CARDIAC ARRYTHMIA AND ITS MANAGEMENT For Anaesthesiology

1. CARDIAC ARRYTHMIAAND ITS
MANAGEMENT
Dr. Sandeep Singh Jadon
MBBS MD Anaesthesiology
Gajraraja Medical College Gwalior madhyapradesh

2. DEFINITION
Arrythmia also known as dysrythmia, refers to any
disturbance in the rate, regularity, site of origin, or
conduction of the cardiac electrical impulse.
 Arrhythmias may cause sudden death, syncope,
heart failure, dizziness, palpitations or no
symptoms at all.

4. Arrhythmia pathogenesis
 Disorder of impulse formation:
 Automaticity.
 Triggered activity
• Early after depolarization.
• Delayed after depolarization.
 Disorder of impulse conduction:
 Impulse Block
 Re - entry phenomena

5. Abnormal automaticity
• The SA node is the heart’s natural pacemaker.
• Any impulses fired from elsewhere in the heart before or
concurrently with SA node firing can lead to premature
heartbeats or sustained abnormal heartbeats.
• Problems associated are:
1. Sinus tachyarrhythmia
2. Sinus bradyarrhythmia
3. Abnormality in site of impulse generation (ectopic loci)
4. Escape rhythms

6. Triggered automaticity
• This is an abnormal secondary upstroke which occur only
after a normal initial or “triggering “ upstroke or action
potential.
• These secondary upstrokes are called after depolarization.This
may be of two types:
1. Early after depolarization
2. Delayed after depolarization

7. Abnormal impulse conduction
Conduction block may occur due to depression of impulse conduction
at AV node & bundle of His, due to vagal influence or ischaemia .
Types :
• 1st degree heart block – slowed conduction
• 2nd degree block – some supraventricular complex not conducted
• 3rd degree block – no supraventricular complex are conducted

8. Re-entry phenomena
It can be of two types:
I. Anatomically defined re-entry - Wolf Parkinson White
syndrome(WPW).
II. Functionally defined re-entry -Mostly seen in patients with
ischemic heart disease.

9. Two features of arrhythmias
• Site of origin
1. Atria
2. Atrioventricular node (AV node)
3. Ventricles
• Affect on heart rate
1. Too slow heart rate (bradycardia)
2. Too fast heart rate(tachycardia)

10. Contributing factors and causes
1. Patient related factors-
• preexisting cardiac disease
• central nervous system disease
• Old age
2.Anaesthesia related factors
• Tracheal intubation
• General anaesthesia
• Regional anaesthesia
• Electrolyte imbalance and abnormal arterial blood gases
• Central venous cannulation
3.Surgery related factors-cardiac and non cardiac surgery

11. Reversible cause of arrhythmia
• Hypovolemia
• Hypoxia
• Hypo/Hyperkalemia
• Hypomagnesaemia /Hypocalcaemia
• Hypoglycemia
• Hypothermia
• Acidosis
• Mechanical Irritation (e.g. central venous
lines, pulmonary artery catheter,chest tube)
• Cardiac ischaemia
• Light plane of anaesthesia/pain
• Toxins/ Drugs
• Cardiac Tamponade
• Tension pneumothorax
• Thrombosis (Coronary or pulmonary)
• Trauma

12. Anaesthetic considerations
• All patients undergoing anaesthesia and surgery should have
ECG monitoring.
• Lead II and V 5 are superior for arrhythmia detection and
diagnosis before the appearance of physical signs.

13. Routine measure for all intraoperative arrythmias
• Assure adequate oxygenation and ventilation
• Assure adequate depth of anaesthesia
• Assure optimum Po2,pco2, acid base, electrolyte and temperature
• Re-evaluate cardiac history/pathology
Get ready for
• Anti-Arrythmic drug
• Anti-Ischemic drug
• Pacing and DC shock

14. Normal Sinus Rhythm
• SA Node is the primary pacemaker
• One upright uniform p-wave for every QRS
• Rhythm is regular
• Rate is between 60-100 beats per minute
• PR interval = 0.12 – 0.20 sec
• QRS interval <0.12 sec

15. ARRYTHMIA CLASSIFICATION
1. Bradyarrhythmia
2. Ectopics/ Premature systoles
3. Tachyarrhythmias

16. Bradyarrhythmias
A. SA node Dysfunction
1) Sinus bradycardia
2) Sinus Arrhythmias
3) Sinoatrial block
4) Sick Sinus Syndrome
B. Atrioventricular (AV) node and bundle of His
Atrioventricular block
1) First degree AV block
2) Second degree block
a. Mobitz I
b. Mobitz II
3) Third degree heart block

17. Mechanism of Bradyarrhythmias
A. Slowed SA node pacemaker activity
 Sinus bradycardia, in excessive parasympathetic (vagal) tone.
 Hypothyroidism
 Drugs like β-adrenergic blockers and some L-type calcium channel blockers.
B. Impaired impulse conduction (block)
1. SA Block
2. AV Block
a. In the AV node
b. In the AV bundle, both bundle branches, or all three fascicles

18. Sinus bradycardia
• Defined as a heart rate of less than 60 beats per minute.
• In patients on chronic beta-blocker, defined as a heart rate of less
than 50 beats/min.

19. Sinus bradycardia
Perioperative causes of Sinus Bradycardia are:
1.Vagal stimulation- Oculocardiac reflex, Celiac plexus stimulation (traction
on mesentry),laryngoscopy, Abdominal insufflation.
2. Drugs- Beat blocker, Cal channel blocker,opioids(fentanyl/sufentanyl)
3. Succinylcholine
4.Hypothermia
5. Hypothyroidism
6. Athelets
7. Cholestatic jaundice or raised intracranial pressure
8. During the early stages of MI

20. Sinus bradycardia
Perioperative management
• In asymptomatic pt. no treatment is required.
• In Mildly symptomatic pts, underlying factors should be
eliminated.
• In severly symptomatic pts, those with chest pain or syncope,
immediate transcutaneous/transvenous pacing is required.
• Atropine 0.5 mg i.v. every 3-5 min(max 3mg) may be given.
• An epinephrine or dopamine infusion may be titrated while
awaiting cardiac pacing.

21. Sinus arrhythmia
Inspiration accelerates the heart rate, and expiration slows it down.

22. Sick sinus syndrome
CAUSES:
• Conditions leading to fibrosis of the sinoatrial (SA) node, such as
increased age, atherosclerotic heart disease, hypertension, and
cardiomyopathy
• Trauma to the SA node caused by open heart surgery
• Autonomic disturbances
• Cardioactive medications such as digoxin, beta adrenergic blockers,
and calcium channel blockers.

23. Sick sinus syndrome
Sometimes called the bradycardia-tachycardia syndrome.
When severe, sinus slowing can cause syncope, but rarely sudden death.

24. Sick sinus syndrome
• No treatment required unless symptomatic
• If the patient is symptomatic, however, treatment aims to alleviate signs
and symptoms and correct the underlying cause of the arrhythmia.
• Atropine or epinephrine may be given initially for symptomatic
bradycardia.
• A temporary or permanent pacemaker may be used.
• Tachyarrhythmias may be treated with antiarrhythmic medications, such
as metoprolol and digoxin.

25. AV BLOCK
• Atrial impulse is conducted with
delay or is not conducted at all to the
ventricle when the AV junction is not
physiologically refractory.
• Block can occur in the AV node ,
bundle of his or bundle branches

26. First Degree Heart Block
Causes: Increased vagal tone, digitalis toxicity, inferior wall MI and myocarditis.
Usually asymptomatic and rarely require T/t.

27. Second Degree AV Block Type 1 (Wenckebach)
• Often seen in post inferior MI with AV node ischemia
• No pacing as long as no bradycardia.

28. Second Degree AV Block Type 2
• Diseased bundle of HIS with BBB.
• May be precursor to complete heart block and needs pacing.

29. Third Degree AV Block
Complete heart block where atria and ventricles beat independently and atria beat faster
than ventricles.
Pacemaker is the treatment.

30. Bundle branch blocks
• RBBB: More common and associated with ASD, IHD, valvular
heart disease
ECG : wide QRS, terminal R wave in lead V1(rSR’) , deep S wave
in lead I and V6
Bifascicular HB- RBBB +left anterior /posterior hemiblock
• LBBB : wide QRS, predominantly negative QRS in V1,V2,V3 and
absence of Q waves in lead I and V6.
• Treat underlying causes

31. Bundle branch block

32. Premature systoles
1) Atrial 2) Junctional 3) Ventricular
APC

33. Premature Atrial Contraction (PAC)
• PACs arises from ectopic foci in atria.
• May produce palpitation, pt. complain of skipped beat/irregular pulse.
• Precipitated by excessive caffeine, alcohol, nicotine , anxiety,
hyperthyroidism.
• Often occur at rest and become less frequent by exercise.
• Frequent PAC forerunner of atrial fibrillation, flutter,
• Treatment : Avoidance of ppt. factors and sympathetic stimulation.
• Pharmacological T/t required only if the PACs trigger secondary
dysrhythmias.
• Usually suppressed by calcium channel blocker or Beta blocker.

34. Premature Atrial Contraction (PAC)

35. Junctional Rhythms
• Rhythms that originate at the AV junction
• Junctional rhythms do not have characteristic p-waves
• P-wave can come before or after the QRS complex or lost within
the QRS entirely
• If a p-wave is seen it will be inverted
• Junctional rhythm often result in AV dys-synchrony and a
junctional tachycardia can severly impaired cardiac output.

36. Premature Junctional Contraction

37. Junctional Rhythms
Perioperative T/t-
• Junctional rhythm is not frequent during GA,usually
requires no T/t
• Loss of AV synchrony during a junctional rhythm may
result in MI, heat failure or hypotension
• Atropine 0.5 mg can be used to treat hemodynamically
significant junctional rhythms
• Temporary or permanent pacemaker may be required.

38. Premature Ventricular Contraction (PVC)

39. Premature Ventricular Contraction (PVC)
Two major characteristics of PVCs:
1. They are premature, occurring before the next normal beat is
expected
2. QRS complex is abnormally wide and T wave and QRS complex
usually points in opposite direction.
PVC are significant for two reason-
1. They can lead to more serious arrhythmia- VT/VF( R- on –T
phenomenon)- PVC occur so early that it fall on the T wave
because the cells are not fully repolarized, VT/VF can result.
2. Also decreases CO esp. if ectopic beats are frequent or sustained

40. Premature Ventricular Contraction (PVC)
• Classify as unifocal, or multifocal PVC’s
• – Unifocal-originating from same area- same morphology
• – Multifocal-originating from different area-different morphology
• Causes of PVCs
• Arterial hypoxemia
• MI
• Myocarditis
• Hypokalemia/Hypomagnesemia
• Digitalis toxicity
• Caffeine, cocaine, Alcohol
• Mechanical irritation-(CV or Pulm. Artery catheter)

41. Premature Ventricular Contraction (PVC)
• If pt. asymptomatic- the arrythmia won’t req. t/t
• During anaesthesia, if pt exhibits 6 or more PVCs per minute and
repetitive or multifocal forms, there is increased risk of developing
life-threatening dysrhythmia.
• T/t include identification of possible cause and t/t of that cause.
While t/t of cause, the immediate availability of a defibrillator
should be confirmed.
• Beta blockers are the most successful drug,
• Amiodarone, lidocaine and other antiarrhythmic are indicated if
the PVCs progress to VT or VF to cause hemodynamic instability

42. TACHYARRYTHMIAS

43. Sinus Tachycardia
• Sinus rhythm with HR > 100 beats/min.
• Causes-exercise, pain, stress, anxiety, fever, intravascular volume
loss, shock, anaemia, embolism, sepsis, hyperthyroidism, drugs-
atropine, isoproterenol, aminophylline, dobutamine, epinephrine,
• With sinus tachycardia at very fast rate, P wave may be merge with
the preceding T wave and become difficult to distinguish.
• Myocardial demands for O2 increased can bring episode of chest pain
in CAD pt.
• Can lower C.O by reducing ventricular filling time leads to
hypotension and decrease perfusion.

44. Sinus Tachycardia

45. Sinus Tachycardia
Treatment
• Focus on determining and correcting underlying cause.
• In symptomatic pt. maintaining the adequate C.O and tissue
perfusion.
• Beta blockers may be used to slow the heart rate and decrease
myocardial O2 demand(if pt is not hypovolemic).
• Supplemental O2 to increase supply in response to increase demand.
• Avoidance of vagolytic drug (pancuronium) intraoperatively

46. Paroxysmal Supraventricular Tachycardia
(PSVT)
• Narrow QRS complex tachycardias
• m.c. PSVT is AV nodal re-entrant tachycardia (AVNRT)
• ECG- narrow complex tachycardia with regular rhythm, no visible
P wave.
• Treatment-
• Carotid sinus massage and Valsalva manoeuvre.
• Adenosine-6 mg rapid IV injection.If response inadequate repeat
12mg
• When PSVT not respond to adenosine – CCB-diltiazem/verapamil
can be effective

48. ATRIAL FLUTTER
• Supra ventricular tachycardia.- atrial rate around 300 cycles/min.
• Commonly associated with second degree block.
• Mechanism-Reentrant circuit revolves around the tricuspid valve in
the right atrium.
• Conditions that enlarge atrial tissue and elevate atrial pressure.-sev.
Mitral valve ds., hyperthyroidism, pericardial ds., pt. after cardiac
surgery, pt with MI/ COPD
• AF and flutter can occur in the same patient, transitioning from one
to the other( at a given time usually one or other rhythms present)

49. ATRIAL FLUTTER

50. ATRIAL FLUTTER
• T/t depends on hemodynamic stability of patient.
• If pt. is hemodynamically unstable - T/t is synchronized electrical
Cardioversion starting at 50 J is indicated.
• If pt.is Hemodynamically stable-With normal cardiac function and duration<
48 hrs. -Direct current (DC) cardioversion.
• If duration >48 hrs. DC cardioversion would not be considered b/c increases
the risk of thromboembolism unless pt is adequately anti coagulated.
• Pharmacological control of ventricular response with IV amiodarone,
diltiazem or verapamil may be tried, if vital signs are stable.

51. Atrial Fibrillation (AF)
• Most common cardiac arrhythmia in general population.
• AF is a supraventricular arrhythmia characterized by complete absence of
coordinated atrial contractions.
• Originate in the area of pulmonary vein- left atrial junctions.
• Causes- occurs following cardiac sx., long standing hypotension, pulmonary
embolism, COPD, electrolyte imbalance, MR/MS, hyperthyroidism, CAD, acute MI,
pericarditis.
• Usually, the single best lead to identify the diagnostic irregular atrial activity of AF
is- lead V1
• If AF/flutter can occur with Complete heart block ECG- shows regular slow
ventricular response

52. Atrial Fibrillation (AF)

53. Atrial Fibrillation (AF)
• AF or flutter have two major clinical implications-
1. Increase in thromboembolism risk( whenever AF is present –anticoagulant status
of pt. should be reviewed and appropriate t/t promptly initiated).
2. development of chronic heart failure.
• Treatment-
• Thromboprophylaxis- based on CHADS2 score
• Score=0 no anticoagulation needed
• Score=1 dabigatron 150 mg bd
• Mitral stenosis /coronary ds. = Warfarin target INRof2-3

54. Atrial Fibrillation (AF)
• Rate control can achieved by AV nodal blockings agents( beta blocker, CCB, digoxin) or AV
junction ablation.
• Rhythm control- cardioversion(rhythm restoration)- chemical cardioversion- limited value,
ibutilide (convert up to 50% of AF) cause QT prolongation
• Rhythm maintenance by anti arrhythmic drugs class 1 agents-flecainide, propafenone,)
class 3 drugs- sotalol, amiodarone, dofetilide,
• If patient is hemodynamically stable and, if duration of AF< 48 hrs- pharmacological
cardioversion (amiodarone, ibutilide), if duration of AF >48 hrs -anticoagulation 3 wks prior
to an elective cardioversion and continue anticoagulation for 4 wks after procedure.
• Pt. is hemodynamic unstable- anticoagulation with heparin should be initiated as soon as
possible prior to cardioversion followed by 4 wks of anticoagulation after the procedure

55. Wolf Parkinson White Syndrome (WPW) syndrome
• Extra pathway between atria and ventricle that would bypass the AV
junction(bundle of kent) preexcite the ventricles.
• ECG shows:
- Short PR interval
- Delta wave on the upstroke of the QRS complex
Incidental finding of WPW syndrome- usually do not require specific
intervention.
• Drug treatment includes Procainamide, amiodarone
• Pt who are symptomatic Tachycardia cured by radiofrequency ablation.
• Major concern risk of sudden onset atrial fibrillation lead to ventricular
fibrillation.
• When AF is associated with WPW- drugs that block the AV node(CCB, Beta
blocker, digoxin) is contraindicated.

56. WPW syndrome

57. Ventricular Tachycardia (VT)
• Three or more PVCs occur in a row and the ventricular rate >100 beats/min.
• Classification -based on duration (non-sustained-<30 sec, sustained> 30 sec)
• Based on appearance on lead(Monomorphic/Polymorphic)
• Mechanism - Increased myocardial irritability triggered by enhanced
automacity/re entry in purkinje system or PVCs initiating the R-on- T
phenomenon.
• Monomorphic VT in patient with prior MI is caused by re-entry around the areas
of myocardial scar.
• Torsades pointes is special variant of polymorphic VT

58. Ventricular Tachycardia (VT)

59. Ventricular Tachycardia (VT)
• Treatment:
• In hemodynamically compromised patients- emergency electrical cardioversion
indicated.
• If there is no hemodynamic compromise and diagnosis of VT is certain- I.V
amiodarone used to terminate arrhythmia
• If no hemodynamic compromise diagnosis of VT is uncertain – response to
adenosine helpful(terminate paroxysmal SVT)
• DC cardioversion is necessary if medical therapy is unsuccessful
• Sustained monomorphic VT in pt. structural heart ds. Is indication for implantable
cardioverter defibrillator.

60. Torsades de Pointes
• French term-Means twisting around the points.
• Special form of polymorphic ventricular tachycardia.
• Usually initiated by VPB starting at the peak of T wave ( R on T phenomenon)
• Cause-usually reversible-drugs which lengthen QT interval, myocardial ischemia, electrolyte abn.
• Hereditary long QT syndrome- abn. Ion channel function in the heart result in prolong repolarization
– Treatment-
• Correcting the underlying causes
• I.V Magnesium 2 gm bolus followed by infusion at 2-4mg/min
• Sustained polymorphic VT requires nonsynchronized cardioversion(defibrillation)

61. Ventricular Fibrillation (VF)
• Chaotic pattern of electrical activity in the ventricles in which electrical impulse arise
from many different foci.
• It produces no effective muscular contraction and no cardiac output. If VF continues, it
leads to ventricular standstill and death.
• Causes- myocardial ischemia, infarction, untreated VT, underlying heart ds., acid base
imbalance, sev. Hypothermia, electric shock, sev. Hypoxia,
• Successful resuscitation requires rapid recognition of the problem and prompt
defibrillation.
• Defibrillation is most effective t/t for VF.
• During cardiac surgery internal paddles are used

63. Treatment