May 2, 2021, via Sahriar Lahouti. Peer Reviewed By Mojtaba Chardoli .MD.
- Principles of management of tachydysrhythmias
- Wide Complex Tachyarrhythmias: Challenges
- Definition and Classification of VT
- Prognosis for SCD
- Monomorphic VT
- Electrical storm
- Polymorphic VT
- Going Further
ACLS: Advanced Cardiovascular Life Support
AF: atrial fibrillation
AFL: atrial flutter
AIVR: Accelerated idioventricular rhythm
AMI: acute myocardial infarction
AVCR: atrioventricular conduction ratio
AVNRT: AV node re-entry tachycardia
AANRT: antidromic AV re-entry tachycardia
BB: beta blockers
BBB: bundle branch block
CCB: calcium channel blocker
CPVT: Catecholaminergic polymorphic VT
EAD: early after depolarization
DAD: delayed after depolarization
Focal AT: focal atrial tachycardia
HCMP: hypertrophic cardiomyopathy
ICD: Implantable Cardioverter Defibrillator
IHD: ischemic heart disease
LBBB: left bundle branch block
MAT: multifocal atrial tachycardia
MVT: monomorphic ventricular tachycardia
NCT: narrow complex tachycardia
PMVT: polymorphic ventricular tachycardia
PMT: pace maker mediated tachycardia
pVT: pulseless ventricular tachycardia
PSVT: paroxysmal supraventricular tachycardia
OAVRT:orthodromic AV re-entry tachycardia
OHCA: Out-of-hospital cardiac arrest
RBBB: right bundle branch block
RWMA: regional wall motion abnormality
RVOT VT: right ventricular outflow tract VT
SCA: sudden cardiac arrest
SCD: sudden cardiac death
ST: sinus tachycardia
SVT: supraventricular tachycardia
Tdp: torsade de pointes
VA: ventricular arrhythmia
VT: ventricular tachycardia
VF: ventricular fibrillation
WCT: wide complex tachycardia
WPW: Wolff-Parkinson-White syndrome
Poor perfusion in critical patients with hemodynamic instability stems from problems with either cardiac pump function; pipe, tank or a complex of multiple overlapping problems. Cardiac function (cardiac output) is primarily determined by heart rate and contractility, and is severely impacted by heart rates at extremis (more on this here). When there are multiple overlapping perfusion problems in a patient, oftentimes the priority is given to correction of heart rate and rhythm with few exceptions. The “primacy of the heart rate” simply states that the more abnormal the heart rate, the more likely it is the primary cause of clinical instability. That’s why intervention to correct the abnormal heart rate has priority in resuscitation. In this post tachyarrhythmias is explored with focus on wide complex tachycardia. For commonly used abbreviations in the text, refer to the above pannel.
Tachyarrhythmias, defined as abnormal heart rhythms with a ventricular rate of 100 or more beats per minute. From the diagnostic (and therapeutic) perspective, it is helpful to broadly classify tachyarrhythmias into the 4 categories (figure 1) based on the width, morphology, and regularity of the QRS complex.
In patients who present with any tachyarrhythmias, two fundamental issues should be considered in the ED:
👉1. Hemodynamic Stability: The first priority when evaluating a patient with a tachyarrhythmias is an assessment of patient hemodynamic stability 1. Unstable patients and those in cardiac arrest should be treated immediately (before an extensive diagnostic evaluation). Unstable conditions confer an imminent risk of further deterioration, irreversible organ injury, or cardiac arrest and include 2 3 4:
- Acute altered mental status
- SBP < 90 mmHg (MAP<65 mmHg). 👉Remember that cardiac output can be dangerously low while the patient maintains a “normal” BP. Blood pressure ≠ cardiac output.
- Ischemic chest pain
- Dyspnea from pulmonary congestion
- Extremely rapid ventricular rates approaching >220-240/min in adult , as seen with PMVT and AF with ventricular pre-excitation
👉2. Cause or Effect: Clinicians should judge whether the heart rate is the primary cause of the clinical symptoms or a compensatory response to another pathology. The “Primacy of the Heart Rate” implies that heart rate at extremis should be considered for intervention in unstable patients with multiple overlaping perfusion problems; though there are some exceptions (see below). Although this is a tough decision, by enlarge abnormal heart rate might be assumed as a primary cause of clinical instability when:
- Non-sinus tachycardia at > 170 bpm
- AF with rapid ventricular response > 130-150 bpm
- HR < 30 bpm (discussed separately)
Generally Heart rates less than 150 bpm are unlikely to be the cause of unstable symptoms unless the patient has abnormal myocardium at baseline due to valvular disease, cardiomyopathy, etc. If sinus tachycardia or AF with rapid ventricular response are present, the provider should identify and treat the underlying cause (i.e. hemorrhage, pulmonary embolism, volume depletion, sepsis or cardiac tamponade,).
👉AF with rapid ventricular response (in the range of 110-150) is often an innocent bystander especially in patients with chronic AF. In such patients one should investigate for other causes of instability such as blood loss, sepsis etc (more on this here ).
Obtain a 12-lead ECG as it plays a pivotal role in diagnosis of arrhythmias, acute ischemia, some electrolyte disturbances as well as certain drugs intoxication. Categorization of the QRS as wide vs. narrow and the rate as regular vs. irregular offers an immediate approach to differential diagnosis (figure 1 above).
Bedside ultrasound provides critical information virtually in any patients (through wide range of clinical spectrum). It can help providers for making decision whether the tachycardia is the primary cause of instability or is a compensatory response to another pathology. For example evidence of volume overload often implies that the rapid response is primary, whereas evidence of volume depletion may point toward a compensatory response (e.g., hemorrhage, sepsis). Moreover ultrasound (echo) can also provide useful information for common causes of patient’s hemodynamic deterioration such as:
- Cardiac tamponade
- Pulmonary embolism (more on this here and here)
- Decompensated heart failure
- AMI (visualizing RWMA)
- Devastating conditions such as aortic dissection
- Valvular emergencies such as acute mitral valve regurgitation and aortic regurgitation
There are several ultrasound protocols for evaluation of patients with signs and symptoms of poor perfusion in ED (e.g., Rapid Ultrasound in Shock(RUSH)30 Abdominal and Cardiac Evaluation in Shock (ACES)31 and Search 8Es 32 etc). The latter is incorporated in our diagnostic approach to patients with tachydysrhythmias below (figure 2). For sonographic findings in each category of the SEARCH 8Es protocol see appendix.
The application of bedside ultrasound during cardiac arrest has gained favor and several studies have shown promising results 33. This will be discussed seperately.
Patient with OHCA whose cardiac monitoring reaveled asystole, while echo shows quivering mitral valves. This is fine VF and patient should be defibrillated immidiately.
Order CBC , electrolytes, renal function. Use clinical context to decide for requesting other labs:
- Troponin: It is reasonable to request troponin for ventricular tachycardia. Note that most patients with PSVT does not require troponin.
- TSH: may be requested in selected patients.
- Other labs may be requested based on underlying conditions and comorbidities.
The most commonly used antiarrhythmic medications in the ED for select patients with hemodynamic stability are summarized in the following table (figure 3). For more on mechanism of antiarrhythmic drugs see appendix.
👉Stable NCT due to AVNRT can be terminated by adenosine, BBs, CCBs and amiodarone. Selecting the first line of pharmacological treatment depends on patients comorbidities, drug side effect profile. However verapamil is strongly effective in termination of AVNRT.
👉For ventricular rate control in the setting of AF, AFL; medications such as BBs, CCBs, amiodarone and digoxin can be selected based on patients comorbidities and drug side effect. Diltiazem is the most frequently used drug in patients with relatively normal LVEF. Hypotension is less common than verapamil.
👉AF + WPW (EKG:irregular WCT): Electrical cardioversion is often selected. All AV nodal blocking agents including beta blockers, calcium channel blocker, adenosine, digoxin and amiodarone are contraindicated. Procainamide is safe.
Generally it is more safe and effective treatment than any antiarrhythmic medications if performed in appropriate setting. Do not affraid of electricity!
Synchronized cardioversion is indicated for all unstable tachycardia (HR > 150 bpm). In critical condition go immediately to unsynchronized shock. To deliver sync shock; engage sync mode before each attempt and look for sync markers on the R wave.Ensure that the device is not syncing to the T-wave (to avoid the R-on-T phenomenon) 5 .
- Regular NCT: Start with 50-100 J. If it fails, increase in stepwise fashion.
- Irregular NCT: Start with 200j monophasic or 120-200j biphasic and then increase in stepwise fashion.
- Regular WCT: Start with 100j, and if fails; increase in stepwise fashion.
- Irregular WCT: Unsynchronized 360j monophasic, or biphasic device specific defibrillation dose
If there is any concern for hyperkalemia as the cause of WCT, immediate treatment with CaCl 1g IV bolus should be given, regardless of patient stability, followed by reassessment of the EKG and laboratory confirmation.
If sodium chanel blockers intoxication is suspected to be the cause of WCT; immidiate treatment with sodium bicarbonate 150 mEq IV bolus should be started and response to treatment be assessed.
Wide complex tachycardia (QRS duration ≧ 120 msec) 6 represents a unique clinical challenge for two reasons:
#1. Diagnosing the arrhythmia is difficult: Although most WCTs are due to VT, the differential diagnosis includes a variety of SVTs (figure 1). Diagnostic algorithms to differentiate these two etiologies are complex and imperfect 7 8 . (see below)
#2. Urgent therapy is often required – Patients may be unstable at the onset of the arrhythmia or deteriorate rapidly at any time, particularly if the WCT is VT or SVT at an extremely rapid rate (e.g, >200 beats per minute).
Ventricular Tachycardia (VT) is a wide complex tachycardia originating in the ventricles. VT can be classified based on the following parameters 9 (figure 4).
Prognosis of patients presenting with VT depends on several parameters which have been associated with risk for sudden cardiac death (SCD). Indices for poor prognosis may include:
- Sustained VT
- Polymorphic VT/VF
- Clinical presentation with syncope, hemodynamic instability, SCD
- Structural heart disease (e.g. Previous MI, IHD, CMP, HCMP) and syndromic channelopathies
Patients at high risk of “SCD” may be candidate for secondary prophylaxis with ICD or catheter ablation following elecrophysiologic studies 38 .
Monomorphic VT (MVT)
Wide and regular ventricular tachyarrhythmia at rate > 120 bpm is assumed VT until proven otherwise.
Among the ventricular tachydysrhythmias the “classic” VT (monomorphic VT) is overwhelmingly the most common and most important etiology encountered.
The mechanisms of “classic VT” is commonly reentrant, with perhaps the most common etiology being “scar-mediated” reentrant circuit VT (e.g. previous MI) 10.
👉Keep in mind that primary VF and polymorphic VT (PMVT) without the presence of QT prolongation on the baseline ECG most commonly occur in the setting of acute myocardial ischemia or infarction. Most patients with monomorphic VT (MVT) have underlying structural heart disease (e.g., previous MI, HF). Acute ischemia is not associated with MVT, rather it may facilitate conversion of MVT to VF.
Symptoms during VT depend on the ventricular rate, duration of the tachycardia, and the presence and extent of the underlying heart disease and peripheral vascular disease. VT can occur in several forms including; short, asymptomatic, nonsustained episodes; sustained, hemodynamically stable events (generally occurring at slower rates or in otherwise normal hearts); or unstable runs, often resulting in hemodynamic collapse and degenerating into VF. VTs initially nonsustained can later become sustained.
- Regular SVT (e.g. ST) with aberrancy
- Antidromic AVRT
- Hyperkalemia: HR usually is < 120 bpm
- Sodium channel blocker intoxication (often very wide QRS > 200 ms)
- Accelerated Idioventricular Rhythm (AIVR): It is a regular wide complex rhythm with ventricular response at 50-110 bpm. This is a reperfusion rhythm often seen post-lytics for STEMI; Think of “slow VT”. The treatment is observation, not medication. 👉Pitfall: Mistaking AIVR (post-lytics for STEMI) for VT and treating with lidocaine may cause cardiovascular collapse.
- Pace-maker mediated tachycardia
In the absence of hyperkalemia or other toxicologic/metabolic causes of QRS widening, the differential of a wide regular tachycardia is VT vs. supraventricular tachycardia (SVT) with aberrancy.
- VT is far more common than SVT, by a factor of four in unselected populations and by as much as 10-fold in patients with prior myocardial infarction.
- Among patients with WCT, VT is much more common than SVT with aberrant conduction.
- More importantly, inadvertently treating VT as though it were SVT could precipitate hemodynamic collapse and/or cardiac arrest, while “mistreating” SVT as though it were VT will does not cause a clinically significant adverse effect.
- Despite multiple ECG algorithms and rules to distinguish VT from SVT with aberrancy (Brugada, Wellens,etc) none are better than 90% specific to identify SVT with aberrancy. No feature or combination of ECG features is 100% specific for SVT with aberrancy. Hence, using an algorithm/rule, there is a 10% chance that you will label VT as SVT with aberrancy erroneously and if you treat the patient with AV nodal blockers, cardiovascular collapse may result.
👉Useful parameters in history and clinical presentation favoring diagnosis of VT may include:
- Prior MI, history of CABG, stent in place
- Heart failure
- Recent angina
- Advanced age: although advanced age makes a wide complex tachycardia being VT much more likely than SVT with aberrancy, up to 50% of patients under 40 years of age who present with a wide complex regular tachycardia with have VT. So VT is also common in young age group!
- Family history of SCD: suggesting conditions such as HOCM, congenital long QT syndrome, Brugada syndrome or arrhythmogenic right ventricular dysplasia that are associated with episodes of VT.
👉Response to adenosine does not rule out VT.
👉Clinical stability does not differentiate between VT and SVT with aberrancy either. Some patients with monomorphic VT are stable!
👉The presence of hemodynamic stability should not be regarded as diagnostic of SVT.
Management decisions can be stratified into those involved in acute management (or termination of VT) and those involved in long-term therapy (or prevention of recurrence or SCD)
Acute management: The first priority when evaluating a patient with a WCT is assessment of patient stability.
Patient in cardiac arrest: Patients who become unresponsive or pulseless are considered to have a cardiac arrest and are treated according to standard ACLS algorithms (figure 5).
👉Antiarrhythmic drug for refractory VF/VT in cardiac arrest: Amiodarone is the initial drug of choice 11.
Based on a single controlled trial with a survival to hospital admission endpoint, IV amiodarone emerged as the initial treatment of choice. Lidocaine may be given intravenously for patients in whom amiodarone is unsuccessful and possibly for those who have an acute transmural MI as the triggering mechanism for cardiac arrest. IV procainamide is rarely used in this setting.
A recent study, randomizing IV amiodarone or lidocaine against placebo, showed no difference between either drug or placebo for survival to discharge outcomes or survival with favorable neurologic status 12. However, survival to hospital admission was significantly better with both active drugs compared to placebo.
👉Double sequential defibrillation for VF/VT in cardiac arrest? Although some case reports have shown good outcomes, a 2020 ILCOR systematic review found no evidence to support double sequential defibrillation and recommended against its routine use. A recent pilot RCT suggests that changing the direction of defibrillation current by repositioning the pads may be as effective as double sequential defibrillation while avoiding the risks of harm from increased energy and damage to defibrillators. On the basis of current evidence, it is not known whether double sequential defibrillation is beneficial 13 .
Unstable patients: In this setting, emergency synchronized cardioversion (after intravenous sedation, whenever possible) is the treatment of choice regardless of the mechanism of the arrhythmia. This should be done immediately, before an extensive diagnostic evaluation (figure 6).
Stable patients: A stable patient with WCT shows no evidence of hemodynamic compromise despite a sustained rapid heart rate. Such patients should have continuous monitoring and frequent reevaluations due to the potential for rapid deterioration as long as the WCT persists (figure 6).
- MVT (regular WCT) that does not cause hemodynamic decompensation can be treated medically to achieve acute termination by IV administration of adenosine, amiodarone, or procainamide.
- If the arrhythmia does not respond to medical therapy, electrical direct-current (DC) cardioversion can be used.
💌Remember that hanging your hat on mean arterial pressure for determining hemodynamic stability is not reasonable, since tissue perfusion correlates well with cardiac output, but not blood pressure (see here). Many patients with known heart disease and VT may not be considered “unstable” according to ACLS guidelines, but nonetheless may have poor cardiac output and be unable to tolerate antidysrhthmic medications. 👉In patients with known structural heart disease and VT, even with normal BP, consider incipient shock and immediate cardioversion.
Initial evaluation in stable patients: The primary goals of the initial evaluation of a stable patient with WCT are to determine the etiology of the WCT and to elucidate any underlying conditions related to the event (e.g. heart failure, myocardial ischemia, drug reaction, or electrolyte abnormalities). In a stable patient, a focused clinical evaluation should include the following:
History: Age, history of heart disease, presence of an implantable cardioverter-defibrillator (ICD), presence of a pacemaker, medications and comorbidities such as renal insufficiency.
Exam: In addition to vital signs, pay specific attention for signs of poor perfusion such as acute confusion, ↑capillary refill time, diaphoresis, and pulmonary edema. The presence of a fistula should raise suspicion of hyperkalemia contributing to the arrhythmia.
EKG, Labs and POCUS (see above)
Scar mediated MVT is the classic VT seen in older patients with a cardiac history (e.g. past MI). The drug of choice for these patients is Procainamide 14.
Adenosine may be used for undifferentiated Regular Monomorphic Wide Complex Tachycardia 17.
If hyperkalemia is suspected as the cause of VT, immediate treatment with IV CaCl should be given regardless of patient stability, followed by reassessment of the EKG and laboratory confirmation.
If sodium channel blockers intoxication is suspected to be the cause of VT; immediate treatment with sodium bicarbonate IV bolus should be started and response to treatment be assessed.
Despite hemodynamic stability synchronized cardioversion is frequently used as the first option for patients with scar-mediated MVT. If pharmacotherapy fails, cardioversion is selected for appropriate candidates (with procedural sedation when feasible).
It refers to a group of ventricular tachycardia which occurs in patients without apparent structural heart disease, or channelopathies . The basic difference between classic and idiopathic VT is presented in the table below (figure 7).
Three commonly recognized syndromes are repetitive monomorphic VT (a.k.a. right ventricular outflow tract “RVOT” VT), paroxysmal sustained VT and idiopathic left ventricular tachycardia. The characteristic features of each are summarized in the following table (figure 8).
Diagnosis of idiopathic VT may require electrophysiologic study and expert consultation is recommended. oftentimes these patients are young and less symptomatic.
👉Do not administer verapamil or beta blocker to patients with WCT whose clinical presentation may fit into a group of idiopathic VT. Expert consultation is warranted.
Patients with ICD represent a specific high risk population in whom WCT is much more likely to be VT. Patients who have ICD for primary prevention are felt to be at high risk for developing life-threatening ventricular arrhythmia, whereas those patients with ICD for secondary prevention have experienced malignant ventricular arrhythmia or sudden cardiac arrest. Therefore any WCT in patients with ICD should be assumed “VT”. ICD patients with recent electrical shock(s) should be under close observation and continious cardiac monitoring.
ICD patients can present to ED for several related complaints; broadly classified into:
- Appropriately delivered shock by ICD: Patient had true episode(s) of concerning arrhythmia and ICD shocked appropriately.
- Inappropriately delivered shock by ICD: Patient had no arrhythmia on device interrogation and no concerning clinical features. In this situation ICD has delivered shock inappropriately. Application of magnet can put the device into VVI mode (pacing preserved, shocking disabled).
- Inappropriately not delivered shock by ICD: Patient presents with concerning clinical features (palpitation, pre-syncope) but ICD not detected the events.
The systemic approach to ICD patient with recent shock(s) or concerning clinical features is presented below (figure 9)
- When the VT has a slower rate e.g. < 175 bpm (which is below the device detection threshold which is usually set at > 175 bpm). In another word, VT is too slow for ICD to recognize. Manage VT just like any other VTs.
- When recurrent episodes of VT happen (frequent VT happens above the detection threshold e.g. > 175 bpm). In this situation, consider
- Possible causes such as: severe HF, electrolyte imbalance, ICD malfunction
- Prophylactic measures are taken to minimize the frequency and recurrence of VTs including administration of amiodarone, beta blocker and sedation 36.
It occurs in the setting of a dual-chamber pacemaker. Pacemaker-mediated tachycardia can be caused via two mechanisms 18:
- In a patient who has a functional AV node, the PM-mediated tachycardia is initiated by a PVC, which causes a retrograde action potential up the AV node followed by retrograde atrial depolarization.The atrial lead of the dual-chamber pacemaker is designed to detect inherent atrial activity; thus, it detects the retrograde P-wave and triggers an impulse via the ventricular lead. The resulting ventricular action potential starts from the ventricular lead and arrives at the AV node after it has repolarized and is ready to accept another retrograde action potential, thereby continuing the reentrant loop
- Another mechanism of pacemaker-mediated tachycardia occurs when a patient with a dual-chamber pacemaker develops any atrial tachycardia that is sensed by the atrial lead, triggering a matching ventricular-paced beat up to the maximal ventricular output rate setting of the pacemaker
Treatment: Application of a magnet turns off the anti-tachycardia function (including defibrillation and synchronized cardioversion) of an implanted cardiac device, as well as the sensing function of a pacemaker (rendering the device simply a pacemaker at a set rate regardless of the patient’s intrinsic function).
Definition: Generally defined as three or more episodes of VF or sustained VT within 24 hours.
Patients can be shocked out of VT/VF easily, but then they keep flipping back into VT/VF (this differentiates VT storm from refractory VT wherein the patient is continually in VT/VF and never goes back to sinus rhythm) 19 .
👉The problem with VT storm isn’t generally breaking any individual episode of VT. Rather, the problem is often that the VT keeps on coming back – so it’s difficult to keep patients out of VT for a prolonged period of time.
- If a patient has an ICD (implanted cardiac defibrillator), this may present with recurrent ICD firing.
- If a 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.
Pathophysiology: electrical storm is a vicious cycle.
- VT/VF increases intracellular calcium levels, which may be pro-arrhythmic39 .
- Shocks and episodes of cardiac arrest (e.g. treated with epinephrine) may cause myocardial injury.
- Myocardial injury & pain stimulate outpouring of endogenous catecholamines 37, promoting recurrent arrhythmia.
- That’s why medications which suppress sympathetic surge play a key role in management. These may include providing generous amount of analgesic/sedation, beta blockers e.g. propranolol and antiarrhythmic with beta blocker properties i.e. amiodarone.
- Key point: The worst approach is watchful waiting, since the natural history of VT storm is generally to deteriorate (even despite the use of standard ACLS algorithms to interrupt each individual episode of VT). Aggressive therapy is needed to stop this process.
- Remember that therapeutic approach to Tdp storm is different from VT storm (see figure 10).
Most patients have structural heart disease (commonly ischemic cardiomyopathy)20. If the patient has a structurally normal heart, this suggests a rare form of arrhythmia requiring specific management (e.g. Brugada syndrome, catecholaminergic polymorphic VT). However, careful assessment is required as some of the known triggers are reversible, including 21 40
- Drug toxicity
- Electrolyte disturbances (i.e, hypokalemia and hypomagnesemia)
- New or worsened heart failure
- Acute myocardial ischemia
- QT prolongation (which may be related to drug toxicity, electrolyte imbalance, or an underlying syndrome such as long QT syndrome)
- Heart failure exacerbation, volume overload
- Medication toxicity, substance abuse (e.g. sympathomimetics)
- Medication non-adherence
- Sepsis 19
The initial treatment approach to patients with electrical storm or incessant VT is based on hemodynamic stability or instability. Patients with cardiac arrest or hemodynamically unstable ventricular arrhythmias should initially undergo electrical cardioversion according to advanced cardiac life support protocol.
Patients with electrical storm who are hemodynamically stable should be treated with both intravenous (IV) antiarrhythmic therapy and a beta blocker in addition to correcting possible electrolyte abnormalities especially hypokalemia and hypomagnesiemia (figure 10):
- Antiarrhythmic medication: The first line antiarrhythmic drug is “Amiodarone” (rather than lidocaine and procainamide). Amiodarone should be given as 150 mg IV over 10 minutes, followed by 1 mg/minute IV infusion for 6 hours, followed by 0.5 mg/minute IV infusion for 18 additional hours.
- Beta blocker: Non-selective beta blocker “Propranolol” is superior to metoprolol because of antagonizing both beta-1 and beta-2 receptors 22. As an alternative, IV esmolol infusion is supported by evidence as well 23.
- Propranolol: IV regimen: Bolus 0.15 mg/kg IV over 10 minutes, then 3-5 mg IV Q6hr 24. Oral regimen: Propranolol 40 mg PO q6hrs has been proven superior to metoprolol (50 mg q6hr) 22.
Esmolol: IV Loading dose is 0.3-0.5 mg/kg IV (~30 mg).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.Max dose is 0.3 mg/kg/min. The advantage of esmolol is titratability. From a mechanistic standpoint, it may be less effective than propranolol because it lacks efficacy at beta-2 receptors.
Sedation: It can break VT storm if provided adequately. Propofol or benzodiazepine (if cannot intolerable to propofol) may be choosen.
Stellate ganglion block: A systematic review and meta-analysis of 22 unique case series with a total of 35 patients has shown a dramatic reduction in arrhythmia burden 25 .Other studies have shown its safety and efficacy in termination of VT storm 26. For performing the procedure, you can see here and here for ultrasound guided approach.
Treatment of the causes of electrical storm
- Revascularization & therapy for myocardial infarction: AMI is an important cause of VT storm. In an appropriate setting where active ischemia is felt to be a contributing factor, additional therapies for ACS should also be considered (e.g. aspirin, P2Y12 inhibitor) and emergent coronary revascularization should be pursued.
- ICD optimization: Any patient with an ICD requires device interrogation. Ensure that the device is truly detecting VT (rather than over-responding to artifact). Anti-tachycardia overdrive pacing may be optimized to break episodes of VT without requiring shocks 36.
- Catheter ablation of VT/VF: Once patient is stabilized, ablation may be considered especially for monomorphic VT storm
- Decompensated heart failure: beta blockers, ACE inhibitors and diuretic are considered and titrated to maximally tolerated doses
- Correction of any identified inciting factors should occur. This may include removal of any offending drugs (eg, prescription or illicit drugs which prolong the QT interval) and correction of any electrolyte disturbances (ie, hypokalemia, hypomagnesemia, etc).
Irregular Wide QRS Tachycardia with rapidly changing QRS morphology and shape from beat to beat. PMVT is usually a non perfusing rhythm; hence patients are hemodynamically unstable. Immediate treatment is unsynchronized cardioversion. However treatment for intermittent or recurrent PMVT depends on the patient’s presentation and the QTc interval during the intermittent sinus rhythm.
Pathophysiology: There is often an underlying “Dynamic Unstable” myocardium e.g. AMI, myocarditis, dynamic changes in QTc.
#1. PMVT with normal QT (a.k.a. Spontaneous PMVT). Etiologies may include:
- Acquired: Unstable myocardium e.g. AMI, cardiomyopathies including takotsubo’s
- Congenital: Catecholaminergic polymorphic VT (CPVT)
#2. PMVT with prolonged QT (torsade de pointes)
- Acquired: Medications that cause prolongation of QT, ↓K, ↓Mg. Refer here for list of QT prolonging drugs
- Congenital: congenital long QT syndrome.
👉Catecholaminergic polymorphic VT (CPVT): Is a genetic disorder presenting as familial and sporadic form. Patients are either asymptomatic (identified by familial screening) or they may present with syncope or stress-induced (emotional or physical stress)27 cardiac arrest precipitated by VT/VF.
EKG is unremarkable during normal sinus rhythm. However during the episode of PMVT, the tachydysrhythmia has two major features:
- The PMVT is not associated with prolonged QTc.
- Bidirectional VT: once thought to be pathognomonic for digital intoxication; it can happen in CPVT 28. It happens due to intracellular calcium overload which in turn leads to DADs and triggered activity.
Diagnosis is confirmed by exercise stress test or epinephrine infusion test; upon which increasing frequency of PVCs with increasing exercise severity is noticed, although both sustained and non-sustained VT may happen.
- Unstable or pulseless patients should receive unsynchronized defibrillation.
- In stable patients, acute suppression of Recurrent PMVT is achieved by “Propranolol”. If it fails, CCBs such as verapamil or flecainide are helpful 29.
- Long-term management of patients with sustained PMVT involves ICD placement and administration of beta blocker to minimize arrhythmia and ICD shock delivery.
👉Torsades de pointes is polymorphic VT that occurs in the setting of a long-QT interval and is characterized by a waxing and waning QRS amplitude. It commonly happens in the setting of underlying bradycardia (including high-grade AV block) that leads to a long-short sequence initiating Tdp. The twisting of the points, although characteristic, may not always be seen, especially if the episode is nonsustained or if only a limited number of leads are available. Therefore the morphology of Tdp (twisting around a point) is not reliable and sufficient enough to distinguish PMVT with normal QT vs. PMVT with prolonged QT (Tdp). The diagnosis of Tdp is only made when tachyarrhythmia is broken and you can appreciate the prolonged QTc during normal sinus rhythm.
👉It is practically impossible to differentiate PMVT from VF on monitor.
- Several studies have shown that pulseless rhythm appeared to be Tdp (twisting around a point) turned out to be VF.
- This distinction has no implication for immediate management (since both will receive defibrillation), however it has implicatication for preventing further dysrhythmia.
- AF + WPW: characterized by irregularly irregular polymorphic wide complex tachycardia with characteristically high rate (>200-250 bpm) and changing QRS shape, width, amplitude from beat to beat.
- Management: The first line treatment regardless of hemodynamic stability is synchronized cardioversion. Otherwise “Procainamide” is recommended in this situation.
- 👉👉All AV nodal blocking agents (e.g. BB, CCBs, amiodarone, digoxin, adenosin) are contraindicated in this situation.
- AF + BBB: The irregular WCT has the characteristic of RBBB-shaped or LBBB-shaped. If diagnosed definitively, treatment with any AV nodal blocking agent is suitable and safe.
- Hyperkalemia (sine wave)
Despite that unsynchronized cardioversion is the first therapeutic measures to most patients with irregular WCT; diagnosis and management of irregular WCT is challenging for two reasons:
#1. AF + WPW: Failure to recognize this pattern is unforgiving. In this condition, all AV nodal blocking agents including amiodarone are absolutely contraindicated. All these medications may lead to degenerating dysrhythmia into VF. The only possible safe antiarrhythmic medication is “Procainamide”.
#2. PMVT: Failure to identify Tdp (as a subtype of PMVT), since the principles of therapeutic approach for Tdp is different from PMVT with normal QTc.
👉Identifying PMVT with normal QTc signals for a thorough evaluation for possible underlying ischemia, cardiomyopathy. Moreover the antiarrhythmic medications which are allowed in this setting including amiodarone, beta blockers are contraindicated in patients with Tdp. The diagnostic approach to PMVT is shown below (figure 11).
1. Immidiate defibrillation if patient has ongoing PMVT (unsynchronized initially started at 200 J biphasic).
2. Once PMVT is broken and QTc prolongation is noted in sinus rhythm, then all attempts should be focused on administration of magnesium (even if serum Mg is normal) as per following protocol 34 35 and correction of hypokalemia. More on rationale for magnesium infusion here.
3. Stop all medications with QT prolonging effects.
4. If despite all measures, Tdp recurs, first defibrilate it (as mentioned). Then employ following steps for prevention of Tdp recurrence including:
- Make sure that patient has received adequate amount of magnesium. one may consider re-loading magnesium with 2-4 grams IV immidiately, if the patient was bolused with magnesium a few hours ago without an infusion.
- Target serum potasium level to > 4.5 mEq/L.
- For some patients with baseline bradycardia, speeding up the heart rate with target HR > 100-110 bpm may seems reasonable except for few patients with some forms of congenital Tdp). This can be achieved by medical or electrical treatment.
- Medical chronotropy: This is the easiest and fastest approach 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.
- Electrical chronotropy may be used if medical chronotropy fails:
- 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.
- Medical chronotropy: This is the easiest and fastest approach to stabilize the patient. The ideal chronotrope depends on the patient’s hemodynamics and baseline blood pressure:
- If all above measures were ineffective, one may consider administration of antiarrhythmic. The drug of choice is “Lidocaine” (since it has no QT prolonging effect). Do Not give amiodarone, procainamide, beta-blockers, or most other antiarrhythmics.
- If patient failed to respond and Tdp recurred, then one may consider alternative diagnosis such as PMVT due to ischemia or catecholaminergic ventricular tachycardia.
- Two fundamental principles in initial evaluation of patients with tachyarrhythmias include determining hemodynamic stability and recognizing whether the arrhythmia is the cause of clinical presentation.
- By enlarge abnormal HR might be assumed as a primary cause of clinical instability when; non-sinus tachycardia at > 170 bpmor AF with rapid ventricular response > 130-150 bpm.
- AF with rapid ventricular response (in the range of 110-150) is often an innocent bystander especially in patients with chronic AF. In such patients one should investigate for other causes of instability such as blood loss, sepsis etc.
- Generally tachyarrhythmia in patients with hemodynamic instability calls for electrical cardioversion/defibrillation while patients who are stable can be treated by antiarrhythmic medications.
- Electrical cardioversion/defibrillation is the easiest and fastest approach to stabilize the patients if indicated and practiced appropriately. It is safer than any other antiarrhythmic medications.
- It is safest to assume regular WCT as VT until proven otherwise.
- PMVT can not be distinguished from Tdp unless the rhythm is broken and QT prolongation is noted on baseline EKG.
- The worst approach to patients with VT/VF storm (electrical storm) is watchful waitting. Electrical storm is a vicious cycle and VT/CF will recur.
- If Tdp is recognized, appropriate administration of magnesium and correction of hypokalemia (if exists) play pivotal roles in prevention of recurrence of Tdp. Failure to administer magnesium infusion often leads to recurrence of the tachydysrhythmia events.
- Procainamide is the drug of choice for most stable patients with WCT. It is also safe in patients with (AF +WPW). However there are still certain conditions in the setting of VT; where “Amiodarone” is superior to procainamide. These include:
- VT/VF in cardiac arrest
- Electrical storm
- ICD patient with VT above detect rate
- Acute MI with PMVT (👌keep in mind that patients with AMI benefit from the beta-antagonist effect of a medication. Amiodarone has beta-antagonist effect in addition to Na, K channel blockade properties)
- Avoid giving medication with AV nodal blocking property such as BBs, CCBs, adenosine, amiodarone and digoxin to patients with Irregularly irregular WCT (at very fast rates usually > 250-300).
- Avoid giving procainamide, BBs, amiodarone to patients with Tdp. These medications will further prolong QTc. If a decision is made to give an antiarrhythmic medication as a last ditch attempt, “Lidocaine” is preferred over other drugs.
- Tachydysrhythmias with Amal Mattu (emergency medicine cases)
- ECG Course: The Paced ECG (EM:RAP)
- Non-torsade VT/VF storm (IBCC)
- Torsades de Pointes
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