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The hemodynamic effects of prolonged mechanical ventilation with positive end-expiratory pressure (PEEP), with and without blood volume augmentation, were studied in 18 beagles anesthetized with halothane (0.7 per cent end-tidal). Addition of 12 cm H2O PEEP during mechanical ventilation in normavolemic dogs was associated with reductions of transmural cardiac filling pressures, cardiac index and stroke index to 50 per cent of control values. Circulatory adaptation did not occur. Filling pressures and flow remained unchanged during the ensuing 8 hours when PEEP was maintained. They returned to control levels when PEEP was discontinued, except for the transmural right ventricular end-diastolic pressure, which remained elevated above control levels. Systemic vascular resistance was unchanged, but pulmonary vascular resistance doubled upon addition of PEEP. Following autologous whole blood transfusion (25 ml/kg) during mechanical ventilation with PEEP, cardiac index returned to, and remained at, control levels. After PEEP was discontinued, cardiac index increased acutely and remained elevated for the remainder of the study period (as long as 7 hours). Comparable transfusion during mechanical ventilation without PEEP elevated cardiac index only transiently. Right atrial, pulmonary capillary wedge, and right and left ventricular end-diastolic pressures showed marked increases relative to atmospheric with PEEP and after transfusion. Calculated transmural pressures demonstrated clear reductions with application of PEEP, followed by increases to control levels with transfusion and further increases to above control when PEEP was discontinued. Study of ventricular function curves revealed that changes in filling pressures and not to changes in ventricular contractility. Transmural pulmonary arterial diastolic pressure rose throughout the 12 hours of study, despite return of pulmonary vascular resistance to control level with removal of PEEP. Thus, acute decreases in cardiac filling pressure, cardiac index, and stroke index persist consequent to application of PEEP, and circulatory adaptation does not occur. The apparent hemodynamic deterioration may be reversed by blood volume augmentation, but when PEEP is discontinued, hypervolemia with consequent increases in filling pressures and a move along a ventricular function curve will occur. Changes in cardiac index will depend upon the overall state of right and left ventricular contractility.
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PMID:Hemodynamic responses to mechanical ventilation with PEEP: the effect of hypervolemia. 23 10

Left ventricular function was studied in 14 patients with end-stage chronic renal failure using non-invasive methods (echocardiography and systolic time intervals). Patients were divided into 3 groups. Group 1 consisted of 5 patients who were normotensive at the time of study and group 2 of 7 patients who were hypertensive when studied. Group 3 consisted of 2 patients: one was receiving propranolol and the other, studied 302 days after renal transplantation, was receiving digitalis for recurrent episodes of cardiac failure. All except the patient receiving propranolol had normal left ventricular function in systole with normal measurements of fractional fibre shortening (% delta S, EF) and normal measurements relating to the velocity of ventricular contraction (mean Vcf, mean velocity of posterior wall motion). Stroke volume and cardiac output were normal in some patients but were increased in patients with fluid overload. Early diastolic compliance of the left ventricle seemed to be normal except in the patient with recurrent cardiac failure. The study provided no evidence for the existence of a specific uraemic cardiomyopathy.
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PMID:Left ventricular function in chronic renal failure. 100 67

Red cell mass and plasma volume were simultaneously measured by Cr51 and J125-albumine, respectively, in 36 patients with chronic obstructive lung disease and cor pulmonale. Additionally, pulmonary function tests and arterial blood gas analyses as well as pulmonary circulatory and right ventricular hemodynamic measurements were performed the same day. Patients were divided into 3 clinical subgroups: 1. a predominantely emphysematous A-type (n =12), 2. a predominantly bronchial B-type (n = 12), and 3. an intermediate type (n = 12) with about equal scores for A and B. With regard to the cardiac state, A-patients were clinically characterized by small ptotic hearts on chest x-ray and the absence of overt cardiac failure during the whole course of illness whereas B-patients generally showed radiological evidence of heart dilatation associated with recurrent episodes of manifest right ventricular failure. Patients of the intermediate type mostly had recovered from cardiac failure. The following results were obtained: 1. Red cell volume, plasma volume, and total blood volume were within normal limits in A-patients and in patients of the intermediate type. A marked hypervolemia in B-patients was almost entirely due to an increased red cell volume. 2. Close correlations of the red cell volume and total blood volume, respectively, to the arterial PO2 as well as to the arterial PCO2 could be established. 3. Total blood volume was significantly correlated to certain hemodynamic parameters, including cardiac output, stroke volume, pulmonary artery pressure, and right ventricular enddiastolic pressure. 4. The quotient body hematocrit/venous hematocrit was lowered to a significant degree as compared to normal subjects. As a consequence, indirect determination of red cell volume and total blood volume from plasma volume and venous hematocrit leads to a consistent overestimation of both parameters, amounting to 28% in the mean for the red cell mass and to 12% for the total blood volume in the present series.
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PMID:[Red cell mass and plasma volume in chronic cor pulmonale (author's transl)]. 119 61

Plasma volume expansion usually occurs with acute endurance exercise and endurance training both in humans and in animals. In most cases, the increase in plasma volume is associated with lower haematocrit without red cell mass change or an actual reduction in red cell mass, causing relative or true anaemia, respectively. The combination of exercise and heat acclimation (which produces also hypervolaemia, but at a lesser degree than exercise) enhances hypervolaemia induced by exercise training alone. The onset of the phenomenon is extremely rapid: hypervolaemia is observed within minutes or hours of the cessation of exercise. However, 2 days are necessary to reach peak plasma volume expansion after a marathon run or longer race. The magnitude of this natural expansion ranges from 9 to 25%, corresponding to an additional 300 to 700 ml of plasma. The magnitude of this alteration depends on preceding exercise: ambient conditions, intensity and duration of exercise, body posture and frequency of the exercise bouts. The larger the reduction in plasma volume during exercise, the greater the subsequent hypervolaemia. The hydration status of the subjects before and during exercise might modify also plasma volume changes: sufficient fluid ingestion can lead to plasma volume expansion even during prolonged exercise. Fluid-regulating hormones (aldosterone, arginine vasopressin and atrial natriuretic factor) in conjunction with an elevation in plasma protein content promote hypervolaemia. However, the role and the mechanism of the increase in protein mass remain unclear and the hormonal role in the induction of chronic hypervolaemia is still an open question. Hypervolaemia can improve performance by inducing better muscle perfusion, and by increasing stroke volume and maximal cardiac output. By increasing skin blood flow, plasma volume expansion also enhances thermoregulatory responses to exercise. This leads to the important concept of optimal plasma volume and haematocrit, and performance.
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PMID:Hormonal and plasma volume alterations following endurance exercise. A brief review. 155 54

Expansion of blood volume (hypervolemia) has been well documented in both cross-sectional and longitudinal studies as a consequence of endurance exercise training. Plasma volume expansion can account for nearly all of the exercise-induced hypervolemia up to 2-4 wk; after this time expansion may be distributed equally between plasma and red cell volumes. The exercise stimulus for hypervolemia has both thermal and nonthermal components that increase total circulating plasma levels of electrolytes and proteins. Although protein and fluid shifts from the extravascular to intravascular space may provide a mechanism for rapid hypervolemia immediately after exercise, evidence supports the notion that chronic hypervolemia associated with exercise training represents a net expansion of total body water and solutes. This net increase of body fluids with exercise training is associated with increased water intake and decreased urine volume output. The mechanism of reduced urine output appears to be increased renal tubular reabsorption of sodium through a more sensitive aldosterone action in man. Exercise training-induced hypervolemia appears to be universal among most animal species, although the mechanisms may be quite different. The hypervolemia may provide advantages of greater body fluid for heat dissipation and thermoregulatory stability as well as larger vascular volume and filling pressure for greater cardiac stroke volume and lower heart rates during exercise.
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PMID:Blood volume: its adaptation to endurance training. 179 75

Basic parameters of central and intracardiac hemodynamics were studied in 49 urological patients 24 of which with urolithiasis entered group I, 13 with hypertension-group II and 12 with varicocele-group III. The patients' age averaged 46.4, 41.6 and 28.6 years, respectively. The data were provided by routine clinical and laboratory examinations, ECG, one-passage radionuclide cardiography with 132I-albumin using a radiocirculographer of Hungarian manufacture and radiocardioanalyzer RKAZ-01 made in this country. Neither marked ischemic disturbances of the myocardium nor valvular defects were revealed. Ambiguous group-specific shifts presented in central and intracardiac hemodynamics. Total peripheral vascular resistance exhibited a moderate increase while left ventricular circulation time grew 1.5-2-fold. The greater resistance can be attributed to activation of renin-angiotensin system in prolonged ischemia of renal parenchyma due to nephrolithiasis. Group II patients demonstrated parallel elevation of arterial pressure, peripheral resistance, left ventricular performance and output suggesting myocardial functional stress. In group III there was a rise in blood volume, left ventricular performance and output, cardiac index, stroke volume. This myocardial overloading may result from changes in intravascular volumetric relations characteristic of hypervolemia. These hemodynamic changes reflect adaptation in urological patients and should be accounted for in treatment and operative interventions.
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PMID:[The radionuclide assessment of the central hemodynamic indices in patients with urolithiasis, arterial hypertension and varicocele]. 194 10

In anesthesiology and intensive care medicine it is often necessary to treat disorders involving cardiac failure or low-output syndrome. However, in patients who are endangered by ischemic heart disease, any pharmacologic therapy with positive inotropic agents should improve cardiac output without increasing myocardial oxygen demand significantly: the heart should perform its task as efficiently as possible. In the present study a mathematical model of myocardial efficiency was developed. The implications of this theoretical concept of myocardial efficiency were evaluated in animal experiments. THEORETICAL MODEL. Cardiac efficiency is predominantly dependent on preload, afterload, and inotropic state. Quantitatively, it can be calculated from end-diastolic volume, left ventricular systolic pressure (Psyst), stroke volume (SV), and ejection time. The implications of the theoretical analysis are: (1) the inotropic state, which leads to optimal myocardial efficiency, is specifically determined by preload and afterload: for each preload and afterload one matched inotropic state is necessary to achieve optimal efficiency; (2) an increase in blood pressure leads to a decrease in myocardial efficiency even if the inotropic state is optimally matched to preload and afterload; and (3) an increase in end-diastolic volume improves the efficiency of myocardial pump work. ANIMAL EXPERIMENTS. The validity of the theoretical model was studied in animal experiments with emphasis on the following items: (1) is theoretically optimal efficiency of myocardial pump work achieved by physiologic regulation of myocardial performance? (2) how does sympathetic stimulation influence myocardial efficiency? and (3) how do cardiodepressive agents such as beta-blockers or volatile anesthetics influence myocardial efficiency? METHODS. Experiments were performed on nine mongrel dogs after induction of piritramide--nitrous oxide anesthesia. Standard hemodynamics: heart rate, Psyst, maximum left ventricular pressure rise (dP/dtmax), and SV (thermodilution) as well as coronary blood flow (pressure difference catheter) and myocardial oxygen consumption (Fick principle) were measured. In order to create a broad range of different hemodynamic settings, blood withdrawal and retransfusion of blood and/or colloid osmotic solutions were used to modify intravascular volume. Additionally, the inotropic state was varied by infusion of catecholamines (isoproterenol 0.4-0.8 microgram.kg-1.min-1 or norepinephrine 1-2 micrograms.kg-1.min-1). Experimental myocardial failure was induced by adding halothane (0.8-1.5 MAC) to the basic anesthesia, beta-blockade with propranolol (125-250 micrograms.kg-1), and combination of beta-blockade with a pressure load imposed on the myocardium (propranolol 125-250 micrograms.kg-1 + norepinephrine 1-2 micrograms.kg-1.min-1). RESULTS. During variation of the intravascular blood volume by normo-, hypo-, and hypervolemia, the myocardial efficiency very closely matched the theoretically predicted values of optimal efficiency: the average observed efficiency was 98.8% of predicted optimal efficiency. Increasing afterload with norepinephrine did not alter this close relationship, although absolute values of efficiency decreased as predicted by the theoretical model. Application of isoproterenol resulted in SVs that exceeded optimal values by 41.5%. In contrast, during experimental myocardial failure SVs were too small to achieve the necessary values for optimal pump work; observed myocardial efficiency was therefore significantly lower than optimal efficiency. CONCLUSIONS. For pharmacological interventions, it can be concluded that maximal efficiency of cardiac pump work requires maximal end-diastolic filling in combination with minimal afterload. (ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The energetics and economics of the cardiac pump function]. 195 41

Cardiogenic shock comprises peripheral hypoperfusion and pulmonary vascular overload. The goals of therapy are to reduce pulmonary congestion by lowering pulmonary capillary wedge pressure and to increase cardiac index. Volume loading is the first step of treatment. It helps to place the patient on the Franck-Starling relationship. This challenge studies the effects of an increased preload on stroke volume. It has to be done even in case of major heart failure. The main effect of venous vasodilators is to decrease myocardial oxygen consumption. Arteriolar vasodilators also decrease left ventricular end systolic volume. Fluid overload may be treated by diuretics or by extra renal devices: peritoneal dialysis or hemofiltration. Intractable cardiogenic shock may respond to cardiac assist devices (intra aortic balloon pump, pump assistance) as a bridge to surgery.
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PMID:[Treatment of cardiogenic shock with exclusion of inotropic drugs]. 206 79

To elucidate the effect of blood volume on the circulatory adjustment to heat stress, we studied alpha-chloralose-anesthetized rats at three levels of blood volume: normovolemia (NBV), hypervolemia (HBV; +32% plasma volume by isotonic albumin solution infusion), and hypovolemia (LBV; -16% plasma volume by furosemide administration). Body surface heating was performed with an infrared lamp to raise arterial blood temperature (Tb) at the rate of approximately 0.1 degree C/min. Before heating, central venous pressure (CVP) was significantly higher in HBV (0.41 +/- 0.25 mmHg) and lower in LBV (-1.44 +/- 0.22 mmHg) than in NBV (-0.41 +/- 0.10 mmHg). The Tb at which CVP started to decrease was approximately 40 degrees C in HBV, approximately 41 degrees C in NBV, and approximately 42 degrees C in LBV, and it decreased by 1.53 +/- 0.14, 1.92 +/- 0.24, and 0.62 +/- 0.14 mmHg from 37 to 43 degrees C of Tb in HBV, NBV, and LBV, respectively. Stroke volume was closely correlated with CVP, and this relationship was not affected by Tb. Heart rate responses to the raised Tb were similar among the three groups. Mean arterial pressure (MAP) was not affected by blood volume modification or CVP and was maintained at preheating (Tb 37 degrees C) level until Tb rose to 40 degrees C. Above this Tb, MAP increased until Tb reached 43 degrees C (+30-40 mmHg) for all three groups. Total peripheral resistance (TPR) was inversely correlated with CVP, and the slope of the linear relationship between TPR and CVP in LBV was three- to fourfold steeper than in NBV or HBV.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Control of total peripheral resistance during hyperthermia in rats. 224 57

We evaluated the effects of the use of 1.2% isoflurane (group A) in a group of patients (n = 13) referred for mitral valve surgery, with pulmonary hypertension and right ventricular failure. We evaluated the hemodynamic status in baseline conditions, after isoflurane ++ administration and in relative hyper- and hypovolemia. We compared the results with those in 17 patients (group B) in identical clinical state who did not receive isoflurane during anesthesia. The evaluated parameters were: mixed venous Hb saturation (SvO2), heart rate (HR), pulmonary capillary pressure (PCP), central venous pressure (CVP), mean blood pressure (mBP), mean pulmonary arterial pressure (mPAP), cardiac index (CI), arteriolar pulmonary resistances (APR), peripheral vascular resistances (SVR), stroke index (SI), left ventricular work (LVW), right ventricular work (RVW), and O2 consumption (VO2). In group A, after isoflurane ++ administration, CI was 107.05% and 80% of baseline values in relative hypervolemia and hypovolemia, respectively. In group B (control), CI was 121.48% and 88.28% of basal values in relative hypervolemia and hypovolemia, respectively. In group A, SVR were 73.59% and 76.72% in hypervolemia and hypovolemia, respectively, while in group B they were 86.21% and 106.80%. In group A, APR were 90.85% and 89.96% in hypervolemia and hypovolemia, while they were 80.72% and 102.34% in group B. We found that isoflurane results in a greater peripheral than pulmonary vasodilation with a greater impairment in right ventricular function.
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PMID:[Isoflurane in pulmonary hypertension and failure of the right ventricle]. 238 73


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