Mechanisms of Decreased Left Ventricular Preload during Continuous Positive Pressure Ventilation in ARDS

CHEST Journal ◽  
1986 ◽  
Vol 90 (1) ◽  
pp. 74-80 ◽  
Author(s):  
Jean F. Dhainaut ◽  
Jean Y. Devaux ◽  
Julien F. Monsallier ◽  
Fabrice Brunet ◽  
Didier Villemant ◽  
...  
Keyword(s):  
Positive Pressure Ventilation ◽  
Left Ventricular ◽  
Positive Pressure ◽  
Continuous Positive Pressure ◽  
Left Ventricular Preload

Continuous positive-pressure ventilation does not alter ventricular pressure-volume relationship

1981 ◽  
Vol 240 (6) ◽  
pp. H821-H826 ◽  
Author(s):  
J. E. Fewell ◽  
D. R. Abendschein ◽  
C. J. Carlson ◽  
E. Rapaport ◽  
J. F. Murray
Keyword(s):  
Mechanical Properties ◽  
Positive Pressure Ventilation ◽  
Venous Return ◽  
Intermittent Positive Pressure Ventilation ◽  
Left Ventricular ◽  
Positive Pressure ◽  
Volume Relationship ◽  
Pressure Volume Relationship ◽  
The Right ◽  
Continuous Positive Pressure

To determine whether alterations in the mechanical properties (i.e., stiffening) of the right and left ventricles contribute to the decrease in right and left ventricular end-diastolic volumes during continuous positive-pressure ventilation (CPPV), we studied six dogs anesthetized with chloralose urethane and ventilated with a volume ventilator. We varied ventricular volumes by withdrawing or infusing blood. Pressure-volume curves, constructed by plotting transmural ventricular end-diastolic pressures against ventricular end-diastolic volumes, did not change during CPPV (12 cmH2O positive end-expiratory pressure) compared to intermittent positive-pressure ventilation (IPPV, 0 cmH2O end-expiratory pressure). We conclude that decreased ventricular end-diastolic volumes during CPPV result primarily from a decrease in venous return. Alterations in the mechanical properties of the ventricles do not play a significant role in this response.

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

1980 ◽  
Vol 46 (1) ◽  
pp. 125-132 ◽  
Author(s):  
J E Fewell ◽  
D R Abendschein ◽  
C J Carlson ◽  
J F Murray ◽  
E Rapaport
Keyword(s):  
Positive Pressure Ventilation ◽  
Left Ventricular ◽  
Positive Pressure ◽  
Continuous Positive Pressure

Lung volume and pleural pressure effects on ventricular function

1981 ◽  
Vol 50 (3) ◽  
pp. 630-635 ◽  
Author(s):  
B. H. Culver ◽  
J. J. Marini ◽  
J. Butler
Keyword(s):  
Right Ventricular ◽  
Ventricular Function ◽  
Lung Volume ◽  
Positive Pressure Ventilation ◽  
Left Ventricular ◽  
Pleural Pressure ◽  
Positive Pressure ◽  
Right Ventricular Afterload ◽  
Ventricular Afterload ◽  
Continuous Positive Pressure

To investigate the changes in ventricular function that occur during continuous positive-pressure ventilation, we studied the effects of separate increases in lung volume, pleural pressure, and right ventricular afterload in 15 dogs. Isovolume increases of pleural pressure caused changes in right and left ventricular hemodynamics indistinguishable from those induced by preload reduction. Lung distension with the chest open to atmosphere caused both right and left atrial intracavitary pressures to rise as cardiac output fell, suggesting altered function of both ventricles. Raising right ventricular afterload by pulmonary artery constriction did not reproduce the hemodynamic changes observed during increases of lung volume. These data indicate that the apparent alteration of ventricular function that occurs during continuous positive-pressure ventilation is produced by the associated increase in lung volume and that a right ventricular afterload-ventricular interdependence effect is not the responsible mechanism.

LEFT VENTRICULAR PERFORMANCE DURING CONTINUOUS POSITIVE PRESSURE VENTILATION

1981 ◽  
Vol 9 (3) ◽  
pp. 178 ◽  
Author(s):  
Jean F. Dhainaut ◽  
Jean Y. Devaux ◽  
François J. Monsallier ◽  
Odile Salmon ◽  
Christian Bricard ◽  
...  
Keyword(s):  
Positive Pressure Ventilation ◽  
Left Ventricular ◽  
Positive Pressure ◽  
Left Ventricular Performance ◽  
Ventricular Performance ◽  
Continuous Positive Pressure

Combination of constant-flow and continuous positive-pressure ventilation in canine pulmonary edema

1989 ◽  
Vol 67 (2) ◽  
pp. 817-823 ◽  
Author(s):  
J. I. Sznajder ◽  
C. J. Becker ◽  
G. P. Crawford ◽  
L. D. Wood
Keyword(s):  
Pulmonary Edema ◽  
Positive Pressure Ventilation ◽  
Alveolar Ventilation ◽  
Positive Pressure ◽  
Constant Flow ◽  
Positive End Expiratory Pressure ◽  
Ventilatory Mode ◽  
Continuous Positive Pressure ◽  
Bronchoscopic Guidance ◽  
Normal Lungs

Constant-flow ventilation (CFV) maintains alveolar ventilation without tidal excursion in dogs with normal lungs, but this ventilatory mode requires high CFV and bronchoscopic guidance for effective subcarinal placement of two inflow catheters. We designed a circuit that combines CFV with continuous positive-pressure ventilation (CPPV; CFV-CPPV), which negates the need for bronchoscopic positioning of CFV cannula, and tested this system in seven dogs having oleic acid-induced pulmonary edema. Addition of positive end-expiratory pressure (PEEP, 10 cmH2O) reduced venous admixture from 44 +/- 17 to 10.4 +/- 5.4% and kept arterial CO2 tension (PaCO2) normal. With the innovative CFV-CPPV circuit at the same PEEP and respiratory rate (RR), we were able to reduce tidal volume (VT) from 437 +/- 28 to 184 +/- 18 ml (P less than 0.001) and elastic end-inspiratory pressures (PEI) from 25.6 +/- 4.6 to 17.7 +/- 2.8 cmH2O (P less than 0.001) without adverse effects on cardiac output or pulmonary exchange of O2 or CO2; indeed, PaCO2 remained at 35 +/- 4 Torr even though CFV was delivered above the carina and at lower (1.6 l.kg-1.min-1) flows than usually required to maintain eucapnia during CFV alone. At the same PEEP and RR, reduction of VT in the CPPV mode without CFV resulted in CO2 retention (PaCO2 59 +/- 8 Torr). We conclude that CFV-CPPV allows CFV to effectively mix alveolar and dead spaces by a small bulk flow bypassing the zone of increased resistance to gas mixing, thereby allowing reduction of the CFV rate, VT, and PEI for adequate gas exchange.

Mechanisms of blood flow during pneumatic vest cardiopulmonary resuscitation

1991 ◽  
Vol 70 (1) ◽  
pp. 454-465 ◽  
Author(s):  
C. Beattie ◽  
A. D. Guerci ◽  
T. Hall ◽  
A. M. Borkon ◽  
W. Baumgartner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Resuscitation ◽  
Positive Pressure Ventilation ◽  
Pulmonary Veins ◽  
Left Ventricular ◽  
Aortic Flow ◽  
Positive Pressure ◽  
Compression Rate ◽  
Compression Phase ◽  
Cardiac Compression

Mechanisms of blood flow during cardiopulmonary resuscitation (CPR) were studied in a canine model with implanted mitral and aortic flow probes and by use of cineangiography. Intrathoracic pressure (ITP) fluctuations were induced by a circumferential pneumatic vest, with and without simultaneous ventilation, and by use of positive-pressure ventilation alone. Vascular volume and compression rate were altered with each CPR mode. Antegrade mitral flow was interpreted as left ventricular (LV) inflow, and antegrade aortic flow was interpreted as LV outflow. The pneumatic vest was expected to elevate ITP uniformly and thus produce simultaneous LV inflow and LV outflow throughout compression. This pattern, the passive conduit of "thoracic pump" physiology, was unequivocally demonstrated only during ITP elevation with positive-pressure ventilation alone at slow rates. During vest CPR, LV outflow started promptly with the onset of compression, whereas LV inflow was delayed. At compression rates of 50 times/min and normal vascular filling pressures, the delay was sufficiently long that all LV filling occurred with release of compression. This is the pattern that would be expected with direct LV compression or "cardiac pump" physiology. During the early part of the compression phase, catheter tip transducer LV and left atrial pressure measurements demonstrated gradients necessitating mitral valve closure, while cineangiography showed dye droplets moving from the large pulmonary veins retrograde to the small pulmonary veins. When the compression rate was reduced and/or when intravascular pressures were raised with volume infusion, LV inflow was observed at some point during the compressive phase. Thus, under these conditions, features of both thoracic pump and cardiac pump physiology occurred within the same compression. Our findings are not explained by the conventional conceptions of either thoracic pump or cardiac compression CPR mechanisms alone.

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