Tissue Death by Deprivation: The Mechanism of Infarction

Introduction

Infarction is a pathological condition that refers to the death (necrosis) of tissue due to inadequate blood supply. This process occurs when the flow of oxygenated blood to a specific region is either completely blocked or severely reduced. The lack of oxygen (hypoxia) and nutrients leads to irreversible damage and death of the affected cells. Infarction is a major cause of morbidity and mortality worldwide, forming the underlying basis of many critical conditions such as myocardial infarction (heart attack), cerebral infarction (stroke), and pulmonary infarction.

The term “infarct” describes the actual area of dead tissue resulting from the interrupted blood flow. The severity and extent of infarction depend on the duration of ischemia, the type of tissue involved, and the availability of collateral circulation.


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Pathophysiology

The development of infarction begins with ischemia, a state where the blood flow to a tissue is insufficient to meet its metabolic demands. When ischemia persists, cells are deprived of oxygen and nutrients, leading to a switch from aerobic to anaerobic metabolism. This change causes accumulation of lactic acid, decreased ATP production, and failure of ion pumps in cell membranes. As a result, cells swell, lose membrane integrity, and eventually undergo necrosis.

The body’s response to this injury involves inflammation and repair. Initially, the necrotic area becomes pale or hemorrhagic depending on the type of infarction. Later, macrophages remove the dead tissue, and fibroblasts and new blood vessels invade the area, forming granulation tissue. Ultimately, the infarcted area is replaced by fibrous scar tissue, which is non-functional.


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Causes of Infarction

Infarction can be caused by various conditions that impede blood flow. The most common causes include:

1. Thrombosis:
Formation of a blood clot within a vessel, often due to atherosclerosis. This is the most frequent cause of infarction in arteries supplying the heart, brain, and other organs.


2. Embolism:
A clot or foreign material (fat, air, amniotic fluid) that travels through the bloodstream and lodges in a vessel, blocking blood flow downstream.


3. Atherosclerosis:
Progressive narrowing of arteries by fatty plaques reduces blood flow and increases the risk of complete occlusion.


4. Vasospasm:
Sudden constriction of a blood vessel, which can transiently stop blood flow (e.g., in variant angina).


5. External compression:
Pressure from tumors, edema, or torsion (as seen in volvulus or testicular torsion) can cut off blood supply to tissues.


6. Trauma or rupture of vessels:
Physical injury or rupture can directly interrupt circulation, leading to localized infarction.

1. Infarction: Causes, Types, and Morphology Classification, Factors Influencing Development, and Pathophysiological Basis

2. Definition of Infarction Localized area of ischemic necrosis caused by occlusion of arterial supply or venous drainage.

3. Causes of Infarction Arterial thrombosis or embolism (most common). Venous thrombosis. Twisting of vessels (torsion). Compression by tumor or edema.

4. Types of Infarction (By Color) White (pale) infarct – arterial occlusion in solid organs (heart, spleen, kidney). Red (hemorrhagic) infarct – venous occlusion or dual blood supply organs (lungs, liver).

5. White or Pale Infarct Due to arterial occlusion in end-arterial organs. Reason for pallor: Lack of RBC seepage into necrotic area. Becomes firm and sharply demarcated.

6. Red or Hemorrhagic Infarct Occurs in lungs, intestine, or organs with dual blood supply. Blood leaks into infarcted tissue giving red color. May also occur after reperfusion of an occluded artery.

7. Morphology of Infarct Ischemic coagulative necrosis (except brain). Wedge-shaped, apex points to occluded vessel. Inflammatory reaction develops at margins within hours.

8. Factors Influencing Development 1. Nature of vascular supply. 2. Rate of occlusion development. 3. Vulnerability of tissue to hypoxia. 4. Oxygen content of blood.

9. Rate of Development of Occlusion Slowly developing occlusions allow collateral circulation. Sudden occlusion → infarction due to lack of time for adaptation.

10. Vulnerability to Hypoxia Neurons: Irreversible injury after 3–4 minutes. Myocardial cells: 20–30 minutes. Skeletal muscle: Several hours.

11. Oxygen Content of Blood Low oxygen levels increase infarction risk. Anemic or cyanotic patients more prone to infarction.