Why the study?
Cardiac output determines the speed and intensity of infused anesthetic drugs, but the effects of changes in cardiac output on the pharmacokinetics and pharmacodynamics of general anesthetics require clarification across all phases of anesthesia.
How do changes in cardiac output affect the pharmacokinetics and pharmacodynamics of general anesthetics?
How do changes in cardiac output affect the pharmacokinetics and pharmacodynamics of general anesthetics?
Understanding the impact of cardiac output on anesthetic pharmacology is crucial for anesthesiologists to optimize dosing and prevent complications like intraoperative awakening.
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Cardiac output variations warrant dosing adjustments at induction; extends PK/PD models but leaves clinical adoption hypothesis-generating.
The relationship between cardiac output and anesthetic drugs is important to anesthesiologists, since cardiac output determines the speed with which a drug infused into the bloodstream reaches its target and the intensity of the drug’s effect. But rather than focus on how anesthetic drugs affect cardiac output, this narrative review focuses on how changes in cardiac output affect the pharmacokinetics and pharmacodynamics of general anesthetics during the three phases of anesthesia. At induction, an increase in cardiac output shortens both the onset time of propofol for hypnosis and the neuromuscular blocking effect of rapid-acting neuromuscular blockers, favoring the conditions for rapid sequence intubation. During maintenance, changes in cardiac output are followed by opposite changes in the drug plasma concentration of anesthetic drugs. Thus, an increase in cardiac output followed by a decrease in the plasma concentration of the anesthetic could expose the patient to a real risk of intraoperative awakening, which can be avoided by increasing the dose of hypnotic drugs. At emergence, an increase in cardiac output secondary to an increase in pCO2 allows for a more rapid recovery from anesthesia. The pCO2 can be increased by adding CO2 to the respiratory circuit, lowering the ventilatory rate, or placing the patient on partial rebreathing. Finally, the reversal action of sugammadex for rocuronium-induced neuromuscular block can be shortened by increasing the cardiac output.
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Simón-Polo et al. (2023) studied this question.
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