Systemic filling pressure in the intact circulation determined with a slow inflation procedure

In eight mechanically ventilated, anaesthetized pigs weighing 10.3 ± 0.8 kg (mean ± SD) we studied the effect of the inflation time of the lung on the estimation of the mean systemic filling pressure (P _sf) from the changes in venous return and central venous pressure during inflation of the lung. For this purpose we applied slow inflation procedures (SIP) to the lung with inflation times of 2.4, 4.8, 7.2, 9.6 and 12 s at tidal volumes (V _T) of 15 and 30 ml/kg. The data were compared with the values of P _sf obtained from inspiratory pause procedures (IPPs). A linear regression between venous return and central venous pressure applied during a SIP underestimated P _sf compared with the value obtained with IPPs. An exponential fit through the values of P _sf obtained from the different SIPs predicted an inflation time of about 15 s for an estimation of P _sf that is not different from the P _sf (IPP). The advantage of the SIP method is that the P _sf can be determined much faster than with the method based on IPPs. However, due to the rather long inflation time needed, the method may be only applicable under circumstances where neurohumoral control mechanisms are suppressed as during intensive care and anaesthesia. Received: 18 July 1995/Received after revision: 22 November 1995 /Accepted: 15 December 1995     

Relationship between venous return and right-atrial pressure

The dynamics and amplitude of changes in venous return and right atrial pressure (central venous pressure) in response to pressor stimuli were studied in acute experiments on cats. The increase in venous return was accompanied by either increase, or decrease in the central venous pressure. Thus, shifts in systemic venous return were not accompanied by simultaneous and co-directed changes in the central venous pressure. These findings suggest the absence of a direct relationship between these parameters.     

Tidal variation of pulmonary blood flow and blood volume in piglets during mechanical ventilation during hyper-, normo- and hypovolaemia

Effects of changes in blood volume on changes in pulmonary blood flow and pulmonary blood volume during the ventilatory cycle during mechanical ventilation with a positive end-expiratory pressure of 2 cm H₂O were determined in six pentobarbital anaesthetized, curarized pigs weighing about 10 kg. Haemodynamic variables were analysed for each cardiac cycle in eight ventilatory cycles in four consecutive series under hyper-, normo- and hypovolaemic conditions. Cardiac output was highest in hypervolaemia. Compared with normo- and hypovolaemia, it decreased less during inflation, due to a smaller rise in central venous pressure and presumably a larger filling state of the venous system. The smaller decrease in right ventricular output in hypervolaemia coincided with a larger fall in transmural central venous pressure (right ventricular filling pressure), due to right ventricular action at a higher, less steep part of its function curve. The difference between right ventricular-output (electromagnetic flow measurement) and left ventricular-output (pulse contour) indicated changes in pulmonary blood volume. In hypervolaemia less blood shifted from the pulmonary circulation into the systemic system during inflation than in normo- and hypovolaemia. This difference can be explained by two mechanisms namely, the smaller fall in input into the pulmonary vascular beds and a smaller pulmonary vascular volume decrease as a result of transmural pressure fall at a steeper part of the pressure-volume curve.     

The effect of decreased intrathoracic pressure on ventricular function

SUMMARY  Large decreases in inspiratory intrathoracic pressure (ITP) occur during obstructive apnoeas. The cardiac effects of apnoea-associated decreased ITP come from the interaction of increased preload (venous return) on the right ventricle (RV) and increased afterload on the left ventricle (LV), and are modulated by the autonomic effects of shifts in blood volume and hypoxaemia. During obstructed breathing, venous return increases by as much as three-fold during inspiration even though mean flow may change little. This leads to a substantial inspiratory increase in RV end-diastolic and stroke volume. Because of ventricular interdependence, there is a decrease in LV diastolic compliance and corresponding decrease LV preload.
Sustained decreases in ITP (Müller manoeuvre) inhibit LV ejection, and hence increase LV afterload. However, breathing against an obstructed airway (repetitive short Müller manoeuvre) is not necessarily modelled by the sustained manoeuvre. Animal studies indicate that with airway obstruction, for the first beat or two of inspiration the primary effect on the LV is a reduction in stroke volume related to a decrease in preload, and afterload, if anything, decreases. In fact, afterload only increases during early expiration when stroke volume increases. When obstructive and central apnoeas are paired for duration and blood-gas alterations, there are increases in pulmonary blood volume with central apnoeas and in RV volume with obstructive apnoeas, consistent with the postulation that the primary effect of obstructive apnoeas is on venous return.
In conclusion, the putative role of decreased ITP in increasing LV afterload under conditions appropriate to OSA is not well supported by experimental studies. However, effects with very large swings in ITP as might be seen under the most extreme forms of OSA, and differences in timing of the swings between diastole and systole have yet to be investigated.     

Measurement of hemodynamic changes with the axial flow blood pump installed in descending aorta

We have developed various axial flow blood pumps to realize the concept of the Valvo pump, and we have studied hemodynamic changes under cardiac assistance using an axial flow blood pump in series with the natural heart. In this study, we measured hemodynamic changes of not only systemic circulation but also cerebral circulation and coronary circulation under cardiac support using our latest axial flow blood pump placed in the descending aorta in an acute animal experiment. The axial flow blood pump was installed at the thoracic descending aorta through a left thoracotomy of a goat (43.8 kg, female). When the pump was on, the aortic pressure and aortic flow downstream of the pump increased with preservation of pulsatilities. The pressure drop upstream of the pump caused reduction of afterload pressure, and it may lead to reduction of left ventricular wall stress. However, cerebral blood flow and coronary blood flow were decreased when the pump was on. The axial flow blood pump enables more effective blood perfusion into systemic circulation, but it has the potential risk of blood perfusion disturbance into cerebral circulation and coronary circulation. The results indicate that the position before the coronary ostia might be suitable for implantation of the axial flow blood pump in series with the natural heart to avoid blood perfusion disturbances.     

Role of Relative Changes in Caval Flows for Evaluation of Right Atrial Pressure Shifts Induced by Nitroglycerin

Experiments on cats treated with nitroglycerin showed dynamic relationship between changes in caval venous flows: blood flow increased in the superior vena cava and decreased in the inferior vena cava. Blood pressure in the right atrium either decreased, or increased. No significant changes in total venous return were observed during maximum shifts in right atrial pressure, while contractility of the right ventricular myocardium usually decreased. Our findings suggest that the direction of the right atrial pressure shifts induced by nitroglycerin does not depend on venous return, but is determined by the prevalence of flow changes in the superior vena cava or inferior vena cava.     

Effects of graded pulsatile pressure on the reflex vasomotor responses elicited by changes of mean pressure in the perfused carotid sinus-aortic arch regions of the dog

1. In the anaesthetized dog, the carotid sinuses and aortic arch were isolated from the circulation and separately perfused with blood by a method which enabled the mean pressure, pulse pressure and pulse frequency to be varied independently in each vasosensory area. The systemic circulation was perfused at constant blood flow by means of a pump and the systemic venous blood was oxygenated by an extracorporeal isolated pump-perfused donor lung preparation.2. We have confirmed our previous observations that under steadystate conditions the vasomotor responses elicited reflexly by changes in mean carotid sinus pressure are modified by alterations in carotid sinus pulse pressure, whereas those evoked by changes of mean aortic arch pressure are only weakly affected by modifications of aortic pulse pressure.3. When the carotid sinus and aortic arch regions are perfused in combination at constant pulse frequency (110 c/min), the relationship between mean carotid sinus-aortic arch pressure and systemic arterial perfusion pressure is dependent on the size of the pulse pressure.4. Increasing the pulse pressure alters the curve relating the mean carotid sinus-aortic arch pressure to systemic arterial perfusion pressure in such a way that the perfusion pressure is lower at a given carotid sinus-aortic arch pressure within the range 80-150 mm Hg. The larger the pulse pressure, up to about 60 mm Hg, the greater the fall in systemic arterial perfusion pressure. Above a mean carotid sinus-aortic arch pressure of about 150 mm Hg, alterations of pulse pressure have little effect.5. There is a family of curves representing the relation between mean carotid sinus-aortic arch pressure and systemic vascular resistance, depending on the pulse pressure.     

Influence of pleural pressure variations on cardiovascular system dynamics: a model study

A mathematical model of the human cardiovascular system (CVS) is used to study the effect of different respiratory manoeuvres on the circulation. The model simulates the normal CVS and the interaction between the heart and the intrathoracic pressure. The vascular system is represented by resistive, capacitive and inertial elements whereas the ventricles are assumed to function according to the time-varying elastance concept based on their transmural pressures. The model predicts that normal inspiratory effeort effects an increase in the venous return, an increase in the pulmonary flow and a slight decrease in the left ventricular stroke volume (LVSV), which represents a decrease in ejection due to the increased LV transmural pressure. A step decrease in pleural pressure to −40 mm Hg, representing the Müller manoeuvre (MM), accentuates these findings, showing a decrease in LVSV in spite of an increase in the LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV) and the LV filling pressure, expressed as the mean left atrial transmural pressure. Simulating intermittent positive pressure ventilation (IPPV) with added positive end expiratory pressure (PEEP) shows an 18·6 per cent decrease in the cardiac output compared with quiet respiration. The calculated results of the model are in good agreement with available experimental data, suggesting that most of these findings may be explained by basic haemodynamic principles in the uncontrolled CVS.     

Reflex vascular responses to changes in left ventricular pressures, heart rate and inotropic state in dogs.

Dogs were anaesthetized with chloralose, artificially ventilated and the chests widely opened. Left ventricular mechanoreceptors, including those in or near the coronary arteries, were stimulated by changing the pressure in the aortic root. The pressures distending the left atrium and the aortic and carotid baroreceptors were controlled. Reflex vascular responses were assessed from changes in perfusion pressures to a hind limb and to the rest of the systemic circulation, which were perfused independently at constant flows. Physiological increases in peak left ventricular and coronary arterial pressures resulted in vasodilatation in both regions. These responses were not influenced by changes in the heart rate. Stimulation of the left cardiac sympathetic nerves resulted in increases in peak ventricular pressure and in the maximal rate of change of pressure (dP/dtmax). This also resulted in increases in perfusion pressures (vasoconstriction) at all levels of peak ventricular pressure although there was little effect on the responses to changes in ventricular pressure. Sympathetic stimulation had little effect on the relationship between perfusion pressures and aortic root pressure. Increases in ventricular filling also resulted in vasoconstriction at all levels of peak ventricular pressure. Increases in filling, however, did not affect the relationship between either perfusion pressure and aortic root pressure. Conversely, decreases in left ventricular filling, by bypassing some of the left atrial blood, resulted in vasodilatation at all levels of peak ventricular pressures but had no effect on the perfusion pressures at any aortic root pressure. The combination of sympathetic stimulation with decreased ventricular filling resulted in little effect on perfusion pressures or on their responses to changes in either aortic root or ventricular systolic pressures. We conclude that the vascular responses to stimulation of left ventricular mechanoreceptors are not enhanced by sympathetic stimulation, decreases in ventricular filling or the combination of the two. The apparent effects of each of these interventions alone on the relationships between perfusion pressures and ventricular, but not aortic root, pressure, could be explained if the receptors responsible were sensitive more to changes in aortic root and coronary arterial pressures than to pressure changes in the ventricle itself.     

Hemodynamic and pressure-volume responses to continuous and pulsatile ventricular assist in an adult mock circulation

This study investigated the hemodynamic and left ventricular (LV) pressure-volume loop responses to continuous versus pulsatile assist techniques at 50% and 100% bypass flow rates during simulated ventricular pathophysiologic states (normal, failing, recovery) with Starling response behavior in an adult mock circulation. The rationale for this approach was the desire to conduct a preliminary investigation in a well controlled environment that cannot be as easily produced in an animal model or clinical setting. Continuous and pulsatile flow ventricular assist devices (VADs) were connected to ventricular apical and aortic root return cannulae. The mock circulation was instrumented with a pressure-volume conductance catheter for simultaneous measurement of aortic root pressure and LV pressure and volume; a left atrial pressure catheter; a distal aortic pressure catheter; and aortic root, aortic distal, VAD output, and coronary flow probes. Filling pressures (mean left atrial and LV end diastolic) were reduced with each assist technique; continuous assist reduced filling pressures by 50% more than pulsatile. This reduction, however, was at the expense of a higher mean distal aortic pressure and lower diastolic to systolic coronary artery flow ratio. At full bypass flow (100%) for both assist devices, there was a pronounced effect on hemodynamic parameters, whereas the lesser bypass flow (50%) had only a slight influence. Hemodynamic responses to continuous and pulsatile assist during simulated heart failure differed from normal and recovery states. These findings suggest the potential for differences in endocardial perfusion between assist techniques that may warrant further investigation in an in vivo model, the need for controlling the amount of bypass flow, and the importance in considering the choice of in vivo model.     

体外反搏对休克狗循环紊乱的治疗作用

复制狗重症失血性休克模型,用彩色显微电视录相装置和微循环多参数分析系统,观察体外反搏对失血性休克大循环与微循环效应。结果,体外反搏使休克时下降的中心静脉压和平均动脉压迅速回升。反搏后120分钟,休克时紊乱的球结膜微循环(口径、流速、流量)恢复到接近正常,半数动物存活3天以上。提示体外反搏可改善失血性休克循环功能。显著提高存活率。     

Influence of body position and pneumoperitoneum on respiratory variation of venous return in anesthetized dogs

Summary Blood flow in the vena cava was measured in anesthetized dogs in supine, lateral, or prone position by a catheter velocity probe at four levels, i. e., above and below the veno-atrial junction and above and below the confluence of the renal veins, with the diameter of the vena cava fixed Teflon rings placed around it. Also the influence of pneumoperitoneum at atmospheric pressure on venous return was examined in supine position. In supine position there was an increase of venous return in the thoracic venae cavae and of calculated hepatic outflow during inspiration, whereas flow in the abdominal vena cava showed less and reversed variations as compared with the thoracic inferior caval venous pattern, i.e., a trough during inspiration and a peak during early expiration. Pneumoperitoneum reduced the inspiratory increase of thoracic inferior vena cava flow and of hepatic outflow. Lateral and prone positions induced a decrease or early leveling off of the inspiratory increase of flow in the thoracic inferior vena cava and of hepatic outflow. Superior caval venous flow remained almost unchanged with postural change. In all positions renal outflow did not show any clear-cut relationship with respiration. These variations of pattern of vena cava flow and hepatic outflow were attributed to an increase in the resistance of the vena cava in the infradiaphragmatic part, induced by the change of body position, as shown by an increase of the preinspiratory caval venous pressure difference between thorax and abdomen to 5.3±0.92 cm H₂O (mean±S.D.,n=14) in lateral position, and to 6.5±0.81 cm H₂O (n=4) in prone position from 2.0±0.85 cm H₂O (n=18) in supine position (p<0.001 for the increase from supine position).     

Cardiac contractility, central haemodynamics and blood pressure regulation during semistarvation.

Eight obese patients were studied before and after 2 weeks of treatment by a very-low-calorie diet (VLCD). Cardiac output and central blood volume (pulmonary blood volume and left atrial volume) were determined by indicator dilution (125I-albumin) and radionuclide angiocardiography (first pass and equilibrium technique by [99Tcm]red blood cells). Cardiac output decreased concomitantly with the reduction in oxygen uptake as the calculated systemic arteriovenous difference of oxygen was unaltered. There were no significant decreases in left ventricular contractility indices, i.e. the ejection fraction, the peak ejection rate and changes in end-systolic volume. Also the diastolic function evaluated by the peak filling rate remained normal. Furthermore, no sign of backward failure could be demonstrated since the central blood volume was not significantly increased. Both systolic and diastolic blood pressure (BP) declined. The fall in BP was caused by the reduction in cardiac output as the total peripheral resistance was unchanged. Finally, the decline in total blood volume was not significant. These findings together with a reduction in heart rate indicated that a reduced sympathetic tone via increased capacitance of the venous bed was the main operator of a reduced venous return. Thus, the haemodynamic alterations in obese patients during short-term semistarvation may be caused by the fall in oxygen uptake and produced mainly by changes in the sympathetic tone.     

Vascular characteristics influence the aortic ultrasound Doppler signal: computer and hydraulic model simulations

There is an increasing demand for non-invasive methods for the assessment of left ventricular function. Ultrasound Doppler methods are promising, and the early systolic flow velocity signal immediately distal to the aortic valve has been used clinically for this purpose. However, the signal is influenced not only by left ventricular ejection but also by systemic vascular characteristics. Their relative contribution to the timevelocity signal has not been analysed in depth previously. A theoretical analysis, based on a three-element Windkessel model, neglecting peripheral outflow in early systole and assuming linear pressure rise, was therefore tested in computer and hydraulic model simulations where peripheral outflow was included. Significant changes in early aortic flow velocity parameters were found when vascular characteristics were altered. As predicted by the theory, with a standardized aortic valve area and aortic pressure change, the simulations confirmed that maximal flow velocity is related to compliance of the aorta and the large arteries, and that maximal acceleration is inversely related to the characteristic impedance of the aorta. Therefore, maximal velocity and acceleration can be used for assessment of left ventricular function only in situations where vascular characteristics can be considered relatively constant or where they can be estimated.     

Cardiovascular changes in conscious dogs during spontaneous deep breaths

Cardiovascular functions were evaluated beat by beat during 29 spontaneous deep breaths in three conscious dogs. When pleural pressure was significantly lower than during quiet breathing, stroke volume was reduced, heart rate elevated, as well as transmural pressure in the pulmonary artery (PPA-Ppl) and in the thoracic aorta (PAO-Ppl); the left ventricular filling pressure (LVEDP-Ppl) did not decrease. The authors suggest that these findings are not consistent with the classical hypothesis which explains the decrease in left ventricular output primarily by a reduction in the venous return to the left heart. The results indicate that the decrease in pleural pressure is responsible for an increase in the afterload on the left heart and suggest that this is the predominate factor in the reduction of the stroke volume without decrease in left ventricular filling pressure.     

体外反搏对失血性休克狗循环紊乱的治疗作用

用彩色显微电视录像和微循环图象分析系统,观察体外反搏对重症失血性休克狗大循环和微循环的效应。结果查明,体外反搏使休克早期下降的中心静脉压和平均动脉压迅速回升。反搏后120分钟,休克时紊乱的球结膜微循环恢复到接近正常,半数动物存活3天以上。证明体外反搏可改善失血性休克循环功能,显著提高存活率。     

Effects of endotoxin infusion on mean systemic filling pressure and flow resistance to venous return

Mean systemic filling pressure (P _sf) is an indicator of the filling state of the systemic circulation. Cardiac output (Q) is related linearly to the difference betweenP _sf and central venous pressure (P _cv), according to:Q = (P _sf –P _cv)/R _sf, whereR _sf is the flow resistance downstream from the sites where blood pressure is equal toP _sf In 16 anaesthetized pigs we evaluatedP _sf,R _sf andQ during baseline conditions, continuous endotoxin infusion and after subsequent fluid loading.P _sf andR _sf were determined from simultaneous measurements ofQ andP _cv at seven levels of lung inflation. The following results were obtained.P _sf was 8.1 ±1.8 mm Hg (mean ± SD) during baseline conditions, increased after endotoxin infusion to 9.9 ± 3.2 mm Hg (P = 0.04) and remained the same after infusion of 18 ml · kg^–1 of Ringer's lactate.R _sf increased from 0.34 ± 0.07 to 0.80 ± 0.34 mm Hg · ml^–1 · s by endotoxin and decreased after fluid infusion to 0.58 ± 0.14.Q changed inversely proportional toR _sf (P = 0.001).R _sf changes were highly correlated with the changes in total systemic flow resistance (R _S) (P < 0.001). Endotoxin caused haemoconcentration and a decrease in plasma volume. The stability ofP _sf during endotoxin infusion and after volume loading indicate that the stressed volume was well maintained and changes in blood volume are compensated by changes in nonstressed volume. The increase inR _sf can be attributed to arteriolar vasoconstriction, venous vasoconstriction and haemoconcentration.     

Left ventricular pressure transmission to myocardial lymph vessels is different during systole and diastole

In six open-thorax-anaesthetized dogs with paced hearts and a retrogradely cannulated epicardial lymph vessel, the sensitivity of myocardial lymph pressure to left ventricular pressure during systole and during diastole was determined. The lymph vessels were cannulated using PE-90 tubing, and lymph pressure was measured by connecting the cannula to a microtip pressure transducer. To obtain the systolic sensitivity, left ventricular pressure was changed by clamping the descending aorta, which caused left ventricular pressure to increase. The diastolic sensitivity was obtained from natural variation to left ventricular pressure caused by atrial contractions during induced long diastoles. The mean ratio of the pulse in lymph pressure to the pulse in left ventricular pressure was determined: systole: 0.069±0.013, n=213, diastole: 0.76±0.16, n=249 and, if possible, linear regression analysis between lymph and left ventricular pressure was performed. The systolic regression coefficients could be determined in six dogs and the diastolic coefficients in three dogs. During long diastoles lymph pressure variations are on average 76 per cent of those in the left ventricle. However, during systole, the sensitivity of lymph pressure to left ventricular pressure is more than ten times lower. It is not unlikely that the structural embedment of lymph vessels within the myocardium is such that volume variations by cardiac contraction are limited.     

Human cardiovascular dose-response to supplemental oxygen

Aim: The aim of the study was to examine the central and peripheral cardiovascular adaptation and its coupling during increasing levels of hyperoxaemia. We hypothesized a dose‐related effect of hyperoxaemia on left ventricular performance and the vascular properties of the arterial tree. Methods: Oscillometrically calibrated arterial subclavian pulse trace data were combined with echocardiographic recordings to obtain non‐invasive estimates of left ventricular volumes, aortic root pressure and flow data. For complementary vascular parameters and control purposes whole‐body impedance cardiography was applied. In nine (seven males) supine, resting healthy volunteers, aged 23–48 years, data was collected after 15 min of air breathing and at increasing transcutaneous oxygen tensions (20, 40 and 60 kPa), accomplished by a two group, random order and blinded hyperoxemic protocol. Results: Left ventricular stroke volume [86 ± 13 to 75 ± 9 mL (mean ± SD)] and end‐diastolic area (19.3 ± 4.4 to 16.8 ± 4.3 cm²) declined (P < 0.05), and showed a linear, negative dose–response relationship to increasing arterial oxygen levels in a regression model. Peripheral resistance and characteristic impedance increased in a similar manner. Heart rate, left ventricular fractional area change, end‐systolic area, mean arterial pressure, arterial compliance or carbon dioxide levels did not change. Conclusion: There is a linear dose–response relationship between arterial oxygen and cardiovascular parameters when the systemic oxygen tension increases above normal. A direct effect of supplemental oxygen on the vessels may therefore not be excluded. Proximal aortic and peripheral resistance increases from hyperoxaemia, but a decrease of venous return implies extra cardiac blood‐pooling and compensatory relaxation of the capacitance vessels.     

Left ventricular mechanoreceptors: a haemodynamic study

1. To study the function of the left ventricular mechanoreceptors, a working left ventricle preparation was devised in dogs which permitted control of pressure and flow of the isolated perfused coronary circulation and of the flow of the isolated, separately perfused systemic circulation. The systemic circulation was perfused at a constant rate so that changes in systemic pressure reflected changes in systemic resistance.2. Increases in myocardial contractility produced by injection of catecholamines into the isolated, perfused coronary circulation produced a fall in the pressure (resistance) of the isolated, separately perfused (at a constant rate) systemic circulation.3. Completeness of isolation of the coronary and systemic circulations was shown by the marked difference in appearance times between the reflex hypotensive responses from catecholamine injections into the isolated coronary circulation and the direct hypertensive response from a similar injection when the circulations were connected as well as by the marked difference between the pressure pulses recorded simultaneously on both sides of the aortic balloon separating the two circulations.4. Myocardial beta receptor blockade produced by injection of propranolol into the isolated coronary circulation abolished or attenuated the changes in left ventricular myocardial contractility as well as the subsequent hypotensive responses following the similar injection of catecholamines.5. Electrical stimulation of a sympathetic nerve innervating the heart resulted in increases in left ventricular myocardial contractility and subsequent systemic hypotensive responses indistinguishable from those following injection of catecholamines.6. That distortion of the mechano- or stretch receptors in the left ventricular myocardium was the cause of the hypotensive responses was demonstrated by increasing left ventricular myocardial contractility by mechanically obstructing the left ventricular outflow which produced hypotensive responses similar to those following the injection of catecholamines or nerve stimulation.7. Bilateral high cervical vagotomy abolished the hypotensive responses following injection of catecholamines into the isolated coronary circulation or following left ventricular outflow obstruction in all but one instance, indicating the importance of vagal fibres to the afferent arm of the reflex.8. It is suggested that the left ventricular mechanoreceptors function normally to reduce the peripheral resistance in order to prepare the systemic circulation to receive the left ventricular output and, especially during exercise, to prepare the systemic circulation to receive the augmented cardiac output with a minimum alteration in the systemic blood pressure and to distribute this augmented output preferentially to the skeletal muscles.