Document Detail


Pathophysiology of dialysis hypotension: an update.
MedLine Citation:
PMID:  11602456     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Dialysis hypotension occurs because a large volume of blood water and solutes are removed over a short period of time, overwhelming normal compensatory mechanisms, including plasma refilling and reduction of venous capacity, due to reduction of pressure transmission to veins. In some patients, seemingly paradoxical and inappropriate reduction of sympathetic tone may occur, causing reduction of arteriolar resistance, increased transmission of pressure to veins, and corresponding increase in venous capacity. Increased sequestration of blood in veins under conditions of hypovolemia reduces cardiac filling, cardiac output, and, ultimately, blood pressure. Adenosine release due to tissue ischemia may participate in reducing norepinephrine release locally, and activation of the Bezold-Jarisch reflex, perhaps in patients with certain but as yet undefined cardiac pathology, may be responsible for sudden dialysis hypotension. Patients with diastolic dysfunction may be more sensitive to the effects of reduced cardiac filling. The ultimate solution is reducing the ultrafiltration rate by use of longer dialysis sessions, more frequent dialysis, or reduction in salt intake. Increasing dialysis solution sodium chloride levels helps maintain blood volume and refilling but ultimately increases thirst and interdialytic weight gain, with a possible adverse effect on hypertension. Blood volume monitoring with ultrafiltration or dialysis solution sodium feedback loops are promising new strategies. Maintaining tissue oxygenation via an adequate blood hemoglobin level seems to be important. Use of adenosine antagonists remains experimental. Given the importance of sympathetic withdrawal, the use of pharmacologic sympathetic agonists is theoretically an attractive therapeutic strategy.
Authors:
J T Daugirdas
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  American journal of kidney diseases : the official journal of the National Kidney Foundation     Volume:  38     ISSN:  1523-6838     ISO Abbreviation:  Am. J. Kidney Dis.     Publication Date:  2001 Oct 
Date Detail:
Created Date:  2001-10-16     Completed Date:  2001-10-25     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  8110075     Medline TA:  Am J Kidney Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  S11-7     Citation Subset:  IM    
Affiliation:
University of Illinois at Chicago, VA Chicago Hospital-West Side, Chicago, IL 60612, USA. jtdaugir@uic.edu
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MeSH Terms
Descriptor/Qualifier:
Arterioles / physiology
Blood Volume
Cardiac Output / physiology
Heart Rate / physiology
Humans
Hypotension / etiology,  physiopathology*,  prevention & control
Kidney / physiopathology
Kidney Failure, Chronic / physiopathology,  therapy*
Renal Dialysis / adverse effects*
Splanchnic Circulation
Vascular Resistance

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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