CONTENTS

approach to wide-complex monomorphic tachycardia

• Diagnostic approach to wide complex tachycardia
  • [1] Consider pretest probability for VT
  • [2] Compare to old ECG if available
  • [3] Initiation of wide complex tachycardia
  • [4] Signs of potential VT mimic
  • [5] Evidence of AV dissociation?
  • [6] Morphology in Leads II & aVR
  • Morphology rules
    • [7a] RBBB-type
    • [7b] LBBB-type
    • [7c] Neither RBBB or LBBB-like 
• Therapeutic approach to undifferentiated monomorphic tachycardia
• Specific types of monomorphic VT:
  • Post-MI monomorphic VT ➡️
  • Outflow tract ventricular tachycardia
  • Fascicular VT 
  • Bundle branch reentry VT

monomorphic VT storm (& polymorphic VT storm 2/2 MI)

• Definition
• TREATMENT
  • [1] Antiarrhythmics
    • Amiodarone
    • Beta blockers
    • Lidocaine
  • [2] Intubation, sedation, vasoconstrictors
  • [3] Treat the cause
    • CAUSES & investigation of etiology
    • EP interventions
  • (Stellate ganglion block)

approach to polymorphic VT

• Definition & causes of polymorphic VT
• Therapeutic approach to polymorphic VT
• Specific types of polymorphic VT:
  • QT prolongation
  • Congenital long QT syndrome (LQTS)
  • Catecholaminergic polymorphic VT
  • Post-MI polymorphic VT ➡️

torsade de pointes (& torsade storm)

• [1] Basic treatment to prevent torsade recurrence
• [2] Treatment of torsade storm

other wide-complex rhythms

• Bidirectional ventricular tachycardia
• AIVR (accelerated idioventricular rhythm)
• Ventricular parasystole

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approach to wide complex tachycardia

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Caution! 

• 🛑 This section is NOT intended to assist in management of wide complex tachycardia in real time if the patient is unstable. For unstable patients: obtain an ECG, stabilize with cardioversion, and pontificate about the ECG later on. 
• 🛑 Algorithms for sorting out VT from SVT are notoriously fallible.
• 🛑 When in doubt, it is safer to err on the side of over-diagnosing VT and treating the patient accordingly. Treatments for VT will be safe and effective (regardless of whether the patient has VT or SVT).
• Causes of algorithm failure:
  • (1) Most algorithms won't work with accessory pathways. Depending on the placement of the accessory pathway, these can generate very close mimics of VT.
  • (2) Antiarrhythmic medications and/or sodium-channel blocking medications may stretch out intervals, confounding algorithms.

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[#1/7] consider pretest probability for VT

• Adult → 80% pre-test probability for VT.
• History of MI → 98% pre-test probability for VT. (Griffin 2022)

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[#2/7] compare to old ECG (if possible)

• Old ECG shows same exact morphology in sinus rhythm → not VT.
• Current ECG matches PVCs in a prior ECG → VT extremely likely.
• Old ECG shows Q-wave MI → VT is likely.
• Old ECG shows a bundle-branch block that is contralateral to current ECG morphology → VT is likely.

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[#3/7] look at initiation of tachycardia (if possible)

clues to supraventricular origin:

• Often triggered by a PAC.
• May start with a narrow complex → transition to wide complex at the same rate.

clues to ventricular tachycardia:

• Initiation with a PVC suggests ventricular tachycardia. (Griffin 2022)

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[#4/7] consider signs of VT mimic

[a] Substantial irregularity 

• Monomorphic VT should generally be regular.
• Irregularity suggests one of the following possibilities:
• (1) AF with WPW, especially if:
  • Rate is >200.
  • Complex morphology is variable.
• (2) AF with bundle-branch block (either chronic or rate-related).

[b] Heart rate <~120 b/m

• VT usually is faster.
• Slow VT is possible (especially among patients on antiarrhythmic medications), but low heart rates should increase suspicion for a VT mimic.

[c] QRS >>200 ms (>>5 boxes)

• This raises the possibilities of hyperkalemia or a sodium channel blocker (although it is still consistent with the possibility of VT).
• Consider a therapeutic trial of IV calcium (for hyperkalemia) or IV bicarbonate (for sodium channel blocker), depending on ECG morphology and clinical history.

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[#5/7] is there evidence of AV dissociation?

[a] fusion beats

• Features of fusion beats in VT:
  • [1] Come a little early.
  • [2] Different morphology (should be narrower).
  • [3] Doesn't reset the tachycardia.
• Definite fusion beats are essentially diagnostic for VT. However, fusion beats may rarely also occur in the following scenarios:
  • AF with an accessory pathway
  • Rarely occur with supraventricular arrhythmias due to synchronously occurring PVCs. 🌊

[b] capture beats

• Key feature of capture: the QRS complex should be normal (and match the baseline ECG).
• Definite capture beat(s) are diagnostic for VT.

[c] unequivocal dissociation of P-waves (P-waves march out)

• This is essentially diagnostic of VT (99% specificity). (Griffin 2022)
  • Theoretically, dissociated P-waves could also be seen in junctional tachycardia with aberrancy, due to dissociation between atria and AV node.
  • In practice, unequivocal P-wave dissociation is effectively diagnostic of VT.
• (Note that lack of AV dissociation doesn't indicate whether the patient is in SVT or VT. VT can cause retrograde activation of the atria – so VT can exist alongside AV association!)

[d] Lewis lead ECG

• If the patient is stable, consider obtaining a Lewis Lead ECG. 📖 Revealing P-wave activity may clarify the diagnosis: (31504425)
  • (i) If P-waves are seen preceding each QRS → sinus tach.
  • (ii) If P-waves are dissociated from the QRS complex → ventricular tachycardia.

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[#6/7] morphology in Lead II and aVR

Basel algorithm: VT is likely if at least two of the following are present:

• [1] Known structural heart disease:
  • History of myocardial infarction.
  • Systolic heart failure (EF <35%).
  • Device (ICD, CRT).
• [2] Lead-II: Time to first peak >40 ms.
• [3] Lead aVR: Time to first peak >40 ms.

morphology in aVR: VT is likely if any of the following are present (Vereckei algorithm)

• [1] Initial R wave in aVR.
• [2] Initial R or Q-wave >40 ms.
• [3] Notching on the initial downstroke of a predominantly negative QRS complex.
• [4] Vi/Vt <1 (initial slope of the QRS complex is shallower than the final slope at the end of the QRS complex). (18180024)

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[#7a/7] RBBB-type morphology: VT vs. aberrancy

V1

• Morphologies favoring VT
  • Monophasic R.
  • R (>30 ms) + any S.
  • qR or QR. 
  • 🐰 Taller left bunny ear (Rsr').
• Morphologies favoring SVT
  • Truly triphasic conduction (RSR' with S-wave below the baseline).
  • 🐰 Taller right bunny ear (rSR') – but this doesn't exclude VT. (31504425)

V6

• Morphologies favoring VT
  • rS (with r < S).
  • QS, Qrs.
  • QR.
  • Monophasic R.
• Morphologies favoring SVT
  • Triphasic.
  • Rs (with R > s).
  • qRs.

other features that suggest VT

• Axis to the left of -30 suggests VT (negative in Lead II).
• QRS >140 ms. (31504425)

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[#7b/7] LBBB-type morphology: VT vs. aberrancy

⚠️ Only 20% of rate-related aberrancy has a LBBB pattern, so be cautious about diagnosing rate-related LBBB aberrancy. (Griffin 2022)

V1

• Morphologies favoring VT:
  • rS with broad R-wave (>~30 ms) – this may represent RVOT VT.
  • Slurred downstroke (e.g. >60-70 ms from onset of R-wave to nadir of S-wave in V1-V3).
  • Notched downstroke of S-wave.
• Morphologies favoring SVT
  • Narrow R and quick S wave downstroke in V1-V3 (e.g. <<60 ms from onset of R-wave to nadir of S-wave in V1-V3).

V6

• Morphologies favoring VT:
  • Any Q-wave or QS complex (QR, QS, QrS, qR).
  • Rr'
• Morphologies favoring SVT:
  • rR'
  • Monophasic R.

other features that suggest VT

• Axis to the right of +90 degrees suggests VT (negative in Lead I).
• QRS >160 ms. (31504425)

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[#7c/7] morphology that is neither RBBB-like or LBBB-like morphology 

• This is probably VT.
• Concordance in V1-V6:
  • Upright concordance: Almost always VT or antidromic AVRT.
  • Negative concordance: At least 90% likelihood of VT.
  • Absence of any precordial RS pattern: almost 100% specific for VT.

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therapy for wide-complex tachycardia in the absence of an established diagnosis

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indications for immediate DC cardioversion include: (31504425)

• Hemodynamic instability.
• Altered mental status.
• Chest pain.
• Acute heart failure symptoms.
• Signs of shock.

midazolam sedation for cardioversion: protocol

• Note: There are numerous potential sedation strategies for cardioversion. The use of midazolam monotherapy has been well validated to be safe and effective, even when performed by cardiologists. (32842955, 26734338, 25176628, 24157233, 17461869, 17312434) Other options include propofol, ketamine, or etomidate. 
• [0] Optimal candidates:
  • (a) No chronic use of benzodiazepines or alcohol.
  • (b) No history of seizures.
• [1] Load with midazolam 3-5 mg IV bolus (depending on age, weight).
• [2] Give 2 mg IV midazolam q2min PRN to target adequate sedation:
  • Eyes closed.
  • No response to gentle verbal/tactile stimuli.
  • Sluggish response to loud verbal commands or stronger tactile stimuli.
• [3] Perform cardioversion.
• [4] Reversal with 0.5-1 mg flumazenil IV if adverse effects result from sedation (e.g., mild hypoxemia, excessive somnolence, laryngospasm).

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outflow tract ventricular tachycardia

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clinical aspects

• Outflow tract VT is an idiopathic form of VT that occurs in structurally normal hearts, due to an automaticity focus that is usually within the RVOT (with a mechanism involving cAMP triggered activity from delayed afterdepolarization).
• This is frequently seen in young to middle-aged patients.
• Arrhythmia may be triggered by:
  • Hypercalcemia, hypokalemia, digoxin.
  • Caffeine.
  • Exercise, emotional stress.
  • Premenstrual, perimenopausal, and gestational periods in women. (Hurst 15th ed)
• Clinically, arrhythmias usually cause syncope but don't degenerate into VF. Thus, the prognosis is fairly benign.
• Differential diagnosis includes myocarditis, sarcoidosis, and arrhythmogenic right ventricular cardiomyopathy. (Hurst 15th ed)
• Management:
  • VT is usually sensitive to adenosine, and may also be terminated by vagal activity.
  • Beta-blockers or calcium channel blockers are often modestly effective.
  • Ablation is highly effective (with a cure rate >90%).

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ECG in LV outflow tract tachycardia 

RVOT VT (90% of patients) 

• Key findings:
  • LBBB pattern.
  • Wide septal R-wave in V1.
  • Inferior axis (QRS positive with tall R-waves in II, III, aVF – indicating activation from base of the heart).
• Other findings
  • QRS is often narrower than other forms of VT (e.g., in the neighborhood of 120-140 ms).
  • QRS complexes are often relatively smooth (lack fragmentation).
• Arrhythmias may include:
  • Sustained monomorphic VT.
  • Frequent salvos of nonsustained monomorphic VT.
  • Frequent, symptomatic PVCs. (Griffin 2022)

LVOT VT (10% of patients)

• Can occur with:
  • RBBB morphology, inferior axis.
  • LBBB morphology, inferior axis.

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fascicular VT

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(Known by several names: idiopathic fascicular VT, verapamil-sensitive VT.)

clinical features

• Basics:
  • Mechanism of arrhythmia involves reentry.
  • Typically occurs in young, healthy people without structural heart disease.
• Clinical presentation:
  • Paroxysmal VT usually seen in men between ~15-40 years old.
  • Generally not associated with sudden cardiac death.
  • May cause an incessant VT leading to tachycardia-mediated cardiomyopathy. (Hurst 15e)
• Management:
  • Doesn't respond to adenosine, vagal maneuvers, or beta-blockers (it involves a reentrant circuit that doesn't involve the AV node).
  • Highly sensitive to verapamil.
  • Long-term therapy may involve either verapamil or catheter ablation.

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ECG features

key features:

• 🔑 May resemble RBBB + LAFB (with tall, wide R-waves in V1).
• 🔑 QRS is relatively narrow (100-140 ms), so it can masquerade as narrow-complex tachycardia.
• 🔑 Capture and/or fusion beats may help clarify diagnosis as VT.

ECG findings

• RBBB pattern (which overall looks more like SVT with aberrancy than VT).
• Relatively narrow complex:
  • QRS duration of 100-140 ms (narrower than most VT).
  • Short RS interval (onset R to nadir S) of 60-80 ms (normally >100 ms in other types of VT).
• Axis:
  • Posterior fascicular VT (95% of cases) – Left, superior axis (RBBB with LAFB).
  • Anterior fascicular VT (5% of cases) – Right axis deviation.

differential diagnosis

• Digoxin toxicity may cause VT with a similar appearance (but the mechanism involves enhanced automaticity).

Other sites of origin have been described, but they are less common (e.g., anterior fascicular, upper septal fascicular, and interfascicular variants). (Hurst 15e)

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bundle branch reentry VT

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• A macro-reentrant circuit usually involves antegrade transmission via the right bundle and retrograde transmission via the left bundle.
• ECG:
  • VT generally has a LBBB configuration with a rapid rate.
  • Sinus rhythm ECG usually shows an intraventricular conduction delay or LBBB. (Hurst 15e)
• Treatment ideally involves ablation, with or without an ICD (for patients with EF <35%). (Hurst 15e)

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definition of VT storm (aka electrical storm)

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what is VT/VF storm?

• Definition:
  • Generally defined as three or more episodes of VF or sustained VT requiring intervention (e.g., defibrillation or ICD shocks) within 24 hours.
  • Patients can be shocked out of VT/VF reasonably easily, but then they keep flipping back into to VT/VF. This differentiates VT storm from refractory VT – wherein the patient is continually in VT/VF and never goes back to sinus rhythm.
• Clinical presentation is typically dramatic:
  • (a) If patient has an ICD (implanted cardiac defibrillator), this may present with recurrent ICD firing.
  • (b) If patient doesn't have an ICD, this may cause recurrent symptoms. Depending on the heart rate and cardiac function, symptoms may range from palpitations to recurrent cardiac arrest.

this section is about monomorphic VT, or polymorphic VT due to ischemia

• The general approach to polymorphic VT is discussed above:
  • Definition and causes of polymorphic VT: ⚡️
  • Initial therapeutic approach to polymorphic VT: ⚡️
• Most polymorphic VT is due to acquired torsade de pointes. This requires a specific management strategy which is described in a different part of this chapter:
  • Basic treatment of torsade: ⚡️
  • Treatment of torsade storm: ⚡️
• The following treatment strategy is for monomorphic VT, or polymorphic VT due to acute myocardial ischemia. The treatment of these entities is very similar, although there is a greater urgency to pursue revascularization in the context of polymorphic VT due to acute ischemia.

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treatment

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🔑 Call for help early and try to think a couple steps ahead (e.g., order IV propranolol early).

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antiarrhythmics

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magnesium & electrolyte repletion 

• 2-4 grams of IV magnesium sulfate may be considered, particularly if the patient is deficient.
  • There is no strong evidence to support the use of magnesium. Given that intracellular calcium overload may be implicated in VT/VF storm, magnesium might be expected to alleviate this problem, given that magnesium may antagonize some of calcium's effects.
• Hypokalemia should be aggressively corrected.

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1st line antiarrhythmic: amiodarone 

• Backbone regimen: 300 mg bolus, then 1 mg/min x6 hours, then 0.5 mg/min.
• Additional boluses can be given for recurrence (up to a total of ~900 mg in boluses).
  • Avoid >2.2 grams total dose within 24 hours (i.e., >900 mg in bolus doses).
• If the patient is on chronic oral amiodarone, they should still be reloaded with IV amiodarone. (34257075)

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2nd line antiarrhythmic: beta-blockers (may actually be the most effective therapy)

propranolol 💊

• Propranolol is probably superior to metoprolol and esmolol because it antagonizes both beta-1 and beta-2 receptors. Patients often have chronic heart failure, which may lead to down-regulation of beta-1 receptors and up-regulation of beta-2 receptors. (36837606) Propranolol may also have superior CNS penetration, further reducing sympathetic outflow. (37257955)
• IV regimen: (10942741, 25745472, 32345562)
  • Loading infusion 0.15 mg/kg IV over 10 minutes (~10 mg). Follow heart rate and hold the infusion if the heart rate falls <45 b/m.
  • Maintenance: 3-5 mg IV Q6hr.
• Oral regimen:
  • Propranolol 40 mg PO q6hrs has been proven superior to metoprolol (50 mg q6hr), with a 2.7-fold reduction in arrhythmia. (29699616)
  • Dose may be increased as tolerated by blood pressure, up to ~80 mg PO q6hr. (36837606) 

esmolol infusion 💊

• Loading dose is 0.5 mg/kg IV (~30 mg) over one minute.
• Start infusion at 0.050 mg/kg/min (~3 mg/min).
• May re-load & up-titrate infusion in increments of 0.05 mg/kg/min every 10 minutes, up to a maximal dose of 0.3 mg/kg/min (~20 mg/min).
• The advantage of esmolol is titratability. From a mechanistic standpoint, esmolol may be less effective than propranolol because it lacks efficacy at beta-2 receptors. (25033747, 10942741)

IV metoprolol 💊

• May be used if nothing else is readily available.
• Dose: 5 mg IV every 5 minutes for total of 15 mg.

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3rd line antiarrhythmic: lidocaine 💊

 utility

• Lidocaine is traditionally recommended as the third-line antiarrhythmic, after amiodarone and beta-blockers.
• Lidocaine is only modestly effective in scar-related monomorphic VT, but it may be more useful in the context of acute ischemia. (28706587; 31352528)
• Lidocaine is relatively hemodynamically stable, but class-I antiarrhythmics can worsen cardiac function due to negative inotropic effects – so exercise some caution. (30554598)

dose

• Bolus with 1-1.5 mg/kg and then infuse at a rate of 0.02 mg/kg/min (~1.5 mg/min). (28706587)
• May re-bolus with 0.5-0.75 mg/kg IV, up to a total dose of 3 mg/kg.
• May titrate the lidocaine infusion up to ~4 mg/min.

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intubation & sedation

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⚠️ Myocardial injury and pain stimulate an outpouring of endogenous catecholamines, promoting recurrent arrhythmia.

intubation

• This is generally required for a true VT storm. Intubation offers numerous benefits:
  • Patients may lose airway control during episodes of VT/VF.
  • Sedation itself is therapeutic.
  • Intubation may facilitate safe performance of procedures (e.g., VT ablation).

analgesia

• Analgesia is important for any intubated patient, but it's especially important in VT storm because untreated pain can drive sympathetic tone and promote recurrent arrhythmia.
• Initially err on the side of over-aggressive analgesia (until the VT storm is controlled).

sedation

• Deep sedation can help break the VT storm.
• Propofol seems to work particularly well here. (12419728) Propofol may cause hypotension due to vasodilation; this may be counteracted with the use of vasoconstrictors (e.g., phenylephrine).
• Dexmedetomidine may also reduce sympathetic tone, so it's not a terrible choice here. However, dexmedetomidine has some drawbacks which probably make it 2nd line here (at least initially until the storm has abated):
  • Dexmedetomidine is sluggish to titrate.
  • Dexmedetomidine can't achieve the same depth of deep sedation that propofol can.
  • To date, there is no evidence on using dexmedetomidine in VT storm.
• Benzodiazepine:
  • May be used if the patient is unable to tolerate propofol/dexmedetomidine due to severe hypotension.
  • Light sedation with benzodiazepine may be utilized for an occasional patient who isn't intubated.

arterial line

• These patients are often very hemodynamically labile (e.g., with recurrent episodes of cardiac arrest). Additionally, we will usually be aggressively titrating medications that cause hypotension (e.g., propofol, amiodarone, beta-blockers).
• An arterial line is often helpful.

pressors

• Phenylephrine may be the best choice, because it won't stimulate cardiac beta-receptors.
• Pressor support may facilitate the use of propofol and beta-blockers to treat VT storm.
• The left ventricle coronary circulation is perfused in diastole, so don't allow the diastolic Bp to decrease too much.

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treatment of cause

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causes & investigation of ventricular ectopy & VT

causes of ventricular ectopy & monomorphic VT

• Acute MI:
  • Recurrent VT/VF should always prompt consideration for emergent cardiac catheterization.
  • Additional therapies for acute coronary syndrome should also be considered (e.g., aspirin, P2Y12 inhibitor). More on the treatment of Type I MI: 📖
• Electrolyte abnormalities, especially:
  • Hypokalemia.
  • Hypomagnesemia.
• Medications:
  • Sympathomimetics.
  • Inotropes.
  • Withdrawal of antidysrhythmic medication (including medication nonadherence).
  • Pro-arrhythmic drug toxicity.
  • Substance abuse (e.g., sympathomimetics).
• Misplaced device: Right heart catheter that has migrated into the right ventricle.
• Thyrotoxicosis.
• Sepsis. (30554598)
• Volume overload.
• Severe anemia.
• Myocarditis, especially:
  • Giant cell myocarditis.
  • Viral or lymphocytic myocarditis.
  • Cardiac sarcoidosis.

investigation of cause

• Interrogation of any pacemaker or ICD.
• Evaluation of ECGs (ideally baseline and during arrhythmia).
• Echocardiography.
• Laboratory studies:
  • Complete electrolytes (including Mg).
  • TSH (thyroid stimulating hormone).
  • Troponin.
  • Brain natriuretic peptide.
  • Relevant drug levels (e.g., digoxin).
  • Liver function tests. (37257955)
• Cardiac catheterization if ischemia is possible.
• Cardiac MRI may be considered once the patient stabilizes.

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EP interventions for VT/VF

ICD (implanted cardioverter-defibrillator) optimization

• Any patient with an ICD requires device interrogation.
• Ensure that the device is truly detecting VT (rather than over-responding to artifact). Additionally this may help clarify whether the patient has monomorphic or polymorphic VT.
• Anti-tachycardia overdrive pacing should be optimized to break episodes of VT without requiring shocks.

catheter ablation of VT/VF

• Recent meta-analysis of 417 patients with VT storm demonstrated clinical arrhythmia suppression in 92% of patients, with an impressive safety profile (complication rate of 1% and periprocedural mortality of <1%). (23264584)
• Urgent ablation is recommended by numerous society guidelines for the management of refractory VT. (34257075)

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stellate ganglion block

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basics of the stellate ganglion block

• Nerve block in the neck cuts off sympathetic outflow to the myocardium.
• Supported by case-study level data, which show a dramatic reduction in arrhythmia burden. (30554598)
• Seems fairly safe (e.g. used as an outpatient procedure for control of neuropathic pain).
• Sensible intervention for patients failing to respond to intubation & anti-arrhythmics.
• The block should cause an ipsilateral Horner's syndrome (pupillary constriction), which is evidence of a successful block.

left stellate ganglion block versus bilateral blocks?

• The left stellate ganglion is more important in autonomic regulation of the heart, so most literature has described unilateral left-sided blockade.
  • In a recent systematic review of the literature, 34/38 reported cases received left-sided block, with the remaining four receiving bilateral blocks. (29270467)
• However, bilateral blockade may be most effective. Some authors are currently advocating for bilateral blockade. (28471068)

basic anatomic principles

• (1) Operate at the level of the C6 transverse process (Chassaignac's tubercle; figure above).
  • This bony structure might be appreciated with deep palpation adjacent to the trachea at the level of the cricoid membrane.
  • The C6 transverse process should be visible during the procedure as a bright, bony signal.
  • The C6 transverse process provides a back-stop which blocks the needle from hitting the vertebral artery (although ideally you should never hit the bone).
• (2) The injection target is just anterior to the longus coli muscle, which runs underneath carotid artery.

overview of two different techniques

Two general techniques may be used. There's no firm evidence regarding which is better, so both will be described here.

“landmark technique” approach

• Traditionally, stellate ganglion blocks were performed using a landmark technique as follows:
  • Palpate the neck adjacent to the trachea to locate the lateral process of C6 (Chassaignac's tubercle)
  • Insert a needle straight into the neck until it hits Chassaignac's tubercle.
  • Inject some local anesthetic, then withdraw 1-2 mm and inject some more anesthetic.
• This is a fast and simple technique (see video below). The problem is that if you're off a little (either too cephalad or caudad) the needle could slip past Chassaignac's tubercle and hit the vertebral artery.
• This approach can be replicated using ultrasonography, which allows needle visualization and prevents going too deep. Ideally anesthetic should be placed just anterior to the longus coli muscle.

lateral approach

• In this approach, the patient's head is turned to the contralateral side. The longus coli is approached lateral to the carotid artery (figure below). As with any technique, the goal is to deposit anesthetic just anterior to the longus coli muscle.
• This technique has the advantage of providing a greater margin of safety between the needle and vital structures (e.g. the carotid artery and thyroid).

A more detailed illustration of the sono-anatomy at the level of C6 is shown below:(24760493)

• The key sono-landmarks are the carotid artery and the Chassaignac's tubercle (marked “at” in the figure below).
• The longus coli (with the ganglion anterior to it) are sandwiched between the carotid artery and the anterior tubercle.
• Using some gentle posterio-medial pressure with the ultrasound probe may displace the carotid artery medially, opening up this space between the carotid and Chassaignac's tubercle. (28455598)

The following video illustrates this general approach, albeit at the C7 level (not my preferred level because, as you can see in the video, incorrect angulation of the needle could risk laceration of the vertebral artery)

Another short video to reinforce the anatomic structures:

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definition & causes of polymorphic ventricular tachycardia

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definitions

• Polymorphic ventricular tachycardia: Defined as ventricular tachycardia with varying QRS amplitude and axis.
  • This is often equated to as torsade de pointes, but it's actually not the same thing. Polymorphic VT may be caused by several etiologies as outlined below.
• Torsade de pointes (TdP) is polymorphic ventricular tachycardia caused by an underlying prolongation of the QT interval (either congenital or acquired long QT interval). The vast majority of torsade results from acquired long-QT syndrome (due to electrolyte abnormalities and/or medications).

ECG mimics of polymorphic VT

• Severe hyperkalemia causing a “sine wave” pattern.
• Coarse ventricular fibrillation.
• Atrial fibrillation with Wolff Parkinson White (varying morphology may create polymorphic appearance).

causes of polymorphic VT

• [1] Torsade de Pointes (QT prolongation is the primary abnormality):
  • Congenital long QT syndromes (LQTS).
  • Acquired QT prolongation.
• [2] J-wave syndromes (QT is generally normal, but can be prolonged in MI, Takotsubo, or hypothermia):
  • Acute myocardial ischemia.
  • Takotsubo cardiomyopathy (acute phase).
  • Brugada syndrome.
  • Early repolarization.
  • Hypothermia.
• [3] Catecholaminergic polymorphic ventricular tachycardia.

etiological clues from the initiation of polymorphic VT

• Torsade de Pointes:
  • Typically this process begins with a “short-long-short” RR sequence. This starts with a PVC (short R-R length), leading to a compensatory pause (long R-R length), followed by a supraventricular beat (short).
  • Then a late-coupled PVC occurs (at end-diastole).
  • This may explain why TdP is a pause-dependent arrhythmia, and why speeding up the heart rate protects patients against recurrent TdP.
• Early-coupled PVC is associated with:
  • Ischemic polymorphic VT. (O'Keefe 2021)
  • Catecholaminergic polymorphic ventricular tachycardia.

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initial approach to polymorphic ventricular tachycardia

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[#1] conversion into sinus rhythm

• Polymorphic VT is never truly stable. This is a short-lived transitional state that usually flips back into sinus rhythm, or less commonly degenerates into ventricular fibrillation. Even if the patient looks OK, they're not really stable: attach pads and don't leave the room.
• The best approach to polymorphic ventricular tachycardia is probably immediate defibrillation. The defibrillator will often be unable to lock onto any QRS complexes, so you generally need to perform an unsynchronized defibrillation.
• If the patient looks exceptionally stable, it might be reasonable give to IV magnesium rather than proceeding immediately to defibrillation. However, there should be immediate readiness to defibrillate the patient if degeneration into ventricular fibrillation occurs.
  • (Note that most treatments associated with torsade are used for the prevention of VT, not breaking an episode of VT. Thus treatments such as isoproterenol or pacing have no role here.)

[#2] evaluate the ECG in sinus rhythm

• Once the patient has converted into sinus rhythm, obtain an ECG. Key points of interest include:
• (a) QTc interval (QT prolongation suggests torsade de pointes).
• (b) Any signs of active myocardial ischemia.
• (c) Any signs of J-waves or J-wave syndromes (listed above).

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QT prolongation

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identifying QT prolongation

• ⚠️ The computer may under-call QT prolongation.
• Measuring the QT interval:
  • [1] Look for the lead with the longest QT interval.
  • [2] Look for a lead with a tall T-wave with a distinct termination.
• Rough rule of thumb: if QT is >1/2 the RR interval, then the QT is probably prolonged.
  • Tachycardia: this will over-call QT prolongation.
  • Bradycardia: this will under-call QT prolongation.

QTc calculation & interpretation

• MDCalc online calculator here.
  • Frederica formula may be best.
  • Bazett formula tends to underestimate QTc in bradycardia & overestimate QTc in tachycardia.
• Interpretation:
  • QTc >~475 ms is statistically elevated (above the 99th percentile).
  • Torsade is unusual unless QTc is >500 ms. (26183037, de Luna 2022)
• QRS prolongation (e.g., bundle branch blocks) will prolong the QT without increasing the risk of torsade. (20142454) Interpretation of QT intervals here is challenging. A common approach is to subtract the excessive duration of the QRS interval (e.g., QRS – 120 ms) from the QT interval. This may be done using the Mayo Clinic corrected QT calculator here: 🧮
• Risk factors for TdP include: (Sadhu 2023)
  • ⚠️ Female sex.
  • ⚠️ Hypokalemia.
  • ⚠️ Hypomagnesemia.
  • ⚠️ Bradycardia.
  • ⚠️ Recent cardioversion from atrial fibrillation (especially with a QT-prolonging medication).
  • ⚠️ Heart failure.
  • ⚠️ Digoxin use.
  • ⚠️ Baseline QT prolongation.

causes of QTc prolongation

• Secondary to conduction abnormality and prolonged QRS complex (e.g. bundle branch block).
• Electrolyte abnormality:
  • Hypocalcemia (prolongation of the ST segment duration). ⚡️
  • Hypokalemia.
  • Hypomagnesemia.
• Medications.
  • TdP risk is often highest with antiarrhythmic medications that prolong the QT interval (with a notable exception of amiodarone, which doesn't tend to cause TdP). (Sadhu 2023)
• Hypothermia.
• Hypothyroidism.
• Takotsubo cardiomyopathy. 📖
• Myocarditis.
• Septic cardiomyopathy.
• Congenital long QT syndromes (see section below).
• (Acute MI can cause slight increase in QT, but this usually isn't grossly noticeable.)

some clues from the ECG:

• QRS prolongation: suggests QT prolongation due to conduction abnormality (QTc should be recalculated to account for the QRS prolongation as described above).
• T-wave with a double-hump morphology may suggest:
  • Hypokalemia.
  • Medications (inhibition of the IKr channel).
  • Congenital LQTS type II. (O'Keefe 2021)

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long QT syndrome

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LQT1

• ECG:
  • Least obvious morphologically.
  • Broad base could look a bit like a hyperacute T-wave.
• Clinically:
  • Most common form of LQTS (~50% of patients).
  • Arrhythmias may be tachycardia-dependent, mostly following physical or emotional stress (e.g., exercise, swimming). (de Luna 2022) Arrhythmias are more common, but less lethal. 
  • Sometimes associated with deafness (Jervell and Lange-Nielsen syndrome).

LQT2 (HERG gene)

• ECG:
  • Broad, bifid T-waves.
  • Will mimic hypokalemia.
• Clinically:
  • Second most common form of LQTS (~35%).
  • Arrhythmias are mostly related to rest, sleep, postpartum period, acoustic stimuli, or cognitive stress (pause-dependent). (de Luna 2022) Arrhythmias are more common, but less lethal. 
  • Many medications prolong the QT interval by inhibiting the HERG gene, so this form of LQTS may have some similarities with drug-induced TdP.

LQT3

• ECG:
  • Long ST segment.
  • Will mimic hypocalcemia.
• Clinically:
  • Least common form of LQTS (~7%).
  • Arrhythmias mostly related to rest, sleep, or acoustic stimuli (pause-dependent). (de Luna 2022)
  • Arrhythmias are less common, but more likely to cause death.

clinical features may include:

• Syncope.
• Family history of sudden death.
• Congenital deafness (some variants).

diagnostic criteria for LQTS: any one of the following

• QTc > 500 on repeated ECGs without secondary causes.
• QTc 480-500 ms on repeated ECGs in a patient with unexplained syncope in the absence of a secondary cause.
• Unequivocally pathologic mutations in one of the LQTS genes.
• Schwartz score of ≧3.5, based on a sum of:
  • Clinical history:
    • Syncope with stress: 2 points.
    • Syncope without stress: 1 point.
    • Congenital deafness: 0.5 points.
  • ECG findings:
    • QTc >480 ms: 3 points.
    • QTc 460-479: 2 points.
    • QTc 450-459 in men: 1 point.
    • Torsades de pointes: 2 points.
    • T-wave alternans: 1 point.
    • Notched T-waves in three leads: 1 point.
    • Low heart rate for age: 0.5 points.
  • Family history:
    • Family member with LQTS: 1 point
    • Immediate family member with sudden unexplained cardiac death before age 30: 0.5 points.

management of LQTS

• Aggressive repletion of potassium, magnesium. Consider chronic oral supplementation of magnesium and/or potassium.
• Avoid problematic medications:
  • Medications that tend to decrease potassium and/or magnesium.
  • Avoid QT prolonging medications.
• Antiarrhythmics depend on the type of LQTS:
  • LQTS1: Beta-blockade is used (ideally nonselective agents such as propranolol or nadolol). (Sadhu 2023)
  • LQTS3: mexiletine may be useful (gain-of-function mutation in SCN5A causes voltage-gated sodium channels to remain open). (Griffin 2022)
• Exercise restriction may be considered in LQTS1 and LQTS2, but this is controversial.
• Consider ICD (e.g., if history of cardiac arrest or recurrent syncope). (Gaggin 2021)

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catecholaminergic polymorphic VT

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ECG findings

• Baseline ECG is normal.
• Evolution may include the following progression:
• [1] Rapid supraventricular arrhythmia.
• [2] Frequent PVCs.
• [3] Runs of bidirectional VT with an alternating QRS axis (e.g., alternating RBBB / LBBB morphology).
• [4] Polymorphic VT.
  • May be initiated following a short coupling interval.
• [5] VF. (de Luna 2022)

clinical aspects

• Catecholaminergic polymorphic VT is a channelopathy that predisposes to VT (despite a structurally normal heart). It results from mutations that increase intracellular calcium levels, leading to delayed afterdepolarizations and triggered activity.
• Transmission may be autosomal dominant or autosomal recessive.
• Onset is usually before ~40 years old, but patients can present at any age. (Griffin 2022)
• VT caused by catecholamine stimulation (e.g., emotional or physical stress).
• Patients are at high risk of VT storm (because defibrillation releases more catecholamines, leading to a vicious cycle.)

management

• [1] Nonselective beta-blockers are front-line therapy:
  • IV propranolol may be useful for acute management (dosing of propranolol is discussed above: ⚡️).
  • PO nadolol has a longer half-life than propranolol (10-24 hours versus 3-6 hours, respectively), so nadolol may be a better option to achieve uninterrupted sympatholysis in a hemodynamically stable patient.
• [2] Sedation is a fundamental therapy of acutely unstable patients. Since anxiety/distress can trigger arrhythmias, there should be a low threshold for sedation/intubation.
• [3] Flecainide is second-line medical therapy that may be especially useful in catecholaminergic polymorphic VT.
• [4] Sympathetic denervation:
  • For acute therapy, stellate ganglion block could be a rational therapy for refractory arrhythmias.
  • For chronic management, surgical sympathetic denervation may be utilized.
• [5] ICD implantation may be considered for patients who are refractory to beta-blockade and/or surgical sympathetic denervation. (Hurst 15th ed)

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Basic treatment to prevent recurrent torsade

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If the ECG shows a prolonged QT-interval and a prior ECG shows a normal QT-interval, then the patient is diagnosed with torsade due to acquired QT prolongation. If you simply break torsade but do nothing else, it is likely to recur. The following therapies will prevent recurrence:

[#1/3] magnesium is 1st line therapy

• Patients with torsade should receive magnesium, even if they have a normal magnesium level.
• Four grams magnesium sulfate IV (16 mM) is a reasonable place to start. Unfortunately, if you stop after four grams then the magnesium level will fall over several hours and torsade may recur. (29169799)
• Additional magnesium should be provided based on the patient's renal function:
  • (a) If GFR > 30 ml/min, a magnesium infusion is useful (see protocol below).
  • (b) If GFR < 30 ml/min, cycle magnesium levels and bolus intermittently to target a magnesium level of 3.5-5 mg/dL (1.5-2 mM).
• Magnesium has a very wide safety margin. A protocoled magnesium infusion may seem aggressive, but overall this is far safer than the risk of recurrent cardiac arrest.
• Below is a magnesium protocol (one version in American units, one in SI units). (7587256, 18320707) This will work best if pasted directly into the patient's chart so that everyone is literally on the same page.🌊

[#2/3] treat any other precipitating factors:

• Hypokalemia, should be treated aggressively, targeting a high-normal potassium level (>4.5 mEq/L). (29084733)
• Hypocalcemia may promote torsade and should be treated if present.📖
• Hypothermia should be aggressively reversed.📖

[#3/3] cessation of all QT-prolonging medications

• The medication list should be carefully reviewed for any medications which may prolong QT interval. Patients are often on several QT-prolonging medications, all of which should be stopped if possible.
• Evidence regarding which drugs cause torsade is extremely murky. In some cases it seems that drugs have been incorrectly maligned (e.g. azithromycin, olanzapine). One complicating factor is that there isn't a simple relationship between QT prolongation and torsade (some drugs such as amiodarone increase the QT, without causing much torsade).

more common medications linked to torsade (26183037, 20142454, 29084733)

• Antiarrhythmics:
  • Class IA: Quinidine, disopyramide, procainamide.
  • Class IC: Flecainide.
  • Class III: Dofetilide, ibutilide, sotalol, dronedarone.
• Psychotropic:
  • Haloperidol, droperidol, chlorpromazine, pimozide.
  • Citalopram, escitalopram.
  • Tricyclic antidepressants.
• Antibiotics:
  • Clarithromycin, erythromycin.
  • Fluoroquinolones.
  • Fluconazole, itraconazole, voriconazole, posaconazole.
  • Pentamidine.
• Other:
  • Methadone.
  • Cocaine, loperamide (when abused in massive doses).
  • Ondansetron (primarily when pushed rapidly).
  • Propofol.
  • Arsenic trioxide, sunitinib, vandetanib.

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Treatment of torsade storm

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Occasional patients will have recurrent episodes of torsade (“Torsade storm”). Each individual episode may be treated with magnesium or defibrillation, if needed (Treatment step #1 above). However, additional therapies are required to stop recurrence and end the storm.

re-load magnesium if needed

• Recurrent torsade may reflects inadequate magnesium dosing (e.g., patient is bolused with 2-4 grams, without an infusion). The first step when managing recurrent torsade is therefore to ensure that the patient has truly received an adequate dose of magnesium.
• If the patient was bolused with magnesium a few hours ago without an infusion, re-load with 2-4 grams IV immediately (8-16 mM).
• If the patient is a candidate for magnesium infusion (GFR >30 ml/hr), this should be started.
• If the patient has renal failure and has already received 4-6 grams of magnesium (16-24 mM), then check magnesium levels and ensure that a high level is achieved. Note that a therapeutic level for torsade is roughly 3.5-5 mg/dL (1.5-2 mM) – not a “normal” level.
• More on magnesium above.📖

treat any other precipitating factors

• Hypokalemia, should be treated aggressively, targeting a high-normal potassium level (>4.5 mEq/L). (29084733)
• Hypocalcemia may promote torsade and should be treated if present.📖
• Hypothermia should be aggressively reversed.📖

speed up the heart

• Speeding up the heart rate will generally decrease the QT interval and reduce the risk of acquired torsade. However, this probably doesn't work in Type-I congenital long-QT syndrome, which is not a pause-dependent arrhythmia. 📄 (34039680)
• The usefulness of chronotropy depends on the patient's baseline heart rate.
  • Chronotropy is most beneficial for patients starting out with bradycardia.
  • If the patient is already significantly tachycardic, chronotropy is unlikely to provide benefit. The usual target heart rate is 100-110 b/m, but occasionally heart rates up to 140 b/m may be needed. (26183037) There's no high-quality data on this.
• Medical chronotropy is generally the easiest & fastest way to stabilize the patient. The ideal chronotrope depends on the patient's hemodynamics and baseline blood pressure.
  • Baseline severe hypotension: epinephrine infusion.
  • Baseline normotension or mild hypotension: dobutamine or isoproterenol infusion.
  • ⚠️ Caution: If chronotropic therapy causes lots of premature ventricular complexes, this may be counterproductive (since premature ventricular complexes can trigger torsade). (31114687) In this situation, consider transvenous pacing and/or lidocaine.
  • ⚠️ Caution: Beta-adrenergic agonists are contraindicated in patients with congenital long-QT syndrome.
• Electrical chronotropy may be used if medical chronotropy fails or is contraindicated:
  • Transcutaneous pacing may work, but this is painful for conscious patients.
  • Transvenous pacing is more comfortable, but this is more invasive and takes a bit longer to achieve.
  • Patients with a pacemaker may have the device rate increased.

lidocaine 💊

• Lidocaine is the preferred antiarrhythmic drug for torsade, although there isn't a ton of evidence supporting its use.
  • Do not use amiodarone, procainamide, beta-blockers, or most other antiarrhythmics. Most of these will stretch out the QT interval even further! Beta-blockers will slow down the heart rate, increasing the risk of torsade (although beta-blockers may be beneficial in some patients with congenital long-QT syndrome).📄 (34039680)
• Start with a loading dose of 1-1.5 mg/kg lidocaine followed by a 1 mg/min infusion. For recurrent arrhythmias, re-load with another 1 mg/kg bolus and increase the maintenance infusion to 2-3 mg/min.

consider an alternative diagnosis

• Acquired torsade is generally fairly easy to control with a combination of high-dose magnesium, heart rate augmentation, and occasionally some lidocaine. Failure to respond to these interventions suggests an alternative diagnosis (e.g. polymorphic VT due to ischemia, catecholaminergic ventricular tachycardia, or congenital long-QT syndrome).

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bidirectional ventricular tachycardia

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The definition of bidirectional tachycardia: alternating frontal plane axis, or alternating LBBB and RBBB

ECG differential diagnosis of bidirectional ventricular tachycardia

• (1) Bidirectional ventricular tachycardia (typically digoxin)
• (2) SVT with bidirectional aberrancy
  • RBBB with alternating LAFB and LPFB
  • Alternating RBBB and LBBB

causes of bidirectional tachycardia

• [1] Digoxin poisoning.
• [2] CPVT (catecholaminergic polymorphic ventricular tachycardia).
• [3] Hypokalemia.
• [4] Herbal aconite poisoning.

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AIVR (accelerated idioventricular rhythm)

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ECG features

• Wide complex rhythm (with morphological features similar to VT as discussed above).
• Heart rate is usually between ~55-110.
  • Faster than ventricular escape (>50 b/m).
  • Slower than VT (<~110 b/m).
• AV dissociation may occur:
  • If P-waves are faster than idioventricular rhythm: AIVR can only occur if there is 3rd degree AV block.
  • If P-waves are slower than idioventricular rhythm: may have AV dissociation.
• AIVR is due to increased automaticity, so it may have a gradual onset, acceleration (warm up), and deceleration prior to termination. (This differentiates AIVR from most forms of ventricular tachycardia.)
• Usually AIVR is relatively brief (self-terminating within a few minutes).
• ⚠️ In a patient with cardiomyopathy who is already on antiarrhythmic medications, reentry VT may masquerade as AIVR (i.e., “slow VT”). (Hurst 15e)

clinical symptoms

• AIVR is generally asymptomatic.
• However, loss of atrial kick may cause hypotension in some patients.

causes

• Usually in acute MI, especially following reperfusion.
• Cardiac surgery.
• Medications:
  • Digoxin intoxication.
  • Sympathomimetic intoxication.
• Dilated cardiomyopathy.
• Acute myocarditis.
• Rheumatic heart disease.
• High vagal tone:
  • Occasionally may be seen in normal individuals (e.g., highly conditioned athletes).
  • Gastrointestinal distress/procedures. (O'Keefe 2021; Hurst 15e)

treatment

• AIVR is generally benign (degeneration into VT/VF is rare).
• Traditional antiarrhythmic therapy such as amiodarone is not indicated and might be dangerous (it might theoretically slow down the AIVR and perhaps even lead to asystole).
• If treatment is needed, preferred therapy may be atropine or glycopyrrolate (to speed up the AV node and thereby achieve capture of the ventricles from above).

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ventricular parasystole

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Ventricular parasystole occurs when there is an ectopic ventricular focus firing at a regular interval that is protected from depolarization by an entrance block.

ECG findings

• Monomorphic PVC occuring at regular intervals (usually along with sinus rhythm).
• Ventricular firing rate is usually 30-55 b/m. (O'Keefe 2021)
• PVCs are not coupled with the sinus beats (differentiating this from bigeminy).
• Some ventricular beats may be blocked, or fusion complexes may occur.

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questions & discussion

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To keep this page small and fast, questions & discussion about this post can be found on another page here.

• Monomorphic VT storm pitfalls:
  • Unawareness of the entity of VT storm and its specific treatment pathway.
  • Failing to differentiate between torsade de pointes (TdP) versus non-torsade electrical storm This distinction is critical, because a torsade storm requires entirely different management.
  • A wait-and-see approach, which will often fail these patients (VT storm is a vicious cycle which often deteriorates without aggressive management). Once a patient has had two-three episodes of VT within a day, strongly consider progressing down the VT storm pathway (with intubation and sedation).
  • Under-utilization of sedation, analgesia, and beta-blockers.
• Torsade de pointes pitfalls:
  • Under-dosing magnesium (e.g. giving two-four grams magnesium and walking away). This will often cause recurrence of ventricular tachycardia in a few hours after the serum magnesium levels fall.
  • Leaving patients on QT-prolonging meds (make sure to scour the medication list for any problematic drugs).
  • Don't give amiodarone or other QT-prolonging antiarrhythmics (e.g. procainamide). These may actually aggravate the situation.
  • Recognize that polymorphic VT with a normal QT interval isn't torsade, this requires an entirely different treatment strategy.

Guide to emoji hyperlinks

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• = Link to IBCC section about a drug.
• = Link to IBCC section covering that topic.
• = Link to FOAMed site with related information.
• 📄 = Link to open-access journal article.
• = Link to supplemental media.