Hypotension pathophysiology

Pathophysiology Hypotension associated with hemodialysis manifests as a symptomatic sudden drop of more than 30 mm Hg in mean arterial or systolic pressure or a systolic pressure drop to less than 90 mm Hg during the dialysis session. The primary cause is fluid removal from the bloodstream. Ultrafiltration removes fluid from the plasma, which... 

Pathophysiology Muscle cramps can occur with up to 20% of dialysis sessions.48 The cause is often related to excessive ultrafiltration, which causes hypoperfusion of the muscles. Other contributing factors to the development of muscle cramps include hypotension and electrolyte and acid-base imbalances that occur during hemodialysis sessions. 

Nearly all cells express kinin receptors that mediate the activities of both bradykinin and kallidin. The activation of these G-protein coupled receptors causes relaxation of venular smooth muscle and hypotension, increased vascular permeability, contraction of smooth muscle of the gut and airway leading to increased airway resistance, stimulation of sensory neurons, alteration of ion secretion of epithelial cells, production of nitric oxide, release of cytokines from leukocytes, and the production of eicosanoids from various cell types [11,12]. Because of this broad spectrum of activity, kinins have been implicated as an important mediator in many pathophysiologies including pain, sepsis, asthma, rheumatoid arthritis, pancreatitis, and a wide variety of other inflammatory diseases. Moreover, a recent report demonstrated that bradykinin B2 receptors on the surface of human fibroblasts were upregulated three-fold beyond normal in patients with Alzheimer s disease, implicating bradykinin as a participant in the peripheral inflammatory processes associated with that disease [13]. 

The syndrome of acute hypotension, adult respiratory distress syndrome, non-cardiogenic pulmonary edema, anemia, coagulopathy, and anaphylactic reactions after the administration of dextran 70 is referred to as the dextran syndrome (36-39). Factors other than acute volume overload due to intravascular absorption of dextran are thought to account for the syndrome. A combination of diverse pathophysiological factors may be responsible, namely direct pulmonary toxicity, activation of the coagulation cascade, release of vasoactive mediators, hypotension, pulmonary edema, intravascular intravasation of fluids, dilution of blood, and impaired renal and hepatic clearance. Cases of pulmonary edema are described under the section Respiratory. 

The treatment of restrictive cardiomyopathy is complex becanse of the heterogeneity of the pathophysiologic abnormalities. Dinretics are used for the symptoms of venous congestion in the presence of restrictive cardiomyopathy, but caution is advised because these patients require high filling pressures to maintain an adequate stroke volume and cardiac output. Hypotension and hypoperfusion may occur as a result of the excessive use of diuretics. Because systolic function is often normal, digoxin is of little benefit and may be proarrhyth-... 

GERD may be due to an extremely hypotensive sphincter, and this was the rationale for the use of metoclopramide in the past. But it is now appreciated that this abnormality is rare and that most GERD is probably due to spontaneous but excessively prolonged (30 to 60 seconds) relaxation of the LES. The issue of transient LES relaxation (TLESR) and its role in GERD is an exciting area of pathophysiology and potentially important therapeutic development. 

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