Donald G. Breazeale

Relationship of Pericardial to Pleural Pressure During Quiet Respiration and Cardiac Tamponade

Pericardial pressure was studied in chronic experiments on dogs with relation to intrathoracic pressure in the normal state and in cardiac tamponade. In the normal resting animal, the two pressures were in good agreement throughout the respiratory cycle. The cardiac cycle produced superimposed pressure fluctuations amounting to 30% of the respiratory swings. Adding saline to the pericardial sac produced sigmoid pressure-volume curves; tamponade required 100 to 330 ml of fluid. Although during tamponade the pericardial pressure greatly exceeded the intrathoracic pressure, the pericardial pressure invariably fell with inspiration, generally by the same amount as the intrathoracic pressure. The cardiac cycle produced greater pressure fluctuations (50% of the respiratory pressure fluctuations). The superior vena caval pressure always fell with inspiration in the normal state and during tamponade. Hypovolemia did not change the resting pericardial pressure, but decreased the slope of the pressure-volume curve measured during cardiac tamponade. Hypervolemia increased the resting pericardial pressure considerably, and increased the slope of the pericardial pressure-volume curve. The results suggest that pleural pressure is a reasonable approximation of the pericardial pressure in normal dogs. There appears to be no substantial evidence that pulsus paradoxus is due to failure of the pericardial sac to transmit inspiratory reductions of pleural pressure.

Effect of Respiration on Venous Return and Stroke Volume in Cardiac Tamponade

In 40 lightly anesthetized dogs, 5 to 30 days after surgical preparation, flow was measured simultaneously in the venae cavae, pulmonary artery, pulmonary vein, and aorta with ultrasonic flowmeters. Intrapleural and pericardial pressures were measured via silastic cannulas. Pulmonary vein diameter was monitored by miniature mutual inductance coils. In the resting animal with sinus arrhythmia, inspiration increased heart rate and flow in the vena cava, and to a lesser extent, in the pulmonary vein. Left ventricular stroke volume (LVSV) varied directly with the right ventricular stroke volume (RVSV) in dogs with slow heart rates. Cardiac tamponade invariably caused tachycardia and a marked decrease in cardiac output, arterial pressure, pulse pressure, and stroke volume; venous pressure and diameter increased. Pericardial pressure, although markedly elevated, fell with inspiration paralleling the fall in intrapleural pressure. Flow in the pulmonary vein rose or remained constant with inspiration. Pulmonary vein diameter frequently increased with inspiration during tamponade, but only after the pulmonary artery diameter increased with the inspiratory surge. LVSV did not decline sharply with inspiration, and actually increased within 2 beats of the increase in RVSV. The sum of LVSV plus RVSV increased markedly with inspiration, contradicting the concept of fixed intrapericardial volume. Almost all of the changes of pulsus paradoxus reflect the normal respiratory effects on the RVSV, delayed by transit through the pulmonary bed and exaggerated by the small LVSV in a vasoconstricted state.

Whole body protection during three hours of total circulatory arrest: An experimental study☆

Survival following 3 hr of total circulatory arrest under profound hypothermic conditions was explored in 19 adult mongrel dogs. Thermoregulatory management included combined surface/perfusion hypothermia and azeotrope anesthesia in 95% O2/5% CO2. All animals were resuscitated and survived for at least 12 hr. During the last seven trials (Group II) the following principles were applied: uniform whole-body cooling where differences between rectal, esophageal, and pharyngeal temperatures averaged less than 1 degree C, induction of circulatory arrest at approximately 3 degrees C, constant lung inflation (10-12 cm H2O between 20 degrees C cooling and 20 degrees C rewarming, including the 3-hr arrest period) and ventilation assistance with positive end-expiratory pressure (4 cm H2O) after 20 degrees C rewarming, intraoperative maintenance of colloid osmotic pressure (COP) above 11 mm Hg, replacement of the cooling perfusate with a colloid-rich rewarming prime (COP = 15 mm Hg) and restoration of hemostasis with fresh whole blood transfusions. The application of these principles resulted in the long-term survival of five animals with four survivors displaying no clinically detectable neurological abnormalities. However, two animals developed optic impairment and one animal died from intusseption on the fourth postoperative day. Despite the improved results, it should also be noted that during pilot (Group I) studies (from which the aforementioned principles were derived) fatalities from complications attributed to systemic edema, central nervous system, or pulmonary or coagulation dysfunctions occurred in 9 out of 12 trials. We conclude that whole body protection following 3 hr of total circulatory arrest at a uniform temperature less than 5 degrees C can be successfully accomplished.

Effect of verapamil on regional myocardial contraction during graded ischemia in the dog.

Summary: Verapamil benefits patients with angina pectoris during exercise. The mechanism underlying this effect is controversial. A direct oxygen-sparing effect on ischemic myocardium has been proposed, but previous studies seeking to demonstrate this effect have been inconclusive because of inadequate control of systemic hemodynamics. This study has assessed the direct effects of verapamil on regional myocardial contraction during graded coronary flow reductions while blood pressure and heart rate were held constant. Verapamil caused a decrease in regional contraction at normal levels of coronary flow, a finding consistent with a negative inotropic effect. At lower coronary flows, however, ischemic dysfunction was similar in the presence and absence of verapamil. These findings fail to support the concept that verapamil either selectively depresses ischemic myocardium or enhances myocardial function during ischemia. Thus, these direct mechanisms would seem unlikely causes of the observed beneficial effect during excercise in patients with coronary artery disease.

Whole-body temperature gradients under surface, perfusion, and combined surface/perfusion hypothermia

Using various methods of hypothermia and halothane-diethyl ether azeotrope anesthesia whole-body temperature gradients were evaluated in 20 adult mongrel dogs. Simultaneous measurements were taken of brain, rectal, esophageal, pharyngeal, liver, jugular vein, shoulder muscle, thigh muscle, and subcutaneous temperatures during (i) surface, (ii) perfusion (slow and rapid cooling), and (iii) combined surface/perfusion methods of hypothermia. Throughout cooling and rewarming core temperature gradients averaged 1.2 °C and during circulatory arrest core temperatures decreased an average of 0.3 °C under pure surface hypothermia. Animals, thermoregulated by extracorporeal methods only, developed larger core temperature gradients during cooling and a significant increase (average = 3.1 °C) was noted in core temperatures during circulatory arrest. This pattern was particularly pronounced during rapid perfusion cooling. Hypothermia induction by combined surface/perfusion, in contrast to pure perfusion methods, resulted in smaller gradients without remarkable increase in core temperature (average = 1.3 °C) during the arrest period. These findings when correlated with the shorter total operating time and ease of operative management and resuscitation lead us to the conclusion that combined surface/ perfusion hypothermia techniques have certain advantages over either pure surface or pure perfusion techniques alone.