Oral Boards Flashcards
What are the signs of venous air embolism? What is the treatmfent algorithm?
Symptoms: decreased ETCO2, decreased O2 saturation, hypotension, “sporadic roaring sounds” on precordial doppler, and a “millwheel murmur”
Treatment algorithm:
1) Call for help and code cart
2) Turn FiO2 to 100%
3) Stop source of air entry by flooding wound with irrigation, compressing proximal vein if possible, and using bone wax
4) Attempt to aspirate air through CVP catheter
5) Provide cardiovascular support with fluid, vasoconstrictors, and inotropes
6) Treat bronchospasm with beta-2-agonists
- Reflex bronchospasm may occur with entry of air into PA
7) Consider positioning patient with left side down (left lateral decubitus) to prevent air from entering the PA
What are the signs of anaphylaxis? What are the common causative agents? What is the treatment algorithm?
Symptoms: hypotension, bronchospasm, high peak-airway pressures, decreased breath sounds, tachycardia, urticaria
Common causes: NMBs, antibiotics, latex products, IV contrast
Treatment algorithm:
1) Call for help and code cart
2) Ventilate with 100% O2
3) Turn off any infusions and inhalational agents
4) Open IV fluids/give fluid bolus
5) Give IV epinephrine (10 - 100 mcg)
- Alpha agonist activity causes vasoconstriction and reverses hypotension
- Beta agonst activity relaxes bronchial smooth muscle and decreases the release of inflammatory mediators
6) Give corticosteroids, anti-histamines, H2-blocker
7) Support hemodynamics
8) Consider:
- Repeating Epi dose until satisfactory BP is reached
- Vasopressin (1-2 units IV) if pt remains hypotensive after repeated doses of epi
- Check tryptase levels: 1st hr, 4 hrs, 24 hr post-reaction
What are the signs of unstable bradycardia? What is the treatment algorithm?
Symptoms: HR less than 50 bpm with hypotension, AMS, shock, chest discomfort, or acute heart failure
Treatment algorithm:
1) Call for help and code cart
2) Turn FIO2 to 100% and verify that oxygenation/ventilation are adequate
3) Give atropine (0.5 mg IV, repeated up to 3 mg total)
4) Stop any form of surgical stimulation
5) If atropine ineffective:
- Start epi (2-10 mcg/min) or dopamine (2-10 mcg/min) infusion
- Start transcutaneous pacing
6) Consider:
- Turning off volatiles if pt remains unstable
- Assess for drug induced causes (B blockers, Ca channel blockers, digoxin)
- Call for expert cardiology consult
What rhythms during cardiac arrest are considered non-shockable? What is the treatment algorithm?
Non-shockable rhythms: asystole and PEA
Treatment algorithm:
1) Call for help and code cart
2) Place pt supine on backboard
3) Turn FIO2 to 100% and turn off volatiles
4) Start CPR and assessment cycle:
- Perform CPR (“hard and fast” 100 compressions/min)
- Give epi (1 mg IV) every 3-5 minutes
- Assess rhythm every 2 minutes and change compression provider
5) Consider:
- ROSC if ETCO2 > 40 mm Hg
- H’s and T’s as causes
What are the “H’s and T’s” of cardiac arrest?
Hydrogen ions (acidosis) Hyper- or Hypo-kalemia Hypothermia Hypovolemia Hypoxia Hypoglycemia Tamponade Tension pneumothorax Thrombosis Toxins
What is the treatment algorithm for severe hyperkalemia?
1) Calcium gluconate or calcium chloride
2) Insulin (10 units regular IV) with 1-2 amps D50W
3) Sodium bicarbonate if pH under 7.2 (1-2 mEq/kg slowly)
What rhythms during cardiac arrest are considered shockable? What is the treatment algorithm?
Shockable rhythms: pulseless Vtach and Vfib
Treatment algorithm:
1) Call for help and code cart
2) Place pt supine on backboard
3) Turn FIO2 to 100% and turn off volatiles
4) Start CPR and assessment cycle:
- Perform CPR (“hard and fast” 100 compressions/min)
- Defibrillate (biphasic 120-200 Joules)
- Give epi (1 mg IV) every 3-5 minutes
- Consider giving amiodarone for refractory VF/VT (300 mg first then 150 mg)
- Assess rhythm every 2 minutes and change compression provider
5) Consider:
- ROSC if ETCO2 > 40 mm Hg
- H’s and T’s as causes
What defines a failed airway? What is the difficult airway algorithm? What is the incidence of “cannot ventilate, cannot intubate”? What is the incidence of difficult DL?
Failed airway = 2 unsuccessful attempts
Treatment algorithm:
1) Call for extra help
2) Get difficult airway cart and video laryngoscope
3) Bag-mask ventilate with 100% O2
4) Figure out if ventilation is adequate
If ventilation is NOT adequate
- optimize ventilation by repositioning pt, using oral/nasal airway, two-handed masking
- check that equipment is proper and working
- attempt to place LMA
- attempt intubation via video laryngoscopy
- surgical airway
If ventilation IS adequate
- take time to consider other options or even waking pt up
“Cannot ventilate, cannot intubate” occur 1 in 5,000 cases
Difficult DL occurs in up to 10% of cases
What is the treatment algorithm for intra-op hemorrhage?
1) Call for help and code cart
2) Open IV fluids and assess for adequate IV access
3) Turn FIO2 to 100% and turn off volatiles
4) Call blood bank and activate massive transfusion protocol (4 FFP: 4 PRBC: 1 Cryo: 1 Plt) - can give uncrossmatched type O blood if crossmatched not available
5) Request rapid infuser or pressure bags
6) Discuss plan with surgical team and consider packing/closure
7) Keep pt warm
9) Send labs to assess for coagulopathy and electrolyte disturbances (hypocalcemia and hyperkalemia)
10) special populations:
- Obstetric (empirical administration of 1 pool of cryo)
- Trauma (give TXA 10 mg/kg q3h)
- Non-surgical bleeding (consider recombinant Factor VIIa 40 mcg/kg)
What is your differential diagnosis for intraop hypotension?
1) Pulmonary: hypoxia, hypercarbia, tension pneumo
2) Hypovolemia: fluid deficit, acute blood loss
3) Cardiac: arrhythmia, HF, MI, tamponade
4) Shock: hypovolemia, cardiogenic, septic
5) Surgical compression
6) Embolus: pulmonary, air, fat, amniotic
7) Electrolyte/hormonal: hypoglycemia, hypocalcemia, hypermagnesemia, adrenal insufficiency
8) Anaphylaxis
9) Deep anesthesia
10) Hypothermia
11) Sympathetic blockade or neuraxial block
12) Venodilation
13) Laparoscopy: hypercarbia, increased vagal tone, compression, venous gas embolism
What are the side effects of lithium treatment? How would a pt being on lithium effect your anesthetic management?
Side effects: polyuria, DI, skeletal muscle weakness, wide QRS, AV block, hypotension, cognitive changes, ataxia, seizures
Anesthetic management:
- Check lithium level pre-op
- Avoid drugs that lead to toxicity (thiazide diuretics, NSAIDs, ACE inhibitors)
- Monitor anesthetic depth and neuromuscular blockade (lithium can decrease MAC requirements and potentiate NMB)
How should you evaluate a pt for possible airway obstruction? How would you interpret flow-volume loops?
Evaluation:
- Determine history and severity of symptoms
- Exam pt in multiple positions (supine vs prone vs upright)
- Review imaging to assess degree of airway compression
Flow-volume loops:
- Fixed obstruction - decreases both inspiratory and expiratory components
- Extrathoracic obstruction - decreases inspiratory component
- Intrathoracic obstruction - decreases expiratory component
What are the risks of non-obstetric surgery in a pregnant pt? When is the safest time to perform surgery?
Risks to the mother:
- Failed intubation
- Pulmonary aspiration
- Hemorrhage
- Infection
- Thromboembolism
Risks to the fetus:
- Preterm labor/delivery
- Teratogenesis
- Fetal hypoxia
- IUGR
- Miscarriage
Ideal time for surgery is 2nd trimester
- Avoids miscarriage and teratogenesis of 1st trimester and risk of preterm labor in 3rd trimester
What is the utility of prophylactic glucocorticoids in pregnant patients undergoing non-obstetric surgery? When should they be given?
Prophylactic glucocorticoids have been shown to significantly decrease the incidence of:
- Respiratory distress syndrome
- Intraventricular hemmorhage
- Neonatal death
Current recommendation is to give a single course of glucocorticoids between weeks 24 and 34, when there is a significant risk of preterm labor
What are the signs/symptoms of DKA? What is the physiologic basis? How is it diagnosed? What is the treatment?
Signs/symptoms: high blood glucose, abdominal pain, nausea/vomiting, AMS
Due to absolute or relative deficiency of insulin that results in ketone acids in the blood
- Hyperglycemia, glucosuria, dehydration, acidosis, and electrolyte imbalance
Diagnosis:
- Serum ketones over 7
- Serum bicarbonate under 10
- pH under 7.25 (check ABG and determine anion gap [(Na+) + (K+)] - [(Cl-) + (HCO3-)] , as usually an increased anion gap metabolic acidosis in DKA)
Treatment:
- Fluid resuscitation
- 10 to 20 units of insulin followed by infusion to reduce glucose by 50-75 mg/dL/hr (too fast and you will get cerebral edema)
- Add 5% dextrose to insulin infusion when blood glucose reaches 250 (to prevent hypoglycemia and provide energy source)
- Replace potassium, phosphate, and magnesium
- Sodium bicarbonate to correct severe acidosis
- Monitor for closing of the anion gap
What is the acronym for diagnosing obstructive sleep apnea?
STOP-BANG: Snoring (loud) Tiredness (daytime) Observed apnea (during sleep) Pressure (high BP) BMI over 35 Age over 50 Neck circumference over 40 cm Gender (Male)
Less than 3 = low risk
More than 3 = high risk
More than 5 = high risk of mod-severe OSA
What is the proper way to anesthetize the airway for an awake intubation?
Administer nebulized lidocaine to the oropharanx (numbs above epiglottis)
Superior laryngeal nerve block (numbs epiglottis to vocal cords)
Trans-tracheal recurrent laryngeal nerve block (numbs below vocal cords)
Care must be taken in situations in which pts do not have normal anatomy or underlying tumors
What are the signs/symptoms of intra-op bronchospasm? What should you do? How should it be treated?
Signs/symptoms: hypoxia and expiratory wheezing
Immediate steps:
- Turn FIO2 to 100%
- Auscultate chest
- Hand ventilate to check compliance
- Check airway pressures and check circuit/machine
- Take pt out of trendelenburg position
Treatment:
1) 100% FIO2
2) Increase volatile concentration to deepen anesthetic
3) Administer albuterol via ETT
4) Small dose of epi
What are some indications for intubation?
- Unstable vital signs
- Inability of pt to protect own airway
- Respiratory rate over 35
- Vital capacity under 15 mL/kg
- NIF less than 20-25 cm H2O
- PaO2 less than 60 on 50% FiO2
- A-a gradient over 350 on 100% FiO2
- PaCO2 over 55
What are some criteria for extubation?
- Stable vital signs
- Minimal end-expiratory concentration of volatile
- Adequately reversed NMB (sustained head lift over 5 seconds)
- Adequate gag and cough
- Awake and following commands
- PaO2 over 60 and PaCO2 under 55 on 40% FiO2
- A-a gradient under 350 on 100% FiO2
- FVC over 10-15 mL/kg
- FEV1 over 10 mL/kg
- Tidal volume over 4-6 mL/kg
- NIF greater than 20 cm H2O
How would you treat intra-op laryngospasm?
1) Turn off any inhaled agents and turn to 100% FiO2
2) Remove any stimulating factors
3) Apply jaw thrust
4) Apply CPAP via tight mask fit
5) Increase depth of anesthetic via IV agent
6) Call for help
7) Give rapid-acting muscle relaxant
8) Attempt to intubate from above if laryngospasm ongoing
9) Eventually, hypoxia results in less vigorous glottic closure and reversal of laryngospasm
What are the treatment options for post-op stridor?
1) Emergent intubation if pt unstable
2) Oxygen via facemask
3) Sit pt up
4) Nebulized racemic epinephrine
5) Heliox (70% helium, 30% oxygen)
What are the indications for a bronchial blocker? What are the limitations?
Indications:
- Critically ill pt in whom it may not be feasible to place a DLT
- Intubated pts
- Pts with known/suspected difficult airway
- Expected post-op ventilator
Limitations:
- Slow lung deflation/re-inflation times
- Difficulty suctioning of operative lung
During one-lung ventilation, what is treatment algorithm for hypoxia?
- Check position of DLT with fiber-optic scope
- Bronchodilators and suctioning
- CPAP to the non-dependent, non-ventilated lung (decreases shunt from atelectasis)
- PEEP to the dependent, ventilated lung
- Occluding the PA of the non-ventilated lung
- If severe and emergent, switch back to two-lung ventilation!
At the end of a one-lung ventilation case, the DLT is usually switched back to a single-lumen tube if the pt requires post-op mechanical ventilation? What are the strategies if initial placement was difficult?
1) Leave DLT in place and withdraw bronchial lumen into trachea
- Avoids further airway manipulation but not viable long term and not all ICUs are comfortable with DLT in place
2) Exchange DLT for single-lumen tube via an extended tube exchanger
- Requires assistance during direct laryngoscopy
How exactly would you perform an RSI?What are the contraindications to RSI? What are the remaining options?
Steps of an RSI:
1) Apply standard ASA monitors plus any additional necessary
2) Apply cricoid pressure
3) Give IV induction agent
4) Immediately give paralytic
- Succinylcholine or “double-dose Rocuronium”
5) Skip ventilation and perform direct laryngoscopy
6) Maintain cricoid pressure until EtCO2 is confirmed and bilateral breath sounds are auscultated
Contraindications to RSI:
- Known or suspected difficult airway
- Cricoid pressure should be avoided in cervical spine injury (and make sure to use in-line stabilization)
If RSI is contraindicated, then the risk of failed intubation takes primary concern over risk of aspiration
Remaining options:
- Awake fiberoptic
- Awake DL
- Blind nasal intubation
What are your concerns in a pt with a burn injury?
Difficult airway
- Inhalation injury
- Airway obstruction secondary to swelling and edema
Carbon monoxide toxicity
- 250 times greater affinity for hemoglobin
- Results in tissue hypoxia and metabolic acidosis
- Diagnosed with co-oximeter blood analysis (pulse oximetry and arterial saturation will be falsely elevated)
- Treated with Oxygen
Anesthetic concerns
- Adequate IV access since fluid resuscitation is vital to prevent hypovolemic shock
- Foley for monitoring UOP
- Arterial line for frequent sampling
- Important to watch for hypothermia (use fluid warmers, blankets, and heat lamps)
- Succinylcholine contraindicated after 24-48 hours due to potential hyperkalemia
- Pt likely with decreased sensitivity to non-depolarize NMBs so will require larger dose and frequent monitoring
What is the treatment algorithm for a post-op change in mental status?
1) Examine the pt, check response to stimuli, and check vital signs
2) review pt’s pre-op mental status and what drugs were given during case
3) Ensure adequate oxygenation/ventilation, hemodynamics, and temperature
3) Check ABG, electrolytes, and tox screen and correct any abnormalities
4) Reversal agents
- residual NMB –> neostigmine and glyco
- over narcotized –> 0.04 mg naloxone q2m
- too much benzo –> 0.2 mg flumazenil q1m
- physostigmine to attempt to reverse sedatives and volatiles
5) If condition is persistent:
- CT scan
- Neurology consult
How can you prevent post-op nausea and vomiting? How would you treat a PACU pt with PONV?
Prevention via aspiration prophylaxis:
1) Metaclopramide
- Dopamine antagonist
- Acts as a prokinetic, reduces gastric volume, and increases lower esophageal sphincter tone (no effect on gastric pH)
- Can result in extrapyramidal symptoms (dyskinesias, akathisia, and/or dystonia)
2) H2 receptor antagonist
- Increases gastric pH
- May decrease gastric volume by inhibiting gastric acid secretion
3) Non-particulate antacid (sodium citrate)
- Increases gastric pH (no effect on gastric volume)
- Effect only lasts for 30-60 minutes after ingestion
- Unpleasant taste may stimulate vomiting in some pts
Intra-op prevention:
1) Adequate hydration
2) Dexamethasone
3) Limit volatiles and nitrous
Post-op treatment:
1) IV fluids
2) Medications
- Ondansetron (serotonin receptor antagonist)
- Promethazine (dopamine receptor antagonist in CTZ, but risks extrapyramidal side effects)
3) Check labs, order EKG, and notify surgical team
What is the nomenclature or code for AICDs/PPMs?
Comprehensive identification combines the defibrillator and pacemaker codes:
1st three letters - AICD function
Last 5 letters - PPM function
Example code: 123-45678
1) Chamber shocked by AICD
2) Chamber used for antitachycardia pacing
3) Source of tachycardia detection
- E for electrocardiogram
- H for hemodynamic
4) Chamber being paced
5) Chamber being sensed
6) Response to sensing [O(none), T(triggered), I(inhibited),D(dual)]
7) Presence of absence of rate responsiveness (R or O)
8) Multisite pacing
Ideally, how would you evaluate a pt’s AICD preoperatively?
Via chart check and pt history, I’d like to know:
- Indication for placement/underlying rhythm
- Which manufacturer
- How many and what type of leads
- Battery/generator status or last check
- How device responds to magnet (usually disables AICD function and preserves PPM function, but NOT always consistent between manufacturers)
Ideally, have a pacemaker representative interrogate AICD/PPM preoperatively:
- Assess and ensure adequate function
- Ensure adequate safety margins
- Get history of rhythm abnormalities
- Set device to asynchronous pacing (DOO)
- Disable tachydysrhythmia detection and therapy
External pacer pads or paddles need to be available both in the OR and afterwards, until AICD is re-interrogated and turned on
Walk me through a standard induction in a presumably healthy pt.
1) Attach ASA standard monitors
2) Administer narcotics and lidocaine to blunt the sympathetic response to laryngoscopy
3) Pre-oxygenate with 100% O2 for several minutes via gentle facemask application
4) Induce anesthesia with propofol
5) Ensure ability to ventilate with 1 or 2 breaths via hand-bang keeping in mind to keep airway pressures low in order to not overcome the lower esophageal sphincter
6) Administer non-depolarizing muscle relaxant
7) Continue to hand-bag ventilate pt to give muscle relaxant time to work
8) Perform DL and place ETT
9) Ensure endotracheal intubation via visible bilateral chest rise, auscultation of bilateral breath sounds, and visualization of EtCO2 waveform
Walk me through emergence of a generally healthy pt.
1) Empty stomach with an OG tube and suction pharynx while pt still deeply anesthetized
2) Fully reverse any residual neuromuscular blockade
3) Administer 100% O2 and turn off any volatile agent
4) Administer IV lidocaine to hopefully prevent coughing/bucking during emergency
5) Extubate pt only after they have regained full consciousness and are able to follow commands and display the ability to protect their own airway
What characteristics of Down syndrome can complicate airway management?
- Short neck
- Large tongue
- Subglottic stenosis
- Mandibular hypoplasia
- Palatal abnormalities
- Atlanto-occipital dislocation
What is the Glascow Coma Scale? How is it scored?
The GCS is a scoring system based on eye opening, best motor response, and best verbal response that has a strong correlation with severity of head injury and pt outcome.
Motor response: Follows commands - 6 Localizes pain - 5 Withdraws from pain - 4 Flexion posture - 3 Extension posture - 2 No response - 1
Verbal response: Oriented - 5 Confused - 4 Inappropriate - 3 Incomprehensible sounds - 2 No response - 1
Eye opening: Spontaneous - 4 To speech - 3 To pain - 2 Nothing - 1
How would you induce and intubate a pt with a known/suspected difficult airway, but is is unwilling or unable to cooperate with an awake intubation?
1) Ensure availability of difficult airway equipment
2) Have surgeon at bedside and ready to perform surgical tracheostomy if necessary
3) Place pt in slight reverse-trendelenburg to improve respiratory mechanics, facilitate intubation, and reduce risk of passive regurgitation
4) Adequately pre-oxygenate the pt
5) Carefully titrate IV ketamine, attempting to achieve adequate plane of anesthesia while maintaining spontaneous respiration (can also consider inhalation induction with sevoflurane)
6) If necessary, remove front of c-collar and apply gentle cricoid pressure, while maintaining in-line manual stabilization
7) Perform careful DL and place ETT
What type of fluids should be used for resuscitation in pt’s with head injury?
Ideally, isotonic solutions, such as normal saline, should be used for resuscitation
- Small amount of free water found in solutions like LR could result in increased brain edema
- Glucose containing solutions should be avoided as hyperglycemia may augment ischemic brain injury
What is cerebral autoregulation? Is it always present?
Cerebral autoregulation maintains cerebral blood flow at a constant rate with MAPs ranging from 50 - 150 mmHg
- Autoregulation may be abolished in the prescense of head trauma or intra-cranial pathology
What is the equation for cerebral perfusion pressure (CPP)? What is normal CPP? What is ideal in a pt with traumatic head injury?
CPP = MAP - ICP
Normal CPP is 80-100 mmHg
Optimal CPP in pt’s with traumatic head injury is not fully known
- Generally accepted to maintain CPP of 60-70 mmHg to avoid cerebral ischemia below CPP of 50 and risk of increased incidence of ARDS with CPP above 70
What is the proper initial assessment in a trauma pt?
1) Rapid overview - determine whether pt is stable, unstable, dying, or dead
2) Primary survey - airway, breathing, circulation, disability, exposure
3) Secondary survey - systematically evaluate pt from head-to-toe for additional injuries, and obtain imaging, diagnostic procedures, and labs as indicated
What formula is used to calculate fluid resuscitate in burn pts? Are there risks of over-resuscitation? What end-points could be used to guide fluid resuscitation in addition to this formula?
The Parkland formula = LR at a volume of (4 mL/Kg per % burned body surface area) over initial 24 hours
- First half of volume over 1st 8 hours
- Second half of volume over remaining 16 hours
Over-agressive fluid resuscitation may lead to:
- Impaired respiration (airway/chest wall/pulmonary edema)
- Impaired peripheral perfusion (increased tissue pressure)
- Abdominal compartment syndrome (fluid-induced increases in intra-abdominal pressure)
End-points for fluid resuscitation:
- UOP of 0.5 to 1 mL/Kg/hr
- HR of 80 to 140 bpm
- MAP over 60 mmHg
What are the signs/symptoms of compartment syndrome? How is it confirmed? How is it treated?
“P’s of compartment syndrome”
- Pain
- Pulselessness
- Pallor
- Parasthesia
- Paresis
Can also be diagnosed with arteriography or trasducer measurement of intra-compartmental pressures (pressure over 30 to 40 mm Hg indicates immediate need for treatment)
Treated via surgical decompression to avoid irreversible muscle and nerve damage
What is malignant hyperthermia? What are the signs/symptoms? What can be done to prevent MH in a susceptible pt? What is the treatment algorithm?
MH is a disorder where intracellular hypercalcemia in skeletal muscle activates metabolic pathways that result in ATP depletion, acidosis, membrane destruction, and cell death
Signs/Symptoms: increased EtCO2, tachycardia, HTN , masseter muscle spasm, hyperkalemia, hypercalcemia, hyperthermia (late sign), elevated CK, myoglobinuric renal failure
Preperation for MH susceptible pt:
1) Fully stocked MH cart (dantrolene, sterile water, etc.)
2) Remove or turn off vaporizers
3) Change CO2 absorbent
4) Set O2 flow to 10 L/min for at least 20 minutes
5) Use a clean, new, disposable breathing circuit
Treatment algorithm:
1) Call for help and code cart
2) Get MH kit, call MH hotline, and have someone start mixing Dantrolene
4) Discontinue any triggering agents
5) Change to a clean circuit, with a new machine or with an oxygen tank and ambu bag
6) Hyperventilate with 100% O2 at flows over 10 L/min
7) Give Dantrolene (2.5 mg/kg IV q5min) then transition to 1 mg/kg q6h for 24-48 hours
8) Give bicarbonate for metabolic acidosis (1-2 mEq/kg slowly)
9) Treat hyperkalemia and dysrhythmias
10) Cooling pt with cold IV saline, ice, etc.
11) Monitor and support UOP with furosemid and mannitol
12) Send labs
What are the signs/symptoms of local anesthetic toxicity? What is the treatment algorithm?
Signs/symptoms (in general order):
- Nonspecific neurologic symptoms (metallic taste, perioral parasthesia, tinnitus, dizziness)
- Hyperdynamic (hypertension, tachycardia)
- Hypotension, bradycardia, arrhythmias
- Seizure and loss of consciousness
Treatment:
1) Call for help and code cart
2) Turn to 100% FiO2
3) Seizure suppression with benzos
4) Succinylcholine and intubation to secure airway
5) Lipid emulsion (20%) therapy
- Bolus 1.5 mg/kg over 1 minute
- Continuous infusion at 0.25 mL/kg/min
What is your differential for hypertension?
1) Pre-existing HTN
2) “White coat” hypertension
3) Pulmonary: hypoxia, hypercarbia, pulmonary edema, OSA
4) Renal: renovascular disease, parenchymal disease, renin-secreting tumor, PCKD
5) Neurologic: elevated ICP, spinal cord injury, autonomic instability
6) Cardiac: ischemia, fluid overload
7) Endocrine: Cushing’s, pheo, thyrotoxicosis, hyperaldosteronism
8) Vascular: aortic coarctation, vasculitis
9) Drugs
10) Pain, anxiety, inadequate anesthesia
11) Bladder distension
12) Malignant hyperthermia
13) Hypothermia
14) Electrolyte abnormalities
What is the treatment algorithm for supraventricular tachycardias?
1) Vagal maneuvers
2) Administer IV adenosine (6 mg rapid bolus, followed by 12 mg if needed)
3) Start Amiodarone 150 mg IV over 10 minutes
4) Bolus Verapamil 2.5-10 mg
5) Esmolol bolus followed by infusion
6) Synchronized cardioversion if pt is non-responsive to medications or unstable
For each region of the EKG, what is the blood supply and what area of the myocardium does it correspond to? What are the complications of ischemia/necrosis of this region?
V1-V2
- Left coronary artery, specifically the LAD and septal branch
- Septum, AV bundle, and bundle branches
- Complications: infranodal and bundle branch blocks
V3-V4
- Left coronary artery, specifically the LAD and diagonal branch
- Anterior wall of left ventricle
- Complications: LV dysfunction, CHF, heart block, PVCs
V5-V6, I and aVL
- Left coronary artery, specifically the circumflex branch
- Lateral wall of left ventricle
- Complications: LV dysfunction and AV nodal block
II, III, and aVF
- Right coronary artery, specifically the posterior descending branch
- Inferior and posterior walls of left ventricle
- Complications: hypotension
What are the signs of ischemia on TEE?
Reduced systolic wall thickening - most sensitive
Reduced endocardial excursion - most easily recognizable
Wall motion abnormalities - not always specific
Describe fat emboli syndrome? What is the classic triad? How is it treated?
Fat emboli syndrome occurs when fat embolizes to the venous and pulmonary circulation
- Occurs most commonly during orthopedic surgeries and in trauma pts
Classic triad:
1) Hypoxemia
2) Neurological abnormalities (AMS)
3) Petechiae
Treatment is purely supportive
What are considered “active cardiac conditions”? What is the revised cardiac risk index (RCRI)?
Active cardiac conditions:
- Unstable coronary syndromes
- Significant arrhythmias
- Severe valvular disease
- Decompensated heart failure
RCRI is a tool used to assess a pt’s risk of perioperative cardiac complications
- Ischemic heart disease
- Congestive heart failure
- Cerebral vascular disease
- Diabetes requiring insulin
- Renal insufficiency
- Vascular, intraperitoneal, and intrathoracic procedures
What are some reasons a pacemaker may “fail to capture”?
Pacemaker malfunction
Lead dislodgement
Ischemia
Acidosis
Anti-arrhythmic drugs
Electrolyte disturbances
What is the normal aortic valve area? How does valve area and pressure gradient change in mild/moderate/severe aortic stenosis?
Normal AV area is about 2 cm
Mild AS
- Valve area: less than 1.5 cm
- Gradient: less than 20 mm Hg
Moderate AS
- Valve area: less than 1.0 cm
- Gradient: greater than 50 mm Hg
Severe AS
- Valve area: less than 0.8 cm
- Gradient: can be as high as 100 mm Hg
In regards to the main physiologic parameters (rhythm, rate, preload, contractility, and afterload), what are the optimal management strategies for:
- Aortic stenosis
- Aortic insufficiency
- Mitral stenosis
- Mitral insufficiency
Aortic Stenosis
- Rhythm: maintain SR (importance of left atrial kick is exaggerated in pts with AS)
- Rate: maintain baseline rate (70-90 bpm) and avoid tachycardia (to avoid increase myocardial oxygen demand)
- Preload: maintain PL (pts are volume dependent but also at risk for pulmonary edema with over-resuscitation)
- Contractility: maintain
- Afterload: must maintain! (pts rely on high afterload for coronary pefusion and any drop may lead to ischemia)
Aortic Insufficiency
- Rhythm: maintain SR
- Rate: slight tachycardia (90-110 bpm) to decrease time for regurgitation
- Preload: maintain
- Contractility: maintain or improve
- Afterload: slight decreases in AL promote forward flow and decrease regurgitation
Mitral Stenosis
- Rhythm: maintain SR (although many pts will be in Afib)
- Rate: maintain normal rate (70-90 bpm) and avoid tachycardia
- Preload: maintain or slightly increase preload
- Contractility: maintain
- Afterload: maintain AL (to avoid reflex tachycardia and decreased filling times in response to hypotension)
Mitral Insufficiency
- Rhythm: maintain SR
- Rate: slight tachycardia (90-110 bpm) to decrease time for regurgitation
- Preload: maintain and avoid over resuscitating (as LA may already be fluid overloaded)
- Contractility: maintain or improve
- Afterload: slight decreases in AL promote forward flow and decrease regurgitation
Despite a full dose of heparin, pt’s ACT does not reach adequate level? What is the likely reason and how would you treat?
Heparin acts by enhancing the activity of anti-thrombin III, leading to enhanced destruction of thrombin and difficulty forming a clot
Some pts, especially those who have been on pre-operative heparin infusions, may have decreases levels or decreased activity of anti-thrombin III
FFP (1-2 units) contains coagulation factors as well as ATIII and can adequately replace the level and activity of ATIII
Protamine is primarily used for the reversal of heparin. What are some potential adverse reactions to protamine and how would you treat them?
Anaphylaxis
- Can occur in pts with previous protamine exposure, fish allergies, diabetics on NPH insulin, or men who have undergone vasectomies
- Pts with risk factors should be given a “test dose” first and monitored for any sign of reaction
- Treatment is via epinephrine and supportive measures
Fulminant pulmonary vasoconstriction and RV failure
- Pts with elevated pulmonary pressures may be at risk
- Stop administration of protamine and supportive measures
- Methylene blue may have a role
Decreased intra-vascular calcium and histamine release, leading to severe hypotension
- Directly related to speed at which protamine is given
- Fluid/vasopressors and supportive measures
Describe some anti-fibrinolytic drugs
Transexamic acid and Amicar
- Lysine analogs that reversibly bind to plasminogen, preventing its activation, and stopping fibronlysis
Aprotinin
- Serine protease, that binds to both plasminogen (decreasing fibrinolysis) and to kallikrein (limiting activation of clotting pathway)
What anesthetic options are possibilities for carotid endarterectomy? What are the options for neuromonitoring? What specific medications should be available?
Anesthetic options:
1) Regional (awake pt)
- Superficial and/or deep cervical plexus block
- Allows monitoring of neuro function of awake pt (gold standard) and improved hemodynamics
- Unsecured airway, requires pt cooperation
2) General anesthesia with ETT
- May facilitate better surgical exposure and conditions
- TIVA (with prop and remi) for superior hemodynamic stability and rapid emergency
- Inhalational technique with isoflurane (theoretical cerebral protection) combined with remi for fast titration and rapid emergence
- Requires additional neuromonitoring techniques!
Options for neuromonitoring:
1) 16-channel EEG
- Reliable and correlated with cerebral ischemia
- Need trained tech, high false positive rate, may be effected by anesthetic agents, and does not detect subcortical ischemia
2) Processed EEG (BIS monitor)
- Available, easy, and can identify severe cerebral ischemia
- Not always reliable, cannot detect focal ischemia
3) Somatosensory evoked potentials (SSEP)
- Same efficacy as EEG, can detect deep brain structure injury
- Need trained tech, effected by anesthetic agents
4) Transcranial doppler (TCD)
- Can assess cerebral blood flow and embolic phenomena
- Requires monitor placement and interpretation
5) Cerebral oximetry
- Simple to use
- Low sensitivity and specificity
6) Carotid stump pressure (CSP)
- Simple technique measuring mean arterial carotid pressure distal to cross-clamp (50 mm Hg cutoff before placement of shunt)
- Lack of validation or agreement on cutoff
Phenylephrine and Nitroglycerine should be available and ready to help manage hemodynamics
What methods are available to reduce ICP in pts with trauma or intracranial masses?
1) Intraventricular catheter (ventriculostomy)
- Allows ICP monitoring and drainage of CSF
2) Elevate pt’s head 15-30 degrees
- Increases venous drainage and improves ventilatory mechanics
3) Administer mannitol
- Reduces ICP by osmotically shifting fluid from brain into intravascular space
4) Administer furosemide
- Diuresis to remove volume
5) Hyperventilation to a EtCO2 of 30-35
- Induces cerebral vasoconstriction
- Risk of exacerbating cerebral ischemia so no longer recommended, unless absolutely necessary
- Changes are only temporary (24-48 hrs)
6) Barbituate coma
- Only used in pts with intractable elevations in ICP
- Lowers CMR and decreases excitatory neurotransmitter release
What is required for the diagnosis of acute respiratory distress syndrome (ARDS)? What is the treatment?
Diagnosis:
- Acute onset
- Bilateral infiltrates on CXR or CT
- PaO2:FiO2 ratio < 300
- Cannot be due to cardiac causes
Treatment:
- Treat cause if known
- Treat any reversible pathology such as DIC, sepsis, or hypotension
- Low tidal volumes (6 mL/kg or less) with sufficient PEEP (permissive hypercapnia may be necessary)
- FiO2 less than 50%
- Steroids are not indicated
Describe bone-cement implantation syndrome
Syndrome of hypoxia, hypotension, and other concerning symptoms associated with the use of methylmethacrylate bone cement
1) Hardening and expansion of bone cement results in increase intra-medullary pressure –> embolization of bone marrow debris
2) Emboli can lead to increase pulmonary vascular resistance, right ventricular strain, and ventricular dysfunction
3) Circulating methylmethacrylate leads to decreased SVR
4) Release of cytokines during reaming of long bones may lead to microthrombus and pulmonary hypertension
How are PFTs useful in thoracic surgery?
PFTs help provide information and evaluation regarding respiratory function, mechanics, and volumes
Can be used to help predict which pts might benefit from bronchodilator therapy and which pts may be at increased risk of post-operative pulmonary complications
High risk factors include:
1) Forced expiratory volume (FEV1) less than 40% predicted
- Evaluates pulmonary mechanics
2) Diffusion capacity of lungs for carbon monoxide (DLCO) less than 40% predicted
- Evaluates lunch parenchymal function
3) Maximal oxygen uptake (VO2 max) less than 10 mL/kg/min
- Evaluates cardio-pulmonary reserve
What are the indications for one-lung ventilation?
Lung isolation to prevent damage or contamination of healthy lung
- pulmonary hemorrhage or lung abscess
Control of distribution of ventilation
- bronchpleural fistula, bronchial disruption from trauma, or major cyst or bulla
Single lung lavage
Surgical exposure
What are the ACC/AHA recommendations for perioperative beta blockade?
Continue beta blockade therapy in patients using them chronically
NEVER START ON DAY OF SURGERY (should be titrated 2-7 days pre-op with goal HR of 60-80)
- Preop initiation may reduce CV morbidity and mortality, but it increases overall risks of hypotension, bradycardia, stroke, and death
Start pre-op titration of beta blockade in:
- Pts with 3 or more factors on the RCRI index
- Pts with less than 3 factors on the RCRI index, but who are found to have long term indication (CAD, HF, HTN)
Describe the specificity and timing of CK-MB and Troponin enzymes
CK-MB is a widespread enzyme found in many tissues of the body
- Not sensitive or specific
- Levels elevate 4-6 hours after MI
- Levels return to baseline within 2-3 days
Troponin is cardiac specific
- Much more sensitive/specific
- Levels elevate 2-6 hours after MI
- Levels stay elevated for 7-10 days
Describe the determinants of myocardial oxygen supply versus demand
Determinants of supply:
- Coronary perfusion pressure (= Aortic diastolic pressure - left ventricular end diastolic pressure)
- Amount of time spent in diastole
Determinants of demand:
- Heart rate
- Contractility
- Myocardial wall tension
- Afterload
What monitors would be required for a typical thoracic case?
Standard ASA monitors
Arterial line
- for close BP measurement and frequent measurement of ABGs
Central line
- to allow central infusion of vasoactive drugs and to provide access for transvenous pacer or PA catheter
Fiberoptic bronchoscope
Is there a preference between a right- or left-sided DLT?
Usually, prefer to use a left-sided DLT
- RUL bronchus’ close proximity to carina increases risk of RUL obstruction with right-sided DLT
For left-sided pathology:
- Have to carefully withdraw bronchial lumen of left-sided DLT into a tracheal position at time of resection to avoid interference with sugery
- Have to avoid inadvertent advancement of left-sided DLT after surgical closure as to now disrupt stump
Can always use right-sided DLT, or SLT with bronchial blocker
What monitors would be required for a typical cardiac case?
Standard ASA monitors
Arterial line
- for close BP measurement and frequent measurement of ABGs
Central line
- to allow central infusion of vasoactive drugs and to provide access for transvenous pacer or PA catheter
TEE
- to provide additional monitor of cardiac function during surgery
BIS monitor
- to help ensure adequate anesthesia during CPB
What is the most likely cause of hypotension following initiation of CPB? What are some other possible causes?
Hypotension following CPB is often due to hemodilution and sudden decrease in SVR due to injection of dilute priming solution of the bypass machine
Other possible causes:
- Monitor malfunction
- Anesthetic-induced decreases in SVR
- Inadequate venous return to CPB pump (hypovolemia, caval obstruction, malposition of venous cannula)
- Aortic disection
- Kinking, clamping, or malposition of arterial cannula
Why is hyperglycemia common during CPB? What are the potential complications? What are the management goals?
Hyperglycemia during CPB is due to:
- Decreased glucose metabolism
- Increase in stress hormones, catecholamines, and cortisol
Hyperglycemia is an independent risk factor for increased short-term and long-term morbidity and mortality following cardiovascular surgery
Goal is to maintain blood glucose levels below 150 mg/dL
What steps must be taken during preparation to wean off of CPB?
1) Ensure normothermia
2) Correct any anemia, electrolyte abnormalities, or metabolic disturbances
3) Turn on and check anesthetic alarms and monitors
4) Check lung compliance and initiate ventilation
5) Ensure heart is de-aired
6) Ensure adequate cardiac function using TEE
7) Ensure availability of pacing device and resuscitation drugs
How exactly would you perform superficial and deep cervical plexus blocks? What are the potential complications?
Superficial cervical plexus block
- Inject 10 mL of local along the posterior border of the sternocleidomastoid
Deep cervical plexus block
- Draw a line from the mastoid process to Chassaignac’s tubercle at the level of the cricoid cartilage
- C2, C3, and C4 transverse processes can be palpated at 1.5 cm intervals below the mastoid process
- Inject 10 mL of local at each transverse process
Potential complications:
- Local anesthetic toxicity
- Epidural and subarachnoid injection
- Phrenic nerve blockade
- Intravascular injection
- Recurrent laryngeal nerve injury
- Horner’s syndrome
Discuss SSEPs vs MEPs
SSEPs
- Evaluate the integrity of the ascending sensory pathways
- Stimulate peripherally and record centrally
MEPs
- Evaluate the integrity of the descending motor pathway
- Stimulate centrally and record peripherally
- Eliminate the need for any sort of “wake up test”
For a crani, discuss sitting vs horizontal position
Sitting position PROS - Superior surgical exposure (less post-op deficits) - Improved venous and CSF drainage - Improved ventilatory mechanics - Easier access to airway, chest, and extremities CONS - High risk of venous air embolism - Hypotension and CV instability - Hyperflexion of neck can occur (jugular compression, paralysis, ETT migration) - Peripheral nerve injuries - Pneumocephalus
Horizontal (lateral/prone) position PROS - Decreases risk of venous air embolism - Improved CV stability CONS - Challenging surgical exposure (more post-op deficits) - Increased bleeding and edema - Prone position carries risks of facial swelling and ischemic optic neuropathy
How are SAHs classified? What are the primary anesthetic goals for their management? What are the post-op concerns?
Graded by the Hunt and Hess classification:
Grade 0 - asymptomatic/non-ruptured
Grade I - minimal headache
Grade II - moderate to severe headache, CN palsy
Grade III - drowsiness, confusion, focal deficity
Grade IV - stupor, hemiparesis
Grade V - coma, moribund, decerebrate rigidity
Anesthetic goals:
- Maintain transmural aneurysm pressure (to avoid rupture)
- Maintain cerebral perfusion pressure
- Provide “slack brain”
Post-op concerns:
1) Re-bleed - usually in the first few days
2) Cerebral vasospasm - occurs 3-12 days after
- Presents with neurologic deterioration and drowsiness
- Causes cerebral ischmia
- Diagnosed with cerebral angiogram or transcranial doppler
- Treatment options include Nimodipine, “Triple H Therapy” (hypertension, hypervolemia, and hemodilution), or transluminal angioplasty
Discuss SIADH vs CSWS vs DI
Both SIADH and cerebral salt-wasting syndomre (CSWS) present with:
- Hyponatremia
- Decreased serum osmolality (<270)
- Elevated urine sodium concentration (>20)
- Elevated urine osmolality (>100)
The difference between SIADH and CSWS is volume:
SAIDH is euvolemic to hypervolemic
- Treated with fluid restriction, IV saline, diuretics, and demeclocycline
CSWS is hypovolemic
- Treated with fluids, sodium replacement, and steroids
Diabetes insipidus (DI) is a state of hypernatremia
- Due to either decreased ADH secretion or resistance to ADH
- Diagnosed via elevated serum osmolality (>287) and decreased urine osmolality (<200)
- Central DI treated with desmopressin and hydration, while nephrogenic DI is treated with diuretics, indomethacin, and hydration
What is autonomic dysreflexia? What are the risks? What anesthetic techniques are best? How do you manage an acute episode?
Autonomic dysreflexia is a disorder of sympathetic dysinhibition seen after spinal cord transection at T6 or above
- Stimulation below the level can result in generalized vasoconstriction and hypertension
- Bradycardia can occur secondary to activation of baroreceptor reflexes
Above lesion, parasympathetic predominantly - flushing and sweating
Below lesion, sympathetic predominantly - pale, cool, and goosebumps
Anesthetic technique should involve deep general or spinal/epidural with local anesthetic
Treatment of acute episode is with alpha-antagonists and vasodilators
- beta-blockers should not be used
What is TURP syndrome? What are the other potential complications of a TURP?
TURP syndrome is a group of signs/symptoms that occur due to over-absorption of irrigating fluids into the prostatic veins:
1) Neurologic - headache, irritability, confusion, somnolence
2) Cardiovascular - HTN, bradycardia, arrhythmias, CV collapse
3) Respiratory - tachypnea, hypoxia, pulmonary edema
4) Metabolic - hyponatremia, hyperglycinemia, hyperammonemia, hypo-osmolality, metabolic acidosis
Other potential complications of TURP:
1) Bladder perforation
- Decreased return of irrigation fluid, nausea/vomiting, abdominal/shoulder pain, hypotension
2) Bleeding / coagulopathy
3) Transient bacteremia and sepsis
- Due to bacteria entering circulation via disrupted prostatic sinuses
- Manifests as fever/chills, hypotension, tachycardia
4) Hypothermia
- Due to room temperature irrigating fluids
5) Toxicity from irrigating fluids
- Glycine toxicity: transient blindness
- Ammonia toxicity: nausea/vomiting, AMS
- Distilled water: hemolysis, hyponatremia
List the ASA NPO guidelines
2 hours: clear liquids
4 hours: breast milk
6 hours: infant formula, full liquids, light non-fatty meals
8 hours: heavy meals
Describe the effects of end-stage liver disease
1) Portal hypertension secondary to increased hepatic resistance to flow as a result of cirrhotic changes
- Esophageal/gastric varices, ascites, pulmonary effusion, and edema
2) Electrolyte abnormalities - hypo-Na, hypo-/hyper-K
3) Neurologic
- Increased ICP due to cerebral edema
- Hepatic encephalopathy
4) Cardiovascular
- Hyperdynamic, low SVR state
- Cardiomyopathy
5) Coagulopathies
- Decreased levels of factors II, VII, IX, X, proteins C/S, and anti-thrombin III (prolonged PT/INR)
- Decreased platelets, platelet dysfunction, and disorders of the fibrinolytic system
- Pts are at risk for both bleeding and increased clotting
6) Hypoalbuminemia
- Can lead to exaggerated effects of some drugs that are normally albumin-bound
7) Hepatopulmonary syndrome
- Triad of liver disease, arterial hypoxemia, and intrapulmonary vascular dilatations
- Platypnea (worsening dyspnea in the upright position) and Orthodeoxia (hypoxemia in the upright position)
- Often resolves spontaneously after transplant
8) Portopulmonary syndrome
- Triad of elevated mean PAP (over 25), elevated PVR (over 120), and elevated PCWP (over 15)
- Progresses rapidly with a very high morbidity and mortality rate
- May worsen after transplant
9) Hepatorenal syndrome
- Caused by persistent splanchnic vasodilation and reduced perfusion of the kidney
- Type I develops rapidly and is progressive with a high mortality rate
- Type II is less acute
Describe the overall anesthetic plan and case management for a liver transplant
Pre-op
- Review all forms of cardiac workup
- – pHTN should be treated prior to transplantation
- – Aortic stenosis should be treated with valvuloplasty prior to transplantation
- Head CT for AMS to evaluate cause
- Pre-op labs (H/H, electrolytes, bilirubin, albumin, coags, type/cross)
- Notify blood bank to have products (RBC, FFP, platelets, and cryo) available and ready
Access/Monitors:
- Standard ASA monitors
- 2 large bore IVs + RIC line
- Arterial line
- CVP +/- PA catheter (or TEE)
- Foley catheter
Intra-op
1) Dissection Phase (dissection and mobilization of liver until it is only attached by the IVC, portal vein, hepatic artery, and CBD)
- Manipulation of liver and decompression of ascites may result in hypotension
- Potentially high blood loss during this phase
- Fluid replacement is important
2) Anhepatic Phase (from clamping of the hepatic artery up to implantation of donor liver)
- Many physiologic alterations (hyperkalemia, acidosis, hypocalcemia, hypomagnesemia, hypo-/hyper-glycemia)
- Careful fluid management
3) Reperfusion Phase (completion of anastomoses and resumption of hepatic blood flow)
- Post-reperfusion syndrome: hypotension, bradycardia, elevated PAP, arrhythmias
- - Due to excessive K+ load with graft flushing, release of vasoactive substances and acid metabolites from the LE or graft, deleterious effect of cold blood on the heart, and inflammatory cytokines
- Prior to clamp removal, pt should be on 100% O2, have adequate CVP, and hematocrit in the mid-30s
- – Have bicarbonate ready to treat acid load, calcium ready to treat hyperkalemia, glucose, and lidocaine
Post-op
- Normal extubation criteria
- ICU admission
- Frequent checks on cardiopulmonary function, electrolytes, renal and liver function, and coagulation
For cerebral aneurysms, what is the purpose of deliberate hypotension? Is it necessary?
Deliberate hypotension is done to decrease transmural pressure in order to prevent aneurysm rupture during direct clip placement
If pt has other cardiac risk factors that would be worrisome with hypotension, clips can instead be placed on supplying arteries
- No need for deliberate hypotension
Describe the physiologic changes of pregnancy
Cardiovascular
- Increased HR, SV, CO, and blood volume
- Decreased SVR, systemic blood pressure, and PVR
- CVP, PCWP, PAP, left ventricular function, and EF do not change
- Sinus tachycardia, t-wave inversions, q waves in III all normal
Hemotologic
- Physiologic anemia (plasma volume increases more than cell volume)
- – Normal oxygen delivery due to increased CO and right-shifted oxyhemoglobin-dissociation curve
- Platelet count unchanged
- Hypercoaguable state
- – Increase in most factors, especially VII and fibrinogen
- Decreased Albumin leads to decreased oncotic pressure
Respiratory
- Increased TV, minute ventilation, work of breathing, and pulmonary blood flow
- Decreased FRC, expiratory reserve volume, and chest wall compliance
- Respiratory rate, closing capacity, vital capacity, and FEV1 do not change
- Pts will have a compensated respiratory alkalosis
Gastrointestinal
- Increased gastric pH due to placental gastrine
- Reduced lower esophageal sphincter tone
- Impaired intestinal motility
- Normal gastric motility until labor
- Elevated alk phos / Decreased serum transaminases
Renal
- Increased renal blood flow, clearance, GFR
- Decreased creatinine and urea
CNS
- Increased sensitivity to both regional and general anesthetics (decreased MAC)
How do most uterotonic agents work? Describe some commonly used agents.
Most uterotonics cause contraction of myometrial smooth muscle by increasing intracellular calcium levels
Oxytocin (Pitocin)
- Given IM or IV
- Can cause hypotension
Prostaglandin F2alpha (Hemabate/Carboprost)
- Given IM or intrauterine
- Can cause bronchospasm
- Contraindicated in asthmatics
Prostaglandin E (Misoprostol)
- Given PO or rectally
- Can cause tachycardia or fever
Methylergonovine (Methergine)
- Given IM or intrauterine
- Can cause profound hypertension
- Contraindicated in pts with HTN
Describe the function of the pituitary
Anterior pituitary is responsible for the synthesis, storage, and secretion of:
1) ACTH - stimulates adrenal cortex secretion
2) Prolactin - stimulates breast milk and inhibits ovulation
3) HGH - responsible for body growth
4) TSH - stimulates thyroid secretion
5) FSH - responsible for ovarian follicle growth / spermatogenesis
6) LH - stimulates ovulation / testosterone secretion
Posterior pituitary stores and secretes two hormones that are initially synthesized in the hypothalamus:
1) ADH - promotes water retention and regulates plasma osmolarity
2) Oxytocin - causes uterine contraction and ejection of breast milk
What are Bromocriptine and Octreotide used for? How do they work?
Both used in the treatment of pituitary adenomas
Bromocriptine is a dopamine agonist
- Inhibits the secretion of both GH and prolactin
Octreotide is a somatostatin analog
- Inhibits the release of GH and may shrink the size of pituitary tumors
What is Acromegaly? What are the manifestations? How is it diagnosed? What are your anesthetic concerns?
Acromegaly is a condition caused by excessive release of growth hormone
Characteristic manifestations:
- Skeletal overgrowth (large body, hands, feet, and jaw)
- Soft tissue overgrowth (large lips, tongue, epiglottis, vocal cords)
- Peripheral neuropathy
- Visceromegaly
- Glucose intolerance
- Osteoarthritis
- Osteoporosis
Usually diagnosed clinically, but there are tests:
- Measurement of serum IGF-I
- Measurement of serum GH
- Oral glucose tolerance test
Anesthetic concerns:
1) Potential for difficult airway
- Distorted facial anatomy
- Enlargement of tongue and epiglottis
- Overgrowth of mandible
- Narrowed glottic opening
- Recurrent laryngeal nerve paralysis
2) Increased incidence of CAD
Why would you want a TEE prior to a neuro case in the sitting position?
Increased risk of VAE during intracranial cases performed in the sitting position
TEE with bubble study can rule out a patent foramen ovale, which would place pt at risk for paradoxical embolism to the coronary or cerebral circulations
- PFO is a relative contraindication to procedures in the sitting position
What are the systemic effects of chronic renal failure?
Metabolic
- Hyperkalemia, hyponatremia, hypocalcemia, hypermagnesemia, hypoalbuminemia, uric acid accumulation, and metabolic acidosis
- Long standing metabolic alterations can lead to neuropathy, uric encephalopathy, seizures, cardiac arrhythmias, accelerated atherosclerosis, and pericarditis
Cardiac
- Retention of sodium and water combined with activation of the RAAS leads to HTN, LVH, CHF, CAD, and CVD
Pulmonary
- Volume overload may lead to pulmonary edema and restrictive pulmonary dysfunction
Immune
- Impaired phagocytosis leads to increased susceptibility to infections
Hematologic
- Anemia due to decreased production of erythropoetin, bone marrow suppression, GI bleeding, and hemodilution
- Impaired platelet function secondary to uremia
What is von Willebrand’s disease (vWD)?
The most common inherited coagulation disorder
Caused by qualitative or quantitative defects of von Willebrand Factor (vWF)
- vWF plays an important role in hemostasis and coagulation by mediating platelet adhesion and aggregation, and by functioning as a carrier and stabilizer of factor VIII
Type I
- Most common and mildest form
- Due to a quantitative defect in plasma levels of vWF
Type II
- A variety of qualitative defects in plasma vWF
Type III
- Most rare and severe form
- Extremely low levels of vWF
- Severe bleeding secondary to abnormalities in both primary hemostasis and coagulation
Multiple tests for diagnosis and classification - vWF antigen, vWF activity, factor VIII activity, vWF multimer distribution by electrophoresis
DDAVP can be used to stimulate release of vWF in pts with Type I vWD, but is not adequate for surgical procedures and does not work for other types of vWD
- Treatment should be with cryo and Humate P (purified factor VIII-vWF concentrate)
- Prophylaxis for major surgery = vWF levels at least 100 IU/dL
What are the current recommendations for periop antibiotics in a pt with mitral disease?
Prophylaxis is reserved for pts with cardiac conditions associated with increased risk for adverse outcomes from infective endocarditis (IE):
1) Prosthetic cardiac vaves
2) Previous episode of IE
3) Unrepaired cyanotic congenital heart disease or repaired disease with residual defects
4) Cardiac transplant recipients with valvulopathy
What are the risk factors for peripheral nerve injury? What are the most commonly injured nerves? What is the prognosis of peripheral nerve injury?
Risk factors:
- Male gender
- Very thin or obese body habitus
- Hospital stay over 14 days
- Vascular disease or HTN
- Diabetes
- Smoking
Most commonly injured nerves are the sciatic and common peroneal (usually from sitting or lithotomy position)
Most cases of peripheral nerve injury resolve within 6-12 weeks
What are the classic features of pheochromocytoma? How are they diagnosed? What are the anesthetic concerns?
Classic triad: paroxysmal sweating, HTN, and headache
Diagnosis:
- Urine analysis for vanillylmandelic acid (metabolite of Norepi) or metanephrines (metabolite of Epi)
- Glucagon provocation testing
- Clonidine suppression testing
Pre-op:
1) Pre-op workup looking for catecholamine-related cardiomyopathy in addition to standard labs (pts often hyperglycemic)
2) Volume resuscitation (pts often Volume depleted)
3) Alpha blockades for 10-14 days pre-op
- Ideally, no pressures over 160/90, no orthostatic HTN, and no ST-T changes on EKG
Intra-op:
1) ASA monitors plus pre-induction a-line, CVP, +/- PAC/TEE
2) Pre-op sedation critical to avoid sympathetically surge
3) Have short acting hypotensive agents (esmolol, NTG, nicardipine) available
4) Expect spikes in BP due to tumor manipulation and potential hypotension after tumor removal
Post-op:
1) Pts often hypotensive
2) Pts may be hypoglycemic
3) ICU monitoring
Describe the anesthetic concerns related to uncontrolled hyperthyroidism
Pre-op:
1) Elective surgeries should be delayed until hyperthyroid is controlled
2) Consider pre-treatment for emergent/urgent cases:
- Propylthiouracil (PTU) and potassium iodide decrease the release of thyroid hormone
- Glucocorticoids block the peripheral conversion of T3 to T4
- Beta blockers used to treat symptoms including tachycardia, sweating, and anxiety
3) Assess for airway compromise from obstructing thyroid gland
Intra-op:
1) Large-bore IVs and pre-induction a-line
2) Be ready for large swings in hemodynamics
3) When applicable, neuraxial anesthesia may block sympathetics
Post-op:
1) Careful consideration of extubation given potential airway concerns
2) Avoid aspirin as it may raise free thyroid hormone levels by displacing protein-bound fraction
What is the MELD risk score?
The “model for end-stage liver disease” (MELD) is used to rank pts on the liver transplant list
- The higher the score, the higher the short-term mortality
MELD score can range from 6 to 40 and is calculated using:
- INR
- Creatinine
- Bilirubin
What are the types of fetal decelerations? Which type is most concerning? How would you treat it?
Three forms of declerations: early, late, and variable
- Late decerlations are the most concerning
Early decelerations
- Shallow, symmetric decelerations that occur and peak at the same time as contractions
- Caused by fetal head compression by the cervix (altered fetal CBF leads to vagal response, causing bradycardia)
Variable decelerations
- Variable in size, shape, duration, and timing
- Caused by umbilical cord compression (leads to increased fetal CO2 and ultimately acidosis)
Late decelerations
- Begin a bit after the onset of contraction and peak after the peak of contraction
- Always indicate fetal hypoxia!
- Caused by uteroplacental insufficiency (any compromise in delivery, exchange, or uptake in fetal oxygen):
1) Excessive uterine contractions
2) Spinal/epidural anesthesia - hypoperfusion/hypotension
3) Post-maturity
4) Maternal hypertension
5) Collagen vascular disease
6) Placental abruption
7) Maternal/fetal anemia
Decelerations can be diagnosed via fetal scalp pH
- Technically difficult and infrequently used
- pH less than 7.20 indicates severe fetal acidosis and requires emergent cesarean
Treatment of acute decelerations
1) Administer oxygen to pt
2) Adjust maternal position - left uterine displacement
3) IV fluid bolus
4) Hold oxytocin infusion and consider tocolysis
5) Consider emergent cesarean
What are the potential complications associated with a molar pregnancy?
Anemia
Pregnancy-induced HTN
Pulmonary insufficiency
- Dyspnea and cyanosis
Pulmonary embolism
Congestive heart failure
Hyperthyroidism/thyrotoxicosis
- Secreted hCG is identical to a sub-unit of TSH
- Symptoms must be treated with iodine and beta-blockers
Disseminated intravascular coagulation (DIC)
Describe the stages of labor. What specifics regional blocks could be performed for each stage?
1st Stage
- Includes uterine contractions and dilation of the cervix
- Pain is transported via visceral C-fibers from T10-L1
- Can be blocked with a paracervical block
- Relatively high risk of fetal bradycardia and decreased uteroplacental insufficiency
2nd Stage
- From full cervical dilation until delivery
- Pain is transported via the pudendal nerves (S2-S4)
- Can be blocked via a pudendal block
- Relatively low risk
3rd Stage
- Delivery of the plaenta
Epidural ideally covers everything (T4-S4)
What are the absolute and relative contraindications to neuraxial anesthesia?
Absolute contraindications:
- Pt refusal
- Sepsis
- Infection at needle entry site
- Increased ICP
- Shock or hypovolemia
- Coagulopathy or therapeutic anticoagulation
Relative contraindications:
- Pre-existing neurologic disease
- Psychiatric disorder or dementia
- Aortic stenosis or LVOT obstruction
- Some congenital cardiac disorders
- Spinal deformities or prior spinal surgery
What are the anatomic differences between adult and pediatric airways?
Infant tongue is much larger
- increased risk of obstruction and difficulty visualizing the larynx
Larynx is located more cephalad (C3-C4) in neonates compared with adults (C4-C5)
- more anterior view during direct laryngoscopy
Infant epiglottis is narrow and omega-shaped compared with broad and flat in adults
- can create difficulty during laryngoscopy
Vocal cords are angulated in neonates compared with being perpendicular to the trachea in adults
- can cause difficulty with intubation
Larynx is funnel-shaped in neonates with the cricoid being the narrowest part, while adults have a cylindrical larynx with the glottis opening being the most narrow area
What is the formula for deciding an ETT size in pediatrics?
(16 + age)/4 - 0.5 = cuffed tube size
Describe the pertinent features of pediatric physiology
Pulmonary
1) Infants are prone to peri-op hypoxemia
- Secondary to increased oxygen consumption coupled with a relatively decreased FRC)
2) Faster inhalational induction
- Increased minute ventilation : FRC ratio
- Increased percentage of vessel-rich tissues
Cardiovascular
1) Cardiac output is rate dependent
- Cannot increase contractility so cannot enhance stroke volume
2) Common causes of bradycardia include hypoxemia and vagal stimulation
Temperature regulation
1) Difficult to maintain normothermia secondary to a disproportionately large body surface area, increased metabolic rate, and a thinner layer of subcutaneous insulating body fat
2) Temperature maintained via brown fat nonshivering thermogenesis (infants do not shiver), crying, and movement
Glucose metabolism
1) Prone to hypoglycemia
- Increased metabolic demands and decreased glycogen stores
2) IV dextrose (D5 0.25%NS) should be used in all pts under 6 months of age, and in infants between 6 and 12 months if surgery is anticipated to last over an hour
3) Maintain serum glucose levels over 40 mg/dL
Maintenance fluids = 4 ml/kg/hr for 1st 10 kg, plus 2 ml/kg/hr for 2nd 10 kg, plus 1 ml/kg/hr for each remaining kg
Describe fetal circulation and the changes that occur after birth
Fetal circulation
1) Blood from placenta travels to baby via umbilical vein
2) Umbilical vein travels to the liver and then splits:
- 50% bypasses the liver through the ductus venosus and then travels to the heart via the vena cava
- 50% goes directly to the liver
3) From the right atrium, the blood can take two paths:
- Most blood passes through the foramen ovale into the left ventricle
- Some blood remains in the right heart, traveling to the pulmonary artery, before bypassing the lungs via the ductus arteriosis to the aorta
4) Blood then travels from the aorta to the umbilical arteries, and back to the placenta
Changes at birth
1) Expansion of the lungs occurs as breathing is initiated
2) Inflation of the lungs reduces pulmonary vascular resistance, resulting in increased blood flow from the pulmonary arteries
- PVR can remain elevated (hypoxemia, hypercarbia, hypothermia, hypovolemia, acidosis) resulting in persistent fetal circulation
What is the APGAR score?
The APGAR Score is a subjective scoring system used to evaluate the newborn and is performed at 1 and 5 minutes after delivery
5 categories:
- Appearance (0=pale/blue, 1=blue extremities, 2=pink)
- Pulse (0=absent, 1=under 100 bpm, 2=over 100 bpm)
- Grimace (0=no response, 1=grimace, 2=cough or cry)
- Activity (0=limp, 1=extremity flexion, 2=active motion)
- Respiration (0=absent, 1=slow/irregular, 2=good/crying)
What is the algorithm for neonatal resuscitation?
1) Warm and dry infant
2) Aspirate the mouth, pharynx, and nose
- If suctioning reveals meconium or thick meconium-stained mucus, suction via an ETT before lungs are inflated
3) Stimulate the infant by slapping the soles of the feet or rubbing its back
4) If after stimulation, the infant is still apneic or has a heart rate less than 100, initiate positive pressure ventilation at rate of 30–40 breaths/minute, and place pulse ox on right upper extremity (in order to monitor pre-ductal flow, which is a better indicator of CNS oxygenation)
5) If after 30 seconds of ventilation, the heart rate is still below 60, begin chest compressions at a rate of 100 compressions per minute
6) If after 30 seconds of compressions, heart rate is still below 60, consider IV fluid bolus (10 mL/kg) or medications
Neontal resuscitation medications/doses:
1) Epinephrine (1:10,000 concentration)
- Used for treatment of asystole or bradycardia despite 30 seconds of effective ventilation and compressions (can be repeated every 3–5 minutes as needed)
- 0.01–0.03 mg/kg IV or 0.1 mg/kg via the ETT
2) Atropine
- Used to treat bradycardia
- 0.02 mg/kg may be given IV or 0.03 mg/kg via the ETT
3) Calcium gluconate
- Used to treat low cardiac output
- 100 mg/kg infused over 5–10 minutes
4) Naloxone
- Used to treat respiratory depression secondary to maternal opioid administration (DO NOT give to infants of opioid addicted mothers for fear of precipitating withdrawal)
- 0.01 mg/kg IV, IM, SQ, or via ETT
5) Sodium bicarbonate 4.2%
- Used only if resuscitation is prolonged, with documented acidosis, despite adequate ventilation and perfusion
- 2 mEq/kg via an umbilical catheter
What are the different types of tracheoesophageal fistula? What other congenital anomalies are associated with TEF? What are the anesthetic concerns/management?
Types of TEF:
A - esophageal atresia without fistula
B - esophageal atresia with fistula to upper trachea
C - esophageal atresia with blind upper pouch and lower segment tracheal fistula (MOST COMMON FORM)
D - esophageal atresia with both proximal and distal tracheal fistulas
E - pure tracheoesophageal fistula without esophageal atresia (H-type)
TEF is associated with VACTERL: V - vertebral defects A - anal atresia C - cardiac (ASD, VSD, AV canal defects) TE - tracheoesophageal fistula R - radial/renal L - limb deformities
Pre-op Concerns:
1) Evaluate for respiratory complications
2) Evaluate hydration status
3) Complete evaluation for other congenital problems (C/A/P and spine films, Kidney ultrasound, Echo)
4) Avoid aspiration by preventing feeding, elevating head, and placing suction catheter in proximal pouch
Intra-op Concerns:
1) Awake intubation vs RSI
- Awake intubation has not been proven to prevent bradycardia or decreased arterial hemoglobin oxygen saturation and has largely been replaced by RSI
2) Place ETT in the mainstem bronchus and withdraw until breath sounds are heard bilaterally
- Auscultate to make sure lungs are ventilated and stomach is not being distended
Post-op Concerns:
1) Esophageal anastomosis is under tension and the infant may electively be paralyzed/ventilated for up to 5 days post-op
2) Ventilation with bag/mask should be avoided for several days, secondary to the fragility of the anastomosis
3) Many long term complications (dysphagia, GERD, strictures, infections, recurrent TEF)
What is the most common metabolic derangement associated with pyloric stenosis? Describe the anesthetic concerns regarding this condition.
Hypokalemic, hypochloremic, hyponatremic metabolic alkalosis
Pre-op:
1) MEDICAL emergency, not a surgical emergency
2) Adequately volume-resuscitate and replete electrolytes (electrolyte MUST be normal before proceeding into the OR)
- Sodium at least 130
- Potassium at least 3
- Chloride at least 85
- Urine chloride over 20
Intra-op:
1) Suction stomach in multiple positions to ensure removal of as much contents as possible
2) Assuming normal looking airway, pretreat with Atropine (.02 mg/kg) and perform RSI with propofol/succinylcholine
3) Maintain anesthesia with volatile/N2O/O2
4) Muscle relaxants not usually needed
Post-op:
1) Extubate the patient when fully awake with regular and adequate breathing patterns
2) Rectal acetaminophen for pain control
3) Monitoring is vital
- Persistence of electrolyte and fluid imbalances
- Pts are less than 60 weeks post-conceptual age and are therefore more likely to exhibit post-op ventilatory depression
What is veno-venous bypass (VVBP)? Are there any alternatives? What are the benefits and risks?
During VVBP ,femoral (or distal IVC) and portal veins are cannulated to reroute blood flow from below the diaphragm to the suprahepatic vena cava (via the axillary, subclavian, or jugular vein) during the anhepatic phase
- Alternative is to use piggyback technique where the IVC is preserved and there is not complete interruption in caval blood flow (technically more difficult and increased surgical complications)
Advantages - improved hemodynamic stability, better organ perfusion, improved cardiac filling, decreased blood and fluid requirements, splanchnic decompression (earlier return of gut motility), preserved drainage of renal veins (potentially reducing renal impairment), limited metabolic impairment, improved surgical field (decompression of portal pressures), less pulmonary edema
Disadvantages - increased risk of air embolism, thromboembolism, arm lymphedema, hematoma, vascular injury, nerve injury
Your almost full-term pregnant pt codes? What do you do? Should you deliver the baby before starting CPR?
Normal ACLS with left uterine displacement
If resuscitative efforts were not successful within the first couple of minutes, deliver baby via emergency c-section
- Delivery of baby within 5 minutes of cardiac arrest improves the chances of survival for both mother and baby by:
1) Relieving aortocaval compression (improving venous return)
2) Decreasing metabolic demands
3) Allowing more effective chest compressions
What are the concerns regarding anesthetizing a child with a URI? What are the general recommendations for when to proceed with an elective case? ETT or LMA?
Pts with acute or recent URI are at increased risk of peri-op respiratory complications such as laryngospasm, bronchospasm, and oxygen desaturation
Mild symptoms (sneezing, nasal congestion, nonproductive cough)
- Delay surgery for 2-4 weeks if surgery requires ETT
- Can proceed with surgery if ETT is not required (regional or GA with mask/LMA)
Severe symptoms (fever over 38.5, productive cough, purulent secretions, malaise, pulmonary involvement) - Delay surgery for 4-6 weeks
Have to balance benefit of decreased airway hyperactivity vs risk of child developing another URI
Using an LMA in pts with acute/recent URI is associated with fewer periop respiratory complications compared to ETT
What is myasthenia gravis (MG)? What are the main types of symptoms seen? What are the anesthetic concerns?
MG is an autoimmune disease in which antibodies are produced against post-synaptic nicotinic acetylcholine receptors
Two types of muscle weakness:
1) Ocular - ptosis and diplopia
2) Generalized (bulbar) - respiratory insufficiency, weakness with chewing, head drop, “expresionless look”
- Symptoms are usually worse later in the day or after exertion
Pre-op:
1) Detailed history on duration, severity, and treatment
2) MG medications should be continued
3) If bulbar symptoms are present, may need PFTs
- Pts at increased risk for aspiration
4) Look for predictors for need for post-op mechanical ventilation
- MG for over 6 years
- COPD
- Pyridostigmine dose over 750 mg/day
- Vital capacity less than 40 mL/kg
5) Discuss the need of NMB with surgeon
Intra-op:
1) If possible, avoid muscle relaxation
2) If muscle relaxation must be used:
- MG pts are resistant to succinylcholine
- MG pts are more sensitive to non-depolarizing NMBs
- NMB reversal may precipitate cholinergic crisis if pt is being treated for MG (consider allowing muscular recovery without reversal)
3) Judicious narcotic use considering potential respiratory insufficiency (consider Remi infusion)
4) Extubate only if pt meets stringent criteria
Post-op:
1) Gradual weaning off of mechanical ventilation in an ICU setting
2) Continue anti-cholinesterase therapy throughout
Describe mild vs severe preeclampsia? What is the volume status of pts with preeclampsia? What is the treatment?
Mild
- BP over 140/90
- Proteinuria over 300 mg/24hrs
- Edema
Severe
- BP over 160/110
- Proteinuria > 5g/day
- Liver dysfunction, pulmonary edema, AMS (HA or visual changes), RUQ pain, oliguria, and/or HELLP (hemolysis, elvated liver enzymes, and low platelets)
Volume Status: relative hypovolemia from increased SVR and increased vascular permeability
- At risk for pulmonary and cerebral edema with over aggressive fluid resuscitation
Treatment is with IV magnesium infusion (anticonvulsant and tocolytic)
- Therapeutic Level: 4-7 meq/L
- – Over 7: Loss of DTRs, hypotension
- – Over 10: Respiratory depression
- – Over 15: EKG changes
- – Over 20: Cardiac Arrest
- Relative contraindications include cardiac pathology (risk of deleterious cardiac effects), myasthenia gravis (will worsen symptoms due to decrased release of acetylcholine), impaired renal function (mag is renally excreted), and current use of calcium channel blockers (potentiates cardiotoxic effects)
In general, what are the normal areas of concern when regarding discharge criteria?
Stable vital signs Normal ambulation No nausea/vomiting Appropriate pain No unexpected surgical bleeding
Which medications should be dose based on ideal body weight?
Propofol (infusion)
Vecuronium
Rocuronium
Remifentanil
What is sickle cell anemia? What are the triggers? Describe the anesthetic concerns.
SS is a hereditary hemoglobin disorder that results in vaso-occlusive crises when RBCs with irreversibly sickled hemoglobin aggregate in blood vessels
Triggers of sickling: hypoxia, acidosis, hypo-/hyperthermia, infection, stress, physical exertion, alcohol consumption, dehydration
Pre-op:
1) Detailed history regarding disease, treatment, and complications
2) Labs: HCT, percent Hb S via electrophoresis (should have less than 40%), BUN/Cr, Ua, type and screen
3) Pre-op transfusion guidelines
- IV fluids:
- – Any minor or brief procedure, or anything under local
- – GA less than 60 minutes
- Simple transfusion to goal Hct 30-35%:
- – Higher risk pts
- – Non-tonsillectomy, non-laparotomy, non-thoracotomy cases
- – Elective procedures involving airway, thoracotomy, or any GA longer than 90 minutes
- Exchange transfusion
- – Urgent procedures, especially involving airway, thorax, or GA longer than 90 minutes
- – Pts with history of acute chest syndrome or COPD
- – Goal Hb S less than 30%
Intra-op:
1) Maintain normothermia, avoid hypoxia/hypovolemia/acidemia
2) Avoid tourniquet if possible
Post-op:
1) Early mobilization
2) Incentive spirometry
Which pts would be considered to have HPA axis suppression? What does of stress dose steroids should be given?
Pts considered to have HPA axis suppression:
- Any pt who has received more than 20 mg/day of prednisone for more than 3 weeks within the previous year
Stress dose steroids:
1) Minor surgeries
- Take normal morning steroid dose
2) Moderate stress surgery
- Take normal morning steroid dose
- 50 mg Hydrocortisone IV before induction and then 25 mg q8h for 24 hours
3) Major stress surgery
- Take normal morning steroid dose
- 100 mg Hydrocortisone IV before induction and then 50 mg q8h for 24 hours
- Taper dose by half per day until maintenance level is reached
Describe some of the potential complications of normal transfusions. What about side effects from massive transfusion?
Infectious
1) Bacterial - usually from platelets stored at room temperature
2) Viral - CMV, Hep B/C, HIV, HTLV, and West Nile
Febrile transfusion reaction
1) Due to reaction to donor leukocytes
2) Mild and self-limited
Acute hemolytic reaction
1) Due to ABO incompatibility (antibody in recipient’s circulation against antigen on transfused cells)
2) Tachycardia, hypotension, hemoglobinuria
3) Diagnosed via direct coombs test, decrease serum haptoglobin, increased serum bilirubin
4) Treatment - stop transfusion, recheck blood and repeat cross-match, support BP, and support renal function
Allergic reactions
1) Due to proteins in donor plasma
2) Treatment is supportive
Transfusion-related acute lung injury (TRALI)
1) Due to activation of recipient leukocytes by donor antibodies
2) Appears clinically like ARDS
3) Treatment is supportive including mechanical ventilation
Complications of massive transfusion:
1) Hypothermia
2) Volume overload
3) Dilutional coagulopathy
4) Decreased 2,3-DPG causing left shift of O2-Hb dissociation curve
5) Citrate toxicity - hypocalcemia leading to hypotension, narrow pulse pressure, elevated CVP, and prolonged QT
6) Hyperkalemia
7) Acid-base disturbances
What special concerns regarding monitoring would you have for mediastinoscopy? What are the potential complications?
During mediastinoscopy, intermittent compression of the innominate vein commonly occurs
- Arterial line and pulse oximetry should be placed on the right arm as early indicators of potential occlusion/disruption of flow
- BP cuff should be placed on left arm to offer consistent BP readings through the case
Potential complications:
1) Pneumothorax
2) Nerve injury (recurrent laryngeal or phrenic)
3) Trauma to adjacent structures (pleura, trachea, esophagus, multiple vascular structures)
- Should a major vascular structure be perforated, bleeding can be severe and rapid, needing emergent sternotomy
- Plan for lower extremity IV access in case of upper vascular disruption otherwise fluids and medications will pool in chest
What is needed in order to clear a trauma pt’s cervical spine?
1) Absence of cervical pain/tenderness
2) Absence of paresthesia or neurological deficit
3) Normal mental status
4) No distracting pain
5) Must be over 4 years old
IF ABOVE NOT MET: cross-table lateral film showing C1 through T1, open mouth odontoid view, and AP view required
- 7% of fx still missed, ligaments not evaluated (CT may be of use)
What is the utility of a lumbar drain? What are the potential complications?
A lumbar drain would allow measurement of CSF pressure and drainage if necessary
- Used in cases in which you are concerned about spinal cord ischemia
- Spinal cord perfusion = MAP - CSF pressure
Potential complications
- Headache
- Hematoma
- Meningitis
- CSF leak
What are the effects of aortic cross-clamping?
Increased afterload proximal to clamp
- Increased BP, coronary blood flow, ventricular wall tension, CVP, and pulmonary capillary wedge pressure
Decreased pressure and perfusion distal to the clamp
- Decreased renal blood flow (not an issue if clamping is infrarenal)
Decreased venous return, ejection fraction, and cardiac output
Increased mixed venous O2 saturation and catecholamine release
Decreased total body oxygen consumption
Metabolic acidosis
What is a TEG used for? What are the common measurements and how would you treat abnormal values?
a TEG measures the viscoelastic properties of blood during clot formation, allowing evaluation of clot formation kinetics and growth, as well as strength and stability of clot
Common parameters
1) R value - time to initial clot formation due to activation of clotting factors
- Treat with FFP
2) K value and alpha angle - speed of fibrin buildup and strengthening due to thrombin
- Treat with cryo
3) Maximum amplitude (MA) - maximum strength of clot due to platelet adhesion
- Treat with platelets
What is cystic fibrosis (CF)? In general, what are the anesthetic concerns?
CF is a disease in which a specific gene mutation leads to abnormal movement of sodium in and out of cells
- Results in development of thick, viscous secretions that are associated with luminal obstruction and glandular destruction of multiple systems
General anesthetic concerns in a pt with CF:
1) Pulmonary
- Mucous plugging
- Hypoxia due to V/Q mismatching
- Bronchospasm due to bronchial hyperreactivity
- Pneumothorax due to bullae formation
- Potential need for post-op mechanical ventilation
2) Cardiac
- Risk for pHTN
- Potential right-sided HF (cor pulmonale)
3) Coagulopathy due to hepatic involvement and malabsorption
4) Diabetes and electrolyte abnormalities due to enzyme insufficiency
What are the potential benefits of thoracic epidural for pain control?
1) Improved pain scores
2) Greater mobility
3) Reduced opioid requirements
- Decreased risk of respiratory depression
- Decrease incidence of ileus
4) Decreased pulmonary splinting
- Decreased incidence of atelectasis and pneumonia
Are there any concerns regarding RSI in a pt with asthma?
RSI carries a significant risk for light anesthesia during induction/intubation and can potentially lead to bronchoconstriction
- Safely securing airway takes precedence over pure aspiration concerns
Perform a “modified RSI”
- Administer short-acting beta-agonist like Albuterol
- Pre-treat with Metoclopramide and Ondansetron
- Pre-oxygenate with 100% O2
- Treat with small amounts of fentanyl and lidocaine to avoid light anesthesia and decrease potential response to laryngoscopy
- Apply cricoid presure
- Induce with Ketamine and Propofol (both are bronchodilators)
- Use succinylcholine, but be aware of potential histamine-induced bronchospasm
- Secure airway with ETT
What is a dibucaine number? How is it clinically relevant?
The dibucaine number represents the function of a pt’s pseudocholinesterase, which is the enzyme responsible for metabolism after a dose of succinylcholine
80 - normal function (up to 10 minutes of paralysis)
50 to 60 - heterozygous (up to 30 minutes of paralysis)
20 - atypical pseudocholinesterase (4-8 hours of paralysis)
You use a peripheral nerve stimulator on your pt and see fade with train-of-four. What do you think is happening?
Fade with train-of-four is normal with residual non-depolarizing neuromuscular blockade
If succinylcholine had been used, this may represent Phase II blockade
- May be due to excessive dose, prolonged infusion, or abnormal metabolism
Discuss the various causes of post-op vision loss and their associated findings.
Corneal abrasion - eye pain worsened with blinking or movement; sensation of foreign body in eye; tearing; conjunctivitis
Acute glaucoma - severe and diffuse periorbital pain; dry and pale eye; dilated pupil
Glycine toxicity - elevated serum glycine over 17; dilated and non-reactive pupil
Cortical blindness - unilateral or bilateral vision loss; normal pupillary response and eye motility, but no response to visual threat
Hemorrhagic retinopathy - floaters; blurred vission; retinal edema
Retinal ischemia from artery occlusion - painless vision loss; cherry red macula
Ischemic optic neuropathy - painless visual loss; absent/impaired light reflex
Describe epiglottitis
An airway emergency that usually occurs in children aged 2-5 years
Caused by Haemophilus influenzae type B
Signs and symptoms include fever, profuse drooling, stridor, and inability to lay supine
- characteristic radiology finding is the “thumb sign” which shows swollen epiglottis along with prevertebral edema
Treatment includes ENT consult, early intubation, and antibiotics
- no attempts at stimulation or suction should be made as excessive agitation, anxiety, or crying can worsen airway obstruction
Anesthetic management involves maintenance of spontaneous respiration and safely securing the airway
- Have surgeon and emergency airway equipment, including multiple ETT sizes, available
- Keep child in the sitting position
- Adminster 100% oxygen
- Inhalational induction with Sevoflurane or IV titration of Ketamine to maintain spontaneous respiration
- Gentle laryngoscopy and placement of small ETT
- Extubation only after child’s fever, neutrophilia, and epiglottic swelling is resolved (evidenced by spontaneous swallowing and a positive leak)
What are the negative consequences of sodium bicarb administration? What are the indications for its use?
Negative effects:
1) Generation of additional CO2, which can temporarily worsen acidosis
2) Left shift of oxyhemoglobin dissociation curve, decreasing oxygen unloading and worsening tissue hypoxia
3) Potential hyperosmolar state due to excessive sodium
4) Potential hypokalemia from intracellular shift of K
Indications:
1) Severe acidosis (pH less than 7.2)
2) Life threatening hyperkalemia
After placement of a CSE, your labor pt experiences tetanic uterine contractions and the fetal heart tones decrease. What is the most likely cause? How will you treat it? Does this alter labor plans?
Most likely cause is a sudden decrease in circulating epinephrine, leading to tetanic uterine contraction and uterine hypoperfusion:
1) Spinal anesthesia leads to rapid decrease in pain
2) Abrupt decrease in plasma epinephrine
3) Decreased stimulation of beta2 receptors in uterus
4) Increased uterine tone, reducing uterine blood flow
5) Diminished fetal oxygen delivery leading to fetal bradycardia
Treatment:
1) Supplemental oxygen
2) Place pt in left uterine displacement
3) Discontinue oxytocin if running
4) Treat any maternal hypotension
5) Administer 100 mcg of IV nitroglycerine to attempt to break contraction
Of note, fetal bradycardia following neuraxial anesthesia is usually transient and readily treated, and it does not increase the incidence of emergency cesarean
