Level 2 of 6Must-remember

Acute coronary syndrome: ECG, antiplatelets and reperfusion

Assess, manage and stay safe — enough on its own

1 / 9

The card — assess, manage, caution

Assessment— look, ask, measure

Get a 12-lead ECG within 10 minutes of first medical contact in anyone with chest discomfort, and in any elderly, diabetic or female patient with unexplained breathlessness, sweating or collapse. The ECG separates STEMI from everything else before any laboratory result exists, and only that distinction changes what happens in the next hour.
The characteristic symptom is central or substernal discomfort — heaviness, pressure, squeezing, smothering or choking, only rarely frank pain. The patient places a flat hand or a clenched fist over the sternum (Levine's sign); discomfort that can be indicated with one fingertip is rarely ischaemic.
It is crescendo–decrescendo and not maximal at onset — a key discriminator from aortic dissection. It radiates to either shoulder, both arms (particularly the ulnar forearm and hand), the back, the interscapular region, the root of the neck, the jaw or teeth, and the epigastrium. Angina is rarely localised below the umbilicus or above the mandible, and radiation to the trapezius ridge is characteristic of pericarditis, not ischaemia.
Duration and nitrate response separate the syndromes: stable exertional angina lasts 2–5 minutes and is relieved within 1–5 minutes by rest or sublingual nitrate, whereas severe chest discomfort lasting > 20 minutes may be an infarct, does not usually respond to sublingual glyceryl trinitrate, and requires opiate analgesia.
Three histories are ACS until disproved: new-onset chest pain; chest pain at rest; and deterioration of pre-existing angina — at lower workloads, more frequently, or waking the patient from sleep. Autonomic features are a genuine severity marker: pallor, cold clammy skin, marked sweating, nausea and vomiting.
Anginal equivalents get sent home: dyspnoea, nausea, fatigue, faintness, pre-syncope and syncope, or a complaint of indigestion or pleuritic pain. They are commonest in the elderly and in diabetes, where autonomic neuropathy blunts ischaemic pain. Around 25% of patients who survive an acute myocardial infarction never come to medical attention, and their prognosis is as adverse as that of those who present classically.
Examine for the alternative diagnosis and for the adverse signs. Hypotension, thready pulse, tachycardia or bradycardia; basal crackles (the physical basis of the Killip class); a fourth heart sound from a stiff ischaemic ventricle, or a third reflecting failure; any murmur — a new one is a mechanical complication until proved otherwise; and raised jugular venous pressure with clear lung fields and hypotension, which in an inferior infarct is the signature of right ventricular involvement. Record the blood pressure in both arms.
Exclude aortic dissection before any antithrombotic is given: pain that is sudden, tearing, maximal at onset and interscapular, with unequal pulses or an inter-arm blood pressure difference. Antiplatelets and anticoagulants may be lethal in dissection, and the whole cost of asking is one question and a blood pressure in each arm.
STEMI criteria: new ST elevation of 0.2 mV (2 mm) or more at the J point in leads V1–V3, or 0.1 mV (1 mm) or more in any other lead, in two contiguous leads; or new, or presumed new, left bundle branch block, which mandates the same urgent reperfusion pathway.
Record two extra lead sets deliberately. V4R at minimum in every inferior infarct, before any nitrate is given, because right ventricular infarction produces a preload-dependent circulation. V7–V9 whenever there is ST depression in V1–V3 with a dominant R wave — a posterior STEMI is a STEMI.
A single normal tracing never excludes an acute coronary syndrome. Repeat the ECG every 15 minutes while the patient remains in pain, and immediately with any change in symptoms, rhythm or blood pressure, with continuous cardiac monitoring throughout. In a ventricular paced rhythm or right bundle branch block, infarction cannot be excluded electrocardiographically.
In non-ST-elevation ACS, dynamic changes — appearing with pain and resolving between episodes — are the most specific finding available. ST depression and T-wave inversion are highly suggestive; transient ST elevation occurs with coronary vasospasm as well as with ACS.
Troponin: treatment of STEMI is never deferred for it. A value below 5 ng/L on a high-sensitivity assay has a negative predictive value of 99.4%, but a negative initial assay must be repeated at 3 hours — it is the rise or fall across serial samples, not a single value, that identifies acute injury. Troponin remains elevated for at least 7–10 days after infarction, and a raised troponin is not synonymous with type 1 myocardial infarction.Not available at your setup — Cardiac troponin.
Assign a Killip class at the bedside with a stethoscope, and reassess it serially: I, no crackles and no third heart sound; II, crackles in less than 50% of the lung fields or a third heart sound; III, crackles in more than 50% of the lung fields — frank pulmonary oedema; IV, cardiogenic shock, with an in-hospital mortality of 40–60%.
Red flags: discomfort persisting beyond 20 minutes or recurring at rest; sweating, pallor or vomiting; systolic pressure below 90 mmHg or a fall of more than 30 mmHg from the patient's usual pressure; new crackles, a third heart sound or frank pulmonary oedema; a new murmur; ventricular tachycardia or fibrillation, complete heart block or symptomatic bradycardia; syncope with the pain; pain persisting despite full anti-ischaemic therapy; and raised JVP with clear lungs and hypotension.
In children atherosclerotic ACS does not occur. Get a 12-lead ECG and cardiology assessment for chest pain or syncope on exertion; chest pain with palpitations; a family history of sudden cardiac death under 40 years; a known cardiac condition or previous cardiac surgery; past Kawasaki disease; a new murmur or gallop; and a child who is unwell, tachycardic at rest, or has hepatomegaly.

Management— do this, in order

Classify on the 12-lead ECG within 10 minutes, then relieve ischaemia and pain, arrest thrombus propagation, restore coronary patency, and anticipate and treat complications while starting secondary prevention before discharge.
Continuous cardiac monitoring with immediate access to a defibrillator, since ventricular fibrillation in the first hours is the commonest mode of death. Two large-bore cannulae, with all blood samples drawn before anything is infused. Sit the breathless patient up; lie the hypotensive patient flat with the legs elevated. Bed rest for the first 6–12 hours and clear fluids only for the first 4–12 hours.Not available at your setup — Defibrillator.
Oxygen is a treatment for hypoxaemia, not for chest pain: give it only if saturations fall below 90%, targeting 94–98% (88–92% in chronic obstructive pulmonary disease with carbon dioxide retention). Routine oxygen in a normoxaemic patient confers no benefit and may cause coronary vasoconstriction.
Aspirin 150–300 mg chewed or dispersed in water (300 mg unless already taken today), then 75–100 mg orally daily; a dispersible tablet per rectum if the patient cannot swallow. Give it before the opioid, since opioids delay gastric emptying and antiplatelet absorption. It is the highest-value single intervention in the chapter.
Add an ADP-receptor antagonist — dual antiplatelet therapy is standard in every acute coronary syndrome. Clopidogrel 300 mg orally loading (600 mg where primary PCI is planned), then 75 mg daily — and clopidogrel is the recommended partner for thrombolysis and the safe default where the strategy is unsettled. Ticagrelor 180 mg loading then 90 mg twice daily, or prasugrel 60 mg loading then 10 mg daily (5 mg if under 60 kg or over 75 years), are preferred where primary PCI is planned; neither is used with planned thrombolysis.Doctor
Glyceryl trinitrate 500 microgram sublingual tablet or 400 microgram spray, repeated every 5 minutes to three doses; if pain persists, 2–10 mg/hour intravenously, titrated. Keep systolic BP above 90 mmHg. Withhold in right ventricular infarction, hypotension, marked bradycardia or tachycardia, or within 24 hours of sildenafil or vardenafil or 48 hours of tadalafil.
Morphine 2.5–5 mg by slow intravenous injection, titrated and repeated (diamorphine 2.5–5 mg IV is equivalent), with metoclopramide 10 mg intravenously; use ondansetron instead in the young because of extrapyramidal reactions. Take care in inferior and right ventricular infarction.Doctor / Nurse
Antithrombin therapy alongside dual antiplatelets. Enoxaparin 1 mg/kg subcutaneously twice daily (once daily if eGFR < 30 mL/min) is the usual choice; unfractionated heparin 5000 units intravenously then 0.25 units/kg/hour by infusion with the APTT checked at 6 hours where rapid reversibility is wanted or renal function is very poor; fondaparinux 2.5 mg subcutaneously daily for up to 8 days; bivalirudin 0.75 mg/kg intravenously then 1.75 mg/kg/hour for 4 hours after PCI peri-procedurally.Doctor / Nurse
Beta-blockade orally, titrated to a resting heart rate of 50–60 beats per minute: metoprolol 25–50 mg orally twice daily, or atenolol 25–50 mg orally daily. Check first for asthma, atrioventricular block, acute pulmonary oedema, hypotension, bradyarrhythmia and any low-output state. Intravenous beta-blockade (metoprolol 5 mg IV repeated to a maximum of 15 mg; atenolol 5 mg IV repeated after 15 minutes) has a narrow role and must never be used in a patient who is hypotensive, in failure, or at risk of shock.Doctor
STEMI — primary PCI is the preferred reperfusion therapy, targeting 60 minutes from diagnosis to wire-crossing of the culprit vessel. Radial access is preferred to femoral, drug-eluting to bare-metal stents; routine thrombus aspiration is not recommended; complete revascularisation during the index admission is now favoured.Doctor
Thrombolysis when primary PCI cannot be delivered within 120 minutes of STEMI diagnosis, targeting less than 10 minutes from decision to delivery of the bolus. Within 6 hours of symptom onset it prevents 30 deaths per 1000 treated; between 7 and 12 hours, 20 per 1000; beyond 12 hours the benefit is limited. Aspirin and clopidogrel are the recommended antiplatelet pair for thrombolysed patients, with unfractionated heparin, enoxaparin or fondaparinux as the anticoagulant.Doctor
Judge reperfusion at 60–90 minutes: resolution of pain and of ST elevation, sometimes with an accelerated idioventricular rhythm. Less than 50% resolution of ST elevation is failed reperfusion and an indication for re-thrombolysis or, preferably, rescue coronary angioplasty; recurrence of pain and ST elevation after initial resolution means reocclusion and demands the same response.Doctor
Non-ST-elevation ACS — time the angiogram by risk. Within 2 hours for persistent or recurrent pain unresponsive to medical therapy, heart failure, haemodynamic instability or cardiogenic shock, or life-threatening arrhythmia. Within 24 hours for a rising or falling troponin, dynamic ST- or T-wave change, or GRACE > 140. Within 72 hours for diabetes, eGFR < 60 mL/min, ejection fraction < 40%, congestive cardiac failure, early post-infarction angina, previous PCI or bypass grafting, or GRACE 109–140.Doctor
Right ventricular infarction — inferior ST elevation with hypotension, raised JVP and clear lungs, confirmed on V4R — is treated with cautious intravenous fluid in 250 mL increments, reassessing the chest after each, while withholding nitrates, diuretics and large opioid boluses. In any hypotensive patient the first decision is between right ventricular infarction, hypovolaemia and pump failure, and hypovolaemia should be corrected by cautious fluid administration under continuous monitoring before more vigorous therapy is begun.
Killip II–III (heart failure and pulmonary oedema): sit the patient up, give oxygen with monitoring and furosemide 40–80 mg intravenously, add glyceryl trinitrate if systolic pressure exceeds 90 mmHg, and an ACE inhibitor within 24–48 hours. Continuous positive airway pressure improves oxygenation and reduces the need for intubation.Doctor / Nurse
Killip IV (cardiogenic shock): noradrenaline is the usual first-line vasopressor and dobutamine the first-line inotrope, both a bridge rather than a treatment since both raise myocardial oxygen demand. The definitive treatment is revascularisation, with or without mechanical circulatory support, and around 80% of these patients eventually require mechanical ventilation.DoctorNot available at your setup — Infusion pump.
Arrhythmia: ventricular fibrillation or pulseless VT requires immediate defibrillation, after which potassium and magnesium are corrected — keep serum potassium at approximately 4.5 mmol/L and magnesium at approximately 2.0 mmol/L. Sporadic ventricular premature depolarisations occur in almost all patients with STEMI and require no treatment. Symptomatic bradycardia or high-grade block: atropine 0.6 mg intravenously repeated to a total of 3 mg, with temporary pacing if atropine fails.DoctorNot available at your setup — Defibrillator, Serum electrolytes.
Start plaque stabilisation during the admission, because that is what determines whether the patient ever receives it. Atorvastatin 80 mg orally daily (or rosuvastatin 20–40 mg, or pravastatin 20–40 mg daily) with dietary advice; ramipril 2.5–10 mg orally daily or lisinopril 5–10 mg orally daily, started within 24–48 hours provided the systolic pressure is above 100 mmHg, with renal function monitored; aspirin 75–100 mg daily indefinitely, which after STEMI reduces recurrent infarction, stroke or cardiovascular death by approximately 25%; dual antiplatelet therapy generally for 12 months; long-term beta-blockade, smoking cessation, cardiac rehabilitation, glycaemic and blood pressure control.Doctor
Paediatric: estimate weight as (age in years + 4) × 2 kg for ages 1–10 years. Morphine 100 microgram/kg (0.1 mg/kg) by slow intravenous injection, maximum initial dose 5 mg; ondansetron 100 microgram/kg (0.1 mg/kg) intravenously, maximum 4 mg; atropine 20 microgram/kg intravenously (minimum 100 microgram, maximum 600 microgram) for bradycardia with poor perfusion; furosemide 0.5–1 mg/kg intravenously; and a crystalloid bolus of 10 mL/kg — not 20 mL/kg — in any child with known or suspected cardiac disease, reassessing the chest and liver edge after each.Doctor / Nurse

Caution— what harms

Never give antiplatelet or antithrombin therapy until aortic dissection has been considered and, where the question is open, excluded. Pain maximal at onset, tearing and interscapular, with unequal pulses or an inter-arm pressure difference, is dissection until proven otherwise.
Never give a nitrate in an inferior infarct before recording V4R. Right ventricular infarction is preload-dependent, and vasodilatation can precipitate an unrecoverable fall in cardiac output. Fluid yes; nitrates, diuretics and large opioid boluses no.
Never accept a single normal ECG as excluding ACS, and never assume infarction can be excluded electrocardiographically in a paced rhythm or right bundle branch block.
Never miss the posterior infarct: ST depression with a dominant R wave in V1–V3 needs V7–V9, and a posterior STEMI requires the same reperfusion pathway as any other STEMI.
Never defer treatment of a STEMI for a troponin, and never treat a raised troponin as proof of type 1 infarction — consider type 2 infarction and non-coronary injury from pulmonary embolism, myocarditis, sepsis, renal failure, decompensated heart failure, tachyarrhythmia and takotsubo syndrome.
Never give glucocorticoids or non-steroidal anti-inflammatory drugs, with the sole exception of aspirin, since they impair infarct healing and increase the risk of rupture and reinfarction.
Never give intravenous beta-blockade to a patient who is hypotensive, in failure, or at risk of shock — it reduces reinfarction and ventricular fibrillation but at the cost of an excess of cardiogenic shock in exactly those patients.
Never treat refractory ischaemia with another dose of morphine. Pain persisting despite nitrate and opioid is a very-high-risk feature demanding urgent angiography; re-record the ECG immediately, because recurrent discomfort heralds infarct extension or reinfarction and carries a near tripling of mortality.
Never treat type 2 infarction as type 1. In supply–demand mismatch the correct treatment is to correct the precipitant — transfuse the anaemia, slow the tachyarrhythmia, restore the blood pressure — and reflex dual antiplatelet therapy with anticoagulation may do more harm than good.
Never let relief by nitrate or antacid reassure you, and never let reproduction of pain on palpation exclude ischaemia in a high-risk patient.
Never treat low risk as no risk: such a patient still requires monitoring, a repeat ECG and a repeat troponin at 3 hours before any decision about discharge.
Never give aspirin to a child under 16 years because of the risk of Reye's syndrome, except on explicit paediatric cardiology instruction for Kawasaki disease or another established cardiac indication — the exact inverse of the adult rule. Avoid metoclopramide under 20 years, and leave nitrates, beta-blockers, ADP-receptor antagonists, anticoagulants and thrombolysis in a child to paediatric cardiology.
Never let a patient with a coronary stent stop dual antiplatelet therapy prematurely, because of the risk of stent thrombosis.
Never explain away a genuinely septic patient with post-infarct fever, and never work one up unnecessarily: temperature elevations up to 38°C may be observed during the first week as part of the inflammatory response to necrosis.

Refer / escalate

Activate the primary PCI pathway immediately on a STEMI ECG — target 60 minutes from diagnosis to wire-crossing, and give thrombolysis instead only if PCI cannot be delivered within 120 minutes of diagnosis; in non-ST-elevation ACS refer for angiography within 2 hours for refractory pain, heart failure, haemodynamic instability, cardiogenic shock or life-threatening arrhythmia, within 24 hours for dynamic ECG change, a rising troponin or GRACE > 140, and within 72 hours for the intermediate-risk group — and refer urgently to cardiac surgery for any sudden deterioration with a new murmur between days 2 and 7.

The card — assess, manage, caution

Acute coronary syndrome: ECG, antiplatelets and reperfusion — Level 1: CorePrevious Acute coronary syndrome: ECG, antiplatelets and reperfusion — Level 3: Core practiceNext

Read the full lesson free

Create a free account to unlock every page, the level exams, and progress tracking.