Determinants of pulmonary blood volume. Effects of acute changes in pulmonary vascular pressures and flow (original) (raw)
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Determinants of pulmonary blood volume
Journal of Clinical Investigation, 1970
Pulmonary blood volume was determined by the radiocardiographic technique in 49 patients coming to cardiac catheterization. Since this method has not been directly compared with the more commonly used double injection of dye. 25 comparisons were carried out in 13 patients of the series. Agreement was good over a range of 4.5-21.1 heart cycles since there was no statistically significant difference between transit time values measured by the two methods. The relation of pulmonary blood volume to other hemodynamic factors in these 49 patients, with and without cardiac or pulmonary disease, was evaluated by means of multiple regression analysis. The analysis carried out for mean transit time indicates that this parameter varies predominately with flow. Pulmonary blood volume, in this series of resting recumbent individuals, varies to a significant degree only with total blood volume and with pulmonary venous pressure. No parameters of vascular distensibility, such as pulmonary vascular resistance, were found to affect the volume of blood in the lungs. The fact that variations in pulmonary blood volume among the subjects could be described by a multiple regression equation linear with respect to total blood volume and pulmonary venous pressure indicates that these variations are the result of passive distention of components of the vascular bed.
Pfl�gers Archiv European Journal of Physiology, 1997
Quantitative information about the effects of pulmonary blood volume (Q p ) on pulmonary haemodynamics is lacking since Q p changes inevitably with flow. To separate flow-dependent from volume-dependent changes in intravascular pressures we imposed changes in Q p (measured continuously) by altering outflow pressure in seven isolated, blood-perfused rabbit lungs and studied the effects of Q p on the relations between arteriovenous pressure gradient (∆P) and blood flow (Q · ) under two conditions: flow-dependent volume changes were either permitted or compensated. In the latter circumstances, ∆P changed more for a given change in Q · .
The role of increased pulmonary blood flow in pulmonary arterial hypertension
European Respiratory Journal, 2005
Chronic increased pulmonary blood flow is considered a prerequisite for the induction of advanced vascular lesions in pulmonary arterial hypertension in congenital heart defects. The aim of the present study was to characterise the effects of increased pulmonary flow induced by an aortocaval shunt in the monocrotaline rat model for pulmonary hypertension in terms of survival, haemodynamics, pathology and histology. Male Wistar rats were injected with monocrotaline followed by the creation of an abdominal aortocaval shunt. Animals were sacrificed when displaying symptoms of weight loss or dyspnoea, 4-5 weeks after the creation of the shunt. Echocardiography identified increased ventricular dimensions in shunted rats and right ventricular hypertrophy in monocrotaline-treated rats. At similar pulmonary artery pressures, shunted monocrotaline rats displayed higher morbidity and mortality, increased pulmonary-tosystemic artery pressure ratios and increased right ventricular hypertrophy compared with nonshunted monocrotaline rats. Histological assessment demonstrated increased number and diameter of pre-acinar pulmonary arteries. Intra-acinar vessel remodelling and occlusion occurred to a similar extent in shunted and nonshunted monocrotaline rats. In conclusion, increased pulmonary blood flow in monocrotaline-induced pulmonary hypertension is associated with increased morbidity, mortality, and unfavourable haemodynamic and cardiac effects. These effects could be attributed to more pronounced right heart failure rather than to altered intra-acinar pulmonary vessel remodelling.
Effect of thoracic blood volume changes on steady state cardiac output
Circulation Research, 1976
We have investigated the extent to which shifts of blood volume out of or into the thoracic region influence the steady state cardiac output. The systemic circulation of anesthetized dogs was replaced with an artificial circuit which stimulated the pertinent mechanical characteristics of an intact circulation. As in the normal animal, the steady state venous return was proportional to the pressure gradient for venous return (i.e, mean systemic minus right atrial pressure). Cardiac function was altered either by administration of epinephrine or by changes in left ventricular afterload. At a constant mean aortic pressure of 100 mm Hg, epinephrine administration increased the steady state cardiac output by 55%. Half of this increase resulted from the lowered mean right atrial pressure (caused by improved cardiac function); the remainder resulted from an increased mean systemic pressure (caused by the volume shift to the systemic circulation). Increases in afterload transferred sufficie...
Negative effect of insufflation on cardiac output and pulmonary blood volume
Acta Anaesthesiologica Scandinavica, 1990
In 14 anaesthetized young pigs the changes in pulmonary blood flow and pulmonary blood volume (Q,) during mechanical ventilation were quantified. Ventilation was performed at 10 cycles per min and tidal volume (V,) was adjusted to an arterial Pco, of about 40 mmHg (5.3 kPa). In 4 animals, 7 ventilatory cycles with an inspiratory pause (IP) of 7.2 s but different tidal volumes were inserted at intervals of 5 min to determine the decrease in Q, (AQ,) from the differences between right ventricular (QI,N) and left ventricular (Q,,") stroke volume, and to relate A Q , to VF We measured pressure in the aorta (PJ, central veins (Pcv), right and left ventricles (P,,, Pi.) pericardium (P,,), and trachea (P,). Blood flow was measured electromagnetically (EM) in the pulmonary artery (Q'pa) and aorta (Q'a,,). Stroke volumes were derived from the EM-flow curves. In the other 10 experiments, as,, was derived from the aortic pulse contour. Beatto-beat analyses of Qs,N and Q+ and blood pressures during the normal ventilatory cycles and those with an I P revealed the following: 1) The end-expiratory RV output and LV output were constant and were defined as baseline values. 2) The accumulated decrease in Qs,N during insumation caused a mean deficit in cardiac output of 10.3+3.2% (s.d.), n = 135; the same was found for Q+, indicating the pulse contour as a useful method to estimate the variations in cardiac output during a ventilatory cycle. 3) Part of the pulmonary blood volume shifted into the systemic circulation during insumation and recovered during expiration with a maximum of about 1.5 ml. kg-' body weight for a V, above 20 ml. kg-'. The decreases in cardiac output and pulmonary blood volume were attributed to an accumulation of blood in the compliant systemic venous system due to the increased intrathoracic pressure. The decreased aortic pressure at early expiration contributed to the decrease in cardiac output. A squeezing effect on the pulmonary circulation during insumation contributed to the decrease in pulmonary blood volume.
Characteristics of blood flow velocity in the hypertensive canine pulmonary artery
Ultrasound in Medicine & Biology, 1986
Pulmonary artery blood flow velocity was measured in 15 dogs by a recently developed direct intraluminal pulsed Doppler technique. Changes in velocity characteristics under conditions of experimentally induced hypoxic pulmonary hypertension were observed. Experimental conditions (fractional inspired oxygen concentration = 0.10) produced significant increases in mean pulmonary artery pressure and pulmonary vascular resistance. Overall and maximal negative velocity increased with pulmonary hypertension. Negative velocity occurred predominantly in the posterior half of the pulmonary artery during both control and experimental conditions. With pulmonary hypertension, diastolic negative velocity increased only in the posterior half of the pulmonary artery and systolic negative velocity decreased only in the anterior half. More basic knowledge of pulmonary artery blood flow characteristics may facilitate an informed approach to noninvasive detection of pulmonary hypertension. Direct measurements by this recently developed intraluminal technique will be useful in studying various conditions with altered pulmonary blood flow.
Cardiovascular effects of increasing airway pressure in the dog
American Journal of Physiology-Heart and Circulatory Physiology, 1977
In paralyzed anesthetized dogs the cardiovascular effects of increasing positive end-expiratory pressure (PEEP) were explored under two conditions: a) end-expiratory lung volume increasing, b) end-expiratory lung volume kept nearly constant by matching pleural pressure rise to end-expiratory airway pressure rise. Two series of experiments were done: I) xenous return was allowed to fall, II) venous return was kept constant by infusion of volume. Right atrial pressure, pulmonary arterial pressure, and left atrial pressure increased under all conditions when measured relative to atmospheric pressure, but increased relative to pleural pressure only under condition a. The rise in left atrial relative to pleural pressure may indicate a degree of left ventricular dysfunction associated with increasing end-expiratory lung volume. Furthermore, when end-expiratory lung volume increased, inequality of the rise in pulmonary artery wedge pressure exceeded the rise in left atrial pressure in seri...