- Inhaled anesthetic agents cause dose-dependent decreases in mean arterial pressure primarily by decreasing systemic vascular resistance.
- Inhaled anesthetics depress ventilation and can blunt the ventilatory response to hypoxia and hypercapnia.
- Increases in cerebral blood flow and intracranial pressure, with reductions in cerebral metabolic rate, can occur with inhaled anesthetics at 1.0 minimum alveolar concentration (MAC).
- Inhaled anesthetic agents produce muscular relaxation and attenuate neuromuscular blockade. They can also trigger malignant hyperthermia in susceptible patients.
Effects on Organ Systems
- Mean arterial pressure (MAP)
- There is a dose-dependent decrease with all volatile agents due to a decrease in systemic vascular resistance (SVR), and a minimal decrease in cardiac output (CO).1
- Halothane decreases MAP entirely by depressed cardiac output.
- Nitrous oxide has minimal effect on MAPs due to sympathetic stimulation.
- Heart rate (HR)
- Heart rate increases with isoflurane (>0.25 MAC), desflurane (>1.0 MAC), and less effect seen with sevoflurane due to attenuation of the baroreceptor reflex (>1.5 MAC).2
- Rapid increases in inspired concentrations of desflurane and isoflurane can lead to transiently increased HR, MAP, and catecholamine levels.
- Cardiac index (CI)
- Cardiac index is minimally affected by inhaled anesthetics and mild increase in ejection fraction with desflurane.
- Nitrous oxide is a direct myocardial depressant in vitro. However, in vivo, cardiac output, MAP, and HR are unchanged or mildly increased due to sympathetic stimulation.
- Pulmonary vascular resistance (PVR) is increased with nitrous oxide.
- QT interval: inhaled anesthetics can prolong QT interval and should be used carefully in susceptible patients (long QT syndrome).3
- Inhaled anesthetic agents decrease myocardial oxygen consumption and coronary vasodilation (seen more with isoflurane) to improve myocardial oxygenation.
- Inhaled anesthetics have been shown to exert a protective effect on myocardial tissue against ischemic injury.4
- Minute ventilation
- ↑ respiratory rate (RR), ↓ tidal volume (TV) → overall decrease in alveolar ventilation leading to increasing PaCO2 levels.
- Airway reflexes: the pungency of desflurane and isoflurane can irritate the airways and precipitate coughing, laryngospasm, or bronchospasm on induction.
- Bronchial effects: inhaled anesthetics can produce mild bronchodilation at higher concentrations due to beta-2 receptor stimulation.5 This effect is most pronounced with sevoflurane.
- All inhaled anesthetics blunt the ventilatory response to hypoxia and hypercapnia.
- Inhaled anesthetics may attenuate hypoxic pulmonary vasoconstriction.6
- Inhaled anesthetics may depress mucociliary function in the airway.
- Cerebral blood flow (CBF): increased with inhaled anesthetics at 1.0 MAC.
- Intracranial pressure (ICP): increased with inhaled anesthetics above 1.0 MAC.
- Cerebral metabolic rate of oxygen (CMRO2): decreased with isoflurane, sevoflurane, and desflurane. CMRO2 is mildly increased with nitrous oxide.
- Inhaled anesthetics preserve cerebral vasculature response to changes in PaCO2.
- Electroencephalogram (EEG): inhaled anesthetics can produce burst suppression or an isoelectric EEG pattern at more than 2 MAC.
- Evoked potentials: ↓ in amplitude, ↑ latency of all cortical somatosensory evoked potentials with inhaled anesthetics. Motor evoked potentials are significantly depressed.
- Analgesia: some effect with nitrous oxide.
- Inhaled anesthetics produce dose-dependent relaxation of skeletal and smooth muscle by inhibiting nicotinic acetylcholine receptors.
- All inhaled anesthetics potentiate and reduce the required dose of neuromuscular blockers. Nitrous oxide has minimal effect on neuromuscular blockade.
- Desflurane > sevoflurane > isoflurane
- Uterine smooth muscle
- All inhaled anesthetics are potent dose-dependent uterine relaxants.
- Nitrous oxide has minimal effect on uterine musculature.
- Malignant hyperthermia: triggered by all inhaled anesthetics except nitrous oxide.
- Inhaled anesthetics can decrease renal blood flow, glomerular filtration rate, and urinary output.
- Inhaled anesthetics cause a dose-dependent decrease in portal vein flow proportional to cardiac output, while hepatic blood flow and total oxygen delivery are maintained.
- Nitrous oxide: possible decrease in hepatic blood flow, less than inhaled anesthetics.
- Although inhaled anesthetics can cause transient changes in liver function tests, persistent changes and severe immune-mediated liver injury is very rare.
- All inhaled anesthetics increase the risk of postoperative nausea and vomiting.
- Gastrointestinal smooth muscle contraction can contribute to nausea, emesis, and ileus.
- Inhaled anesthetics may decrease intraocular pressure (IOP).
- Nitrous oxide may increase IOP.
- McKay RE. Inhaled Anesthetics. In: Pardo MC, Miller RD. Basics of Anesthesia. Philadelphia, PA 7th ed. Elsevier. 2018: 83-103.
- Malan Jr. PT, DiNardo JA, Isner JR, et al. Cardiovascular effects of sevoflurane compared with those of isoflurane in volunteers. Anesthesiology. 1995;83(5):918-28. PubMed
- Booker PD, Whyte SD, Ladusans EJ. Long QT syndrome and anaesthesia. Br J Anaesth. 2003;90(3):349-366. PubMed
- De Hert SG, Cromheecke S, ten Broecke PW, et al. Effects of propofol, desflurane, and sevoflurane on recovery of myocardial function after coronary surgery in elderly high-risk patients. Anesthesiology. 2003;99(2):314-23. PubMed
- Rooke GA, Choi J-H, Bishop MJ. The effect of isoflurane, halothane, sevoflurane, and thiopental/nitrous oxide on respiratory system resistance after tracheal intubation. Anesthesiology. 1997;86(6):1294-99. PubMed
- 6. Lumb AB, Slinger P. Hypoxic pulmonary vasoconstriction: physiology and anesthetic implications. Anesthesiology. 2015;122(4):932-46. PubMed
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