Pulmonary vascular impedance analysis of adaptation to chronically elevated blood flow in the awake dog.

SUMMARY. Investigators model noncardiogenic pulmonary hypertension by constricting the pulmonary artery to increase right ventricular afterload. To investigate this model's validity, we compared the right ventricular afterload, quantified as pulmonary input impedance, created by constricting the pulmonary artery and by inducing a pulmonary microvascular injury (with glass beads infused into the pulmonary circulation). The pulmonary injury constriction produced a different right ventricular afterload than the microvascular injury. The constriction increased both the input resistance and the characteristic impedance. Mircrovascular injury increased only input resistance. Physiological levels of lung inflation did not influence pulmonary impedance, but lung hyperinflation increased input resistance both before and while constricting the pulmonary artery or after producing microvascular injury. Total right ventricular power output and stroke work were unchanged during each vascular intervention. Pulmonary artery constriction did not affect power output distribution, whereas microvascular injury decreased oscillatory power and its relative contribution to total power. Lung hyperinflation dramatically reduced right ventricular power and left ventricular stroke work. These effects appeared mediated by right ventricular afterload increase uncompensated for by right ventricular preload increase. These observations help explain the hemodynamic consequences of acute pulmonary hypertension and the effects of lung hyperinflation with positive end-expiratory pressure respiration in such patients. (Circ Res 56: 40-56, 1985)

Section: Effects Of Vascular Interventionssupporting

confidence: 91%

Pulmonary artery constriction produces a greater right ventricular dynamic afterload than lung microvascular injury in the open chest dog.

Calvin¹,

Baer²,

Glantz³

1985

“…Previous studies of pulmonary artery input impedance have been primarily restricted to animal experiments (Caro and McDonald, 1961;Patel et al, 1963;Bergel and Milnor, 1965;Milnor et al, 1966;O'Rourke, 1968;Elkins and Milnor, 1971;Reuben et al, 1971;Pace, 1971;Elkins et al, 1974;Piene, 1976aPiene, , 1976bHopkins et al, 1979Hopkins et al, , 1980. Pouleur et al (1978) analyzed the effects of artificial lung inflation on anesthetized dogs, but the effects of normal respiratory mechanics on the input impedance of the pulmonary arterial system have not been studied.…”

Section: Input Impedance Of the Pulmonary Arterial System In Normal Manmentioning

confidence: 99%

Input impedance of the pulmonary arterial system in normal man. Effects of respiration and comparison to systemic impedance.

Murgo¹,

Westerhof

1984

SUMMARY. Input impedance of the pulmonary arterial system was determined in 10 subjects undergoing elective cardiac catheterization. No cardiovascular or pulmonary disease was found in these patients. In five of the subjects, systemic arterial input impedance was also obtained, so that both systems could be compared. Pulmonary and systemic peripheral resistances were 79 ± 9 dynes sec/cm 5 (mean ± SEM) and 1016 ± 50 dynes sec/cm 5 , respectively. Characteristic impedance of the pulmonary circulation was lower than the characteristic impedance of the systemic circulation: 20 ± 1 dynes sec/cm 5 vs. 47 ± 9 dynes sec/cm ! , respectively. Pulmonary pressure and flow spectra for both systems are also presented. The amplitudes of the harmonics of pressure and flow are smaller for the pulmonary circulation, which is consistent with the lower pressures and more rounded waveforms of the normal pulmonary circulation. In all 10 subjects, input impedance of the pulmonary system was examined during both the inspiratory and expiratory phases of respiration. There was no difference between inspiration and expiration in either pulmonary vascular resistance (77 ± 10 dynes sec/cm ! vs. 80 ± 9 dynes sec/cm 5 , respectively), characteristic impedance (20 ± 1 dynes sec/cm 5 vs. 20 ± 1 dynes sec/cm 5 ) or in the overall impedance spectrum. Quiet respiration, thus, has no effect on the pulmonary arterial load, and changes in pressure and flow must result from alterations in right ventricular performance. (CircRes 54: 666-673, 1984) UNLIKE the systemic circulation, the pulmonary vascular system in normal man is a low pressure system which is entirely exposed to changes in intrathoracic pressure during respiration. The effects of these changes on the physical characteristics of the human pulmonary circulation are unknown. It is of physiological and clinical importance to know how the pulmonary vasculature is affected by respiration, especially when evaluating the relationships between this vascular bed and right ventricular function. To study such effects, it is necessary to describe the pulmonary circulation in quantitative terms. One method is to calculate pulmonary input impedance. The input impedance of a vascular bed not only provides information about the pulsatile pressure-flow relationships, but also yields information regarding the physical characteristics of that bed (Randall and

“…The characteristics of the ventricles differ (Rushmer, 1964;Elzinga et al, 1980). Although a comparative study has not been done, the literature indicates that pulmonary and systemic input impedances are also different (Milnor et al, 1966;Noble et al, 1967;Reuben et al, 1971;Westerhof et al, 1973;Pouleur et al, 1978;Hopkins et al, 1979Hopkins et al, , 1980. Consequently, resemblance of pulmonary and aortic flow waves is small; the same is true for pulmonary and aortic pressure waves (Fig.…”

mentioning

confidence: 99%

Pulse wave reflection: can it explain the differences between systemic and pulmonary pressure and flow waves? A study in dogs.

Bos¹,

Westerhof²,

Randall³

1982

SUMMARY. We have studied the effect of changes in pulse wave reflection on the configurations of pressure and flow in systemic and pulmonary circulation. Electromagnetic flow transducers, atrial catheters, and pacing leads were implanted in 10 dogs. In four animals, the flow transducer was placed on the pulmonary artery, in another four on the ascending aorta, and in two additional dogs on both vessels. One week later, ascending aortic and/or pulmonary artery flow and pressure (catheter tip manometer) were measured under general anesthesia (Nembutal, 30 mg/kg, iv). When the pulmonary circulation was studied (six dogs), measurements were made before and during serotonin infusion (0.5-0.75 mg/min). When the systemic circulation was studied (six dogs), measurements were made before and during nitroprusside infusion (50-200 jug/min). To quantify the arterial load, we calculated pulmonary and systemic input impedances. To estimate the amount of reflection, we used a reflection index which we defined as the amplitude ratio of reflected and forward wave. Nitroprusside decreased total peripheral resistance, increased total arterial compliance, and decreased the reflection index; similarity between aortic pressure and flow wave shapes increased, and they looked more like their pulmonary counterparts. Serotonin increased pulmonary vascular resistance, decreased pulmonary arterial compliance, and increased the reflection index. Resemblance of pressure and flow waves decreased. The differences in wave shapes can thus be explained by the amount of reflection: the less reflection the more pressure and flow resemble each other. (Circ Res 51: 479-485, 1982)