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Anaesthesiology
Inhaled Anesthetics
Built from Barash Clinical Anesthesia, 9th Edition
What’s inside
14 sections · 199 slides
Overview
- Scope of this topic
- Why inhaled agents remain popular
- Agent selection in practice
Pharmacokinetic principles
- Pharmacodynamics and pharmacokinetics
- Compartments and redistribution
- Speed, gas state, and route of administration
- Equilibration of anesthetic partial pressures
- Chemical structures of the inhaled anesthetics
- Structure and its consequences
- Vapor pressure and boiling point
- Physiochemical properties of the volatile anesthetics
- Key numbers from the properties table
- Dalton's law and partial pressure
- Solubility and Henry's law
- Partial pressure in solution
- Why end-tidal concentration reflects brain level
- Anesthetic transfer from machine to brain
- Dilution steps between machine and alveolus
- The three physiologic tissue groups
- Tissues of desired and undesired effect
- Distribution of cardiac output by tissue group
- Reading the tissue-group table
Uptake and distribution
- The FA/FI ratio
- Rate of rise of alveolar concentration
- Rise of the inspired fraction in the circuit
- Methods to speed the rise in inspired fraction
- Rise in alveolar fraction without uptake
- Why children induce faster
- Uptake into blood and its time constant
- Solubility worked example: halothane versus desflurane
- Determinants of blood uptake
- Factors that change the rate of rise of alveolar concentration
- Tissue uptake and the shape of the curve
- Muscle uptake
- Fat uptake and its effect on emergence
- Nitrous oxide as a distribution exception
- Overpressurization
- The concentration effect
- Augmented gas inflow
- Mechanism of the concentration effect
- The second gas effect
- Ventilation effects on uptake
- Cardiac output effects on uptake
- Effect of intrapulmonary shunt on alveolar and arterial partial pressures
- Ventilation-perfusion mismatching
- Effect of solubility on shunt
Elimination and recovery
- Percutaneous and visceral loss
- Intertissue diffusion
- Washout of anesthetic after discontinuation
- Determinants of recovery
- Two differences between recovery and induction
- Continued tissue uptake after discontinuation
- Extent of washout needed for emergence
- Recovery time and duration of anesthesia
- Diffusion hypoxia
The individual agents
- Isoflurane
- Desflurane: physicochemistry
- Desflurane: clinical profile
- Sevoflurane
- Sevoflurane metabolism and degradation
- Comparing desflurane and sevoflurane
- Xenon
- Limits and promise of xenon
- Nitrous oxide: basic properties
- Nitrous oxide: four areas of controversy
- Expansion of closed gas spaces
- Practical consequences of gas-space expansion
Minimum alveolar concentration
- Definition of minimum alveolar concentration
- Clinical use of MAC multiples
- Evidence for the awareness threshold
- Cerebral metabolic rate against end-tidal isoflurane concentration
- Variants of MAC
- Additivity of MAC values
- Factors that increase minimum alveolar concentration
- Reading the factors that raise MAC
- Factors that decrease minimum alveolar concentration
- Factors that decrease minimum alveolar concentration (continued)
- Factors that decrease minimum alveolar concentration (continued)
- Themes among the factors that lower MAC
- Factors that do not alter MAC
- Genetic influences on MAC
- Effect of age on minimum alveolar concentration
Effects on the brain
- Overview of neurophysiologic effects
- Cerebral metabolic rate and the electroencephalogram
- A property unique to desflurane
- Sevoflurane and epileptiform activity
- Cerebral blood flow
- Cerebral blood flow during halothane and isoflurane anesthesia
- Flow-metabolism uncoupling
- Cerebral autoregulation
- Intracranial pressure
- Agent choice in neurosurgery
- Carbon dioxide vasoreactivity
- Cerebral protection
- Postoperative cognitive dysfunction
- Evidence against a causal role
- Effects on the processed electroencephalogram
- Effects on evoked potentials
- Nitrous oxide and cerebral physiology
The circulatory system
- Blood pressure and vascular resistance
- Heart rate and blood pressure during volatile anesthesia
- Heart rate effects
- Cardiac index, filling pressure and vascular resistance
- Myocardial contractility
- Diastolic function
- Spontaneous versus controlled ventilation
- Cardiovascular effects of nitrous oxide
- Oxygen consumption and regional blood flow
- Epinephrine dose needed to provoke arrhythmia
- Effects on conduction and repolarization
- Corrected QT interval in children given sevoflurane or desflurane
- Comparative QT data
- Coronary steal
- Evidence against clinically important steal
- Anesthetic preconditioning
- Mechanism of cardioprotection
- Clinical evidence on cardioprotection
- Baroreflex control of the circulation
- Sympathetic nerve activity during sevoflurane and desflurane
- Sympathetic activation by desflurane
- Stress hormone response to a rapid rise in anesthetic concentration
- The neuroendocrine surge and how to blunt it
The pulmonary system
- General ventilatory effects
- Resting carbon dioxide, tidal volume, rate and minute ventilation
- Nitrous oxide and ventilation
- Ventilatory mechanics under anesthesia
- Loaded expiration under anesthesia
- Ventilatory response to carbon dioxide
- Clinical relevance of the apneic threshold
- Ventilatory response to hypoxia at subanesthetic concentrations
- Depression of the hypoxic ventilatory response
- Causes of bronchoconstriction under anesthesia
- Bronchodilation by volatile anesthetics
- Airway resistance after desflurane and sevoflurane
- Mucociliary function
- Hypoxic pulmonary vasoconstriction
- One-lung ventilation as a clinical test
Liver, muscle, and uterus
- Hepatic effects
- Neuromuscular effects
- Malignant hyperthermia
- Uterine tone
- Managing uterine tone at caesarean section
- Occupational exposure and genotoxicity
- Teratogenicity and nitrous oxide
- Spontaneous abortion in theatre personnel
- Neonatal effects after caesarean section
- Anesthetic neurotoxicity in the developing brain
- Human evidence on developmental neurotoxicity
Degradation, metabolism, and the environment
- Formation of compound A
- Renal safety of compound A
- Carbon monoxide from desiccated absorbent
- Determinants of carbon monoxide formation
- Reported poisoning and the heat hazard
- Compound A production with different absorbents
- Fluoride-induced nephrotoxicity
- Why sevoflurane escapes fluoride toxicity
- Global warming potential of the volatile agents
- Environmental cost of volatile anesthetics
- Driving equivalents of one MAC-hour
- Strategies to lessen the environmental impact of potent volatile anesthetics
- Applying the sustainability checklist
Clinical utility
- Indications for inhalation induction
- Technique and timings for sevoflurane induction
- Sevoflurane for the difficult adult airway
- Advantages for maintenance of anesthesia
- Drawbacks of volatile maintenance
- Choosing between the three agents
Key points
- Key points: pharmacokinetics
- Key points: dose and the brain
- Key points: organ systems
- Key points: safety and environment
References
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- References (continued)
- Barash, Cullen, and Stoelting's Clinical Anesthesia, 9th Edition