Embryonic stroke volume and cardiac output in the chick

Cine recordings of the hearts of chick embryos of 3 days and 2 hr to 4 days and 21 hr incubation were projected and measured. The measurements were converted to volumes. Stroke volume was determined from the difference in end diastolic and end systolic volume and multiplied by heart rate to yield cardiac output. Mean stroke volume was 0.0058 (±0.00036 SEM) mm³ per mg body wt; mean cardiac output was 0.956 (± 0.061 SEM) mm³/min per mg body wt. Stroke volume and cardiac output rose above their control values after intravascular injection of Ringer's solution, and even more so after the injection of dextran solution. The increases in stroke volume were due to increases in end diastolic volume, in the case of dextran injected embryos they occurred in spite of a simultaneous increase in end systolic volume. It is concluded that the rise in cardiac output with growth of the embryo is in large part due to an increase in stroke volume, and that the increase in stroke volume depends in part on the known increase in embryonic blood volume. The experiments further suggest that a rapid hydrostatic and osmotic equilibrium exists between embryonic blood plasma and an extra vascular compartment.     

Estimation of cardiac output and stroke volume from thermal equilibration and heartbeat rates in fish

Cardiac output and stroke volume were estimated for a 200 g largemouth blackbass (Micropterus salmoides) by a modified whole-body thermodilution method using the relation between thermal equilibration rates and heartbeat frequencies. The reciprocal of the thermal time constant, k (min^–1), was related to the heartbeat frequency, F (beats min^–1), by the equation k=0.00146 F + 0.309; the slope is the weight-specific stroke volume (ml g^–1) and the intercept is the weight-specific heat transfer constant (cal °C^–1 min^–1 g^–1). Stroke volume was 0.292 ml (0.00146 ml/g body weight), yielding cardiac output values ranging from 44 ml kg^–1 min^–1 (at 30 beats min) to 158 ml kg^–1 min^–1 (at 108 beats min^–1), or 4.4 to 15.8% of body weight. Active (convective) heat transfer due to blood flow constituted an estimated 11 to 34% (mean 22.5%) of total heat transfer, depending on heartbeat frequency; this variability constitutes physiological thermoregulation.     

Blood volume, the venous system, preload, and cardiac output

Cardiac output is determined by heart rate, by contractility (maximum systolic elastance, Emax) and afterload, and by diastolic ventricular compliance and preload. These relationships are illustrated using the pressure-volume loop. Diastolic compliance and Emax place limits determined by the heart within which the pressure-volume loop must lie. End-diastolic and end-systolic pressures and hence the exact position of the loop within these limits are determined by the peripheral circulation. In the presence of minimal sympathetic tone, some 60% of total blood volume is hemodynamically inactive and constitutes a blood volume reserve (the unstressed volume). The remainder of the blood volume (the stressed volume) and the compliance of the venous system determine the venous pressure. This venous pressure together with venous resistance determines venous return, right atrial pressure, cardiac preload, and hence cardiac output. Venoconstriction causes conversion of unstressed volume to the stressed volume, the blood volume reserve is converted into hemodynamically active blood volume. After hemorrhage this replaces the lost stressed volume, while in other situations where total blood volume is not reduced, it allows a sustained increase in cardiac output. The major blood volume reserve is in the splanchnic bed: the liver and intestine, and in animals but not man, the spleen. A major unsolved problem is how the conversion of unstressed volume to stressed volume by venoconstriction is reflexly controlled.     

Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans

Nóbrega, Antonio C. L., Jon W. Williamson, Jorge A. Garcia, and Jere H. Mitchell. Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans. J. Appl. Physiol. 83(3): 712-717, 1997.Ten patients with preserved inotropic function having adual-chamber (right atrium and right ventricle) pacemaker placed forcomplete heart block were studied. They performed static one-leggedknee extension at 20% of their maximal voluntary contraction for 5 minduring three conditions: 1)atrioventricular sensing and pacing mode [normal increase in heart rate (HR; DDD)], 2) HRfixed at the resting value (DOO-Rest; 73 ± 3 beats/min), and3) HR fixed at peak exercise rate(DOO-Ex; 107 ± 4 beats/min). During control exercise (DDD mode),mean arterial pressure (MAP) increased by 25 mmHg with no change instroke volume (SV) or systemic vascular resistance. During DOO-Rest andDOO-Ex, MAP increased (+25 and +29 mmHg, respectively) because of aSV-dependent increase in cardiac output (+1.3 and +1.8 l/min,respectively). The increase in SV during DOO-Rest utilized acombination of increased contractility and the Frank-Starling mechanism(end-diastolic volume 118-136 ml). However, during DOO-Ex, agreater left ventricular contractility (end-systolic volume 55-38ml) mediated the increase in SV.

     

Spontaneous baroreflex control of heart rate versus cardiac output: altered coupling in heart failure

Dynamic cardiac baroreflex responses are frequently investigated by analyzing the spontaneous reciprocal changes in arterial pressure and heart rate (HR). However, whether the spontaneous baroreflex-induced changes in HR translate into changes in cardiac output (CO) is unknown. In addition, this linkage between changes in HR and changes in CO may be different in subjects with heart failure (HF). We examined these questions using conscious dogs before and after pacing-induced HF. Spontaneous baroreflex sensitivity in the control of HR and CO was evaluated as the slopes of the linear relationships between HR or CO and left ventricular systolic pressure (LVSP) during spontaneous sequences of greater or equal to three consecutive beats when HR or CO changed inversely versus pressure. Furthermore, the translation of baroreflex HR responses into CO responses (HR-CO translation) was examined by computing the overlap between HR and CO sequences. In normal resting conditions, 44.0 +/- 4.4% of HR sequences overlapped with CO sequences, suggesting that only around half of the baroreflex HR responses cause CO responses. In HF, HR-LVSP, CO-LVSP, and the HR-CO translation significantly decreased compared with the normal condition (-2.29 +/- 0.5 vs. -5.78 +/- 0.7 beats.min(-1).mmHg(-1); -70.95 +/- 11.8 vs. -229.89 +/- 29.6 ml.min(-1).mmHg(-1); and 19.66 +/- 4.9 vs. 44.0 +/- 4.4%, respectively). We conclude that spontaneous baroreflex HR responses do not always cause changes in CO. In addition, HF significantly decreases HR-LVSP, CO-LVSP, and HR-CO translation.     

Peak exercise stroke volume: associations with cardiac structure and diastolic function.

One of the most debilitating effects of primary aging is the decline in aerobic exercise capacity. One of its causes is an age-related decline in peak exercise stroke volume. This study's main purpose was to determine the cardiovascular adaptations to aging that most influence peak exercise stroke volume in the elderly. We hypothesized that increased left ventricular (LV) filling and mild concentric LV remodeling would be associated with an increase in peak exercise stroke volume corrected for lean body mass (LBM) and that an increased augmentation index (AI), which is a marker of arterial stiffness, would be associated with a decrease. A second aim was to determine the adaptations to aging that most influence LV concentric remodeling in the elderly. We hypothesized that AI would be a predictor of LV mass/LBM and the LV posterior wall thickness-to-LV radius ratio (h/r). We performed a cross-sectional study of cardiac and vascular adaptations to aging in 52 sedentary, elderly subjects. LV filling [as measured by the early-to-late transmitral flow velocity ratio (E/A)] was inversely correlated with and was an independent predictor of peak exercise stroke volume/LBM and was also a predictor of LV remodeling. AI was a predictor of LV remodeling (LV mass/LBM) but not of peak exercise stroke volume/LBM. We conclude that 1) maintenance of LV filling (E/A <1) is associated with a higher peak exercise stroke volume/LBM in very elderly subjects and thus may be a useful adaptation that enhances stroke volume during peak exercise, 2) LV remodeling and AI are less influential on peak exercise stroke volume/LBM, and 3) AI was the most important predictor of LV remodeling.     

Cardiac output and stroke volume in swimming harbor seals

Summary Cardiac output was measured by the thermodilution method in three young harbor seals, at rest and while swimming up to the maximum effort for which they could be trained. Stroke volume was determined by counting heart rate simultaneously with determination of cardiac output. Cardiac outputs varied widely between surface breathing (7.8 ml · kg^–1 · s^–1) and breath-holding while swimming under water (1.8 ml · kg^–1 · s^–1). Stroke volume while at the surface was almost twice the volume white submerged. Surface cardiac output was always near maximal despite work effort, whereas submerged cardiac output gradually increased at higher work efforts. The cardiovascular performance of seals at the maximum MO₂ we could induce from them is equivalent to that of the domestic goat.Abbreviations CO Cardiac output - HR Heart rate - SV Stroke volume - MO ₂ Metabolic rate - FS Forced sumersion - V Velocity - C _DF Frontal drag coefficient - CV Cardiovascular Present address: Institute of Marine Science, University of Alaska, Fairbanks, AK, USA     

Pulmonary tissue volume, cardiac output, and diffusing capacity in sustained microgravity

Verbanck, Sylvia, Hans Larsson, Dag Linnarsson, G. KimPrisk, John B. West, and Manuel Paiva. Pulmonary tissue volume, cardiac output and diffusing capacity in sustained microgravity. J. Appl. Physiol. 83(3): 810-816, 1997.In microgravity (µG) humans have marked changes in bodyfluids, with a combination of an overall fluid loss and aredistribution of fluids in the cranial direction. We investigatedwhether interstitial pulmonary edema develops as a result of a headwardfluid shift or whether pulmonary tissue fluid volume is reduced as aresult of the overall loss of body fluid. We measured pulmonary tissuevolume (Vti), capillary blood flow, and diffusing capacity in foursubjects before, during, and after 10 days of exposure to µG duringspaceflight. Measurements were made by rebreathing a gas mixturecontaining small amounts of acetylene, carbon monoxide, and argon.Measurements made early in flight in two subjects showed no change inVti despite large increases in stroke volume (40%) and diffusingcapacity (13%) consistent with increased pulmonary capillary bloodvolume. Late in-flight measurements in four subjects showed a 25%reduction in Vti compared with preflight controls(P < 0.001). There was aconcomittant reduction in stroke volume, to the extent that it was nolonger significantly different from preflight control. Diffusingcapacity remained elevated (11%; P < 0.05) late in flight. These findings suggest that, despiteincreased pulmonary perfusion and pulmonary capillary blood volume,interstitial pulmonary edema does not result from exposure to µG.

     

Comparative radionuclide and thermodilution determinations of cardiac output and stroke volume in the baboon (Papio ursinus)

Thermodilution cardiac output determinations and multigated equilibrium blood-pool scintigraphy were performed in ten healthy chacma baboons (Papio ursinus). The correlation was moderately good between both the radionuclide and thermodilution stroke volume (r = 0.58, SEE = 3 ml; SVth = 0.78SVr + 15.6 ml) as well as the cardiac output (r = 0.72, SEE = 0.2 liter/min; COth = 0.56 Cor + 2.1 liter/min). The attenuation depth dr as determined by radionuclide techniques was found to correlate well with the radiologically determined values dx (r = 0.8, SEE = 0.4 cm; dx = 0.87dr + 0.72 cm) which validated the depth values used in the calculations.