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Orthopedics Torniquets....The Physiological cost..part 1




Tourniquets have significant risks, and these risks and the strategies to minimize them should be part of the knowledge base of all practicing anesthesiologists.

Limb exsanguination causes an increase in central blood volume that is reflected as a transient rise in central venous pressure.
Tourniquet inflation also causes an increase in afterload. Patients with diminished cardiac function may not be able to tolerate this combined insult of increased preload and afterload.

After tourniquet deflation, preload decreases acutely as blood reenters the affected extremity, which undergoes a period of postischemic reactive hyperemia. This
is accompanied by an acute decrease in afterload that often produces hypotension.

During limb ischemia, oxygen and high-energy phosphate stores decrease progressively, and carbon dioxide and lactic acid levels rise as ischemic tissues convert to anaerobic metabolism.

The pH of the ischemic limb decreases as the duration of ischemia increases.

After tourniquet deflation, aerobic metabolism resumes, with marked increases in oxygen consumption and carbon dioxide production.

Systemic partial pressure of carbon dioxide increases in this interval, and pH transiently decreases as a result of combined metabolic and respiratory acidosis.

Ultrastructural changes within the endothelium of the ischemic capillaries lead to diffuse capillary leak after reperfusion.

In conjunction with reactive hyperemia, significant edema can develop after tourniquet deflation. This can even lead to a compartment syndrome in the affected extremity.
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