Mechanical function of the main pulmonary artery

Patel, Dali J.; Freitas, Flavio M. De; Mallos, Alexander J.

doi:10.1152/jappl.1962.17.2.205

Cited by 40 publications

(18 citation statements)

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“…Since the whole pulmonary arterial system has a compliance of ,4 mL?mmHg -1 (table 1), a large part of arterial compliance is located in the periphery. This estimate is in line with earlier publications showing that a considerable proportion of the pulmonary arterial compliance is distal to the proximal large arteries [30,[40][41][42][43][44][45][46]. Thus, with an embolus (large) part of peripheral arteries is lost meaning that their compliance is lost resulting in a decrease of the total compliance, and by the loss of vessels the resistance is increased.…”

Section: Why the Product Of Resistance And Compliance Is Constantsupporting

confidence: 91%

The arterial load in pulmonary hypertension

Saouti¹,

Westerhof²,

Postmus³

et al. 2010

Eur Respir Rev

186

153

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The anatomical differences between the pulmonary and systemic arterial system are the main cause of the difference in distribution of compliance. In the pulmonary arterial system compliance is distributed over the entire arterial system, and stands at the basis of the constancy of the RC-time. This distribution depends on the number of peripheral vessels, which is ,8-10 times more in the pulmonary system than the systemic tree. In the systemic arterial tree the compliance is mainly located in the aorta (80% of total compliance in thoracic-abdominal aorta).The constant RC-time in the pulmonary bed results in proportionality of systolic and diastolic pressure with mean pressure and, in turn, in the constant ratio of oscillatory and mean power.KEYWORDS: Compliance, pulmonary hypertension, resistance, systemic circulation, Windkessel T he common feature of pulmonary and the systemic circulation is that both transport an equal amount of blood. However, a major difference is that the pulmonary circulation works at much lower pressures than the systemic circulation. Pulmonary pressure is lower as resistance is lower and the pulmonary vasculature is more compliant. In pulmonary hypertension, the right ventricular load increases due to an increase in pulmonary vascular resistance and decrease in pulmonary vascular compliance, ultimately leading to right ventricular failure. In recent years it has become clear that in pulmonary hypertension not only the contribution of resistance is of importance but that the decrease in arterial compliance plays an equally important role. In addition, in pulmonary hypertension the changes in resistance and compliance are fundamentally and quantitatively different from those in systemic hypertension. Therefore, changes in the pulmonary arterial tree and in pressure are considerably larger than in the systemic arterial tree.This review describes the most important components of the arterial load on the right ventricle (RV) in terms of resistance and arterial compliance, and the consequences of load changes for right ventricular work and function. We will conclude with a short comparison of the pulmonary and systemic circulation in health and hypertension. While the hydraulic load describes the load that the ventricular pump experiences, the muscles generate and feel wall stress, which is considered the muscular afterload. In general higher impedance relates to higher wall stress.

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Section: Why the Product Of Resistance And Compliance Is Constantsupporting

confidence: 91%

The arterial load in pulmonary hypertension

Saouti¹,

Westerhof²,

Postmus³

et al. 2010

Eur Respir Rev

186

153

View full text Add to dashboard Cite

show abstract

“…Increased wall stiffness in established pulmonary hypertension has been reported by several authors (Milnor et al, 1969;Patel et al, 1962;Elkins et al, 1974;Caro and Harrison, 1962). Milnor et al (1969) reported impedance data on seven patients with mitral valve disease and pulmonary hypertension showing higher Z o and C o with progressive elevations of pulmonary artery pressures; all of these patients had elevated left atrial pressures and normal or decreased blood flows.…”

Section: Pulmonary Hypertension and Chronic High-flow Stressmentioning

confidence: 71%

“…It is well accepted that significant vasomotor activity exists in small precapillary resistance ves- sels; however, there also is evidence of changes in mechanical properties of the larger pulmonary arteries under physiological stress and adrenergic stimulation (Ingram et al, 1968). Patel et al (1962) showed that the main pulmonary artery has huge volume distensibility. It has been demonstrated that the dynamic transmission characteristics of the proximal vessels have a contributory role in the control of regional pulmonary flow patterns (Maloney et al, 1968).…”

Section: Resistance and Impedancementioning

confidence: 99%

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

Hopkins¹,

Hammon²,

Modesti³

et al. 1979

Circulation Research

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Pulsatile pulmonary hemodynamics were analyzed in a chronic awake canine high flow model. Standard mean flow and pulsatile flow hemodynamics were measured and alterations in the proximal pulmonary vascular physical properties were quantified by the characteristic impedance (Zo). Pulmonary vascular resistance (PVR), which assesses arteriolar-capillary recruitment of perfusing radius and measures a more distal pulmonary vascular response to changing flows, also was calculated. Twelve control dogs were studied and had mean Qpa (pulmonary blood flow) = 2.02 +/- 0.15 liters/min, Zo = 193 +/- 20 dyne sec cm-5 and PVR = 416 +/- 32 dyne sec cm-5. Ten dogs were studied awake 20 weeks after creation of bilateral arteriovenous fistulae. Five of these shunted dogs, designated group A, developed Qpa = 3-4 liters/min (mean = 3.80 +/- 0.09, P less than 0.001 different from control group); the other five dogs (group B) developed Qpa = 4-8 liters/min (mean = 5.87 +/- 0.16, P less than 0.001). In group A, Zo = 143 +/- 8 (P less than 0.05) and PVR = 249 +/- 6 (P less than 0.10). In group B, Zo = 90 +/- 5 (P less than 0.005) and PVR = 126 +/- 14 (P less than 0.01). The total input power (potential and kinetic) was 125% above the controls for group A (P less than 0.001) and 264% for group B (P less than 0.001), but the mean energy components increased significantly more than did the pulsatile components. These data demonstrate a lower impedance to pulsatile flow during chronically elevated total flow which effects a reduction in both the work load of the right ventricle and the transmission of energy to the precapillary bed. Analysis of the alterations in characteristic impedance suggests a distinct proximal pulmonary vascular mechanism of decreased vessel stiffness (decreased elastic moduli) for adaptation to chronically elevated flow loads which is in addition to the two geometric alterations of proximal arterial dilation and distal vascular channel recruitment.

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“…Although smooth muscle fibers cannot be regarded as perfect elastic structures, the net behavior of major pulmonary arterial walls up to transmural pressures of approximately 40 mm Hg is that of a perfect elastic structure (19). It seems reasonable to conclude that the acute reversible changes in volume-distensibility characteristics of pulmonary vessels during the brief changes in pump rate would be due to changes in smooth muscle behavior.…”

Section: Effect Of Sympathetic Nerve Stimulation In Adjusting Vascularmentioning

confidence: 99%

Effects of Sympathetic Nerve Stimulation on the Pulmonary Arterial Tree of the Isolated Lobe Perfused in Situ

Ingram

Szidon

Skalak

et al. 1968

Circulation Research

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The hemodynamic response to sympathetic nerve stimulation (SNS) was studied in canine lung lobes isolated in situ and perfused with a pulsatile pump. For the same input pulse, both the rate of rise and the rate of fall of pulmonary arterial pressure increased during SNS; the peak systolic pressure was also higher during SNS, whereas diastolic pressure levels were either at, or below, control levels. The increase in pulse pressure produced little or no change in mean pulmonary artery pressure and resistance. During SNS, compliance per unit length in large arteries fell, pulse wave velocity increased, and elastic modulus increased. Phenoxybenzamine produced opposite changes. Norepinephrine injections increased resistance and produced smaller compliance changes than SNS.Flow loads imposed by short bursts of rapid pump rate at constant stroke volume caused increments of vascular volume which returned to control levels after return to the slower rate. Volume increments were smaller and restoration rates faster during SNS than during control. After phenoxybenzamine, volume increments were larger and restoration rates slower than control.The results indicate that the distensibility of the large pulmonary arteries and the precapillary bed is decreased during sympathetic stimulation, while calculated resistance is not changed. Accepted for publication April 18, 1968. nerves supplying the thoracic viscera results in an increase in pulmonary arterial pressure as well as in heart rate (1). However, the experiments were too incomplete to be more than suggestive of pulmonary vasoconstriction. In 1904, Plumier (2) and more recently I. deB. Daly and associates (3, 4) performed a series of experiments which took into account many of the cardiac and respiratory changes on the pulmonary vascular bed during sympathetic nerve stimulation (SNS) which Francois-Franck did not measure. These workers used nonpulsatile perfusion of the isolated lung and demonstrated a modest but definite vasoconstriction and thus established that stimulation of the sympathetic nerves could produce a direct pulmonary vasomotor response.

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Mechanical function of the main pulmonary artery

Cited by 40 publications

References 0 publications

The arterial load in pulmonary hypertension

The arterial load in pulmonary hypertension

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

Effects of Sympathetic Nerve Stimulation on the Pulmonary Arterial Tree of the Isolated Lobe Perfused in Situ

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