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.

Effects of continuous positive-pressure ventilation in experimental pulmonary edema

1976 ◽  
Vol 40 (4) ◽  
pp. 568-574 ◽  
Author(s):  
P. C. Hopewell ◽  
J. F. Murray
Keyword(s):  
Pulmonary Edema ◽  
Left Atrial ◽  
Positive Pressure Ventilation ◽  
Colloid Osmotic Pressure ◽  
Intermittent Positive Pressure Ventilation ◽  
Water Volume ◽  
Positive Pressure ◽  
Positive End Expiratory Pressure ◽  
Continuous Positive Pressure ◽  
Double Isotope

We compared the effects of continuous positive-pressure ventilation (CPPV), using 10 cmH2O positive end-expiratory pressure (PEEP), with intermittent positive-pressure ventilation (IPPV), on pulmonary extravascular water volume (PEWV) and lung function in dogs with pulmonary edema caused by elevated left atrial pressure and decreased colloid osmotic pressure. The PEWV was measured by gravimetric and double-isotope indicator dilution methods. Animals with high (22–33 mmHg), moderately elevated (12–20 mmHg), and normal (3–11 mmHg) left atrial pressures (Pla) were studied. The PEWV by both methods was significantly increased in the high and moderate Pla groups, the former greater than the latter (P less than 0.05). There was no difference in the PEWV between animals receiving CPPV and those receiving IPPV in both the high and moderately elevated Pla groups. However, in animals with high Pla, the Pao2 was significantly better maintained and the inflation pressure required to deliver a tidal volume of 12 ml/kg was significantly less with the use of CPPV than with IPPV. We conclude that in pulmonary edema associated with high Pla, PEEP does not reduce PEWV but does improve pulmonary function.

Left ventricular geometry during intermittent positive pressure ventilation in dogs

1987 ◽  
Vol 2 (4) ◽  
pp. 230-244 ◽  
Author(s):  
Randall C. Bell ◽  
James L. Robotham ◽  
Frederick R. Badke ◽  
William C. Little ◽  
Mary K. Kindred
Keyword(s):  
Positive Pressure Ventilation ◽  
Intermittent Positive Pressure Ventilation ◽  
Left Ventricular ◽  
Left Ventricular Geometry ◽  
Positive Pressure ◽  
Ventricular Geometry

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

End-respiratory pressure ventilation and sulfobromophthalein sodium excretion in dogs

1977 ◽  
Vol 43 (4) ◽  
pp. 714-720 ◽  
Author(s):  
E. E. Johnson ◽  
J. Hedley-Whyte ◽  
S. V. Hall
Keyword(s):  
Positive Pressure Ventilation ◽  
Total Concentration ◽  
Venous Pressure ◽  
Serum Levels ◽  
Intermittent Positive Pressure Ventilation ◽  
Positive Pressure ◽  
Central Venous ◽  
Serum Samples ◽  
Cholecystokinin Octapeptide ◽  
Continuous Positive Pressure

Sulfobromophthalein sodium (BSP) 25 mg/kg body wt was given as a single iv injection to 32 fasted dogs. Serum samples at 3, 5, 10, 20, 30, 45, 60, 80, and 120 min postinjection were analyzed for total concentration of BSP and from 30 to 120 min for percent conjugated BSP. Four groups were compared: spontaneous ventilation; intermittent positive-pressure ventilation (IPPV) and continuous positive-pressure ventilation (CPPV) (2 groups). During CPPV, one group of dogs was given a continuous infusion of cholecystokinin octapeptide (CCK-8, 1 ng/kg per min). Central venous pressure averaged 11.3 +/- 0.7 (SE) cmH2O in dogs with CPPV + CCK-8 and 11.8 +/- 0.8 (SE) cmH2O in dogs with CPPV alone. At 3, 5, and 10 min postinjection serum BSP levels were similar in all groups. From 30 to 120 min postinjection serum levels of both free and conjugated BSP were higher in dogs ventilated with CPPV alone than in any other group (P less than 0.01). Dogs given CCK-8 during CPPV had serum BSP levels that were statistically similar to dogs breathing spontaneously or ventilated with IPPV. We conclude that CPPV impairs BSP excretion. This effect is counteracted by CCK-8.

Elevated mean systemic filling pressure due to intermittent positive-pressure ventilation

1992 ◽  
Vol 262 (4) ◽  
pp. H1116-H1121 ◽  
Author(s):  
E. Chihara ◽  
S. Hashimoto ◽  
T. Kinoshita ◽  
M. Hirose ◽  
Y. Tanaka ◽  
...  
Keyword(s):  
Blood Volume ◽  
Positive Pressure Ventilation ◽  
Venous Return ◽  
Intermittent Positive Pressure Ventilation ◽  
Spontaneous Respiration ◽  
Positive Pressure ◽  
Circulating Blood Volume ◽  
Mean Systemic Filling Pressure ◽  
Systemic Filling ◽  
Systemic Filling Pressure

To clarify the effect of intermittent positive-pressure ventilation (IPPV) on systemic circulation, mean systemic filling pressure (Psf) and circulating blood volume were measured together with other hemodynamic parameters of capacitance vessel. Change in circulating blood volume was determined by dilution with 51Cr-labeled erythrocytes. Vascular compliance (Cvas) was measured from the change in Psf caused by a bolus injection of blood. These parameters were measured during both spontaneous respiration and IPPV in male Wistar rats anesthetized with pentobarbital sodium. The shift from spontaneous respiration to IPPV reduced cardiac output (CO) by 20.9%. Psf increased significantly, from 7.1 +/- 1.2 to 8.6 +/- 1.1 mmHg. Central venous pressure (Pcv) also increased significantly. The pressure gradient for venous return decreased by 15.6% (from 6.4 to 5.4 mmHg). The resistance to venous return did not change significantly, but there was a significant increase in total peripheral resistance. Neither Cvas nor circulating blood volume was changed significantly by IPPV. These results indicate that during IPPV the increased Pcv attenuates the pressure gradient for venous return and decreases CO and that the compensatory increase in Psf is caused by a blood shift from unstressed to stressed blood volume.

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

Effect of negative-pressure ventilation on lung water in permeability pulmonary edema

1989 ◽  
Vol 66 (5) ◽  
pp. 2223-2230 ◽  
Author(s):  
M. Skaburskis ◽  
R. P. Michel ◽  
A. Gatensby ◽  
A. Zidulka
Keyword(s):  
Cardiac Output ◽  
Pulmonary Edema ◽  
Positive Pressure Ventilation ◽  
Intermittent Positive Pressure Ventilation ◽  
Positive Pressure ◽  
Lung Water ◽  
Anesthetized Dogs ◽  
Water Accumulation ◽  
Permeability Pulmonary Edema ◽  
Continuous Positive Pressure

We have previously shown (Am. Rev. Respir. Dis. 136: 886–891, 1987) improved cardiac output in dogs with pulmonary edema ventilated with external continuous negative chest pressure ventilation (CNPV) using negative end-expiratory pressure (NEEP), compared with continuous positive-pressure ventilation (CPPV) using equivalent positive end-expiratory pressure (PEEP). The present study examined the effect on lung water of CNPV compared with CPPV to determine whether the increased venous return created by NEEP worsened pulmonary edema in dogs with acute lung injury. Oleic acid (0.06 ml/kg) was administered to 27 anesthetized dogs. Supine animals were then divided into three groups and ventilated for 6 h. The first group (n = 10) was treated with intermittent positive-pressure ventilation (IPPV) alone; the second (n = 9) received CNPV with 10 cmH2O NEEP; the third (n = 8) received CPPV with 10 cmH2O PEEP. CNPV and CPPV produced similar improvements in oxygenation over IPPV. However, cardiac output was significantly depressed by CPPV, but not by CNPV, when compared with IPPV. Although there were no differences in extravascular lung water (Qwl/dQl) between CNPV and CPPV, both significantly increased Qwl/dQl compared with IPPV (7.81 +/- 0.21 and 7.87 +/- 0.31 vs. 6.71 +/- 0.25, respectively, P less than 0.01 in both instances). CNPV and CPPV, but not IPPV, enhanced lung water accumulation in the perihilar areas where interstitial pressures may be most negative at higher lung volumes.

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.

From Continuous Positive-pressure Breathing to Ventilator-induced Lung Injury

2004 ◽  
Vol 101 (4) ◽  
pp. 1015-1017 ◽  
Author(s):  
Henning Pontoppidan ◽  
Srinivasa N. Raja
Keyword(s):  
Respiratory Failure ◽  
Acute Respiratory Failure ◽  
Positive Pressure Ventilation ◽  
Arterial Oxygen Tension ◽  
Intermittent Positive Pressure Ventilation ◽  
Arterial Oxygen ◽  
Positive Pressure ◽  
Residual Capacity ◽  
The Mean ◽  
Continuous Positive Pressure

Continuous positive-pressure ventilation in acute respiratory failure. By Kumar A, Falke KJ, Geffin B, Aldredge CF, Laver MB, Lowentein E, Pontoppidan H. N Engl J Med 1970; 283:1430-6. Reprinted with permission. Continuous positive-pressure ventilation was used in eight patients with severe acute respiratory failure. Cardiac output and lung function were studied during continuous positive-pressure ventilation (mean end-expiratory pressure, 13 cm H2O) and a 30-min interval of intermittent positive-pressure ventilation. Although the mean cardiac index increased from 3.6 to 4.5 l/min per square meter of body surface area, the mean intrapulmonary shunt increased by 9% with changeover to intermittent positive-pressure ventilation. Satisfactory oxygenation was maintained in all patients during continuous positive-pressure ventilation with 50% inspired oxygen or less. With intermittent positive-pressure ventilation, arterial oxygen tension promptly fell by 161 mm of mercury, 79% occurring within 1 min. Prevention of air-space collapse during expiration and an increase in functional residual capacity probably explain improved oxygenation with continuous positive-pressure ventilation. In four patients, subcutaneous emphysema or pneumothorax developed. Weighed against the effects of prolonged hypoxemia, these complications were not severe enough to warrant cessation of continuous positive-pressure ventilation.

Continuous positive-pressure ventilation and choledochoduodenal flow resistance

1975 ◽  
Vol 39 (6) ◽  
pp. 937-942 ◽  
Author(s):  
E. E. Johnson ◽  
J. Hedley-Whyte
Keyword(s):  
Bile Duct ◽  
Common Bile Duct ◽  
Positive Pressure Ventilation ◽  
Venous Pressure ◽  
Intermittent Positive Pressure Ventilation ◽  
Intravenous Fluid ◽  
Positive Pressure ◽  
Flow Through ◽  
The Common ◽  
Continuous Positive Pressure

Resistance to flow through the choledochoduodenal junction was measured during constant perfusion (0.8 ml saline/min). In eight dogs, intermittent positive-pressure ventilation (IPPV) and continuous positive-pressure ventilation (CPPV) were compared. Pressure in the common bile duct was always higher during JPPV than IPPV. With the first application of CPPV the rate of intravenous fluid was adjusted to maintain constant Hct. Mean hepatic venous pressure (Phv) increased from 6.6 to 11.5 cmH2O (P less than 0.001). Mean pressure in the common bile duct increased (P less than 0.001) from 11.6 to 14.1 cmH2O. The average increase in resistance was 21%. Changes reversed with return to IPPV. During the second application of CPPV, intravenous fluid was increased to maintain constant arterial pressure. Phv increased to 12.8 cmH2O and pressure in the common bile duct increased to 15.0 cmH2O (30% increase). In four additional dogs, choledochoduodenal resistance during continuous CPPV was reduced by intravenous vasopressin, intravenous norepinephrine and intraducta phenylephrine. CPPV increases resistance to flow through the choledochoduodenal junction, probably by vascular engorgement.

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