🫀 High-yield overview: Cardiology is easiest when you link structure → physiology → ECG → clinical syndrome → management. For exams, always ask: is the problem mainly pump failure, pipe disease, valve disease, electrical instability, or pericardial constraint? This version adds emojis, exam pearls, UK-style clinical reasoning and “why it matters” explanations while keeping the original HTML structure.

🧠 Think in systems	Clinical meaning
Pump	Heart failure, cardiomyopathy, cardiogenic shock
Pipes	Coronary artery disease, hypertension, aortic disease, PE
Valves	Stenosis/regurgitation, murmurs, endocarditis
Electrics	ECG interpretation, AF, SVT, VT, heart block
Pericardium	Pericarditis, tamponade, constriction

🫀 1. Anatomy of the Heart

🧠 Exam pearl: Anatomy becomes clinically useful when you map each structure to a common presentation: LAD occlusion causes anterior STEMI, mitral disease gives apical murmurs, and pericardial fluid can rapidly impair filling. The heart is not just a pump; it is a pressure-generating chamber system with valves, vessels and electrical wiring packed into a very small space.

✅ 1.1 Position and Orientation

The heart is a hollow, muscular, four-chambered organ situated in the middle mediastinum, within the thoracic cavity. It lies obliquely, with approximately two-thirds of its mass to the left of the midline. It is bordered anteriorly by the sternum and costal cartilages, posteriorly by the oesophagus and descending aorta, inferiorly by the diaphragm, and laterally by the lungs and pleura.

Apex: located at the 5th intercostal space, midclavicular line (left side)
Base: posterosuperior surface formed by the left atrium and parts of the right atrium
Weight: 250–350 g in adults; heavier in men than women
Size: approximately the size of a clenched fist
The long axis of the heart runs from the base (superior-right) to the apex (inferior-left)

✅ 1.2 Chambers

The heart is divided into four chambers. The right side receives deoxygenated blood from the body and pumps it to the lungs; the left side receives oxygenated blood from the lungs and pumps it to the body.

Right atrium (RA): receives deoxygenated blood via the superior vena cava (SVC), inferior vena cava (IVC), and coronary sinus; contains the sinoatrial (SA) node
Right ventricle (RV): thin-walled, crescent-shaped; pumps blood into the pulmonary artery; normal systolic pressure 15–30 mmHg
Left atrium (LA): receives oxygenated blood from four pulmonary veins; posterior chamber with thick walls; LA pressure 5–12 mmHg
Left ventricle (LV): thick-walled, ellipsoid; generates high pressure (120 mmHg systolic); wall thickness ~10–12 mm
Interventricular septum: muscular wall separating the two ventricles; contributes to LV contraction
Interatrial septum: contains the fossa ovalis, the remnant of the foramen ovale

🚪 1.3 Valves

The four cardiac valves ensure unidirectional flow of blood through the heart. They are divided into atrioventricular (AV) valves and semilunar valves.

Mitral valve (bicuspid): between LA and LV; two leaflets (anterior and posterior); supported by chordae tendineae and papillary muscles
Tricuspid valve: between RA and RV; three leaflets (anterior, posterior, septal); more prone to IE in IV drug users
Aortic valve: semilunar; three cusps (left, right, non-coronary); guards the left ventricular outflow tract
Pulmonary valve: semilunar; three cusps; guards the right ventricular outflow tract; least commonly diseased valve
Valve surface area - aortic: 2–4 cm²; mitral: 4–6 cm²; critical stenosis when <1 cm² (aortic) or <1.5 cm² (mitral)

✅ 1.4 Coronary Arteries

The coronary arteries are the first branches of the aorta, arising from the aortic sinuses just above the aortic valve. They supply the myocardium with oxygenated blood during diastole.

Left main coronary artery (LMCA): short trunk dividing into LAD and LCx; occlusion is catastrophic ("widow maker")
Left anterior descending (LAD): supplies anterior LV wall, anterior interventricular septum, and apex; most commonly occluded artery in STEMI
Left circumflex (LCx): supplies lateral and posterior LV wall; gives rise to obtuse marginal branches
Right coronary artery (RCA): supplies RA, RV, inferior LV wall, SA node (60%), AV node (80–90%); gives posterior descending artery (PDA) in right-dominant systems
Dominance: right-dominant in ~85% of people (RCA gives PDA), left-dominant in ~8%, co-dominant in ~7%
Venous drainage: coronary veins drain into the coronary sinus, which empties into the RA

✅ 1.5 Pericardium

The pericardium is a fibroserous sac that encloses the heart and the roots of the great vessels. It has two layers: the outer fibrous pericardium and the inner serous pericardium (which itself consists of parietal and visceral layers).

Fibrous pericardium: tough, inelastic outer layer; limits acute cardiac distension
Parietal pericardium: lines the inner surface of the fibrous pericardium
Visceral pericardium (epicardium): adherent to the heart surface
Pericardial cavity: potential space between parietal and visceral layers; normally contains 15–50 mL of serous fluid
Functions: protects the heart from infection, reduces friction, maintains cardiac position, prevents overdistension

⚙️ 2. Cardiac Physiology

⚙️ Core idea: Most cardiology physiology comes back to preload, afterload, contractility and rhythm. A patient with sepsis may have low afterload, aortic stenosis has high afterload, AF loses atrial kick, and HFrEF has impaired contractility.

✅ 2.1 The Cardiac Cycle

The cardiac cycle refers to the sequence of events that occur during one complete heartbeat, including both systole and diastole. At a resting HR of 75 bpm, one cycle lasts approximately 0.8 seconds.

Isovolumetric contraction: all valves closed; LV pressure rises rapidly; no change in volume
Rapid ejection: aortic valve opens as LV pressure exceeds aortic pressure; ~70% of stroke volume ejected
Reduced ejection: continued ejection but at a slower rate; LV pressure begins to fall
Isovolumetric relaxation: aortic valve closes; LV pressure falls; all valves closed; no change in volume
Rapid ventricular filling: mitral valve opens; passive flow of blood into LV; ~70–80% of filling occurs here
Diastasis: slow ventricular filling; minimal blood flow
Atrial systole: atrial contraction accounts for ~20–30% of ventricular filling ("atrial kick"); lost in AF

✅ 2.2 Cardiac Output and Determinants

Cardiac output (CO) is the volume of blood pumped by each ventricle per minute. Normal resting CO is 4–8 L/min.

CO = Heart Rate (HR) × Stroke Volume (SV)
Cardiac index = CO / body surface area; normal 2.5–4.0 L/min/m²
Preload: end-diastolic volume (EDV); determined by venous return, filling pressure; increased by fluid, lying flat
Afterload: resistance against which the ventricle ejects; determined by SVR and aortic pressure; increased in hypertension and aortic stenosis
Contractility (inotropy): intrinsic myocardial force of contraction; increased by sympathetic stimulation, catecholamines, digoxin
Frank-Starling law: increased preload → increased sarcomere stretch → increased force of contraction → increased SV (up to a point)
Ejection fraction (EF): SV/EDV × 100; normal LV EF ≥55%; reduced in systolic HF

🚨 2.3 Action Potentials in the Heart

Cardiac cells generate action potentials that drive depolarisation and contraction. There are two main types: fast-response (ventricular/atrial myocytes) and slow-response (SA/AV nodes).

Phase 0 (fast AP): rapid depolarisation due to fast Na+ channel opening; absent in nodal cells (use slow Ca2+ channels)
Phase 1: partial repolarisation due to K+ efflux and Na+ channel inactivation
Phase 2 (plateau): Ca2+ influx via L-type Ca2+ channels balances K+ efflux; prolonged depolarisation triggers muscle contraction
Phase 3: rapid repolarisation; K+ efflux via delayed rectifier K+ channels; Ca2+ channels close
Phase 4: resting membrane potential (−90 mV in myocytes); slow spontaneous depolarisation in pacemaker cells (automaticity)
SA node resting potential: −60 mV (more depolarised); fastest spontaneous rate → drives pacemaking
Refractory period: prevents re-excitation during systole; absolute refractory period covers plateau phase

✅ 2.4 Conduction System

The cardiac conduction system is a specialised network of cells that generates and transmits electrical impulses to coordinate myocardial contraction.

SA node: primary pacemaker; located in the RA near the SVC; inherent rate 60–100 bpm; innervated by ANS
Internodal pathways: conduct impulses from SA to AV node via anterior (Bachmann), middle (Wenckebach), and posterior (Thorel) tracts
AV node: located at the base of the interatrial septum (Koch's triangle); delays impulse by 0.1 s (allows atrial emptying); inherent rate 40–60 bpm
Bundle of His: passes through the fibrous skeleton of the heart; only electrical connection between atria and ventricles
Right bundle branch (RBB): conducts impulse down right side of interventricular septum to RV
Left bundle branch (LBB): divides into anterior and posterior fascicles; supplies LV
Purkinje fibres: terminal conduction network; spreads impulse rapidly throughout ventricular myocardium; inherent rate 20–40 bpm

📈 3. Electrocardiogram (ECG)

📈 ECG approach: Use a fixed order every time: rate, rhythm, axis, intervals, QRS width, ST/T changes, then compare with old ECGs. This prevents missing dangerous diagnoses such as hyperkalaemia, STEMI, complete heart block or broad-complex tachycardia.

🔬 3.1 ECG Basics and Lead Placement

The ECG records the electrical activity of the heart as electrical potential differences between electrodes placed on the body surface. The standard 12-lead ECG uses 10 electrodes to produce 12 views of cardiac electrical activity.

Limb leads: I, II, III (bipolar); aVR, aVL, aVF (augmented unipolar)
Precordial leads: V1–V6 (unipolar chest leads)
V1–V2: right ventricle and interventricular septum
V3–V4: anterior wall of LV
V5–V6: lateral LV wall
II, III, aVF: inferior wall (RCA territory)
I, aVL: high lateral LV wall (LCx territory)
Paper speed: 25 mm/s; 1 small square = 0.04 s; 1 large square = 0.2 s
Voltage: 1 mV = 10 mm at standard calibration

🔬 3.2 ECG Waveforms and Intervals

Each component of the ECG corresponds to a specific event in the cardiac cycle. Abnormalities in waveform shape, amplitude, or duration provide diagnostic clues.

P wave: atrial depolarisation; duration <0.12 s; amplitude <2.5 mm; upright in II, inverted in aVR
PR interval: time from onset of P wave to onset of QRS; normal 0.12–0.20 s; prolonged in heart block
QRS complex: ventricular depolarisation; normal duration <0.12 s; broad if BBB or ventricular rhythm
Q wave: normal if <0.04 s duration and <25% R wave height; pathological Q waves indicate old MI
R wave progression: should increase in amplitude from V1 to V5; poor R wave progression suggests anterior MI
ST segment: isoelectric; connects QRS to T wave; elevation suggests STEMI or pericarditis; depression suggests ischaemia or NSTEMI
T wave: ventricular repolarisation; normally upright in I, II, V3–V6; inverted T waves suggest ischaemia or ventricular strain
QT interval: onset of QRS to end of T wave; corrected using Bazett formula: QTc = QT/√RR; normal QTc <440 ms (men), <460 ms (women)
U wave: follows T wave; most visible in V2–V3; prominent in hypokalaemia

🔬 3.3 ECG Axis

The cardiac axis describes the overall direction of ventricular depolarisation. It is calculated from the limb leads and expressed in degrees.

Normal axis: −30° to +90°
Left axis deviation (LAD): <−30°; causes: LBBB, LVH, inferior MI, left anterior fascicular block
Right axis deviation (RAD): >+90°; causes: RBBB, RVH, lateral MI, left posterior fascicular block, PE, dextrocardia
Extreme axis deviation: −90° to ±180°; rare; seen in ventricular tachycardia
Quick method: if QRS predominantly positive in leads I and aVF → normal axis

✅ 3.4 Bundle Branch Blocks

Bundle branch block (BBB) occurs when conduction through either the right or left bundle branch is impaired, resulting in a broad QRS complex (≥0.12 s).

RBBB: RSR' pattern ("M-shaped") in V1; wide S wave in I and V6; right axis deviation; may be normal variant or due to PE, RVH, ASD
LBBB: broad notched ("M-shaped") QRS in V5–V6; deep wide S in V1; always pathological; causes: IHD, HF, hypertension, cardiomyopathy
New or presumed-new LBBB with convincing ischaemic symptoms is high risk; assess urgently with senior/PCI input, serial ECGs, troponins and criteria for occlusion MI rather than dismissing as “just LBBB”
Left anterior fascicular block (LAFB): LAD (−45° to −90°); small Q in I/aVL; small R in II/III/aVF; narrow QRS
Left posterior fascicular block (LPFB): RAD; small R in I/aVL; small Q in II/III/aVF; diagnosis of exclusion
Bifascicular block: RBBB + LAFB or LPFB; may progress to complete heart block

🩺 4. Hypertension

🩺 Why it matters: Hypertension silently damages end-organs by increasing arterial wall stress, promoting endothelial dysfunction and accelerating atherosclerosis. In older adults, isolated systolic hypertension is common because stiff arteries raise systolic pressure while diastolic pressure may fall.

📖 4.1 Definition and Classification

🇬🇧 UK exam note: Confirm persistent hypertension with ABPM or HBPM unless urgent same-day assessment is needed. Severe hypertension becomes an emergency when there is acute end-organ damage such as encephalopathy, pulmonary oedema, ACS, AKI, papilloedema, aortic dissection or stroke features.

Hypertension is defined as a persistently elevated blood pressure that increases the risk of cardiovascular events. It is classified by stage based on blood pressure readings taken on multiple occasions.

Stage 1: clinic BP ≥140/90 mmHg + daytime ABPM/HBPM ≥135/85 mmHg
Stage 2: clinic BP ≥160/100 mmHg + daytime ABPM/HBPM ≥150/95 mmHg
Stage 3 (severe): clinic systolic BP ≥180 mmHg or clinic diastolic BP ≥120 mmHg
Isolated systolic hypertension: systolic ≥140 mmHg + diastolic <90 mmHg; common in elderly due to reduced arterial compliance
White-coat hypertension: elevated clinic BP but normal ABPM; does not require treatment but warrants monitoring
Masked hypertension: normal clinic BP but elevated ABPM; associated with increased cardiovascular risk

🧬 4.2 Pathophysiology and Causes

Blood pressure is determined by cardiac output and total peripheral resistance (TPR). Hypertension results when either or both are persistently elevated.

Primary (essential) hypertension (~95%): multifactorial; genetic predisposition + environmental factors; no identifiable single cause
Renal causes (~2–3%): renal artery stenosis (atherosclerotic or fibromuscular dysplasia), CKD, polycystic kidney disease, renal parenchymal disease
Endocrine causes: primary hyperaldosteronism (Conn's syndrome), phaeochromocytoma, Cushing's syndrome, hyperthyroidism, acromegaly
Coarctation of the aorta: upper limb hypertension with radio-femoral delay; rib notching on CXR
Drug-induced: NSAIDs, combined oral contraceptive pill, steroids, sympathomimetics, ciclosporin, cocaine
RAAS activation: renin → angiotensin I → ACE → angiotensin II → aldosterone → Na+ and water retention → increased BP

✅ 4.3 End-Organ Damage

Chronic hypertension damages target organs through a combination of mechanical stress, endothelial dysfunction, and accelerated atherosclerosis.

Heart: LVH (increased wall thickness), diastolic dysfunction, HFpEF, accelerated CAD, AF
Brain: hypertensive encephalopathy, lacunar infarcts, intracerebral haemorrhage, vascular dementia
Kidneys: nephrosclerosis, proteinuria, progressive CKD; hypertension is second commonest cause of ESRD
Eyes: hypertensive retinopathy (grades I–IV); papilloedema in malignant hypertension
Peripheral arteries: accelerated atherosclerosis, aortic aneurysm, peripheral arterial disease
Aorta: thoracic and abdominal aortic aneurysm; aortic dissection (especially type A)

🔬 4.4 Investigation of Hypertension

ABPM or HBPM: gold standard for confirming diagnosis; ABPM preferred
Urinalysis: check for proteinuria, haematuria (renal cause)
Blood tests: U&E (renal function), fasting glucose, HbA1c, lipid profile, eGFR
ECG: LVH (Sokolow-Lyon criteria: SV1 + RV5/V6 >35 mm); strain pattern
Echocardiogram: if ECG suggests LVH; assess diastolic function
Renal imaging: Doppler ultrasound or MRA for renal artery stenosis if secondary cause suspected
Urine catecholamines/metanephrines: if phaeochromocytoma suspected
Aldosterone:renin ratio: if Conn's syndrome suspected (hypokalaemia + refractory hypertension)
24-hour urinary cortisol: if Cushing's syndrome suspected

💊 4.5 Treatment of Hypertension

💊 Practical prescribing: ACE inhibitors/ARBs can increase creatinine and potassium, so check U&E before starting and after dose changes. Calcium-channel blockers may cause ankle oedema, thiazide-like diuretics may cause hyponatraemia or gout, and spironolactone is useful in resistant hypertension but can cause hyperkalaemia.

Treatment is guided by NICE guidelines (2023) and aims to reduce cardiovascular morbidity and mortality. The target BP in most patients is <140/90 mmHg (<130/80 mmHg in diabetics and high-risk patients).

Step 1 (age <55, not black African/Caribbean): ACE inhibitor (or ARB if ACE inhibitor not tolerated)
Step 1 (age ≥55 or black African/Caribbean): calcium channel blocker (CCB)
Step 2: ACE inhibitor/ARB + CCB
Step 3: ACE inhibitor/ARB + CCB + thiazide-like diuretic (e.g. indapamide or chlortalidone)
Step 4 (resistant hypertension): add spironolactone 25 mg (if K+ <4.5 mmol/L) or alpha-blocker or beta-blocker; refer to specialist
Lifestyle: weight loss, DASH diet (low Na+, high K+, fruits/vegetables), regular aerobic exercise, reduce alcohol, smoking cessation
Hypertensive urgency (Stage 3, no symptoms): oral antihypertensives; do not reduce BP too rapidly
Hypertensive emergency (Stage 3 + end-organ damage): IV labetalol or sodium nitroprusside; aim to reduce MAP by 25% in first hour, then gradually

🫀 5. Coronary Artery Disease (CAD)

🫀 Pathology link: Stable angina is usually a fixed supply problem during exertion, whereas ACS is usually an unstable plaque problem with thrombosis. That is why stable angina management focuses on symptom control and risk reduction, while ACS management prioritises urgent antithrombotic therapy and reperfusion/risk stratification.

🧬 5.1 Pathophysiology of Atherosclerosis

Atherosclerosis is a chronic inflammatory disease of arterial walls involving the accumulation of lipids, fibrous tissue, and inflammatory cells. It is the underlying pathology in the majority of coronary artery disease.

Endothelial dysfunction: earliest event; triggered by dyslipidaemia, hypertension, smoking, diabetes, shear stress
Monocyte recruitment: monocytes adhere to dysfunctional endothelium and migrate into the intima, becoming macrophages
Foam cell formation: macrophages engulf oxidised LDL via scavenger receptors, forming foam cells
Fatty streak: earliest macroscopic lesion; collections of foam cells beneath the intima; reversible
Fibrous plaque: smooth muscle cell migration from media; collagen cap formation; plaque growth narrows lumen
Vulnerable plaque: thin fibrous cap, large lipid core, high macrophage density; prone to rupture
Plaque rupture/erosion: exposes thrombogenic material; platelet aggregation and thrombus formation → ACS
Stable plaque: thick fibrous cap; calcification; causes stable angina (flow limitation on exertion)

⚠️ 5.2 Risk Factors for CAD

Non-modifiable: age (men >45, women >55), male sex, family history of premature CAD (<55 in 1st degree male relative, <65 female)
Modifiable: smoking (doubles risk), hypertension, dyslipidaemia (elevated LDL, low HDL), type 2 diabetes, obesity, physical inactivity
Emerging risk factors: CKD, chronic inflammatory conditions (RA, SLE, psoriasis), obstructive sleep apnoea, air pollution, psychosocial stress
Protective factors: high HDL (>1.6 mmol/L), Mediterranean diet, regular exercise, moderate alcohol (controversial)
Risk calculators: QRISK3 (UK), Framingham, SCORE2; used to guide primary prevention therapy
High risk: 10-year cardiovascular risk >10% (QRISK3); statin therapy recommended

✅ 5.3 Stable Angina

Stable angina is a clinical syndrome caused by reversible myocardial ischaemia, occurring predictably on exertion or emotional stress and relieved by rest or GTN within a few minutes.

Mechanism: fixed coronary stenosis (>70% luminal narrowing) limits coronary blood flow on increased demand
Symptoms: central, crushing, or tight chest pain; radiation to left arm, jaw, or epigastrium; associated dyspnoea and diaphoresis
Canadian Cardiovascular Society (CCS) grading: Class I (no symptoms with ordinary activity) to Class IV (symptoms at rest)
ECG changes during ischaemia: horizontal or downsloping ST depression ≥1 mm; T wave inversion
Investigation: exercise ECG (Bruce protocol), myocardial perfusion imaging, stress echo, CTCA, coronary angiography
Acute relief: sublingual GTN spray 400 mcg; repeat after 5 min if no relief; 999 if no relief after two doses
Medical management: beta-blocker (1st line), CCB (alternative); add long-acting nitrate, ivabradine, ranolazine, nicorandil
Revascularisation: PCI (stenting) for single/double vessel disease; CABG preferred for triple vessel disease or LMCA disease

🫀 6. Acute Coronary Syndrome (ACS)

📖 6.1 Classification and Pathophysiology

ACS encompasses a spectrum of conditions caused by acute myocardial ischaemia, typically due to coronary plaque rupture and superimposed thrombosis. Prompt recognition and treatment are critical to minimise myocardial necrosis.

Unstable angina (UA): ischaemia without myocardial necrosis; troponin negative; requires urgent evaluation
NSTEMI: partial occlusion or distal embolism; subendocardial infarction; troponin positive; no ST elevation
STEMI: complete coronary occlusion; transmural infarction; ST elevation or new LBBB; troponin positive; requires immediate reperfusion
Type 1 MI: spontaneous plaque rupture/erosion with thrombus
Type 2 MI: supply-demand mismatch (e.g. tachycardia, hypotension, severe anaemia, vasospasm); no plaque rupture

🔍 6.2 Clinical Presentation of ACS

⚠️ Red flags: Treat chest pain as high risk if it is prolonged, associated with sweating/vomiting/syncope, occurs at rest, has dynamic ECG changes, or occurs in a patient with diabetes, CKD or previous coronary disease.

Typical chest pain: central, crushing, pressure-like; radiation to left arm, jaw, neck, back; duration >20 min; not relieved by GTN or rest
Associated symptoms: diaphoresis, nausea/vomiting, dyspnoea, palpitations, pre-syncope
Atypical presentations: epigastric pain, isolated dyspnoea, fatigue (common in women, elderly, diabetics)
Silent MI: completely asymptomatic; more common in diabetics and elderly; detected on ECG or echo
Killip classification of haemodynamic status: Class I (no HF) to Class IV (cardiogenic shock)
Signs: pallor, diaphoresis, tachycardia, hypotension (if haemodynamically compromised), new murmur (MR from papillary muscle rupture, VSD)

🔬 6.3 STEMI - ECG Changes and Territories

Hyperacute T waves: tall, peaked T waves; earliest STEMI change (minutes)
ST elevation: ≥1 mm in two contiguous limb leads or ≥2 mm in two contiguous precordial leads; appears within minutes to hours
Reciprocal ST depression: in leads facing opposite wall; confirms STEMI (e.g. inferior STEMI → ST depression in V1–V4)
Pathological Q waves: develop within hours; permanent marker of myocardial necrosis
T wave inversion: follows ST elevation resolution; may persist permanently
Anterior STEMI: ST elevation V1–V4; LAD occlusion
Inferior STEMI: ST elevation II, III, aVF; RCA or LCx occlusion; check for RV involvement (V4R)
Lateral STEMI: ST elevation I, aVL, V5–V6; LCx or diagonal branch
Posterior STEMI: ST depression V1–V3; tall R wave V1–V2; confirm with posterior leads (V7–V9)
High-risk STEMI-equivalent patterns: posterior MI pattern, de Winter T waves (proximal LAD occlusion), and concerning new/presumed-new LBBB with ischaemic symptoms

💊 6.4 Management of STEMI

🕒 Why reperfusion is urgent: The longer a coronary artery remains occluded, the more myocardium becomes irreversibly necrotic. Early reperfusion preserves LV function, reduces cardiogenic shock and lowers mortality.

STEMI management prioritises rapid coronary reperfusion to limit infarct size. The primary treatment modality is primary percutaneous coronary intervention (PPCI).

Call 999 immediately; administer aspirin 300 mg (if not contraindicated)
PPCI: gold standard; target door-to-balloon time <90 min (or <120 min from first medical contact); superior to thrombolysis
Thrombolysis: used if PPCI unavailable within 120 min; agents: alteplase, reteplase, tenecteplase; contraindicated in haemorrhagic stroke, active bleeding, recent surgery, uncontrolled hypertension
Antiplatelet therapy: aspirin 300 mg loading + ticagrelor 180 mg or prasugrel 60 mg (clopidogrel 600 mg if others contraindicated)
Anticoagulation: unfractionated heparin during PPCI; bivalirudin or fondaparinux are alternatives
Oxygen: only if SpO2 <94%; hyperoxia may worsen outcomes
Morphine: 5–10 mg IV for pain; but may delay P2Y12 inhibitor absorption - use antiemetic (metoclopramide) with it
GTN: contraindicated if systolic BP <90 mmHg, right ventricular MI, or recent PDE5 inhibitor use
Monitoring: continuous ECG; watch for reperfusion arrhythmias (accelerated idioventricular rhythm = benign)
Secondary prevention: lifelong aspirin + P2Y12 for 12 months; high-intensity statin; ACE inhibitor; beta-blocker; cardiac rehabilitation

💊 6.5 Management of NSTEMI and UA

Risk stratify using GRACE score: >140 = high risk → early invasive strategy (<24 h); 109–140 = intermediate; <109 = low
Antiplatelet: aspirin + ticagrelor or clopidogrel
Anticoagulation: fondaparinux (preferred) or LMWH; stop before angiography
Beta-blocker: reduces HR and O2 demand; avoid if haemodynamically unstable or cardiogenic shock
High-dose statin: atorvastatin 80 mg immediately
Coronary angiography: within 24 h (high risk) or 72 h (intermediate); revascularise as appropriate
Conservative management: in very low risk (GRACE <109); medical therapy + non-invasive testing

✅ 6.6 Complications of MI

Arrhythmias: VF (commonest cause of death in first hour); VT; AF; sinus bradycardia (inferior MI → vagal); complete heart block
LV failure and cardiogenic shock: Killip IV; mortality >50%; requires inotropes ± IABP ± Impella
Mechanical complications: papillary muscle rupture (acute severe MR - days 2–7); VSD (interventricular rupture); free wall rupture (sudden haemopericardium, death)
Pericarditis: Dressler syndrome (weeks to months post-MI); treat with aspirin + colchicine
LV aneurysm: persistent ST elevation; paradoxical pulsation; risk of mural thrombus and systemic embolism
RV infarction (complication of inferior STEMI): hypotension + raised JVP + clear lungs; treat with IV fluids; avoid nitrates and diuretics

💧 7. Heart Failure

💧 Clinical reasoning: Heart failure is a syndrome, not a single diagnosis. Always identify the phenotype, trigger and cause: HFrEF after MI, HFpEF from hypertension/AF, acute pulmonary oedema from ischaemia, or right heart failure from pulmonary hypertension.

📖 7.1 Definition and Classification

Heart failure (HF) is a clinical syndrome characterised by typical symptoms (dyspnoea, fatigue, oedema) caused by a structural or functional abnormality of the heart, resulting in reduced cardiac output or elevated intracardiac pressures at rest or on exertion.

HFrEF (heart failure with reduced ejection fraction): EF <40%; impaired systolic function; most evidence for therapy
HFmrEF (mildly reduced EF): EF 40–49%; "grey zone"; emerging evidence for treatment
HFpEF (preserved EF): EF ≥50%; diastolic dysfunction; common in elderly women with hypertension
High-output HF: elevated CO but inadequate for tissue demands; causes: severe anaemia, thyrotoxicosis, AV fistula, Paget's disease, beriberi
Acute HF: sudden onset; de novo or acute-on-chronic; requires immediate intervention
Chronic HF: gradual onset; compensated or decompensated

✅ 7.2 Causes of Heart Failure

Ischaemic cardiomyopathy: most common cause in developed world; post-MI LV dysfunction
Hypertensive heart disease: pressure overload → LVH → diastolic dysfunction → HFpEF
Dilated cardiomyopathy (DCM): idiopathic, genetic, alcoholic, peripartum, viral myocarditis, drugs (doxorubicin)
Valvular heart disease: aortic stenosis (pressure overload), aortic/mitral regurgitation (volume overload)
Hypertrophic cardiomyopathy (HCM): genetic; asymmetric septal hypertrophy; diastolic dysfunction
Arrhythmias: persistent AF; tachycardia-mediated cardiomyopathy
Infiltrative diseases: amyloidosis, sarcoidosis, haemochromatosis
Congenital heart disease, pericardial disease, endocrine causes (hypothyroidism)

🔍 7.3 Symptoms and Signs

The clinical presentation of HF depends on whether the left, right, or both ventricles are primarily affected.

Left-sided HF (pulmonary congestion): dyspnoea on exertion (earliest), orthopnoea (number of pillows), paroxysmal nocturnal dyspnoea (PND), cough (pink frothy sputum in acute pulmonary oedema), fatigue
Right-sided HF (systemic venous congestion): ankle/leg oedema (pitting), ascites, hepatomegaly (pulsatile in TR), abdominal discomfort, anorexia, raised JVP (with hepatojugular reflux)
Bilateral HF: combination of above; most common presentation is biventricular failure
Signs: tachycardia, displaced apex beat (LV dilatation), S3 gallop (volume overload), S4 (stiff ventricle), bibasal crackles, pleural effusions, peripheral cyanosis
NYHA Classification: Class I (no limitation) → Class II (slight limitation) → Class III (marked limitation) → Class IV (symptoms at rest)

🔬 7.4 Investigation of Heart Failure

BNP/NT-proBNP: key biomarker; NT-proBNP >125 pg/mL (chronic HF) or >300 pg/mL (acute HF) supports diagnosis; very high levels = poor prognosis
ECG: LVH, LBBB, AF, Q waves (ischaemia), poor R wave progression
CXR: cardiomegaly (cardiothoracic ratio >50%), upper lobe venous diversion, Kerley B lines, bat-wing pulmonary oedema, pleural effusions
Echocardiogram: gold standard for diagnosis; measures EF, wall motion, valve function, filling pressures
Cardiac MRI: best for cardiomyopathy assessment; late gadolinium enhancement identifies fibrosis/scar
Coronary angiography: if ischaemic aetiology suspected
Cardiopulmonary exercise test (CPEX): peak VO2 useful for transplant assessment
Blood tests: FBC (anaemia), U&E (renal function, electrolytes), LFTs, TFTs, iron studies, HbA1c

💊 7.5 Pharmacological Management of HFrEF

🧠 Teaching point: Diuretics make patients feel better by relieving congestion, but the mortality benefit in HFrEF comes mainly from neurohormonal blockade and SGLT2 inhibition. Start low, titrate carefully, and monitor BP, renal function and potassium.

The "foundational four" drugs have been shown to reduce mortality in HFrEF. All four should be initiated and up-titrated as tolerated in all patients with HFrEF.

ACE inhibitor (e.g. ramipril) or ARB (e.g. candesartan): reduces afterload and preload; reduces mortality by ~25%; monitor K+ and eGFR; contraindicated in bilateral renal artery stenosis, pregnancy, angioedema
ARNI (sacubitril/valsartan): superior to ACEi in reducing mortality in HFrEF; replaces ACEi (36 h washout required)
Beta-blocker (bisoprolol, carvedilol, metoprolol succinate): reduces mortality by ~34%; start at low dose and titrate up; avoid in acute decompensation
Mineralocorticoid receptor antagonist (MRA) - spironolactone/eplerenone: reduces mortality; monitor K+; avoid if eGFR <30 or K+ >5.0 mmol/L
SGLT2 inhibitor (dapagliflozin, empagliflozin): reduces hospitalisation and cardiovascular death; renal and cardiac protective; now fourth pillar of HFrEF therapy
Ivabradine: reduces HR in sinus rhythm >70 bpm if intolerant of beta-blocker; reduces hospitalisation
Diuretics: loop diuretics (furosemide) for symptom relief and fluid overload; do not reduce mortality alone

💊 7.6 Device Therapy in HF

ICD (implantable cardioverter-defibrillator): indicated if EF ≤35% and NYHA Class II–III despite optimal therapy; prevents SCD from VT/VF
CRT (cardiac resynchronisation therapy): indicated if EF ≤35% + LBBB + QRS ≥150 ms; improves symptoms, EF, and survival; CRT-D if ICD also needed
LVAD (left ventricular assist device): mechanical circulatory support; bridge to transplant or destination therapy
Cardiac transplantation: definitive treatment for end-stage HF; NYHA Class IV; peak VO2 <12 mL/kg/min; 1-year survival ~85%
Wearable cardioverter defibrillator (WCD): for newly diagnosed HFrEF (EF ≤35%); used while waiting for optimisation before ICD decision

⚡ 8. Arrhythmias

⚡ Safe first step: In any arrhythmia, decide whether the patient is stable or unstable. Shock, syncope, ischaemic chest pain, severe breathlessness or hypotension usually means urgent senior help and electrical treatment rather than slow diagnostic debate.

✅ 8.1 Sinus Node Dysfunction

Sinus bradycardia: HR <60 bpm; causes: athletes, vagal tone, hypothyroidism, beta-blockers, inferior MI; symptomatic → atropine 500 mcg IV or transcutaneous pacing
Sinus tachycardia: HR >100 bpm; physiological response; treat underlying cause (pain, fever, hypovolaemia, PE, anaemia)
Sick sinus syndrome: dysfunction of SA node; alternating bradycardia and tachycardia; symptoms: syncope, palpitations; may need pacemaker
Sinus arrest: SA node fails to fire; pause on ECG; >3 s symptomatic → pacemaker

✅ 8.2 Atrial Fibrillation (AF)

AF is the most common sustained cardiac arrhythmia, affecting ~3% of adults over 65. It causes irregularly irregular heart rate and loss of atrial systole, with significant thromboembolic risk.

Mechanism: multiple re-entrant wavelets within the atria; chaotic, rapid atrial activity (350–600/min); irregular ventricular response
ECG: absent P waves, irregularly irregular QRS, fibrillatory baseline
Classification: first-detected, paroxysmal (<7 days, self-terminating), persistent (>7 days), long-standing persistent (>1 year), permanent
Causes: hypertension (commonest), valvular disease, IHD, HF, thyrotoxicosis, alcohol, PE, pneumonia, post-cardiac surgery, electrolyte disturbance, lone AF (no cause found)
Symptoms: palpitations, dyspnoea, fatigue, reduced exercise tolerance, presyncope; may be asymptomatic
Rate control: beta-blocker or rate-limiting CCB (diltiazem, verapamil); digoxin in sedentary patients or HFrEF; target resting HR <110 bpm
Rhythm control: DC cardioversion (synchronised); flecainide ("pill-in-pocket" if no structural heart disease); amiodarone (if structural HD); catheter ablation (pulmonary vein isolation)
Anticoagulation: CHA₂DS₂-VASc ≥2 (men) or ≥3 (women) → anticoagulate; use DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) in preference to warfarin unless valvular AF (mitral stenosis or mechanical valve → warfarin)
HAS-BLED score: assesses bleeding risk; used to identify and correct modifiable bleeding risk factors; should not be used to withhold anticoagulation
Cardioversion precautions: if AF >48 h duration → anticoagulate for ≥3 weeks before and ≥4 weeks after cardioversion (or transoesophageal echo to exclude LA thrombus)

✅ 8.3 Heart Block

First-degree AV block: prolonged PR >0.20 s; all P waves conducted; benign; no treatment needed
Second-degree AV block Mobitz type I (Wenckebach): progressive PR prolongation until P wave not conducted; repeating cycles; usually benign; AV node level
Second-degree AV block Mobitz type II: fixed PR interval; sudden non-conducted P waves; below AV node (His-Purkinje); risk of complete block; may need pacemaker
2:1 AV block: every other P wave not conducted; difficult to distinguish Mobitz I from II; requires EP study or Holter
Third-degree (complete) heart block: no relationship between P waves and QRS; complete dissociation; ventricular escape rhythm (broad QRS 20–40 bpm); causes: inferior MI (RCA), digoxin toxicity, Lyme disease, congenital; requires permanent pacemaker
Acute complete heart block: temporary transvenous pacing while awaiting permanent PPM

✅ 8.4 Supraventricular Tachycardia (SVT)

AVNRT (AV nodal re-entrant tachycardia): most common SVT; re-entry circuit within AV node; regular narrow complex tachycardia ~150–250 bpm; P waves hidden in or just after QRS
AVRT (AV re-entrant tachycardia): re-entry involving accessory pathway; orthodromic (narrow QRS) or antidromic (broad QRS)
WPW (Wolff-Parkinson-White syndrome): accessory pathway (Bundle of Kent); delta wave + short PR + broad QRS on resting ECG; risk of AF conducting rapidly to ventricles → VF → SCD; ablation of pathway recommended
Acute management: vagal manoeuvres (Valsalva, carotid sinus massage); adenosine 6 mg rapid IV bolus (12 mg if unsuccessful); if haemodynamically unstable → synchronised DC cardioversion
Prevention: beta-blocker, CCB, ablation (definitive)

✅ 8.5 Ventricular Arrhythmias

PVCs (premature ventricular complexes): broad complex early beats; compensatory pause; benign if no structural heart disease; frequent/symptomatic → beta-blocker
VT (ventricular tachycardia): ≥3 consecutive ventricular beats at >100 bpm; broad complex (QRS >0.12 s); may or may not have pulse; consider if AV dissociation, fusion beats, capture beats present
Sustained VT: >30 s or causing haemodynamic compromise; haemodynamically stable → IV amiodarone; unstable → synchronised DC cardioversion
Pulseless VT: treated as VF; immediate unsynchronised defibrillation
VF: chaotic ventricular activity; no cardiac output; fatal without immediate CPR and defibrillation
Torsades de pointes: polymorphic VT with rotating QRS axis; associated with prolonged QTc; causes: hypokalaemia, hypomagnesaemia, drugs (antiarrhythmics, antipsychotics, antibiotics); treat with IV magnesium 2 g + correct electrolytes; stop QT-prolonging drugs
Long QT syndrome (LQTS): congenital (LQT1–LQT3 most common) or acquired; risk of torsades and SCD; beta-blocker; avoid triggers; ICD if high risk
Brugada syndrome: genetic Na channel mutation; ST elevation V1–V3 with RBBB morphology; risk of VF/SCD; ICD if symptomatic
Catecholaminergic polymorphic VT (CPVT): exercise/stress-induced bidirectional VT; beta-blocker; ICD + flecainide

🚪 9. Valvular Heart Disease

🚪 Murmur logic: Stenosis is a valve that will not open; regurgitation is a valve that will not close. The timing of the murmur tells you the valve: aortic/mitral stenosis and regurgitation map to whether the valve is meant to be open in systole or diastole.

🚪 9.1 Aortic Stenosis (AS)

🧠 Why symptoms are ominous: In severe AS, the LV cannot increase output across the fixed obstruction during exertion. Syncope, angina and heart failure therefore indicate limited cardiac reserve and high mortality without valve intervention.

Aortic stenosis is the most common valvular heart disease in developed countries, occurring in ~3% of people over 75. The natural history involves a long asymptomatic period followed by rapid deterioration once symptoms develop.

Causes: degenerative calcification (most common, elderly), congenital bicuspid aortic valve (younger patients, peak symptoms 50–60s), rheumatic heart disease
Haemodynamics: fixed outflow obstruction → LV pressure overload → concentric LVH → diastolic dysfunction → reduced CO
Symptoms (SAD triad): Syncope (exertional), Angina, Dyspnoea; survival: syncope/angina 2–3 years; HF 1–2 years without intervention
Signs: slow-rising (anacrotic) pulse, narrow pulse pressure, heaving/non-displaced apex beat, ejection systolic murmur at right 2nd ICS radiating to carotids, soft/absent A2, reversed splitting of S2, S4
ECG: LVH + strain; CXR: cardiomegaly, calcified aortic valve, post-stenotic aortic root dilatation
Echo: valve area (severe <1.0 cm²), mean gradient (severe >40 mmHg), peak velocity (severe >4 m/s), EF
Severe low-flow low-gradient AS: EF <40%, low gradient despite severe stenosis; dobutamine stress echo or CT calcium scoring to confirm
Treatment: surgical AVR (SAVR) - gold standard for most patients; TAVI (transcatheter aortic valve implantation) - for high or intermediate surgical risk; balloon valvuloplasty - bridge to definitive treatment only

🚪 9.2 Aortic Regurgitation (AR)

Causes (acute): aortic dissection, IE, blunt chest trauma; medical emergency
Causes (chronic): bicuspid aortic valve, rheumatic fever, Marfan syndrome, ankylosing spondylitis, syphilitic aortitis, hypertension
Haemodynamics: diastolic regurgitation → LV volume overload → eccentric LVH → LV dilatation → LV failure
Symptoms: usually asymptomatic for years; exertional dyspnoea, orthopnoea, angina; acute AR presents with sudden severe pulmonary oedema
Signs: wide pulse pressure, collapsing (water-hammer) pulse, Corrigan's sign (visible carotid pulsations), de Musset's sign (head nodding), Quincke's sign (nail pulsations), Duroziez's sign (femoral bruit), Traube's sign (pistol-shot femoral pulse), high-pitched early diastolic murmur at left sternal edge (leaning forward, end expiration), Austin Flint murmur (low-pitched apical mid-diastolic)
Echocardiogram: quantifies severity; monitors LV dimensions; surgical referral when LV ESD >50 mm or LVEDD >70 mm or EF falls <50%
Medical: vasodilators (nifedipine, ACEi) can slow LV dilatation; no proven mortality benefit
Surgery: AVR (indicated for symptoms, or LV dysfunction, regardless of symptoms)

🚪 9.3 Mitral Stenosis (MS)

Cause: almost always rheumatic fever → leaflet thickening, commissural fusion, chordal shortening; rare: congenital, carcinoid, SLE, mucopolysaccharidoses
Haemodynamics: obstruction to LA emptying → elevated LA pressure → pulmonary hypertension → RV failure; fixed CO
Symptoms: progressive exertional dyspnoea, orthopnoea, haemoptysis (pulmonary hypertension or rupture of bronchial veins), AF (large LA), systemic emboli, recurrent chest infections
Signs: malar flush, irregularly irregular pulse (AF), tapping non-displaced apex beat, loud S1, opening snap (closer to S2 = more severe), rumbling mid-diastolic murmur at apex with pre-systolic accentuation (absent in AF), signs of pulmonary hypertension (loud P2, RV heave)
Echo: MVA (severe <1.5 cm²), mean gradient (severe >10 mmHg), pressure half-time; assess valve morphology (Wilkins score) to guide intervention type
Treatment: rate control (beta-blocker, CCB) + anticoagulation (AF or emboli); balloon mitral valvuloplasty (BMV) - if pliable valve, low Wilkins score, no MR or LA thrombus; surgical mitral valvotomy/valve replacement - for calcified or heavily diseased valves

🚪 9.4 Mitral Regurgitation (MR)

Primary MR (organic): intrinsic valve pathology - mitral valve prolapse (most common in developed world), rheumatic fever, IE, connective tissue diseases, papillary muscle rupture (post-MI)
Secondary MR (functional): normal valve leaflets but abnormal LV geometry → failure of leaflet coaptation; due to IHD or DCM
Haemodynamics: volume overload → LA and LV dilatation → LV failure
Signs: pansystolic murmur at apex radiating to axilla, displaced hyperdynamic apex, soft S1, S3, signs of LV failure; acute MR: pulmonary oedema with soft murmur (low gradient across valve)
Echo: quantifies severity (EROA, regurgitant volume), mechanism (Carpentier classification), LV function
Surgical: mitral valve repair (preferred) or replacement; indications - symptoms, EF <60%, LVESD >45 mm, new AF or PAH
MitraClip: transcatheter leaflet repair; for high-risk surgical candidates with primary MR or secondary MR refractory to medical therapy

🦠 10. Infective Endocarditis (IE)

🦠 Do not miss: IE is a diagnosis of persistent suspicion: fever plus a murmur, embolic phenomena, prosthetic material, IVDU or positive blood cultures should trigger blood cultures before antibiotics where safe. The vegetation is both an infection source and an embolic/thrombotic risk.

🧬 10.1 Pathogenesis and Microbiology

Infective endocarditis involves infection of the endocardial surface, most commonly the valve leaflets, leading to formation of vegetations - masses of fibrin, platelets, and microorganisms.

Predisposing factors: structural heart disease (valvular disease, congenital HD, previous IE, prosthetic valve), IV drug use, indwelling cardiac devices, poor dentition, immunosuppression, haemodialysis
Bacteraemia: transient bacteraemia → bacterial adherence to damaged endothelium or non-bacterial thrombotic endocarditis (NBTE)
Streptococcus viridans (S. sanguinis, S. mitis): most common in community-acquired native valve IE; source - dental procedures/oral flora; subacute course
Staphylococcus aureus: most common cause of acute IE; prosthetic valve IE; IV drug use; healthcare-associated; aggressive, rapid destruction; MRSA increasingly common
Enterococcus faecalis: elderly, GI/GU source; difficult to treat due to resistance
HACEK organisms: Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella; slow-growing, culture-negative; sensitive to ceftriaxone
Staphylococcus epidermidis: most common cause of early prosthetic valve IE (<1 year post-surgery); biofilm formation
Culture-negative IE (~5–10%): prior antibiotics, slow-growing organisms (Coxiella burnetii Q fever, Bartonella, Tropheryma whipplei, Brucella); requires serology + PCR
Fungal IE: Candida (prosthetic valves, IV drug users, immunosuppressed); high mortality; often requires surgery

🔍 10.2 Clinical Features

Fever: most common symptom; may be low-grade and persistent in subacute IE
New or changed murmur: important sign; absence does not exclude IE
Embolic phenomena: stroke (left-sided IE), renal infarcts, splenic infarcts, septic pulmonary emboli (right-sided IE), retinal artery occlusion
Osler's nodes: painful, tender, purplish nodules on finger/toe pads; immune complex deposition
Janeway lesions: painless, haemorrhagic macules on palms/soles; septic emboli (more common in S. aureus)
Splinter haemorrhages: linear subungual haemorrhages (also seen in trauma)
Roth spots: retinal haemorrhages with pale centres; visible on fundoscopy
Clubbing: found in prolonged, subacute IE
Splenomegaly: common in subacute IE
Immunological manifestations: glomerulonephritis, RF positive, raised ESR/CRP, anaemia of chronic disease

✅ 10.3 Duke Criteria for Diagnosis

Definite IE: 2 major criteria, OR 1 major + 3 minor criteria, OR 5 minor criteria
Possible IE: 1 major + 1 minor, OR 3 minor criteria
Major criteria: (1) positive blood cultures - typical organism in 2 separate cultures, or persistently positive cultures; (2) echocardiographic evidence - vegetation, abscess, prosthetic valve dehiscence, or new valvular regurgitation
Minor criteria: predisposing heart condition or IV drug use; fever >38°C; vascular phenomena (arterial emboli, Janeway lesions, etc.); immunological phenomena (Osler's nodes, Roth spots, RF); microbiological evidence not meeting major criteria
Blood cultures: 3 sets from different sites, >1 h apart, before antibiotics; capture ~90% of bacteraemia
Echo: TOE (transoesophageal echo) superior to TTE for vegetations, abscess, prosthetic valves; sensitivity ~95%

💊 10.4 Treatment of IE

Empirical antibiotics: amoxicillin 2 g IV 4-hourly + gentamicin (for native valve); vancomycin + gentamicin (if prosthetic valve or penicillin allergy); adjusted once cultures available
Native valve S. viridans: penicillin G/amoxicillin for 4 weeks (or 2 weeks with gentamicin); ceftriaxone is alternative
S. aureus native valve: flucloxacillin 2 g IV 4-hourly for 4–6 weeks; MRSA → vancomycin
Prosthetic valve IE: requires at least 6 weeks of treatment; typically triple therapy; often requires surgery
Surgical indications: heart failure due to valve destruction, periannular abscess or fistula, fungal IE, persistent bacteraemia despite antibiotics, large mobile vegetations (>10 mm), prosthetic valve IE with complications
Monitoring: daily bloods (CRP, FBC, U&E, LFTs, drug levels); repeat echo at 1 week and end of treatment; watch for embolic events

🧬 11. Cardiomyopathies

🧬 Pattern recognition: Cardiomyopathies are best separated by ventricular shape and physiology: dilated = weak and enlarged, hypertrophic = thick and stiff ± obstruction, restrictive = stiff filling, arrhythmogenic = scar/fat with ventricular arrhythmia risk.

✅ 11.1 Dilated Cardiomyopathy (DCM)

DCM is characterised by LV dilatation and systolic dysfunction in the absence of abnormal loading conditions (hypertension, valvular disease) or coronary artery disease sufficient to explain the degree of dysfunction.

Prevalence: 1 in 2500; second most common cause of HF after IHD
Genetic: ~35–50% familial; TTN (titin gene) mutation most common; autosomal dominant; screen first-degree relatives
Acquired causes: alcohol (toxic, dose-dependent), viral myocarditis (Coxsackievirus B, adenovirus, parvovirus B19, HIV), peripartum (last month to 5 months postpartum), chemotherapy (doxorubicin, trastuzumab), autoimmune, thyroid disease, selenium/thiamine deficiency
Features: HFrEF; dilated, globally hypokinetic LV; EF often <30–35%; functional MR common; AF common; LV thrombus risk
CMR: typically diffuse fibrosis in mid-wall pattern (vs. subendocardial in ischaemic); distinguishes from ischaemic CMP
Management: HFrEF therapy (foundational four) + anticoagulation if EF <35% + ICD/CRT as appropriate; alcohol abstinence; immunosuppression for autoimmune myocarditis

✅ 11.2 Hypertrophic Cardiomyopathy (HCM)

HCM is the most common inherited cardiac condition (1 in 500), characterised by LV hypertrophy (usually asymmetric septal) in the absence of a secondary cause. It is the commonest cause of sudden cardiac death in young athletes.

Genetics: autosomal dominant; mutations in sarcomeric protein genes (MYH7, MYBPC3 most common); 60–70% of cases; variable penetrance and expressivity
Pathology: myocyte hypertrophy + disarray + interstitial fibrosis; impaired diastolic function; LVOTO in ~25–30%
LVOTO (left ventricular outflow tract obstruction): dynamic; worsened by reduced preload, reduced afterload, increased contractility; systolic anterior motion (SAM) of mitral valve contributes
Symptoms: dyspnoea, exertional chest pain, pre-syncope/syncope (especially on exertion), palpitations; sudden cardiac death (ventricular arrhythmia)
Signs: jerky (bisferiens) pulse, double apical impulse, ejection systolic murmur at left sternal edge (increases with Valsalva/standing), pan-systolic murmur (MR from SAM)
ECG: LVH, deep T-wave inversions V1–V6, giant negative T waves (apical HCM), short PR, delta-like waves; pathological Q waves in inferior/lateral leads
Echo: septal thickness ≥15 mm (or ≥13 mm with family history); SAM; LVOTO gradient >30 mmHg at rest or >50 mmHg on provocation is obstructive HCM
SCD risk stratification: HCM Risk-SCD calculator; ICD if 5-year risk ≥6%; individual risk factors: family history of SCD, unexplained syncope, maximal wall thickness ≥30 mm, NSVT, abnormal BP response to exercise
Medical treatment: beta-blocker or verapamil for symptomatic relief; disopyramide for LVOTO; avoid nitrates, vasodilators, digoxin in LVOTO
Septal reduction: surgical myectomy (gold standard for severe LVOTO) or alcohol septal ablation (for high surgical risk)
Mavacamten: cardiac myosin inhibitor; reduces contractility and LVOTO; novel targeted therapy for obstructive HCM
Lifestyle: avoidance of competitive sport in most patients; low-intensity exercise generally encouraged

✅ 11.3 Arrhythmogenic Cardiomyopathy (ACM / ARVC)

Definition: inherited cardiomyopathy characterised by fibrofatty replacement of myocardium, predominantly affecting the RV (and increasingly LV in biventricular form)
Genetics: autosomal dominant; desmosomal gene mutations (PKP2, DSP, DSG2, DSC2, JUP); loss of desmosome integrity → myocyte death → fibrous/fatty replacement
Features: RV enlargement, reduced RV systolic function, ventricular arrhythmias (LBBB morphology = RV origin), SCD in young athletes
ECG: epsilon waves (terminal notching after QRS in V1–V3), T-wave inversion V1–V3, LBBB morphology VT
CMR: fibrofatty infiltration of RV wall; regional RV wall motion abnormalities
Management: ICD for high-risk patients; beta-blocker; sotalol/amiodarone; catheter ablation for VT; restriction from competitive sport

✅ 11.4 Restrictive Cardiomyopathy

Characterized by reduced ventricular compliance with normal or reduced volume; diastolic dysfunction predominates; systolic function usually preserved (until late)
Amyloidosis: most common cause; AL (light chain) or ATTR (transthyretin) amyloid; "sparkling" myocardium on echo; low voltage ECG + thick walls; technetium scintigraphy for ATTR; tafamidis (ATTR stabiliser) reduces mortality in ATTR-CM
Sarcoidosis: granulomatous infiltration; conduction abnormalities, VT, HF; immunosuppression; ICD if indicated
Haemochromatosis: iron deposition; DCM or restrictive pattern; phlebotomy or deferasirox
Löffler endocarditis/eosinophilic: hypereosinophilia → endocardial fibrosis; treat with steroids and hydroxyurea
Differentiation from constrictive pericarditis: CMR, invasive haemodynamics (constrictive shows ventricular interdependence)

🛡️ 12. Pericardial Disease

🛡️ Key concept: The pericardium normally protects and stabilises the heart, but when inflamed or tense it becomes the problem. Tamponade is primarily a filling problem, so diuretics and vasodilators can worsen haemodynamics.

✅ 12.1 Acute Pericarditis

Acute pericarditis is inflammation of the pericardium, most commonly caused by viral infection. It presents with sharp, pleuritic chest pain and may cause a pericardial friction rub.

Causes: viral (Coxsackievirus, echovirus, adenovirus, EBV, CMV, HIV) most common (~80–90%); bacterial (TB - especially in endemic areas; S. aureus; streptococcal); autoimmune (SLE, RA, scleroderma); post-MI (Dressler's syndrome); uraemia; malignancy; drugs (hydralazine, isoniazid, procainamide)
Diagnostic criteria (≥2 of 4): pleuritic chest pain, pericardial friction rub, new widespread ST elevation/PR depression on ECG, new or worsening pericardial effusion
ECG stages: Stage I - saddle-shaped ST elevation in multiple leads + PR depression; Stage II - ST normalises; Stage III - T wave inversions; Stage IV - ECG normalises
Troponin: may be mildly elevated (myopericarditis); significantly elevated troponin suggests myocarditis component
CRP: elevated; useful for monitoring response to treatment
Treatment: NSAIDs (ibuprofen 600 mg TDS or aspirin 750–1000 mg TDS) + colchicine 0.5 mg BD for 3 months (halves recurrence risk); gastroprotection with PPI; restrict activity until symptom-free and CRP normal
Steroids: reserved for refractory cases or specific aetiology (autoimmune, uraemic); low-dose prednisolone; associated with increased recurrence risk
Hospital admission: if high-risk features - fever >38°C, large effusion, immunosuppressed, anticoagulated, acute trauma, no response to NSAID after 7 days

✅ 12.2 Cardiac Tamponade

Cardiac tamponade is a life-threatening emergency occurring when pericardial fluid accumulates under pressure, compressing the heart and reducing ventricular filling and CO.

Causes: malignancy (most common cause of large effusions in developed world), TB (common worldwide), iatrogenic (post-procedure), trauma, aortic dissection, post-MI (free wall rupture), uraemia, radiation
Haemodynamics: as effusion pressure rises → equalisation of diastolic pressures across all chambers → reduced filling → reduced CO → shock
Beck's triad: hypotension + raised JVP + muffled heart sounds (only present together in ~30%)
Pulsus paradoxus: inspiratory fall in systolic BP >10 mmHg due to increased RV filling reducing LV filling; measured with BP cuff
ECG: sinus tachycardia, low voltage QRS, electrical alternans (alternating QRS amplitude due to swinging heart)
CXR: large globular "water bottle" shaped heart shadow
Echo: pericardial effusion + right atrial and right ventricular diastolic collapse; respiratory variation in valve flow velocities
Treatment: urgent pericardiocentesis (needle aspiration under echo guidance); surgical drainage if loculated/clotted; haemodynamic support with IV fluids; avoid vasodilators, diuretics, and IPPV if possible

✅ 12.3 Constrictive Pericarditis

Pathophysiology: chronic fibrous thickening and calcification of pericardium → rigid shell → impaired ventricular filling → equalization of diastolic pressures
Causes: previous pericarditis (viral or idiopathic most common in West), TB (most common worldwide), post-radiation, post-cardiac surgery, malignancy
Symptoms: progressive right HF (oedema, ascites, hepatomegaly, raised JVP); fatigue; exertional dyspnoea
Signs: Kussmaul sign (JVP rises with inspiration - opposite to normal); pericardial knock (early diastolic sound); Friedrich sign (rapid y-descent in JVP waveform)
Investigations: CXR/CT - pericardial calcification (best seen on CT); CMR - pericardial thickening >4 mm; invasive haemodynamics - equalization of end-diastolic pressures; ventricular interdependence; discordance of LV/RV pressures with respiration
Treatment: surgical pericardiectomy (definitive); anti-TB therapy if tuberculous aetiology; anti-inflammatory therapy for subacute/inflammatory constrictive pericarditis

👶 13. Congenital Heart Disease (CHD)

👶 Exam framework: Divide CHD into cyanotic and acyanotic lesions, then ask whether there is left-to-right shunt, right-to-left shunt, obstruction, or mixing. Large untreated left-to-right shunts can eventually reverse through pulmonary hypertension, causing Eisenmenger physiology.

✅ 13.1 General Principles

CHD affects ~8–9 per 1000 live births and encompasses a wide range of structural cardiac malformations. With improved surgical techniques, over 90% of children with CHD now survive to adulthood (grown-up congenital heart disease - GUCH).

Cyanotic CHD: deoxygenated blood enters systemic circulation (right-to-left shunt or mixing); central cyanosis, clubbing
Acyanotic CHD: no right-to-left shunt initially; may develop Eisenmenger syndrome (shunt reversal) if untreated large left-to-right shunt
Eisenmenger syndrome: large L-to-R shunt → pulmonary hypertension → reversal to R-to-L shunt → cyanosis; irreversible; heart-lung transplant may be considered
Associated conditions: Down syndrome (AVSD, VSD), Turner syndrome (coarctation, bicuspid AV), Noonan syndrome (pulmonary stenosis, HCM), DiGeorge syndrome (interrupted aortic arch, truncus arteriosus), Marfan syndrome (aortic root dilatation, AR)

✅ 13.2 Ventricular Septal Defect (VSD)

Most common congenital heart defect (~30% of CHD)
Types: perimembranous (most common, ~80%), muscular, outlet (subarterial), inlet (AV canal type)
Physiology: L-to-R shunt → pulmonary overcirculation → LV volume overload; size determines haemodynamic significance
Symptoms: small VSDs often asymptomatic ("maladie de Roger"); large VSDs → failure to thrive, recurrent chest infections, HF in infancy
Signs: harsh pansystolic murmur at left sternal edge (4th ICS); thrill; signs of HF (large defect)
Investigations: Echo (definitive); CXR (cardiomegaly, plethoric lung fields if large); ECG (biventricular hypertrophy if large)
Management: small VSDs may close spontaneously (especially muscular); symptomatic/large defects → surgical repair or transcatheter closure; prophylactic endocarditis cover no longer routinely recommended

✅ 13.3 Atrial Septal Defect (ASD)

Types: secundum (most common, ~75%, fossa ovalis region), primum (atrioventricular canal defect, associated with Down syndrome), sinus venosus (near SVC), coronary sinus
Physiology: L-to-R shunt → RV volume overload → RV dilatation → pulmonary hypertension if large and untreated
Symptoms: often asymptomatic in childhood; adult presentation with exertional dyspnoea, AF, paradoxical emboli
Signs: wide, fixed split S2; soft ejection systolic murmur at pulmonary area (increased flow across normal pulmonary valve); mid-diastolic tricuspid flow murmur if large shunt
ECG: RBBB (incomplete); RAD in secundum ASD; LAD in primum ASD
Management: close if Qp:Qs >1.5:1 or paradoxical embolism; transcatheter device closure (Amplatzer) for secundum ASDs; surgical repair for primum/sinus venosus ASDs

✅ 13.4 Patent Ductus Arteriosus (PDA)

Ductus arteriosus normally closes within 48 h of birth (functional) and 3 weeks (anatomical)
Persistent in premature infants (lack of smooth muscle response to O2) and in maternal rubella infection
Physiology: continuous L-to-R shunt from aorta to pulmonary artery → LV volume overload
Signs: continuous ("machinery") murmur below left clavicle; collapsing pulse; active precordium
Management in premature infants: indomethacin or ibuprofen (inhibit prostaglandin E2 which keeps duct open); surgical ligation if fails; transcatheter coil/device closure in full-term infants and children

✅ 13.5 Tetralogy of Fallot (ToF)

Most common cyanotic CHD after the neonatal period; accounts for ~10% of CHD
Four components: large perimembranous VSD, overriding aorta, pulmonary stenosis (subvalvular, valvular, or both), RVH (compensatory)
Haemodynamics: pulmonary stenosis → obstruction to RV outflow → R-to-L shunt through VSD → desaturated blood into aorta → cyanosis
Degree of cyanosis proportional to severity of RVOTO; mild RVOTO → "pink Tet"
Tet spells (hypercyanotic spells): acute worsening of cyanosis due to increased RVOTO; triggers - crying, feeding, fever; management: knee-chest position, morphine, propranolol, IV fluids, phenylephrine, oxygen
CXR: boot-shaped heart (coeur en sabot), reduced pulmonary vascular markings, right aortic arch (25%)
ECG: RVH, RAD
Echo: all four features; coronary artery anatomy (anomalous LAD from RCA crosses RVOT in ~5%)
Surgery: complete repair in infancy (VSD closure + RVOTO relief); or palliated with Blalock-Taussig shunt first if too small; long-term complications include pulmonary regurgitation → RV dilatation → arrhythmia → SCD

✅ 13.6 Coarctation of the Aorta

Discrete narrowing of the aorta, usually at the isthmus (junction of aortic arch and descending aorta, near ductus arteriosus)
Associated with bicuspid aortic valve (50–85%), VSD, intracranial aneurysms (berry aneurysms); associated with Turner syndrome
Presentation: neonates - severe HF and shock if duct-dependent (duct closes → acute obstruction); older children/adults - hypertension in upper limbs, headaches, epistaxis, claudication; incidental radiological finding
Signs: BP differential between right arm and legs (>20 mmHg); radio-femoral delay; ejection systolic murmur over left scapula; collateral vessel murmur
CXR: rib notching (3rd–8th ribs, from collateral arteries, develops after age 5); "figure of 3" sign (indentation of aorta at coarctation site)
Management: balloon angioplasty + stenting (first-line in most older children and adults); surgical repair (end-to-end anastomosis, subclavian flap, interposition graft) - preferred in neonates; correct BP after repair; monitor for recoarctation, persistent hypertension, aortic root dilatation

🩸 14. Aortic Disease

🩸 Danger signal: Aortic catastrophes are often pain diagnoses before they are imaging diagnoses. Sudden tearing chest/back pain, pulse deficit, neurological signs, syncope or shock should raise concern for dissection or rupture.

✅ 14.1 Aortic Aneurysm

An aortic aneurysm is a permanent, localised dilation of the aorta to more than 1.5 times its normal diameter. They are classified as thoracic (TAA) or abdominal (AAA) and as true (all three layers) or false (pseudoaneurysm).

AAA: aortic diameter ≥3.0 cm; rupture risk increases markedly at ≥5.5 cm; risk of rupture at 5.5–6 cm ~25%/year; ruptured AAA mortality ~80%
AAA causes: atherosclerosis (most common), smoking, hypertension, family history, COPD; male sex (5:1)
AAA screening: NHS AAA screening programme offers one-off ultrasound to all men aged 65
AAA surveillance: 3.0–4.4 cm → scan every 1 year; 4.5–5.4 cm → every 3 months; ≥5.5 cm → refer for surgery
AAA repair: EVAR (endovascular aortic repair) - preferred if anatomy suitable; open surgical repair for complex anatomy or young patients; elective repair at ≥5.5 cm (men) or ≥5.0 cm (women) or growth >1 cm/year
TAA: most common cause - cystic medial necrosis (Marfan, bicuspid AV, Ehlers-Danlos); atherosclerosis; aortitis; family history; repair at 5.5 cm (ascending) or 6.0 cm (descending)

✅ 14.2 Aortic Dissection

Aortic dissection involves a tear in the aortic intima, allowing blood to enter and propagate through the medial layer, creating a false lumen. It is a cardiothoracic emergency with high early mortality.

Stanford Type A: involves the ascending aorta (regardless of origin); surgical emergency; mortality 1–2% per hour without surgery
Stanford Type B: confined to the descending aorta (distal to left subclavian); managed medically in uncomplicated cases; endovascular treatment (TEVAR) for complicated Type B
Risk factors: hypertension (most common), bicuspid aortic valve, Marfan/Loeys-Dietz/Ehlers-Danlos syndrome, pregnancy, cocaine use, trauma, aortic instrumentation
Symptoms: sudden severe "tearing" or "ripping" chest pain, maximal at onset; radiates to back (descending dissection); may radiate to jaw, abdomen, or legs depending on extent
Signs: BP differential between arms (>20 mmHg); pulse deficits; aortic regurgitation (Type A); Horner syndrome (compression of cervical sympathetic chain); neurological deficits; MI (RCA involvement - inferior STEMI); abdominal ischaemia; acute limb ischaemia
Investigations: CXR - widened mediastinum (>8 cm); loss of aortic knuckle; displaced trachea; CT aortography (CT with contrast) - gold standard; confirms extent, true/false lumen, branch vessel involvement; TTE/TOE useful but CT faster
Medical management (all types initially): target systolic BP 100–120 mmHg with IV labetalol or esmolol; HR <60 bpm; adequate analgesia (morphine)
Type A surgery: emergent surgical repair under cardiopulmonary bypass; Bentall procedure if aortic root involved
Complicated Type B: TEVAR; complications include malperfusion (renal, visceral, limb), uncontrolled hypertension, ongoing pain, rapid expansion

🩺 15. Pulmonary Hypertension (PH)

📖 15.1 Definition and Classification

Pulmonary hypertension is defined as a resting mean pulmonary artery pressure (mPAP) ≥20 mmHg on right heart catheterisation. It is classified into five groups based on aetiology.

Group 1 - Pulmonary arterial hypertension (PAH): idiopathic, heritable, drug/toxin-induced (anorexigens), associated with CTD (SSc, SLE), HIV, portal hypertension, CHD
Group 2 - PH due to left heart disease: most common cause; HFpEF, HFrEF, valvular disease; treat underlying cause
Group 3 - PH due to lung disease/hypoxia: COPD, ILD, OSA; treat underlying lung disease + supplemental O2
Group 4 - Chronic thromboembolic PH (CTEPH): organised thromboembolic obstruction; treated with pulmonary endarterectomy or balloon pulmonary angioplasty + riociguat
Group 5 - Miscellaneous: haematological disorders, systemic disorders, metabolic disorders

🔍 15.2 Clinical Features and Investigation

Symptoms: progressive exertional dyspnoea (earliest and most common), fatigue, chest pain (RV ischaemia), presyncope/syncope on exertion, haemoptysis
Signs: loud P2, right-sided S4, RV heave, elevated JVP, peripheral oedema, hepatomegaly, cyanosis (late), Tricuspid regurgitation murmur
ECG: RVH (R > S in V1), RAD, P pulmonale (peaked P in II), RBBB
Echo: estimates RVSP from TR jet velocity; assesses RV size/function; rules out LHD and CHD
CT pulmonary angiography: excludes CTEPH
V/Q scan: preferred for CTEPH diagnosis (CT may miss distal disease)
Right heart catheterisation (RHC): gold standard; measures mPAP, PAWP, PVR, CO; required before PAH-specific therapy
Vasoreactivity testing (during RHC): acute vasodilator challenge with inhaled NO or IV adenosine; identifies ~10% of IPAH with favourable response → high-dose CCB therapy
6-minute walk test: monitors exercise capacity and treatment response

💊 15.3 Treatment of PAH (Group 1)

General measures: supervised exercise, avoid pregnancy, avoid high altitude and extreme exertion, annual influenza and pneumococcal vaccination, supplemental O2 if hypoxic
Anticoagulation: historically recommended for IPAH (mural thrombi); now controversial; not routinely recommended in CTD-PAH (higher bleeding risk)
Diuretics: for RV failure and fluid overload; monitor renal function and electrolytes
PAH-specific therapy - three pathways: Endothelin pathway: endothelin receptor antagonists (ERAs) - ambrisentan, bosentan, macitentan; oral; teratogenic; hepatotoxic (bosentan) Prostacyclin pathway: prostacyclin analogues - epoprostenol (IV, gold standard for severe PAH), treprostinil (IV/SC/inhaled), iloprost (inhaled); prostacyclin receptor agonist - selexipag (oral) NO/cGMP pathway: PDE5 inhibitors - sildenafil, tadalafil; soluble guanylate cyclase stimulator - riociguat
Upfront combination therapy (ERA + PDE5i) now standard of care for most newly diagnosed PAH patients
Lung transplantation: for WHO functional class III–IV despite maximal medical therapy

🫁 16. Pulmonary Embolism (PE)

🫁 Exam pearl: PE is a clot burden plus physiology problem: small PE may cause pleuritic pain, but large PE causes acute RV pressure overload, hypotension and obstructive shock. Risk stratification determines whether anticoagulation alone is enough or reperfusion is needed.

🧬 16.1 Pathophysiology and Risk Factors

PE occurs when a blood clot (usually arising from deep vein thrombosis in the legs or pelvis) occludes the pulmonary vasculature. It is part of the venous thromboembolism (VTE) spectrum.

Virchow's triad: venous stasis, endothelial damage, hypercoagulability
Risk factors - provoked: surgery (especially orthopaedic), immobility, pregnancy/puerperium, oral contraceptive/HRT, long-haul travel, trauma
Risk factors - unprovoked/constitutional: malignancy, thrombophilia (Factor V Leiden, protein C/S deficiency, antiphospholipid syndrome), previous VTE, obesity, inflammatory bowel disease
Massive PE: obstructs >50% of pulmonary vascular bed → acute RV failure → obstructive shock

🔍 16.2 Clinical Presentation

Symptoms range from asymptomatic to haemodynamic collapse
Classic triad: dyspnoea + pleuritic chest pain + haemoptysis (in only ~20% of cases)
Other symptoms: tachycardia, tachypnoea, cough, fever, syncope (massive PE)
Submassive PE: normal BP but RV dysfunction (echo evidence or raised troponin/BNP)
Massive PE: haemodynamic instability (SBP <90 mmHg or shock); requires immediate treatment
Signs: tachycardia (most common sign), tachypnoea, reduced O2 saturation, pleuritic rub, calf tenderness/swelling (DVT), RV heave, loud P2, signs of shock

🔬 16.3 Investigation and Risk Stratification

Clinical probability: Wells score or Geneva score; stratifies into low, intermediate, or high pre-test probability
D-dimer: if low/intermediate probability → D-dimer; negative result (<500 ng/mL, or age-adjusted threshold: age × 10 if >50 years) reliably excludes PE; elevated D-dimer is non-specific
CT pulmonary angiography (CTPA): gold standard; confirms PE to segmental level; also detects alternative diagnoses
V/Q scan: alternative if renal impairment or contrast allergy; more sensitive than CTPA for subsegmental PE
ECG: most common finding - sinus tachycardia; S1Q3T3 pattern (S wave in I, Q wave + T-wave inversion in III) - specific but insensitive; RBBB; AF
ABG: hypoxia, hypocapnia (increased respiratory rate), respiratory alkalosis; widened A-a gradient
Echo: RV dilatation/hypokinesia; D-shaped septum (McConnell sign - apical RV wall motion with free wall hypokinesia); elevated RVSP; useful if CTPA not immediately available
Troponin: elevated in massive/submassive PE (RV ischaemia); associated with worse prognosis
BNP/NT-proBNP: elevated in PE with RV dysfunction; prognostic marker
PESI score: used to risk-stratify confirmed PE → guides outpatient vs inpatient management

💊 16.4 Management of PE

🫁 Management logic: Anticoagulation prevents clot extension while endogenous fibrinolysis resolves clot. Thrombolysis is reserved for massive/high-risk PE with shock or severe haemodynamic compromise because bleeding risk is significant.

Massive PE (shock/arrest): immediate thrombolysis (alteplase 100 mg IV over 2 h); or surgical embolectomy; or catheter-directed thrombolysis/thrombectomy; CPR with minimal interruption
Submassive PE (RV dysfunction, haemodynamically stable): consider thrombolysis vs anticoagulation alone; escalate if deteriorates
Low-risk PE: outpatient treatment if PESI Class I–II; anticoagulation alone
Anticoagulation: DOAC (rivaroxaban or apixaban) first-line; rivaroxaban 15 mg BD for 3 weeks then 20 mg OD; apixaban 10 mg BD for 7 days then 5 mg BD; LMWH + warfarin alternative; unfractionated heparin if thrombolysis planned or renal impairment
Duration: provoked PE (surgery) → 3 months; provoked PE (non-surgical/persistent risk factor) → 3–6 months; unprovoked PE → ≥3 months, consider indefinite if high recurrence risk; active malignancy → DOAC (edoxaban, rivaroxaban) preferred
IVC filter: only if anticoagulation absolutely contraindicated + high risk; not routinely recommended
Thrombophilia screen: in unprovoked PE - test after anticoagulation completed (DOAC affects some assays); test for antiphospholipid syndrome, protein C/S, antithrombin, Factor V Leiden, prothrombin mutation

🧈 17. Lipid Disorders and Statin Therapy

🧈 Risk reduction: Lipid management is about lifetime vascular risk, not just the number on a blood test. LDL particles drive plaque formation, so reducing LDL reduces future MI and stroke risk.

⚠️ 17.1 Lipid Metabolism and Cardiovascular Risk

LDL-cholesterol: primary atherogenic lipoprotein; target in primary and secondary prevention; calculated using Friedewald equation or directly measured
HDL-cholesterol: inverse relationship with CVD risk; >1.0 mmol/L (men), >1.2 mmol/L (women) considered protective
Triglycerides: fasting level >1.7 mmol/L associated with increased CV risk; >10 mmol/L → pancreatitis risk
Non-HDL cholesterol: total cholesterol minus HDL; includes all atherogenic lipoproteins; preferred treatment target in some guidelines
ApoB: reflects number of atherogenic particles; superior to LDL for risk assessment; 1 ApoB per LDL, IDL, VLDL, and Lp(a) particle
Lp(a): inherited; independent cardiovascular risk factor; elevated levels associated with atherosclerosis and aortic stenosis; not currently modifiable with standard therapies (RNA-based therapies in trials)

✅ 17.2 Familial Hypercholesterolaemia (FH)

Autosomal dominant; mutations in LDLR, ApoB, PCSK9 genes
Heterozygous FH (HeFH): 1 in 250; LDL typically 5–10 mmol/L; xanthelasmata, corneal arcus before 45 years, tendon xanthomata
Homozygous FH (HoFH): 1 in 1,000,000; LDL >13 mmol/L; severe premature CAD; may need LDL apheresis
Simon Broome criteria for diagnosis: definite FH if tendon xanthomata in patient or 1st degree relative + LDL >4.9 mmol/L (adult) or DNA mutation
Treatment: high-intensity statin; add ezetimibe; PCSK9 inhibitors (evolocumab, alirocumab) if target not achieved; target LDL <2.5 mmol/L (primary prevention) or <1.4 mmol/L (established CVD)
Cascade screening: all first-degree relatives should be screened

💊 17.3 Statins and Lipid-Lowering Therapy

Statins: inhibit HMG-CoA reductase → reduce hepatic cholesterol synthesis → upregulate LDL receptors → reduce circulating LDL
High-intensity statins: atorvastatin 40–80 mg or rosuvastatin 20–40 mg (reduce LDL by ≥50%)
Primary prevention: offer high-intensity statin if 10-year CVD risk ≥10% (QRISK3); also offer if diabetes, CKD, or FH
Secondary prevention: all patients with established CVD (IHD, stroke, PAD) → atorvastatin 80 mg; target LDL <1.4 mmol/L or ≥50% reduction
Ezetimibe: inhibits intestinal cholesterol absorption (NPC1L1); reduces LDL by ~20% additional; add-on to statin
PCSK9 inhibitors (evolocumab, alirocumab): monoclonal antibodies; reduce LDL by 50–60%; subcutaneous injection every 2–4 weeks; for very high-risk patients or statin intolerance/FH
Inclisiran: siRNA against PCSK9; reduces LDL by ~50%; given twice yearly by injection; approved for FH and secondary prevention
Bempedoic acid: inhibits ATP-citrate lyase; reduces LDL by ~18%; oral; for statin-intolerant patients
Statin side effects: myopathy (rare), rhabdomyolysis (<0.01%), transaminitis (usually mild), new-onset diabetes (small risk), statin-associated muscle symptoms (SAMS) in ~5–10% of users
Fibrates: reduce triglycerides by 30–50%; modestly raise HDL; role in severe hypertriglyceridaemia; fenofibrate added if TG >5.6 mmol/L despite statin

💊 18. Cardiac Pharmacology

💊 Prescribing logic: Cardiac drugs work by changing rate, rhythm, preload, afterload, contractility, thrombosis or cholesterol. Always check renal function, potassium, heart rate, BP and drug interactions before escalation.

✅ 18.1 Beta-Blockers

Mechanism: competitive antagonism of beta-adrenoreceptors → reduced HR (negative chronotropy), reduced contractility (negative inotropy), reduced AV conduction (negative dromotropy)
Cardioselective (beta-1): bisoprolol, metoprolol, atenolol - less bronchospasm; preferred in asthma/COPD (though still use with caution)
Non-selective: carvedilol (also alpha-1 blocker), propranolol, labetalol
Uses: HFrEF (bisoprolol, carvedilol, metoprolol succinate), angina, hypertension, AF rate control, post-MI, arrhythmias (SVT, VT), anxiety, thyrotoxicosis (propranolol), migraine prophylaxis, portal hypertension
Side effects: bradycardia, hypotension, fatigue, cold extremities, bronchospasm, erectile dysfunction, masking hypoglycaemia, nightmares (lipophilic: propranolol), impaired glucose metabolism
Contraindications: acute decompensated HF, severe asthma, 2nd/3rd degree AV block (without pacemaker), cardiogenic shock, severe bradycardia
Withdrawal: taper gradually - abrupt cessation can precipitate rebound tachycardia, hypertension, and angina

✅ 18.2 ACE Inhibitors and ARBs

ACE inhibitors: block ACE → prevent conversion of angiotensin I to angiotensin II → reduced aldosterone → reduced Na+/water retention + vasodilation; also increase bradykinin (→ cough)
Examples: ramipril, lisinopril, perindopril, enalapril, captopril
Uses: HFrEF, post-MI LV dysfunction, hypertension, diabetic nephropathy, CKD with proteinuria, secondary prevention of CVD
Side effects: dry cough (bradykinin, 10–15%); angioedema (rare but serious - 0.1–0.3%); hyperkalaemia; hypotension (first dose); AKI (bilateral RAS, dehydration)
Contraindications: pregnancy (teratogenic), bilateral renal artery stenosis, prior angioedema, hyperkalaemia, severe hypotension
ARBs (angiotensin II receptor blockers): block AT1 receptor; do not increase bradykinin → no cough; same indications as ACEi; used if ACEi not tolerated; examples: candesartan, losartan, valsartan, irbesartan
Monitor: K+, eGFR at baseline, 1–2 weeks after starting/dose change, then annually; up to 30% rise in creatinine acceptable; if >30% or K+ >5.5 → withhold and investigate

✅ 18.3 Calcium Channel Blockers

Block L-type Ca2+ channels; two classes: dihydropyridines (mainly vascular smooth muscle) and non-dihydropyridines (cardiac + vascular)
Dihydropyridines: amlodipine, nifedipine, felodipine → arterial vasodilation; used for hypertension, angina; reflex tachycardia may occur with short-acting formulations; do NOT use non-DHP CCBs with beta-blockers
Non-dihydropyridines: verapamil (most cardiac), diltiazem → negative chronotropy and dromotropy; used for AF rate control, SVT, angina; avoid in HFrEF; avoid combination with beta-blocker (risk of complete heart block)
Side effects: amlodipine - peripheral oedema (most common), flushing, headache; verapamil - constipation, bradycardia, AV block; all - hypotension

✅ 18.4 Diuretics

Loop diuretics: furosemide, bumetanide - inhibit Na-K-2Cl cotransporter in thick ascending loop of Henle; most potent; used in acute and chronic HF; pulmonary oedema; side effects: hypokalaemia, hyponatraemia, dehydration, ototoxicity (high dose IV)
Thiazide diuretics: bendroflumethiazide, indapamide, chlortalidone - inhibit Na-Cl cotransporter in distal convoluted tubule; used in hypertension; less effective if eGFR <30; side effects: hypokalaemia, hyponatraemia, hyperuricaemia (gout), hyperglycaemia, dyslipidaemia
Potassium-sparing diuretics: amiloride - blocks ENaC; spironolactone/eplerenone - MRA; used in HF, resistant hypertension, Conn's syndrome, cirrhotic ascites; risk of hyperkalaemia; spironolactone side effects - gynaecomastia, menstrual irregularities (eplerenone more selective)
Acetazolamide: carbonic anhydrase inhibitor; used for altitude sickness, glaucoma, metabolic alkalosis in HF

📖 18.5 Antiarrhythmic Drugs (Vaughan Williams Classification)

Class I - Na channel blockers: IA (quinidine, procainamide) - moderate rate block, prolong APD; IB (lidocaine, mexiletine) - fast rate block, shorten APD; IC (flecainide, propafenone) - slow rate block, minimal APD effect; flecainide used in AF/SVT (only in structurally normal hearts - avoid post-MI)
Class II - Beta-blockers: discussed above
Class III - K channel blockers: amiodarone, sotalol, dronedarone; prolong APD and QT; amiodarone - most effective antiarrhythmic; used in VT, VF, AF/flutter; multiple class effects; side effects: pulmonary toxicity, thyroid dysfunction (hyper and hypo), corneal microdeposits, photosensitivity, hepatotoxicity, neuropathy, bradycardia; check TFTs/LFTs/CXR regularly; sotalol - also Class II; QT prolongation/torsades risk; dronedarone - less toxic than amiodarone but less effective; do not use in permanent AF or HFrEF
Class IV - Ca channel blockers: verapamil, diltiazem; discussed above
Other: adenosine - first-line for SVT; half-life <10 seconds; transiently blocks AV node; contraindicated in asthma, WPW with AF (may cause degeneration to VF); digoxin - inhibits Na-K ATPase → increased intracellular Ca2+ → positive inotropy + negative chronotropy/dromotropy (via vagal stimulation); narrow therapeutic window; toxic at K+ <3.0 mmol/L; toxicity: nausea, visual changes (yellow-green), arrhythmias (PAT with block, VT); isoprenaline - beta agonist; used in complete heart block/bradycardia awaiting pacemaker

🔬 19. Key Cardiac Investigations

🔬 Choose the right test: ECG is electrical, echo is structural/functional, CTCA is coronary anatomy, CMR is tissue characterisation, and nuclear imaging is perfusion/viability. Matching the question to the test avoids unnecessary investigations.

🔬 19.1 Echocardiography

Transthoracic echo (TTE): standard first-line imaging; assesses LV/RV structure and function, valve morphology, pericardium, aortic root; measures EF (Simpson's biplane method)
Transoesophageal echo (TOE): higher resolution; better for posterior structures (LA, LAA, aorta, prosthetic valves); gold standard for IE vegetation/abscess, LA thrombus, aortic dissection
Stress echo: exercise or dobutamine; assesses inducible wall motion abnormalities (ischaemia); evaluates valve gradients under stress (e.g. MS, low-flow low-gradient AS)
3D echo: improves volumetric measurements and valve assessment; useful in MV disease (planning repair)
Speckle tracking/strain imaging: myocardial deformation analysis; detects subclinical LV dysfunction (early HF, chemotherapy cardiotoxicity)
Contrast echo: improves endocardial border definition; detects LV thrombus, intracardiac shunts (bubble study for ASD/PFO), LVNC

🔬 19.2 Cardiac MRI (CMR)

Gold standard for: cardiac volumes and EF (most accurate), cardiomyopathy characterisation, myocardial viability, pericardial disease, congenital HD assessment
Late gadolinium enhancement (LGE): detects fibrosis and scar; ischaemic LGE - subendocardial; non-ischaemic LGE patterns - mid-wall (DCM), patchy (sarcoid), diffuse subendocardial (amyloid)
T1 mapping: quantifies diffuse fibrosis (ECV - extracellular volume fraction); elevated in amyloid, HCM, DCM
T2 mapping: assesses oedema/inflammation; elevated in acute myocarditis, acute MI
CMR-specific indications: HCM (wall thickness, SAM, LGE for SCD risk), ARVC (fibrofatty replacement), myocarditis (Lake Louise criteria - T2 + LGE + T1), cardiac sarcoidosis, iron overload (T2* mapping), ATTR amyloid, pericardial constriction vs restriction
Limitations: cannot be used in patients with non-MRI-compatible implants (some PPMs, cochlear implants); claustrophobia; renal impairment (gadolinium NSF risk); prolonged scan time; limited in arrhythmias

✅ 19.3 Nuclear Cardiology

Myocardial perfusion imaging (MPI): SPECT or PET; uses radiotracers (Tc-99m sestamibi/tetrofosmin for SPECT; Rb-82 or N-13 NH3 for PET); stress + rest imaging
Reversible perfusion defect: stress defect that fills in on rest = ischaemia
Fixed perfusion defect: present at rest and stress = scar/infarction
PET perfusion: higher sensitivity and specificity than SPECT; quantifies absolute myocardial blood flow (MBF) and flow reserve (MFR); useful in balanced ischaemia (multivessel CAD), obese patients
Technetium-99m DPD/PYP scan: hot-spot imaging for ATTR cardiac amyloidosis; highly sensitive and specific; allows non-invasive diagnosis without biopsy if AL excluded

🔬 19.4 Coronary Artery Investigations

CTCA: non-invasive coronary artery imaging; Agatston calcium score; first-line investigation for stable chest pain with low-intermediate pre-test probability of CAD (NICE 2016); high sensitivity (~97%), lower specificity
Invasive coronary angiography (ICA): gold standard; visualises lumen; allows IVUS and FFR measurement; required before revascularisation
FFR (fractional flow reserve): pressure wire measurement across stenosis; FFR <0.80 = haemodynamically significant → guides PCI decision
iFR (instantaneous wave-free ratio): similar to FFR but no adenosine required; <0.89 = significant
IVUS/OCT: intracoronary imaging; guides PCI; assesses plaque morphology, stent deployment, stent expansion
Coronary artery calcium (CAC) score: CT-based; Agatston score; >100 = moderate risk; >400 = high risk; useful for risk reclassification in intermediate-risk patients; score 0 = very low event rate (calcium scan "warranty period" 10 years)

🚨 20. Cardiac Emergencies and Resuscitation

🚨 ABCDE first: In cardiac emergencies, stabilisation and diagnosis happen together. Oxygen only helps if hypoxic, fluids help some shock states but harm pulmonary oedema, and early defibrillation is the key treatment for VF/pulseless VT.

🚨 20.1 Adult Advanced Life Support (ALS)

⚡ ALS memory: Shockable rhythms are VF and pulseless VT; non-shockable rhythms are PEA and asystole. High-quality CPR and early defibrillation matter more than most drugs in the first minutes of arrest.

The ALS algorithm provides a structured approach to managing cardiac arrest. It is based on the 2021 European Resuscitation Council (ERC) guidelines and uses a loop structure based on rhythm analysis.

Recognition of cardiac arrest: unresponsive + absent/abnormal breathing + no pulse; activate emergency services; start CPR immediately
CPR: 30:2 compressions to ventilations ratio; compression depth 5–6 cm; rate 100–120/min; allow full recoil; minimise interruptions (<5 s); use 100% O2; continuous compressions with supraglottic airway/ETT
Shockable rhythms (VF/pulseless VT): defibrillate (200 J biphasic) → 2 min CPR → rhythm check; adrenaline 1 mg IV after 3rd shock, then every 3–5 min; amiodarone 300 mg IV after 3rd shock, 150 mg after 5th shock
Non-shockable rhythms (PEA/asystole): adrenaline 1 mg IV immediately, then every 3–5 min; CPR 2 min cycles; no defibrillation
4Hs: Hypoxia, Hypovolaemia, Hypo/Hyperkalaemia (and other metabolic), Hypothermia
4Ts: Thrombosis (MI/PE), Tension pneumothorax, Tamponade, Toxins
Post-resuscitation care (ROSC): target SpO2 94–98%; normocapnia; avoid hypotension (MAP >65 mmHg); targeted temperature management (TTM) if comatose (32–36°C for 24 h, now mostly normothermia - HYPERION trial); early coronary angiography if STEMI suspected; neuroprotective care; glucose control (4–10 mmol/L)
Deciding when to stop: no ROSC after ≥20 min (in absence of reversible causes); clinical judgement; TFTs and toxicology screen

🚨 20.2 Cardiogenic Shock

Cardiogenic shock is a state of reduced cardiac output causing end-organ hypoperfusion despite adequate filling pressures. It carries a mortality of 30–50% even with modern treatment.

Definition: SBP <90 mmHg >30 min (or vasopressors required) + signs of hypoperfusion (oliguria, cool peripheries, altered consciousness, elevated lactate) + evidence of cardiac dysfunction
Haemodynamic profile: low CO/CI (<1.8 L/min/m² without support); low MAP; elevated PAWP (>15 mmHg - "wet and cold"); high SVR
Causes: acute MI with LV failure (most common, ~75%); acute severe MR or VSD (mechanical complication); RV infarction; fulminant myocarditis; end-stage DCM; massive PE; tension pneumothorax; cardiac tamponade
SCAI stages: A (at risk) → B (beginning) → C (classic cardiogenic shock) → D (deteriorating) → E (extremis)
Treatment: treat underlying cause (PPCI for MI); oxygen and ventilation if needed; cautious IV fluids (unless clearly volume-depleted); vasopressors (noradrenaline preferred - if MAP <65 mmHg); inotropes (dobutamine, milrinone) for low-output state; monitor with arterial line + urinary catheter ± PA catheter
Mechanical circulatory support: IABP (intra-aortic balloon pump - reduces afterload, improves coronary perfusion; modest benefit); Impella (axial flow pump from LV to aorta; more powerful unloading); VA-ECMO (venoarterial extracorporeal membrane oxygenation - complete cardiopulmonary bypass; used in refractory shock); bridge to recovery or transplant
Multidisciplinary shock team: cardiologist, cardiac surgeon, intensivist, cardiac nurse specialist - structured decision-making improves outcomes

🚨 20.3 Acute Pulmonary Oedema

Causes: acute LV failure (post-MI, acute severe MR, hypertensive emergency, acute myocarditis), fluid overload, acute severe AS/MR/AR
Symptoms: severe dyspnoea, orthopnoea, pink frothy sputum, cough, extreme distress, fear of dying
Signs: tachypnoea, tachycardia, hypertension (usually) or hypotension (if cardiogenic shock), diaphoresis, bilateral crackles, wheeze ("cardiac asthma"), S3 gallop
CXR: bilateral perihilar "bat-wing" shadowing, Kerley B lines, upper lobe venous diversion, pleural effusions, cardiomegaly
ABG: type I respiratory failure (low PaO2, low/normal PaCO2); if severe → CO2 retention (type II)
CPAP/NIV (BiPAP): reduces work of breathing; decreases preload; improves oxygenation; first-line respiratory support; reduces need for intubation
IV furosemide: 40–80 mg IV; immediate venodilatation then diuresis; monitor urine output and electrolytes
Opiates (morphine): anxiolysis and mild venodilatation; use cautiously (respiratory depression)
IV nitrates: if SBP >110 mmHg; venodilator; reduces preload and afterload rapidly; GTN infusion titrated to BP
Position: sit patient upright (reduces venous return)
Intubation and ventilation: if unable to maintain airway or failing on NIV

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