PERIOPERATIVE ARRYTHMIAS IN ANAESTHESIA

1. DR ASHISH NAIR
MBBS, MD ANAESTHESIA
PERIOPERATIVE
ARRHYTHMIAS
IN
ANAESTHESIA

2. Definition-Arrhythmia
 Abnormality of cardiac rate, rhythm or conduction which
can be either lethal(sudden cardiac death),or symptomatic
(syncope, near syncope, dizziness or palpitations) or
asymptomatic.

3. Topics covered
 A normal ECG and the myocardial conduction pathways
 Narrow complex arrhythmias
 Sinus arrhythmia
 Sinus bradycardia
 Atrial ectopics

4.  Narrow complex tachycardias
 Sinus tachycardia
 Supraventricular and junctional tachycardia
 Atrial flutter
 Atrial fibrillation
 Sick sinus syndrome
 Wolff Parkinson White syndrome
 Broad complex arrhythmias
 Ventricular ectopics
 Ventricular tachycardia
 Supraventricular tachycardia with aberrant conduction
 Ventricular fibrillation
 Torsades de pointes
 Anti-arrhythmic drugs

5. ABC patient assessment:
Determine if the arrhythmia is causing serious cardiovascular compromise with
altered heart
rate, cardiac output, and blood pressure.
Obtain senior help if needed
senior help if needed
Assess the anaesthetic. Check:
• Oxygenation
• Ventilation and end tidal CO2
• Is anaesthetic too light for surgery?
• Drug error/interaction?
Assess the surgery. Check for:
• Vagal stimulation from ocular/peritoneal traction
• Possible air/fat embolism
• Unexpected haemorrhage & hypovolaemia
• Mediastinal manipulation
• Adrenaline injection
Record a 12 lead ECG where possible and correct the
underlying cause

6. Normal ECG

7.  Series of waves and deflections recording the heart’s electrical
activity from a certain “view.”
 Many views, each called a lead, monitor voltage changes
between electrodes placed in different positions on the body.

8.  Leads I, II, and III are bipolar leads:
 Consist of two electrodes of opposite polarity (positive and
negative)
 The third (ground) electrode minimizes electrical activity from
other sources.

9.  Leads aVR, aVL, and aVF:
 are unipolar leads,
 consist of a single positive electrode and
 a reference point (with zero electrical potential) that lies in
the centre of the heart’s electrical field.

10.  Leads V1–V6:
 are unipolar leads
 consist of a single positive electrode with a negative reference point
found at the electrical centre of the heart.

12. The standard paper speed is 25mm/sec:
1mm (small square) = 0.04 sec (40ms)
5mm (large square) = 0.2 sec (200ms)

13. Estimating the rate
 At a paper speed of 25 mm/second
 1 SMALL square = 0.04 seconds
 5 SMALL squares = 1 LARGE square = 0.2 seconds
 5 LARGE squares = 1 second
 ECG rhythm strip:
 = 250 SMALL squares = 50 LARGE squares = 10 seconds
 To calculate beats per minute (bpm):
 1500 SMALL squares = 300 LARGE squares = 1 minute

14. Analyzing a rhythm
Component Characteristic
Rate The bpm is commonly the ventricular rate.
If atrial and ventricular rates differ, as in a
3rd-degree block, measure both rates.
Normal: 60–100 bpm
Slow (bradycardia): 60 bpm
Fast (tachycardia): 100 bpm
Regularity Measure R-R intervals and P-P intervals.
Regular: Intervals consistent
Regularly irregular: Repeating pattern
Irregular: No pattern

15. Component Characteristic
P Waves If present: Same in size, shape, position?
Does each QRS have a P wave?
Normal: Upright (positive) and uniform
Inverted: Negative
Notched: P′
None: Rhythm is junctional or ventricular.
PR Interval Constant: Intervals are the same.
Variable: Intervals differ.
Normal: 0.12–0.20 sec and constant
QRS interval Normal: 0.06–0.10 sec
Wide: 0.10 sec
None: Absent
QT interval Beginning of R wave to end of T wave
Varies with HR.
Normal: Less than half the R-R interval

17. Conduction pathway

18. Sinoatrial (SA) node
Atrial
Ventricular(AV)
node
AV bundle of His
L and R bundle
branches
Purkinje fibres

19. Structure Function and Location
Sinoatrial (SA)
node
Dominant pacemaker of the heart, located in
upper portion of right atrium. Intrinsic rate
60–100 bpm.
Internodal
pathways
Direct electrical impulses between SA and AV
nodes.
Atrioventricular
(AV) node
Part of AV junctional tissue. Slows
conduction, creating a slight delay before
impulses reach ventricles. Intrinsic rate
40–60 bpm.
Bundle of His Transmits impulses to bundle branches.
Located below AV node.
Left bundle
branch
Conducts impulses that lead to left ventricle
Right bundle
branch
Conducts impulses that lead to right ventricle
Purkinje system Network of fibers that spreads impulses
rapidly throughout ventricular walls.
Located at terminals of bundle branches.
Intrinsic rate 20–40 bpm

20. Narrow complex arrhythmias

21. Sinus arrhythmia
 Sinus rhythm with a beat-to-beat variation in the P-P interval (the time
between successive P waves), producing an irregular ventricular rate
 Normal rate (>60bpm and <100bpm)
 Normal complexes and P-R intervals
 Irregularly spaced R-R intervals
 Sinus arrhythmia alters with respiration and can be a normal
finding, especially in young patients

22. •Variation in the P-P interval of more than 120 ms (3 small boxes).
•The P-P interval gradually lengthens and shortens in a cyclical fashion,
usually corresponding to the phases of the respiratory cycle.
•Normal sinus P waves with a constant morphology (i.e. no evidence of
premature atrial contractions).
•Constant P-R interval (i.e. no evidence of Mobitz I AV block).

23. Sinus bradycardia
 Sinus rhythm with normal P-QRS-T complexes and
morphology
 Rate <60bpm.
 Normal finding in athletic patients or patients with high vagal
tone
 Seldom necessary to correct in fit patients until the rate is
<40bpm

24.  Surgical factors
 vagal stimulation by anal or genitocervical dilatation.
 Medical causes
 Cardiac in origin- (myocardial infarction, sick sinus
syndrome)
 Non-cardiac in origin-hypothermia, raised intracranial
pressure, or hypothyroidism.
 Pharmaceutical causes
 Direct e.g beta-blockers or digoxin,
 Indirect effects from specific drug side effects of halothane
or anticholinesterases such as neostigmine.

25.  Management:
 Correct reversible causes first.
 Then consider atropine (up to 20μg/kg) (0.02mg/kg) or glycopyrolate
(10μg/kg) (0.01mg/kg) by the IV route.
 If the bradycardia is resistant to the above and the patient is known to take
beta-blockers, consider
 ADRENALINE 1mg/ml-1amp
5mg in 45ml NS (100mcg/cc)……dose- 2-10mcg/min
- ISOPRENALINE by infusion 1amp/2mg in 50ml NS
Dose- 5mcg/min…..start @0.9cc/hr……(0.5-10μg/min).
 If the bradycardia is entirely drug resistant, a pacemaker is required.
 If emergency surgery is indicated, the insertion of a temporary pacing wire will
suffice, before formal pacemaker insertion.

26. Atrial ectopics
 Atrial ectopics are usually common and benign.
 These arise from ectopic pacemaking tissue within the atria. There
is an abnormal P wave, usually followed by a normal QRS complex
 Before attributing these to a benign cause, other causes should be
excluded.These include a side effect of the:
 Anaesthetic drugs used,
 Light depth of anaesthesia,
 Sepsis, shock
 Ischaemia.

27. ECG Features of Premature Atrial Complex (PAC)
PACs usually have the following features:
• 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).

28. • 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”).
• PACs arriving early in the cycle may be conducted aberrantly,
usually with a RBBB morphology (as the right bundle branch has
a longer refractory period than the left). They can be
differentiated from PVCs by the presence of a preceding P
wave.
• 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.

29. Classification of Premature Atrial Complex (PAC)
PACs may be either:
 Unifocal – Arising from a single ectopic focus; each PAC is identical.
 Multifocal – Arising from two or more ectopic foci; multiple P-wave
morphology
PACs often occur in repeating patterns:
 Bigeminy — every other beat is a PAC.
 Trigeminy — every third beat is a PAC.
 Quadrigeminy — every fourth beat is a PAC.
 Couplet – two consecutive PACs.
 Triplet — three consecutive PACs.

30. RED ARROW INDICATES A PREMATURE ATRIAL COMPLEX WHICH IS THEN CONDUCTED AND FOLLOWED
BY AN ATRIAL PAUSE.
BLOCKED PAC(BELOW)
•THIS HIDDEN PAC GIVES A PEAKED APPEARANCE TO THE T WAVE (CIRCLED).
•THE PAC IS NOT NOT FOLLOWED BY A QRS COMPLEX, INDICATING THAT IT HAS NOT BEEN CONDUCTED TO THE VENTRICLES (“BLOCKED PAC”).
•IT IS FOLLOWED BY A COMPENSATORY PAUSE.
Clinical Significance of Premature Atrial Complex (PAC)
•PACs are a normal electrophysiological phenomenon not usually requiring
investigation or treatment.
•Frequent PACs may cause palpitations and a sense of the heart “skipping a beat”.
•In patients with underlying predispositions (e.g. left atrial enlargement, ischaemic
heart disease, WPW), a PAC may be the trigger for the onset of a re-entrant
tachydysrhythmia — e.g. Atrial fibrillation, atrial flutter, AVNRT, AVRT.

31. Causes of Premature Atrial Complex (PAC)
 Frequent or symptomatic PACs may occur due to:
• Anxiety.
• Sympathomimetics.
• Beta-agonists.
• Excess caffeine.
• Hypokalaemia.
• Hypomagnesaemia.
• Digoxin toxicity.
• Myocardial ischaemia
Management
 Exclusion of correctable and serious causes,
 Modification of clinical management if necessary.
 Specific treatment is unnecessary unless consistent runs of atrial tachycardias occur.

32. Narrow complex tachycardias
 The differential diagnosis:
 Sinus tachycardia
 Supraventricular tachycardias (SVT) such as atrial flutter,
atrial tachycardia, multifocal atrial tachycardia and
junctional tachycardias
 Paroxysmal supraventricular tachycardia (PSVT)
 Atrial fibrillation (AF)
 Sick sinus syndrome
 Wolff-Parkinson-White syndrome

33. Sinus tachycardia
 Sinus tachycardia is a sinus rhythm with normal P-QRS-T
complexes and morphology
 Rate >100bpm.
 Causes can be multi-factorial.
 Operative causes - pain, surgical stimulation and light depth
of anaesthesia.
 Pharmacological factors - administration of
catecholamines, atropine, or ketamine.
 Medical factors -sepsis, hypovolaemia, heart failure,
anaemia, and thyrotoxicosis
 Management -correct the precipitating cause.

34. Supra-ventricular and junctional tachycardia

35.  Any tachycardia originating from above the ventricles.
 Sinus rhythm, atrial rhythm and junctional rhythm together
constitute the ‘supraventricular’ rhythms
 The nature of a SVT depends on the origin of the electrical
impulse.

36.  On the basis of origin of impulse
 Impulses from the sino-atrial node -sinus tachycardias,
sino-atrial re-entrant tachycardias and atrial flutter.
 Impulses from the atrial myocardium itself -ectopic
unifocal tachycardias, multifocal atrial tachycardias, and
atrial flutter or fibrillation.
 Atrioventricular (junctional) electrical sources -AV re-
entrant tachycardias, atrioventricular reciprocating
tachycardia, and junctional ectopic tachycardias.

37. Atrial tachycardia is a form of supraventricular tachycardia, originating within the atria
but outside of the sinus node. Both atrial flutter and multifocal atrial tachycardia are
specific types of atrial tachycardia.
ECG Features of Atrial Tachycardia
•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”).

38. Junctional rhythms are arbitrarily
classified by their rate:
1. Junctional Escape Rhythm:
40-60 bpm
2. Accelerated Junctional
Rhythm: 60-100 bpm
3. Junctional Tachycardia: > 100
bpm
No p wave so
junctional
tachycardia…and not
sinus tacchy
Accelerated Junctional Rhythm is a very regular rhythm,
and any QRS that occurs with a shorter R-R interval is not
from the junction, but is a beat conducted from above

39. They may also be classified by aetiology:
• Automatic Junctional Rhythms (e.g. AJR) = Due to enhanced
automaticity in AV nodal cells
• Re-entrant Junctional Rhythms (e.g. AVNRT) = Due to re-entrant loop
involving AV node
Automatic Junctional Rhythms
Re-entrant Junctional Rhythms

40. ECG Features of AJR
• 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.

41. Junctional Tachycardia
•Narrow complex tachycardia at 115 bpm.
•Retrograde P waves — inverted in II, III and aVF; upright in V1
and aVR.
•Short PR interval (< 120 ms) indicates a junctional rather than
atrial focus

42. SVT
Vagal maneuvers
and /or IV
adenosine
If ineffective or not feasible
Hemodynamically
stable
Iv beta blockers
Iv diltiazem or
iv verapamil
Synchronised
cardioversion
Synchronised
cardioversion
yes no
If ineffective,not feasible
injectable solution
•6mg/2mL prefilled
syringe
•12mg/4mL prefilled
syringe
ADENOSINE- 6 mg
IVP over 1-3 seconds
(maybe given IO)
followed by rapid flush
with 20 mL NS, if no
conversion within 1-2
minutes give 12 mg IVP,
repeat a second time if
necessary (30 mg total)
DILTIAZEM – 0.25mg/kg over 3-5mins f/b infusion 5-15mg/hr
VERAPAMIL – 5-10mg/kg over 3-5 mins f/b 2.5-10mg/hr

44.  Medical management:
 Adenosine 6mg IV bolus, given as a fast push and
followed with a 20ml 0.9% saline flush.
 This rapidly blocks AV node conduction therefore slows the ventricular rate,
cardioverting a junctional rhythm to sinus or terminating a re-entry SVT.
 If a second and third dose is needed,
 12mg with an interval period of at least 1 minute between doses.
 The effects only last for 10-15s
 Ensure recording of an ECG rhythm strip during
administration.

45.  Beta-blockers e.g. esmolol 50-200ug/Kg/min IV, or
metoprolol 3-5mg IV over 10 minutes every 6 hours.
 Verapamil 5-10mg IV over 2 minutes, with a second dose
of 5mg after 10 minutes if needed. Useful with SVT who
relapse post-adenosine. Do not use with beta-blockers.
 Amiodarone 300mg IV over 1hour via a central line should
be considered when the above interventions have failed.

46. Atrial flutter
 Atrial rate >250/min and there is no flat baseline between the P
waves ‘atrial flutter’ is present
 A narrow complex tachycardia with a ventricular rate of about 125–
150/min –atrial flutter with 2:1 block.
 Ventricular rate is determined by the AV conduction ratio (“degree of
AV block”). The commonest AV ratio is 2:1, resulting in a ventricular
rate of ~150 bpm

47. Classification
 This is based on the anatomical location and direction of the re-entry circuit
Typical Atrial Flutter (Common, or Type I Atrial Flutter)
Involves the IVC & tricuspid isthmus in the reentry circuit. Can be further classified based on the direction of the reentry circuit (anticlockwise or clockwise):
Anticlockwise Reentry: Commonest form of atrial flutter (90% of cases). Retrograde atrial conduction produces:
 Inverted flutter waves in leads II,III, aVF
 Positive flutter waves in V1 – may resemble upright P waves
Clockwise Reentry. This uncommon variant produces the opposite pattern:
 Positive flutter waves in leads II, III, aVF
 Broad, inverted flutter waves in V1
Atypical Atrial flutter (Uncommon, or Type II Atrial Flutter)
 Does not fulfill criteria for typical atrial flutter.
 Often associated with higher atrial rates and rhythm instability.
 Less amenable to treatment with ablation.

48. General Features
•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
•In atrial flutter with variable block the R-R intervals will be multiples of the P-P interval — e.g. assuming an atrial rate
of 300bpm (P-P interval of 200 ms), the R-R interval would be 400 ms with 2:1 block, 600 ms with 3:1 block, and 800
ms with 4:1 block.

49. Atrial Flutter with 2:1 Block
This is the classic appearance of anticlockwise flutter.
•There are inverted flutter waves in II, III + aVF at a rate of 300 bpm (one
per big square)
•There are upright flutter waves in V1 simulating P waves
•There is a 2:1 AV block resulting in a ventricular rate of 150 bpm
•Note the occasional irregularity, with a 3:1 cycle seen in V1-3

50. Atrial Flutter with 1:1 Block
•There is a very rapid, regular narrow-complex tachycardia at 250-300 bpm.
•Flutter waves are not clearly seen, but there is an undulation to the baseline in the
inferior leads suggestive of flutter with a 1:1 block.
•Alternatively, this may just be rapid SVT (AVNRT / AVRT) with rate-related ST
depression.
With ventricular rates as rapid as this, spending any further time evaluating the ECG
is unwise! Resuscitation is the priority… This patient will almost certainly be
haemodynamically unstable, requiring emergent DC cardioversion.

54. Atrial fibrillation
 When the atrial muscle fibres contract independently there
are no P waves on the ECG, only an irregular line
 Clinical features -irregularly irregular pulse, with no ‘a’ waves
or ‘x’ descent seen in the jugular venous pulse.
 On auscultation, there is first heart sound variance and a
discrepancy between apical pulse and radial pulse.
 ECG - chaotic atrial activity with no discernible P-waves and
irregular R-R intervals

55. ECG Features of Atrial Fibrillation
•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

56.  The most common complaint is fatigue.
 Signs and symptoms –
 generalized weakness,
 palpitations,
 hypotension,
 syncope,
 angina pectoris,
 shortness of breath,
 orthopnea,
 hypotension
 Common underlying comorbid disease conditions-
 Systemic hypertension, ischemic heart disease, hyperlipidemia, heart
failure, diabetes, anemia,arthritis, chronic kidney disease, and
chronic obstructive lung disease.
Causes of Atrial
Fibrillation
•Ischaemic heart disease
•Hypertension
•Valvular heart disease (esp. mitral
stenosis / regurgitation)
•Acute infections
•Electrolyte disturbance
(hypokalaemia, hypomagnesaemia)
•Thyrotoxicosis
•Drugs (e.g. sympathomimetics)
•Pulmonary embolus
•Pericardial disease
•Acid-base disturbance
•Pre-excitation syndromes
•Cardiomyopathies: dilated, hypertro
phic.
•Phaeochromocytoma

58. Uncontrolled chronic AF
management
 Digoxin loading 1-2 days preoperatively unless already
digitalised.
 This can be achieved with oral preparations but may
need to be IV if urgent surgery is indicated.
 Check serum digoxin levels (0.8-2.0μg/L)

59. Sick sinus syndrome
 Etiology- Familial, congenital, rheumatic, ischaemic, and/or
hypertensive
 Presentation is normally due to non-specific symptoms secondary to
vital organ hypoperfusion
 Severe bradycardia resistant to atropine is a hallmark of SSS
 The ECG appearances are of sinus bradycardia, alternating sinus
bradycardia with tachycardia (tachybrady
syndrome), sino-atrial block, atrial flutter or AF.
 A permanent pacemaker, either atrial or dual chamber is required if
symptomatic or suffering tachy-brady syndrome.

61. Wolff-parkinson white syndrome
 In WPW an accessory conduction pathway is present between the
atria and the ventricles.
 Electrical impulses are rapidly conducted to the ventricles.
 Ventricular pre-excitation causes an earlier-than-normal deflection
of the QRS complex called a delta wave
 These preexcitation ECG changes are a form of conduction block.
 The ECG criteria in adults are
a) PR interval less than 120 ms
b) Slurring of the initial portion of the QRS (delta wave),
c) QRS longer than 120 ms in adults,
d) Secondary ST-segment and T-wave changes.

63.  Patients with known WPW syndrome coming for surgery
should continue to receive their anti-dysrhythmic medications.
 The goal during management of anesthesia is to avoid:
 any event (e.g., increased sympathetic nervous system
activity due to pain, anxiety, or hypovolemia) or
 drug (digoxin, verapamil) that could enhance anterograde
conduction of cardiac impulses through an accessory
pathway.
 Appropriate antidysrhythmic drugs and equipment for
electrical cardioversion defibrillation must be immediately
available.

64. Broad complex arrhythmias

65. Ventricular Ectopics
 Benign in the absence of structural heart disease.
 Causes-
 Hypokalaemia or hypercarbia
 Dental surgery
 Anal stretch
 Use of halothane
 Light depth of anaesthesia.
Causes
Frequent or symptomatic
PVCs may be due to:
•Anxiety
•Sympathomimetics
•Beta-agonists
•Excess caffeine
•Hypokalaemia
•Hypomagnesaemia
•Digoxin toxicity
•Myocardial ischemia

66. Ventricular Ectopics
•Ectopic firing of a focus within the ventricles bypasses the His-Purkinje system and depolarises the
ventricles directly.
•This disrupts the normal sequence of cardiac activation, leading to asynchronous activation of the two
ventricles.
•The consequent interventricular conduction delay produces QRS complexes with prolonged duration
and abnormal morphology.

67. Ventricular bigeminy

68. Classification
PVCs may be either:
• Unifocal — Arising from a single ectopic focus; each PVC is identical.
• Multifocal — Arising from two or more ectopic foci; multiple QRS morphologies.
The origin of each PVC can be discerned from the QRS morphology:
• PVCs arising from the right ventricle have a left bundle branch block morphology (dominant S
wave in V1).
• PVCs arising from the left ventricle have a right bundle branch block morphology (dominant R
wave in V1).
PVCs often occur in repeating patterns:
• Bigeminy — every other beat is a PVC.
• Trigeminy — every third beat is a PVC.
• Quadrigeminy — every fourth beat is a PVC.
• Couplet — two consecutive PVCs.
• NSVT — three-thirty consecutive PVCs

69.  Management:
 Graded doses of IV beta-blocker such as metoprolol 3-5mg used
once other factors have been normalised.
 If bradycardia <50bpm ectopics may in fact be ventricular escape
beats.
 In this instance, a trial of an anticholinergic such as atropine or
glycopyrolate to increase ventricular rate, can be used.
PVCs have the following features:
•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.
•After a VPC in the compensatory pause if there is a p wave and is at equal
interval as the other p wave in the rhythm ..we can say that its sinus rhythm

70. Ventricular Tachycardia
 High frequency electrical depolarisation from a central focus within the ventricular muscle
causing a fast (>100bpm) widened QRS (>0.12s) of variable shape
Clinical Significance
• Ventricular tachycardia may impair cardiac output with consequent hypotension, collapse,
and acute cardiac failure. This is due to extreme heart rates and lack of coordinated atrial
contraction (loss of “atrial kick”).
• The presence of pre-existing poor ventricular function is strongly associated with
cardiovascular compromise.
• Decreased cardiac output may result in decreased myocardial perfusion with degeneration
to VF.
• Prompt recognition and initiation of treatment (e.g. electrical cardioversion) is required in all
cases of VT.
 Wide and abnormal complexes are seen in all 12 leads of the standard ECG
 Ventricular Tachycardia (VT) is a broad complex tachycardia originating in the ventricles.
There are several different varieties of VT — the most common being Monomorphic VT.
 Severe ,potentially life-threatening arrhythmia, which needs urgent diagnosis and
management.

71. VENTRICULAR TACHYCARDIA CLASSIFICATION IS BASED ON:
1. Morphology
• Monomorphic
• Polymorphic VT
• Torsades De Pointes (Polymorphic with QT prolongation)
• Right Ventricular Outflow Tract Tachycardia
• Fascicular Tachycardia
• Bidirectional VT
• Ventricular Flutter
• Ventricular Fibrillation
2. Duration
• Sustained = Duration > 30 seconds or requiring intervention due to
hemodynamic compromise.
• Non-sustained = Three or more consecutive ventricular complexes
terminating spontaneously in < 30 seconds.
3. Clinical Presentation
• Haemodynamically stable.
• Haemodynamically unstable — e.g hypotension, chest pain, cardiac
failure, decreased conscious level.

72.  Electrophysiologists may also describe the location within the ventricles from where
theVT is originating.This can be determined by the morphology of the QRS
complex.
 For example,VT that has a LBBB morphology must come somewhere from the right
ventricle; this is because the electrical potential takes a long time to reach the left
ventricle, similar to what occurs with a simple LBBB.
 PolymorphicVT (Torsades de Pointes) is a form ofVT with multipleQRS
morphologies.
 PolymorphicVT is best treated with intravenous magnesium. Patients with
a prolonged QT interval have a higher risk for developing polymorphicVT.
 Ventricular tachycardia can be difficult to distinguish from SVT with aberrancy.The
Brugada Criteria are most commonly used to differentiate between these two
entities — a clinically important distinction.
 If present, “fusion beats” and “capture beats” can also be helpful to diagnoseVT.
 A fusion beat — also known as Dressler’s beat — occurs when sinus node activity (P wave)
begins to conduct through the normal conduction pathway during an episode ofVT.The
abnormal ventricular impulse then conducts retrograde (backward) across the atrioventricular
node, colliding with the sinus impulse. The resulting QRS is a fusion of the normal QRS
morphology and the ventricular morphology from theVT.

73. The Brugada Criteria
commonly used to determine whether a wide complex tachycardia is from ventricular tachycardia or
tachycardia with aberrancy.
The Brugada criteria/algorithm is as follows:
1. Is there concordance present in the precordial leads (leads V1-V6)?
 Also explained as the absence of an RS complex, concordance is diagnostic of ventricular
simple way to think of this would be to ask the question, "Are all of the QRS complexes
completely downward in the precordial leads?" If the answer is yes, then VT is the diagnosis.
2. Is the R to S interval > 100 ms in any one precordial lead?
 If present, then VT is the diagnosis. Simply use calipers to measure the distance between the R
wave in each precordial lead, and see if it exceeds 100 ms.

74. 3. Is AV dissociation present?
 If present, the diagnosis is VT.
 AV dissociation occurs when P waves (represents atrial depolarization) are
different rates than the QRS complex. This is present in only a small
ECG tracings, but is diagnostic of VT. Frequently, this is difficult to see
rate of the QRS complex.
A wide QRS tachycardia is VT until proven otherwise (1). Features suggesting VT include:-
•evidence of AV dissociation
•independent P waves (shown by arrows here)
•capture or fusion beats
•beat to beat variability of the QRS morphology
•very wide complexes (> 140 ms)
•the same morphology in tachycardia as in ventricular ectopics
•history of ischaemic heart disease
•absence of any rS, RS or Rs complexes in the chest leads (2)
•concordance (chest leads all positive or negative)

75. 4. Examine the morphology of the QRS complex to see if it meets the specific
criteria for VT, as below.
 VT is frequently either in a right bundle branch block pattern (upright in V1) or
branch block pattern (downward in V1).
If upward in lead V1 (RBBB pattern), then VT is present in the following situations:
• A monophasic R or biphasic qR complex in V1.
• If an RSR' pattern (“bunny-ear”) is present in V1, with the R peak being higher
than the R’ peak, then VT is present.
• An rS complex in lead V6 favors VT.
If downward in lead V1 (LBBB pattern), then VT is present in the following
situations:
• The presence of any Q or QS wave in lead V6 favors VT.
• A wide R wave in lead V1 or V2 of 40 ms or more favors VT.
• Slurred or notched downstroke of the S wave in V1 or V2 favors VT.
• Duration of onset of the QRS complex to peak of QS or S wave > 60 ms favors

77. Mechanisms of Ventricular
Tachycardia
Three mechanisms exist for initiation
and propagation of ventricular
tachycardia:
1. Reentry
•Commonest mechanism.
•Requires two distinct conduction
pathways with a conduction block in
one pathway, and a region of slow
conduction in the other.
•Develops due to abnormal myocardial
scarring usually due to prior ischemia
or infarction.
2. Triggered Activity
•Occurs due to early or late after-
depolarisations.
•Examples include Torsades and
digitalis toxicity.
3. Abnormal Automaticity
•Accelerated abnormal impulse
generation by a region of ventricular
cells

79. Electrocardiographic Features of Ventricular Tachycardia
 Ventricular tachycardia can be difficult to differentiate from other causes of broad complex tachycardia.
The following characteristics aid in the identification of VT.
Features common to any broad complex tachycardia
• Rapid heart rate (> 100 bpm).
• Broad QRS complexes (> 120 ms).
Features suggestive of VT
• 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.

81.  The intra-operative causes-
 Electrolyte imbalance (hypokalaemia and
hypomagnesaemia) must be excluded.
 Myocardial ischaemia
 Hypoxia,
 Hypotension,
 Fluid overload,
 IV use of adrenaline and other chatecholamines.

82. Ventricular fibrillation
 Characterised by fast, chaotic, irregular and disorganised broad complexes on the ECG
 No palpable peripheral or central pulses due to the lack of cardiac output.
 Risk factors –
 Recent myocardial infarction
 Pre-existing ischaemic heart disease
 Hypokalaemia,
 Excessive endogenous or exogenous catecholamine levels
 Myocardial irritation e.g. from a guide-wire during the insertion of a central venous catheter.
ECG Findings
• 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)

83. CAUSES OF VENTRICULAR FIBRILLATION (VF)
Cardiac
• Myocardial ischemia / infarction
• Cardiomyopathy (dilated, hypertrophic, restrictive)
• Channelopathies e.g. Long QT (acquired / congenital) causing TdP –> VF and Brugada syndrome
• Aortic stenosis
• Aortic dissection
• Myocarditis
• Cardiac tamponade
• Blunt trauma (Commotio Cordis)
Respiratory
• Tension pneumothorax
• Pulmonary embolism
• Primary pulmonary hypertension
• Sleep apnoea
• Bronchospasm
• Aspiration
Toxic and Metabolic
• Drugs (e.g. verapamil in patients with AF+WPW)
• Drug-induced QT prolongation with torsades de pointes
Environmental
• Electrical shocks, drowning, hypothermia
• Sepsis
Neurological
• Seizure
• CVA

84. • No QRS complex can be identified,
• The ECG is totally disorganized
• The diagnosis is easy as the patient will usually have lost consciousness by the
time you have realized that the change in the ECG pattern is not just due to a
loose connection

86. Torsades de pointes
 Atypical polymorphic form of VT characterised by
 Beat-to beat variation,
 Prolonged QT interval
 Constantly changing/twisting QRS axis around the baseline
 A severe non-uniform delay in repolarisation, illustrated by QT prolongation
 Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia in which there
are multiple ventricular foci with the resultant QRS complexes varying in amplitude, axis and
duration. The commonest cause of PVT is myocardial ischaemia.
 Torsades de pointes (TdP) is a specific form of polymorphic ventricular tachycardia occurring in
the context of QT prolongation; it has a characteristic morphology in which the QRS complexes
“twist” around the isoelectric line.
 For TdP to be diagnosed, the patient has to have evidence of both PVT and QT prolongation.
 Bidirectional VT is another type of polymorphic VT, most commonly associated with digoxin toxicity.

87. Pathophysiology of TdP
• A prolonged QT reflects prolonged myocyte repolarisation due to ion channel malfunction.
• This prolonged repolarisation period also gives rise to early after-depolarisations (EADs).
• EADs may manifest on the ECG as tall U waves; if these reach threshold amplitude they may manifest as
premature ventricular contractions (PVCs).
• TdP is initiated when a PVC occurs during the preceeding T wave, known as ‘R on T’ phenomenon.
• The onset of TdP is often preceded by a sequence of short-long-short R-R intervals, so called “pause
dependent” TDP, with longer pauses associated with faster runs of TdP.
Electrocardiographic Pearls
• During short runs of TdP or single lead recording the characteristic “twisting” morphology may not be apparent.
• Bigeminy in a patient with a known long QT syndrome may herald imminent TdP.
• TdP with heart rates > 220 beats/min are of longer duration and more likely to degenerate into VF.
• Presence of abnormal (“giant”) T-U waves may precede TdP
Drug-induced Torsades
• In the context of acute poisoning with QT-prolonging agents, the risk of TdP is better described by
the absolute rather than corrected QT.
• More precisely, the risk of TdP is determined by considering both the absolute QT interval and the
simultaneous heart rate (i.e. on the same ECG tracing).
• These values are then plotted on the QT nomogram (below) to determine whether the patient is at risk of TdP.
• A QT interval-heart rate pair that plots above the line indicates that the patient is at risk of TdP.

88. Torsades de Pointes:
•Frequent PVCs with ‘R on T’ phenomenon trigger a run of polymorphic VT which subsequently begins to
degenerate to VF.
•QT is difficult to see because of artefact but appears slightly prolonged (QTc ~480ms), making this likely
to be TdP.
•This combination of mildly prolonged QTc and frequent PVCs / bigeminy is commonly seen in acute
myocardial ischaemia and is high-risk for deterioration to PVT / VF

90.  Causes:
 Metabolic: Hypokalaemia, hypomagnesaemia
 Drugs: Phenothiazine, procainamide, quinidine, dispyramide
 Cardiac: Bradycardia, acute ischemia, infarction.
R on T phenomenon:
•There is sinus rhythm with frequent PVCs in
a pattern of ventricular bigeminy.
•The QT interval is markedly prolonged (at
least 600ms), with each PVC falling on the
preceding T wave (= ‘R on T’ phenomenon).
•This ECG is extremely high risk for TdP – in
fact this patient had a TdP cardiac arrest
shortly after this ECG was taken.

91.  Management:
 Any electrolyte disturbance is corrected.
 Causative drug and precipitating factors should be
stopped and removed.
 Intravenous isoprenaline may be effective when QT
prolongation is acquired.
 β Blockade is advised if the QT prologation is congenital

92. Antiarrhythmic drugs

94. Class I drugs
 Membrane-depressant drugs that reduce the rate of
entry of sodium into the cell.
 They may slow conduction, delay recovery or reduce the
spontaneous discharge rate of myocardial cells.
 Class 1a-lengthen the action potential
 Class 1b-shorten action potential
 Class Ic do not affect the duration of the action potential.

95. Class II drugs
 Antisympathetic drugs prevent the effects of
catecholamines on the action potential.
 Most are B-adrenergic antagonists. Cardioselective B-
blockers (B1 ) include metoprolol, atenolol, and
acebutalol.

96. Class III drugs
 Prolong the action potential and do not affect sodium
transport through the membrane.
 Two major drugs in this class; amiodarone and sotalol.

97. Class IV drugs
 The non-dihydropyridine calcium antagonists that
reduce the plateau phase of the action potential are
particularly effective at slowing conduction in nodal
tissue.
 Verapamil and diltiazem are the most important drugs in
this group.