Intermittent claudication--pathophysiological considerations.
Intermittent claudication is a non-pathognomic symptom elicited by an inbalance between the metabolic demands of the exercising skeletal muscle and its blood supply. In normal conditions hyperemia to the working muscles will be impaired during the exercise by mechanical compression of the microvessels. The resulting anaerobic metabolism will cause further vasodilatation. Both phenomena (exercise and reactive hyperemia) contribute to a maximal increase in local blood flow as soon as the exercise is stopped. If the local circulation is impaired by occluding arterial disease (eventually complicated by aggravating factors) the tolerance to skeletal work is lowered and the circulatory reserves are entirely exhausted as demonstrated by the ischemic exercise-test. In the case of a major obstruction and poor collateralisation, a "steel phenomenon" may occur. The pharmacotherapeutic possibilities to cope with in this situation are briefly discussed.
D000255:Adenosine Triphosphate / Q000378:metabolism; D003097:Collateral Circulation; D006801:Humans; D007383:Intermittent Claudication / Q000378:metabolism / Q000503:physiopathology*; D009119:Muscle Contraction; D009132:Muscles / Q000098:blood supply / Q000378:metabolism; D010100:Oxygen / Q000097:blood; D012039:Regional Blood Flow
D000255:Adenosine Triphosphate; D010100:Oxygen