340 SECTION IV Pediatric Critical Care Cardiovascular Wenckebach behavior and avoid an acute drop in pacing rate by 50% when the UTR is reached However, it is also important to distinguish appropriate[.]
340 S E C T I O N I V Pediatric Critical Care: Cardiovascular I • Fig 33.10 Initiation of orthodromic reciprocating tachycardia with a single atrial paced beat that falls at a vulnerable time After several narrow-complex beats, bundle branch block in tachycardia results in a wide-complex rhythm Wenckebach behavior and avoid an acute drop in pacing rate by 50% when the UTR is reached However, it is also important to distinguish appropriate pacemaker Wenckebach from failure to sense the atrium or failure to pace the ventricle When initiating dual-chamber pacing, it is important to be sure that the atrial lead senses appropriately and that the rates, intervals, and refractory periods are set appropriately to allow the pacemaker to track the spontaneous atrial rate If the intrinsic atrial activity is not appropriately sensed and the dual-chamber temporary pacemaker’s low rate is lower than the patient’s intrinsic atrial rate, you may falsely assume that dual-chamber pacing is occurring when it is not The presence of cannon A waves on central venous pressure tracing may provide a clue that AV synchrony is not occurring Reversing the atrial leads, lowering the numeric atrial sensitivity, or adjusting the AV interval, UTR, or PVARP may remedy this situation If the atrium still cannot be sensed appropriately, setting the pacemaker’s low rate higher than the patient’s own atrial rate will allow AV synchrony In effect, this is pacing in DVI mode: pacing atrium and ventricle, sensing the ventricle, and inhibiting pacemaker output when spontaneous ventricular beats occur, avoiding asynchronous pacing by maintaining a higher atrial-paced rate Occasionally, a reentrant arrhythmia known as pacemakermediated tachycardia (PMT) may be seen, in which a DDD pacemaker (temporary or permanent) senses the atrium and paces the ventricle, with the patient’s own AV node conducting the impulse up from the ventricle to the atrium and the cycle repeating again Thus, the pacemaker acts as the antegrade limb of the reentrant circuit, while the patient’s own AV node acts as the retrograde limb Usually, PMT can be avoided with careful adjustment of the pacemaker’s AV interval and PVARP In a permanent pacing system, PMT can usually be terminated acutely by placing a magnet over the pacemaker; the resultant asynchronous pacing effectively interrupts the antegrade limb of the reentrant circuit Fig 33.11 shows initiation of PMT by loss of atrial capture with termination of the tachycardia by a spontaneous ventricular beat The selection of optimal temporary pacing mode and rate must be individualized for each patient Usually, atrial pacing (AAI) is preferred over dual-chamber pacing when AV conduction is intact However, marked first-degree AV block may unfavorably affect ventricular filling such that dual-chamber pacing provides better hemodynamics Periodic reassessment of pacing and sensing thresholds, as well as underlying rhythm, should be performed at least twice daily, and hemodynamic responses to changes in mode or timing parameters should be performed as needed with changes in clinical status Permanent Pacing—Indications and Selection The two most common indications for permanent pacing are high-grade AV block and sinus node dysfunction AV block may be congenital or acquired, with surgical damage to the conduction system the most common cause of acquired AV block In patients with surgical AV block, there may be recovery of normal conduction with resolution of edema In general, permanent pacing is not recommended unless there has been no recovery for to 14 days.23 Occasionally, if the surgeon is confident that the conduction system has been permanently damaged or if temporary pacing is not reliable, permanent pacemakers may be implanted within days after the initial injury Elective pacing for congenital AV block in the first decade of life is usually prompted by symptoms, low ventricular rates, or ventricular ectopy Elective pacing is commonly recommended in the second decade of life even for asymptomatic patients with congenital heart block on the basis of studies showing that the first symptom in teenagers and adults may be catastrophic.24 Pacing for sinus node dysfunction is most commonly performed in patients with structural heart disease, usually following extensive atrial surgery such as the Fontan operation or atrial repair of transposition of the great arteries In older children and adults, transvenous pacing is preferred due to lower morbidity of implantation, optimized lead placement, and lower susceptibility to lead fractures as compared with epicardial leads, unless intracardiac shunting is present In younger children, however, concern about venous occlusion in a patient who will require many decades of pacing often favors placement of epicardial pacemaker leads The development of epicardial leads that elute a small amount of dexamethasone appears to improve epicardial lead performance,25 although epicardial lead fractures remain a problem that is cause for concern In patients requiring a lifetime of pacing, various approaches to allow atrial and ventricular pacing are commonly needed Lower-profile lumenless pacing leads provide an alternative to epicardial pacing in 341 CHAPTER 33 Disorders of Cardiac Rhythm A P A P B V A P B V A S A S B V B V 0.40 ms A P B V B V A S A S B V A P B V A S B V A R B V A S B V A P A S B V A P V S A S B V A S B V A P B V B V A P B V A P B V • Fig 33.11 Initiation and termination of pacemaker-mediated tachycardia Top, Two atrial pacing stimuli fail to capture, followed by ventriculoatrial conduction of a ventricular paced beat The resulting atrial beat (AS) is sensed and triggers another ventricular beat, and the process repeats Had the retrograde atrial beat occurred during the postventricular atrial refractory period, it would not have triggered a ventricular paced beat Bottom, Spontaneous ventricular beat inhibits the ventricular pacing, terminating the process Atrial electrogram tracings are shown at the bottom of each panel AP, Atrial pace; AR, atrial refractory; BV, biventricular pace; VS, ventricular sense smaller patients and appear to perform comparably to more traditional pacing leads over time.25a The recent development of leadless pacemakers represents an exciting prospect for future pacing options However, in their current design, they are not suitable for younger patients and are available only for single-chamber right ventricular pacing.26 Ongoing advances, including leadless designs for dual-chamber or left ventricular pacing, may prove much more useful in patients with abnormal anatomy requiring dualchamber or biventricular pacing in whom a standard transvenous option is not available Other Indications for Pacing Considerable data have shown that a prolonged QRS duration (either due to conduction delay or chronic pacing) results in mechanical dyssynchrony, which further impairs ventricular function Biventricular pacing, with independent stimulation of the right and left ventricles, can reverse this dyssynchrony and improve ventricular function in some patients Limited large-scale data are available in the pediatric population on this approach to heart failure treatment (often referred to as cardiac resynchronization therapy), but small studies suggest benefit.27 Certainly, if pacing is otherwise required in a patient with impaired ventricular function, a biventricular pacing system should be considered Alternatively, with epicardial pacing, placement of the ventricular lead on the left ventricular apex rather than right ventricular apex may achieve similar benefit However, identifying patients most likely to benefit from this modality and the best technique for optimizing the timing of activation between the ventricles remains unresolved Tachycardia Therapies Vagal Maneuvers Vagal maneuvers were once the most commonly used intervention for terminating SVTs They occasionally terminate VTs as well Mechanical maneuvers, such as the Valsalva maneuver or carotid sinus massage, usually produce effective vagal stimulation beyond infancy In infants, a similar reflex vagal response can be elicited sometimes by applying firm, steady abdominal pressure or by applying an ice pack to the face These maneuvers should be attempted for 15 to 30 seconds Endotracheal suctioning may also terminate tachycardias by this mechanism Acute Pharmacologic Therapies Adenosine An endogenous nucleoside with profound effects on SA node and AV node conduction, adenosine has become a mainstay in the acute treatment of SVT with normal QRS duration.16 Administered as a rapid bolus, it produces transient but profound depression of AV nodal conduction and should reliably terminate reciprocating tachycardias (AV nodal reentry, AV reentry) Given the prevalence of AV reentry and AV nodal reentry among otherwise healthy young patients, adenosine is often advocated for wide QRS tachycardias as a therapeutic and/or diagnostic maneuver It usually causes transient AV block without terminating most primary atrial tachycardias but may transiently suppress atrial automatic tachycardias (ectopic atrial or junctional) and occasionally may terminate atrial reentrant tachycardias Certain VTs may be adenosine sensitive, particularly those originating because of abnormal triggering in the right ventricular outflow tract (RVOT) 342 S E C T I O N I V Pediatric Critical Care: Cardiovascular Adenosine (100–300 mg/kg) must be administered rapidly because of rapid metabolism by erythrocytes If tachycardia is not terminated, determination must be made regarding whether a larger dose is warranted, the dose was given too slowly, or VA or AV conduction was altered without terminating tachycardia (see discussion on diagnosis) Therefore, it is important to record an ECG strip during adenosine administration so that important diagnostic or therapeutic clues are not missed Because of its brief effect (half-life of 8–10 seconds), tachycardias sometimes immediately reinitiate following successful termination If they reinitiate, readministration of the same dose should be attempted rather than increasing the dose further In addition to effects on the AV node, adenosine can produce sinus arrest, which may be prolonged in the setting of intrinsic SA nodal dysfunction after heart transplant; in the presence of drugs that interfere with its metabolism, such as dipyridamole and diazepam; or with drugs that may exaggerate its effects, such as class I, II, or III antiarrhythmic drugs High doses should not be used indiscriminately in these situations The use of adenosine in patients with reactive airway disease may be problematic because adenosine occasionally triggers severe bronchospasm Conversely, its effects may be antagonized by aminophylline and other methylxanthines that the patient may be receiving Adenosine produces dramatic but transient chest pain, along with systemic vasodilation, both of which tend to increase sympathetic tone As a result, adenosine may paradoxically accelerate tachycardias if termination is unsuccessful or, in the case of primary atrial tachycardias (atrial flutter or fibrillation), may produce more rapid conduction over the AV node (after initially slowing the ventricular rate) Various secondary arrhythmias may occur following administration of adenosine—particularly, ventricular ectopy, atrial fibrillation, or, rarely, ventricular fibrillation Although these effects are usually transient, emergency external cardioversion should always be available whenever adenosine is administered The appropriateness of adenosine has been questioned in patients with known ventricular preexcitation syndromes (WPW syndrome) or suspected VTs Nevertheless, its thoughtful and careful use remains invaluable for both diagnosis and treatment of many tachycardias Antiarrhythmic Agents The addition of pharmacologic agents following adenosine administration should be guided by the clinical situation, known or suspected tachycardia mechanism, and response to adenosine administration In some cases (such as in patients with wide QRS tachycardia or in hemodynamically compromised patients), it may be most appropriate to proceed directly to pacing termination or cardioversion if adenosine is unsuccessful in restoring sinus rhythm In other instances, acute antiarrhythmic drug therapy may be warranted.29 The Vaughan Williams classification divides drugs according to their surface ECG effects, which often correlate closely with their cellular electrophysiologic effects: those that block cardiac sodium channels (class I); block b-adrenoreceptors (class II); prolong repolarization (class III); and block calcium channels (class IV) Digoxin and adenosine, which are not included in this classification scheme, exert their primary antiarrhythmic effects on the AV node Magnesium also has depressant effects on the AV node and suppresses early and late afterdepolarizations (triggered activity) Many of the available drugs manifest properties of more than one class, which contribute collectively to their antiarrhythmic action.30 In general, class I drugs (particularly IA and IC) slow conduction in atrial, ventricular, or accessory pathway tissue and class III drugs prolong refractoriness in these same tissues Class IA drugs usually accomplish both effects b-Adrenergic antagonists, calcium channel antagonists, digoxin, and adenosine act primarily by slowing AV nodal conduction or inhibiting abnormal automaticity Thus, the latter group of drugs is primarily used for reciprocating tachycardias using the AV node (ART, ORT, AVNRT) or to induce second-degree AV block during a primary atrial tachycardia In contrast, classes IA, IC, and III drugs may be more effective in terminating or directly suppressing primary atrial tachycardias and may be effective for reciprocating tachycardias.6,29 Despite the various antiarrhythmic agents available for chronic therapy, relatively few are suitable for acute administration to the critically ill patient either because the drugs are not available in IV formulation or they have significant negative inotropic effects when administered IV (Table 33.3) This discussion is limited to agents suitable for acute and short-term parenteral administration All antiarrhythmic agents have the potential for producing bradycardia, particularly when administered acutely, and most have negative inotropic and/or hypotensive effects Careful observation is required during initial administration and subsequent infusion of all IV antiarrhythmic agents Although many are contraindicated in cases of heart failure or hypotension, therapy may be necessary if the arrhythmia is contributing significantly to the patient’s hemodynamic compromise Procainamide. Procainamide is useful for various SVTs and VTs in the intensive care setting Its broad electrophysiologic effects include both conduction slowing and increased refractoriness in atrial tissue, ventricular tissue, and accessory AV connections Unlike quinidine, procainamide can be administered IV Effective plasma concentrations (6–10 mg/dL) can be readily achieved with a total loading dose of 15 mg/kg over 15 minutes (or in smallbolus increments at a similar rate) Careful and repeated blood pressure monitoring is required because of potential negative inotropic and direct vasodilator effects If hypotension complicates infusion, administration should be momentarily interrupted until blood pressure returns to normal In primary atrial tachycardias, a vagolytic effect may increase the ventricular response over the AV node Occasionally, atrial tachycardia that is conducting 2:1 to the ventricle slows sufficiently to allow 1:1 conduction, converting a hemodynamically stable rhythm to an unstable rhythm Thus, one should always be prepared to use cardioversion if necessary Procainamide, like other class IA and class III drugs, is contraindicated in patients with the congenital or acquired long QT syndromes Regular monitoring of plasma concentration every to 12 hours is necessary during IV administration to maintain levels between and 10 mg/dL The active metabolite N-acetylprocainamide contributes to the antiarrhythmic action; higher levels of the parent drug may be necessary in patients lacking the enzyme to produce this metabolite Lidocaine. Intravenously administered lidocaine is useful for suppressing and sometimes terminating VTs in children Although somewhat less likely to acutely terminate VTs than procainamide or amiodarone, lidocaine’s lack of significant negative inotropic effect makes it attractive for this indication The usual loading dose is to mg/kg acutely or mg/kg over 20 to 30 minutes, followed by a 20 to 50 µg/kg per minute infusion Lidocaine levels should be monitored to prevent central nervous system (CNS) toxicity With chronic use (4–7 days), accumulation of the metabolite glycine xylide may impair drug efficacy by interfering with the parent drug effect at the sodium channel Despite traditional recommendations for its use in ventricular fibrillation, lidocaine increases defibrillation energy requirements CHAPTER 33 Disorders of Cardiac Rhythm 343 TABLE Treatment of Bradycardias, Supraventricular Tachycardias, and Ventricular Tachycardias 33.3 Primary Therapies Secondary Therapies Long-Term Therapies Sinus bradycardia Atropine 0.01 mg/kg Epinephrine 0.1 mg/kg Transcutaneous pacemaker Temporary pacemaker Isoproterenol infusion Permanent pacemaker (AAIR, DDDR) AV block (high grade) Transcutaneous pacemaker Temporary pacemaker Permanent pacemaker (DDDR) Sinus tachycardia Identify cause(s) Sedation, pain control Adjust catecholamines Respiratory support b-Blockers, if chronic Consider nonsinus mechanism Paroxysmal supraventricular tachycardia, AV nodal reentrant tachycardia Vagal maneuvers Adenosine Transesophageal termination Procainamide Esmolol Verapamil Procainamide (IV) Amiodarone (IV) Class I, class III b-Blockers, class I, class III Amiodarone Radiofrequency ablation Radiofrequency ablation AET and other incessant supraventricular tachycardia Amiodarone Esmolol Avoid cardioversion b-blockers Amiodarone Atrial flutter ,24 h Rate control (diltiazem IV) Procainamide Pace termination with pacemaker DC cardioversion Ibutilide (transesophageal echocardiography if duration unknown of 24 h to rule out thrombus) Pace termination (Transesophageal, intracardiac) Radiofrequency ablation Antitachycardia pacemaker Atrial fibrillation ,24 h Same as above, except pace termination not feasible) Chaotic atrial tachycardia Procainamide, amiodarone b-Blocker (rate control) Propafenone, amiodarone Monomorphic (conscious, stable) Procainamide/lidocaine DC cardioversion Pace termination if PM, ICD Procainamide/lidocaine Amiodarone Defined by substrate Known heart disease Same as above Amiodarone ICD, radiofrequency ablation Amiodarone Known idiopathic Consider IV verapamil Avoid cardioversion b-Blocker Calcium channel blocker b-Blocker Radiofrequency ablation Pulseless (monomorphic, polymorphic) DC cardioversion b-Blocker Amiodarone Amiodarone (unless long QT) b-Blocker Magnesium ICD Ventricular fibrillation Defibrillation Epinephrine Vasopressin ICD Bradycardias Supraventricular Tachycardias Ventricular Tachycardias AET, Atrial ectopic tachycardia; AV, atrioventricular; ICD, implantable cardioverter-defibrillator; PM, pacemaker b-Blocking agents. A limited number of b-blocking agents are useful for IV treatment of tachycardias Acutely, their role is generally limited to incessant tachycardias, which seem to be dependent on sympathetic tone, and VTs related to myocarditis, ischemia/reperfusion injury, or congenital long QT syndromes In hemodynamically unstable patients, b-blocking agents should be used cautiously because of hypotension and potential sinus bradycardia once tachycardia terminates All may produce bronchospasm, hypotension, or bradycardia or may depress ventricular function Esmolol, a short-acting, nonselective b-blocker with a half-life of to minutes, can be administered as a continuous infusion A loading dose of 250 to 500 mg over to minutes followed by an infusion of 50 to 300 mg/kg per minute The infusion can be titrated upward by doubling every to minutes up to 500 mg/kg per minute Repeat loading doses may be useful as the infusion is 344 S E C T I O N I V Pediatric Critical Care: Cardiovascular increased Its very short half-life is excellent for short-term use, but extended efficacy is limited by tachyphylaxis For longer-term IV administration, metoprolol (0.05–0.10 mg/kg) is administered by slow IV infusion every to hours, while carefully observing for hypotension (or bradycardia) Amiodarone. Amiodarone is arguably the single most potent antiarrhythmic drug available both in the acute IV setting and when administered chronically At sufficient doses, it is often effective in controlling various tachycardias refractory to other antiarrhythmic agents.31 Although typically regarded as a class III agent, its effects are considerably more diverse It not only prolongs repolarization (by blocking potassium channels) but, to varying degrees, it blocks some sodium channel (class I effect), calcium channel (class IV effect), and b-receptors (class II effect) Amiodarone is administered as a total loading dose of mg/kg divided into 1-mg/kg aliquots given at 5- to 10-minute intervals The loading can be truncated if arrhythmia control is achieved If hypotension ensues, volume expansion or calcium chloride (10–30 mg/kg) should be administered If arrhythmia control is not achieved, a second loading dose can be administered 30 to 60 minutes later A continuous infusion of to mg/kg/min can be initiated (5–10 mg/day) Other QT Prolonging (Class III) Antiarrhythmic Drugs Intravenous sotalol. Sotalol is a class III (i.e., QT prolonging) antiarrhythmic drug with significant b-blocking properties used extensively in its oral form for a variety of supraventricular and ventricular arrhythmias It is now available in IV form and has been used effectively in children for termination of a variety of atrial and ventricular arrhythmias.32,33 It can also be used to continue maintenance antiarrhythmic therapy in patients unable to take the oral form It is infused as a 1-mg/kg bolus (maximum 80 mg) over hour, closely monitoring blood pressure and rhythm The dose can be repeated if termination does not result with the first bolus It should be noted that mean times to termination have varied widely, from 33 minutes to up to 12 hours It is important to ensure normal serum levels of potassium and magnesium before administration Hypotension is the main acute side effect, and it should be used in caution in the setting of depressed ventricular function Ibutilide. Ibutilide is a class III antiarrhythmic drug available only intravenously due to extensive first-pass metabolism of the oral form It is cleared rapidly (elimination time 3–6 hours), and pharmacokinetics are not altered by age, sex, or hepatic or renal dysfunction.34 Ibutilide is used for termination of atrial fibrillation or atrial flutter, with acute success rates as high as 76%.35 In children and patients with congenital heart disease, ibutilide has been reported to successfully terminate atrial flutter or fibrillation in 71%, with rare episodes of torsades de pointes and nonsustained ventricular tachycardia.36 Prior to administration, serum potassium and magnesium should be checked and repleted if low, and preexisting QT prolongation is a relative contraindication The standard dose is 0.01 mg/kg for patients less than 60 kg and mg for patients heavier than 60 kg infused over 10 minutes, with a repeat dose if necessary Calcium Channel–Blocking Agents Verapamil and diltiazem have proved useful for terminating SVT involving the AV node (AV reentry, AV nodal reentry) However, their acute efficacy is no greater than that of adenosine, and both may cause hypotension or cardiovascular collapse in young infants or patients with poor ventricular function.37 Either drug can be useful as an alternative to adenosine when tachycardias have repeatedly reinitiated following termination with adenosine Both agents may help slow the ventricular response over the AV node during atrial flutter or fibrillation Verapamil is administered as a bolus of 0.15 mg/kg Diltiazem can be administered as a bolus of 0.15 to 0.35 mg/kg and can be infused continuously at 0.05 to 0.2 mg/kg per hour if ongoing effect is necessary In addition to vasodilation and negative inotropic effects, both can accelerate antegrade conduction over accessory pathways in patients with WPW syndrome Therefore, they are contraindicated for preexcited atrial fibrillation and, generally, they should not be administered during uncharacterized wide QRS tachycardias Likewise, oral calcium channel blockers generally should not be used as maintenance therapy for patients with WPW syndrome If hemodynamic compromise develops, IV calcium gluconate should be administered immediately Magnesium Sulfate Magnesium (administered as 25–50 mg/kg magnesium sulfate) has proved useful in the treatment of certain ventricular and supraventricular arrhythmias Its actions appear to be mediated through depression of early and late afterdepolarizations; depressant effects on AV nodal conduction; and, at high doses, indirect inhibition of sodium-potassium adenosine triphosphatase It is most effective in the acute treatment of torsades de pointes and as a temporizing measure in the treatment of arrhythmias associated with digoxin toxicity.38 Therapeutic efficacy is not restricted to situations in which hypomagnesemia is present Although magnesium has efficacy comparable with that of adenosine in the acute termination of SVT resulting from AV reentry and AV nodal reentry, it has more severe and lasting adverse effects It has little demonstrable effect in the acute treatment of monomorphic VTs or polymorphic VTs not associated with QT prolongation Digoxin Digoxin has been used for various supraventricular arrhythmias, including AV reentry, AV nodal reentry, and primary atrial tachycardias In a randomized controlled trial of infants younger than months with SVT, recurrence rates were similar between digoxin and propranolol.39 Digoxin may increase the risk of rapid antegrade conduction during atrial fibrillation in older patients and possibly infants with preexcitation Like calcium channel– blocking agents, it should be avoided altogether in the treatment of patients with ventricular preexcitation (WPW syndrome) Its use is further confounded by potentially dangerous interactions with other medications, including quinidine, verapamil, amiodarone, flecainide, phenytoin, and warfarin At toxic dosages, its direct cellular effects may predispose to dangerous tachycardias and bradycardias Dexmedetomidine Dexmedetomidine is a selective a2-adrenergic receptor agonist that provides sedation, anxiolysis, and analgesia with minimal to no respiratory depression As a result, it has become widely used in a variety of settings, including the pediatric ICU Dexmedetomidine acts as a peripheral parasympathomimetic and a central sympatholytic, with electrophysiologic effects, including sinus and atrioventricular node depression.40 Studies have suggested that dexmedetomidine is effective for acute termination of SVT in children, with fewer side effects compared with adenosine.41 Serious adverse events—including sudden pauses, asystole, and ... left ventricles, can reverse this dyssynchrony and improve ventricular function in some patients Limited large-scale data are available in the pediatric population on this approach to heart failure... ventricular apex may achieve similar benefit However, identifying patients most likely to benefit from this modality and the best technique for optimizing the timing of activation between the ventricles... should be attempted for 15 to 30 seconds Endotracheal suctioning may also terminate tachycardias by this mechanism Acute Pharmacologic Therapies Adenosine An endogenous nucleoside with profound effects