The incidence of anesthetic complications can be as high as 12% in small animals and occurs more frequently in dogs when compared to cats.^1,2 Brachycephalic and specific breeds such as Weimaraner, Pekingese, Jack Russell Terrier, and Himalayan cats are reportedly at increased risk for anesthetic complications.¹ Common complications observed perioperatively include hypotension, bradycardia, tachycardia, hypoxemia, hypoventilation, prolonged emergence, and postoperative delirium. Hypotension and respiratory depression have been reported as the most common.^1,2 The primary objective of this lecture is to identify and trouble shoot complications that occur during the perioperative period. Particular attention will be placed on cause, diagnosis, and treatment.

Perioperative Cardiovascular Morbidities

Hypotension-Hypovolemia, Vasodilation, Bradycardia, Negative Inotropy

Hypotension under anesthesia has been recently suggested by the American and European College of Veterinary Anesthesia and Analgesia as a systolic (SAP) and mean (MAP) arterial blood pressure below 87 mm Hg and 62 mm Hg, respectively.³ It has been reported in 38% of all dogs placed under anesthesia and those of ASA PS of > III are more likely to become hypotensive intraoperatively.⁴ The author recommends that SAP and MAP be maintained above 90 mm Hg and 70 mm Hg, respectively. Blood pressure is affected by several factors: 1) heart rate 2) contractility 3) systemic vascular resistance. During hypotension (MAP < 60–70 mm Hg), vital organs such as the brain and kidney cannot autoregulate their blood supply resulting in organ ischemia. MAP is the most important determinant of organ perfusion. A diastolic arterial pressure (DAP) of greater than 50 mm Hg is important when maintaining coronary perfusion. A decrease in heart rate, contractility, or systemic vascular resistance can result in decreases in MAP. The most common causes for hypotension in anesthetized patients include hypovolemia, vasodilation, bradycardia, and reduced myocardial contractility.⁵

Diagnosis of hypotension can be made via non-invasive blood pressure (oscillometric, Doppler) or invasive blood pressure (arterial catheter and transducer) devices. Treatment of hypotension should be aimed at the most likely cause as inappropriate fluid resuscitation or cardiac drugs could result in further deterioration in patient's status increasing the likelihood for morbidity and/or mortality.

Hypovolemia can occur from blood loss, dehydration, abdominal compartment syndrome, addisonian crisis, diarrhea, or vomiting. Treatment includes volume resuscitation with crystalloids, colloids, or blood products. Alterations in pulse pressure amplitude on the plethysmograph during positive pressure ventilation can be a good indicator of hypovolemia. Vasodilation occurs secondary to anesthetic drugs (inhalant anesthetics, acepromazine, propofol, alfaxalone). Reduction of anesthetic depth or dose is the first step in treatment of anesthesia related vasodilation. A crystalloid bolus (10–20 ml/kg), assuming no cardiac disease, can help fill the intravascular compartment and increase cardiac output. Vasopressor support drugs like phenylephrine, ephedrine, or dopamine (high-dose) would be other alternatives. Sepsis, anaphylaxis, acidosis, systemic inflammatory response syndrome (SIRS), and cardiac drugs (ACE inhibitors, Ca₂⁺ channel blockers) are other causes of vasodilation. Treatment is dependent on the cause and situation. A decrease in DAP and MAP during anesthesia is suggestive of a vasodilatory or hypovolemic hypotension. Bradycardia during anesthesia can reduce cardiac output, resulting in decreased blood pressure. Greater than a 50% reduction in baseline heart rate is considered bradycardic for most patients. α₂-agonists, opioids, and an overdose of inhalant anesthetics decrease heart rate. Treatment of bradycardia induced hypotension includes the reduction or reversal of anesthetics or the use of anticholinergics. Vagal stimulation, hypothermia, hyperkalemia, negative chronotropes (digoxin, ß-blockers), and heart disease also result in bradycardia and should be treated based on etiology. Anticholinergics can be administered in hypotensive cases due to bradycardia of unknown origin. Hypothermic patients will not respond to anticholinergic therapy and require rewarming. Decreases in contractility often decrease SAP and MAP and are a result of inhalant anesthetics, propofol, barbiturates, and ketamine (direct effect). Cardiac drugs, acidosis, electrolyte abnormalities, sepsis, SIRS, and primary cardiac disease also decrease contractility. Positive inotropes such as dobutamine, dopamine, or ephedrine increase contractile force via ß-adrenergic stimulation.

Tachycardia

Tachycardia occurs less commonly than bradycardia, however it can act as a reflex to maintain adequate cardiac output and increase oxygen delivery during hypotension and hypoxia. Catecholamine release during light planes of anesthesia, stress, noxious stimulus, anticholinergics, ß-agonists (ephedrine, dobutamine, dopamine), ketamine (indirect effect), and cardiovascular disease also may contribute to tachycardia. Treatment involves addressing the primary cause or with ß-blockers.

Perioperative Respiratory Morbidities

Hypoxia and Hypoxemia

Hypoxia is a low oxygen partial pressure within the tissues, whereas hypoxemia is low oxygen partial pressure in the blood. Oxygen partial pressure <60 mm Hg can result in arrhythmias, lactic acidosis, and organ damage due to decreased oxygen delivery. Mucous membranes, pulse oximetry, and arterial blood gas are used to detect hypoxemia. The development of cyanosis is dependent on the patient having sufficient amounts of unbound hemoglobin (Hb>5 g/dl).

The clinician must understand the primary causes for hypoxia or hypoxemia to guide treatment.

Causes of Hypoxemia

1.  Low fractional inspired oxygen

2.  Hypoventilation

3.  Right to left anatomical shunt

4.  Ventilation:perfusion (V/Q) mismatching

5.  Diffusion impairment

Causes of Hypoxia

1.  Circulatory shock

2.  Anemia

3.  Decreased blood oxygen (hypoxemia)

4.  Hemoglobin-binding disorders (histotoxic)

Evaluation begins with inspired oxygen delivery, end tidal carbon dioxide, blood pressure, cardiopulmonary auscultation for crackles, wheezes, or murmurs, and PCV. This will help in eliminating differential diagnoses, leading to other causes such as V/Q mismatch or diffusion impairment. Common causes for unexpected hypoxia seen in practice include bronchial intubation, obstructed endotracheal tube (mucous, kinking), laryngeal spasm, upper airway obstruction in brachycephalic breeds, and respiratory depression from anesthetics. Pulmonary edema, aspiration pneumonia, and pneumothorax occur but less frequently. Clinical signs of hypoxia include tachypnea, tachycardia, hypotension, and lightening of anesthetic depth.

Hypoventilation

Hypoventilation, an increased in end tidal carbon dioxide levels >45 mm Hg, can be a result of decreased respiratory rate and/or tidal volume. Causes for hypoventilation include anesthetic drugs (inhalants, propofol, alfaxalone, dexmedetomidine, opioids), patient positioning (dorsal recumbency), obesity, neurological dysfunction, thoracic pain, and pulmonary disease. Diagnosis can be made via capnography and arterial or venous blood gas. A Wright respirometer can be used to determine minute ventilation. Treatment includes intubation and positive pressure ventilation. If necessary reverse or decrease anesthetic agents.

Post-operative Morbidities

Recovery is an important part of the perioperative period. In some species morbidity and mortality is highest in recovery when compared to the intraoperative/anesthetic period. Anesthetists should be aware of the most common phenomena during the recovery phase: 1) prolonged emergence and 2) emergence delirium.

Prolonged Emergence

Prolonged emergence can be associated with residual drugs or overdose, changes in drug pharmacokinetics due to patient's physical state, metabolic derangements, and neurological disease. When prolonged emergence from anesthesia is diagnosed, the anesthesia provider should systematically evaluate the patient to determine the most likely cause. This algorithm using letters A-H (A-Airway, B-Breathing, C-Circulation, D-Drugs, F-Failure of neurologic function, G-Get up, H-Hypothermia) can aid in diagnosing and treating cases of delayed emergence. All preoperative co-morbidities and medications, types of operations, types and doses of anesthetic drugs, drugs administered by the surgical team, and the duration and complications during the anesthetic event should be taken into consideration.

Emergence Delirium

Postoperative delirium is an acute onset of hyperarousal, agitation, hyperactivity, and psychosis upon awakening from general anesthesia. Little research has evaluated this phenomenon in veterinary medicine and much of what is discussed pertains to drug-induced post- anesthetic delirium associated with dissociatives, benzodiazepines, and opioids. There are several risk factors that may potentiate delirium post-anesthesia. The most effective way in managing post-operative delirium is via prevention. The goal of treatment is to ensure patient safety and if necessary physical restraint or placing the patient in a small confined area. Physiologic causes of delirium should be considered first (distended bladder, nausea, uncomfortable positioning). Next, reversal agents (flumazenil, naloxone) may help minimize drug induced delirium from opioids and benzodiazepines. Sedatives such as α₂ agonists, acepromazine, and propofol can be used to prevent or treat emergence delirium.

References

1.  Dyson DH, Maxie MG, Schnurr D. Morbidity and mortality associated with anesthetic management in small animal veterinary practice in Ontario. J Am Anim Hosp Assoc. 1998;34(4):325–335.

2.  Gaynor JS, Dunlop CI, Wagner AE, Wertz EM, Golden AE, Demme WC. Complications and mortality associated with anesthesia in dogs and cats. J Am Anim Hosp Assoc. 1999;35(1):13–17.

3.  Ruffato M, Novello L, Clark L. What is the definition of intraoperative hypotension in dogs? Results from a survey of diplomates of the ACVAA and ECVAA. Vet Anaesth Analg. 2015;42(1):55–64.

4.  Redondo JI, Rubio M, Soler G, Serra I, Soler C, Gomez-Villamandos RJ. Normal values and incidence of cardiorespiratory complications in dogs during general anaesthesia. A review of 1281 cases. J Vet Med A Physiol Pathol Clin Med. 2007;54(9):470–477.

5.  Hunyady KG, Johnson RA. Anesthesia case of the month. Hypotension. J Am Vet Med Assoc. 2006;229(8):1250–1253.