Symptoms and Signs

Patients usually present with sudden onset central crushing chest pain, which may radiate down either arm (but more commonly the left) to the jaw, back or neck. The pain lasts longer than 20 min and is not relieved by glyceryl trinitrate (GTN). The pain is often associated with dyspnoea, nausea, sweatiness and palpitations. Intense feelings of impending doom (angor animi) are common. Some individuals present atypically, with no symptoms (silent infarct, most common in diabetic patients with diabetic neuropathy), unusual locations of the pain, syncope or pulmonary oedema. The pulse may demonstrate a tachycardia or bradycardia. The blood pressure is usually normal. The rest of the cardiovascular system examination may be unremarkable, but there may be a third or fourth heart sound audible on auscultation as well as a new and/or worsening murmur, which may be due to papillary muscle rupture in the left heart.

Investigations

• ECG: ECG changes associated with myocardial infarction (MI) indicate the site and thickness of the infarct. The first ECG change is peaking of the T wave. ST segment elevation then follows rapidly in a ST elevation myocardial infarction (STEMI).
  
• Troponin I: elevated plasma concentrations of troponin I indicates that myocardial necrosis has occurred. Troponins begin to rise within 3–12 h of the onset of chest pain and peak at 24–48 h and then clear in about 2 weeks. It is important that a troponin level is interpreted in the clinical context, because conditions other than MI can damage cardiac muscle (e.g. heart failure, myocarditis, pericarditis, pulmonary embolism or renal failure). Patients presenting with suspected acute coronary syndromes (ACS) should have troponin measured at presentation. If it is negative, it should be repeated 12 hours later. If the 12 h troponin is also negative, then MI but not unstable angina can be excluded.

Management

Immediate 

In the ambulance or on first medical contact, individuals with suspected MI are immediately given 300 mg chewable aspirin and 300 mg clopidogrel to block further platelet aggregation. Two puffs of GTN are sprayed underneath the tongue. The patient is assessed by brief history and a clinical examination, and a 12-lead ECG is recorded. The patient is given oxygen via a face mask. Morphine, which has vasodilator properties, together with an anti-emetic (e.g. metoclopramide) is administered to relieve pain and anxiety, thus reducing the tachycardia that these cause. A β-blocker (e.g. metoprolol) should be given unless contraindicated (e.g. LV failure or moderate to severe asthma) because β-blockers decrease infarct size and have a positive effect on mortality. The preferred treatment of a confirmed STEMI is revascularization with percutaneous coronary intervention

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