Its crucial to diagnose arrythmias quickly and treat it promptly. Here i have made small attempt to diagnose tachyarrythmias briefly and proceeds with its immediate managenent..

1. DR. HARSHAD WANKHADE
EMERGENCY MEDICINE AND
CRITICAL CARE.

2.  TACHYCARDIA-RHYTHM THAT
PRODUCES VENTRICULAR RATE MORE
THAN 100 BEATS PER MINUTE.
 TACHARRHYTHMIAS ARE ISOLATED
PREMATURE COMPLEXES OR
NONSUSTAINED OR SUSTAINED FORM OF
TACHYCARDIA ORIGINATING FROM
MYOCARDIAL FOCI OR REENTRANT
CIRCUIT.

3.  Physiological
 Pathological:
 Valvular heart disease.
 Electrolyte disturbances.
 Structural heart disease.
 Ischemic heart disease.
 Hypertensive heart diseases.
 Congenital heart disease.
 Cardiomyopathies.
 Carditis.
 RV dysplasia.
 Drug related.
 Pericarditis.
 Pulmonary diseases.
 Others.

4.  Palpitation.
 Dizziness.
 Chest Pain.
 Syncope.
 Irregularity in pulse.
 Dyspnea.
 Fainting.
 Hemodynamic collaps.
 Sudden cardiac death.

5.  ECG
 24h Holter monitor
 Echocardiogram
 Stress test
 Coronary angiography
 Electrophysiology study

12.  ECG CHANGES—
 Regular rhythm at a rate of 60-100 bpm (or age-
appropriate rate in children).
 Each QRS complex is preceded by a normal P
wave.
 Normal P wave axis: P waves should be
upright in leads I and II, inverted in aVR.
 The PR interval remains constant.
 QRS complexes are < 100 ms wide (unless a co-
existent interventricular conduction delay is
present).

14.  TREATMENT
 USUALLY NOT REQUIRED
 UNDERLYING CAUSE-
 INCREASE HYDRATION
 SALT LOADING 10-15 GMS OF SODIUM/DAY
 DRUG THERAPY-
 PROPRANOLOL- 20 mg TDS
 CCB-
 MINERALOCORTICOIDS
 FLUDROCORTISONE 0.1-0.3mg PO
 ADRENOCORTICO RECEPTOR ANTAGONIST
 MICLODRINE 2.5-10 mg TDS
 SSRI
 CATHETER ABLATION
 ATRIAL PACING THERAPY

16.  An abnormal (non-sinus) P wave is followed by a QRS complex.
 The P wave typically has a different morphology and axis to the
sinus P waves.
 The abnormal P wave may be hidden in the preceding T wave,
producing a “peaked” or “camel hump” appearance — if this is
not appreciated the PAC may be mistaken for a PJC.
 PACS arising close to the AV node (“low atrial” ectopics) activate
the atria retrogradely, producing an inverted P wave with a
relatively short PR interval ≥ 120 ms (PR interval < 120 ms is
classified as a PJC).
 PACs that reach the SA node may depolarise it, causing the SA
node to “reset” — this results in a longer-than-normal interval
before the next sinus beat arrives (“post-extrasystolic pause”).
Unlike with PVCs, this pause is not equal to double the preceding
RR interval (i.e. not a “full compensatory pause”).
 Similarly, PACs arriving very early in the cycle may not be
conducted to the ventricles at all. In this case, you will see an
abnormal P wave that is not followed by a QRS complex (“blocked
PAC”). It is usually followed by a compensatory pause as the
sinus node resets.
 TREATMENT – BETA BOCKERS.

18.  Narrow QRS complex, either (1) without a
preceding P wave or (2) preceded by an
abnormal P wave with a PR interval of < 120
ms (these “retrograde” P wave are usually
inverted in leads II, III and aVF).
 Occurs sooner than would be expected for the
next sinus impulse.
 Followed by a compensatory pause.
 PJCs that arrive early in the cycle may be
conducted aberrantly, most commonly with a
RBBB morphology.

20.  Irregularly irregular rhythm.
 No P waves.
 Absence of an isoelectric baseline.
 Variable ventricular rate.
 QRS complexes usually < 120 ms unless pre-
existing bundle branch block, accessory
pathway, or rate related aberrant conduction.
 Fibrillatory waves may be present and can be
either fine (amplitude < 0.5mm) or coarse
(amplitude >0.5mm).
 Fibrillatory waves may mimic P waves leading
to misdiagnosis

21.  Ashman’s Phenomenon – presences of
aberrantly conducted beats, usually of RBBB
morpholo, due a long refractory period as
determined by the preceding R-R interval.
 Commonly AF is associated with a ventricular
rate ~ 110 – 160.
 AF is often described as having ‘rapid
ventricular response’ once the ventricular rate
is > 100 bpm.
 ‘Slow’ AF is a term often used to describe AF
with a ventricular rate < 60 bpm.
 Causes of ‘slow’ AF
include hypothermia, digoxin toxicity,
medications, and sinus node dysfunction.

23.  TREATMENT
 RATE CONTROL=
 NORMAL SYSTOLIC FUNCTION-
 CCB- DILTIAZEM 15mg then 20 mg over 2 min f/b
infusion 5-15 mg/hrfor 24 hr shift to oral 120-360 mg
daily
 Beta blockers- Metoprolol 5-5-5 mg over 2min f/b oral
50 mg bd
 Propranolol-0.15mg/kgIV UPTO 10mg over 1 min f/b oral
80-240 mg daily.
 Digoxin
 amiodarone
 LV Dysfunction-
 Digoxin – 0.25mg iv over 2min max 1.5mg in 24hrs f/b
oral 0.125-0.375 mg daily (other drug dose half
reduction)
 Amiodarone- 150 mg stat over 10 minf/b 360 mg
infusion over6 hrs f/b 540 mg over 18 hrs.
 NON-PHARMACOLGICAL- AV node ablation

24. RHYTHM CONTROL-
 AF <7 DAYS
 SYSTOLIC FUNCTION PRESERVED-
 PILL IN POCKET
 FLECAINIDE 200-300 mg OD
 PROPAFENONE- 600 mg OD
 IBUTILIDE 1mg IV over 10 min
 AMIODARONE- 200-400 mg daily
 LV DYSFUNCTION-
 AMIODARONE-
 DOFETILIDE
 AF >7 DAYS
 AMOIDARONE
 DOFETILIDE
 Digoxin and sotalol are NOT preffered for rhythm
control.

25.  ELECTRICAL CARDIOVERSION-
 200 J SYNC
 If > 48 hrs then antocoagulation for 3 wks then
electively dc cardioversion
 SURGICAL ABLATION- Maze procedure.
 ANTICOAGULATION-
 Inj. heparin 1.5MU SC BD for 8 days then tab
warfarine.
 INR-
 RHD /mirtal valve repair 2-3
 Mitral valve replacement 2.5-3.5

27.  Narrow complex tachycardia
 Regular atrial activity at ~300 bpm
 Flutter waves (“saw-tooth” pattern) best seen
in leads II, III, aVF — may be more easily
spotted by turning the ECG upside down!
 Flutter waves in V1 may resemble P waves
 Loss of the isoelectric baseline
 Venrticular rate is constant.

28. TREATMENT:-
 Similar to AF.
 DC cardio version( 50 J) preferred as it causes
more hemodynamic compromised.

30.  TREATMENT:-
 CCB- preferred b/o MAT is associated with COPD
 PROPAFENONE
 FLECAININDE
 AMIODARONE
 NO ANTICOAGULATION
 NO CARDIOVERSION, beta blockers,
 Digoxin narrow margin of safety.

32.  ECG-
 Regular tachycardia ~140-280 bpm.
 QRS complexes usually narrow (< 120 ms) unless pre-existing
bundle branch block, accessory pathway, or rate related aberrant
conduction.
 ST-segment depression may be seen with or without underlying
coronary artery disease.
 QRS alternans – phasic variation in QRS amplitude associated
with AVNRT and AVRT, distinguished from electrical
alternans by a normal QRS amplitude.
 P waves if visible exhibit retrograde conduction with P-wave
inversion in leads II, III, aVF.
 P waves may be buried in the QRS complex, visible after the QRS
complex, or very rarely visible before the QRS complex.
 P waves are often hidden – being embedded in the QRS
complexes.
 Pseudo R’ wave may be seen in V1 or V2.
 Pseudo S waves may be seen in leads II, III or aVF.
 In most cases this results in a ‘typical’ SVT appearance with absent
P waves and tachycardia

34.  LONG TERM THERAPY:
 DIGOXIN
 BETA BLOCKER
 CCB
 CLASS IA OR IC AGENTS
 CATHETER ABLATION

36.  IN ORTHODROMIC CONDUCTION
 ECG-
 Rate usually 200 – 300 bpm
 P waves and QRS complex seperated and inverted in
lead II, III AVF
 RP interval >0.08 sec
 QRS Alternans – phasic variation in QRS amplitude
associated with AVNRT and AVRT, distinguished
from electrical alternans.
 AV block not possible
 IN ANTIDROMIC CONDUCTION-
 ECG changes looks similar to VT.

37.  TREATMENT-
 IN ORTHODROMIC CONDUCTION-SIMILAR TO
AVNRT.
 IN ANTIDROMIC CONDUCTION- TRAET
SIMILAR AVNRT OTHERWISE VT PROTOCOL.

39.  ECG-Narrow complex rhythm; QRS duration <
120ms (unless pre-existing bundle branch block or
rate-related aberrant conduction).
 Ventricular rate usually 60 – 100 bpm.
 Retrograde P waves may be present and can
appear before, during or after the QRS complex.
 Retrograde P waves are usually inverted in the
inferior leads (II, III, aVF), upright in aVR + V1.
 AV dissociation may be present with the
ventricular rate usually greater than the atrial rate.
 There may be associated ECG features of digoxin
effect or digoxin toxicity.
 TREATMENT- REMOVE DIGOXIN

41.  ECG -Atrial rate > 100 bpm.
 P wave morphology is abnormal when compared with sinus
P wave due to ectopic origin.
 There is usually an abnormal P-wave axis (e.g. inverted in
the inferior leads II, III and aVF)
 At least three consecutive identical ectopic p waves.
 QRS complexes usually normal morphology unless pre-
existing bundle branch block, accessory pathway, or rate
related aberrant conduction.
 Isoelectric baseline (unlike atrial flutter).
 AV block may be present — this is generally a physiological
response to the rapid atrial rate, except in the case of digoxin
toxicity where there is actually AV node suppression due to
the vagotonic effects of digoxin, resulting in a slow
ventricular rate (“PAT with block”)
 TRATMENT-
 DIGITALIS TOXICITY- discontinue , DIGIBIND
 ELECTROLYE IMBALANCE – CORRECT
 hypokalemia
 hypocalcemia
 REST SIMILAR TO AVNRT

43.  ECG-
 Broad QRS complex (≥ 120 ms) with abnormal
morphology.
 Premature — i.e. occurs earlier than would be expected
for the next sinus impulse.
 Discordant ST segment and T wave changes.
 Usually followed by a full compensatory pause.
 Retrograde capture of the atria may or may not occur.
Sinus rhythm with PVCs of two different morphologies
(arrows).
 Note the appropriately discordant ST segments / T
waves.
 The pause surrounding the PVC is equal to double the
preceding R-R interval (= a full compensatory pause
 TREATMENT- REMOVE STIMULENT

45.  ECG-
 Regular rhythm.
 Rate 50-110 bpm.
 Three or more ventricular complexes.
 QRS complexes >120ms.
 Fusion and capture beats
 TREATMENT-
 AIVR is a benign rhythm in most settings and does not
usually require treatment.
 Usually self limiting and resolves when sinus rate exceeds
that of the ventricular foci.
 Administration of anti-arrhythmics may cause precipitous
haemodynamic deterioration and should be avoided.
 Treat the underlying cause: e.g. correct electrolytes, restore
myocardial perfusion.
 Patients with low-cardiac-output states (e.g. severe
biventricular failure) may benefit from restoration of AV
synchrony to restore atrial kick – in this case atropine may be
trialled in an attempt to increase sinus rate and AV
conduction.

47.  ECG
 Very broad complexes (>160ms).
 Absence of typical RBBB or LBBB morphology.
 Extreme axis deviation (“northwest axis”) — QRS is positive
in aVR and negative in I + aVF.
 AV dissociation (P and QRS complexes at different rates).
 Capture beats — occur when the sinoatrial node transiently
‘captures’ the ventricles, in the midst of AV dissociation, to
produce a QRS complex of normal duration.
 Fusion beats — occur when a sinus and ventricular beat
coincide to produce a hybrid complex of intermediate
morphology.
 Positive or negative concordance throughout the chest leads,
i.e. leads V1-6 show entirely positive (R) or entirely negative
(QS) complexes, with no RS complexes seen.
 Brugada’s sign – The distance from the onset of the QRS
complex to the nadir of the S-wave is > 100ms.
 Josephson’s sign – Notching near the nadir of the S-wave.
 RSR’ complexes with a taller “left rabbit ear”. This is the
most specific finding in favour of VT. This is in contrast to
RBBB, where the right rabbit ear is taller.

48.  JOSEPHSON SIGN BLUE
 BRUGADAQ SIGN RED

50.  ECG
 Chaotic irregular deflections of varying
amplitude
 No identifiable P waves, QRS complexes, or T
waves
 Rate 150 to 500 per minute
 Amplitude decreases with duration (coarse VF
-> fine VF)

52.  ECG-
 A premature atrial complex (beat #9 of the
rhythm strip) lands on the end of the T wave,
causing ‘R on T’ phenomenon and initiating a
paroxysm of polymorphic VT. QT interval
slightly prolong
 QT interval slightly prolonged.

54.  TREATMENT-
 SUSTAINED MONOMORPHIC VT-
 UNSTABLE –
 Monophasic shock 200-300-360 J
 STABLE-
 Good LV Function-
 Procainamide
 Amiodarone
 Lidocaine – 1mg/kgbolus – 0.5mg/kg -0.5- 0.5
 Other –
 Electrical cardioversion
 Temprary pacing
 Impaired LV function-
 Amiodarone
 Lignocaine-

55.  SUSTAINED POLYMORPHIC VT-
 Mostly unstable pt.
 Electrical cardioversion 200-200-360 J
 REGULAR PVT (QT< 0.44sec)
 Cause MI
 Beta blocker.
 IABCounterpusation
 Coronary angiography
 Emergency myocardial revascularization.
 TORSADES DE POINTES (QT>0.44 sec)
 MI- beta blockers
 Electrolytes- hypokalemia hypomagnesemia
 Antiarrythmics-
 Mg- 2 gm diluted 100 mi of 5%dextrose over 1 hr.
 Lignocaine
 Isoprenaline – 2-10 mcg/ min drip.
 Temprary pacemaker.

56.  V FIB.
 360 J cardioversion
 5 cycle CPR
 2ND shock
 5 cycle CPR
 3RD shock
 Precordial thump
 CPR.
 Vasopresin 40 U IV.
 LONG TERM THERAPY-
 V. FIB AND SUSTAINED VT-
 Automatic d fib.
 NONSUSTAINED
 Beta blockers.
 ACE inhibitors
 NO ANTIARRTHMIC THERAPY.

60.  CAUSES-
 drugs: amiodarone, TCA’s, many antibiotics,
fluconazole, erythromycin, metoclopramide,
quinidine, haloperidol, droperidol, methadone,
ondansetron, SSRI’s
 genetic: cardiac ion channel mutation (Na+,
K+)
 myocardial disease: MI, RF, 3rd degree HB,
cardiomyopathy
 electrolytes: low Ca2+, low K+, low Mg2+
 Congenital long QT syndrome.

61.  TREATMENT-
 beta-blockade
 avoidance of increased sympathetic tone
 cardiac pacing
 treat cause
 ICD

63.  ECG-ST segment elevation >2mm in >1 of V1-
V3 followed by a negative T wave
 This ECG abnormality must be associated with
one of the following clinical criteria to make
the diagnosis:
 Documented ventricular fibrillation (VF) or
polymorphic ventricular tachycardia (VT).
 Family history of sudden cardiac death at <45 years
old .
 Coved-type ECGs in family members.
 Inducibility of VT with programmed electrical
stimulation .
 Syncope.
 Nocturnal agonal respiration.
 TREATMENT- ICD

66.  HOCM ECG CHANGES
 Left atrial enlargement (P MITRALE)
 Left ventricular hypertrophy with associated ST
segment / T-wave abnormalities
 Deep, narrow (“dagger-like”) Q waves in the
lateral > inferior leads
 Giant precordial T-wave inversions in apical HCM
 Signs of WPW (short PR, delta wave).
 Dysrhythmias: atrial fibrillation, supraventricular
tachycardias, PACs, PVCs, VT

68.  ECG-
 Sinus rhythm with a very short PR interval (< 120
ms).
 Broad QRS complexes with a slurred upstroke to
the QRS complex — the delta wave.
 Dominant R wave in V1 — this pattern is known
as “Type A” WPW and is associated with a left-
sided accessory pathway.
 Tall R waves and inverted T waves in V1-3
mimicking right ventricular hypertrophy — these
changes are due to WPW and do not indicate
underlying RVH.
 Negative delta wave in aVL simulating the Q
waves of lateral infarction — this is referred to as
the “pseudo-infarction” pattern.

70.  Rapid, irregular, broad complex tachycardia
(overall rate ~ 200 bpm) with
a LBBB morphology (dominant S wave in V1).
 This could easily be mistaken for AF with
LBBB.
 However, the morphology is not typical of
LBBB, the rate is too rapid (up to 300 bpm in
places, i.e. too rapid to be conducted via the
AV node) and there is a subtle beat-to-beat
variation in the QRS width which is more
typical of WPW (LBBB usually has fixed width
QRS complexes)

71.  TREATMENT-
 WITH AVRT
 PROCAINAMIDE 10-12 mg/kg max 1000 mg in 30
min
 Ibutilide – 1mg over 10 min in 10 ml dilution of
dextrose.
 Adenosine- not effective.
 ELECTRICAL CARDIOVERSION.
 INTRACARDIAC PACING.
 RADIOFREQUENCY ABLATION
 WITH AF-
 STABLE-Procainamide
 UNSTABLE- DC cardioversion
 CCB, BETABLOCKERS, DIGOXIN contraindicated.

73. ECG AVRMCM/D
 Epsilon wave (most specific finding, seen in 30% of
patients)
 T wave inversions in V1-3 (85% of patients)
 Prolonged S-wave upstroke of 55ms in V1-3 (95% of
patients)
 Localised QRS widening of 110ms in V1-3
 Paroxysmal episodes of ventricular tachycardia with
a LBBB morphology
 TREATMENT-
 ICD treatment of choice.
 Catheter ablation
 Beta blockers with other antiarrhythmic drugs.