Management of Anesthetic Complications
World Small Animal Veterinary Association World Congress Proceedings, 2003
Luisito S. Pablo, DVM, MS, DACVA
College of Veterinary Medicine University of Florida
Gainesville, FL, USA

Safety of the patient during anesthesia should always be a priority. However, there are very few instances when morbidity and mortality occur despite the conscious effort to follow good anesthetic practice. As A.S. Keats puts it: "Some adverse events during anesthesia occur for which no explanation based on current knowledge is possible, yet no negligence, error, or fault is demonstrable."

Absence or lack of oxygen delivery to the vital organs of the body will result in mortality and morbidity. To prevent anesthetic complications, efforts should be made to maintain oxygen delivery to the tissue. Oxygen delivery to the tissue is dependent on oxygen content of the blood and cardiac output. Some specific conditions known to decrease oxygen delivery during anesthesia include reduced cardiac output, hypotension, hypoxemia, certain dysrhythmias, and severe hypoventilation. The focus of this presentation will be on these anesthetic complications with emphasis on the cardiovascular and respiratory systems.


Arterial hypotension is one of the most common anesthetic complications. Hypotension occurs when mean arterial pressure (MAP) is below 60 mmHg or the systolic blood pressure is below 80 mmHg (using Doppler). It may be manifested as a weak peripheral pulses. However, a strong peripheral pulse does not guarantee a normal MAP. The pulse felt by the anesthetist is the difference between the systolic and diastolic pressures. A large difference between the two pressures will result in a very strong pulse and yet the MAP may be low. A helpful guide in the decision making is the use of an indirect or direct blood pressure monitor. It is important to maintain a normal MAP to ensure perfusion to the vital organs.

To manage hypotension during anesthesia, one has to determine the possible cause(s) of the problem. A hypotensive episode may be due to one or a combination of the following: 1) reduced inflow to the heart, 2) reduced pumping function of the heart, and 3) reduced vascular resistance. In a healthy dog or cat presented for elective procedure, the anesthetics administered are the most cause of arterial hypotension. Blood loss during surgery can also result in hypotension. Preexisting conditions that can result in hypotension during anesthesia include hypovolemia, shock, cardiomyopathy, valvular heart disease, arrhythmias, hypothyroidism, hypoxemia and Addisonian crisis. Drugs, blood or blood products administered during anesthesia can cause anaphylactoid reaction. The most common manifestation of anaphylactoid reaction during anesthesia is hypotension.

If the patient does not have any preexisting problem(s) and the hypotension is more likely anesthetic-induced, the vaporizer setting or infusion rate of the IV anesthetic should be reduced. In severe hypotension, stopping anesthetic administration for 1-2 minutes may be necessary. IV bolus administration of crystalloid at 5.0-10 ml/kg should also be done. If hypotension persists, the administration of positive inotrope should be considered. Dopamine is the most common inotrope we use in our practice. To stimulate the beta-1 receptors, dopamine is given at 5.0 ug/kg/min. Further increase in the infusion rate is needed if hypotension persists. A rate of up to 10 ug/kg/min may be necessary in some cases. If this high rate of infusion is required, reduced vascular resistance may be the dominant cause of hypotension. An alternative is the use of ephedrine, a mixed alpha and beta agonist. It is given as a bolus injection at 0.03-0.1 mg/kg. This drug will increase myocardial contractility and peripheral resistance. Because of the highly concentrated preparation of ephedrine (50.0 mg/ml), the author dilutes 5.0 mg of ephedrine with saline to make a total volume of 10.0 ml. The lower dosage should be used first because sinus tachycardia may accompany the higher dose. If the hypotension does not improve, another dose can be given 5 minutes after the initial dose.

If the cause of hypotension is known, it is important to treat the primary problem. Blood loss during surgery should be replaced initially with crystalloid (Lactated Ringers', saline, or Normosol). The volume of crystalloid administered should be 3 times the volume of blood lost. If more than 20% of the blood volume is lost, whole blood or packed red blood cells is indicated. Colloid preparation is indicated in hypoproteinemic patient.

It is important to ensure adequate oxygenation and ventilation in hypotensive patients. If inhalation anesthetic is being used, check the O2 saturation. If the patient is not intubated and receiving injectable anesthetic agents, intubate the patient and assist ventilation.


Hypoxemia may be the most common cause of mortality in our patients under anesthesia. It is defined as a lower than normal partial pressure of oxygen in arterial blood (PaO2 < 60 mmHg). Using the pulse oximeter, hypoxemia is present if the SpO2 is 90% and below. It is important to realize that hypoxemia can occur without obvious cyanosis. If the oral mucous membrane turns bluish, it is an indication of severe hypoxemia. The naked eyes will fail to recognize most hypoxemic episodes by just looking at the mucous membrane. Anesthetized patients may not show any change in respiratory rate, heart rate and blood pressure. Severe and terminal hypoxemia may be signaled by bradycardia. In some cases, cardiac dysrhythmias will be manifested.

Recognizing the cause of hypoxemia during anesthesia is important in the management and treatment. There are 5 main causes of hypoxemia, namely 1) reduced inspired concentration of O2 , 2) hypoventilation, 3) ventilation-perfusion mismatch, 4) shunt or venous admixture, and 5) diffusion barrier.

If the patient does not have any preexisting pulmonary and cardiovascular problem, the possible causes of hypoxemia in practice are anesthetic machine problems, hypoventilation in animals breathing room air, closed pop-valves, endobronchial intubation, aspiration of gastric contents, and inappropriate use of nitrous oxide.

If a patient becomes cyanotic, immediately check for pulse. If there is a pulse, make sure the patient is breathing 100% oxygen. If the patient is apneic, intubate the trachea and control ventilation immediately. While supporting ventilation, try to ascertain the exact cause of the problem. For healthy patients, make sure that the endotracheal tube (ETT) is not in the bronchus. Pulling the ETT slightly may solve the problem. Always look for anesthetic machine and breathing circuit problems. If nitrous oxide is available, make sure that the flow meter is turned off. Look for disconnections in the breathing circuit and machine. If the problem is a closed pop-valve resulting in pneumothorax, aspirating air from the chest should be done and in severe cases, a chest tube is kept in place for about 2 days.

If the patient has preexisting pulmonary problem, management will be more difficult. Anesthetics are known to worsen shunting and ventilation-perfusion mismatching. These animals may require controlled ventilation and the application of positive end-expiratory pressure (PEEP) during anesthesia. The hypoxemia may also worsen as they recover from anesthesia requiring ventilatory support in recovery.

If the patient turns cyanotic and there is no palpable pulse, cardiopulmonary resuscitation (CPR) should be initiated.

In a practice setting where patients are mostly of physical status ASA 1 and 2 (healthy or with minor systemtic disturbance), thorough check up of the anesthetic machine and breathing circuit will prevent hypoxemia. Adherence to good anesthetic techniques like the use of the proper length of ETT, keeping pop-valve open, and providing 100% O2 will prevent most hypoxemic episodes.


Hypercapnia is present if there is an abnormally high levels of CO2 in the blood or end-tidal gas. Almost all anesthetics will depress the respiratory function in a dose-dependent manner. It is not surprising then to see hypercapnia during anesthesia. The more important concern is when we intervene to correct hypercapnia. The upper limits of abnormally high CO2 that jeopardize the safety of our patient is still open to debate. Mild hypercapnia in anesthetized patients has been shown to increase blood pressure, cardiac output, and heart rate. However, hypercapnia that leads to a pH below 7.2 has been associated with cardiovascular depression. Severe hypercapnia can also result in cardiac dysrhythmias. Without the monitoring equipment the decision when to intervene becomes more difficult.

Hypercapnia is mostly associated with decreased CO2 elimination during anesthesia, not increased CO2 production. Depression of the respiratory center by the perianesthetic drugs is the most common cause of hypercapnia. Respiratory obstruction may also result in hypercapnia. Faulty unidirectional valves, exhausted soda lime, and inadequate O2 flow in non-rebreathing systems are machine-related problems that lead to hypercapnia.

Since hypercapnia is more commonly associated with the anesthetic agents, keeping the animal at an anesthetic plane compatible with the requirement of procedure should be done. If dysrhythmias occur secondary to the hypercapnia, controlled ventilation is required. A good example is a healthy cat undergoing ovariohysterectomy which shows premature ventricular complexes on ECG. By simply controlling the ventilation of this cat, the PVCs will disappear. If an anesthetized patient is not receiving a high concentration of O2 and it develops hypercapnia, hypoxemia may ensue. It is good practice to always ensure adequate oxygenation in hypercapnic patients. Tracheal intubation and assisted ventilation will be needed in patients with respiratory obstruction. Over-inflated cuff and ETT kinking should be ruled out. The anesthetic machine should be checked regularly to detect faulty unidirectional valves and exhausted soda lime.


Dysrhythmias during anesthesia become clinically significant if the hemodynamic state of the patient is affected. Not all dysrhythmias that occur during anesthesia should be treated. However, other dysrhythmias are potentially lethal and should be treated immediately.

Sinus bradycardia with or without 2nd degree AV block is commonly seen during anesthesia. It may be due to drugs that increase the vagal tone, vagally mediated reflexes, hypothermia, and deep anesthesia. Bradycardia may decrease both cardiac output and blood pressure. Anticholinergic (atropine, 0.02-0.04 mg/kg IV or glycopyrrolate, 0.005-0.01 mg/kg IV) are effective in treating sinus bradycardia or other bradyarrhythmias associated with high vagal tone. If the bradycardia is caused by an anesthetic overdose or severe hypothermia, atropine may not be effective. Other forms of support will be needed to increase the heart rate. Specific reversal agents, if available, for the anesthetic agents used will help correct the bradycardia. Support of body temperature in hypothermic patients will slowly correct the sinus bradycardia.

Sinus tachycardia occurs during light plane of anesthesia. It is also associated with hypovolemia, shock, drugs with chronotropic effect (dopamine, anticholinergic, epinephrine), and uncontrolled hyperthyroidism. Administration of more anesthetic (either IV or inhalant) and analgesic (opiates like oxymorphone, fentanyl, morphine or hydromorphone) will reduce the heart rate if the animal is in a light plane of anesthesia. Epidural morphine and/or local anesthetic before the surgery can prevent the sympathetic response to the surgical stimulation. Tachycardia due to hypovolemia or shock should be managed with fluid administration. Beta blocking agent (propranolol or esmolol) can be given in hyperthyroid cats with persistent tachycardia (heart rate >200 beats per minute).

Supraventricular dysrhythmias are tolerated by most anesthetized patients and do not require drug therapy. In some cases, deterioration of the hemodynamic state necessitates the use of drugs. Beta blocking drugs (esmolol, 50-200 ug/kg/min constant rate infusion or 50-100 ug/kg slow IV or propranolol, 0.04-.06 mg/kg IV) or diltiazem (10-15 ug/kg/min) can be used for supraventricular tachycardia and atrial flutter/fibrillation. Quinidine (0.2-0.5 mg/kg IV) can be used to treat atrial flutter/fibrillation). Premature atrial complexes can occur during anesthesia and specific treatment for these dysrhythmias is not needed. However, ventilation and oxygenation should be assessed and improved if needed.

Premature ventricular complexes are the most common ventricular dysrhythmias during anesthesia. They are well tolerated in healthy patients and do not require therapy in most cases. Lidocaine (1.0-2.0 mg/kg IV dogs; 0.5 mg/kg cats IV) is indicated if PVCs are multiform and sustained, occur in rapid succession, and result in cardiovascular compromise. It is important to ensure adequate oxygenation and ventilation in these patients. Adequate anesthesia and analgesia will also eliminate some PVCs. Another ventricular dysrhythmia of concern will be ventricular tachycardia. This dysrhythmia can progress to ventricular fibrillation. Lidocaine is also the drug of choice for ventricular tachycardia.

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Luisito S. Pablo, DVM, MS, DACVA
College of Veterinary Medicine, University of Florida
Gainesville, FL, USA

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