Effect of autonomic blockade on the hemodynamic findings in acute cardiac tamponade.
Twenty-three closed-chest, alpha-chloralose-anesthetized, volume-expanded, alpha- and beta-adrenergic-blockaded dogs with rate fixed by atrial pacing had 30-90 ml of saline at 37 degrees C infused into the pericardial sac a) with vagus intact, b) after vagotomy, and c) with vagus intact but with systolic pressure augmented with a balloon. A significant reduction in left ventricular (LV) systolic pressure (SP), and cardiac output (CO) occurred at a pericardial volume of 30-60 ml, when LV end-diastolic (ED) and right atrial (RA) pressures were not increased. Whereas the percentage decline of CO, LVSP, maximum negative and maximum positive dP/dt was greater in group A (vagus intact) than in group B (vagus cut), significant residual depressed performance was demonstrated only in group B. In four paced, atropinized, beta-blockaded dogs, response to tamponade was similar to that in intact dogs; vagotomy at 90 ml in these dogs resulted in a fall in CO, a rise of LVSP and a significant elevation in LVED and RA pressures. Thus, in the early phases of cardiac tamponade a sympathetic neurohumoral response supports cardiac performance while the vagus nerve exerts a myocardial protective effect. Vagal afferents appear to modulate this response.
Effect of autonomic blockade on the hemodynamic findings in acute cardiac tamponade. Twenty-three closed-chest, alpha-chloralose-anesthetized, volume-expanded, alpha- and beta-adrenergic-blockaded dogs with rate fixed by atrial pacing had 30-90 ml of saline at 37 degrees C infused into the pericardial sac a) with vagus intact, b) after vagotomy, and c) with vagus intact but with systolic pressure augmented with a balloon. A significant reduction in left ventricular (LV) systolic pressure (SP), and cardiac output (CO) occurred at a pericardial volume of 30-60 ml, when LV end-diastolic (ED) and right atrial (RA) pressures were not increased. Whereas the percentage decline of CO, LVSP, maximum negative and maximum positive dP/dt was greater in group A (vagus intact) than in group B (vagus cut), significant residual depressed performance was demonstrated only in group B. In four paced, atropinized, beta-blockaded dogs, response to tamponade was similar to that in intact dogs; vagotomy at 90 ml in these dogs resulted in a fall in CO, a rise of LVSP and a significant elevation in LVED and RA pressures. Thus, in the early phases of cardiac tamponade a sympathetic neurohumoral response supports cardiac performance while the vagus nerve exerts a myocardial protective effect. Vagal afferents appear to modulate this response.