Palpitations and Arrhythmias (Case 6)

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Palpitations and Arrhythmias (Case 6)

Arzhang Fallahi MD and Michael Kim MD

Case: A 75-year-old man with a history of hypertension and hyperlipidemia presents to the emergency department complaining of palpitations. He states that for the past day he has felt a strange feeling in his chest, like his heart is racing, and says he is mildly short of breath. He has had similar episodes in the past, but they went away with rest and tended to “come and go.” He reports some light-headedness. He denies any chest pain, cough, or history of thyroid disease. He has never seen a cardiologist before and has never had “serious heart problems.” His only medications are aspirin 81 mg, hydrochlorothiazide 25 mg, and simvastatin 40 mg, all taken once daily. There is no family history of heart disease. His pulse is 135 bpm, and his BP is 145/70 mm Hg. On exam he seems to be in no acute distress but appears anxious. He has clear lung fields bilaterally and an irregular heart rate with no obvious murmurs, rubs, or gallops and no elevated neck veins. He has trace edema in his lower extremities.

An ECG reveals a narrow complex tachycardia at 135 bpm, irregularly irregular with no P waves and no delta waves; aVL shows a QRS complex of 12 little boxes in height; no other ST elevations or depressions are noted.

Differential Diagnosis

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Speaking Intelligently

The approach to a patient with palpitations is as follows:

1. Assess airway, breathing, and circulation with IV access, oxygen administration, and cardiac monitoring; with a 12-lead ECG; and with initial blood work (including troponin concentrations).

2. Clinically assess associated signs of the tachycardia: hypotension, heart failure or pulmonary congestion, shortness of breath, renal failure, shock, altered mental status, angina, or acute myocardial infarction. A quick assessment of vital signs must be made even before one takes a detailed history. Ultimately, is the patient stable or unstable? Arrhythmias such as ventricular tachycardia, ventricular fibrillation, or any heart rhythm with profound hypotension are a medical emergency, which may require immediate management.

3. The history of the palpitations is a key point. Is this new? Does the patient have a history of cardiac arrhythmias? Is the patient on any medications that may contribute? Are the palpitations associated with any chest pain? Is there any history of thyroid disease? The underlying cause of the tachycardia must be determined from the very outset. Is the patient having an acute coronary event? Does the patient have signs of heart failure or pulmonary disease? Is the patient hypo- or hypervolemic? Is the process acute or chronic in nature?

4. Assess for comorbidities: lung disease (asthma, chronic obstructive pulmonary disease [COPD], pulmonary hypertension, restrictive lung disease), cardiac disease, hypertension, age, diabetes, history of stroke. Comorbidities will help in risk-stratifying the patient, as well as in guiding management.

5. The tachyarrhythmia must be quickly assessed using the four main categories listed above to guide subsequent management.

PATIENT CARE

Clinical Thinking

• First and foremost, the patient must be quickly assessed systematically for airway, breathing, and circulation. Prompt IV access, administration of oxygen, and cardiac monitoring should be instituted. A STAT ECG is also critical to guide subsequent management of the tachyarrhythmia.

• Given the clinical presentation, the patient appears to be stable, but with such an elevated heart rate at rest, his condition is tenuous and requires prompt management. The irregular narrow complex tachycardia limits our main differential to atrial fibrillation, atrial flutter, and multifocal atrial tachycardia. Given the complete absence of P waves and no mention of flutter waves, this patient most likely has atrial fibrillation with a rapid ventricular response. This is the most common tachyarrhythmia seen, and given the patient’s age and history of hypertension, with a suggestion of LVH on the ECG, we can be even more confident in our diagnosis.

• The next two steps are to control the rate and determine the underlying cause of the atrial fibrillation. Certain history will help determine therapeutic options. Does the patient have normal LV function? Does the patient have Wolff-Parkinson-White syndrome? Is the duration of symptoms less than or more than 48 hours? Is anticoagulation indicated? Can the patient undergo electrical cardioversion safely, or would pharmacologic conversion be preferable? What is the risk of embolization? Is the ventricular rate too high?

• The patient is not hypotensive and shows no signs of heart failure. However, given his age and chronic symptoms, it is unclear if his symptoms have been going on for 48 hours or more. Together, this increases his risk for embolization; therefore, electrical cardioversion would not be the best initial option. One must look at comorbidities in determining which pharmacologic agent to use. Atrioventricular (AV) nodal agents such as β-blockers or calcium channel blockers are important for rate control, while amiodarone is one of the main agents used for rhythm control. In patients with severe asthma, β-blockers may exacerbate the condition, and in patients with heart failure and hypotension, calcium channel blockers can result in decompensation. In patients with severely reduced ejection fraction, agents such as digoxin, in combination with AV nodal agents, may be of benefit.

• There are various precipitants of atrial fibrillation, but initially acute coronary syndrome must be ruled out. Monitoring for signs of angina and elevated cardiac markers is crucial. Hypo- or hypervolemia may also trigger atrial fibrillation. Use of sympathomimetic agents such as caffeine, amphetamines, and cocaine can also trigger tachycardia and must be considered.

History

• Determine when the palpitations started and what triggered them. Associated symptoms, such as chest pain, may suggest an acute coronary event. Other contributing symptoms such as shortness of breath, leg swelling, and paroxysmal nocturnal dyspnea may suggest CHF. Symptoms such as weight loss and heat intolerance may suggest an endocrine etiology such as hyperthyroidism. The time course of symptoms is also important. Is this acute, chronic, or intermittent?

• Risk stratification, such as patient age, history of CHF, diabetes, and history of stroke, will help guide subsequent management.

• Medications, diet, and social history: Has the patient taken any medications that may have contributed to tachycardia? Does the patient have a history of illicit drug use?

Physical Examination

• Vital signs: Assess the patient’s heart rate, and check for hypertension or hypotension. The patient should also be assessed for respiratory distress and oxygen saturation. Monitor the patient’s temperature to see if infection may be the cause for the underlying condition.

• General appearance: Examine for diaphoresis, respiratory distress, and signs of shock for potential hypotension requiring immediate intervention.

• Respiratory exam: Listen to breath sounds bilaterally to make sure they are symmetric, and listen for any signs of fluid accumulation from either pulmonary and/or cardiac dysfunction or other diseases. Percussion may help identify areas of consolidation.

• Cardiac auscultation (to determine if rate is regular or irregular): Determine whether the heart sounds appear distant, which may suggest a pericardial effusion; assess for murmurs and abnormal heart sounds, since an S3 gallop may indicate CHF or a dilated chamber, while an S4 gallop may indicate the stiff LV of hypertensive heart disease. Look at neck veins to see if they are elevated, which may indicate volume overload or an inability to adequately distribute blood volume.

• Vascular auscultation (carotid bruits): to assess atherosclerotic status.

• Abdominal examination: Assess that there is no evidence of an acute abdomen or possible gastrointestinal hemorrhage, which could have led to the tachycardia.

• Neurologic examination: Quickly assess patient’s mental status to determine if there is adequate perfusion of the brain. A screening neurologic exam should be performed to see if there are any focal deficits that might preclude use of anticoagulation therapy.

• Extremities: Check to see if extremities are warm to assess perfusion.

Tests for Consideration

• ECG is critical to obtain in all patients promptly.
ECG can be used to categorize the type of tachyarrhythmia, which will help guide management.

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• Cardiac markers (serum troponins and/or CK-MB) are needed to determine if an acute coronary syndrome is precipitating the event.

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• Metabolic panel with thyroid-stimulating hormone (TSH), creatinine, and electrolytes will help determine if an underlying metabolic disturbance is resulting in cardiac dysfunction. An acute decompensation in renal function may be a sign of shock. A low TSH concentration may suggest hyperthyroidism.

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• Complete blood count: to determine if the patient has an underlying infection, which may contribute to the tachyarrhythmia. Hemoglobin and hematocrit are important to determine if the patient is anemic.

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• Liver function tests may be helpful to help ascertain if there is a hepatic cause of infection.

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• Coagulation tests are helpful to see whether the patient is prone to thrombosis or at high risk of bleeding. They are also helpful if the patient is to have a procedure, such as ablation to treat the arrhythmia.

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• A urine toxicology screen should be obtained in patients suspected of using illicit drugs as a precipitant of the arrhythmia.

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IMAGING CONSIDERATIONS

→ Chest radiography is helpful to see if any pulmonary disease or process such as a pneumonia, effusion, or pneumothorax is present. Cardiomegaly can be assessed, but quality may be suboptimal with a portable chest radiograph. Radiography can also help determine if there is a widened mediastinum, which may be suggestive of an aortic dissection.

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→ Echocardiography is helpful not only to assess ventricular and valvular dysfunction, but also possibly to help determine if there is a thrombus, which may embolize if the patient is cardioverted.

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Clinical Entities Medical Knowledge

Atrial Fibrillation/Atrial Flutter

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Atrial fibrillation and atrial flutter are often caused by underlying heart disease (of any etiology), which contributes to heart failure and atrial enlargement, an increase in atrial pressure, or infiltration or inflammation of the atria. Metabolic causes such as hyperthyroidism can also precipitate atrial fibrillation or flutter, as can cardiac surgery. Often episodes of paroxysmal atrial fibrillation are triggered by premature atrial beats, while other episodes are triggered by atrial tachycardia or atrial flutter. Ectopic foci are mostly located in the pulmonary vein in atrial fibrillation, while in atrial flutter the conducting reentrant circuit can be located in the low right atrial isthmus between the orifice of the inferior vena cava and annulus of the tricuspid valve.

TP

Classically the patient presents with palpitations, dyspnea, dizziness, and reduced exercise capacity and may exhibit chest pain (which may suggest acute coronary syndrome as a precipitant).

Dx

Diagnosis is made on clinical grounds, but the most informative test is the ECG. Patients in atrial fibrillation will have a complete absence of P waves and irregularly irregular RR intervals with varying amplitude and morphology. Atrial fibrillation is typically a narrow-complex tachycardia unless accompanied by fascicular block, preexcitation via an accessory pathway, or aberration. In atrial flutter, P waves are absent, with F waves or “sawtooth”-appearing flutter waves at a rate most typically 300 bpm. The ventricular response is usually one half the atrial rate (2 : 1 AV nodal conduction). Atrial flutter should always be considered when the ventricular rate is around 150 bpm.

Tx

Management of atrial fibrillation or flutter depends on the clinical presentation. Patients with severe hypotension or shock secondary to their underlying rhythm should undergo immediate cardioversion. In more stable patients, consider whether to use rate control or rhythm control (attempt to convert the patient to normal sinus rhythm), and consider prevention of systemic embolization. Treatment is also guided by the type of atrial fibrillation, whether it is paroxysmal (self-terminating), persistent (fails to self-terminate within 7 days), permanent (lasts for more than 1 year and cardioversion has not been attempted or failed), or lone (which describes paroxysmal, persistent, or permanent atrial fibrillation in patients without structural heart disease).

Rate control with chronic anticoagulation is recommended for most patients. The most common agents for rate control are AV nodal agents such as β-blockers and calcium channel blockers (diltiazem or verapamil). In patients with heart failure or hypotension, digoxin may be helpful, although it has a longer onset of action. Amiodarone can also control rate but is not used as a primary therapy.

Rhythm control can be divided into external synchronized DC cardioversion and pharmacologic cardioversion. Caution should be exercised in patients with symptoms lasting more than 48 hours, as they are at higher risk of embolization from atrial thrombi, which can form due to turbulent flow in the atria while the patient is in atrial fibrillation; in these patients, anticoagulation is required or thrombi should be excluded with transesophageal echocardiography. In patients with minimal heart disease, agents such as flecainide or propafenone can be used, while amiodarone and dofetilide are preferred for patients with reduced LV ejection fraction or heart failure.
 

Radiofrequency catheter ablation is another modality to treat atrial fibrillation and atrial flutter. In most cases of atrial fibrillation, the focus is located inside the pulmonary veins, with the left superior vein being the most common site. In patients with atrial flutter, the macroreentrant pathway is located in the right atrium and is generally more amenable to ablation than in atrial fibrillation.

The annual risk for stroke in patients can be estimated using the CHADS2 score, which assigns a point for every comorbidity—CHF, hypertension, age over 75 years, diabetes—and 2 points for prior stroke. A higher CHADS2 score means patients would benefit from anticoagulation with agents such as warfarin sodium (Coumadin), although patient comorbidities must be taken into account especially in patients with a history of bleeding. A new class of agents, the direct thrombin inhibitors (e.g., dabigatran), is now available for anticoagulation in patients with atrial fibrillation; use of these agents does not require INR monitoring. See Cecil Essentials 10.

Multifocal Atrial Tachycardia (MAT)

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In most cases the different P-wave morphologies seen on the ECG suggest that a pacemaker arises in different locations within the atria. Cardiac disease (coronary, valvular, and congestive heart failure) is associated with MAT. Pulmonary disease, especially COPD, is also associated with MAT. Pulmonary arterial hypertension results in increased right atrial stretch, which can result in ectopic atrial activity. Hypokalemia and hypomagnesemia can also contribute to MAT.

TP

Patients may not have symptoms or may complain of palpitations. One must always consider the underlying cause that is contributing to the arrhythmia.

Dx

Diagnosis is made by ECG, which reveals P waves with three different morphologies (best seen in leads II, III, and V1), atrial rate over 100 bpm, P waves separated by isoelectric intervals, and PP, PR, and RR intervals that vary.

Tx

Treatment should be focused the underlying disorder. β-Blockers and calcium channel blockers (i.e., verapamil) have been shown to be effective. Due to risk of bronchospasm in patients with pulmonary disease, verapamil is most commonly used, although in the absence of such comorbidities, agents such as metoprolol can also be effective. Repletion in those with low magnesium (and even in those with normal magnesium) may be of some benefit. Repletion of potassium may also be of benefit. Ablation may be an option in some patients with MAT. See Cecil Essentials 10.

Atrioventricular Nodal Reentrant Tachycardia (Junctional Reciprocating Tachycardia)

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Structural heart disease is not required for AVNRT, and most times AVNRT develops in patients with otherwise normal hearts, although it can also occur in patients with organic heart disease. While there are usually no precipitating factors, AVNRT can be brought on by nicotine, alcohol, stimulants, or surges in vagal tone.

In patients with normal sinus rhythm, a normal sinus beat enters the AV node and passes down both fast and slow pathways. The fast pathway reaches the His bundle, creating a refractory wake. Consequently this blocks the impulse from the slow pathway, since the area in the final common pathway is refractory because of the fast pathway that just traveled through it. In the most common form of AVNRT, a critically timed premature beat goes down the slow pathway (which has recovered excitability), and the beat conducts down through the final common pathway to the bundle of His. Meanwhile, if the fast pathway has recovered excitability, the impulse via the slow pathway can conduct retrograde up the fast pathway. This creates a circuit, which then conducts down the slow pathway following retrograde conduction up the fast pathway, resulting in a sustained tachycardia.

TP

Patients typically present with palpitations, a strange feeling in the chest, and possible dizziness. In severe cases, patients may feel dyspnea and chest pain, and possibly fatigue or syncope.

Dx

Diagnosis is made by ECG. Usually the rate is between 120 and 220 bpm. In most cases, the retrograde atrial activation causes the P wave to be buried or fused with the QRS complex. If the P wave occurs shortly after the QRS complex, a fused waveform can appear as a pseudo-R’ in lead V1 and a pseudo-S wave in the inferior leads. The axis of the P wave, because of retrograde activation, is typically inverted in leads I, II, III, and aVF.

Tx

In unstable patients with evidence of hemodynamic collapse, DC cardioversion is the treatment of choice. In the absence of severe symptoms or hemodynamic collapse, vagal maneuvers (carotid massage, cough, Valsalva) can be used to break the rhythm. Adenosine can be used for rapid conversion to sinus rhythm. Non-dihydropyridine calcium channel blockers or β-blockers can also be used. For chronic cases of AVNRT, patients can undergo catheter ablation. See Cecil Essentials 10.

Atrioventricular Reentrant (or Reciprocating) Tachycardia

Pφ

In AVRT a defined circuit exists consisting of two distinct pathways: the normal AV conduction system and an AV accessory pathway, which are linked by proximal tissue (the atria) and distal tissue (the ventricles). The two major forms of this type of arrhythmia are orthodromic AVRT and antidromic AVRT.

In orthodromic AVRT (OAVRT), a premature atrial or ventricular beat is blocked in the bypass tract but conducts slowly to the ventricle over the AV node/His-Purkinje system. The impulse may travel retrograde into the AV accessory pathway, and back down anterograde down the normal AV conduction system, which completes a reentrant circuit resulting in a sustained tachycardia.

In antidromic AVRT (AAVRT), the ventricles become activated anterogradely via the AV accessory pathway, which is then followed by retrograde conduction over the AV node/His-Purkinje system, which then completes the reentrant circuit.

TP

Similar to symptoms in patients with AVNRT.

Dx

In OAVRT the ECG shows a narrow-complex tachycardia, typically 150 to 250 bpm, with P waves inscribed within the ST-T segment with an RP interval usually less than one-half the tachycardic RR interval. The RP interval remains constant. In AAVRT, the ECG shows a wide QRS complex (retrograde conduction over the AV node/His-Purkinje system), with regular RR intervals and ventricular rates of up to 250 bpm. This wide-complex tachycardia with an up-sloping “delta wave” is called Wolff-Parkinson-White (WPW) syndrome.

Tx

For OAVRT, acute termination may be achieved with increases in vagal tone, such as carotid sinus massage and the Valsalva maneuver. If these do not terminate the tachycardia, IV verapamil or adenosine may be used and are the preferred agents. Procainamide and β-blockers can be used but are second-line agents. If the etiology of the wide QRS tachycardia is unknown, IV procainamide is the drug of choice.

AAVRT must first be distinguished from other wide-complex tachycardias, mainly VT. The drug of choice is procainamide. Unless the diagnosis is certain, β-blockers, calcium channel blockers, adenosine, and digoxin should be avoided to prevent an undiagnosed wide-QRS tachycardia, such as ventricular tachycardia, from degrading into ventricular fibrillation. Patients with WPW who have atrial fibrillation will have preferential conduction via the accessory pathway with these agents, and thus the agents should be avoided. See Cecil Essentials 10.

Ventricular Tachycardia

Pφ

VT occurs within the ventricular myocardium distinct from the normal conduction system. Compared to a normal supraventricular beat, ventricular activation is slower and results in a wide QRS complex. VT is the most common wide-complex tachycardia, especially in patients with a history of cardiac disease.

TP

Symptoms are important for assessing the severity of hemodynamic compromise and may consist of chest pain, syncope, shock, seizure, and cardiac arrest. Comorbidities such as prior cardiac disease may also be a key factor in the typical presentation of VT.

Dx

Wide-complex tachycardias, especially in patients with coronary disease, should be treated as VT unless proven otherwise. VT presents as a wide-complex tachycardia but may also be confused as supraventricular tachycardia [SVT] with aberrancy (an SVT with slow conduction down the AV node or His-Purkinje system). Findings that suggest VT are concordance (QRS complex that is monophasic with the same polarity), AV dissociation (atrial rate slower than the ventricular rate), and the presence of fusion beats (supraventricular beat following a P wave that fuses with a complex originating in the ventricle).

Tx

In unstable patients, immediate synchronized external cardioversion should be performed. In stable patients with known or presumed VT, external cardioversion may also be used. In refractory or recurrent VT, IV amiodarone (recommended in most settings because it acts on both atrial and ventricular arrhythmias), procainamide or lidocaine may be used. See Cecil Essentials 10.

 

Practice-Based Learning and Improvement: Evidence-Based Medicine

Title
A comparison of rate control and rhythm control in patients with atrial fibrillation

Authors
Van Gelder IC, Hagens VE, Bosker HA, et al.; Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation Study Group

Institution
AFFIRM Clinical Trial Center, Axio Research, 2601 4th Avenue, Suite 200, Seattle, Washington 98121, USA

Reference
N Engl J Med 2002;347:1834–1840

Problem
The treatment of atrial fibrillation has relied on two basic strategies: rhythm and rate control. Rhythm control offers the prospect of maintaining sinus rhythm, while rate control can be achieved with drugs that are generally less toxic. A comparison of these two strategies with respect to mortality before this trial had not been performed.

Intervention
A total of 4060 patients with atrial fibrillation were randomized to receive either rate control (with β-blockers, calcium channel blockers, digoxin, or combinations of these drugs) or rhythm control (amiodarone, sotalol, propafenone, procainamide, quinidine, flecainide, disopyramide, moricizine, dofetilide, or combinations of these drugs). Average length of follow-up was 3.5 years.

Quality of evidence
Level I

Outcome/effect
The primary end point was overall mortality. The composite secondary end points were death, disabling stroke, disabling anoxic encephalopathy, major bleeding, and cardiac arrest. The overall mortality between the two groups was not statistically significant. The rates of composite end points were also similar in both groups. The rhythm control group did have higher rates of bradycardic arrest and TdP.

Historical significance/comments
This was an important trial that showed that rhythm and rate control are associated with no difference in mortality. Since the rhythm control group had more complications and used drugs with higher potential toxicity, this trial was instrumental in physicians adopting a rate control strategy initially in most patients with atrial fibrillation.

 

Interpersonal and Communication Skills

Assist Patients in Making Informed Decisions

In patients diagnosed with atrial fibrillation, use of anticoagulation raises many issues of balancing the benefits and risks. The patient should understand that the reason for use of anticoagulation is to prevent stroke, but must also be made to realize that with this comes a risk of bleeding and the need for careful monitoring. These concerns should be factored into the decision to choose this therapy. Patients must be given complete information to make informed decisions about this treatment modality, and their decisions must be respected.

 

Professionalism

Ensure Access to Care for the Medically Vulnerable

Management of cardiac arrhythmias requires long-term follow-up with either a primary-care physician or cardiologist (or both). When patients with atrial fibrillation are started on a rate control strategy, they need to be followed to determine how effectively the medication is working and how well they are tolerating it. Furthermore, with the need for anticoagulation, patients must be closely monitored to be sure they are anticoagulated at the appropriate level (INR of 2–3 if on warfarin) and to be monitored for signs of bleeding. Access to health care and to proper follow-up is an important issue in these patients and should be a major concern for physicians.

 

Systems-Based Practice

Anticoagulation: Coordinating Care in the Outpatient Setting to Reduce Costs and Complications

The decision to begin anticoagulation for a patient with atrial fibrillation has important considerations at the outset of therapy. Many patients are started on anticoagulation as part of an inpatient hospital admission. Traditionally, these patients had remained in the hospital until their INRs were therapeutic, at times adding multiple days to an inpatient stay without the acuity to warrant continued hospitalization. Most hospitals now have instituted pathways to bridge patients at home until they are fully anticoagulated. These programs involve the coordinated use of subcutaneous injections of a low-molecular-weight heparin in conjunction with oral warfarin. INRs are monitored at home through a visiting nurse or home care agency. Cost and access to both the subcutaneous injections and the home care services may be a barrier for some patients. Many hospital-based programs, however, have now rectified this by providing the medication to the patients from hospital funds. The cost of care from the hospital perspective is reduced when the patient is discharged home with appropriate follow-up, and the risk of hospital-related health complications is decreased. Newer anticoagulants (such as dabigatran) may also help to reduce unnecessary length of stay for some patients by eliminating the need for continuous blood draws to assess the efficacy of oral anticoagulation.

Suggested Readings

Arnsdorf MF. Treatment of multifocal atrial tachycardia. Article in UpToDate version 17.2 last updated January 11, 2006.

Arnsdorf MF, Ganz LI. Approach to the diagnosis of narrow QRS complex tachycardias. Article in UpToDate version 17.2 last updated February 14, 2008.

Arnsdorf MF, Podrid PJ. Tachyarrhythmias associated with accessory pathways. Article in UpToDate version 17.2 last updated April 29, 2005.

Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients with Supraventricular Arrhythmias). J Am Coll Cardiol 2003;42:1493–1531.

Fuster V, Rydén LE, Cannom DS, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients with Atrial Fibrillation). J Am Coll Cardiol 2006;48:149–246.

Podrid PJ. Overview of the acute management of tachyarrhythmias. Article in UpToDate version 17.2 last updated February 10, 2008.

Podrid PJ, Ganz LI. Approach to the diagnosis and treatment of wide QRS complex tachycardia. Article in UpToDate version 17.2 last updated March 31, 2009.

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