Physiologic correlates of right ventricular ejection fraction in chronic obstructive pulmonary disease: A combined radionuclide and hemodynamic study

Brent, Bruce N.; Berger, Harvey J.; Matthay, Richard A.; Mahler, Donald A.; Pytlik, Linda; Zaret, Barry L.

doi:10.1016/0002-9149(82)90174-6

Cited by 190 publications

(54 citation statements)

References 22 publications

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“…[17][18][19] However, in the present study, the ESPVR defined by these estimates of RV end systole had an inferior goodness of fit and consequently had less statistical power to detect changes in RV function produced by inotropic interventions compared with the ESPVR defined by maximal elastance.…”

Section: Modifications Of Rv Espvrcontrasting

confidence: 60%

Human right ventricular end-systolic pressure-volume relation defined by maximal elastance.

Brown

Ditchey

1988

Circulation

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This study was undertaken to determine 1) whether a combined radionuclide-hemodynamic technique could define the right ventricular end-systolic pressure-volume relation (RV ESPVR) in the clinical setting, 2) whether the human RV ESPVR defined by maximal elastance is linear and responsive to inotropic interventions, and 3) whether more easily measured modifications of the ESPVR are reliable substitutes as an index of RV function. Eight patients with normal RV function were studied with simultaneous micromanometer RV pressure measurements and radionuclide ventriculography to construct RV pressure-volume loops. Data were collected at baseline and after at least two alterations in loading conditions with nitroglycerin, phenylephrine, or saline. End systole was defined by maximal elastance (E(t) = P(t)I [V(t) -VO]). Data were also obtained during administration of dobutamine in four patients and after atrial pacing tachycardia in one patient. The RV ESPVR defined by maximal elastance was highly linear (r=0.988-0.999) throughout the range of pressures and volumes tested. Furthermore, the linear correlations were significantly higher (p<0.005), and the linear regression standard error of the estimate (SEE) was significantly lower (p<0.005) for the RV ESPVR defined by maximal elastance compared with modifications of the ESPVR with the ratio of pulmonary artery-dicrotic notch pressure or RV peak pressure to end-ejection volume. Dobutamine or atrial pacing tachycardia produced a leftward shift of the entire RV pressure-volume loop, and in each patient (five of five), the point of maximal elastance fell outside the 95% confidence interval defined by the baseline ESPVR. However, because of the larger SEE, the leftward shift with modifications of the ESPVR was not statistically significant in any patient by the pulmonary artery-dicrotic notch pressure: end-ejection volume ratio and was significant in only one of five patients by the RV peak pressure: end-ejection volume ratio (p<0.03). Therefore, it appears that the steady-state RV ESPVR defined by maximal elastance in patients with normal RV function is responsive to alterations in inotropic state and is more sensitive to alterations in RV function than the frequently used, more easily measured modifications of the RV ESPVR. (Circulation 1988;78:81-91) T he concept of the left ventricular (LV) endsystolic pressure-volume relation (ESPVR) has evolved substantially in complexity in recent years. However, there is a large body of experimental and clinical data showing that the LV ESPVR is relatively load independent and sensitive to changes in LV contractility and, hence, can serve as a clinically useful index of LV function. 1-15 In the isolated heart, the right ven-

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Section: Modifications Of Rv Espvrcontrasting

confidence: 60%

Human right ventricular end-systolic pressure-volume relation defined by maximal elastance.

Brown

Ditchey

1988

Circulation

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“…Systolic ventricular dysfunction is generally defined by a decrease in RVEF. In COPD, RVEF can be reduced and its value is inversely related to Ppa [53]. Nonetheless, a decrease in RVEF does not mean that there is true ventricular dysfunction [54].…”

Section: Right-ventricular Functionmentioning

confidence: 99%

Pulmonary hypertension in chronic obstructive pulmonary disease

Barberà

Peinado²,

Santos³

2003

Eur Respir J

390

299

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Pulmonary hypertension in chronic obstructive pulmonary disease. J.A. Barberà, V.I. Peinado, S. Santos. #ERS Journals Ltd 2003. ABSTRACT: Pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD). Its presence is associated with shorter survival and worse clinical evolution. In COPD, pulmonary hypertension tends to be of moderate severity and progresses slowly. However, transitory increases of pulmonary artery pressure may occur during exacerbations, exercise and sleep. Right ventricular function is only mildly impaired with preservation of the cardiac output.Structural and functional changes of pulmonary circulation are apparent at the initial stages of COPD. Recent investigations have shown endothelial dysfunction and changes in the expression of endothelium-derived mediators that regulate vascular tone and cell growth in the pulmonary arteries of patients with mild disease. Some of these changes are also present in smokers with normal lung function. Accordingly, it has been postulated that the initial event in the natural history of pulmonary hypertension in COPD could be the lesion of pulmonary endothelium by cigarettesmoke products.Long-term oxygen administration is the only treatment that slows down the progression of pulmonary hypertension in chronic obstructive pulmonary disease. Nevertheless, with this treatment pulmonary artery pressure rarely returns to normal values and the structural abnormalities of pulmonary vessels remain unaltered. Vasodilators are not recommended on the basis of their minimal clinical efficacy and because they impair pulmonary gas exchange. Recognition of the role of endothelial dysfunction in the physiopathology of pulmonary hypertension in chronic obstructive pulmonary disease opens new perspectives for the treatment of this complication. Eur Respir J 2003; 21: 892-905.

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“…Right ventricular ejection fraction (RVEF) is much more sensitive to changes in ventricular afterload than LV ejection fraction [28]. The RVEF has been found to augment with exercise in healthy subjects given the decreased PVRI and increased contractility of the RV free wall [29,30].…”

Section: Right Ventricular Functionmentioning

confidence: 99%

Haemodynamic evaluation of pulmonary hypertension

Chemla¹,

Castelain²,

Hervé³

et al. 2002

Eur Respir J

304

188

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Haemodynamic evaluation of pulmonary hypertension. D. Chemla, V. Castelain, P. Hervé, Y. Lecarpentier, S. Brimioulle. #ERS Journals Ltd 2002. ABSTRACT: Pulmonary hypertension is characterised by the chronic elevation of pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) leading to right ventricular enlargement and hypertrophy. Pulmonary hypertension may result from respiratory and cardiac diseases, the most severe forms occurring in thromboembolic and primary pulmonary hypertension.Pulmonary hypertension is most often defined as a mean PAP w25 mmHg at rest or w30 mmHg during exercise, the pressure being measured invasively with a pulmonary artery catheter. Doppler echocardiography allows serial, noninvasive follow-up of PAPs and right heart function. When the adaptive mechanisms of right ventricular dilatation and hypertrophy cannot compensate for the haemodynamic burden, right heart failure occurs and is associated with poor prognosis.The haemodynamic profile is the major determinant of prognosis. In both primary and secondary pulmonary hypertension, special attention must be paid to the assessment of pulmonary vascular resistance index (PVRI), right heart function and pulmonary vasodilatory reserve.Recent studies have stressed the prognostic values of exercise capacity (6-min walk test), right atrial pressure, stroke index and vasodilator challenge responses, as well as an interest in new imaging techniques and natriuretic peptide determinations. Overall, careful haemodynamic evaluation may optimise new diagnostic and therapeutic strategies in pulmonary hypertension.

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Physiologic correlates of right ventricular ejection fraction in chronic obstructive pulmonary disease: A combined radionuclide and hemodynamic study

Cited by 190 publications

References 22 publications

Human right ventricular end-systolic pressure-volume relation defined by maximal elastance.

Human right ventricular end-systolic pressure-volume relation defined by maximal elastance.

Pulmonary hypertension in chronic obstructive pulmonary disease

Haemodynamic evaluation of pulmonary hypertension

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