Right and left ventricular pressure-volume response to positive end-expiratory pressure

1984 ◽  
Vol 246 (1) ◽  
pp. H114-H119 ◽  
Author(s):  
W. P. Santamore ◽  
A. A. Bove ◽  
J. L. Heckman
Keyword(s):  
Right Ventricular ◽  
Left Ventricular Pressure ◽  
Cardiovascular Effects ◽  
Left Ventricular ◽  
Positive End Expiratory Pressure ◽  
End Diastolic Volume ◽  
Diastolic Stiffness ◽  
Volume Response ◽  
Volume Measurements ◽  
Left And Right

Cardiovascular effects of positive end-expiratory pressure (PEEP) at 20 cmH2O were examined in six mongrel dogs (11.3-15.0 kg). The dogs were anesthetized through a combination of intramuscular Innovar and gaseous anesthesia (60% N2O-40% O2). For volume measurements, radiodense tantalum screws were placed on the endocardial surface of the left and right ventricle. Esophageal and left and right ventricular pressures were measured. With the use of this preparation, the effects of positive end-expiratory pressure (PEEP = 20 cmH2O) on cardiovascular function were examined. PEEP caused right ventricular transmural pressures to decrease, 3.4 +/- 1.0 to 2.0 +/- 1.0 mmHg end-diastolic (P less than 0.05) and 29.2 +/- 2.2 to 27.9 + 2.2 mmHg peak systolic; left ventricular transmural pressures decreased, 5.9 +/- 1.6 to 1.2 +/- 1.4 mmHg end-diastolic (P less than 0.05) and 117.2 +/- 8.0 to 76.2 +/- 7.4 mmHg peak systolic (P less than 0.05). After volume loading the animal (500 ml dextran), PEEP caused similar changes in right and left ventricular pressures. Plots of end-diastolic volume versus pressure showed an increase in the apparent diastolic stiffness in both ventricles with decreased end-diastolic volume.

Malignant Hyperthermia Phenotype

2000 ◽  
Vol 92 (6) ◽  
pp. 1777-1788 ◽  
Author(s):  
Daniel C. Sigg ◽  
Paul A. Iaizzo
Keyword(s):  
Malignant Hyperthermia ◽  
Right Ventricular ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
High Dose ◽  
Central Venous ◽  
Induced Hypotension ◽  
Arterial Blood ◽  
Left And Right

Background Succinylcholine causes immediate and severe arterial hypotension in swine with the malignant hyperthermia phenotype. The underlying mechanisms are unknown. Methods Malignant hyperthermia-susceptible (MHS; n = 10) and normal swine (n = 5) were anesthetized with thiopental. The following were monitored: electrocardiogram; arterial blood pressure; pulmonary artery, central venous, and left and right ventricular pressure; cardiac output; end-tidal carbon dioxide; core temperature; peripheral-blood flows; and arterial blood gases. After a control period, 2 mg/kg succinylcholine was given intravenously. Three MHS animals received 1 mg/kg vecuronium and two MHS animals received 2.5 mg/kg dantrolene intravenously. The effects of succinylcholine on left and right ventricular pressure and contractility were analyzed in isolated hearts. The effects of 0.06 mm succinylcholine on isometric tension development were recorded in isolated femoral artery rings. Results Succinylcholine caused an early, severe decrease in blood pressure, cardiac output, left ventricular pressure, and left ventricular contractility in MHS swine but not in normal swine; no significant differences were found in heart rate, right ventricular parameters, systemic vascular resistance, and preload (pulmonary diastolic pressure, central venous pressure). The succinylcholine-induced hypotension and associated effects were not prevented by dantrolene. However, pretreatment with high-dose vecuronium prevented not only the cardiovascular depression, but also MH. In addition, no phenotypic differences of succinylcholine on contractility or left ventricular pressure were observed in the isolated working hearts. Similary, succinylcholine did not cause a significantly different relaxation in rings in either phenotype. Conclusion Succinylcholine-induced hypotension occurred before muscle hypermetabolism in MHS swine. Succinylcholine had no differential physiologic effects on either the isolated heart or on isolated arteries. This hypotension could not be prevented by dantrolene but was prevented by pretreatment with high-dose vecuronium. Thus, an indirect mechanism such as the release of a cardiac depressant from skeletal muscle may have caused this hypotensive response.

Dimensional analysis of right and left ventricles during positive-pressure ventilation in dogs

1982 ◽  
Vol 242 (4) ◽  
pp. H549-H556 ◽  
Author(s):  
S. S. Cassidy ◽  
J. H. Mitchell ◽  
R. L. Johnson
Keyword(s):  
Left Ventricle ◽  
Stroke Volume ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Left Ventricular Volumes ◽  
Ventricular Volumes ◽  
End Diastolic Volume ◽  
Left And Right ◽  
The Right ◽  
Ventricular Dimensions

Our purpose was to determine the effects of controlled ventilation with positive end-expired pressure (PEEP) on ventricular dimensions and to relate changes in shape to changes in stroke volume and left ventricular volumes. Left and right ventricular dimensions were measured using biplane cinefluorography of dogs with radiopaque markers implanted in their hearts, and left ventricular volumes were derived from left ventricular dimensions by assuming that the left ventricle conformed to the shape of a nonprolate ellipsoid. As PEEP increased from 0 to 5, 10, and 15 cmH2O, stroke volume fell 36%, and all three left ventricular end-diastolic dimensions fell, with apex-base falling 5%, anterior-posterior falling 7%, and septal-lateral falling nearly twice as much, 12%. This resulted in a 11.3 cm3 fall in left ventricular end-diastolic volume. The right ventricular end-diastolic dimensions changed in opposite directions with respect to each other as the level and PEEP was raised to 15 cmH2O; one axis fell 3.2 mm, and the midpoint of the right ventricular free wall moved outward by 1.7 mm. Thus the fall in cardiac output (and stroke volume) during PEEP was associated with a fall in left ventricular end-diastolic volume and a change both left and right ventricular configurations. It is not known whether the left ventricular septal-lateral narrowing is the consequence of lateral wall compression by the lungs or encroachment on the left ventricle by the septum.

Effects of regional ischemia and ventricular pacing on LV dP/dtmax-end-diastolic volume relation

1987 ◽  
Vol 252 (5) ◽  
pp. H933-H940 ◽  
Author(s):  
W. C. Little ◽  
R. C. Park ◽  
G. L. Freeman
Keyword(s):  
Coronary Artery ◽  
Right Ventricular ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Ventricular Pressure ◽  
Free Wall ◽  
Ventricular Pacing ◽  
End Diastolic Volume ◽  
The Right

We investigated the effects of coronary artery occlusion and pacing from ventricular sites on the relation of the maximum rate of rise of left ventricular pressure (dP/dtmax) to the end-diastolic volume (VED) in dogs previously instrumented to measure left ventricular pressure and to determine left ventricular volume from three ultrasonically measured dimensions. The dP/dtmax-VED relation was generated by vena caval occlusion and compared with the simultaneously produced end-systolic pressure-end-systolic volume (PES-VES) relation. The dP/dtmax-VED relation was described by a straight line during all conditions. Occlusion of the left circumflex coronary artery produced a rightward shift of the dP/dtmax-VED relation, increasing the volume intercept by 11.3 +/- 5.3 (SD) ml (P less than 0.05). Compared with atrial pacing, the dP/dtmax-VED relation was shifted to the right with the volume intercept increasing by 4.8 +/- 4.4 ml (P less than 0.05) during pacing from the right ventricular free wall, 3.7 +/- 5.0 ml (P less than 0.05) during pacing from the right ventricular apex, and 3.7 +/- 2.4 ml (P less than 0.05) during pacing from the left ventricular free wall. Similar increases were observed in the volume intercepts of the PES-VES relations during coronary occlusion or ventricular pacing. These results are consistent with the predictions of the time-varying elastance model and support its use as a conceptual framework to understand left ventricular performance during isovolumic contraction and at end systole, both in the normal ventricle and the ventricle with regional abnormalities of contraction.

Right and left ventricular pressure-volume response to respiratory maneuvers

1984 ◽  
Vol 57 (5) ◽  
pp. 1520-1527 ◽  
Author(s):  
W. P. Santamore ◽  
J. L. Heckman ◽  
A. A. Bove
Keyword(s):  
Right Ventricular ◽  
Diastolic Pressure ◽  
Valsalva Maneuver ◽  
Left Ventricular Pressure ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Left Ventricular Volumes ◽  
Right Ventricular Volume ◽  
Ventricular Volumes ◽  
End Diastolic Volume

With respiration, right ventricular end-diastolic volume fluctuates. We examined the importance of these right ventricular volume changes on left ventricular function. In six mongrel dogs, right and left ventricular volumes and pressures and esophageal pressure were simultaneously measured during normal respiration, Valsalva maneuver, and Mueller maneuver. The right and left ventricular volumes were calculated from cineradiographic positions of endocardial radiopaque markers. Increases in right ventricular volume were associated with changes in the left ventricular (LV) pressure-volume relationship. With normal respiration, right ventricular end-diastolic volume increased 2.3 +/- 0.7 ml during inspiration, LV transmural diastolic pressure was unchanged, and LV diastolic volume decreased slightly. This effect was accentuated by the Mueller maneuver; right ventricular end-diastolic volume increased 10.4 +/- 2.3 ml (P less than 0.05), while left ventricular end-diastolic pressure increased 3.6 mmHg (P less than 0.05) without a significant change in left ventricular end-diastolic volume. Conversely, with a Valsalva maneuver, right ventricular volume decreased 6.5 +/- 1.2 ml (P less than 0.05), and left ventricular end-diastolic pressure decreased 2.2 +/- 0.5 mmHg (P less than 0.05) despite an unchanged left ventricular end-diastolic volume. These changes in the left ventricular pressure-volume relationship, secondary to changes in right ventricular volumes, are probably due to ventricular interdependence. Ventricular interdependence may also be an additional factor for the decrease in left ventricular stroke volume during inspiration.

Effects of intravenous anesthetic agents on left ventricular function in dogs

1977 ◽  
Vol 232 (1) ◽  
pp. H44-H48
Author(s):  
L. D. Horwitz
Keyword(s):  
Left Ventricular Pressure ◽  
Cardiovascular Effects ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Intravenous Anesthetic ◽  
First Derivative ◽  
Anesthetic Agents ◽  
Thiopental Sodium ◽  
Stimulation Of ◽  
Mean Heart Rate

The cardiovascular effects of ketamine hydrochloride and thiopental sodium were studied in 11 dogs. During anesthesia, mean heart rate rose to 185 beats/min with ketamine and 147 beats/min with thiopental. Cardiac output was increased with ketamine but unchanged by thiopental. The maximum first derivative of the left ventricular pressure (dP/dt max) fell by 14% with thiopental but did not change significantly with ketamine. Propranolol resulted in attenuation of the tachycardia and a fall of 10% in dP/dt max with ketamine but had little effect on the response to thiopental. Phentolamine had no consistent effects on either drug. With pentolinium both drugs decreased dP/dt max. Intracoronary injection of ketamine decreased dP/dt max. Adrenalectomy had little effect on the responses to either anesthetic. The results lead to the conclusion that both ketamine and thiopental have myocardial depressant effects, but, whereas thiopental does not alter sympathetic tone, the depressive effects of ketamine are obscured by stimulation of cardiac sympathetic nerves.

Regulation of β myosin heavy chain, c-myc and c-fos proto-oncogenes in thyroid hormone-induced hypertrophy of the rat myocardium

1993 ◽  
Vol 84 (1) ◽  
pp. 61-67 ◽  
Author(s):  
N. K. Green ◽  
M. D. Gammage ◽  
J. A. Franklyn ◽  
A. M. Heagerty ◽  
M. C. Sheppard
Keyword(s):  
Thyroid Hormone ◽  
Right Ventricular ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Molecular Mechanisms ◽  
Left Ventricular ◽  
Transcriptional Level ◽  
Messenger Rnas ◽  
Hypertrophic Response ◽  
Left And Right

1. In order to investigate the molecular mechanisms determining the hypertrophic response of the ventricular myocardium to thyroid hormone administration, changes in left and right ventricular expression of the c-myc, c-fos and H-ras proto-oncogenes in response to treatment with 3,3′,5-tri-iodothyronine were defined. 2. Adult female Wistar rats were treated with daily subcutaneous injections of 3,3′,5-tri-iodothyronine (50 μg) for 1, 3, 7 or 14 days (n = 6 in each treatment group) and the results from 3,3′,5-tri-iodothyronine-treated animals were compared with those obtained from untreated controls (n = 6). Changes in the weight of the left and right ventricles in response to 3,3′,5-tri-iodothyronine treatment were measured; changes in expression of the c-myc, c-fos and H-ras proto-oncogenes were determined in parallel by measurement of specific messenger RNAs by Northern and dot hybridization, as well as changes in expression of β myosin heavy chain messenger RNA. 3. Treatment with 3,3′,5-tri-iodothyronine resulted in increases in both left and right ventricular weights after 3 days, an effect maintained up to 14 days. Despite an increase in left ventricular weight, levels of β myosin heavy chain, c-myc, c-fos and H-ras mRNAs in the left ventricle were unchanged; in contrast, an increase in right ventricular weight was associated with increased expression of β myosin heavy chain, c-myc and c-fos messenger RNAs. 4. These specific ventricular changes in gene expression, in the face of a hypertrophic response of both ventricles to 3,3′,5-tri-iodothyronine, suggest that the cardiac growth response to thyroid hormones reflects the well-documented secondary haemodynamic influences rather than direct gene regulatory actions of 3,3′,5-tri-iodothyronine at the transcriptional level on the genes studied. Changes in right ventricular proto-oncogene and β myosin heavy chain expression may in turn reflect an increase in right ventricular pressure load.

Levels of brain natriuretic peptide in children with right ventricular overload due to congenital cardiac disease

2005 ◽  
Vol 15 (4) ◽  
pp. 396-401 ◽  
Author(s):  
Thomas S. Mir ◽  
Jan Falkenberg ◽  
Bernd Friedrich ◽  
Urda Gottschalk ◽  
Throng Phi Lê ◽  
...  
Keyword(s):  
Right Ventricle ◽  
Brain Natriuretic Peptide ◽  
Right Ventricular ◽  
Natriuretic Peptide ◽  
Cardiac Disease ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Congenital Cardiac Disease ◽  
The Right

Objective:To evaluate the role of the concentration of brain natriuretic peptide in the plasma, and its correlation with haemodynamic right ventricular parameters, in children with overload of the right ventricle due to congenital cardiac disease.Methods:We studied 31 children, with a mean age of 4.8 years, with volume or pressure overload of the right ventricle caused by congenital cardiac disease. Of the patients, 19 had undergone surgical biventricular correction of tetralogy of Fallot, 11 with pulmonary stenosis and 8 with pulmonary atresia, and 12 patients were studied prior to operations, 7 with atrial septal defects and 5 with anomalous pulmonary venous connections. We measured brain natriuretic peptide using Triage®, from Biosite, United States of America. We determined end-diastolic pressures of the right ventricle, and the peak ratio of right to left ventricular pressures, by cardiac catheterization and correlated them with concentrations of brain natriuretic peptide in the plasma.Results:The mean concentrations of brain natriuretic peptide were 87.7, with a range from 5 to 316, picograms per millilitre. Mean end-diastolic pressure in the right ventricle was 5.6, with a range from 2 to 10, millimetres of mercury, and the mean ratio of right to left ventricular pressure was 0.56, with a range from 0.24 to 1.03. There was a positive correlation between the concentrations of brain natriuretic peptide and the ratio of right to left ventricular pressure (r equal to 0.7844, p less than 0.0001) in all patients. These positive correlations remained when the children with tetralogy of Fallot, and those with atrial septal defects or anomalous pulmonary venous connection, were analysed as separate groups. We also found a weak correlation was shown between end-diastolic right ventricular pressure and concentrations of brain natriuretic peptide in the plasma (r equal to 0.5947, p equal to 0.0004).Conclusion:There is a significant correlation between right ventricular haemodynamic parameters and concentrations of brain natriuretic peptide in the plasma of children with right ventricular overload due to different types of congenital cardiac disease. The monitoring of brain natriuretic peptide may provide a non-invasive and safe quantitative follow up of the right ventricular pressure and volume overload in these patients.

Norepinephrine and dobutamine improve cardiac index equally by supporting opposite sides of the heart in an experimental model of chronic pulmonary hypertension

2021 ◽  
Author(s):  
Janus Adler Hyldebrandt ◽  
Nikolaj Bøgh ◽  
Camilla Omann Christensen ◽  
Peter Agger
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Index ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
End Diastolic Volume ◽  
Chronic Pulmonary Hypertension ◽  
Blood Pressures ◽  
The Right

Abstract Background: Pulmonary hypertension is a significant risk factor in patients undergoing surgery. The combined effects of general anaesthesia and positive pressure ventilation can aggravate this condition and cause increased pulmonary blood pressures, reduced systemic blood pressures and ventricular contractility. Although perioperative use of inotropic support or vasopressors is almost mandatory for these patients, preference is disputed. In this study, we investigated the effects of norepinephrine and dobutamine and their ability to improve the arterio-ventricular relationship and haemodynamics in pigs suffering from chronic pulmonary hypertension.Method: Pulmonary hypertension was induced in five pigs by banding the pulmonary artery at 2–3 weeks of age. Six pigs served as controls. After 16 weeks of pulmonary artery banding, the animals were re-examined under general anaesthesia using biventricular conductance catheters and a pulmonary artery catheter. After baseline measurements, the animals were exposed to both norepinephrine and dobutamine infusions in incremental doses, with a stabilizing period in between the infusions. The hypothesis of differences between norepinephrine and dobutamine with incremental doses was tested using repeated two-way ANOVA and Bonferroni multiple comparisons post-test. Results: At baseline, pulmonary artery banded animals had increased right ventricular pressure (+39%, p=0.04), lower cardiac index (-23% p=0.04), lower systolic blood pressure (-13%, p=0.02) and reduced left ventricular end-diastolic volume (-33%, p=0.02). When incremental doses of norepinephrine and dobutamine were administered, the right ventricular arterio-ventricular coupling was improved only by dobutamine (p<0.05). Norepinephrine increased both left ventricular end-diastolic volume and left ventricular contractility to a greater extent (p<0.05) in pulmonary artery banded animals. While the cardiac index was improved equally by norepinephrine and dobutamine treatments in pulmonary artery banded animals, norepinephrine had a significantly greater effect on mean arterial pressure (p<0.05) and diastolic arterial pressure (p<0.05).Conclusion: While norepinephrine and dobutamine improved cardiac index equally, it was obtained in different manners. Dobutamine significantly improved the right ventricular function and the arterio-ventricular coupling. Norepinephrine increased systemic resistance, thereby improving arterial pressures and left ventricular systolic function by maintaining left ventricular end-diastolic volume.

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