MCEM B CVS TACHY |1

@ Resus council UK 2010 & Resus council UK 2015

o TACHYCARDIAS
 TACHYCARDIA
o @ TYPES
 Broad
 Regular
o VT
o SVT with BBB
 Irregular
o AF with BBB ( most likely cause)
o Other possible causes are
 AF with ventricular pre-excitation (in patients with WPW
syndrome), or
 polymorphic VT (e.g. torsade de pointes)
 narrow
 irregular
o AF (most probable)
o Atrial flutter with variable AV conduction (‘variable block’).
 Regular
o Sinus tachycardia (not an arrhythmia)
o AV nodal re-entry tachycardia (AVNRT) (SVT) – the commonest type of
regular narrow-complex tachyarrhythmia;
o AV re-entry tachycardia (AVRT) – due to WPW syndrome;
o Atrial flutter with regular AV conduction (usually 2:1).
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 Sequence of actions &
o ABCDE: Assess a patient with a suspected arrhythmia using the ABCDE approach
 In particular, note the presence or absence of ‘adverse features’
o O2:Give oxygen immediately to hypoxaemic patients and adjust delivery according to observed arterial oxygen saturations
o Insert an intravenous (IV) cannula
o Whenever possible, record a 12-lead ECG
o Correct any electrolyte abnormalities (e.g. K+, Mg2+, Ca2+).
 Adverse features (Unstable) &
o Shock – hypotension (systolic blood pressure <90 mm Hg), pallor, sweating, cold, clammy extremities, confusion
or impaired consciousness
o Syncope – transient loss of consciousness due to global reduction in blood flow to the brain
o Myocardial ischaemia – typical ischaemic chest pain and/or evidence of myocardial ischaemia on 12-lead ECG
o Heart failure – pulmonary oedema and/or raised jugular venous pressure (with or without peripheral oedema
and liver enlargement).
 If a patient is Unstable &
o Synchronised cardioversion is the treatment of choice.
o If cardioversion fails to restore sinus rhythm, and the patient remains unstable,
 Give amiodarone 300 mg IV over 10–20 min and re-attempt electrical cardioversion.
 The loading dose of amiodarone may be followed by an infusion of 900 mg over 24 h.
o Synchronised cardioversion
 If the patient is conscious,
 Carry out cardioversion under sedation or general anaesthesia
 For a broad-complex tachycardia or atrial fibrillation
 Start with 120–150 J and increase in increments if this fails.
 Atrial flutter and regular narrow-complex tachycardia will often be terminated by lower energies:
 Start with 70–120 J.
 Rhythms &
 Broad-complex tachycardia
o Regular
 Ventricular tachycardia (VT) or
 Supraventricular rhythm with bundle branch block.
 In an UNSTABLE patient
 Assume that rythm is ventricular in origin & attempt synchronised cardioversion
 In a STABLE patient,
 If the broad-complex tachycardia is thought to be VT, treat with amiodarone 300
mg IV over 20–60 min, followed by an infusion of 900 mg over 24 h.
 If a regular broad-complex tachycardia is known to be a supraventricular
arrhythmia with bundle branch block (usually after expert assessment of
previous episodes of identical rhythm) and the patient is stable use the strategy
indicated for regular, narrow-complex tachycardia
 Where there is uncertainty, seek urgent expert help whenever possible.
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o Irregular
 This is most likely to be AF with BBB,
 Other possible causes are
o AF with ventricular pre-excitation (in patients with WPW syndrome), or
o Polymorphic VT (e.g. torsade de pointes),
 but sustained polymorphic VT is unlikely to be present without
adverse features.
 Seek expert help with the assessment and treatment of irregular broad-complex
tachyarrhythmia.
 Torsade de pointes VT
 Rx
o Stop all drugs known to prolong the QT interval.
o Do not give amiodarone for definite torsade de pointes.
o Correct electrolyte abnormalities, especially hypokalaemia.
o Give magnesium sulfate 2 g IV over 10 min (= 8 mmol, 4 mL of 50%
magnesium sulfate).
o Obtain expert help, as other treatment (e.g. overdrive pacing) may be
indicated to prevent relapse once the arrhythmia has been corrected.
o If adverse features are present, which is common, arrange immediate
synchronised cardioversion.
o If the patient becomes pulseless, attempt defibrillation immediately (ALS
algorithm).
 Narrow-complex tachycardia
o Regular
 Sinus tachycardia
 AVNRT and AVRT (paroxysmal supraventricular tachycardia)
 AV nodal re-entry tachycardia
o Commonest type of paroxysmal supraventricular tachycardia (SVT)
o It is usually benign (unless there is additional, co-incidental, structural
heart disease or coronary disease) but it may cause symptoms that the
patient finds frightening.
 AV re-entry tachycardia
o occurs in patients with the WPW syndrome, and is also usually benign,
unless there is additional structural heart disease. The common type of
AVRT is a regular narrow-complex tachycardia, usually having no visible
atrial activity on the ECG.
 Atrial flutter with regular AV conduction (often 2:1)
 This produces a regular narrow-complex tachycardia. It may be difficult to see
atrial activity and identify flutter waves in the ECG with confidence, so the
rhythm may be indistinguishable, at least initially, from AVNRT or AVRT.
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 Typical atrial flutter has an atrial rate of about 300 min-1, so atrial flutter with 2:1 conduction
produces a tachycardia of about 150 min-1. Much faster rates (>160 min-1) are unlikely
to be caused by atrial flutter with 2:1 conduction. Regular tachycardia with slower
rates (e.g. 125–150 min-1) may be due to atrial flutter with 2:1 conduction, usually when the rate
of the atrial flutter has been slowed by drug therapy.
 Treatment
o Regular narrow-complex tachycardia
 Unstable
 Attempt synchronised electrical cardioversion.
 It is reasonable to apply vagal manoeuvres and/or give adenosine to an unstable
patient with a regular narrow-complex tachycardia while preparations are being
made urgently for synchronised cardioversion. Do not delay electrical
cardioversion if adenosine fails to restore sinus rhythm.
 Stable
 Start with vagal manoeuvres.
o Carotid sinus massage or the Valsalva manoeuvre will terminate up to a
quarter of episodes of paroxysmal SVT.
o Record an ECG (preferably multi-lead) during each manoeuvre. If the
rhythm is atrial flutter, slowing of the ventricular response will often
occur and reveal flutter waves.
 If the arrhythmia persists and is not atrial flutter,
o Give adenosine 6 mg as a rapid IV bolus.
 Use a relatively large cannula and large (e.g. antecubital) vein. Warn the patient that they will feel
unwell and probably experience chest discomfort for a few seconds after the injection. Record an
ECG (preferably multi-lead) during the injection. If the ventricular rate slows transiently, but then
speeds up again, look for atrial activity, such as atrial flutter or other atrial tachycardia, and treat
accordingly.
 If there is no response (i.e. no transient slowing or termination of
the tachyarrhythmia) to adenosine 6 mg IV, give a 12 mg IV bolus.
If there is no response give one further 12 mg IV bolus. Apparent
lack of response to adenosine will occur if the bolus is given too
slowly or into a peripheral vein.
 Vagal manoeuvres or adenosine will terminate almost all AVNRT or AVRT within
seconds. Termination of a regular narrow-complex tachycardia in these ways
identifies it as being AVNRT or AVRT.
 Failure to terminate a regular narrow-complex tachycardia with adenosine
suggests
o An atrial tachycardia such as atrial flutter (unless the adenosine has been
injected too slowly or into a small peripheral vein).
 If adenosine is contra-indicated, or fails to terminate a regular narrow-complex
tachycardia without demonstrating that it is atrial flutter,
o Consider giving Verapamil 2.5–5 mg IV over 2 min.
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o Irregular narrow-complex tachycardia
 Most likely to be AF with an uncontrolled ventricular response or,
 Less commonly, Atrial flutter with variable AV block.
 Record a 12-lead ECG to identify the rhythm.
 If the patient is UNSTABLE
 Start antithrombotic therapy & attempt synchronised cardioversion.
 If the patient is STABLE
 Immediate treatment options include:
o No treatment
o Rate control by drug therapy
o Rhythm control using drugs to encourage chemical cardioversion
o Rhythm control by electrical cardioversion
o Treatment to prevent complications (e.g. Anticoagulation).
 Obtain expert help to determine the most appropriate treatment for the
individual patient.
 The longer a patient remains in AF the greater is the likelihood of atrial thrombus
developing.
 In general, patients who have been in AF for > 48 h
o Should not be treated by cardioversion (electrical or chemical) until
 They have been fully anticoagulated for at least three weeks, or
 Unless Trans-Oesophageal Echocardiography has shown the
absence of atrial thrombus.
o If the clinical situation dictates that cardioversion is needed more
urgently,
 Give either
 Low-molecular-weight heparin in weight-adjusted
therapeutic dose or
 IV bolus injection of unfractionated heparin followed by a
continuous infusion to maintain the activated partial
thromboplastin time (APTT) at 1.5 to 2 times the reference
control value.
 Continue heparin therapy and commence oral anticoagulation
after attempted cardioversion, whether or not it is successful.
 Seek expert advice on the duration of anticoagulation, which
should be a minimum of four weeks, often substantially longer,
unless the risk of bleeding is prohibitive.
 Use of scoring systems to assess thromboembolic risk (e.g. the
CHA2DS2-VASc score) and the risk of bleeding (e.g. the HAS-BLED
score) are recommended when considering the balance of risk
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and benefit from anticoagulant therapy in people with AF (and
atrial flutter).
o Rate control
 Usual drug of choice is a Beta-Blocker.
 Diltiazem Or Verapamil may be used in patients in whom beta-blockade is
contraindicated or not tolerated. An IV preparation of diltiazem is available in some countries
but not in the UK.
 Digoxin or Amiodarone may be used in patients with heart failure.
 Amiodarone may be used to assist with rate control but is more useful in
maintaining rhythm control.
 Whenever possible seek expert help in selecting the best choice of
treatment for rate control in each individual patient.
 If the duration of AF is < 48 h and rhythm control is considered appropriate,
 Chemical cardioversion may be attempted.
o Seek expert help with use of drugs such as Flecainide Or Propafenone.
 Do not use flecainide or propafenone in the presence of
 Heart failure, known left ventricular impairment or
ischaemic heart disease, or a prolonged QT interval.
o Amiodarone (300 mg IV over 20–60 min followed by 900 mg over 24 h)
may also be used (unless the QT interval is prolonged) but is less likely to
achieve prompt cardioversion.
o Electrical cardioversion remains an option in this setting and will restore
sinus rhythm in more patients than chemical cardioversion.
 AF is known to or found to have ventricular pre-excitation (WPW syndrome).
o Seek expert help
o Avoid using adenosine, diltiazem, verapamil, or digoxin in patients with pre-
excited AF or atrial flutter as these drugs block the AV node and cause a relative increase in pre-excitation.

o Treatment of tachycardia():
 Common managements of all tachyarrhythmia
 ABC, O2
 Monitor and 12 lead ECG
 Identify and treat reversible cause
 Synchronized Cardioversion if 5 adverse signs present
 Unstable patient:
 Synchronised cardioversion
o Carry out cardioversion under general anaesthesia or conscious sedation.
o For a broad-complex tachycardia or atrial fibrillation,
 start with 120-150 J biphasic shock (200 J monophasic) and
increase inincrements if this fails.
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o Atrial flutter and regular narrow-complex tachycardia will often be
terminated by lower energies:
 start with 70-120 J biphasic (100 J monophasic).
 Stable
o Broad complex
 Regular
 Irregular
 Treat torsade de pointes VT immediately by
o stopping all drugs known to prolong the QT interval.
o Correct electrolyte abnormalities, especially
hypokalaemia.
o Give magnesium sulphate 2 g IV over 10 min (= 8
mmol, 4 ml of 50% magnesium sulphate).
o Seek expert help
 Stable patients:
 Narrow
 Wide
o Regular
 Monomorphic VT ()62
 1ST Line: Amiodarone
 2nd Line:
o Lignocaine
o B Blocker (esp. in MI/ischemia)
 Correct Reversible causes ():
o Correct ischemia in post infarct VT.
 B Blockers & Revascularisation
o Electrolytes:
 Aim K ≥4-4.5, Mg ≥1
o Acidosis. If pH < 7.1
 Give Bicarbonates
 8.4% Na Bicarbonate 50 ml over 20 min IV
central.
 If recurrent or persistant VT:
o Synchronized DC shock
o Over drive pacing using temprory Transvenous wire
 Once acute episode of VT is over, consider cardiologist
referral for:
o Holter monitoring
o Exercise test
o Coronary angiography
o VT stimulation (provocation) test
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o Irregular
 Polymorphic VT (eg Torsades de pointes)
 IV Magnesium Sulphate
o 2g = 8 mmol = 4 ml of 50% Mg
 over 10 min
 Referactory cases require
o Overdrive Pacing
o Synchronized Cardioversion
o See YouTube
 http://www.youtube.com/watch?v=CpoubRYVdhs
 Also stored in u tube videos
 See technique $123
 () Hemodynamically compromised pt needs defibrillation. The only exception is
chronic AF with uncontrolled ventricular rate, defibrillation is unlikely to
cardiovert to SR. rate control and treatment of precipitant is first line.
 Sedate awake pt with
o Midazolam (2.5 – 10 mg) IV
 According to OHEM in unstable tachycardia
 Give 3 sync shocks
 If unsuccessful give Amiodarone 300 mg IV over 10-20 min
 Repeat the shock
 Then give Amiodarone 900 mg IV over 24 hrs
o DRUGS
 ADENOSINE
 Indications
o SVT $164
o AVNRT $
o Regular and monomorphic broad complex tachy $
o Does not convert $
 AF
 Atrial Flutter
 VT
 Transient AV block produce 3 effects : ()60
o If tachycardia terminates:
 It suggests SVT with abberancy
o Ventricular rate slows unmasking atrial activity:
 AF or Atrial Flutter appears
o If no effect
 VT
 Dose $165
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o 1st :
6 mg IV followed by 20 ml N/S push
nd
o 2 : 12 mg after 1-2 min if no effect
o 3rd : 12 mg
o Half the dose if on dipyridamole or carbamazepine
o Inc the dose if taking Theophylline or Caffeine
 Alternate
o If contraindicated consider
 Verapamil 2.5 – 5 mg over 2 min
 Avoid Verapamil in
 Cardiac failure
 Hypotension
 WPW
 Concomitment with B Blockers
 SE ( all symptoms brief for 30 sec)
o Flushing
o Chest pain or tightness, bronchospasm
o Bradycardia or asystole.
o It is safe in pregnancy
 -Rx:
o 2nd or 3rd degree block
o WPW
o Asthma
o
o BROAD COMPLEX TACHYCARDIA
 Broad complex tachy associated with TCA
o ABC, O2
o Correct metabolic disorder: IV Bicarbonate
o Avoid Antiarrhythmics
 VT vs SVT with abberent pathway.
 VT has
o Pt >60 yrs
o Hx of IHD or Cardiomyopathy
o Clinical evidence of AV dissociation
 Intermittent canon ‘a’ wave on JVP
 S1 of variable intensity
o Inverted P wave in II
o QRS > .13 sec
o Capture beats
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 Some time sinus rhythm when reach AV node find entire
ventricular conduction system receptive to depolarization and
produce a normal appearing QRS. &155
o Fusion beat
 In VT an Atrial depolarization finds a receptive AV node, but
ventricular depolarization only proceeds so far before it meets
ventricular depolarization progressing from the ventricular focus
producing fusion beat which is blending on ECG of a normal QRS
with a PVC like complex. &155
o QRS bizarre not resembling bundle branch block
o All chest leads (v1-6) are concordant(QRS complexes point the same way)
 In SVT has mixed +ve & -ve QRS deflection in chest leads
o Deep S wave in V6
o Marked LAD ()60
o Cycle length stability (<40 ms R-R variation) ()60

o
o Brugada’s sign – The distance from the onset of the QRS complex to the nadir
of the S-wave is > 100ms.
 Brugada's Sign is characteristic of Ventricular tachycardia.
o Josephson’s sign is a small notch near the low point of the S wave.
 characteristic of ventricular tachycardia
o
 Factors favouring SVT ()60:
o Grossly irregular broad complex tachycardia >200/min, suggest AF with
conduction with accessory pathway
o Terminate by vagotonic maneuver
o Evidence of AV coupling eg 1:2 AV block

WPW syndrome (Wolff –Parkinson–White

 Caused by congenital accessoryconduction pathway between atria and ventricles.
 Resting ECG shows
o Short PR interval,
o Wide QRS complex (due to slurred upstroke or ‘delta wave’) and
o ST-T changes.
 2 types:
o WPW type A (+ve  wave in V1),
o WPW type B (–ve  wave in V1).
 If WPW is the underlying cause of AF, avoid AV node blockers such as adenosine, diltiazem, verapamil
and digoxin—but flecainide may be used.
 Treatment
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o Amiodarone
o Electric cardioversion
o Flecainide (if no cardiac structural disease)