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PubMed1989

[Heart growth in the human embryonic period (a study related to the 2d month of gestation)].

The growth of the heart was studied in 27 human staged embryos of post-somitic period (stages from 15 to 23, Carnegie Institution of Washington). The volume of the heart was determined multiplying the cardiac profiles areas (evaluated by point counting planimetry on serial sections) by the thickness of microtomy. Cardiac volume increase was examined relative to age, to crownrump length, and to body weight. The data were transformed into logarithms and bivariate relations were analysed according allometric equations of the form (log y = k log x + log b). The data were fitted according to three techniques: least squares, major axis, and reduced major axis. The slopes of the allometric regressions indicate positive allometry of the cardiac volume relative to embryonic age and to C-R length, and isometry relative to body weight.

Cardiac Volume↗
PubMed2001

In vitro determination of cardiac ventricular volumes using MRI at 1.0 T in a porcine heart model.

PURPOSE: To determine the accuracy of a 1.0 T MR system with a standard gradient system for quantification of left and right ventricular volumes. A porcine heart model in vitro was used. METHODS: In eight explanted porcine hearts the atria were removed and the aorta and the pulmonary truncus were cannulated. Defined volumes were injected into the ventricles. Magnetic resonance imaging (MRI): FFE-EPI (Multishot EPI) was used. Papillary muscles and trabeculae were excluded. True volumes and MR measurements were analysed separately for both ventricles and by both investigators. RESULTS: The correlation of the true volumes and MR measurements was >0.99. MRI was found to be investigator independent in assessing right and left ventricular volumes in vitro. CONCLUSIONS: MRI at 1.0 T using standard equipment can be used to quantitate cardiac ventricular volumes in vitro with high accuracy.

Animals↗
PubMed1990

Effect of changes in circulating blood volume on cardiac output and arterial and ventricular blood pressure in the stage 18, 24, and 29 chick embryo.

We studied the hemodynamic effects of changing volume loading in the chick embryo, before autonomic innervation, to test the hypothesis that the Frank-Starling mechanism functions in the embryonic myocardium. Dorsal aortic blood velocity was measured by pulsed Doppler. Heart rate and aortic diameter were also measured to calculate cardiac output and stroke volume index. Vitelline arterial and ventricular pressures were measured with a servo-null micropressure system in stage 24 embryos. Infusing isotonic solution intravenously resulted in linear increases in stroke volume index for stages 18 (y = 388x + 6.89), 24 (y = 466x + 7.86), and 29 (y = 549x + 4.96). The slopes and intercepts were statistically the same for all three stages. Similar volume loading in stage 24 embryos initially increased mean arterial pressure linearly, but at higher loading conditions, the rate of rise lessens. Thus, volume loading resulted in a decrease in vascular resistance. Withdrawing blood from stage 24 embryos resulted in a decrease in ventricular peak systolic and end-diastolic pressures. With reinfusion of the blood, systolic and end-diastolic pressures initially rose above baseline levels and later returned to normal. We conclude that a length-tension relation is present in the preinnervated embryonic heart and that vascular resistance changes inversely with loading conditions. We speculate that these mechanisms are the primary hemodynamic control mechanism in the early chick embryo.

Animals↗
PubMed2006

The cellular basis for enhanced volume-modulated cardiac output in fish hearts.

During vertebrate evolution there has been a shift in the way in which the heart varies cardiac output (the product of heart rate and stroke volume). While mammals, birds, and amphibians increase cardiac output through large increases in heart rate and only modest increases (approximately 30%) in stroke volume, fish and some reptiles use modest increases in heart rate and very large increases in stroke volume (up to 300%). The cellular mechanisms underlying these fundamentally different approaches to cardiac output modulation are unknown. We hypothesized that the divergence between volume modulation and frequency modulation lies in the response of different vertebrate myocardium to stretch. We tested this by progressively stretching individual cardiac myocytes from the fish heart while measuring sarcomere length (SL), developed tension, and intracellular Ca2+ ([Ca2+]i) transients. We show that in fish cardiac myocytes, active tension increases at SLs greater than those previously demonstrated for intact mammalian myocytes, representing a twofold increase in the functional ascending limb of the length-tension relationship. The mechanism of action is a length-dependent increase in myofilament Ca2+ sensitivity, rather than changes in the [Ca2+]i transient or actin filament length in the fish cell. The capacity for greater sarcomere extension in fish myocardium may be linked to the low resting tension that is developed during stretch. These adaptations allow the fish heart to volume modulate and thus underpin the fundamental difference between the way fish and higher vertebrates vary cardiac output.

Animals↗
PubMed1976

[Changes in the morphology of the normal left ventricle during the phases of isovolumic contraction and relaxation. Consequences on the calculation of the volume and cardiac output by cineangiocardiographic methods].

It is well known that the left ventricular volume, as measured by the cineangiographic method, decreases during the phase of isometric contraction. What is more, the cardiac index and the ejection fraction measured by this method are definitely larger than those derived from dilution methods. These discrepancies can be explained by movements of the mitral valve during the phases of isometric contraction and relaxation. The systolic ejection volume (SEV) was measured by three different methods: 1. End-diastolic volume (EDV) -end-systolic volume (ESV) ; 2. EDV - pre-filling volume (PFV) ; 3. Pre-ejection volume (PEV) - ESV. It has emerged that the results given by the methods (2) and (3) correspond closely, and differ significantly from those given by method (1); they are also close to those obtained by the dilution method. This difference seems to arise from the fact that the movements of the mitral valve during the phase of isometric relaxation are diametrically opposite to those which occur during isometric contraction; thus, when the values EDV-ESV are used in the calculation of SEV, an overestimate is made because the mitral valve is not to be found in the same position within the ventricular cavity for both values.

Adolescent↗
PubMed1990

Red cell volume and cardiac output in anaemic preterm infants.

To test the hypothesis that haemoglobin concentration is a poor predictor of benefit from transfusion in preterm infants, and that red cell volume is the most important indicator of anaemia, 24 preterm infants receiving red cell transfusions had red cell volume, haemoglobin concentration, and cardiac output measured before and after transfusion. Red cell volume was measured either using dilution of autologous fetal haemoglobin with donor adult haemoglobin, or with a new technique using biotin as a red cell label. The two techniques give similar results. Mean (SD) values before transfusion were 27.4 (13.3), and after transfusion 45.0 (13.7) ml/kg. Cardiac output was measured using imaging and Doppler ultrasonography, and fell with transfusion from mean 286 (121) to 251 (95.6) ml/kg/min. The red cell volume before transfusion correlated well with changes in cardiac output following transfusion, infants with a red cell volume before transfusion of less than 25 ml/kg showing a fall in cardiac output, and those with a red cell volume of greater than 25 ml/kg not showing a significant fall. There was no correlation between haemoglobin concentration, packed cell volume, or change in packed cell volume with changes in cardiac output after transfusion. A red cell volume of 25 ml/kg seems to be critical in preterm infants with anaemia, and infants with values below this are those most likely to benefit from transfusion.

Anemia, Neonatal↗
PubMed1991

The effect of meal size on postprandial increase in cardiac output.

Heart rate, stroke volume, cardiac output and mean arterial blood pressure were followed from the resting pre-meal situation and for 2 hours after intake of standardized meals in four healthy individuals. Continuous records of stroke volume and cardiac output were achieved with an improved method of Doppler ultrasonography. A smallish meal and one 2 1/2 times larger were both given twice and in random order to each of the four test persons. The consumption of a meal invariably resulted in a cardiac output increase, which developed gradually to reach a maximum level 30 to 60 min after end of the meal. The postprandial cardiac output increase resulted from significant increases in both heart rate and stroke volume. There were distinct and significant differences between the circulatory responses to small and large meals. The increase in cardiac output after a large meal was considerably larger and lasted for longer than the increase after a small meal. Two hours after a small meal cardiac output was nearly or fully back to pre-meal values, while cardiac output was still markedly elevated 2 hours after a large meal. Consequently, the total 'extra' amount of blood delivered by the heart over 2 post-meal hours was significantly--about 100%--larger after the large meal than after the small one. Mean arterial blood pressure either fell or remained almost unchanged in the hour after a meal, so that total peripheral resistance was consistently and significantly reduced in the postprandial period--and considerably more so after a large meal than after a small one.

Adult↗
PubMed1994

Effect of body fat on exercise hemodynamics in sedentary older men.

Morbid obesity is often associated with cardiac dilatation and left ventricular dysfunction. The present study investigated whether a similar relationship exists between mild and moderate obesity and left ventricular reserve function in 28 middle aged and older men (58.6 +/- 6.1 years, mean +/- SD). Subjects had a body mass index of 26.4 +/- 2.9 kg/m2, a percent body fat determined by hydrodensitometry ranging from 9.5% to 33.8%, and were carefully screened to exclude cardiovascular disease. Left ventricular function was assessed by gated blood pool scans at rest and during exhaustive upright cycle exercise. There were no significant relationships between resting or exercise cardiac volumes or ejection fraction with percent body fat; however, peak work rate/kg correlated inversely with percent body fat (r = -0.68, p < 0.0001). Heart rate reserve, defined as heart rate at peak work rate minus resting heart rate, declined significantly with increasing percent body fat (r = -0.47, p = 0.01). End diastolic volume index reserve also tended to decline with increasing percent body fat, but stroke volume index and cardiac index reserve were maintained because the decrease in end systolic volume index from rest to maximal exercise was greatest in those subjects with highest percent body fat (r = -0.41, p = 0.03). Therefore, rest and exercise left ventricular function are not related to percent body fat in healthy older men. However, older more obese men have a smaller increase in heart rate and end diastolic volume and a greater decrease in end systolic volume from rest to peak effort as a mechanism to augment exercise cardiac output.

Body Mass Index↗
PubMed2001

Mathematical coupling does not explain the relationship between right ventricular end-diastolic volume and cardiac output.

OBJECTIVE: To evaluate the clinical significance of mathematical coupling on the correlation between cardiac output and right ventricular end-diastolic volume (RVEDV) through measurement of cardiac output by two independent techniques. DESIGN: Prospective, observational study. SETTING: Surgical intensive care unit in a level 1 trauma center. PATIENTS: Twenty-eight critically ill surgical patients who received mechanical ventilation and hemodynamic monitoring with a pulmonary artery catheter. INTERVENTIONS: A pulmonary artery catheter designed to measure right ventricular ejection fraction (RVEF) and cardiac output by the intermittent bolus thermodilution (TDCO) method and continuous cardiac output by the pulsed thermal energy technique was placed. A computerized data logger was used to collect data simultaneously from the RVEF/TDCO system and the continuous cardiac output system. MEASUREMENTS AND MAIN RESULTS: Two hundred forty-nine data sets from 28 patients were compared. There is statistical correlation between TDCO and continuous cardiac output measurements (r = 0.95, p < 0.0001) with an acceptable bias (-0.11 L/min) and precision (+/-0.74 L/min). The correlation was maintained over a wide range of cardiac outputs (2.3-17.8 L/min). There is a high degree of correlation between RVEDV and both TDCO (r = 0.72, p < 0.0001) and independently measured continuous cardiac output (r = 0.68, p < 0.0001). These correlation coefficients are not statistically different (p = 0.15). CONCLUSIONS: The continuous cardiac output technique accurately approximates cardiac output measured by the TDCO method. RVEDV calculated from TDCO correlates well with both TDCO and independently measured continuous cardiac output. Because random measurement errors of the two techniques differ, mathematical coupling alone does not explain the correlation between RVEDV estimates of preload and cardiac output.

Adult↗
PubMed1988

Cardiopulmonary receptor modulation of plasma renin activity in normotensive and hypertensive subjects.

Cardiopulmonary receptors modulate renin release in several animals species. However, their involvement in reflex control of this humoral substance in humans is controversial. Furthermore, no information is available on the alteration of this control in hypertension. We studied the modulation of plasma renin activity (radioimmunoassay) in 12 normotensive subjects and in 12 age-matched subjects with untreated hypertension of mild or moderate degree. Cardiopulmonary receptors were stimulated by increasing central venous pressure (right atrial catheter) and cardiac volume (echocardiographic measurement) through passive leg raising and deactivated by reducing central venous pressure and cardiac volume through lower body negative pressure. The stimuli were maintained for 20 to 30 minutes, and their degree was set to avoid changes in blood pressure (indirect or direct measurements) and heart rate, thus avoiding involvement of arterial baroreceptors. In normotensive subjects, deactivation of cardiopulmonary receptors induced a progressive rise in plasma renin activity and stimulation of cardiopulmonary receptors induced a progressive fall. The reflex gain (ratio between plasma renin activity and central venous pressure or cardiac volume changes) was similar for deactivation and stimulation. During cardiopulmonary receptor deactivation, the gain corresponded to that obtained by dividing the increase in plasma renin by the reduction in central venous pressure induced by tilting. Cardiopulmonary receptor deactivation and stimulation also induced clear-cut changes in plasma renin activity in hypertensive subjects, but the percent magnitude of the reflex plasma renin activity excursion was less than that in normotensive subjects. These observations indicate that cardiopulmonary receptors modulate plasma renin activity in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Vascular, volume, and cardiac response to normal and hypertensive pregnancy.

Cardiovascular adaptations to the circulatory and volume changes of pregnancy have been studied in late normal and hypertensive pregnancy and postpartum. There has been evidence of a marked plasma volume expansion in normal pregnancy, blunted in preeclampsia; an increased capillary permeability during normal pregnancy; augmented left ventricular mass, which is increased in mild preeclampsia; and similar increases in peripheral venous distensibility during normal and preeclamptic pregnancy. In mild preeclampsia the enlarged ventricle has been shown to be capable of maintaining a normal cardiac output despite elevated afterload. The forearm vascular bed appears to play little part in these adjustments, because forearm venous distensibility has been shown to be higher during normal pregnancy than during postpartum; in hypertensive individuals there was no difference during pregnancy and postpartum. It is evident from this brief review that it is too early to draw clear-cut conclusions regarding the vascular, volume, and cardiac response to normal and hypertensive pregnancy. Research in this field, including two-dimensional echocardiography and plethysmography in larger homogeneous groups, will probably lead to a better understanding of the pathophysiological mechanism of pregnancy hypertension.

Arm↗
PubMed1979

Augmented venous return: protection of the ischemic myocardium during endotoxemia.

The effects of gram-negative endotoxin (Escherichia coli 4 mg/kg) induced myocardial failure in the pentobarbital-anesthesized dog were examined by monitoring its influence on coronary and systemic hemodynamics and correlating these results with myofibrillar ATPase activity. An identical series of studies was performed incorporating a femoral-femoral arterial-venous shunt to augment venous return. Over a five-hour period, gram-negative endotoxemia was associated with a progressive fall in arterial pressure, stroke volume, cardiac output, coronary flow, and a rise in total peripheral resistance and diastolic coronary vascular resistance. Augmenting venous return by 313 +/- 71 ml/min significantly increased cardiac output, stroke volume, and coronary flow and substantially reduced total peripheral resistance and coronary vascular resistance. Myofibrillar ATPase activity from both endocardium and epicardium was significantly depressed in the endotoxin-shocked preparations. However, with the augmentation of venous return with the A-V shunt in the endotoxin-treated animal, myofibrillar ATPase activity is normal. It appears that endotoxin causes a decrease both in venous return and in cardiac contractility by increasing total peripheral resistance, coronary vascular resistance, and impedance to left ventricular ejection. Augmenting venous return by optimizing preload and reducing afterload prevents any significant increase in total peripheral resistance, coronary vascular resistance, or impedance to left ventricular ejection. This is manifested by a rise in cardiac output, stroke volume, and coronary flow and the preservation of myocardial function. This is the first successful application of left ventricular afterload reduction in noncardiogenic shock.

Adenosine Triphosphatases↗
PubMedDate not supplied

Echocardiographic analysis of human left ventricular diastolic volume and cardiac performance during halothane anesthesia.

Using M-mode echocardiography we found that 0.5, 1.0, and 1.5% end-tidal halothane induced dose-related increases in left ventricular volume and decreases in left ventricular performance in seven normal unpremedicated subjects. During controlled respiration with normocarbia, the diastolic minor axis of the heart, which is related to the cube root of left ventricular volume, increased to a maximum of 107. 7 +/- 1.9 (% +/- SE of control) at 1.5% end-tidal halothane from a control value of 43.5 +/- 1.3 (mm +/- SE). Two ejection-phase performance variables, percentage shortening and mean velocity of circumferential shortening decreased to 60.1 +/- 6.1 (% +/- SE of control) and 62.4 +/- 6.5, (% +/- SE of control) at 1.5% halothane from respective control values of 29.7 +/- 2.61 (% +/- SE) and 0.94 +/- 0.08 (circumferences/second +/- SE). Surgical stimulation did not significantly affect these changes. Under these experimental conditions, we conclude that halothane dilates the heart, and that echocardiography can be used to monitor the depressant effect of halothane on the heart.

Adult↗