Cardiovascular adjustments in dogs during continuous pressure breathing

1960 ◽  
Vol 15 (3) ◽  
pp. 425-428 ◽  
Author(s):  
Claude Lenfant ◽  
Barbara J. Howell
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Vena Cava ◽  
Pulmonary Vessels ◽  
Pulmonary Flow ◽  
Airway Pressures ◽  
Anesthetized Dogs ◽  
Pressure Changes ◽  
Flow Resistances

Pressure changes in the pulmonary artery and vein, thoracic vena cava, aorta and intrapleural space as well as the cardiac output were measured in anesthetized dogs subjected to continuous airway pressures varying between -25 to +25 cm H2O. Pulmonary and systemic resistances were calculated. During positive airway pressures the pulmonary artery, vein and vena cava pressures approximately paralleled changes in intrapleural pressures. Cardiac output and aorta pressures decreased; systemic and pulmonary flow resistances markedly increased. During negative airway pressures the pulmonary vessels and vena cava pressures decreased but no longer paralleled the changes in intrapleural pressures. It is assumed that these vessels reached their limit of distensibility. While aortic pressures decreased, cardiac output, systemic and pulmonary resistances remained essentially unchanged. Submitted on January 14, 1960

Effect of small doses of 5-hydroxytryptamine (serotonin) on pulmonary circulation in the closed-chest dog

1959 ◽  
Vol 197 (5) ◽  
pp. 963-967 ◽  
Author(s):  
John T. Shepherd ◽  
David E. Donald ◽  
Erland Linder ◽  
H. J. C. Swan
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Pulmonary Veins ◽  
Pulmonary Vessels ◽  
Isolated Perfused Lung ◽  
Small Doses ◽  
Perfused Lung ◽  
Anesthetized Dogs ◽  
Flow Through ◽  
The Difference

5-Hydroxytryptamine (serotonin) was infused into anesthetized dogs at a rate of 20 µg/kg/min. In nine sets of observations on three dogs the increase in the difference of pressure between the pulmonary artery and the left atrium, which averaged 55%, consistently exceeded the increase in pulmonary blood flow, which averaged 16%. 5-HT therefore is a potent constrictor of pulmonary vessels, even in small concentrations. No changes in the pulmonary-artery wedge and pulmonary-vein pressures were detected during the infusions of 5-HT, nor was there any change in the volume of blood between the pulmonary artery and the root of the aorta. With this dose of 5-HT the principal site of the increased resistance to flow through the lungs appeared to be in the precapillary vessels. In the isolated perfused lung, moderate constriction of pulmonary veins also was produced by large doses of 5-HT.

Unequal right and left ventricular ejection with ectopic beats

1962 ◽  
Vol 203 (6) ◽  
pp. 1141-1144 ◽  
Author(s):  
Jay M. Levy ◽  
Emmanuel Mesel ◽  
Abraham M. Rudolph
Keyword(s):  
Pulmonary Artery ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Pulmonary Flow ◽  
Anesthetized Dogs ◽  
Ectopic Beats ◽  
The Difference ◽  
The Right ◽  
Ventricular Depolarization

Simultaneous right and left ventricular stroke volumes were measured with electromagnetic flow probes in open-chest, anesthetized dogs. Atrial ectopic beats with normal ventricular depolarization produced differences between right and left ventricular stroke output, although the right and left ventricular pressures were proportionately reduced to an equal extent. This imbalance in volume ejected was a result of the differences in diastolic level, related to peak systolic pressure, in the aorta compared with pulmonary artery. With ventricular ectopic beats, the stimulated ventricle failed to develop the same percentage of control pressure as did the contralateral ventricle. The difference between aortic and pulmonary flow was thus less marked with right ventricular ectopic beats, and exaggerated with left ventricular ectopic beats.

Pulmonary capillary recruitment during airway hypoxia in the dog

1975 ◽  
Vol 39 (6) ◽  
pp. 900-905 ◽  
Author(s):  
W. W. Wagner ◽  
L. P. Latham
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Left Atrial ◽  
Weak Correlation ◽  
Capillary Length ◽  
Capillary Recruitment ◽  
Pulmonary Capillaries ◽  
Pulmonary Capillary ◽  
Anesthetized Dogs ◽  
Measuring Tool

To study the effect of hypoxia on the pulmonary capillaries, windows were inserted in the chest wall of 9 pentobarbital-anesthetized dogs. A microscope with an image-superimposing device was used to make drawings of the perfused capillaries. Summed lengths of individual perfused capillaries in the drawing were determined with a map-measuring tool. Total capillary length was constant between PaO2 of 160 and 70 Torr. As PaO2 fell below 70 Torr, recruitment of previously unperfused capillaries occurred in every case; at PaO2 of 40 Torr, the total length of perfused capillaries was about 4 times greater than during normoxia. There was no correlation between the recruitment of capillaries and alterations in left atrial pressure, only a weak correlation with cardiac output changes, but a very strong correlation with increased pulmonary artery pressure. This implies that recruitment was probably caused by vasoconstriction within the lung.

Effect of PEEP on discharge of pulmonary C-fibers in dogs

1985 ◽  
Vol 59 (4) ◽  
pp. 1085-1089 ◽  
Author(s):  
M. P. Kaufman ◽  
G. A. Ordway ◽  
T. G. Waldrop
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Impulse Activity ◽  
Vena Cava ◽  
Laboratory Animals ◽  
Positive End Expiratory Pressure ◽  
Firing Rates ◽  
C Fibers ◽  
Anesthetized Dogs ◽  
Stimulation Of

Although positive end-expiratory pressure (PEEP) is believed to depress cardiac output and arterial pressure by compressing the vena cava and the heart, it is unclear whether PEEP also depresses these variables by a reflex arising from an inflation-induced stimulation of pulmonary C-fibers. We therefore recorded the impulse activity of 17 pulmonary C-fibers in barbiturate-anesthetized dogs with closed chests, while we placed the expiratory outlet of a ventilator under 5–30 cmH2O. Increasing PEEP in a ramp-like manner stimulated 12 of the 17 pulmonary C-fibers, with activity increasing from 0.0 +/- 0.1 to 0.9 +/- 0.2 imp/s when end-expiratory pressure equaled 15 cmH2O. When PEEP was increased in a stepwise manner to 15–20 cmH2O and maintained at this pressure for 15 min, pulmonary C-fibers increased their firing rates, but the effect was small averaging 0.2–0.3 imp/s after the 1st min of this maneuver. We conclude that pulmonary C-fibers are unlikely to be responsible for causing much of the decreases in cardiac output and arterial pressure evoked by sustained periods of PEEP in both patients and laboratory animals. These C-fibers, however, are likely to be responsible for causing the reflex decreases in these variables evoked by sudden application of PEEP.

Large venous compliance in carboxyhemoglobinemia and hemodilutional anemia

1986 ◽  
Vol 64 (5) ◽  
pp. 556-560 ◽  
Author(s):  
George P. Biro
Keyword(s):  
Inferior Vena Cava ◽  
Inferior Vena ◽  
Venous Return ◽  
Vena Cava ◽  
Transverse Diameter ◽  
Venous Compliance ◽  
Reduced Viscosity ◽  
Anesthetized Dogs ◽  
Pressure Changes ◽  
Made In

Anesthetized dogs were prepared for the measurement of compliance of the inferior vena cava by placement of a catheter for pressure measurement and a pair of ultrasonic dimension transducers for the measurement of transverse diameter. Measurements of compliance were made in a control state, after the induction of carboxyhemoglobinemia or hemodilutional anemia, by measuring pressure changes and diameter changes during brief occlusions of the inferior vena cava downstream from the transducers. Carboxyhemoglobinemia cuased an upward shift of the averaged pressure–diameter curve while there was a negligible shift in the hemodiluted group. These results indicate that in carboxyhemoglobinemia a change in the compliance of the vena cava occurs, which favours augmented venous return by improved conductance rather than by a dislocation of blood by constriction of the large venous reservoir. In hemodilutional anemia the change in compliance is insignificant, but venous return is favoured by the reduced viscosity.

scholarly journals Pulmonary Hemodynamics and Ventilation in Patients With COVID-19-related Respiratory Failure and ARDS

2020 ◽  
Author(s):  
André Becker ◽  
Frederik Seiler ◽  
Ralf M. Muellenbach ◽  
Guy Danziger ◽  
Sebastian Mang ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Respiratory Failure ◽  
Pulmonary Artery ◽  
Distress Syndrome ◽  
Respiratory Infections ◽  
Severe Respiratory Failure ◽  
Shunt Fraction ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Vessels ◽  
Microcirculatory Dysfunction

Abstract Background: It has been suggested that COVID-19-associated severe respiratory failure (CARDS) might differ from usual acute respiratory distress syndrome (ARDS) due to failing auto-regulation of pulmonary vessels and higher shunt. We sought to investigate pulmonary hemodynamics and ventilation properties in patients with CARDS compared to patients with ARDS of pulmonary origin. Methods: Retrospective analysis of prospectively collected data of consecutive adults with laboratory-confirmed severe acute respiratory syndrome coronavirus 2 patients treated on our ICU in 04/2020 and comparison of the data to matched controls with ARDS due to respiratory infections treated on our ICU from 01/2014 to 08/2019 and for whom pulmonary artery catheter data were available. Results: CARDS patients (n = 10) had similar ventilation characteristics as compared to ARDS (n = 10) patients. Still, mechanical power applied by ventilation was significantly higher in CARDS patients (23.4 ± 8.9 J/min) than in ARDS (15.9 ± 4.3 J/min; p<0.05). COVID-19 patients had similar pulmonary artery pressure but significantly lower pulmonary vascular resistance, as cardiac output was higher in CARDS vs. ARDS patients (p<0.05). Shunt fraction and dead space were similar in CARDS compared to ARDS (p>0.05) and was in both groups correlated with hypoxemia. The arterio-venous pCO2 difference (DpCO2) was elevated (CARDS 5.5±2.8 mmHg vs. ARDS 4.7±1.1 mmHg; p>0.05) as was P(v-a)CO2/C(a-v)O2 ratio (CARDS mean 2.2±1.5 vs. ARDS 1.7±0.8; p>0.05). Conclusions: Respiratory failure in COVID-19 patients seems to differ only slightly from ARDS regarding ventilation characteristics and pulmonary hemodynamics. Differences are mainly due to increased CO2 production in CARDS patients. Our data indicate microcirculatory dysfunction. More data needs to be collected to assure these findings and gain more pathophysiological insights in COVID-19 and respiratory failure.

Limitations of thermodilution cardiac output measurements in the rat

1984 ◽  
Vol 246 (6) ◽  
pp. H754-H760 ◽  
Author(s):  
B. E. Hayes ◽  
J. A. Will ◽  
W. C. Zarnstorff ◽  
G. E. Bisgard
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Heat Loss ◽  
Thoracic Aorta ◽  
Vascular System ◽  
Vena Cava ◽  
Right Atrial ◽  
Thermodilution Cardiac Output ◽  
The Right

Heat loss from the vascular system could introduce an error in thermodilution cardiac output determinations. Cardiac output measured in the rat via the thermodilution technique following right atrial injection yielded different values (P less than 0.001), depending whether sampling was from the pulmonary artery (460 +/- 31 ml X min-1 X kg-1), right ventricle (311 +/- 19), or thoracic aorta (245 +/- 15). Recirculation errors could not account for the differences. Heat loss from the vascular system was measured from extravascular thermistors within both the thorax and the abdomen. These dilutions were 22-57% in peak height of aortic curves recorded at approximately the same location. Differences in calculated cardiac output between sampling sites could be attributed to rapid heat conduction directly from the right atrium and inferior vena cava to the thoracic aorta with progressive loss of indicator from both the right ventricle and pulmonary artery.

Stability of pulmonary artery pressure during emboli-induced pulmonary edema in dogs

1965 ◽  
Vol 208 (6) ◽  
pp. 1263-1266
Author(s):  
H. Weisberg ◽  
R. T. Jortner ◽  
I. K. Kline ◽  
A. Ellis ◽  
L. N. Katz
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Edema ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Pressure Rise ◽  
Vascular Effects ◽  
Artery Pressure ◽  
Pressure Changes

Changes in some facets of cardiovascular hemodynamics occurring after acute unilateral pulmonary starch embolization were studied in the anesthetized closed-chest dog. While bilateral pulmonary edema and reduced cardiac output occurred in starch-embolized dogs, these phenomena were not seen in control animals. Pulmonary arterial pressure changes were not significant during the present experiments, but the consistent rise in pulmonary vascular resistance after embolization indicates that the latter may be a better index of pulmonary vascular effects of emboli than are pressure changes. The fall in cardiac output was of sufficient magnitude to more completely neutralize the pulmonary artery pressure rise usually expected with increased pulmonary vascular resistance following pulmonary embolization.

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