Monitoring and management of perioperative problems (Proceedings)
All commercially available sedatives and anesthetics are safe when properly administered to normal animals. Physiologically compromised patients, however, are predisposed to complications, and the risks are increased when the pharmacodynamic effects of the anesthetic conflict with the physiologic compromise of the patient. Although there are no absolute contra-indications to any specific anesthetic drug, it is preferable to implement an anesthetic plan which best complements the physiologic compromise of the patient.
The organ systems about which we are most concerned in the critically ill patient are the cardiovascular, respiratory, central nervous system, and visceral. Pre-existing dehydration or hypovolemia, anesthesia-induced vasodilation, or intra-operative blood loss or plasma exudation may contribute to perioperative hypovolemia. Myocardial contractility can be reduced by pre-existing myocardial disease and many anesthetic drugs. Stroke volume can be decreased by incompetent atrioventricular valves, stenotic outflow valves, and by ventricular arrhythmias. Excessive bradycardia can be caused by anesthetic drugs or high vagal tone, and can diminish cardiac output. Excessive hypotension diminishes cerebral and coronary perfusion. Excessive vasodilation causes hypotension; excessive vasoconstriction reduces visceral organ perfusion. Anemia diminishes oxygen content and oxygen delivery; hypoxemia diminishes the partial pressure gradients between the plasma and the mitochondria.
Cardiovascular evaluation always begins with an evaluation of venous return and preload pressure; adequate diastolic filling is a prerequisite to an adequate stroke volume. The most common cause of poor venous return is hypovolemia. Once the heart is properly filled, it must then contract with sufficient force to create a useful stroke volume. Most anesthetic drugs are generally considered to decrease preload and afterload independent myocardial contractility. The inhalational anesthetics, as a class group of drugs appear to be more depressant than are the injectables, at all dosages. Of the inhalants, the least depressant appears to be desflurane followed by sevoflurane and isoflurane followed by halothane; enflurane appears to be the most depressant. Of the injectable anestheics, propofol is notably depressant while the barbiturates, opioids, etomidate, and ketamine have minimal effects but could decrease myocardial contractility at high dosages or at normal dosages in patients with debilitated hearts.Alterations in heart rate would cause a linear change in cardiac output if stroke volume remained unchanged. Stroke volume, however, increases at slower heart rates and vice versa which offsets heart rate-induced changes in cardiac output or oxygen delivery. Animals also compensate for bradycardia-induced decreases in cardiac output with systemic vasoconstriction so as to maintain arterial blood pressure. The administration of atropine increases heart rate in bradycardic patients and increases arterial blood pressure, cardiac index, oxygen delivery, and venous partial pressure of oxygen (PvO2) from a low to a high normal value, and decreases systemic vascular resistance and oxygen extraction. Heart rate is decreased by anesthetic dosages of alpha2-agonists (xylazine, metdetomidine, and romifidine) in a dose-related manner and opioids. Benzodiazepines and phenothizines generally minimally increase heart rate although if the benzodiazepine or opioid cause CNS excitation, the heart rate will increase. The cyclohexanones and inhalational anesthetics generally increase heart rate. The barbiturates, etomidate and propofol generally increase heart rate slightly. Tachycardia can impair stroke volume by limiting the amount of time available for diastolic filling and ventricular arrhythmias can impair stroke volume by causing an uncoordinated myocardial contraction.
Cardiac output is the product of preload, contractility, and heart rate, and is an important systemic forward flow parameter. Cardiac output is generally decreased by the alpha2-agonists in a dose-related manner. Benzodiazepines and phenothiazines generally have minimal, but variable, effects on cardiac output. Anesthetic dosages of opioids appear to decrease cardiac output. The cyclohexanones generally increase cardiac output although very high dosages can decrease cardiac output. Cardiac output is generally well maintained during inhalational anesthesia, although there is a gradual decrease with increasing dosages. The barbiturates and propofol are generally associated with a decrease in cardiac output.
Arterial blood pressure is primarily determined by the balance between cardiac output and systemic vascular resistance with the latter being the most potent determinant. Blood pressure is important to cerebral and coronary perfusion. The alpha2-agonists typically, initially increase blood pressure in a dose-related manner, and subsequently decrease blood pressure. Benzodiazepines generally have minimal effects on blood pressure although if the benzodiazepine causes CNS excitation, blood pressure may increase. Phenothiazines tend to decrease arterial blood pressure. Anesthetic dosages of opioids have variable effects; oxymorphone was associated with an increase, morphine with no change after a transient decrease. The cyclohexanones are generally associated with an increase in arterial blood pressure, although large dosages may cause a decrease. The barbiturates are generally associated with an increased arterial blood pressure (after a very transient initial decrease). Etomidate may be associated with no change to a slight increase while propofol usually causes a significant decrease in arterial blood pressure. The inhalational anesthetics are associated with a dose-dependent decrease in arterial blood pressure.