Idioventricular Rhythm: Ventricular Frequency, Causes, Management and Medical Care

Definition: it is very similar to ventricular tachycardia except that the ventricular rate is less than 60 beats per minute.

All other features apply; this includes the presence of atrioventricular dissociation, as observed in the electrocardiogram, and the Brugada criteria.

An idioventricular rhythm is often referred to as one for this reason.

Idioventricular rhythm is a form of heart rhythm that originates in the ventricles.

It is recognized in the electrocardiogram by a broad QRS complex (representing electrical activation of the ventricles) and absence of preceding P waves (representing electrical activation of the atria).

In general, the speed of the idioventricular rhythm is slow, in the order of 20 to 40 beats per minute.

The idioventricular rhythm occurs when the dominant heart pacemaker (sinus node or sinoatrial node or SA node) is not functioning or when the pulses of the sinus node are blocked in the AV node (atrioventricular node) or lower.

Since the idioventricular rhythm is not a stable rhythm, the heart rate has to be stabilized by pacemaker implantation if the rhythm is permanent.

The artificial pacemaker is usually implanted under the skin over the chest and the electrodes are inserted into the heart through a vein (a blood vessel that carries deoxygenated blood to the heart).

The artificial pacemaker gives electrical pulses to stimulate the heart whenever it is needed.

Temporal stimulation can be done when the idioventricular rhythm has occurred due to a reversible cause such as in a heart attack (myocardial infarction).

The idioventricular rhythm can also be accelerated for a short period using infusions of drugs such as isoprenaline that accelerate the ventricular rhythm.

But the efficacy of isoprenaline infusion is limited and can sometimes cause more serious disturbances in heart rhythm.

Thoroughly

It is currently defined as an improved ectopic ventricular rhythm with at least 3 consecutive ventricular beats, which is faster than the normal intrinsic ventricular escape rhythm (≤ 40 ppm), but slower than ventricular tachycardia (at least 100-120 ppm) .

It is important to note that there is potential overlap of rates between the ventricular rhythm and some slow ventricular tachycardias. It should not be diagnosed solely based on the ventricular rate; The context is important.

Other characteristics of the idioventricular rhythm are useful for its correct diagnosis.

The idioventricular rhythm is generally a transient rhythm, rarely causing hemodynamic instability and rarely requires treatment.

However, misdiagnosis of idioventricular rhythm such as slow ventricular tachycardia or complete heart block can lead to inappropriate therapies with potential complications.

Idioventricular rhythm is often a clue to certain underlying conditions, such as myocardial ischemia-reperfusion, Digoxin toxicity, and cardiomyopathies.

When the ventricular rate is between 60 and 100 ppm, it is called accelerated idioventricular rhythm.

This is a hemodynamically stable rhythm that commonly occurs after myocardial infarction and no treatment is needed.

The idioventricular rhythm results when the rate of an ectopic ventricular pacemaker exceeds that of the sinus node. Often associated with increased vagal tone and decreased sympathetic tone.

The proposed mechanism is the improved automaticity of the ventricular pacemaker, although the triggered activity may play a role especially in the ischemia and toxicity of Digoxin.

The idioventricular rhythm is classically observed in the reperfusion phase of an acute STEMI, for example, after thrombolysis. It is generally a well-tolerated, benign and self-limiting arrhythmia.

Characteristics of the Electrocardiogram

  • Regular rhythm.
  • Speed ​​50-110 ppm.
  • Three or more ventricular complexes.
  • Complejos QRS> 120 ms.
  • Fusion and capture of beats.
  • Isorhythmic AV dissociation.

This refers to AV dissociation with the breast and ventricular complexes that occur at identical rates.

This is in contrast to complete heart block, where the atrial rate is usually faster than the ventricular rate.

Isorhythmic AV dissociation is usually due to functional blockage in the AV node due to retrograde ventricular impulses.

These ventricular impulses depolarize the AV node, leaving it refractory to the incoming sinus impulses (= “interference-dissociation”).

Ventricular frequency

The rate of idioventricular rhythm distinguishes it from other rhythms of similar morphology.

Rates <50 ppm consistent with a ventricular escape rhythm.

Rate> 110 ppm consistent with ventricular tachycardia.

Causes of idioventricular rhythm

There are multiple causes of idioventricular rhythm including:

  • Reperfusion phase of an acute myocardial infarction (most common cause).
  • Beta-sympathomimetics such as isoprenaline or adrenaline.
  • Pharmacological toxicity, especially Digoxin, cocaine and volatile anesthetics such as desflurane.
  • Electrolyte abnormalities.
  • Cardiomyopathy, congenital heart disease, myocarditis.
  • Return of spontaneous circulation (ROSC) after cardiac arrest.
  • Athlete’s heart

Management of idioventricular rhythm

Idioventricular rhythm is a benign rhythm in most settings and usually does not require treatment. It usually self-limits and resolves when the sinus frequency exceeds that of ventricular foci.

The administration of antiarrhythmics may cause precipitated hemodynamic deterioration and should be avoided. The underlying cause must be treated: for example, correct electrolytes, restore myocardial perfusion.

Patients with low cardiac output states (eg, severe biventricular failure) may benefit from the restoration of AV synchrony to restore the atrial drive.

In this case, atropine can be tested in an attempt to increase sinus frequency and AV conduction.

Medical care

Treatment for idioventricular rhythm does not change the prognosis. The most important therapy for patients with idioventricular rhythm is to treat the underlying etiology.

The idioventricular rhythm is usually tolerated hemodynamically and self-limited; Therefore, it rarely requires treatment.

Occasionally, patients may not tolerate idioventricular rhythm due to:

(1) Loss of atrial-ventricular synchrony,

(2) Relative fast ventricular rate, or

(3) ventricular tachycardia or degenerated ventricular fibrillation of idioventricular rhythm (extremely rare).

Under these situations, atropine can be used to increase the underlying sinus rate to inhibit the idioventricular rhythm.

Other treatments for idioventricular rhythm, which include isoproterenol, verapamil, antiarrhythmic drugs such as lidocaine and amiodarone, and atrial pacing are only occasionally used nowadays.

Patients with an idioventricular rhythm should be treated mainly for its underlying causes, such as Digoxin toxicity, myocardial ischemia and diseases of the heart structure.

Beta-blockers are often used in patients with myocardial ischemia-reperfusion and cardiomyopathy. The transfer to an advanced care center depends on the associated conditions.