14 Acute myocardial infarction
Salient features
History
• Family history of cardiovascular disease, hyperlipidaemia, gout
• Past history of diabetes mellitus, hypertension, stroke, myocardial infarction (MI), intermittent claudication and hyperlipidaemia
• History of oral contraceptives in young women
Examination
• Hands: nicotine staining of fingers
• Pulse: check pulse rate (keeping in mind heart block and tachycardia), rhythm (keeping in mind atrial fibrillation, ventricular arrhythmias)
• JVP may be raised in cardiac failure or right ventricular infarction
• Eyes: look for arcus senilis, xanthelasma
• Cardiac apex: look for double apical impulse (ventricular aneurysm)
• Auscultate for fourth heart sound, pericardial rub, pansystolic murmur of papillary muscle dysfunction (or ventricular septal defect)
Questions
What is Levine’s sign?
In acute myocardial infarction the patient often describes the pain by illustrating a clenched fist.
What is the clinical classification of myocardial infarction?
Type 1: spontaneous MI related to ischaemia caused by a primary coronary event such as plaque erosion and/or rupture, fissuring or dissection.
Type 2: MI secondary to ischaemia caused by either increased oxygen demand or decreased supply, such as coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension.
How would you use the ECG to localize STEMI?
• Anterior or anteroseptal: The QS complexes in leads V1 and V2 indicate anteroseptal infarction. A characteristic notching of the QS complex, often seen with infarcts, is present in lead V2. The septum is supplied with blood by the left anterior descending coronary artery. Septal infarction generally suggests this artery or one of its branches is occluded, whereas a strictly anterior infarct generally results from occlusion of the left anterior descending coronary artery.
• Anterolateral: ST segment elevation in leads I, L, and V1 to V6 with Q waves in V1 to V4. (Fig. 14.1B,C)
• Posterior: tall R waves in leads V1 and V2. In most cases of posterior infarctions, the infarct extends either to the lateral wall of the LV (resulting in characteristic changes in lead V6) or to the inferior wall of that ventricle (resulting in characteristic changes in leads II, III and aVF). Because of the overlap between inferior and posterior infarctions, the more general term inferoposterior is used when the ECG shows changes consistent with either inferior or posterior infarction.
• Inferior: ST elevations in leads II, III, and aVF and the reciprocal ST depressions in leads I and aVL. Inferior wall infarction is generally caused by occlusion of the right coronary artery. Less commonly, it occurs because of a left circumflex coronary obstruction.
• Right ventricular infarction: Q waves and ST segment elevations in leads II, III and aVF are accompanied by ST elevations in the right precordial leads.
This classification is not absolute, and infarct types often overlap.
How would you manage a patient with acute MI?
• In A&E, a patient with chest pain should have a quick clinical examination and an ECG done within 10 min of arrival to hospital.
• Aspirin: chewable non-coated 160–325 mg should be administered immediately and then 160–325 mg daily. In the ISIS-2 and ISIS-3 trials, 160 mg dosage was effective whereas a 325 mg dose was used successfully in GISSI-2. An initial large dose of aspirin of 325 mg orally or 160 mg chewable aspirin is preferred because lower doses may still allow significant thromboxane activity and may take a few days.
• Pain relief: immediate relief of pain should be a top priority because severe pain can result in autonomic disturbances that can result in sudden death.
• Reperfusion strategies: either thrombolysis or primary PTCA should be performed within 30 min of the patient’s arrival in hospital.
• Beta-blockers: patient should receive beta-blockers when there are no contraindications within 12 h of onset of infarction, irrespective of administration of concomitant thrombolytic therapy or performance of primary angioplasty.
• ACE inhibitors: should be administered within the first 24 h of a suspected acute STEMI in ≥2 anterior precordial leads or with clinical heart failure in the absence of hypotension (systolic BP <100 mmHg) and known contraindications to use of ACE inhibitors.
