Download Ablation of Ventricular Tachycardia

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 usually use 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 stenotic valvular 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.
-
Maintenance of 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 proceduralist ahead 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
a. Performed in sinus rhythm
b. 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)
c. Frequently, pacing is performed at various sites within the
endocardium to better identify potential areas of interest that may be
targeted for ablation
d. Additionally, the following may be caused from catheter stimulation:
i. Isolated PVCs
ii. Runs of NSVT
2.
3.
4.
5.
iii. Occasional sustained arrhythmias that may require forced
overdrive pacing (“ATP”) or external shock to terminate
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:
a. Activation mapping
i. While VT is ongoing, the catheter is moved to various regions
of the heart to gather information about potential sites of
ablation
ii. If possible, VT is allowed to continue as long as
hemodynamically tolerated, with blood pressure support
provided as needed
iii. If unstable and unable to be supported pharmacologically, VT
is terminated, either by rapid pacing (ATP) or with external
cardioversion
iv. ECMO has been used on occasion for mechanical support,
although not usually only for the purpose of mapping in VT
b. ATP or shock
i. Done if poorly tolerated from the outset
ii. Provides indirect information about sites to target – valuable
especially if there is no clear area of scarring
Ablation, based on data from above
a. 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)
b. 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
c. Can be extensive, based on amount of substrate targeted
Endpoint assessment (can be performed multiple times throughout the
course of ablation)
a. Attempt to re-induce arrhythmia (#2)
b. Pacing at various sites within ablated region(s)
Epicardial access and ablation
a. Attempted if
i. VT still inducible after comprehensive endocardial ablation,
and/or VT morphology appears consistent with epicardial exit
ii. Prior failed endocardial ablation
iii. Suspicion of mid-myocardial substrate, thus requiring
additional epicardial ablation opposite endocardial ablation
site
b. Usually though not always performed under GETA (for pt comfort and
to minimize movement during pericardial access)
6. Hemodynamic considerations in addition to above
a. Hypotension
i. Always prompts assessment for pericardial effusion and
impending tamponade
ii. Alternative causes considered:
1. Cardiogenic shock
2. Acute bleeding from other source
3. Drug effect
iii. Important for the EP physician to be alerted for new drops in
BP and/or need for blood pressure support.
iv. Attempt to avoid/minimize agents that are negatively effect
cardiac output.
b. Volume overload
i. Can be significant, and I/O’s are assessed hourly, diuretics
given in response
ii. Updates on ABG, oxygenation needs are useful to help guide
therapies
Table from Mittnacht article.