Treatment Of Circulatory Shock Research Articles

Tissue perfusion pressure enables continuous hemodynamic evaluation and risk prediction in the intensive care unit.

Treatment of circulatory shock in critically ill patients requires management of blood pressure using invasive monitoring, but uncertainty remains as to optimal individual blood pressure targets. Critical closing pressure, which refers to the arterial pressure when blood flow stops, can provide a fundamental measure of vascular tone in response to disease and therapy, but it has not previously been possible to measure this parameter routinely in clinical care. Here we describe a method to continuously measure critical closing pressure in the systemic circulation using readily available blood pressure monitors and then show that tissue perfusion pressure (TPP), defined as the difference between mean arterial pressure and critical closing pressure, provides unique information compared to other hemodynamic parameters. Using analyses of 5,988 admissions to a modern cardiac intensive care unit, and externally validated with 864 admissions to another institution, we show that TPP can predict the risk of mortality, length of hospital stay and peak blood lactate levels. These results indicate that TPP may provide an additional target for blood pressure optimization in patients with circulatory shock.

Circulating biomarkers to assess cardiovascular function in critically ill.

Circulatory shock is one of the most common reasons for ICU admission. Mortality rates in excess of 40% necessitate the rapid identification of high-risk patients, as well as the early assessment of effects of initiated treatments. There is an unmet medical need for circulating biomarkers that may improve patient stratification, predict responses to treatment interventions and may even be a target for novel therapies, enabling a better biological rationale to personalize therapy. Apart from established biomarkers such as lactate, ScvO2 or NT-pro-BNP, novel biomarkers, including adrenomedullin, angiopoietins, angiotensin I/II ratios, renin and DPP3 show promise, as they are all associated with well defined, therapeutically addressable molecular pathways that are dysregulated during circulatory shock. Although some of the therapies related to these biomarkers are still in preclinical stages of development, they may represent personalized treatment opportunities for patients in circulatory shock. From a molecular perspective, shock represents a highly heterologous syndrome, in which multiple unique pathways are dysregulated. Assessment of the status of these pathways with circulating biomarkers may provide a unique opportunity to detect specific phenotypes and implement personalized medicine in the treatment of circulatory shock.

Physiological comparison of hemorrhagic shock and O2max: A conceptual framework for defining the limitation of oxygen delivery.

Disturbance of normal homeostasis occurs when oxygen delivery and energy stores to the body's tissues fail to meet the energy requirement of cells. The work submitted in this review is important because it advances the understanding of inadequate oxygen delivery as it relates to early diagnosis and treatment of circulatory shock and its relationship to disturbance of normal functioning of cellular metabolism in life-threatening conditions of hemorrhage. We explored data from the clinical and exercise literature to construct for the first time a conceptual framework for defining the limitation of inadequate delivery of oxygen by comparing the physiology of hemorrhagic shock caused by severe blood loss to maximal oxygen uptake induced by intense physical exercise. We also provide a translational framework in which understanding the fundamental relationship between the body's reserve to compensate for conditions of inadequate oxygen delivery as a limiting factor to O2max helps to re-evaluate paradigms of triage for improved monitoring of accurate resuscitation in patients suffering from hemorrhagic shock.

Noradrenaline versus Dopamine in the Treatment of Circulatory Shock

There is no difference in the rate of death between individuals randomised to receive dopamine or noradrenaline as first-line treatment of circulatory shock. However, the use of dopamine was associated with a greater incidence of adverse events, especially in those patients with cardiogenic shock.

Pulmonary Artery Catheter: Does the Problem Lie in the Users?

The aims of this study were to look for the variability in the treatment of circulatory shock and to assess the extent to which this variability was reduced by pulmonary artery catheterization (PAC). At three international conferences in 1997-1998 (European Society of Critical Care Medicine, French Language Society for Critical Care [Société de Réanimation de Langue Française], and Society of Critical Care Medicine), a real-life clinical case was discussed in meetings among physicians and a panel of experts, with assistance from an expert computer program. A total of 417 physicians took part in the discussions. Following the clinical presentation, only 38% of physicians suggested the same treatment as the experts, and 35% suggested potentially harmful treatments. Complete hemodynamic data from PAC significantly decreased the range of suggested treatments, improved agreement among physicians themselves as well as the agreement between physicians and experts, and decreased the number of potentially harmful propositions. However, whereas almost 80% of participants finally agreed on the treatment after one to three invasive hemodynamic sets of measurements, at least 10% persisted in suggesting potentially harmful treatments. PAC improved interphysician agreement, but our data suggest that yet greater agreement could be achieved by improving the theoretical training of practitioners.

Novel Insights Into the Pathogenesis and Therapy of Circulatory Shock

Several lines of evidence suggest central roles for nitric oxide, oxygen free radicals, cytokines, and adhesion molecules in circulatory shock. Lipid peroxidation fre quently accompanies ischemia-reperfusion injury; re cruitment of leukocytes exposed to ischemia-reperfu sion injury is largely dependent on leukocytes and endothelial cell adhesion interaction, enhanced nitric oxide stimulation by proinflammatory cytokines contrib utes to increased gut mucosal permeability in sepsis, and tumor necrosis factor (TNF) administration mimics the hemodynamic changes characteristic of circulatory shock. Recent advances in molecular and cellular biol ogy have paved the way for innovative approaches to the treatment of circulatory shock. Novel pharmaco logic approaches are being directed at three distinct levels of the inflammatory cascade: the inciting insult (ie, endotoxin), the mediators (ie, TNF, interleukin-1, oxygen free radicals), and the effector cells (ie, neutro phils). The intent of this review is to discuss the biology of mediators in circulatory shock as well as the experi mental and clinical evidence implicating their role in development and pathogenesis of the injury. Current status of novel adjunctive therapies for circulatory shock is reviewed.

Pathophysiology and Treatment of Circulatory Shock

Circulatory shock is a syndrome characterized by imbalance between oxygen supply and demand. Myriad different mediators are responsible for the systemic manifestations of shock. The therapeutic approach requires initial interventions directed at increasing oxygen delivery followed by definitive therapy for the causative process. Areas of ongoing research involve mediated-directed therapy, reperfusion injury, and immunologic interventions directed at reducing infectious complications in the survivors of circulatory shock.

Beneficial effect of norepinephrine in the treatment of circulatory shock caused by tricyclic antidepressant overdose

The beneficial effect of dopamine in circulatory shock induced by tricyclic antidepressants (TCA) overdose may be decreased due to compromise of the endogenous stores of norepinephrine caused by TCA. The successful outcome of two cases of TCA overdose complicated by hypotension, unresponsive to an initial treatment with physostigmine fluid challenge and dopamine (>15 μg/kg/min) but subsequently responsive to an infusion of norepinephrine is reported.

Use and misuse of vasoactive agents in acute circulatory failure.

AbstractThe challenging aspect in the treatment of circulatory shock, which is a life-threatening situation, is essentially to look for medications that can improve survival. Among vasoactive agents, none of the currently used catecholamines has been shown to increase survival from circulatory shock, and especially not isoproterenol, noradrenaline or adrenaline. Even with dopamine, that we have known for more than ten years, there is no evidence that survival can be increased. Dobutamine is a younger drug but it does not show any such evidence either at the present time. Therefore, we still need to improve treatment of acute circulatory failure by finding other agents that could increase survival in these conditions.

Treatment of Circulatory Shock

Treatment of Circulatory Shock

Treatment of circulatory shock with dopamine. Studies on survival

Treatment of circulatory shock with dopamine. Studies on survival

Treatment of Circulatory Shock With Dopamine

Therapeutic effects of dopamine hydrochloride on the peripheral and metabolic defects of shock were investigated in 34 patients with circulatory shock associated with myocardial infarction, bacteremia, or hypovolemia. Severity of the circulatory defect characterized by hypotension, reduced cardiac output, oliguria, and notably reduced skin (toe) temperature before treatment with dopamine was not directly related to survival. However, the arterial blood concentration of lactate before treatment with dopamine indicated the likelihood of survival. Patients who ultimately survived following treatment with dopamine had normal or only mildly elevated levels of arterial blood lactate before therapy. No patients with established shock states in whom perfusion failure was associated with substantial increases in the level of arterial blood lactate survived regardless of treatment with dopamine. Increases in toe temperature during dopamine treatment also emerged as a uniquely good indicator of favorable outcome during therapy.

Neonatal and Pediatric Cardiovascular Crises

CRISES of the cardiovascular system in the pediatric age group occur most often in the infant, whose size makes monitoring blood pressure difficult and the dosage of fluids and medications critical. Therefore, some general comments about monitoring and drug dosage may serve well as an introduction to the critical care of infants and children. Blood Pressure Determination The blood pressure determination is crucial to the diagnosis as well as to the treatment of circulatory shock. No matter whether auscultation or ultrasonic or other electronic methods are employed,the cuff size is of enormous significance. A cuff that is too small will indicate systolic pressures higher than the true value of the intra-arterial pressure, and a cuff too large will produce readings that may suggest shock in the presence of a normal circulatory state. The width of the air bladder in the cuff should be 20% to 25% wider than the

Treatment of circulatory shock. Use of sympathomimetic and related vasoactive agents

Treatment of circulatory shock. Use of sympathomimetic and related vasoactive agents

Treatment of Circulatory Shock

Reduction of effective blood flow represents the primary disturbance accounting for circulatory shock. Four categories of circulatory shock are identified: cardiogenic, hypovolemic, distributive, and obstructive. The pharmacology and clinical implications for treatment of shock with vasoactive drugs are reviewed in this context. Except for epinephrine, when it is used for treatment of anaphylactic shock, there is no specific indication for the routine use of alpha- or beta-adrenergic receptor agonists. These agents may increase blood pressure or cardiac output, but nutritive flow is not necessarily improved. Comparable limitations are observed with alpha-adrenergic receptor blocking agents. However, selective effects on the myocardium and on the resistance, exchange, and capacitance vessels may be advantageous as an interim and complementary measure. Since vasoactive drugs frequently intensify the fundamental defect accounting for perfusion failure, their selective rather than routine employment is mandatory.

HEMODYNAMIC SPECTRUM OF VASOPRESSOR AND VASODILATOR DRUGS

Hemodynamic effects of vasopressor agents and vasodilator drugs were compared in order to clarify differences which would be of practical significance for their use in treatment of circulatory shock. The alpha-adrenergic agents, methoxamine and phenylephrine hydrochloride, increased arterial pressure and decreased heart rate and venous return. The beta-adrenergic agents, mephentermine and isoproterenol hydrochloride, and the alphaadrenergic blocking agents, phentolamine mesylate and phenoxybenzamine hydrochloride, produced similar hemodynamic effects. Both groups of drugs increased heart rate and venous return. An intermediate response was observed with epinephrine, levarterenol bitartrate, and metaraminol bitartrate, drugs which have both alphaand beta-adrenergic actions. In these studies, the limited significance of a classification which is based on the pressor response became apparent. When the effects are viewed as a spectrum of hemodynamic actions, the apparent paradox between vasopressor and vasodilator therapy for shock is largely resolved.

Hemodynamic Spectrum of Vasopressor and Vasodilator Drugs

Hemodynamic effects of vasopressor agents and vasodilator drugs were compared in order to clarify differences which would be of practical significance for their use in treatment of circulatory shock. The alpha-adrenergic agents, methoxamine and phenylephrine hydrochloride, increased arterial pressure and decreased heart rate and venous return. The beta-adrenergic agents, mephentermine and isoproterenol hydrochloride, and the alphaadrenergic blocking agents, phentolamine mesylate and phenoxybenzamine hydrochloride, produced similar hemodynamic effects. Both groups of drugs increased heart rate and venous return. An intermediate response was observed with epinephrine, levarterenol bitartrate, and metaraminol bitartrate, drugs which have both alphaand beta-adrenergic actions. In these studies, the limited significance of a classification which is based on the pressor response became apparent. When the effects are viewed as a spectrum of hemodynamic actions, the apparent paradox between vasopressor and vasodilator therapy for shock is largely resolved.