Augmentation of cardiac function by elevation of intrathoracic pressure.
We studied the cardiovascular effects of increasing intrathoracic pressure in an acute pentobarbital-anesthetized canine model of acute ventricular failure induced by large doses of propranolol. Left ventricular (LV) function curves were generated by volume loading from LV filling pressures of 5-20 Torr. The animals were ventilated by using intermittent positive-pressure ventilation with large tidal volumes (30 ml/kg). Chest and abdominal pneumatic binders were used to increase intrathoracic pressure. When compared with the control state, acute ventricular failure was associated with a decrease in the slope of the LV function curves (P less than 0.01). After binding the increase in intrathoracic pressure (1.1 +/- 1.6 to 12.1 +/- 2.4 Torr, P less than 0.01) was associated with an improvement in both right ventricular and LV function. Our study demonstrates that in this model of acute ventricular failure, increasing intrathoracic pressure improves cardiac function. We postulate that this observed improvement with increased intrathoracic pressure is due to reduced LV wall stress in a manner analogous to that seen with arterial vasodilator therapy in congestive heart failure.
D000208:Acute Disease; D000818:Animals; D001011:Aorta / Q000503:physiopathology; D001794:Blood Pressure; D002302:Cardiac Output; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D006331:Heart Diseases / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles; D011312:Pressure; D011433:Propranolol / Q000494:pharmacology; D013909:Thorax / Q000502:physiology*
D011433:Propranolol