Continuous positive-pressure ventilation decreases right and left ventricular end-diastolic volumes in the dog.

Abstract

SUMMARY We investigated the mechanism(s) responsible for the decreased cardiac output during continuous positive-pressure ventilation (CPPV). Seven dogs were anesthetized with chloralose-urethane, intubated, and ventilated using a volume ventilator. We measured heart rate, stroke volume, and the determinants of stroke volume: left and right ventricular end-diastolic volumes, isovolumic and ejection phase indices of myocardial contractility, and pulmonary and systemic arterial pressures. Myocardial blood flow was estimated using radioactive microspheres. Variables were measured during a control period of intermittent positive-pressure ventilation (IPPV), 8-20 minutes after the initiation of CPPV using 12 cm H 2 O positive end-expiratory pressure (PEEP), and 8-20 minutes after the removal of PEEP. CPPV decreased cardiac output but did not affect total or regional myocardial blood flow or the ratio of subendocardial to subepicardial blood flow. Isovolumic and ejection phase indices of myocardial contractility, heart rate, and systemic arterial pressure did not change during CPPV. Right and left ventricular end-diastolic and end-systolic volumes decreased markedly during CPPV. We conclude that CPPV decreases cardiac output in accordance with Starling's law by decreasing preload. Circ Res 46: 125-132, 1980CONTINUOUS positive-pressure ventilation (CPPV) is used to increase the arterial Po 2 in patients with acute respiratory failure and hypoxemia refractory to usual oxygen therapy (Ashbaugh et al., 1969;Mclntyre et al., 1969;Kumar et al., 1972;Falke et al., 1972). Although CPPV usually improves the arterial Po-2, it also decreases cardiac output and may actually decrease the amount of oxygen transported to the tissues (Lutch and Murray, 1972).Studies on animals (Tucker and Murray, 1972;Jones and King, 1973) and humans (Cournand et al., 1948;Powers et al., 1973) have demonstrated that CPPV decreases the cardiac output, but the mechanism is unclear. It generally was believed that cardiac output falls due to decreased venous return (Cournand et al., 1948;Ashbaugh and Petty, 1973;Qvist et al., 1975). If this were true, the effective or transmural filling pressure of the right atrium (right atrial pressure minus pleural pressure) would be expected to decrease during CPPV. However, several investigators have reported that transmural right and left atrial pressures, measured rel- ative to lateral pleural or esophageal pressure, do not decrease, but stay the same or actually increase during CPPV (Scharf et al., 1977;Zarins et al., 1977;Cassidy et al., 1978). This suggests that decreased venous return is not the primary factor producing the decrease in cardiac output. A decrease in cardiac output in the presence of constant or increasing transmural atrial pressures may indicate a decrease in myocardial contractility. Lozman et al. (1974) and Powers and Dutton (1975) have suggested that ventricular dysfunction occurs during CPPV and may be related to decreased subendocardial blood flow.The purpose of the present study was to c...

Pulmonary artery constriction produces a greater right ventricular dynamic afterload than lung microvascular injury in the open chest dog.

“…We believe that these changes probably were due to an increase in the contact pressure between the lungs and the heart when the lungs are hyperinflated such that both ventricles' diastolic pressure-volume curves were changed. Similar increases in extracardiac contact pressure have been reported during studies of PEEP (Prewitt et al, 1979;Fewell et al, 1980Fewell et al, , 1981. We cannot rule out a direct interaction between both ventricles mediated by shifting of the interventricular septum, however, because we did not measure septal-free wall dimension.…”

The Effects of Lung Distension, Oxygenation, and Gestational Age on Fetal Behavior and Breathing Movements in Sheep

“…An increase in intrathoracic pressure induced by CPAP would be more profound in relatively mature fetuses due to an increase in pulmonary compliance. This decrease in pH (metabolic acidemia) might have resulted from decreased cardiac output, leading to poor tissue perfusion and impaired O2 delivery to meet the fetal metabolic demands (anerobic metabolism), and from decreased umbilical and renal blood flows, leading to an accumulation of metabolic end products (28,29). A decrease in fetal tissue Po2 in response to increased Pao2 has been reported by Towel1 et al (30).…”

Haemodynamic effects of nasal continuous positive airway pressure in severe congestive heart failure

“…When contractility is normal, a reduction in preload decreases LV ejection by the Frank-Starling mechanism. As a result, the normal heart is considered to be preload-dependent [5,6,27], and normal subjects usually [15,21], but not always [28], experience a consistent fall in CO with NCPAP. In contrast, CO in the failing heart is thought to be more responsive to changes in afterload, as LV contractility is reduced and is relatively unresponsive to changes in diastolic volume [5,6].…”