Effect of acute intravenous volume loading on haemodynamics and aortic baroreceptor activity in dogs

This study evaluates the effect of acute intravenous volume loading on haemodynamics and aortic baroreceptor activity in order to determine the mechanistic factors responsible for divergent heart rate responses to volume loading. Eleven beagles were anaesthetized and instrumented for the recording of aortic pressure, diameter, flow and aortic baroreceptor activity. Isotonic saline, equal to 20% of the estimated blood volume, was infused intravenously within 60-90 s. The animals were divided into tachycardiac and bradycardic groups according to their heart rate response to volume loading. In the group developing the tachycardic response, aortic baroreceptor activity increased. Total peripheral resistance was reduced by 31% and variables representing aortic stretch, mean aortic pressure, diameter and tension remained unchanged. In contrast, in the group developing the bradycardiac response, aortic baroreceptor activity increased markedly. Also in this group peripheral resistance decreased, but only by 15%, which was significantly less than in the tachycardiac group. Factors determining aortic stretch, mean aortic pressure, diameter and tension also increased significantly. Earlier studies show that regardless of the resulting heart rate response, atrial receptor activity increases during volume loading. Thus, we conclude that during cardiac acceleration, marked peripheral vasodilation eliminates the stimulation of baroreceptors and therefore the tachycardic response caused by atrial receptors develops. In the case of cardiac slowing, vasodilation also takes place, but is not sufficient to prevent activation of baroreceptors. In consequence, increased baroreceptor activity overrides the tachycardic drive coming from the atrial receptors and a typical baroreceptor reflex becomes manifested.     

Acute effects of low aortic pressure on cardiac performance

Summary Aortic pressure has dual effects on the heart: One as the afterload pressure for the left heart and the other as a determinant of coronary perfusion pressure. As aortic pressure becomes subphysiological, these two effects may come to an imbalance. In dogs in which aortic pressure, aortic flow and heart rate were controlled at constant levels, a critical level of low aortic pressure (CAP) was studied below which an acute and progressive rise of left atrial pressure was observed. In normal heart, an elevation of CAP was observed from 15 to 36 mm Hg, as aortic flow was increased from 30 to 180 ml/min/kg. The elevation was less marked in response to the increase of heart rate from 100 to 250 beats/min. Coronary ligation or administration of a large amount of propranolol (1 to 2 mg/kg) caused a significant elevation of CAP. The results obtained from the present study is suggestive of the role of low aortic pressure in the development of cardiac deterioration during shock.     

The influence of hyperventilation on the measurement of stroke volume using a CO2 rebreathing method

Summary The influence of different degrees of hyperventilation on stroke volume measured with a CO₂ rebreathing method was studied in seven normal subjects and seven patients with aortic regurgitation. Hyperventilation was initially performed with a rebreathing rate of 30 min^–1 and a tidal volume corresponding to 60% of the subject's vital capacity. The tidal volume was then randomly decreased or increased by 0.5 and 1.01 and the procedure was repeated with rebreathing rates of 25 and 35 min^–1. The possible influence of habituation to repeated measurements was tested in seven of the subjects. No significant differences in response to hyperventilation of stroke volume, cardiac output or heart rate were found between normal subjects and patients. When the tidal volume was increased, there was a significant increase in heart rate and also an increase in cardiac output, which was significant when comparing measurements performed with the lowest and highest tidal volumes. When comparing initial and final measurements, there was a significant decrease in heart rate and a tendency to decrease in cardiac output. Stroke volume was not affected by variations in rebreathing rate from 25 to 35 min^–1 or tidal volume changes of ±0.51 and was also unaffected by repeated measurements.     

Quantitative assessment of cardiac pump performance.

1. A means of quantitating left ventricular performance in the conscious dog is presented. Changes in heart rate, stroke volume and cardiac output during elevation of left atrial pressure by acute volume expansion were measured in the conscious dog. 2. The changes in heart rate and stroke volume could be described by y = ym - (ym-yi)e-kp, where yi and ym are initial and maximum values of the variable and p is the change in mean left atrial pressure. 3. Because cardiac output is a derived variable (stroke volume X heart rate) its response is described by a multiple exponential relationship. 4. For a given initial heart rate and inotropic state, the stroke volume response is determined by the Frank-Starling mechanism and the pressure-volume characteristics of the myocardium.     

Right-left ventricular output balance in the totally implantable artificial heart

Pneumatically powered artificial hearts readily accommodated the higher net stroke volumes by the right ventricle than from the left ventricle. We published that this discrepancy was approximately 8% of the left ventricular cardiac output. A variety of methods have been used to achieve balance between the right and left atrial pressures. Relatively large volume-displacement chambers (VDC) present potential problems, but do provide balance. The VDC in volumetrically coupled right-left stroke volumes was eliminated by using a small-diameter interatrial shunt (IAS). Preliminary studies demonstrated excellent balance in contracted and expanded blood volume (preload) and by hypotension and hypertension created with vasoactive drugs (afterload). At a mean aortic pressure of 120 mmHg, heart rate of 120 BPM, cardiac output of 8 L/minute and right atrial pressure of 13 mmHg, the peak IAS flow was 3.2 ml/beat in a right to left direction and 8.0 ml/beat in a left to right direction. The net left to right flow was 4.8 ml/beat. Over a wide range of preload (2 to 20 mmHg) and afterload (45 to 180 mmHg), the left atrial pressure was routinely 5 mm Hg more than the right atrial pressure. Elimination of the VDC reduces the number of components, volume, and weight of the totally implantable artificial heart. The IAS offers a simple solution to a very complex problem and provides a device that is simpler to implant and is possible to explant.     

Effects of voluntary physical exercise on cardiac function and energetics in spontaneously hypertensive rats

The influence of voluntary physical exercise in running wheels on myocardial function, cardiac oxygen utilization and cardiovascular response to emotional stress was analysed in the spontaneously hypertensive rat. After 6 weeks of exercise, a significant increase in resting cardiac output was found, which was due to an elevation of stroke volume. However, voluntary training for 12 weeks had no effect on resting blood pressure or on the blood-pressure response to mental stress. Cardiac function was also examined in vitro. At a low aortic diastolic pressure, it was markedly augmented in trained spontaneously hypertensive rats. At high aortic diastolic pressure, maximal cardiac function was similar in the two groups. Myocardial oxygen consumption (mumol min-1 g-1) for a given level of external work was reduced in trained, compared with non-exercised control spontaneously hypertensive rats. Chronic physical exercise thus greatly improved myocardial function at a subnormal perfusion pressure, suggesting better nutritional supply to the myocardium, probably created by an increased capillary surface area.     

Can a linear electrical analog model of a mechanical valve predict flow by using a pressure gradient?

The objective was to determine whether a previously developed technique for biological aortic valves could predict flow through a mechanical valve. An electrical analog model of the aortic valve that includes compliance, resistance, and inertance parameters, and corresponding second order differential equations was used to predict flow given a pressure gradient, as previously reported. Simulated pressures and flow were recorded by using a pulse duplicator system. The heart rate was varied from 60 to 180 bpm, and the stroke volume was varied from 22 to 67 cc. Resistance, inertance, and compliance parameters of the governing differential equation were estimated by using a least-squares fit to the measured flow at 120 bpm and 50 cc stroke volume. By using these parameter estimates, flow was calculated for other heart rates and stroke volumes. To achieve a better flow prediction, a nonlinear filter (third order polynomial range calibration equation) was applied to the output of the linear model (flow). The mean error, full-scale error, and spectral error in magnitude and phase between measured and predicted flow were compared. Error in mean flow ranged from 3% at medium flow rates to 90% at low flow rates. The maximum and minimum full scale errors were 12% and 5%, respectively. Error in the harmonics of measured and calculated flow ranged from 0% to 55%. Larger errors were usually present at the higher harmonics. The agreement between measured and calculated flow was better at normal and high flows but rather poor at low flows. The nonlinear filter (range calibration equation) was unable to account for the discrepancies between the measured and calculated flow over all flow ranges. It seems that this linear model and nonlinear filter have limited application, and an alternate nonlinear approach may produce better results.     

Cardiovascular patterns associated with appetitive and defensive activation during affective picture viewing

In this study we assessed blood pressure (BP), heart rate (HR), stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) in response to 13 picture series in 37 participants in order to investigate their hemodynamic response associated with activation of the appetitive and defensive motivational systems underlying emotional experience. BP and SV, but not TPR, increased with increasing self‐rated arousal, whereas HR decelerated more in response to negative than positive and neutral pictures. These findings suggest that modulation of the cardiovascular response to pictures is primarily myocardial. The observed response pattern is consistent with a configuration of cardiac sympathetic–parasympathetic coactivation. The relationships between self‐rated arousal, BP, and SV were mainly exhibited by men, suggesting that increases in the sympathetic inotropic effect to the heart with self‐rated arousal may be larger in men than in women.     

Stroke volume response to incremental submaximal exercise in aerobically trained, active, and sedentary men.

Stroke volume response of trained cyclists (n = 10; Trained), active but untrained men (n = 10; Active), and sedentary men (n = 10; Sedentary) was determined by impedance cardiography during cycle ergometer exercise. For the Trained, at a heart rate of 90 beats. min(-1), stroke volume increased by 27% compared to baseline levels, whereas stroke volume of Active and Sedentary groups did not significantly increase. Throughout exercise indices of ventricular emptying and filling of Trained were significantly greater than that of the other two groups whereas ventricular rates of the Active were significantly greater than those of the Sedentary. Throughout exercise cardiac contractility of the Trained was significantly greater than the other two groups. Results indicate that despite similar resting heart rate, stroke volume, and body mass, Trained compared to Active men significantly enhanced stroke volume, ventricular filling, and cardiac contractility during incremental ergometry exercise. Active compared to Sedentary men, however, displayed significantly larger stroke volume and ventricular filling rates during ergometry. We conclude that impedance cardiography indices of ventricular performance of aerobically trained men were superior to those of active, untrained men possessing similar resting stroke volume and heart rate. Furthermore, the ventricular performance of the active men possessing large resting stroke volume was superior to that of sedentary men.     

Hydrodynamics of a Newly China-Made Jiuling Bileaflet Heart Valve Prostheses

INTRODUCTION　　 Implantation of heart valve substitute has become the standard treatment forend-stage valvular heart disease since the1 960 s.There are two different types ofmechanical heart valve in widespread use at present,the tilting disc valve and t…     

The cold pressor test: Vascular and myocardial response patterns and their stability

The purposes of the present study were to compare the cardiovascular response patterns evoked by three versions of the cold pressor test (either forehead stimulation or hand or foot immersion) and to determine the reproducibility of the responses over a 2-week interval. Blood pressure, heart rate, stroke volume, cardiac output, total peripheral resistance, and systolic time intervals were obtained during rest and during the cold pressor test in 42 young men. Across conditions, the pressor response was supported by peripheral resistance increases with concomitant stroke volume decreases. Although the response panerns were generally similar across sites, exceptions were apparent for heart rate. Forehead stimulation was characterized by no significant change in heart rate, whereas limb (hand or foot) immersion was associated with significant heart rate acceleration. The responses elicited by the three cold pressor test conditions were reliable and showed little evidence of attenuation over the test-retest interval.     

Cardiovascular responses to salt-loading in conscious domestic geese

1. The intravenous injection of large volumes of 0.5 M-NaCl that are usually used to induce nasal gland secretion in marine birds has been shown in geese to increase greatly plasma volume, cardiac output, heart rate and stroke volume at the time secretion commences after 2-8 min.2. There were no consistent changes in mean arterial blood pressure or in the distribution of the cardiac output to major organs except to the salt-glands whose share increased approximately fourteenfold. Salt-gland blood flow remained high for 10-20 min after cardiac output and heart rate had returned to nearly normal levels.3. The increases in plasma volume and venous return are unlikely to be the stimuli for salt-gland secretion because secretion was also initiated by giving artificial sea water into the proventriculus and this produced no changes in these variables at the time secretion commenced, 5-14 min later.4. At the start of secretion in orally loaded birds, the only detectable changes in the plasma were small increases in osmolality (from 1.3 to 4.6%), Na (from 0.3 to 6%) and Cl (from 1.3 to 7.1%) concentrations.     

Der Einfluß einer konstanten Herzfrequenz auf den Carotis-Sinus-Reflex am wachen Hund

Summary In healty, conscious dogs the heart rate was kept constant at 144 to 146 beats per minute either by vagal blockade with Atropine (0,5 mg/kg i.v.) or by electrical pacing of the heart. In the resting dog a carotid-sinus-reflex was elicited clamping both common carotid arteries with implanted pneumatic cuffs. Velocity in the ascending aorta (electromagnetic flowmeter), pressure in the descending thoracic aorta (implanted miniature pressure transducer) and pressure in the right carotid sinus using a catheter were measured. By analogue processing acceleration in the ascending aorta, stroke volume and stroke work of the left ventricle, and mean values were derived. Compared to the reflex under normal resting heart rates (64 beats per minute) the results show, that with a constant heart rate (144–146 beats per minute) blood pressure rises by about the same amount induced by a larger increase of the peripheral resistance. Because the fast increase of cardiac output regularly observed under normal conditions was eliminated, the time course of pressure elevation was slower when heart rate was kept constant. The elevated stroke work of the left ventricle during carotid occlusion cannot be explained by an increase of contractility due to enhanced sympathetic activity, because no such increase in contractility was found.It is suggested, that a low control heart rate allows fast reflex adjustment of blood pressure mediated by increases of cardiac output due to vagal inhibition. In contrast, when heart rate is high due to vagal blockade or electrical pacing, the reflex response is determined by slow changes of the total peripheral resistance.

Mit dankenswerter Unterstützung der Deutschen Forschungsgemeinschaft (S.F.B. 90).     

Factors contributing to blood pressure elevation during norepinephrine and phenylephrine infusions in dogs

To examine the factors contributing to the rise in systemic blood pressure during α- and β- adrenergic stimulation, phenylephrine, an α-adrenergic agonist, and norepinephrine, an α- and β-adrenergic agonist, were infused intravenously to anesthetized dogs until mean aortic blood pressure was raised equally by 40–60 mmHg. Changes in preload were estimated by changes in left ventricular end-diastolic pressure or segment length recorded by an ultrasonic technique. By obstructing the inferior vena cava (IVC), the increase in preload could be reduced to control level during phenylephrine and norepinephrine infusions without altering peripheral resistance (mean aortic blood pressure/cardiac output). Normalization of preload reduced the pressure response by 2/3 during phenylephrine infusion and by 1/4 during norepinephrine infusion. However, after β-adrenergic blockade by propranolol, normalization of preload reduced the pressure response by 2/3 during both phenylephrine and norepinephrine infusions. Thus, during α-adrenergic stimulation, the increase in preload is a more important factor than the increase in peripheral resistance. Norepinephrine raised stroke volume by 24±5%. When the increase in stroke volume was prevented by IVC obstruction, the pressure response to norepinephrine was halved. Thus, during norepinephrine infusion the rise in stroke volume caused by β-adrenergic stimulation is as important as α-adrenergic stimulation for the pressure response.     

Hemodynamics of the carotid sinus reflex elicited by bilateral carotid occlusion in the conscious dog

Summary Flow velocity in the ascending aorta and aortic blood pressure were recorded continuously in healthy conscious dogs. Using implanted pneumatic cuffs the effect of bilateral carotid occlusion on heart rate, stroke volume, cardiac output, peak velocity, maximum acceleration, blood pressure, and total peripheral resistance (T.P.R.) was studied in the resting animal.Following carotid occlusion heart rate rose within 3–4 sec by 13 beats/min; during the steady state it exceeded the control by 8 beats/min.Cardiac output closely followed heart rate, since stroke volume decreased slightly (3–4%), mainly because of the elevated aortic pressure. During the first 3–4 sec cardiac output increased by 10–15% reaching a steady state level 8% above control.The initial fast increase of cardiac output caused mean aortic pressure to rise rapidly, while T.P.R. transiently decreased. Subsequently T.P.R. rose, causing a secondary slow increase of pressure. During the steady state blood pressure was elevated by 27 mm Hg (26%), T.P.R. by 12.1 mm Hg×l^–1×min (20%).Maximum acceleration did not change with heart rate and was hardly affected (–1.5%) by the pressure rise. Peak velocity was little influenced by heart rate; it decreased by 7% mainly because of the elevated aortic pressure.-blockade (0.5 mg/kg propranolol) affected T.P.R. only during control (+18%), but did not modify the time course of the reflex and its steady state changes.-blockade (5.0 mg/kg phenoxybenzamine) decreased aortic mean pressure (5 mm Hg) and T.P.R. (7%) during control. Following carotid occlusion T.P.R. rose by the same amount, but much more slowly. Starting from the lower control the same pressure level was now obtained by a higher reflex increase of heart rate and cardiac output.It is concluded that the initial pressor response is initiated by an increase of cardiac output mediated by vagal inhibition. The secondary rise of blood pressure is predominantly caused by an increase of T.P.R. due to autoregulation in some vascular beds. The higher stroke work during the reflex is not accomplished by an increased contractility due to sympathetic activation.This study was supported by the Deutsche Forschungsgemeinschaft.A preliminary report of a portion of this work was presented before the Deutsche Physiologische Gesellschaft, Mainz, March 1969.     

Cardiovascular effects of anti-G suit inflation at 1 and 2 G

We sought to determine to which pressure a full-coverage anti-G suit needs to be inflated in order to obtain the same stroke volume during a brief exposure to twice the normal gravity (2 G) as that at 1 G without anti-G suit inflation. Nine sitting subjects were studied at normal (1 G) and during 20 s of exposure to 2 G. They wore anti-G suits, which were inflated at both G-levels to the following target pressures: 0, 70, 140 and 210 mmHg. Stroke volume was computed from cardiac output, which was measured by rebreathing. Heart rate and mean arterial pressure at heart level were recorded. Inflation to 70 mmHg compensated for the decrease in stroke volume and cardiac output caused by hypergravity. Mean arterial pressure at heart level was comparable at 1 G and at 2 G and increased gradually and similarly with inflation (P<0.001) at both gravity levels. Thus, anti-G suits act by increasing both preload and afterload but the two effects counteract each other in terms of cardiac output, so that cardiac output at 2 G is maintained at its 1 G level. This effect is reached already at 70 mmHg of inflation. Greater inflation pressure further increases mean arterial pressure at heart level and compensates for the increased difference in hydrostatic pressure between heart and head in moderate hypergravity.     

Contributions of blood drainage from the liver,spleen and intestines to cardiac effects of aortic occlusion in the dog

By occluding the descending thoracic aorta, blood transferred from the lower to the upper part of the body increases left ventricular end-diastolic volume and maintains stroke volume despite a rise in systolic left ventricular pressure (LVP) of about 60 mmHg. Seventy percent of the blood drained stems from the splanchnic circulation. To examine which splanchnic organs contribute to the cardiac effects, selective occlusions were performed during ultrasonic measurements of spleen and liver dimensions and left ventricular myocardial chord length (MCL) in atropinized, open-chest dogs. Drainage of 15±2 ml from the spleen accounted for 18±4% of the increase in end-diastolic MCL, whereas liver dimensions remained unaltered. Similar results were obtained during aortic occlusion at high inotropy (isoproterenol infusion). it was ascertained by occlusion of the coeliac and mesenteric arteries that about 50% of the cardiac response to aortic occlusion was due to drainage from the intestines and the aorta. Liver blood volume could be reduced by combined occlusion of the aorta and portal vein or coeliac and mesentenc arteries and was sensitive to changes in pressure in the inferior vena cava, but did not contribute to the cardiac response to aortic occlusion.     

A system for providing an on-line analogue display of beat-by-beat cardiac output

A system for an on-line analogue display of beat-by-beat cardiac output and other cardiovascular functions is described. The phasic aortic blood flow signal, derived from an electromagnetic flowmeter with the flow probe implanted around the ascending aorta, drives a multi-channel recorder with a combination of associated signal conditioning input couplers and peripheral electronic circuitry, to provide a continuous analogue display of beat-by-beat phasic stroke volume, integrated stroke volume, heart rate, and cardiac output. These cardiovascular functions, which permit instantaneous on-line feedback of these parameters, were all derived from the single aortic flow measurement.     

Cardiovascular and blood gas responses to shivering produced by external and central cooling in the pigeon

Cardiovascular and blood gas responses of pigeons to spinal cord cooling (35-36 degrees C) were measured at thermoneutral (28 degrees C) and low (5 degrees C) ambient temperatures. Spinal cord cooling at thermoneutral temperatures caused immediate shivering and increases in heat production (223%), heart rate (152%) and cardiac output (169%), but blood pressure and stroke volume did not change. PaCO2 and PvCO2 increased slightly during the cooling; PaO2 and CaO2 decreased slightly while PvO2 and CvO2 decreased considerably (10 Torr and 1.7 mmol . l-1, respectively), resulting in a greater a-v difference in O2 content. Ambient cooling produced responses comparable to spinal cord cooling. Simultaneous spinal cord and ambient cooling produced similar responses that were generally greater in magnitude than either kind of cooling alone. Consequently, heart rate, cardiac output and O2 extraction from the blood were all significantly, linearly related to heat production over the wide range studied. Comparisons are made between cardiovascular responses of birds to shivering and exercise in regards to the relative importance of increases in heart rate, stroke volume and blood pressure. It is suggested that exercise and shivering may effect cardiovascular responses through similar receptor mechanisms.     

Hemodynamic determinants of chronic hypotension and their modification through vasopressor application

Chronic low blood pressure is typically accompanied by symptoms such as fatigue, reduced drive, dizziness, headaches and cold limbs. Reduced cognitive performance, diminished cerebral blood flow and autonomic dysregulation have been furthermore documented in this condition. The present contribution reports two studies exploring systemic hemodynamics in chronic hypotension and their modification through vasopressor application. In study I, effects of the alpha-sympathomimetic midodrine were examined in 54 hypotensive individuals using a placebo-controlled double-blind design. Hemodynamic parameters were assessed at rest and during mental stress. They were derived from continuous blood pressure recordings using Modelflow analysis. The drug led to marked increases in blood pressure, total peripheral resistance and stroke volume. However, due to strong heart rate deceleration, cardiac output remained virtually unchanged. In study II, 40 hypotensive and 40 normotensive control persons were compared with respect to hemodynamics. While groups did not differ in total peripheral resistance, hypotensives exhibited markedly diminished stroke volume and heart rate, resulting in a reduction in cardiac output of 25% at rest and of 33% during mental stress. The data provide relevant knowledge about the hemodynamic mediation of chronic hypotension. In contrast to elevated blood pressure, which is mainly determined by increased peripheral resistance, reduced cardiac output may be the cardinal hemodynamic aberration in chronic hypotension. Midodrine proved to be effective in elevating blood pressure. However, given the cardiac origin of chronic hypotension and the lack of drug effect on cardiac output, alpha-sympathomimetic treatment may be suboptimal.