Cause of death after acute coronary occlusion

2021-05-17 04:54 PM

When the heart becomes unable to generate enough force to pump enough blood to the arterial branches, heart failure and necrosis of peripheral tissues ensue as a result of peripheral ischemia.

(1) decreased cardiac output (2) pulmonary oedema, pulmonary oedema (3) ventricular fibrillation (4) rupture of the heart wall.

Decreased cardiac output - cardiogenic shock

When some heart muscle fibres do not work and others are too weak to exert a great force, the ventricles cannot pump enough blood. Indeed, the overall pumping power of the ischemic heart often decreases, a phenomenon known as systolic strain. That is, when the normal portion of the ventricular muscle, the ischemic portion of the heart muscle, whether it is dead or simply not functioning, replaces pressure on the outside of the artery with lateral growth. in the ventricles. Thus, much of the pumping force of the ventricles is dissipated by the distension of non-functional areas of the myocardium.

When the heart becomes unable to generate enough force to pump enough blood to the arterial branches, heart failure and necrosis of peripheral tissues ensue as a result of peripheral ischemia. This condition is called coronary shock, cardiogenic shock, circulatory shock. The cardiogenic shock almost always occurs when more than 40 percent of the left ventricular muscle is ischemic, and death occurs in more than 70 percent of patients with cardiogenic shock.

Figure. Systolic strain in ischemic myocardium.

Venous system stasis

When the heart is not pumping blood forward, it must prevent blood from returning to the heart from the blood vessels of the lungs or in the circulatory system. This leads to increased capillary pressure, especially in the lungs.

Blocking blood in the veins is usually less of a problem in the first few hours after a heart attack. Symptoms are aggravated by: decreased cardiac output resulting in decreased blood flow to the kidneys. The kidneys do not excrete an insufficient amount of urine which increases the blood volume leading to congestion. Consequently, many patients are well after the sudden onset of heart failure leading to acute pulmonary oedema and will usually die within a few hours of the onset of pulmonary symptoms.

Ventricular fibrillation

Many people die from coronary occlusion, death occurs due to sudden ventricular fibrillation. There is a predisposition to ventricular fibrillation after a large infarct, but sometimes ventricular fibrillation can occur after small vessel occlusion. Indeed, some patients with chronic coronary insufficiency die suddenly from ventricular fibrillation without any acute infarction.

Ventricular fibrillation undergoes two phases after a coronary infarct. The first phase is within 10 minutes after the infarction occurs. There is then a relatively safe short period, followed by a second phase, which stimulates the heart for 1 hour or so and lasts for a few hours. Ventricular fibrillation can also occur days after infarction, but that is less likely.

At least 4 factors in ventricular fibrillation:

1. Loss of blood supply to the myocardium causes a rapid depletion of potassium in the myocardium. This also increases the concentration of potassium in the extracellular fluid surrounding the myocardium. In experiments, increased extracellular fluid K concentration increased the possibility of ventricular fibrillation.

2. Myocardial ischemia due to "traumatic" causes related to the electrocardiogram of patients with acute myocardial infarction. Because muscles often do not respond to the pulse after each heartbeat. Thus, pulses emitted from the sinus node cross the ischemic region to the normal areas and ventricular fibrillation can occur.

3. The sympathetic reflex usually develops after a major infarction, mainly because the heart does not pump an adequate volume of blood into the arteries, resulting in a drop in blood pressure. Sympathetic stimulation is increased and the myocardium is easily excitable, so ventricular fibrillation occurs.

4. Excessive myocardial dilation during infarction often causes excessive ventricular dilatation. This over-dilation increases the length of impulse conduction from the sinus node and frequently causes abnormal conduction pathways around the ischemic area.

Heart wall rupture in the area of ‚Äč‚Äčischemia

During the first day or after acute infarction, there is little risk of rupture of the heart wall in the ischemic portion. But a few days later, the muscle fibres begin to degenerate, and the heart wall is stretched thin. When this happens, the necrotic myocardium bulges out to such an extent that with each contraction of the heart, the systolic blood pressure increases more and more until the heart wall ruptures. In practice, ultrasound is used to assess myocardial infarction severity.

When the ventricular wall ruptures, blood rushes into the pericardium causing cardiac tamponade and blood cannot enter the right atrium, and the patient dies from a sudden decrease in cardiac output.