Alterations in central blood volume and cardiac output induced by positive pressure breathing and counteracted by metaraminol (aramine).
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Based on model calculations a mathematical approach has been developed which permits an analysis and approximative evaluation of the significance of geometric and various muscle physiological factors for cardiac stroke volume with respect to anatomical ventricular size. Despite increasing wall stress the stroke volume generally increases with growing anatomical heart size, reaching a maximum beyond which it falls off. On the basis of the model of a thick-walled sphere for the left ventricle, stroke-volume-radius relations have been calculated for three different types of chronic ventricular enlargement (constancy of wall thickness, wall volume, or of the ratio of wall thickness to inner radius) in particular. In all three cases stroke volume increases with chronic enlargement of the heart, at least to a certain extent. Thus, stroke volume can be augmented with increasing anatomical heart size under constant contractile conditions despite decreasing ejection fraction. This fact has to be considered in the assessment of ventricular function. Nomograms are obtained by varying contractility, wall thickness, or end-systolic pressure while keeping the other contractile conditions constant, thus permitting the evaluation of the effect of therapeutic measures in the presence of cardiac dilatation.
We measured hemodynamic responses during 4 days of head-down tilt (HDT) and during graded lower body negative pressure (LBNP) in invasively instrumented rhesus monkeys to test the hypotheses that exposure to simulated microgravity increases cardiac compliance and that decreased stroke volume, cardiac output, and orthostatic tolerance are associated with reduced left ventricular peak dP/dt. Six monkeys underwent two 4-day (96 h) experimental conditions separated by 9 days of ambulatory activities in a crossover counterbalance design: 1) continuous exposure to 10 degrees HDT and 2) approximately 12-14 h per day of 80 degrees head-up tilt and 10-12 h supine (control condition). Each animal underwent measurements of central venous pressure (CVP), left ventricular and aortic pressures, stroke volume, esophageal pressure (EsP), plasma volume, alpha1- and beta1-adrenergic responsiveness, and tolerance to LBNP. HDT induced a hypovolemic and hypoadrenergic state with reduced LBNP tolerance compared with the control condition. Decreased LBNP tolerance with HDT was associated with reduced stroke volume, cardiac output, and peak dP/dt. Compared with the control condition, a 34% reduction in CVP (P = 0.010) and no change in left ventricular end-diastolic area during HDT was associated with increased ventricular compliance (P = 0.0053). Increased cardiac compliance could not be explained by reduced intrathoracic pressure since EsP was unaltered by HDT. Our data provide the first direct evidence that increased cardiac compliance was associated with headward fluid shifts similar to those induced by exposure to spaceflight and that reduced orthostatic tolerance was associated with lower cardiac contractility.
OBJECTIVE: The number of cardiac transplant programs continues to increase despite no increase in the number of hearts available for transplantation. As a result, the majority of heart transplant centers perform extremely small numbers of transplant operations annually. To determine the effect of small transplantation volume on transplant outcome, the following study was performed. DESIGN: Using the Scientific Registry of the United Network for Organ Sharing, all cardiac transplant procedures from October 1987 through December 1991 were analyzed to determine whether center volumes affected cardiac transplant outcome. Patient survival rates for each center were determined, and the survival rates were modeled for the following patient variables: first transplantation or retransplantation, patient condition at the time of transplantation, patient underlying cardiac disease (congenital vs all others), and time. SETTING: All cardiac transplant centers in the United States were included in the analysis. PATIENTS: All patients undergoing cardiac transplantation in the United States from October 1987 through December 1991 were included in the analysis. MAIN OUTCOME MEASURE: The primary end point in this analysis was mortality. RESULTS: Throughout the entire study, of the 150 cardiac transplant centers, 35.3% of the centers were performing fewer than five cardiac transplantations per year, 53.3% were performing fewer than nine transplantations per year, and 61.3% were performing fewer than 12 transplantations per year, the minimum required for Medicare payment eligibility. Using the modeled survival rates, the risk of mortality decreased to a basal level in those centers performing between eight and 10 transplant operations per year. In centers performing fewer than nine transplantations, mortality increased sharply and exponentially. Dividing centers into those that performed nine or more transplantations per year (70 centers) and fewer than nine transplantations per year (80 centers), the increased risk of mortality at 1 month and 12 months was 40.3% and 33.1%, respectively, in centers performing fewer than nine cardiac transplantations per year (P < .001). Once the threshold of nine transplant procedures was met, those centers that were eligible for Medicare payment did not have significantly better survival than those centers not eligible for Medicare coverage. CONCLUSIONS: These data demonstrate that the risk of mortality at early and intermediate time points is substantially higher in low-volume cardiac transplant centers, which make up more than half of the centers performing cardiac transplantation in the United States.
In six volunteers (5 male, 1 female) it has been shown that normal respiration made no statistical difference to the estimates of the mean stroke volume and the mean cardiac output as determined by the electrical impedance method of Kubicek et al, (1966). The coefficient of variation was usually increased by respiration. The use of those stroke volumes which occur only at end-expiration was not shown to yield a greater reproducibility with 3 other male volunteers. In the female subject it was found that the use of a digital averager triggered from the preceding R-wave of the ECG gave values for the mean stroke volume and cardiac output which were always lower than the conventional mean values obtained from a number of strokes. The expense of either of these approaches does not appear to be justified as a means of compensating for the effects of normal respiration on the impedance dZ/dt waveform.
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On the basis of model and clinical investigations using differential rheograms , a conclusion was drawn that in measuring the curve of Ad amplitude from the isoelectric line, the cardiac stroke volume ( SHV ) averaging 30-80 ml as determined by the method of tetrapolar chest rheography and calculated by the formula of Kubi cek et al. (formula see text) was in full agreement with the SHV determined by Fick's method for the same heart rate. When calculated by formula (formula see text) or (formula see text) which used (formula see text) or delta Z found by extrapolating the rheographic curve according to the method of A. A. Kedrov or N. R. Paleev , the SHV proved to be lower and, therefore, in order to obtain more accurate values of the SHV , corrective coefficient K should be introduced into these formulae. The value of K is determined by an inverse dependence between the volumetric rate of the cardiac output and the resilient-viscous properties of vessels, and it varies with different heart rates.
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The applicability of the finger pressure-derived pulse contour (PC) technique was evaluated in the measurement of stroke volume (SV), cardiac output (CO) and their changes in different phases of the tilt-table test. The reference method was whole-body impedance cardiography (ICG). A total number of 40 physically active patients, aged 41 +/- 19 years, were randomly chosen from a pool of 230. Specifically speaking, 20 of the patients experienced (pre)syncope (tilt+ patients) during the head-up tilt (HUT), and 20 did not (tilt-). A total number of three measurement periods, 30-60 s each, were analysed: supine position, 5 min after the commencement of HUT, and 1 min before set down. SV and CO values measured by PC underestimated significantly those measured by ICG (biases +/- SD 19 +/- 14 ml and 1.55 +/- 1.14 l min-1, respectively) in agreement with earlier reports. The bias between the methods was almost the same in the different phases of the test. However, the SD of the bias was bigger for tilt+ (P < 0.05). When the bias between the methods was eliminated by scaling the first measurement to 100%, the agreement between the methods in the second and third measurements was clearly better than without scaling. Both methods showed a physiological drop in SV after the commencement of HUT. These results indicate that PC suffices in tracking the changes in CO and SV, but for absolute values it is not reliable.
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Glomerular volume has been reported to be increased in patients with congenital cyanotic heart disease and cor pulmonale; however it has not been systematically studied in patients with congestive cardiac failure (CCF). Glomerular volume was therefore measured by point-counting serially sectioned glomerular profiles of 25 randomly selected glomeruli using the Cavalieri principle in autopsy specimens from 8 patients dying from CCF and 6 age-matched controls with no renal or cardiac pathology. Mean glomerular volume was not different between patients dying from CCF and controls, 2.49 (0.21) vs. 2.25 (0.26) x 10(6) microm3, and the distribution of individual glomerular volumes was similar in the two groups. We conclude that severe CCF is not associated with significant glomerular enlargement and that the previously reported glomerular enlargement in cyanotic heart disease is likely to be mediated through hypoxemia.
The ECG, chest x-ray and haemodynamic parameters were investigated preoperatively in 19 patients subjected to surgery for renal artery stenosis (RAS) and in a control group comprising 19 normotensive patients subjected to other forms of major vascular surgery. Increased cardiac volume was demonstrated in 13 (68%) RAS patients and in two (11%) patients from the control group. Abnormal ECG (i.e. left ventricular hypertrophy or atrial fibrillation) was observed in 11 (58%) RAS patients and in one (5%) patient from the control group. In the RAS patients the following haemodynamic parameters were found to be statistically significantly increased, compared to the control group: systemic blood pressure, (systolic arterial pressure: +43%, diastolic arterial pressure: +38%, mean arterial pressure: +41%), pulmonary artery mean pressure (+64%), pulmonary capillary wedge pressure (+107%), heart rate (+15%), systemic vascular resistance (+27%), left ventricular minute work index (+46%) and right ventricular minute work index (+67%). The presence of increased cardiac volume and abnormal ECG were more closely related to the level of the pathologically increased pulmonary artery mean and wedge pressures than to the systemic blood pressure or central venous pressure. A preoperative haemodynamic evaluation is recommended to determine the degree of heart failure in RAS patients with: left ventricular hypertrophy and increased cardiac volume, or atrial fibrillation.
Impedance cardiography (IC) is an inexpensive, reliable and noninvasive technique for determining stroke volume (SV) and cardiac output (CO). It relies on the measurement of phasic changes in transthoracic electrical resistivity, related to ejection of blood into the ascending aorta with each heart beat. Because of its non-invasive nature, IC is becoming increasingly used in clinical settings, as well as in many areas of physiological research. This paper discusses IC in terms of its theoretical basis, the components of the impedance signal and how impedance data is mathematically processed. One of the major controversies surrounding IC concerns how well it compares with conventional methods of determining SV and CO, such as thermodilution. A literature review of such comparative studies demonstrated that the controversy is far from settled, but that IC is generally agreed to be capable of accurately monitoring trends in cardiovascular dynamics. The question of accuracy of IC in terms of absolute values of SV and CO remains to be determined. The methodological limitations, accuracy, reliability and reproducibility of IC are examined, as are some of the methods developed to improve these aspects of the technique. The application and utility of IC in aerospace medicine research is also addressed.
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Single-dimension left ventricular echocardiographic measurements are currently being used in investigational studies as the basis for evaluating cardiac output parameters in normal subjects, even though validity of the method for normal subjects has not been established. We prospectively compared stroke volume derived from M mode left ventricular dimensions (LVID) to Fick stroke volume in 20 patients with no objective evidence of cardiac disease. Based on simultaneous studies, stroke volume by Fick ranged from 39 to 121 ml and cardiac output ranged from 3.9 to 10.4 L/min. Comparing the LVID cubed method with Fick, the correlation coefficient was r = .47 for stroke volume and r = .36 for cardiac output. LVID absolute error in cardiac output ranged -2.11 to +3.21 L/min. Use of other published formulas for calculating stroke volume from LVID did not improve accuracy. These data indicate that stroke volume and cardiac output cannot be accurately measured or reliably estimated from M mode left ventricular internal dimensions.
The clinical applicability of a method for quantifying pericardial effusion (PE) was studied. The pericardial and cardiac volumes were determined from border tracings of 2-dimensional echocardiograms fitted with 3-dimensional disk models. The PE volume was the difference between pericardial and cardiac volumes. A phantom study included 54 cases with different volumes and viewing geometry showed a correlation coefficient r = 0.98 and an accuracy of +/- 6%. A clinical study included 20 cases showing that the estimated PE volume correlated well with that drained surgically (between 100 mL and 1200 mL): y = 0.81 x + 120 mL; r = 0.91, P <.0001. The percent error, determined by the standard error of the estimate (114 mL) over mean (548 mL), was 20%. Intraobserver variability was 4% and interobserver variability 6%. The 3-dimensional disk method provides a quick and convenient way to quantify PE from 2-dimensional echocardiograms with acceptable accuracy and reproducibility.
The volume-sensitive chloride current (ICl,swell) is found in the mammalian myocardium and is activated by osmotic swelling. The goal of this study was to examine the importance of the tyrosine kinases focal adhesion kinase (FAK) and Src kinase in cardiac ICl,swell regulation. Neonatal rat ventricular myocytes were cultured on collagen membranes and infected with adenovirus expressing beta-galactosidase (AdLacZ), FAK, or FAK-related nonkinase. FAK-related nonkinase (FRNK) is an endogenous cardiac protein, which functions as an inhibitor of FAK. Whole cell patch-clamp recordings demonstrated that osmotic swelling was associated with the activation of an outward rectifying current in uninfected and AdLacZ-infected cells. Consistent with the properties of ICl,swell, this current displayed a reversal potential close to the equilibrium potential for Cl-; was inhibited by the Cl- channel blockers 4,4'-dinitrostilbene-2,2'-disulfonic acid, 5-nitro-2-(3-phenylpropylamino)-benzoic acid, and tamoxifen; and was eliminated in hypertonic solution. In addition to activating ICl,swell, hypotonic swelling enhanced the tyrosine phosphorylation of multiple cardiac proteins including those in the range of 68-70 and 120-130 kDa. Pretreatment of the cells with the drug 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine, an inhibitor of FAK and Src, diminished swelling-induced phosphorylation of these proteins but paradoxically increased ICl,swell. Furthermore, overexpression of FRNK but not FAK caused a twofold augmentation in I(Cl,swell) and increased the rate of current activation. Thus the tyrosine kinases FAK and Src contribute to the regulation of ICl,swell.