BASIC RHYTHM INTERPRETATION
Electrocardiograms (ECGs) of normal infants and children are different from those of normal adults. Neonates and infants will demonstrate right ventricular (RV) dominance related to the relative hypertrophy of the RV caused by the fetal circulation. Left ventricular (LV) dominance develops over the course of childhood.
Sequence of Interpretation: Specific order is less important than having your own systematic approach to rhythm interpretation (Figure 33-1). Here is one example:
Rate: Heart rate
Clinical Tip: Estimated HR = 300 / # of big boxes
Rhythm: Sinus or nonsinus
Clinical Tip: Normal sinus rhythm requires the presence of:
P before every QRS
Regular PR interval
NL P wave axis (0–90 degrees) – P wave upright in I and aVF
Axes: QRS axis, T wave axis. An upright wave in any given lead means the vector forces travel towards that lead.
Intervals: Measure the PR, QRS, QTc intervals
Morphology: P wave amplitude and duration, QRS amplitude and duration, presence of abnormal Q waves, ST and T wave morphology
Telemetry: Continuous monitoring of the cardiac rhythm is standard of care in the cardiac intensive care unit (CICU)
Cardiac monitoring is used to identify pathologic rhythms in patients at risk for arrhythmia.
Real-time cardiac monitoring is not an ECG. Full interpretation of axis and morphology cannot be performed due to differences in electrode positioning compared to standard 12-lead ECG.
Continuous cardiac monitoring is indicated in patients who have undergone cardiac surgery; have a history of heart failure or arrhythmias; or have been admitted to the ICU for major trauma, acute respiratory failure, shock, pulmonary embolus, renal failure with electrolyte abnormalities, or toxic ingestion. Also used for monitoring in patients receiving proarrhythmic medications.
Sinus Tachycardia: An elevated heart rate for age with the rhythm still originating from the sinus node. May be caused by cardiac pathology or systemic disease. Treat underlying cause.
Premature Beats: Premature beats are common in patients admitted to the PICU (Figure 33-2).
Premature atrial contractions (PACs)
Description: An early heartbeat caused by premature activation of atrial tissue outside of the sinus node.
Appearance: P wave with an abnormal morphology will occur sooner than the anticipated sinus beat. This may be obscured by the preceding T wave. The PR interval may be prolonged. If the beat is very early, the QRS complex may be abnormally wide (PAC with aberrancy) or even absent (nonconducted PAC).
Treatment: Usually no treatment necessary for isolated PACs.
Premature ventricular contractions (PVCs)
Description: An early heartbeat caused by premature activation of ventricular tissue.
Appearance: Wide QRS complex will occur sooner than the anticipated sinus beat. T wave typically points in the opposite direction. Multiple PVCs can occur at regular intervals (bigeminy, trigeminy) or in a row (couplets, triplets) and can be uniform (monomorphic) or variable in morphology (polymorphic or multifocal).
Treatment: Treat underlying cause. In children with otherwise normal hearts, isolated monomorphic PVCs often do not require treatment. Symptomatic, frequent, or sustained ventricular ectopy may require intervention (see “Ventricular Tachycardia” later).
Clinical Tip: Both PACs and PVCs can have a wide QRS. With PACs there is typically an incomplete compensatory pause (the length from the beat preceding the PAC to the beat following is less than the length of two normal cycles). With PVCs a complete compensatory pause frequently occurs (the length from the beat preceding the PVC to the beat following is the same as that of two normal cycles). In other words, a PAC will typically “reset” the sinus cycle length, whereas a PVC usually does not.
Atrioventricular reentrant tachycardia (AVRT):
Description: Most common type of SVT in children. Reentrant circuit formed using the AV node and an anatomically separate accessory pathway. If the accessory pathway has anterograde conduction properties, the patient will demonstrate ventricular preexcitation (Wolff-Parkinson-White [WPW] pattern) in sinus rhythm (Figure 33-3B).
Appearance: Paroxysmal onset and termination with fast, regular heart rate. If a P wave is visible, it will be retrograde (just after the QRS complex).
Clinical Tip: QRS is usually narrow. If the reentrant circuit conducts down the atrioventricular (AV) node and up the accessory pathway (orthodromic, most common), the QRS will be narrow (Figure 33-3D). If the reentrant circuit conducts down the accessory pathway and up the AV node (antidromic, less common), the QRS will be wide (Figure 33-3E). The QRS may also be wide if there is aberrant conduction.
Acute Termination: Vagal maneuvers, adenosine, rapid atrial pacing (temporary pacing wires or transesophageal pacing leads).
Unstable SVT: Synchronized cardioversion.
Incessant or recurrent SVT: Beta blockers, sodium channel blockers (procainamide acutely, flecainide for chronic/refractory), or amiodarone. Avoid digoxin if pre-excitation present.
AV nodal reentrant tachycardia (AVNRT):
Description: Rare in infants. More common in older children. Reentrant circuit formed within the AV node due to the presence of dual AV nodal pathways: one with fast and the other with slow conduction properties (Figure 33-3F). Most often, the reentrant circuit conducts down the slow pathway and up the fast pathway (typical).
Appearance: Heart rate is usually rapid and regular. Rapid onset and termination (paroxysmal). In typical AVNRT, the P wave may be invisible because the retrograde P will be hidden in the QRS complex.
Acute Termination: Vagal maneuvers, adenosine, rapid atrial pacing (temporary pacing wires or transesophageal pacing leads)
Unstable SVT: Synchronized cardioversion
Incessant or recurrent SVT: Beta blockers, sodium channel blockers, amiodarone, or digoxin
Junctional ectopic tachycardia (JET)
Description: Most frequently seen in the early postoperative period after surgery for congenital heart disease. Occurs due to activation of an automatic focus in or near the AV node. May result in hemodynamic instability due to loss of AV synchrony in patients with poor cardiac reserve.
Appearance: Narrow QRS complex at a rate of 180 to 240 bpm. There may be ventriculoatrial (VA) dissociation (with ventricular rate faster than atrial rate) or retrograde VA conduction.
Clinical Tip: If temporary atrial pacing wires are present, an atrial electrogram may help make the diagnosis.
Clinical Tip: In patients with a bundle branch block at baseline, the QRS may be wide, making it difficult to distinguish from ventricular tachycardia.
Decrease sympathetic stimulation: Wean inotropes if possible, antipyretics, therapeutic cooling, avoid acidosis, initiate sedation/paralysis.
Drugs that decrease automaticity: Procainamide or amiodarone.
Pace the atrium at a rate faster than the junctional tachycardia to restore AV synchrony. Unlike reentrant SVT, this will not break the tachycardia.
Ectopic Atrial Tachycardia (EAT)
Description: Tachycardia triggered by an abnormal focus within the atrium. Because it is often incessant and relatively slow tachyarrhthmia, it may lead to associated cardiac dysfunction.
Appearance: Often gradual onset and resolution (warm-up and cool-down). Although it may appear similar to sinus tachycardia, P wave morphology will differ from normal sinus appearance. PR interval may be prolonged.
Clinical Tip: Like sinus rhythms, the heart rate (HR) in EAT will increase in response to catecholamines.
Decrease sympathetic stimulation: Wean inotropes if possible, antipyretics, therapeutic cooling, avoid acidosis, increase sedation/paralysis.
Drugs that slow conduction: Digoxin, beta blockers, amiodarone.
Drugs that decrease automaticity: Sodium channel blockers.
Description: Reentrant circuit formed within the atrium itself that triggers ventricular activation at intervals that are multiples of the atrial circuit. The atrial rate is fast enough that not every P wave will be able to be transmitted through the AV node.
Appearance: Classic sawtooth pattern may be visible beneath the QRS complexes. Atrial rate typically approaches 300 bpm. AV nodal block results in ventricular activation in a 2:1, 3:1, 4:1, etc., pattern. QRS will be narrow and may be regular (if consistently conducting at a particular ratio) or irregular (if variably conducting).
Clinical Tip: Although adenosine will not break the tachycardia, it may unmask difficult-to-see flutter waves.
Clinical Tip: Intra-atrial reentrant tachycardia (IART) is a reentrant atrial rhythm that may be seen in patients who have undergone prior congenital heart surgery. Atrial rate is often slower, and sawtooth pattern may be absent.
Treatment: Must first assess duration of arrhythmia. Prolonged (>24–48 hr) atrial flutter is associated with formation of intracardiac thrombi. May need transesophageal echo prior to therapy to assess risk of clot embolization.
Cardioversion: Synchronized cardioversion or rapid atrial pacing; drugs that decrease automaticity: class I and class III antiarrhythmics (ex: procainamide, ibutilide).
Clinical Tip: Procainamide’s anticholinergic properties may enhance AV nodal conduction and lead to a 1:1 ventricular response and severe tachycardia, especially as the flutter circuit slows. Consider pre-administration of a beta blocker or digoxin to avoid this effect.
Rate Control: Drugs that slow AV conduction: beta blocker, calcium channel blocker, digoxin, amiodarone.
Anticoagulation: IV anticoagulation if concern for intracardiac thrombus.
Description: Chaotic atrial activation resulting in irregular activation of the ventricle. Relatively rare in young, healthy patients.
Appearance: Irregularly irregular rhythm without clear P waves.
Clinical Tip: QRS may be wide in the presence of an accessory pathway (WPW) that can conduct antegrade to the ventricle. Risk of deterioration to ventricular fibrillation and sudden death in these patients.
Treatment: Must first assess duration of arrhythmia. Prolonged (>24–48 hr) atrial fibrillation is associated with formation of intracardiac thrombi. May need transesophageal echo prior to therapy to assess risk of clot embolization.
Cardioversion: Synchronized cardioversion; drugs that decrease automaticity: Class I (procainamide, flecainide) and class III antiarrhythmics (ex: sotalol, ibutilide).
Clinical Tip: Avoid digoxin and calcium channel blockers in patients with atrial fibrillation and WPW, as this may enhance conduction down the accessory pathway.
Rate Control: Drugs that slow AV conduction: Beta blocker, calcium channel blocker, digoxin, amiodarone.
Anticoagulation: IV anticoagulation if concern for intracardiac thrombus.
Multifocal Atrial Tachycardia (MAT)
Description: Tachycardia results from multiple ectopic foci within the atrium. Most commonly seen in patients with underlying systemic critical illness (respiratory failure, pulmonary embolism, sepsis, etc.).
Appearance: Irregular rhythm with three or more separate non-sinus P wave morphologies. Variable PR, PP, and RR intervals.
Treat underlying systemic illness.
Beta blockers, drugs that decrease automaticity (class Ia, Ic, or III), amiodarone.
Ventricular tachycardia (VT) (Figure 33-4):
Description: Series of three or more PVCs. VT that lasts >30 seconds is labeled “sustained.” Although VT can be benign, it is often associated with ventricular dysfunction/cardiomyopathy, metabolic/electrolyte abnormalities, or toxic exposures.
Appearance: Usually complete VA dissociation. P waves may be absent or buried in QRS. HR typically 120 to 200 bpm. Wide QRS complex will have a distinct morphology compared to sinus QRS. Uniform QRS morphology in VT is monomorphic. Variable QRS morphology is polymorphic.
Clinical Tip: Torsades de pointes is a form of polymorphic VT caused by a prolonged QT interval. The QRS complex repetitively twists around the baseline. If sustained, will deteriorate into ventricular fibrillation.
Correct reversible causes (acidosis, electrolyte abnormalities, etc.).
Pulseless VT: Defibrillation and PALS algorithm (see Chapter 7).
Unstable VT: Synchronized cardioversion.
Stable VT: Amiodarone, beta blockers, sodium channel blockers.
Torsades de pointes: IV magnesium, remove QT-prolonging agents, correct electrolytes, PALS algorithm.
SVT with aberrancy:
Description: Rate-dependent bundle branch block that results in a wide QRS complex. Can be seen in particularly rapid SVT or in patients with conduction abnormalities.
Appearance: See “Narrow Complex” earlier.
Clinical Tip: SVT with aberrancy can be extremely difficult to distinguish from VT. VA dissociation (i.e., more QRS complexes than P waves) is diagnostic of VT. Generally, a wide complex rhythm should be treated like VT until proven otherwise.