Extrapericardial and esophageal pressures with positive end-expiratory pressure in dogs

1981 ◽  
Vol 51 (4) ◽  
pp. 798-805 ◽  
Author(s):  
K. D. Craven ◽  
L. D. Wood
Keyword(s):  
Stroke Volume ◽  
Esophageal Pressure ◽  
Confidence Limits ◽  
Positive End Expiratory Pressure ◽  
Local Surface ◽  
Closed Chest ◽  
Increase Stroke Volume ◽  
Anesthetized Dogs ◽  
Lateral Decubitus ◽  
The Right

Using flat balloon techniques to minimize distortion and artifacts, we studied the effect of positive end-expiratory pressure (PEEP) on local surface pressures between the lung and pericardium overlying the right (R) and left (L) ventricles of ventilated closed-chest anesthetized dogs in right lateral decubitus position. To test the hypothesis that local extrapericardial [Pep(L) and Pep(R)] and average pleural pressures change equally with PEEP, we also measured esophageal pressure (Pes). When 10-cmH2O PEEP was applied, mean increases in Pes, Pep(L), and Pep(R) were 6.2, 5.6, and 5.3 cmH2O, respectively. When PEEP was raised to 20 cmH2O, further average increases in Pes, Pep(L), and Pep(R) were 5.8, 5.0, and 5.4 cmH2O. At each level of PEEP, volume infusion was used to increase stroke volume. Volume infusion at 20-cmH2O PEEP was associated with small 1.0- and 1.5-cmH2O increases in Pep but no change in Pes. Analysis of confidence limits showed that application of up to 20-cmH2O PEEP, with or without volume infusion to restore stroke volume, is associated with nearly equal changes in esophageal and local extrapericardial pressures.

Constancy of stroke volume in ventricular responses to exertion

1959 ◽  
Vol 196 (4) ◽  
pp. 745-750 ◽  
Author(s):  
Robert F. Rushmer
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Cardiac Response ◽  
Indirect Measurements ◽  
Increase Stroke Volume ◽  
Normal Man ◽  
The Right ◽  
Response To Exercise ◽  
Indicator Dilution Techniques

Diastolic and systolic dimensions of the left ventricle and the free wall of the right ventricle in intact dogs are affected little by spontaneous exercise. The concept that stroke volume and heart rate in normal man increase by about the same relative amounts was derived from estimations of cardiac output, particularly in athletes, based upon indirect measurements using foreign gases or CO2. Data for man obtained with the modern cardiac catheterization or indicator dilution techniques confirm the impression derived from intact dogs that increased stroke volume is neither an essential nor a characteristic feature of the normal cardiac response to exercise. Stroke volume undoubtedly increases whenever cardiac output is increased with little change in heart rate (e.g. in athletes or in patients with chronic volume loads on the heart). Tachycardia produced experimentally with an artificial pacemaker in a resting dog causes a marked reduction in diastolic and systolic dimensions and in the stroke change of dimensions. The factors generally postulated to increase stroke volume during normal exercise may prevent the reduction in stroke volume accompanying tachycardia.

Effect of positive end-expiratory pressure on canine ventricular function curves

1981 ◽  
Vol 51 (6) ◽  
pp. 1367-1374 ◽  
Author(s):  
J. J. Marini ◽  
B. H. Culver ◽  
J. Butler
Keyword(s):  
Ventricular Function ◽  
Ventricular Dysfunction ◽  
Transmural Pressure ◽  
Positive End Expiratory Pressure ◽  
Hemodynamic Changes ◽  
Venous Flow ◽  
Cardiac Depression ◽  
Before And After ◽  
Anesthetized Dogs ◽  
The Right

Recent observations have been interpreted to suggest altered ventricular function during ventilation with positive end-expiratory pressure (PEEP), apart from the effect of reduced preload. We constructed ventricular function curves in 14 anesthetized dogs as PEEP was varied under closed- and open-chest conditions. The systemic venous flow of the animal was diverted through an external circuit so that blood return to the right atrium could be varied stepwise from 1--4.5 l/min before and after 15 cmH2O PEEP was applied to the airway. Pressures adjacent to the heart were measured with thin fluid-filled water sensors to enable estimation of transmural pressure. Alterations in ventricular function were assessed by comparing tangential slopes as well as the atrial pressure differences separating the curves at high and low stroke volumes. Sensitivity of this method to cardiac depression was demonstrated by similar comparisons made before and after propranolol. Curves using transmural pressure on and off PEEP were statistically indistinguishable. We conclude that hemodynamic changes resulting from PEEP are attributable to the combined effects of reduced preload and raised juxtacardiac pressure, without ventricular dysfunction.

Influence of the pericardium on ventricular loading during respiration

1990 ◽  
Vol 68 (4) ◽  
pp. 1640-1650 ◽  
Author(s):  
M. Takata ◽  
W. Mitzner ◽  
J. L. Robotham
Keyword(s):  
Intrathoracic Pressure ◽  
Ventricular Volume ◽  
Esophageal Pressure ◽  
Inferior Vena Caval ◽  
Early Systole ◽  
Anesthetized Dogs ◽  
Acute Changes ◽  
The Right ◽  
Pulmonary Artery Constriction ◽  
Ventricular Dimensions

The influence of the pericardium on ventricular loading during respiration was studied in 17 acutely instrumented anesthetized dogs. Changes in intrapericardial surface pressures (Ppe) on the ventricles were measured by use of air-filled flat latex balloons during acute changes in ventricular loading with the chest open or during negative intrathoracic pressure (NITP) produced by phrenic nerve stimulation with the chest closed. Ppe always demonstrated a phasic change within a cardiac cycle, with its maximum near end diastole and minimum near end systole, and a waveform similar to ventricular dimensions measured by sonomicrometer crystals. With the chest open we found that 1) inferior vena caval constriction decreased Ppe on both ventricles at end diastole (P less than 0.01), 2) aortic constriction increased Ppe on both ventricles at end systole and end diastole (P less than 0.05), and 3) pulmonary artery constriction increased Ppe on the right ventricle (RV) (P less than 0.01) while decreasing Ppe on the left ventricle (LV) at end diastole (P less than 0.05). Thus regional Ppe over a ventricle is influenced by changes in ventricular loading conditions. During NITP with lung volume either constant or increased, Ppe over the anterolateral LV decreased less than two independent extrapericardial measures of intrathoracic pressure, and this resulted in an increased transpericardial pressure at end systole (P less than 0.05) and end diastole (P less than 0.01). During NITP with increased transpericardial pressure, Ppe over the anterior LV, lateral LV, and RV inflow showed small regional differences, but all decreased less than esophageal pressure (P less than 0.01). These results sugges that the increase in transpericardial pressure during late diastole to early systole, produced by increases in ventricular volume during NITP, could effectively attenuate the increases in ventricular preload and afterload caused by respiration, analogous to a negative feedback loop.

End-systolic pressure-volume relationships in dogs during ventilation with PEEP

1988 ◽  
Vol 254 (4) ◽  
pp. H664-H670 ◽  
Author(s):  
A. J. Crottogini ◽  
P. Willshaw ◽  
J. G. Barra ◽  
G. J. Breitbart ◽  
R. H. Pichel
Keyword(s):  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Positive End Expiratory Pressure ◽  
Closed Chest ◽  
Inotropic State ◽  
Anesthetized Dogs ◽  
Lv Volume

Whether left ventricular (LV) contractility changes during ventilation with positive end-expiratory pressure (PEEP) remains controversial. To assess LV inotropic state during PEEP using a load-independent index, we generated end-systolic pressure-volume relationships (ESPVRs) in eight closed-chest, chronically instrumented, anesthetized dogs undergoing 0 [zero end-expiratory pressure for the 1st time (ZEEP1)], 5 (PEEP-5), 10 (PEEP-10), and again 0 (ZEEP2) cmH2O PEEP. LV volume was calculated from three orthogonal internal diameters (sonomicrometry), and LV pressure was measured using an implanted transducer. ESPVRs at each level of PEEP were generated by transient inflation of a vena caval occluder. Despite significant decreases in cardiac output with PEEP-5 (1.81 +/- 0.38 l/min, means +/- SE; P less than 0.05) and PEEP-10 (1.70 +/- 0.46; P less than 0.01) with respect to ZEEP1 (2.12 +/- 0.41), no change was found in the slope (ZEEP1: 6.99 +/- 1.03 mmHg/ml; PEEP-5: 7.48 +/- 1.20; PEEP-10: 7.17 +/- 1.02; ZEEP2: 7.38 +/- 1.02), the volume intercept (ZEEP1: 7.4 +/- 3.4 ml; PEEP-5: 6.6 +/- 3.0; PEEP-10: 7.2 +/- 4.0; ZEEP2: 6.6 +/- 3.6), or the new index area beneath the ESPVR (ZEEP1: 304 +/- 98; PEEP-5: 329 +/- 104; PEEP-10: 310 +/- 98; ZEEP2: 343 +/- 114). We conclude that these levels of PEEP do not affect LV contractility as assessed by the ESPVR.

Effect of positive end-expiratory pressure on hypoxic pulmonary vasoconstriction in the dog

1990 ◽  
Vol 259 (3) ◽  
pp. H697-H705 ◽  
Author(s):  
K. B. Domino ◽  
M. R. Pinsky
Keyword(s):  
Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Linear Regression Analysis ◽  
Left Lung ◽  
Vena Cava ◽  
Positive End Expiratory Pressure ◽  
Anesthetized Dogs ◽  
Alveolar Hypoxia ◽  
Lung Blood Flow ◽  
The Right

We studied the effects of uni- and bilateral positive end-expiratory pressure (PEEP) on pulmonary artery pressure-flow (Ppa/Q) relationships during unilateral hypoxia in anesthetized dogs. A bronchial divider was inserted, the right lung was ventilated with 100% O2, and the left lung was ventilated with either 100% O2 (hyperoxia) or a hypoxic gas mixture (hypoxia). Left lung blood flow (QL) and aortic flow (QT) were measured by electromagnetic flow probes. Simultaneous Ppa/Q relations for both lungs, with Q on the ordinate, were obtained by altering QT via an arteriovenous fistula and an inferior vena cava occluder. Ppa/Q slopes (delta Q/delta Ppa) and extrapolated zero-flow Ppa intercepts (Pzf) were obtained by linear regression analysis. Bilateral PEEP increased Pzf for both lungs (P less than 0.01) but did not alter delta Q/delta Ppa of either lung. Unilateral PEEP decreased ipsilateral blood flow (P less than 0.001) and increased Pzf for the ipsilateral lung (P less than 0.05). Left lung PEEP did not affect the slope of the left lung Ppa/Q relationship (delta QL/delta Ppa). Hypoxic ventilation of the left lung decreased QL (P less than 0.001), increased Pzf (P less than 0.05), and decreased delta QL/delta Ppa (P less than 0.001). Neither uni- nor bilateral PEEP altered this flow diversion away from the left lung or the reduction in delta QL/delta Ppa with left lung hypoxia. We conclude that PEEP and alveolar hypoxia increase pulmonary vascular resistance at different loci, such that their effects are additive. A net increase in 10 cmH2O of PEEP does not inhibit the pulmonary vascular response to regional alveolar hypoxia.

Control of breathing in anesthetized dogs by a left-heart baroreflex

1986 ◽  
Vol 61 (6) ◽  
pp. 2095-2101 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Pulmonary Veins ◽  
Vagal Afferents ◽  
Low Flow ◽  
Base Line ◽  
Left Heart ◽  
Breathing Frequency ◽  
Autonomic Ganglion ◽  
Anesthetized Dogs ◽  
The Right ◽  
Vagal Cooling

Anesthetized open-chest dogs on cardiopulmonary bypass were used to test the hypothesis that breathing reflexly responds to distension of the left-heart chambers. Bypass perfusion withdrew systemic flow from the right atrium and returned it to the aorta after gas exchange. Ventricles were fibrillated. The left heart was isolated by tying all pulmonary veins, and it was perfused separately at low flow admitted through one pulmonary vein and withdrawn from the ventricle. Left-heart pressure was intermittently raised abruptly from a nominal base line of 0 by partial occlusion of outflow. Pressures from approximately 10 to 50 cmH2O caused proportional increases in breathing frequency and decreases in expiratory and inspiratory times. Changes occurred immediately, reached a plateau within approximately 20 s, and were sustained for periods of observation as long as 3 min. Recovery to base line followed stimulus removal. Vagal cooling to 8 degrees C prevented responses, but autonomic ganglion blockade with hexamethonium had no effect. I conclude that breathing may be stimulated by left-heart distension and that this is mediated by large myelinated vagal afferents.

Pericardial mechanoreceptors with phrenic afferents

1993 ◽  
Vol 264 (6) ◽  
pp. H1836-H1846 ◽  
Author(s):  
D. R. Kostreva ◽  
S. P. Pontus
Keyword(s):  
Phrenic Nerve ◽  
Cardiac Rhythm ◽  
Afferent Activity ◽  
Fibrous Layer ◽  
Anesthetized Dogs ◽  
Anatomic Distribution ◽  
Phrenic Nerves ◽  
The Right

Pericardial mechanoreceptors with afferents in the phrenic nerves were studied in anesthetized dogs. The specific aims determined 1) if pericardial receptors with phrenic afferents exist in the dog; 2) the stimuli needed to activate these receptors; 3) the anatomic distribution of these pericardial receptors; and 4) which pericardial layer contains the receptors. Afferent activity was recorded from the phrenic nerves while the pericardium was probed. In 15 of 18 animals, pericardial receptors were found on the right side. In 12 of 18 animals pericardial receptors were located on the left side. Most of the mechanoreceptors were found in a band that paralleled the pericardiophrenic attachment, in the fibrous layer of the pericardium, overlying the atria and atrioventricular grooves. Some receptors had a cardiac rhythm, whereas others were stimulated by the inflating lung. None of the receptors were chemosensitive to capsaicin, bradykinin, or saline. This study is the first to demonstrate that the pericardium of the dog contains mechanosensitive receptors which are innervated by the phrenic nerve.

Sign in / Sign up

Export Citation Format

Share Document