Infarcted tissue is an area that has suffered cell death, known as necrosis, because its blood supply was severely reduced or completely cut off. This lack of blood flow, or ischemia, deprives the tissue of the oxygen and nutrients necessary for survival. The resulting lesion of dead tissue is specifically called an infarct. This condition signifies a serious medical event, as the loss of blood flow can quickly lead to irreversible damage and loss of function.
The Cellular Process of Ischemic Necrosis
The immediate consequence of a blocked blood vessel is oxygen deprivation, or hypoxia, which initiates a cascade of destructive events within the cells. Cells normally rely on oxygen to produce the vast majority of their energy (ATP). With the oxygen supply interrupted, the cell is forced to switch to a less efficient energy production method that rapidly depletes its ATP reserves.
The failure to maintain adequate ATP levels causes the cell’s internal pumps, particularly the sodium-potassium pump, to fail. This pump regulates the balance of fluids and electrolytes, and its collapse leads to an influx of water and calcium into the cell. The cell and its internal components, the organelles, begin to swell dramatically.
This swelling marks the transition to irreversible cell death, or necrosis, as the cell membrane ultimately ruptures. The rupture releases the cell’s contents, including destructive enzymes, into the surrounding tissue. This spillage triggers a strong inflammatory reaction as the body attempts to clear the cellular debris.
Triggers and Causes of Vascular Occlusion
The event that physically stops the blood flow and leads to infarction is known as vascular occlusion. These blockages can broadly be categorized into two main groups, each with a distinct mechanism of formation and travel.
Thrombosis occurs when a blood clot, or thrombus, forms locally within a blood vessel, typically at the site of a pre-existing problem. The most common cause is atherosclerosis, where fatty deposits, or plaque, build up on the inner walls of an artery, causing the vessel to narrow and create a rough surface. If this plaque ruptures, a blood clot can quickly form over the damaged area, completely blocking the artery.
Embolism, in contrast, involves a traveling mass, called an embolus, that originates elsewhere in the body and lodges in a smaller blood vessel downstream. The embolus is often a piece of a blood clot that has broken off from a distant thrombus. However, an embolus can also consist of other materials, such as fat globules, air bubbles, or pieces of foreign material.
Other, less frequent causes of occlusion include severe, prolonged tightening of the blood vessel, known as vasospasm, which can restrict flow enough to cause tissue death. External compression from a tumor, severe swelling, or the twisting of an organ, like in testicular torsion, can also mechanically block the blood supply.
Major Organ Systems Affected by Infarction
Infarction can occur in almost any organ, but it is most commonly associated with major systems where the blockage causes immediate and life-threatening consequences. The heart is the primary site, where an obstruction in a coronary artery results in a myocardial infarction, commonly called a heart attack. This event causes a section of the heart muscle to die, which severely compromises the organ’s ability to pump blood.
The brain is the second most common location, where a blockage in an artery supplying the brain tissue leads to a cerebral infarction, also known as an ischemic stroke. The rapid death of brain cells in the affected area can cause sudden loss of function, such as weakness, paralysis, or speech difficulties.
Infarctions also affect the lungs, resulting in a pulmonary infarction, which often occurs when an embolus travels from the legs and lodges in a lung artery. This event prevents a portion of the lung from receiving blood, causing chest pain and shortness of breath. Furthermore, the kidneys can suffer a renal infarction, typically from a traveling clot that lodges in one of the renal arteries, presenting with flank pain and nausea.
Tissue Repair and Scar Formation
After the initial event and the death of the tissue, the body initiates a healing process focused on clearing the dead cells and sealing the damaged area. This response begins with an inflammatory phase where specialized immune cells invade the site to break down and remove the necrotic debris.
In most vital organs, including the heart and brain, the infarcted tissue is replaced by non-functional fibrous tissue, commonly referred to as scar tissue. Specialized cells called fibroblasts migrate into the area, proliferate, and begin to lay down a dense matrix of collagen. This scarring process structurally reinforces the wall of the organ, which is particularly important in the heart to prevent rupture.
The main consequence of scar formation is a permanent loss of function in the affected area. For example, heart muscle replaced by a collagen scar cannot contract, leading to a reduction in the heart’s overall pumping capacity. The size of this scar determines the long-term outcome, as a larger scar results in a greater functional deficit for the organ.