Knowledge Gaps Flashcards
Describe the difference between roller and centrifugal pumps used in cardiopulmonary bypass?
Roller pumps produce a FIXED pulsatile forward flow based on the speed that is set. This flow is not sensitive to preload or afterload, can cause lots of hemolysis, and has the potential for large amounts of air entrainment.
Centrifugal pumps use rotational force to induce forward flow. These pumps are sensitive to preload and afterload and cause less damage to RBCs and will stop working if there is a lot of air entrained. But the disadvantage is a lack of PULSATILE flow.
Would you use alpha stat or pH stat management in moderate hypothermia?
alpha stat in adults because neurological injury is usually an embolic event (rather than ischemia), and the enhanced cerebral blood flow that results from pH stat management is not ideal.
**the best strategy in deep hypothermia with or without circ arrest is unknown
Would you use alpha stat or pH stat management for moderate hypothermia in the pediatric patient?
pH stat because the primary mechanism for neurological injury in children is ischemia (not embolic events). Therefore, the addition of CO2 to maintain a PaCO2 of 40 would enhance cerebral blood flow which is ideal.
Does it matter if mitral regurgitation is acute or chronic?
Yes - an acute mitral regurg would lead to volume overload 2/2 increased left atrial and ventricular pressures, decreased cardiac output, pulmonary edema and eventually R heart failure. The associated tachycardia could also lead to myocardial ischemia.
Chronic MR is less concerning because there is usually compensatory ventricular dilation.
Explain the normal pulmonary capillary wedge tracing?
ACXVY
C-wave reflects ELEVATION of the mitral valve during early systole
X descent occurs with the DOWNWARD displacement of the atrium during ventricular contraction
V-wave reflects VENOUS RETURN against a closed mitral valve
Y descent represents a DECLINING atrial pressure as the mitral valve opens
**In MR, CV becomes one combined wave with X disappearing
Induction goals in mitral regurgitation with CAD?
Avoid hypertension and bradycardia which will worsen MR
Avoid hypotension and tachycardia which could lead to inadequate coronary perfusion
**Laryngoscopy often causes hypertension and tachycardia –> this worsens MR causing atrial dilation and increased myocardial demand –> both can lead to atrial fibrillation
Atrial contribution in regurgitant lesions versus stenotic lesions? (Lost in A-fib)
Significant in stenotic lesions, less critical in regurgitant lesions. Rate control if HD stable in regurgitant lesions. Low threshold for pharmacological or electrical cardioversion in stenotic lesions.
What would you do if the venous reservoir level is decreasing during cardiopulmonary bypass?
Ask the perfusionist to reduce pump flows and add fluid to the blood volume while simultaneously looking for causes of decreased venous return. Perhaps there is a problem with the venous cannula (kinking or malpositioning) or the surgeon is compressing the heart.
Why does the surgeon ask you to vigorously inflate the lungs prior to coming off the cardiopulmonary bypass pump?
To remove air from the pulmonary vasculature into the left heart where it is vented. This prevents air embolization to the cerebrum and coronaries. It also recruits the collapsed alveoli.
What is happening if the pulmonary pressures increase and systemic pressures decrease coming off of cardiopulmonary bypass?
This is an indication of left heart failure. Many things could cause this including increased afterload, graft failure (kinking, clot, air), poor coronary perfusion (hypotension, emboli, spasm, tachy), valve failure, reperfusion injury, acidemia
How might mitral valve replacement contribute to risk of left ventricular failure coming off bypass?
There is a loss of passive (reguritant) flow into the left atrium which leads to an acute increase in volume load for the LV which can lead to left ventricular dysfunction. Inotropes, afterload reduction, and/or increase in preload may be needed for the propogation of the extra volume.
Can an IABP help facilitate weaning from cardiopulmonary bypass in the setting of LV failure?
Yes an IABP is the only intervention which increases coronary perfusion (increases oxygen supply) and decreases afterload (decreases oxygen demand)!
Where should an IABP be positioned? When should it inflate?
The tip should be at the junction of the aortic arch and the descending aorta (below the left subclavian artery) to prevent cerebral emboli.
It should inflate during early diastole (dicrotic notch of arterial wave form or middle of the T-wave on ECG),
What is pulsus paradoxus?
An exaggerated (>10 mmHg) drop in systolic pressure with inspiration. Classically seen with cardiac tamponade.
inspiration causes a negative intrathoracic pressure –> increased venous return to the heart –> increased RV volume and bulging of septum into the LV –> resultant drop in systolic pressure (normally <10)
How would you evaluate postop vision deficits?
Determine if it is painful or painless first.
PainFUL vision problems includes corneal abrasions and acute glaucoma. Corneal abrasions often have a foreign body sensation while acute glaucoma will present with a dilated pupil.
PainLESS vision problems most commonly include ischemic optic neuropathy (anterior vs posterior), central retinal artery occlusion, and cortical blindness (ALL are due to ischemia from impaired blood flow from some cause)
cortical blindness results in vision loss with normal pupils and normal fundoscopy.
CRAO has abnormal fundoscopy –> unilateral vision loss with a cherry red macula
Anterior ischemic optic neuropathy –> unilateral or bilateral vision loss with optic disc edema
posterior ischemic optic neuropathy –> unilateral or bilat vision loss with a normal optic disc
Other: glycine toxicity –> TEMPORARY blindness with dilated non-reactive pupils; lasts approx 24 hours
What is TRALI vs TACO?
TRALI is clinically similar to ARDS. It is a noncardiogenic edema that occurs within 1-6 hours after blood products. Results in acute onset hypoxemia with bilat chest infiltrates on CXR in the ABSENCE of cardiac failure or fluid overload. Symptoms might include frothy pulmonary secretions, tachycardia, dyspnea, cyanosis, chills, and hypOtension. Treatment is supportive.
Pathophysiology? neutrophil activation to DONOR leukocyte antibodies in the pulmonary vessels.
TACO is a CARDIOGENIC pulmonary edema from transient volume overload during transfusion. It usually occurs in the setting of impaired cardiac function. Signs may include JVD, peripheral edema, HTN. Treatment includes inotropes, diuretics, and afterload reduction.
Major complications in TURP?
bladder perforation –> abdominal and referred shoulder pain
prostatic capsule perforation –> lower abdominal pain and back pain
sepsis
TURP syndrome which will show multiple end organ dysfunction
What is TURP syndrome?
Multiple end organ dysfunction caused by large amounts of HYPOtonic fluid that is absorbed via surgically disrupted venous sinuses that leads to HYPOosmolality, hyponatremia, and solute toxicity
neruo: cerebral edema and increased ICP resulting in confusion, restlessness, seizures, visual changes, coma, death
CV: HTN, bradycardia
Resp: tachypnea and decreased saturations 2/2 pulmonary edema
hematologic: hemolysis and DIC
renal: metabolic acidosis and renal failure 2/2 glycine toxicity
What is the ideal irrigation for B-TURP?
isotonic so that it is non-hemolytic
electrically inert to prevent electrical dispersion
transparent for surgical visualization
non-toxic so that it requires minimal metabolism and can be easily and rapidly excreted
**M-TURP requires hypotonic solution to prevent electrical dispersion
Problems with various TURP solutions (glycine, sorbitol and mannitol)
glycine becomes ammonia (both are toxic)
sorbitol leads to hyperglycemia
mannitol leads to too much intravascular volume expansion
Who is at risk for TURP syndrome?
Monopolar cautery because hypotonic solutions must be used to prevent electrical dispersion
Prolonged surgical resections (>1 hour)
Suspension of fluid > 40 centimeters due to increased hydrostatic pressures
When the prostatic capsule is disrupted
How should TURP syndrome be managed?
Ensure adequate oxygenation and circulatory support. initiate invasive monitoring if cardiovascular instability. ABGs. 12-lead EKG.
Correct hyponatremia with fluid restriction, diuretics, and hypertonic saline. Anticonvulsants if seizures.
What are the ACC/AHA guidelines for establishing beta blocker therapy?
It should occur at least 2-7 days prior to surgery.
What is the significance of a negative CK-MB but positive troponin enzymes?
It is suggestive that an acute MI occurred over 2-3 days ago and that the patient has not suffered a recurrent MI in the interval.
CK-MB is a non specific marker for myocardial damage. It usually elevates within 4-6 hours whereas troponin elevates within 2-6 hours. CK-MB peaks in 12-24 hours (same as troponin) BUT RETURNS TO BASELINE within 2-3 days (whereas troponin stays elevated for 7-10 days).
What is the significance of ST-segment depression on the EKG?
ST-segment depression in two or more contiguous leads is highly suggestive of subendocardial ischemia, i.e. unstable angina or NSTEMI. The presence of elevated cardiac biomarkers establishes the diagnosis of NSTEMI.
What are some contributing factors to myocardial ischemia?
Stems from a supply and demand mismatch. Supply issues stem from reduced oxygen delivery and can include tachycardia, anemia, hypoxia and decreased CPP. Demand issues stem from an increased workload so include tachycardia, increased wall tension, increased contractility and increased afterload.
The surgeon declares a case emergent. What are your options to optimize pulmonary status in a patient with severe atelectasis seen on CXR?
Perioperative bronchodilator therapy. Post intubation alveolar recruitment maneuvers and diuretics if there was evidence of pulmonary edema. Postoperative chest physiotherapy and incentive spirometry.
What are therapeutic levels of Digoxin?
0.5-2 ng/mL
How does digoxin toxicity present? What is the ideal management strategy for Digoxin toxicity (levels greater than 2 ng/mL)?
EKG changes, arrhythmias, fatigue, hypersalivation, confusion, N/V, and visual changes. Even in therapeutic ranges, mild ST depression in multiple ECG leads can be seen making it difficult to monitor for cardiac ischemia.
I would discuss discontinuing digoxin until after surgery and avoid any factors that might potentiate the toxcicity such as hypokalemia, hypomagnesemia, and hypercalcemia.
Which EKG leads are best to monitor ischemia vs. arrhythmias?
V5 - best for ischemia
II - best for arrhythmias
Does a TEE eliminate the need for a PA catheter?
Not necessarily. The TEE provides more accurate determinations of filling volumes and contractility as well as being the most sensitive indicator of myocardial ischemia BUT it is not available during induction and intubation and is usually not continued postoperatively in the ICU where HD instability can persist.
Where would you place a central line in a patient with a right carotid bruit?
If the patient has asymptomatic carotid disease, my preference would be to use the left IJ with ultrasound guidance to minimize complications. However if the patient’s carotid disease were severe or symptomatic, I would consider using the brachial or subclavian v. approach.
What would you do if the BP drops to 80/50 and HR is 50 immediately after induction and prior to chest incision during a CABG?
it is likely attributable to cardiac depression secondary to induction drugs and volatile anesthetics. However I would quickly rule out other critical causes first such as arrhythmia, cardiac ischemia, and pneumothorax. If I believed my initial assessment was correct, i would treat conservatively by reducing the anesthetic depth and temporizing until incision with a direct acting vasopressor such as NE.
What can cause low blood pressure with the initiation of cardiopulmonary bypass?
Often due to dilute priming solution. However consideration should be given to pump malfunction, malposition/kinking/clamping of the arterial cannula, inadequate venous return to the pump such as caval obstruction, hypovolemia, malposition of the venous cannula.
What constellation of symptoms are consistent with malpositioning of the arterial cannula during cardiopulmonary bypass?
unilateral face blanching and right sided mydriasis/chemosis. This happens with the malposition of the arterial cannula directs flows of the priming solution toward the innominate artery. increased systemic line pressures in the CPB circuit and higher right sided arterial pressures (relative to the left side) are other signs consistent with this complication.
**This has a high potential for cerebral injury so take steps to reduce cerebral edema such as mannitol, head-up positioning and preserve adequate cerebral perfusion IF CASE MUST BE CONTINUED.
Would you treat a glucose of 250 mg/dL during CABG?
Yes it is particularly important in these cases which are prone to cerebral ischemia and hyperglycemia worsens neuronal injury under these conditions. I would start an insulin infusion an closely monitor blood sugar with a goal of glucose levels between 140-18).
How do you prepare a patient to come off of CPB?
Begin rewarming to normothermia and correct acid/base and electrolyte abnormalities; turn on anesthetic alarms and monitors; initiate ventilation; ensure the heart is adequately de-aired; ensure the availability of a pacing device and inotropes and vasopressors.
Chest tube drainage after CABG is 250mL in the first 2 hours after surgery. How would you determine the cause of this postop bleeding?
I would repeat an ACT and order labs including CBC, fibrinogen, and TEG if available. If these studies failed to explain the excessive post op bleeding, the patient should return to the operating room for exploration.
What is a normal SvO2?
approximately 75%. Low mixed venous oxygen saturation usually reflects inadequate tissue perfusion.
What would you tell a patient and family that experienced recall during anesthesia?
I would explain that intraoperative awareness is a rare and poorly understood complication of anesthesia. I would also explain the precautions that were taken (or why they were not taken) to prevent recall. I would document the incident and arrange counseling.
What is the most common type of TE fistula?
Type C - a blind esophageal pouch with lower segment tracheal fistula.
Does prematurity concern you in the setting of a TE fistula?
Yes - Maintaining ventilation and oxygenation in these infants can be extremely challenging especially during surgery. Premature infants have underdeveloped lungs and decreased pulmonary compliance AT BASELINE. This is particularly challenging in the setting of a TE fistula with superimposed aspiration pneumonitis +/- congenital cardiac abnormalities and other VACTERL findings.
What are the congenital abnormalities associated with esophageal atresia and TEF?
VACTERL: vertebral defects, anal atresia, cardiac anomalies, TE fistula, radial and renal dysplasia and limb abnormalities.
Pre-surgical ECHO is a must in these infants.
How do you evaluate a newborn with a TE fistula preoperatively?
Start with identifying/optimizing the respiratory status, releasing any gastric distention with a gastrostomy, and replete volume as these patients are often dehydrated. Studies I would want include an ECHO to look for cardiac abnormalities, CXR to rule out penumonitis or pneumonia, renal ultrasound to look for hydronephrosis, and spinal films to evaluate for scoliosis and plan for epidural.
I would correct any electrolyte abnormalities and evaluate the infants starting hematocrit. Ideally I would obtain adequate access and preductal/postductal O2 saturations.
How would you induce a neonate with a TE fistula?
Ensure proper monitoring and IV access. Place infant in head up position to minimize risk of aspiration. Suction the proximal esophagus and the gastrostomy tube.
I would induce with sevoflurane with a goal to maintain spontaneous respiration until I had confirmation of adequate mask ventilation without gastric distention.
If rigid bronchoscopy was necessary, I might supplement sevoflurane induction with a propofol infusion (50-150 mcg/kg/min).
The tip of the ETT would ideally be between the fistula and the carina so I would initially mainstem the tube and then withdraw while auscultating until air was seen/heard from the gastrostomy. i would then advance the tube 1 centimeter distal to this point and confirm bilat chest rise and breath sounds as well as adequate end tidal CO2.
If this was not possible, I would consider retrograde insertion of a Fogarty through the gastrostomy to occlude the fistula. This could be confirmed with a fiberoptic scope.
Would you use a cuffed endotracheal tube in an infant?
Yes I would not hesitate to use an adequately sized cuffed ETT. However, I would ensure there is a leak around the inflated cuff at 30-40 cmH20.
During TEF repair, the SpO2 gradually declines to 89% and airway pressures increase. What do you think is going on?
Most likely the tube has migrated to a mainstem position. The thoracotomy approach is usually from the right side which would augment these changes.
Other causes may be gastric distention and reduced pulmonary compliance if the fistula is not yet ligated. Bronchospasm, pneumothorax, and obstruction of the ETT could also cause this type of picture.
Intraoperative fluid management in the neonate?
insensible losses should be replaced with an isotonic solution at 6 mL/kg/hour while maintenance fluids should be 4 mL/kg/hour so total of 10mL/kg/hour.
Blood loss should be replaced 1:1 with 5% albumin or pRBCs.
Would you extubate immediately after TE fistula repair?
Likely no. At the end of surgery, there will be significant atelectasis in an infant who may already have baseline aspiration pneumonitis and poor pulmonary compliance +/- cardiac abnormalities.
Do you agree with mechanical ventilation settings of PIP 30, PEEP 2, IMV=35 and FiO2 100% in a premature neonate?
No PIP seems too high (risk for barotrauma)
Also FiO2 should be the minimal necessary to maintain a paO2 of 60-80mmHg
What is the ideal hematocrit for a neonate?
it is unknown but a healthy full term neonate typically has a HCT around 55% so my goal would be to maintain a HCT of at least 35%.
**Remember fetal Hgb is approximately 75% at birth causing a leftward shift of the Hb-O2 dissociation curve.
Two hours after extubation of an infant, the patient develops a barking cough with inspiratory stridor. What is your differential diagnosis? How would you treat?
This is most consistent with post intubation croup 2/2 glottic or tracheal edema. Treatment is racemic epi and dexamethasone.
other differentials might be bronchitis or epiglottitis.
What are the risk factors for developing post-intubation croup?
traumatic intubation, excessively tight ETT, prolonged intubation, history of croup, head/neck procedures, intraoperative changes to the child’s position, and coughing with the ETT in place.
Postoperative pain management plan after TEF repair?
thoracic epidural with 0.1% ropiviaine @ 0.1 mL/kg/hour continuously.
Continuous thoracic epidural rate for an infant 3 months to 1 year?
0.15 mL/kg/hour
Continuous thoracic epidural rate for a child?
0.2 mL/kg/hour
What is the MELD score?
A scoring system based on serum creatinine, bilirubin and INR. It is a tool used to prioritize organ allocation to those who are at greatest risk for mortality. The higher the score, the higher the risk of impending mortality.
Common causes of dyspnea in liver failure?
(alcoholic or cirrhotic) cardiomyopathy, ascites, plerural effusions, hepatopulmonary syndrome or a combination
What is hepatopulmonary syndrome?
Triad of
1 - intraPULMonary vascular dilatations (diagnosed via echo, perfusion lung scanning or pulm arteriography)
2 - setting of portal hypertension
3 - leading to right-to-left shunts and hypoxia (decreased oxygenation PaO2 < 80 on room air, A-a gradient > 20)
**this is an indication for liver transplant unless completely unresponsive to supplemental oxygen indicating unacceptable perioperative risk of graft hypoxia/failure
What do you think of a tense/distended abdomen in the setting of marked ascites?
This level of intra-abdominal pressure would likely compromise pulmonary mechanics and gas exchange; as well as make this person a high aspiration risk.
Should a preoperative paracentesis be performed prior to a liver transplant?
Preferable if time permits. Removing fluid may improve cardiac output (by relieving compression of the IVC), pulmonary gas exchange (increased pulmonary compliance and reduced V/Q mismatch, also reduction of pulm effusions), and decrease risk of aspiration.
If performed, ensure adequate volume expansion to prevent circulatory collapse with the progressive reaccumulation of ascitic fluid in the peritonieal space (especially with removal of >5L). Use 50% colloid solution at the time of paracentesis and remainder 6 hours later.
Most common signs of hepatopulmonary syndrome?
1 - Worsening dyspnea and hypoxia
2 - Orthodeoxia (oxygen desaturation with movement from supine to upright position)
3 - platypnea (dyspnea with movement from supine to upright position) may also be present
The mainstay of treatment is supplemental oxygen. The disease can be reversed completely with successful liver transplant.
What is hepatorenal syndrome? Signs?
Cirrhosis and portal hypertension cause the release of vasodilators, which then lead to systemic and splanchnic vasodilation. This “decreased” pressure is sensed by the kidneys and leads to compensatory activation of the renin-angiotensin-aldosterone cascade causing profound renal vasoconstriction.
It is a diagnosis of exclusion so prerenal, parenchymal, obstructive, and nephrotoxic causes should be ruled out first. Common signs include high creatinine, decreased creatinine clearance, decreased UOP, and low urine sodium.
Any treatment for hepatorenal syndrome?
Definitive treatment is liver transplantation. medical therapy with volume expansion (albumin), vasoconstrictors (particularly midodrine), and ocreotide (inhibits splanchnic vasodilation) can help.
What is portopulmonary hypertension?
Defined as a mean PAP > 25 mmHg or PVR > 120 dyne/sec/cm-5 in the presence of a normal pulmonary capillary wedge pressure
mild PPH = 25-35 mmHg
mod PPH = 35-45 mmHg
Severe PPH > 45 mmHg
How does veno-venous bypass during liver transplant work?
it diverts blood from the IVC and portal vein to suprahepatic veins such as the axillary v. This attenuates the decrease in preload, improves renal perfusion, decreases splanchnic congestion and delays development of metabolic acidosis.
Describe the 3 stages of liver transplantation?
1 - pre-anhepatic - liver is dissected and mobilized until it is only attached by the IVC, portal vein, hepatic artery and common bile duct.
2 - anhepatic - begins with clamping of the hepatic artery and proceeds through the removal of the native liver and implantation of the donor liver
3 - neohepatic - completion of anastamosis and ensuring adequate hemostasis
At the start of the anhepatic phase of a liver transplant, the surgeon clamps the IVC and the blood pressure drops to 78/44. What will you do?
I would communicate with the surgeon to remove the clamp since the timing of the hypotension suggests reduced cardiac preload. I would volume load the patient to a target CVP of 10-20 mmHg and ensure the availability of vasopressors prior to replacing the clamp.
Consideration could also be given to veno-venous bypass if that was an available option.
During the anhepatic phase of liver transplantation, the patient’s ECG begins to exhibit peaked T-waves and widening QRS? What do you think is going on and how would you manage?
This is most consistent with hyperkalemia which is very common in liver tranplantation. I would notify my surgeon, check the potassium and begin to treat by first stabilizing the myocardium with calcium gluconate or calcium chloride. I would correct anything that could be contributing to hyperkalemia such as acidosis. I would give insulin and glucose, beta-adrenergic drugs, and sodium bicarb to facilitate intracellular movement of potassium and hyperventilate the patient to blow off CO2. I would consider hemodialysis if these measures did not work.
What is citrate toxicity?
Hypocalcemia induced by citrate chelation after FFP and platelet transfusion. This is very rare but more likely during liver failure as citrate undergoes hepatic metabolism. Hypothermia can also contribute to citrate toxicity.
Signs: hypotension, decreased pulse pressure, arrhythmias, increased LVEDP and CVP
Treatment: calcium (based on T-wave changes) and treat arrhythmias
At the beginning of the reperfusion phase of liver transplantation, the BP drops to 64/37. What do you think is going on?
This is likely due to the removal of the vascular clamps with subsequent development of post-perfusion syndrome. It is usually associated with hypotension, bradycardia, cardiac arrhythmias, and elevated pulmonary artery pressures.
Other considerations might include bleeding, CHF, pneumothorax.
What causes reperfusion syndrome during liver transplantation?
Multifactorial - potassium load with flushing of the graft perfusate into the systemic circulation; release of vasoactive metabolites from the graft and lower extremities; release of cold blood from the graft stunning the heart.
Administer bicarb to counter acid load; administer calcium to counter the effects of potassium on the heart; give inotropes and vasoconstrictors
Post operative complications that should be anticipated following liver transplantation?
coagulopathic bleeding, anastomotic leakage or failure, renal dysfunction, congestive heart failure, TRALI, pulmonary edema, encephalopathy, infection, acute graft failure or rejection, metabolic abnormalities
How would you evaluate a patient’s cardiac implantable electronic device preoperatively?
Consult with the CIED management team for the following information:
indication for placement
model and type of device
is the patient PM dependent
programmed mode
patient’s underlying rhythm/rate
behavior when exposed to a magnet
age of leads (<3 mos, dislodging risk)
battery status (should be at least 3 months)
The hand surgeon wants to use electrocautery in a patient with an AICD who is pacemaker dependent. Would you agree to this?
Yes I would agree despite the potential complications including inhibition of pacing function, reprogramming of the AICD, triggering tachydysrhythmia treatment, microschock or internal damage to the device.
I would recommend bipolar cautery (the two blades of the electrocautery forceps act as the active and return electrodes making a remote return plate unnecessary).
If bipolar is not an option, then the return plate should be as close to the operative site but as far away as possible from the CIED (goal for presumed path should be at least 6 inches away from CIED).
I would also disable the tachydysrhythmia detection and therapy and since the patient is PM dependent, set the pacer to an asynchronous mode via reprogramming.
I would also recommend the surgeon use short, intermittent and irregular bursts at the lowest feasible energy levels.
Would you agree to skip the CIED interrogation and proceed with a magnet in someone who has an AICD and is pacemaker dependent?
My preference if time permits is to interrogate the device because a magnet in an AICD turns off the antitachydysrhthmia sensing but does not put the pacemaker in asynchronous mode which could lead to inhibition of the PM (due to EMI) in this patient who is dependent. Ideally the representative would put the pacer in asynchronous mode and use the magnet to disable/enable antitachydysrhythmia sensing.
If time did not permit, I would use the magnet to inhibit tachydysrhythmia sensing and have external pacing/defibrillator pads on the patient.
induction goals in a trauma patient with an open globe?
have difficult AW cart available
aspiration prophylaxis
preoxygenate well
ensure adequate plane of anesthesia AND muscle relaxation (use nerve stimulator) to prevent extrusion of intraocular contents
Would you extubate a trauma patient after open globe repair?
If the patient has a full stomach or NPO time is unknown, I would wake the patient up while trying to avoid coughing/retching. Lidocaine 1.5 mg/kg could help prevent any tracheal reflexes.
If there was no concern for aspiration, I would extubate this patient deep while spontaneously breathing.
How to calculate mean ocular perfusion pressure? (MOPP).
MOPP = Mean opthalmic artery pressure - IOP
mean opthalmic artery pressure = 2/3*MAP
normal IOP = 10-20
normal MOPP = 45-55
Good choices for premedication, induction, and maintenance in ocular injuries? Which medications should be avoided?
premedications:
midazolam
dexmedetomidine 0.7 mcg/kg x 10 minutes
induction meds:
RSI with video laryngoscopy is preferred
remifentanil 3-5 mcg/kg
propofol 2-3 mg/kg
with coadministration of ephedrine
maintenance with sevoflurane (promotes flow of aqueous humor)
***propofol TIVA if hx of PONV
drugs to avoid:
ketamine: can cause nystagmus and blepharospasm
etomidate: can cause myoclonus with incr IOP
nitrous oxide
Wide complex VT with a pulse - how do you manage?
Assess hemodynamic stability
If stable:
12-lead EKG to determine if monomorphic or polymorphic…
Confirm that it is wide complex (>0.12 sec) in all leads?
Is there a P-wave?
Compare the Q-wave morphology to a previous EKG if there is any doubt: if morphology is different, then presume VT (not SVT)
Tx:
Administer adenosine
If no resolution, add amiodarone 300 mg (or procainamide)
Correct any other fctrs like hypoxemia, acidosis, electrolytes, glucose, mag
If unstable:
synchronized cardioversion if monomorphic
unsynchronized shock if polymorphic (120-200 J with biphasic; 360 J with monophasic)
Start chest compressions
2nd shock –> no pulse?
Continue chest compressions and give epi 1 mg q 3-5 minutes
3rd shock –> no pulse?
Continue chest compressions and give amiodarone 300 mg (or lido 1.5 mg/kg)
Give 1-2 Grams mag if torsades or hypoMg
If hyperkalemia:
calcium chloride 1 g
sodium bicarb 1 amp
5-10 U regular insulin with 1 amp D50
STOP BANG criteria?
S - snoring
T - tiredness daytime
O - observed apnea
P - high blood pressure
B - BMI > 35
A - Age > 50
N - neck > 40cm
G - gender male
<3 factors = low risk
5-8 = mod to severe OSA
do you have any concerns with the beach chair position in a patient with a BP of 168/98?
yes - i am concerned about the increased risk of cerebral ischemia with a beach chair position in the setting of general anesthesia. I would be very vigilant in maintaining adequate end-organ perfusion throughout the case.
Would you recommend smoking cessation 2 days preoperatively?
I would not recommend cessation 2 days prior because the benefits of smoking cessation are not seen for approximately 4 weeks. Furthermore, during the first several days of abstinence, there is increased mucous secretions which could complicate AW and respiratory management despite an improvement in CO levels and reduction in nicotine levels
Parkland formula
flow volume loops
Also consider that highest risk for complications for mediastinal masses:
cardiopulmonary symptoms at baseline
obstructive and restrictive obstruction on PFTs
tracheal compression > 50%
coronary distribution by EKG leads?
