Effects of respiratory alkalosis and acidosis on myocardial excitation.
In anesthetized dogs electrocardiogram and monophasic action potentials (MAPs) were recorded from the right atrium and the right ventricle by intracardiac suction electrode technique. The animals were subjected, by means of ventilation with CO2 and hyperventilation, to periods of respiratory acidosis and respiratory alkalosis, respectively. Pronounced respiratory acidosis induced an increased sympathetic activity followed by a decrease in heart rate and prolongation of the A-V conduction time whereas the shape and duration of the atrial and ventricular MAPs remained unaltered. Arterial hypoxia in combination with pronounced respiratory acidosis did not influence the MAP durations. Respiratory alkalosis resulted in an increased sympathetic influence on the heart activity whereas the shape and duration of the atrial and the ventricular MAPs remained unaffected. During pronounced hyperventilation with increasing central venous pressure an increased parasympathetic influence on the heart activity with decrease in the heart rate, prolongation of the A-V conduction time and shortening of the atrial MAP duration was recorded.
D000142:Acidosis, Respiratory / Q000503:physiopathology*; D000200:Action Potentials; D000472:Alkalosis, Respiratory / Q000503:physiopathology*; D000818:Animals; D016275:Atrial Function; D004285:Dogs; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology*; D006339:Heart Rate; D008297:Male; D009200:Myocardial Contraction; D013997:Time Factors; D016276:Ventricular Function