[Pathophysiological mechanisms in stagnant hypoxia with special reference to myocardial ischaemia (author's transl)].
The extent of biochemical changes arising from hypoxia due to slowed circulation and the rate at which they occur are closely related to the degree of functional and morphological impairment of the affected organ. The pathophysiological mechanisms operating in stagnant-type hypoxia are reviewed with special reference, on account of its practical importance, to myocardiac ischaemia. Differences between regional hypoxia and damage to the whole organ, and also the additional damage caused by stoppage of the circulation are discussed in detail. The importance of adjusting the therapeutic measures to the pathophysiological regulatory mechanisms when treating ischaemic cardiac arrest or myocardiac infarction is stressed.
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000777:Anesthetics / Q000009:adverse effects; D003327:Coronary Disease / Q000150:complications*; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism; D006321:Heart / Q000503:physiopathology; D006323:Heart Arrest / Q000628:therapy; D006336:Heart Massage; D006801:Humans; D000860:Hypoxia / Q000209:etiology / Q000503:physiopathology*; D007773:Lactates / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D005996:Nitroglycerin / Q000627:therapeutic use; D009599:Nitroprusside / Q000627:therapeutic use; D012121:Respiration, Artificial
D000777:Anesthetics; D007773:Lactates; D009599:Nitroprusside; D000255:Adenosine Triphosphate; D005996:Nitroglycerin; D005947:Glucose
Stagnationshypoxie Pathophysiologische Mechanismen am Beispiel der myokardialen Ischämie.