c_broadcomplextachy
Table of Contents
broad complex tachycardias
see also:
AV nodal blockers, particularly, verapamil, but also adenosine, may cause VF if given to patients with WPW with broad complex tachyarrythmias unless it is definetely antidromic AVRT and not AF or atrial flutter
- is it really a broad complex tachy?
- if there is at least one lead with narrow complexes then it is NOT a broad complex tachy as the appearance may be due to either:
- sinus tachy with large ST elevation acute myocardial infarction (AMI/STEMI/NSTEMI)
- artefactual patterns
acute Mx of broad complex tachycardia:
- oxygen, cardiac monitor, resuscitation facilities on hand, correct electrolyte disturbances if present
- could it be sinus tachy with wide QRS?
- look for notches in T waves to indicate presence of P waves and rate < 150
- if unlikely to be sinus tachy, but is haemodynamically unstable then immediate DC reversion
- if haemodynamically stable then:
- if really wide QRS, consider hyperkalaemia and Rx accordingly if it is
- if definitely supraventricular then Mx as for Supraventricular tachycardia (SVT)
- if uncertain, for pharmacologic termination of a stable wide QRS-complex tachycardia, the following are options:
- if digoxin toxicity then
- iv Digibind
- whilst waiting for Digibind, iv magnesium sulphate may be life saving if VT/VF present - give 2g bolus then 1-2g/hr and check serum levels of Mg every 2hours aiming for Rx range of 4-5mEq/L.
- treat hyperkalaemia if K+ > 5.5mEq/L
- do not give calcium to Rx hyperkalaemia as VT/VF may be precipitated
- iv lignocaine 100mg boluses, if successful then maintenance infusion 1-4mg/min
- or iv phenytoin 100mg boluses every 5-10min up to load dose of 15mg/kg
- avoid procainamide and bretylium
- do not give calcium channel blockers such as verapamil (Isoptin) as they may increase digoxin toxicity
- short-acting beta blockers such as esmolol may be helpful, but may precipitate advanced or complete AV block
- else if irregular, wide complex tachy (eg. pre-excited AF such as in pre-excitation syndromes such as WPW) then
- DC reversion is preferred, or if stable AND LV function not impaired, then:
- iv flecainide (or ibutilide or procainamide)
- else if impaired LV function or signs of heart failure then
- iv amiodarone, or,
- otherwise:
- iv procainamide and/or
- iv sotalol
- alternatively, as for impaired LV function
- NB. verapamil (Isoptin) may be used as first-line Rx for LV fascicular VT
DDx of wide complex tachycardias:
- see https://lifeinthefastlane.com/ecg-library/basics/vt_vs_svt/ for VT vs SVT with aberrancy algorithms
- if rate <120 then NOT VT!
- QRS duration > 120msec
- if REALLY WIDE QRS ⇒ consider hyperkalaemia as cause and Rx accordingly
- if becomes unconscious then assume VT ⇒ DC reversion ASAP
- classical twisting axis pattern then torsade de pointes VT
- if alternate beats have QRS axis 180deg rotated from previous then it is called bidirectional VT
- this is mainly seen in:
- digoxin toxicity - Rx as for digoxin overdose
- patients with familial catecholaminergic polymorphic ventricular tachycardia (CPVT)
- onset usually in childhood mean age 7-9yrs; FH sudden death; arrhythmia usually reproducible on exercise stress testing when sinus tachy reaches 120bpm and recede with recovery from exercise
- Rx with DC reversion, then beta adrenergic blockers
- if patient is on flecainide but not a beta blocker or calcium channel blocker (or recently ceased these) then there is a risk of them developing either:
- “slow atrial flutter” with 1:1 conduction rates of arpound 200/min and widened QRS which may “fit” usual VT criteria 1)
- monomorphic sinusoidal wide QRS tachycardia VT
- polymorphic ventricular tachycardia or fibrillation
- if irregular then:
- AF, or,
- atrial flutter or AT with variable conduction and BBB or antegrade conduction via accessory pathway such as WPW
- if regular then:
- if QRS identical to that in SR then SVT with BBB or antidromic AVRT
- otherwise:
- if PH ischaemic heart disease or structural heart disease then VT likely
- if V rate faster than atrial rate then VT
- if atrial rate faster than V rate then atrial tachycardia or atrial flutter
- otherwise:
- check QRS morphology in precordial leads:
- otherwise probable VT see elsewhere
- note:
- An RS (from the initial R to the nadir of S) interval longer than 100 ms in any precordial lead is highly suggestive of VT.
- A QRS pattern with negative concordance in the precordial leads is diagnostic for VT (“negative concordance” means that the QRS patterns in all of the precordial leads are similar, and with QS complexes). Positive concordance does not exclude antidromic AVRT over a left posterior accessory pathway.
- The presence of ventricular fusion beats indicates a ventricular origin of the tachycardia.
- QR complexes indicate a myocardial scar and are present in approximately 40% of patients with VTs after myocardial infarction.
c_broadcomplextachy.txt · Last modified: 2024/05/04 02:24 by gary1