Wide QRS Complex Tachycardia

Etiology

If a patient is clinically stable and time permits, knowing the cause of wide QRS complex tachycardia provides an opportunity to appropriately manage the patient and significantly reduce the potential for morbidity and mortality. Below are some of the known causes of WCT, which also consists of the differential diagnosis.[1][2]

• Sodium channel blockade
• Hyperkalemia
• Hyper- or hypo-magnesemia
• Supraventricular tachycardia (SVT) with pre-existing or a rate-related bundle branch block (BBB)
• SVT with aberrant conduction
• Atrial fibrillation (Afib) with Wolff-Parkinson-White syndrome (WPWS)
• Mono-morphic ventricular tachycardia (VT)
• Ventricular fibrillation (VFib)
• Polymorphic VT (torsades de pointes)
• Pacemaker mediated tachycardia (PMT)
• Drug overdose and toxicities (i.e., TCA’s, digitalis, cocaine, lithium, diphenhydramine)
• Post-resuscitation (ROSC)
• EKG artifact

Epidemiology

Out of all the known causes for wide QRS complex tachycardia, there are two etiologies (VT, VF) that account for the most cardiac deaths in the U.S. It is estimated that there are 300,000 deaths per year due to these cardiac dysrhythmias. Between these two ventricular etiologies, VT tends to be the most common cause, accounting for approximately 80% of WCTs. This is especially true in patients with a history of cardiovascular disease (i.e., myocardial infarctions, coronary artery disease) and increases the likelihood to 90%. SVT is the third most likely cause of WCT, although it occurs less frequently. Out of the different causes of SVT, conduction with aberrancy appears to be the most likely cause of WCT. SVT with aberrancy accounts for approximately 21% of WCTs.[3][4][5]

History and Physical

When first assessing these patients, the physician must act quickly and determine whether the patient is stable or unstable. It is critical to first evaluate the patient’s ABCs (airway, breathing, circulation), which will guide your management. Patients who are unstable due to WCT present with a myriad of symptoms such as altered mental status, hypotension, pulmonary edema, or other signs of low end-organ perfusion (i.e., pallor, cyanosis, decreased body temperature). Once a patient is deemed stable, a focused history and physical exam should be made quickly as a patient’s clinical status can deteriorate suddenly. During an episode of WCT, patients will typically present with persistent chest pain that may be accompanied by one or more of the following symptoms, such as shortness of breath, diaphoresis, dizziness, and nausea. 

A patient’s medical history provides significant information that can help the physician to determine the potential cause of a WCT. Having a history of cardiovascular disease (i.e., myocardial infarction, coronary artery disease, congestive heart failure) will predispose patients to have WCTs secondary to ventricular etiologies. A small retrospective study concluded that there is a greater than 95% positive predictive value of VT for patients who had a history of previous myocardial infarction, congestive heart failure, or a recent episode of chest pain.[6] Additionally, physicians should thoroughly inquire about a patient’s medication history, particularly if they are taking any antiarrhythmics. These medications are known to prolong the QRS complex (which can be misinterpreted as WCTs), but more importantly and ironically, they can also cause arrhythmias. It is also imperative to ask patients if they have a pacemaker or to identify it on a physical exam. If a patient with a known permanent pacemaker were to present with a WCT, the device could be a cause of this arrhythmia and would change management/treatment.

Although subtle, a careful and scrupulous physical exam can strongly suggest the diagnosis of VT. During the physical exam, the physician should focus on signs of atrioventricular dissociation, which includes: irregular cannon A waves, changes in S1 heart sound, and labile systolic blood pressure with respect to heartbeats. All of these exam findings occur during VT because they indicate that the atria and ventricles are functioning independently of one another. It is important to know that the absence of these exam findings does not exclude VT as the cause of WCT, nor does it confirm SVT as an etiology. Some physical exam maneuvers can be helpful in distinguishing between SVT and VT. These are known as vagal maneuvers, which include: carotid sinus massage, Valsalva, coughing, breath holding, squatting, water immersion, and many others. SVT responds to vagal maneuvers by slowing down the heart rate and allowing atrial activity (p waves) to be easily seen. VT will typically not respond at all these maneuvers.[1]

Evaluation

Physicians should always remain vigilant when managing WCT as these patients can quickly become unstable and experience sudden cardiovascular collapse. The EKG will be an essential diagnostic tool that will assist in diagnosing the etiology of WCTs. A good rule of thumb is that any EKG with WCT is VT until proven otherwise. Rapidly and accurately diagnosing WCT still remains a problem because there are numerous algorithms and complicated criteria that can be difficult to remember in an emergency situation. Approximately 90% of WCTs can be diagnosed with almost absolute certainty, but despite the availability of numerous algorithms and criteria available, 10% of cases are still misdiagnosed. For the differentiation of WCTs, this article will review the most well-known approaches but will not discuss them in detail, given that they are complicated, and its use would be challenging in an urgent setting. 

Prior to the development of distinguished algorithms, WCTs were differentiated using the Traditional Criteria, which was created through the contribution of several authors such as Sandler, Swanick, Marriott, Wellens, Coumel, and Kindwall. The established subsequent step-wise algorithms would incorporate principles from the Traditional Criteria as well as developing new ones. The most famous and commonly used algorithm to date is the Brugada algorithm. Vereckei published two algorithms which proved to be superior to Brugada but were limited, given that they were more time consuming compared to Brugada. The ACC (American College of Cardiology), AHA (American Heart Association), and ESC (European Society of Cardiology) have developed an algorithm for the practical approach and evaluation of WCTs in otherwise hemodynamically stable patients. Important things to keep in mind are key aspects of the medical history (i.e., previous heart attack, history of congestive heart failure, chest pain, older age, structural heart disease) and physical exam (i.e., signs of atrioventricular dissociation) that have been discussed previously.

Morphology on EKG that is strongly suggestive for VT is AV dissociation, the finding of fusion beats and capture beats which signify AV dissociation, extreme axis deviation (NW axis), initial R or Rs wave in limb lead aVR, absence of RS complexes in precordial leads (leads V1-V6), positive or negative concordance across the precordial leads, and an R wave peak time >50 ms in limb lead II. The diagnosis of SVT as the cause for WCT would be more indicative if there is evidence of a typical BBB or fascicular block. Interestingly, if the QRS morphology during sinus rhythm is similar to the QRS morphology during an episode of WCT, this can either be SVT or VT. VT will usually be a regular rhythm depending on the timing of the WCT episode, history of anti-arrhythmic medication use, and history (or undiagnosed) focal idiopathic VT. Also, if a WCT appears to have an irregular rhythm, caution should be advised as the underlying etiology could be Afib with WPWS (or Afib with aberrancy), and mismanagement could lead to serious consequences. In concordance with EKGs, exam maneuvers can be helpful in distinguishing between SVT and VT. Vagal maneuvers (i.e., carotid sinus massage, Valsalva, coughing, etc.) cause an increase in parasympathetic tone/response, which would normally lower one’s heart rate. Tachycardia, which is resolved by vagal maneuvers, is most likely to be SVT. WCT caused by VT is typically known to not resolve with vagal maneuvers. However, interestingly enough, idiopathic outflow tract VT can be terminated from these maneuvers.[2][7][8][2]

Treatment / Management

Physicians must act quickly and determine whether a patient is stable or unstable when during their initial evaluation of WCT. It is critical to first evaluate both the patient’s ABCs (airway, breathing, circulation) and hemodynamic status because it will guide your management in the emergency setting. If the patient is unresponsive, not protecting their airway, or not breathing (but has a pulse) then they should be immediately intubated in order to secure their airway. If a patient has low oxygen saturation on the pulse ox, then supplemental oxygen should be initiated. If a patient does not have a pulse, immediately begin chest compressions and follow ACLS protocol guidelines. Intravenous access, EKG, cardiac rhythm monitoring, and blood pressure monitoring should be started immediately on all patients who complain of chest discomfort. Once a hemodynamically unstable patient is found to have a WCT, emergent cardioversion (or defibrillation) should be your next immediate step as it will reduce morbidity and mortality. It is critical to know how to cardiovert an unstable patient as these two methods of delivering electrical shocks are quite different. The presence or absence of an unstable patient’s pulse is what determines which type of cardioversion will be used. If the patient has a pulse, then synchronized cardioversion will be preferred as it will be coordinated with the heart’s electrical activity (QRS complex) to reduce the risk of inducing cardiac arrest. If the patient does not have a pulse, then this will be considered a cardiac arrest and requires immediate defibrillation.[9][10]

In stable patients, pharmacologic treatment should be based on the most updated AHA ACLS guideline along with cardioversion. Below you will find a modified algorithm from AHA guidelines for the emergency management and resuscitation of hemodynamically unstable patients presenting with WCT. It is important to always consider reversible causes (i.e. acute ischemia, myocardial infarction, electrolyte abnormalities, drug toxicities) in unstable patients because some can be easily corrected. As mentioned previously, if uncertain regarding the etiology of WCT, it is better to err on the side of caution and treat arrhythmia as VT given that it is the most common cause and has more detrimental consequences if managed inappropriately. During the emergent setting, it is necessary to stabilize the patient, treat any reversible causes, and leave the process of refining the diagnosis once the patient is admitted and stable. 

When considering a pharmacologic intervention, it is important to have some clinical suspicion about whether the origin of the WCT is coming from the atria or the ventricles.

• SVT will typically be managed with adenosine, Afib with WPWS will be treated with amiodarone, and Afib with aberrancy with either diltiazem or a beta-blocker.
• Typically, amiodarone will be the first-line drug of choice for all ventricular arrhythmias (VT, polymorphic VT, Vfib, etc.) Lidocaine can also be considered as a potential 2nd line medication but it should never be used for WCT of unknown origin.
• If the EKG shows evidence of Torsades de Pointes, then it is essential to give magnesium as this will be the most effective way to treat this ventricular arrhythmia. If Torsades is refractory to magnesium, one could perform overdrive pacing (heart rate of 90 to 130 bpm) which is generally successful in these circumstances.

If a patient is clinically stable and time permits, knowing the cause of their WCT will allow the physician to correctly treat/manage the etiology and further reduce the potential risk for morbidity and mortality. For example, VT (with pulses) is normally treated with either anti-arrhythmic medications or electrical cardioversion. If one were to mistake Afib for VT and treat with electrical cardioversion, this could have some serious consequences. When the atria beat irregularly/spastically, this increases the risk of clot formation on the atrial walls. A patient who is not anti-coagulated and was to receive cardioversion in the setting of Afib, their risk of possible stroke will be 1.5% due to clot dislodgement.[11] Another example is mistaking VT for SVT. As stated previously, SVT can be managed conservatively with vagal maneuvers or with medications (i.e. adenosine, diltiazem, verapamil). Adenosine effectively resolves tachycardia caused by SVT by blocking electrical conduction through the AV node. Giving adenosine in VT can effectively slow the rate which can aid in diagnosis and in some rare instances, can cardiovert.[12][13](A1)

One of the most important factors to consider when administering pharmacologic treatment for WCT is the possibility that a patient may have an alternative conduction pathway that is atypical of normal cardiac anatomy. These alternative pathways can either be outside of the AV node or within the AV node. These alternative pathways are problematic due to their faster electrical conduction velocities compared to the AV node. When these pathways are used, they result in faster activation of the ventricular myocardium and can create a positive feedback loop and lead to very high ventricular rates. The complications of these pathways could be potentiated by AV nodal blockade medications (i.e. adenosine, calcium channel blockers, and beta-blockers).

Erroneously giving adenosine in irregular WCT (or when there is a concern for an aberrant pathway) can cause coronary ischemia or precipitate dangerous arrhythmias such as Afib with RVR (rapid ventricular response), Vfib, or torsades de pointes.[3][5][14] With respect to calcium channel blockers (i.e. diltiazem and verapamil), these medications weaken the strength of cardiac contractions (negative ionotropy) and slow down the electrical conduction via the AV node. If a patient has an alternative conduction pathway, complications from these medications result in the use use of aberrant pathways which can lead to significant hemodynamic collapse from profound vasodilation, increased rate of VT, or degeneration to Vfib. (A1)

Patients with a known permanent pacemaker who presents with a WCT, the device should be considered as a potential cause of arrhythmia and would be managed differently. A magnet would be placed directly over the pacemaker and would likely terminate this arrhythmia. The magnet works by disabling the pacemaker’s atrial sensing capability and essentially reprograms it to an asynchronous form of pacing.[1][2][15](B3)

Differential Diagnosis

Below is a broad differential diagnosis for WCT, which also consists of potential etiologies.[1][2]

• Supraventricular tachycardia (SVT) with pre-existing bundle branch block (BBB)
• SVT with rate-related BBB
• SVT with aberrant conduction  
• Atrial fibrillation (Afib) with Wolff-Parkinson-White syndrome (WPWS)
• Ventricular tachycardia (VT)  
• Ventricular fibrillation (VFib)   
• Polymorphic VT (torsades de pointes)   
• Pacemaker mediated tachycardia (PMT)   
• Drug overdose (i.e., TCA’s, digitalis, cocaine, lithium, diphenhydramine) 
• Sodium channel blockers  
• Hyperkalemia  
• Hyper or hypo-magnesemia
• Post-resuscitation (ROSC)
• EKG artifact
• Genetic disorders 

• Long QT syndrome
• Short QT syndrome
• Hypertrophic cardiomyopathy
• Familial dilated cardiomyopathy
• Brugada syndrome
• Catecholaminergic polymorphic ventricular tachycardia
• Arrhythmogenic right ventricular dysplasia

Prognosis

Although there is a wide differential for the causes of WCT, the prognosis of all these etiologies is dependent on the duration of the arrhythmia, how it affected the hemodynamic stability of the patient during the episode, and if the patient had any subsequent complications from the event. Patients who are hemodynamically stable on initial presentation and their WCT is quickly terminated typically tend to have a better prognosis than those who are unstable because of the lower incidence of complications. Prognosis is also dependent on preventing the recurrence of WCT. Patients with a history of VT (or at increased risk for it) may be eligible for placement of implantable cardioverter-defibrillator (ICD) devices, which can help improve morbidity and mortality. Catheter ablation is also another potential treatment option for some etiologies of WCT, which can improve prognosis. Myocardial infarction is a potential complication during a WCT event, which can further worsen a patient’s prognosis due to the increased risk for sudden death. Left ventricular ejection fraction (LVEF) is strongly associated with a patient’s prognosis and can help determine those who are at risk for sudden cardiac death. Patients with an LVEF of < 30% are considered to have an overall annual mortality rate that approaches 10%.[2][15]

Complications

VT is the most common cause of WCT, and the severity of its complications is determined by the duration and frequency of the arrhythmia and predisposing risk factors. VT most commonly occurs in patients with a history of cardiovascular disease (i.e., coronary artery disease, myocardial infarctions, structural heart disease). Common complications of VT include frequent episodes of syncope (and associated physical injuries sustained during the syncopal event) as well as decreased efficiency of the heart to pump blood, which could lead to heart failure. Although a history of cardiovascular disease poses its own risk for complications, this, in conjunction with VT, has increased risk for the most feared complication - sudden cardiac death. This fatal complication is defined as a death that occurs unexpectedly, immediately or an abrupt change in a patient’s clinical presentation within one hour from the onset. Sudden cardiac death is believed to be secondary to VT deteriorating to the lethal Vfib arrhythmia.

In the United States, sudden cardiac death consists of 15% of the total causes of mortality and greater than half of all cardiac-related deaths. It is also important to keep in mind that a small portion of sudden cardiac deaths are from inherited familial disorders and should be carefully evaluated in patients with family members who were young, and died suddenly/unexpectedly.[15]