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
