Blood Volume Shifts Research Articles

Effect of head-out water immersion on cardiorespiratory response to dynamic exercise

Head-out water immersion is known to produce several cardiopulmonary adjustments at rest due to a cephalad shift in blood volume. The purpose of this study was to determine the effect of head-out water immersion on the cardiorespiratory response to graded dynamic exercise. Nineteen healthy middle-aged men performed upright cycling exercise at 40, 60 and 80% of maximal oxygen consumption on land and in water (31.0 +/- 1.0 degrees C) to the shoulders. Cardiac output (measured by the carbon dioxide rebreathing technique) was significantly greater in water at 40 and 80% maximal oxygen consumption. Stroke volume was significantly elevated at all stages of exercise. Heart rate did not differ significantly at 40 and 60% maximal oxygen consumption but was significantly lower in water at 80% maximal oxygen consumption. Total ventilation did not differ significantly in water and on land at any stage of exercise. The results suggest that the central redistribution of blood volume with head-out water immersion leads to an increase in stroke volume. Because there is not a proportional decrease in heart rate with the elevated stroke volume, cardiac output is regulated at a higher level during upright exercise in water compared with that on land. In conclusion, there are serious limitations of available, prerecorded rhythm data bases for designing and testing of automatic external defibrillators. Performance can be adequately assessed only by extensive clinical tests, which seem mandatory for this new and important type of defibrillator.

Cardiovascular Effects of Anesthesia and Operation

Anesthesia and surgery have a wide range of effects on the cardiovascular system. Even in healthy patients having minor operations, anesthetic agents can cause significant cardiac depression and hemodynamic instability. Virtually all anesthetic agents have intrinsic myocardial depressant properties, although some may mask this with sympathetic stimulation. The vasodilatory effects of the volatile agents can result in serious hypotension when combined with this negative inotropy. In the patient with pre-existing cardiac disease, these cardiovascular anesthetic effects become much more serious. These patients will not tolerate wide swings of hemodynamic variables, and the cardiodepressant effects of anesthetics are more pronounced in them. The stress of anesthesia and surgery frequently unmasks previously undiagnosed heart disease. Surgery itself provides many insults to the cardiovascular system, and these may be additive with the effects of anesthesia. These include loss of blood and other volume shifts, release of various substances into the circulation, hypothermia, sudden changes in cardiac preload and afterload, myocardial ischemia, and effects of drugs or blood products given for surgical reasons. The signs and symptoms of these surgical stresses to the cardiovascular system are often masked by anesthesia.

Circulatory Adaptations of Snakes to Gravity

Comparative investigations of diverse taxa of snakes demonstrate numerous adaptations for counteracting effects of gravity on the circulation, including morphological, physiological and behavioral specializations. Arboreal and terrestrial snakes that are normally subjected to stresses from gravity are characterized by relatively high arterial pressures and ability to regulate pressure by physiological adjustments of flow and flow resistance. The heart occupies an anterior position, and the arterial blood column between the heart and head is comparatively short. Terrestrial snakes characteristically possess short vascular lungs which eliminate risks of pulmonary edema due to gravity effects during vertical posture. Problems of blood pooling in peripheral systemic vasculature are counteracted by relatively non-compliant body tissue, vasomotor adjustments, and specific movements that facilitate the venous cardiac return. Anatomical valves appear to be absent from major venous channels, but gravity, acting in concert withspecific features of venous morphology, can create valving actions that impede shifts of blood volume to dependent segments of these vessels. Nearly all of these characteristics are absent or deficient in several independent lineages of aquatic snakes that are far less subject to gravitational disturbance of hydrostatic pressures. Thus, snakes provide diverse and particularly useful models for examining cardiovascular adaptations to gravity, including mechanisms of function and the evolution of cardiovascular design.

Immediate hemodynamic response to furosemide in patients undergoing chronic hemodialysis.

To evaluate the effect of furosemide on cardiovascular hemodynamics in patients with end-stage renal failure, we studied ten patients undergoing hemodialysis three times a week. Arterial pressure, heart rate, and cardiac output (indocyanine green dye) were measured in triplicate; total peripheral resistance and central blood volume were calculated by standard formulas. Hemodynamics were determined at baseline and 5, 10, 15, and 30 minutes after intravenous (IV) bolus injection of furosemide 60 mg. Furosemide produced a decrease in central blood volume of -13% +/- 2.2% from pretreatment values (P less than .01) that was most pronounced five minutes after injection, together with a fall in cardiac output (from 6.76 +/- 0.59 to 6.17 +/- 0.52 L/min, P less than .10). Stroke volume decreased with a maximum fall occurring after 15 minutes (from 84 +/- 7 to 79 +/- 7 mL/min, P less than .05), and total peripheral resistance increased (from 15.8 +/- 2.1 to 17.8 +/- 2.3 units, P less than .05) after furosemide. Arterial pressure and heart rate did not change. The decrease in central blood volume reflects a shift of the total blood volume from the cardiopulmonary circulation to the periphery, suggesting dilation of the peripheral venous bed. Thus, even in patients undergoing hemodialysis, furosemide acutely decreases left ventricular preload by venous dilation and should therefore prove to be beneficial in acute volume overload.

Graphic analysis of serotonin effects in dog heart-lung preparation.

Graphical analysis of the effects of serotonin on cardiac function and pulmonary circulation was performed, using the dog heart-lung preparation. The equilibrium points, at which the cardiac output (CO)-curve and venous return (VR)-curve cross in the right atrial pressure (RAP) or left atrial pressure (LAP)-CO relations, were directly recorded on two X-Y recorders. CO- and VR-curves were directly depicted by changing the blood level in the reservoir, and by inducing ventricular fibrillation and simultaneously occluding pulmonary arterial trunk, respectively. Single injections of serotonin, 300 micrograms, into the right or left atrium, induced a negative inotropic response. Low rate (less than 30 micrograms/min) of infusion of serotonin had no effect on the CO-curve or on the slope-gradient of VR-curve in the LAP-CO relation. At a rate of 60 or 120 micrograms/min, however, the CO-curve was moved downwards to the right, indicating a negative inotropic effect. Pulmonary mean filling pressure increased and the slope-gradient of pulmonary VR-curve decreased, indicating an increased resistance to venous return from the pulmonary circulation. Pulmonary arterial pressure was markedly elevated. In order to obtain the capacitance ratio between the extracorporeal circuit and the pulmonary circulation, a shift of blood volume to the pulmonary circulation was induced by elevating the aortic pressure, which also decreased the slope-gradient. The calculated capacitance ratio became greater during the infusion of serotonin, indicating that the capacitance in the pulmonary circulation was lowered. It is likely that serotonin has contractile effects on the pulmonary arterial and venous vascular beds, elevating the pulmonary filling pressure and resistance to venous return.

Effect of head-out water immersion on response to exercise training.

During spaceflight and head-out water immersion (WI) there is a cephalad shift in blood volume. We have recently shown that left ventricular end-diastolic dimension is significantly greater during moderate cycling exercise with WI compared with on land. The purpose of this study was to determine whether the cephalad shift in blood volume and accompanying increase in cardiac preload with WI alters the normal cardiovascular adaptations to aerobic exercise training. Nine middle-aged healthy men trained on cycle ergometers in water, nine trained on land, and four served as controls for 12 wk. Following training, both training groups showed similar increase (P less than 0.05) in stroke volume and similar decreases in heart rate (P less than 0.01) and blood pressure (P less than 0.05) at a given submaximal exercise O2 consumption (VO2). Maximal VO2 increased (P less than 0.01) similarly for both training groups. The control group did not demonstrate any significant changes in submaximal or maximal exercise responses. We conclude that the cephalad shift in blood volume with WI does not alter the normal cardiovascular adaptation to aerobic exercise training.

Pressure-volume conditions in patients with subarachnoid and/or intraventricular hemorrhage.

Pressure-volume conditions were studied in 17 patients with subarachnoid and/or intraventricular hemorrhage, who underwent continuous intracranial pressure (ICP) monitoring. The pressure-volume index (PVI) technique was used. The interrelationship between the ICP pulse amplitude and compliance was also examined. All patients were admitted in Hunt and Hess Grades II to V, and 11 had a proven aneurysm. The ICP was above 15 mm Hg in all patients during some part of the monitoring period. The pressure-volume conditions were abnormal in all patients. Median PVI was 12.7 ml (5.8 to 40.0 ml). The PVI did not correlate with ICP: the PVI based on bolus injection was significantly greater than PVI based on fluid withdrawal. The ICP pulse amplitude varied from 1.5 to 15 mm Hg and rose concomitantly with increasing ICP. Considering the pulsatile shift in intracranial blood volume as an endogenous bolus that increases ICP from the diastolic (Pdiast) to the systolic (Psyst) level, an equation was derived from the PVI model that describes the relationship between the Psyst:Pdiast ratio and the PVI.

The effect of long-term intraarterial norepinephrine infusion on transcapillary fluid and protein transport

The effect of long-term (4 hr) intraarterial norepinephrine (NOR) infusion on vascular resistance ( R), transcapillary fluid movement ( J v), and protein transport ( J s) was determined in the isolated hindlimb of the dog. The limb was isolated by an occluding tourniquet and perfused at constant pressure with blood from the opposite femoral artery. Tissue volume changes were detected with a Whitney (1953) mercury-in-rubber strain gauge and protein transport assessed by direct monitoring of the rate of accumulation of 125 I-albumin in the tissue. Periodically venous pressure ( P v) was elevated 20 mm Hg in order to estimate the capillary filtration coefficient ( K f) and to determine whether or not prolonged NOR exposure modified the microcirculatory response to increased pressure. Infusing NOR at a delivered dose ranging from 0.026 to 0.13 μg/ml significantly elevated R for the entire infusion period. Tissue volume and radioactivity declined transiently and then returned to the control level within 15 min and remained at this level for the remainder of the infusion period. These changes were attributed to blood volume shifts. Elevating P v during NOR infusion further increased R to an extent which exceeded that during control. Jv and Js were elevated to a greater extent than during control with the ΔJ s exceeding ΔJ v. The changes in J v are probably due to an increase in microvascular surface area as reflected in an elevated K f. The greater increase in J s is due in part to an increase in convective transport across a greater microvascular surface area. However, since the ratio of J s J v increased with P v elevation following NOR, the increased J s may represent a change in microvascular permeability produced by the increased P v. It is also possible that due to myogenic activity or a venous-arteriolar reflex, the microvascular pressure profile was shifted toward the venous side where the reflection coefficient is lower.

Cardiovascular responses to heat stress and blood volume displacements during exercise in man.

Subjects exercised in the upright position at approximately 50% of maximal oxygen consumption in four situations: in 25 degrees C air, in 45 degrees C air [mean skin temperature (Tsk) 35 degrees C], in 35 degrees C water immersed to the level of the xiphoid process, and finally wearing a suit perfused with 35 degrees C water. The water immersion prevented gravitational shifts of blood volume to the legs. In this situation the forearm blood flow (FBF) rose continually with increasing core temperature (Tes) in contrast to the attenuation in rise above 38 degrees C Tes in 45 degrees C air. The differences were significant above 38.6 degrees C Tes in experiments in eight subjects. The effects of immersion on cardiac output (CO), stroke volume (SV), and heart rate (HR) were studied in five of the subjects in relation to Tes, since the rate of rise of Tes was different in the four situations. CO and SV tended to be higher during both rest and exercise in the water than in the other three conditions, while HR rose in the same manner with increasing core temperature, except that it was lower in 25 degrees C air, where Tsk was lower. Thus, the prevention of hydrostatic shifts of peripheral venous volume permitted the maintenance of a higher SV and peripheral blood flow, and enhanced the ability of the circulation to deal with the combined exercise and heat stress.

Ventricular diastolic pressure-volume shifts during acute ischemic left ventricular failure in dogs

Ischemic left ventricular failure was produced in eight acutely instrumented, anesthetized dogs to study the contribution of changing myocardial compliance and pericardial pressure to shifts in right and left ventricular diastolic pressure-volume relations. Right and left ventricular and pericardial volumes were measured by ungated computed tomography. Cardiac volumes were manipulated by infusion of saline solution, hemorrhage, phenylephrine infusion and, during failure only, nitroglycerin administration. During both control and failure periods, these interventions shifted the left and right ventricular pressure-volume relations by changing pericardial pressure only; that is, these interventions caused no change in the ventricular transmural pressure-volume relation. The induction of failure as such increased pericardial pressure only minimally and did not change the left ventricular or right ventricular transmural pressure-volume relations significantly. Volume loading during the control period caused an apparent pericardial creep which attenuated the pericardial effect on ventricular pressure-volume relations. During failure, volume loading caused an increase of right ventricular volume, but tended to decrease left ventricular volume; this was associated with a leftward displacement of the interventricular septum. In conclusion, in the presence of ischemic left ventricular failure as well as normally, changes in preload, afterload and circulating blood volume shift ventricular diastolic pressure-volume relations by stretching or relaxing the pericardium, thus changing pericardial pressure. In these circumstances, there were no consistent changes in myocardial compliance.

Total body vascular capacitance changes during high intracranial pressure in dogs.

The active capacitance response to increased intracranial pressure (Pic) was studied in nine chloralose-anesthetized dogs. The vena cavae were cannulated and drained into a reservoir as blood was pumped at a constant flow (Q) into the right atrium. Central blood volume was determined as Q times the mean transit time of dye from the right atrium to the aortic root. Arterial compliance (Ca) was determined from the monoexponential decay of systemic arterial pressure (SAP) during vagal cardiac arrest to compute changes in arterial volume (delta SAP X Ca). Atropine was administered to prevent bradycardia and dangerous, constant cardiac output-induced increases in pulmonary arterial (PAP) and right and left atrial pressures. Blood volume shifts indicative of active venoconstriction, included changes in reservoir, central, and arterial volumes during Pic of 100-200 mmHg. Raised Pic, after atropine, induced a tachycardia, increased systemic and pulmonary resistances, and increased SAP and PAP. Venoconstriction caused marked blood shifts between 125 and 200 mmHg Pic. The extrapolated response threshold was about 112 mmHg. In the most sensitive range, venoconstriction amounted to 3.9 ml X kg-1 per 25-mmHg change in Pic. These results indicate that intense active capacitance vessel constriction is an important part of cardiovascular hemostasis during rapidly increased intracranial pressure.

Mechanical heart-lung interaction with positive end-expiratory pressure.

Recent reports have suggested that positive end-expiratory pressure (PEEP) depresses left ventricular (LV) function or shifts LV pressure-volume (PV) relationships due to neural, humoral, or mechanical events. These studies have usually utilized pressures measured during expiration. To study the mechanical effects of PEEP in expiration and inspiration, the circulation was arrested in 12 open-chest dogs, and the coronaries were perfused with a cold cardioplegic agent. Balloons were placed in the ventricles to measure ventricular pressures. Shifts in cardiopulmonary blood volume were prevented by venting the atria to atmosphere. Having ablated neural reflexes and humoral changes, we varied ventricular volumes, chest wall compliance, tidal volume, and PEEP. We found that isovolumic ventricular pressures (relative to atmosphere) increase with PEEP (P less than 0.001), and heart-lung interaction with PEEP is significantly greater in inspiration (P less than 0.001). The effect of PEEP is modified by heart volume (P less than 0.01) and respiratory system compliance (P less than 0.01). We conclude that a mechanical compressive force can be applied to the heart by the lungs as they expand, and this may explain the previous reports of diminished LV function or LV diastolic compliance with PEEP and, in part, explain the decreased cardiac output associated with PEEP. The marked increase in mechanical compressive forces applied to the heart during inspiration with PEEP may have far greater hemodynamic consequences than events during expiration.

Mechanisms of cardiac contraction. What roles for preload, afterload and inotropic state in heart failure?

There is evidence that sarcomere length is maximal and changes little during chronic cardiac enlargement, and that the failing heart does not operate on a true descending limb of the Frank-Starling curve. However, increases of ventricular end-diastolic volume over time clearly are important at the geometrical level in maintaining stroke volume. When the preload reserve is fully utilized, afterload mismatch can exist in the steady state to produce operation of the heart on an apparent descending limb of cardiac function, and further afterload mismatch can be produced by pressure loading under these conditions. The treatment of acute experimental heart failure with a mixed vasodilator (nitroprusside) can lead to an increased cardiac output by afterload reduction only when the venous return curve does not shift downward; thus, the threefold larger shift of central blood volume to the periphery in heart failure (compared to normal) counter balances the venodilator action of nitroprusside. Whether or not the inotropic ceiling of failing myocardium can be reached by positive inotropic agents is unclear, but major hemodynamic benefits in heart failure with many potent inotropic drugs are associated with the direct vasodilating properties of these agents. Thus, there appears to be little role for the Frank-Starling mechanism at the sarcomere level, whereas afterload mismatch and its correction are of major importance provided the venous return can be increased. A degree of inotropic reserve also is available, even in the severely failing myocardium, but more research is needed on the potential costs and benefits of marked sustained inotropic stimulation.

Participation of lung innervation in pulmonary edema formation.

The plasma leakage in neurogenic pulmonary edema (NPE) is generally thought to be a result of an elevation in the intravascular pressure induced by a shift of blood volume from systemic to pulmonary circulation. Besides such a mechanism, a possibility that the central nervous system directly affects the pulmonary vascular bed to increase the vascular permeability was demonstrated in this study. NPE was induced with brain ischemia in anesthetized dogs. Supplementary blood was collected from another dog and mixed with 10 % solution of dextran 40. Right and left atria (RA and LA) and pulmonary arterial trunk were cannulated. At first, we made a right heart bypass preparation. The venous return to the reservoir from the systemic circulation via RA was suddenly changed to that from the pulmonary circulation via LA. By this procedure, a complete artificial pulmonary perfusion preparation was made, while the brain circulation ceased. Perfusion pressure was 20-30 cmH2O, and left atrial pressure was in the range of 7-11 cmH2O. Initial peak inspiratory pressure was 8-10 cmH2O. Even under these conditions which were considered not to induce a hydrostatic pulmonary edema, edema still occurred, indicating an increased vascular permeability. Elimination of lung innervation inhibited the decrease in the reservoir blood volume, suggesting a physiological role of lung innervation on the pulmonary vascular permeability.

Abnormalities of cerebral oxidative metabolism in animal models of Parkinson disease.

Abnormalities of cerebral oxidative metabolism were investigated in "animal models" of Parkinson disease by in situ optical measurements of local cerebral blood volume and cytochrome oxidase redox shifts in rats two weeks after unilateral 6-hydroxydopamine lesions of the substantia nigra with or without interruption of ascending noradrenergic pathways. The data demonstrate oxidative metabolic dysfunction of ipsilateral cerebral hemispheres caused by lesions that involve both dopaminergic and noradrenergic systems but not when dopaminergic neurons only are affected. We speculate that the dementia of Parkinson disease may be more prevalent when degeneration of catecholaminergic systems is widespread and not restricted to the dopaminergic system.

Hemodynamic Effects of Medical Anti-Shock Trousers (MAST Garment)

Despite widespread use of the Medical Anti-Shock Trousers (MAST) little is known about the exact mechanism by which they increase arterial pressure. It is assumed that an autotransfusion occurs. To examine this question, blood pressure, heart rate, forearm blood flow, cardiac output, and stroke volume were measured in ten healthy adults, supine and during 60 degree headup tilt with MAST garment pressures of 409 and 100 mm Hg. Supine, the garment produced no net 'autotransfusion,' but raised blood pressure (27%) by increasing peripheral resistance (48%) with decreased stroke volume and cardiac output (18%). During headup tilt without the MAST device, venous pooling in the legs decreased stroke volume (52%), cardiac output (30%), and increased total peripheral resistance (40%). Application of the garment during tilt shifted this blood centrally, producing increased stroke volume (52%), cardiac output (30%), and increased total peripheral resistance (40%). Application of the garment during tilt shifted this blood centrally, producing increased stroke volume (14%). In supine normovolemic subjects, the garment raised pressure almost exclusively by increased systemic afterload. Forearm vascular resistance did not change and the increased pressure augmented flow to the arm, i.e., to noncompressed tissue. With increased venous pooling during tilt, the MAST garment acted as a 'G-suit' and caused a central shift of blood volume. These findings could explain: 1) why fluid replacement is not always adequate to maintain pressure when deflating the trousers; 2) why the trousers should not be used if one wishes to avoid increasing afterload (e.g., certain patients with acute myocardial infarction). We conclude that the MAST garment acts as a local, effective, nonpharmacologic vasoconstrictor and should be used when such an effect is clinically appropriate.

Effects of central venous blood volume shifts on arterial baroreflex control of heart rate

The purpose of this study was to investigate the effects of anesthesia, body position, and blood volume expansion on baroreflex control of heart rate. Five male rhesus monkeys (7.0-10.5 kg) were given bolus injection of 4.0 micrograms/kg phenylephrine during each of the following situations: awake sitting, anesthetized (AN) (10 mg/kg ketamine-HCl) sitting, AN recumbent, AN 90 degrees head down tilt, and AN 50% blood volume expansion with normal saline. beta-Receptor blockade was also performed on each treatment after anesthesia. Four additional animals were similarly treated after 20% blood volume expansion. R-R interval was plotted against systolic aortic pressure, and the slope was determined by linear regression. Baroreflex slope was significantly (P less than 0.05) reduced by 90 degrees head down tilt and 50% volume expansion both before and after beta-receptor blockade. A similar trend was seen after 20% volume expansion. These data are consistent with the thesis that baroreflex control of heart rate is reduced by central blood volume shifts.

The importance of the spleen in blood volume shifts of the systemic vascular bed caused by the carotid sinus baroreceptor reflex in the dog.

The importance of the spleen in blood volume shifts of the systemic vascular bed caused by the carotid sinus baroreceptor reflex in the dog.

Cerebral compensation for chronic noradrenergic denervation induced by locus ceruleus lesion: recovery of receptor binding, isoproterenol- induced adenylate cyclase activity, and oxidative metabolism

The long term effects of specific noradrenergic denervation of rat cerebral cortex were considered in parallel studies of in vitro noradrenergic receptor binding and isoproterenol-induced adenosine 3':5'-monophosphate (cycle AMP) generation and of in vivo oxidative metabolism. Noradrenergic denervation was achieved by the local, unilateral injection of 6-hydroxydopamine into the locus ceruleus. Cerebral noradrenaline remained depleted throughout the 8-week duration of the study. Ligand-binding assays showed increased beta-adrenergic receptors 2 weeks after locus ceruleus lesion with recovery occurring by 4 weeks. There were no changes in alpha 1-adrenergic receptors. Isoproterenol-induced cyclic AMP generation increased at 2 weeks after lesion but recovered at 8 weeks. Dual wavelength reflection spectrophotometric measurements of cytochrome oxidase reduction/oxidation and local blood volume shifts, provoked in situ by direct cortical stimulation, also demonstrated abnormalities at 2 weeks with recovery by 4 weeks after lesion. Thus, in vivo and in vitro changes after locus ceruleus lesion are reversible and the time course of these changes is related temporally. These data suggest that cerebral cortex has adaptive capabilities which are activated to compensate for prolonged noradrenaline depletion. We also speculate that there may be a causal relationship between the in vitro and in vivo parameters studied.

Rib cage and abdominal restrictions have different effects on lung mechanics

The effects of a variety of restrictive procedures on lung mechanics were studied in eight healthy subjects. Rib cage restriction decreased total lung capacity (TLC) by 43% and significantly increased elastic recoil and maximum expiratory flow (MEF). Subsequent immersion of four subjects with rib cage restriction resulted in no further change in either parameter; shifts of blood volume did not reverse recoil changes during rib cage restriction. Abdominal restriction decreased TLC by 40% and increased MEF and elastic recoil, but recoil was increased significantly less than was the case with rib cage restriction. Further, at a given recoil pressure, MEF was less during rib cage restriction than during either abdominal restriction or no restriction. Measurements of the unevenness of inspired gas distribution by the single-breath nitrogen technique showed increased unevenness during rib cage restriction, which was significantly greater than that during abdominal restriction. We conclude that lung volume restriction induces changes in lung function, but the nature of these changes depends on how the restriction is applied and therefore cannot be ascribed to low lung volume breathing per se.