Influence of the right ventricle on canine left ventricular function with PEEP

1982 ◽  
Vol 52 (1) ◽  
pp. 254-259 ◽  
Author(s):  
S. M. Scharf ◽  
R. Brown
Keyword(s):  
Pulmonary Arterial Pressure ◽  
Arterial Occlusion ◽  
Left Ventricular ◽  
Right Atrial ◽  
Lv Function ◽  
Stroke Work ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
The Right ◽  
Extracorporeal Bypass

In anesthetized dogs we evaluated the influence of increased right ventricular (RV) pressures on left ventricular (LV) function by comparing the hemodynamic effects of increases in RV afterload (pulmonary arterial pressure) produced by positive end-expiratory pressure (PEEP) with those due to pulmonary arterial occlusion (PAO). Left atrial (Pla) and right atrial (Pra) pressures increased with PEEP and PAO [for Pla: 3.1 +/- 0.7 Torr (PEEP), 2.4 +/- 0.9 Torr (PAO); for Pra: 2.9 +/- 0.4 Torr (PEEP), 3.1 +/- 1.2 Torr (PAO)]. RV septal-free wall dimension (RVD) increased, and LV septal-posterolateral dimension (L2) decreased with both conditions [increases in RVD: 1.9 +/- 0.3 mm (PEEP), 2.2 +/- 0.5 mm (PAO); decrease in L2: 1.1 +/- 0.4 mm (PEEP), 0.9 +/- 0.3 mm (PAO)]. Extracorporeal bypass of the great veins did not alter these findings. LV function curves showed less stroke work at any Pla during PEEP, this being unaffected by vagotomy. When the RV was bypassed, there were no PEEP or PAO related changes in Pla or LV function. Thus diminished LV function with PEEP is probably due to the influence on the LV of a stressed RV in this situation.

Opening the pericardium during pulmonary artery constriction improves cardiac function

2004 ◽  
Vol 96 (3) ◽  
pp. 917-922 ◽  
Author(s):  
Israel Belenkie ◽  
Rozsa Sas ◽  
Jamie Mitchell ◽  
Eldon R. Smith ◽  
John V. Tyberg
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
End Diastolic Volume ◽  
Anesthetized Dogs ◽  
Acute Pulmonary Hypertension ◽  
The Right ◽  
Pulmonary Artery Constriction

During acute pulmonary hypertension, both the pericardium and the right ventricle (RV) constrain left ventricular (LV) filling; therefore, pericardiotomy should improve LV function. LV, RV, and pericardial pressures and RV and LV dimensions and LV stroke volume (SV) were measured in six anesthetized dogs. The pericardium was closed, the chest was left open, and the lungs were held away from the heart. Data were collected at baseline, during pulmonary artery constriction (PAC), and after pericardiotomy with PAC maintained. PAC decreased SV by one-half. RV diameter increased, and septum-to-LV free wall diameter and LV area (our index of LV end-diastolic volume) decreased. Compared with during PAC, pericardiotomy increased LV area and SV increased 35%. LV and RV compliance (pressure-dimension relations) and LV contractility (stroke work-LV area relations) were unchanged. Although series interaction accounts for much of the decreased cardiac output during acute pulmonary hypertension, pericardial constraint and leftward septal shift are also important. Pericardiotomy can improve LV function in the absence of other sources of external constraint to LV filling.

Optimal matching between canine left ventricle and afterload

1988 ◽  
Vol 254 (6) ◽  
pp. H1051-H1058
Author(s):  
E. S. Myhre ◽  
A. Johansen ◽  
H. Piene
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Stroke Work ◽  
External Work ◽  
Volume Load ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Pressure Volume Relationship ◽  
Optimal Values

A parabolic relationship exists between ventricular external work and arterial load at given preload and contractility. Previous data indicate that the working point falls close to the parabola optimum. By combining the left ventricular (LV) end-systolic pressure-volume relationship (ESPVR) and an equation describing external stroke work, optimum values of stroke volume (SV), the slope (Emax) of the ESPVR, and arterial resistance (Rp) corresponding with the optimum (i.e., mSV, mEmax, mRp) were obtained. Experiments in anesthetized dogs were performed to test whether mSV, mEmax, and mRp also correspond to observed SV, Emax, and Rp at three different levels of volume load (right atrial pressure, RAP) before and after acute depression of LV contractility. Comparisons of observed and optimal values of SV, Emax, and Rp were made before and after LV depression. Before embolization, the ratios were SV/mSV 1.10–1.20 (RAP 5–15 mmHg); Emax/mEmax 1.21–1.41; and Rp/mRp 0.84–0.69. After LV depression, SV/mSV was 0.80–0.83, Emax/mEmax was 0.78–0.71, and Rp/mRp was 1.56–1.46. The ratios were all significantly changed (P less than 0.01) by the induced LV depression. The present analysis may offer a new tool to detect nonoptimal relations between cardiac and arterial functions.

Cardiovascular regulation during head-out water immersion exercise

1990 ◽  
Vol 69 (2) ◽  
pp. 657-664 ◽  
Author(s):  
J. L. Christie ◽  
L. M. Sheldahl ◽  
F. E. Tristani ◽  
L. S. Wann ◽  
K. B. Sagar ◽  
...  
Keyword(s):  
Pulmonary Arterial Pressure ◽  
Water Immersion ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Dynamic Exercise ◽  
Right Atrial ◽  
Stroke Index ◽  
Suprasternal Notch ◽  
Pulmonary Arterial ◽  
Cardiac Filling

Head-out water immersion is known to increase cardiac filling pressure and volume in humans at rest. The purpose of the present study was to assess whether these alterations persist during dynamic exercise. Ten men performed upright cycling exercise on land and in water to the suprasternal notch at work loads corresponding to 40, 60, 80, and 100% maximal O2 consumption (VO2max). A Swan-Ganz catheter was used to measure right atrial pressure (PAP), pulmonary arterial pressure (PAP), and cardiac index (CI). Left ventricular end-diastolic (LVED) and end-systolic (LVES) volume indexes were assessed with echocardiography. VO2max did not differ between land and water. RAP, PAP, CI, stroke index, and LVED and LVES volume indexes were significantly greater (P less than 0.05) during exercise in water than on land. Stroke index did not change significantly from rest to exercise in water but increased (P less than 0.05) on land. Arterial systolic blood pressure did not differ between land and water at rest or during exercise. Heart rates were significantly lower (P less than 0.05) in water only during the two highest work intensities. The results indicate that indexes of cardiac preload are greater during exercise in water than on land.

Inconstancy Of PGI2 Administration In Preventing Attacks Of Prinzmetal Angina

1981 ◽  
Author(s):  
S Chierchia ◽  
R De Caterina ◽  
F Crea ◽  
W Bernini ◽  
A Distante ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Pulmonary Arterial Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Local Defects ◽  
Ecg Leads

It has been proposed that vasospastic angina, eventually due to local defects of PGI2 production, might benefit from PGI2 administration. We therefore investigated the effects of PGI2 in healthy volunteers and, then, in patients with frequent ischemic episodes (IE) of Prinzmetal angina, to detennine 1. hemodynamic, antiplatelet and possible side effects of the drug and 2. its possible therapeutic usefulness in the management of IE. In 6 healthy volunteers PGI2 was infused i.v. at doses of 2.5,5,10 and 20 ng/kg/min during consecutive periods of 30 min each. Heart rate (HR) and right atrial pressure were monitored continuously; cardiac output (thermodilution in 2 subjects, indirectly by a Doppler technique in all), arterial blood pressure (BP) and in-vitro platelet aggre- gability (PA) by ADP (Born), intermittently. In 2 subjects we also measured pulmonary arterial pressure and, in one, left ventricular pressure, during the infusion and in control conditions. PGI2 was then infused in 6 pts with frequent IE at maximal well tolerable rate (6-26 ng/kg/min) for periods of 3 hours alternated with equal periods of placebo (P), continuosly recording 2 ECG leads to detect ST-T changes, and sampling blood for PA as before. In all healthy volunteers PGI2, at the highest rates of infusion, decreased significantly (p < .001) both systolic BP (-10 ± 3%, mean ± SD) and diastolic BP (-19 ± 5%) increasing HR (+ 21 ± 5%); no significant changes were observed in the other hemodynamic parameters. The maximal decrease in PA was 58 ± 30%(p <. 001). Skin flushing, restlessness and headache, sometimes observed at the highest doses, rapidly disappeared decreasing the infusion rate. In the 6 pts the same trend in BP, HR and PA was evident. 106 IE were observed. PGI2 did not affect severity, duration and number of IE (44 during P, 62 during PGI2 infusion). One of the pts, however,not clinically different from the others, showed a reduction at 10 ng/ kg/min (6 IE during P, 2 during PGI2) and a complete abolition in the 3 following periods at 20 ng/kg/min (4,3,5 IE during P vs. none duringPGI2). We conclude that 1. PGI2 can be safely administered to humans and 2. it may prevent IE is some vasospastic pts, but not in others. Different pathogenetic mechanisms are perhaps involved in apparently similar Prinzmetal anginas.

Effects of arteriovenous fistula on systemic and pulmonary circulations

1964 ◽  
Vol 207 (6) ◽  
pp. 1319-1324 ◽  
Author(s):  
Jiro Nakano ◽  
Christian De Schryver
Keyword(s):  
Cardiac Output ◽  
Blood Transfusion ◽  
Arterial Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Pulmonary Arterial

The effects of arteriovenous fistulas of different magnitudes on cardiovascular dynamics were studied in anesthetized dogs. It was found that A-V fistula decreases mean systemic arterial pressure, effective systemic blood flow, total and pulmonary peripheral resistances, whereas it increases heart rate, total cardiac output, stroke volume, left atrial pressure, pulmonary arterial pressure, and systemic peripheral resistance. The magnitude of the above hemodynamic changes was essentially proportional to the size of the fistula. At equivalent increments in total cardiac output produced by A-V fistula and blood transfusion, the former condition causes a greater increase in pulmonary arterial pressure than the latter, although both conditions decrease the pulmonary peripheral resistance by the same degree. It was also found that, at equivalent left atrial pressures, left ventricular stroke work with A-V fistula was greater than that with blood transfusion.

Transmural metabolic gradients in the normal dog left ventricle: effect of right atrial pacing

1977 ◽  
Vol 233 (2) ◽  
pp. H217-H221 ◽  
Author(s):  
T. B. Allison ◽  
J. W. Holsinger
Keyword(s):  
Right Atrial ◽  
Control Group ◽  
Base Line ◽  
Atrial Pacing ◽  
Stroke Work ◽  
Ischemic Insult ◽  
Circumflex Artery ◽  
Heart Work ◽  
Anesthetized Dogs ◽  
The Right

The effects of atrial pacing on tissue metabolite levels known to be sensitive to ischemia were examined. Anesthetized dogs were thoracotomized and a pacing electrode was sutured to the right atrium. Pacing at rates of 200 or 250 beats/min (10 animals per group) was performed for 15 min after base-line hemodynamic data had been obtained. At the end of the pacing period, a transmural biopsy was taken, frozen in liquid nitrogen, and sectioned into subepicardial, midmyocardial, and subendocardial layers. ATP, phosphocreatine, lactate, and glycogen were extracted and analyzed. Significant (P less than 0.001) transmural gradients of each of these metabolites existed in the control group. Pacing had no significant (P greater than 0.2) effect on any metabolite from layer to layer at 200 or 250 beats/min. However, indices of heart work (i.e., contractility (dP/dt), stroke work, and stroke volume) demonstrated significant reductions (P less than 0.01) due to pacing, while circumflex artery blood flow increased more than twofold (P less than 0.001) at the highest rate. These data suggest that physiologic autoregulation occurred during pacing and protected the subendocardium from stress-induced ischemic insult.

Enhanced systolic function of the right ventricle during respiratory distress syndrome in newborn lambs

2001 ◽  
Vol 280 (1) ◽  
pp. H392-H400 ◽  
Author(s):  
Maartje De Vroomen ◽  
Paul Steendijk ◽  
Robbert H. Lopes Cardozo ◽  
Hens H. A. Brouwers ◽  
Frank Van Bel ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Distress Syndrome ◽  
Pulmonary Arterial Pressure ◽  
Systolic Function ◽  
Systolic Pressure ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
Ventricular Systolic Function ◽  
Pulmonary Arterial ◽  
The Right

Respiratory distress syndrome (RDS) causes pulmonary hypertension. It is often suggested that this increased afterload for the right ventricle (RV) might lead to cardiac dysfunction. To examine this, we studied biventricular function in an experimental model. RDS was induced by lung lavages in seven newborn lambs. Five additional lambs served as controls. Cardiac function was quantified by indexes derived from end-systolic pressure-volume relations obtained by pressure-conductance catheters. After lung lavages, a twofold increase of mean pulmonary arterial pressure (from 15 to 34 mmHg) was obtained and lasted for the full 4-h study period. Stroke volume was maintained (5.2 ± 0.6 ml at baseline and 6.1 ± 1.4 ml at 4 h of RDS), while RV end-diastolic volume showed only a slight increase (from 6.5 ± 2.3 ml at baseline to 7.7 ± 1.3 ml at 4 h RDS). RV systolic function improved significantly, as indicated by a leftward shift and increased slope of the end-systolic pressure-volume relation. Left ventricular systolic function showed no changes. In control animals, pulmonary arterial pressure did not increase and right and left ventricular systolic function remained unaffected. In the face of increased RV afterload, the newborn heart is able to maintain cardiac output, primarily by improving systolic RV function through homeometric autoregulation.

Effects of angiotensin on pulmonary and systemic hemodynamics

1962 ◽  
Vol 202 (4) ◽  
pp. 690-694 ◽  
Author(s):  
John E. Chimoskey ◽  
Pedro C. Blaquier ◽  
A. C. Taquini ◽  
David F. Bohr
Keyword(s):  
Heart Rate ◽  
Renin Angiotensin System ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Pulmonary Resistance ◽  
Angiotensin System ◽  
Arterial Resistance ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial

In ten morphine-urethan anesthetized dogs single injections of 2.0 µg/kg of synthetic valine 5 angiotensin II amide elevated systemic and pulmonary arterial pressures and depressed heart rate. Thirty-minute intravenous infusions of angiotensin (0.4 and 1.0 µg/kg/min) in eight dogs elevated systemic arterial pressure and diminished heart rate. Pulmonary arterial, pulmonary wedge, left ventricular end-diastolic, and right atrial pressures were all slightly elevated; mean cardiac output did not change. Calculated total pulmonary resistance and pulmonary arterial resistance were diminished; central blood volume was elevated. These findings suggest that elevated systemic pressure and resistance increase myocardial work and induce reflex bradycardia, thereby elevating left ventricular end-diastolic, pulmonary wedge, and pulmonary arterial pressures. Systemic vasoconstriction also contributes to the elevated right atrial pressure and distention of the pulmonary vascular bed, which diminishes total pulmonary and pulmonary arterial resistance. These findings are not incompatible with the theory that the renin-angiotensin system is active in essential hypertension.

scholarly journals Elevated plasma endocan and BOC in heart failure patients decrease after heart transplantation in association with improved hemodynamics

2020 ◽  
Vol 35 (11) ◽  
pp. 1614-1628
Author(s):  
Salaheldin Ahmed ◽  
Abdulla Ahmed ◽  
Habib Bouzina ◽  
Jakob Lundgren ◽  
Göran Rådegran
Keyword(s):  
Heart Failure ◽  
Heart Transplantation ◽  
Plasma Levels ◽  
Left Ventricular ◽  
Right Atrial ◽  
Ageing Population ◽  
Stroke Work ◽  
Major Health Problem ◽  
Pulmonary Arterial ◽  
Related Proteins

Abstract Background The prevalence of heart failure (HF) is rising with ageing population and constitutes a major health problem globally. A common complication of HF is pulmonary hypertension (PH) which negatively impacts survival. A pathophysiological association between HF and PH with tumorigenic processes has been suggested. We aimed to identify the plasma levels of, and the association between tumour-related proteins and hemodynamic improvements in patients with HF and PH due to left heart disease (LHD) before and 1-year after heart transplantation (HT). Methods Forty-eight tumour-related proteins were measured with proximity extension assay in plasma from 20 controls and 26 HF patients before and 1-year after HT. Patients’ hemodynamics were measured with right heart catheterization. Results Out of 48 proteins, specifically, plasma levels of endocan and brother of CDO (BOC) were elevated in end-stage HF patients compared to controls (p < 0.001), but decreased after HT (p < 0.01), towards controls’ levels. The decrease of endocan levels after HT correlated with improved mean pulmonary arterial pressure (rs = 0.80, p < 0.0001), pulmonary arterial wedge pressure (rs = 0.63, p = 0.0012), and pulmonary vascular resistance (rs = 0.70, p < 0.001). The decrease and normalization of BOC after HT correlated with decreased mean right atrial pressure (rs = 0.61 p = 0.0015) and NT-proBNP (rs = 0.57, p = 0.0022), as well as increased cardiac index (rs = − 0.51, p = 0.0086) and left-ventricular stroke work index (rs = − 0.57, p = 0.0039). Conclusion Our results suggest that (i) plasma endocan in HF may reflect the state of pulmonary vascular congestion and PH-LHD, whereas (ii) plasma BOC may reflect the cardiac function and the hemodynamic overload in HF. The exact role of these proteins and their clinical applicability as biomarkers in HF and PH-LHD ought to be investigated in larger cohorts.

Absence of right ventricular isovolumic relaxation in open-chest anesthetized dogs

1992 ◽  
Vol 263 (5) ◽  
pp. H1587-H1590 ◽  
Author(s):  
E. S. Myhre ◽  
B. K. Slinker ◽  
M. M. LeWinter
Keyword(s):  
Right Ventricular ◽  
Left Ventricular ◽  
Right Atrial ◽  
Relative Timing ◽  
Relaxation Period ◽  
First Derivative ◽  
Open Chest ◽  
Anesthetized Dogs ◽  
The Right ◽  
Isovolumic Relaxation

During the left ventricular (LV) pump cycle, peak negative first derivative of pressure vs. time (dP/dt) occurs very close to the end of LV ejection, and there is a well-defined isovolumic relaxation period. Despite similarities between the right ventricular (RV) and LV pump cycles, recent studies indicate uncertainty as to whether peak negative RV dP/dt occurs simultaneously with RV end ejection and whether there is an isovolumic relaxation period during the RV pump cycle. To study these questions, we recorded relative timing of peak negative RV dP/dt, RV end ejection, and right atrial-RV pressure crossover in the open-chest anesthetized dog. The data demonstrate that peak negative RV dP/dt occurs an average of 60 ms before end ejection and that there is no RV isovolumic relaxation period. These findings have implications for the possible use of peak negative RV dP/dt as a marker of RV end ejection and for how time constants of pressure decay obtained during RV relaxation can be interpreted.

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