Fast Rhythms_The Tachycardias

Fast rhythms >100 beats per minute: The Tachycardias

Tachycardias are in the first instance subdivided into those with wide QRS complexes (>0.12s or 3 small boxes on the ECG) and those with narrow QRS complexes.  For simplicity and safety, broad complex tachycardias are generally treated as ventricular in origin.

Monomorphic regular ventricular tachycardia with a broad-

complex QRS complex

     Normal Sinus Rhythm for comparison 

Sinus Tachycardia: 
  There’s fewer than 3 large boxes  between adjacent QRS complexes. QRS complexes are regular and narrow and there’s a normal P-wave before every QRS complex

                                                      Supraventricular tachycardia:

                                               no obvious p-waves, narrow QRS, regular

                                                                       Atrial flutter

    normal rate of ventricular response. Note narrow QRS and saw-toothed atrial flutter waves

Narrow complex tachycardia if regular should be differentiated into sinus tachycardia, supraventricular (atrial) tachycardia, or atrial flutter.  Junctional tachycardias may also fall into this group.

Tachycardias are further subdivided into regular and irregular.  Irregular broad-complex tachycardias with variable morphology on the monitor are treated as “Torsades de pointes”.  Irregularly irregular narrow complex tachycardias with no identifiable p-waves are treated as atrial fibrillation (a. fib).  In addition, atrial flutters are sometimes irregular.  Multifocal atrial tachycardias may also fall into this group.

Polymorphic irregular ventricular tachycardia, with broad-

complex QRS complexes all of which appear different.

           Atrial fibrillation: 
note irregularly irregular narrow - complex tachycardia, and absence of normal P-waves. There are fibrillatory f waves on the ECG isoelectric line.

Management of STABLE tachycardias:

If narrow complex regular tachycardias can be distinguished as sinus tachycardia, supraventricular tachycardia, or atrial flutter, treatment should be tailored to the specific rhythm.

If these rhythms cannot be distinguished on screen or on an ECG strip, empirical treatment using vagal manoeuvres and IV adenosine may slow the rhythm sufficiently to allow specific rhythm identification.

SINUS TACHYCARDIA: treatment is of the cause. 

SUPRAVENTRICULAR TACHYCARDIA: vagal manoeuvres (eg blowing into syringe followed by trendelenberg) should be tried initially.  Following ANY treatment or intervention, a full set of vital signs should be rechecked, starting with the pulse.  If vagal manoeuvres fail, the patient may be treated with adenosine 6mg by rapid IV injection followed by a 20ml saline flush.  Make sure the patient is not a brittle asthmatic or on drug therapy that may interfere with adenosine prior to treatment*.  If 6mg adenosine fails, 12mg may be tried.  The half-life of adenosine is approximately 10 seconds, so rapid administration is imperative.  Because of this short half-life, alternative drug therapy with either beta-blockers or calcium channel blockers may be considered if adenosine fails to abort the arrhythmia.  Request expert help before progressing beyond the adenosine steps.

ATRIAL FLUTTER: Considerations in the management of atrial flutter are the same as for management of atrial fibrillation. See below.

ATRIAL FIBRILLATION: This is one of the commonest arrhythmias seen by healthcare personnel, but management is often difficult.  Seek expert help if a patient presents with atrial fibrillation, because underlying pathologies, chronicity and left ventricular function will all impact on patient management.  As it is usually difficult to ascertain how long the patient has been in atrial fibrillation, initial recommended management is rate control with either a beta blocker (eg metoprolol 2.5-5mg by slow IV injection) or calcium channel blocker (eg diltiazem, verapamil), and commence anticoagulation.  If the patient becomes unstable, there may be no choice other than to perform synchronised cardioversion as a life-saving measure.  If time permits, a trans-oesophageal echo should be performed to rule out any thrombus in the left atrial appendage, and the patient should be covered with a heparin bolus.

SUMMARY:

·         If stable: rate control with beta blocker or calcium channel blocker

·         If unstable: synchronised cardioversion

Additional considerations with atrial fibrillation are left ventricular function (if LV function poor, consider treatment with digoxin, which is a positive inotrope) and length of time present (avoid synchronised cardioversion unless critically ill because of risk of embolization causing stroke.  Similarly, avoid chemical cardioversion with amiodarone if a. fib present >48hours). 

VENTRICULAR TACHYCARDIA – MONOMORPHIC:  A single dose of 6mg adenosine can be used to differentiate SVT with aberrancy from ventricular tachycardia in broad complex, regular, monomorphic tachycardias.  However, this may be dangerous in certain types of broad-complex tachycardia (eg very rapid atrial fibrillation with delta wave: Wolff-Parkinson-White syndrome), and establishing whether a very rapid ventricular tachycardia is regular or monomorphic may be difficult on ECG.  Broad-complex tachycardias may be treated safely as ventricular tachycardias.

Stable ventricular tachycardia may be treated with 150mg amiodarone in 5% dextrose, administered over 10-20 minutes.  As amiodarone has a vasodilatory effect and can drop the blood pressure markedly, the slower administration is safer.  Lignocaine, procainamide or sotolol are other drugs that may be considered as first-line therapy; procainamide and sotolol should be avoided with prolonged QT.  Polypharmacy should be avoided, so choose your drug and stick with it until expert help arrives.

VENTRICULAR TACHYCARDIA – POLYMORPHIC:  polymorphic VT is frequently associated with hypomagnesaemia, therefore serum chemistry should be checked and corrected.  MgSO4 1-2g by slow IV injection may be given instead of amiodarone.

Management of UNSTABLE tachycardias:

Management of unstable sinus tachycardia is of the cause.

Unstable monomorphic VT, SVT, atrial flutter and atrial fibrillation may all be treated with synchronised cardioversion.  In this procedure, a low-energy synchronised shock is delivered on the R wave in an attempt to return the patient to sinus rhythm.  Failure to synchronise may cause the shock to be delivered on the T wave, which may precipitate ventricular fibrillation and cardiac arrest.  Because the machine has to hunt for the R wave before the shock is delivered, there may be a delay between pressing the shock button and delivery of the shock.  For this reason, one needs to continue to press the shock button and maintain clearance until the shock is delivered.  This is a painful procedure, so if time and patient condition allows, an anaesthetist should be called, and the patient should be sedated, with appropriate respiratory management.

Narrow complex regular rhythms: cardioversion dose may start at 50J, and if unsuccessful the energy may be increased in 50J steps for subsequent cardioversions.  The rhythms treatable with 50J are SVT and atrial flutter

Broad complex regular rhythms require higher doses of energy to convert.  Cardioversion of monomorphic VT should commence at 100J.

Narrow complex irregular rhythm cardioversion requires higher doses of energy.  Doses for atrial fibrillation are 120-200J, depending on machine.

Broad complex irregular tachycardia (polymorphic VT) may not respond to synchronised cardioversion because the defibrillator may not be able to identify the r wave, on which synchronised cardioversion is usually delivered.  Therefore, an unsynchronised (defibrillation) shock may be  required to abort polymorphic VT

To perform synchronised cardioversion, the following steps should be performed:

1.  Call anaesthetist to administer sedation and manage airway if time permits, but this should not   delay cardioversion in a critically ill patient.  Call cardiology (ie SEEK EXPERT HELP)
2.  Place pads on patient’s chest
3.  Select joules appropriate to rhythm
4.  Press “Sync”
5.  Run a strip showing that Sync mode is working, and that markers co-incide with R waves
6.  Charge the machine. 
7.  Remove oxygen.
8.  Clear the patient.
9.  Deliver synchronised cardioversion.
10.  Take “Sync” mode off if it has not gone off automatically, and immediately check patient’s pulse 

Possible outcomes:

•        If pulseless with shockable rhythm: defibrillate immediately and call a code.
•        If pulseless with non-shockable rhythm: commence CPR and call a code
•        If pulse present: look at monitor to see if sinus rhythm present.  If cardiovertible            rhythm persists, check full vitals, and prepare to cardiovert at higher energy
•        If sinus rhythm present: check vitals, refer to cardiology for review.