Showing papers on "Hypovolemia published in 1970"

Shock after acute myocardial infarction: A clinical and hemodynamic profile

Abstract: Clinical features, predisposing factors, precipitating events, laboratory and hemodynamic observations, pathologic findings, prognostic indicators and the results of therapy are surveyed for 73 patients in whom shock developed after acute myocardial infarction. The incidence of shock was 15 percent, and the mortality 86 percent. It was not possible to differentiate patients with shock from those with acute infarction alone on the basis of age, anamnestic data, delay before hospitalization or anatomic location of infarction. No precipitating cause for shock other than acute infarction itself was consistently present. Hypovolemia, anemia, arrhythmia and drugs could not be incriminated as important factors in the genesis of shock. Extensive myocardial damage, coronary atherosclerosis and left ventricular hypertrophy were found at postmortem examination in most patients who died, but similar findings were noted in a group of patients in the coronary care unit who died without evidence of shock during the period of the study. Delay in onset of shock in many cases suggested progression of cardiac damage after the initial clinical event. Hemodynamic studies in 19 patients showed that cardiac index was less than half of the normal index, stroke volume index about a third of normal, and peripheral resistance generally increased. We conclude that patients who have the highest risk can be identified from various clinical and hemodynamic observations. It is appropriate to consider such patients for unconventional therapy.

Restoration of intravascular fluid volume following acute hypovolemia in rats.

Abstract: i~~yavas~ula~ Juid vohme following acute hypovolemia in rats. Am. 3. Physiol. 218(l): 191496. 1970.-Subcutaneous injection of hyperoncotic polyethylene glycol (PC) solution produced hypovolemia in rats by gradually withdrawing isosmotic plasma fluid into the local interstitium, Significant drinking was observed for 6-8 hr, although water ingestion subsequently diminished despite persistent hypovolemia. This inhibition of thirst in the presence of substantial plasma deficits has been attributed to osmotic dilution of body fluids. When 0.5 1 M NaCl solution was additionally present, rats manifested a sodium appetite 6-9 hr after treatment and water intake progressed without evident inhibition. Apparently, osmotic dilution potentiated a sodium appetite in the hypovolemic rats, which removed the inhibition of thirst by increasing body fluid osmolality. Because of the increased fluid intakes and low urine volumes and sodium concentrations, increasing amounts of nearisotonic fluid were retained and eventually plasma deficits were repaired. These results indicate that thirst and sodium appetite are interdependent behavioral mechanisms of volume regulation which complement well-known antidiuretic and antinatriuretic processes in providing for the restoration of intravascular Auid volume in hypovolemic rats.

Evaluation of the pharmacologic basis for the therapy of circulatory shock.

Abstract: In circulatory shock, pathogenesis of severe irreversible shock is partly due to activation of the sympathoadrenal system as a reflex compensatory response to hypotension or hypovolemia, and if sustained and ineffective in restoring adequate tissue perfusion, it results in tissue hypoxia resulting in further hypotension and hypovolemia. Objectives of therapy are: (1) to restore blood volume; (2) to open channels for perfusion of certain critical tissues; and (3) to augment the head of perfusion pressure. If the first objective is not met, drugs may be ineffective. Objectives 2 and 3 are contradictory if only generalized vasodilatation or only generalized vasoconstriction is considered without regard to the balance of flow and pressure head. If reflex sympathetic vasoconstriction is deleterious, then it is not reasonable to produce greater generalized vasoconstriction but to inhibit ongoing vasoconstriction selectively by the use of an alpha adrenergic blocking drug. A combination of actions is theoretically desirable in which blood flow to “essential” organs (such as kidneys, myocardium and brain) is augmented (vasodilatation), and the head of pressure is raised by increased cardiac output or by vasoconstriction in less essential organs (such as skin and skeletal muscle). If restoration of blood volume is not sufficient, drugs should be used according to their selective actions, such as alpha adrenergic blocking agents, beta adrenergic vasodilators, other adrenergic and non-adrenergic vasodilators, and vasoconstrictors (both alpha adrenergic and nonadrenergic). The value of glucocorticoid drugs in the treatment of shock has not yet been definitely established.

On the cardiovascular effect of propranolol during halothane anaesthesia en normovolaemic and hypovolaemic dogs

Abstract: SUMMARY The circulatory effects of propranolol during halothane anaesthesia were investigated in fifteen dogs, in eight of which a moderate hypovolaemia was produced. Mean aortic pressure and flow, stroke volume, cardiac performance, and time of presssure rise showing infusion of adrenaline were measured or derived. The investigation led to the following findings: (1) The circulatory responses were similar in normo- and hypovolaemic animals. The ability of the latter to maintain an adequate cardiac output was markedly restricted. (2) Halothane significantly reduced flow, pressure, cardiac performance in both groups, and heart rate in the normovolaemic group. There was a non-significant decrease of heart rate in the hypovolaemic group and of stroke volume in both groups. (3) Propranolol significantly prolonged the time of pressure rise, slowed down and stabilized the heart rate and reduced the flow. The fall of stroke volume was significant in the normovolaemic group and the fall of cardiac performance was significant in the hypovolaemic group only. There was no significant change of pressure. (4) Adrenaline significantly increased pressure and cardiac performance after beta blockade but caused non-significant changes in other parameters except stroke volume in the hypovolaemic group. Two hypovolaemic animals had an irreversible asystole. It is emphasized that, particularly in hypovolaemia and under propranolol during halothane anaesthesia, reliance on estimation of the arterial pressure may lead to completely false conclusions.

Role of hypovolemia in the impaired water diuresis of adrenal insufficiency.

Abstract: Impaired water diuresis in adrenal insufficiency is rapidly corrected by glucocorticoid. The defect in water excretion has been attributed to hypovolemia consequent to sodium deficit. The role of hypovolemia in this defect was evaluated by observing the effect of corticoids on water diuresis in normal subjects made hypovolemic by sodium depletion. In addition the patterns of diuresis in these subjects were compared with those of patients with adrenal insufficiency maintained on mineralocorticoid but not given glucocorticoid. It was found that hypovolemia significantly impaired water diuresis in normal subjects, but that glucocorticoid had no effect on this change. The impaired water diuresis observed in patients with Addison's disease differed from that of the hypovolemic subjects. In normals made hypovolemic most of the change in water diuresis was due to increased reabsorption of fluid in the proximal nephron. In Addisonians, however, a major portion of the impairment was due to diffusion of wa...

Fluid therapy in hemorrhagic shock: experimental evaluation.

Abstract: A model for the production of hemorrhagic shock in the rat was found to offer advantages over canine models. The ready availability of uniform inexpensive animals permitted evaluation of fluid therapy for hypovolemia. After 120 min of hypovolemia, reinfusion of the shed blood or infusion of Ringer's lactate or normal saline in a volume equal to three times the volume of the shed blood reduced mortality equally. The addition of 5% dextrose to Ringer's lactate produced a deleterious effect probably due to increased osmolarity.

Problems of Clinical Research in Shock

Abstract: The vascular pattern of hypovolemia with diminished cardiac output in the early stages of shock syndromes is well recognized and has been extensively studied by many investigators. However, with the development of techniques for rapid performing hemodynamic and respiratory measurements at the bedside, a new range of altered physiologic responses in shock syndromes has been observed. These recently recognized circulatory patterns consist of a hyperkinetic circulation with high cardiac output and rapid mean circulation time in the presence of arterial hypotension and progressive clinical deterioration (Mac — Lean et al. 1965; Khe and Shoemaker 1968; Duff et al. 1969).