Knowledge Gaps Flashcards
1
Q
Describe the difference between roller and centrifugal pumps used in cardiopulmonary bypass?
A
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.
2
Q
Would you use alpha stat or pH stat management in moderate hypothermia?
A
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
3
Q
Would you use alpha stat or pH stat management for moderate hypothermia in the pediatric patient?
A
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.
4
Q
Does it matter if mitral regurgitation is acute or chronic?
A
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.
5
Q
Explain the normal pulmonary capillary wedge tracing?
A
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
6
Q
Induction goals in mitral regurgitation with CAD?
A
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
7
Q
Atrial contribution in regurgitant lesions versus stenotic lesions? (Lost in A-fib)
A
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.
8
Q
What would you do if the venous reservoir level is decreasing during cardiopulmonary bypass?
A
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.
9
Q
Why does the surgeon ask you to vigorously inflate the lungs prior to coming off the cardiopulmonary bypass pump?
A
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.
10
Q
What is happening if the pulmonary pressures increase and systemic pressures decrease coming off of cardiopulmonary bypass?
A
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
11
Q
How might mitral valve replacement contribute to risk of left ventricular failure coming off bypass?
A
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.
12
Q
Can an IABP help facilitate weaning from cardiopulmonary bypass in the setting of LV failure?
A
Yes an IABP is the only intervention which increases coronary perfusion (increases oxygen supply) and decreases afterload (decreases oxygen demand)!
13
Q
Where should an IABP be positioned? When should it inflate?
A
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),
14
Q
What is pulsus paradoxus?
A
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)
15
Q
How would you evaluate postop vision deficits?
A
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
16
Q
What is TRALI vs TACO?
A
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.
17
Q
Major complications in TURP?
A
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
18
Q
What is TURP syndrome?
A
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
19
Q
What is the ideal irrigation for B-TURP?
A
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
21
Q
Problems with various TURP solutions (glycine, sorbitol and mannitol)
A
glycine becomes ammonia (both are toxic)
sorbitol leads to hyperglycemia
mannitol leads to too much intravascular volume expansion
21
Q
Who is at risk for TURP syndrome?
A
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
22
Q
How should TURP syndrome be managed?
A
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.
23
Q
What are the ACC/AHA guidelines for establishing beta blocker therapy?
A
It should occur at least 2-7 days prior to surgery.
24
Q
What is the significance of a negative CK-MB but positive troponin enzymes?
A
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).
25
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.
26
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.
27
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.
28
What are therapeutic levels of Digoxin?
0.5-2 ng/mL
29
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.
30
Which EKG leads are best to monitor ischemia vs. arrhythmias?
V5 - best for ischemia
II - best for arrhythmias
31
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.
32
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.
33
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.
34
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.
35
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.
36
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).
37
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.
38
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.
39
What is a normal SvO2?
approximately 75%. Low mixed venous oxygen saturation usually reflects inadequate tissue perfusion.
40
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.
41
What is the most common type of TE fistula?
Type C - a blind esophageal pouch with lower segment tracheal fistula.
42
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.
43
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.
44
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.
45
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.
46
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.
47
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.
48
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.
49
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.
50
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
51
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.
52
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.
53
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.
54
Postoperative pain management plan after TEF repair?
thoracic epidural with 0.1% ropiviaine @ 0.1 mL/kg/hour continuously.
55
Continuous thoracic epidural rate for an infant 3 months to 1 year?
0.15 mL/kg/hour
56
Continuous thoracic epidural rate for a child?
0.2 mL/kg/hour
57
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.
58
Common causes of dyspnea in liver failure?
(alcoholic or cirrhotic) cardiomyopathy, ascites, plerural effusions, hepatopulmonary syndrome or a combination
59
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
60
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.
61
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.
62
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.
63
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.
64
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.
65
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
66
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.
67
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
68
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.
69
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.
70
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
71
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.
72
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
73
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
74
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)
75
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.
76
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.
77
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
78
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.
79
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
80
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
81
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
82
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
83
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.
84
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
85
What is a Bezold-Jarisch reflex?
Stimulation of inhibitory cardiac receptors (mechanical or chemical) leading to a PANS activation --> subsequent bradycardia, vasodilation and hypotension.
86
pathophysiology of aspiration pneumonitis?
The aspiration of significant gastric contents results in damage to the surfactant producing cells and the pulmonary capillary endothelium with subsequent atelectasis, pulmonary edema, bronchospasm, hypoxemia, increased pulmonary vascular resistance and increased work of breathing.
87
What is the significance of CPAP in a patient with OSA?
it is continuous positive airway pressure that counteracts the recurrent episodes of upper airway collapse during sleep that severely limit airflow despite breathing efforts. Whenever possible, CPAP should be continued in the postoperative period.
88
Associated comorbidities with morbid obesity?
Increased risk for
-HTN
-heart disease and atherosclerosis
-diabetes and metabolic syndrome
-breathing problems such as sleep apnea and obesity hypoventilation syndrome
-osteoarthritis
89
What level of neuroaxial blockade for a total knee arthroplasty?
L1 level to adequately block the lumbar plexus - particularly the femoral nerve, lateral femoral cutaneous nerve, and the obturator nerve.
(Alternatively lumbar plexus block, fascia iliaca block, femoral nerve block, femoral triangle block, or adductur canal block. Proximal block will have more motor involvement and relaxation, while distal blocks will provide more sensory coverage with less motor block)
90
Fetal bradycardia immediately after placement of a labor CSE - what is going on and what should be done about it?
Labour analgesia induction can result in fetal heart rate changes and even severe fetal bradycardia. This is most likely due to uterine hypertonus secondary to an acute drop in circulating epinephrine (leads to decreased uterine blood flow in setting of uterine hypertonus). If the uterus is quickly relaxed and fetus properly resuscitated, this should not affect the outcome of the delivery or neonatal health.
* Uterine displacement. Remember this any time there is significant fetal or maternal resuscitation! Practitioners often forget about uterine displacement.
* Correct any hypotension. I give ephedrine if the systolic blood pressure is less than baseline.
* Supplemental oxygen. This may increase the supply to the fetus.
* Turn off oxytocin. May help relax the uterus.
* Fetal scalp stimulation.
* Change maternal position.
* Nitroglycerin 200 to 400 μg iv or sl. It's quick, easy, few side effects, and labour will quickly return to normal after giving it. However, if it does not work quickly (two to four minutes) I give terbutaline.
* Terbutaline 250 mcg SC (may cause uncomfortable maternal tachycardia for approx 30 minutes)
91
Hunt-Hess Scoring?
Grade 0: Unruptured aneurysm
Grade I: Asymptomatic or minimal headache and slight nuchal rigidity
Grade Ia: Fixed neurological deficit without other signs of SAH
Grade II: Moderate to severe headache, nuchal rigidity, no deficit other than cranial nerve palsy
Grade III: Drowsiness, confusion, or mild focal deficit
Grade IV: Stupor, moderate to severe hemiparesis, early decerebrate rigidity, and vegetative state
Grade V: Deep coma, decerebrate rigidity, moribund appearance
92
Cardiac complications of SAH?
Can cause catecholamine-mediated REVERSIBLE myocardial "stunning" injury
-Troponinemia is common
-Severe, acute heart failure can develop similar to Takotsubo cardiomyopathy with ejection fractions commonly 10-30%; GOOD recovery profile!
-Ventricular dysfunction is often associated with ECG patterns also seen in myocardial ischemia: ST depression, prolonged QT (550 ms), canyon T-waves, U waves.
-If no ventricular dysfunction, then look for aberrant rhythms on the ECG
93
What are the priorities of critical care management of a SAH?
-maintenance of adequate CPP (60-70 mmHg)
-prevention of brain herniation from incr ICP
-monitoring and treatment of cerebral vasospasm to prevent delayed cerebral ischemia
-monitoring and treatment for rebleed
94
When is an EVD or lumbar drain appropriate in SAH?
Common thresholds:
ventriculomegaly with GCS < 12
Hunt Hess >2
95
Goal blood pressure in SAH?
systolic < 160 and MAP < 110 (CPP at least 60-70)
96
Mechanism for reduced vasospasm with nimodipine?
dilation of smaller arteries
decr calcium-mediated excitotoxicity
decr platelet aggregation
(give 60mg PO QID within 48 hours and for 3 weeks)
97
Induction and maintenance of anesthesia during clipping of SAH?
Induction goals: minimize large swings in blood pressure with laryngoscopy (fentanyl, nicardipine, esmolol, lidocaine, and hypnotic of choice). Preferrably preinduction a-line to guide titration. Roc or Sux but give defasiculating dose. Have pressors ready if hypotension.
Maintenance: Ideally there would be SSEP and MEP monitoring so use a balanced technique with IV infusions and inhalational anes <0.5 MAC to prevent decoupling of CMRO2 and CBF.
During temporary clip placement, the patient’s blood pressure should be raised by 10-20% to ensure perfusion through collateral vessels. Blood pressures can be normalized after the aneurysm is secured.
98
How can surgical exposure be facilitated during clipping of SAH?
strategies for intraoperative brain relaxation include:
-Maintaining an adequate depth of anesthesia and analgesia
-Optimizing hemodynamic parameters
-Optimizing patient positioning to facilitate cerebral venous drainage
-Maintaining normocarbia to moderate hypocarbia (PaCO2 30-35 mm Hg). Brief hyperventilation to PaCO2 of less than 30 mm Hg may be used if other ICP reduction maneuvers fail.
-Hyperosmolar therapy such as intravenous mannitol, furosemide, or hypertonic saline
Cerebrospinal fluid (CSF) drainage via an external ventricular drain
99
Strategies to prevent ischemic damage during temporary clipping include:
-Inducing temporary hypertension to promote collateral flow (10-20% increase in SBP)
-Avoiding prolonged temporary clipping (usually greater than 10 minutes)
-Reducing CMRO2 using burst suppression
-Using IONM to detect ischemia and alert a signal change
100
Facilitating surgical exposure if bleeding begins during clipping of SAH?
Deliberate hypotension
Adenosine-Induced Temporary Flow Arrest
A dose of 0.3–0.5 mg/kg leads to approximately 1 minute of moderate hypotension.
101
Strategies to reduce airway reactivity during extubation after SAH?
short acting opioids titrated to spontaneous ventilation rate
;
lidocaine 1.5mg/kg
infusions of remifentanil or dexmedetomidine during emergence. **detomidine may have added benefit of reduced hypertension in the postop period
102
Early complications after clipping or coiling of SAH?
1) rebleeding
2) delayed cerebral ischemia 2/2 vasospasm that typically occurs between days 3-14 post-hemorrhage (rule out other causes with urgent CT)
3) hydrocephalus from decreased CSF absorption and obstruction of flow - often require an EVD
4) hypERnatremia and diabetes insipidus - presents with incr UOP 12-48h postop with Na>140 and low urine osmolarity; treatment=DDAVP
5) hypOnatremia - usually 2/2 cerebral salt wasting syndrome or SIADH
6) cardiac - stress induced cardiomyopathy and/or arrhythmias
103
Management of cerebral vasospasm after SAH? (may also occur after arteriovenous malformation rupture, nonaneurysmal SAH, traumatic brain injury, or secondary to inflammatory conditions)
1) prophylaxis with nimoidipine
2) normovolemia (CVP 8-10, hb>9, sats>95, optimal ICP)
3) forced HTN (SBP >180-220 or CPP > 80) - NE or phenylephrine infusions
4) endovascular therapy with ballooning or intra-arterial vasodilators (nicardipine) - may need to increase vasopressor infusion as some systemic circulation is expected
Triple H therapy (falling out of favor): induced hypertension, hypervolemia, and hemodilution
104
pathophys of cerebral vasospasm after SAH?
1) breakdown products of hemoglobin --> vasoconstriction
2) release of calcium from smooth muscle --> vasospasm
3) inflammatory mediated remodeling
105
what happened to triple H therapy?
While effective in reversing vasospasm, triple H therapy is associated with many complications (e.g., pulmonary edema), and its use is no longer supported by current evidence.
Replaced with normovolemia, forced HTN, and endovascular therapy
106
Could scleral icterus be caused by anesthesia?
yes - anesthesia can cause a combination of reduced hepatic blood flow with decreased O2 delivery/ischemia and subsequent reperfusion injury can lead to post op liver disfunction (POLD).
107
Causes of post operative jaundice?
pre-hepatic - usually hemoglobin load that overwhelms the liver's capacity to conjugate bilirubin - will resolve over time
intrahepatic - inability to conjugate bilirubin (hepatocellular dysfunction) or obstruction (as in cirrhosis); hepatocellular dysfunction is usually do to ischemia or drug induced and improves once offender is removed; both conjugated and unconjugated bilirubin will be high
post-hepatic - direct injury to liver
108
Absolute indications for double lumen tube?
To prevent contamination of one lung to the other in instances such as empyema, purulent secretions, hemorrhage, lung lavage, bronchopleural fistula or pulmonary alveolar proteinosis
109
Advantages and disadvantages of a DLT?
Advantages:
1) easy isolation and conversion to two-lung ventilation
2) access to the isolated lung for suctioning
3) ability to add PEEP and CPAP
4) once in position, less likelihood of dislodgment
Disadvantages:
1) selecting proper size can be difficult
2) placement can be more challenging than a single lumen tube
3) needs to be replaced with single lumen tube if not extubating patient
4) major tracheobronchial injuries (although rare)
110
Sizing of DLT?
35 or 37 Fr for females
39 or 41 for males
(based on height and sex typically)
Can do ultrasound to look at tracheal diameter...
111
Indications for a right sided DLT?
When there is compression or distortion of the left mainstem bronchus (tumor, descending thoracic aortic aneurysm)
Also possibly left sided pneumonectomy
112
How does etomidate cause adrenal suppression?
suppresses production of cortisol in the adrenal cortex via inhibition of 11-beta-hydroxylase; cortisol levels are decreased for 24-48 hours
113
induction dose of etomidate? Mechanism of action? Common side effects of etomidate?
0.2-0.6 mg/kg
MOA: potentiates GABA-A receptor
SE: pain on injection, myoclonus, n/v, adrenal suppression
114
treatment options for shivering?
meperidine (via opioid and alpha2 R's), clonidine, dexmedetomidine, propofol, tramadol, ondansetron, sufentanil, alfentanil
115
What is RhoGam?
anti-Rh antibodies that destroy FETAL rhesus positive erythrocytes before a maternal immune response occurs.
116
What is rhesus isosensitization?
When blood from an Rh positive baby enters the maternal circulation of a Rh negative mother -- this leads to an IgG antibody production against the Rhesus antigens across the placenta. Reactions can range from mild anemia to hemolytic disease of the newborn, to hydrops fetalis or even stillbirth during current and future pregnancies.
117
Normal FHR variability is a surrogate for ______?
a normally functioning autonomic nervous system and fetal well being. FHR variability develops around the 25th to 27th week of gestation.
118
Difference between spina bifida occulta and spina bifida cystica?
occulta is incomplete midline formation over the back withOUT herniation of neural elements -- asymptomatic
cystica is incomplete midline formation over the back WITH herniation of meninges +/- neural elements. Meningocele (herniation of meninges only) is usually asymptomatic with a NORMAL spinal cord. Myelomeningocele is often associated with an ABNORMAL spinal cord (tethered cord, scoliosis, neurodeficits).
119
Difference between omphalocele and gastroschisis?
both are abdominal wall defects with externalization of the abdominal viscera. Omphalocele has a membranous covering around the herniated sac while gastroschisis involves expsed viscera.
omphalocele is usually associated with congenital defects while gastroschisis is usually an isolated anomaly.
120
preop mgmt of an omphalocele?
address respiratory insufficiency bc these babies sometimes have lung hypoplasia
protect the exposed viscera and prevent further insensible losses
obtain IV access and optimize volume status
rule out other congenital abnormalities
121
What is Beckwith-Wiedemann syndrome?
macrosomia (large birth weight)
macroglossia
midline abdominal wall defects (omphalocele, umbilical hernia)
neonatal hypoglycemia
**potential difficult airway
122
Monitoring for an omphalocele?
standard monitors plus
core temp bc more susceptible to heat loss from herniated viscera and
nerve monitor for adequate relaxation during reduction of viscera
123
pathophys of autonomic hyperreflexia?
Usually seen in T7 or higher injuries
bladder/rectal stimulation or pain below the level of spinal cord injury leads to an UNINHIBITED reflex --> intense vasoconstriction below lesion and vasoDILation above lesion --> presents as hypertension with reflex bradycardia (carotid sinus stimulation)
Normally, this reflex is inhibited by descending cortical pathways.
124
MOA of amiodarone? SEs?
K+ channel blocker --> lengthens cardiac action potential by prolonging repolarization and slows conduction speed through SA node
LFTs: direct pulmonary tox, hepatotox, thyroid tox
hypotension
125
Effect of high altitude on volatiles?
Sevo and Iso: volume percent increases but partial pressure remains the same so NO ADJUSTMENTS need to be made
Des: pressurized so decreased partial pressure at lower barometric pressures --> increase dose
new dose = (% desired x 760) / new barometric P
126
narrOw complex tachycardia in setting of WPW?
Orthodromic reentrant tachycrdia -->
circuit goes through AV node to ventricle and then returns to atria via accessory pathway
goal is to slow AV node conduction!!
give beta blockers or calcium channel blockers
try adenosine or amiodarone 6 mg or amiodarone 150 mg over 10 minutes
lidocaine 1-1.5 mg/kg can be tried
127
WIDE complex tachycardia in setting of WPW?
ANTIdromic reentrant tachycardia -->
circuit uses accessory pathway to ventricle and returns to atria via AV node
slowing AV nodal conduction is CONTRAINDICATED!!
try procainamide @ 20-50 mg/min
try amiodarone 150 mg over 10 min
try ibutilide 1 mg over 10 min
128
advantages/disadvantages of a spinal
advantages:
reliable, dense blockade
technically easy and fast
small dose of drug to achieve adequate blockade
low risk of LAST and drug transfer to placenta
disadvantages:
limited duration with inability to supplement/titrate
abrupt sympathectomy may not be tolerated in cardiac disease
129
TIVA or inhalational anesthesia during one lung ventilation?
Either can be used but TIVA may have slight advantage because volatiles inhibit hypoxic pulmonary vasoconstriction whereas IV anesthetics do not. HPV is important in maintaining V/Q matching
130
Appropriate demand doses for PCA in opioid naive patients? (70 kg)
Morphine 0.5 mg
Dilauded 0.1 mg
Fentanyl 5-10 mcg
130
Should a basal dose be used for a PCA?
Avoid use in opioid naive patients
Can be used in opioid tolerant patients
Calculate total daily dosing, decr 50%
Divide this number by 24 for hourly basal rate
demand dose would be 10% of total daily dose
131
Anes concerns in Neurofibromatosis?
endocrine changes, tumors everywhere, poss difficult AW and neuroaxial, restrictive lung disease from pulmonary changes and scoliosis, and sometimes essential HTN from activation of RAS (but be weary of pheochromocytoma)!!
tumors anywhere (can be vascular) including but not limited to brain (incr ICP/seizures/cognition changes), AW (including VCs and tongue), heart (dysrhythmias, RV outflow tract), lungs (pulm fibrosis), mediastinum, spine (diff neuroaxial), and near peripheral nerves.
endocrine: association with PHEOchromocytoma (HTN, palpitations) and intestinal CARCINOID (flushing, bronchospasm). Also check electrolytes and regular glucose for long cases.
kyphoscoliosis and pulmonary fibrosis that can cause restrictive lung disease --> RV strain and PHTN eventually possible
incr incidence of seizure disorders, cognitive dysfunction, and deafness
132
fentanyl dosing for epidural?
2 mcg/mL
133
spinal anesthesia dosing?
1/10 of epidural dosing
so for single shot spinal dose is between 1.2-1.6 mL (plus 15 mcg fentanyl and 0.4 mL duramorph)
spinal catheter would be approx 1 mL per hour
134
Mechanism of pulmonary edema in setting of pregnancy induced hypertension?
increased hydrostatic pressure and decreased osmotic pressures
135
Opioid reversal drugs and mechanism?
Naloxone: pure μ, κ, and δ antagonist. 20-40 μcg IV, onset 1-2 mins. May cause extreme pain, HTN, arrhythmias, pulmonary edema, and death
Naltrexone: pure antagonist, oral equivalent of naloxone
Nalbuphine: μ-antagonist, κ-agonist (possible δ activity). Reduces itching after intrathecal opioid administration
Butorphanol: antagonist/partial agonist of μ receptors, κ-agonist
Buprenorphine: partial agonist of μ receptors, no or antagonist at κ receptors. Shows resistance to reversal from naloxone.
136
Contraindications to CPAP or BIPAP
Unstable hemodynamics
Aspiration risk
Altered mental status
Facial trauma
137
Exclusion criteria for fast-track CABG?
emergency, re-do, transplant, ACLS, IABP, inhaled pulm dilators, open chest, bleeding >200 in 1 hour, significant lactic acidosis, heart failure, resp insuff, excessive inotropic support
138
receptors in the chemoreceptor trigger zone?
D2, 5HT3, NK1, muscarinic cholinergic, histamine
this is why dopamine antagonists (droperidol), serotonin antagonists (ondansetron), anticholinergics (scopolamine), and histamine blockers (promethazine, diphenhydramine) help!
139
EKG signs of pulmonary HTN or cor pulmonale?
RVH (large R in V1 V2) & R atria enlargement (P wave>2.5mm in II, III, aVF)
140
lung signs on TTE? PTX on TTE?
PRESENCE of lung sliding and lung pulse in 2D view
seashore sign in M-mode
ABSENCE of lung sliding, lung pulse, B-lines (indicate "dense" diseased lungs), and PRESENCE of a lung point (point PTX with air btn parietal and visceral pleura NEXT to normal lung)
PRESENCE of lung point can be visualized in M-mode as a barcode sign
141
citrate toxicity MOA and presentation
citrate (found in FFP, plts, cell saver) chelates Ca/Mg
Citrate usually metabolized by liver so more pronounced in liver failure
p/w hypotension, myocardial depression, dysrhythmias, and neuronal excitability (tetany, laryngospasm)
Replace Ca and Mg
142
Trousseau's sign and Chvostek’s sign (hypOcalcemia)
Trousseau's - carpopedal spasm in response to ischemia induced by BP cuff
Chvostek's sign - facial muscle twitching in response to tapping of facial n.
143
mgmt of regular wide-complex tachyarrhythmia?
unstable? ACLS and defibrillate 200J biphasic 360J monophasic ASAP, epi after 2 rounds q 3-5 min, then amiodarone, then lidocaine
if stable, could be VT or SVT with aberrancy.
Try adenosine 6 mg bc if SVT, it will break.
If VT, nothing will change, then try SLOW AMIODARONE 150 mg
144
mgmt of regular narrow-complex tachyarrhythmia vs irregular narrow-complex tachyarrhythmia?
regular narrow complex:
rhythm control with adenosine, then rate control with b-blkr/ca ch blkr
irregular narrow complex: rate control and then try amiodarone 150 mg
145
mgmt of regular wide-complex tachyarrhythmia?
unstable? ACLS and defibrillate 200J biphasic 360J monophasic ASAP, epi after 2 rounds q 3-5 min, then amiodarone, then lidocaine
if stable, could be VT or SVT with aberrancy.
Try adenosine 6 mg bc if SVT, it will break.
If VT, nothing will change, then try SLOW AMIODARONE 150 mg
146
What is PRIS?
mitochondrial dysfunction in setting of prolonged propofol infusions --> metabolic acidosis, rhabdo, hyperkalemia, and myocardial depression
147
sarcoidosis concerns in anesthesia?
multisystem granulomas that can lead to fibrosis. commonly affects AW, myocardium, lungs, kidneys and leads to hypercalcemia. can also affect CNS and peripheral nerves.
evaluate for dysphonia, dysphagia, stridor or noisy breathing during AW exam. look at ECG for right heart strain or conduction abnormalities. lungs for restrictive (or obstructive) disease 2/2 fibrosis (also decr DLCO). can have seizures, cranial nerve palsies or peripheral neuropathies.
148
Fat embolism syndrome (FES) mechanism, anes concerns, diagnosis and treatment?
Mechanism:
Fat droplets in blood circulation that activate two pathways: (1) inflammatory cascade: free fatty acids induce release of cytokines and pulmonary endothelial damage (sometimes progressing to ARDS)
(2) mechanical obstruction of end organ capillaries from fat debris
anes concerns: early presentation is hypoxemia but can progress to resp failure, CNS changes, cutaneous and hematological signs and symptoms
diagnosis based pulm edema, pulmonary infiltrates on CXR, petechiae (pathognomenic), confusion, anemia/thrombocytopenia, fever, tachycardia
(1 major & 4 minor criteria or score > 5 depending on index used)
treatment is supportive: early stabilization of fracture, resuscitation w fluids (esp albumin), oxygenation/ventilation, and circulatory support. Steroids not recommended!
**Albumin thought to bind free fatty acids
149
GCS 9-12 indicates ______?
moderate brain injury
GCS <9 severe
GCS>12 mild
150
How to clear C-spine?
AOx3, non-tender, non-focal, and no distracting pain
151
ideal CPP in TBI?
around 60-70 (normal is 70-85)
152
pathophys of ARDS?
SIRS in the lungs --> capillary alveolar membrane damage leading to bilat pulmonary infiltrates, severe dyspnea and hypoxemia
153
diagnostic criteria for ARDS and treatment
P/F ratio < 300
acute onset (w/i 7 days of an inciting event such as aspiration, trauma, sepsis) RESPIRATORY FAILURE "not fully explained by cardiac failure or fluid overload" in setting of radiographic evidence of bilat pulm infiltrates
Usually a diagnostic echo is also done
Treatment: supportive mechanical ventilation while aggressively treating cause
lung protective strategy, PEEP as tolerated to improve oxygenation, low airway pressures <30, and permissive hypercapnea
154
How to tell difference between SIADH and cerebral salt wasting? (both present with hyponatremia and high urine sodium)
volume status - CSW is hypovolemic while SIADH is euvolemic
also urinary sodium profoundly high in CSW (>100) and less high in SIADH (<100)
ADH high in SIADH
***Important bc treatment is different. Volume restriction, lasix, and desmopressin in SIADH vs. normal saline or hypertonic saline in CSW until normal volume and Na>125 (correct SLOW no more than 1 mEq/hr)
155
volume replacement and timing after paracentesis?
6-8 mL/dL of colloid per mL of ascitic fluid that is removed. Give 50% at time of paracentesis and remaining 50% 6 hours later.
156
Diagnosis of OSA vs. OSH vs. Pickwickian?
OSA: complete sessation of airflow >10 seconds (5 episodes/hr) with desat > 4%
OSH: milder form of OSH with 50% decreased airflow >10 seconds (15 episodes/hr) with desat > 4%
Pickwickian: OSH with cor pulmonale
157
Cardiac changes in OSA?
chronic hypoxemia and hypercarbia --> increased catecholamines:
(1) HPV, PHTN with associated RVH, RAE, and cor pulmonale
(2) systemic hypertension with end-organ changes (CNS, LVH)
(3) arrhythmias
(4) polycythemia
158
problems with nitrous oxide?
decreased FiO2 (this can be an advantage in some scenarios)
diffusion into air filled spaces
incr nausea/vomiting
INCR PULM VASCULAR RESISTANCE
159
an appropriate maintenance strategy in OSA?
balanced anesthetic technique with short acting agents including desflurane, remifentanil (IBW dosing), and rocuronium (IBW dosing)
160
buprenorphine management in minimally painful procedures?
Continue buprenorphine. Use Sufentanil and hydromorphone intraop (because binds mu receptors with similar affinity). Can also add regional/local infiltration, lidocaine infusion, magnesium infusion, and ketamine.
Postop maximize non-opioids on a scheduled basis (acetaminophen, NSAIDS, gabapentanoids) plus PRN hydromorphone for breakthrough pain.
161
buprenorphine management in moderate to severely painful procedures?
Stop buprenorphine. Maximize all non-opioids: regional, local infiltration, tylenol, NSAIDs, gabapentanoids, lidocaine, magnesium, and ketamine. Sufentanil is a good short acting agent to supplement 2/2 similar binding affinity at Mu receptors.
Then PCA with limited to no basal dose of hydromorphone (hydromorphone has similar binding affinity to Mu opioid receptors).
162
best med to target opioid induced pruritis?
nalbuphine
naloxone - but can cause profound rebound pain leading to catecholamine surge
163
Possible mechanisms for nimodipine's neuroprotective benefits include?
dilation of small arteries not visible on angiograms;
reduction of calcium-dependent excitotoxicity;
and decreased platelet aggregation.
164
Most common complications after carotid endarterectomy?
(1) thrombosis or embolism
(2) hypertension 2/2 surgical denervation of the carotid sinus
(3) cerebral hyperperfusion from altered cerebral autoregulation --> HA, edema, hemorrhage, seizures
(4) wound hematomoa - most are from slow ooze and require external compression but if rapidly expanding, then secure airway and surgically drain (also consider getting coagulation profile, platelets, ACT to find etiology)
165
advantages/disadvantages of regional in CEA?
advantages:
-awake patient is the gold standard for monitoring (despite GALA trial showing no difference btn RA and GETA)
-less hemodynamic stability
-less need for shunt
-shorter hospital length of stay
disadvantages:
-inability of controlled ventilation
-unsecured AW
-requires good mental status and no language barrier
-patient discomfort and anxiety
166
BP goals in CEA
-Mostly near patient's baseline
-incr BP to 20% above baseline during cross clamp to maximize CPP via collateral circulation
-decr BP to 20% below baseline when unclamping to decrease shearing force
-near patient's baseline if shunt is placed
-avoid coughing/bucking during emergence
167
DDx for stridor?
edema
laryngospasm
bronchospasm
recurrent laryngeal n injury
neck wond hematoma
if critical, call for help, difficult AW cart, and CRICOTHYROTOMY kit!!
168
Diagnostic criteria for DKA
gluc > 250
urine ketones 3+ (dipstick)
serum ketones
metabolic acidosis pH < 7.3
incr AG
bicarb < 15
AGGRESSIVE fluid replacement and replace electrolytes (first with isotonic fluid then switch to 1/2 NSS)
Insulin with 30-minute glucose readings
169
Pyloric Stenosis resuscitation to what end point?
bicarb < 28
chloride > 100
170
at what cervical process is the deep cervical plexus block?
C2, C3, C4
171
option for preventing tourniquet pain with axillary block?
ring block, decr length of tourniquet time
172
Maintenance for CEA?
Isoflurane a good choice if it will not affect cerebral monitoring (decr cardiac steal and more cardiac stable)
173
acute coronary sydnrome workup includes?
serial EKGs
serial troponins/CK-MB
MONA (A for anticoagulation)
B-blockers
vasopressors/antihypertensives as needed
174
how to rule out pulmonary infection in COPD?
history, physical and labs. signs of infection include
worsening dyspnea
assessing respiratory mechanics
evaluating sputum volume and color
lab studies such as WBCs, CRP and procalcitonin
treat with antibiotics for 5-7 days if COPD exacerbation due to bacterial cause is suspected
175
would you continue albuterol and ipratropium in COPD? why/why not?
Yes continue both. Both increase bronchial smooth muscle relaxation via different pathways (beta agonism and anticholinergic).
Ipratropium also reduces mucous secretion.
176
regional anesthesia as sole technique for shoulder surgery?
If no contraindications to interscalene (usually cardiopulmonary or neurological), then can be done with tremendous patient cooperation and coaching. pt should be advised of potential need to convert to GA.
Would need to be ultrasound guided interscalene block in combination with supraclavicular n and dorsal scapular n for cutaneous and acromioclavicular joint coverage. Alternatively with interscalene and surgeon infiltration.
Be aware of Bezold Jarisch reflex in beach chair position so it can be treated early if it occurs.
177
coronary distribution on EKG
II, III, aVF: RCA
I, aVL, V5, V6: LCX
V1-V4: LAD
178
Physiological effects of CRF
HTN/LVF
Fluid accumulation with electrolyte abnormalities (hyperK, hypoNa)
Uremia with platelet dysfunction, metabolic acidosis, pericarditis, and encephalopathy
Anemia
179
How to evaluate fluid status in CRF?
H&P, chart review including dialysis record and dry weight
volume overload signs:
JVD, dependent anemia, incr weight, fluid on CXR, rales on auscultation
volume depletion signs: dry mucous membranes, hypotension, tachycardia, orthostasis
180
Pharmacological effect of CRF?
depends on drug mode of elimination
renal excretion: prolonged duration
redistribution: unchanged duration
protein binding is decr: so CRF patients more sensitive to certain drugs
181
indications for dialysis?
AEIOU
Acidosis
electrolytes
intoxication
overload
uremia
182
methods of antepartum fetal surveillance?
fetal movement assessment, nonstress test, contraction stress test, fetal biophysical profile, modified biophysical profile and umbilical artery Doppler velocimetry.
fetal movement assessment: mother counts fetal "kicks"
nonstress test: fetal HR variability associated with fetal movement; can be low during fetal sleep cycle
contraction stress test: assessing for late decels or variable decels associated with uterine contraction
biophysical profile: five components - fetal breathing, fetal kicks, fetal extension/return to flexion, non-stress test (fetal HR variability), and amniotic fluid volume (pocket > 2cm is normal)
modified biophysical profile: nonstress test plus amniotic fluid volume (reassuring is positive FHR variability and fluid INDEX > 5cm)
umbilical arter doppler velocity: normal fetus=high velocity
183
Intrapartum fetal monitoring (during labor) options:
fetal HR monitoring (external or internal); intermittent auscultation or doppler; fetal scalp stimulation; fetal scalp pH or lactate
184
at what MAC of gas does cerebral autoregulation become linear?
5-6 MAC! (otherwise autoregulation is blunted but not linear with inhalational agents)
185
advantages of isoflurane?
cost effective
cardiac stable
less cardiac steal
reduces CMRO2 the most of all gases
decr CBF the least
186
difference between anaphylaxis and anaphylactoid reactions?
clinical presentation is the same
treatment is the same
pathophys is different:
anaphylaxis is type I IgE mediated mast cell release of inflammatory mediators such as histamine & kallikrien
anaphylactoid is not IgE mediated
187
stages of delivery:
stage 1 includes latent and active; active dilation is regular contractions with 1 centimeter dilation per hour; complete at 10 centimeters
stage 2 full dilation until delivery of baby
stage 3 delivery of fetus
188
definition of accreta and risk factors
abnormal implantation of placenta to the myometrium rather than being restricted within the decidua basalis.
risk factors:
any uterine scar (cesearean, myomectomy)
plus placenta previa
fibroids
advanced maternal age
multiparity
pregnancy induced hypertension
smoking
189
risk factors for atony:
big, sick, tired:
multiparity
chorioamnionitis,
prolonged labor
drugs (mag)
retained placenta
inversion
190
situations where profound uterine relaxation is needed:
1) manual removal of a retained placenta
2) breech delivery: obstructed after coming head or shoulders
3) multiple pregnancy: second twin in transverse-lie
4) inadvertent oxytocic overdose prior to delivery
5) uterine constriction ring
6) inverted uterus
7) (some cases of) fetal distress.
191
Risk factors for placental abruption?
HTN/PIH
smoking
cocaine
alcohol
trauma
multiparity
multiple gestation
192
indication to repair AAA?
size > 5.5 centimeters
symptomatic
rapidly expanding
other aneurysms concurrent: iliac, femoral, popliteal
193
Risk factors for uterine rupture and signs that it is occurring?
risks: VBAC (~1%)
previous C/S (esp w/ classical)
myomectomy
multiple gestation
hydaditiform mole/choriocarcinoma
signs:
fetal bradycardia (most sensitive sign)
abdominal pain
lower baseline uterine pressure
hypotension/shock
recession of presenting part or protrusion of the fetus, placenta, or both into the abdominal cavity
194
Significant Cobb angles and clinical implications?
40-50: surgical correction
60: pulmonary dysfunction
70: pulmonary hypertension with activity
110: pulmonary hypertension with rest
195
pathophys and treatment for refractory hemophilia?
pathophys: IgG antibodies to recombinant VIII aka "factor inhibitors"
treatment: bypass products such as prothrombin complex concentrates or recombinant VIIa
196
Parkland formula
197
Sepsis therapy?
Early goal directed fluid resuscitation
30 mL/kg fluid challenges to mantain a MAP > 65 or (CVP 8-12 or 12-16 if on mechanical ventilation); other goals include adequate urine output (0.5 mL/kg) and SVO2 > 75-75
followed by pressors (NE 1st choice) if fluid refractory hypotension to maintain MAP >65
Other measures:
measure lactate
blood cultures
broad spectrum antibiotics after blood cx
transfuse to maintain Hb > 7
198
What is mnemonic COALS?
Factors that contribute to PvO2 aka mixed venous oxygen TENSION (don't confuse with sVO2 which is mixed venous oxygen SATURATION).
COALS:
Cardiac output
Oxygen consumption
Amount of Hb
Loading of Hb
Saturation of Hb
199
Anesthetic implications of acromegaly?
difficult laryngoscopy and difficult mask ventilation: mandibular overgrowth, excess soft tissue, macroglossia, OSA susceptibility, narrow glottis
consider FOI, videolaryngoscopy with larger blade, smaller ETT
200
TAP block covers which nerves?
Innervation of the anterolateral abdominal wall arises from the anterior rami of spinal nerves T7 to L1. These include the intercostal nerves (T7-T11), the subcostal nerve (T12), and the iliohypogastric and ilioinguinal nerves (L1)
201
carboprost dosing?
250 mcg IM q 15 minutes (8 dose max)
contraindicated in bronchospasm
202
Recommendations for platelet count to do epidural?
>70 ideal
50-70 = patient MAY be at risk for increased epidural hematoma but can be done if risk of bleeding diathesis clinically low
<50 patient IS at risk for epidural hematoma, usually recommended to avoid placement
203
pediatric energy dosing for cardioversion vs defibrillation?
cardioversion: 1 J/kg, incr to 2 J/kg (max 4)
defibrillation: 2 J/kg, incr to 4 J/kg (max 10)
204
pediatric dosing for adenosine or amiodarone in PALS?
Adenosine:
0.1 mg/kg FIRST dose (max 6 mg)
0.2 mg/kg SECOND dose (max 12 mg)
Amiodarone:
5 mg/kg (up to 3 doses)
205
anesthetic management during clamping of main pulmonary artery in pneumonectomy?
promote pulmonary vasodilation and limit right heart strain
high FiO2, avoid hypercarbia by hyperventilating, nitric oxide, pulmonary vasodilators (epoprostenol, terbualine, calcium channel blockers)
206
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%
207
treatment of CENTRAL sleep apnea in infants?
methylxanthines and caffeine
oxygen does NOT help
208
symptoms of ANTIcholinergic crisis? (atropine, scopolamine)
treatment?
hot as a hare (fever)
dry as a bone (
mad as a hatter
blind as a bat (mydriasis)
red as a beet
full as a flask
Treatment: physostigmine (the only anticholinesterase that crosses BBB)
209
coronary distribution by EKG leads?
