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58 year old with chronic fib (developed 4 years ago) for catheter ablation. had palpitations and syncope three weeks ago.

PMH: tobacco, T2DM, GERD, OA, rheumatic fever, CVA last year with residual R weakness

Meds: diltiazem, coumadin, HCTZ, metformin, naproxen, prilosec, lipitor, MVI

what are your concerns?

1. arrhythmias - impaired CO, and end-organ ischemia
2. MI - secondary to chronic htn (increased afterload), atrial fib (impaired CO) and CAD (HTN, HPLD, DM, obesity, increased age, tobacco, CVA, atrial fib, MV stenosis)
3. acute ischemic stroke - embolic or thrombotic
4. HD instability - chronic htn, atrial fib, MV stenosis
5. CHF - due to ischemia, or RVP overload due to MV stenosis
6. aspiration - GERD, DM
7. complications of smoking - pulm disease, bronchospasm, hypoxia, CVA, prolonged mech vent, infection, impaired wound healing
8. hypo/hyperglycemia
9. coagulopathy due to coumadin
10. complications of procedure - CVA, atrial perf, cardiac tamponade, pericardial effusion, complete AV block, pulm vein stenosis, valve trauma, phrenic nerve paralysis, atrial esophageal fistula


what caused this patients a fib?

can be idiopathic but usually it is associated with valvular disease, LVH, CAD, HTN, CM, SSS, pericarditis. given her HPLD, DM, HTN, obesity, age, tobacco and h/o rheumatic fever it is likely the result of one of these factors.

less frequently, there are non-cardiac factors, such as hyperthyroid, pulm emb, alcohol, or caffeine.


what will your preop eval focus on?

s/s of CAD, CHF, thyroid dysfunction.

- EKG to see her current rhythm and signs of ischemia, prev infarct and LVH, right heart strain
- CXR to check for CM, pulm edema
- ECHO for wall abnormalities, estimate CO, severity of any structural heart disease, thrombus
- H/H, CMP (esp K, Mag with HCTZ), PT/INR (coumadin)
- if her risk of cardiac ischemia remained unclear, i would consider further cardiac testing

exam would focus on severity and scope of her residual weakness.


why is she taking diltiazem?

HR control in chronic afib by slowing conduction through the AV node. should be used with caution in patients with ventricular dysfunction as it has negative inotropic effects. it produces less myocardial depression than verapamil and is the preferred drug in patients with systolic heart failure.


what are the goals of afib treatment?

1. slow HR
2. restore/maintain NSR
3. prevent CVA by anticoagulation


should she continue diltiazem preoperatively?

the decision would depend on her underlying ventricular rate while not on CCB, her risk for myocardial ischemia, and the degree it will interfere with EP mapping.

typically, anti-arrhythmics are discontinued to facilitate the induction of arrhythmias while mapping the conduction pathways and source of excitability. however, since CCB control the ventricular rate by slowing conduction through the AV node, they have minimal effects on EP mapping and usually can be continued preoperatively. if she has MVS, an increase in ventricular rate could be devestational.


what are the indications for catheter ablation?

1. symptomatic SVT due to AVNRT, WPW, unifocal atrial tach
2. atrial fib with lifestyle impairing symptoms and ineffective antiarrhythmic tx
3. symptomatic v tach
4. patient preference
5. noncompliance


what was the cause of her syncopal episode? does she need further eval?

given her h/o chronic a fib, CVA, possible MVS, it was likely due to cardiac arrhythmia/TIA. she also could have had a hypoglycemic episode or MI.

additional workup would be based on the suspected etiology and may include ECG, exercise stress test, ECHO, carotid sinus massage, tilt-table test


echo reveals mitral valve area of 1.1 cm2, dilated LA without thrombus, and mod TR. why is there TR?

secondary to rheumatic disease and pulm htn due to mitral stenosis. decreased flow through stenotic mitral valve leads to increased LAP which are then transmitted to the pulm circ. over time, chronically elevated pressures result in pulm vascular changes that lead to irreversible pulm htn. RVP overload develops, compensatory RVH, and eventually dilation. that can lead to tricuspid regurg.


what is the grading of mitral valve stenosis?

normal: VA 4-6 cm2
mild: VA 1.6-20 cm2, pressure half time 220 ms, pressure gradient >10 mmHg


how does tricuspid regurg effect your management?

i would avoid decreased preload or increased right ventricular after load, such as hypovolemia, decreased SVR, hypoxia (increased PA pressure), acidosis (increased PA pressure), hypercarbia (increased PA pressure), tachycardia (impaired LV filling, increased LA pressures, increased RV after load)

additionally, i would:
1. avoid N2O (exacerbates pulm htn)
2. ensure removal of air in IV lines (increased risk of high pressure RV to low pressure LV shunt through PFO)
3. monitor CVP to guide fluid admin, monitor RV function and detect changes in regurgitant volume
4. avoid excessive airway pressure which can increase after load and decrease preload.


would you place a PAC for this case?

although with mitral stenosis and TR, a PAC to monitor PAP (RV after load), cardiac output and SVR may prove valuable in guiding fluid therapy, ensuring adequate preload, and maintaining CO. However, given the inaccuracies associated with TR and MVS, the difficulty of passing the catheter through the regurgitant valve, the increased risk of massive hemorrhage in the setting of pulm htn (increased risk of PA rupture) and an elevated INR, i would not employ a PAC.


suppose you did place one, what discrepancies could you expect to see?

1. PCWP would overestimate LVDP by at least the amount of the MV pressure gradient
2. tachycardia and elevated CO increase the MV pressure gradient, leading to increased difference in the actual and estimated LVDP
3. thermodilution CO measurements would be inaccurate (falsely elevated) due to a portion of the cold inject ate moving retrograde into the atrium rather than into the pulm art.


what are the contraindications to PAC?

- infection at insertion site
- insertion during CPB
- lack of consent

- coagulopaty
- thrombocytopenia
- electrolyte disturbances
- severe acid-base disturbance

High risk:
- pulm htn, eisenmeger's syndrome
- defib or pacemaker
- prosthetic/stenotic tricuspic/pulmonic valve
- RA/RV mass


would you provide general anesthesia or MAC for this case? what are the advantages of general?

given the importance of maintaining adequate preload in this patient with MVS and TR, i would prefer to perform this case under MAC to avoid the potential reduction in SVR that often occurs under general anesthesia in chronic htn. however, considering her increased risk of aspiration (GERD plus DM) and the potentially detrimental effects of tachycardia in the setting of MVS, i would balance adequate analgesia with minimizing sedation.

general anesthesia can be advantageous. it increases patient comfort, blunts sympathetic stimulation (avoiding tachycardia), airway control and ventilation (reduce hypercarbia which worsens pulm htn), and the option for immediate surgical intervention if a complication occurs.


patient refuses MAC. how would you induce the patient?

goals will be to avoid tachycardia and reductions in SVR. additionally, there is potential for difficult airway management (obesity, decreased cervical ROM) and i would prefer to avoid sch due to her history of significant R-sided weakness and possibly proliferation of exntrajunctional receptors that could cause hyperkalemia. i would
1. ensure presence of difficult airway equipment
2. provide aspiration prophylaxis (pepcid, reglan, bicitra)
3. sniff position (i would avoid reverse trendelenberg to avoid further reductions in preload)
4. pre oxygenate with 100% FiO2
5. administer lidocaine and fentanyl to blunt sympathetic response to laryngoscopy
6. apply cricoid pressure
7. gentle laryngoscopy
8. secure airway as quickly as possible


what about RSI?

usually, this would be desirable in a patient with GERD and DM, however I would avoid it in this patient due to her risk of hemodynamic instability (reduced SVR/preload), inadequate depth of anesthesia (tachycardia) and sch-induced hyperkalemia


after induction the HR increases to 210 bpm. are you concerned? what do you do?

yes i would be concerned as this high of a HR decreases coronary perfusion while increasing myocardial oxygen demand and LV wall tension. this increases the risk of ischemia. moreover, in this patient with MVS, this will decrease LV filling (decreased time for diastolic filling), increase LAP, and possibly lead to pulm edema and heart failure.

i would confirm the rate and rhythm on EKG, cycle the BP cuff, ensure adequate oxygenation/ventilation, attempt to palpate a pulse and administer diltiazem to control the ventricular rate.

since her rate is >150 bpm, i would also begin chest compressions and perform synchronized cardioversion using 100, 200, 300, 360 J as necessary.


would you give a BB?

while they are often used for rate control in afib they should not be combined with CCB due to risk for severe cardiac depression. this would be of particular concern in this patient with signs of right heart strain.


in the case of the unstable patient requiring DC cardioversion, would you require synchronized shocks?

while synchronization of DC shocks with the R we is desirable to prevent the shock being delivered during the vulnerable period of depolarization, i would not require synchronization in the case of an unstable patient.


the patient's condition is stabilized and the case proceeds. during mapping the BP suddenly drops to 44/21. what do you think is the cause?

my ddx would include:
1. arrhythmia: ventricular tachycardia/fibrillation
2. myocardial ischemia
3. acute failure
4. cardiac tamponade
5. cardiac rupture
6. hemorrhage
7. PE
8. air embolism
9. tension PTX


how would you manage this?

1. inform the surgeon
2. discontinue VA
3. evaluate the EKG
4. palpate pulse
5. auscultate chest
6. ensure adequate oxygenation
7. place patient in trendelenberg to increase preload
8. administer fluids, vasopressors, inotropes

consider ECHO, CXR to further evaluate


intervention fails and ablation catheter is noted to be curled up in the left chest under fluoro. what now?

this is consistent with cardiac rupture.
1. inform OR and CV for emergent repair
2. begin fluid resuscitation
3. prepare for massive transfusion
4. vasopressors as indicated
5. arterial line/TEE to guide therapy
6. if tamponade present (RA/RV/LV diastolic collapse) ask surgery to decompress pericardium


pt. undergoes successful ablation with no complications. can she be discharged home?

yes she can, once she meets "safe discharge" criteria.
1. stable vital signs
2. controlled nausea/vomiting
3. absence of unexpected bleeding
4. adequate pain control with oral meds
5. ability to walk without dizziness
6. discharge instructions and prescriptions
7. pt acceptance of discharge
8. responsible escort


what is the PADS system?

PostAnesthetic Discharge Scoring System
9 or higher can go home

Vital Signs:
2 - within 20% of baseline
1 - within 20-40% of baseline
0 - >40% baseline

2 - steady gait, no dizziness, baseline
1 - ambulates with assistance
0 - unable to ambulate

2 - minimal, no tx
1 - moderate, tx effective
0 - severe, tx not effective

2 - VAS = 0-3
1 - VAS = 4-6
0 - VAS = 7-10

Surgical bleeding
2 - minimal
1 - moderate (1-2 dressing changes)
0 - severe


RN informs you the patient meets discharge criteria but i unable to void her bladder. would you allow her to be discharged?

urinary retention can lead to bladder atony and permanently impaired voiding, it is no longer a necessary condition for safe discharge in patient considered low risk for retention.

if the patient is high risk of developing retention (pelvic surgery, personal/family history of retention, spinal cord disease, neuraxial anesthesia with opioids and LA, i would require voiding with residual volume less than 400 mL on ultrasound. moreover, if the patient's bladder volume was greater than 500 mL, i would perform catheterization to empty it.


the patient did not arrange for an escort. what do you do?

i would explain my concerns to the patient and that she may have impaired driving performance for up to 24 hours postop. if an escort still could not be arranged, i would arrange for hospital admission


20 min after surgery, RN informs you patient is having significant PONV. what would you do?

go evaluate the patient. make sure BG is acceptable and that pain is under control. i would also check oxygenation, fluid administration, and HD stability. if PONV were not related to a more serious condition, i would initiate therapy. it is important to keep in mind that it is not recommended to repeat any drugs used for prophylaxis or treatment during the first 6 hours since initial admin. assuming none had been given, i would give ondansetron 1 mg (tx dose is 1/4 prophylactic dose) and provide supplemental oxygen. if she remained nauseous, i would administer a drug from a different class, such as droperidol or promethazine. if these were also inadequate, i would give 20 mg propofol as needed. i would avoid steroids in this diabetic patient.


what are the RF of PONV?

1. patient - female, nonsmoking, anxiety, h/o of PONV or motion sickness
2. anesthetic- VA, N2O, neostigmine, opioids
3. surgery - laparoscopy, ENT, NSGY, breast, strabismus, laparotomy, plastic surgery