Acute ST-Elevation Myocardial Infarction (STEMI) Cardiology Physiotherapy

Clinical Features of Acute ST-Elevation Myocardial Infarction (STEMI)

In this article we will discuss the Clinical Features of Acute ST-Elevation Myocardial Infarction (STEMI)

In this article, we will discuss the Clinical Features of Acute ST-Elevation Myocardial Infarction (STEMI). So, let’s get started.

Clinical Features

The myocardial infarction is characterized by typical anginal pain at rest which is more severe and prolonged, radiates to left arm or to the other sites and is associated with signs and symptoms of sympathetic overactivity i.e. sweating, feel weak and apprehensive. They may have associated symptoms, e.g. vomiting, dyspnea etc. About 25% of AMI may have atypical symptoms such as atypical chest pain, nausea, vomiting, dyspnea, fatigue, exhaustion, etc. Myocardial infarction may also be painless, masquerade as the development or worsening of CHF, appearance of an arrhythmia (more common in anterior MI), an overwhelming sense of apprehension, profound exhaustion, acute indigestion, pericarditis, stroke or peripheral embolism.

The sign and symptoms are given below:


Prolonged and severe retrosternal chest pain radiating to left arm, throat, shoulder, epigastrium and back. Most infarction pain occur at rest and early morning hours.

Anxiety, fear, apprehension of impending death. Patient move about in the bed seeking a position of comfort.

Nausea, vomiting, sweating, feeling of weakness. Dyspnea, orthopnea, cough. Giddiness or syncope or collapse. Painless infarction occur in one-third patient specially in older women and diabetics.


Signs of sympathetic overactivity usually present, e.g. pallor, perspiration, tachycardia.

Signs of vagal stimulation may be present as an inferior wall infarction, e.g. bradycardia.

Signs of myocardial dysfunction and/or left heart failure may be evident if complicated:

Cold extremities, hypotension or shock or fall in BP in patients with hypertension


Low volume pulse, low pulse pressure and arrhythmia (e.g. UPCs)

Quiet first heart sound

Diffuse apical thrust. Midsystolic murmur of papillary muscles dysfunction may be present

Fine crackles at the bases, respiratory distress, and S3 gallop.

Signs of tissue damage, e.g. fever leukocytosis and raised ESR.

Heart examination, e.g. pericardial rub may be present midsystolic or parasystole kamar due to mitral regurgitation aur papillary muscle dysfunction at not com soft heart sounds and atrial gallop (S4) is common than ventricular gallop (S3).

About 50% of patients die before they arrived at hospital the cause of death is cardiac arrest due to ventricular fibrillation.

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