Ventricular systolic pressure-volume area as predictor of cardiac oxygen consumption

1981 ◽  
Vol 240 (1) ◽  
pp. H39-H44 ◽  
Author(s):  
H. Suga ◽  
T. Hayashi ◽  
M. Shirahata
Keyword(s):  
Oxygen Consumption ◽  
Consumption Rate ◽  
Regression Line ◽  
Systolic Pressure ◽  
Specific Area ◽  
Left Ventricular ◽  
Improved Method ◽  
Ventricular Systolic Pressure ◽  
Left Ventricular Systolic Pressure ◽  
Linear Regressions

We scrutinized the recently reported correlation between the canine left ventricular systolic pressure-volume area (PVA) and cardiac oxygen consumption rate per beat (Vo2) by use of an improved method of Vo2 assessment. PVA is the specific area in the pressure-volume (PV) plane bounded by the end-systolic and end-diastolic PV lines and the systolic segment of the PV loop. Different from the previous study in which Vo2-PVA data from isovolumic and ejecting contractions were pooled for analyses, we analyzed Vo2-PVA data from the two different modes separately to examine whether there was any difference of Vo2-PVA relationship between them. The results indicated that the linear regressions of Vo2 on PVA were virtually the same for isovolumic and ejecting contractions. The regression line was Vo2 (ml O2/beat) = a[PVA (mmHg x ml x beat-1)] + b, where a = 1.64 (+/- 0.12 SE) X 10(-5) (ml O2/beat)/(mmHg x ml x beat-1) and b = 0.015 +/- 0.002 ml O2/beat in 10 hearts. We conclude that PVA serves as a reliable predictor of Vo2 regardless of the mode of contraction in a given left ventricle with a stable inotropic background.

Regression of cardiac oxygen consumption on ventricular pressure-volume area in dog

1981 ◽  
Vol 240 (3) ◽  
pp. H320-H325 ◽  
Author(s):  
H. Suga ◽  
T. Hayashi ◽  
M. Shirahata ◽  
S. Suehiro ◽  
R. Hisano
Keyword(s):  
Oxygen Consumption ◽  
Consumption Rate ◽  
Systolic Pressure ◽  
Specific Area ◽  
Left Ventricular ◽  
Optimal Combination ◽  
Ventricular Wall ◽  
Ventricular Systolic Pressure ◽  
Elastic Potential Energy ◽  
Left Ventricular Systolic Pressure

Left ventricular systolic pressure-volume area (PVA) has been reported to be a reliable predictor of cardiac oxygen consumption rate per beat (VO2) in a given heart with a stable inotropic background. PVA is the specific area in the pressure-volume (PV) diagram, consisting of the area (EW) within the PV loop and the area (PE) bound by the end-systolic and end-diastolic PV lines and the relaxation segment of the PV loop. EW and PE correspond to the external mechanical work and the end-systolic elastic potential energy in the ventricular wall, respectively. We determined the optimal combination of EW and PE for the best prediction of VO2, using the linear multiple regression analysis. From EW, PE, and VO2, data of many isovolumic and ejecting contractions, the optimal coefficients of EW and PE were 1.67 +/- 0.43 (SD; 7 hearts) and 1.74 +/- 0.49 (10(-5) ml O2/mmHg . ml), virtually identical to each other, corroborating that PVA, i.e., a simple sum of EW and PE, can reliably predict VO2 of a given heart in a stable contractile state.

Left ventricular systolic pressure-volume area correlates with oxygen consumption

1979 ◽  
Vol 237 (5) ◽  
pp. H566-H569 ◽  
Author(s):  
F. Khalafbeigui ◽  
H. Suga ◽  
K. Sagawa
Keyword(s):  
Oxygen Consumption ◽  
Linear Regression Analysis ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
O2 Consumption ◽  
Specific Pressure ◽  
Average Correlation ◽  
Ventricular Systolic Pressure ◽  
Volume Load ◽  
Left Ventricular Systolic Pressure

In 13 excised, cross-circulated canine hearts, we studied the correlation between left ventricular oxygen consumption per beat (MVO2) and the magnitude of a specific pressure-volume (P-V) area circumscribed by the end-systolic and end-diastolic P-V relationship curves and the systolic segment of the P-V trajectory of a left ventricular contraction. The pressure and volume load of the ventricle were changed with a volume servo pump in order to alter the P-V area, and MVO2 was measured (after each change in the pressure and volume load). In the data collected from both isovolumic and ejecting contractions of each left ventricle contracting with a stable inotropic background, we found a linear correlation between MVO2 and the P-V area. The average correlation coefficient was 0.92 +/- 0.016 (SE). Linear regression analysis yielded the formula: MVO2 (ml/beat) = alpha[P-V area (mmHg.ml/beat)] + b, where alpha, the slope coefficient, was (1.53 +/- 0.14) x 10(-5) and b, which probably represents the basal O2 consumption, was 0.019 +/- 0.003 ml/beta. We propose that the P-V area as defined above may be a good index of ventricular oxygen consumption under a given inotropic background.

Role of reflexes following myocardial necrobiosis

1965 ◽  
Vol 209 (6) ◽  
pp. 1081-1088 ◽  
Author(s):  
G. Ascanio ◽  
F. Barrera ◽  
E. V. Lautsch ◽  
M. J. Oppenheimer
Keyword(s):  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Hemodynamic Changes ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood ◽  
Bilateral Vagotomy ◽  
Left Ventricular Systolic Pressure

Intracoronary administration of hexachlorotetrafluorobutane (Hexa) into non-thoracotomized dogs produced a statistically significant decrease in left ventricular systolic pressure (LVSP), mean femoral arterial blood pressure (MFAP), first derivative of left ventricular pressure pulse (dP/d t), total peripheral resistance (TPR), and cardiac output (C.O.) lasting up to 1 hr after injection. Femoral vascular resistance decreased during the first 3 min after production of necrobiosis. Fifty percent of the dogs died of ventricular fibrillation (VF) after Hexa infarction. Prereserpinized dogs did not show significant changes in the parameters which were significantly changed in normal dogs after Hexa necrobiosis except in the case of VF which was almost absent in this group. Bilateral vagotomy prior to Hexa administration prevented most hemodynamic changes after necrobiosis whereas atropine did not. Bilateral vagotomy and atropine 1 hr after necrobiosis increased MFAP, dP/d t, LVSP, C.O., and TPR. Apparently excitatory efferent sympathetic activity on heart and femoral arterial vessels is reflexly inhibited by the effects of intracoronary injection of Hexa. The afferent pathway is via the vagus nerve.

Increased cardiac contractility in acute uremia: interrelationships with hypertension

1975 ◽  
Vol 229 (2) ◽  
pp. 501-505 ◽  
Author(s):  
T Nivatpumin ◽  
T Yipintsoi ◽  
S Penpargkul ◽  
J Scheuer
Keyword(s):  
Blood Pressure ◽  
Systolic Hypertension ◽  
Diastolic Pressure ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Ventricular Systolic Pressure ◽  
Inotropic State ◽  
Left Ventricular Systolic Pressure

To study the effects of acute uremia on the inotropic state of the rat heart, we subjected rats to bilateral nephrectomy and studied their hearts in the open chest 24 h later. Uremic rats had significantly higher systolic blood pressure than sham-operated animals. Left ventricular systolic pressure and maximum dP/dt, both during ejection and isovolumic contrations, were higher for any given end-diastolic pressure in hearts of uremic rats than in sham-operated animals. This difference in performance charcteristics was not abolished by doses of propranolol that blocked the heart rate response to isoproterenol. The administration of phenoxybenzamine during the 24 h of uremia abolished the blood pressure rise in uremic rats, but the increased contractile state persisted. Treatment of sham-operated animals with methoxamine to produce the same course of blood pressure as observed in uremic rats was also associated with an increased inotropic state. These results indicate that in the rat, acute uremia is associated with an increased inotropic state that is not mediated by beta-adrenergic mechanisms. The systolic hypertension of acute uremia is not the major cause of the increased contractility, although systolic hypertension without uremia can mimic the performance characteristics found in hearts of uremic rats.

Effects of sympathetic stimulation during cooling on hypothermic as well as posthypothermic hemodynamic function

2006 ◽  
Vol 84 (10) ◽  
pp. 985-991 ◽  
Author(s):  
T.V. Kondratiev ◽  
T. Tveita
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Saline Solution ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Mechanical Function ◽  
Ventricular Systolic Pressure ◽  
Hemodynamic Variables ◽  
Left Ventricular Systolic Pressure

This experimental study was performed to explore hemodynamic effects of a moderate dose epinephrine (Epi) during hypothermia and to test the hypothesis whether sympathetic stimulation during cooling affects myocardial function following rewarming. Two groups of male Wistar rats (each, n = 7) were cooled to 15 °C, maintained at this temperature for 1 h, and then rewarmed. Group 1 received 1 μg/min Epi, i.v., for 1 h during cooling to 28 °C, a dose known to elevate cardiac output (CO) by approximately 25% at 37 °C. Group 2 served a saline solution control. At 37 °C, Epi infusion elevated CO, left ventricular systolic pressure, maximum rate of left ventricle pressure rise, and mean arterial pressure. During cooling to 28 °C, these variables, with the exception of mean arterial pressure, decreased in parallel to those in the saline solution group. In contrast, in the Epi group, mean arterial pressure remained increased and total peripheral resistance was significantly elevated at 28 °C. Compared with corresponding prehypothermic values, most hemodynamic variables were lowered after 1 h at 15 °C in both groups (except for stroke volume). After rewarming, alterations in hemodynamic variables in the Epi-treated group were more prominent than in saline solution controls. Thus, before cooling, continuous Epi infusion predominantly stimulates myocardial mechanical function, materialized as elevation of CO, left ventricular systolic pressure, and maximum rate of left ventricle pressure rise. Cooling, on the other hand, apparently eradicates central hemodynamic effects of Epi and during stable hypothermia, elevation of peripheral vascular vasopressor effects seem to take over. In contrast to temperature-matched, non-Epi stimulated control rats, a significant depression of myocardial mechanical function occurs during rewarming following a moderate sympathetic stimulus during initial cooling.

A Physiological Controller for Turbodynamic Ventricular Assist Devices Based on Left Ventricular Systolic Pressure

2016 ◽  
Vol 40 (9) ◽  
pp. 842-855 ◽  
Author(s):  
Anastasios Petrou ◽  
Gregor Ochsner ◽  
Raffael Amacher ◽  
Panagiotis Pergantis ◽  
Mathias Rebholz ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Assist Devices ◽  
Ventricular Assist ◽  
Ventricular Systolic Pressure ◽  
Assist Devices ◽  
Left Ventricular Systolic Pressure
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