Etiological Classification
Depending on the factors causing blood flow reduction, four main types of arterial ischaemia are distinguished:
- Angiospastic. Occurs due to arterial spasm triggered by neural, hormonal, or pharmacological factors (e.g., during stress, angina pectoris, or appendicular colic). The pathogenesis is driven by an excess of vasopressor agents in the blood: angiotensin II, vasopressin, and catecholamines. The clinical course is always acute.
- Obstructive. Associated with partial or complete closure of the arterial lumen from within. The acute form is triggered by a thrombus or embolus, while the chronic form results from the gradual growth of an atherosclerotic plaque.
- Compressional. Develops when a vessel is compressed from the outside. Causes include a tourniquet, severe edema, or a growing tumor. The process can be either acute or chronic.
- Redistribution. Occurs after the rapid release of external compression (e.g., rapid removal of ascetic fluid or a large tumor). Blood rushes abruptly into previously ischaemic vessels, "stealing" flow from adjacent organs. The course is always acute.
Clinical and Pathophysiological Manifestations
Symptoms directly depend on the degree of blood supply reduction and profound microcirculatory disturbances. Ischaemic tissue undergoes a series of characteristic changes:
- Pallor and local hypothermia. The organ becomes pale due to the constriction of superficial vessels and a decrease in the number of functioning capillaries. Tissue temperature drops because of reduced warm arterial inflow and suppressed oxidative processes (decreased heat production).
- Hemodynamic shifts. Arterial pulsation weakens. Hydrodynamic pressure drops, along with linear and volumetric blood flow velocities. Arteries, veins, and microvessels constrict. A sharp pressure drop in capillaries ultimately leads to blood flow arrest — stasis.
- Decreased tissue turgor and volume. Tissue becomes flaccid, and the organ decreases in size. This results from diminished vascular filtration and loss of intercellular fluid.
- Impaired lymph drainage. Lymph formation and outflow processes are significantly diminished.
- Pain syndrome and paresthesias. Patients experience numbness, tingling («pins and needles»), and severe pain. Pain is caused by the accumulation of specific mediators in the hypoxic zone: kinins, histamine, prostaglandins, potassium ions ($K^+$), as well as lactic and pyruvic acids.
Morphology and Outcomes of Ischaemia
The foundation of all ischaemic tissue damage is hypoxia. The nature and severity of morphological changes depend on the duration and degree of blood deficiency, the presence of collateral vessels, and the specific organ's sensitivity to oxygen deprivation.
- In acute ischaemia, dystrophic and necrotic changes develop rapidly in tissues (resulting in infarction).
- In chronic ischaemia, the process is slower, allowing collateral circulation to form, which partially compensates for the hypoxia. Consequently, atrophic and sclerotic changes come to the foreground.
A crucial role belongs to the functional state of the organ, which dictates its metabolic rate and oxygen demand. The higher the functional activity, the more severe the damage. This principle is utilized in medicine: for instance, induced hypothermia reduces tissue $O_2$ demand, enabling safe cardiac surgery under cardiopulmonary bypass.