Effects of respiratory alkalosis on coronary vascular dynamics and myocardial energetics in patients with coronary artery disease.
To determine if respiratory alkalosis produces hemodynamically significant coronary vasoconstriction in coronary artery disease (CAD), we studied the effects of hyperventilation on coronary sinus blood flow (CSBF), myocardial O2 uptake, and lactate extraction in 13 CAD patients. No patient developed chest pain or ischemic ECG changes during hyperventilation. Hyperventilation increased pressure-rate product (myocardial O2 consumption index, MVO2) minimally did not change global CSBF, coronary vascular resistance or lactate extraction. However, hyperventilation increased global myocardial O2 uptake from 14.5 plus or minus 3.2 to 18.7 plus or minus 17.2 ml/min (p less than 0.01) principally due to increased myocardial O2 extraction (65.0 plus or minus 7.4 to 71.6 plus or minus 6.2%, p less than 0.01). The increased pressure-rate product was not sufficient to account for increased myocardial O2 uptake. We conclude that respiratory alkalosis increases myocardial O2 extraction but does not produce hemodynamically significant coronary vasoconstriction in CAD patients.
D000328:Adult; D000472:Alkalosis, Respiratory / Q000503:physiopathology*; D003327:Coronary Disease / Q000503:physiopathology*; D004734:Energy Metabolism; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption