Chapter 82 Arrhythmia (Case 40)
Patient Care
History
• Onset and duration of arrhythmia should be elicited to determine potential for secondary sequelae (myocardial dysfunction, thromboembolism).
• A history of recent viral symptoms should raise concern for myocarditis as the cause of arrhythmia.
Physical Examination
• Heart rate, especially for narrow complex tachycardias, can provide a clue to the etiology of the arrhythmia. Reentrant SVTs are generally faster than sinus tachycardia or ectopic atrial tachycardias (EATs).
• Blood pressure, pulses, and overall perfusion should be monitored closely to assess adequacy of cardiac output. An irregularly irregular pulse is the hallmark of atrial fibrillation.
• Respiratory rate and effort may be increased if pulmonary edema develops as a result of poor cardiac output.
• Cardiac auscultation should focus on the regularity or irregularity of the rhythm and presence of adventitious sounds (murmur, gallop, rub).
Tests for Consideration
• CBC, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP): In the child with possible myocarditis $30
Clinical Entities: Medical Knowledge
| Sinus Tachycardia and Bradycardia | |
|---|---|
| Pϕ | Sinus tachycardia and bradycardia originate from the sinoatrial node, and maintain normal conduction through the heart. Sinus bradycardia can be a manifestation of increased vagal tone, hypothermia, increased intracranial pressure, meningitis, hypothyroidism, anorexia, obstructive jaundice, and medications. Sinus tachycardia may occur in the setting of anemia, dehydration, pain, fever, infection, hypoxia, hypotension, anxiety, myocarditis or cardiomyopathy, hyperthyroidism, ingestion of certain medications, and pheochromocytoma. |
| TP | The child with sinus tachycardia or bradycardia often remains asymptomatic but may experience palpitations, light-headedness, and possibly syncope. |
| Dx | Diagnosis can be made on ECG by identification of P waves preceding each QRS complex and by orientation of the P-wave axis. In sinus rhythm P waves are upright in leads I, II, and aVF. |
| Tx | Treatment is directed by identifying and treating the cause. Medications (atropine, epinephrine) may be needed if bradycardia is severe enough. Very rarely, temporary or permanent cardiac pacing is required if medication fails to adequately improve perfusion. See Nelson Essentials 142. |
| Supraventricular Tachycardia | |
|---|---|
| Pϕ | SVT originating in the atria comprises a large family of arrhythmias. Reentrant tachycardias are perpetuated through accessory bypass tracts that circumvent the atrioventricular node. Ectopic atrial tachycardia (EAT) originates from an atrial focus away from the sinus node and is generally faster than sinus rhythm but slower than SVT. Atrial flutter and fibrillation are rare in children, except those with some forms of acquired heart disease or congenital heart disease. Junctional ectopic tachycardia (JET), a narrow complex tachycardia originating in the atrioventricular (AV) junction, occurs most commonly in postoperative cardiac surgery patients. |
| TP | Children with SVT often experience palpitations and may have chest pain and a fluttering feeling in the neck. Some children experience abdominal pain and nausea or vomiting. Dizziness may precede syncope or near-syncope. If the rate is fast enough, the child may have poor perfusion, delayed capillary refill, and hypotension. |
| Dx | Diagnosis can be made on 12-lead ECG. SVT rates in infants generally range from 220 to 320 beats per minute, and 150 to 250 beats per minute in older children. The ECG demonstrates narrow complex tachycardia. Ectopic atrial tachycardia is marked by P wave morphology, axis, and PR interval that differ from findings on normal sinus ECG. Atrial flutter can be identified by a “sawtooth” pattern of the P waves. In atrial fibrillation, flutter waves may be seen intermittently; however, atrial rate is very irregular. |
| Tx | Treatment is determined by the specific arrhythmia and the patient’s stability or instability. In the stable patient with reentrant tachycardia, one can try vagal maneuvers, such as ice to the face or blowing through an occluded straw. Adenosine can be given if the SVT persists. Synchronized cardioversion should be performed in the hemodynamically unstable patient. The hemodynamically stable patient with atrial flutter or fibrillation should receive anticoagulation and rate control before cardioversion. Medications most commonly given for rate control include calcium channel blockers, beta-blockers, and digoxin (alone or in combination). Treatment of ectopic atrial tachycardia generally begins with beta-blockade. See Nelson Essentials 142. |
| Ventricular Tachycardia | |
|---|---|
| Pϕ | Ventricular tachycardia can be idiopathic in children but also occurs in children with (1) congenital heart disease, (2) cardiomyopathy or myocarditis, (3) tumors or cardiac infiltrates, (4) primary arrhythmias (long QT syndrome, familial ventricular tachycardia), (5) electrolyte abnormalities, (6) medications and toxins (general anesthetics, catecholamines, tricyclic antidepressants, cocaine, and digoxin toxicity), and (7) blunt chest trauma. |
| TP | Palpitations, dyspnea, chest or abdominal pain, dizziness, and syncope or near-syncope are most common in children with rates greater than 150 beats per minute. Sustained arrhythmia can produce signs of congestive heart failure. |
| Dx | ECG features of ventricular tachycardia include wide QRS complexes with either left or right bundle branch block pattern and AV dissociation. Rates of ventricular tachycardia range from 120 to 300 beats per minute in children. |
| Tx | Treatment is determined by the patient’s hemodynamic status. In the stable patient with an identifiable cause that can be corrected, the underlying abnormality should be corrected. If the rhythm persists, patients should be given lidocaine or amiodarone. Patients with cardiac compromise require immediate synchronized cardioversion. Treatment of pulseless ventricular tachycardia follows the same PALS algorithm as ventricular fibrillation. See Nelson Essentials 142. |
| Heart Block | |
|---|---|
| Pϕ | Heart block occurs when conduction of the cardiac impulse from the sinus node to the atrioventricular node, or from the atrioventricular node to the ventricles, is impaired. First-degree AV block, occurs with digoxin toxicity; with inflammatory conditions such as rheumatic heart disease, myocarditis, or Kawasaki disease; with some cardiac malformations; or after cardiac surgery. Second-degree AV block can occur in situations similar to first-degree AV block. Third-degree (complete) heart block is either congenital or acquired. The acquired form results from conditions similar to those causing first-degree AV block and infectious etiologies (Lyme). Maternal connective tissue disease is associated with congenital complete heart block. This can also occur in the setting of L- transposition of the great arteries and heterotaxy syndrome. |
| TP | First- and second-degree AV block are usually asymptomatic. Complete heart block often has hypotension and poor perfusion. Older children can experience exercise intolerance, easy fatigability, syncope, or near-syncope. |
| Dx | Diagnosis of heart block is made by 12-lead ECG. First-degree AV block is identified by prolonged PR interval. Second-degree type I (Wenckebach or Mobitz I) demonstrates progressive prolongation of the PR interval with eventual dropping of a QRS complex. In second-degree type II (Mobitz II), QRS complexes are dropped suddenly, without progressive prolongation of the PR interval. Complete heart block is marked by complete disassociation of P waves and QRS complexes, with the atrial rate faster than the ventricular rate. |
| Tx | Treatment of heart block is similar to that for symptomatic bradycardia (see above). See Nelson Essentials 142. |
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