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Unstable tachyarrhythmias will result in cardiac arrest or irreversible end organ damage if not rapidly diagnosed and treated.
Examples of unstable conditions include:
AMS or obtunded state
Symptomatic hypotension
Ischemic chest pain
Dyspnea from pulmonary congestion/acute HF
Extremely fast HR > 250 bpm (polymorphic VT or atrial fib with pre-excitation)
KEY UNSTABLE MANAGEMENT PEARLS:
KEY UNSTABLE MANAGEMENT PEARLS:
If pulseless with ventricular fibrillation or ventricular tachycardia, perform immediate defibrillation and chest compressions.
If unstable, perform synchronized cardioversion for monomorphic VT or other tachyarrhythmias using sedation when possible unless obtunded (150-200 J biphasic).
Consider a precordial thump if defibrillator is not immediately available, just don't delay compressions.
Unstable polymorphic VT may require defibrillation when cardioversion is not possible due to very rapid rates.
Consider if the tachycardia is the cause of the instability or if it is compensatory
LV overload on POCUS suggests a primary cause
LV depletion suggests a compensatory response
Always consider hyperkalemia and treat with empiric calcium when thought to be a potential cause
Hemodynamic or refractory electrical instability secondary to ACS is an indication for emergent cath
Categorize rhythms based on QRS width (narrow or wide) and rate variation (regular or irregular)
Consider adenosine or vagal maneuvers for narrow complex monomorphic tachycardia if not clinically hypotensive, while prepping for synchronized cardioversion
If known SVT, use synchronized cardioversion when hemodynamically unstable & vagal maneuvers are ineffective or unfeasible.
Differentiate the Rhythm!
Differentiate the Rhythm!
Narrow vs. Wide and Regular vs. Irregular Rhythms
Narrow QRS (<120 ms)
Narrow QRS (<120 ms)
3 main causes of NARROW & REGULAR tachycardias
Sinus tachycardia (single sinus P wave before every QRS)
Supraventricular Tachycardia (No P waves or retrograde P waves after QRS)
Atrial flutter with fixed conduction (Flutter waves)
3 main causes of NARROW & IRREGULAR tachycardias
Atrial fibrillation (fib waves)
Atrial flutter with variable conduction (flutter waves)
Multifocal atrial tachycardia (3 or more distinct P waves)
Looks closely for P waves in all leads (especially V1 & II) to differentiate between the 3 different potential rhythms
Wide QRS (>120 ms)
Wide QRS (>120 ms)
Anything that causes aberrant conduction will turn the narrow complex DDx above into a wide complex DDx.
Main causes of aberrancy include:
Bundle branch blocks, pacemakers, LVH
Electrolyte, metabolic causes (hyperkalemia, acidosis, etc.)
Toxicologic causes, medications (e.g. TCA's)
Accessory pathways
Ventricular rhythms
WIDE & REGULAR tachycardia should be considered to be VT until proven otherwise!
Use the VTACH mnemonic below to remember potential VT mimics that may change your management
Do not rely on the VT vs. SVT criteria, when in doubt, treat for VT
WIDE & IRREGULAR tachycardias should be scrutinized for evidence of afib with WPW
Avoid all AV nodal blockers unless certain that patient has afib with bundle branch block similar in morphology to baseline
Use electrical cardioversion when in doubt, and procainamide when hemodynamically stable
KEY TACHYCARDIA PEARLS
KEY TACHYCARDIA PEARLS
Avoid all AV node blockers (including adenosine, digoxin, & amiodarone) in wide complex irregular tachycardias that are polymorphic, suggestive of AFib with pre-excitation that can rapidly degenerate into ventricular fibrillation!
Obtain an ECG before and after termination of tachyarrhythmias to look for signs of structural disease, ACS, long & short QT syndromes, WPW, ARVD, Brugada syndrome, and HOCM.
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