Pediatric Dysrhythmias - University of New Mexico

Pediatr Clin N Am 53 (2006) 85 ? 105

Pediatric Dysrhythmias

Stephanie J. Doniger, MD, FAAPT, Ghazala Q. Sharieff, MD, FACEP, FAAEM, FAAP

Pediatric Emergency Medicine, Children's Hospital and Health Center/ University of California San Diego, 3020 Children's Way, MC 5075 San Diego, CA 92123-4282, USA

The overall incidence of arrhythmias is 13.9 per 100,000 emergency department (ED) visits and 55.1 per 100,000 pediatric ED visits (children under 18 years of age) [1]. Among children with arrhythmias, the most common dysrhythmias are sinus tachycardia (50%), supraventricular tachycardia (13%), bradycardia (6%), and atrial fibrillation (4.6%) [1].

The presentation of dysrhythmias can serve as a diagnostic challenge to most clinicians because most children present with vague and nonspecific symptoms such as ``fussiness'' or ``difficulty feeding.'' Despite the infrequency and vague presenting symptoms, it is critical to identify and appropriately manage these disorders. When left they are unrecognized and untreated, dysrhythmias can lead to cardiopulmonary compromise and arrest.

The electrocardiogram in pediatrics

The most common reasons for obtaining EKGs in children are chest pain, suspected dysrhythmias, seizures, syncope, drug exposure, electrical burns, electrolyte abnormalities, and abnormal physical examination findings. Of all of these, the most life-threatening findings are those caused by electrolyte disturbances, drug exposure, and burns [2].

Although a complete EKG interpretation is beyond the scope of this chapter, it is advisable to use a systematic approach, with special attention to rate, rhythm, axis, ventricular and atrial hypertrophy, and the presence of any ischemia or

T Corresponding author. E-mail address: sdoniger@ (S.J. Doniger).

0031-3955/06/$ ? see front matter D 2006 Elsevier Inc. All rights reserved.

doi:10.1016/j.pcl.2005.10.004

pediatric.

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Table 1 Pediatric ECG normal intervals

Age

Heart rate (BPM)

PR interval (s)

1st wk 1?3wk 1?2 mo 3?5 mo 6?11 mo 1?2 y 3?4 y 5?7 y 8?11 y 12?15 y 16 y

90?160 100?180 120?180 105?185 110?170 90?165 70?140 65?140 60?130 65?130 50?120

0.08?0.15 0.08?0.15 0.08?0.15 0.08?0.15 0.07?0.16 0.08?0.16 0.09?0.17 0.09?0.17 0.09?0.17 0.09?0.18 0.12?0.20

Courtesy of Ra'id Abdullah, MD, University of Chicago, IL.

QRS interval (s)

0.03?0.08 0.03?0.08 0.03?0.08 0.03?0.08 0.03?0.08 0.03?0.08 0.04?0.08 0.04?0.08 0.04?0.09 0.04?0.09 0.05?0.10

repolarization abnormalities. More specifically, it is essential to interpret pediatric EKG's based on age-specific rates and intervals (Table 1) [3?5]. The EKG can be evaluated further for rhythm, chamber size, and T-wave morphology.

Tachydysrhythmias

Tachycardia is defined as a heart rate beyond the upper limit of normal for the patient's age. In adults, the heart rate is greater than 100 beats per minute (BPM). Tachycardias can be classified broadly into those that originate from loci above the atrioventricular (AV) node (ie, supraventricular), from the AV node (AV node reentrant tachycardias), and from the ventricle. The majority of tachycardias are supraventricular (SVT) in origin. Those that are ventricular in origin are associated typically with hemodynamic compromise [4]. When tachycardia is recognized, step-wise questioning can help evaluate the EKG tracing. Is it regular or irregular? Is the QRS complex narrow or wide? Does every P wave result in a single QRS complex? Once these have been established, the treatment options are considered according to whether the patient has a pulse and the presenting rhythm on EKG (Fig. 1) [6].

Sinus tachycardia

Sinus tachycardia can be differentiated from other tachycardias by a narrow QRS axis and a P wave that precedes every QRS complex. The rate is usually greater than 140 BPM in children and greater than 160 BPM in infants. Sinus tachycardia is typically benign. The pulse rate has been shown to increase linearly with temperature in children older than 2 months of age. For every 18C (1.88F) increase in body temperature, the pulse rate increases by an average of 9.6 BPM [7]. Sinus tachycardia can also be associated with such underlying conditions as

TACHYCARDIA

pediatric dysrhythmias

V- Fib V- Tach

12 LNeoadPuElsCeG 12 Lead ECG

Not V- Fib/ V- Tach Incl. PEA, Asystole

QRS NL (0.08 sec)

DEFIBRILLATION 2J/kg -> 2-4 J/kg -> 4J/kg

CPR, IV,Intubate Epinephrine IV/IO 0.01 mg/kg 1:10,000

DEFIBRILLATION 4 J/kg

Amiodarone^ IV/IO 5 mg/kg OR Lidocaine* IV/IO/TT 1 mg/kg OR Magnesium (Torsades) IV/IO 25-50 mg/kg

DEFIBRILLATION 4 J/kg

Pattern: Drug-CPR-shock (repeat)

Epinephrine IV/IO 0.01 mg/kg 1:10,000

ETT 0.1 mg/kg 1:1000

CPR, IV,Intubate

Epinephrine q 3-5 min

| |

Identify underlying causes PEA:

Hypovolemia

Tamponade

Hypoxia

Tension PTX

H+ (acidosis)

Toxins/poisons

Hypo/Hyperkalemia Thromboembolism

Hypothermia

SVT

UNSTABLE CARDIOVERSION

0.5- 1 J/kg

STABLE Adenosine IV/IO 0.1 mg/kg (max 6 mg)

Adenosine IV/IO 0.2 mg/kg (max 12 mg)

Consider Alternative Medications Amiodarone^ (5 mg/kg IV over 20-60 min) OR Procainamide (15 mg/kg IV over 10- 15 min)

Sinus Tachycardia Treat Underlying Disorder

V- Tach

UNSTABLE CARDIOVERSION

0.5- 1 J/kg

STABLE Amiodarone^ (5 mg/kg IV over 20-60 min) OR Procainamide (15 mg/kg IV over 10- 15 min)

OR Lidocaine* (1 mg/kg IV)

^ For Amiodarone administration: Repeat doses of 1- 5 mg/kg (max imum15 mg/kg/day) may be required depending upon patient stability and clinical scenario.

* For Lidocaine administration: repeat every 5-10 minutes after initial bolus, to total dose 3 mg/kg. After return of perfusion, follow with continuous infusion @ 20- 50 mcg/kg/min.

Fig. 1. Tachycardia algorithm. PEA, pulseless electrical activity; SVT, supraventricular tachycardia; V-Fib, ventricular fibrillation; V-Tach, ventricular tachycardia. (Data from Hazinski M, Zaritsky A, Nadkarini V, et al. PALS provider manual. Dallas (TX): American Heart Association; 2002.)

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hypoxia, anemia, hypovolemia, shock, myocardial ischemia, pulmonary edema, hyperthyroidism, medications (catecholamines), hypocalcemia, and illicit drug use. Most commonly, it is a result of dehydration and hypovolemia [1,4]. Because children augment cardiac output by increasing the heart rate rather than the stroke volume, heart rate increases appear early, whereas hypotension is a late sign of dehydration. Treatment aimed at correcting the heart rate alone may be harmful to the patient because the tachycardia is a compensatory response to sustain adequate cardiac output. For this reason, the treatment of sinus tachycardia is largely targeted at treating the underlying disorder, rather than treating the tachycardia itself.

Ventricular tachycardia

Although it is rare in children, ventricular tachycardia is an important rhythm to recognize and treat promptly. Nonperfusing ventricular rhythms are seen in up to 19% of pediatric cardiac arrests, when sudden infant death syndrome (SIDS) cases are excluded [8]. Although the heart may be contracting and pulses are palpable in some patients who have ventricular tachycardia, those contractions are hemodynamically inefficient and can lead ultimately to syncope and death if left untreated. Furthermore, ventricular tachycardia can decompensate into ventricular fibrillation, which is a nonperfusing, terminal arrhythmia.

Ventricular tachycardia may result from electrolyte disturbances (hyperkalemia, hypokalemia, and hypocalcemia), metabolic abnormalities, congenital heart disorders, myocarditis, or drug toxicity. Other causes include cardiomyopathies, cardiac tumors, acquired heart disease, prolonged QT syndrome, and idiopathic causes.

On electrocardiograms, the QRS complexes have a wide configuration. The QRS duration is prolonged, ranging from 0.06 to 0.14 seconds. Complexes may appear monomorphic with a uniform contour and absent or retrograde P waves. Alternatively, the QRS complexes may appear polymorphic or vary randomly as is seen in torsades de pointes. EKG findings that further support the presence of ventricular tachycardia include the presence of AV dissociation with the ventricular rate exceeding the atrial rate (Fig. 2).

In a patient who has ventricular tachycardia, the urgency of treatment depends on the patient's clinical status. Initially, the airway, breathing, and circulation (ABCs) must be maintained, and it must be determined whether the patient has a pulse and is hemodynamically stable. The American Heart Association has set forth treatment algorithms [6] to facilitate prompt treatment for this potentially fatal rhythm (see Fig. 1).

Ventricular tachycardia with a pulse in an unstable patient warrants immediate synchronized cardioversion at 0.5 to 1 J/kg. It is important to pretreat conscious patients with light sedation (eg, midazolam, 0.1 mg/kg). Pharmacologic interventions include amiodarone (5 mg/kg intravenously [IV] over 20?60 min; maximum single dose, 150 mg; maximum daily dose, 15 mg/kg/d), procainamide (15 mg IV over 30?60 min), or lidocaine (1 mg/kg IV bolus, repeat every

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Fig. 2. Ventricular tachycardia. An example of an extraordinarily fast ventricular tachycardia, with a heart rate of almost 300 BPM. (Courtesy of CDR Jonathan T. Fleenor, MD, Naval Medical Center, San Diego, CA.)

5?10 min, with max total of 3 mg/kg) [9]. When using procainamide, the infusion is stopped once the arrhythmia resolves if the QRS complex widens to 50% over the baseline or if hypotension ensues. Pulseless ventricular tachycardia should be treated as ventricular fibrillation (see below).

After cardioversion, the return to normal sinus rhythm is usually transient. The medication used to achieve sinus rhythm must be given as a continuous infusion using lidocaine (20?50 mg/kg/min), amiodarone (7?15 mg/kg/d), or procainamide (20?80 mg/kg/min [maximum dose of 2 g/24 h]) [6]. In polymorphic ventricular tachycardia, temporary atrial or ventricular pacing may be required. Overall, the treatment goal is to keep the heart rate at less than 150 BPM in infants and less than 130 BPM in older children.

Premature ventricular contractions

A premature ventricular contraction (PVC) is a premature, wide QRS complex that has a distinct configuration and is not preceded by a P wave. They may appear in a pattern of two consecutive PVCs (couplet), an alternating PVC with a normal QRS complex (bigeminy), or in which every third beat is a PVC (trigeminy). The occurrence of three or more consecutive PVCs is considered ventricular tachycardia. The sinoatrial (SA) node maintains a normal conduction pace, and the PVC replaces a normal QRS wave while maintaining a rhythm.

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