertrophy usually asymmetric septal but occasionally concentric or apical
  • Complications: AF ± thromboembolism, mitral valve endocarditis; progressive HF rare — often compatible with normal life-span
36

DCM (Dilated Cardiomyopathy)

C/P
  • Heart failure (dyspnoea, fatigue, oedema)
  • Arrhythmia, conduction defects, thromboembolism, sudden death
  • Apex displaced down-and-out
  • S3 gallop, functional MR/TR
Inves
  • ECG: diffuse non-specific ST/T changes, sinus tachycardia, AF, PVCs, VT, conduction abnormality
  • Echo: dilation of LV ± RV, globular ventricle, poor global systolic function, ↓ ejection fraction
  • CMR: aetiology + fibrosis
  • Coronary angiography/CTCA to exclude CAD (>40 yo)
Mng
  • Standard HF therapy (4 pillars: β-blocker, ACEi/ARNI, MRA, SGLT2i)
  • CRT + ICD for NYHA III/IV
  • Anticoagulation if AF or LV thrombus
  • Cardiac transplant for end-stage
Special
  • Familial DCM mostly autosomal dominant (>20 loci)
  • Aetiologies: idiopathic, alcohol, peripartum, viral myocarditis sequel, doxorubicin, haemochromatosis
  • Most common cardiomyopathy
  • Prognosis: usually slowly progressive HF, ~50% die within 2 years; mural thrombus → systemic embolism
  • Further named aetiologies: endocrine (thyroid), nutritional (thiamine/beri-beri, selenium, carnitine), infections (HIV, Chagas, Lyme), muscular dystrophy (Duchenne/Becker — dystrophin), sarcoidosis, trastuzumab, hypocalcaemia
physiology · background · low-yield
Mechanism
  • Pathology: globular thin-walled balloon-like heart, dilatation masks hypertrophy, ↑ heart weight; micro — myocyte hypertrophy with prominent dark nuclei, interstitial fibrosis, T-lymphocyte infiltrate
Background
  • Family screening of first-degree relatives (family history + pedigree construction) to identify early asymptomatic disease before complications
37

RCM (Restrictive Cardiomyopathy) + Cardiac Amyloidosis

C/P
  • Dyspnoea, fatigue, embolic symptoms
  • Right HF prominent: hepatomegaly, ascites, peripheral oedema
  • Friedreich's sign (raised JVP with diastolic collapse)
  • Kussmaul's sign (JVP rises on inspiration)
  • S3 + S4
  • AF common (atrial enlargement)
  • Amyloid: macroglossia, periorbital bruising, postural hypotension, carpal tunnel, proteinuria
  • Cardiac amyloid: recurrent pericardial + pleural effusions, peripheral (postural) neuropathy
Inves
  • ECG: low voltage QRS, ST/T abnormalities
  • Echo: symmetrical wall thickening, normal EF, impaired filling, biatrial enlargement
  • Amyloidosis: voltage-mass mismatch (low ECG voltage + thickened walls), speckled/ground-glass myocardium
  • CMR: fibrosis pattern (specific in amyloid, sarcoid)
  • Cardiac catheterisation: distinguishes RCM from constrictive pericarditis
  • Endomyocardial biopsy (uniquely useful — amyloid Congo red birefringence)
Mng
  • No specific treatment usually
  • Anti-failure measures, rate control + anticoagulation for AF
  • Amyloid-specific: tafamidis (TTR amyloid); liver transplant for familial; chemo for AL
  • Cardiac transplant for severe (amyloid recurs)
Special
  • Amyloid is most common cause; also sarcoid, Loeffler's, EMF (last two with eosinophilia)
  • Voltage-mass mismatch = amyloid signature
  • Friedreich's + Kussmaul's both seen — overlap with constrictive pericarditis
  • Additional infiltrative/deposition causes: haemochromatosis, Anderson-Fabry, glycogen storage disease, desminopathy, scleroderma, carcinoid heart disease, metastatic tumour, radiation fibrosis, sarcoidosis
physiology · background · low-yield
Background
  • Amyloid subtypes: AL (Ig light chains, plasma-cell neoplasm), AA (SAA, chronic inflammation e.g. TB), ATTR (transthyretin, familial/senile), senile atrial (ANF); Congo red → apple-green birefringence under polarised light
Mechanism
  • Mechanism: pathological infiltration → firm myocardium → failure of relaxation; late pulmonary hypertension + RV hypertrophy/failure
38

ARVC (Arrhythmogenic Right Ventricular Cardiomyopathy)

C/P
  • Young adults; ventricular arrhythmia, syncope, sudden death (especially during exercise)
  • Right HF late
Inves
  • ECG: T inversion V1–V3, epsilon waves (small notch at end of QRS), incomplete/complete RBBB
  • Holter: frequent RV ectopics, NSVT
  • Echo: RV dilation, RV aneurysms (late)
  • CMR: fibro-fatty replacement of RV free wall, RV wall motion abnormalities
  • Genetic testing
  • Task Force criteria for diagnosis
Mng
  • β-blockers (1st line non-life-threatening)
  • Amiodarone / sotalol if symptomatic
  • ICD for refractory or life-threatening arrhythmia
  • Cardiac transplant if intractable
  • Avoid competitive exercise
Special
  • Epsilon wave = pathognomonic
  • Fibro-fatty replacement of RV myocytes (gross + microscopic hallmark)
  • Inherited (autosomal dominant most often, desmosomal proteins)
physiology · background · low-yield
Mechanism
  • Inherited desmosomal (intercalated-disc) protein mutations — plakoglobin, desmoplakin
39

Peripartum Cardiomyopathy

C/P
  • DCM presentation
  • Onset: last trimester or within 5 months postpartum
Inves
  • Echo: dilated LV with poor systolic function
  • Exclude pre-existing CM
Mng
  • Standard HF therapy (ACEi/ARB post-partum only — teratogenic in pregnancy)
  • Anticoagulation (high thromboembolism risk)
Special
  • Risk factors: obese, multiparous, >30 yo, pre-eclampsia
  • ~50% recover normal function within 6 months
  • Subsequent pregnancies high-risk (often contraindicated if no recovery)
40

Tachycardia-induced Cardiomyopathy

C/P
  • DCM picture in patient with prolonged uncontrolled tachyarrhythmia (AF, SVT, VT)
Inves
  • Echo: dilated LV with reduced function
  • Diagnosis of exclusion
Mng
  • Restore sinus rhythm (cardioversion / ablation) — function recovers
  • Rate control if rhythm control fails
Special
  • Reversible cardiomyopathy
  • Diagnosis confirmed retrospectively when rhythm controlled and EF improves
41

LVNC (Left Ventricular Non-Compaction)

C/P
  • Heart failure, thromboembolism, arrhythmia, sudden death
  • Often associated with congenital heart abnormalities
Inves
  • Echo / CMR / LV angiography: sponge-like LV with excessive trabeculations, predominantly apical
  • Ventricular septum spared
Mng
  • HF therapy + anticoagulation + ICD if indicated
Special
  • Familial + spontaneous cases
  • Apical non-compaction with sparing of septum
physiology · background · low-yield
Mechanism
  • Arises from embryologic arrest of myocardial trabeculation (spongy myocardium)
42

Tako-tsubo (Stress) Cardiomyopathy

C/P
  • Acute chest pain + breathlessness mimicking ACS
  • Following emotional or physical stress
  • Middle-aged to elderly women predominantly
Inves
  • ECG changes + elevated troponin (mimics MI)
  • Coronary angio: unobstructed arteries
  • Left ventriculogram: apical ballooning with normal base
  • Echo: apical akinesis with normal basal contraction
Mng
  • Supportive (β-blocker, ACEi)
  • Avoid inotropes (catecholamine-driven)
Special
  • Full recovery typically within 4–6 weeks
  • Recurrences possible
  • Proposed mechanism: transient catecholamine excess
43

Endomyocardial Fibrosis (Obliterative)

C/P
  • Restrictive picture with right-sided HF
  • Hyperéosinophilia association
  • Tropical regions
  • Predominantly affects children and adolescents; involves both LV and RV
Inves
  • Echo: endocardial thickening, obliteration of ventricular apex
  • Eosinophilia
Mng
  • Anti-failure measures
  • Surgical resection of fibrotic endocardium
Special
  • Loeffler's endocarditis = temperate counterpart with eosinophilia
  • Both feature myocardial/endocardial fibrosis + eosinophilia
44

Myocarditis

C/P
  • Recent viral illness (Coxsackie B most common)
  • Chest pain, dyspnoea, palpitations, syncope, sudden death
  • HF features, arrhythmia
  • HR rise out of proportion to fever (>10 bpm per °C)
  • Frequently accompanied by pericarditis (myopericarditis); may cause functional MR
Inves
  • ECG: non-specific ST/T changes, arrhythmia, AV block
  • Troponin elevated
  • CMR: late gadolinium enhancement (subepicardial/mid-wall)
  • Endomyocardial biopsy
  • Viral serology
Mng
  • Supportive: HF therapy, anti-arrhythmics
  • Treat underlying cause (immunosuppression for autoimmune)
  • Restrict exercise during recovery
  • VAD / transplant if severe
Special
  • Causes: viral (Coxsackie B), bacterial, fungal, parasitic (Chagas), autoimmune, drugs (clozapine, doxorubicin), Lyme
  • HR rises disproportionately with fever (unlike other febrile illnesses)
  • Causes expanded: cardioselective viruses Coxsackie A&B, adenovirus, ECHO (commonest); diphtheria (toxin), meningococcus, typhus, Toxoplasma, Trypanosoma; giant cell myocarditis, sarcoidosis, rheumatic fever, SLE, transplant rejection
physiology · background · low-yield
Microbiology
  • Non-selective viruses (usually asymptomatic): HIV, rubella, mumps, CMV, polio; cardioselective viruses also cause skeletal myositis
Mechanism
  • Pathology: mottled pale & haemorrhagic myocardium (severe cases); micro — dense T-lymphocyte infiltrate with necrosis

Pericardial Disease

5 entries
45

Acute Pericarditis

C/P
  • Pleuritic chest pain, relieved by leaning forward, worse on inspiration / lying flat
  • Fever, systemic symptoms of underlying cause
  • Pericardial friction rub (rough scratching, accentuated leaning forward, not related to cardiac cycle, often absent)
Inves
  • ECG: widespread saddle-shaped (concave) ST elevation in all leads except aVR (where ST depressed); PR depression (PR elevation in aVR); T inversion later
  • ECG with large effusion: low voltage + electrical alternans
  • CXR: normal; globular if large effusion
  • Bloods: ESR/CRP, autoimmune screen if indicated
  • Echo: exclude significant effusion
  • Cardiac enzymes (troponin) — to exclude myopericarditis
Mng
  • NSAIDs first-line + colchicine (reduces recurrence)
  • Steroids only for autoimmune / resistant cases
  • Antimicrobials if bacterial/TB/fungal
  • Dialysis for uraemic pericarditis
  • Pericardiocentesis if significant effusion + tamponade signs
Special
  • Mnemonic for causes: RHIM (Radiotherapy, Hemopericardium, Infections/Inflammatory/Idiopathic, Metabolic, Malignancy)
  • Dressler's = 2–10 wk post-MI (autoimmune)
  • No reciprocal ST depression (differentiates from STEMI)
  • Saddle-shape ST elevation = disease-specific
physiology · background · low-yield
Epidemiology/Risk
  • Classically post-viral — recent URTI in a young patient
Background
  • RHIM sub-causes: hemopericardium (trauma, aortic dissection); infections (viral, bacterial, TB, fungal); inflammatory (connective tissue disease, acute rheumatic fever, Dressler's, drug reactions); metabolic (uraemia, hypothyroidism)
46

Pericardial Effusion

C/P
  • Small: asymptomatic
  • Large: dyspnoea, dull chest discomfort
  • Signs of tamponade if hemodynamic compromise (see #47)
Inves
  • CXR: globular heart outline if large
  • ECG: low voltage ± electrical alternans
  • Echo: anechoic space surrounding heart
  • Pericardial fluid analysis: culture, cytology, chemistry (CCC); transudate vs exudate; GeneXpert for TB
Mng
  • Treat underlying cause
  • Pericardiocentesis if tamponade or diagnostic uncertainty
  • Pleuro-pericardial window for recurrent (e.g. malignant)
Special
  • Transudate: HF, renal failure
  • Exudate: inflammation, malignancy, infection
  • Same aetiologies as pericarditis
  • Fluid-character classification: haemorrhagic (trauma, aortic dissection), chylous (lymphatic obstruction), purulent (bacterial infection)
47

Cardiac Tamponade

C/P
  • Beck's triad: hypotension + raised JVP + muffled heart sounds
  • Tachycardia, weak/impalpable pulse, cold clammy peripheries
  • Dyspnoea, syncope
  • Pulsus paradoxus (SBP drop >10 mmHg on inspiration)
  • Kussmaul's sign (JVP rises on inspiration)
  • Absent apex beat, ↑ cardiac dullness
Inves
  • ECG: low voltage + electrical alternans
  • CXR: globular ("water-bottle") heart
  • Echo (gold standard): large anechoic space surrounding heart + RV diastolic collapse, RA collapse, IVC plethora, septal bounce
  • Pre-pericardiocentesis: clotting screen, platelets
Mng
  • Emergency percutaneous pericardiocentesis
  • Emergency surgical drainage if traumatic / blood / inaccessible
  • IV fluids as bridge
  • Treat underlying cause
  • Pleuro-pericardial window for recurrent malignant effusion
Special
  • Beck's triad + pulsus paradoxus + electrical alternans = pathognomonic
  • Rate of accumulation > absolute volume matters
  • RV diastolic collapse on echo = early; RA collapse = sensitive
physiology · background · low-yield
Other
  • Aetiological bloods: thyroid profile, ANA, Quantiferon (TB) to identify underlying cause
Physiology
  • Pulsus paradoxus mechanism: inspiration → marked septal shift to the left → encroaches on LV filling → SBP falls >10 mmHg
48

Constrictive Pericarditis

C/P
  • Right heart failure picture: raised JVP, hepatomegaly, ascites, oedema
  • Dyspnoea, fatigue
  • Kussmaul's sign
  • Pericardial knock (early diastolic high-pitched sound — ventricular filling abruptly halted)
  • Often history of TB / cardiac surgery / radiation
Inves
  • CT/MRI: pericardial thickening/calcification (most sensitive)
  • Egg-shell calcification on CXR/CT (named appearance, best seen on CT)
  • Echo: septal bounce, respiratory variation in MV/TV inflow
  • Cardiac catheterisation: equalisation of diastolic pressures, "square root" / dip-plateau sign
Mng
  • Diuretics for symptomatic relief
  • Pericardiectomy (definitive)
Special
  • TB = most common cause globally
  • Pericardial knock = disease-defining
  • Differentiate from RCM (overlapping picture) — both Kussmaul +, both ↑ JVP; CT/MRI shows thickened pericardium in constrictive
49

Adhesive Pericarditis

C/P
  • Rare; minimal clinical manifestations
Inves
  • Imaging shows pericardial adhesion to surrounding mediastinal structures
Mng
  • Treat underlying cause (rheumatic fever historically)
Special
  • Adhesion of pericardium to mediastinum/chest wall — usually post-inflammatory
  • No significant hemodynamic compromise

Hypertension

7 entries
50

Essential (Primary) HTN

C/P
  • Usually asymptomatic ("silent killer")
  • Headache, dizziness only at very high BP
  • Found incidentally / on screening
Inves
  • Office BP ≥140/90 on ≥2 visits, OR
  • ABPM 24h avg ≥130/80 / daytime ≥135/85 / night-time ≥120/70
  • HBPM avg ≥135/85
  • Confirm with out-of-office BP measurement (preferred)
  • Initial work-up: U&E, fasting glucose, lipids, urinalysis (proteinuria), ECG, fundoscopy
  • Echo if LVH suspected
  • White-coat HTN (high clinic / normal out-of-office BP, often anxiety) and masked HTN (normal clinic / high out-of-office BP — missed without home/ambulatory monitoring)
Mng
  • Lifestyle: salt restriction, weight loss, DASH diet, exercise, ↓ alcohol, smoking cessation
  • Pharmacology (per ACC/AHA, ESC):
    • <55 / non-Black: ACEi or ARB
    • ≥55 / Black: CCB or thiazide
    • Step 2: combine A+C / A+D
    • Step 3: A+C+D
    • Step 4 (resistant): + spironolactone
  • Target <140/90 (most), <130/80 if diabetic/CKD/high-risk
  • Start drugs immediately once confirmed (≥140/90) regardless of CVD risk, preferably as a low-dose two-drug combination (ACEi/ARB + CCB or thiazide), with follow-up every 1–3 months
  • Target SBP 120–129 and DBP 70–79 mmHg if tolerated (ALARA principle); more lenient <140/90 if age ≥85, frail, or symptomatic orthostatic hypotension
  • Beta-blockers not first-line unless a compelling indication (arrhythmia, pregnancy, CAD, heart failure)
Special
  • 90% of all HTN; multifactorial (genetic + lifestyle)
  • Mostly >40 yo, gradual onset
  • Female sex hormones protect pre-menopause; equalises post-menopause
  • Benign (chronic) HTN pathology: hyaline arteriolosclerosis of vessels and benign nephrosclerosis — small, finely granular contracted kidney → proteinuria + progressive chronic renal failure
physiology · background · low-yield
Epidemiology/Risk
  • Affects ~one-third of adults; most common condition treated in primary care; leading global risk factor for death; <50% reach target; leading risk factor for AF, stroke, MI & end-stage kidney disease
  • CVD risk stratified with SCORE2 (40–69 yo) / SCORE2-OP (≥70 yo): ≥10% = high risk, 5–<10% = borderline (needs risk modifiers)
  • Evidence: a 10/5 mmHg BP reduction → 15% ↓ all-cause mortality, 35% ↓ stroke, 40% ↓ HF, 20% ↓ MI
Background
  • "Elevated BP" (120–139/70–89): lifestyle only if low/moderate CVD risk; add drugs after 3 months if high CVD risk and BP remains ≥130/80
Exam technique
  • Office BP: 5 min rest, correct cuff (bladder ≥80% arm length, ≥40% width), ≥2 readings/visit, deflate 3 mmHg/s, Korotkoff phase V for diastolic (phase IV in children), both arms initially → use higher; palpate pulse for AF
51

Secondary HTN

C/P
  • Suspect if: <40 with grade 2 HTN, abrupt onset, resistant HTN, grade 3 or emergency, extensive HMOD, clinical features of endocrine/CKD/OSA/pheo
  • Cushingoid features, abdominal bruit (RAS), hypokalaemia (hyperaldo), paroxysmal headache + sweating + palpitations (pheo)
  • Flash (recurrent) pulmonary oedema + new HTN after age 55 + abdominal bruit → renal artery stenosis; confirm with duplex Doppler renal ultrasonography
Inves
  • Renal: U&E, eGFR, urinalysis, urine ACR, renal US, renal Doppler / CT / MR angiography
  • Endocrine: aldosterone-to-renin ratio (Conn's), 24-h urinary metanephrines (pheo), 24-h urinary cortisol + low-dose dexamethasone (Cushing's), TSH, PTH/Ca/PO4
  • Sleep: polysomnography (OSA)
  • Coarctation: echo + aortic CT angiogram
Mng
  • Treat underlying cause (potentially curable)
  • BP control with antihypertensives meanwhile
Special
  • 10% of HTN cases
  • Drug causes: OCP, NSAIDs, decongestants, stimulants, liquorice (mimics hyperaldo), immunosuppressants, VEGF inhibitors
physiology · background · low-yield
Background
  • Further causes: thyroid disease (hypo/hyper), acromegaly, primary hyperparathyroidism, pre-eclampsia; further drug causes: diet pills (phenylpropanolamine/sibutramine), anabolic steroids, erythropoietin, herbal (ephedra/ma huang)
52

Malignant HTN / Hypertensive Emergency

C/P
  • BP ≥180/120 + acute end-organ damage
  • Severe headache, visual disturbance, encephalopathy, seizure
  • Acute LV failure with pulmonary oedema
  • AKI, haematuria
  • Papilloedema, flame haemorrhages, cotton-wool spots (grade IV retinopathy)
  • Microangiopathic haemolytic anaemia
Inves
  • BP repeat
  • Fundoscopy: papilloedema
  • U&E, urinalysis (RBC casts, proteinuria), creatinine
  • ECG, CXR (pulmonary oedema)
  • CT brain if neuro signs (exclude stroke)
  • Echo if HF
Mng
  • ICU + IV antihypertensives
  • Sodium nitroprusside, labetalol, GTN, nicardipine
  • Reduce BP carefully: max 25% in first hour, then to 160/100 over 2–6 h (rapid drop → stroke / coronary ischaemia)
  • Exception: aortic dissection → BP <120 systolic ASAP
  • Treat end-organ complications
  • IV options also include clevidipine and fenoldopam; nitroprusside carries cyanide-toxicity risk with prolonged use
Special
  • Fibrinoid necrosis of arterioles = pathological hallmark
  • Hypertensive encephalopathy
  • "Onion-skinning" of arterioles in kidney
  • Flea-bitten kidney — smooth surface with pin-point haemorrhages (ruptured arterioles/glomerular capillaries); kidneys normal-sized (shrunken only if accelerated)
  • Accelerated HTN = malignant HTN arising suddenly in a patient with prior benign HTN; de novo malignant HTN classically in young Afro-Caribbean males (BP usually >200/120)
physiology · background · low-yield
Mechanism
  • Malignant vascular lesions: fibrinoid necrosis (necrotizing arteriolitis — endothelial injury, plasma-protein leakage, platelet deposition) and hyperplastic arteriolosclerosis (PDGF-driven concentric intimal SMC hyperplasia → onion-skin)
53

Resistant HTN

C/P
  • BP above target despite ≥3 antihypertensives of different classes (including diuretic) at maximum/tolerated doses
Inves
  • Confirm adherence
  • ABPM/HBPM (exclude white-coat)
  • Investigate secondary causes
  • Salt diet review, drug-induced HTN screen
Mng
  • Optimise lifestyle
  • Add spironolactone (or eplerenone) as 4th-line
  • Consider renal denervation if refractory
  • Refer to specialist hypertension centre (exclude pseudo-/secondary resistance, optimise to 3-drug single-pill); sequential add-ons after spironolactone: beta-blocker, then alpha-blocker or centrally-acting agent (e.g. clonidine)
Special
  • Workup for secondary cause mandatory
54

Isolated Systolic HTN

C/P
  • SBP ≥140 with DBP <90
  • Elderly patients (>50)
  • Wide pulse pressure (often >50 mmHg)
Inves
  • Routine HTN workup
  • Echo to assess aortic incompetence (can cause ISH)
Mng
  • Same approach as combined HTN
  • Do not reduce DBP <60 mmHg (compromises coronary perfusion)
Special
  • Age-related arterial stiffening
  • Wide pulse pressure ↑ vascular damage
  • Aortic regurgitation can present as ISH — auscultate
55

Orthostatic Hypotension

C/P
  • Within 1–3 min of standing: SBP drop >20 mmHg or DBP drop >10 mmHg
  • Postural intolerance, dizziness, falls, syncope
  • Often asymptomatic
Inves
  • Lying + standing BP at 1 and 3 min
  • Screen for autonomic neuropathy (DM, Parkinson's)
  • Medication review
Mng
  • Stand slowly, compression stockings
  • ↑ salt + fluid intake
  • Adjust offending medications
  • Use standing BP to guide antihypertensive therapy
Special
  • Associated with older age, DM, Parkinson's, autonomic dysfunction
56

Hypertensive Heart Disease (End-organ damage)

C/P
  • LVH → diastolic dysfunction → HFpEF → HFrEF
  • Angina, arrhythmia (AF), sudden cardiac death
  • Hypertensive retinopathy, CKD, stroke
  • Brain HMOD: cognitive impairment / vascular dementia, silent microinfarcts, microbleeds, white-matter lesions, brain atrophy (beyond overt stroke)
Inves
  • ECG: LVH (Sokolow-Lyon S V1 + R V5/V6 > 35 mm)
  • Echo: concentric LVH, diastolic dysfunction → progressive LV dilation
  • Fundoscopy: AV nipping, silver wiring, haemorrhages, exudates, papilloedema (grade IV)
  • Urine ACR, eGFR (CKD)
Mng
  • Aggressive BP control
  • Standard HF therapy if developed
  • Treat associated CV risk factors
Special
  • HMOD = Hypertension-Mediated Organ Damage (eye, brain, heart, kidney, arteries)
  • LVH = strongest predictor of CV event in HTN
  • "Heart failure cells" = haemosiderin-laden macrophages in alveoli (from pulmonary oedema of LV failure)
physiology · background · low-yield
Mechanism
  • Microcirculation HMOD: endothelial dysfunction, ↑ peripheral vascular resistance, vascular remodelling/fibrosis; large-artery HMOD: atherosclerosis, vascular calcification, arterial stiffness

Hyperlipidaemia

2 entries
57

Hyperlipidaemia (general)

C/P
  • Usually asymptomatic until CV event
  • Xanthelasma, corneal arcus
  • Eruptive xanthomas if severe ↑TG
  • Acute pancreatitis if TG >500 mg/dL
Inves
  • Fasting lipid profile if TG >400 mg/dL or FH
  • Total cholesterol, LDL-C, HDL-C, TG, non-HDL-C
  • Friedewald: LDL-C = TC − (HDL + TG/5) — invalid if TG >400
  • Screen for secondary causes: TSH, glucose, urinalysis, LFTs
  • SCORE2 / SCORE2-OP for 10-yr CV risk
  • Lipoprotein(a) once in lifetime
Mng
  • Lifestyle first: Mediterranean diet, exercise, weight loss, alcohol moderation, smoking cessation
  • Statin (high-intensity for established CVD / very high risk)
  • Add ezetimibe if not at goal
  • Add PCSK9 inhibitor (alirocumab, evolocumab) if still not at goal
  • Bempedoic acid as alternative
  • Fibrates for high TG (or omega-3); niacin niche
  • LDL targets: <55 mg/dL very-high-risk, <70 high-risk, <100 moderate, <116 low-risk
  • Extreme risk (recurrent events on max statin / poly-vascular disease): LDL-C goal <40 mg/dL
  • Very-high & high risk also require ≥50% LDL-C reduction from baseline (in addition to the absolute goal)
  • Non-HDL-C targets: <85 very-high, <100 high, <130 moderate (rule of thumb: LDL target + 30)
  • Persisting high TG despite max statin (TG 135–499 mg/dL): add icosapent ethyl 2 g BID (preferred) or fenofibrate (if TG >200)
  • Before starting statin: baseline lipids, LFTs, CK; recheck lipids q3 months until target then annually. Stop statin if ALT >3× or CK >10× normal
Special
  • 95% of Western population has raised cholesterol
  • Diet primarily affects TG (only 15% of LDL is diet-modifiable)
  • Post-MI: measure lipids within 24 h OR ≥1 month later (acute illness ↓ lipids up to 3 months)
physiology · background · low-yield
Epidemiology/Risk
  • Dyslipidaemia contributes up to half of population CVD risk worldwide
  • Drug causes of secondary hyperlipidaemia: antiretrovirals, β-blockers, OCP, corticosteroids, thiazide diuretics
  • Opportunistic screening indications: FHx CHD / lipid disorder, xanthoma/arcus, DM, HTN, obesity, acute pancreatitis, renal replacement therapy (systematic screening if >40 yr)
  • Lp(a) >180 mg/dL (>430 nmol/L) confers a lifetime ASCVD risk equivalent to HeFH
Background
  • Statin intensity: high (≥50% LDL↓) = atorvastatin 40–80 / rosuvastatin 20–40; moderate = 30–49%; low = <30%
Mechanism
  • Bempedoic acid = ATP-citrate lyase inhibitor prodrug (activating enzyme absent in skeletal muscle → no myopathy); inclisiran = siRNA inhibiting PCSK9 synthesis
Physiology
  • CV-risk gradient: LDL-C/non-HDL-C strong risk (esp. CHD); HDL-C protective; VLDL/IDL weak added risk; chylomicrons confer no excess CVD risk
58

Familial Hypercholesterolaemia (FH)

C/P
  • Premature CAD (HeFH: 30–60 yr; HoFH: childhood)
  • Tendinous xanthomata (Achilles, knuckles, knees)
  • Corneal arcus before age 45 (abnormal in young = FH suspect)
  • Xanthelasma
  • FHx premature CAD (men <55, women <60) or sudden death
Inves
  • LDL-C: HeFH >190 mg/dL; HoFH >400 mg/dL
  • Dutch Lipid Clinic Network score:
    • Family hx (1–2 points), clinical hx (1–2), exam (4–6 — xanthoma exclusive with arcus), LDL-C levels (1–8), DNA mutation (8)
    • Definite >8, Probable 6–8, Possible 3–5
  • Genetic testing: LDLR, ApoB, PCSK9 mutations
  • Cascade screening of 1st-degree relatives
Mng
  • High-intensity statin from diagnosis (childhood in HoFH)
  • Add ezetimibe; PCSK9 inhibitor essential in HoFH
  • LDL apheresis for refractory HoFH
  • Lomitapide / evinacumab (HoFH-specific)
  • Family screening mandatory
Special
  • Autosomal dominant; HeFH 1 in 250 (one of commonest AD disorders)
  • HoFH 1 in 300,000 — poor response to standard therapy
  • Tendinous xanthomata = pathognomonic
  • Corneal arcus in <45 yo = highly suggestive
  • FH is a SCORE2/SCORE2-OP exclusion — automatically classified as High / Very-high CV risk
physiology · background · low-yield
Background
  • FHx clues: consanguinity, early death, similar symptoms in relatives

Other (cardio-relevant DDx)

1 entry
59

Pulmonary Embolism (+ DVT)

C/P
  • Sudden pleuritic chest pain, dyspnoea, haemoptysis
  • Tachycardia, tachypnoea, hypotension if massive
  • DVT signs: unilateral leg swelling, calf tenderness, ↑ warmth
  • ± Syncope, hypoxia
  • Risk: immobility, recent surgery, malignancy, OCP, pregnancy, thrombophilia
Inves
  • CT pulmonary angiography (CTPA) = definitive
  • V/Q scan if CTPA contraindicated
  • ECG: sinus tachycardia (most common); S1Q3T3 (classic but uncommon); RBBB, RAD, T inversion V1–V3
  • ABG: hypoxaemia, hypocapnia (respiratory alkalosis)
  • Echo: RV strain (dilation), tricuspid regurgitation, ↑ PAP
  • Doppler US lower limbs for DVT
Mng
  • Anticoagulation: LMWH → DOAC or warfarin
  • Massive PE (hemodynamically unstable): systemic thrombolysis (alteplase) ± mechanical thrombectomy
  • IVC filter if anticoagulation contraindicated
  • ICU admission for confirmed acute PE with lower-limb DVT
  • Supplemental oxygen (respiratory support)
  • Correct the precipitant: stop combined OCP and switch to another contraceptive method
Special
  • S1Q3T3 + new RBBB = classic but rare PE ECG
  • Saddle PE at pulmonary artery bifurcation = massive

Additions — Approach & OSCE

3 entries
60

Multifocal Atrial Tachycardia (MAT) / Wandering Atrial Pacemaker

C/P
  • Palpitations; classically seen in severe COPD exacerbation
Inves
  • ECG: narrow QRS <120 ms, irregular rhythm, tachycardia (HR >100), ≥3 different P-wave morphologies
  • Wandering atrial pacemaker (WAP) = same multiple P morphologies but HR <100 (no tachycardia)
Mng
  • Treat the underlying cause (hypoxia / COPD)
Special
  • ≥3 distinct P-wave morphologies distinguishes MAT from AF (which has no P waves); tachycardia distinguishes MAT from WAP
61

Sinus Arrhythmia

C/P
  • Usually asymptomatic; common and of no clinical significance in young healthy individuals
Inves
  • ECG: irregular rhythm with normal sinus P waves; R-R interval varies by ≥120 ms between longest and shortest
  • HR increases on inspiration, decreases on expiration (Bainbridge reflex)
Mng
  • None required — benign in the young
Special
  • In older patients, or if unrelated to respiration → may indicate sick sinus syndrome (SSS)
62

Junctional (AV Nodal) Rhythms

C/P
  • Often asymptomatic / incidental
Inves
  • ECG: retrograde P waves — inverted in lead II, upright in aVR (opposite to sinus); P may precede, hide within, or follow the QRS; narrow QRS
  • Rates: escape/junctional bradycardia <60, accelerated junctional 60–100, junctional tachycardia >100
Mng
  • Treat the underlying cause
Special
  • Retrograde P wave (inverted II / upright aVR) is the hallmark of a junctional pacemaker

Diagnostic Criteria

4 entries
1

Modified Duke Criteria 2000 — Infective Endocarditis

Major (need 2)

  • Positive blood cultures or organisms seen at histology
  • Vegetation on echo

Minor

  • Predisposition or IV drug abuse
  • Fever ≥38 °C
  • Vascular phenomena
  • Immunological phenomena
  • Serological / minor culture evidence (uncharacterised organism or fungus = minor)

Definitive IE

  • 2 Major
  • 1 Major + 3 Minor
  • 5 Minor

Possible IE

  • 1 Major + 1 Minor
  • 1 Major + 2 Minor
  • 3–4 Minor
2

2023 ESC Diagnostic Criteria — Infective Endocarditis

Major — Blood Cultures

  • (a) Typical organisms from 2 separate cultures: Oral streptococci · Strep gallolyticus (S. bovis) · HACEK · S. aureus · E. faecalis
  • (b) Continuously positive: ≥2 positive >12 h apart, OR all 3 / majority of ≥4 with first/last ≥1 h apart
  • (c) Single positive C. burnetii culture OR phase I IgG titre >1:800

Major — Imaging

  • Echocardiography (TTE + TOE)
  • Cardiac CT
  • [18F]-FDG-PET/CT(A)
  • WBC SPECT/CT

Minor (5 categories)

  • (i) Predisposing conditions — high/intermediate-risk cardiac condition OR PWID
  • (ii) Fever >38 °C
  • (iii) Embolic vascular dissemination (6 signs): systemic/pulmonary emboli/infarcts/abscesses · haematogenous osteoarticular complications (spondylodiscitis) · mycotic aneurysms · intracranial ischaemic/haemorrhagic lesions · conjunctival haemorrhages · Janeway lesions
  • (iv) Immunological phenomena (3): glomerulonephritis · Osler nodes + Roth spots · rheumatoid factor
  • (v) Microbiological: positive culture not meeting major OR serological evidence

Classification

  • Definite IE: 2 Major · 1 Major + ≥3 Minor · 5 Minor
  • Possible IE: 1 Major + 1–2 Minor · 3–4 Minor
  • Rejected IE: does not meet definite/possible, ± alternative diagnosis
3

Dutch Lipid Clinic Network — Familial Hypercholesterolaemia

Family History

  • 1 pt — 1st-degree relative with premature CAD (♂ <55, ♀ <60) OR LDL-C >95th percentile
  • 2 pts — 1st-degree relative with tendinous xanthomata/arcus OR children <18 with LDL-C >95th percentile

Clinical History

  • 2 pts — premature CAD
  • 1 pt — premature cerebral/peripheral vascular disease

Physical Examination (mutually exclusive — max 6)

  • 6 pts — tendinous xanthomata
  • 4 pts — arcus cornealis before age 45

LDL-C (untreated, mg/dL)

  • 8 pts — ≥325
  • 5 pts — 251–325
  • 3 pts — 191–250
  • 1 pt — 155–190

DNA Analysis

  • 8 pts — functional mutation in LDLR, ApoB, or PCSK9

Diagnosis

  • Definite >8
  • Probable 6–8
  • Possible 3–5

Rule: Choose only one score per group (highest applicable).

4

Task Force Criteria — ARVC

5 Categories

  • Structural — RV dilation + abnormal wall motion (echo / MRI)
  • Tissue biopsy — fibro-fatty replacement of myocytes
  • ECG / signal-averaged ECG — repolarisation + conduction abnormalities
  • Holter — VT or frequent ventricular extrasystoles
  • Family history — 1st/2nd-degree relative + premature sudden death (<35 yr)

Risk Scores

5 entries
5

CHA₂DS₂-VA — AF Stroke Risk

Components

LetterCriterionPts
CChronic HF (sx/signs OR asymptomatic LVEF ≤40%)1
HHypertension (BP >140/90 on ≥2 occasions OR on tx)1
A₂Age ≥752
DDiabetes (T1/T2 OR glucose-lowering tx)1
S₂Prior Stroke / TIA / arterial thromboembolism2
VVascular disease (CAD, PVD)1
AAge 65–741
ScSex category (female)1

Recommendations (2024 ESC)

  • Score ≥2 → OAC recommended
  • Score = 1 → OAC should be considered
  • Score = 0 → no OAC (bleeding risk outweighs benefit)
6

HAS-BLED — Bleeding Risk on OAC

9 Components

  • H — Hypertension (SBP ≥160 mmHg)
  • A — Abnormal renal function
  • A — Abnormal liver function
  • S — prior Stroke
  • B — Bleeding history
  • L — Labile INRs
  • E — Elderly (≥65)
  • D — Drugs (NSAIDs etc.)
  • A — Alcohol intake

Risk Stratification

  • Score 0 → ~1 %/yr major bleeding (low)
  • Score ≥3 → >5 %/yr (high) — modify reversible factors (BP, alcohol), do NOT withhold OAC
7

ACS Risk Stratification — GRACE / HEART / TIMI

GRACE Score

Predicts in-hospital + 6-month mortality / recurrent MI.

  • Age
  • Heart rate
  • Systolic BP
  • Creatinine
  • Heart failure
  • Cardiac arrest
  • ST deviation
  • Cardiac enzymes / troponin

HEART Score (5 components)

  • History
  • EKG
  • Age
  • Risk factors
  • Troponin

TIMI

Third option for ACS risk stratification.

8

SCORE2 / SCORE2-OP — 10-yr CVD Risk

  • SCORE2 — age 40–69
  • SCORE2-OP — age ≥70
  • Estimates 10-yr fatal + non-fatal CV events
  • Stratifies into low / moderate / high / very-high risk
9

HCM — Sudden Cardiac Death Risk Factors

ICD if ≥2 of:

  • Massive LVH >30 mm
  • FHx SCD <50 yr
  • Non-sustained VT (Holter, <30 s)
  • Prior unexplained syncope
  • Abnormal BP response on exercise (flat or hypotensive)

If <2 factors → amiodarone.

Anatomical Classifications

5 entries
10

Aortic Dissection — Stanford + DeBakey

Stanford

  • A (proximal) — involves ascending aorta (regardless of tear site) → surgical emergency
  • B (distal) — does NOT involve ascending → medical (BP control)

DeBakey (Relative Frequency)

TypeFrequencyStanford
I60%A
II10–15%A
III25–30%B
11

MI — Universal Classification

  • Type 1 — Plaque rupture with thrombus (classic acute MI)
  • Type 2a — Vasospasm / endothelial dysfunction
  • Type 2b — Fixed atherosclerosis + supply-demand imbalance
  • Type 2c — Supply-demand imbalance alone (severe anaemia, hypotension)
12

ACS — Classification

TypeTroponinECG
UANegativeST depression / T-wave changes (or normal)
NSTEMIPositiveST depression / T-wave changes (or normal)
STEMIPositiveST elevation

NSTE-ACS = UA + NSTEMI

13

AF — Clinical Classification

  • First detected — any duration / severity
  • Paroxysmal — stops spontaneously within 7 days
  • Persistent — continuous >7 days
  • Longstanding persistent — continuous >1 year
  • Permanent — joint physician–patient decision to stop rhythm-control attempts

Utility: dictates choice between rate and rhythm control.

14

Hyperlipidaemia — Fredrickson Types

Primary (Familial)

TypeLipoprotein ↑Synonym
IChylomicronsFamilial chylomicronaemia
IIaLDLFamilial hypercholesterolaemia (most common)
IIbLDL + VLDLFamilial combined hyperlipidaemia
IIIIDLFamilial dysbetalipoproteinaemia
IVVLDLFamilial hypertriglyceridaemia
VVLDL + chylomicronsFamilial mixed hyperlipidaemia

Secondary Causes

  • Hypercholesterolaemia: hypothyroidism, nephrotic syndrome, drugs
  • Hypertriglyceridaemia: DM, alcohol, gout, CRF

Severity Classifications

8 entries
15

NYHA Functional Classification — Heart Failure

Based on symptom severity + exertion needed to provoke.

3 provoking symptoms: fatigue · palpitation · dyspnoea

ClassDefinition
INo limitation of physical activity
IISlight limitation; ordinary activity → fatigue/palpitation/dyspnoea; comfortable at rest
IIIMarked limitation; less-than-ordinary activity → symptoms; comfortable at rest
IVSymptoms at rest; any activity increases discomfort
16

LVEF Classification — Heart Failure

CategoryLVEF
HFrEF≤40%
HFmrEF41–49%
HFpEF≥50%

Population split: 50% HFrEF / 50% HFpEF + HFmrEF

HFpEF / HFmrEF Diagnostic Criteria (BOTH required)

  • Symptoms ± signs
  • Evidence of raised LV filling pressures (↑ natriuretic peptide OR invasive/non-invasive haemodynamic measurement)

HFrEF doesn't require criterion 2 (LVEF ≤40% + symptoms suffices).

17

ACC/AHA Stages — Heart Failure

Stage A — At Risk for HF

Asymptomatic, no structural disease, no biomarker stretch injury.

Risk factors: HTN · ASCVD · DM · metabolic syndrome / obesity · cardiotoxic agents · genetic CM variant · +FHx CM

Stage B — Pre-HF

No symptoms/signs but structural disease, raised filling pressures, OR raised biomarkers.

  • Structural (6): ↓ LV/RV systolic function · ↓ EF / strain · LVH · enlarged chamber · wall-motion anomalies · valvular disease
  • Biomarkers: ↑ BNP · persistently ↑ troponin
  • Exclusions (4): ACS · CKD · PE · myopericarditis

Stage C — Symptomatic HF

Structural disease + current or previous HF symptoms.

Stage D — Advanced (Refractory) HF

Marked symptoms interfering with daily life + repeated admissions despite optimal GDMT → consider LVAD / transplant.

18

ACC/AHA Stages ↔ NYHA Mapping

  • ACC/AHA captures structural progression (one-way; cannot move back)
  • NYHA captures functional symptom severity (bidirectional; improves/worsens with treatment)
ACC/AHA StageNYHA Equivalent
ANone (asymptomatic, no structural disease)
BNYHA I
CNYHA II–IV
DNYHA IV

Therapeutic Implications

  • Stage B + NYHA I → start ACEi/ARB + β-blocker even though asymptomatic
  • Stage D + NYHA IV → advanced therapies (LVAD, transplant, palliative)
19

HTN — BP Cutoffs

Office BP

CategoryCutoff
Non-elevated<120/70
Elevated120–139 / 70–89
Hypertension≥140/90

Out-of-Office Cutoffs for HTN Diagnosis

  • ABPM 24-h avg ≥130/80
  • ABPM daytime ≥135/85
  • ABPM night-time ≥120/70
  • HBPM avg ≥135/85
20

HTN — Primary vs Secondary

PrimarySecondary
CauseNone identifiable (multifactorial)Identifiable
Prevalence90%10%
Age of onsetMostly >40 yrMostly <40 yr
OnsetGradualAbrupt / severe
TreatmentLifestyle + antihypertensivesTreat cause + BP control
PrognosisChronic managementPotentially curable / reversible
21

HTN — Benign vs Malignant (Pathological)

Benign

  • Gradual onset
  • Hyaline arteriolosclerosis
  • Slow nephrosclerosis progression

Malignant

  • Hyperplastic arteriolosclerosis (onion-skinning)
  • Fibrinoid necrosis
  • Rapid renal failure
  • Papilloedema, encephalopathy
  • Microangiopathic haemolytic anaemia (MAHA)
22

Cardiomyopathies — Classification

  • Hypertrophic (HCM)
  • Dilated (DCM)
  • Restrictive (RCM) — incl. amyloidosis, sarcoid, Loeffler's, EMF
  • Arrhythmogenic RV (ARVC)
  • Other: LVNC, Tako-tsubo, peripartum, tachycardia-induced, obliterative (EMF)

ECG Criteria

7 entries
23

Chamberlain's 10 Rules — Normal ECG

  1. PR interval 120–200 ms (3–5 small squares)
  2. QRS width <110 ms (<3 small squares)
  3. QRS dominantly upright in I, II, III
  4. QRS + T wave same general direction in limb leads
  5. aVR all waves negative
  6. R wave grows V1→V4; S wave grows V1→V3 then disappears by V6
  7. ST segment isoelectric (except V1, V2 may be slightly elevated)
  8. P waves upright in I, II, V2–V6
  9. No Q wave or only small q <0.04 s wide in I, II, V2–V6
  10. T waves upright in I, II, V2–V6
24

LBBB — ECG Criteria

  • QRS ≥0.12 s (complete) or 0.10–0.12 s (incomplete)
  • V1, V2: QS or rS
  • V5, V6, I: monophasic R (± notched)
  • V5, V6: secondary T inversion

Cannot Diagnose in LBBB

  • MI
  • Ischaemia
  • Ventricular enlargement
  • Hemiblock
25

RBBB — ECG Criteria

  • QRS ≥0.12 s (complete) or 0.10–0.12 s (incomplete)
  • V1, V2: RsR' or RR' (rabbit ears)
  • V5, V6, I: QRS with slurred S
  • V1, V2: secondary T inversion (normal in V1–V3 in RBBB)

Cannot Diagnose in RBBB

  • Ischaemia
  • Ventricular enlargement

(MI still diagnosable, unlike LBBB)

26

LVH — Voltage Criteria

Sokolow-Lyon

  • S in V1 + R in V5 >35 mm

Cornell

  • S in V3 + R in aVL >28 mm (♂) or >20 mm (♀)

R wave in aVL

  • ≥11 mm

Strain pattern

  • ST depression ± T inversion in V5–V6 (pressure overload)
27

RVH — Voltage Criteria

  • V1: tall R >7 mm OR R/S ≥1
  • V6: deep S
  • Strain pattern: ST depression ± T inversion in V1–V2
28

WPW — ECG Criteria

  • Short PR <120 ms
  • Wide QRS >120 ms
  • Delta wave (slurred QRS upstroke)
  • ST-T changes opposite to QRS
  • Type A — dominant R in V1 (left-sided accessory pathway)
  • Type B — dominant S in V1 (right-sided accessory pathway)
  • Pre-excited AF — irregular wide QRS, ~300 bpm
29

HCM — ECG Findings

  • LVH (often massive)
  • ST / T-wave changes
  • Abnormal Q waves in inferolateral leads

Surgical / Procedural Indications

5 entries
30

Aortic Stenosis — AVR Indications

All symptomatic severe AS → AVR

Asymptomatic Severe AS (any one)

  • Symptoms or hypotension during exercise test
  • EF <50%
  • Undergoing CABG or other cardiac/aortic surgery
  • Peak velocity through aortic valve >5.5 m/s
  • Systolic PA pressure >60 mmHg
  • Velocity ↑ >0.3 m/s/yr

Bicuspid AV Concurrent Indications

  • Ascending aorta >50 mm OR expansion >5 mm/yr
31

Aortic Regurgitation — Surgery Indications

Acute Severe AR

(e.g. endocarditis) — indicated

Symptomatic Chronic Severe AR

Dyspnoea, NYHA II–IV, angina

Asymptomatic

  • LVEF ≤50%
  • End-diastolic dimension >70 mm OR end-systolic >50 mm
  • Concurrent CABG / ascending aorta / other valve surgery
32

Mitral Regurgitation — Surgery Indications (ESC)

  • Symptomatic severe MR
  • Asymptomatic: end-systolic >40 mm
  • Asymptomatic: EF <60%
  • Asymptomatic preserved LV function + AF OR pulmonary HTN
  • Torrential MR (papillary/chordal rupture, IE) → emergency MVR

Stricter EF/dimension thresholds than aortic valve (LV unloads into LA → EF artificially preserved).

33

Mitral Stenosis — Surgery / BMV

  • Surgery threshold: MVA ≤1.5 cm² + persistent symptoms OR pulmonary HTN
  • BMV preferred if: pliable valve, minimal subvalvular involvement, minimal MR
  • BMV contraindications: heavy calcification, more than mild MR, LA thrombus
  • Pre-BMV: TOE mandatory (exclude LA thrombus)
  • Open valvotomy / MVR for calcified or regurgitant valves
34

IE — V-HEART Surgical Indications

LetterIndication
VVegetation (>10 mm, esp. mobile / after embolism)
HHeart failure
EExtension — perivalvular (abscess / fistula / pseudoaneurysm)
AAV block (conduction disturbance)
RResistant / difficult organism
TTreatment failure (persistent bacteraemia ~10 days)

Timing & Specifics

  • 24–72 h if S. aureus / GN bacillus / fungus + worsening HF
  • Prosthetic-specific: TOE valve dehiscence, paravalvular abscess, recurrent emboli, valve dysfunction → HF, antimicrobial-resistant organism
  • Right-sided IE: medical preferred; if surgery, repair > replacement (avoids re-infection in continued IVDU)
  • Post-stroke surgery: delay 1 month

ECG — How to Read (Fundamentals)

7 entries
35

ECG Paper & Calibration

  • Small square: 1 mm — 0.04 s (40 ms) wide, 0.1 mV tall
  • Big square (5 small): 5 mm — 0.2 s (200 ms) wide
  • 5 big squares = 1 s · 300 big squares = 1 min
  • Standard calibration: 10 mm = 1 mV (2 big squares tall), speed 25 mm/s
  • Non-standard: double speed 50 mm/s, or half voltage (0.5 mV = 1 big square) when complexes too large/small

Pearl — check before interpreting

  • Voltage calibration = 2 big squares
  • Speed = 25 mm/s
  • aVR negative (if not → limb-lead reversal)
36

Leads → Territory & Coronary Artery

LeadsTerritoryArtery
II, III, aVFInferiorRCA
I, aVLHigh lateralLCx
V5, V6Low lateralLCx
V1, V2SeptalLAD
V3, V4AnteriorLAD
  • Limb leads = frontal (vertical) plane · Chest leads = horizontal plane
  • Lead II best represents the cardiac axis · aVR is a cavity lead
37

Rate Calculation

  • Regular: 300 ÷ (big squares between two R waves), OR 1500 ÷ (small squares between two R waves)
  • Irregular (e.g. AF): count QRS in 30 big squares (6 s) × 10 = rate/min
  • Bradycardia <60 · Tachycardia >100
38

Cardiac Axis — Quadrant Method

AxisRangeLead ILead III
Normal−30 to +90PositivePositive
Left (LAD)−30 to −90PositiveNegative
Right (RAD)+90 to +180NegativePositive
Extreme−90 to ±180NegativeNegative
  • Assess in leads I, III (± aVF)
  • Most common cause of RAD = RV hypertrophy
  • Most common cause of LAD = conduction abnormality (e.g. LAFB)
39

Systematic Interpretation & Report

Reading Sequence

  • Rhythm strip (lead II) → rate, rhythm, arrhythmia/heart block (key = PR interval)
  • 12-lead → atrial enlargement (II, V1); BBB (wide QRS, V1/V6)
  • If BBB present, do NOT look for MI/ischaemia (except RBBB), hemiblock (except RBBB), or ventricular enlargement — BBB masks them
  • Then: ventricular enlargement (V1, V6) → axis (I, III, aVF) → hemiblock → MI/ischaemia

Miscellaneous — "PLED"

  • Pre-excitation · Pulmonary embolism · Pericarditis · Pacemaker · Prolonged QT · Low voltage · Electrolytes · Drug (digitalis)

Report Order

  • Rate → Rhythm → Axis → P wave → PR → QRS (axis/width/amplitude/waves) → ST → T → QT → Final diagnosis
40

Normal ECG Values

ItemNormal value
P waveHeight ≤2.5 mm (taller = P-pulmonale/RAE), width <3 mm (wider = P-mitrale/LAE); upright all leads, neg aVR, biphasic V1
PR interval120–200 ms (3–5 small squares)
QRSWidth <110–120 ms (<3 small squares); sum I+II+III >15 mm (else low voltage); small septal q <1 mm normal in I/aVL/V5/V6
ST segmentIsoelectric ±1 mm
T wave≤1 big square (limb), ≤2 big squares (chest); same direction as QRS
QTQTc prolonged >440 ms (♂) / >460 ms (♀); >500 → torsades risk; <350 abnormally short. Rule of thumb: normal QT <½ preceding RR
41

R Wave Progression & Rotation

  • Normal: R amplitude grows V1→V4; transition zone (R>S) at V3–V4
  • Poor R progression (transition after V4; R<S in V4) = clockwise rotation → COPD or old anteroseptal MI
  • Early progression (transition at/before V2) = counterclockwise rotation → RV enlargement

ECG — Ischaemia & Infarction

5 entries
42

Acute Ischaemia — ST / T Criteria

(in the absence of LVH and BBB)

ST Elevation

  • New STE at the J-point in 2 contiguous leads
  • ≥1 mm in all leads except V2–V3, where: ≥2 mm (♂ ≥40 y), ≥2.5 mm (♂ <40 y), ≥1.5 mm (♀ any age)

ST Depression / T Changes

  • New horizontal or downsloping ST depression ≥0.5 mm in 2 contiguous leads
  • T inversion >1 mm in 2 contiguous leads with dominant R (R/S >1)

Pattern Clues

  • Ischaemic T inversion is symmetrical (LVH strain = asymmetrical)
  • Downsloping/horizontal ST classic for ischaemia; upsloping is not
43

STEMI — Age / Evolution

StageECG
Hyperacute (0–6 h)ST elevation ± hyperacute T (T may be the earliest sign, before elevation)
Acute (6–24 h)Pathological Q / poor R progression begin (Q appears 8–12 h after pain onset)
Subacute / evolving (24 h–3 wk)Persistent ST elevation, biphasic T, pathological Q
Chronic (>3 wk)ST back to baseline, T inverts then normalises; pathological Q persists (only permanent change)
  • Persistent ST elevation >3 wk = LV aneurysm (normal enzymes, no chest pain, unchanged from old ECG)
44

Pathological Q Waves

  • >1 mm wide (>0.04 s) AND >2 mm deep, OR >25% of the following R wave depth
  • Present in 2 contiguous leads of the same territory
  • Indicate current/prior MI
  • Non-ischaemic causes: HCM (most common cause of sudden death in the young), lead malposition
45

MI Localisation → Territory & Artery

Territory → Coronary Artery

MIST elevation in
AnteroseptalV1–V4 (LAD)
AnterolateralV3–V6, I, aVL
Extensive anteriorI, aVL, V1–V6 (most dangerous)
InferiorII, III, aVF (RCA) — always check RV

Posterior MI

  • V1–V3: tall R, ST depression, tall T (mirror image)
  • Place posterior leads → true ST elevation; do NOT call NSTEMI; usually with inferior = infero-posterior

RV Infarction

  • ST elevation in V3R, V4R (V3/V4 mirrored to right chest)
  • Suspect in any inferior MI (RCA); NO NITRATES
46

Reciprocal Changes

  • ST depression in leads opposite the ST-elevation territory
  • Inferior MI (II/III/aVF) → reciprocal in lateral (I/aVL)
  • Anterior MI (V3/V4) → reciprocal in inferior (II/III/aVF)

Why it matters

  • Confirms the ST elevation is significant (esp. early/subtle infarcts)
  • Differentiates MI (reciprocal present) from pericarditis (reciprocal absent)

ECG — Enlargement & Conduction

3 entries
47

Atrial Enlargement

Right (RAE) — P pulmonale

  • Lead II: tall peaked P >2.5 mm
  • V1: positive deflection >1.5 mm
  • e.g. tricuspid disease, pulmonary HTN

Left (LAE) — P mitrale

  • Lead II: broad (>3 mm / >120 ms) ± notched P
  • V1: deep wide negative terminal deflection >1 mm
  • e.g. mitral valve disease

P wave: initial part = right atrium, terminal part = left atrium.

48

Fascicular & Bi/Trifascicular Blocks

LAFBLPFB
AxisLADRAD
I, aVLqRrS
Inferior leadsrSqR
  • LAFB also: prolonged R-wave peak time in aVL; LPFB is rarer (exclude RVH first)
  • Bifascicular: RBBB + LAFB (or + LPFB)
  • Trifascicular: bifascicular + 1st-degree AV block
49

Heart Block — Diagnostic Algorithm

PR / conductionDiagnosis
PR uniform >200 ms, all P conducted, regular1st-degree
PR progressively lengthens then dropped beat, R-R irregularMobitz I (Wenckebach)
PR fixed, intermittent dropped beats (e.g. 2:1), wide QRSMobitz II
PR variable, P-P & R-R each regular but dissociated3rd-degree (complete) — AV dissociation

ECG — Rhythm, Patterns & Emergencies

6 entries
50

Electrolyte & QT Abnormalities

Hyperkalaemia

  • Tall peaked (tented) T → flat/lost P → wide QRS → sine wave (QRS merges with P & T). Hyperacute T is sharp/pointed (STEMI T is round)

Hypokalaemia

  • U waves, flat T, ST depression

Hypocalcaemia vs hypercalcaemia (QT)

  • Hypocalcaemia: long QT · Hypercalcaemia: short QT (QTc <330)

Long QT electrolyte causes

  • Hypokalaemia, hypocalcaemia, hypomagnesaemia (+ drugs) → torsades

Osborn (J) wave

  • Hypothermia
51

Low Voltage & Electrical Alternans

Low Voltage Criteria

  • QRS <5 mm in all limb leads and/or <10 mm in all chest leads
  • Sum of QRS in I + II + III <15 mm

Causes (= impalpable apex)

  • Pleural effusion, pericardial effusion, emphysema, pneumothorax, myxoedema, obesity, dilated cardiomyopathy

Electrical Alternans

  • Beat-to-beat QRS amplitude variation; with low voltage → massive pericardial effusion / tamponade
52

Digoxin Effect

  • Sagging / scooped ("reverse tick") ST depression = digitalis effect (therapeutic — not toxicity)
53

Pacemaker ECG

  • Atrial pacing (single chamber): spike before P wave
  • Ventricular pacing (single chamber): spike before QRS; wide QRS
  • Dual chamber: spike before P AND before QRS
54

Named Emergency Patterns

  • PE: sinus tachycardia + RBBB + RAD + S1Q3T3 (may be normal); ± ST depression V1–V2
  • Acute pericarditis: widespread concave-up ST elevation + PR depression; reciprocal ST depression + PR elevation in aVR (± V1); no MI-type reciprocal changes
  • Left main / triple-vessel: diffuse ST depression + ST elevation in aVR
  • Cardiac tamponade: low voltage + electrical alternans + sinus tachycardia
  • R-on-T PVC: premature beat on preceding T → risk of malignant ventricular arrhythmia

4 Life-threatening Causes of Acute Chest Pain

  • MI · aortic dissection · PE · tension pneumothorax
  • Dissection → NO antiplatelet / anticoagulant / thrombolysis (catastrophic)
55

Arrhythmia Recognition — by Pacemaker Origin

PacemakerECG signatureRhythm
SA nodeP upright in II, biphasic V1, negative aVRSinus rhythm / tachy / brady / arrhythmia / pause
Atrial (narrow, QRS <120 ms)No P, regular, HR >100SVT
No P, fibrillatory waves, irregularAtrial fibrillation
Flutter (sawtooth) waves, regular (irregular if variable block)Atrial flutter
3 different P morphologies, HR <100Wandering atrial pacemaker
3 different P morphologies, HR >100Multifocal atrial tachycardia
Junctional (AV node)Retrograde P (neg II, upright aVR; before/in/after QRS)Junctional tachy (>100) / brady (<60) / accelerated (60–100)
Ventricular (wide, QRS ≥120 ms)T opposite QRS + AV dissociation (no fixed P–QRS relation)VT (mono/polymorphic)
Chaotic irregular deflections, varying amplitude, no identifiable P/QRS/TVF

Causes of Arrhythmia

  • HF, myocarditis · HTN, HCM · hyper-/hypothyroidism · hypoxia · ischaemia/MI · infection · electrolytes · elderly (degenerative) · valvular (MS → AF)
56

Cardiovascular Drug Classes (Clinical Therapeutics)

Antihypertensives

  • CCBs (-dipine; non-dihydro = verapamil/diltiazem) — SE ankle oedema; negative inotropes → contraindicated in HF & bradycardia (esp. non-dihydro)
  • ACEi (-pril) — ↑bradykinin → dry cough, angioedema; ARB (-sartan) — no cough (avoid ACEi/ARB in pregnancy, bilateral RAS, hyperkalaemia)

Diuretics

  • Loop (-ide, furosemide) — most potent; SE ototoxicity · Thiazide (-thiazide/-thalidone) — 1st-line in HTN · K-sparing / MRA (spironolactone) — weak, HF benefit (SE gynaecomastia; myocardial anti-fibrotic) · carbonic anhydrase inhibitors (-zolamide) · mannitol (osmotic)

Antianginal

  • Nitrates (coronary vasodilator; SE headache), + beta-blockers, CCBs

Antihyperlipidaemics

  • Statins (-statin, 1st line, HMG-CoA reductase inhibitor) → add ezetimibe → bempedoic acid / PCSK9 (-cumab); also bile-acid resins, fibrates, niacin, fish oil (omega-3)

Heart failure (HFrEF)

  • Sacubitril/Valsartan (ARNI) — sacubitril inhibits neprilysin (↑ANP/natriuretic peptides) + valsartan (ARB)
  • SGLT2 inhibitors (-flozin) — SE UTI/genital candida, euglycaemic DKA
  • Digoxin; inotropes — milrinone/inamrinone (PDE inhibitor → ↑cAMP: inotrope + vasodilator), dobutamine (β1/α agonist) & dopamine (used in acute HF / cardiogenic shock)

Antiarrhythmics (Vaughan-Williams)

  • I — Na⁺ blockers · II — beta-blockers (-olol) · III — K⁺ blockers (amiodarone, sotalol) · IV — Ca²⁺ blockers · V — unclassified (magnesium, adenosine)

Blood thinners

  • Anticoagulants + antiplatelets — see the haematology anticoagulant/antiplatelet cards