Q-wave myocardial infarction on ECG

Morphological basis and ECG criteria

The evolution of diagnostic approaches to acute coronary events has led to a close correlation between anatomical changes and the ECG pattern.

Historically and clinically, two main types of injury are distinguished:

• Transmural myocardial infarction (Q-wave MI). In this variant, necrosis extends through the entire thickness of the ventricular muscle wall. Dead tissue loses its ability to conduct electrical impulses, creating a sort of "electrical window". On the ECG, this is manifested by the appearance of a deep and wide pathological Q wave. Additionally, an upward displacement of the ST segment from the isoelectric line is recorded.
• Nontransmural (small focal) infarction. The necrosis zone is limited and typically located in the subendocardial layers. Since a significant portion of the wall remains viable, a pathological Q wave does not form. Electrical anomalies exclusively affect the terminal part of the ventricular complex—changes are recorded in the ST segment and T wave.

The role of the disease in the Acute Coronary Syndrome (ACS) concept

At the initial patient contact stage, physicians face a major challenge in early diagnosis. The clinical picture and initial ECG changes in various types of ischemia can be absolutely identical. Pain syndrome (pressing, squeezing retrosternal pain) is often prolonged (more than 30 minutes) in both myocardial infarction and unstable angina attacks. Moreover, specific ECG signs (ST elevation, Q wave formation) and elevated blood enzyme levels can be significantly delayed.

This is why, until the diagnosis is definitively clarified, the working term Acute Coronary Syndrome (ACS) is used. This group encompasses unstable angina, non-Q-wave myocardial infarction, and Q-wave myocardial infarction.

Initial ACS diagnosis is based on three pillars:

1. Pain characteristics: typical pressing or squeezing retrosternal localization.
2. History: history of prior infarctions or angina.
3. Risk factors: presence of arterial hypertension, diabetes mellitus, positive family history.

Differential diagnosis algorithm

The diagnosis is definitively verified within several hours or days. The basis is dynamic ECG monitoring and blood tests for cardiospecific markers (myoglobin, troponins, CK-MB fraction).

• Large focal infarction: characterized by the appearance of a pathological Q wave and ST-segment elevation. Necrosis markers are significantly elevated.
• Non-Q-wave infarction: pathological ST and Q changes are absent, but enzymes exceed the normal limit by more than two times.
• Unstable angina: no specific ECG changes, enzyme levels remain within normal limits.

Particular attention is required for differentiation from non-coronary pain, which may be of neuromuscular origin. Important nuance: such patients may have old scar changes on the electrocardiogram from previous conditions. These traces should not mislead the physician when evaluating the current pain attack.

ECG differences between infarction and acute pericarditis

In clinical practice, it is often necessary to differentiate ischemic injury from pericardial inflammation.

Assessment of background pathology and heart failure

Transmural necrosis often leads to a decrease in cardiac pumping function. Although the ECG has no specific signs of heart failure (HF) itself, it reveals background pathology: myocardial hypertrophy, bundle branch blocks, arrhythmias, and old scars (persistent Q wave).

To confirm HF and assess hemodynamics, instrumental methods are used:

• Echocardiography (Ultrasound of the heart): reveals chamber dilation (primarily the left ventricle), increased end-diastolic and end-systolic dimensions, as well as a reduced ejection fraction (EF).
• Chest X-ray: shows signs of congestion (root dilatation, enhanced markings, blurred contours due to perivascular tissue edema), pleural effusion, and cardiomegaly (cardiothoracic index > 50%).
• Blood flow velocity assessment: in HF, blood flow is slowed. In addition to complex scintigraphy, the magnesium sulfate test is used. 2 ml of a 25% solution is administered intravenously; normally, a sensation of warmth in the tongue occurs no later than 14 seconds later.
• Invasive catheterization: makes it possible to record an increase in left ventricular end-diastolic pressure (LVEDP) and elevated pressure in the pulmonary artery system.

To monitor treatment efficacy and assess the body's functional reserves, stress tests (such as bicycle ergometry) and repeat measurement of the magnesia time are additionally used.

Class and exam questions

What else to study on this topic

• Cardiospecific necrosis markers: troponins, myoglobin, and CK-MB
• Echocardiographic criteria for systolic dysfunction and ejection fraction (EF) assessment
• Radiological signs of pulmonary congestion
• Performing and interpreting the magnesium sulfate test
• Stress testing in cardiology: bicycle ergometry technique

Other topics in the "Cardiovascular system" section

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