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Ventricular tachycardia

In ventricular tachycardia, commonly called V-tach, three or more PVCs occur in a row and the ventricular rate exceeds 100 beats/minute. This arrhythmia may precede ventricular fibrillation and sudden cardiac death, especially if the patient isn’t in a health care facility.

Ventricular tachycardia is an extremely unstable rhythm. It can occur in short, paroxysmal bursts lasting

fewer than 30 seconds and causing few or no symptoms. Alternatively, it can be sustained, requiring immediate treatment to prevent death, even in patients initially able to maintain adequate cardiac output.

How it happens

Ventricular tachycardia usually results from increased myocardial irritability, which may be triggered by enhanced automaticity or reentry within the Purkinje system or by PVCs initiating the R-on-T phenomenon. Conditions that can cause ventricular tachycardia include:

•myocardial ischemia

•MI

•coronary artery disease

•valvular heart disease

•heart failure

•cardiomyopathy

•electrolyte imbalances such as hypokalemia

•drug intoxication from digoxin (Lanoxin), procainamide, quinidine, or cocaine

•proarrhythmic effects of some antiarrhythmics.

Unpredictable V-tach

V-tach is unstable and can occur in short paroxysmal bursts.

Ventricular tachycardia is significant because of its unpredictability and potential to cause death. A patient may be stable with

a normal pulse and adequate hemodynamics or unstable with hypotension and no detectable pulse. Because of reduced ventricular filling time and the drop in cardiac output, the patient’s condition can quickly deteriorate to ventricular fibrillation and complete cardiac collapse.

What to look for

On the ECG strip, the atrial rhythm and rate can’t be determined. The ventricular rhythm is usually regular but may be slightly

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irregular. The ventricular rate is usually rapid—100 to 250 beats/ minute.

The P wave is usually absent but may be obscured by the QRS complex. Retrograde P waves may be present. Because the P wave can’t be seen in most cases, you can’t measure the PR interval. The QRS complex is wide and bizarre, usually with an increased amplitude and a duration of longer than 0.12 second.

All about uniformity

QRS complexes in monomorphic ventricular tachycardia have a uniform shape. In polymorphic ventricular tachycardia, the shape of the QRS complex constantly changes. If the T wave is visible, it occurs opposite the QRS complex. The QT interval isn’t measurable. (See Identifying ventricular tachycardia.)

Torsades de pointes is a special variation of polymorphic ventricular tachycardia. (See Torsades de pointes and Pediatric torsades de pointes.)

Don’t skip this strip

Identifying ventricular tachycardia

This rhythm strip illustrates ventricular tachycardia. Look for these distinguishing characteristics.

The QRS complex is

wide and bizarre.

	The ventricular rate is
	100 to 250 beats/minute.
• Rhythm: Regular	• QRS complex: 0.16 second; wide	• QT interval: Unmeasurable
• Rate: 187 beats/minute	and bizarre	• Other: None
• P wave: Absent	• T wave: Opposite direction of QRS
• PR interval: Unmeasurable	complex

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Quick work prevents collapse

Although some patients have only minor symptoms at first, they still need rapid intervention and treatment to prevent cardiac

Don’t skip this strip

Torsades de pointes

Torsades de pointes, which means “twisting about the points,” is a special form of polymorphic ventricular tachycardia. The hallmark characteristics of this rhythm, shown below, are QRS complexes that rotate about the baseline, deflecting downward and upward for several beats.

The rate is 150 to 250 beats/minute, usually with an irregular rhythm, and the QRS complexes are wide with changing amplitude. The P wave is usually absent.

Paroxysmal rhythm

This arrhythmia may be paroxysmal, starting and stopping suddenly, and may deteriorate into ventricular fibrillation. It should be considered when ventricular tachycardia doesn’t respond to antiarrhythmic therapy or other treatments.

Reversible causes

The cause of this form of ventricular tachycardia is usually reversible. The most common causes are drugs that lengthen the QT interval, such as amiodarone, ibutilide, erythromycin, haloperidol, droperidol, and sotalol. Other causes include myocardial ischemia and electrolyte abnormalities, such as hypokalemia, hypomagnesemia, and hypocalcemia.

Going into overdrive

Torsades de pointes is treated by correcting the underlying cause, especially if the cause is related to specific drug therapy. The practitioner may order mechanical overdrive pacing, which overrides the ventricular rate and breaks the triggered mechanism for the arrhythmia. Magnesium sulfate may also be effective. Electrical cardioversion may be used when torsades de pointes doesn’t respond to other treatment.

The ventricular rate

is 150 to 250 beats/minute.

Ages

and stages

Pediatric torsades de pointes

Torsades de pointes at an early age is usually due to congenital long QT syndrome. Ask the parents about a family history of sudden cardiac death or sudden infant death syndrome.

The QRS complexes are wide, with phasic variation that seems to twist around the baseline.

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collapse. Most patients with ventricular tachycardia have weak or absent pulses. Low cardiac output will cause hypotension and a decreased level of consciousness (LOC) leading to unresponsiveness. Ventricular tachycardia may precipitate angina, heart failure, or a substantial decrease in organ perfusion.

How you intervene

Treatment depends on whether the patient’s pulse is detectable or undetectable. A patient with pulseless ventricular tachycardia receives the same treatment as one with ventricular fibrillation and requires immediate defibrillation and CPR. Treatment for the patient with a detectable pulse depends on whether his condition is stable or unstable and has monomorphic or polymorphic QRS complexes.

Unstable patients generally have heart rates greater than 150 beats/minute. They may also have hypotension, shortness of breath, an altered LOC, heart failure, angina, or MI—conditions that indicate cardiac decompensation. These patients are treated immediately with direct-current synchronized cardioversion.

Typical tachycardia complex

A hemodynamically stable patient with monomorphic ventricular tachycardia is treated differently. First, administer amiodarone following advanced cardiac life support (ACLS) protocols to correct the rhythm disturbance. If the drug doesn’t correct the disturbance, prepare the patient for synchronized cardioversion.

If the patient has polymorphic ventricular tachycardia with a normal QT interval, correct ischemia and electrolyte imbalances. Then adminster beta-adrenergic blockers, lidocaine, amiodarone, or procainamide following ACLS protocol. Again, if drug therapy is unsuccessful, synchronized cardioversion is performed.

Correct electrolyte abnormalities in the patient with polymorphic ventricular tachycardia with a prolonged QT interval and administer magnesium I.V. If the rhythm persists, prepare the patient for overdrive pacing.

Patients with chronic, recurrent episodes of ventricular tachycardia who are unresponsive to drug therapy may have a cardio- verter-defibrillator implanted. This device is a more permanent solution to recurrent episodes of ventricular tachycardia. (For more information about the implantable cardioverter-defibrillator [ICD], see chapter 9.)

Treatment for the patient in V-tach depends on whether his pulse is detectable or undetectable.