Anesthetic Emergencies And Disaster Prevention
William W. Muir, III, DVM, PhD, DACVECC, DACVA
One of the most alarming if not frustrating and often times disappointing challenges the veterinary surgeon must be prepared to respond to is the anesthetic related emergency. All to often drugs used to produce chemical restraint or anesthesia cause the development of untoward side effects some of which are potentially life threatening. The most common life threatening emergencies associated with small animal anesthesia and surgery are (in order of occurrence) hypoventilation and apnea, sinus bradycardia with or without hypotension, hypotension and cardiac arrhythmias. Hypovolemia either prior to or during surgery (hemorrhage) can become life threatening if it leads to low cardiac output and hypotension but is generally easily recognized prior to (dehydration, tachycardia, weakness, etc.) or during (blood loss) anesthesia and surgery.
Hypoventilation and Apnea:
Apnea is easily recognized by the absence of breathing and is relatively common following the acute bolus administration of an intravenous anesthetic drug. Its occurrence during or after surgery however may be more difficult to detect particularly if the patient is totally covered with surgical drapes or warming blankets, patient monitoring is infrequent or a respiratory is not used. Regardless of whether or not frequent patient monitoring is practiced or a respiratory monitor is used hypoventilation can occur and depending upon its duration can produce the same effects as apnea (just not as fast). Hypoventilation is an insidious and technically difficult problem because most veterinarians and veterinary technicians assume that an adequate respiratory rate and respiratory efforts equate with adequate alveolar ventilation. It must be remembered that the amount of gas exchanges with each breath (tidal volume; VT) is composed of two components: dead space gas (VD) and alveolar ventilation (VA) such that VT=VD+VA. The most important point in understanding this relationship is that VD is relatively constant and is always the first gas to be exchanged since it represents the movement of gas in and out of the mouth or nasal passages, trachea and other conducting (non gas exchanging units) of the respiratory tree. Said another way if VT decreases and VD cannot change then VA must decrease leading to the development of hypoxia and hypercarbia.
The treatment of apnea or hypoventilation regardless of cause is to control, assist or in some way support ventilation. Ventilator support is relatively easily accomplished in anesthetized patients following orotracheal intubation by connecting the patient to an anesthetic machine and inflating the rebreathing bag, connecting the patient to a ventilatory assist device (respirator) or connecting the patient to a self inflating (Ambu) bag connected to an oxygen supply source. Whether breathing is assisted (VT controlled) or controlled (both VT and respiratory rate controlled) normal respiratory rate should be between 8-12 breaths/min and VT between 12-15 ml/kg for most small animal patients. The single or multiple bolus administration of respiratory stimulants (ex. doxapram; Dopram-V) are not indicated for most anesthetic related causes of apnea and/or hypoventilation because they frequently produce a transient period of hyperventilation causing hypocarbia (remember CO2 is the major drive to ventilation) and another period of apnea or hypoventilation and must be given by constant rate infusion to be truly effective. Suffice it to say that the administration of doxapram during the post anesthetic/surgery recovery period may produce a false sense of security if the patient begins to breathe more frequently or deeply. This is usually followed however by a longer period of hypoventilation and/or apnea.
Bradyarrhythmias make themselves apparent in several different forms during anesthesia and surgery. Sinus bradycardia is easily the most common cardiac arrhythmia encountered during anesthesia and may produce important hemodynamic effects. Heart rate (HR) is important in maintaining both an adequate blood flow (cardiac output; Q) to peripheral tissues and an adequate arterial blood pressure (ABP) in order to maintain tissue perfusion. The importance of heart rate in maintaining normal hemodynamics is emphasized by knowing that Q=SV x HR where SV is the amount of blood pumped (stroke volume) by the heart during each contraction. Furthermore, ABP=Q x PVR where PVR is peripheral vascular resistance. Therefore, ABP = (SV x HR) x PVR. In practical terms the maintenance of normal heart rate is important for the maintenance of both cardiac output and arterial blood pressure. Decreases in heart rate decrease both cardiac output and arterial blood pressure. The important question during anesthesia is what is an acceptable lower heart rate? The answer to this question varies depending on many factors including the patientís age, medical history and current health status, but whatever the value selected, it is usually higher than if the patient were not receiving anesthetic drugs. The reason for this is that anesthetic drugs not only depress heart rate, but also decrease venous return (preload) and cardiac contractile force, two other very important determinants of cardiac output. Lower acceptable heart rates for normal anesthetized dogs and cats are 60-70 and 80-90, respectively. Heart rates lower than these values are usually associated with decreases in cardiac output or hypotension in anesthetized patients.
The decision to treat sinus bradycardia during anesthesia is not always straightforward. The obvious first response to the treatment of sinus bradycardia is to administer an anticholinergic drug (atropine, glycopyrrolate). Anticholinergic drugs are very effective for treating sinus bradycardia or other cardiac bradyarrhythmias caused by increases in parasympathetic (vagal) tone, but are less effective and often ineffective in treating bradyarrhythmias caused by anesthetic drugs or circulating toxins. Furthermore, the use of anticholinergics for the treatment of cardiac bradyarrhythmias is not without consequence. Anticholinergics can produce sinus tachycardia and other cardiac tachyarrhythmias. Although the latter are relatively rare, increases in heart rate above normal values increases myocardial work and myocardial oxygen consumption, which predisposes to myocardial ischemia and can lead to heart failure in patients with compromised cardiovascular function. Drugs which are noted for their ability to increase parasympathetic tone and their ability to produce sinus bradycardia and other bradyarrhythmias include the opioids (morphine, oxymorphone, fentanyl), alpha-2 agonists (xylazine, detomidine, medetomidine) and occasionally the phenothiazine tranquilizer, acepromazine. Bradyarrhythmias produced by any of these drugs almost always respond favorably to anticholinergic therapy. Sinus bradycardia and other bradyarrhythmias caused by inadvertent anesthetic overdose or an adverse response to anesthetic drugs almost never or only partially respond to the administration of anticholinergic drugs. The reason for this should be obvious in that increases in parasympathetic tone plays very little or no role in producing the bradyarrhythmia and that the real problem is direct drug induced depression of cardiac automatic or conduction (in the case of 1st, 2nd or 3rd degree heart block) properties. It should be noted that direct drug induced depression of heart rate is generally associated with myocardial depression resulting in decreases in cardiac output and arterial blood pressure.
Anesthetic drug (intravenous or inhalation) induced decreases in heart rate that are not caused by increases in parasympathetic tone or are associated with low cardiac output and/or hypotension are best treated with catecholamines. Dopamine is a positive chronotrope and inotrope that can be administered to treat bradyarrhythmias and hypotension in dogs or cats. Although bolus dosages can be given, the drug is usually administered by infusion (1-5 mg/kg/min) in order to maintain drug effects. If bradycardia (>50% reduction from normal heart rate) or hypotension become life threatening epinephrine should be administered (0.01 mg/kg). Although epinephrine is potentially arrhythmogenic, especially in the presence of some inhalation anesthetics (halothane, methoxyflurane), it is the best first choice for the emergency treatment of life threatening bradyarrhythmias or hypotension. If cardiac arrhythmias are caused by epinephrine, lidocaine (2 mg/kg dogs; 0.5 mg/kg cats) is the drug of choice.
Hypotension without sinus bradycardia or other cardiac arrhythmias oftentimes goes undetected during anesthesia unless direct or indirect blood pressure monitoring devices are being used. Although palpation of a peripheral pulse indicates the presence of a heart beat, it is frequently misleading as an estimate of arterial blood pressure, particularly when arterial blood pressure is low. The question that is often asked in this situation is: When is a weak peripheral pulse too weak to provide adequate perfusion of the tissues? The best answer to this question in quantitative terms is whenever the mean arterial blood pressure is below 60 mmHg. This answer, however, implies the ability to accurately assess arterial blood pressure using direct (arterial catheterization) or indirect (doppler, oscillometric) methods. The best answer to this question when quantitative methods for measuring arterial blood pressure are not available is whenever a weak peripheral pulse leads to poor capillary refill time (>2 sec) pale pink, white, gray or blue mucous membranes.
The major factors which govern the treatment of hypotension during anesthesia are anesthetic depth, blood loss, PCV, TP, heart rate and cardiac contractile force. Patients with a normal heart rate and palpable apex beat usually respond favorably by lightening the plane of anesthesia (if possible) and fluid therapy (10-20 ml/kg of crystalloid). Patients with a normal heart rate and weak apex beat may or may not respond to a reduction in anesthetic depth and fluid therapy, oftentimes requiring the administration of a catecholamine (dopamine, dobutamine). Dopamine (1-5 mg/kg/min) is the preferred drug if the patient is hypotensive and has a low normal or low heart rate. Dobutamine (1-5 mg/kg/min) is the preferred drug if the heart rate is normal or elevated. The dosages of both drugs may need to be increased in patients with poor myocardial contractile performance due to anesthetic depression, heart disease or during shock (poor myocardial blood flow). The administration of blood (1:1 for blood loss) is indicated when the PCV falls below 20%. Plasma or colloids (dextrans) are generally indicated when the TP falls below 3.5 g/dl.
Both supraventricular and ventricular arrhythmias are common during anesthesia and surgery. Supraventricular arrhythmias are generally well tolerated by most patients unless the ventricular rate becomes too slow or too rapid (see above). The treatment of supraventricular tachycardia, whether a sinus or subsidiary pacemaker, usually involves the use of drugs that suppress sympathetic tone (beta adrenoceptor blockers), directly depress automaticity (Class I and IV antiarrhythmics) or prolong conduction through the AV node. Both propranolol (0.05-0.1 mg/kg IV) and esmolol (10-15 mg/kg/min) have been successfully used to treat sinus tachycardia during anesthesia. Quinidine (0.02-0.5 mg/kg IV) is used to treat the acute onset of atrial flutter/fibrillation and beta adrenoceptor blocking drugs and diltiazem (10-15 mg/kg/min) have been used to prolong conduction through the AV node, and thereby, slow ventricular response (slow ventricular rate) during supraventricular tachycardia and atrial flutter/fibrillation. Diltiazem has also been used during anesthesia for the treatment of flutter/fibrillation.
Ventricular arrhythmias may be of little consequence in otherwise normal, healthy patients but should be treated in any patient when they comprise more than 50% of the ventricular beats, occur in rapid succession, are sustained, are multiform or multifocal and produce poor hemodynamics (poor perfusion and mucous membrane color). The best first choice antiarrhythmic for almost all ventricular arrhythmias during anesthesia is lidocaine (2.0 mg/kg dogs; 0.5 mg/kg cats IV). Lidocaine can be administered by infusion (25-50 mg/kg/min) throughout the anesthetic period and during recovery if necessary. Diazepam (0.1-0.2 mg/kg) is helpful in reducing central nervous system sympathetic tone, which may contribute to the development of ventricular arrhythmias during anesthesia or the recovery period.