Complications of Anesthesia Study Guide.docx

**[Complications of Anesthesia Study Guide]** 1. **What are some possible causes of VT?** a. Hypoxemia, MI, acidosis, hypokalemia, hypomagnesemia, and irritation due to CVL b. Hs & Ts i. Heart rate (vagal stimulus), Hypovolemia, hypoxemia, hydrogen ion aci...

**[Complications of Anesthesia Study Guide]** 1. **What are some possible causes of VT?** a. Hypoxemia, MI, acidosis, hypokalemia, hypomagnesemia, and irritation due to CVL b. Hs & Ts i. Heart rate (vagal stimulus), Hypovolemia, hypoxemia, hydrogen ion acidosis, hyperkalemia, hypokalemia, hypoglycemia, hypocalcemia, hypothermia, hyperthermia (MH) ii. Toxins, tamponade, tension pneumothorax, thrombosis (coronary & pulmonary) 2. What is appropriate treatment for VT? c. Stable/unsustained Vtach \--\> no immediate treatment; just try to reverse causes d. Stable sustained Vtach iii. Synchronized cardioversion (150-200 biphasic; 360 j monophasic) iv. Beta blockers: Esmolol 10-100 mg IV or 25-300 mcg/kg/min (can also use metoprolol/propranolol) v. Amiodarone: 150 mg over 10 min then 1 mg/min for 6 hrs vi. Lidocaine: 1.5 mg/kg IV \--\> infusion @ 1-4 mg/min e. Unstable ACLS , Lil bit of CPR 3. What are common causes of perioperative cardiac arrest related to the following categories: medication, respiratory, and cardiovascular? f. Found this from a recent article () vii. *Medication* \--\> anaphylaxis to medications (Sux, Roc) viii. *Respiratory* \--\> airway obstruction, difficult intubation, laryngospasm ix. *Cardiovascular* \--\> severe hemorrhage, bradycardia, venous embolism, MI, vasovagal syndrome, sepsis hemodynamic instability 4. What are the initial steps of resuscitation for intraoperative cardiac arrest? ACLS 5. What are some drugs used in the OR that can precipitate an anaphylactic reaction? g. **Neuromuscular Blocking Agents** x. 50-70% of cases xi. Succinylcholine /rocuronium most frequently reported xii. Atracurium, mivacurium and doxacurium- anaphylactoid reactions h. **Latex** (20%) xiii. High risk: health care workers, those having multiple surgeries (spina bifida), atopic individuals, and those allergic to mango, kiwi, bananas, and other fruits i. **Antibiotics** xiv. Β lactam ring antibiotics, penicillin, cephalosporin xv. Cross reactivity btw penicillin & 1st-gen cephalosporins about 10% xvi. Red man syndrome (vancomycin) -rapid admin d/t histamine release j. Propofol xvii. Egg lecithin (egg yolk) allergy k. Narcotics xviii. Morphine and meperidine \--\> anaphylactoid reactions (fentanyl rare) l. Injectable Dyes xix. Isosulfan blue (methylene blue reactions very rare) & Iodinated contrast material m. Paraaminobenzoic Acid xx. Ester local anesthetic preservative causing anaylphylactic reactions (procaine, chloroprocaine, tetracaine, cocaine) n. Colloid Volume Expanders xxi. Dextrans with highest risk, hetastarch safest xxii. No cross-sensitivity between different colloids 6. What is the treatment for intraoperative anaphylaxis? o. Discontinue causative agent p. Inform surgeons q. Maintain airway and support oxygenation and ventilation r. Decrease or stop anesthetic agents if hypotension is present s. Expand circulating volume rapidly t. Administer epinephrine IV (epi, epi, epi) u. Administer H1 antagonist (benadryl) v. Administer corticosteroids (solumedrol or solucortef) w. Administer H2 antagonist (cimetidine) -- competitively blocks action of histamine on myocardium and peripheral cells x. Invasive monitoring if necessary 7. What is the treatment for an intraoperative gas embolism? y. S/s: sudden decrease in ETCO2, BP, or SpO2; sudden increase in CVP, dyspnea, respiratory distress in awake patient z. Treatment: xxiii. 100% FiO2 10-15 LPM xxiv. Turn off volatile anesthetics + vasodilating drips xxv. Give IV vasopressor bolus to support circulation & consider rapid fluid bolus xxvi. Evaluate right heart w/ TEE/TTE \-\--\> maintain sinus rhythm, normal RV volume status, RV contractility, decrease RV afterload xxvii. Place patient in left lateral decubitus position xxviii. Attempt removal of air -- aspirate from central line if present 8. What is the treatment for local anesthetic toxicity? See \#9 9. How should cardiovascular collapse in a patient that has received neuraxial anesthesia be managed? a. First xxix. Airway management + seizure suppression b. Manage arrythmias xxx. ACLS/BLS xxxi. Avoid: Vaso, CCBs, Beta blockers, Lidocaine xxxii. Propofol will worsen contractility/vasodilation xxxiii. Reduce Epi to \< 1 mcg/kg c. Lipids!! 20% xxxiv. Bolus: 1.5 ml/Kg over 1 min xxxv. Drip: 0.25 ml/kg/min for at least 10 mins AFTER regaining cardiac stability 10. What are the 5 standards for post anesthesia care? 1. All patients who have received general anesthesia, regional anesthesia or monitored anesthesia care shall receive appropriate post anesthesia management. 2. A patient transported to the pacu shall be accompanied by a member of the anesthesia care team who is knowledgeable about the patient's condition. The patient shall be continually evaluated and treated during transport with monitoring and support appropriate to the patient's condition. 3. Upon arrival in the pacu, the patient shall be re-evaluated, and a verbal report provided to the responsible pacu nurse by the member of the anesthesia care team who accompanies the patient. 4. The patient's condition shall be evaluated continually in the pacu. 5. Physician is responsible for the discharge of the patient from the post anesthesia care unit 11. **What is the minimum time interval requirement for VS measurement and recording in the PACU? \*tricky\*** d. Recording = 15 min e. Measurement = continuously HR, SpO2; intermittent BP 12. What are some postop physiologic disorders that may manifest in the PACU? f. Most common = PONV, hypoxia, hypothermia, shivering, cardiovascular instability 13. What is the most frequent cause and usual mechanism of upper airway obstruction in the PACU? g. Most often caused by inadequate recovery of the airway reflexes and tone and is seen commonly in patients with obesity and/or preexisting obstructive sleep apnea (OSA) (from mass gen textbook). 14. How does upper airway obstruction present clinically? xxxvi. lack of adequate air movement xxxvii. Intercostal/suprasternal retractions xxxviii. Paradoxical abdominal & chest wall motion during inspiration xxxix. COMPLETE obstruction = silent xl. Partial: snoring (obstruction above larynx) or stridor (if perilaryngeal) 15. Why might residual neuromuscular blockade not manifest until the patient is in the PACU? h. Insidious hypoventilation leading to respiratory acidosis/regurgitation can occur/show up later in recovery i. (idk thats what i found in NAgelhout) j. Miller (pg. 2928): **Residual neuromuscular blockade may not be evident on arrival in the PACU because the diaphragm recovers from neuromuscular blockade before the pharyngeal muscles do.** 16. **What are two potential reasons for inadequate reversal of neuromuscular blockade?** k. Pseudocholinesterase deficiency (dibucaine \#\ tracheotomy 25. How can upper airway obstruction secondary to opioids or benzodiazepines be treated in the PACU? i. Opioids -- reverse with Naloxone 0.04 mg IV; Benzos -- reverse with Flumazenil 0.2 mg IV 26. How can upper airway obstruction secondary to residual neuromuscular blockade be treated? j. If Rocuronium or Vecuronium used: Sugammadex 22. 2 mg/kg IV for TOF 2/4; 4 mg/kg IV for TOF 0/4 or 1-2 PTC 23. If Roc RSI dose just given -- 16 mg/kg IV k. If Succinylcholine used: no reversal supportive care -- chin lift, jaw thrust, 100% fio2, CPAP l. If Atracurium or Cisatracurium used: 24. Neostigmine: 0.05-0.07 mg/kg (max 5 mg) 25. Glycopyrrolate: 0.16-0.2 mg/mg of Neostigmine 27. How can upper airway obstruction in the PACU after thyroid or carotid surgery be managed? m. Decompress airway by releasing clips or sutures on wound + evacuating hematoma; Emergency tracheostomy if needed 28. What are some methods to monitor for upper airway obstruction during transport from OR to PACU? n. Listen for patient **snoring, stridor, or absent breath sounds** o. Keep vigilant watch of O2 saturation and waveform p. Look for fogging in face mask q. Observe for labored breathing pattern -- retractions, paradoxical abd/chest wall movements 29. **What are some common causes of hypoxemia in the PACU? [POPPA, Ur BAHD]!** liv. Pulmonary embolism lv. OSA lvi. Pneumothorax lvii. Pulmonary edema lviii. \*Atelectasis lix. Upper airway obstruction lx. Bronchospasm lxi. Aspiration of gastric contents lxii. \*Hypoventilation lxiii. Diffusion hypoxia r. Most common = **atelectasis + alveolar hypoventilation** 30. What are some potential causes of postop hypoventilation? s. ↓ ventilatory drive t. Pulmonary and respiratory muscle deficiency u. Inadequate reversal of neuromuscular blockade v. Inadequate analgesia w. Bronchospasm x. Pneumothorax  31. **What is the normal ventilatory response to elevated carbon dioxide levels? How is this affected by residual anesthetic drugs?** y. Normal ventilatory response = breathe faster & deeper to blow off CO2 z. Anesthesia drugs \-- we move CO2 response curve to the **right** = decreased alveolar ventilation for increased PaCO2 \-\--\> takes more CO2 to respond with increased RR and increased volume lxiv. Only to a point (setpoint)! lxv. At some point your body can't respond -- different for everyone lxvi. There's a point at which your CO2 is so high that it causes sedation lxvii. Shifting curve to right = increases apnea threshold, so patient needs even higher CO2 build up to kick in respiratory drive \... but then they may develop CO2 narcosis 32. In the PACU, how can arterial hypoxemia secondary to hypercapnia be reversed? a. Reversed by administration of supplemental oxygen or by normalizing patient's PaCO2 by external stimulation of the patient to wakefulness, pharmacologic reversal of opioid or benzo effect, or controlled mechanical ventilation of patient's lungs b. If hypercapnia caused by: lxviii. Over-sedation from narcotics or benzos \-\--\> admin reversal agents (cautiously so you don't take away full pain-relieving effects) lxix. Lack of adequate analgesia \-\--\> admin more pain meds so patient can breathe deeper/stop breath holding lxx. Inadequate reversal of NMBA \-\--\> admin Sugammadex or Neostigmine/Glycopyrrolate lxxi. Neurologic injury sustained during surgery \-\--\> neuro consult immediately, intubate patient for airway protection lxxii. COPD \-\--\> non-invasive ventilation (face mask, NC, opti-flow, CPAP) lxxiii. Bronchospasm \-\--\> admin 100% FiO2 10-15 LPM, Epinephrine 5-10 mcg IV, Albuterol or Ipratropium for bronchodilation, Hydrocortisone 100 mg IV, nebulized racemic Epi lxxiv. Pneumothorax \-\--\> get CXR stat, need chest tube insertion if hemodynamically compromised 33. What is diffusion hypoxia? c. May occur during washout of nitrous oxide upon emergence from GA \-\--\> nitrous rapidly diffuses out of blood into alveoli when it's discontinued, producing dilution of alveolar oxygen tension and hypoxemia d. High inspired FiO2 by face mask can prevent hypoxemia 34. Describe the hypoxic pulmonary vasoconstriction response and identify some drugs that may inhibit it. e. Hypoxic pulmonary vasoconstriction lxxv. Pulmonary vascular mechanism that diverts blood flow away from poorly ventilated areas of the lung to minimize V/Q mismatch \[reduces perfusion of the under ventilated lung\] f. Drugs that inhibit HPV: lxxvi. All inhaled anesthetics -- Nitrous Oxide, Sevoflurane, Isoflurane, Desflurane, Halothane 26. Vasodilation produced by these agents blunts body's HPV mechanism lxxvii. Nitroprusside -- vasodilation blunts HPV mechanism 35. What coexisting lung diseases may result in a decreased diffusion capacity and subsequent arterial hypoxemia in the PACU? g. Emphysema h. Interstitial lung disease i. Primary pulmonary hypertension j. Pulmonary fibrosis 36. What are the typical causes of cardiogenic and noncardiogenic pulmonary edema in the PACU? k. Cardiogenic \-\--\> caused by intravascular volume overload, CHF l. Noncardiogenic \-\--\> airway obstruction (postobstructive pulmonary edema), sepsis, transfusion (TRALI) 37. What is postobstructive pulmonary edema? m. Transudative edema produced by the exaggerated negative intrathoracic pressure generated by an inspiratory effort against a closed glottis \-\--\> negative intrathoracic pressure and increased venous return escalate hydrostatic pressure gradient across the pulmonary vascular bed, promoting the transudation of fluid 38. What are some causes of postobstructive pulmonary edema presenting in the PACU? n. Most common = laryngospasm o. Can also be caused by any condition that occludes the upper airway 39. How might postobstructive pulmonary edema present in the PACU? p. Arterial hypoxemia observed within 90 minutes of the upper airway obstruction q. Bilateral fluffy infiltrates on CSR 40. How is postoperative pulmonary edema diagnosed and treated? r. Diagnosed via CXR s. Treatment = supportive, supplemental oxygen, diuresis, positive-pressure ventilation (if severe) 41. What is transfusion related lung injury (TRALI)? When is it likely to be presented? How is TRALI distinguished from transfusion associated circulatory overload? t. TRALI -- acute, noncardiogenic pulmonary edema associated with hypoxia that occurs during or after a blood transfusion lxxviii. Presentation 27. Typically exhibited 1-2 hours after the transfusion of plasma-containing blood products \[PRBCs, whole blood, FFP, PLTs\] 28. Fever 29. Systemic hypotension lxxix. Distinguished from transfusion-associated circulatory overload via following criteria 42. What is the FiO2 that can be delivered through a simple nasal canula? What are other options of O2 delivery in the PACU? 43. What is a high flow nasal canula? What is its advantage? u. Deliver FiO2 equal to that delivered by traditional mask devices lxxx. 40 LPM, 37 degrees Celsius, 99.9% relative humidity lxxxi. Vapotherm = 10-40 LPM v. Advantage: deliver high-flow oxygen directly to nasopharynx throughout the respiratory cycle 44. **Is there a role for CPAP and non-invasive positive pressure ventilation (NIPPV) in the PACU?** w. Yes -- OSA patients. x. Wouldn\'t put it on patients that weren't already on it though 45. What are some factors associated with hypertension in the PACU? y. Preoperative hypertension z. Arterial hypoxemia a. Hypervolemia b. Emergence excitement c. Shivering d. Drug rebound e. Increased ICP f. Increased SNS activity g. Hypercapnia h. Pain i. Agitation j. Bowel distension k. Urinary retention 46. What are some complications that can result from hypertension in the PACU? l. Heart failure, MI m. Arrythmias n. Bleeding, Stroke o. AKI 47. What are some causes of hypotension in the PACU? p. Intravascular volume depletion \--\> persistent fluid losses, ongoing third-space translocation of fluid, bowel preparation, GI losses, surgical bleeding q. Increased capillary permeability \--\> sepsis, burns, TRALI r. Decreased cardiac output \--\> myocardial ischemia or infarction, cardiomyopathy, valvular disease, pericardial disease, cardiac tamponade, cardiac dysrhythmias, pulmonary embolus, tension pneumothorax, drug induced (beta blockers, calcium channel blockers) s. Decreased vascular tone \--\> sepsis, allergic reactions (anaphylactic, anaphylactoid), spinal shock (cord injury, iatrogenic high spinal), adrenal insufficiency  48. What are the most common causes of allergic reactions leading to hypotension in the perioperative setting? t. **So I\'m going to go with NMBs -- as they're \#1?** lxxxii. Succinylcholine, Rocuronium = anaphylaxis lxxxiii. Atracurium, Mivacurium, Doxacurium = anaphylactoid u. I think just know all the drugs associated with allergic rxns 49. How is myocardial ischemia detected in the PACU? (Miller 8^th^ edition pg. 2937) v. Interpretation of changes on the ECG in the PACU is influenced by the patient's cardiac history and risk index. w. PATIENTS AT LOW RISK (\< 45, with no known cardiac dz, and only 1 risk factor) lxxxiv. Postop ST-segment changes on the ECG do not usually indicate myocardial ischemia. lxxxv. Relatively benign causes of ST changes in patients at low risk include: anxiety, esophageal reflux, hyperventilation, and hypokalemia. lxxxvi. In general, these patients require only routine PACU observation unless associated signs and symptoms warrant further clinical evaluation. lxxxvii. A more aggressive evaluation is indicated if the changes are accompanied by cardiac rhythm disturbances or hemodynamic instability (or both) x. PATIENTS AT HIGH RISK lxxxviii. In contrast to patients at low risk, ST-segment and T-wave changes on the ECG in patients at high risk can be significant even in the absence of typical signs or symptoms. lxxxix. In this patient population, any ST or T-wave changes that are compatible with myocardial ischemia should prompt further evaluation to rule out myocardial ischemia. xc. Determination of serum troponin levels is indicated when myocardial ischemia or infarction is suspected in the PACU. Once blood samples for measurement of **troponin** are obtained and a **12-lead ECG** is completed, arrangements must be made for the appropriate **cardiac monitoring and cardiology follow-up.** y. CARDIAC MONITORING xci. In the immediate postoperative period, myocardial ischemia is rarely accompanied by chest pain, and confirming myocardial ischemia in a patient in the PACU is **dependent on the sensitivity of the cardiac monitoring** xcii. Although a combination of leads II and V5 will reflect 80% of the ischemic events detected on a 12-lead ECG, visual interpretation of the cardiac monitor is often inaccurate. xciii. Because of human error, the American College of Cardiology guidelines recommend that **computerized ST-segment analysis** be used (if available) to monitor this patient population in the immediate postoperative period. xciv. A recent study suggests that a postoperative 12-lead ECG obtained in the PACU may be a valuable tool to adjust risk stratification in patients older than 50 years of age who are at low risk for cardiac ischemia. xcv. However, at this time a **routine postoperative 12-lead ECG is recommended only for patients with known or suspected coronary artery disease who have undergone high- or intermediate-risk surgery** 50. What are some factors that may contribute to cardiac arrythmias in the PACU? (Miller) z. Hypoxemia, hypoventilation and associated hypercapnia, endogenous/exogenous catecholamines, electrolyte abnormalities, acidemia, fluid overload, anemia, substance withdrawal 51. What are some possible causes of ST in the PACU? (Miller) a. Pain, agitation, hypoventilation associated w/hypercapnia, hypovolemia, shivering = common b. Bleeding, cardiogenic/septic shock, pulmonary embolism, thyroid storm, malignant hyperthermia = less common 52. How should new onset a-fib be managed in the PACU? (Miller) c. Control of the ventricular response rate is the immediate goal of tx of new onset afib d. **Patients who are hemodynamically unstable may required prompt electrical cardioversion, but most can be pharmacologically treated w/IV beta blocker/CCB** e. **Diltiazem = CCB of choice for pts that can't take BBs** f. **If hemodynamic instability is a concern, then short acting BB esmolol is an option** g. Rate control with these agents is often enough to result in chemical cardioversion for the postop pt who's arrhythmia may be catecholamine driven h. For chemical cardioversion, then **amiodarone** load can be started in PACU knowing that QT prolongation, bradycardia, and hypotension may accompany 53. What drugs may contribute to VT in the PACU? (Miller) i. True VT is rare and indicative of an underlying cardiac pathologic condition j. In the case of torsades de pointes, QT prolongation on the EKG may be intrinsic or drug related (amiodarone, procainamide, droperidol) 54. What are some possible causes of bradycardia in the PACU? (Miller) k. Bradycardia in PACU is often iatrogenic l. Drugs: beta blockers, anticholinesterase reversal of NMBs, opioids, dexmedetomidine m. Procedure/patient: bowel distention, increased ICP or IOP, spinal anesthesia xcvi. High spinal block that blocks cardioaccelerator fibers (T1-T4) can produce severe bradycardia xcvii. The resulting sympathectomy, bradycardia, and possible IV fluid volume depletion and associated decreased venous return can produce sudden bradycardia and cardiac arrest even in young healthy patients 55. What is the incidence of postoperative delirium? n. **\> 50 years old** xcviii. **Elective surgery = 10%** will experience some degree of postoperative delirium within the first 5 postoperative days xcix. **Repair of hip fracture = \>35%** c. **Bilateral knee replacement = 41%** o. Although the majority of these patients are older adults who develop delirium within the first several postoperative days, the percentage who become delirious while recovering in the PACU is not well known; 56. What are some risk factors and causes of postoperative delirium be managed? p. Preop risk factors ci. \(1) advancing age (70 years and older), cii. \(2) preoperative cognitive impairment, ciii. \(3) decreased functional status, civ. \(4) alcohol abuse, cv. \(5) history of delirium. q. Intraop risk actors cvi. Surgical blood loss, hematocrit less than 30%, and the number of intraoperative blood transfusions. cvii. In adults, intraoperative hemodynamic derangements (hypotension), the administration of nitrous oxide, and the anesthetic technique (general versus regional) have not been shown to increase the risk of postoperative delirium or longer-term POCD. r. Clinical evaluation of a patient with delirium in the PACU includes a thorough evaluation of any underlying disease or metabolic derangement, such as **hepatic and/ or renal encephalopathy.** The workup for postoperative delirium must exclude or treat iatrogenic factors, including **inadequate hydration, perioperative medications, arterial hypoxemia, hypercapnia, pain, sepsis, and electrolyte abnormalities.** 57. What is emergence delirium? s. The American Psychiatric Association defines delirium as an acute change in cognition or disturbance of consciousness that cannot be attributed to a preexisting medical condition, substance intoxication, or medication; however, preexisting conditions such as age, functional status, and substance abuse influence the risk of immediate postoperative delirium. 58. **What is the differential diagnosis of postoperative renal dysfunction?** t. Differential dx of postop renal dysfunction includes = prerenal, intrarenal, postrenal causes u. Frequently, the cause is multifactorial with an intraop insult exacerbating a preexisting renal insufficiency v. In the PACU, dx efforts should focus on ID and tx of the readily reversible causes of oliguria w. When appropriate, one should confer with the surgical team regarding the details of the surgical procedure (uro/gyno) to rule out anatomic obstruction or disruption of the ureters, bladder, or urethra x. \*Notice: she didn't say "oliguria, polyuria, anuria" - gotta think through all those things (this list below is shit she said in class reviewing this doc) cviii. Hypotension cix. Hypovolemia cx. AKI cxi. ATN cxii. Blocked catheter cxiii. Opioid urinary retention (more common in M \> F; esp young males) \-- straight cath and see cxiv. Blood in urine? Figure out if it's trauma related (foley insertion/removal) or if it's higher up (bladder/kidneys) 59. How is oliguria defined? What is the most common cause of oliguria in the PACU? (Miller) y. **Oliguria = UOP \< 0.5 mL/kg/hr** z. Most common cause of oliguria in PACU = depletion of intravascular fluid volume 60. How should oliguria due to decreased intravascular volume be managed in the PACU? (Miller) a. **A fluid challenge (500-1000 mL of crystalloid) is usually effective in restoring UOP** b. Hct is indicated when surgical blood loss is suspected and repeated volume boluses are required to maintain UOP c. Volume resuscitation to maximize renal perfusion is particularly important to prevent ongoing ischemic injury and the development of ATN d. If a fluid challenge is contraindicated or oliguria persists, then assessment of intravascular fluid volume status and cardiac function is indicated to differentiate hypovolemia from sepsis and low CO states e. Fractional excretion of Na+ can be useful in determining the adequacy of renal perfusion, assuming diuretics haven't been given f. However, dx of prerenal azotemia will not differentiate hypovolemia, CHF, or hepatorenal syndrome g. further evaluation w/central venous monitoring or ECHO or both may facilitate the differential diagnosis 61. What are the risk factors for postoperative urinary retention? (Miller pg. 2939) h. Urinary retention = bladder volume \> 600 mL in conjunction with an inability to void within 30 minutes i. **Age \> 50 years, intraop fluid \> 750 mL, bladder volume on entry to the PACU \> 270 mL** j. Use ultrasound to ID patients at high risk for possible urinary retention 62. Which patients are at risk for acute renal dysfunction due to intra-abdominal hypertension? (Miller) k. Intraabdominal HTN should be considered in any patient with oliguria + tense abdomen after surgery l. Elevated IAP can impede renal perfusion and lead to renal ischemia and postop renal dysfunction m. **Normal IAP (not obese) = \~5 mmHg** n. IAP HTN is graded into 4 categories cxv. 1: 12-15 mmHg cxvi. 2: 16-20 mmHg cxvii. 3: 21-25 mmHg cxviii. 4: \> 25 mmHg o. Abdominal compartment syndrome = IAP \> 20 mmHg with or without abdominal perfusion pressure \< 50 mmHg p. IAP HTN accounted for 40% of new onset renal insufficiency in a study \--\> postop renal impairment independently associated with 4 factors: cxix. **Hypotension, sepsis, older age, increased IAP** q. Bladder pressure (an indirect measure of IAP) should be measured in pts whom IAHTN is suspected to ensure initiation of prompt intervention to relieve the pressure and restore renal perfusion r. Bladder pressure is measured at end expiration with the pt in supine position and in absence of abdominal muscle contractions s. Transducer is placed in the midaxillary line (like art line) 63. Which patients are at risk for acute renal dysfunction due to rhabdomyolysis? How should it be managed? t. Risk cxx. Rhabdomyolysis may complicate the postoperative course of patients who have suffered **major crush or thermal injury.** cxxi. The incidence is also significantly increased in patients who are **morbidly obese and who undergo bariatric surgery.** cxxii. Rhabdomyolysis has been reported to occur in 22.7% of 66 consecutive patients undergoing **laparoscopic bariatric surgery.** cxxiii. Risk factors include **increased BMI and the length of the surgery.** u. Management cxxiv. Patient history and the operative course should guide the decision to measure **creatine phosphokinase** in the PACU. cxxv. **Early aggressive hydration** to maintain urine output is the [mainstay] of treatment. cxxvi. **Loop diuretics** can be used to flush the renal tubules and to avoid fluid overload. cxxvii. The infusion of **mannitol** to enhance the elimination of myoglobin casts from the renal tubules and **bicarbonate** to protect against myoglobin toxicity is commonly practiced but may not provide further benefit. 30. In a study of more than 2000 trauma patients with rhabdomyolysis, the infusion of bicarbonate and mannitol did not further decrease the incidence of acute renal failure cxxviii. No evidence suggests that **renal dose dopamine** affords renal protection in this setting. cxxix. In severe cases, an attempt can be made to **remove myoglobin** by **CRRT** 31. Unlike conventional hemodialysis filters that do not remove circulating myoglobin, **high-flux membranes** can be effective. Continuous renal replacement modes typically use high-flux membranes. 32. Additionally, convection (i.e., the mechanism of solute removal in continuous hemofiltration) removes larger molecular weight solutes than diffusion (i.e., the mechanism of solute removal in conventional hemodialysis) 64. Which patients are at risk for acute renal dysfunction due to contrast nephropathy? How should it be managed? (Miller) v. **Angiography with intravascular stent placement** is replacing open surgical procedures to treat [carotid stenosis, aortic aneurysm, and peripheral vascular disease]. As a result, contrast nephropathy will be more frequently included in the differential diagnosis of postoperative renal dysfunction. w. Perioperative attention to **adequate hydration** is indicated in any patient who has received an intravenous contrast agent. Aggressive hydration **with normal saline provides the single most effective protection against contrast nephropathy.** x. Alkalinization of the urine with **sodium bicarbonate** has been shown to provide additional protection. cxxx. If bicarbonate is used for renal protection, then 154 mEq/L should be infused at a rate of 3 mL/kg/hr for 1 hour before injection of a contrast agent, followed by 1 mL/kg/hr for 6 hours. y. **Mucomyst** is a relatively inexpensive and easily administered medication (single oral dose before and after procedure) that may also provide protection. 65. **What is the incidence of post-operative shivering? How should it be treated? (pg. 3902 Barash)** z. Incidence cxxxi. 5-65% after GA cxxxii. 33% after epidural a. DLG cxxxiii. **Forced air-warming devices = most efficacious for treating hypothermia** cxxxiv. IV fluids and blood should be warmed cxxxv. For most patients, shivering from mild-to-moderate hypothermia is uncomfortable but self-limited, and needs no treatment other than rewarming and reassurance cxxxvi. Wrap their heads cxxxvii. **Meperidine = most effective in conjunction rewarming \--\> can use fentanyl when meperidine is contraindicated** cxxxviii. Make sure you fully reverse them (withholding reversal of relaxants in ventilated, sedated patients attenuates shivering but increases rewarming time) cxxxix. Dexmedetomidine, clonidine (Barash) cxl. Propofol is the most common b. Causes of shivering (Barash) cxli. **Propofol** \> penthothal cxlii. During emergence, hypothalamic regulation generates shivering to increase endogenous heat production cxliii. Shivering is accentuated by tremors r/t emergence from inhalational anesthesia \--\> tremors exhibit clonic & tonic components, likely reflect decreased cortical influence on spinal cord reflexes cxliv. Pain cxlv. SNS stimulation cxlvi. Nervous -- release of their nerves cxlvii. OB hormones "birth quakes" c. Consequences of shivering (Barash) cxlviii. Incidental trauma cxlix. Disrupts medical devices cl. Interferes w/EKG and pulse ox cli. O2 consumption and CO2 production can increase 200% \--\> increases in MV and CO might precipitate ventilatory failure in pts w/limited reserve or MI in those with CAD d. Treatment (Miller) clii. Intervention includes the identification and treatment of **hypothermia**, if present. cliii. Accurate **core body temperatures** can be most easily obtained at the **tympanic membrane.** Axillary, rectal, and nasopharyngeal temperature measurements are less accurate and may underestimate the core temperature. cliv. **Forced air warmers** are used to warm patients with hypothermia. clv. Most commonly used opioid: **meperidine, 0.35 to 0.4 mg/kg (12.5 to 25 mg IV)** clvi. Other drugs: 33. **Ondansetron** 34. **Clonidine** 35. **Low-dose ketamine (0.5 mg/kg IV)** infusion before general and regional anesthesia has been shown to be an effective prophylactic measure. 66. What are some adverse effects of postoperative hypothermia? (Barash pg. 3902) e. Complicates and prolongs care in PACU by 40-90 min f. Increases SNS activity w/increased epi and NE levels g. Elevates PVR h. Decreases venous capacitance i. Risk of myocardial ischemia and dysrhythmia from mechanical myocardial stimulation is increased j. Vasoconstriction interferes w/reliability of pulse ok and art line k. Hypoperfusion jeopardizes marginal tissue grafts and promotes tissue hypoxia and metabolic acidemia l. The higher affinity of Hgb compromises O2 unloading to hypothermic tissues m. Platelet sequestration, decreased platelet function, reduced clotting factor function \--\> coagulopathy n. Moderate hyperglycemia, cellular immune responses compromised, postop infection rates increase o. Decrease in MAC of inhaled anesthetics (5- 7% per 1 degree C cooling) accentuates residual sedation \--\> prolonged inhaled anesthesia p. Low perfusion and impaired biotransformation might increase DOA of NMBs & sedatives q. **Moderate hypothermia (28-32 C) = cardiac dysrhythmias** r. **Severe hypothermia (≤ 28 C) = interferes w/cardiac rhythm generation and impulse conduction** clvii. **EKG: PR, QRS, QT intervals lengthen, J waves appear** s. **Temps \< 28 C = spontaneous vfib** t. Miller clviii. Mild-to-moderate hypothermia (33° C to 35° C) 36. Inhibits platelet function, coagulation factor activity, and drug metabolism. 37. It exacerbates postoperative bleeding, prolongs neuromuscular blockade, and may delay awakening. 38. Whereas these immediate consequences are associated with a prolonged PACU stay, long-term deleterious effects include an increased incidence of myocardial ischemia and myocardial infarction, delayed wound healing, and increased perioperative mortality. 67. What are some factors associated with an increased incidence of PONV? (Barash pg. 3910) u. Patient factors clix. Females of childbearing age clx. Non-smokers clxi. Hx PONV clxii. Hx motion sickness clxiii. Menstruating females clxiv. Obese clxv. "Children over the age of 2" v. Surgeries clxvi. Longer duration (↑exposure to lipophilic drugs) clxvii. Eye procedures \*Strabismus surgery clxviii. ENT procedures \*T&A clxix. Peritoneal or intestinal irritation 39. Cholecystectomy 40. Gynecological 41. Laparoscopic 42. \*Herniorrhaphy 43. \*Male genitalia clxx. Cosmetic/plastic procedures clxxi. Breast clxxii. Orthopedic w. Periop factors clxxiii. NPO (starvation, dehydration) clxxiv. Autonomic imbalance clxxv. Pain clxxvi. Drugs 44. Anesthetics \--\> chemotaxic center 45. Opioids 46. All inhaled gases (sevo & des most) 47. GA \> regional 48. Etomidate/ketamine *\> propofol/barbs* 49. Neostigmine x. More serious preop causes that should be addressed prior to treatment: clxxvii. Hypotension, hypoxia, hypoglycemia, increased ICP, gastric bleeding 68. What is the simplified risk score for identifying patients at risk for PONV? 69. How can PONV be prevented or treated? y. Preventing PONV = easier than treating established N/V z. Multimodal approach works best because of its multifactorial etiology a. Preop clxxviii. Meclizine 25 mg (hx motion sickness) clxxix. Aprepitant 40 mg PO before anesthesia (substance P antagonist that blocks NK1 receptor) can work in very high risk patients w/refractory N/V clxxx. Scopolamine b. Intraop clxxxi. TIVA w/prop best 😊 clxxxii. 1 of these 50. Ondansetron 4-8 mg IV prior to emergence \--\> caution w/prolonged QT 51. Dexamethasone 4-8 mg IV prior to emergence 52. Droperidol (prolonged QT) = 0.625 mg IV \--\> EKG monitoring 2-3 hours after admin clxxxiii. Propofol (instead of gas) clxxxiv. Benzos clxxxv. Hydration c. Postop/rescue clxxxvi. Promethazine (nonselective antihistamine) \--\> caution w/increased sedation in children and pts w/OSA d. Acupuncture, acupressure, TENS 70. What are some common causes of delayed awakening in the PACU? How should it be managed? e. Even after prolonged surgery and anesthesia, a response to stimulation in **60 to 90 minutes** should occur f. When delayed awakening occurs, evaluating the **vital signs** (e.g., systemic arterial blood pressure, arterial oxygenation, ECG, body temperature) and performing a **neurologic examination** are important steps; patients may be hyperreflexia in the early postoperative period. g. Monitoring with **pulse oximetry** and analysis of **arterial blood gases** and pH can detect problems of oxygenation and ventilation. h. Additional blood studies may be indicated to evaluate possible **electrolyte derangements** and **metabolic disturbances (e.g., blood glucose concentration).** i. Most common causes clxxxvii. **Residual sedation from drugs used during anesthesia is the most frequent cause of delayed awakening in the PACU.** 53. If residual effects of **opioids** are a possible cause of delayed awakening, then titrated intravenous doses of **naloxone (20- to 40-μg increments in adults)** should be carefully administered while keeping in mind that this treatment will also antagonize opioid-induced analgesia. 54. **Physostigmine** may be effective in reversing the central nervous system sedative effects of anticholinergic drugs, especially **scopolamine**. 55. **Flumazenil** is a specific antagonist for the residual depressant effects of **benzodiazepines**. clxxxviii. H**ypothermia** (especially a body temperature lower than 33° C) clxxxix. **Hypoglycemia \--\>** stat measurement of serum glucose is indicated if hypoglycemia is a possibility, as in patients with known insulin-dependent diabetes mellitus. cxc. **increased intracranial pressure**, is important. \--\> Computed tomography may be indicated in patients in whom a central nervous system cause of delayed awakening is a consideration. cxci. **Residual neuromuscular block** may appear to be delayed awakening \--\> Confirmation with **peripheral nerve stimulation** and administration of a **reversal agent** should correct this situation 71. **What are the principles used to determine PACU discharge criteria?** j. Although specific PACU discharge criteria may vary, certain general principles are universally applicable (Box 96-10). k. To summarize, a mandatory minimum stay in the PACU is not required. cxcii. Patients must be observed until they are **no longer at risk for ventilatory depression** and their **mental status is clear or has returned to baseline.** cxciii. Hemodynamic criteria are based on the **patient's baseline hemodynamics** without specific systemic blood pressure and heart rate requirements. l. An assessment and written documentation of the patient's peripheral nerve function on discharge from the PACU may become useful information should a new peripheral neuropathy develop in the later postoperative period.