FIGURE 86.4 Narrow complex tachycardia due to atrial flutter: This shows atrial flutter at 240 BPM Flutter waves are subtle, but may be discerned in a 2:1 ratio to QRS complexes especially in lead V1 through V4 and in the right-sided chest leads V3R and V4R FIGURE 86.5 Atrial flutter with 3:1 and 4:1 atrioventricular block If AV conduction occurs in a 1:1 or 1:2 ratio (as in Fig 86.4 ) adenosine may make flutter waves more visible as seen here Adenosine is absolutely contraindicated in patients with WPW syndrome presenting in atrial fibrillation (i.e., wide complex, irregular rhythm) Blocking the AV node may then cause atrial fibrillation to be conducted rapidly to the ventricle via the accessory connection leading to VF and possibly death Adenosine is relatively contraindicated in heart transplant recipients due to prolonged sinus pauses in the transplanted heart, which is denervated from the autonomic nervous system Besides prolonged asystole, the heart is vulnerable to malignant escape rhythms Starting with one-third the recommended dose, and increasing if necessary may mitigate the effect of adenosine on the transplanted heart Finally, there are rare reports of adenosine causing bronchospasm in asthmatics Wide Complex Regular Tachycardia A wide complex regular tachycardia may be VT, SVT with aberrancy, antidromic WPW, or sinus tachycardia with aberrancy/bundle branch block A quick history including symptoms, previous tachycardia, baseline EKG, and any cardiac surgery or CHD will guide treatment The EKG and rhythm strip should be scrutinized to identify P waves and establish the mechanism of tachycardia Assess for hemodynamic stability and proceed according to the PALS algorithms Adenosine may be given with continuous rhythm strip recording in a nonsinus regular tachycardia Cardiology should be consulted early to guide therapy While VT in adults is commonly due to ischemia secondary to coronary artery disease, in children, ischemic VT is usually due to congenital coronary anomalies or postoperative complications Nonischemic VT may be due to scars in postoperative CHD, ion channelopathies (LQTS, catecholaminergic polymorphic ventricular tachycardia [CPVT] or Brugada syndrome), cardiomyopathies (myocarditis, DCM, HCM, and arrhythmogenic right ventricular dysplasia [ARVD]), cardiac tumors, or drugs Idiopathic VF is diagnosed after cardiac arrest when no cause for VF is identified in spite of a complete workup There are two types of monomorphic VT commonly encountered in the normal heart One is VT arising from the RVOT (LBBB, inferior axis) and the other is Belhassen VT a left fascicular tachycardia (RBBB and left axis) Both are relatively benign and may be treated with medication or cured by catheter ablation Belhassen VT usually responds to verapamil Scars in the heart from CHD surgery may provide a more malignant substrate for VT as can electrolyte and metabolic disturbances (acidosis) When wide complex tachycardia is only 15% to 20% faster than the underlying sinus rhythm, it is called idioventricular tachycardia This is generally a benign condition and should be evaluated by a cardiologist Management/Diagnostic Testing of Wide Complex VT The EM provider must be able to identify, record, and treat VT in the pediatric population Generally, wide complex tachycardia is assumed to be VT, although a few other rhythms may look wide For the differential diagnosis, see Table 86.7 and Figure 86.6 The first step is to assess hemodynamic stability If the patient is unstable, management is straightforward, with rapid defibrillation and attention to ABC’s The energy dose for defibrillation is J/kg increasing to J/kg, if necessary Synchronize if VT is organized or monomorphic Do not synchronize defibrillation of VF If at all possible, an EKG should be performed before, during, and after conversion The origin of VT may be discerned from the morphology of the QRS on EKG This information will be useful in long-term management of the dysrhythmia TABLE 86.7 DIFFERENTIAL DIAGNOSIS FOR WIDE COMPLEX TACHYCARDIA Differential diagnosis Description Ventricular P waves slower and not related to QRS, although they tachycardia may be conducted retrograde Sinus tachycardia with Frequently seen in postoperative CHD BBB SVT with aberrancy Usually aberrant for several beats and then narrows (functional BBB) Wolff–Parkinson– Ventricular pre-excitation: usually seen in sinus rhythm White If tachycardia is pre-excited and irregular, not give adenosine Electrolyte P waves precede QRS and rate is not fast disturbance/acidosis Myocardial infarction ST segment changes progress to VT or BBB associated with MI BBB, bundle branch block; CHD, congenital heart disease; SVT, supraventricular tachycardia; VT, ventricular tachycardia; MI, myocardial infarction If wide complex tachycardia is hemodynamically stable and regular, IV access may be obtained and a dose of adenosine administered Some forms of SVT appear wide and will respond to adenosine Conversely, some VT in children is relatively narrow See Figures 86.7 and 86.8 Management/Diagnostic Testing of Channelopathies Long QT presents as syncope due to torsades de pointes (TdP) CPR and airway management are instituted Defibrillation is rapidly performed If patient continues to go back into TdP, magnesium sulfate can be given, 30 to 50 mg/kg/dose over to 20 minutes For adults a dose of to g over to 20 minutes, followed by a drip of 0.5 to g/hr may be used Isoproterenol (Isuprel) infusion may also be effective Avoid amiodarone, as this further prolongs the QT interval Management/Diagnostic Testing of Bradycardia In pediatrics, bradycardia associated with cardiovascular collapse is usually due to respiratory compromise and responds to adequate ventilation Asymptomatic bradycardia is not an emergency A patient with bradycardia due to a primary dysrhythmia may be agitated and combative due to poor cardiac output Care must be taken not to sedate these combative patients because doing so may precipitate cardiac arrest Causes of symptomatic bradycardia include pacemaker malfunction, complete AV block due to Lyme disease, late onset postoperative complication, or idiopathic causes Sinus bradycardia may be due to sick sinus syndrome, drug ingestion (i.e., beta-blocker, sedating medications, opioids, and seizure medications), hypothyroidism, anorexia nervosa with or without cardiomyopathy, myocarditis, or frequent blocked premature atrial contractions (PACs) ( Figs 86.9 and 86.10 ) Infants discovered to have bradycardia due to 2:1 AV block should be assumed to have LQTS until proven otherwise by a pediatric electrophysiologist EKG and long rhythm strip should be obtained These patients should be monitored on telemetry in case TdP develops ... 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