Clinical Presentation and Diagnosis

Suspect atrial fibrillation when the pulse is “irregularly irregular.” Heart sounds may vary in intensity, a pulse deficit may be present, and the cardiac impulse is markedly variable. The ECG shows chaotic fibrillatory waves of varying amplitude, morphology, and duration, causing variation of the baseline. The RR interval is irregularly irregular. The atrial rate is generally >350 bpm, while the ventricular rate varies between 100 and 200 bpm (Figure 3.1). Sporadic aberrant ventricular conduction can result in random wide QRS complexes.

Figure 3.1 Atrial fibrillation.

ED Management

Treatment can usually be delayed until the patient is admitted to an intensive care setting, where therapy is aimed at control of ventricular rate, conversion to sinus rhythm, and prevention of stroke. However, in the ED, treat acute atrial fibrillation associated with a rapid ventricular rate and signs of hemodynamic compromise with synchronized cardioversion (0.5–2 J/kg).

If the patient is hemodynamically stable, consult a pediatric cardiologist before initiating pharmacologic cardioversion, which can most frequently be accomplished with amiodarone, sotalol, or procainamide. Rate control is best accomplished with diltiazem, digitalis, or esmolol. However, digitalis and verapamil are contraindicated if the patient is known to have WPW syndrome, since they may facilitate conduction through an accessory AV connection, leading to ventricular fibrillation.

Although atrial thrombus is uncommon in children with atrial fibrillation, give anticoagulation prior to cardioversion if the fibrillation has lasted for >48 hours. To document the presence of a thrombus, obtain a standard transthoracic echocardiogram, and if no thrombus is detected, a transesophageal study.

Indications for Admission

• 
  

  Acute onset of atrial fibrillation

  
  
• 
  

  Chronic atrial fibrillation with an increase in ventricular rate requiring treatment with a new anti-arrhythmic medication

  
  
• 
  

  Intracardiac thrombus documented on echocardiogram

Clinical Presentation and Diagnosis

Since normal hemodynamics are generally maintained, ST is usually an incidental finding in a patient with a noncardiac disease process. The rate is generally between 100 and 180 bpm, although in infants the rate may reach 240 bpm.

Sinus tachycardia must be differentiated from supraventricular tachycardia, in which the rates are generally faster with little to no variability and the QRS complexes may not be preceded by recognizable P-waves of sinus origin. In some cases of SVT, the QRS complexes may follow abnormally directed P-waves. Increasing the ECG paper speed to 50 mm/second may help to identify normal P-waves.

ED Management

Most often, ST is encountered in the settings mentioned above, so therapy is directed toward identifying and treating these conditions.

Clinical Presentation

The presentation depends on the age of the patient, the rate and duration of the tachycardia, and whether there is associated heart disease. Common clinical findings include palpitations, shortness of breath, chest pain, respiratory distress, dizziness, syncope, irritability, pallor, and poor feeding in infants. The heart rate is usually between 150 and 300 bpm. Heart failure is uncommon in patients >1 year of age and is usually associated with congenital heart disease, SVT for >24 hours, and heart rates >200 bpm.

Diagnosis

The electrocardiogram in SVT typically reveals a narrow complex tachycardia at a rate of 150–300 bpm. The P-wave may not be seen; it may be inverted just after the QRS complex; or it may precede the QRS, but have an abnormal axis (negative in leads I or AVF). The ventricular complexes are usually normal in contour, although aberrant rate-dependent conduction can cause slight widening. In SVT the atrial rate is 180–240 bpm, with 1:1 AV conduction and a fixed RR interval (Figure 3.2).

Figure 3.2 Supraventricular tachycardia.

Supraventricular tachycardia must be differentiated from ST. In the latter, the rate is usually <180 bpm (240 bpm in infants), a P-wave with normal axis precedes the QRS complex, and some variation in the RR interval may be present.

Supraventricular tachycardia with wide QRS complexes due to aberrant conduction may be difficult to differentiate from ventricular tachycardia. Ventricular tachycardia is suggested by the presence of atrioventricular dissociation, “fusion beats” (when the sinus and ventricular beats coincide to produce a hybrid beat), “capture beats” (when a conducted sinus beat transiently captures the ventricles to produce a narrow QRS complex beat), and very broad QRS complexes (>160 ms). In addition the patient will appear sicker, and possibly the tachycardia will be slower. Assume that all wide complex tachycardias in children are ventricular tachycardia unless the diagnosis of SVT is absolutely certain.

ED Management

Perform a history and physical examination, carefully evaluate the patient’s hemodynamic status, and continuously monitor the ECG and blood pressure. Congestive heart failure or hemodynamic compromise are indications for rapid termination of the arrhythmia with DC cardioversion. After successful conversion to a sinus rhythm, obtain a complete ECG looking for WPW and refer the patient to a pediatric cardiologist.

Vagal Maneuvers

Vagal nerve stimulation increases the effective refractory period of the AV node, thus interrupting the reentrant circuit. Continuously monitor the ECG when vagal maneuvers are attempted. If successful, the tachycardia breaks abruptly and is replaced by a normal sinus rhythm (Figure 3.3). Transient slowing of the ventricular rate suggests that either sinus tachycardia or atrial flutter (Figure 3.4) was misdiagnosed as SVT. Do not use eyeball pressure, which can cause retinal detachment. Gagging and inducing vomiting can be effective, but may lead to aspiration in infants or agitated patients. Commonly employed vagal techniques include the following.

Figure 3.3 SVT response to treatment.

Figure 3.4 Atrial flutter.

Eliciting the Diving Reflex. Submerge the face of an older child in ice-cold water or place an ice bag with equal volumes of ice and water over the entire face for 10–20 seconds.

Unilateral Carotid Massage. Perform the massage at the junction of the carotid artery and the mandible. This is much more likely to be successful in the older child or adolescent.

Valsalva Maneuver. Ask the patient to “bear down,” or “strain,” as if attempting to move his or her bowels. If this is unsuccessful, have the patient stand on his or her head for 15–30 seconds.

Cardioversion

Synchronous cardioversion is indicated when there is hemodynamic compromise (heart failure, shock, acidosis) or, rarely, if other treatment modalities have failed. The dose is 0.5–1 J/kg, which can be repeated, doubling the dose to a maximum of 2 J/kg. Sedate older patients with midazolam (0.1 mg/kg IV) prior to cardioversion. To prevent ventricular dysrhythmias, give lidocaine (1 mg/kg IV) to digitalized patients prior to attempting cardioversion. Prior to cardioversion, be certain of synchronized mode setting, to avoid precipitating a potentially lethal ventricular arrhythmia.

Conversion to sinus rhythm using vagal maneuvers, adenosine, verapamil, and/or cardioversion is within the realm of the ED physician. If the SVT is refractory, consult with a pediatric cardiologist who will determine the choice of second-line medications. Also consult after conversion is accomplished, to arrange appropriate evaluation and follow-up. It is imperative that a rhythm strip be running at the time of either adenosine infusion or cardioversion to document termination of the SVT, as this will aid in the categorization of the SVT subtype and is crucial in the prompt detection of degeneration of the rhythm. The Pediatric Advanced Life Support algorithms for tachycardia with adequate and poor perfusion are summarized in Figures 3.5 and 3.6.

Figure 3.5 PALS algorithm for tachycardia with adequate perfusion.

Figure 3.6 PALS algorithm for tachycardia with poor perfusion.

Follow-up

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  SVT without hemodynamic compromise, terminated in ED: consult a pediatric cardiologist to determine appropriate follow-up

Indications for Admission

• 
  

  SVT causing hemodynamic compromise

  
  
• 
  

  Initiation of a medication with proarrhythmia potential (flecainide, sotalol, amiodarone)

Clinical Presentation

Most cases are discovered during the routine examination of an asymptomatic patient, when an irregular heart beat is noted. However, some patients complain of chest discomfort, palpitations, chest pain, or syncope.

Diagnosis

Ventricular premature contractions are characterized by bizarre, widened QRS complexes which are not preceded by a P-wave (Figure 3.7). They may occur in a fixed ratio with normal beats (bigeminy 1:1; trigeminy 2:1) (Figure 3.8). They can be uniform (identical electrocardiographic appearance with consistent interval from the preceding QRS) or multiform (dissimilar ECG appearances with varying coupling intervals with the preceding QRS). It is possible for a VPC with a short coupling interval to fall on the T-wave of the preceding normal complex (R-on-T phenomenon) and initiate ventricular tachycardia.

Figure 3.7 Ventricular premature contraction.

Figure 3.8 VPC in trigeminal pattern.

Ventricular premature contractions can also be divided into benign and ominous categories. Benign VPCs are uniform in morphology, with an otherwise normal resting ECG, including the QTc interval, and are not associated with an R-on-T phenomenon or structural heart disease. Benign VPCs can normally be suppressed by exercise, such as 20 seconds of jumping jacks.

Ominous VPCs may be multiform or short-coupled, and may be associated with a prolonged QTc interval, an R-on-T phenomenon, or structural heart disease. Exercise either has no effect or increases the VPC frequency and the number of VPCs can worsen during the recovery phase of activity. Ominous VPCs indicate an increased risk of ventricular tachycardia (three or more consecutive VPCs).

ED Management

Follow-up

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  Benign VPCs: primary care follow-up in 1–2 weeks

Indications for Admission

• 
  

  Ominous VPCs

Clinical Presentation

The symptomatology depends on the rate and duration of the tachycardia and the presence or absence of underlying structural heart disease. Occasional patients are asymptomatic, although chest pain, syncope, and palpitations are common, and lethargy, disorientation, hypotension, and sudden death with hemodynamic collapse can occur.

Diagnosis

Ventricular tachycardia is a wide QRS complex tachycardia. The rate of VT (Figure 3.9) is 120–200 bpm, which is slower than SVT with aberrant conduction. Ventricular tachycardia is suggested by AV dissociation, or QRS morphology that resembles a single VPC present during sinus rhythm elsewhere on the ECG.

Figure 3.9 Ventricular tachycardia.

ED Management

Regardless of the patient’s status, consult a pediatric cardiologist.

Indications for Admission

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  Newly diagnosed or difficult to control VT

  
  
• 
  

  Presumed or documented VT with long QT syndrome

Clinical Presentation

Patients with ventricular fibrillation are generally unresponsive and pulseless.

Diagnosis

In ventricular fibrillation (Figure 3.10) there is a wavy, sinusoidal line, without any true QRS complexes.

Figure 3.10 Ventricular fibrillation.

ED Management

If the VT degenerates into ventricular fibrillation, immediately defibrillate using 2 J/kg. If unsuccessful, double to 4 J/kg for three consecutive defibrillations. If unsuccessful, also give IV lidocaine (1 mg/kg) alternating with epinephrine (0.1 mL/kg of 1:10,000 IV or 0.1 mL/kg of 1:1000 ET). If fibrillation recurs, start a lidocaine continuous infusion (20–50 mcg/kg/min).

Indications for Admission

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  Any patient who survives after treatment for ventricular fibrillation

Bibliography

Cannon BC, Snyder CS. Disorders of cardiac rhythm and conduction. In Allen HD, Shaddy RE, Penny DJ, Feltes TF, Cetta F (eds.) Moss and Adams’ Heart Disease in Infants, Children, and Adolescents, Including the Fetus and Young Adult (9th edn.). Philadelphia, PA: Lippincott Williams & Wilkins, 2016; 623–654.

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