Anesthetic Management of Commonly Encountered Complications
Elizabeth Goudie-DeAngelis, DVM, MS
The anesthetic plan was carefully formulated specifically for your patient. You took into account underlying pathologies and the procedure you are performing. The induction went well, but now that your patient is under general anesthesia you are encountering complications. Chances are your patient has hypotension, hypothermia, hypoventilation or a combination of the three. The best way to keep your procedures moving forward and your patient stable is to know how to predict, prevent and treat these three common anesthetic complications.
We do not have a way to easily, non-invasively, or accurately measure perfusion (the oxygenation of tissues at the capillary level), so in combination with hemoglobin saturation, we use blood pressure to make an approximation of tissue perfusion. Hypotension is defined as a systolic arterial blood pressure (SAP) under 90 mmHg. Ideally, we attempt to keep this number between 90 – 110 mmHg under general anesthesia because an SAP greater than 90 mmHg correlates to a mean arterial blood pressure (MAP) of 60 mmHg. The MAP is the number we are concerned with. With a MAP in the range of 60-120 mmHg the capillary beds of the kidneys and brain can autoregulate; outside of this range there is concern for inadequate perfusion to these and other important tissues. Hypotension under general anesthesia is caused by some premedications, induction agents (e.g. propofol, alfaxalone) and the inhaled anesthetics.
When faced with low blood pressure, it is easiest to go back to basic physiology to determine what to do next:
Blood pressure= cardiac output *systemic vascular resistance
Cardiac output= heart rate *stroke volume
Stroke volume is determined by preload, afterload and contractility.
If you encounter hypotension, the next step is to determine the cause. If we look at the equation above, a decrease in blood pressure is due to a decrease in output and/or vasodilation. Since inhaled anesthetics cause vasodilation, it is important to minimize their use when hypotension is encountered or expected.
- Minimizing the inhaled anesthetics can be achieved by MAC reducing drugs (e.g. opioids, ketamine, lidocaine) as CRIs or boluses. The use of nerve blocks (e.g. epidurals, dental blocks, ring blocks) can also minimize inhalant requirements.
- A crystalloid fluid bolus of 5 mL/kg for cats and 10 mL/kg for dogs can be used to combat the relative hypovolemia caused by the vasodilation. Fluids support can be administered concurrently with inhalant reduction especially if the patient has indications of hypovolemia (e.g. hemoconcentration).
The heart rate should also be evaluated. While a heart rate of 70 bpm for a dog under general anesthesia is not abnormal, it is always important to also consider what the patient’s resting heart rate was, especially when a low blood pressure is observed. If the heart rate is relatively low for your patient, an anticholinergic can be administered:
- Atropine 0.02-0.04 mg/kg IV
- Glycopyrrolate 0.005 mg/kg -0.015 mg/kg IV
Finally, if minimizing inhalants, addition of fluids, and normalization of the heart rate has not successfully treated the hypotension, the addition of a vasopressor agent can be considered:
- Dopamine: alpha1, beta1, dopaminergic receptors. Increases heart rate and causes vasoconstriction. 5-10 ug/kg/min
- Dobutamine: beta1, beta2 receptors. Increases heart rate and contractility. Causes mild vasodilation. 3-5 ug/kg/min
- Norepinephrine: alpha1, alpha2. Potent vasoconstrictor 0.01 ug/kg/min-0.03 ug/kg/min
- Ephedrine: effects at all adrenergic receptors, possibly greater effects at alpha1. Tachyphylaxis with repeated dosing. 0.01-0.05 mg/kg IV
Hypothermia can cause a number of negative sequelae, especially in the surgical patient. It can occur during general anesthesia because of vasodilation, open abdominal or thoracic cavities, resetting of the thermoregulatory center by general anesthesia, and contact with a cool surface and room. Hypothermia is defined by a rectal temperature less than 990F in dogs and cats.
Perioperative side effects of hypothermia include coagulopathies, prolonged anesthetic recovery, increased metabolic oxygen demand, reduced wound healing, increased rate of infection, alterations of protein/enzymatic function, and changes to the metabolism and pharmacokinetics of a variety of drugs. Intraoperatively, patients require less inhaled anesthetics due to changes in solubility of the inhalants. Hypothermia causes profound bradycardia that is often nonresponsive to anticholinergic agents as well as decreased response to alpha1 receptor agonists. Ventilation is impaired by a number of mechanisms, and there is an increased risk of acute lung injury, pneumonia and pulmonary edema.
There are three phases to heat loss due to general anesthesia: 1) An initial and marked drop in core temperature is noted during the first 30 minutes to hour of general anesthesia. 2) The second phase occurs over the next 2-3 hours at a more gradual, linear manner. 3) There is a plateau phase in which there is minimal temperature change. Prevention and early intervention are key to maintaining normothermia throughout an anesthetic episode. Mechanisms to counteract heat loss include warm water blankets on the induction table and surgical table, forced air blankets intraoperatively, and the use of towels and blankets between the patient and metal tables. For patients undergoing celiotomies the use of warmed abdominal lavage can increase the core temperature significantly when the flush is allowed to have contact with the abdomen for 2-6 minutes.
Warming of patients should continue post-operatively, and regular assessment of post-anesthetic patients’ rectal temperatures should be performed particularly if the patient is still sedate, inactive and/or suffered from hypothermia during the anesthetic episode.
Hypoventilation is defined as a partial pressure of carbon dioxide in the arterial system greater than 45 mmHg or an end-tidal carbon dioxide greater than 45 mmHg. Hypoventilation under general anesthesia occurs because of a decrease in tidal volume caused by positioning of patients in dorsal recumbency (particularly over-conditioned patients) and resetting of the medullary respiratory center chemoreceptors by anesthetic drugs. Carbon dioxide levels can be used to evaluate tissue perfusion, gas exchange and cardiac output.
Why are we concerned about hypercapnea under general anesthesia? Aside from the necessity of normal ventilation to ensure appropriate gas exchange including the inhaled anesthetics being used to maintain the patient asleep, we also worry about various pathophysiologic changes. Ventilation gives an indication of tissue perfusion, efficiency of gas exchange and cardiac output. Changes that occur with an increased arterial carbon dioxide level include respiratory acidosis, vasodilation, elevated heart rate and hypnosis with levels greater than 90 mmHg.
Carbon dioxide can be measured using a capnometer or by drawing blood gas samples. A capnometer allows for minute-to-minute measurement of end-tidal carbon dioxide and can be used to easily and rapidly to monitor ventilation. If assisted ventilation via manual IPPV or a mechanical ventilator is being used, evaluation of carbon dioxide levels is paramount to ensure neither hyper or hypoventilation is occurring.
Regardless of the method of ventilation (manual or mechanical) airway pressure should not exceed 20 cmH2O to prevent barotrauma or volutrauma to the patient.
Dr. Goudie-DeAngelis always welcomes anesthesia related questions and would be happy to discuss any of the complications described here. In addition she is available for consults relating to pain management and for anesthesia case management.