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Propedeutics · Additional topics

First aid for myocardial infarction

Angina pectoris

The fundamental cause of an acute coronary event is a severe imbalance between the myocardial oxygen demand and the actual delivery volume. In nearly half of patients with acute coronary insufficiency, myocardial infarction—which can lead to fatal complications—is the first manifestation of the pathology.

CHD mortalityaccounts for 54.4% of all cardiovascular deaths
Critical stenosisNarrowing of the lumen of at least one coronary artery by more than 75%
MarkersTroponins T and I, as well as the CK-MB fraction, are the main laboratory signs of necrosis
Cardiogenic shockOccurs due to a sharp decline in the heart's pumping function with a preserved circulating blood volume (CBV)
3 min readFor medical studentsUpdated 10.10.2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesPending instructor review

Causes and mechanisms of coronary insufficiency

The underlying mechanism of the attack is coronary artery disease (CAD), whose primary clinical syndrome is traditionally angina pectoris (formerly known as "breast pang"). Most cases (over 90%) are associated with stenosing atherosclerosis of the coronary vessels. When an atherosclerotic plaque blocks the arterial lumen by more than 75%, critical stenosis develops. Under such conditions, adequate blood flow is impossible even with minimal physical activity, leading to severe ischemia, infarction, or sudden cardiac death.

The European Society of Cardiology (ESC, 2019) proposes using the term Chronic Coronary Syndromes (CCS) to describe stable forms of the disease, emphasizing its dynamic nature. Several CCS scenarios are distinguished, including patients with dyspnea, left ventricular dysfunction, as well as individuals with a history of acute coronary syndrome (ACS) or revascularization. Despite this, CAD remains the leading term in domestic practice. The epidemiological picture shows that the prevalence of this pathology steadily increases with age: in older men it reaches 14%, and in women, 12%.

Emergency and routine diagnostic methods

The primary step in providing care and establishing a diagnosis remains history taking and physical examination. A thorough medical history allows for the suspicion of acute ischemia even before lab results are available.

To confirm myocardial infarction (especially in the absence of a pathognomonic Q wave on the ECG), laboratory diagnostics is critically vital. In the first hours after the onset of the pain attack, an increase in specific markers is registered:

  • Troponin T and Troponin I;
  • Titer of the creatine kinase MB fraction (CK-MB).

Additionally, the lipid profile (LDL, HDL, VLDL, triglycerides, and total cholesterol) and carbohydrate metabolism (hyperglycemia) are assessed, which is especially important for patients with obesity.

Among instrumental methods, ECG remains the gold standard, registering changes in the electrical field of the heart. For advanced analysis, the following are used:

  1. Echocardiography (ultrasound) — reveals decreased contractile activity, diastolic relaxation abnormalities, and valvular changes.
  2. Holter monitoring — dynamic rhythm assessment.
  3. Invasive coronary angiography — the decisive method for visualizing arterial atherosclerosis.
  4. Radionuclide methods (thallium-201 Tl scintigraphy) — allow differentiation between viable (hibernating) myocardium and irreversibly damaged tissue.
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Acute vascular failure and complications

The severe course of myocardial infarction can be complicated by critical conditions requiring immediate intervention.

Syncope (fainting) — brief loss of consciousness due to transient reduction of cerebral blood flow. Cardiogenic syncope often occurs against the background of arrhythmias or acute infarction. Important rule: any fainting episode occurring during physical exertion is initially regarded as a manifestation of cardiac pathology.

Collapse is characterized by a pronounced mismatch between the circulating blood volume (CBV) and the vascular bed capacity. Unlike syncope, the patient is conscious during collapse, although consciousness may be altered. The cause of cardiogenic collapse is acute myocardial weakness.

The most formidable complication is shock — circulatory collapse developing after an overwhelming impact on homeostasis. In myocardial infarction, cardiogenic shock occurs. Its pathogenesis consists of a primary drop in cardiac output (due to myocardial necrosis or cardiac tamponade) with initially preserved CBV. This fundamentally distinguishes it from hypovolemic or distributive (vascular) shock, where fluid loss or total vasodilation is the leading factor.

Class and exam questions

What is the main cause of angina pectoris and myocardial infarction?

The main cause is stenosing atherosclerosis of the coronary arteries. It leads to an imbalance between myocardial oxygen demand and its actual delivery.

Which laboratory parameters confirm myocardial cell death?

When infarction is suspected (especially without a Q wave), the levels of Troponin T, Troponin I, and the creatine kinase MB fraction (CK-MB) are examined.

How does cardiogenic shock differ from hypovolemic shock?

In cardiogenic shock, there is a sharp drop in the heart's pumping function, but the circulating blood volume (CBV) remains preserved. In hypovolemic shock, there is an absolute decrease in CBV due to blood loss or dehydration.

What is the significance of syncope during physical exertion?

Any syncopal episode (fainting) occurring during physical exertion must be regarded primarily as a sign of serious cardiac pathology.

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What else to study on this topic

  • Clinical scenarios of chronic coronary syndromes (CCS)
  • Pathogenesis and types of syncope (vasovagal, orthostatic, sinocarotid)
  • Principles of echocardiography and assessment of LV contractility
  • Myocardial scintigraphy: distinguishing hibernating myocardium from scar tissue
  • Septic and anaphylactic shock: mechanisms of vasodilation

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