Saturday, April 3, 2021

Wide Complex Tachycardia Case File

Posted By: Medical Group - 4/03/2021 Post Author : Medical Group Post Date : Saturday, April 3, 2021 Post Time : 4/03/2021
Wide Complex Tachycardia Case File
Eugene C. Toy, Md, Michael d . Faulx, Md

Case 15
A 54-year-old man presents to the emergency department complaining of tachypalpitations and lightheadedness. He denies syncope, chest pain, exertional dyspnea, orthopnea, lower extremity edema, nausea, vomiting, or diaphoresis. His symptoms have been intermittent for several weeks, usually lasting less than 1 minute. However, today his symptoms have persisted for several hours. His medical history includes coronary artery disease with a remote inferior myocardial infarction requiring stenting, hypertension. hyperlipidemia. diabetes mellitus, and a 40-pack/year history of smoking with moderate to severe chronic obstructive lung disease. His medications are aspirin, atorvastatin, metoprolol succinate, lisinopril, metformin, and an inhaled long-acting β-agonist and anti cholinergic bronchodilator. On exam, he is mentating appropriately but appears anxious. His blood pressure is 105/68 mmHg. his pulse is 175 bpm. his oxygen saturation is 93%, and he is afebrile. There is no jugular venous distention. Pulmonary exam demonstrates a few scattered expiratory wheezes bilaterally but no rales. Cardiac exam is pertinent for tachycardia but no murmurs or rubs. The abdominal, musculoskeletal, neurologic, and skin exams are benign. Labs are normal, including potassium, magnesium, and a point-of-care troponin T (TpT). Baseline ECG (Figure 15-1) and ECG obtained on presentation (Figure 15-2) are shown.
  • What is the most likely diagnosis?
  • What is the best next diagnostic step?
  • What is the best next step in therapy ?
ECG Wide Complex Tachycardia

Figure 15-1. Baseline ECG for the main subject of this case.


Wide Complex Tachycardia ECG

Figure 15-2. Presenting ECG for the main subject of this case.


Answer to Case 15:
Wide Complex Tachycardia

Summary: A 54-year-old-man with a history of coronary artery disease and myocardial infarction presents to the emergency room with sustained tachypalpitations. He has been having intermittent symptoms of the same palpitations over the preceding several weeks, but this is the first time it has lasted more than a minute. He denies symptoms of presyncope, syncope, chest pain at rest or with exertion, dyspnea on exertion, orthopnea, lower extremity edema, nausea, vomiting, or diaphoresis. His blood pressure is 105/68 mmHg, his pulse is 175 bpm, his oxygen saturation is 93%, and he is afebrile. His exam demonstrates tachycardia and is without signs of heart failure. Lab work is normal. His ECG is shown in Figure 15-1.
  • Most likely diagnosis: Ventricular tachycardia.
  • Next diagnostic step: Review ECG for Brugada’s criteria.
  • Next step in therapy: If the patient is unstable in any manner, perform emergent synchronized cardioversion. If the patient is stable, consider administration of an IV antiarrhythmic drug such as amiodarone and/or urgent cardioversion.
ANALYSIS

Objectives
  1. Be able to identify a wide complex tachycardia (WCT) and know the next immediate steps in treatment.
  2. Become familiar with the differential diagnosis for wide complex tachycardia, and understand the criteria used to differentiate ventricular tachycardia (VT) from supraventricular tachycardia (SVT) with aberrancy.
  3. Understand the criteria for placement of an implantable defibrillator for primary and secondary prevention.
Considerations
This patient’s ECG shows a wide complex tachycardia (WCT). While there is a differential diagnosis that needs to be considered, the clinical status of patients in a WCT can vary from stable to cardiac arrest, and status may change rapidly. Therefore, the first priority for any patient in a WCT is to assess their clinical status. If there is no pulse, there should be immediate initiation of CPR along with advanced cardiovascular life support (ACLS) or basic life support (BLS) algorithms, including cardioversion. Even in the setting where a pulse is present, if there are signs of clinical instability, defined as hypotension (SBP < 90 mmHg), altered mental status, angina, or heart failure, the patient requires immediate cardioversion. In both cases, cardioversion should be synchronized if possible, reserving unsynchronized cardioversion for ventricular fibrillation (VF). In settings where the patient is stable, such as the one described in this case, the etiology of the WCT should be assessed through an evaluation of the ECG and history taking.

In an unselected patient population presenting with a WCT, the rhythm is ultimately determined to be ventricular tachycardia (VT) in 80% of cases. This number increases to >90% in patients with a prior myocardial infarction. VT is also more common in adult patients, compared to pediatric patients. Therefore, in an adult patient presenting with a WCT, if the rhythm cannot be determined, it is reasonable to treat them as if it is VT. This is especially true because treating a SVT as a VT is safe, while treating a VT as SVT can be harmful.

Approach To:
Wide Complex Tachycardias

DEFINITIONS

WIDE COMPLEX TACHYCARDIA (WCT): A rhythm with a rate >150 bpm and a QRS duration of >120 ms.

VENTRICULAR TACHYCARDIA (VT): A rhythm originating below the level of the AV node. Most commonly, this rhythm originates within the ventricular tissue itself and is associated with scarring in the ventricle. On the ECG this generally produces a wide QRS as the electrical signal propagates cell to cell through the ventricles without the aid of the His-Purkinje system.

SUPRAVENTRICULAR TACHYCARDIA (SVT): A rhythm originating at the level of the AV node or higher, namely, the SA node, atria, or the AV node itself. These rhythms tend to produce a narrow QRS complex as the electrical signal from the AV node propagates via the His-Purkinje system. However, the QRS can be wide if there is an accessory pathway or aberrant conduction.

ACCESSORY PATHWAY: A connection between the atrium and the ventricle that is not part of the AV node. Accessory pathways can result in preexcitation of ventricular tissue, characterized by a delta wave as is seen in Wolff-Parkinson- White (WPW) syndrome. An accessory pathway can also result in atrioventricular reentrant tachycardia (AVRT) in which a circuit is created as the signal from the SA node travels down the accessory pathway, up the AV node, and back down the accessory pathway–or the reverse.

ABERRANT CONDUCTION: Conduction of a supraventricular impulse into the ventricle in an abnormal manner, such as is seen with a right or left bundle branch block. This abnormal conduction produces a wide QRS.


CLINICAL APPROACH

Etiologies
Wide complex tachycardias are the result of a rhythm originating in the ventricle or a SVT conducting aberrantly or via an accessory pathway. However, by far the most common WCT is VT. VT is described as either sustained (episodes lasting >30 seconds) or nonsustained VT. VT is further divided into monomorphic VT (MMVT) and polymorphic VT (PMVT). In MMVT all the beats look the same because they are all coming from the same source (Figure 15-3a). This source is either an area within the ventricle with increased automaticity or, more typically, from a reentrant circuit. The reentrant circuit is similar to those found in atrial flutter or AVNRT, and classically occurs around an area of scar from a myocardial infarction. This is why WCTs are more likely to be VT in patients with known CAD, as they are the patients with the substrate to form these circuits. Patients with cardiomyopathy and decreased left ventricular ejection fractions are also at high risk for VT.

Polymorphic VT is a WCT where the QRS changes morphology, axis, or both (Figure 15.3b). Unlike the scenario in MMVT, where there is one source initiating the rhythm, in PMVT there are multiple simultaneous circuits. The changes in morphology seen on the ECG are the summed vectors of these multiple electric circuits within the ventricle. PMVT is often categorized into those without prolonged QT and those with prolonged QT.

The QT interval is measured from the onset of the Q wave to the end of the T wave, and represents ventricular repolarization. It is affected by heart rate, and is corrected using Bazett’s formula, dividing the QT interval by the square root of the RR interval (QTc = QT/√RR), where QTc is the corrected QT interval. The QTc is prolonged for men if it lasts for >450 ms and for females, for >470 ms. QTc prolongation can be inherited or acquired through electrolyte abnormalities or medication use. Hypokalemia and hypomagnesemia can cause QTc prolongation, as can the use of medications such as quinolone antibiotics (ciprofloxacin), antipsychotics (Haldol), antiarrhythmic drugs (amiodarone, flecanide, sotalol), and many other medications.

In patients with a normal QTc and PMVT, most cases are related to myocardial ischemia (Figure 15-3b). In patients with a prolonged QTc and PMVT, it is called torsades de pointes (TdP), which translates to “twisting of the points.” This description is derived from the “twisting” of the QRS complex around the isoelectric baseline. Long QT is a predisposition for an R-on-T phenomenon, which occurs when a premature ventricular contraction lands on the T wave. At this point in the cardiac cycle the ventricle is in a relative refractory period, and the extra stimuli from the PVC can initiate TdP (Figure 15-3c).

Ventricular fibrillation (VF) occurs when there is uncoordinated contraction of the ventricle. This is always a nonperfusing rhythm and a dire medical emergency (Figure 15-3d). This should be treated with immediate initiation of CPR along with advanced cardiovascular life support (ACLS) or basic life support (BLS) algorithms, including defibrillation. VF is seen in cardiac ischemia, severe electrolyte disturbances, and overdoses of cardiotoxic medications.

Supraventricular tachycardias are rhythms originating at the level of the AV node or higher, namely, the SA node, atria, or the AV node itself. These rhythms tend to produce a narrow QRS complex as the electrical signal from the AV node propagates via the His-Purkinje system. However, in two specific circumstances a SVT can cause a WC: when there is an accessory pathway, or when there is aberrant conduction. If there is an accessory pathway, the signal can reach the ventricle through this access point before the signal from the AV node. These two eventually meet and form the QRS, but the signal from the accessory pathway comes earlier

Monomorphic ventricular tachycardia
Monomorphic ventricular tachycardia ECG

Polymorphic ventricular tachycardia
Polymorphic ventricular tachycardia ECG

Torsades de pointes
Torsades de pointes ECG

Ventricular fibrillation
Ventricular fibrillation ECG

Atrial fibrillation with a Wolf-Parkinson-White accessory pathway
Atrial fibrillation with a Wolf-Parkinson-White accessory pathway

Antidromic AVRT

Atrial flutter with aberrant conduction
Atrial flutter with aberrant conduction ECG

Atrial fibrillation with aberrant conduction
Atrial fibrillation with aberrant conduction ECG

Figure 15-3. Examples of wide complex tachycardias.

than that from the AV node, resulting in a slurring of the QRS called a delta wave. When a patient with an accessory pathway develops an atrial arrhythmia such as atrial fibrillation or atrial flutter, it can appear as a WCT (Figure 15-3e).

Accessory pathways can also result in AVRT. AVRT is classified as antidromic or orthodromic depending on the pathway that initially depolarizes the ventricle. Antidromic AVRT is a rhythm where a signal from the SA node travels down the accessory pathway into the ventricle, up the AV node, and back down the accessory pathway. Because the ventricle depolarization is being initiated via the accessory pathway, and not the AV node and His-Purkinje system, the QRS will be wide. Alternatively, in orthodromic AVRT the signal initially propagates normally through the AV node and down the His-Purkinje system, but returns through the accessory pathway and back down the AV node. This will produce a narrow complex tachycardia because the His-Purkinje system is involved in the initial ventricular depolarization.

Another instance when a SVT can produce a WCT is in the presence of aberrancy. Patients with a bundle branch block who develop atrial flutter or atrial fibrillation will have WCT (Figure 15-3 f, g). In these cases, an ECG obtained prior to the tachycardia is very helpful. It is important to know that aberrant conduction can either develop or become more pronounced heart rate increases. For example, a patient with an incomplete right bundle branch block and a QRS of 100 at a heart rate of 70 bpm may have a complete bundle branch and a QRS of 130 at a rate of 120 bpm.

Diagnosis
The diagnosis of VT can be difficult. Several algorithms have been developed to help differentiate VT from SVT, the most common of which is the Brugada criteria (Figure 15-4). This is a four-step decision tree in which if any of the criteria are met, the rhythm is VT. Overall, the algorithm’s sensitivity and specificity are 98.7% and 96.5%, respectively. Step 1 is to evaluate the morphology of the precordial leads (V1–V6) for concordance. If the QRS complex in all these leads is monophasic with the same polarity, or if there is a QS complex, they are said to be concordant. They are not concordant if there is a QR or RS complex in any of the leads. If concordance is present, the rhythm is VT; if not, continue to step 2. The next step is to evaluate the duration of the RS interval. If the RS interval is >100 ms in any of the precordial leads, then the rhythm is VT; if not, continue to the next step. Step 3 requires evaluating for evidence of AV dissociation. If P waves can be identified, and march out separately from the QRS complexes, there is AV dissociation. Also, if fusion beats are present, there is AV dissociation and the rhythm is VT. If there is no AV dissociation, then continue to step 4 and evaluate the morphology of the QRS complexes. In this step the QRS is first determined to be either a left bundle branch block (LBBB) morphology or a right bundle branch block (RBBB) morphology. Once this is determined, the criteria outlined in Figure 15-3 are applied, and if the QRS meets the criteria, the rhythm is VT; if not, it is an SVT.

Clinical Presentation
Patients with a WCT can be in a relatively benign rhythm, like atrial flutter with aberrancy, or life-threatening rhythm, like VT or VF. Likewise, the presentation of

Brugada criteria for ventricular tachycardia

Brugada criteria for ventricular tachycardia

Figure 15-4. Brugada criteria for the diagnosis of ventricular tachycardia.

patients with a WCT can vary dramatically from stable to pulseless. The majority of patients who present with, or develop, a WCT will need immediate intervention to save their lives. These interventions, along with treatments for more stable patients, and prophylactic measures will be discussed in the next section. Here we discuss historical, exam, and laboratory information that is pertinent in the assessment of a WCT patient.

In an unselected patient population presenting with a WCT, the rhythm will ultimately be determined to be VT in 80% of cases. This number increases to more than 90% in patients with a prior myocardial infarction. Therefore it is helpful to know whether the patient has a history of coronary artery disease. Patients with structural heart disease, particularly those with a decreased ejection fraction, are also more likely to have VT, making a history of congestive heart failure important. Other comorbidities, such as renal disease, can predispose to electrolyte abnormalities and subsequent arrhythmias. Recent medication changes can also cause electrolyte abnormalities, such as hypokalemia and hypomagnesiema from new or increased diuretic dose, or hyperkalemia from ACE inhibitors or aldosterone antagonists.

Long QT can be induced by new medications, including quinolone antibiotics (ciprofloxacin), macrolide antibiotics (erythromycin), antipsychotics, antiarrhythmic drugs (amiodarone, flecanide, sotalol), antiemetics (ondansetron, promethazine), and many others. Additionally, a history of WPW, atrial fibrillation, or atrial flutter may be helpful in determining the etiology of the patient’s WCT, but a history of these does not exclude VT.

Symptoms experienced by a patient in a WCT are variable. Excluding those with cardiac arrest, symptoms can include palpitations, fatigue, presyncope, or syncope. People may also have angina, either as the provoking stimulus for their arrhythmia or from the increased myocardial oxygen demand in the setting of the tachycardia. The tachyarrhythmia can also result in heart failure and symptoms of shortness of breath, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, weight gain, and lower extremity edema.

The exam of a patient with WCT, depending on the situation, may be extremely cursory. However, despite limited time, certain obvious findings can be helpful. A sternotomy scar likely indicates prior cardiac surgery and probable coronary artery disease. Similarly, amputations (particularly lower extremity) are most commonly related to peripheral vascular disease, and greatly increase the likelihood of coronary artery disease. Finally, the presence of an arteriovenous fistula (generally on the upper extremity) indicates end-stage renal disease and hence a predisposition to electrolyte abnormalities.

Lab work should be obtained on all patients with a WCT and should be evaluated for electrolyte abnormalities and cardiac ischemia. One should also consider checking thyroid studies.

Treatment
The first priority for any patient in a WCT is to assess their clinical status. If there is no pulse, there should be immediate initiation of CPR along with advanced cardiovascular life support (ACLS) or basic life support (BLS) algorithms, including cardioversion. Even in the setting where a pulse is present, if there are signs of clinical instability–defined as: hypotension, altered mental status, angina, or heart failure–the patient requires immediate cardioversion. In both cases, cardioversion should be synchronized if possible, reserving unsynchronized cardioversion for VF. If possible, an ECG should be obtained and evaluated using the Brugada criteria. A prior ECG can be very helpful in evaluating for a history of atrial arrhythmia, preexcitation, or aberrant conduction. However, even in a stable patient with VT, urgent cardioversion is reasonable.

The immediate medical treatment for VT generally consists in correcting any electrolyte abnormalities and administering IV antiarrhythmic drugs such as amiodarone or lidocaine. Amiodarone is effective for both VT and SVTs, and is administered 150 mg IV over 10 minutes followed by an infusion of 1 mg/min for 6 hours, then 0.5 mg/min. Lidocaine is particularly effective in treating VT related to cardiac ischemia and is administered as a bolus of 1–1.5 mg/kg over 2–3 minutes. Chronic medical therapy for VT should be performed with guidance of a specialist. For patients in whom VT reoccurs despite medical therapy, or in whom medical therapy is not tolerated, a catheter-based VT ablation can be considered.

Patients who survive an episode of VT or VF may warrant placement of an implantable cardioverter defibrillator (ICD). The indications for a secondary prevention ICD are (1) patients who are resuscitated from a VT/VF arrest in whom a completely reversible cause cannot be identified–patients with VT/VF limited to the first 48 hours after an acute myocardial infarction do not qualify for an ICD and (2) patients with spontaneous VT in the setting of hypertrophic, valvular, ischemic, or infiltrative heart disease. The indications for a primary prevention ICD are patients with (1) a prior myocardial infarction (>40 days prior) and an ejection fraction ≤30%; (2) nonischemic cardiomyopathy, NYHA class II or III symptoms, and an ejection fraction persistently ≤ 35% despite guideline-directed medical management for 3 months; (3) structural heart disease, syncope, and VT induced during an electrophysiology study; and (4) patients underlying disorders at high risk for VT/ VF such as congenital long QT or arrhythmogenic right ventricular cardiomyopathy. An ICD is contraindicated in patients with a life expectancy of less than 1 year, even if they otherwise meet ICD implantation criteria.

CASE CORRELATION
  • See also Case 13 (narrow complex tachycardias), and Case 14 (sudden cardiac death).

COMPREHENSION QUESTIONS
15.1 A 70-year-old woman with a history of Wolff-Parkinson-White (WPW) pattern noted on numerous prior ECGs presents to the emergency department with palpitations and near-syncope. Her ECG on presentation reveals a wide complex irregular tachycardia with a rate of 200 bpm. What is the most appropriate therapy for this patient?
A. Metoprolol
B. Diltiazem
C. Digoxin
D. Cardioversion
E. Adenosine

15.2 A 25-year-old man presents from a group home for schizophrenic patients after an episode of syncope. His ECG on presentation reveals QT prolongation to 630 ms. Which of the following arrhythmias most likely caused his syncope?
A. Monomorphic VT
B. AV nodal reentrant tachycardia
C. Atrial fibrillation with aberrancy
D. Ventricular fibrillation
E. Torsades de pointes (TdP)

15.3 An ICD is indicated in which of the following situations?
A. A patient with ischemic cardiomyopathy, NYHA class II symptoms, and an ejection fraction of 45%
B. A patient who experienced VF arrest at the time of a myocardial infarction, but has not had any arrhythmias since
C. A patient with a nonischemic cardiomyopathy, on guideline-directed medical therapy for the last 3 months, whose ejection fraction has persistently been 30%
D. A patient who developed QTc prolongation and TdP after starting ciprofloxacin, and whose QTc returned to normal once the medication was stopped


ANSWERS

15.1 D. Prompt cardioversion would be the best move here. This patient has atrial fibrillation in the setting of a known accessory pathway. The wide complex appearance is due to conduction down the accessory pathway into the ventricle, where it conducts cell to cell and produces a wide QRS. Cardioversion is required to abort conduction down the bypass tract, which is generally quite rapid. Sodium channel blockers can also do this. The remaining choices are all drugs that can block the AV node, which can be dangerous in atrial fibrillation with an accessory pathway because it can force all conduction down the accessory pathway and precipitate ventricular fibrillation.

15.2 E. A prolonged QTc predisposes to an R-on-T phenomenon and TdP. QT prolongation can be caused by a number of medications, and antipsychotic drugs are common offenders. Although all of the rhythm disorders listed can potentially cause syncope, the one most closely associated with prolonged QT intervals is TdP.

15.3 C. A patient with a nonischemic cardiomyopathy, on guideline-directed medical therapy for the last 3 months, whose ejection fraction has persistently been ≤35%, qualifies for an ICD. Patients with an ischemic cardiomyopathies do not qualify for ICDs unless their EFs are persistently ≤30% and they are on guideline-directed medical therapy for at least 3 months. Patients who experience VT/VF at the time of myocardial infarction are not candidates for an ICD unless the arrhythmia reoccurs >48 hours from the time of the infarction. An ICD is not indicated if a reversible cause can be identified.


CLINICAL PEARLS
  • Most WCTs are VT.
  • VT is more common in patients with a history ofmyocardial infarction or a decreased ejection fraction.
  • Differentiating VT from SVT can be difficult, and Brugada’s criteria can be helpfiul.
  • Treatment of WCTs often requires emergent intervention, including cardioversion.
  • There are guidelines outlining the indications for ICd use in primary and secondary prevention.
References

Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/ AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. Circulation. 2008;117(21):e350–e408.

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