Pathophysiology of anaphylactic shock

The effects of histamine are shown in TabieJ. The presence of bronchospasm does not appear to be related to blood levels.

ididltart lc-rtt ikn^ tt rjchvevta <3

ficiKiud ¡¡uiTri: uciAtoii cj

hHi r'L»-' i-fry* * > . iWJ >->: Lfvj (w^ ,

Table 1 Plasma histamine levels and symptoms in humans

Equivalent histamine plasma levels have been noted without cardiovascular effects. The state of and quantity of receptors may be important in these responses, and recent work shows that subpopulations of mast cells react differently to different stimuli in terms of histamine release, suggesting that significant reactions may occur without elevating plasma histamine.

There appears to be no correlation between a drug's ability to release histamine and its ability to cause severe reactions. For example, morphine is a potent histamine releaser but a rare cause of anaphylaxis, whereas penicillin does not release histamine yet causes anaphylaxis.

The role of histamine in the cardiovascular system is complex. Histamine receptors include H -,, H2, and H3 receptors. Owing to the large mast cell population in the perivascular spaces and around the heart, histamine may have an unknown physiological role as part of host defense mechanisms. Histamine can also produce either vasoconstriction or vasodilation depending on the state of the endothelium. IgE-mediated hypersensitivity in human cardiac muscle in vitro produces increases in inotropic and chronotropic effects. The difficulty with the extrapolation of in vitro data to the human heart is the complex interaction of the response to anaphylactic mediators, the sympathetic adrenal response, and the secondary effects of hypoxia and acidosis.

The majority of observations in humans with normal hearts undergoing anaphylactic reactions show that hypotension and reduced cardiac output are primarily related to plasma volume loss and vasodilation, although persistent ventricular dysfunction can occur particularly with pre-existing coronary artery disease.

Observations in non-b-blocked humans with anaphylaxis show reduced left venticular filling pressure and decreased preload and afterload, with no evidence of cardiac dysfunction.

Le.vy.eL§i (19.89). reported anaphylaxis to protamine as part of two studies evaluating the incidence of reactions during cardiac surgery. In an IgE-mediated reaction, profound vasodilation and decreased systemic vascular resistance were found without increases in pulmonary artery pressure. Another reaction was characterized by acute pulmonary vasoconstriction, right ventricular dysfunction, and systemic hypotension.

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