335CHAPTER 33 Disorders of Cardiac Rhythm duration, and AV relationship (Table 33 2), which collectively should provide an initial differential diagnosis (Fig 33 5) Ideally, multiple ECG monitoring le[.]
CHAPTER 33 Disorders of Cardiac Rhythm duration, and AV relationship (Table 33.2), which collectively should provide an initial differential diagnosis (Fig 33.5) Ideally, multiple ECG monitoring leads should be inspected Rate trends should be reviewed for abruptness of onset to help discriminate between sinus and nonsinus tachycardias in the critically ill patient TABLE Electrocardiographic Patterns 33.2 Pattern Description AV Block Mobitz type I Shortened PR of first conducted beat after block Mobitz type II No change in PR before/after block Periods of high-grade block Third-degree Fixed, rather than variable, RR interval Supraventricular Tachycardias AV reentrant supraventricular tachycardia P waves obscured or buried in ST segment AV nodal reentrant supraventricular tachycardia P waves obscured by terminal QRS Pseudo R9 in lead V1 during tachycardia, not sinus Junctional ectopic tachycardia Narrow QRS tachycardia, VA dissociation RR periodically shortened because of sinus capture complexesa Atrial ectopic tachycardia Monotonous rate, inappropriately fast Abnormal P-wave morphology (may be subtle) Intraatrial reentrant tachycardia Inappropriately fast rate, discrete P waves, variable AV conduction in postoperative patient with congenital heart disease Atrial flutter Variable RR interval Rapid, sawtooth flutter waves (.280 beats/min) Atrial fibrillation Irregular ventricular rate Coarse baseline with no discernible P waves Chaotic atrial tachycardia 3 P-wave morphologies, irregular atrial rate, variable AV conduction (periods of atrial flutter or fibrillation common) Ventricular Tachycardias Monomorphic Wide QRS for age, different from baseline Slurred upstroke of QRS Variable VA conductionb Sinus capture complexesb Idiopathic types Left bundle branch block, inferior axis (right ventricular outflow tract origin) Right bundle branch block, left superior axis (left ventricular septal origin) Bidirectional Alternating QRS axis (beat-to-beat) Torsades des pointes Initiation with short-long-short sequence QT-interval prolongation before onset Twisting of QRS axis AV, Atrioventricular; VA, ventriculoatrial a Junctional ectopic tachycardia may be associated with third-degree AV block b Helpful when seen; absent if 1:1 VA relationship 335 While the surface ECG usually is sufficient to characterize most bradycardias, additional diagnostic maneuvers, sometimes coupled with direct recording of atrial activity, may be required to accurately characterize tachycardias Changes in ventricular rate and regularity, QRS duration and morphology, and atrial-toventricular relationship must be actively sought When available, temporary atrial pacing wires or an esophageal ECG can facilitate the diagnosis (Fig 33.6) Likewise, observing the response of an arrhythmia following perturbations such as premature atrial contractions (PACs) or premature ventricular contractions (PVCs) may be informative Repetitive patterns in ventricular activation referred to as grouped beating always provide important clues to the diagnosis Bradycardias Perhaps the most important diagnostic issues in bradycardias are determination of whether AV conduction occurs and recognizing the presence and rate of any underlying intrinsic escape rhythms This should usually be straightforward when the atrial rate exceeds the ventricular rate during second-degree or third-degree AV block In complete AV block, the resultant escape rhythm is usually regular; in second-degree AV block, the ventricular intervals vary (see Fig 33.1) This is especially helpful when sinus node disease and AV block coexist; variation of the RR interval typically implies some degree of AV conduction When atrial pacing is feasible (as in patients with recent cardiac surgery), AV conduction can be more directly characterized The distinction between bradycardia resulting from AV block and sinus node dysfunction may have important therapeutic implications, particularly with respect to pacing If AV nodal conduction is fully intact, it is usually desirable to pace the atrium only (see AAI mode) rather than perform dual-chamber pacing In contrast, isolated AV block is best managed by sensing and tracking the intrinsic atrial rate (see DDD mode) and pacing the ventricle Other variations in pacing modes are discussed elsewhere in this chapter Extrasystoles Extrasystoles, or premature beats, are defined as supraventricular (supraventricular premature beats or premature atrial or junctional complexes) or ventricular (premature ventricular complexes, ventricular premature beats [VPBs]) in origin True junctional extrasystoles are uncommon Isolated premature QRS complexes with prolonged QRS duration may represent either ventricular extrasystoles or aberrantly conducted atrial extrasystoles Distinguishing the two may be difficult from a single rhythm strip When the extrasystole results in an early QRS with normal morphology and duration, a supraventricular extrasystole may be presumed Usually, an early P wave can be discerned, but it may be obscured by the preceding T wave in certain leads The ensuing sinus beat is usually advanced by the atrial extrasystole, but entrance block can often result in a full compensatory pause, which is usually more characteristic of ventricular extrasystoles It is important to view multiple leads, since a ventricular extrasystole may resemble the normal QRS in one lead but appear totally dissimilar and broader in others The ECG can also help discern unifocal versus multifocal PVCs and also help localize the site of PVC origin The ECG features favoring ventricular extrasystoles over aberrantly conducted atrial extrasystoles include (1) wide QRS morphology, (2) a full compensatory pause prior to the ensuing sinus beat, (3) presence of fusion beats, and (4) absence of a discernible premature P wave A full compensatory pause indicates failure of 336 S E C T I O N I V Pediatric Critical Care: Cardiovascular • Fig 33.5 Ventricular tachycardia in an 8-year-old with previous muscular ventricular septal defect repair Note transient ventriculoatrial block (arrows), excluding a supraventricular mechanism with aberrant conduction aVR aVL aVF A B 150– 100– 50 • Fig 33.6 (A) Narrow QRS tachycardia in an infant following a stage I Norwood operation Possible atrioventricular (AV) dissociation is suggested, but P waves are not easily discerned on the surface electrocardiogram (B) Atrial recording from the same patient (after rate increased) using an epicardial atrial pacing wire AV dissociation with faster junctional rate is demonstrated, typical of junctional ectopic tachycardia Absence of clearly shortened RR intervals because of sinus capture might indicate associated AV block the sinus node to be reset by the ventricular depolarization, though a very premature beat may occasionally reset the sinus node because of retrograde (VA) conduction over the AV node to the atrium Fusion indicates a QRS morphology intermediate between a fully anomalous QRS and the normal QRS Fusion is also seen in patients with ventricular preexcitation (WPW) and in whom PACs often result in a widened QRS due to selective delay in conduction of the premature impulse through the AV node but not the accessory pathway The distinction between atrial and ventricular extrasystoles may be somewhat academic in otherwise asymptomatic individuals because neither generally warrants therapy However, either might be a harbinger for myocardial irritability and should prompt a search for underlying causes Occasionally, measures to suppress ectopy may appear to improve cardiac output by regularizing filling time in an otherwise tenuous patient The relative advantages and risks of any such measure, whether achieved with medications or temporary pacing, need to be considered individually Tachycardias With Normal QRS In otherwise healthy infants, children, and adolescents, SVT usually represents AV reentrant tachycardia or AVNRT (Fig 33.7) Further distinction between these two mechanisms has little impact on acute management However, in the ICU setting, primary atrial tachycardias (including sinus tachycardia) and junctional tachycardias are considerably more prevalent (particularly following cardiac surgery) The finding of abnormal P-wave morphology (determined by 12-lead ECG), a PR interval greater than 50% of the RR interval, or completely obscured P waves favors a nonsinus mechanism Finally, ensuring normal QRS duration for age, rather than simply relying on adult standards, is essential in discriminating from VTs Distinguishing sinus tachycardia from various types of SVT may be difficult In young patients, intraarterial reentry, atrial flutter, and atrial fibrillation are usually seen following surgical treatment for congenital heart defects involving the atrium (atrial septal defects, atrial repair of transposition of the great arteries, or the Fontan operation).15 The term intraatrial reentrant tachycardia is often used in this setting when a reentrant tachycardia displays discrete P waves rather than the usual sawtooth flutter waves Because the atrial rate is often relatively slow in comparison with typical atrial flutter, a high index of suspicion is essential in distinguishing this rhythm from sinus rhythm or sinus tachycardia, especially when fixed 1:1 conduction or 2:1 conduction (with blocked P waves obscured by the QRS or T wave) Again, direct atrial recordings using transesophageal electrocardiography or temporary epicardial atrial pacing wires usually facilitate the diagnosis and characterize the AV relationship (see Fig 33.6B), as can vagal maneuvers, administration of adenosine to temporally interrupt AV conduction, or—in ambulatory patients—simply changing position from supine to standing to assess for changes in the ventricular response Tachycardias with Prolonged QRS Tachycardia with prolonged QRS can represent VT, an SVT with aberrancy, or, occasionally, a preexcited tachycardia in a patient with ventricular preexcitation (WPW, Mahaim fiber) VA dissociation, the hallmark and most specific ECG feature of VT, may not be seen in childhood because of rapid retrograde conduction over the AV node (see Fig 33.5) The distinction between VT and SVT with aberrant conduction can be difficult and may ultimately require invasive electrophysiologic study Other features favoring VT are the presence of fusion complexes (implying AV dissociation), a superior QRS axis, or a concordant QRS axis across the precordium (i.e., pure R waves or pure S waves) However, these criteria may be unreliable in patients with CHD where normal conduction axes may be abnormal at baseline CHAPTER 33 Disorders of Cardiac Rhythm I aVR V1 V4 II aVL V2 V5 III aVF V3 V6 337 V4R • Fig 33.7 Supraventricular tachycardia resulting from atrioventricular nodal reentry in an infant Although considerably less common than orthodromic reciprocating tachycardia in this age group, the P wave on the terminal portion of the QRS complex results in a pseudo rSr9 pattern During sinus rhythm, this terminal deflection on the QRS was absent; the transesophageal recording confirmed the mechanism Generally, tachycardias with prolonged QRS should be presumed to be VTs until or unless evidence of an alternative diagnosis is clearly demonstrated Prolonged attempts to differentiate SVT from VT by noninvasive means may simply delay treatment, and the wrong conclusion may prove disastrous: acute treatment based on a presumed diagnosis of VT is rarely deleterious even when the mechanism subsequently proves to be supraventricular However, an erroneous presumption of SVT with aberrant conduction may result in rapid clinical deterioration When feasible, a full 12-lead ECG may aid in the diagnosis, particularly when a baseline ECG in normal rhythm is available for comparison Apparent hemodynamic stability should not be mistaken as evidence of SVT over VT whether in an otherwise healthy child or in a patient with known cardiac disease Assessment of Atrial Activation When the AV relationship during a tachycardia is unclear, sometimes it can be inferred indirectly by other available monitoring Invasive arterial and venous pressure waveforms can help define atrial contractile action in some situations For example, cannon A waves are commonly noted in patients with atrial flutter or JET Direct recording of atrial activity may clarify the AV relationship when it cannot be determined from the surface ECG or other means Patients recovering from cardiac surgery may have temporary atrial epicardial pacing wires that can be used to record atrial electrograms directly while simultaneously recording the surface ECG (see Fig 33.6B) Attachment of the atrial wires to a unipolar precordial lead (V lead) on the monitor is an easy way to observe atrial activation Alternatively, the atrial wire can simply be placed beneath a limb lead, producing a larger/sharper atrial signal of atrial activation (which can be further accentuated by placing the bedside monitor to detect pacing events) When necessary equipment is available, a bipolar esophageal catheter inserted in the esophagus behind the left atrium can also demonstrate atrial activation Diagnostic Uses of Adenosine Although most widely used as an acute therapy for terminating SVT that involves the AV node, adenosine administration also may yield important diagnostic clues to the underlying arrhythmia mechanism.16 By producing transient block in the AV node during tachycardia, it is often possible to distinguish AV reentrant tachycardias and AVNRTs (either of which should terminate) from atrial tachycardias and VTs However, adenosine’s effects are not always confined to the AV node Ectopic (automatic) atrial and junctional tachycardias, intraatrial reentry, and certain VTs may also terminate with adenosine Extreme caution should be taken when administering adenosine during wide QRS tachycardia Adenosine produces vasodilation, which theoretically can result in hemodynamic deterioration and tachycardia acceleration, or even fibrillation, if tachycardia fails to terminate Ventricular fibrillation has been rarely observed when adenosine is administered in the setting of WPW syndrome, probably as a result of atrial fibrillation that is then conducted rapidly to the ventricles Cardiac defibrillation capability should always be readily at hand when administering adenosine for diagnostic or therapeutic purposes 338 S E C T I O N I V Pediatric Critical Care: Cardiovascular Treatment of Rhythm Disturbances The approach to treatment of cardiac arrhythmias is influenced by the clinical setting, but several important considerations help guide therapy in any given situation The first and most important concern is the degree of hemodynamic compromise associated with a particular arrhythmia At one extreme, minor rhythm disturbances may be more readily recognized in the intensive care setting than in other situations simply because of the level of monitoring, which may prompt undue attention and unnecessary treatment At the other extreme, otherwise life-threatening arrhythmias ordinarily requiring acute therapy may be of little acute consequence in the setting of extracorporeal life support (ECLS) or mechanical ventricular assist devices Indeed, ECLS may serve as adjunctive therapy for refractory arrhythmias Even ventricular fibrillation in a patient with a ventricular assist device (VAD) rarely results in immediate decompensation In contrast, arrhythmias that might ordinarily be well tolerated may be acutely destabilizing in an already critically ill patient and require immediate intervention A second important consideration in critically ill patients, particularly in those after cardiac surgery, is to favor therapies that maintain appropriate AV synchrony whenever feasible In the setting of marginal hemodynamics, the practice of medically slowing the ventricular rate during arrhythmias such as atrial tachycardias and fibrillation, junctional tachycardia, or AV block may be inadequate to preserve cardiac output (Fig 33.8) A third consideration in the management of arrhythmias in the ICU is the recognition that many arrhythmias in this setting are iatrogenic Even minor arrhythmias may herald more serious issues, such as electrolyte disturbances, acidosis, subendocardial ischemia, excessive catecholamine infusions, or increased intracranial pressure It is important to identify and correct any such underlying causes because therapies directed at the rhythm itself may not protect from more serious rhythm decompensation Finally, whenever feasible, acute and short-term measures with limited potential to impair hemodynamics generally should be favored over chronic therapies Thus, nonpharmacologic therapies (such as pacing or cardioversion) or ultra-short-acting drugs (such as adenosine or esmolol) may be preferable to chronic antiarrhythmic therapy Whether chronic therapy is warranted for a given arrhythmia is determined more by its underlying mechanism, clinical setting, and frequency than by the severity of the arrhythmias encountered in the intensive care setting Before beginning chronic antiarrhythmic therapy, consultation with a mm/sec PACING ON P P P P P P P P P P PP P P P P 20 10 75 55 • Fig 33.8 Junctional 30 85 65 ectopic tachycardia with hypotension immediately improved with faster atrial pacing—in this case, resulting in 2:1 atrioventricular (AV) block and AV synchrony cardiologist versed in the spectrum of arrhythmias seen in childhood is advisable The impact of acute measures on chronic arrhythmia management becomes increasingly crucial with the emergence of amiodarone use in the ICU and the increasing availability of nonpharmacologic therapies such as radiofrequency catheter ablation and implantable defibrillators for a broader spectrum of arrhythmias and patient populations.17–19 Bradycardia Therapies Whenever treatment is instituted for a rhythm disturbance, an underlying cause should be sought and corrected This is especially important for bradycardias that occur in the intensive care setting, where airway compromise and respiratory insufficiency probably are the most common causes of acute bradycardias Increased intracranial pressure, hypothermia, or iatrogenic causes also may produce bradycardias that require specific interventions beyond those outlined here Emergency interventions for AV nodal and sinus nodal dysfunction are essentially identical Chest compressions should be administered if there is no effective underlying rhythm Pharmacologic Treatment of Bradycardias After appropriate confirmation or restoration of airway integrity and ventilatory function, initial treatment of symptomatic bradycardias is usually pharmacologic, whether the cause is sinus node slowing or AV nodal block Atropine (0.01–0.04 mg/kg intravenously [IV] or, if necessary, intramuscularly or via endotracheal tube) may transiently ameliorate bradycardia caused by hypoxia (or other vagal stimulants), digoxin, intracranial hypertension, or AV block as a result of Lyme disease Atropine is less likely to reverse bradycardic effects of b-blocking agents or other antiarrhythmic drugs, particularly in the setting of underlying sinus node disease Epinephrine (0.1 µg/kg) can be administered by various routes to accelerate the heart rate Continuous infusions of epinephrine (0.05–2 mg/kg per minute) or isoproterenol (0.02–0.2 mg/kg per minute) may be instituted In general, highdose epinephrine or isoproterenol infusions should be replaced by temporary pacing as soon as feasible Even if lower doses of these agents prove adequate, temporary pacing should be available as a backup Occasionally, methylxanthines are useful as an alternative to pacing for nonlethal bradycardias Glycopyrrolate and ketamine may help augment rates in bradycardic patients, requiring sedation or anesthesia Temporary and Permanent Pacing for Bradycardias Pacing is an essential adjunct to medical management of arrhythmias in the ICU Several reviews of pacing in children are available.20,21 Pacing can be accomplished using permanently implanted pacemaker and lead systems, temporary epicardial leads attached to the heart at the time of cardiac surgery, transvenous placement of a temporary pacing lead, or transcutaneous patches Most pacing is performed for bradyarrhythmias, although temporary pacing may be used to terminate reentrant tachyarrhythmias Principles of Pacing All pacing requires a complete circuit with at least one lead on or near each chamber that is to be paced Often, two leads are placed on each chamber (bipolar leads), although sometimes only the cathode is attached to the heart (unipolar leads), with a subcutaneous electrode acting as the anode The metal can of a permanent CHAPTER 33 Disorders of Cardiac Rhythm pacemaker can also serve as the anode The intensity of the pacing stimulus is related to the stimulus duration (pulse width) and its amplitude, which can be expressed as either current (mA) or voltage (V) Energy is proportional to the pulse width and the square of the amplitude Most temporary pacemakers provide a fixed pulse width, with an adjustable current output (mA) Permanent pacemakers generally have both an adjustable pulse width and amplitude Sensing intrinsic activity of the chamber being paced is important to prevent asynchronous pacing that may inadvertently induce an atrial or ventricular tachycardia The sensitivity of permanent and temporary pacemakers is adjustable The sensitivity setting (mV) refers to a sensing threshold for detection of spontaneous cardiac activity The spontaneous activity must exceed that threshold to be detected by the pacemaker Thus, a lower numeric sensitivity setting makes the pacemaker more sensitive to both spontaneous activity of the atrium or ventricle (appropriate sensing) and other electrical signals (oversensing) The programmed mode and timing circuits of the pacemaker determine when the pacemaker paces and its response to sensed events A simplified pacing code uses three letters to describe pacing modes.22 The first two letters refer to the chamber(s) paced and chamber(s) sensed, respectively (A, atrium; V, ventricle; D, dual) The third letter refers to the response to sensed events (I, inhibit; T, trigger or track; D, dual) Thus, a single-chamber atrial or ventricular pacing demand mode is AAI or VVI mode, whereas dual-chamber pacing is generally DDD mode Corresponding asynchronous modes are AOO, VOO, or DOO and may be important to prevent inadvertent inhibition of pacing due to electrical interference, such as with electrocautery Other pacing modes may be employed with permanent pacing systems Recognizing the peculiarities of these modes is important when distinguishing observed pacing behaviors as appropriate or dysfunctional Timing intervals most readily adjusted include low rate, AV delay, upper tracking rate (UTR), and postventricular atrial refractory period (PVARP) The sum of the AV delay and the PVARP in milliseconds determines the minimum atrial cycle length (60,000 divided by heart rate) and thus the maximum rate, which can be tracked and paced in the ventricle (UTR) Temporary Pacing In the pediatric ICU, temporary pacing is most commonly used in patients after surgical treatment of CHD Temporary epicardial pacing wires are usually placed on the atria and ventricles, allowing pacing of either chamber As previously noted, direct atrial recording (by attaching the wire to an ECG lead) may also aid in the diagnosis of tachyarrhythmias Atrial burst pacing can be used to terminate reentrant supraventricular arrhythmias such as IART, AVNRT, and ORT Pace termination of ORT is shown in Fig 33.9 • Fig 33.9 Pace termination of orthodromic reciprocating tachycardia with a burst of atrial pacing 339 Although JET generally cannot be terminated with burst pacing, atrial pacing at a rate faster than the JET rate often improves hemodynamics by allowing AV synchrony until the JET resolves or is pharmacologically controlled (see Fig 33.8) In bradycardic patients who not have temporary epicardial pacing wires, transcutaneous pacing can be performed acutely It is important that electrodes and output are appropriate for patient size, and positioning may be critical to maintaining capture In general, transcutaneous pacing is used only for a short time while a temporary transvenous pacing lead is placed At the bedside, placement of a balloon-tipped temporary transvenous lead is best accomplished via the internal jugular or subclavian vein because the catheter often can be directed to the ventricle blindly When fluoroscopy is available, a temporary active fixation may be preferred, allowing more secure positioning and the choice of pacing the atrium, ventricle, or both (in dual-chamber mode) Setting Temporary Pacing Parameters For AAI or VVI demand pacing, the pacemaker is usually initially set at a rate higher than the patient’s intrinsic atrial or ventricular rate The pacing threshold (lowest output that captures the chamber being paced) should be determined by decreasing the pacing current (mA) just until capture is lost and then setting output to at least twice threshold Similarly, sensing threshold is determined by first lowering to a rate below the intrinsic rate of the chamber being paced, then adjusting the sensitivity to a higher numeric setting (less sensitive) until the pacemaker stops sensing the intrinsic activity as indicated by loss of blinking markers on the device and/or inappropriate pacing on the monitor The sensitivity is then adjusted to a lower numeric value (more sensitive) to determine the highest numeric value at which the pacemaker senses appropriately (sensing threshold) Ideally, the sensitivity is programmed to one-half the sensing threshold, but this is not always possible, especially for temporary atrial leads Failure to sense can result in inappropriate pacing, which can induce tachyarrhythmias Fig 33.10 shows a single inappropriate atrial stimulus initiating sustained ORT Dual-chamber pacing is more complex The atrial and ventricular sensitivity and output are set using basically the same process described for single-chamber pacing The other timing parameters discussed earlier must also be set, including the UTR, AV delay, and PVARP Atrial events occurring during the PVARP will be ignored by the pacemaker and will not result in a ventricular paced event The pacemaker is also refractory to spontaneous atrial events during the AV interval Thus, the total atrial refractory period (TARP) includes both the AV interval and the PVARP and limits the UTR (which cannot exceed the TARP) Thus, increasing the UTR often requires shortening the AV interval and/or the PVARP, thus decreasing the TARP The TARP also determines high-rate behavior when atrial rates exceed the UTR If the spontaneous atrial cycle length (60,000 ms/min divided by the spontaneous atrial rate in beats/min) is less than the TARP, only half of the spontaneous atrial beats will result in pacing The point at which this occurs is known as the 2:1 block rate In contrast, if the intrinsic atrial cycle length is greater than the sum of the AV delay and PVARP, atrial events exceeding the UTR will still be noted by the pacemaker The resulting pattern of ventricular pacing resembles Wenckebach AV conduction and is referred to as pacemaker Wenckebach Thus, it is desirable to program the AV delay and PVARP such that the resulting sum (TARP) is less than the upper tracking limit in milliseconds (60,000 divided by upper programmed rate) to favor pacemaker ... orthodromic reciprocating tachycardia in this age group, the P wave on the terminal portion of the QRS complex results in a pseudo rSr9 pattern During sinus rhythm, this terminal deflection on the QRS... inadequate to preserve cardiac output (Fig 33.8) A third consideration in the management of arrhythmias in the ICU is the recognition that many arrhythmias in this setting are iatrogenic Even minor arrhythmias... arteries, or the Fontan operation).15 The term intraatrial reentrant tachycardia is often used in this setting when a reentrant tachycardia displays discrete P waves rather than the usual sawtooth