Pulmonary artery catheterization is used to patients with known or suspected pulmonary artery hypertension and for patients with a low cardiac ejection fraction.
Transesophageal echocardiography is a sensitive monitor for the assessment of preload, contractility, ejection fraction, regional wall motion abnormalities, and emboli.
Thromboelastography, if available, may be a useful guide for coagulation management.
Selection of Anesthetic Technique
Neuraxial vs. General Anesthesia (GA). The effect of neuraxial anesthesia on hepatic blood flow appears related to alterations of systemic blood pressure. High (T5) neuraxial blocks appear to reduce hepatic blood flow, and this effect may not be reversed when block-related hypotension is corrected with catecholamines. Thus, avoidance of high neuraxial block and hypotension seems prudent in patients with advance liver disease.
Volatile anesthetics decrease hepatic blood flow to a variable degree. (Isoflurane and sevoflurane have less significant effects on hepatic blood flow than halothane.)
In addition to variable effects on hepatic blood flow, concern exists regarding the production of reactive intermediates during the metabolism of volatile anesthetics.
With the exception of sevoflurane, volatile anesthetics undergo metabolism that yields reactive trifluoroacetylated (TFA) intermediates. These bind to hepatic proteins and produce an immunologic reaction.
The incidence of liver injury correlates with the extent to which inhaled anesthetics undergo oxidative metabolism. Although 20% of halothane and 2.5% of enflurane are metabolized to TFA intermediates, the corresponding percentages for isoflurane and desflurane are 0.2% and 0.02%, respectively.
Because there is no pathognomonic liver pathology, the diagnosis is based on the exclusion of other causes and a history of recent exposure.
In distinction to the other agents, sevoflurane does not produce reactive TFA metabolites or fluoroacetylated liver proteins, suggesting that patients sensitized to other volatile anesthetics could be safely anesthetized with sevoflurane.
Nitrous oxide administration has not been shown to cause hepatocellular injury in the absence of hepatic hypoxemia.
Because of sympathomimetic effects, nitrous oxide can lead to decreased hepatic blood flow, and inhibition of methionine synthase can occur after even brief exposures. (The clinical significance of these effects is unclear.)
Repeated exposure could induce a vitamin B12 deficiency.
Intravenous anesthetics such as propofol, etomidate, and midazolam do not appear to alter hepatic function when given for a short duration during minor procedures.
A rare syndrome of lactic acidosis, lipemia, rhabdomyolysis, hyperkalemia, myocardial failure, and death has been reported after prolonged infusions of propofol.
Liver dysfunction resulting in altered lipid metabolism may predispose to the propofol infusion syndrome, as may genetic defects. Patients on prolonged propofol infusions should be monitored for worsening lactic acidosis and escalating vasopressor requirements.
There is no evidence that opioids have an effect on hepatic function that is independent of hepatic blood flow. All opioids increase sphincter of Oddi pressure.