Rapid review: cardiovascular

• Cardiovascular presentations sort into a handful of high-yield pictures: chest pain, collapse, breathlessness with oedema, palpitations, murmurs, severe hypertension, infective endocarditis, and late congenital disease.
• For each picture, name the single most dangerous diagnosis first, do the one test that changes management, and give the one treatment that must not be delayed.
• Common examination traps are predictable: attribute chest pain to gastro-oesophageal reflux before excluding acute coronary syndrome; collapse to a vasovagal episode before excluding cardiac syncope; a murmur to innocent flow before excluding aortic stenosis; severe hypertension to anxiety before excluding end-organ damage.
• Every presentation here is linked, in plain text, to the full topic page for deeper study.

By the end of this revision page you should be able to:

1. For each major cardiovascular presentation, state the most likely dangerous diagnosis, the best first test, the best first treatment and the commonest wrong answer.
2. Distinguish the main causes of chest pain (acute coronary syndrome, aortic dissection, pericarditis, pulmonary embolism) by presentation.
3. Separate syncope, dyspnoea and palpitations into cardiac and non-cardiac mechanisms.
4. Recognise murmurs that require intervention and plan the next investigation.
5. Define a hypertensive emergency and outline its initial management.
6. Select the first test and first treatment for suspected infective endocarditis, adult congenital heart disease and cardiac arrest.

This is a revision sheet, not a textbook. Each block below gives five things for one classic presentation: the presenting picture in clinical words, the single most likely diagnosis, the best first test, the best first treatment, and the commonest wrong answer, followed by the location of the full topic. Numbers are taken from the same guideline editions cited by the full topic pages.

Presenting picture. Central, pressure-like chest pain, often with sweating, nausea, breathlessness or radiation to the arm or jaw, lasting more than 20 minutes or recurring at rest, with ST-segment depression or T-wave change on the electrocardiogram (ECG), and a rise and fall of high-sensitivity troponin.^[7]

Single most likely diagnosis. Acute coronary syndrome, most often non-ST-elevation myocardial infarction (NSTEMI) or unstable angina when there is no persistent ST elevation.

Best first test. A 12-lead ECG within minutes of presentation, repeated serially, plus high-sensitivity cardiac troponin taken at presentation and again at 1 or 2 hours, interpreted with the clinical picture.^[7]

Best first treatment. Aspirin, a P2Y12 inhibitor (ticagrelor or prasugrel preferred when a percutaneous coronary intervention is planned), systemic anticoagulation, a high-intensity statin, and secondary prevention, with invasive timing governed by risk score.^[7]

Commonest wrong answer. To assume a normal first troponin or a normal first ECG excludes an infarct, or to load anticoagulation when the picture is actually an aortic dissection before that diagnosis has been excluded. See the full unstable angina and NSTEMI and STEMI topics.

Presenting picture. Sudden, severe, tearing pain in the chest or back, sometimes with unequal pulses or blood pressures between the arms, a new aortic regurgitation murmur, or neurological or limb symptoms.^[4]

Single most likely diagnosis. Acute aortic dissection, most often Stanford type A, which involves the ascending aorta.

Best first test. Electrocardiogram-gated computed tomography (CT) angiography of the whole aorta. Chest radiograph may show mediastinal widening but is neither sensitive nor specific.

Best first treatment. Urgent surgical assessment for an ascending dissection, with initial medical stabilisation: control heart rate with short-acting beta-blockade and reduce systolic blood pressure rapidly to strictly under 120 mm Hg with a heart rate of about 60 to 80 beats per minute, adding a calcium channel blocker or nitrate if necessary.^[4]

Commonest wrong answer. To treat the hypertension with vasodilatation alone, which can worsen a dissection by increasing shear stress, or to anticoagulate for a suspected pulmonary embolism before the aorta has been imaged. See the full aortic dissection topic.

Presenting picture. Sharp, central or left-sided chest pain that is worse on inspiration or when lying flat, often better when leaning forward, sometimes with a fever, with a pericardial friction rub and widespread ST-segment elevation with PR-segment depression on the ECG. Two of pericardial pain, pericardial rub, new ST-segment elevation or PR depression, or a new or worsening pericardial effusion make the diagnosis.^[2]

Single most likely diagnosis. Acute viral or idiopathic pericarditis.

Best first test. A 12-lead ECG plus an echocardiogram, which shows the effusion and excludes tamponade; full blood count, C-reactive protein and troponin are usually measured.

Best first treatment. First-line anti-inflammatory therapy: ibuprofen 600 to 800 milligrams three times daily, or aspirin 750 to 1000 milligrams three times daily, for 1 to 2 weeks with gradual taper, plus colchicine 0.5 milligrams twice daily for 3 months.^[2]

Commonest wrong answer. To treat like an acute coronary syndrome with anticoagulation, which risks a haemorrhagic pericardial effusion and tamponade, or to reach for corticosteroids as first treatment rather than as a reserve for non-steroidal anti-inflammatory drug failure or autoimmune disease. See the full acute pericarditis and cardiac tamponade topics.

Presenting picture. Pleuritic chest pain, breathlessness, tachypnoea, tachycardia, hypoxia and sometimes haemoptysis or syncope, especially after a period of immobility, surgery, pregnancy or in active cancer.^[3]

Single most likely diagnosis. Pulmonary embolism, often massive or submassive when there is hypotension or right ventricular strain.

Best first test. Computed tomography pulmonary angiography (CTPA) in most patients; a ventilation-perfusion scan when CTPA is contraindicated, with CTPA or leg ultrasound sometimes arranged from a chest radiograph and D-dimer pathway.^[3]

Best first treatment. Anticoagulation. A direct oral anticoagulant (apixaban or rivaroxaban) is preferred for confirmed proximal thrombus, with low-molecular-weight heparin bridging to dabigatran, edoxaban or a vitamin K antagonist where needed; continuous unfractionated heparin with consideration of thrombolysis in haemodynamic instability. Anticoagulation is continued for at least 3 months.^[3]

Commonest wrong answer. To dismiss pleuritic chest pain as musculoskeletal before excluding embolism, or to give thrombolysis to a stable patient with an intermediate scan result. See the full pulmonary embolism topic.

Presenting picture. A sudden, brief loss of consciousness with complete and rapid recovery, often with a prodrome of nausea, sweating or dimming vision in reflex syncope, or with warning palpitations or chest pain in cardiac syncope.

Single most likely diagnosis. Reflex (vasovagal or situational) syncope in a young person; cardiac syncope, from an arrhythmia or structural lesion, in an older person or anyone with heart disease.

Best first test. A careful history from the patient and a witness, a 12-lead ECG and orthostatic lying and standing blood pressure. These three steps outrank most investigations.

Best first treatment. Treat the mechanism: education, triggers, salt and fluids, and counter-pressure manoeuvres for reflex syncope; stopping hypotensive drugs and compression for orthostatic hypotension; and treating the rhythm or the valve or structural lesion for cardiac syncope, with pacemaker or implantable cardioverter-defibrillator when indicated.

Commonest wrong answer. To call an episode a seizure (and order brain imaging) without asking what happened before and after, or to reassure a patient with exertional syncope and an abnormal electrocardiogram that it was vasovagal. See the full syncope topic.

Presenting picture. Breathlessness on exertion or at rest, orthopnoea and paroxysmal nocturnal dyspnoea, with ankle or sacral oedema, raised jugular venous pressure and fine basal crackles, often after a myocardial infarction, hypertension or valve disease.

Single most likely diagnosis. Heart failure, most often acute decompensation of chronic heart failure.

Best first test. Clinical assessment with natriuretic peptide and an echocardiogram to assess left ventricular function; a chest radiograph to identify pulmonary oedema.

Best first treatment. Intravenous diuretic therapy, started as a bolus or infusion, with a higher dose than the patient's admission dose if already on a diuretic and it is safe to do so.^[8] Add oxygen if hypoxaemic, vasodilators when blood pressure allows, and guideline-directed medical therapy (ACE inhibitor or ARB, beta-blocker, mineralocorticoid receptor antagonist and SGLT2 inhibitor) once the patient is stable.

Commonest wrong answer. To give large volumes of intravenous fluid for "dehydration" when the problem is congested, not dry, or to withhold guideline-directed therapy because of a single borderline blood pressure. See the full heart failure topic.

Presenting picture. Awareness of a rapid, irregular or strong heartbeat, sometimes with breathlessness, chest discomfort, dizziness or syncope; atrial fibrillation is irregularly irregular with no P waves, ventricular tachycardia is broad-complex and potentially unstable, and supraventricular tachycardia is regular and sudden in onset and offset.

Single most likely diagnosis. Atrial fibrillation, the commonest arrhythmia in adults; persistent ventricular arrhythmia if the rhythm is broad-complex or the patient is compromised.

Best first test. A 12-lead ECG, and if the rhythm comes and goes, an ambulatory monitor or an implantable loop recorder.

Best first treatment. For an acutely unstable patient, immediate synchronised electrical cardioversion. For stable atrial fibrillation, rate control with a beta-blocker (the most effective single agent in trials) or digoxin, and anticoagulation when indicated by risk score, because anticoagulation matters more than rate versus rhythm for long-term outcome.^[7]

Commonest wrong answer. To cardiovert paroxysmal atrial fibrillation without assessing how long it has been present and thrombo-embolic risk, or to miss ventricular tachycardia because the patient is still talking. See the full approach to tachyarrhythmias, atrial fibrillation and flutter, supraventricular tachycardias and ventricular arrhythmias topics.

Presenting picture. Exertional dyspnoea, angina or syncope in an older adult, with a slow-rising pulse, a sustained apex and a harsh crescendo-decrescendo systolic ejection murmur loudest at the right upper sternal edge and radiating to the carotids.

Single most likely diagnosis. Degenerative calcific aortic stenosis, occasionally bicuspid or rheumatic in a younger adult.

Best first test. Transthoracic echocardiography, which grades severity (severe: peak velocity at least 4.0 metres per second, mean gradient at least 40 millimetres of mercury, valve area 1.0 square centimetre or less).^[5]

Best first treatment. No drug slows progression. Valve intervention with surgical aortic valve replacement or transcatheter aortic valve implantation is indicated for symptomatic severe disease; the choice between them depends on age, surgical risk and anatomy.^[5]

Commonest wrong answer. To assume the murmur is innocent because the patient is elderly, or to withhold intervention because the patient describes only mild symptoms while the ventricle is already failing. See the full valvular heart disease topic.

Presenting picture. Heart-failure symptoms with a holosystolic murmur at the apex, often radiating to the axilla, with or without atrial fibrillation.

Single most likely diagnosis. Primary (degenerative) mitral regurgitation, often from prolapse or a flail leaflet; secondary mitral regurgitation from ventricular or atrial disease is an equally important possibility.

Best first test. Transthoracic echocardiography for mechanism and severity; transoesophageal echocardiography for anatomy before repair.

Best first treatment. Guideline-directed medical therapy for heart failure while assessing; surgical repair is preferred for primary disease when indicated; transcatheter edge-to-edge repair is an option for selected high-risk or secondary disease after optimisation.^[6]

Commonest wrong answer. To call any holosystolic apical murmur mitral regurgitation without considering a ventricular septal defect, or to list a patient for replacement when repair is the better operation. See the full valvular heart disease topic.

Presenting picture and approach. Mitral stenosis gives a low-pitched mid-diastolic rumble with an opening snap; aortic regurgitation an early diastolic decrescendo murmur with a collapsing pulse; hypertrophic cardiomyopathy a systolic murmur that increases with Valsalva; tricuspid regurgitation a systolic murmur at the left lower sternal edge that increases on inspiration.

Single most likely diagnosis. Match the sound to the lesion above, and ask whether the lesion is primary or secondary.

Best first test. Transthoracic echocardiography in every case that is not clearly innocent.

Best first treatment. Follow the lesion-specific triggers; most severe lesions require intervention only when symptoms or ventricular change appear.

Commonest wrong answer. To forget that an innocent flow murmur is a diagnosis of exclusion in an adult, or to manage a murmur without imaging. See the full cardiac physical examination and valvular heart disease topics.

Presenting picture. A severely raised blood pressure in a patient with acute organ damage: chest pain, breathlessness or pulmonary oedema, confusion, stroke signs, visible bleeding or papilloedema, acute kidney injury, or an aortic syndrome.

Single most likely diagnosis. A hypertensive emergency, defined as blood pressure at least 180 over 110 millimetres of mercury by European criteria or at least 180 over 120 by North American criteria, with acute target-organ damage; a severe uncomplicated (urgency) rise is not an emergency.^[4]

Best first test. Repeated blood pressure measurement, urinalysis, basic blood tests including creatinine and troponin, an electrocardiogram and funduscopy; targeted imaging for suspected aortic, cerebral or cardiac complications.^[4]

Best first treatment. Intravenous antihypertensive therapy, chosen by the organ involved: labetalol 0.25 to 0.5 milligrams per kilogram over one minute with an infusion of 2 to 4 milligrams per minute, nicardipine 5 to 15 milligrams per hour, or esmolol 0.5 to 1 milligrams per kilogram bolus with 50 to 300 micrograms per kilogram per minute, titrated to the target for that organ and reassessed frequently.^[4]

Commonest wrong answer. To lower the blood pressure by half in the first hour regardless of cause, or to call severe but uncomplicated hypertension an emergency and arrange unnecessary admission. Antihypertensive therapy in aortic dissection should drive the pressure under 120 millimetres of mercury systolic with a heart rate of 60 to 80 beats per minute, with short-acting beta-blockers such as esmolol preferred.^[4] See the full hypertensive crises and aortic dissection topics.

Presenting picture. Fever with a new or changing murmur, often after a dental or invasive procedure or in injecting drug use, with embolic phenomena (stroke, splinter haemorrhages, septic emboli) and regurgitant valve disease; the presentation can be indolent and mimic rheumatic disease.

Single most likely diagnosis. Infective endocarditis, most often staphylococcal or streptococcal in origin.

Best first test. At least three sets of peripheral blood cultures, 10 millilitres each about 30 minutes apart, before giving antibiotics, plus transthoracic echocardiography (transoesophageal when the transthoracic image is inadequate, with prosthetic material, or for better resolution). The diagnosis is supported by the modified Duke criteria, which combine clinical, microbiological and imaging findings.^[9]

Best first treatment. Empirical intravenous antibiotic therapy started after cultures, tailored to the organism and the valve, with early surgery for heart failure, uncontrolled infection or large vegetations with embolic risk. Antibiotic choice depends on local guidelines and the organism grown; do not guess a regimen without a source for the dose.

Commonest wrong answer. To give a single dose of antibiotics before taking cultures, which renders them useless, or to discount a normal transthoracic echocardiogram in early disease or prosthetic valve endocarditis. See the full infective endocarditis topic.

Presenting picture. A murmur, cyanosis, clubbing, limited exercise, paradoxical embolism or right heart failure in an adult who had a repaired or unrepaired childhood lesion, often surfacing in early adult life; common lesions include atrial septal defect, ventricular septal defect, patent ductus arteriosus, tetralogy of Fallot after repair, coarctation of the aorta and complex cyanotic disease.

Single most likely diagnosis. A simple acyanotic lesion if the patient is well grown and pink; a complex or cyanotic lesion if there is cyanosis, desaturation, clubbing or Eisenmenger physiology.

Best first test. Transthoracic echocardiography with bubble study where a shunt is suspected; cardiac magnetic resonance or computed tomography for complex anatomy, and diagnostic catheterisation when non-invasive imaging is insufficient.

Best first treatment. Management by an adult congenital heart disease service, following the 2020 AHA/ACC and 2020 ESC adult congenital heart disease guidance and national practice, with device or surgical closure of significant shunts, repair of coarctation, catheter or surgical management of valve lesions, treatment of pulmonary hypertension, and lifelong surveillance for repaired tetralogy of Fallot.^[10]

Commonest wrong answer. To assume the problem was cured in childhood, or to apply standard adult acquired heart disease pathways (such as routine coronary angiography or conventional valve replacement) to a congenital substrate without specialist input. See the full congenital heart disease in adults topic.

Presenting picture. Sudden collapse, unresponsiveness and absent or abnormal breathing, often with a brief run of arrhythmia preceding it; check the carotid pulse for no more than 10 seconds while help is called.

Single most likely diagnosis. A cardiac arrhythmia (ventricular fibrillation or pulseless ventricular tachycardia) in a witnessed monitored arrest; asystole or pulseless electrical activity in most out-of-hospital arrests.

Best first test. None before starting treatment; rhythm assessment follows once a monitor is attached, and point-of-care ultrasound may identify treatable causes such as cardiac tamponade or tension pneumothorax.^[1]

Best first treatment. High-quality cardiopulmonary resuscitation plus early defibrillation for shockable rhythms: recognise, call for help, start chest compressions, defibrillate within roughly 3 minutes for shockable rhythms, give adrenaline 1 milligram as soon as possible for non-shockable rhythms and after the third shock for shockable rhythms, repeated every 3 to 5 minutes; amiodarone 300 milligrams intravenously after three shocks and 150 milligrams after five shocks. Give fluids only for hypovolaemia, do not routinely give calcium or sodium bicarbonate, and identify and treat reversible causes without delay.## An approach flowchart: unexplained or severe chest discomfort ^[1]

• Heart failure topic
• Syncope topic
• Atrial fibrillation and flutter topic
• Approach to tachyarrhythmias topic
• Unstable angina and NSTEMI topic
• ST-elevation myocardial infarction topic
• Aortic dissection topic
• Acute pericarditis topic
• Cardiac tamponade topic
• Pulmonary embolism topic
• Valvular heart disease topic
• Hypertensive crises topic
• Aortic aneurysm topic
• Infective endocarditis topic
• Congenital heart disease in adults topic
• Cardiac arrest and advanced life support topic
• Cardiac physical examination topic
• ECG interpretation topic

When any of the following is present, the diagnosis is dangerous until excluded:

• Chest pain with haemodynamic instability, new ST-segment elevation, or a suspected aortic syndrome: image the aorta, rule out dissection, and involve cardiology or cardiothoracic surgery at once. ^[4]
• Syncope with exertion, while supine, or with an abnormal electrocardiogram: treat as cardiac syncope until the contrary is proven, and avoid the temptation to label the episode vasovagal.
• Breathlessness with oedema, hypotension or hypoxia: consider acute decompensated heart failure, massive pulmonary embolism or tamponade, and avoid routine fluid resuscitation unless hypovolaemia is clear.
• Palpitations with a broad-complex or irregularly irregular rhythm in an unwell patient: assume instability and cardiovert rather than waiting for a definitive rhythm diagnosis.
• A murmur with exertional symptoms, heart-failure signs, or reduced exercise tolerance: grade the lesion and assess for intervention, rather than observing it without imaging.
• Severe hypertension with neurological signs, chest pain, breathlessness, or acute renal impairment: investigate and treat as a hypertensive emergency with intravenous therapy chosen for the organ. ^[4]
• Fever with a changing murmur or embolic phenomenon: begin the endocarditis pathway with cultures before antibiotics and echocardiography, including transoesophageal imaging when the first study is normal. ^[9]
• Collapse, especially if the pulse or rhythm is unobtainable: call for help, start compressions, defibrillate for shockable rhythms, and treat reversible causes during the arrest. ^[1]

The principles above change less with setting than the logistics:

• A 12-lead ECG and a basic echocardiogram carry more diagnostic weight than most sophisticated tests, and should be the first resources protected. A single transthoracic echocardiogram diagnosing rheumatic mitral stenosis, aortic stenosis, pericardial tamponade and many adult congenital lesions is high value.
• In aortic dissection and massive pulmonary embolism, imaging and transfer pathways matter more than drug choice: know the nearest centre that can image the aorta and provide reperfusion, and call early rather than after repeated tests.
• In heart failure, intravenous diuretics and oxygen save lives when echocardiography is unavailable; guideline-directed oral therapy is inexpensive and effective once congestion is resolved. ^[8]
• In hypertension, the distinction between emergency and urgency depends on organ damage rather than the number on the manometer, so urinalysis, creatinine and funduscopy can be as informative as imaging.
• Infective endocarditis needs blood cultures and echocardiography wherever possible; empirical therapy without cultures is sometimes unavoidable, but it should be the exception, not the plan.
• Cardiac arrest outcomes depend most on recognition, early defibrillation and high-quality compressions. Adrenaline and amiodarone formulation choices are secondary to these basics and to treating reversible causes. ^[1]
• When a definitive procedure is unavailable locally, stabilise, give the best medical therapy supported by evidence, and arrange safe transfer. Good notes, a clear diagnosis, and early contact with the receiving team are themselves useful interventions.

• Acute coronary syndrome and aortic dissection both cause severe chest pain and both can invalidate ECGs; the difference is in the quality of the pain (pressure versus tearing), radiation (arm or jaw versus back or abdomen), the peripheral pulses and the aortic regurgitation murmur. Hypotension should prompt suspicion of dissection rather than a larger infarct.
• Pericarditis and myocardial infarction both produce ST elevation; pericarditis gives widespread elevation with PR depression and positional pain, while infarction gives territory-appropriate elevation with reciprocal change. Pericarditis should not receive anticoagulation.
• Pulmonary embolism mimics musculoskeletal pain, pneumonia and anxiety. A raised respiratory rate, tachycardia and clear lung fields should prompt D-dimer testing or imaging, not reassurance, especially after immobility or surgery.
• Vasovagal syncope is common and benign; cardiac syncope is not. Red flags include exertional onset, supine onset, palpitations or chest pain, known cardiac disease and an abnormal ECG. Risk scores are checklists rather than verdicts.
• Dyspnoea with ankle oedema is often treated as fluid overload but can be cor pulmonale, nephrotic syndrome, venous insufficiency, pulmonary embolism or anaemia. An echocardiogram and natriuretic peptide measurement separate cardiac from non-cardiac dyspnoea.
• A systolic murmur in an adult is not innocent until imaging says so. Aortic stenosis, hypertrophic cardiomyopathy, mitral regurgitation and tricuspid regurgitation each has characteristic associated findings, but all require echocardiography.
• Severe hypertension without symptoms does not need intravenous treatment; conversely, a pressure that is only modestly raised but accompanied by headache, vomiting or visual change may be encephalopathy and needs care.
• Fever plus murmur plus emboli is infective endocarditis until a urine, throat, blood, joint or imaging diagnosis explains everything else; negative early blood cultures and a normal transthoracic echo do not close the question.

These distinctions are the reason this revision page separates presentations rather than diagnoses. Learn the pictures, test the dangerous diagnosis first, and the common mistakes stop being common.

• Chest pain: ECG before diagnosis, diagnosis before drugs. If it is tearing and radiates to the back, image the aorta first.
• Chest pain: ST elevation in V1-V4 is anterior STEMI, not pericarditis, until the other clues (positional pain, widespread changes, absence of reciprocal change) genuinely point that way.
• Collapse: reflex syncope is a diagnosis of exclusion after red flags, not a label to use because the patient is young and the ECG is hard to get.
• Dyspnoea: treat decompensated heart failure with diuretics, oxygen and nitrates; do not chase filling pressures with fluids.
• Palpitations: the rhythm at the time of symptoms is the diagnosis. If a smart-watch trace or an ambulatory recording is available, read it before ordering more tests.
• Murmur: valve area, gradient and regurgitant volume on echocardiography determine severity and timing, not how loud the sound is.
• Hypertension: urgency can be treated in clinic over days; emergency needs organ involvement and intravenous drugs.
• Endocarditis: cultures first, echo second, antibiotics third, surgery when the haemodynamics or infection dictate.
• Congenital disease: ask about blue lips as a child, and if the answer is yes, refer rather than investigate again.
• Cardiac arrest: compress well, shock early, give adrenaline on time, look for reversible causes throughout.

Each of these pairs prevents the error most commonly marked in accounts of cardiovascular medicine practice. Knowing the pair is the revision; acting on it is the doctor.