Influence of right ventricular hemodynamics on left ventricular diastolic pressure-volume relations in man.

Ludbrook, Philip A.; Byrne, Joseph D.; McKnight, Robert C.

doi:10.1161/01.cir.59.1.21

Cited by 122 publications

(27 citation statements)

References 56 publications

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“…In particular, T has been used to describe how various diseases or interventions, including angina (Mann et al, 1979;Sharma et al, 1979), left ventricular hypertrophy (Ring et al, 1979), postextrasystolic potentiation (Blaustein et al, 1979), sinus tachycardia (Fioretti et al, 1980), and vasodilators (Ludbrook et al, 1977(Ludbrook et al, , 1979, affect ventricular relaxation in intact animals or humans.…”

mentioning

confidence: 99%

Volume loading slows left ventricular isovolumic relaxation rate. Evidence of load-dependent relaxation in the intact dog heart.

Raff¹,

Glantz²

1981

Circulation Research

426

131

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SUMMARY We studied the effects of volume loading on left ventricular isovolumic relaxation rate in 16 intact anesthetized dogs. End-diastolic pressure, mean aortic systolic pressure, dp/dt mnx , and heart rate were measured at end expiration and end inspiration. Volume loading to approximately 5, 10, 15, and 20 mm Hg above initial end-diastolic pressure was performed. In nine dogs, simultaneous ventricular dimensions were measured with previously implanted tantalum screws using biplane cineangiography. Similar volume loading was done in open-chest and open-pericardium states. Relaxation rate was measured in 3413 beats using T, the time constant of exponential isovolumic pressure fall. T was calculated as reported previously by others and also from a linear regression of dp/dt against p, to eliminate the effects of extracavity pressure changes. T always increased significantly with volume loading, indicating slower relaxation. (For example, with the chest intact, mean T increased from 26 ± 2 (SEM) msec before volume loading to 41.5 ± 4 msec after volume loading.) Using multiple linear regression analysis, we found, in agreement with previous reports, that T decreased significantly as dp/dt,,., and heart rate increased. In contrast to previous reports, we also found that T increased significantly as end-diastolic and mean aortic systolic pressure increased. These four variables taken together accurately predicted T [SEE (standard error of estimate) = 3.2 msec, R = 0.94, P < 0.001]. Geometric variables, including ventricular dimensions and ejection fraction, did not have a statistically significant effect on T independent of the hemodynamic variables. Opening the chest or pericardium did not have a consistent effect on T. Volume loading slows isovolumic relaxation rate in the intact canine heart. This effect appears to be a reflection of the dependence of relaxation on both end-diastolic and mean aortic systolic pressures. Circ Res 48: [813][814][815][816][817][818][819][820][821][822][823][824] 1981 STUDIES of the hemodynamic determinants of left ventricular isovolumic relaxation grew out of interest in the effects of ischemia on diastolic pressure. Following the observation of Barry et al. (1974) that left ventricular diastolic pressure increased without significant increases in end-diastolic volume during angina pectoris, McLaurin et al. (1973) investigated the hypothesis, first suggested by Mitchell et al. (1960), that incomplete relaxtion during diastole might cause an apparent acute stiffening of the left ventricle on the next beat. McLaurin et al. (1973) observed that angina produced a significant decrease in the magnitude of dp/dtmin (also called -dp/dtmax) and suggested that this response indicated impaired relaxation. However, the interpretation of this and similar clinical studies (Papapietro et al., 1979) is clouded by the complex interaction of many changes that occur during ischemia, including depressed inotropic state, increased preload, and increased afterload. Studies of the determinants of dp/d...

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mentioning

confidence: 99%

Volume loading slows left ventricular isovolumic relaxation rate. Evidence of load-dependent relaxation in the intact dog heart.

Raff¹,

Glantz²

1981

Circulation Research

426

131

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“…" Several studies have demonstrated that vasodilators produce a downward, parallel shift of the left ventricular diastolic pressure-volume curve. [12][13][14][15][16][17] This shift in the left ventricular pressure-volume curve is not clearly attributable to the systemic vascular effects of vasodilators, since in isolated heart preparations, no such effect of changing impedance has been noted. Several studies suggest that events in the right heart have an important influence on the altered left ventricular pressure-volume relationship, especially with an intact pericardium.…”

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confidence: 99%

Effect of nitroprusside on hydraulic vascular loads on the right and left ventricle of patients with heart failure.

et al. 1983

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SUMMARY We studied the effect of nitroprusside on the hydraulic vascular load of the right and left ventricle in seven patients with severe left ventricular failure. At doses of 0.25-0.75 ,ug/kg/min, stroke volume increased progressively from 40.1 to 48.6 ml and left ventricular end-diastolic pressure decreased from 24.5 to 11.2 mm Hg. Accompanying this improvement in left ventricular performance were doserelated decreases in mean ventricular pressures, pulmonic and systemic resistances and the lower-frequency components of input impedance moduli. Characteristic impedance and both total and oscillatory external power were decreased in the pulmonic, but not the aortic, vasculature. We sought to determine the mechanism and magnitude of right ventricular unloading and the dose-response relationship of right relative to left ventricular hydraulic unloading with nitroprusside in patients with severe left ventricular failure. A primary concern was whether this agent, in doses just sufficient to produce a measurable alteration in systemic resistance and left ventricular performance, had a primary effect on right ventricular load through a direct effect on pulmonary vascular resistance and impedance. Methods PatientsWe studied patients with severe, chronic left ventricular failure from various causes. Clinically overt left ventricular congestive heart failure was manifested by pulmonary vascular congestion on chest x-ray, ventricular gallop sounds and recent history of both dyspnea and shortness of breath at rest. Patients who were scheduled to undergo diagnostic cardiac catheterization were asked to participate in the study. Any patient with suspected valvular or congenital heart disease was excluded. From this population, 20 patients were entered into the study after they gave informed consent.

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“…However, Ludbrook et al 4 have demonstrated the importance of right ventricular filling pressure in determining the left ventricular diastolic pressure-volume relation. 4 In their study amyl nitrite caused no downward displacement of the left ventricular diastolic pressure-volume relation when compared with nitroglycerin, which produced a similar reduction in mean arterial pressure but shifted the pressure-volume relation downward. This phenomenon was attributed to the failure of amyl nitrite to decrease right ventricular diastolic pressure in contrast to the significant decrease in right ventricular filling pressure resulting from nitroglycerin infusion.…”

Section: Methodsmentioning

confidence: 99%

Right ventricular diastolic pressure-volume relations and regional dimensions during acute alterations in loading conditions.

Dell’Italia

Walsh

1988

Circulation

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Acute pharmacologically mediated parallel shifts in the left ventricular diastolic pressure-volume relation may be due to the restraining effect of the pericardium and/or leftward displacement of the interventricular septum. The existence and cause of this phenomenon in the right ventricle has not been studied in animals or in man. Accordingly, we altered right ventricular pressure with intravenous phenylephrine (0.2 to 0.3 mg) and nitroprusside (0.5 to 1.5 ,g/kg/min) to achieve three disparate peak right ventricular pressures in nine normal subjects after partial autonomic blockade with atropine (1 mg) and propranolol (0.15 mg/kg). Simultaneous high-fidelity right ventricular pressures and biplane cineventriculographic volumes were acquired during the three resultant loading conditions. Right atrial pacing maintained heart rate constant at each pressure level.

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Influence of right ventricular hemodynamics on left ventricular diastolic pressure-volume relations in man.

Cited by 122 publications

References 56 publications

Volume loading slows left ventricular isovolumic relaxation rate. Evidence of load-dependent relaxation in the intact dog heart.

Volume loading slows left ventricular isovolumic relaxation rate. Evidence of load-dependent relaxation in the intact dog heart.

Effect of nitroprusside on hydraulic vascular loads on the right and left ventricle of patients with heart failure.

Right ventricular diastolic pressure-volume relations and regional dimensions during acute alterations in loading conditions.

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