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The effect of cardiac output on the pharmacokinetics and pharmacodynamics of propofol during closed-loop induction of anesthesia.

07:00 EST 19th February 2020 | BioPortfolio

Summary of "The effect of cardiac output on the pharmacokinetics and pharmacodynamics of propofol during closed-loop induction of anesthesia."

Intraoperative hemodynamic stability is essential to safety and post-operative well-being of patients and should be optimized in closed-loop control of anesthesia. Cardiovascular changes inducing variations in pharmacokinetics may require dose modification. Rigorous investigational tools can strengthen current knowledge of the anesthesiologists and support clinical practice. We quantify the cardiovascular response of high-risk patients to closed-loop anesthesia and propose a new application of physiologically-based pharmacokinetic-pharmacodynamic (PBPK-PD) simulations to examine the effect of hemodynamic changes on the depth of hypnosis (DoH).

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This article was published in the following journal.

Name: Computer methods and programs in biomedicine
ISSN: 1872-7565
Pages: 105406

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Medical and Biotech [MESH] Definitions

A state of elevated cardiac output due to conditions of either increased hemodynamic demand or reduced cardiac oxygen output. These conditions may include ANEMIA; ARTERIOVENOUS FISTULA; THYROTOXICOSIS; PREGNANCY; EXERCISE; FEVER; and ANOXIA. In time, compensatory changes of the heart can lead to pathological form of high cardiac output and eventual HEART FAILURE.

A state of subnormal or depressed cardiac output at rest or during stress. It is a characteristic of CARDIOVASCULAR DISEASES, including congenital, valvular, rheumatic, hypertensive, coronary, and cardiomyopathic. The serious form of low cardiac output is characterized by marked reduction in STROKE VOLUME, and systemic vasoconstriction resulting in cold, pale, and sometimes cyanotic extremities.

Rare and often fatal drug complication which affects patients undergoing long-term treatment with high doses of PROPOFOL. It is characterized by METABOLIC ACIDOSIS; HYPERLIPIDEMIA; RHABDOMYOLYSIS; cardiovascular CIRCULATORY COLLAPSE; CARDIAC FAILURE; and KIDNEY FAILURE.

Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE).

Naturally occurring genetic variations associated with drug response (e.g., dosage, extent and rate of metabolic processes). While these variants are not markers for GENETIC PREDISPOSITION TO DISEASE they influence PHARMACOKINETICS and pharmacodynamics and often occur on genes encoding drug metabolism enzymes and transporters (e.g., ANGIOTENSIN CONVERTING ENZYME; CYTOCHROME P-450 CYP2D6).

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