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Cardiology — Disease Index + Criteria

ICC-1 finals revision · 59 diseases + 34 criteria · Compiled from StudyFix deck

C/P

Inves

Mng

Special — pathognomonic

Ischaemic Heart Disease / ACS

5 entries

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

Inves

Stress ECG, stress echo, CT coronary angiography
Lipids, glucose, U&E, LFT
Resting ECG (rule out resting ischaemia)

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

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

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

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

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)

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

Aortic Disease

1 entry

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

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)

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

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

Valvular Heart Disease

6 entries

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)

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

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)

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)

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)

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

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

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

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

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

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

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: Valve dysfunction (HF), Heart failure, Embolism (recurrent), Abscess (paravalvular), Resistant organism, large vegetation (>10 mm)
IVDU right-sided: medical preferred; if surgery, repair > replacement
Prophylaxis (high-risk only): pre-dental procedures

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

Arrhythmias

17 entries

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

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)

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

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

Special

AF prevalence: ~2% general, 15% over 75
Hypertension = most important cause
AF + mitral stenosis = warfarin only

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

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

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)

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

VF

C/P

Cardiac arrest, unresponsive, no pulse, no breathing

Inves

ECG: chaotic irregular deflections, no identifiable P/QRS/T, varying amplitude

Mng

Unsynchronised defibrillation (CPR + ACLS)
Post-arrest: IV amiodarone + therapeutic hypothermia
Long-term: ICD

Special

VF = cardiac arrest = immediate defibrillation, not synchronised cardioversion

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

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

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)

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"

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

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

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

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

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

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)

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

Heart Failure

4 entries

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

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

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 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)

Special

Mortality high; reverse cause + mechanical support

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)

Cardiomyopathies

10 entries

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

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%)

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

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

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

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)

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)

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

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

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

Endomyocardial Fibrosis (Obliterative)

C/P

Restrictive picture with right-sided HF
Hyperéosinophilia association
Tropical regions

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

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)

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)

Pericardial Disease

5 entries

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

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

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

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

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

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

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

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

Special

90% of all HTN; multifactorial (genetic + lifestyle)
Mostly >40 yo, gradual onset
Female sex hormones protect pre-menopause; equalises post-menopause

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)

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

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

Special

Fibrinoid necrosis of arterioles = pathological hallmark
Hypertensive encephalopathy
"Onion-skinning" of arterioles in kidney

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

Special

Workup for secondary cause mandatory

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

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

Hypertensive Heart Disease (End-organ damage)

C/P

LVH → diastolic dysfunction → HFpEF → HFrEF
Angina, arrhythmia (AF), sudden cardiac death
Hypertensive retinopathy, CKD, 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

Hyperlipidaemia

2 entries

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

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)

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

Other (cardio-relevant DDx)

1 entry

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

D-dimer (rule-out in low/intermediate Wells score)
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

Special

S1Q3T3 + new RBBB = classic but rare PE ECG
Wells score for pre-test probability
Saddle PE at pulmonary artery bifurcation = massive

Diagnostic Criteria

4 entries

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

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

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).

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

CHA₂DS₂-VA(Sc) — AF Stroke Risk

Components

Letter	Criterion	Pts
C	Chronic HF (sx/signs OR asymptomatic LVEF ≤40%)	1
H	Hypertension (BP >140/90 on ≥2 occasions OR on tx)	1
A₂	Age ≥75	2
D	Diabetes (T1/T2 OR glucose-lowering tx)	1
S₂	Prior Stroke / TIA / arterial thromboembolism	2
V	Vascular disease (CAD, PVD)	1
A	Age 65–74	1
Sc	Sex category (female)	1

Recommendations (2024 ESC)

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

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

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.

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

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

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)

Type	Frequency	Stanford
I	60%	A
II	10–15%	A
III	25–30%	B

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)

ACS — Classification

Type	Troponin	ECG
UA	Negative	ST depression / T-wave changes (or normal)
NSTEMI	Positive	ST depression / T-wave changes (or normal)
STEMI	Positive	ST elevation

NSTE-ACS = UA + NSTEMI

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.

Hyperlipidaemia — Fredrickson Types

Primary (Familial)

Type	Lipoprotein ↑	Synonym
I	Chylomicrons	Familial chylomicronaemia
IIa	LDL	Familial hypercholesterolaemia (most common)
IIb	LDL + VLDL	Familial combined hyperlipidaemia
III	IDL	Familial dysbetalipoproteinaemia
IV	VLDL	Familial hypertriglyceridaemia
V	VLDL + chylomicrons	Familial mixed hyperlipidaemia

Secondary Causes

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

Severity Classifications

8 entries

NYHA Functional Classification — Heart Failure

Based on symptom severity + exertion needed to provoke.

3 provoking symptoms: fatigue · palpitation · dyspnoea

Class	Definition
I	No limitation of physical activity
II	Slight limitation; ordinary activity → fatigue/palpitation/dyspnoea; comfortable at rest
III	Marked limitation; less-than-ordinary activity → symptoms; comfortable at rest
IV	Symptoms at rest; any activity increases discomfort

LVEF Classification — Heart Failure

Category	LVEF
HFrEF	≤40%
HFmrEF	41–49%
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).

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.

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 Stage	NYHA Equivalent
A	None (asymptomatic, no structural disease)
B	NYHA I
C	NYHA II–IV
D	NYHA IV

Therapeutic Implications

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

HTN — BP Cutoffs

Office BP

Category	Cutoff
Non-elevated	<120/70
Elevated	120–139 / 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

HTN — Primary vs Secondary

	Primary	Secondary
Cause	None identifiable (multifactorial)	Identifiable
Prevalence	90%	10%
Age of onset	Mostly >40 yr	Mostly <40 yr
Onset	Gradual	Abrupt / severe
Treatment	Lifestyle + antihypertensives	Treat cause + BP control
Prognosis	Chronic management	Potentially curable / reversible

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)

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

Chamberlain's 10 Rules — Normal ECG

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

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

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)

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)

RVH — Voltage Criteria

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

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

HCM — ECG Findings

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

Surgical / Procedural Indications

5 entries

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

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

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).

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

IE — V-HEART Surgical Indications

Letter	Indication
V	Valve dysfunction → HF
H	Heart failure
E	Embolism (recurrent)
A	Abscess (paravalvular)
R	Resistant organism
T	large vegeTation (>10 mm)

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