PATHOPHYSIOLOGY AND NATURAL HISTORY VENTRICULAR PERFORMANCE Immediate effect of expiratory loading on left ventricular stroke volume

While the steady-state effects of positive pleural pressure on the circulation have been extensively studied, less is known about the immediate effects of positive intrathoracic pressure on cardiac dynamics. Therefore, we performed electrocardiographically gated radionuclide ventriculography with a respiratory gating technique in nine healthy subjects during quiet breathing and during expiration against a 24 cm H20 expiratory threshold load. During expiration, respiratory loading caused an increase in stroke counts by 29.4% (p < .001) due to an increase in end-diastolic counts of 26.1% (p < .001). End-systolic counts also rose 18.8% (p < .05). The ejection fraction did not change significantly. These findings indicate that the increase in left ventricular stroke volume that occurs during the first 1 or 2 beats of a loaded expiration is due to an increase in left ventricular filling and not to augmentation of left ventricular ejection. This immediate increase in pulmonary venous return may reflect increased distensibility of the left ventricle due to decreased filling of the right ventricle. Circulation 75, No. 1, 139-145, 1987. A SUDDEN INCREASE in pleural pressure such as occurs with coughing or a Valsalva maneuver causes an immediate increase in aortic pulse pressure, but the mechanism for this is not known. 1 Although some animal studies have shown that left ventricular stroke volume transiently increases during positive pressure inflation of the lung,2other animal and human studies have shown no increase in stroke volume during the early phase of a Valsalva maneuver' 5-7 in which pleural pressure is increased during an expiratory maneuver at constant lung volume. An increase in pulse pressure could reflect an increase in arterial impedance as well as an increase in stroke volume. We wanted to determine if stroke volume was, in fact, transiently increased during forced expiration, such as might occur during a cough, or with expiratory obstruction of the upper airway. In addition, a knowledge of the physiologic mechanism for changes in pulse pressure or stroke volume may lead to insights with respect to From the Division of Nuclear Medicine of the Russel H. Morgan Department of Radiology, Division of Radiation Health Sciences and Department of Medicine, Johns Hopkins Medical Institutions, Baltimore. Supported in part by NIH grant Nos. CA32845, HL10342, and HL00914. Address for correspondence: Robert A. Wise, M.D., Division of Pulmonary Medicine, Francis Scott Key Hospital, 4940 Eastern Ave., Baltimore, MD 21224. Received July 9, 1985; revision accepted Sept. 25, 1986. Vol. 75, No. 1, January 1987 the use of diagnostic respiratory maneuvers in patients with abnormal hemodynamics. If stroke volume is increased, we wanted to determine wether this was due to an increase in end-diastolic volume or to an improvement in left ventricular ejection. In a previous study using techniques similar to those employed here, we had demonstrated that a sudden fall in pleural pressure with loaded inspiration caused a fall in stroke volume attributable to an increase in end-systolic volume, which we proposed was due to the negative pleural pressure impeding left ventricular ejection.8 Therefore, we postulated that the opposite would occur with a sudden elevation of pleural pressure; that is, the increased pleural pressure would increase stroke volume of the left ventricle by assisting ejection. To determine the mechanism of this increase in pulse pressure with an expiratory increase in pleural pressure, we studied the effects of forced expiration against an expiratory threshold load on left ventricular hemodynamics. Specifically, we measured the immediate effects of expiratory loading on left ventricular stroke volume, end-diastolic volume, and end-systolic volume in nine norrnal subjects by radionuclide ventriculography gated for both the cardiac and respiratory cycles. Our results indicate that the increase in stroke volume accompanying a sudden expiratory elevation of pleural pressure is due to increased filling of the left ventricle. 139 by gest on Sptem er 6, 2017 http://ciajournals.org/ D ow nladed from