Anesthesia Oral Boards Flashcards
Side effects of glucagon
Increased heart rate and transient hyperglycemia
Rx for SIADH
Fluid restriction and demeclocycline: inhibits renal action of ADH, induces diabetes insipidus, alternative to demeclocycline is tolvaptan, a vasopressin receptor antagonist
Hyponatremia, euvolemia
SIADH, postop pain/stress, diuretics, hypothyroidism
Hyponatremia, hypovolemia, urine Na less than 10 mEq/L
Non renal solute loss: GI losses, skin, insensible
Hyponatremia, hypervolemia, urine Na greater than 20 mEq/L
Renal failure
Clinical features of hypernatremia
Lethargy, confusion, irritability, coma, seizures, nausea, myoclonus, tremors, muscle weakness, intracerebral bleeding
Clinical features of hyponatremia
Asymptomatic: greater than 125
Anorexia, nausea, malaise: 120-125
Headache, lethargy, confusion, agitation, obtundation: 110-120
Stupor, seizures, coma: less than 110
Drugs that cause hyperkalemia
Succinylcholine, beta blocker, ACE inhibitors, heparin, severe digitalis toxicity, cyclosporine
Diagnosis of DKA
Serum ketones > 7 mmol, serum bicarbonate < 10 meq/L, pH < 7.25
Labs to order when suspecting DKA
Urinalysis, glucose, electrolytes to determine anion gap, ABG, CBC to check for infection
Treatment for DKA
IV fluids, insulin bolus then gtt, potassium as acidosis is corrected, antibiotics for sepsis
Diagnosis and treatment of nonketotic hyperosmolar coma
Severe dehydration, no ketoacidosis, glucose very high like 1000 mg/dL, mental status changes.
Treatment: IVFs, insulin, dextrose, potassium
Anesthetic considerations for diabetic patients
Renal dysfunction; increased risk of CAD and CVA and PVD; autonomic dysfunction: delayed gastric emptying, orthostatic hypotension, resting tachycardia; infection and poor wound healing; stiff joints; poor response to ephedrine
Drugs that precipitate when mixed with barbiturates
Vecuronium, atracurium, midazolam, sufentanil, alfentanil
Sevoflurane has potential for emergence delirium and can be switched to what agent after induction?
Isoflurane
Sevoflurane given at flow rates less than 2 liters can cause what?
Formation of compound A with is nephrotoxic
Which volatile agent has greatest risk of degrading to form carbon monoxide in extremely dry CO2 absorber?
Desflurane
Virchow’s triad for venous thromboembolism
Venous stasis, vessel wall damage, hypercoagulability
Diagnostic triad for fat embolism syndrome, ways to reduce incidence/severity.
Hypoxemia, altered mental status, petechiae (12-72 hours after initial trauma), pulmonary edema. Early immobilization of fractures, limit intraosseus pressure, operative correction rather than traction alone
Triad of symptoms for severe aortic stenosis
Syncope (3 yr mortality rate is 50%), angina (5 yr mortality rate is 50%), dyspnea (2 yr mortality rate is 50%). Valve area < 1.0 cm^2, mean gradient > 40 mmHg, aortic jet velocity > 4.0 m/s
Risk of occurrence of venous air embolism in sitting crani, and why is risk greater in sitting vs prone position?
76%. Horizontal position still has 12% risk of occurrence. Sitting position increases the pressure gradient favoring entry of gas into the veins that now have less than atmospheric pressure because they are above the heart.
Why is nitrous oxide avoided in surgical procedures where there are closed air spaces
Nitrous oxide has blood gas coefficient of 0.47 compared to 0.015 of nitrogen, so nitrous oxide will enter closed gas filled spaces 34 times faster than nitrogen can diffuse out.
Oliguria is < 0.5 mL/kg/hour of urine for how many hours?
6 hours, or < 500 mL in 24 hours for adults, or < 1 mL/kg/hr for an infant.
Intraoperative narcotic of choice for ESRD patient
Fentanyl: primary liver metabolism and no active metabolites
Morphine: one small dose is okay but its metabolite 6-glucuronide can lead to prolonged respiratory depression
Meperidine: do not use. Its metabolite normeperidine is neurotoxic, leading to convulsions.
Signs associated with post-op jaundice due to halothane anesthetic toxicity
Fever, rash, eosinophilia
Antepartum bleeding and maternal cocaine use
Placental abruption. Also associated with excessive alcohol use and smoking
Anesthesia of choice for obstetrical antepartum bleeding in setting of coagulopathies, uncontrolled hemorrhage, and hemodynamic instability
General anesthesia with arterial line to guide volume resuscitation and frequent blood draws
3 C’s of signs and symptoms associated with tracheoesophageal fistula
Coughing, choking, cyanosis
How would you induce anesthesia for epiglottitis and when would you extubate?
Inhalational induction with sevoflurane and nitrous oxide to maintain spontaneous ventilation. Extubate after 24-48 hours of antibiotics and steroids, and epiglottic swelling and clinical signs resolved.
Paroxysmal sweating, hypertension, and headache is the classic triad for?
Pheochromocytoma, other signs include flushing, tremors
Treatment for thyroid storm
Large doses of propylthiouracil, fever reduction, IV fluids, steroids, beta blockers, sodium iodide, cdigoxin for afib with RVR
How is cervical spine cleared?
Alert, non-intoxicated patient without neck pain, tenderness to palpation, depressed level of consciousness, distracting injury, or neurological abnormality or symptoms can be clinically cleared
How would you assess volume status?
Vital signs, mucous membranes, cap refill, skin turgor, listen to lungs, urine output, blood loss, CXR, arterial line pulse pressure variation or systolic pressure variation, ultrasound of IVC looking at collapsibility
Methods to reduce ICP
No venous obstruction, elevating head, mannitol, furosemide, barbiturate, hyperventilation, hypothermia.
Adverse effects of hypothermia
Coagulopathy, cardiac dysrhythmias, impaired renal function, poor wound healing, delayed emergence, impaired enzyme function, shivering leading to increased oxygen demand by 400%
What would you do if patient becomes hypotensive, desats, high peak pressures
100% O2, hand ventilate, check machine, auscultate chest, verify correct position of ETT, check depth of anesthesia. Consider vasopressors, CXR, ABG, TEE.
Diagnosis of ARDS
Identifiable cause, acute onset, diffuse bilateral infiltrates, PaO2 to FiO2 ratio less than 200, PAOP < 18
Deleterious effects of supraphysiologic doses of steroids
Sepsis, hyperglycemia, pneumonia, poor wound healing, immunosuppression, electrolyte imbalance
How to assess pulmonary status of a COPD patient
I would perform a history and physical, focusing assessing severity of COPD by asking about cough, sputum production, frequency of infections/exacerbations, exercise tolerance, hospitalizations, efficacy of past treatments. If severe signs and symptoms, consider ordering CXR, PFTs, ABG, pulmonary consult.
How can PFTs help assess pulmonary status
Type and severity of disease, baseline function, responsiveness to bronchodilators (12-15% increase in FEV1)
Risks of poor perioperative glucose control (hyperglycemia)
Poor wound healing, increased rate of infection (high glucose impairs WBC activity), osmotic diuresis, worse neurological outcomes following traumatic brain injury (increased inflammation, ischemia, edema, and vasospasm).
Preop lab work for diabetic person
Identify end organ disease associated with poorly controlled diabetes: CBC, BUN/Cr, K, glucose, urinalysis, recent EKG
How to assess risk of perioperative alcohol withdrawal symptoms
History of consumption; signs of cirrhosis, hepatic encephalopathy, cardiomyopathy; labs including electrolytes and LFTs; EKG and CXR
Anesthetic concerns of chronic alcohol abuse
Increased MAC, cognitive impairment, cardiomyopathy, cirrhosis, electrolyte abnormalities, GI bleeding, thrombocytopenia
What to do if there is significant reduction of SSEP/MEP signals
1) Optimize oxygen delivery: oxygenation, ventilation, circulation, hematocrit.
2) make sure anesthesia depth has remained stable. 3) Ask surgeon to rule out surgical cause.
What to do if delayed emergence is unknown after ruling out residual anesthesia, residual neuromuscular blockade (twitch monitor), metabolic derangements (check electrolytes, glucose, ABG, lactic acid), hypothermia.
Perform neuro test of reflexes, consult neurologist, order EEG, order CT of head and neck
Which patients are at high risk for developing posterior ischemic optic neuropathy?
Prolonged procedure (> 6.5 hours), substantial blood loss (> 45% of estimated blood volume)
How can you reduce risk of perioperative vision loss for high risk patient undergoing prone surgery
Place head in neutral position at or higher level of heart, arterial line to maintain blood pressure near baseline, monitor hematocrit levels
How would you evaluate cardiac status of a patient with CAD and CHF
I would start with a focused H&P, from the history I would want to know functional status; signs and symptoms of angina, JVD, pedal or pulmonary edema; previous medical interventions. From the physical, I would assess vital signs and listen to the heart and lungs for murmurs and rhonchi. Finally, I would obtain further cardiac testing if it would change my anesthetic management.
Advantages and disadvantages of regional anesthesia for CEA
Advantages: Greater hemodynamic stability, avoiding intubation and associated sympathetic response, continuous neurological assessment of an awake patient.
Disadvantages: Requires high level of patient cooperation, difficulty of converting to GA
Options for neurological monitoring for cerebral ischemia in a patient under GA for CEA
Stump pressure, EEG, SSEP, transcranial Doppler, cerebral oximetry
What is pharmacologic preconditioning?
Drugs such as volatile agents as low as 0.25 MAC may limit infarct size, prevent dysrhythmias, and preserve myocardial function.
What causes barking cough with inspiratory stridor post extubation
Post-intubation croup, which develops secondary to edema formation (tx: racemic epi, decadron). Differential includes other extrathoracic airway obstructions like epiglottitis, foreign body, laryngotracheobronchitis
Anesthetic concerns in someone with ESRD
Electrolyte abnormalities, metabolic acidosis, cardiac conduction blockade, LVH/CHF, hyperglycemia, altered drug clearance, anemia, platelet dysfunction, volume status
How is chronic anemia well tolerated in a patient with ESRD?
metabolic acidosis and increased levels of 2,3-DPG cause rightward shift of the hemoglobin-oxygen dissociation curve, which facilitates offloading of oxygen from hemoglobin
Routine labs for patient with ESRD
CBC for anemia; electrolytes for Na, Ca, K; EKG for hypertrophy, arrhythmia, ischemia; CXR for fluid overload and pulmonary status; coagulation studies if doing a regional anesthetic.
What to do when blood pressure decreases intraoperatively?
Recheck BP, ensure adequate ventilation and oxygenation, check appropriate depth of anesthesia, check EKG for signs of ischemia or arrhythmias, check surgical field for bleeding, place patient in trendelenburg position, give fluid bolus, give vasopressor
How can capnography identify cause of hypoxia?
CO2 waveform can identify esophageal intubation, obstructive lung disease, inadequate muscle relaxant, incompetent ventilatory valves
Causes of hypoxia shortly after intubation, and what would you do
Inadequate ventilation, esophageal intubation, right mainstem bronchial intubation, bronchospasm, atelectasis, poor pulmonary compliance, ETT obstruction/kink. To do: Check monitors, hand ventilate with 100% fio2, auscultate lungs, deepen anesthetic, suction ETT, pull back ETT, give albuterol, give recruitment breath, place patient in reverse trendelenberg
Anesthetic plan to prevent perioperative sickling in a patient with sickle cell disease.
Avoid hypoxemia, hypotension, hypothermia, hypovolemia, and acidosis. Maintain hematocrit above 30% and provide adequate pain control.
Succinylcholine causes severe masseter muscle rigidity, what is the likelihood of malignant hyperthermia and what would you do?
50%, if caused by volatile anesthetic then it is 100%. Overall, 1% of children develop masseter spasm. If ventilation difficult, call for help, attempt nasal intubation, prepare for surgical airway, monitor temperature and etCO2, cancel case, monitor patient for 12-24 hours, check CK and acid-base status and electrolytes, place foley and arterial line, followup testing for MH susceptibility.
How would you prepare a hyperthyroidism patient for emergent surgery?
Minimize risk of hemodynamic instability (fluid resuscitate), cardiac arrhythmias (beta blockers), and thyroid storm by continuing PTU, giving beta blockers and glucocorticoids and sodium iodide
Preop workup for cirrhosis patient
Determine severity of hepatic disease by performing thorough history and physical, jaundice, bleeding, ascites, encephalopathy. Labs including CBC, liver enzymes, electrolytes, bilirubin, albumin, coags, ammonia
Signs and symptom of a post dural puncture headache (PDPH)
Frontal-occipital headache that is postural, nausea, vomiting, neck stiffness, back pain, visual and auditory disturbances
Clinical symptoms and diagnostic testing of a pulmonary embolism
Tachycardia, dyspnea, cough, fever, hypoxemia, JVD, hemodynamic instability, EKG changes such as new RBBB or ST changes. Testing: CT, CXR, d-dimer, echocardiogram, pulmonary angiography (gold standard)
Differential for postpartum headache
Tension headache (most common), migraine, lactation, pneumocephalus, pre-eclamtpsia, meningitis, subdural hematoma, caffeine withdrawal, sinusitis, PDPH
Concerns following cervical spinal cord injury
Respiratory dysfunction, hypotension from loss of cardioaccelerator fibers, aspiration, difficult airway, loss of thermal regulation, arrhythmia, end organ ischemia. Long term: autonomic dysfunction, risk of hyperkalemia, risk of pneumonia
What is spinal shock?
Following acute spinal cord transection, there is flaccid paralysis, ileus, loss of sensation and reflexes and sympathetic tone and temperature regulation. It usually lasts 1-3 weeks.
Why is hydroxyurea used to treat sickle cell anemia?
It increases circulating HbF, which reduces rate and extent of HbS. Reduces sickle cell crises by reducing adhesion of sickled RBC to endothelium, reducing neutrophil activation, and causing nitric oxide-induced vasodilation.
Pathophysiology of sickle cell disease
Genetic hemoglobinopathy with mutation of chromosome 11, substituting amino acid valine for glutamic acid. HbS molecules polymerize in presence of hypoxemia (paO2 < 50) causing deformation of RBC into a sickle shape, leading to hemolysis and microvascular occlusion and ischemic end organ injury.
How would do you evaluate a sickle cell anemia patient?
I would start with a focused HandP. From the history I would want to know the severity and frequency of vaso-occlusive crises, history of acute chest syndrome or complications from transfusions, cardiac sequelae (CHF, MI, arrhythmias), lung sequelae (pHTN, pulmonary fibrosis), renal insufficiency, CNS sequelae (CVA, seizures, ICH). From the physical I would assess the vital signs, check volume status, and listen to the heart and lungs. Finally I would obtain studies such as BUN/Cr, hgb, EKG to help determine severity of multi organ dysfunction.
How would you evaluate a patient with preeclampsia
I would start with a focused HandP. From the history I would want to know recent BPs and platelet counts, signs and symptoms of coagulopathy, any headaches.
From the physical, I would assess the vital signs, perform a careful airway exam, and check volume status.
Finally I would obtain studies such as platelet level, hemoglobin, coags, type and screen.
How would you evaluate an obese patient
I would start with a focused H&P. From the history I would want to know NPO status, functional status, h/o OSA (restrictive lung disease), pHTN, difficult airway, early satiety. From the physical I would assess the vital signs, perform a careful airway exam (rapid desaturation and decreased FRC), listen to the heart and lungs. Finally I would obtain studies such as EKG, CXR, and depending on comorbidities.
Minutes after delivery, mother complains of dyspnea and then begins seizing. Differential?
Amniotic fluid embolism, LAST, eclampsia, intracranial hemorrhage, hypoglycemia
Signs and symptoms of amniotic fluid embolism.
Abrupt and rapid deterioration with hypoxia, hypotension, DIC, pulmonary edema, altered mental status and seizures. Tx: ABCs, supportive care.
Nitrous oxide should be avoided for how many days following retinal detachment surgery?
Depends on type of gas injected:
5 days for air
10 days for sulfur hexafluoride
30 days for perfluoropropane
Clinical presentation and treatment of acute chest syndrome in a sickle cell patient
Wheezing, chest pain, fever, tachypnea, cough, hypoxemia, pulmonary infiltrate. Rx: O2, bronchodilators, incentive spirometry, chest PT, antibiotics, adequate pain control, correct anemia.
Tx for pseudotumor cerebri
Carbonic anhydrase inhibitor (acetazolamide) to decrease CSF production, furosemide, corticosteroids, serial lumbar punctures, ventriculoperitoneal shunt
Abdominal compartment syndrome diagnosis triad
Elevated intra-abdominal pressures (NGT or foley), significant abdominal distension, end organ dysfunction (renal, cardiac, hepatic)
Universal blood type of FFP (fresh frozen plasma) donor
AB blood type
Do platelets have to be ABO compatible?
Not necessarily, whole blood derived platelets have very little plasma so non-ABO compatible is not clinically significant. Platelets in apheresis packs are suspended in plasma so ABO compatibility is necessary.
Propofol infusion syndrome clinical presentation, treatment, prognosis.
Metabolic acidosis, bradycardia, rhabdomyolysis, lipemia, fatty liver, renal failure, cardiovascular collapse. Tx: discontinue propofol, supportive care, possibly hemodialysis. Prognosis: poor, 80% mortality
Why should you be concerned if the drainage bag of an external ventricular device falls from the bed to the floor?
Significant change in the height of the bag places patient at risk for sudden and dangerous changes in intracranial pressure
Downsides to treating acidosis with sodium bicarbonate
More CO2 formation, excessive sodium load, development of hypokalemia, leftward shift of oxyhemoglobin dissociation curve
What issues can significant acidosis cause?
Dysrhythmias, hypotension, myocardial depression, catecholamine resistance.
Patient conditions needed to reliability use pulse pressure variation to assess volume status
Sinus rhythm, mechanical ventilation of at least 8 mL/kg of tidal volume, no significant changes to chest wall compliance.
Large A-a gradient in neonate with congenital diaphragmatic hernia is caused by what?
Hypoplastic lung causing intrapulmonary shunting and pulmonary hypertension, then pHTN causing extrapulmonary shunting. A-a gradient > 500 predicts poor prognosis. A-a gradient < 400 predicts survival.
Initial treatment for patient with congenital diaphragmatic hernia
Medical stabilization to reduce pulmonary hypertension and achieve preductal oxygen saturation > 85%. Mechanical ventilation to help resolve hypoxia and hypercarbia and acidosis, all of which exacerbate pHTN. Consider pulmonary vasodilator like nitric oxide, inotrope like milrinone. Last resort to initiate ECMO.
Complications and contraindications of ECMO, extracorporeal membrane oxygenation
Complications: Intracranial bleeding and pulmonary hemorrhage, emboli, infection, vascular trauma.
Contraindications: gestation < 34 weeks, weight < 2kg, significant intracranial hemorrhage, congenital heart disease
Complications associated with umbilical vein catheterization
Infection, hemorrhage, vein thrombosis, portal cirrhosis, endocarditis, liver abscess
Complications associated with using umbilical artery for drug administration
Air embolism, vasospasm, exsanguination
How does pregnancy in a trauma patient affect management?
Left uterine displacement, difficult airway, aspiration risk, low O2 reserve from decreased FRC and increased O2 demand, hypercoagulability, fetal monitoring, fetal affects of opioids and ionizing radiation.
Rhogam (anti-Rh antibodies) are given within how many hours of delivery or trauma?
72 hours. Rhogam prevents Rh isosensitization which is when maternal IgG antibodies are produced by a Rh negative mother when blood from a Rh positive fetus enters maternal circulation
Difference between omphalocele and gastrochisis
Omphalocele occurs at base of umbilicus, has membranous covering around herniated viscera, associated with diaphragmatic hernia and trisomy 21 and exstrophy of the bladder and cardiac abnormalities. Gastroschisis occurs lateral to the umbilicus, exposed viscera, less likely associated with congenital abnormalities.
How would you intubate a neonate with an omphalocele?
First perform a careful airway exam, recognizing possible macroglossia. Then ensure presence of appropriate airway equipment, intravenous access, and monitoring. Next, decompress stomach with NG tube given increased risk of regurgitation and aspiration. Assuming reassuring airway exam, perform rapid sequence induction and secure airway with an appropriately sized cuffed endotracheal tube. If airway was not reassuring, I would perform an awake intubation.
What is the pathophysiology of retinopathy of prematurity
Abnormal neovascularization of the retina in premature infants less than 44 weeks postconception age, can lead to blindness or retinal detachment. Risk factors include prematurity, underweight, hyperoxia, hypotension, sepsis, hyperglycemia. Retinopathy of prematurity can occur in absence of oxygen supplementation.
Cause of significant difference between pre and post ductal oxygen saturation in a newborn
Coarctation of the aorta, significant right to left shunting
When does fetal heart rate variability begin to develop?
25-27th week of gestation
How long should you continue giving dantrolene to treat malignant hyperthermia?
24-48 hrs because up to 25% of patients relapse within the first 24 hours, max dose is 10 mg/kg
Advantages and disadvantages of using centrifugal or roller pumps for CPB
Roller advantage: pulsatile flow (theoretically improves renal and cerebral perfusion), not sensitive to preload or afterload. Roller disadvantage: more damage to RBCs, potential to deliver air to patient.
What is alpha stat and pH stat strategies?
These are strategies to manage CO2 in a hypothermic patient when CO2 solubility increases so pH increases and paCO2 decreases. pH stat strategy is to add CO2 to maintain pH of 7.4 and paCO2 of 40. Alpha stat strategy is to not add CO2. In adults, brain injury is thought to be caused by embolic events, alpha stat is preferred because pH stat would increase cerebral blood flow. In kids, brain injury is thought to be caused by ischemia, pH stat is preferred because it increases cerebral blood flow to help facilitate cerebral cooling. Most practitioners use pH stat.
Why monitor core and peripheral temperature during CPB?
Ensure adequate cerebral cooling prior to bypass and adequate normothermia prior to weaning off bypass. Also a temperature gradient develops during cooling and rewarming, gradient > 10C can lead to formation of gas bubbles in the blood
Causes of CPB venous reservoir level decreasing and what would you do?
Problems with venous cannulation, inadequate diameter, kinking, malpositioning, obstruction by thrombotic material, surgeon lifting the heart. I would ask perfusionist to add fluid to blood volume to prevent reservoir from emptying, which could cause massive arterial air embolism.
Causes of increased pulmonary artery pressure and decreased systemic pressure during weaning of CPB
This scenario is left ventricular failure, which can be caused by: graft failure (air, kink, clot), inadequate myocardial preservation, inadequate coronary perfusion (hypotension, emboli, spasm, decreases diastolic time), MI, valve failure, inadequate preload (hypovolemia, loss of atrial kick), hypoxemia, acidemia, electrolyte abnormalities, reperfusion injury.
What electrolyte abnormalities are seen in a patient with pyloric stenosis?
Hypokalemic, hyponatremic, hypochloremic metabolic alkalosis
Causes of atrial fibrillation and preop evaluation
Valvular disease, LVH, CAD, cardiomyopathy, sick sinus syndrome, pericarditis, idiopathic, hyperthyroidism, PE, excessive alcohol or caffeine intake. Preop: evaluate CAD, CHF, thyroid dysfunction by reviewing EKG, CXR, any previous cardiac testing
Indications for cardiac catheter ablation.
Symptomatic SVT, inefficacy or intolerance of antiarrhythmic drug, patient preference, noncompliance to drug regimen.
Causes of syncope
Cardiac arrhythmia, TIA, hypoglycemia, MI, vasovagal, orthostatic hypotension, aortic stenosis, vertigo, seizure, hypertrophic cardiomyopathy
Treatment of status asthmaticus
Supplemental O2, inhaled bronchodilators like albuterol and atrovent and aminophylline, IV steroids, IV epinephrine, order PFTs and ABGs to monitor adequacy of oxygenation and ventilation and response to treatment, consider mechanical ventilation if patient fatigues or oxygenation/ventilation is inadequate, low TVs and peak pressures and prolonged expiratory phase and consider PEEP.
How would you prepare a severe asthmatic for emergency surgery
Optimize asthma by continuing current meds, give a stress dose of steroids, benadryl to prevent histamine-induced bronchoconstriction and anxiety-induced bronchospasm, give albuterol prior to induction; control pain with fentanyl, avoiding histamine releasing narcotics; minimize risk of aspiration by giving metoclopramide; prevent/treat nausea with ondansetron
How would you induce general anesthesia in a severe asthmatic for emergency surgery
Goal is achieve adequate depth of anesthesia to avoid bronchoconstriction while minimizing risk of aspiration. Ensure premeds given to reduce risk of aspiration and nausea and bronchospasm, proper airway equipment, IV access, monitors. Assuming reassuring airway, give albuterol, preoxygenate with 100% O2, give fentanyl and lidocaine to blunt sympathetic surge from laryngoscopy, cricoid pressure, RSI with propofol and succinylcholine.
Anesthetic goals in a patient with mitral valve prolapse
Goal is to avoid left ventricular emptying because reduction in diameter of the left ventricle can worsen MVP which would exacerbate mitral regurgitation. Thus, avoid sympathetic activation, maintain SVR and preload (avoid hypovolemia, upright positioning, and aggressive positive pressure ventilation).
Pathophysiology of anaphylaxis
Second exposure to an antigen that previously caused production of antigen-specific IgE antibodies, degranulation of mast cells and basophils releases histamine, leukotrienes, prostaglandins. Leading to increased capillary permeability, peripheral vasodilation, bronchoconstriction, negative inotropy, coronary artery vasoconstriction.
Treatment of anaphylaxis
Tell surgeon, stop all current medication administration, call for help, decrease anesthesia, 100% O2, open up IV fluids, give IV epinephrine (start at 100 mcg if complete cardiac collapse, 10 mcg if just hypotensive), IV steroids, diphenhydramine, H2 blocker like famotidine, inhaled beta2 agonist, consider vasopressin or bicarb if hypotension refractory. Send for serum tryptase and histamine levels.
Significance of abnormal fetal heart rate variability
Can be sign of fetal hypoxia, fetal sleep state, fetal tachycardia, prematurity, congenital anomalies, CNS depressants like opioids or magnesium
what is carcinoid syndrome and how is it diagnosed?
carcinoid tumor releases hormones such as serotonin, histamine, and bradykinin that cause symptoms including skin flushing, bronchoconstriction, diarrhea, right sided heart failure, hemodynamic instability. Dx: 24 hour urine levels of 5-hydroxyindoleacetic acid (5-HIAA), a breakdown product of serotonin. Imaging can also help localize the tumors.
what to do preoperatively to reduce risk of carcinoid crisis in a patient with carcinoid syndrome?
start octreotide (reduces secretion of serotonin), optimize intravascular volume, anti-histamines, alpha and beta blockers, steroids
pathophysiology of aspiration pneumonitis
gastric material cause atelectasis, pulmonary edema, alveolar hemorrhage, hypoxic pulmonary vasoconstriction. signs include hypoxemia, tachypnea, wheezing, tachycardia, coughing, bronchospasm, taking 6-12 hours to show up in radiographic findings.
what to do if line-isolation monitor alarms
LIM alarms when potential flow of current from power supply to ground may place patient at risk for macroshock. Check gauge, if between 2 mA and 5 mA, too many pieces of electrical equipment plugged in, creating leakage current. If gauge > 5 mA, likely a faulty piece of equipment is plugged in, so start unplugging until alarm stops. Does not protect from microshock (10 microAmps) that can disrupt cardiac function
How does ESWL, extracorporeal shock wave lithotripsy, disintegrate renal calculi?
Sudden vaporization of water by an energy source generates a pressure wave that releases compressive energy causing shear forces when it encounters a sudden change in impedance like the tissue-stone interface. Tissue injury can occur, like bruising and hematuria
AICDs and pacemakers are recommended to be checked within the last how many months?
6 months for AICD
12 months for pacemakers
Most postpartum peripheral nerve palsies are obstetric in nature due to?
Extreme positioning, instrumentation during vaginal delivery, baby’s head compressing nerves while crossing pelvic brim.
Options for regional anesthesia other than epidural for vaginal delivery
Paracervical block for 1st stage of labor, pudendal block for 2nd stage of labor. Paracervical blocks have high risk of fetal bradycardia and decreases uteroplacental perfusion. Pudendal blocks have low risk of hematoma and abscess formation.
Risk factors for disseminated intravascular coagulopathy (DIC) in peripartum setting and non-obstetric.
Amniotic fluid exposure, hypovolemia, preeclampsia. Burn, trauma, sepsis, blood transfusion, cancer
What is disseminated intravascular coagulopathy (DIC)?
Pathological activation of coagulation cascade leading to consumption of coagulation factors, increased PT and PTT, decreased fibrinogen and platelets. Treat hypovolemia, hypoxemia, and acidosis while starting replacement of coagulation factors.
what is respiratory distress syndrome?
premature infants usually < 35 wks gestation will have insufficient surfactant production leading to tachypnea, intercostal retractions, tachycardia, rales, cyanosis
Potential complications with a premature neonate undergoing surgery?
retinopathy of prematurity, postoperative apnea, intraventricular hemorrhage, hypothermia, hypoglycemia (reduced renal tubular reabsorption of glucose when < 34 wks)
FiO2 should be decreased to minimize risk of retinopathy of prematurity for a neonate so PaO2 and O2sat are maintained at what levels?
PaO2 50-80 mmHg, O2sat 87-95%
Risk factors for retinopathy of prematurity
prematurity, low birth weight, major fluctuations in oxygen saturation, hyperoxia, hypoxia, mechanical ventilation, respiratory distress, acidosis, anemia, hypercarbia, blood transfusion, bradycardia, infection,
What are your considerations for transfusing blood in a premature neonate with a patent ductus arteriosus
Presence of fetal hemoglobin, increased O2 demand, decreased cardiopulmonary reserve, acuity and persistence of blood loss, hemodynamic stability
Causes of post-operative hypertension in a neonate
inaccurate measurement, pain, hypervolemia, hypoxemia, hypercarbia, bladder distension, increased intracranial pressure, undiagnosed coarctation of the aorta
differential and treatment for neonatal seizure
intracranial hemorrhage, hypoxic-ischemic encephalopathy, cerebral edema, hypoglycemia, hypocalcemia, sepsis, obstetric history of TORCH (toxoplasmosis, rubella, cytomegalovirus, herpes). tx: ensure adequate oxygenation, ventilation, and circulation, give barbiturate or benzodiazepine, order electrolytes, notify neonatologist
Common functional pituitary adenomas
prolactinoma, excessive ACTH (Cushing’s disease), excessive growth hormone (acromegaly), excessive TSH (hyperthyroidism)
How would you maintain general anesthesia if you are monitoring visual evoked potentials?
Visual evoked potentials monitor integrity of optic nerves, VEPs are extremely sensitive to inhalational and intravenous anesthetics so I would use a balanced technique with low concentration volatile agent, low concentration propofol infusion, and remifentanil infusion to minimize interference.
Cocaine injected into nasal mucosa and patient suddenly loses consciousness. What is going on and what would you do?
Local anesthetic systemic toxicity, high spinal, or cocaine induced dysrhythmia. I would intubate, give 100% O2, fluids, and medications to ensure adequate oxygenation, ventilation, and circulation. If this was LAST, then give benzodiazepine, consider intralipid infusion, and CPR if cardiovascular collapse
Causes of sudden drop in blood pressure during a transphenoidal resection of a pituitary adenoma in the sitting position
venous air embolism, massive hemorrhage, myocardial infarction, anaphylaxis, anesthetic overdose, cardiac dysrhythmia, tension pneumothorax. I would recheck BP, check for adequate oxygenation and ventilation by verifying proper ETT placement, auscultate the chest, look at EKG and etCO2, look at surgical field, consider TTE to confirm diagnosis.
What to do if there is a venous air embolism in a patient undergoing surgery in a sitting position
Ask surgeon to flood field with saline, deliver 100% O2, apply direct jugular venous compression to increase venous pressure at surgical site, provide hemodynamic support with fluids and vasopressors, try moving patient to trendelenberg and right side up position to reduce chance of air lock in the right ventricle
How would you extubate a patient who is high risk for difficult airway management
Place patient in slight reverse trendelenberg position, ensure adequate oxygenation, ventilation, and circulation, normothermic, fully reversed from paralysis, awake, alert, following commands, intact airway reflexes
Obese patient in PACU is obtunded and desaturating, what’s going on?DD
airway obstruction and apnea, overnarcotized, atelectasis, pulmonary edema, aspiration, inadequate reversal of paralysis, residual anesthesia, electrolyte abnormality, arrhythmia, MI, stroke
How is diabetes insipidus diagnosed and treated?
Polyuria, increased serum osmolality, decreased urine osmolality (urine specific gravity < 1.005), and urine osmolality increases wi
th administration of ADH. Tx: Central: Replace fluids and give DDAVP, Nephrogenic: Replace fluids and give thiazide or NSAIDs, consider amiloride (K-sparing diuretic) for lithium induced DI
what does normal PT and elevated PTT mean?
hemophilia A (VIII), hemophilia B (IX), hemophilia C(XI), von willebrand deficiency, low dose heparin, lupus anticoagulant
mechanism of desmopressin (DDAVP) in treating factor deficiency
DDAVP induces release of factor VIII and vWF from endothelial cells, is most effective when factor VIII levels are > 5%
To what level would you correct factor VIII preoperatively and how long do you continue giving factor VIII after surgery?
50-100% of normal, half life of factor VIII is about 6 hours, continue replacement for up to 2 weeks.
Pulmonary function tests that are best for pre-thoracotomy assessment
ppoFEV1 (respiratory mechanics) > 40% is low risk, ppoDLCO (lung parenchymal function) > 40% is low risk, VO2max (cardiopulmonary reserve) > 15 mL/kg/min is low risk. 2 flights = VO2max of 12. Extra info: PaO2 > 60 and PaCO2 < 45 are low risk
Normal PaO2 on room air can be estimated knowing patient’s age with what equation?
102 - (age / 3)
what are your anesthetic management goals for a particular case?
Preoperatively evaluate nature and severity of comorbidities, optimize cardiopulmonary functions, and plan for anticipated complications. Intraoperatively I want to maintain stable hemodynamics and oxygenation and ventilation, provide adequate level of anesthesia, secure the airway, reduce risk of complications, facilitate surgical exposure. Postoperatively I want to maintain ventilatory support, adequate pain control, and be vigilant for postoperative complications
Genetic mode of inheritance of malignant hyperthermia
Autosomal dominant with reduced penetrance and variable expression
how would you deliver jet ventilation?
Ensure adequate muscle relaxation and depth of anesthesia to prevent bronchospasm, initiate jet ventilation at low pressures until adequate chest rise and fall is noted, keeping in mind complications such as pneumothorax, subcutaneous emphysema, gastric distention, and aspiration of surgical debris.
Would you extubate a patient after an intraoperative airway fire?
No, inhalational injury can progress rapidly to life threatening airway obstruction, so I would give steroids, humidified oxygen, and monitor patient for at least 24 hours with continuous pulse oximetry and serial CXRs
Differential for hypoxia and high airway pressures in a patient still intubated postoperatively, and what would you do?
bronchospasm, pulmonary edema, kinked or plugged ETT, right mainstem intubation, pneumothorax. Tx: hand ventilate with 100% O2, suction ETT, auscultate lungs, ensure adequate placement of ETT, CXR, ABG
What is the pathophysiology and treatment of TRALI
Donor leukocyte antibodies activate neutrophils that lead to endothelial damage, capillary leakage, acute lung injury, pulmonary edema. Signs and symptoms include fever, tachycardia, dyspnea, cyanosis, hypotension. Tx: supportive, most patients recover within 96 hours.
Possible causes of decreased energy in a patient with pheochromocytoma
Catecholamine-induced cardiomyopathy or congestive heart failure, CVA, MI, acute renal failure, hypothyroidism, electrolyte abnormalities
Diagnosis of pheochromocytoma
Free metanephrines in plasma (most reliable test), plasma catecholamines, urinary catecholamines or metanephrines, urinary vanillymandelic acid.
Alpha blockade should be started how many weeks prior to pheochromocytoma surgery
2 weeks
Medications to avoid during pheochromocytoma surgery
Histamine releasing drugs (succinylcholine, morphine, atracurium), drugs causing significant hypertension (droperidol, metoclopramide, ephedrine), drugs that increase sympathetic activity (ketamine, atropine, pancuronium)
Why avoid inhalational induction in a patient with muscular dystrophy?
Volatile agents may induce rhabdomyolysis and hyperkalemia even in the absence of succinylcholine
what is considered a clinically significant reduction in SSEP or MEP signals?
50% decrease in amplitude or 10% increase in latency
what is hepatopulmonary syndrome?
triad of liver disease, hypoxemia, and intrapulmonary vascular dilation. symptoms of worsening dyspnea in the upright position. is an indication for liver transplantation
how would you determine if elevated creatinine level is secondary to hepatorenal syndrome?
Give a fluid challenge, if renal function improves, then likely pre-renal cause. Also check urine electrolytes, review medications.
what is the pathophysiology of hepatorenal syndrome?
Increased levels of vasodilators like nitric oxide lead to splanchnic arterial vasodilation, causing compensatory activation of the renin-angiotensin-aldosterone system, leading to systemic and renal vasoconstriction. Definitive treatment is liver transplantation.
Liver transplantation is contraindicated in patients with pulmonary artery pressures above what level?
mean PAP > 50 mmHg, Portopulmonary hypertension is defined as mean PAP > 25 mmHg
why is hepatic encephalopathy a concern?
Because it is associated with GI bleeding, infection, anemia, increased ICP. I would be careful giving any sedation drugs like benzodiazepines because they may exacerbate the encephalopathy
Reasons for hyperkalemia in the anhepatic phase of liver transplantation case
Acidosis causing K to move from intracellular to extracellular, high K in transfused rbcs, renal insufficiency due to hepatorenal syndrome
Proposed mechanisms for reperfusion syndrome, and how to manage it.
High K load from graft perfusate, release of vasoactive substances and metabolites from clamped off region. Correct acidosis, give calcium, give vasopressors or inotropes.
What toxicity can occur with nitroprusside infusion and how to treat?
Cyanide binds to tissue cytochrome oxidase (enzyme of the electron transport chain), impairing oxygen utilization, leading to metabolic acidosis, cardiac arrhythmias, and tachyphylaxis. Tx: 100% O2, give sodium thiosulfate or sodium nitrate or amyl nitrate which all remove cyanide ions from circulation
How would you evaluate and manage postop oliguria?
I would start with a focused H&P. From the history I would want to review the chart for fluids and meds given, the anesthetic record. From the physical I would assess the vital signs and check the foley catheter, check volume status. I would give a fluid bolus if appropriate, order serum and urine electrolytes, consider renal consult.
Risk factors and causes of perioperative acute renal failure
Risk factors: Advanced age, prolonged cross clamp time, cardiac disease, preexisting renal disease. Causes: renal ischemia, nephrotoxins, air embolization, activation of renin-angiotensin system.
Difference between narcotic abuse, dependence, addiction
Abuse: use that is detrimental to the individual or society
Dependence: physiologic state of adaptation to a substance that leads to withdrawal
Addiction: medical disease, abuse of addictive drug with loss of control and irrepressible craving
Why might a patient be difficult to wean off ventilator while getting TPN?
Patient on TPN may have hypophosphatemia or hypokalemia or hypermagnesemia, which leads to muscle weakness
During laparoscopic surgery, ABG shows PaCO2 is elevated, what would you do?
Review monitor (BP, EKG, etCO2, temperature), verify proper ETT placement, auscultate chest, review ABG. Look for signs of subcutaneous emphysema, tension pneumothorax, CO2 embolism, CHF, MH
Which antihypertensive meds to give during pheochromocytoma surgery
Use rapid onset and short acting meds such as esmolol, nitroglycerine, nitroprusside, nicardipine, labetalol, and phentolamine
Signs of elevated intracranial pressure
headache, nausea, altered mental status, papilledema, Cushing’s triad (HTN, bradycardia, irregular respirations) Cushing causes gastric ulcer so risk of bleeding and aspiration (tx: PPI)
During cerebral aneurysm surgery, ST changes on EKG can be a sign of what?
subarachnoid hemorrhage, myocardial ischemia. Check CKMB and troponins to differentiate.
How do you differentiate SIADH (syndrome of inappropriate antidiuretic hormone) and CSWS (cerebral salt wasting syndrome)?
SIADH is euvolemic and urine sodium levels are < 100 meq/L while CSWS is hypovolemic and urine sodium levels > 100 meq/L. Treatment for SIADH is fluid restriction and diuresis, while treatment for CSWS is fluid replacement
What is ankle brachial index (ABI) ?
Ratio of ankle to brachial systolic pressures using doppler, claudication is associated with ABI < 0.9. Rest pain at ABI < 0.5, ulceration at ABI < 0.25
Differential for delayed emergence specifically after a craniotomy
Hematoma formation, tension pneumocephalus, cerebral edema, cerebral ischemia, hypoxia, hypercarbia, seizure, obstructive hydrocephalus
Anesthetic concerns for a cystic fibrosis patient? Preop labs?
Concerns for decreased pulmonary function such as of hypoxia, bronchospasm, pneumothorax, postoperative respiratory failure, pHTN leading to right heart failure. Also hepatic, pancreatic, and GI involvement leading to coagulopathy, pseudocholinesterase deficiency, diabetes, electrolyte abnormalities. I would order CBC, BMP, coags, ABG, possibly CXR, EKG, PFTS, TTE, LFTs
Pathophysiology of cystic fibrosis
Recessive genetic disorder with a defective cystic fibrosis transmembrane conductance regulator (CFTR) gene leading to abnormal NaCl movement that causes thick secretions that affect lungs, pancreas, liver, GI: mucous plugging, inflammation, chronic infections, emphysema, hypoxemia, cor pulmonale, cardiomegaly, hepatomegaly, respiratory failure, malnutrition, diabetes, coagulopathy, decreased cholinesterase.
Treatment for cystic fibrosis
Prevention and control of pulmonary infections, antibiotics, physical therapy, enzyme replacement, adequate nutrition
Risk factors for emergence delirium and methods to prevent it
Preop anxiety, young age, postop pain, less soluble volatile agents like sevo and des, prolonged surgery, patient temperament. Reduce preop anxiety, good pain control, sedative like midazolam propofol or dexmedetomidine
Treatment for extrapyramidal symptoms caused by metoclopramide
Ensure adequate oxygenation and ventilation, give diphenhydramine or benztropine (anticholinergics)
What causes a phase 2 blockade with use of succinylcholine?
Excessive doses, prolonged infusions, or abnormal metabolism of succinylcholine leading to larger dose of succinylcholine reaching the neuromuscular junction.
What does it mean when troponin is positive but Ck-mb is negative?
MI occurred more than 2-3 days ago. CK-MB is elevated 4-6 hours after MI and returns to baseline within 2-3 days. Troponin is elevated 2-6 hours after MI and returns to baseline after 7-10 days.
ST segment depression can be caused by what?
NSTEMI, subendocardial ischemia, digoxin use, hypokalemia
Therapeutic levels of digoxin, factors that potentiate digoxin toxicity, treatment for digoxin toxicity?
0.5-2.0 ng/mL. Hypokalemia, hypomagnesemia, and hypercalcemia can potentiate digoxin toxicity (nausea, blood stools, blurred vision, confusion, muscle weakness, ventricular arrhythmias). Tx: check digoxin level, digibind is antidote (10-20 vials), supportive care
Most likely cause of coagulopathy following cardiopulmonary bypass?
Platelet dysfunction. Differential includes thrombocytopenia, dilutional coagulopathy, DIC, hypothermia, fibrinolysis
What is the American academy of dermatology recommended maximum dose of lidocaine for liposuction? And what can you do to reduce risk of local anesthetic systemic toxicity?
55 mg/kg. Use diluted solution with epinephrine, limit volume of fat removal to 3000 mL, have intralipid available
Diagnosis of CRPS
Clinical diagnosis with inciting event, followed by burning pain, allodynia, hyperalgesia, cyanosis, edema, sweating, glossy skin, hair loss, osteoporosis, stiff joints. Type 1 is nonspecific area of injury while type 2 is specific nerve injury
Treatment for CRPS
Opioids (CRPS doesn’t respond well to opioids), gabapentin, antidepressants, physical therapy, sympathetic nerve block, ketamine. Prognosis: most patients are still in pain with some degree of functional dysfunction after one year, even with intensive therapy.
Causes of premature ventricular contractions (PVCs)
Increased levels of adrenaline (caffeine, tobacco, anxiety, exercise), epinephrine, hypoxia, cardiac ischemia, electrolyte abnormalities, anesthesia induced cardiac depression.
Intralipid dosing
20% lipid solution. 1.5 mL/kg bolus over 1 minute, then infusion rate of 0.25 mL/kg/min. Repeat bolus and increase infusion rate if cardiovascular instability persists. Max dose of intralipid is 8 mL/kg bolus.
What is aplastic crisis?
Decreased RBC production caused bone marrow suppression secondary to infection or folate deficiency.
Decision to give a blood transfusion is based on what criteria?
Patient comorbidities (CAD, sickle cell, coagulation deficiencies), current surgical hemostasis and likelihood of continued blood loss, hemodynamic stability, signs of decreased tissue perfusion (lactic acid, mixed venous oxygen saturation, pulse oximetry, etco2, circulation, cap refill)
Pathophysiology of bone cement implantation syndrome
Hardening and expansion of cement leads to increased intramedullary pressure and embolization of bone debris leading to pulmonary hypertension, hypotension, hypoxia, dysrhythmias, cardiac arrest. Also release of cytokines during reaming lead to microthrombi formation.
Why not initiate beta blockers on day of surgery and how many days prior to surgery should they be started?
Initiation of beta blockers without careful titration may increase overall morbidity and mortality secondary to hypotension, bradycardia, stroke, and death. Ideally begin beta blockers 2-7 days before surgery, but even better to give 6-8 weeks to allow HR to decrease close to 60
What is the pathophysiology of autonomic hyperreflexia?
Stimuli below the level of spinal cord injury results in reflex sympathetic discharge without inhibition from higher central nervous system centers, leading to vasoconstriction below level and reflex vasodilation above level that is insufficient to prevent systemic hypertension.
What are the subsequent complications of autonomic hyperreflexia if it is not treated?
MI, intracranial hemorrhage, seizure, dysrhythmias, pulmonary edema
Differential for no twitches of peripheral nerve stimulator at the end of a case when succinylcholine and a nondepolarizing agent given
Drug error, defective nerve stimulator, pseudocholinesterase deficiency, electrolyte abnormality, hypothermia, acidosis, hypercarbia, aminoglycoside administration, neuromuscular disease such as myasthenia gravis, eaton lambert syndrome, ALS.
How to differentiate between myasthenia or cholinergic crisis?
Both have muscle weakness, salivation, and sweating. Myasthenia has mydriasis (large pupils) and improved strength with edrophonium. Cholinergic crisis has miosis (small pupils) and increased weakness with edrophonium.
What is hypertrophic obstructive cardiomyopathy?
Genetic condition characterized by left ventricular hypertrophy, dynamic left ventricular outflow tract obstruction, systolic anterior movement of the mitral valve, diastolic dysfunction, myocardial ischemia, dysrhythmias leading to sudden death.
Pyloric stenosis diagnosis
Ultrasound or X-ray with barium
Why is rehydration important in correcting metabolic alkalosis caused by emesis?
It’s important because dehydration and hyponatremia causes kidneys to conserve sodium which leads to reabsorption of bicarbonate, which worsens the metabolic alkalosis
Anesthetic considerations for obstructive sleep apnea (OSA)
Coexisting comorbidities such as HTN, CAD, pHTN, arrhythmias, right heart failure. As well as airway difficulties, sensitivity to narcotics, extubation criteria, postoperative pain control, ASA guidelines recommend monitoring OSA patients 3 hours longer than non-OSA patients and 7 hours after last episode of airway obstruction or hypoxemia.
Causes of hypertension in a young adult
Pain, hypoxia, hypercarbia, anxiety, illicit drug use, hyperthyroidism, hypercalcemia, pheochromocytoma, coarctation of the aorta, elevated ICP, polycystic kidney disease
Why would a surgeon ask for a lumbar drain for a cerebral aneurysm surgery?
To treat hydrocephalus, reduce brain bulk to facilitate access to aneurysm, control intracranial pressure, and may reduce symptomatic vasospasm
What things can you do if cerebral aneurysm ruptures during clipping procedure?
Induce hypotension to reduce blood loss, manual pressure on ipsilateral carotid, consider hypothermic arrest
Is it necessary to get a serum sodium level for an ESRD patient?
Yes, because renal failure can lead to hyponatremia which can cause cerebral edema, seizures, lethargy, mental status changes, muscle weakness
what is systemic lupus erythematosus (SLE)?
autoimmune disease causing systemic chronic inflammation (ie. vasculitis, which can increase risk of intracerebral hemorrhage) and tissue damage. antinuclear antibodies (ANA), malar rash, nephritis, arthritis, pericarditis, seizures, peripheral neuropathy, thrombocytopenia, hemolytic anemia, coagulation factor deficiency, antiphospholipid antibodies (prolonged PTT) causing thromboembolic events like fetal demise. medications: steroids, immunosuppresants, anticoagulants, NSAIDS
What can you do to attenuate the hypotension caused by rapid administration of vancomycin?
Vancomycin administration leads to histamine release causing drop in systemic vascular resistance, so you can give antihistamines prior to giving vancomycin
what type of acute aortic dissection requires immediate surgical repair?
acute aortic dissection involving the ascending aorta; proximal propagation can lead to aortic insufficiency, tamponade, and coronary artery dissection.
what hemodynamic changes occur with placement of an aortic cross-clamp?
Increased afterload leading to increase in blood pressure, left ventricular wall tension, central venous pressure. Decrease in ejection fraction, cardiac output, renal blood flow, and distal perfusion pressure. HR and MAP usually elevated unless underlying poor ejection fraction can lead to hypotension and bradycardia so do not start vasodilators prior to cross clamp
how does hypothermia cause coagulopathy?
Mild hypothermia (33-35C) causes defects in platelet aggregation and adhesion. More severe hypothermia (> 33C) also causes abnormal coagulation enzyme activity.
How does thromboelastography (TEG) measure coagulation?
TEG measures viscoelastic properties of blood during induced clot formation, clinically identifying coagulation factor activity (R time, time to initial clot formation), fibrin formation (K time and alpha angle, speed of clot formation), platelet function/concentration (MA, clot strength), fibrinolysis activity (LY30, degree of fibrinolysis).
Increased R time -> give FFP
Decreased alpha angle -> give cryoprecipitate
Decreased MA -> give platelets, consider DDAVP
Decreased LY30 -> give tranexamic acid
Treatment for a bleeding patient with uremic platelet dysfunction
Desmopressin (DDAVP), which induces release of vWF factor and factor VIII from endothelial cells that leads to improvement of platelet adhesion and aggregation. Also consider giving EPO, cryoprecipitate, platelets, and performing dialysis to remove uremic acid.
How would you manage a patient who is taking lithium?
Preoperatively I would evaluate for signs of toxicity like muscle weakness, seizures, polyuria, widened QRS, AV block, hypotension. Check most recent lithium level and EKG. Intraoperatively, I would closely monitor neuromuscular blockade and anesthetic depth because lithium prolongs paralysis and reduces MAC. Postoperatively, I would ensure patient is fully awake and meeting all extubation criteria.
How would to evaluate whether a hyperthyroidism patient’s condition is controlled adequately?
First perform history and physical looking for signs of hyperthyroidism such as diarrhea, warm moist skin, heat intolerance, cardiac arrhythmias, fatigue, muscle weakness, fine tremor. Consider ordering TSH, free T3 and T4 levels.
What conditions cause thyroxine binding globulin (TBG) to increase, leading to elevated total T4 levels?
Pregnancy, birth control pills, acute liver disease
Differential diagnosis for inspiratory stridor, restlessness, and tingling around mouth 3 hours after total thyroidectomy
Hypocalcemia secondary to removal of parathyroid glands (typically 24-96 hours after surgery), hematoma, post-intubation croup, residual neuromuscular blockade, recurrent laryngeal nerve injury, hypoxia, hypercarbia, hypoglycemia.
Why would you not administer aspirin in a patient with thyrotoxicosis?
aspirin displaces thyroid hormones from binding proteins which would exacerbate the condition
How to distinguish between neuroleptic malignant syndrome (NMS) and malignant hyperthermia (MH)?
1) NMS exhibits slower progression to critical temperature and multi organ failure
2) Non depolarizing muscle relaxants will produce flaccid paralysis in NMS patients. Difficult to differentiate, so initiate dantrolene, active cooling, consider bromocriptine (dopamine agonist)
What are your concerns and evaluation of a patient with elevated hypertension prior to surgery?
Concerns with increased perioperative risk of hemodynamic lability, myocardial ischemia, dysrhythmias, congestive heart failure, stroke, renal insufficiency, and other end-organ ischemia. I would perform a focused HandP to identify end organ damage by asking about baseline BP, medications, symptoms of angina and dyspnea, exercise tolerance, neuro symptoms, assess other vital signs, volume status, listen to heart and lungs, consider obtaining an EKG (LVH), CXR, electrolytes, BUN/Cr. Stage 1 (140/90), Stage 2 (160/100), Stage 3 (180/110), would prefer to delay surgery 6-8 wks if stage 3 or stage 1/2 with end-organ damage.
Signs of hypervolemia and hypovolemia
Hypervolemia: HTN, pulmonary edema, peripheral edema, JVD
Hypovolemia: hypotension, tachycardia, dry mucous membranes, orthostasis
Differential for sudden drop in blood pressure (hypotension) intraoperatively
Monitor error, decreased contractility, rate/rhythm abnormality, MI, CHF, valvular disease, hypoxia, hypercarbia, acidosis, electrolyte abnormality (hyperkalemia, hypocalcemia, hyponatremia, hypoglycemia), hypovolemia, blood loss, sepsis, anaphylaxis, anesthetic overdose, tension pneumothorax, pulmonary embolism (clot, air, fat, amniotic), tamponade, hypothermia
Most common cause of post-operative coagulopathy
Platelet dysfunction caused by uremia, hypothermia, severe anemia, or drug effect. Differential includes residual heparin effect, inadequate surgical hemostasis, metabolic acidosis, thrombocytopenia, DIC. I would check platelet count, INR, PTT, fibrinogen, CBC, possibly TEG.
Why would you not recommend treating patient’s oliguria with dopamine?
Dopamine does not reliably improve renal function, in addition, the inotropic effects may increase myocardial oxygen demand and increase risk of MI. May consider fenoldopam which is a D1-selective agonist.
What are anesthetic considerations for a patient with rheumatoid arthritis?
Airway: cervical stiffness, TMJ stiffness, consider awake fiberoptic intubation
Cardiac: pericarditis, arrhythmias, myocardial ischemia, valvular disease
Pulmonary: fibrosis, pleural effusions
GI: ulcers from anti-RA meds
Renal: dysfunction from anti-RA meds
Neuro: peripheral neuropathy, joint deformity
What are drug treatments of rheumatoid arthritis and how do they affect anesthetic management?
NSAIDS: renal insufficiency (vasoconstriction of afferent arteriole leading to decreased renal blood flow)p, platelet dysfunction, GI ulcers
corticosteroids: need for stress dose
DMARDs (disease modifying anti-rheumatic drugs): increased risk of infection
what’s the difference between type and screen and type and cross?
type and screen mixes recipient plasma with panel of commercial RBCs while type and cross mixes recipient plasma with the donor RBCs
what would you do if a hemolytic transfusion reaction occurs?
stop transfusion, 100% FiO2, treat hypotension with fluids and vasopressors, recheck prbc unit number, notify blood bank, consider diuretic and sodium bicarb to prevent renal injury
What is the pathogenesis of acute intermittent porphyria?
Deficiency of one of the enzymes in the heme biosynthesis pathway leads to overproduction of porphyrins. Various drugs or anemia can induce AIP, causing severe abdominal pain, nausea, muscle weakness, respiratory failure, peripheral neuropathy, electrolyte abnormalities, psychiatric disturbance
what can you do to reduce the risk of acute intermittent porphyria and how would you treat it?
I would avoid fasting, dehydration, stress, infection, anemia, certain drugs like ketorolac and etomidate. To treat, I would ensure adequate oxygenation, ventilation, hydration, analgesia, anxiolysis, give carbs, give anti-emetics, correct any electrolyte abnormalities, give hematin (a porphyrin).
What equipment is required for a non-operating room conscious sedation room?
2 sources of oxygen, ASA standard monitors (BP, pulse ox, EKG, etCO2, temp), airway equipment, emergency meds, crash cart, flashlight, and CPR-certified personnel
what are the risk factors for late stent thrombosis following placement of a drug eluting stent (DES)?
Premature discontinuation of antiplatelet therapy, multiple lesions, long stents, overlapping stents, low EF, advanced age, DM, renal failure
What’s the only definitive treatment for HELLP syndrome?
Delivery of baby
