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CHAPTER 24 Electrical Storm and Incessant Ventricular Tachycardia 245

Vereckei Algorithm

Brugada Algorithm

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in Lead aVR

Presence of an initial R wave?

Presence of an inltial R or Q

wave >40 ms?

Presence of a notch on the

descending limb of a negative

onset and predominantly

negative QRS?

vi/vt ≤1?

SVT diagnosed

Fig. 24.1 The Vereckei and Brugada algorithms for differentiation of ventricular tachycardia from

supraventricular tachycardia. SN, Sensitivity; SP, speciﬁcity; SVT, supraventricular tachycardia with aberrancy; vi/vt, initial (vi) and terminal (vt) ventricular activation velocity ratio; VT, ventricular tachycardia. (From Baxi RP, Hart KW, Vereckei A, et al. Vereckei criteria as a diagnostic tool amongst emergency medicine residents to distinguish between ventricular tachycardia and supra-ventricular tachycardia with aberrancy. J Cardiol. 2012;59:307–312.)

Ye s

VT diagnosed

Absence or an R2 complex

in all precordial leads

R to S interval >100 ms in

one precordial lead

AV dissociation?

Morphology criteria for VT present both in precordial

leads V

to V2 and V

SVT SN = .965 SP = .987

Ye s

VT SN = .21 SP = 1. 0

VT SN = .82 SP = .98

VT SN = .987 SP = .965

algorithms are available to help differentiate VT from SVT. Two algorithms are presented in Fig. 24.1.24 Since no algorithm is perfect, a wide-complex tachycardia in patients with underlying structural heart disease should be assumed to be VT until proven otherwise. The administration of treatments for SVT, such as adenosine or calcium channel blockers, can precipitate cardiac arrest in patients with VT who were otherwise hemodynamically tolerating the arrhythmia. In most cases, continuous telemetry monitoring or ICD interrogation of intracardiac electrograms are required to document the VT. On interrogation of ICDs of patients with electrical storm, 86% to 97% have monomorphic VT, 1% to 21% have primary VF, 3% to 14% have combined VT/VF, and 2% to 8% have polymorphic VT.

5–7,9,10,12,13,16,18,25,26

Patients with these arrhythmias can be further divided into those with and without structural heart disease to facilitate diagnosis and treatment (Fig. 24.2).

Monomorphic VT storm (Fig. 24.3) is usually associated with structural heart disease and is due to electrical wavefront reentry around a ﬁxed anatomic barrier, most commonly scar tissue following a prior MI, ﬁbrosis in nonischemic cardiomyopathies, arrhythmogenic right ventricular cardiomyopathy/dysplasia, sarcoidosis, amyloidosis, Chagas disease, or a prior surgical incision. Surviving myocytes within the dense scar lead to a zone of slow conduction and, combined with areas of anatomic or functional conduction block, give rise to electrical reentry circuits for reentry that can be triggered by a premature ventricular depolarization.

When monomorphic VT occurs in structurally normal hearts, it is referred to as idiopathic VT. The characteristics of idiopathic VT depend on the origin of the VT. VT arising from the outﬂow tract is the most common form of idiopathic VT and characteristically will present with a left bundle branch block and inferior axis (Fig. 24.4). The usual mechanism involves triggered activity due to cyclic adenosine monophosphate (cAMP)-mediated delayed afterdepolarizations. β-Adrenergic stimulation increases intracellular cAMP and intracellular calcium levels, resulting in spontaneous calcium release from the sarcoplasmic reticulum, delayed afterdepolarizations, and triggered activity.

Fascicular (or idiopathic) VT is the second most common cause of monomorphic VT in the absence of structural heart disease. The mechanism is thought to involve macro-reentry involving the Purkinje ﬁber network, which connects to the left fascicle. Fascicular VT is classiﬁed according to the ECG morphology (right bundle branch pattern and superior or inferior QRS axis) and corresponding fascicle coupled to the reentrant circuit: left posterior fascicular VT, left anterior fascicular VT, and left upper septal VT. Left posterior fascicular VT is most common (Fig.

24.5). The fascicular VTs have characteristic ECGs demonstrating

a relatively narrow QRS that results from rapid spread of depolarization using the specialized conduction system. Other less common causes of monomorphic VT storm in structurally normal hearts include nonreentrant focal Purkinje VT, papillary muscle VT, and mitral/tricuspid annular VT. It is important to realize that these patients may have depressed LV function when they

3,27,28

246 PART IV Noncoronary Diseases: Diagnosis and Management

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Recurrent VT/VF (≥3 episodes or appropriate ICD therapies in 24 hours) or shock-refractory VT/VF

Electrical or pharmacologic cardioversion/defibrillation

Sedation, respiratory, and circulatory support if necessary

12-lead ECG, transthoracic echocardiography

Routine labs (electrolytes, thyroid function, etc.)

Structural heart disease

Monomorphic VT Polymorphic VT/VF

Myocardial ischemia

β-blockers

Amiodarone

ICD reprogramming

Ablation

CSD

Discontinue offending drugs

Temporary mechanical circulatory

β-blockers

Amiodarone

Revascularization

Ablation

CSD

With QT prolongation

Magnesium

Pacing

Heart failure

Amiodarone

β-blockers

Heart failure treatment

support

Ablation

Medical and drug history

Structurally normal heart

Monomorphic VT Polymorphic VT/VF

OT-VT PM-VT

Annular VT

Focal Purkinje VT

β-blockers

antagonists

ClassIC or III AADs

Ablation

Fascicular VT

Verapamil

Ablation

Congenital LQTS

β-blockers

Magnesium

Verapamil

CSD

Late Na

Discontinue offending drugs

blockade (LQT3)

Acquired LQTS

Magnesium

Pacing

SQTS

Class IA or III AADs

Isoproterenol

Brugada syndrome

Isoproterenol

Quinidine

Ablation

Fig. 24.2 Management of electrical storm. ADDs, Antidysrhythmic drugs; CPVT, catecholaminergic

polymorphic ventricular tachycardia; CSD, cardiac sympathetic denervation; ICD, implantable cardioverter deﬁbrillator; LQTS, long QT syndrome; OT-VT, outﬂow ventricular tachycardia; PM-VT, papillary muscle ventricular tachycardia; SQTS, short QT syndrome; VF, ventricular ﬁbrillation; VT, ventricular tachycardia. (Modiﬁed from Maruyama M. Management of electrical storm: the mechanism matters. J Arrhythmia. 2014;30:242–249.)

come to medical attention that is due to the detrimental impact of incessant VT on LV function rather than an indication of structural heart disease. The LV dysfunction in such situations tends to be global as opposed to segmental3 and usually recovers after the VT is terminated.

VF is fatal if not treated immediately. Following deﬁbrillation, VF may recur repeatedly and present as electrical storm. Mortality rates in this setting are 85% to 97%.

29,30

Since ischemia is the primary mechanism of VF storm, patients should be emergently triaged to coronary angiography and revascularization. Patients

CPVT (normal baseline ECG)

β-blockers

Verapamil

CSD

Idiopathic VF (normal baseline ECG)

Verapamil

Ablation

with a structurally normal heart can develop VF storm triggered by closely coupled monomorphic PVCs. Brugada syndrome, an inherited arrhythmia syndrome caused by mutations in the cardiac sodium channel gene, can present as recurrent VF or electrical storm and a characteristic ECG pattern of right bundle branch block and ST segment elevation in leads V1 to V3 (Fig. 24.6).

Polymorphic and monomorphic VT reﬂect different arrhythmogenic mechanisms. For polymorphic QRS complexes to be present on the surface ECG, multiple wavefronts must propagate throughout the heart or appear simultaneously in different areas

CHAPTER 24 Electrical Storm and Incessant Ventricular Tachycardia 247

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Fig. 24.3 Monomorphic ventricular tachycardia storm. Continuous

electrocardiographic strips in a patient with recurrent syncopal episodes are shown. (From Maruyama M. Management of electrical storm: the mechanism matters. J Arrhythmia. 2014;30:242–249.)

Fig. 24.4 A 12-lead electrocardiogram (ECG) of right ventricular

outﬂow tract (RVOT) ventricular tachycardia demonstrating a left bundle branch block pattern in the precordial leads with transition from a small r wave to a large R wave at V a right-sided site of origin. Also consistent with the outﬂow tract site is the inferior ECG axis. (From Prystowsky EN, Padanilam BJ, Joshi S, Fogel RI. Ventricular arrhythmias in the absence of structural heart disease. J Am Coll Cardiol. 2012;59:1733–1744.)

Fig. 24.5 A 12-lead electrocardiogram of left posterior fascicular

ventricular tachycardia demonstrating a right bundle branch block pattern with a superior axis. This type of tachycardia has a site of origin near the left posterior fascicle. (From Prystowsky EN, Padanilam BJ, Joshi S, Fogel RI. Ventricular arrhythmias in the absence of structural heart disease. J Am Coll Cardiol. 2012;59:1733–1744.)

to V4 consistent with

Fig. 24.6 A 12-lead electrocardiogram of Brugada syndrome

demonstrating coving of the ST segment in the early precordial leads and right bundle branch block pattern. (From Prystowsky EN, Padanilam BJ, Joshi S, Fogel RI. Ventricular arrhythmias in the absence of structural heart disease. J Am Coll Cardiol. 2012;59:1733–1744.)

Fig. 24.7 Drug-induced torsades de pointes following quinidine

treatment. (From Schwartz PF, Woosley RL. Predicting the unpredictable. Drug-induced QT prolongation and torsades de pointes. J Am Coll Cardiol. 2016;67:1639–1650.)

of the heart.32 Polymorphic VT, which can occur with a normal or prolonged QT interval (Fig. 24.7), is most often encountered in patients with acute coronary syndromes. As such, electrical storm can be the initial manifestation of acute ischemia. In acute MI, polymorphic VT can be caused by ischemia, altered membrane potentials, triggered activity, necrosis, or scar formation. Ischemia may cause dispersion of electrical refractory periods between the endocardium and epicardium, which is required for multiple waves of reentry.33 Ischemia increases Purkinje cell automaticity, leading to spontaneous ﬁring of these ﬁbers, which triggers polymorphic VT or VF.34 However, patients without acute ischemia, such as those with acute myocarditis or hypertrophic cardiomyopathy, can also develop polymorphic VT storm.

Polymorphic VT storm is rare in structurally normal hearts but can occur in patients with primary genetic abnormalities, due to secondary causes or with no discernible cause, referred to as idiopathic VF. The treatment strategies differ greatly among patients with polymorphic VT storm. The baseline ECG is of critical importance in making the diagnosis. If the QT interval is markedly prolonged, the polymorphic VT is most likely torsades de pointes due to congenital or acquired LQTS.

The congenital LQTS is an ion channel disorder characterized by abnormally prolonged QT intervals (corrected QT interval >440 ms in men and >460 ms in women) with or without morphologic abnormalities of the T waves35 (Fig. 24.8). A decrease in outward potassium currents or an increase in inward sodium currents prolongs the repolarization phase of the cardiac action potential, resulting in prolongation of the QT interval and

248 PART IV Noncoronary Diseases: Diagnosis and Management

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and idiopathic VF.3 CPVT is an inherited abnormality of intracellular calcium handling and is commonly seen in young patients with stress- or exertion-induced syncope. The hallmark of CPVT is alternating left bundle branch and right bundle branch QRS complexes. Idiopathic VF presents as syncope or aborted sudden cardiac death in young people with normal hearts and no identiﬁable genetic syndrome. The events are typically unrelated to stress or activity but may occur in clusters characterized by frequent ventricular ectopy and short episodes of VF or polymorphic VT. The spontaneous VF or polymorphic VT events

Fig. 24.8 A 12-lead electrocardiogram of long QT syndrome

demonstrating a QT interval of 580 ms and a corrected QT interval of 513 ms. Genetic testing revealed an LQT1 syndrome. (From Prystowsky EN, Padanilam BJ, Joshi S, Fogel RI. Ventricular arrhythmias in the absence of structural heart disease. J Am Coll Cardiol. 2012;59:1733–1744.)

are triggered by premature ventricular contractions (PVCs), generally with a short coupling interval, often referred to as short coupled torsade. The PVCs triggering the events may arise from the Purkinje ﬁbers or the myocardium; the former generally has shorter coupling intervals. Isoproterenol may be effective in suppressing VF storms in the acute setting.

predisposition to early afterdepolarizations and torsade de pointes. At least 15 different genes involved in inherited LQTS have been described. The ﬁrst 3—LQT1, LQT2, and LQT3—account for 60% to 75% of the genotyped LQTS cases.3 The remainder involve mutations related to other channel subunits or their regulator proteins. Approximately 25% of affected patients have no identiﬁable gene mutations.

Acquired LQTS is caused by QT-prolonging drugs. As of 2016, 48 medications were on the list of drugs known to cause torsades de pointes (including 10 removed from the United States market but which may still be available in other countries). Another 72 were on the list for possible risk and 32 were on the list for conditional risk. A list of drugs that have a risk of QT prolongation and/or torsades des pointes can be found on the CredibleMeds website (https://www.crediblemeds.org/).36 Electrolyte abnormalities or drugs that induce hypokalemia, hypocalcemia, or hypomagnesemia can also lead to torsades de pointes in patients with or without genetic susceptibility.

Short QT syndrome is rare but should be considered if the QT interval is markedly truncated with a nearly absent ST segment along with peaked and symmetrical T waves.3 Brugada syndrome—which is characterized by a distinct ECG pattern, the absence of structural heart disease, and a high risk of polymorphic VT/VF and sudden death—can present as electrical storm.3 In addition to over 100 different mutations of the sodium channel itself, mutations of genes that modulate sodium channel function are also associated with Brugada syndrome.37 Hypokalemia, high vagal tone, and fever are predisposing factors for electrical storm. Three different types of ECG changes have been associated with Brugada syndrome based on the morphology in V1 and V2.37 Type 1 ECG is characterized by a 2 mm or greater J-point elevation, coved type ST-T segment elevation, and inverted T wave in leads V1 and V2 (see Fig. 24.6). Type 2 ECG is characterized by a 2 mm or greater J-point elevation, 1 mm or greater ST segment elevation, saddleback ST-T segment, and a positive or biphasic T wave. Type 3 ECG is the same as type 2, except that the ST segment elevation is less than 1 mm. Among these three types of ECGs, only type 1 is diagnostic of Brugada syndrome.

In patients with a normal ECG and a structurally normal heart who present with polymorphic VT/VF storm, the possible diagnoses include catecholaminergic polymorphic VT (CPVT)

MANAGEMENT

Patients with electrical storm or incessant VT should be rapidly assessed for hemodynamic instability. Pulseless patients or those with clinical evidence of hemodynamic compromise manifested by hypotension, chest pain, dyspnea, or altered mental status should be immediately treated according to advanced cardiac life support (ACLS) protocols with electrical cardioversion.

PHARMACOLOGIC THERAPY

In hemodynamically stable patients with electrical storm or incessant VT, urgent pharmacologic therapy is indicated to both terminate the ventricular arrhythmia and to interrupt the detrimental effect of the associated intense adrenergic stimulation on the heart. Intravenous amiodarone is the most commonly used agent to treat patients with electrical storm or incessant VT in patients with structural heart disease (see Fig. 24.2). The usual dose is 150 mg by IV bolus followed by 1 mg/min IV infusion for 6 hours, followed by 0.5 mg/min for an additional 18 hours. Rapid intravenous infusion of amiodarone blocks fast sodium channels in a use-dependent fashion, meaning there is more channel blockade at faster heart rates. It also inhibits norepinephrine release and blocks L-type calcium channels without prolonging ventricular refractoriness. minimal negative inotropic effects and is therefore safe in patients with depressed LVEF. In addition, despite the potential for causing QT prolongation, the incidence of torsades de pointes is low. About 60% of patients will have their electrical storm terminated by intravenous amiodarone.

Because of the adrenergic stimulation associated with electri-

cal storm, incessant VT, or ICD shocks, β-blockers should be administered along with amiodarone. Although metoprolol is the more commonly used agent, propranolol may suppress electrical storm that is refractory to metoprolol.39 In patients with congestive heart failure, propranolol decreases sympathetic outﬂow more than metoprolol. Furthermore, the lipophilic nature

of propranolol enables penetration of the central nervous system, allowing blockade of central and prejunctional receptors in addition to peripheral β receptors.

40,41

propranolol is 1 to 3 mg every 5 minutes to a total of 5 mg. The

Amiodarone has

The dose of intravenous

CHAPTER 24 Electrical Storm and Incessant Ventricular Tachycardia 249

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dose of intravenous metoprolol is 2.5 to 5 mg over 5 minutes, which can be repeated to a maximum dose of 15 mg over 15 minutes. Oral amiodarone and β-blockers should be initiated once the patient is stable.

Lidocaine binds to fast sodium channels in a use-dependent fashion.34 However, outside of the setting of ischemia, lidocaine has relatively weak antiarrhythmic properties. Conversion rates from VT are 8% to 30% and a randomized trial has demonstrated that survival is signiﬁcantly greater with amiodarone than lidocaine for treatment of out-of-hospital, shock-resistant VT or VF.42 Thus, amiodarone has replaced lidocaine as ﬁrst-line therapy for refractory VT and VF. The 2017 American College of Cardiology/American Heart Association guidelines gives a IIa recommendation for intravenous lidocaine as a less effective alternative to amiodarone in the treatment of polymorphic VT associated with no reversible causes.2 If lidocaine is used, it is administered as an IV bolus of 1 to 1.5 mg/kg followed by an initial bolus of 0.5 to 0.75 mg/kg that can be repeated every 5 to 10 minutes as needed to a total dose of 3 mg/kg. A continuous IV infusion of 1 to 4 mg/min is used to maintain therapeutic levels.

In patients without structural heart disease, the treatment should be tailored to the speciﬁc underlying cause. Outﬂow tract VT can be suppressed by β-blockers that lower stimulated levels of cAMP and thus decrease intracellular calcium. Alternatively, nondihydropyridine calcium channel blockers, such as verapamil or diltiazem, may be effective at suppressing outﬂow tract VT by directly reducing intracellular calcium. The distinctive feature of fascicular VT is its sensitivity to intravenous verapamil, which is the preferred therapy. The response to class I antidysrhythmic drugs or β-blockers is variable.

The initial treatment of polymorphic VT storm in patients with LQTS is discontinuation of QT-prolonging medications and/or rapid correction of electrolyte abnormalities. β-Blockers are primary pharmacologic therapy for congenital long QT syndromes types 1 and 2. Intravenous verapamil effectively suppresses polymorphic VT in patients who are refractory to β-blockers. Intravenous magnesium may facilitate termination of polymorphic VT associated with LQTS. If the long QT syndrome genotype is known to be type 3, drugs with late sodium current blocking effects—such as mexiletine, ranolazine, and propranolol—are helpful. However, in patients with acquired LQTS, β-blockers may promote VT by inducing bradycardia. Temporary pacing is the treatment of choice in patients with bradycardia-dependent polymorphic VT in LQTS. Isoproterenol can be used while awaiting pacemaker insertion. In patients with short QT syndrome, class I and class III antidysrhythmic drugs—such as quinidine, disopyramide, and amiodarone—are effective at prolonging the QT interval. Isoproterenol suppresses VT storm in Brugada syndrome. Quinidine may also prevent VT/VF in Brugada syndrome.

The trauma that patients with electrical storm or incessant VT experience from multiple electrical cardioversions can have short-term and long-term physical and emotional consequences. Thus, all patients with electrical storm should be sedated. Shortacting agents—such as propofol, benzodiazepines, and some general anesthetics—have been shown to convert or suppress VT.43 Left stellate ganglion blockade and thoracic epidural

anesthesia have been reported to suppress electrical storm that was refractory to multiple antidysrhythmic therapies.

44,45

General

anesthesia may also be helpful.

NONPHARMACOLOGIC THERAPIES

For patients with electrical storm and incessant VT in whom acute myocardial ischemia is thought to be an inciting factor, coronary angiography and percutaneous revascularization should be urgently performed as restoration of coronary perfusion may terminate arrhythmias.

46,47

An intraaortic balloon pump or other temporary percutaneous LV mechanical support device may also be placed while in the catheterization laboratory. These devices may suppress ventricular arrhythmias by increasing coronary perfusion pressure or unloading a failing LV. Balloon counterpulsation has been reported to terminate electrical storm even in the absence of ischemia,48 presumably by reducing afterload, LV size, and wall tension. In extreme cases of refractory arrhythmias, extracorporeal membrane oxygenation can be considered but should be implemented early in the course before irreversible end-organ damage has occurred.34 Ultimately, recurrent refractory ventricular arrhythmias may be an indication to place an LVAD or list a patient for cardiac transplantation.

Catheter ablation is effective therapy for many patients with electrical storm or incessant VT refractory to or intolerant of medical therapy.

49–51

In one series, radiofrequency (RF) ablation completely suppressed drug-refractory electrical storm in 95 of 95 patients, many of whom were hypotensive and required hemodynamic support. Long-term suppression of electrical storm was achieved in 92% of patients and 66% were free of VT at 22

months.49 Notably, the endpoint of ablation was the elimination of all clinical VTs. Of the 10 patients who continued to have inducible VT, eight had recurrent electrical storm and four died despite ICD therapy. RF ablation is also indicated in recurrent polymorphic VT when speciﬁc triggers such as monomorphic PVCs can be identiﬁed and targeted.34 This approach has been successful in suppressing electrical storm in patients with both ischemic and nonischemic cardiomyopathies.

52–55

Antiarrhythmic therapy should be continued in CICU patients who have undergone RF ablation. Withdrawal of antidysrhythmic medications may be considered later.

CONCLUSION

Electrical storm and incessant VT are increasingly common lifethreatening syndromes characterized by poor short- and long-term outcomes. A diagnostic approach based on the ECG morphology of the ventricular arrhythmia (monomorphic versus polymorphic) and the presence or absence of structural heart disease facilitates

selection of the most appropriate therapies for these patients. The initial management consists of identifying and treating underlying ischemia, electrolyte imbalances, or other inciting factors. Amiodarone and β-blockers are appropriate initial therapy in most, but not all, patients. RF ablation may be helpful in patients who are refractory to appropriate antidysrhythmic medications.

The full reference list for this chapter is available at

ExpertConsult.com.

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35. Prystowsky EN, Padanilam BJ, Joshi S, Fogel RI. Ventricular arrhythmias in the absence of structural heart disease. J Am Coll Cardiol. 2012;59:1733–1744.

36. Schwartz PF, Woosley RL. Predicting the unpredictable. Druginduced QT prolongation and torsades de pointes. J Am Coll Cardiol. 2016;67:1639–1650.

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40. Tsagalou EP, Kanakakis J, Rokas S, Anastasiou-Nana MI. Suppression by propranolol and amiodarone of an electrical storm refractory to metoprolol and amiodarone. Int J Cardiol. 2005;99(2):341–342.

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Diagnosis and Treatment of Unstable Supraventricular Tachycardia

Nimesh Patel, Mark S. Link

OUTLINE

Introduction, 250 Epidemiology, 250

Diagnosis, 250 Therapy, 255

INTRODUCTION

Supraventricular tachycardias (SVTs) occur frequently in critically ill patients and are associated with increased morbidity and mortality. Immediate exact diagnosis is not necessary and initial management should focus on ensuring hemodynamic stability. Tachycardias should be characterized by QRS complex width, rate, regularity, and rapidity of onset, as initial treatment can be guided by these characteristics rather than a precise diagnosis.1 Hemodynamically stable regular tachycardias should initially be treated with vagal maneuvers or adenosine, as these are generally safe and short-acting interventions that not only terminate many tachycardias but also may provide important diagnostic information. Hemodynamically unstable SVT should be treated with synchronized direct current cardioversion (DCCV). After initial stabilization, focus should transition to establishing the etiology of SVT and considering the need for antiarrhythmic drugs or ablation.

EPIDEMIOLOGY

SVT occurs in up to 10% to 20% of critically ill intensive care unit (ICU) patients.2 While not usually life threatening, SVT is associated with increased morbidity and mortality, especially in patients who are critically ill. Several medical conditions frequently encountered in the ICU are associated with SVT, including sepsis, acute coronary syndrome, decompensated heart failure, hemorrhagic shock, pulmonary embolism, respiratory failure, and thyrotoxicosis. Any medical condition that stimulates a sympathetic response will enhance cellular automaticity and trigger premature ventricular or atrial contractions that promote arrhythmogenesis. In addition, atrial and atrioventricular (AV) nodal conductions are enhanced, which allows for reentrant arrhythmias.

DIAGNOSIS

Although the precise diagnosis of SVT is not necessary in its initial management, a differential can be generated by

assessing the QRS width, rate, regularity, and rapidity of onset (Table 25.1).

Wide complex tachycardias (WCTs) may be ventricular in origin (i.e., ventricular tachycardia [VT] or ventricular ﬁbrillation [VF]) or SVTs with left or right bundle aberrancy, preexcitation, or pacemaker tracking. If there is underlying heart disease, WCT is much more likely ventricular in origin and should be treated as such. In stable WCT, adenosine is useful diagnostically and therapeutically. VTs, but will not perturb reentrant VT.

Sinus tachycardia is characterized by a gradual onset of a regular tachycardia and generally reaches a maximum rate of around 220 beats/min minus the patient’s age (Fig. 25.1). The rhythm originates from the sinus node and the ventricular rate is proportional to the degree of hemodynamic stress. Sinus tachycardia is treated by addressing the underlying condition and is not considered to be pathologic itself; thus patients should not be given pharmacologic agents to control sinus tachycardia.

Atrial ﬁbrillation (Fig. 25.2) is the most common tachyarrhythmia encountered in critically ill patients. It is seen particularly in men, older patients, and in patients with underlying hypertension or cardiopulmonary disease. It occurs secondary to simultaneous depolarization of multiple wavelets within the atria, with variable conduction to the ventricle via the AV node and HisPurkinje system. Acute onset atrial ﬁbrillation is characterized by a rapid rise in ventricular rate and an irregular ventricular response. In patients who have chronic atrial ﬁbrillation, the ventricular rate rises gradually proportional to the degree of sympathetic activation from physiologic stress. In the absence of severe systolic left ventricular dysfunction or disorders that severely impair left ventricular ﬁlling, such as hypertrophic cardiomyopathy or severe left ventricular hypertrophy, atrial ﬁbrillation rarely causes hemodynamic instability. The surface electrocardiogram (ECG) shows an absence of discernable P waves and an irregular ventricular rhythm.

Atrial ﬂutter (Fig. 25.3) is the second most common pathologic SVT and, in its typical form, involves a reentry circuit around the tricuspid valve in the right atrium. Atypical atrial ﬂutters

It will terminate many of SVTs and idiopathic

250

CHAPTER 25 Diagnosis and Treatment of Unstable Supraventricular Tachycardia 250.e1

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Keywords

supraventricular tachycardia narrow complex tachycardia AVNRT AVRT atrial tachycardia atrial ﬁbrillation atrial ﬂutter

CHAPTER 25 Diagnosis and Treatment of Unstable Supraventricular Tachycardia 251

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TABLE 25.1 Differential Diagnosis of the Supraventricular Tachycardias (SVTs), Arranged

by Regularity

Rate

SVT

Atrial ﬁbrillation

(AF)

Multifocal atrial

tachycardia (MAT)

Underlying Conditions Regularity

Cardiac disease,

pulmonary disease, pulmonary embolism, hyperthyroidism, postoperative

Pulmonary disease,

theophylline

Irregular 100–220 Acute

Irregular 100–150 Gradual Changing P

(beats/ min) Onset P:QRS Ratio

None Transient gradual (if in chronic AF)

morphology prior to QRS

Adenosine Response ECG

slowing of ventricular rate

None

Frequent atrial

premature contractions (APC)

Sinus

tachycardia (ST)

Atrial ﬂutter

(Aﬂutter)

Atrioventricular

(AV) nodal reentrant tachycardia (AVNRT)

AV reentrant

tachycardia (AVRT)

Caffeine stimulants Irregular 100–150 Gradual P prior to QRS None

Sepsis,

hypovolemia, anemia, pulmonary embolism, pain, fear, fright, exertion, myocardial ischemia, hyperthyroidism, heart failure

Cardiac disease Regular

None Regular 150–250 Acute No apparent atrial

Rarely, Epstein

anomaly

Regular Up to 220

– Age

150 Acute Flutter waves Transient (occasionally irregular if variable AV conduction)

Regular 150–250 Acute Orthdromic AVRT:

Gradual P prior to QRS Transient

activity or R′ at termination of QRS

retrograde P wave

Antidromic AVRT:

P wave usually not seen

AF with WPW: no

P waves present

slowing

slowing of ventricular rate

Terminate

Terminate Orthodromic AVRT

Antidromic AVRT

Atrial

tachycardia (AT)

From Link MS. Clinical practice. Evaluation and initial treatment of supraventricular tachycardia. N Engl J Med. 2012 Oct 11;367(15):1438-1448. ECG, Electrocardiogram; WPW, Wolff-Parkinson-White syndrome.

Cardiac disease, pulmonary disease

AFib with WPW

Regular 150–250 Acute P prior to QRS Terminates

60%–80%

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