350 SECTION IV Pediatric Critical Care Cardiovascular Junctional Ectopic Tachycardia JET immediately following cardiac surgery may be mistaken for third degree AV block; however, on rewarming, ventric[.]
350 S E C T I O N I V Pediatric Critical Care: Cardiovascular Junctional Ectopic Tachycardia JET immediately following cardiac surgery may be mistaken for third-degree AV block; however, on rewarming, ventricular rates approach or exceed 200 beats/min Atrial wires or esophageal electrography confirms the key diagnostic features: AV dissociation with normal QRS and the regular ventricular rate faster than the atrial rate Appropriately timed atrial systoles conducted to the ventricle result in advancement of the tachycardia (without a change in QRS morphology or subsequent pause) If the QRS is normal but the RR interval does not shorten with appropriately timed atrial systoles, JET with retrograde (VA) conduction or third-degree AV block with JET as the escape rhythm should be suspected Infants with JET usually are often severely ill, and b-adrenergic agonists, fever, and endogenous catecholamines accelerate the tachycardia Initial treatment of postoperative JET includes sedation and analgesia, withdrawal of adrenergic stimulants (to the extent possible), and cooling The tachycardia may be suppressed by temporary overdrive (atrial) pacing, by pacing at a rate sufficient to produce 2:1 AV block, or by AVT mode pacing to provide AV synchrony.62 A variety of medications have been used for postoperative JET, including procainamide, lidocaine, dexmedetomidine, and, recently, ivabradine IV amiodarone has been used with perhaps the greatest efficacy.63 Although emergency radiofrequency ablation has been performed in rare instances, aggressive temporizing measures, including extracorporeal membrane oxygenation, appear warranted given the transient nature of this arrhythmia Late Postoperative Arrhythmias Atrial tachycardia and bradycardia are common late sequelae following the Senning and Mustard operations for d-transposition of the great arteries, atrial septal defect closure, and the Fontan procedure for tricuspid atresia and single ventricle.15 Patients with these arrhythmias appear to be at increased risk for sudden death, although whether death is the result of atrial tachycardia itself, associated bradycardia, degeneration to VT, or even nondysrhythmic events remains unclear Likewise, in patients with repaired or palliated CHD, ventricular arrhythmias that are associated with risk for sudden death may develop There seems to be little justification for empirical drug therapy to suppress asymptomatic ventricular arrhythmias in these patients Earlier repair is believed to decrease the incidence of serious problems Still, the relative contributions of postoperative hemodynamic abnormalities, natural history of the unrepaired lesions, and surgical technique to the development of late arrhythmias remain uncertain Similarly, the roles of pacemaker/defibrillator therapy, prospective electrophysiologic study, and antiarrhythmic drug testing are not well established Because both bradycardias and tachycardias develop in many patients, the correlation of symptoms with electrophysiologic abnormality is important in guiding therapy Metabolic Derangements Electrolyte Disturbances Hyperkalemia causes characteristically tall (peaked or tented) T waves with a narrow base with progressive changes at higher concentrations, including decreased P-wave amplitude, QRS prolongation, SA nodal and AV nodal block, and, ultimately, ventricular fibrillation Mild to moderate hypokalemia may cause prominent U waves, diminished T-wave amplitude, T-wave inversion, and fusion of the T wave and U wave, along with increased spontaneous ventricular ectopy and inducible ventricular arrhythmias Arrhythmias caused by hypokalemia are potentiated by catecholamines, and hypokalemia itself potentiates the toxic effects of digoxin and the proarrhythmic effects of drugs associated with drug-induced long QT syndrome.64 Severe hypokalemia is associated with ventricular fibrillation Hypercalcemia produces T-wave inversion and shortens the QT interval Hypocalcemia prolongs the time to the peak of the T wave but not the QT interval itself Isolated calcium abnormalities are uncommon, and arrhythmias caused by such abnormalities are rare, although hypercalcemia may aggravate digitalis toxicity.2 Endocrine Disorders (Thyroid) Hyperthyroidism exerts both sympathetic-like and direct cardiovascular actions that produce sinus tachycardia and atrial fibrillation, but ventricular arrhythmias are uncommon These arrhythmias respond to b-blockers and resolve when the euthyroid state is restored Combination treatment with digoxin potentiates AV nodal block while minimizing negative inotropic effects Hypothyroidism causes sinus bradycardia and AV conduction disturbances; QT interval prolongation is common but rarely associated with torsades de pointes.65 Central Nervous System Injury The most common ECG change associated with CNS trauma and increased intracranial pressure is sinus bradycardia, usually with associated hypertension These bradycardias appear to be vagally mediated and usually respond to atropine However, potentially serious arrhythmias may occur within 24 hours following blunt trauma to the head, subdural hematoma, and subarachnoid hemorrhage QT-interval prolongation is common and, in combination with bradycardia and hypokalemia, may provoke torsades de pointes Hypothermia and Hyperthermia Mild hypothermia can cause a range of reversible ECG changes, including sinus bradycardia; prolongation of the PR, QRS, and QT intervals; and a characteristic secondary deflection on the terminal portion of the QRS (Osborn wave).66 Severe hypothermia may cause more significant bradycardias, including AV block and asystole or VTs and ventricular fibrillation Therapeutic hypothermia is associated with QT prolongation, and torsades de pointes has been reported.67 In contrast, hyperthermia causes sinus tachycardia and may enhance other tachycardias, such as PSVT, ectopic atrial arrhythmias, and especially JET in susceptible patients Acute Myocardial Infarction Acute myocardial infarction is uncommon in young patients but may occur in cases of anomalous origin of the left coronary artery, when there is perinatal stress, following Kawasaki disease, with blunt chest wall trauma, and following cardiac transplantation and the arterial switch procedure It can occur after air embolism in cyanotic CHD or after open-heart operations The diagnosis may be overlooked in infants and children because of the inconsistency of symptoms and relatively poor (60%) clinical recognition by electrocardiography.68 Nevertheless, acute infarction may result in various rhythm disturbances, including sinus bradycardia (as a result of the Bezold-Jarisch reflex), AV conduction disturbances, intraventricular block, and asystole Arrhythmias Resulting From Drug Toxicity Digoxin Digoxin toxicity may cause various arrhythmias and should be suspected in any patient in whom a new arrhythmia develops during digoxin therapy Likewise, digoxin ingestion should be considered in patients with acute arrhythmias, particularly those associated CHAPTER 33 Disorders of Cardiac Rhythm 494 544 611 516 477 444 444 455 444 450 444 411 1538 455 • Fig 33.16 Bidirectional ventricular tachycardia This unusual arrhythmia is seen only in patients with digoxin toxicity and two rare genetic arrhythmia syndromes: Andersen-Tawil syndrome (periodic paralysis and ventricular arrhythmias) and catecholaminergic polymorphic ventricular tachycardia The patient is asymptomatic during this arrhythmia, but patients appear to be at risk for ventricular fibrillation with CNS and gastrointestinal symptoms Accelerated junctional rhythm may be the first arrhythmia seen Progressive AV block is common Sinus bradycardia resulting from either SA node exit block or sinus arrest may occur, as can atrial fibrillation (but usually not atrial flutter) Ectopic atrial arrhythmias may occur Nearly any ventricular arrhythmia may occur, including multiform ventricular extrasystoles, bigeminy, VT (particularly bidirectional VT, otherwise only seen in rare genetic arrhythmia syndromes; Fig 33.16), and ventricular fibrillation.69 In general, digoxin concentrations less than ng/mL are considered nontoxic Neonates usually tolerate levels as high as 3.5 ng/mL Nevertheless, neonates and other ICU patients may be more susceptible to digoxin toxicity because of renal dysfunction, electrolyte imbalances, and hypoxia Hypokalemia, excessive calcium infusions, and rapid sinus rates exacerbate digitalisrelated arrhythmias Purified digoxin-specific Fab antibody fragment, which binds the drug and is eliminated in the urine, is used to treat digoxin toxicity Prophylactic treatment with this preparation should be gauged according to the quantity ingested, time since ingestion, and serum digoxin level Magnesium sulfate is a useful temporizing treatment while specific antibody treatment is being implemented Cardioversion should be reserved for life-threatening tachycardias or those unresponsive to these therapies Cocaine Life-threatening ventricular arrhythmias, cardiac arrest, and myocardial infarction can occur in healthy individuals with normal coronary arteries following cocaine ingestion and in prenatally exposed neonates.70,71 Cocaine produces myocardial ischemia and infarction by inducing severe local coronary vasoconstriction, increasing myocardial-metabolic demand through its potent chronotropic effects, and increasing afterload In infarct models, cocaine directly potentiates arrhythmias induced by catecholamines.72 These factors favor the use of b-adrenergic antagonists as first-line treatment for cocaine-related arrhythmias Additionally, cocaine blocks fast inward sodium channels, similar to class I antiarrhythmic agents.73 QT prolongation and torsades de pointes have been observed Tricyclic Antidepressants and Phenothiazine Phenothiazines and tricyclic antidepressants produce electrophysiologic (and potentially antiarrhythmic) effects similar to quinidine and procainamide They slow conduction velocity in atrial and ventricular tissue, prolong repolarization, and exert anticholinergic effects, accounting for the observed ECG changes of conduction disturbances, prolonged QT intervals and QRS 351 duration, and various tachycardias and bradycardias.74 Sinus tachycardia, atrial tachycardias and VTs, and AV conduction disturbances distal to the AV node occur occasionally during normal therapeutic administration and may reflect individual susceptibility to QT-prolonging agents Arrhythmias commonly follow intentional overdose, resulting in hypotension (due to a-blocking effects), severe anticholinergic effects (neuromuscular and mucosal), seizures, and coma Quinidine and procainamide are contraindicated for tachycardias because of these agents In patients manifesting early cardiotoxicity, arrhythmias may develop to days following ingestion, apparently because of release of tissue stores Therefore, ECG monitoring should be continued for at least 24 to 48 hours after apparent ECG and rhythm normalization and longer if severe arrhythmias are observed Infections Myocarditis may cause atrial tachycardias and VTs or acquired heart block Lyme disease may produce high-grade acute AV block Although AV conduction usually normalizes with appropriate antibiotic therapy, temporary pacing may be required.75 Antibiotic treatment should be instituted on the basis of the history and electrocardiographic findings alone while awaiting confirmatory serology Bacterial endocarditis can cause AV conduction disturbances, particularly when the aortic valve is involved Unstable or persisting conduction abnormalities (.7 days) carry a high risk of mortality (43%–80%) and are indications for early valve replacement.76 Myocarditis may be responsible for some cases of VT in otherwise healthy individuals and may range from chronic ventricular ectopy or tachycardia to fulminant and refractory arrhythmias leading to electromechanical dissociation Chaotic atrial tachycardia may occur in the setting of infection with respiratory syncytial virus, although the cause of this association is unclear Finally, paroxysmal tachycardias of any etiology may be exacerbated by acute infections that cause fever, dehydration, and increased sympathetic tone Short-term modifications of chronic therapy may be necessary, particularly when oral administration becomes impractical Key References Gikonyo BM, Dunnigan A, Benson Jr DW Cardiovascular collapse in infants: association with paroxysmal atrial tachycardia Pediatrics 1985;76:922-926 Kang KT, Potts JE, Radbill AE, et al Permanent junctional reciprocating tachycardia in children: a multicenter experience Heart Rhythm 2014;11:1426-1432 Moore JP, Patel PA, Shannon KM Predictors of myocardial recovery in pediatric tachycardia-induced cardiomyopathy Heart Rhythm 2014;11:1163-1169 Pinto DS Cardiac manifestations of Lyme disease Med Clin North Am 2002;86:285-296 Valsangiacomo E, Schmid ER, Schupbach RW, et al Early postoperative arrhythmias after cardiac operation in children Ann Thorac Surg 2002;4:792-796 Walsh EP, Cecchin F Recent advances in pacemaker and implantable defibrillator therapy for young patients Curr Opin Cardiol 2004; 19:91-96 Weindling SN, Saul JP, Walsh EP Efficacy and risks of medical therapy for supraventricular tachycardia in neonates and infants Am Heart J 1996;131:66-72 The full reference list for this chapter is available at ExpertConsult.com e1 References Valsangiacomo E, Schmid ER, Schupbach RW, et al Early postoperative arrhythmias after cardiac operation in children Ann Thorac Surg 2002;4:792-796 Ramaswamy K, Hamdan MH Ischemia, metabolic disturbances, and arrhythmogenesis: mechanisms and management Crit Care Med 2000;28:N151-N157 Benson DW, Wand DW, Dyment M, et al Congenital sick sinus syndrome caused by recessive mutation in the cardiac sodium channel gene (SCN5A) J Clin Invest 2003;12:1019-1028 Lupoglazoff JM, Denjoy I, Villain E, et al 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Yang T, Roden DM Extracellular potassium modulation of drug block of IKr Implications for torsades de pointes and reverse usedependence Circulation 1996;93:407-411 65 Klein I, Ojamaa K Thyroid hormone and the cardiovascular system N Engl J Med 2001;344:501-509 66 Mattu A, Brady WJ, Perron AD Electrocardiographic manifestations of hypothermia Am J Emerg Med 2002;20:314-326 67 Huang CH, Tsai MS, Hsu CY, et al Images in cardiovascular medicine Therapeutic hypothermia-related torsades de pointes Circulation 2006;114:e521-e522 68 Towbin JA, Bricker JT, Garson Jr A Electrocardiographic criteria for diagnosis of acute myocardial infarction in childhood Am J Cardiol 1992;69:1545-1548 69 Hastreiter AR, van der Horst RL, Chow-Tung E Digitalis toxicity in infants and children Pediatr Cardiol 1984;5:131-148 70 Kloner RA, Rezkalla SH Cocaine and the heart N Engl J Med 2003;348:487-488 71 Frassica JJ, Orav EJ, Walsh EP, et al Arrhythmias in children prenatally exposed to cocaine Arch Pediatr Adolesc Med 1994;148:11631169 72 Inoue H, Zipes DP Cocaine-induced supersensitivity and arrhythmogenesis J Am Coll Cardiol 1988;11:867-874 73 Chakko S Arrhythmias associated with cocaine abuse Card Electrophysiol Rev 2002;6:168-169 74 Witchel HJ, Hancox JC, Nutt DJ Psychotropic drugs, cardiac arrhythmia, and sudden death J Clin Psychopharmacol 2003;23: 58-77 75 Pinto DS Cardiac manifestations of Lyme disease Med Clin North Am 2002;86:285-296 76 DiNubile MJ, Calderwood SB, Steinhaus DM, et al Cardiac conduction abnormalities complicating native valve active infective endocarditis Am J Cardiol 1986;58:1213-1217 e3 Abstract: Arrhythmias are frequently encountered in the intensive care setting, either as the primary problem requiring care or in the setting of other cardiac or noncardiac disease processes The acute approach to diagnosis, treatments, and identification of underlying etiologies is crucial to appropriate stabilization of the patient and direction of ongoing management Likewise, recognition of specific arrhythmia mechanisms is often important in the selection of treatment choices This chapter attempts to provide an overview of the approach to treatment of an array of arrhythmias in the intensive care unit setting Key words: AV block, supraventricular tachycardia, junctional ectopic tachycardia, atrial flutter, ventricular tachycardia, adenosine, temporary pacemakers, permanent pacemakers, antiarrhythmic drugs ... prolongation and torsades de pointes have been observed Tricyclic Antidepressants and Phenothiazine Phenothiazines and tricyclic antidepressants produce electrophysiologic (and potentially antiarrhythmic)... arrhythmias) and catecholaminergic polymorphic ventricular tachycardia The patient is asymptomatic during this arrhythmia, but patients appear to be at risk for ventricular fibrillation with CNS and gastrointestinal... drug and is eliminated in the urine, is used to treat digoxin toxicity Prophylactic treatment with this preparation should be gauged according to the quantity ingested, time since ingestion, and