Both hypoxemia and acidosis stimulate vasopressin release. In cases of prolonged shock, vasopressin is rapidly released and then depleted. This suggests that, especially in early shock states, vasopressin may be a useful adjunct to norepinephrine. Furthermore, vasopressin maintains its potency in the setting of acidosis and hypoxia, while catecholamines may not. Vasopressin may be particularly beneficial in acidotic states as it may inhibit KATP channels more effectively than catecholamines. However, these effects have been observed only in animal models. These rationales have formed the basis for large randomized controlled studies in patients with shock. In general, vasopressin has been shown to be a safe and appropriate alternative to norepinephrine in septic, cardioplegic, and hemorrhagic shock states.
References
- Landry DW, Oliver JA. The ATP-sensitive K+ channel mediates hypotension in endotoxemia and hypoxic lactic acidosis in dog. J Clin Invest 1992; 89: 2071-4. PubMed Link
- Wakatsuki T, Nakaya Y, Inoue I. Vasopressin modulates K(+)-channel activities of cultured smooth muscle cells from porcine coronary artery. Am J Physiol 1992; 263: H491-6. PubMed Link
Other References
- Gkisioti S, Mentzelopoulos SD. Vasogenic shock physiology. Open access emergency medicine : OAEM 2011; 3: 1-6. Link
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