[Fluid balance and postoperative lung function].

J A Sturm

Home/Archive/PubMed

PubMed · 1983490

[Fluid balance and postoperative lung function].

J A Sturm

View original source ↗Export metadata ↓

Abstract

Postoperative volume therapy: 1. Replacement of fluid loss. 2. Therapy of intravasal hypovolaemia in case of permeability damage or intracellular fluid shift. Monitoring: 1. Circulation (HR, CVP, art. pressure). 2. Homeostasis (Na, K). 3. Metabolic changes (BE, pH). 4. Kidney function. In complications like sepsis or ARDS with pulmonary problems and increase of pulmonary vascular resistance the use of a pulmonary artery catheter is necessary. Differential treatment has to be based on additional measurement of cardiac output and pulmonary capillary pressure. Volume treatment in postoperative complications is essential because of intravasal hypovolaemia. Kidney and cardiac failure have to be ruled out.

Explore related subjects

Acid-Base Equilibrium Blood Volume Fluid Therapy Hemodynamics Humans Monitoring, Physiologic Postoperative Complications Respiratory Distress Syndrome Respiratory Function Tests Water-Electrolyte Balance Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

J A Sturm. 1990. [Fluid balance and postoperative lung function].. https://pubmed.ncbi.nlm.nih.gov/1983490/

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

KEEP EXPLORING

Related citations

PubMed1992

ATP-driven Ca2+/H+ antiport in acid vesicles from Dictyostelium.

Amoebae of the cellular slime mold Dictyostelium discoideum possess an extensive and dynamic endomembrane system that includes many types of acidic vacuoles. A light membrane fraction from Dictyostelium, rich in vacuolar-type H(+)-ATPase, has been described [Padh, H., Lavasa, M. & Steck, T.L. (1989) J. Cell Biol. 108, 865-874]. Here, we show that this "acidosomal" fraction also contains a high-affinity vanadate-sensitive Ca2+ uptake activity that is stimulated by the pH gradient formed by the H(+)-ATPase. We attribute this Ca2+ uptake to the presence of a H(+)-countertransporting Ca(2+)-ATPase, pumping Ca2+ into an acidic compartment.

Acid-Base Equilibrium↗

PubMed1992

Episodic weakness associated with exertional lactic acidosis and myopathy in Old English sheepdog littermates.

Two Old English Sheepdog littermates were evaluated for weakness that developed during periods of minimally intense exercise. Lactic acidosis accompanied by increased muscle enzyme activity, an increased lactate/pyruvate ratio, and increased venous PO2 supported the possibility of defective mitochondrial oxygen use. Electromyographic abnormalities included increased insertional activity and complex repetitive discharges. Muscle alterations included scattered myofiber necrosis, abundant endomysial connective tissue, excessive glycogen accumulation, and greater than normal numbers and vacuolation of mitochondria. A distinctive pattern of subsarcolemmal mitochondrial aggregates, referred to as "ragged red fibers" in human mitochondrial myopathies, was observed in muscle biopsy samples from 1 dog. Several features of the disease in these dogs, including onset of weakness during early life, simultaneous disease in littermates, subtle nonprogressive weakness of at least 3 years' duration, and partial reversibility of lactic acidosis following rest were suggestive of an inborn error of metabolism, consistent with mitochondrial myopathy.

Acid-Base Equilibrium↗

PubMed1992

Mechanisms of ion and acid-base regulation at the gills of freshwater fish.

This review examines the branchial mechanisms utilized by freshwater fish to regulate internal acid-base status and presents a model to explain the underlying basis of the compensatory processes. Rainbow trout, Oncorhynchus mykiss, and brown bullhead, Ictalurus nebulosus, were examined under a variety of experimental treatments which induced respiratory and metabolic acid-base disturbances. Acid-base regulation was achieved by appropriate adjustments of Na+ and Cl- net fluxes across the gills which, in turn, were accomplished by variable contributions of three different branchial mechanisms: 1) differential changes in Na+ and Cl- diffusive effluxes, 2) changes in internal substrate (H+, HCO3-) availability, and 3) morphological adjustments to the gill epithelium. Differential diffusive efflux of Na+ over Cl- was involved only during periods of metabolic alkalosis. The importance of internal substrate availability was demonstrated using a two-substrate model. According to the model, ionic flux rates (J(in)Cl-, J(in)Na+) are determined not only by the concentration of the external ion (Na+, Cl-) but also by the concentration of the internal counterion (H+, HCO3-). This system provides for an "automatic negative feedback" to aid in the compensation of metabolic acid-base disturbances. Morphological alteration of the gill epithelia and the associated regulation of chloride cell (CC) fractional area is an essential third mechanism which is especially important during respiratory acid-base disturbances. Specifically, fish vary the availability of the CC associated Cl-/HCO3- exchange mechanism by physical covering/uncovering of CCs by adjacent pavement cells.

Acid-Base Equilibrium↗