First-Line Treatment for Ventricular Tachycardia? What the Guidelines and Evidence Say

by Sana Kathawala, MD MBA

It’s a quiet day in the ED. You’re twiddling your thumbs wondering whether you should get a second cup of coffee to keep awake when the notification phone rings.

“68-year-old male with history of diabetes, hypertension, and ESRD with witnessed syncope after hemodialysis earlier today. HR 270s, BP stable, IV access obtained, 500 cc NS and 150 mg amiodarone given in the field.”

You quickly go to your resuscitation bay and get set up. You have your monitor, the defibrillator is at bedside, and the nurse has the IV set up and blood tubes ready. The junior resident is preparing the airway tray.

5 minutes later, the patient is wheeled in with EMS at bedside, providing the history and rhythm strip. Immediately, you run through your ABCs.

Airway: Intact
Breathing: Clear bilaterally
Circulation: Normal mental status, tachycardia

You take a moment to view the rhythm strip (below) while you ask more about your patient’s medical history. His cardiac history includes CHF, Paroxysmal Afib, and recent admission for “SVT” as per family. He is compliant with his home meds.

EMS Rhythm Strip

What are your initial steps?

Cardiac monitor, ECG

Assess end organ perfusion – decide whether the patient is stable vs unstable. Your patient is alert and oriented without chest pain, shortness of breath, diaphoresis or pallor; normotensive. Conclusion: stable.
After concluding that the patient is stable, you decide to treat for stable, wide QRS complex tachycardia (WCT). However, being the astute ED clinician you are, you have the defibrillator pads placed on the patient for electrical therapy in case of any decompensation – VERY IMPORTANT!

You then complete the physical exam:

VS: BP 112/53 mm Hg, P 223/min, RR 14/min, POx 96% on RA, T 97.1 F
Gen: AAO x 3, speaking in full sentences
HEENT: No external signs of trauma
Chest: CTAB, no wheezes/rales/rhonchi
Heart: Tachycardia
Abd: Soft, non-tender, non-distended
Extremities: warm, 2+ pulses radial and DP
Skin: No cyanosis, warm, no diaphoresis

Initial ECG

Approach to the ECG: What rhythm is this?

Ventricular Tachycardia (VT) versus Supraventricular Tachycardia (SVT) with aberrancy can be extremely hard to differentiate – what to do when you’re not sure?

The initial approach to a stable, regular WCT can seem uncertain if there is strong suspicion for SVT w/aberrancy. This patient has had a recent admission for SVT, and keeping anchoring bias in mind, you consider SVT highest on your differential and decide to use adenosine.¹ You push 6 mg, but the rhythm does not revert to sinus or uncover P waves. You push 12 mg, and again, no effect. At this point, you decide that this may be stable VT. You treat with Procainamide 1 gm infusion over 30 minutes, and after 15 minutes, the rhythm reverts to normal sinus rhythm.

ECG after procainamide; note the prolonged QTc, which is a common side effect of procainamide

The patient is admitted to the CCU for further telemetry monitoring and serial cardiac enzymes. Cardiology starts an amiodarone infusion.

THE LITERATURE – WHAT DO WE KNOW, WHAT SHOULD BE OUR APPROACH, AND WHAT ARE THE SUPPORTING GUIDELINES?

Ventricular Dysrhythmias – Definition & Electrophysiology

Ventricular Dysrhythmias represent a broad spectrum from ectopic beats to sustained ventricular tachycardia and ventricular fibrillation (VF), thus spanning from the benign to life-threatening. If the rhythm lasts > 30 seconds or the patient shows signs of instability, the rhythm is considered “sustained.” The majority of cases of sustained ventricular dysrhythmias are due to structural and/or ischemic heart disease.²

There are several mechanisms in which these rhythms can arise and propagate. Scarred myocardium from previous infarction can provide a substrate for reentrant circuits within the myocardium. Other mechanisms include early or late afterdepolarization (triggered activity) and abnormal automaticity (a group of ventricular cells produce an ectopic focus).³

Structural heart disease such as hypertrophic obstructive cardiomyopathy and congenital channelopathies such as Long QT Syndrome, Short QT Syndrome, and Brugada Syndrome also predispose patients to sustained VT and VF. Remember to get a thorough history, and if the patient has any of these diseases, treat the specific etiology and consult their cardiologist early.

Remember to look for and treat other causes of WCT: toxidromes including TCA overdose and hyperkalemia (typically seen in ESRD patients).⁴

ECG Features suggestive of a ventricular dysrhythmia:^5,6

AV Dissociation – also suggested by fusion and capture beats
QRS > 160 ms
QRS concordance across precordial leads (spec 90-100%)
Extreme Axis Deviation (-180° to -90°)
No clear RBBB/LBBB pattern
V1 – RBBB-like morphology BUT with higher L rabbit ear (as opposed to higher R ear in RBBB) – very specific
Brugada’s Sign: RS interval > 100 ms
Josephson’s Sign: notching towards the nadir of the S wave
Regular: Monomorphic
Irregular: Polymorphic

Quick tip – Brugada and Vereckei Methods:

Recognize that quick diagnosis can lead to more efficient and judicious use of medications as well as diagnostic accuracy. Two 4-step methods – the Brugada and Vereckei methods – have been proposed to assist in diagnosing VT. In a recent comparison of the two methods, both had similar utility in diagnosing VT, but the first step of the Vereckei method (the presence of an initial R in aVR) proved to be both fast and accurate (when compared to the gold standard of electrophysiologic study).^7,8

An important caveat:

In the ED patient with stable WCT, making the diagnosis of VT takes second priority to treatment. Delaying treatment to determine the exact etiology is NOT advised – instead consider antidysrhythmic medications and be prepared to use synchronized cardioversion if the drugs do not work or if the patient decompensates.

Management:

The initial approach to any patient in the resuscitation bay should be our good ol’ ABCs. Once we complete our primary and secondary surveys and immediate measures such as IV access, supplemental oxygen as needed, telemetry monitoring and an ECG, we then focus on the most important initial aspect of VT – determining stability.

A patient is unstable if there are any signs of end-organ hypoperfusion: altered mental status, ischemic chest pain, dyspnea, or clammy/diaphoretic skin (do not rely solely on hypotension). If this is the case, the patient should immediately be treated with synchronized cardioversion at 100 joules.

The stable patient, however, can be managed with the following medications:

Procainamide:

AHA Class IIa recommendation
Mechanism of action – sodium channel blockade
Administered as a slow infusion at 10 mg/kg IV (max dose 17 mg/kg or 100 mg/min depending on guidelines used)
Discontinue at conversion to sinus rhythm conversion or at the onset of hypotension

The current literature and guidelines both support Procainamide as a first-line agent. The PROCAMIO trial was the first randomized trial to compare the use of procainamide and amiodarone in stable, sustained, monomorphic wide complex tachycardia (most likely ventricular).⁹ This was a multicenter, prospective trial that included 74 patients with regular WCT who presented to the ED and met the inclusion criteria:

HR > 120/min
SBP > 90 mm Hg
QRS > 120 ms
Age > 18 yrs
No dyspnea at rest
No peripheral signs of hypoperfusion
No severe angina.

Patients were then randomized to receive either IV amiodarone (5 mg/kg over 20 min) or IV procainamide (10 mg/kg over 20 min – note that this infusion was more rapid than the typical rate).

Primary endpoint
- Major adverse cardiac events
Secondary endpoints
- Termination of tachycardia episode within 40 min of drug administration
- Incidence of total adverse events in a 24 hr observation period

The study results were promising in favor of procainamide. Compared to amiodarone, procainamide had a statistically significant lower rate of major cardiac events (OR 0.1, 95% CI 0.03 to 0.6, P=0.006) and terminated VT more frequently (OR 3.3, 95% CI 1.2 to 9.3, P=0.026). There was no difference in total adverse events.

Limitations: Not blinded, small sample size.

Amiodarone:

AHA Class IIb recommendation
Complex mechanism of action – initial beta-blocking effect, then later prolongs phase 3 cardiac action potential and increases the refractory phase
Administered at 150 mg over 10 minutes, followed by an infusion for 24 hours

Amiodarone had been the favored antidysrhythmic for stable VT due to its possible benefit in patients with pulseless VT.¹⁰ However, PROCAMIO and other prior studies have steered us away from the use of amiodarone.^11,12 It still may be considered for VT that occurs as a consequence of acute MI (abnormal automaticity).¹³

Sotalol:

AHA Class IIb recommendation
Mechanism of action: Potassium channel blocker + non-selective beta-blocker properties
Administered as 1.5 mg/kg IV over 4 min

Lidocaine:

Considered the least effective except perhaps in setting of acute MI (abnormal automaticity)

Note: Direct current cardioversion is the most effective therapy for stable or unstable VT. It is reasonable to proceed directly to procedural sedation and electrical cardioversion for stable VT.

Long-term management will be up to our cardiology colleagues – typically a combination of long-term antidysrhythmics, ablation therapy, and AICD placement.

Summary:

For stable, regular WCT, it is reasonable to treat with adenosine first
If adenosine does not terminate the stable WCT, assume VT and consider drug treatment
Use synchronized cardioversion for the unstable patient
Major clues for VT:
- Initial R in aVR (Vereckei method)
- AV Dissociation
Limited evidence suggests that Procainamide may be superior to Amiodarone for stable VT

REFERENCES:

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Rithvik Balakrishnan

Resident Physician, EM/IM

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2 Comments

Joe · March 6, 2019 at 4:29 pm

Adenosine-Sensitive Ventricular Tachycardia
Right Ventricular Abnormalities Delineated by Magnetic Resonance Imaging
Steven M. Markowitz , Bonnie L. Litvak , Elizabeth A. Ramirez de Arellano , John A. Markisz , Kenneth M. Stein , and Bruce B. Lerman
Originally published19 Aug 1997https://doi.org/10.1161/01.CIR.96.4.1192Circulation. 1997;96:1192–1200

Doyou see risk in presuming that termination of tachycardia after adenosine means the rhythm was SVT?

deSouza · March 16, 2019 at 10:35 am

This is a good point. Following treatment and stabilization (as well and diagnosis and treatment of any possible underlying etiology), a close inspection of the ECGs and discussion of further management with an electrophysiologist, if necessary, would be wise. Adenosine-sensitive VT (right ventricular outflow tract tachycardia) often has typical ECG characteristics (inferior axis, LBBB). If the diagnoses of the initial rhythm remains in question, further observation/telemetry in the hospital may be warranted.