Decline In Cardiac Output Research Articles

Acceleration stress and effects of propranolol on cardiovascular responses.

AbstractHeart rate, arterial pressure and cardiac output were recorded in six physically well‐trained, young male volunteers in the sitting position at normal gravity and at 3 G acting in the head‐seat direction, before and after beta‐adrenergic blockade by propranolol. Studies were performed both at rest and during leg exercise at a load corresponding to 50 % of the maximal oxygen uptake. After propranolol, the heart rate response to increased G at rest averaged 38 % of that observed without blockade, indicating that G‐induced cardioaccelera‐tion is predominantly due to sympathetic stimulation. G‐induced decline of cardiac output was more marked after propranolol, this effect being entirely due to the reduced response of the heart rate. In spite of the cardioinhibitory effects of propranolol, subjective G tolerance was well preserved; the response of the arterial mean pressure to increased G was unaffected due to a 65 % rise in systemic vascular resistance as against 43 % before propranolol. Hence, sympathetic chronotropic stimulation of the heart is not essential for the circulatory defense against increased gravitational stress. Transition from rest to exercise at 3 G produced a larger increase in stroke volume than in heart rate; after beta‐adrenergic blockade the dominance of the stroke xolume increase was exaggerated.

Cardiac Performance in the Unanesthetized Senescent Male Rat

The effects of aging on cardiac output in the intact, unanesthetized rat were determined in 50 l2-mo.-old and 45 24-mo.-old male Wistar rats. Heart rate, phasic, and mean blood pressure were measured through an implanted intra-arterial catheter. Cardiac output determinations were made by S0 RbCI indicator dilution technique. In 30 young and 26 old rats studied at rest the heart rate was slightly higher (p < .05) and the mean blood pressure was slightly lower (n < .05) in the old than in the young rats. The cardiac index and the stroke index were significantly lower in the old than in the young rats (p < .005 and n < .001, respectively). In 20 young and 19 old rats studied after beta-adrenergic blockade (propranolol I mg/kg), there were no age differences in heart rate or blood pressure. However, after beta-adrenergic blockade, cardiac index and stroke index remained significantly lower in the old than in the young rats (n < .025 for both indices). Thus, the decline in cardiac output and stroke volume with age was not related to differences in sympathetic nervous system tone.

The effects of tidal-volume change with positive end-expiratory pressure in pulmonary edema.

The effects of variation in tidal volume were studied in 14 dogs with pulmonary edema during mechanical ventilation with a constant positive end-expiratory pressure (PEEP) of 10 cm H2O. Tidal volumes (VT) of 5 ml/kg with PEEP improved PEEP over that seen with a VT of 15 ml/kg without PEEP. Oxygenation improved with PEEP as VT was increased stepwise from 5 to 25 ml/kg. The greatest improvement in oxygenation and ventilation with PEEP occurred when VT was increased from 5 to 10 ml/kg. Thereafter, as VT was increased, improvement in oxygenation was small and was accompanied by a gradual decline in cardiac output. A tidal volume of 10 ml/kg and a positive end-expiratory pressure of 10 cm H2O produced the most effective gas exchange with the least impairment of cardiac output.

CONTINUOUS POSITIVE PRESSURE VENTILATION AND OXYGEN DELIVERY

The effects of intermittent and continuous positive pressure were studied in mechanically ventilated healthy dogs. No statistically significant changes were produced in oxygen tension, carbon dioxide tension, alveolar-arterial gradients or shunts by continuous positive pressure. It did produce a significant reduction in cardiac output and total oxygen delivery which was reversed by the reintroduction of intermittent positive pressure. The decline in cardiac output was not accompanied by hypotension. The application of continuous positive pressure requires careful assessment of systemic effects to determine its usefulness.

Action of acetylstrophanthidin on experimental myocardial infarction.

An experimental animal model with acute myocardial infarction of a size insufficient to produce profound heart failure or shock was used to study the effects of acute infarction on digitalis tolerance and the hemodynamic changes produced by moderate and large doses of acetylstrophanthidin. With acute myocardial infarction, digitalis toxic arrhythmias could be precipitated with significantly lower doses of digitalis than in animals without myocardial infarction. There was no precise correlation between the size of infarction and the toxic dose of glycoside. Coronary artery ligation produced a stable but relatively depressed circulatory state, as evidenced by lowered cardiac output and stroke volume and elevated systemic vascular resistance and left atrial mean pressure. When digitalis was infused, the following significant changes were observed at nontoxic doses: (1) elevation of aortic and left ventricular pressures; (2) further decline in cardiac output; and (3) decreased left atrial mean pressure.

Performance of the right ventricle under stress: relation to right coronary flow.

Right ventricular performance was studied relative to right coronary artery flow in the chloralose-anesthetized, open chest dog. The right coronary artery was cannulated for measurement and control of flow and pressure. Under control conditions, right coronary artery occlusion caused no change in cardiac output, or right and left ventricular pressures, although right ventricular contractile force fell markedly. With right coronary artery flow intact, incremental pulmonary artery obstruction caused a corresponding decline in cardiac output and elevation of right ventricular end-diastolic pressure with eventual total right ventricular failure and systemic shock. With right coronary artery occlusion, identical degrees of pulmonary artery obstruction resulted in more pronounced changes in cardiac output and right ventricular end-diastolic pressure with right ventricular failure occurring at a much lower level of right ventricular stress.However, with right coronary artery flow intact, the right ventricular decompensation induced by pulmonary artery obstruction, could be reversed by raising right coronary artery perfusion to levels above normal, thus increasing right ventricular performance and restoring cardiac output. We conclude that right ventricular failure and resultant systemic hypotension due to severe pulmonary artery obstruction can be reversed simply by right coronary artery hyperperfusion, and that, although a normally contractile right ventricular free wall is not essential to maintain cardiac performance at rest, during right ventricular systolic stress, over-all cardiac performance becomes increasingly dependent on the right ventricle. The data further imply that increased myocardial impingement on right coronary artery flow during systole in right ventricular hypertension may be an important factor leading to right ventricular failure.

Significance of splanchnic proteases in the production of a toxic factor in hemorrhagic shock.

The pathogenesis of circulatory shock has been previously associated with the plasma accumulation of a myocardial depressant factor (MDF). The plasma accumulation of MDF in cats subjected to hemorrhagic shock was associated with marked increases (P &lt;0.01) in activities of plasma cathepsins A-B. The pH optima for three of the five cathepsins were in the range of 4.8-5.2, a pH range close to that found intracellularly during shock. Moreover, pancreatic and hepatic tissue from these cats exhibited significant decreases in total specific activities for these enzymes, compared with minimal changes in heart, duodenum and spleen. Decreases in total pancreatic cathepsin activities were associated with marked ultrastructural changes in pancreatic acinar cells primarily characterized by vacuolization of the lysosomes. Incubation of homogenates of splanchnic viscera of unshocked dogs revealed that significant concentrations of MDF were produced only in incubated pancreatic homogenates. Infusion of MDF in amounts half that produced by a cat pancreas into intact anesthetized cats yielded a significant circulatory depression indicated by a progressive decline in cardiac output and mean arterial blood pressure and a 54% decrease in cardiac work performance within 60 minutes. These data indicate that substantial amounts of lysosomal proteases are released during shock and that they operate in a suitable pH range to account for the production of quantities of MDF that are sufficient to induce a marked degree of cardiac depression.

Sequential effect of angiographic contrast agent on canine renal and systemic hemodynamics

The prolonged effects of angiographic contrast media on systemic hemodynamics, renal function, and solute excretion were compared to saline and mannitol in dogs lightly anesthetized with pentobarbital. Measurements of hemodynamic and renal function were made at intervals from one half hour before to one hour after rapid left ventricular injection. The progressive decline in cardiac output and renal plasma flow, following iothalamate reflected diuresis induced volume depletion since these effects were reversed by replacing urine volume. This latter maneuver did not modify the iothalamate effect on renal solute excretion. Although the rate and pattern of urinary excretion of iothalamate- 131I paralleled mannitol, the magnitude of the iothalamate diuresis significantly exceeded that induced by mannitol. The augmented iothalamate diuresis resulted from an increased urinary content of sodium chloride as confirmed by a significant decrease in tubular chloride reabsorption. Mannitol caused an increased renal plasma flow and a reduced renal vascular resistance, while iothalamate effects were opposite. The effect of iothalamate on renal electrolyte reabsorption may represent a direct effect on renal-tubular sodium transport.

Maternal cardiovascular dynamics: IV. The influence of gestational age on the maternal cardiovascular response to posture and exercise

Serial hemodynamic evaluations were carried out in 11 patients during pregnancy and the postpartum period. The patients were studied at rest in the supine, lateral, and sitting positions as well as during and after exercise on a bicycle ergometer. The cardiac output was found to be elevated to peak levels as early as 20 to 24 weeks of gestation and was maintained at this high level through the thirty-second week of gestation. At 38 to 40 weeks there was a decline in cardiac output in all positions. This fall was most pronounced in the supine position, in which the cardiac output was found to be lower than in the same position during the postpartum period. The heart rate increased only slightly during early gestation but continued to rise throughout pregnancy in the supine and lateral positions. Accordingly, The stroke volume showed a progressive decline from 20 to 24 weeks of gestation to term. The cardiovascular response to mild exercise was constant throughout pregnancy and similar to that encountered in nonpregnant individuals. However, moderate exercise indicated there is a progressive decline in circulatory reserve as pregnancy advances. This is not attributed to any change in cardiac function but rather to peripheral pooling of blood and obstruction to venous return by the large gravid uterus. Following exercise cardiovascular function returned to resting levels with equal rapidity during pregnancy and post partum.

Studies in acute iron poisoning. 3. The hemodynamic alterations in acute experimental iron poisoning.

Extract: One hour after administration of a lethal dose of ferrous sulfate into the intestine, 10 dogs sustained a sharp decline in cardiac output (mean 57%), a lesser reduction of arterial blood pressure (mean 17%), and a marked elevation of total peripheral resistance (mean 100%). Thereafter, the cardiac output decreased more rapidly than did blood pressure. Total peripheral resistance remained elevated until death.

Cardiovascular effects of sustained norepinephrine infusions. 1. Hemodynamics.

Norepinephrine (NE) in graded doses of 1, 2, and 4 µg/kg/min was infused for four hours into 14 dogs; 5 dogs served as controls. The systemic pressure and flow, blood volume, hematocrit, arterial blood pH, and oxygen saturation were measured at selected intervals throughout the infusion period. Cardiovascular performance was augmented during the first 15 minutes of the NE infusions, but this effect was not sustained. Thereafter, there was a dose-related decline in cardiac output, systemic pressure and left ventricular work, and an increase in the calculated peripheral vascular resistance. At the highest NE dose rate employed, significant left ventricular failure developed by the second hour of NE administration. The hematocrit increased during the first 15 minutes of NE infusion and remained elevated throughout the infusion period. Sustained hypovolemia was not found during the prolonged NE administration, and severe acidosis (pH &lt; 7.20) was inconstant. The processes which lead to cardiovascular dysfunction during prolonged NE infusion are discussed.

Cardiovascular responses of the chicken to seasonal and induced temperature changes.

Blood pressure and cardiac output decline as ambient temperature rises in birds acclimatized to both seasonal- and induced-temperature changes, in contrast to the response usually observed in unacclimatized mammals. The decline in chickens is due to a lowered vascular resistance and blood volume. These circulatory adjustments may be related to the fact that excess heat in birds is dissipated through the respiratory system rather than through the skin.

Primary pulmonary hypertension. Review of clinical features and pathologic physiology with a report of pulmonary hemodynamics derived from repeated catheterization.

The clinical features of 16 patients with primary pulmonary hypertension are reviewed. Repeated cardiac catheterizations at intervals of 1 to 4 years during the course of the disease were performed in five patients. In three of the five patients there was a progressive increase in pulmonary artery pressure, total pulmonary resistance, and a decline in cardiac output. In two patients the pulmonary hemodynamics remained unchanged between studies at intervals of 2 and 4 years. Arterial oxygen saturation decreased with progression of the disease, presumably reflecting the appearance of an uneven distribution of pulmonary capillary flow. The course of the illness was variable and unaffected by any mode of therapy, including long-term anticoagulation.

Arteriovenous fistula: Hemodynamic effects of occlusion and exercise

Hemodynamic studies were carried out in 7 patients with arteriovenous fistulas, during rest and exercise, when the fistula was open and closed. A high cardiac output existed in all patients during rest, unless congestive heart failure was present. A uniform decrease in cardiac output was observed upon occlusion of the fistula. Two patients increased their cardiac output supernormally on exercise. Muscular occlusion of the fistula was postulated in 3 patients without heart failure, in whom a decline in cardiac output occurred during exercise. Correlation between the filling pressures of the left ventricle and stroke volume could not be made in the various experimental situations studied.

The effect of digitoxin on sodium excretion, creatinine clearance and apparent cardiac output.

During the initial phase of decline in cardiac output following the administration of digitoxin to normal subjects, sodium excretion did not decline. Several days later, as cardiac output rose toward the normal level, sodium output decreased in most subjects. The possible implication of these re sults in relation to the regulation of sodium excretion is discussed.

Gastrointestinal symptoms of progressive myocardial disease

The condition presented involves a patient who, after coronary occlusion, developed heart failure, the primary symptoms of which were nausea and vomiting, and in whom the significant pathologic changes were multiple areas of myocardial fibrosis. As a result of the experiences with this and other similar cases and a review of the literature, the following conclusions are drawn: 1. 1. When nausea and vomiting are dominant symptoms in a case of heart failure, one should consider as possible factors not only drugs, congestion of the abdominal viscera, and disorders of the blood metabolites (such as occur in uremia), but should also entertain the possibility that progressive myocardial disease may be the cause of the symptoms. 2. 2. The mechanism of the nausea and vomiting induced by progressive myocardial disease is believed to be analogous to that caused by digitalis, which has been shown to be due to a reflex arising in the heart itself. 3. 3. When coronary thrombosis occurs in a patient with pre-existing narrowing of the smaller coronary arterial branches, a vicious cycle may ensue; the decline in cardiac output and small pulse pressure lead to further coronary insufficiency and progressive myocardial fibrosis, which bring about a further decrease in cardiac output and perpetuation of the cycle. 4. 4. In cases of heart failure in which there is a small pulse pressure with a high diastolic pressure, the outlook is poor because of the factors outlined.