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A4. Management of acute rhythm disturbances

Arrhythmias are important for three reasons:

  • They cause suboptimal contraction, reducing cardiac output
  • They may predispose to thromboembolism
  • The arrhythmia may worsen, causing cardiac arrest

Evaluation

  • Is there electrical activity at all?
  • How much is the ventricular rate?
  • Is the rhythm regular or irregular?
  • Evaluation of QRS – is it wide or narrow? – limit is 120 ms
  • Is there atrial activity?
  • Is there a connection between P waves and QRS complexes?
  • Is the patient clinically and haemodynamically stable or unstable?
    • Are signs of peri-arrest (topic 15) present?

Bradyarrhythmias

Bradyarrhythmias are arrhythmias characterised by bradycardia, a ventricular heart rate < 60/min. The most common examples are sinus bradycardia and sick sinus syndrome. Bradyarrhythmias can be life-threatening if the heart rate is too low to sustain cardiac output. They can also degenerate into asystole, causing cardiac arrest. Short-lived paroxysmal bradyarrhythmias can cause syncope.

Types

Etiology

Acute management

If bradyarrhythmias are severe enough to cause haemodynamic instability, atropine (0,5 mg) can be given to increase the heart rate. Atropine can be repeated up to 3 mg. As a second choice, isoprenaline or adrenaline can be given. Transcutaneous pacing may also be used, where pads applied externally to the chest pace the heart like a pacemaker.

Tachyarrhythmias

Tachyarrhythmias are arrhythmias characterised by tachycardia, a heart rate < 60/min. The most common examples are sinus tachycardia and supraventricular tachycardias like atrial fibrillation, AVNRT, and AVRT.

Clinically we distinguish wide complex tachycardias and narrow complex tachycardias based on the width of the QRS complex on the ECG. Tachycardias with wide QRS complexes are ventricular in origin or supraventricular with a concomitant bundle branch block which widens the QRS. Narrow complex tachycardias always originate supraventricularly (from the sinus node or atria). In the acute setting it can be difficult or impossible to determine the exact type of tachycardia based on the ECG, so acute tachyarrhythmias are managed according to whether they are wide complex or narrow complex.

Tachyarrhythmias can be life-threatening if the heart rate is so high that the ventricles don't have enough time to fill in diastole, causing reduced cardiac output and cardiogenic shock. They can also degenerate into ventricular fibrillation or ventricular tachycardia, causing cardiac arrest. Short-lived paroxysmal tachyarrhythmias can cause syncope.

When a patient has a tachyarrhythmia, it's important to feel for a pulse. Pulseless tachyarrhythmia is cardiac arrest and requires cardiopulmonary resuscitation.

Types

Etiology

Clinical features

Tachyarrhythmias can be anywhere from asymptomatic to causing haemodynamic instability and cardiac arrest. Palpitation is a common symptom, as is dizziness. Signs of haemodynamic instability include hypotension, altered mental status, signs of shock, chest pain, or acute decompensated heart failure.

Acute management

Regardless of whether the tachyarrhythmia is wide or narrow complex, the management for tachycardia which causes haemodynamic instability but has a pulse is electrical cardioversion. The cardioverter is put in synchronised mode and an energy level of 150-200 J in biphasic mode. Cardioversion may be attempted 3 times. If there is no effect, a loading dose (300 mg IV) of the anti-arrhythmic amiodarone can be given. It is never wrong to cardiovert an unstable tachycardia, but if the tachycardia is narrow complex one may consider trying to give adenosine first.

For tachyarrhythmias which do no cause haemodynamic instability, the management depends on the morphology:

  • Regular narrow-complex tachycardia
    • Vagal manoeuvres are attempted first. These may terminate the arrhythmia or at least slow it down enough to identify the specific type of arrhythmia
    • If vagal manoeuvres are insufficient, a bolus of adenosine may be tried and repeated up to 3 times with increasing dosage
    • If vagal manoeuvres and adenose are insufficient, verapamil or a beta blocker may be attempted, or one can attempt electrical cardioversion
  • Irregular narrow-complex tachycardia
    • An irregular narrow-complex tachycardia is usually atrial fibrillation. A beta blocker or calcium channel blocker should be given to reduce conduction through the AV node (negative dromotropic effect)
    • If insufficient, digoxin may be used
  • Regular wide complex tachycardia
    • A regular wide complex tachycardia is a ventricular tachycardia (rather than a supraventricular tachycardia with bundle branch block) until definitively proven otherwise
    • The first choice for regular wide complex tachycardia is amiodarone infusion
    • If one is absolutely certain that the rhythm is supraventricular with bundle branch block rather than ventricular tachycardia (because the patient has known SVT and known bundle branch block, etc.), one can attempt vagal manoueuvres or adenosine
  • Irregular wide complex tachycardia
    • Irregular wide complex tachycardia may be atrial fibrillation with bundle branch block or polymorphic ventricular tachycardia (including torsade de pointes)
    • The ECG should be inspected closely, as well as the patient's older ECGs. If atrial fibrillation with BBB is currently suspected, treat as for irregular narrow complex tachycardia
    • If one cannot say for sure that the rhythm is atrial fibrillation, magnesium (2 g IV) should be given for presumed torsade de pointes

If there is no pulse, cardiopulmonary resuscitation must be initiated.

Vagal manouevres

Vagal manouevres increase the vagal tone, which may slow down or terminate supraventricular tachycardias. The best vagal manouevre is the modified Valsalva manouevre:

  • The patient is sitting in a semirecumbent position
  • The patient is asked to exhale forcefully against a closed glottis or a syringe for 15 seconds
  • The patient is rapidly laid back down into supine position and the legs are elevated to 45 degrees

This manouevre increases the arterial pressure in the carotid sinuses and aortic arch, which triggers the baroreceptor reflex, which stimulates parasympathetic output to the heart via the vagus nerve. The parasympathetic stimulation produces negative chronotropic and dromotropic effects, mostly on the AV node, which may terminate the tachycardia.

The "standard" Valsalva manoeuvre involves only exhaling forcefully, while the modified version (including lying down and raising legs) is more effective at terminating supraventricular tachycardias and should be used instead.