Assessment of slope of end-systolic pressure-volume line of in situ dog heart

1986 ◽  
Vol 250 (4) ◽  
pp. H685-H692 ◽  
Author(s):  
Y. Igarashi ◽  
H. Suga
Keyword(s):  
Systolic Pressure ◽  
Electromagnetic Flowmeter ◽  
Left Ventricular ◽  
Aortic Occlusion ◽  
Atrial Pacing ◽  
Ventricular Contractility ◽  
Dog Heart ◽  
End Diastolic Volume ◽  
Isovolumic Contraction

The purpose of this study was to establish a new method of assessment of the slope (Emax) of the end-systolic pressure-volume line (ESPVL) of the in situ heart. In anesthetized open-chest dogs, an isovolumic contraction was produced by an aortic occlusion after steady-state ejecting contractions in the left ventricle. We plotted ventricular pressure measured with a catheter-tip manometer against time integral of aortic flow measured with an electromagnetic flowmeter of the last ejecting and the first isovolumic contraction, assuming the same end-diastolic volume. ESPVL was drawn from the peak isovolumic pressure-volume point tangential to the left upper corner of the +/- 3.0 (SE) mmHg/ml (n = 9 dogs) in control run and was increased by 59 +/- 19% under isoproterenol and decreased by 47 +/- 9% after propranolol. Emax was little changed by atrial pacing. We conclude that Emax by this aortic occlusion method is useful for assessment of left ventricular contractility of the in situ dog heart.

New mechanoenergetic evaluation of left ventricular contractility in in situ rat hearts

1997 ◽  
Vol 272 (6) ◽  
pp. H2671-H2678 ◽  
Author(s):  
H. Tachibana ◽  
M. Takaki ◽  
S. Lee ◽  
H. Ito ◽  
H. Yamaguchi ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Left Ventricular ◽  
Aortic Occlusion ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Rat Hearts ◽  
Total Mechanical Energy ◽  
Work Capability

We recorded a series of ejecting left ventricular (LV) pressure (P)-volume (V) loops of in situ rat hearts during a gradual ascending aortic occlusion. The end-systolic (ES) P-V relationship (ESPVR) was upward convex curvilinear regardless of LV contractility. The ESPVR was shifted upward in an enhanced contractility by dobutamine and downward in a depressed contractility by propranolol; ESP at a midrange V of 0.1 ml/g LV on each ESPVR increased from 131 +/- 11 to 192 +/- 17 mmHg and decreased from 136 +/- 10 to 110 +/- 7 mmHg, respectively. Furthermore, we obtained an upward concave curvilinear pressure-volume area (PVA; a measure of total mechanical energy)-V (preload) relationship to assess LV work capability in each contractility. This relationship also shifted upward in enhanced contractility and downward in depressed contractility; the PVA at midrange V increased from 7.9 +/- 1.2 to 12.3 +/- 1.5 mmHg. ml.beat-1.g-1 and decreased from 8.2 +/- 0.9 to 6.4 +/- 0.8 mmHg.ml.beat-1.g-1. We conclude that the heights of the ESPVR and PVA-V relationship curves can evaluate LV contractility mechanoenergetically.

Sympathetic stimulation alters left ventricular relaxation and chamber size

1993 ◽  
Vol 264 (1) ◽  
pp. R1-R7 ◽  
Author(s):  
I. G. Burwash ◽  
D. E. Morgan ◽  
C. J. Koilpillai ◽  
G. L. Blackmore ◽  
D. E. Johnstone ◽  
...  
Keyword(s):  
Stellate Ganglion ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Wall Stress ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Ventricular Contractility ◽  
Cross Sectional ◽  
Stress Changes ◽  
Neuronal Stimulation

Alterations in left ventricular (LV) contractility, relaxation, and chamber dimensions induced by efferent sympathetic nerve stimulation were investigated in nine anesthetized open-chest dogs in sinus rhythm. Supramaximal stimulation of acutely decentralized left stellate ganglia augmented heart rate, LV systolic pressure, and rate of LV pressure rise (maximum +dP/dt, 1,809 +/- 191 to 6,304 +/- 725 mmHg/s) and fall (maximum -dP/dt, -2,392 +/- 230 to -4,458 +/- 482 mmHg/s). It also reduced the time constant of isovolumic relaxation, tau (36.5 +/- 4.8 to 14.9 +/- 1.1 ms). Simultaneous two-dimensional echocardiography recorded reductions in end-diastolic and end-systolic LV cross-sectional chamber areas (23 and 31%, respectively), an increase in area ejection fraction (32%), and increases in end-diastolic and end-systolic wall thicknesses (14 and 13%, respectively). End-systolic and end-diastolic wall stresses were unchanged by stellate ganglion stimulation (98 +/- 12 to 95 +/- 9 dyn x 10(3)/cm2; 6.4 +/- 2.4 to 2.4 +/- 0.3 dyn x 10(3)/cm2, respectively). Atrial pacing to similar heart rates did not alter monitored indexes of contractility. Dobutamine and isoproterenol induced changes similar to those resulting from sympathetic neuronal stimulation. These data indicate that when the efferent sympathetic nervous system increases left ventricular contractility and relaxation, concomitant reductions in systolic and diastolic dimensions of that chamber occur that are associated with increasing wall thickness such that LV wall stress changes are minimized.

Relation between oxygen consumption and pressure-volume area of in situ dog heart

1987 ◽  
Vol 253 (1) ◽  
pp. H31-H40 ◽  
Author(s):  
T. Nozawa ◽  
Y. Yasumura ◽  
S. Futaki ◽  
N. Tanaka ◽  
Y. Igarashi ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Left Ventricle ◽  
Systolic Pressure ◽  
Ascending Aorta ◽  
Aortic Occlusion ◽  
O2 Consumption ◽  
Loading Conditions ◽  
Contractile State ◽  
Dog Heart

We studied the relation between O2 consumption (VO2) and the systolic pressure-volume area (PVA) in the left ventricle of open-chest dogs. PVA and the slope (Emax) of the end-systolic pressure-volume line were determined by an abrupt occlusion of the ascending aorta. VO2 linearly correlated with PVA in control contractile state, where Emax was 15.8 +/- 4.4 (SD) mmHg/ml with intact reflexes and 11.5 +/- 1.2 mmHg/ml with blocked reflexes. Emax and the VO2 axis intercept of the VO2-PVA line were greater in the in situ heart than in the excised cross-circulated dog heart in our previous study. Enhancement of contractile state by dobutamine increased Emax by 60–80% and shifted the VO2-PVA line upward, increasing the VO2 axis intercept by 38% with intact reflexes and by 79% with blocked reflexes. The slope had a tendency to increase with dobutamine, but the increase was statistically insignificant. We conclude that PVA and Emax obtained by the aortic-occlusion method can account for changes in VO2 with changes in loading conditions and contractility in an in situ dog heart.

Dobutamine improves afterload-induced deterioration of mechanical efficiency toward maximal

1992 ◽  
Vol 263 (4) ◽  
pp. H1201-H1207
Author(s):  
T. Nozawa ◽  
O. Wada ◽  
S. Ishizaka ◽  
H. Asanoi ◽  
M. Fujita ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Electromagnetic Flowmeter ◽  
Mechanical Efficiency ◽  
Ventricular Volume ◽  
Atropine Sulfate ◽  
Left Ventricular ◽  
External Work ◽  
Average Decrease ◽  
Inotropic State ◽  
End Diastolic Volume

We studied the effect of increased afterload on the ratios of O2 consumption (VO2) to external work (EW), VO2 to the systolic pressure-volume area (PVA), and PVA to EW at control state and with dobutamine in the left ventricles of open-chest dogs. Left ventricular volume was measured with a volumetric conductance catheter and coronary flow with an electromagnetic flowmeter. Hexamethonium bromide and atropine sulfate were administered before changes in end-systolic pressure (Pes) with an infusion of nitroprusside or angiotensin II. Dobutamine enhanced ventricular end-systolic elastance by 100%. In the control, with increases in Pes, EW/VO2 remained unchanged, PVA/VO2 increased by 48%, and EW/PVA decreased by 26%. Dobutamine increased both EW/VO2 and EW/PVA at any given Pes but decreased PVA/VO2. During dobutamine, EW/VO2 increased significantly with increases in Pes. The ratio of measured EW/VO2 to the theoretically predicted maximal EW/VO2 value for a given end-diastolic volume and contractility was 0.83 at a Pes of 70 mmHg, and this ratio decreased by 33% with increases in Pes in the control. During dobutamine, measured EW/VO2 values were almost equal to each corresponding theoretical maximal value, and the average decrease in the ratio with increases in Pes was 7%. Thus the enhanced inotropic state by dobutamine can restore the afterload-induced deterioration of EW/VO2 toward the normal maximal level.

Left ventricular ejection activation in the in situ heart

1991 ◽  
Vol 260 (5) ◽  
pp. H1495-H1500
Author(s):  
Y. Igarashi ◽  
C. P. Cheng ◽  
W. C. Little
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Cross Sectional Area ◽  
Aortic Flow ◽  
Aortic Occlusion ◽  
Ventricular Pressure ◽  
Left Ventricular Ejection ◽  
Sectional Area ◽  
Cross Sectional

We tested, in the in situ heart, the hypothesis that the end-systolic pressure (ESP) of small ejecting contraction (EC) is greater than that of an isovolumic contraction (IC) with a similar end-systolic volume. We produced ECs with varying amounts of ejection by partial aortic occlusion while measuring left ventricular pressure, one or two left ventricular dimensions (anteroposterior and septal-lateral), and aortic flow. In 11 dogs, we plotted ventricular pressure against the time integral of aortic flow of ECs and IC with the same end-diastolic anteroposterior dimension. The end-systolic pressure-volume line was drawn from the peak isovolumic pressure-volume point tangential to the left upper corner of the pressure-volume loop of ECs. The slope of the tangential line of the middle EC, whose stroke volume was 51 +/- 8% of that of the control EC, was decreased by 54 +/- 16% compared with that of the control EC. In eight dogs with two pairs of crystals, left ventricular volume was controlled by partial vena caval occlusion, and ICs were produced by total aortic occlusion. The end-systolic pressure of small ejections exceeded (11.3 +/- 7.7 mmHg, P less than 0.01) those of isovolumic contractions with the same end-systolic cross-sectional area, whereas the end-systolic pressure of beats with large ejections was similar (-9.4 +/- 14.4 mmHg, P = NS) to an IC with the same end-systolic cross-sectional area. We conclude that the end-systolic pressure-volume point of beats with a small ejection is located above the isovolumic end-systolic pressure-volume relation in the in situ dog left ventricle.

Inotropic effects of ejection are myocardial properties

1994 ◽  
Vol 266 (3) ◽  
pp. H1202-H1213 ◽  
Author(s):  
P. P. De Tombe ◽  
W. C. Little
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Negative Effects ◽  
Inotropic Effects ◽  
Contraction Duration ◽  
Loading System ◽  
Positive Effect ◽  
Isolated Rat

Recent studies in isolated and in vivo canine hearts have suggested that the left ventricular end-systolic pressure (LVPes) of ejecting beats is the net result of a balance between positive and negative effects of ejection. At present, it is unknown whether these ejection effects are merely a ventricular chamber property or represent a fundamental myocardial property. Accordingly, we examined the effects of ejection in eight isolated rat cardiac trabeculae at the sarcomere level. We approximated in situ sarcomere shortening patterns using an iterative computer loading system. Six isovolumic contractions were compared with four ejecting contractions. The superfusing solution contained either 0.7 mM Ca2+ or 0.65 mM Sr2+ plus 0.15 mM Ca2+. With Ca2+, simulated LVPes ("LVP"es) of ejecting contractions was significantly lower than isovolumic "LVP"es (-5.3 +/- 5.6%), whereas with Sr2+, ejecting "LVP"es was significantly higher than isovolumic "LVP"es (+4.5 +/- 7.5%). Contraction duration and time to end systole were markedly prolonged in ejecting vs. isovolumic contractions with either Ca2+ or Sr2+. As a consequence, comparison of simulated LVP between ejecting and isovolumic beats throughout the contraction, i.e., at the same simulated LVV and time, revealed only a positive effect of ejection with either Ca2+ (+18.8 +/- 5.5%) or Sr2+ (+23.4 +/-9.3%). We conclude that both positive and negative effects of ejection are basic myocardial properties.

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.

Left ventricular-arterial coupling in conscious dogs

1991 ◽  
Vol 261 (1) ◽  
pp. H70-H76 ◽  
Author(s):  
W. C. Little ◽  
C. P. Cheng
Keyword(s):  
Stroke Volume ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Arterial System ◽  
Conscious Dogs ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Inotropic State ◽  
End Diastolic Volume ◽  
Wide Range

We investigated the criteria for the coupling of the left ventricle (LV) and the arterial system to maximize LV stroke work (SW) and the transformation of LV pressure-volume area (PVA) to SW. We studied eight conscious dogs that were instrumented to measure LV pressure and determine LV volume from three ultrasonically determined dimensions. The LV end-systolic pressure (PES)-volume (VES) relation was determined by caval occlusion. Its slope (EES) was compared with the arterial elastance (EA) and determined as PES per stroke volume. At rest, with intact reflexes, EES/EA was 0.96 +/- 0.20 EES/EA was varied over a wide range (0.18-2.59) by the infusion of graded doses of phenylephrine and nitroprusside before and during administration of dobutamine. Maximum LV SW, at constant inotropic state and end-diastolic volume (VED), occurred when EES/EA equaled 0.99 +/- 0.15. At constant VED and contractile state, SW was within 20% of its maximum value when EES/EA was between 0.56 and 2.29. The conversion of LV PVA to SW increased as EES/EA increased. The shape of the observed relations of the SW to EES/EA and SW/PVA to EES/EA was similar to that predicted by the theoretical consideration of LV PES-VES and arterial PES-stroke volume relations. We conclude that the LV and arterial system produce maximum SW at constant VED when EES and EA are equal; however, the relation of SW to EES/EA has a broad plateau. Only when EA greatly exceeds EES does the SW fall substantially. However, the conversion of PVA to SW increases as EES/EA increases. These observations support the utility of analyzing LV-arterial coupling in the pressure-volume plane.

scholarly journals A simulation study of left ventricular decompression using a double lumen arterial cannula prototype during a veno-arterial extracorporeal membrane oxygenation

2019 ◽  
Vol 42 (12) ◽  
pp. 748-756
Author(s):  
Filip Ježek ◽  
Svitlana Strunina ◽  
Brian E Carlson ◽  
Jiří Hozman
Keyword(s):  
Extracorporeal Membrane Oxygenation ◽  
Cardiogenic Shock ◽  
Cardiovascular System ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Double Lumen ◽  
Membrane Oxygenation ◽  
Arterial Cannula

Background: Veno-arterial extracorporeal membrane oxygenation can be vital to support patients in severe or rapidly progressing cardiogenic shock. In cases of left ventricular distension, left ventricular decompression during veno-arterial extracorporeal membrane oxygenation may be a crucial factor influencing the patient outcome. Application of a double lumen arterial cannula for a left ventricular unloading is an alternative, straightforward method for left ventricular decompression during extracorporeal membrane oxygenation in a veno-arterial configuration. Objectives: The purpose of this article is to use a mathematical model of the human adult cardiovascular system to analyze the left ventricular function of a patient in cardiogenic shock supported by veno-arterial extracorporeal membrane oxygenation with and without the application of left ventricular unloading using a novel double lumen arterial cannula. Methods: A lumped model of cardiovascular system hydraulics has been coupled with models of non-pulsatile veno-arterial extracorporeal membrane oxygenation, a standard venous cannula, and a drainage lumen of a double lumen arterial cannula. Cardiogenic shock has been induced by decreasing left ventricular contractility to 10% of baseline normal value. Results: The simulation results indicate that applying double lumen arterial cannula during veno-arterial extracorporeal membrane oxygenation is associated with reduction of left ventricular end-systolic volume, end-diastolic volume, end-systolic pressure, and end-diastolic pressure. Conclusions: A double lumen arterial cannula is a viable alternative less invasive method for left ventricular decompression during veno-arterial extracorporeal membrane oxygenation. However, to allow for satisfactory extracorporeal membrane oxygenation flow, the cannula design has to be revisited.

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