Cardiovascular

Chest pain caused by reversible myocardial ischaemia from fixed coronary artery atheroma — pain on exertion, relieved by rest or GTN. Diagnosis rests on the classic triad and is confirmed with CT coronary angiography (NICE first-line). Managed with secondary prevention (antiplatelet + statin), an anti-anginal (beta-blocker or CCB first-line), and revascularisation for refractory symptoms.

The spectrum of acute myocardial ischaemia from plaque rupture: STEMI (full-thickness, ST elevation, troponin rise), NSTEMI (ST depression/T-wave change + troponin rise) and unstable angina (ischaemic symptoms, no troponin rise). Immediate management is shared (MONA + dual antiplatelet + anticoagulation); the fork is reperfusion — STEMI needs emergency PCI, NSTEMI is risk-stratified (GRACE) for inpatient angiography.

The commonest sustained arrhythmia. AF = chaotic atrial activity with an irregularly irregular pulse and no P waves; flutter = a re-entrant circuit giving sawtooth flutter waves, often 2:1 (ventricular ~150). Management has three arms: rate vs rhythm control, and — crucially — stroke prevention guided by CHA₂DS₂-VASc, with a DOAC first-line.

A regular narrow-complex tachycardia (typically 150–250) from a re-entry circuit involving the AV node — AVNRT (commonest) or AVRT via an accessory pathway (e.g. WPW). Acute termination uses vagal manoeuvres then adenosine; the key trap is pre-excited AF in WPW, where AV-node-blocking drugs are dangerous.

Broad-complex tachycardias arising from the ventricles. Monomorphic VT (often post-MI scar) and polymorphic VT (e.g. torsades de pointes from a long QT) can degenerate into ventricular fibrillation — a non-perfusing rhythm and the commonest cause of cardiac arrest. A broad-complex tachycardia is VT until proven otherwise.

Pathologically slow rhythms from sinus node disease or atrioventricular conduction block. First-degree (long PR), Mobitz I (Wenckebach — progressive PR lengthening then dropped beat), Mobitz II (intermittent dropped QRS, high block risk) and third-degree (complete AV dissociation). Mobitz II and complete block are dangerous and usually need pacing.

Inherited (or acquired) cardiac ion-channel disorders that predispose to malignant ventricular arrhythmias and sudden cardiac death in structurally normal hearts. Long QT syndrome prolongs repolarisation → torsades; Brugada syndrome shows coved ST elevation in V1–V2 → VF; CPVT causes exercise-induced polymorphic VT. Family history of sudden death is the key clue.

A clinical syndrome of breathlessness, fatigue and fluid overload from impaired ventricular function. Split by ejection fraction: HFrEF (≤40%, systolic — the type with prognostic drug therapy) and HFpEF (preserved EF, diastolic). NT-proBNP triages referral; the four-pillar drug therapy (ACEi/ARB/ARNI + beta-blocker + MRA + SGLT2 inhibitor) transforms HFrEF outcomes.

Ventricular dilatation with impaired systolic function not explained by loading or coronary disease. Causes include genetic/familial, alcohol, peripartum, viral myocarditis, chemotherapy (anthracyclines, trastuzumab) and thyroid disease. Presents as heart failure, arrhythmia or thromboembolism, and is treated as HFrEF with the four pillars plus cause-specific measures.

An autosomal-dominant sarcomeric disease causing inappropriate left ventricular hypertrophy (classically asymmetric septal). It is the commonest cause of sudden cardiac death in young athletes. Dynamic LV outflow tract obstruction gives an ejection murmur that increases with Valsalva/standing. Management centres on sudden-death risk stratification and avoiding pre-load reduction.

Two less common cardiomyopathies. Restrictive cardiomyopathy = stiff, poorly compliant ventricles with impaired filling and preserved EF (amyloid, sarcoid, haemochromatosis, endomyocardial fibrosis) — presents like right heart failure and mimics constrictive pericarditis. Arrhythmogenic right ventricular cardiomyopathy (ARVC) = fibrofatty replacement of the RV causing ventricular arrhythmia and sudden death in young people.

Inflammation of the heart muscle, most often post-viral, but also drug/toxin-related, autoimmune or due to immune-checkpoint inhibitors. Presents with chest pain, heart failure or arrhythmia after a viral prodrome, often with a raised troponin and normal coronaries — a key ACS mimic. Can cause fulminant heart failure and is a leading cause of sudden death and dilated cardiomyopathy in the young.

Inflammation of the pericardial sac, usually viral or idiopathic. The classic picture is sharp pleuritic chest pain relieved by sitting forward, a pericardial friction rub, and widespread saddle-shaped ST elevation with PR depression. Treated with NSAIDs plus colchicine; the danger is progression to a significant effusion and tamponade.

Accumulation of fluid (or blood) in the pericardial sac. A slow effusion may be tolerated, but rapid or large accumulation raises intrapericardial pressure and prevents ventricular filling — cardiac tamponade, an obstructive shock. Beck's triad (hypotension, raised JVP, muffled heart sounds) with pulsus paradoxus is the clinical signature; treatment is pericardiocentesis.

Narrowing of the aortic valve causing fixed LV outflow obstruction. The commonest cause is senile calcific degeneration; a bicuspid valve causes it earlier. The classic triad of exertional Syncope, Angina and Dyspnoea (SAD) marks symptomatic severe disease — a turning point, because symptomatic severe AS has a poor prognosis and needs valve replacement.

Diastolic leakage of blood back into the left ventricle from an incompetent aortic valve or dilated aortic root. Chronic AR causes volume overload and a hyperdynamic, wide-pulse-pressure circulation with an early diastolic murmur; acute AR (endocarditis, dissection) is a sudden, poorly tolerated emergency. Causes include bicuspid valve, rheumatic disease, endocarditis, and root dilatation (Marfan, dissection, syphilis).

Systolic leakage of blood back into the left atrium. Primary MR is a valve problem (myxomatous prolapse, rheumatic, endocarditis, ruptured chordae tendineae, papillary muscle rupture post-MI); secondary (functional) MR results from LV dilatation. Chronic MR causes a pansystolic murmur radiating to the axilla and gradual LA/LV dilatation; acute MR (chordae/papillary rupture) causes sudden pulmonary oedema.

Narrowing of the mitral orifice, in the vast majority due to rheumatic heart disease. Obstructed left atrial emptying raises LA pressure → pulmonary congestion, AF and pulmonary hypertension. The signs are a loud S1, an opening snap and a low-pitched mid-diastolic rumble at the apex, with a malar flush.

Disease of the tricuspid and pulmonary valves. Tricuspid regurgitation is usually functional (secondary to RV dilatation/pulmonary hypertension) but can be from endocarditis (IV drug use), rheumatic disease or carcinoid. Pulmonary stenosis is usually congenital. Right-sided lesions present with systemic venous congestion rather than pulmonary symptoms.

Infection of the endocardial surface, usually a heart valve, producing vegetations. Risk factors are prosthetic valves, prior endocarditis, structural/congenital heart disease and IV drug use. Diagnosis uses the modified Duke criteria (positive blood cultures + echo evidence). It is a great mimic — fever with a new murmur and embolic/immunological phenomena — and needs prolonged IV antibiotics ± surgery.

A multisystem autoimmune sequela of group A streptococcal throat infection, 2–4 weeks later, driven by antibody cross-reactivity. Diagnosed with the Jones criteria. Acute carditis can cause valve damage that, with recurrences, leads to chronic rheumatic heart disease (especially mitral stenosis) — still a major cause of valve disease worldwide. Long-term penicillin prophylaxis prevents recurrence.

Persistently raised arterial blood pressure, confirmed with ambulatory/home monitoring. Most is essential (primary); secondary causes (renal, endocrine, drugs, coarctation) matter in the young or treatment-resistant. It is a major modifiable cardiovascular risk factor, and the NICE staged drug algorithm depends on age and ethnicity. Malignant hypertension and the emergencies are the acute danger.

A focal dilatation of the abdominal aorta to ≥3 cm, usually infrarenal and degenerative. Most are asymptomatic and found on screening (the NHS offers a one-off ultrasound to men at 65); the catastrophe is rupture. Elective repair is offered above a size/growth threshold, balancing rupture risk against operative risk.

A tear in the aortic intima lets blood split the media, creating a false lumen. Stanford type A involves the ascending aorta (surgical emergency); type B is distal to the left subclavian (usually managed medically). It presents with sudden tearing chest/back pain and pulse/BP asymmetry; complications follow the branches it occludes (stroke, MI, tamponade, limb/visceral ischaemia).

A tear in the wall of a carotid or vertebral artery, often after minor neck trauma or spontaneously (connective tissue disease), creating an intramural haematoma. It is an important cause of stroke in younger patients. The carotid triad is unilateral head/neck pain, a partial Horner's syndrome and cerebral/retinal ischaemia.

Atherosclerotic narrowing of the lower-limb arteries causing chronic ischaemia. Intermittent claudication (calf/thigh pain on walking, relieved by rest) is the early stage; critical limb ischaemia (rest pain, ulceration, gangrene) is limb-threatening. An ankle-brachial pressure index confirms it. Management is aggressive cardiovascular risk reduction plus supervised exercise, with revascularisation for critical/lifestyle-limiting disease.

Sudden loss of arterial perfusion threatening limb viability, usually from an embolus (often AF) or acute thrombosis of a diseased artery. It is a surgical emergency recognised by the 6 Ps; time to revascularisation determines limb salvage, and reperfusion brings its own risks (compartment syndrome, hyperkalaemia).

Death of tissue, classically of the extremities. Dry gangrene is ischaemic necrosis (PAD, diabetes, embolism) with a demarcated, mummified appearance and no infection. Wet gangrene is infected, spreading necrosis (a surgical emergency); gas gangrene (Clostridium perfringens) is a rapidly fatal myonecrosis. The split — dry vs wet/gas — drives whether the priority is revascularisation or emergency debridement/antibiotics.

Thrombosis of a deep vein, usually the leg, arising from Virchow's triad. The danger is propagation and embolism to the lungs (PE). The two-level Wells score directs whether to image or D-dimer; treatment is anticoagulation, now with a DOAC first-line. Unprovoked or recurrent DVT prompts a search for cancer/thrombophilia.

Obstruction of the pulmonary arteries, usually by an embolised leg DVT. It ranges from small subsegmental clots to massive PE with obstructive shock. The two-level PE Wells score directs CTPA vs D-dimer; massive PE with haemodynamic instability is an indication for thrombolysis. Anticoagulation with a DOAC is first-line for the stable patient.

Incompetent venous valves cause reflux and venous hypertension, producing dilated tortuous superficial veins (varicose veins) and, over time, the skin changes of chronic venous insufficiency that culminate in venous (gravitational) ulceration. Compression is the mainstay; endovenous/surgical treatment is for symptomatic or complicated disease.

A raised mean pulmonary arterial pressure from one of five WHO groups: pulmonary arterial hypertension (group 1), left heart disease (group 2, commonest), lung disease/hypoxia (group 3), chronic thromboembolic (group 4, CTEPH — potentially curable surgically), and miscellaneous (group 5). It causes progressive right heart failure; identifying the group determines whether specific vasodilator therapy or treatment of the underlying cause is appropriate.

Episodic vasospasm of the digital arteries causing the classic triphasic colour change (white → blue → red) on cold/emotion. Primary Raynaud's disease is benign and symmetrical in young women; secondary Raynaud's phenomenon points to an underlying disorder (especially connective tissue disease such as systemic sclerosis) and can cause digital ulceration/ischaemia. Buerger's disease (thromboangiitis obliterans) is a related smoking-related digital ischaemia in young men.

Transient loss of consciousness from global cerebral hypoperfusion, with rapid, complete spontaneous recovery. The central task is separating benign reflex (vasovagal) syncope from dangerous cardiac syncope (arrhythmia, structural disease), and from non-syncopal causes such as seizures. Red-flag features and an ECG drive risk stratification.

A sustained fall in blood pressure on standing (≥20 mmHg systolic or ≥10 mmHg diastolic within 3 minutes), causing light-headedness, dizziness, blurred vision or syncope. Common in the elderly and a major cause of falls. Causes are volume depletion, drugs (antihypertensives, diuretics, alpha-blockers, antidepressants), and autonomic failure (diabetes, Parkinson's, neuropathy).

A life-threatening state of inadequate tissue perfusion. The classification drives treatment: hypovolaemic (haemorrhage/fluid loss), cardiogenic (pump failure — MI, arrhythmia), obstructive (PE, tamponade, tension pneumothorax), and distributive (sepsis, anaphylaxis, neurogenic). Recognising the type — especially separating cardiogenic/obstructive from the rest — is essential because fluids help some and harm others.

Obstruction of the superior vena cava, usually by extrinsic compression from a mediastinal tumour (lung cancer, lymphoma) or thrombosis around an indwelling line/pacemaker. Venous return from the head, neck and arms is impeded, producing facial/arm swelling, distended veins and breathlessness. It is an oncological emergency when there is airway/cerebral compromise.

Structural heart defects that may first declare themselves, or need ongoing care, in adulthood. The framework is acyanotic (left-to-right shunts — ASD/VSD/PDA — and obstructive lesions — coarctation/aortic/pulmonary stenosis) versus cyanotic (right-to-left shunts — tetralogy of Fallot, transposition). Full paediatric detail (presentation, duct-dependent lesions, prostaglandin) lives on the child_health page; this card covers the adult-presentation and shunt-physiology essentials.

A transient, stress-induced cardiomyopathy ('broken-heart syndrome', apical ballooning syndrome) in which an intense emotional or physical stressor triggers acute left ventricular dysfunction that mimics an acute MI — chest pain, ST changes and a raised troponin — but with UNOBSTRUCTED coronary arteries and characteristic apical ballooning. It is usually reversible with supportive care.