cardiac ablation Flashcards
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?
- arrhythmias - impaired CO, and end-organ ischemia
- 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)
- acute ischemic stroke - embolic or thrombotic
- HD instability - chronic htn, atrial fib, MV stenosis
- CHF - due to ischemia, or RVP overload due to MV stenosis
- aspiration - GERD, DM
- complications of smoking - pulm disease, bronchospasm, hypoxia, CVA, prolonged mech vent, infection, impaired wound healing
- hypo/hyperglycemia
- coagulopathy due to coumadin
- 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?
- slow HR
- restore/maintain NSR
- 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?
- symptomatic SVT due to AVNRT, WPW, unifocal atrial tach
- atrial fib with lifestyle impairing symptoms and ineffective antiarrhythmic tx
- symptomatic v tach
- patient preference
- 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:
- avoid N2O (exacerbates pulm htn)
- ensure removal of air in IV lines (increased risk of high pressure RV to low pressure LV shunt through PFO)
- monitor CVP to guide fluid admin, monitor RV function and detect changes in regurgitant volume
- 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?
- PCWP would overestimate LVDP by at least the amount of the MV pressure gradient
- tachycardia and elevated CO increase the MV pressure gradient, leading to increased difference in the actual and estimated LVDP
- 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?
Absolute:
- infection at insertion site
- RVAD
- insertion during CPB
- lack of consent
Relative:
- coagulopaty
- thrombocytopenia
- electrolyte disturbances
- severe acid-base disturbance
High risk:
- pulm htn, eisenmeger’s syndrome
- LBBB, RBBB
- 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.