Volatile Anesthetics: Comprehensive Study Guide
Volatile Anesthetics: Comprehensive Study Guide
Lecture Objectives
Describe the pharmacokinetics and systemic effects of volatile anesthetics.
Explain the uptake and distribution of volatile anesthetics.
Define MAC (minimum alveolar concentration) and identify factors that can modify MAC.
Describe the effects of anesthetic agents on respiratory, cardiovascular, renal, hepatic, and cerebral physiology.
Introduction
Volatile anesthetics exert their action by interacting with receptors in the body.
Agents discussed include:
Nitrous oxide
Sevoflurane
Desflurane
Isoflurane
Halothane (discussed despite it being outdated due to historical relevance)
These agents produce reversible depression in the central nervous system (CNS).
A thorough understanding of inhalational anesthetic pharmacokinetics is essential for safe practice.
History of Volatile Anesthetics
Halothane:
Synthesized in 1951 and introduced in 1956.
Had various drawbacks that led to the search for new anesthetics.
Methoxyflurane:
Introduced in 1960; problematic due to renal toxicity and prolonged recovery times.
Highly lipid soluble with extensive hepatic metabolism leading to nephrotoxicity.
Enflurane:
Methyl ethyl derivative introduced in 1973; less ideal due to CNS stimulation.
Isoflurane:
Introduced in 1981; resistant to metabolism and still used today.
Desflurane:
Introduced in 1992; fully fluorinated, has a high vapor pressure requiring a heated vaporizer.
Sevoflurane:
Introduced in 1994; background information on its properties.
Physiochemical Properties of Volatile Anesthetics
Basic Characteristic Comparisons
All modern volatile anesthetics are ethers except halothane.
Vapor Pressure: Proportional to temperature; higher vapor pressure means faster onset.
Partial Pressure: Defined as the pressure exerted by a single gas in a mix; depth of anesthesia relates to the partial pressure of the agent in the brain, not volume percent.
Identification of Volatile Anesthetics
Isoflurane: 5 fluorine atoms, 1 chlorine atom; potency is increased by chlorine.
Desflurane: 6 fluorine atoms; fully fluorinated, increased MAC due to decreased potency, also requires a heated vaporizer.
Sevoflurane: Heavily fluorinated with no chlorine; roughly three times more potent than desflurane.
Halothane: Only volatile with bromine, associated with liver toxicity risks.
Considerations in Use
Modern volatiles' low blood solubility allows rapid induction and recovery, though costs must be managed by using low fresh gas flow rates.
Low fresh gas flow rates minimize anesthetic loss and reduce overall consumption.
Pharmacokinetics of Volatile Anesthetics
Absorption: Influenced by:
Ventilation rates
Cardiac output
Anesthetic blood solubility
Alveolar Uptake::
Dependent on the uptake from alveoli into pulmonary blood and distribution throughout the body.
Distinct absorption between volatile gases and liquids at atmospheric pressure and room temperature.
Blood-Gas Solubility Coefficients
Indicator of anesthetic speed:
Isoflurane: 1.4
Desflurane: 0.42 (more rapid induction).
Higher coefficients = slower onset, lower = quicker effects.
Minimum Alveolar Concentration (MAC)
Definition of MAC: Minimum alveolar concentration resulting in a 50% movement response to surgical stimulation.
Factors affecting MAC include:
Age (decreases with increased age)
Hair color (redheads require higher dosages)
Co-morbidities like hyponatremia and chronic alcohol use.
Variations of MAC:
MAC Awake: 0.4-0.5 MAC (consciousness)
MAC-bar: Concentration needed to block autonomic responses (approximately 1.5 MAC).
Physiological Effects of Volatile Anesthetics
Respiratory System
Depressants leading to:
Decreased tidal volume
Increased respiratory rate, leading to reduced minute ventilation.
Bronchodilation occurs except for nitrous oxide.
Cardiovascular System
Volatile anesthetics generally cause:
Dose-dependent decrease in systemic vascular resistance (SVR)
Reductions in blood pressure in varying degrees based on the specific agent used.
Desflurane and Isoflurane: Slight increases in HR due to sympathetic activation.
Halothane: Known for myocardial sensitization to catecholamines.
CNS Effects
Decrease cerebral metabolic rate of oxygen consumption (CMR o2).
Increase cerebral blood flow and intracranial pressure if exceeding 1 MAC dosage.
Nitrous oxide: Opposite effects on CMR o2, leading to potential contraindications in neurosurgery.
Renal Effects
Associated reductions in renal blood flow and glomerular filtration rates, largely dependent on systemic blood pressure.
Preoperative hydration may attenuate these effects.
Hepatic Effects
Similar risk concerns across agents; halothane notably associated with hepatitis and significant liver dysfunction in susceptible individuals.
Conclusion
Usage of modern volatile anesthetics has advanced significantly.
Overall, understanding pharmacodynamics, especially regarding the factors affecting induction and recovery, is key for safe and effective anesthetic practices.
Special considerations regarding patient demographics, conditions, and usage of adjuncts can play critical roles in anesthesia management.