Ablation of Ventricular Tachycardia (VT) in the EP Lab

Purpose: The purposes of this document are

1)To provide education pertaining to the process of VT ablation in the EP lab and this population’s common peri-procedure management concerns.

2)To provide peri-procedure management suggestions from some of the Cardiothoracic Anesthesia group at the University of Colorado.

Content: This content is a combination of published literature and peer recommendation. There are no anesthesia society recommendations for this procedure.

Suggested Reading:

Mittnacht A, Dukkipati S, Mhajan A. Ventricular Tachycardia Ablation: A comprehensive review for anesthesiologists. Anesthesia and Analgesia, April 2015, volume 120, #4, pages 737-748.

The patient acuity and procedure invasiveness vary significantly from case to case. The spectrum runs from the patient with a structurally normal heart and isolated monomorphic ventricular tachycardia (MMVT) to the patient with severe ischemic cardiomyopathy with severe biventricular dysfunction in VT storm requiring epicardial ablation.Endocardial ablation is the more common of the two approaches, with access to the heart achieved from the femoral vessels. The right side of the heart is accessed through the femoral vein. The left side of the heart can be accessed via a trans-septal approach or retrograde through the femoral artery. Epicardial ablations done in the EP lab will usuallyuse a subxiphoid approach. We have done some epicardial ablations through a thoracotomy.

The pre-anesthesia assessment starts with a standard evaluation, with careful attention to the following:

1)Left ventricular function.

2)Right ventricular function.

3)Valvular heart disease.

4)Presence or absence of coronary artery disease. If present, is there an ischemic burden?

5)Pulmonary hypertension. If present, does right heart catheterization show vasodilator responsiveness? Is it precapillary or postcapillary?

6)How active is the VT? Nonsustained? Sustained? VT storm? Hemodynamically stable or unstable? See table below.

7)What is the cycle length? Shorter equals faster ventricular rate and generally more hemodynamic instability.

8)Functional capacity.

9)Symptoms during VT.

10)Presence of ICD and/or pacemaker.

11)Presence of congenital heart disease. If present, how does blood flow now?

12)Are they being considered for heart transplant or LVAD? Have a high suspicion for hemodynamic instability if this is the case.

13)How does the EP doc plan to map the VT? Is there mechanical assist back-up planned? Is it necessary?

14)Does the EP doc want sedation or general anesthesia? Many VT ablations can be done under sedation. Complex ablations and epicardial ablations are generally done under general anesthesia.

Room Setup standard set up plus invasive blood pressure monitoring , an additional large bore peripheral IV, pumps for any necessary infusions, heparin.

Anesthesia induction will vary significantly depending upon the patient and approach.

-Patients with normal biventricular function/otherwise structurally normal heart and a straightforward ablation under MAC can probably be managed without invasive monitoring. Avoid Precedex due to significant sympatholysis. Communicate significant changes in hemodynamics with the EP doc.

-Patients with diminished cardiac function &/or structurally ABnormal hearts &/or myocardial ischemic burden having ablations under MAC should have invasive arterial monitoring. If you elect to have cardiology place a femoral arterial line make sure this will not be taken away from you in case of emergency. Avoid Precedex due to significant sympatholysis. Communicate significant changes in hemodynamics with the EP doc.

-Patients with normal biventricular function/otherwise structurally normal heart and straightforward ablation under general anesthesia should have invasive monitoring placed. This can be done before or after induction of anesthesia depending upon physician preference.

-Patients with decreased LV or RV systolic function &/or patients who otherwise have structural heart disease &/or myocardial ischemic burden undergoing VT ablation with general anesthesia should have an arterial line placed prior to anesthesia induction. Inductions should be gentle. Inotropes and vasopressors should be available at the time of induction for rescue. Propofol often results in significant hypotension when used for induction in patients with moderate to severe ventricular dysfunction or severe stenoticvalvular disease/LVOT obstruction therefore its use in this population is discouraged. Vasopressors should be used judiciously in patients with moderate to severely decreased ventricular systolic function as increasing SVR too much can significantly reduce cardiac output. Inotropes are often required in this population.

In patients with pulmonary hypertension it is important to avoid hypoxia, hypercarbia and acidosis with induction as these things can increase pulmonary vascular resistance. If the patient has severe precapillary pulmonary hypertension, RV dysfunction and is known to be vasodilator responsive, consider nitric oxide or Flolan. Avoid Precedex unless in VT storm. If the patient is in VT storm it may be worth discussing Precedex with Cardiology. Consider calling a cardiac anesthesiologist for consultation in these sick patients.

-Maintenanceof general anesthesia with inhaled anesthetics is generally appropriate. Unless the patient is hemodynamically unstable in VT storm avoid Precedex due to significant sympatholysis. If there is VT storm and hemodynamic instability it may be appropriate to discuss Precedex and/or thoracic epidural with EP proceduralist. Communicate significant changes in hemodynamics with the EP proceduralist. Blood pressure management should be a team approach considering both the patient’s underlying physiology and the procedure. Fluid management is important, as these patients easily get volume overloaded. Hourly I/O will be recorded. Neuromuscular blockade may not be appropriate, so please discuss with the EP proceduralistahead of time. Consider Remifentanil if patient movement will be dangerous and you are unable to use neuromuscular blockade.

-Emergence/extubation/disposition is at the discretion of the anesthesia team.

-Procedural risks include damage from vascular access, cardiac perforation, phrenic nerve injury and thromboembolic events. With epicardial ablations direct coronary injury and abdominal organ puncture from access are additional concerns.

A description of the VT ablation procedure is below, provided by Dr. Wendy Tzou:

General strategy for VT ablation

**Note that there may be variations in order and content of what is performed based on patient, situation, and operator. The following is to function only as a very general guide

  1. Voltage map
  2. Performed in sinus rhythm
  3. Involves moving catheter within chamber of interest, collecting electrical and anatomic data to recreate a 3-dimensional shell of the endocardium illustrating areas of probable scar and sites of arrhythmia circuit(s)
  4. Frequently, pacing is performed at various sites within the endocardium to better identify potential areas of interest that may be targeted for ablation
  5. Additionally, the following may be caused from catheter stimulation:
  6. Isolated PVCs
  7. Runs of NSVT
  8. Occasional sustained arrhythmias that may require forced overdrive pacing (“ATP”) or external shock to terminate
  9. Programmed stimulation – pacing with introduction of up to 3 extrastimuli (PVCs) with a goal of arrhythmia induction. Pacing is initiated with 6-8 beats at either 600 or 400 msec, with associated single, double, or triple extrastimuli (typical language: “600 singles”). The most aggressive protocol for stimulation (and most likely to induce an arrhythmia) is pacing at 400 msec with triple extrastimuli (“400 triples”). If monomorphic VT (MMVT) is induced, the following may occur:
  10. Activation mapping
  11. While VT is ongoing, the catheter is moved to various regions of the heart to gather information about potential sites of ablation
  12. If possible, VT is allowed to continue as long as hemodynamically tolerated, with blood pressure support provided as needed
  13. If unstable and unable to be supported pharmacologically, VT is terminated, either by rapid pacing (ATP) or with external cardioversion
  14. ECMO has been used on occasion for mechanical support, although not usually only for the purpose of mapping in VT
  15. ATP or shock
  16. Done if poorly tolerated from the outset
  17. Provides indirect information about sites to target – valuable especially if there is no clear area of scarring
  18. Ablation, based on data from above
  19. Usually performed using open irrigated-tip catheters, with flow rates of 2-30 ml/min (higher flows used while actively ablating; lower flow to prevent blood clots forming during mapping)
  20. In certain cases, we use a catheter with lower ablation flow rates (15 ml/min), although this catheter does not provide the same force feedback information as the higher-flow catheter
  21. Can be extensive, based on amount of substrate targeted
  22. Endpoint assessment (can be performed multiple times throughout the course of ablation)
  23. Attempt to re-induce arrhythmia (#2)
  24. Pacing at various sites within ablated region(s)
  25. Epicardial access and ablation
  26. Attempted if
  27. VT still inducible after comprehensive endocardial ablation, and/or VT morphology appears consistent with epicardial exit
  28. Prior failed endocardial ablation
  29. Suspicion of mid-myocardial substrate, thus requiring additional epicardial ablation opposite endocardial ablation site
  30. Usually though not always performed under GETA (for pt comfort and to minimize movement during pericardial access)
  31. Hemodynamic considerations in addition to above
  32. Hypotension
  33. Always prompts assessment for pericardial effusion and impending tamponade
  34. Alternative causes considered:
  35. Cardiogenic shock
  36. Acute bleeding from other source
  37. Drug effect
  38. Important for the EP physician to be alerted for new drops in BP and/or need for blood pressure support.
  39. Attempt to avoid/minimize agents that are negatively effect cardiac output.
  40. Volume overload
  41. Can be significant, and I/O’s are assessed hourly, diuretics given in response
  42. Updates on ABG, oxygenation needs are useful to help guide therapies

Table from Mittnacht article.