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Anesthetic complications and emergencies and how to handle them (Proceedings)
The most effective way to deal with anesthetic emergencies is to prevent them and appropriate 1) stabilization of the patient, 2) selection of type and dosage of anesthetic drugs, 3) preparation of anesthetic equipment, 4) pre-, post- and intra-operative support of the patient, and 4) physiologic monitoring, will make the anesthetic episode safer and will decrease the likelihood of anesthetic emergencies.
The most effective way to deal with anesthetic emergencies is to prevent them and appropriate 1) stabilization of the patient, 2) selection of type and dosage of anesthetic drugs, 3) preparation of anesthetic equipment, 4) pre-, post- and intra-operative support of the patient, and 4) physiologic monitoring, will make the anesthetic episode safer and will decrease the likelihood of anesthetic emergencies. Anesthetic complications and emergencies can occur during any one of the four phases of anesthesia: premedication, induction, maintenance or recovery. Unfortunately, most unexpected anesthetic complications occur in recovery – and most of those occur because of failure to appropriately monitor and support the patient.
Anesthetic drugs must cause depression of the central nervous system (CNS) in order to produce sleep and, in general, anesthetic dugs also cause depression of cardiac output, arterial blood pressure, alveolar ventilation and oxygen delivery to the tissues. These changes in the CNS, cardiovascular and respiratory systems can become acutely life-threatening if depression is profound (eg, anesthetic overdose) or if the patient is debilitated (eg, patients in shock). Thus, we focus our monitoring and support on these three organ systems. Anesthesia-induced changes in other organ systems (eg, slowing of hepatic metabolism, decreased renal function) are not generally acutely life-threatening, although they can manifest as complications days to weeks postoperatively. Generally, support of the CNS, cardiovascular and respiratory systems provides support for other organ systems.
I. Central nervous system complications/emergencies
• Inadequate anesthetic depth is less common and more easily fixed that excessive anesthetic depth. Again, prevention through diligent monitoring is the key to success.
• Excessive anesthetic depth is one of the most common complications encountered in anesthesia and excessive anesthetic depth can precipitate all of the other complications described here and can rapidly become an emergency rather than a complication. Appropriate patient monitoring – and response to each patient as individuals – is imperative for successful anesthesia.
• Causes of excessive anesthetic depth: Anesthetic drugs (side effects are dose dependent); age and health status of the patient (neonates, geriatrics, compromised patients require lower dosage); duration of surgery (side effects are cumulative over time); hypothermia (causes decreased need for anesthetic drugs)
• Prevention of CNS complications/emergencies
MONITOR – continually assess anesthetic depth. Use response to surgery, eye position, jaw tone, respiratory rate and rhythm, heart rate and rhythm, arterial blood pressure, etc...
A. Treatment of CNS complications/emergencies?
• If the patient is too deep, decrease anesthetic depth IMMEDIATELY. If necessary, turn the vaporizer completely off, fill the rebreathing bag with oxygen and ventilate for the patient.
• If the patient is too light, first assess pain management – addition of analgesia may be more appropriate than increasing the dose of anesthetic agent.
II. Respiratory complications/emergencies
A. Hypoventilation (PaCO2 or ETCO2 > 55 mmHg) is the most common reported anesthetic complication / emergency. However, it often occurs secondary to excessive anesthetic depth.
• Hypoventilation causes hypercarbia which may lead to respiratory acidosis. Hypoxemia may also occur.
B. Causes of hypoventilation
Hypoventilation simply means that gas exchange (removal of CO2/uptake of O2) is impaired and causes of hypoventilation include anesthetic drugs, physical or physiologic issues in the patient and equipment malfunction.
• Anesthetic drugs – almost all anesthetic drugs can cause some degree of respiratory compromise. Primary offenders include thiopental, propofol and inhalant anesthetic drugs. **The degree of respiratory depression is dose-dependent for most drugs and overdose of an anesthetic drug (including inhalant anesthetic drugs) is a common cause of respiratory depression.
• Physical or physiologic issues includes systemic disease, CNS disease, upper airway complications and lower airway complications.
o Diseases that cause hypoventilation include any diseases that impairs CNS function (eg, septicemia) or respiratory function (eg, pneumonia).
o Primary CNS disease, cranial trauma, brain tumors, etc... can all cause hypoventilation.
o Upper airway complications include laryngeal dysfunction and tracheal collapse.
o Lower airway complications include diseases (again, like pneumonia) and physiologic changes like ventilation/perfusion (V/Q) mismatch (eg, due to pulmonary consolidation or tumors, general anesthesia in horses, etc...).
• Equipment malfunction can include anything from the endotracheal tube to the oxygen supply for the hospital.
o Common equipment problems include kinked or plugged endotracheal tubes, malfunctioning inspiratory/expiratory valves and exhausted CO2 absorbent.
C. Hyperventilation (PaCO2 or ETCO2 < 25-30 mmHg) can also occur under anesthesia.
• Hyperventilation is generally due to an underlying cause like pain, inadequate anesthetic depth and elevated CO2 (which can be caused by excessive anesthetic depth so don't automatically administer anesthetic drugs to hyperventilating patients).
• Hyperventilation can lead to respiratory alkalosis.
D. Hypoxemia (The ideal PaO2 = 5x fraction inspired oxygen [FIO2] – true PaO2 is rarely this high and hypoxemia is defined as PaO2 < 50-60 mmHg on room air or <200 mmHg on 100% O2) can occur under anesthesia.
• Hypoxemia can be due to
o Hypoventilation, low FIO2, , ventilation-perfusion mismatch, impaired diffusion of oxygen across the alveolar/arterial membrane, anatomical shunting of blood
E. Prevention of respiratory complications/emergencies
• Respiratory rates (eg, 10-15 breaths/min in cats dogs; 6-10 breaths/min in horses),
• Tidal volume (10-15 ml/kg body weight)
• Mucous membrane color (pink vs 'blue'),
• Oxygen-hemoglobin binding (SpO2 >95%),
• End-tidal CO2 (35-55 mmHg),
• Arterial blood gases
F. Treatment of respiratory complications/emergencies
QUICKLY determine the problem and FIX IT.Case: You notice that the ETCO2 on the patient that you have anesthetized for an OHE is 70 mmHg and that breathing is rapid and very shallow. What do you do?
• Quickly give the dog a breath – as you are delivering the breath you are feeling for resistance in the system watching the machine and the thoracic excursion of the dog to make sure that there are no obstructions or other causes of impaired flow.
• As you are giving the breath, you are also assessing anesthetic depth, looking at the vaporizer setting and thinking about the drugs/dosages that the patient has received.
• LOOK AT THE PATIENT – not only might the cause be patient-related but sometimes electronic monitors give false information. Assess anesthetic depth, recheck the airway, etc
• After you have made the initial assessment described above, start looking deeper. Is the CO2 absorber exhausted? Is the ETCO2 monitor functioning normally?
• If no cause can be found, change machines. Or may need to reintubate if the tube/airway is the suspected problem.
• Finally, ask if there a cause for increased CO2 production rather than decreased CO2 elimination? Uncommon anesthetic emergencies like malignant hyperthermia (and anything that causes hypermetabolism) can cause an increase in CO2 production that may overwhelm the patient's ability to eliminate CO2.
• If no cause can be found, this patient might require ventilator assistance throughout the anesthetic episode. This is uncommon in young, healthy patients but very common in aged or compromised patients.
III. Cardiovascular complications / emergencies
• Hypotension (MAP<60 mmHg in small animals or <70 mmHg in horses) is the second most commonly reported anesthetic complication/emergency. As with hypoventilation, hypotension often occurs secondary to excessive anesthetic depth. Hypotension leads to decreased blood flow (and therefore decreased oxygen delivery) to the tissues.
A. Causes of hypotension
• Hypotension is generally caused by decreased cardiac output. Cardiac output is determined by heart rate (HR) x stroke volume (SV). Stroke volume is dependent on preload (circulating fluid volume), afterload (vascular tone) and myocardial contractility.
• Causes include anesthetic drugs and physical or physiologic issues in the patient.
o Through effects on both HR and SV, almost all anesthetic drugs can cause some degree of cardiovascular compromise.
o Primary offenders include thiopental, propofol and inhalant anesthetic drugs. **The degree of cardiovascular depression is dose-dependent for most drugs and overdose of an anesthetic drug (including inhalant anesthetic drugs) is a common cause of cardiovascular depression.
• Physical or physiologic issues that cause hypotension include anything that causes an impairment of pump function (myocardial contractility), vascular tone, or circulating volume.
o Pump function can be impaired by any cardiac disease (eg, HCM, DCM, mitral insufficiency) and many systemic diseases (eg, septicemia, hypothyroidism).
o Vascular tone is also affected by systemic diseases like septicemia.
o Circulating volume is affected by ANY form of intravascular fluid loss (eg, dehydration, hemorrhage, 'third-spacing' of fluid, etc...).
B. Hypertension (MAP > 150 mmHg? – not well-defined in anesthetized animals) occasionally occurs during general anesthesia.
• Hypertension can be caused by systemic disease (eg, hyperthyroidism).
• Hypertension is generally due to an underlying cause.
o Common causes include pain, inadequate depth of anesthesia, and hypercarbia.
C. Arrhythmias are the third most common anesthetic complication/emergency.
• ANY arrhythmia can occur during anesthesia but the most commonly occurring arrhythmias are bradycardia, tachycardia and ventricular premature contractions (VPCs).
• Arrhythmias are concerning not only because they could be a result of organic cardiac disease but also because they can contribute to hypotension and decreased organ perfusion.
• Bradycardia (see normal heart rates listed under prevention)
o May be caused by certain anesthetic drugs (eg, alpha-2 agonists, opioids and propofol) or by maneuvers that enhance vagal tone (eg, ocular or laryngeal procedures).
• Tachycardia (see normal heart rates listed under prevention)
o Tachycardia generally occurs secondary to an underlying condition. Therefore, treatment of the underlying condition (rather than treatment of the heart rate itself) is usually the correct approach.
o Examples of underlying conditions include pain, inadequate plane of anesthesia, high CO2, cardiac disease, systemic conditions like hyperthyroidism and septicemia, etc...
• Ventricular premature contractions (VPCs)
o VPCs can be caused or exacerbated by pre-existing myocardial disease, by some anesthetic drugs and by physiologic abnormalities like hypoxia, hypercarbia, acidosis and electrolyte abnormalities.
o A low number of VPCs are normal in some patients (eg, geriatric patients) and may not require treatment. Treatment should be initiated if the arrhythmia is affecting the blood pressure or if the number of VPCs is >20% of the total number of ventricular beats.
How do we prevent cardiovascular complications/emergencies?
'Normal' heart rates should be defined as normal for the size of the patient when it is relaxed (rather than excited or scared as often occurs in patients who are being examined at the veterinary clinic). Guidelines are:
Heart rate: 50-60 beats/min for large dogs; 60-80 beats/min for medium dogs; 80-100 beats/min for small dogs; 100-150 beats/min for extremely small dogs and for cats;
mucous membrane color (pink vs pale),
capillary refill time (CRT<2 seconds),
quality/strength of pulse,
arterial blood pressure (MAP >60 mmHg in small animals and 70 mmHg in horses),
oxygen-hemoglobin binding (SpO2; >95%).
How do we treat cardiovascular complications/emergencies?
Determine the problem and FIX IT.
• Hypotension – fix the pump (heart) and the fluids (and the vasculature - but the vasculature is a little harder to treat).
o DECREASE ANESTHETIC DEPTH.
o Increase fluid rate – give a bolus of crystalloids or colloids or both.
o Fix the heart rate (increase or decrease).
o Administer positive inotropic agents (eg, dopamine or dobutamine – the dose of both is roughly 1-10 microg/kg/min).
• Bradycardia is generally vagally mediated and can be treated with anticholinergics (0.04 mg/kg atropine; 0.01mg/kg glycopyrrolate).
o Bradycardia that is unresponsive to anticholinergics can generally be treated with catecholamines like dopamine (1-10 mg/kg/min), epinephrine (0.1-1.0 microg/kg/min) or norepinephrine (0.5-1.0 microg/kg/min).
o Occasionally, unresponsive bradycardia may occur due to cardiac disease, toxemia, profound hypothermia, profound hypoxia, a variety of systemic diseases, etc...
o Bradycardia should be treated anytime that the low heart rate is contributing to low blood pressure. However, remember that the alpha-2 agonists cause low heart rate with high blood pressure and using anticholinergics will cause an unnecessary increase in cardiac work.
• Generally, treat tachycardia by eliminating the underlying cause. (RARELY beta-blockers will be administered to patients under anesthesia to decrease tachycardia from uncommon, uncontrollable causes like pheochromocytoma.)
• The first line of treatment for VPCs is to eliminate all underlying causes (eg, treat electrolyte imbalances, improve oxygenation, etc...).
o Lidocaine or procainamide should be used to treat VPCs due to myocardial disease, arrhythmias that persist after correction of the underlying cause and arrhythmias that are immediately life-threatening.
o Lidocaine is generally the first choice for treatment of VPCs and the dose in dogs is 2-6 mg/kg IV (maximum 8 mg/kg during any 10 minute period) followed by 25-75 microg/kg/min infusion.
o Lidocaine dose in cats is 0.2-0.5 mg/kg IV as an initial bolus followed by 10 microg/kg/min infusion.
o Procainamide dose in dogs is 10 (8-20) mg/kg IV bolus followed by 25-50 microg/kg/min infusion.
o Procainamide dose in cats is 1-2 mg/kg IV SLOW bolus followed by 10-20 microg/kg/min infusion.
o Procainamide can cause profound negative inotropic effects and should not be administered to patients with impaired contractility. Arterial blood pressure should be monitored during the administration of procainamide.