Anesthesia Student Survival Guide.pdf - Index of

62 ● AnesthesiA student survivAl Guide
within the alveoli. This, in turn, leads to an increase in the uptake of the second
agent, which enters the alveoli more readily in response to the partial vacuum
created by rapid absorption of nitrous oxide.
Volatile Anesthetics (Isoflurane, Sevoflurane,
and Desflurane)
The volatile anesthetic agents used in current anesthetic practice share many
similar characteristics and side effects:
● Cardiovascular effects: The volatile anesthetics depress myocardial
contractility and cause peripheral vasodilation (the various agents differ
somewhat in the balance of these two effects). The effect on heart rate is
variable. Arterial blood pressure is decreased in a dose-dependent fashion.
● Respiratory effects: Tidal volume is decreased by the volatile anesthetics.
Respiratory rate increases slightly or remains stable, leading to decreased
minute ventilation. The responses to hypercapnia are blunted (i.e. an
anesthetized patient will increase minute ventilation in response to
hypercapnia less than an awake patient and will remain apneic at a higher
PCO 2 than an awake patient). As with nitrous oxide, hypoxic ventilatory drive
is markedly diminished. Volatile anesthetics also produce bronchodilation.
● Cerebral effects: The volatile anesthetics reduce cerebral oxygen
consumption. At doses above 1 MAC, cerebral blood flow and consequently
intracranial pressure are increased. Hyperventilation reverses the cerebral
vasodilation seen with these agents.
● Musculoskeletal effects: The effects of neuromuscular blockers are
potentiated by volatile anesthetics.
● Obstetric effects: The volatile anesthetics produce a dose-dependent
reduction in uterine smooth muscle contractility.
● Renal and hepatic blood flow: All agents decrease renal blood flow,
glomerular filtration rate, and urinary output. They also decrease hepatic
blood flow.
● Nausea and vomiting: The volatile anesthetic agents are known to cause
postoperative nausea and vomiting.
● Malignant hyperthermia: The volatile anesthetic agents are triggers for
malignant hyperthermia (note: nitrous oxide is not a triggering agent).
● Cardiac preconditioning: Exposure of cardiac tissue to volatile anesthetics
may be protective against the effects of subsequent ischemia and reperfusion.