Effect of continuous pressure breathing on right ventricular volumes

Wong, Maylene; Escobar, E; Martinez, Gilberto; Butler, John; Rapaport, Elliot

doi:10.1152/jappl.1967.22.6.1053

Cited by 15 publications

(3 citation statements)

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“…A study conducted in self-ventilating patients with emphysema (i.e., prone to hyperinflation) described an obstruction of venous return in the inferior vena cava where it enters the thorax during inspiration and normal flow during the expiration (Nakhajavan et al 1966;32). The same phenomenon has been described in dogs with normal lungs when extrathoracic negative pressure was applied with very negative values (Wong 1967;22).…”

Section: Cardiovascular Effectssupporting

confidence: 72%

Mechanical Ventilation

Arnal¹,

Bancalari²,

Clement³

et al. 2014

Pediatric and Neonatal Mechanical Ventilation

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Section: Cardiovascular Effectssupporting

confidence: 72%

Mechanical Ventilation

Arnal¹,

Bancalari²,

Clement³

et al. 2014

Pediatric and Neonatal Mechanical Ventilation

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“…Qvist et al (1975) have shown that CPPV can decrease cardiac output for up to 8 hours. Furthermore, several investigators (Marotta and Harner, 1962;Maulsby and Hoff, 1962;Wong et al, 1967;Scharf et al, 1977) have demonstrated that bilateral cervical vagotomy, which interrupts most afferent nerve fibers from the lungs, does not alter the cardiovascular response to CPPV. It is likely, then, that CPPV decreases cardiac output primarily by reducing right and left ventricular end-diastolic volumes.…”

Section: Discussionmentioning

confidence: 99%

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

Fewell¹,

Abendschein²,

Carlson³

et al. 1980

Circulation Research

178

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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...

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“…A compensatory effect was ascribed to baroreceptor reflexes and humoral control mechanisms (6). Cyclic changes in right and left ventricular output during the ventilatory cycle have been reported by many authors (1,(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19). During insumation, right ven-tricular stroke volume falls synchronously with the rise in intrapulmonary and intrathoracic pressure, whereas left ventricular stroke volume follows the fall in output at the right side with a delay of several beats implying a decrease in pulmonary blood during insumation ( 10).…”

mentioning

confidence: 95%

Negative effect of insufflation on cardiac output and pulmonary blood volume

Versprille

Jansen

Frietman

et al. 1990

Acta Anaesthesiol Scand

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In 14 anaesthetized young pigs the changes in pulmonary blood flow and pulmonary blood volume (Qp) during mechanical ventilation were quantified. Ventilation was performed at 10 cycles per min and tidal volume (VT) was adjusted to an arterial PCO2 of about 40 mmHg (5.3 kPa). In 4 animals, 7 ventilatory cycles with an inspiratory pause (IP) of 7.2 s but different tidal volumes were inserted at intervals of 5 min to determine the decrease in Qp (delta Qp) from the differences between right ventricular (Qs,rv) and left ventricular (Qs,lv) stroke volume, and to relate delta Qp to VT. We measured pressure in the aorta (Pao), central veins (Pcv), right and left ventricles (Prv, Plv) pericardium (Pit), and trachea (PT). Blood flow was measured electromagnetically (EM) in the pulmonary artery (Q'pa) and aorta (Q'ao). Stroke volumes were derived from the EM-flow curves. In the other 10 experiments, Qs,lv was derived from the aortic pulse contour. Beat-to-beat analyses of Qs,rv and Qs,lv and blood pressures during the normal ventilatory cycles and those with an IP revealed the following: 1) The end-expiratory RV output and LV output were constant and were defined as baseline values. 2) The accumulated decrease in Qs,rv during insufflation caused a mean deficit in cardiac output of 10.3 +/- 3.2% (s.d.), n = 135; the same was found for Qs,lv, indicating the pulse contour as a useful method to estimate the variations in cardiac output during a ventilatory cycle.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effect of continuous pressure breathing on right ventricular volumes

Cited by 15 publications

References 0 publications

Mechanical Ventilation

Mechanical Ventilation

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

Negative effect of insufflation on cardiac output and pulmonary blood volume

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