Cardiovascular effects of increasing airway pressure in the dog

Scharf, Steven M.; Caldini, Paolo; Ingram, R. H.

doi:10.1152/ajpheart.1977.232.1.h35

Cited by 60 publications

(38 citation statements)

References 22 publications

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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%

“…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.…”

mentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

mentioning

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

View full text Add to dashboard Cite

show abstract

“…The methods used in this study have been previously used to describe the circu latory changes accompanying the use of positive end-expiratory pressure [22], me chanical positive pressure ventilation [24], and inspiratory loading [20]. In this study, we could not calculate left ventricular volume, since only 2 of the 3 required left ventricular dimensions were measured.…”

Section: Discussionmentioning

confidence: 99%

“…It was expressed in arbitrary units and normalized by dividing by the control value. For the measurement o f Ppl, a brass cannula, previously described [22], 0.25 cm in diameter, was inserted through the chest wall into the left hemithorax. Fluid-Filled catheters (Cordis No.…”

Section: Methodsmentioning

confidence: 99%

Cardiovascular Performance during Bronchospasm in Dogs

Scharf¹,

Brown²,

Ingram³

1987

Respiration

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In 8 anesthetized mongrel dogs, we studied the effects of carbachol-induced bronchoconstriction (BC) on the cardiovascular system. Inhalation of carbachol in an amount sufficient to produce at least a 50% decrease in lung conductance (G_L) did not lead to significant changes in cardiac output, mean transmural left atrial (Pla) or right atrial pressure, end-diastolic left ventricular septal-lateral dimension, left ventricular apex to base dimension, or in end-diastolic right ventricular septal to lateral dimension during expiration. Mean transmural pulmonary arterial pressure rose and mean transmural aortic pressure (Pao) fell during BC. During inspiration, there were significant increases in transmural left atrial pressure, Pla, associated with decreases in end-diastolic left ventricular septal-lateral and apex-base dimensions. End-diastolic right ventricular septal-lateral dimension increased during inspiration. Beat-to-beat aortic flow (Qao) decreased during inspiration, while pulmonary arterial flow increased. There were no changes in transmural Pao during inspiration measured at the nadir of aortic flow. During BC, these changes were exaggerated, but remained qualitatively the same. The magnitude of the inspiratory decrease in pleural pressure (Ppl) was shown to be linearly related to the magnitude of the change in G_L, and the magnitude of the inspiratory decrease in Pao and Qao (pulsus paradoxus) was shown to be linearly related to the magnitude of the inspiratory swing in Ppl. Although vagotomy significantly altered the pattern of respiration such that tidal volume increased and respiratory rate decreased, it did not substantially alter the responses of the cardiovascular system to breathing during BC. We conclude: (1) the inspiratory decrease in Pao and Qao (pulsus paradoxus) is associated with a decrease in left ventricular end-diastolic filling, and a stiffening of the

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“…Our interest in reflex cardiovascular effects of lung hyperinflation arose as a consequence of observations that ventilation with positive end-expiratory pressure that hyperinflates the lung, depresses cardiac output beyond that attributable to mechanical obstruction either to venous return or to pulmonary circulation (1)(2)(3)(4). To study reflex cardiovascular effects of lung hyperinflation, it is necessary to employ a model in which the direct mechanical effects of lung inflation are eliminated.…”

Section: Introductionmentioning

confidence: 99%

Reflex Cardiovascular Depression during Unilateral Lung Hyperinflation in the Dog

Cassidy¹,

Eschenbacher²,

Johnson³

1979

J. Clin. Invest.

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A B S T R A C T We have examined whether lung hyperinflation in the anesthetized dog reflexly depresses cardiac output, stroke volume, heart rate, and blood pressure and whether these changes persist for more than a minute. To eliminate any mechanical restriction to venous return and pulmonary blood flow during lung hyperinflation, a model was developed in which all pulmonary artery blood flow and all ventilation were directed to the right lung in dogs with widely open chest and the left lung was hyperinflated before and after left cervical vagotomy. Heart rate, stroke volume, and blood pressure decreased by 24, 20, and 27%, respectively, within 15 s of left lung inflation to 30 cm H20. Heart rate increased to preinflation levels by 1 min, but stroke volume and blood pressure remained depressed during lung hyperinflation for at least 15 min. Upon deflation, stroke volume and blood pressure returned to control levels within 1 min. Division of the left vagosympathetic trunk at the neck interrupted all autonomic afferent and efferent nerves of the left lung, but left intact the right vagal sympathetic and parasympathetic afferent and efferent nerves ofthe heart. After left cervical vagotomy the transient fall in heart rate, stroke volume, and blood pressure during left lung hyperinflation was greatly reduced or eliminated. These results suggest that unilateral lung hyperinflation reflexly depresses heart rate and blood pressure, which are partially compensated with time, and reflexly flepresses stroke volume, which persists uncompensated until the lung is deflated. These findings may explain the depressed cardiovascular function observed during regional lung overdistention especially when it occurs during positive pressure ventilation.

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Cardiovascular effects of increasing airway pressure in the dog

Cited by 60 publications

References 22 publications

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

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

Cardiovascular Performance during Bronchospasm in Dogs

Reflex Cardiovascular Depression during Unilateral Lung Hyperinflation in the Dog

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