PubMed HealthSearch

PubMed · 3633591

Shock.

Abstract

Inevitably, a patient in shock will present to your office. The findings may be obvious, or they may show the more subtle changes of mild tachypnea, tachycardia, and/or changes in mental status. In either event, the perfusion pressure either has already decompensated or will do so momentarily. Whether you initiate therapy then and there might well determine whether your patient will survive. Accordingly, each office should have available for the pre-hospital management of shock those items listed in Table 3. As clinicians, you must be prepared to begin treatment in your office. Although the hospital, particularly the intensive or coronary care unit, is the appropriate setting for the management of shock, therapy must be initiated as soon as and wherever the diagnosis is made. In this situation, an ounce of prevention is indeed worth a pound of cure. Shock, whether it develops insidiously or precipitously, is a state of inadequate tissue perfusion that, if misdiagnosed or treated inadequately, will inevitably result in death.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J K Bouzoukis. 1986. Shock.. https://pubmed.ncbi.nlm.nih.gov/3633591/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Increased plasma endothelin in cirrhosis. Relationship with systemic endotoxemia and response to changes in effective blood volume.

BACKGROUND/AIMS: Patients with cirrhosis and ascites show high plasma concentrations of endothelin. The aim of the current study was to investigate whether this feature is a compensatory response to effective hypovolemia or a consequence of systemic endotoxemia. METHODS: Protocols 1 and 2 assess the effect of acute changes in effective blood volume on plasma endothelin, and protocol 3 investigates the relationship between plasma endotoxin and endothelin in patients with cirrhosis and ascites. Protocol 1 included nine healthy subjects and 26 patients with cirrhosis studied during supine rest, upright tilt (which decreases effective blood volume) and cycloergometric exercise (which activates vasoactive systems by a baroreceptor independent mechanism). Protocol 2 included six patients studied before and 1 and 3 h after the intravenous administration of a plasma expander. In protocol 3, the plasma levels of endothelin and endotoxin were measured in 17 non-infected patients with cirrhosis and also in four patients with spontaneous bacterial peritonitis at diagnosis and following resolution of infection. RESULTS: Plasma endothelin was 3-5 times higher in patients with cirrhosis than in healthy volunteers. In healthy subjects, upright tilt and exercise were associated with a significant activation of the renin-aldosterone and sympathetic nervous systems and an increase in plasma endothelin. In patients with cirrhosis, upright tilt and exercise were associated with a significant increase and plasma volume expansion with a marked suppression of the renin-aldosterone and sympathetic nervous systems. However, in these patients none of these maneuvers affected plasma endothelin levels. In the patients with cirrhosis in protocol 3, there was no correlation between plasma endotoxin and endothelin. Resolution of peritonitis was associated with a marked fall in plasma endotoxin and no changes in plasma endothelin. CONCLUSIONS: These findings suggest that mechanisms other than effective hypovolemia or systemic endotoxemia are involved in the increased plasma endothelin of cirrhosis with ascites.

Blood Volume

Incorporation of first-order uptake rate constants from simple mammillary models into blood-flow limited physiological pharmacokinetic models via extraction efficiencies.

Incorporation of First-Order Uptake Rate Constants from Simple Mammillary Models into Blood-Flow Limited Physiological Pharmacokinetic Models via Extraction Efficiencies. W. L. Roth, L. W. D. Weber, and K. Rozman (1995). Pharm. Res. 263-269. First-order rate constants obtained from classical pharmacokinetic models correspond to mammillary systems in which all of the blood (or plasma) is assumed to be located in a central compartment. In such models the rate at which chemicals are transported out of this pool and into another compartment is the product of the mass of chemical in the central compartment multiplied by a rate constant, which is not limited in magnitude by the blood flow, or the rate at which chemicals from the blood are delivered to the peripheral compartment. Most of the physiologically-based models published to date dispense with some of the information available from mammillary models by assuming that all of the chemical delivered by the flow of blood rapidly equilibrates and can be taken up by the tissue under the control of a "partition coefficient" (Rij = Cj/Ci). We show that the partition coefficient alone does not retain the uptake rate (kji) information available from a classical mammillary model, but that the uptake rate information can be incorporated via unitless extraction efficiency parameters, epsilon j.

Blood Volume