Managing Anesthetic Complications (Parts 1 & 2) Bonnie Hay Kraus, DVM, DACVS, DACVAA Iowa State University Ames, IA

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1 Managing Anesthetic Complications (Parts 1 & 2) Bonnie Hay Kraus, DVM, DACVS, DACVAA Iowa State University Ames, IA Peri-anesthetic complications Hypotension, arrhythmias, cardiac arrest, hemorrhage, hypoventilation, hypoxemia, upper airway obstruction, gastro-esophageal reflux/aspiration pneumonia, hypothermia/hyperthermia The best way to manage peri-operative complications is prevention.this requires the anesthetist to prepare ahead of time for anticipated complications, monitor for their occurrence and intervene before significant morbidity or mortality can occur. Preoperative patient preparation plays a significant role in avoiding peri-operative complications; correct fluid, acid/base and electrolyte abnormalities, anemia and hypoalbuminemia prior to anesthesia. Placement of an intra-venous catheter for fluid administration and in case of emergency is recommended for all but the briefest anesthetic procedures. Intubation with a properly inflated cuffed endotracheal tube will provide a patent airway, allow positive pressure ventilation and prevent aspiration. Intra-operative monitoring warns the anesthetist of changes in the patient s status and allows for early intervention. Cardiovascular complications Hypotension Adequate delivery of oxygen to tissues is the key to patient survival. Delivery of oxygen to tissues is dependent on cardiac output and the content of oxygen in the blood (DO2 = CO x CaO2). Mean Arterial pressure (MAP) is the driving force for blood flow thru capillaries that supply O2 to organs and tissues. MAP is dependent on cardiac output and systemic vascular resistance (MAP = CO x SVR). In turn, cardiac output is dependent on heart rate and stroke volume (CO = HR x SV). It is important to remember these relationships when considering the underlying cause(s) of hypotension in order to choose the best treatment. Hypotension is defined as MAP < 60 mmhg in SA, MAP < 70 mmhg in LA and SAP < 90 mmhg. Causes of hypotension related to decreased HR Drugs (opioids cause an increase in vagal tone especially when used with acepromazine), hypothermia and physiologic conditions such as cardiac disease, brachycephalic syndrome and neurologic disease. Pediatric patients are more dependent on HR for CO and cannot compensate by increasing SV as well as adults and so are more likely to become hypotensive when bradycardic. Consider including an anti-cholinergic with premedication in brachycephalic breeds, pediatric patients and when using opioids with acepromazine. Anti-cholinergic drugs should be used with caution in geriatric patients and patients with cardiac disease. Sinus tachycardia increases myocardial work and oxygen consumption while decreasing blood flow to the heart which may increase the potential for ventricular arrhythmias in patients with less cardiac reserve. Treat the underlying cause of bradycardia if possible and use anti-cholinergic drugs (atropine, glycopyrrolate). Causes of hypotension related to decreased SV Stroke volume depends on preload, contractility, afterload (vascular tone), therefore factors that affect these will decrease SV: Factors that decrease preload include: decreased blood volume (hemorrhage, dehydration, shock, sepsis) vasodilation (inhalants, acepromazine, propofol) intermittent positive pressure ventilation Factors that decrease contractility include: anesthetic drugs (inhalants, acepromazine, propofol, thiopental), cardiac disease Factors that increase afterload include: increased arterial tone due to sympathetic nervous system stimulation, hyperthyroidism, pheochromocytoma, ketamine, dexmedetomidine (this results in reflex bradycardia) **Anything that reduces systemic vascular resistance, heart rate and/or stroke volume will contribute to hypotension Treatment of hypotension consists of assessing/reducing anesthetic depth, increasing vascular volume and use of positive inotropes or vasopressors. Inhalant anesthetics cause dose dependent cardiovascular depression, therefore, limiting inhalant % by supplementing with opioids, nitrous oxide or other adjunct analgesics will decrease the MAC of inhalant and therefore cause less CV depression. Treatment of vagal induced bradycardia with anti-cholinergic drugs is indicated if the patient is also hypotensive; recommended target HR are >60bpm for medium to large dogs > 80bpm for small dogs, >90bpm for cats. Anticholinergic drugs will be less effective or not effective in the face of moderate to severe hypothermia. Stroke volume can be improved with IV fluids; crystalloid bolus of 5-10mls/kg, hetastarch at 2 5ml/kg (up to 20ml/kg), hypertonic saline at 2-4ml/kg or blood products if indicated (blood loss > 20-30% of blood volume). Positive inotropes may be used to increase contractility and therefore SV and vasopressors are used to counteract drug induced vasodilation. Ephedrine has both direct and indirect sympathomimetic properties, has greater β1>β2 activity leading to positive inotropy, increases contractility and also stimulates α mediated vasoconstriction (dose: mg/kg IV). Dopamine at a dose of <2.5 ug/kg/min stimulates DA1 & DA2 dopamine receptors and causes 1

2 vasodilation especially in the kidney, at a dose of ug/kg/min, it s primary effect is β1 agonist and + inotropy, doses >5-10 ug/kg/min stimulate α1 & α2 receptors leading to vasoconstriction and afterload so, although blood pressure increases so does myocardial work. Dobutamine is a β1 agonist that contractility and does not have an effect on SVR, it has some β2 and α effects (Dose: 1-10 ug/kg/min) Cardiac dysrhythmias Pre-operative cardiac auscultation with simultaneous palpation of peripheral pulses is recommended to identify cardiac arrhythmias prior to anesthesia. A pre-op lead II ECG allows definitive diagnosis of the arrhythmia and can monitor treatment. Further cardiac work-up (chest radiographs, echocardiograph) may be offered to the client or indicated prior to the patient undergoing general anesthesia. Arrhythmias may be seen in patients with CV disease, critical/unstable patients and those with moderate to severe electrolyte and acid/base abnormalities. Causes of cardiac dysrhythmias are many and include Drugs, increased vagal tone, increased sympathetic tone, hypoxemia, hypercapnia, electrolyte & acid/base abnormalities, cardiac disease, systemic disease (GDV, splenic mass), pain, hypovolemia, hypotension. Being familiar with the common arrhythmias associated with anesthesia and underlying diseases allows the anesthetist to quickly identify and treat if needed. Common dysrhythmias seen in peri-operative patients include: sinus bradycardia, sinus tachycardia, 2 nd degree atrioventricular (AV) block, ventricular premature contractions. In addition, the anesthetist should be able to identify the four most common arrest rhythms: Pulseless electrical activity (PEA), asystole, ventricular fibrillation, pulseless ventricular tachycardia to allow early intervention in the case of cardiac arrest. A simple systematic approach is helpful when evaluating for cardiac dysrhythmias: Identify P, QRS, T waves, Is there a P for every QRS? Is there a QRST for every P? Is the R-R interval constant or vary? Is there a pattern to variation? Do complexes come earlier than expected? Sinus bradycardia Since cardiac output is directly reliant on heart rate (CO = SV x HR) and mean arterial pressure (MAP) is dependent on cardiac output (MAP = CO x SVR), then low heart rate can cause decreased cardiac output, leading to decreased MAP. Causes include: increased vagal tone => Opioids, hypothermia, profound hypoxemia, hypoglycemia, hyperkalemia, cardiac disease, brachycephalic breeds. NOTE: dexmedetomidine causes reflex bradycardia due to vasoconstriction and increased blood pressure, do not treat with anticholinergic drugs, partial or full reversal if HR < 30bpm is indicated. Normal range for HR: Dogs bpm, Cats bpm. Treatment is indicate if bradycardia is resulting in hypotension: treat the underlying cause if known, anti-cholinergic drugs (atropine, glycopyrrolate) Sinus tachycardia Severe tachycardia will decrease stroke volume leading to decreased cardiac output and mean arterial pressure. It will also increase myocardial work & O2 consumption while decreasing cardiac perfusion which can lead to ventricular arrhythmias. Causes include: drugs (ketamine, anti-cholinergics), pain, hypovolemia, anemia, hypoxia, hypercarbia and hyperthyroidism. Investigation into the likely underlying cause is indicated. Short term tachycardia caused by IV anti-cholinergic administration can be tolerated in young healthy patients. Treatment with a beta-blocker may be indicated for sustained tachycardia; hypotension may be a side-effect of treatment. Second degree A-V block Many of the same causes as sinus bradycardia since it is also a vagally induced arrhythmia. Treat with anti-cholinergics (atropine, glycopyrrolate). Ventricular premature contractions Identified by no P wave with QRS, R-R interval varies, R wave may be wide and bizarre, there is a compensatory pause after the QRS and the complex comes BEFORE a normally expected QRS (MUST differentiate from ventricular ESCAPE complex). Causes are many and include: cardiac disease, traumatic myocarditis, hypoxemia, ischemia, electrolyte or acid/base abnormalities, GDV, pancreatitis, OSA, splenic hemangiosarcoma, drugs (thiopental, digitalis). Indications to treat include: > 20-30/min, clinical signs (hypotension, dropped pulses ), runs of > 3 in a row, multi-focal, R on T, bigeminy, trigeminy, **Rate > bpm**. These are all indications that this rhythm may progress to pulseless ventricular tachycardia or ventricular fibrillation (which are cardiac arrest rhythms). Treatment entails finding/treating the underlying cause if possible and Lidocaine 2mg/kg IV, repeat then CRI. 2

3 Hemorrhage managing acute intra-operative hemorrhage Delivery of oxygen (DO2) to tissues is essential to patient survival. DO2 is dependent on cardiac output (CO) and the content of oxygen (CaO2) in the blood (DO2 = CO x CaO2). The oxygen content in blood is made up of the O2 bound to hemoglobin (HbO2) and the oxygen dissolved in blood (PaO2). Normal healthy animals with a PCV of 20 can compensate for a decreased O2 content (RBC) by increasing CO via increasing heart rate and vasoconstriction. Anesthesia interferes with the ability to compensate by causing vasodilation and many anesthetic drugs also decrease HR. Therefore, the following pre-operative transfusion triggers are recommended: PCV < 20 => transfusion recommended PCV => maybe, depends on organ reserve, expected losses, chronicity/regeneration, expected blood loss for procedure PCV > 30 => no transfusion Even if a patient has a normal PCV pre-operatively, the anesthetist should be prepared to quantitate and treat intra-operative hemorrhage if it occurs. Induction of general anesthesia decreases PCV, TP and COP even if no crystalloid IV fluids are administered, therefore, a PCV, TP and/or COP should be measured after induction to obtain an accurate starting point for these values. The total blood volume should be calculated for the patient and then increments of loss (10%, 20% and 30%) as this corresponds to modalities of treatment. Calculate total blood volume o Dog 90ml/kg, cat 70ml/kg Examples: 20kg dog x 90ml/kg = 1800ml 2.5kg cat x 70ml/kg = 175mls Then calculate allowable blood loss at 10, 20 & 30% o Examples: 20kg dog, total blood volume = 1800ml =>10% = 180ml, 20% = 360ml, 30% = 540ml 2.5kg cat, total blood volume = 175ml =>10% = 17.5ml, 20% = 35ml, 30% = 52.5mls Clinical signs may be seen when 10% blood loss has occurred; hypotension, +/- tachycardia therefore, blood loss should be replaced as it occurs. Quantitating intra-operative blood loss Q-tip.1ml 4x4 sponge 5-15ml Lap sponge 50ml Weight 1gm = 1ml Suction cannister: mls blood loss = PCV of fluid x Volume of fluid in suction PCV of patient Treatment of blood loss starting with normal PCV 10-15% => replace with crystalloid 15-25% => replace with colloid >25-30% => replace with blood Blood products Whole Blood - RBC, protein, platelets, clotting factors; for severe blood loss (> 30-50%) Packed RBC- RBC, PCV 80-90%; for less severe blood loss or with plasma for severe blood loss mls blood required = blood volume x (desired PCV recipient PCV) Donor PCV Fresh Frozen Plasma - Albumin, plasma proteins, clotting factors; for hypoalbuminemia (along with colloids), prolonged clotting times o Need high doses; 45ml/kg to raise albumin 1g/dl Canine/Human Albumin o Human ½ of dogs have severe, sometimes fatal transfusion reactions o Canine new, no independent, controlled studies Respiratory insufficiency - hypoventilation & hypoxemia Minute ventilation is dependent on tidal volume and frequency of respiration (MV=TV x f). As MV decreases, PaCO2 & EtCO2 will increase. Normal PaCO mmhg, > 45 = hypoventilation. EtCO2 is a non-invasive indicator of PaCO2. Assuming that 3

4 ventilation and perfusion are adequately matched; EtCO2 is usually 3-5mmHg lower than PaCO2. The cause of hypoventilation during anesthesia is most commonly due to the dose dependent respiratory depression caused by anesthetic drugs. Patient factors that contribute to hypoventilation include: obesity, Cushings disease, CNS disease. Monitoring respiratory rate alone is insufficient to identify hypoventilation and therefore, monitoring of EtCO2 is recommended. Normal PaO2 in patients breathing room air is mmHg, however, it may be as high as 500mmHg on 100% O2. Causes of hypoxemia include: hypoventilation, low inspired O2, V/Q mismatch, shunt and diffusion abnormality. Pulse oximetry can be used to monitor SpO2 and is most helpful at induction and during the transition from 100% oxygen to room air at recovery. It is less helpful while patients are breathing 100% oxygen due to the shape of the oxygen dissociation curve (ie. A PaO2 of 200mmHg and 500mmHg will both show an SpO %). Induction Hypoventilation & Hypoxemia are common at induction with all induction agents, the duration/severity may be related to dose/rate of administration of the induction agent. Pre-oxygenation for at least 4minutes prior to induction delays onset of hypoxemia. **Need to recognize => ideally, a place pulse oximeter on patient during induction or as soon as soon as intubated. Treat with low frequency manual IPPV (hand-bagging) with 100% O2. Maintenance Hypoventilation is the primary concern during anesthesia maintenance. Anesthetic drugs, especially inhalant anesthetic cause decreased chemoreceptor responsiveness to PaCO2 which results in decreased respiratory rate and tidal volume, leading to increased PaCO2 and increased EtCO2. Monitoring EtCO2 allows identification of hypercarbia. Permissive hypercarbia is when EtCO2 is allowed up to 55-57mmHg; mild hypercarbia helps increase heart rate and blood pressure due to mild sympathetic stimulation. PaCO2 should be kept 60mmHg because this corresponds to ~ 7.2pH (ph.08/ every 10mmHg increase PaCO2) and cellular enzymes malfunction outside a ph range of Treatment of hypercarbia should consist of lowering the level of inhalant anesthetic and IPPV if needed. Recovery Hypoventilation & Hypoxemia are again a concern as the patient is transitioned from 100% oxygen to room air (21% oxygen). Causes during recovery include residual respiratory depression from gas anesthetics/opioids, ventilation/perfusion mismatch (atelectasis), upper airway obstruction (brachycephalic breeds). Management should include allowing at least 5-10 minutes supplemental O2 after the inhalant vaporizer is turned off, monitoring SpO2 during the transition to room air and providing supplemental oxygen until SpO2 > 95%. Supplemental O2 can be supplied by flow by for the short-term or nasal/nasal tracheal oxygen if it is anticipated to be needed longer term than the immediate post-operative period. Partial reversal may also assist in alleviating respiratory depression due to pure mu agonist opioids (.1ml (1mg) Butorphanol +.9ml NaCl, give in.2ml (.2mg) increments). Brachycephalic breeds need to be observed for evidence of upper airway obstruction after extubation and the anesthetist should be prepared to re-intubate should obstruction occur. Gastroesophageal reflux Occurs when the gastric contents flow orad into the esophagus due to decreased LES tone under anesthesia. The majority of GER is clinically silent and so the anesthetist must always ensure the ET cuff is properly inflated to protect the airway. The consequences of the acidic fluid in the lower esophagus may be esophagitis/stricture and/or aspiration. Prevention of aspiration: intubate patients who undergo general anesthesia, properly inflate ET cuff, check ET cuff for leaks PRIOR to induction, check cuff inflation periodically during procedure, deflate cuff only when patient has a strong swallow reflex. Treatment is indicated if regurgitation if observed from mouth/nose during anesthesia; suction/lavage esophagus, +/- installation of sodium bicarbonate. Hypothermia Defined as a body temperature < 100 F and clinical consequences can be seen at < 95 F. Anesthesia interferes with the body s ability to maintain body temperature by inhibiting vasoconstriction and shivering. Heat loss occurs primarily by redistribution of blood from the core body to the periphery and to some extent by conduction, convection, radiation, evaporation. The consequences of hypothermia include: decrease in MAC of inhalant anesthetics, decreased metabolic rate, prolonged recovery, increased blood viscosity, CNS depression (confusion ~ 95 F, unconscious ~86 F), increased risk of surgical infection, increased metastatsis, impaired coagulation, platelet function and wound healing. Myocardial conduction slows resulting in bradycardia that is non-responsive to anticholinergic drugs, the myocardium becomes irritable leading to ventricular arrhythmias and fibrillation at ~ 68 F. Cats are at increased risk for post-operative hyperthermia with the use of opioids if they are hypothermic intra-operatively. Prevention includes prewarming of patients, minimizing anesthesia/surgery time, warming of IV fluids and monitoring body temperature with a digital 4

5 thermometer or thermistor probe. Active patient warming can be supplied by circulating water blankets, forced warm air blankets and air-free, conductive warming blankets (Hot Dog ). Hyperthermia can be caused by excessive external heating and can occur up to 5 hours post-operatively in cats administered hydromorphone (also other opioid drugs and ketamine). The consequences of hyperthermia include: increased metabolic rate and oxygen consumption leading to increased myocardial work and cellular hypoxia. Hyperthermia due to over-warming of patients can be prevented by intra-operative monitoring of body temperature and turning down or off warming devices BEFORE target temperature is reached. Monitoring of body temperature should continue into the post-operative period. Treatment should include removal of external heat source, supplemental oxygen, IV fluids, tranquilizers and active cooling (alcohol, ice, steel table). Prolonged, dysphoric or rough recovery Lighted gas anesthetic during surgical closing, turn off vaporizer, empty reservoir bag, increase oxygen flow, allow patient to breathe oxygen only for 5-10 minutes before disconnecting from circuit, monitor SpO2 during transition to room air (oxygen wash out will take 2-3 minutes depending on the patients respiratory rate and tidal volume ie. The amount of residual respiratory depression. Even mild hypoventilation (EtCO2 ~ 52-55mmHg) may lead to hypoxemia when the patient is breathing room air. Provide supplemental oxygen until SpO2 > 95%. Supplemental O2 can be supplied by flow by for the short-term or nasal/nasal tracheal oxygen if it is anticipated to be needed longer term than the immediate post-operative period. Partial reversal may also assist in alleviating respiratory depression and sedation due to pure mu agonist opioids (.1ml (1mg) Butorphanol +.9ml NaCl, give in.2ml (.2mg) increments). Dysphoria/rough recovery Emergence delirium is a well known phenomenon in human medicine, occurring in 5% of adults and 12-13% of children. It is defined as a dissociated state of consciousness in which the patient is inconsolable, irritable, uncooperative, typically thrashing, crying, moaning or incoherent and does not recognize familiar objects or people. This condition can also be seen in our veterinary patients, especially in patients that have a short time to awakening at the end of anesthesia. It is often difficult to discern the exact cause of rough recovery in veterinary patients, but some possibilities include: pain, noise sensitivity (due to opioids, dexmedetomidine), hypoxemia, urinary bladder discomfort or emergence agitation. It is important to remember that several life threatening considerations (eg. hypoxia, severe hypercarbia, hypotension, hypoglycemia, increased intracranial pressure) may also result in disorientation and agitation. These entities must be monitored for and treated promptly. Bladder distention may also yield a similar clinical picture. Prevention/preparation Anticipate patient analgesia and sedation needs for recovery. Empty urinary bladder at the end of surgery/procedure Acepromazine => 0.005mg/kg at the time of discontinuing inhalant, especially if dexmedetomidine was included in premedication and > an hour has elapsed. Dexmedetomidine 1.0ug/kg IV very fast onset of action, provides analgesia and sedation in the event that differentiation between pain or emergence is not possible, potent sedation to prevent risk or injury to patient or personnel. 5