Change In End-diastolic Volume Research Articles

Left ventricular hypertrophy and impaired diastolic filling in essential hypertension. Diastolic mechanisms for systolic dysfunction during exercise.

Left ventricular ejection fraction is normal at rest but may respond abnormally to exercise in many patients with essential hypertension. To assess the determinants of the abnormal ejection fraction response to exercise, we performed radionuclide angiography at rest and during exercise in 41 hypertensive patients without coronary artery disease. In 22 patients (group 1), the ejection fraction increased more than 5% during exercise; in the other 19 patients (group 2), the ejection fraction either increased by less than 5% or decreased with exercise. Left ventricular diastolic filling was impaired at rest in patients in group 2 compared with group 1, with reduced peak filling rate (2.5 +/- 0.4 vs. 3.1 +/- 0.7 end-diastolic volume/sec; p less than 0.01) and prolonged time to peak filling rate (175 +/- 28 vs. 153 +/- 22 msec; p less than 0.01). Impaired diastolic filling in group 2 was associated with less augmentation in end-diastolic volume during exercise compared with group 1 (p less than 0.01). These observations were not dependent on the threshold value that was arbitrarily chosen to define an abnormal ejection fraction response, as there were significant correlations for the entire group between the magnitude of change in ejection fraction with exercise and both the resting peak filling rate (r = 0.46) and the change in end-diastolic volume with exercise (r = 0.62).(ABSTRACT TRUNCATED AT 250 WORDS)

Interaction between left ventricular end-diastolic and end-systolic volumes in normal humans

The extent to which the end-systolic volume (ESV) "follows" the end-diastolic volume (EDV) when the latter changes in response to various perturbations is a major determinant of the cardiac ejection fraction (EF) and has not been studied in humans. We measured EDV, ESV, and EF, determined by gated blood pool scans, during a change in posture from the supine to the upright seated position and during graded upright bicycle exercise. The experimental group consisted of 119 healthy individuals (79 males and 40 females) ranging in age from 21 to 81 yr and in physical-conditioning status (75-225 W maximum work load); rigorous screening excluded cardiac disease. Multiple regression analysis showed that the change in ESV (delta ESV) during a postural shift or during graded exercise was highly statistically correlated with the change in EDV (delta EDV) that occurred (r2 ranged from 0.34 to 0.49, correlation is positive) regardless of age, sex, or exercise work load. The correlation of delta ESV with delta EDV observed in this large sample, heterogeneous with respect to age, sex, and physical fitness, was also present in additional 31 subjects who exercised during beta-adrenergic blockade (propranolol 0.15 mg/kg). The delta EF with posture change and exercise in all subjects under all conditions was highly and inversely correlated with the delta ESV (r2 ranged from 0.38 to 0.81). Thus the delta ESV during the circulatory adaptive response to orthostatic and exercise stresses in humans is related to the delta EDV, and this relationship modulates the delta EF in response to these stresses.

Short‐Term and Long‐Term Changes of Left Ventricular Volumes During Rate‐Adaptive and Single‐Rate Pacing

To evaluate the adaptation of the heart to exercise during pacing, 15 patients with permanent endocardial pacemakers were studied; nine patients had atrioventricular universal (DDD) pacemakers (Symbios 7005) and six patients had activity detecting rate-responsive ventricular (VVIR) pacemakers (Activitrax 8403). Left ventricular function in each patient during rate variable pacing was compared to ventricular function during VVI single-rate pacing. End-systolic and end-diastolic volume changes during exercise were measured by radionuclide angiography and the amount of volume change was used to assess left ventricular function. Both short-term (within 4 hours) and long-term measurements (after at least 4 weeks) were made at rest and at 50% of the maximal exercise capacity in DDD or VVIR mode and were compared with VVI single-rate pacing. All patients, when changed from DDD or VVIR mode to VVI single-rate pacing showed a significant increase of the end-diastolic volume during exercise, which increased even more after long-term VVI pacing. During long-term rate variable pacing, there was no increase of the end-diastolic volume during exercise. DDD or VVIR pacing initially showed a substantial increase of the end-systolic volume during exercise combined with a decrease of left ventricular ejection fraction, suggesting a decrease of the left ventricular contractility. After 4 weeks, contractility improved both with DDD and VVIR pacing. We conclude that short-term DDD and VVIR pacing induces a temporary impairment of left ventricular function that improves after 4 weeks, whereas long-term VVI pacing is associated with left ventricular dilatation even at moderate levels of exercise.

Long-term function of human cardiac allografts assessed by two-dimensional echocardiography

Previous studies from our laboratory demonstrated increasing left ventricular mass in cyclosporine-treated cardiac allograft recipients over 30 days after transplantation, but the long-term evolution of this process and possible effects on allograft function are unknown. Accordingly, quantitative two-dimensional echocardiography was performed 2 and 23 days and 15 months postoperatively in 14 recipients treated with cyclosporine and prednisone. Changes in left ventricular ejection fraction, end-diastolic volume, mass, and end-systolic wall stress were analyzed. Comparison of studies at 2 and 23 days revealed significant (p less than 0.01) increases in ejection fraction (54% +/- 8% [standard deviation] to 62% +/- 4%), end-diastolic volume (84% +/- 32 ml to 96 +/- 31 ml), and left ventricular mass (118 +/- 45 gm to 136 +/- 41 gm). Comparison of studies at 23 days and 15 months revealed no significant change in end-diastolic volume or left ventricular mass, whereas ejection fraction decreased slightly (62% +/- 4% to 57% +/- 4%, p less than 0.01). End-systolic wall stress decreased when data at 2 days and 15 months were compared (83 +/- 24 gm/cm2 versus 66 +/- 18 gm/cm2, p less than 0.05), but no change in contractility was apparent from the ejection fraction/end-systolic stress relation. We conclude that left ventricular mass and end-diastolic volume increase early after transplantation in cyclosporine-treated cardiac allograft recipients, but these changes are not predictive of long-term results, which are characterized by no significant late variation in left ventricular mass, end-diastolic volume, or contractility.

Model studies of the contribution of ventricular interdependence to the transient changes in ventricular function with respiratory efforts.

The effects of variations in intrathoracic pressure on left ventricular function were studied using a mathematical model of the circulation. The variations in intrathoracic pressure directly affect the left ventricular afterload, and indirectly alter left ventricular filling by changing the right ventricular volume. The decrease in intrathoracic pressure with sustained inspiratory efforts increased the left ventricular afterload and thus reduced the left ventricular stroke volume. Secondary to the reduction in stroke volume, the left ventricular end systolic and end diastolic volumes increased. Decreasing intrathoracic pressure also increased the systemic venous return, thereby increasing right ventricular volume. The model predicted that an enlarged right ventricular volume would, through diastolic ventricular interdependence, immediately reduce the left ventricular end diastolic volume (which in turn reduced the left ventricular stroke volume), while through systolic ventricular interdependence it would increase left ventricular stroke volume and reduce left ventricular end systolic volume. An increased right ventricular volume would also increase right ventricular stroke volume and after a delay of a few heart beats raise left ventricular end diastolic and stroke volumes. The net effect of respiratory variations in intrathoracic pressure on left ventricular function would be a combination of these effects. Thus on sustained inspiration the left ventricular stroke volume initially decreased (left ventricular afterload and diastolic interdependence secondary to the increase in right ventricular volume partly counteracted by the effects of systolic interdependence), followed by an increase as the increased venous return reached the left ventricle. The model indicated that the response to a forced expiratory effort was not simply the opposite of the inspiratory response, since the increase in intrathoracic pressure during a forced expiration is accompanied by increases in abdominal pressure. On sustained expiration the left ventricular stroke volume initially increased, with no significant initial change in end diastolic volume. The cardiovascular response to respiration is complex, and model studies can help to isolate and identify the various components involved.

Left ventricular myocardial structure in aortic valve disease before, intermediate, and late after aortic valve replacement.

Left ventricular biplane cineangiography, micromanometry, and endomyocardial biopsies were performed in 27 patients with aortic stenosis (AS) and in 17 patients with aortic insufficiency (AI). Twenty-three patients with AS and 15 with AI were restudied at an intermediate time (18 months after successful valve replacement), and nine patients with AS and six with AI were restudied late (70 and 62 months after surgery). Biopsy samples were evaluated for muscle fiber diameter, percent interstitial fibrosis, and volume fraction of myofibrils. In control biopsy samples obtained from five donor hearts at transplantation, these morphometric variables averaged 21.2 microns, 7.0%, and 57.2%, respectively. After surgery, mass determined by cineangiography decreased from 186 to 115 and 94 g/m2 in patients with AS and from 201 to 131 and 93 g/m2 in patients with AI. At the three studies, muscle fiber diameter was 30.9, 28.0, and 28.7 microns in patients with AS and was 31.4, 27.6, and 26.4 microns in patients with AI. Percent interstitial fibrosis was 18.2, 25.8, and 13.7% in patients with AS and was 20.4, 23.7, and 19.2% in patients with AI. Left ventricular fibrous content decreased from 34.2 to 29.8 and to 12.7 g/m2 in patients with AS and from 42.1 to 28.9 and to 18.9 g/m2 in patients with AI. Volume fraction of myofibrils was 57.7, 56.8, and 49.0% in patients with AS and was 56.8, 56.6 and 48.8% in patients with AI. Thus, the decrease of muscle mass determined by cineangiography at the intermediate time after valve replacement is mediated by regression of myocardial cellular hypertrophy in patients with AS and AI and in addition by a decrease of fibrous content in patients with AI. Late after surgery, left ventricular fibrous content also decreases in patients with AS. This late decrease associated with minor changes of end-diastolic volume may be important for improvement of increased diastolic myocardial stiffness. Even 6-7 years after valve replacement, incomplete regression of structural abnormalities of left ventricular hypertrophy still exists compared with the normal myocardium. The residually increased relative interstitial fibrosis and the small late postoperative decrease of volume fraction of myofibrils, associated with a prosthesis-related slight left ventricular pressure increase, are at the origin of a persistent systolic overload at the myofibrillar level.

Left ventricular filling and early diastolic function at rest and during angina in patients with coronary artery disease.

Left ventricular diastolic function was studied in 11 patients with coronary artery disease. Single plane ventriculography (30 degrees right anterior oblique projection) was performed at rest and during an episode of angina immediately after a period of rapid atrial pacing. Left ventricular pressure was recorded simultaneously by a micromanometer tipped catheter. The ventriculograms were digitised frame by frame to derive continuous plots of left ventricular shape, volume, and rate of change of volume. The time constant (tau) of the fall in left ventricular pressure was determined from the exponential portion of pressure decay during isovolumic relaxation. Ventricular pressure-volume loops were constructed to study the left ventricular diastolic pressure-volume relation. The time of minimum left ventricular pressure was used to divide diastole into an early phase and a late phase. Angina was associated with an increase in end systolic volume and a fall in ejection fraction with no significant change in end diastolic volume. Peak left ventricular pressure was unchanged but left ventricular minimum and end diastolic pressures were both increased and the diastolic pressure-volume relation was moved upwards. The time constant of left ventricular pressure fall was prolonged. At rest more than 50% of the stroke volume entered the left ventricle during the period of early diastole. This proportion was significantly reduced during angina and as a consequence a significantly greater proportion of the stroke volume entered the ventricle during late diastole. Despite this, and although the left ventricular diastolic pressure-volume relation was moved upwards with angina, the mean slope of the relation during late diastole--that is, chamber stiffness--was not significantly altered. The upward shift of the left ventricular diastolic pressure-volume relation seen during angina is thus already apparent in early diastole, and its extent does not change during the later phase of diastole, which alone shows the property of passive stiffness. A primary increase in the passive stiffness of the ventricle cannot therefore be the cause of the upward shift of the diastolic pressure-volume relation, and events occurring in early diastole have to be looked to for an explanation. The study findings show that left ventricular function in early diastole is profoundly disturbed during angina pectoris and it is suggested that loss of elastic recoil and dissipation of this restoring force by asynchronous onset of relaxation and abnormal changes in shape are important factors contributing to this disturbance of function.

The insufficient nitrate response: patients' characterization and response to beta and calcium blockade.

Little information has been published regarding the nitrate-induced changes of left ventricular volumes at rest and during exercise in relation to the degree of the anti-ischaemic response. Therefore we assessed the electrocardiographically defined nitrate response to a single tablet of 80 mg isosorbide dinitrate s.r. and compared it to the changes in end-diastolic volumes at rest and during exercise, as determined by radionuclide ventriculography. Thirty-four of the 63 patients were classified as good nitrate responders, whereas 29 patients showed insufficient nitrate response with regard to the reduction of exercise-induced ST-segment depression. The baseline characteristics were quite comparable. At rest the ISDN-induced decrease of the end-diastolic count rate was significantly less (-17%) in patients with insufficient ST-segment response when compared to patients with good ST-segment response (-25%). During exercise, in patients with good ST-segment response, ISDN reduced the end-diastolic volume significantly (-19%), whereas in patients with insufficient ST-segment response the end-diastolic volume remained unchanged. In this special subset of patients with insufficient nitrate response we further evaluated the effects of additional beta or/and calcium blockade. The benefits from verapamil were equivalent to propranolol. However, a considerable part of the patients investigated needed the combination of verapamil and propranolol for an optimal anti-ischaemic drug treatment. Thus, our data support the concept that preload reduction plays a major role for the anti-ischaemic effects of ISDN in patients with exercise-dependent ischaemia. Since, a suboptimal therapeutic effect must be considered, objective control of the nitrate therapy (usually by exercise- and Holter-ECG) must be regarded as obligatory for each individual patient if optimal results are to be expected.

Impaired left ventricular function during exercise in coronary artery disease and exertional hypotension.

To characterize the hemodynamic abnormalities responsible for exertional hypotension coronary artery disease, we studied 11 patients with exertional hypotension during supine cycle ergometer exercise, defined as greater than 10 mm Hg decrease in systolic blood pressure during exercise, and 11 patients without exertional hypotension (controls). Patients were similar with respect to age, left ventricular ejection fraction at rest, and the intensity of exercise relative to maximal treadmill exercise capacity. Peak exercise ejection fraction, determined by radionuclide ventriculography, was significantly lower in patients with, than in those without exertional hypotension (50 +/- 3 vs. 56 +/- 3%; p less than 0.025). Ejection fraction and stroke volume decreased with exercise in patients with exertional hypotension but not in the controls even though changes in end-diastolic volume and mean blood pressure were similar in both groups. Peak exercise systolic blood pressure and rate pressure product were significantly lower in the patients with exertional hypotension than those without. The exercise-induced regional left ventricular contraction abnormalities were more prominent, extensive and frequent in patients with exertional hypotension than controls. Impairment of left ventricular contractile function was further evident by an abnormal end-systolic volume-systolic blood pressure relation in patients with exertional hypotension. These patients attained a much smaller increase in systolic blood pressure compared with controls despite no statistically significant differences in end-systolic volume response to exercise. These findings suggest that exertional hypotension in patients with ischemic heart disease is associated with exercise-induced left ventricular systolic dysfunction secondary to extensive myocardial ischemia.

Factors influencing the variations of ejection fraction during exercise in chronic aortic regurgitation.

The influence of left ventricular volume variations and regurgitant fraction variations upon left ventricular ejection fraction during exercise was examined using equilibrium radionuclide angiography in patients suffering from aortic regurgitation. Ejection fraction (EF), regurgitant fraction (RF), end diastolic volume (EDV) and end systolic volume (ESV) variations from rest to peak exercise were determined in 44 patients suffering from chronic aortic regurgitation (AR) and in 8 healthy volunteers (C). In C, EF increased (+0.10 +/- 0.03, P less than 0.01) and ESV decreased significantly (-23% +/- 12%, P less than 0.01), RF and EDV did not vary significantly. In AR patients, EF, EDV and ESV did not vary significantly because of important scattering of individual values. Changes in EF and ESV were inversely correlated (r = -0.79, P less than 0.01) and RF decreased significantly (-0.12 +/- 0.10, P less than 0.01). Volumes and EF changes during exercise occurred in three different ways. In a 1st subgroup of 7 patients, EF increased (+0.09 +/- 0.03, P less than 0.05) in conjunction with a reduction of ESV (-24% +/- 12%, P less than 0.05) without a significant change in EDV. In a 2nd group of 22 patients, EF decreased (-0.04 +/- 0.07, P less than 0.01) in association with an increase in ESV (+17% +/- 16%, P less than 0.01) and no change in EDV. In a 2nd group of 22 patients, EF decreased (-0.04 +/- 0.07, P less than 0.01) in association with an increase in ESV (+17% +/- 16%, P less than 0.01) and no change in EDV. In a 3rd subgroup of 15 patients, EF decreased (-0.02 +/- 0.06, P less than 0.01) despite a reduction in ESV (-7% +/- 6%, P less than 0.01) because of a dramatic EDV decrease (-10% +/- 6%, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

In utero right ventricular output in the fetal lamb: the effect of heart rate.

1. The effect of heart rate on right ventricular output was examined in six lambs during a period extending from 126 to 139 days of gestation. The fetuses had been surgically instrumented at least four days previously with a main pulmonary artery flow probe, right ventricular dimension transducers and left and right atrial pacing electrodes. 2. During spontaneous variations in heart rate, rate was correlated positively with right ventricular output (P less than 0.0001) and end-diastolic dimension (P less than 0.0001) among the lambs considered as a group, but no significant effect of rate on stroke volume was found. When individual responses were examined, output increased significantly with rate in sixteen out of seventeen observations. 3. With left atrial pacing, heart rate did not affect output. With right atrial pacing, rate correlated negatively with output (P less than 0.0001). With pacing from either site, rate correlated negatively with end-diastolic dimension (P less than 0.0001) and stroke volume (P less than 0.0001). 4. The introduction of a longer period interval during each pacing rate inhibited the rate-related decrease in dimension and allowed the ventricle to fill to the same end-diastolic dimension. The systole following these longer intervals had a greater stroke volume than did the preceding systoles with smaller end-diastolic dimension. The faster the preceding paced rate, the greater was the increase in stroke volume (P less than 0.001). 5. Right ventricular dimensions and volumes were measured in vitro, and the relationship was found to be linear using regression analysis. 6. This study demonstrates that experimentally induced variations in heart rate produce changes in end-diastolic volume and contractility which prominently affect right ventricular stroke volume. As a consequence, rate has, over a broad range, either no significant effect on output or a negative one. With spontaneous variations in rate, additional changes in contractility and venous return occur which affect stroke volume and end-diastolic volume and enhance right ventricular output. These relationships are similar to those in the adult heart, and demonstrate the absence of a maturational change in the effects of rate on ventricular function from the fetus to the adult.

Cardiovascular Effects of Positive Pressure Ventilation in Humans

Pulsus paradoxus is the pathological exaggeration of the normal transient decrease in arterial blood pressure that occurs during spontaneous inspiration. The transient increase in arterial pressure associated with positive pressure inspiration is termed reversed pulsus paradoxus (RPP). Cardiorespiratory interactions and the mechanism of these effects have been studied extensively in animals, and to a lesser extent, in humans. In this clinical investigation pulsus paradoxus and RPP were studied in 10 postoperative cardiac patients with invasive monitoring and mediastinal pressure catheters placed intraoperatively. From end-expiration to end-inspiration, RPP was accompanied by decreased transmural pressures in the right atrium, left atrium, and aorta. Left ventricular end-systolic volume measured by radionuclide studies diminished during a positive pressure inspiration, without a significant change in end-diastolic volume. These results are consistent with decreased left ventricular afterload as the major mechanism of RPP. During spontaneous breathing, inspiration was associated with converse effects, a fall in arterial pressure and an increase in transmural right atrial, left atrial, and aortic pressures from end-expiration to end-inspiration. End-systolic volume was significantly larger at end-expiration than end-inspiration, with no change in end-diastolic volume. These findings suggest that an increase in left ventricular afterload during inspiration is responsible for the observed pulsus paradoxus.

The effect of heart rate on in utero left ventricular output in the fetal sheep.

The effect of heart rate on left ventricular output was examined in seven fetal lambs at ages of 128 to 140 gestational days. The fetuses had been surgically instrumented at least 4 days previously with an ascending aortic flow probe, left ventricular dimension transducers, and left and right atrial pacing electrodes. Natural variations in heart rate of the lambs taken as a group correlated positively with left ventricular output, and negatively with ventricular end-diastolic dimension and stroke volume (P less than 0.0001). Rate did not affect output with right atrial pacing. With left atrial pacing, it correlated negatively with output (P less than 0.0001). At both pacing sites, rate correlated negatively with end-diastolic dimension and stroke volume (P less than 0.0001). The introduction of a longer interval during each pacing rate circumvented the rate-related changes in dimension and allowed the ventricle to fill to the same end-diastolic dimension. The systole at the end of the longer interval had a greater stroke volume than the preceding systoles. The faster the preceding paced rate, the greater was the stroke volume (P less than 0.0001). This study demonstrates that experimentally induced variations in heart rate produce changes in end-diastolic volume and contractility which prominently affect stroke volume. Over a broad range of rates, however, the effect of rate on left ventricular output is either negative or absent. With naturally occurring rate changes, there are additional changes in contractility and venous return which affect stroke volume. These combine to produce a positive relation between heart rate and left ventricular output. These effects of heart rate on output are qualitatively similar to those described for the adult animal.

Left ventricular performance of the athletic heart during upright exercise

This study compares the left ventricular performance of chronically conditioned pentathletes (N = 10) with less-conditioned subjects (N = 10) during dynamic upright exercise. The pentathletes were found to have a superior treadmill performance [24 +/- 4 vs 17 +/- 2 min (SD), P less than 0.01], reduced resting heart rate (41 +/- 13 vs 62 +/- 6 bpm, P less than 0.01), and increased left ventricular mass (254 +/- 85 vs 179 +/- 35 g, P less than 0.05) compared to the control group. Radionuclide ventriculography and heart rate controlled-bicycle ergometry were employed to examine changes in left ventricular ejection fraction, end-diastolic volume, end-systolic volume, and stroke volume. Heart rate was controlled by adjusting the resistance of the ergometer until stable heart rates of 90, 110, 130, and 150 bpm were achieved. Following heart rate stabilization, 99mTc images were acquired during 3-min stages at each target heart rate level. In the pentathletes, left ventricular ejection fraction, end-diastolic volume, and stroke volume increased (P less than 0.01) during exercise, and end-systolic volume tended to decrease. No difference was noted in left ventricular ejection fraction between groups when heart rates were matched. However, the exercise-induced changes in end-diastolic volume and stroke volume were greater (P less than 0.01) in the pentathletes. In conclusion, the athletes studied relied on the same mechanism as the less-conditioned subjects for improving pump performance during exercise stress, but the athletes' ability to mobilize a greater end-diastolic volume accounts for their larger stroke output during each stage of heart rate-matched exercise.

Postural changes in cardiac volumes in men in relation to adult age

Cardiac volumes by equilibrium gated cardiac blood pool scans and heart rate were measured in the supine and sitting positions in 64 male volunteer subjects (age 25–80 yrs) who had been rigorously screened to exclude cardiovascular disease. After the upright position was assumed, the average cardiac output of all subjects was unchanged but heart rate increased and stroke volume decreased due to a decrease in end diastolic volume. Neither the supine or sitting cardiac output nor the average postural change in cardiac output, cardiac volumes or heart rate was age-related. While the average cardiac output among the subjects was unaltered with a change in posture, in some individuals it increased slightly while in others it decreased. The postural change in cardiac output among the individuals correlated by linear regression analysis (1) with a change in heart rate only in younger subjects and (2) with a change in stroke volume in all age groups, but the slope of this relationship was greater in older than in younger subjects. The postural change in stroke volume was strongly correlated with a change in end diastolic volume and this relationship did not vary with age. Thus, although the average postural change in cardiac output among healthy subjects is not age-related, a given change in cardiac output with posture in an older individual depends more on a change in stroke volume and less on a heart rate change than in a younger one. This result, like the response to vigorous upright exercise previously demonstrated to occur with aging, indicates a greater reliance in the elderly on the Frank-Starling mechanism than on heart rate for a given change in cardiac output in response to perturbations from the basal supine state.

Hemodynamic effects of anti-G suit inflation in a 1-G environment.

This study evaluated effects of various anti-G inflation pressures on cardiac volumes and the relationship of these volume changes to mean arterial pressure changes. Ventricular volumes were calculated using two-dimensional echocardiography. An anti-G suit was inflated to 2, 4, and 6 psi in the standing and supine positions for 10 male subjects. In the supine position, mean arterial pressure increased from base line for all three inflation pressures (P = 0.05). The end-diastolic volume increased after 2-psi inflation (P = 0.03). Cardiac output or stroke volume did not change. After standing, mean arterial pressure (P = 0.002), end-diastolic volume (P = 0.002), and stroke volume (P = 0.05) fell after suit deflation. Peripheral vascular resistance fell in the 2- and 4-psi inflation profiles. In the standing protocol, mean arterial pressure, end-diastolic volume, stroke volume, and cardiac output rose with all three inflation pressures (P less than 0.05). After reclining, heart rate increased (P = 0.02) and mean arterial pressure fell (P less than 0.05) in the 4- and 6-psi inflation profiles after suit deflation. Increases in mean arterial pressure are caused by increases in cardiac preload and cardiac output after inflation of the anti-G suit while subjects were standing. Increased cardiac preload was not consistently seen after inflation while subjects were supine. Changes in end-diastolic volume and mean arterial pressure were dependent on the pressure used to inflate the anti-G suit.

The effect of cardiac autonomic blockade on ventricular response to changes in preload

Echocardiographic (E) assessment of left ventricular response to increases (1) and decreases (D) in preload of 9 volunteer male subjects (mean age 25 ± 2.0 years) was made during both control (C) and cardiac blocked (B) conditions. Cardiac autonomic blockade was produced by intravenous administration of atropine (0.04 mg/kg) and propranolol (0.2 mg/kg), while I was produced by 5° head-down tilt (T) for 90 min and D by lower body negative pressure to −40 Torr. Increases in resting heart rate of 44% and diastolic blood pressure of 13% occurred after B, ( P < 0.05). During C, the alterations in preload produced mean changes in end-diastolic volume (EDV) ranging from 135 ± 10 cm 3 for I to 96 ± 9.1 cm 3 for D. Changes in stroke volume during condition C were significantly related to changes in EDV during preload alterations and conformed to a normal LV function curve and were described by SV - 0.6 EDV + 4.5 cm 3 ( r = 0.85; P < 0.001). Similarly during B, SV = 0.43 EDV + 5.8 cm 3 ( r = 0.75; P < 0.001). Comparison of the LV function curves produced during C and B showed that both slope of regression and r were significantly different ( P < 0.01). These data indicate that cardiac autonomic blockade produces a downward shift in the LV function curve indicating a depression in myocardial contractility. In addition, the data indicate that changes observed in LV function during wide variations in preload are independent of autonomic nervous system influences and are independent of the intrinsic heart rate.

Effect of end-diastolic volume on the canine left ventricular ejection fraction

Left ventricular ejection fraction is commonly used in the clinical assessment of ventricular function. However, the effect of changes in end-diastolic volume on ejection fraction is controversial. The present study examines the effect of changes in end-diastolic volume on ejection fraction in 26 anesthetized dogs on right heart bypass with controlled hemodynamics. At the end of each experiment, pressure-volume relationships were obtained in the potassium arrested heart following suturing of the mitral valve leaflets and clamping of the aortic root. This technique allowed determination of the end-diastolic volume from the end-diastolic pressure. Ejection fraction is highly dependent on end-diastolic volume and end-diastolic pressure at lower levels of end-diastolic volume and end-diastolic pressure. Ejection fraction increased from 30 ± 1% (SEM) to 64 ± 2% ( p < 0.001) when end-diastolic pressure was increased from 4 ± 0.5 to 11 ± 0.5 cm H 2O. The corresponding end-diastolic volumes were 22 ± 0.5 and 38 ± 1 ml, respectively ( p < 0.01). Ejection fraction only increased from 64 ± 2% to 71 ± 1% ( p < 0.01) when end-diastolic pressure was increased from 11 ± 0.5 to 18 ± 1 cm H 2O. The corresponding end-diastolic volumes were 38 ± 1 and 50 ± 1 ml ( p < 0.01), respectively. This dependence of ejection fraction on preload is present over a wide range of levels of aortic pressure. Similar directional changes in ejection fraction with preload were present after an adequate autonomic blockade, in the presence of either increased or decreased inotropic state and in the presence of an open or closed pericardium. Thus, the present study demonstrates that ejection fraction can be substantially altered by acute changes in end-diastolic volume. This factor should be taken into account when using ejection fraction for the clinical assessment of ventricular function.

Left Ventricular Function Before and After Reaching the Anaerobic Threshold

Simultaneous pulmonary gas exchange analysis and exercise radionuclide angiography were performed in 24 normal patients (14 supine and ten upright). Left ventricular (LV) volumes and ejection fraction (EF) were measured at rest, anaerobic threshold (point of nonlinear increase in ventilation relative to oxygen uptake), and peak exercise. The anaerobic threshold occurred at a similar heart rate for supine vs upright exercise, 78 percent and 77 percent of peak heart rate, respectively. The anaerobic threshold occurred at a similar workload for supine vs upright exercise, 60 percent and 56 percent of peak workload, respectively. The anaerobic threshold also occurred at a similar oxygen uptake for supine vs upright exercise, 69 percent vs 69 percent of peak oxygen uptake, respectively. For both exercise modes, mean LVEF increased (p less than 0.01) by a similar amount (.06 vs .07) from rest to anaerobic threshold, but there was no further increase from anaerobic threshold to peak exercise. The mechanism of the increase was a reduction in end-systolic volume with little or no change in end-diastolic volume. This increase was not seen in patients with rest LVEF in the high normal range (greater than 0.68). Therefore, for both supine and upright exercise, the major augmentation in LVEF occurs at earlier stages of exercise, prior to the anaerobic threshold. After the anaerobic threshold, the LVEF response may be highly variable, and a uniform increase is not necessarily expected even in normal subjects.

Radionuclide absolute left ventricular volumes during upright exercise: validation in normal subjects by simultaneous hemodynamic measurements.

A nongeometric radionuclide technique for the determination of absolute left ventricular volumes was validated during exercise in nine normal subjects. Simultaneous reference stroke volume and cardiac output measurements were obtained by the Fick method. The reference left ventricular volumes were calculated by combining the Fick stroke volume and the isotopic ejection fraction. Data were collected at rest in the supine and upright positions and during 60 degrees upright exercise, at three levels of increasing severity. At rest, from supine to upright position, the reference end-diastolic volume decreased significantly from 182 +/- 24 ml to 154 +/- 21 ml (mean +/- SD, P less than 0.005); during upright exercise of low intensity, end-diastolic volume increased to 176 +/- 24 ml (P less than 0.05); at maximal exercise, end-diastolic volume was not different from the resting value in upright position. The end-systolic volume gradually decreased at rest from 67 +/- 11 ml in the supine position to 54 +/- 8 ml in the upright position (P less than 0.05). Compared with these reference data, the scintigraphic measurements were significantly lower on average by 23% for stroke volume, 21% for cardiac output, 22% for end-diastolic volume, and 23% for end-systolic volume. The overall changes in stroke volume (P less than 0.05) and end-systolic volume (P less than 0.001) occurring at rest and during exercise were correctly detected by the scintigraphic method but the smaller changes in end-diastolic volume (less than 15%) were not (P less than 0.15) because they were within the range of the precision of the technique.(ABSTRACT TRUNCATED AT 250 WORDS)