Hemodilution significantly decreases tolerance to isoflurane‐induced cardiovascular depression

Abstract

isoflurane-induced cardiovascular depression had adverse effects on cardiac output and oxygen delivery during extreme hemodilution because: 1) The vasodilatory effect of isoflurane was insufficient to compensate for the myocardial depression, and also contributed to a critically low arterial blood pressure; 2) A decrease in cardiac output produced delivery-dependent oxygen consumption and hyperlactemia; and 3) A decrease in myocardial blood flow caused myocardial ischemia which may have exacerbated the myocardial depression.

Influence of crystalloid and colloid replacement solutions on hemodynamic variables during acute normovolemic hemodilution

“…In contrast, another study by the same group in the identical porcine model demonstrated a progressive decrease in CO and SVR resistance with increasing isoflurane concentrations. 18 This decrease in CO and SVR was greater after hemodilution. At isoflurane concentrations greater than 1%, arterial lactate concentrations also increased.…”

Subcutaneous Po2 as an index of the physiological limits for hemodilution in the rat

“…Isoflurane, an anesthetic agent known to promote vasodilatation, causes a depression of CO and Q O 2 and an earlier fall in MAP during extreme hemodilution (49). Increased depth of anesthesia, with halothane or ketamine, also reduces the tolerance for hemodilution in rats (62).…”

Anesthetic management of a patient with β-thalassemia intermedia undergoing splenectomy: a case report

“…Hence, the CI and cardiac output were measured using the Swan-Ganz catheter. Anesthesia was maintained with balanced anesthesia using isoflurane at a low concentration and fentanyl to avoid cardiovascular depression, because with severe anemia tolerance to volatile anesthetic-induced cardiovascular depression might be limited [11][12][13]. In other words, balanced anesthesia with a volatile anesthetic at low concentrations and fentanyl, which is known to decrease the minimum alveolar concentration of volatile anesthetics [14], may help stabilize hemodynamic parameters by minimizing noxious sympathetic responses during surgery [15] and by avoiding a decrease in the cardiac output induced by a high concentration of volatile anesthetic.…”