2. • Definition: Arrhythmia is defined as
"Abnormality of cardiac rate, rhythm or
conduction.
• Cardiac arrhythmias are the most frequent
perioperative cardiovascular abnormalities
in patients undergoing both cardiac and
non-cardiac surgery.
• The occurrence of arrhythmias have been
reported in 70% of patients subjected to
general anaesthesia for various surgical
procedures.
3. Mechanisms of Arrhythmia
Production
• Re-entry (refractory tissue reactivated due to conduction
block, causes abnormal continuous circuit. eg accessory
pathways linking atria and ventricles in Wolff-Parkinson-
White syndrome)
• Injury or damage (pathology) to the cardiac conduction
systems
• Abnormal pacemaker activity/ automaticity in non-
conducting/conducting tissue (eg. ischaemia)
• Delayed after-depolarisation (automatic depolarisation of
cardiac cell triggers ectopic beats, can be caused by drugs
eg digoxin)
4. Contributing factors and causes
1. Patient related factors-
• preexisting cardiac disease
• central nervous system disease
• Old age
2.Anaesthesia related factors
• Tracheal intubation
• general anaesthetics
• regional anaesthesia
• Electrolyte imbalance and abnormal arterial
blood gases
• Central venous cannulation
9. 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.
10.
11. Waveform Analysis
– For each strip it is necessary to go through steps
to correctly identify the rhythm
1. Is there a P-wave for every QRS?
• P-waves are upright and uniform
• One P-wave preceding each QRS
2. Is the rhythm regular?
• Verify by assessing R-R interval
• Confirm by assessing P-P interval
3. What is the rate?
• Count the number of beats occuring in one minute
• Counting the p-waves will give the atrial rate
• Counting QRS will give ventricular rate
12. • Normal
– Heart rate = 60 – 100 bpm
– PR interval = 0.12 – 0.20 sec
– QRS interval <0.12
– SA Node discharge = 60 – 100 / min
– AV Node discharge = 40 – 60 min
– Ventricular Tissue discharge = 20 – 40 min
13. • Cardiac cycle
– P wave = atrial depolarization
– PR interval = pause between atrial and
ventricular depolarization
– QRS = ventricular depolarization
– T wave = ventricular depolarization
15. • Normal Sinus Rhythm
– Sinus Node is the primary pacemaker
– One upright uniform p-wave for every QRS
– Rhythm is regular
– Rate is between 60-100 beats per minute
Sinus Rhythms
17. • Sinus Bradycardia
– One upright uniform p-wave for every QRS
– Rhythm is regular
– Rate less than 60 beats per minute
• SA node firing slower than normal
• Normal for many individuals
• Identify what is normal heart rate for patient
Sinus Rhythms
18. Perioperative causes of Sinus Bradycardia-:
1. Vagal stimulation- Oculocardiac reflex, Celiac
plexus stimulation(traction on mesentry),
laryngoscopy, Abdominal insufflation, Nausea
and ECT
2. Drugs- Beat blocker, Cal channel blocker, opioids
(fentanyl/sufentanyl)
3. Succinylcholine 4.Hypothermia
5. Hypothyroidism 6. Atheletic heart syndrome
7. SA node disease or ischemia
19. Perioperative T/T-
- In asymptomatic pt no t/t requires
- In Mildly symptomatic pts, underlying factors
should be eleminated
- In severly symptomatic pts, those with chest pain
or syncope, immediate
transcutaneous/transvenous pacing is required.
- Atropine 0.5 mg Iv every 3-5 min(max 3mg) may
be given. It should be noted dose of atropine
(<0.5mg) can cause further slowing of HR.
- An epinephrine or dopamine infusion may be
titrated while awaiting cardiac pacing.
21. • Sinus Tachycardia
– One upright uniform p-wave for every QRS
– Rhythm is regular
– Rate is greater than 100 beats per minute due to
increased SA node discharge sec. to sympathetic
stimulation (physiological/pathological
/pharmacological response)
• Usually between 100-160 (>160 SVT)
• Can be high due to anxiety, stress, fever, medications
(anything that increases oxygen consumption)
Sinus Rhythms
22. Treatment-:
-correcting underlying cause of symp. Stimulation.
-Beta blockers may be employed to lower 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
24. • Sinus Arrhythmia
– One upright uniform p-wave for every QRS
– Rhythm is irregular
• Rate increases as the patient breathes in
• Rate decreases as the patient breathes out
– Rate is usually 60-100 (may be slower)
– Variation of normal, not life threatening
Sinus Rhythms
25. Premature Atrial Contraction (PAC)
Heart
Rate
Rhythm P Wave
PR Interval
(sec.)
QRS
(Sec.)
NA Irregular
Premature &
abnormal or
hidden
.12 - .20 <.12
Atrial Rhythms
26. – Premature Atrial Contraction (PAC)
• One P-wave for every QRS
– P-wave may have different morphology on ectopic beat,
but it will be present
• Single ectopic beat will disrupt regularity of
underlying rhythm
• Rate will depend on underlying rhythm
• Underlying rhythm must be identified
• Classified as rare, occasional, or frequent PAC’s
based on frequency
Atrial Rhythms
27. • Sign and symptoms
-PACs arises from ectopic foci in atria. Typical
symptoms include an awareness of a fluttering
or a heavy heart beat.
-Precipitated by excessive caffeine, stress,
alcohol, nicotine and hyperthyroidism.
-Often occur at rest and become less frequent
by exercise.
-second most arrhythmias asso. With MI.
28. Perioperative T/t-:
1. Avoidance of ppt. factors and sympathetic
stimulation.
2. Pharmacological T/t required only if the PACs
trigger sec. dysrhythmias.
3. Usually suppressed by calcium channel
blocker or Beta blocker.
30. • Atrial Fibrillation
– No discernable p-waves preceding the QRS complex
• The atria are not depolarizing effectively, but fibrillating
– Rhythm is grossly irregular
– If the heart rate is <100 it is considered controlled a-
fib, if >100 it is considered to have a “rapid ventricular
response”
– AV node acts as a “filter”, blocking out most of the
impulses sent by the atria in an attempt to control the
heart rate
Atrial Rhythms
31. • Atrial Fibrillation (con’t)
– Often a chronic condition, medical attention only
necessary if patient becomes symptomatic
– Patient will report history of atrial fibrillation.
– Symptoms range from palpitation to angina
pectoris, CHF, pul. Oedema and hypotension
– Often associated with fatigue and generalized
weakness.
– Predisposing factors are :RHD, hypertension,
thyrotoxicosis, IHD, chronic COPD, pericarditis
and pulmonary embolus.
Atrial Rhythms
32. Perioperative management-
-If new onset of AF, surgery should be postponed if possible
untill control of dysrhythmia.
-T/t of AF during Sx depends on hemodynamic stability of pt.
-if hemodynamically significat, the T/t is cardioversion
-Synchronized electrical cardioversion (100 to 200 J) is most
effective.
-Pharmacological cardioversion by IV amiodarone (pref.drug),
diltiazem or verapamil may be attempted.
-Pt with chronic AF should be maintained on their
antidysrhythmic drugs with close attention to serum
electrolyte(K &Mg).
-Manage the transition on and off IV and oral anticoagulation.
33. Atrial Flutter
Heart Rate Rhythm P Wave
PR Interval
(sec.)
QRS
(Sec.)
Atrial=250
– 400
Ventricular
Var.
Irregular Sawtooth
Not
Measur-
able
<.12
Atrial Rhythms
34. • Atrial Flutter
– More than one p-wave for every QRS complex
• Demonstrate a “sawtooth” appearance
– Atrial rhythm is regular. Ventricular rhythm will be
regular if the AV node conducts consistently. If the
pattern varies, the ventricular rate will be irregular
– Rate will depend on the ratio of impulses conducted
through the ventricles
– Most commonly atrial rate compared to ventricular
rate 2:1 (if atrial rate is 300bpm and 2:1 conduction,pt
can present with venticular rate of 150 with sign and
symptoms)
Atrial Rhythms
35. • Peioperative T/t-
-T/t depends on hemodynamic stability of
patient.
-If AF is hemodymamically sig. the T/t is
cardioversion, synchronized elec. Cardioversion
satarting at 50 J is indicated.
-Pharmacological control of ventricular response
with IV amiodarone, diltiazem or verapamil may
be tried, if vital signs are stable.
36. Atrial Rhythms
• Atrial Flutter
– Atrial flutter is classified as a ratio of p-waves
per QRS complexes (ex: 3:1 flutter 3 p-waves
for each QRS)
– Not considered life threatening, consult
physician if patient symptomatic
37. • Rhythms that originate at the AV junction
• Junctional rhythms do not have
characteristic p-waves.
Junctional Rhythms
38. Premature Junctional Contraction PJC
Heart
Rate
Rhythm P Wave
PR Interval
(sec.)
QRS
(Sec.)
Usually
normal
Irregular
Premature,
abnormal, may be
inverted or hidden
Short
<.12
Normal
<.12
Junctional Rhythms
39. • Premature Junctional Contraction (PJC)
– P-wave can come before or after the QRS complex,
or it may lost in the QRS complex
• If visible, the p-wave will be inverted
– Rhythm will be irregular due to single ectopic beat
– Heart rate will depend on underlying rhythm
– Underlying rhythm must be identified
– Classify as rare, occasional, or frequent PJC based
on frequency
– Atria are depolarized via retrograde conduction
Junctional Rhythms
41. • Accelerated Junctional Rhythm
– P-wave can come before or after the QRS
complex, or lost within the QRS complex
• If p-waves are seen they will be inverted
– Rhythm is regular
– Heart rate between 60-100 beats per minute
• Within the normal HR range
• Fast rate for the junction (normally 40-60 bpm)
Junctional Rhythms
43. • Junctional Tachycardia
– 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
– Rhythm is regular
– Rate is between 100-180 beats per minute
• In the tachycardia range, but not originating from SA node
– AV node has sped up to override the SA node for
control of the heart
– Junctional rhythm often result in AV dyssynchrony
and a junctional tachycardia can severly impaired
Cardiac output.
Junctional Rhythms
44. • Perioperative T/t-
-Junctional rhythm is not frquent during GA.
-Transient Junctional rhythm require 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 significat junctional rhythms
45. Ventricular Rhythms
Premature Ventricular Contraction (PVC)
Heart
Rate
Rhythm P Wave
PR
Interval
(sec.)
QRS
(Sec.)
Var. Irregular
No P waves
associated with
premature beat
NA
Wide
>.12
46. Ventricular Rhythms
• Premature Ventricular Contraction (PVC)
– The ectopic beat is not preceded by a p-wave
– Irregular rhythm due to ectopic beat
– Rate will be determined by the underlying rhythm
– QRS is wide and may be bizarre in appearance
– Caused by a irritable focus within the ventricle which
fires prematurely
47. Ventricular Rhythm
• Premature Ventricular Contraction
– Classify as rare, occasional, or frequent
– Classify as unifocal, or multifocal PVC’s
• Unifocal-originating from same area of the
ventricle; distinguished by same morphology
48. Ventricular Rhythm
• Premature Ventricular Contraction
– Classify as unifocal, or multifocal PVC’s
– Unifocal-originating from same area of the
ventricle; distinguished by same morphology
– Multifocal-originating from different areas of the
ventricle; distinguished by different morphology
49. Ventricular Rhythm
• Premature Ventricular Contraction
– Bigeminy
• A PVC occurring every other beat
– Also seen as Trigeminy, Quadrigeminy
51. • Causes of PVCs
- Arterial hypoxemia
- MI
- Myocarditis
- SNS activation
- Hypokalemia/Hypomagnesemia
- Digitalis toxicity
- Caffeine, cocaine,Alcohol
- Mechanical irritation-(CV or Pulm. Artery
catheter)
52. • Prioperative T/t-
-During anaesthesia, if pt exhibits 6 or more PVCs
per minute and repetetive or multifocal forms,
there is increased risk of developing life
threatining dysrhythmia.
-T/t include a D/d 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 antiarhythmic
are indicated if the PVCs progress to VT or
ferquent to cause hemodynamic instability.
54. Ventricular Rhythms
• Ventricular Tachycardia
– No discernable p-waves with QRS
– Rhythm is regular
– Atrial rate cannot be determined, ventricular
rate is between 150-250 beats per minute
– Must see 4-6 beats in a row to classify as v-
tach
55. Ventricular Rhythms
• Ventricular Tachycardia
– THIS IS A DEADLY RHYTHM
• Check patient:
– If patient awake and alert, monitor patient and call physician
– Pt with symptomatic or unstable VT or SVT cardioverted
immediately.
– If vitals signs stable and VT is persistent or recurrent after
cardioversion, Amiodarone 150mg over 10min should be
given, other drugs may be used like procainamide,lignocaine
or sotalol.
– Pulseless VT requires immediate cardioversion/defibrillation
and CPR. (If patient has no vital signs, call code and start
CPR
» Defibrillate)
57. Ventricular Rhythms
• Ventricular Fibrillation
– No discernable p-waves
– No regularity
– Unable to determine rate
– Multiple irritable foci within the ventricles all firing
simultaneously
– May be coarse or fine
– This is a deadly rhythm
• Patient will have no pulse
• Call a code and begin CPR
• Survival is best if defbrillation occcurs within 3-5 min
59. Asystole
• No p-waves
• No regularity
• No Rate
• This rhythm is associated with death
– Check patient and leads
– No pulse
• Begin CPR
60. Heart Block
First Degree Heart Block
Heart
Rate
Rhythm P Wave
PR Interval
(sec.)
QRS
(Sec.)
Norm. Regular
Before each QRS,
Identical
> .20 <.12
61. Heart Block
– First Degree Heart Block
• P-wave for every QRS
• Rhythm is regular
• Rate may vary
• Av Node hold each impulse longer than normal
before conducting normally through the ventricles
• Prolonged PR interval
– Looks just like normal sinus rhythm
Cuases- increased vagal tone, digitalis toxicity, inferior wall
MI and myocarditis.
-Usually asymptomatic and rarely require T/t.
-Elimination of drugs that slows AV conduction or clinical
factors that enhance vagal tone can reverse 1st degree
block.
62. Heart Block
Second Degree Heart Block
Mobitz Type I (Wenckebach)
Heart
Rate
Rhythm P Wave
PR Interval
(sec.)
QRS
(Sec.
)
Norm.
can be
slow
Irregular
Present but some
not followed by
QRS
Progressively
longer
<.12
63. Heart Block
• Second Degree Heart Block
• Mobitz Type I (Wenckebach)
– Some p-waves are not followed by QRS complexes
– Rhythm is irregular
• R-R interval is in a pattern of grouped beating
– Rate 60-100 bpm
– Intermittent Block at the AV Node
• Progressively prolonged p-r interval until a QRS is blocked
completely
64. Heart Block
Second Degree Heart Block
Mobitz Type II (Classical)
Heart
Rate
Rhythm P Wave
PR
Interval
(sec.)
QRS
(Sec.)
Usually
slow
Regular
or
irregular
2 3 or 4 before each
QRS, Identical
.12 - .20
<.12
depends
65. Heart Block
• Second Degree Heart Block
• Mobitz Type II (Classical)
– More p-waves than QRS complexes
– Rhythm is irregular
– Atrial rate 60-100 bpm; Ventricular rate 30-100 bpm
(depending on the ratio on conduction)
– Intermittent block at the AV node
• AV node normally conducts some beats while blocking others
• Mobitz type II block has high rate of progression to 3rd
degree heart block. A cardiac pacemaker is mandatory in this
situation.
66. Heart Block
Third Degree Heart Block
(Complete)
Heart
Rate
Rhythm P Wave
PR
Interval
(sec.)
QRS
(Sec.)
30 –
60
Regular
Present but no
correlation to QRS
may be hidden
Varies
<.12
depends
67. Heart Block
• Third Degree Heart Block (Complete)
– There are more p-waves than QRS
complexes
– Both P-P and R-R intervals are regular
– Atrial rate within normal range; Ventricular
rate between 20-60 bpm
– The block at the AV node is complete
• There is no relationship between the p-waves and
QRS complexes.
• Cardiac pacing is require in cases of 3rd degree
block
68. • Anaesthetic management
-Previous placement of a transvenous pacemacker or
availability of of transcutaneous cardiac pacing is required
before an anesthetic is administered for insertion of
permanent cardiac pacemaker ,
-Isoproterenol may be required to maintain acceptable HR
and acts as “chemical pacemaker” untill the artificial
pacemaker is functional
69. MODALITIES FOR TREATMENT OF
ARRHYTHMIA
• Antiarrhythmic drugs
. All such drugs may aggravate or produce
arrhythmias and they may also depress
ventricular contractility and must, therefore, be
used with caution.
• They are classified according to their effect on
the action potential (Vaughan Williams'
classification)
72. Management of Arrythmia’s
• ECG and rhythm information
• should be interpreted within the context of
total patient assessment
• Providers must evaluate
• Patient’s symptoms
• Clinical signs
• Ventilation, oxygenation, heart rate, blood
pressure, signs of inadequate organ perfusion
73. • In both unstable and symptomatic cases
• Provider must make an assessment whether
it is the arrhythmia that is causing the patient
to be unstable
• Patient in septic shock with sinus
tachycardia 140 / min is unstable
• Electric cardioversion will not improve this
patient’s condition
74. • If patient with severe hypoxemia becomes
hypotensive and develops bradycardia
• Bradycardia is not the primary cause of
instability
• Treating the bradycardia without treating
the hypoxemia is unlikely to improve the
patient’s condition
75.
76.
77. Supraventricular Tachycardia
• (Supraventricular - a rhythm process in which
the ventricles are activated from the atria or
AV node/His bundle region)
• Refers to supraventricular tachycardia other
than afib, aflutter and MAT
• Occurs in 35 per 100,000 person-years
• Usually due to reentry—AVNRT or AVRT
78. • QRS typically narrow (in absence of bundle
branch block); thus, also termed narrow QRS
tachycardia
• Usually paroxysmal, i.e, starting and stopping
abruptly; called PSVT
• Aetiology should be considered before
therapy is instituted
79. Vagal maneuver
• Valsalva maneuver or carotid sinus massage
• Terminate up to 25% of PSVTs
• For other SVTs
• May transiently slow the ventricular rate
• Potentially assist rhythm diagnosis but will
not usually terminate such arrhythmias
80. Adenosine ( if regular)
• If PSVT does not respond to vagal maneuvers
• Give 6 mg of IV adenosine as a rapid IV push
through antecubital vein followed by a 20 mL
saline flush
• If the rhythm does not convert within 1 to 2
minutes
• Give a 12 mg rapid IV push using the method
above
82. Rate Control
• Unstable patients
• Prompt electric cardioversion
• Stable patients
• Ventricular rate control as directed by
patient symptoms
• IV nondihydropyridine calcium channel
blockers
Diltiazem are drugs of choice for acute rate
control in most individuals with atrial
fibrillation and rapid ventricular rate
83. Ventricular arrhythmias
• Non-sustained ventricular
arrhythmias
- routinely seen in the absence of cardiac
disease- may not require drug therapy in the
perioperative period.
- Conversely, in patients with structural heart
disease, these non-sustained rhythms do
predict subsequent life-threatening ventricular
arrhythmias.
84. NSVT after - cardiopulmonary bypass, unstable
patients with marginal perfusion may
deteriorate with recurrent episodes of NSVT
may benefit from suppression with lidocaine or
beta blockade.
repletion of post-bypass hypomagnesaemia
(MgCl2 2 g i.v.) reduces the incidence of NSVT
after cardiac surgery.
85. Sustained VT
• two categories: monomorphic and
polymorphic.
• monomorphic VT - the amplitude of the QRS
complex remains constant
• polymorphic ventricular tachycardia - the QRS
morphology continually changes.
86. Therapy for monomorphic wide
complex tachycardia
• If the etiology of the rhythm cannot be
determined
• QRS monomorphic, regular
• IV adenosine is relatively safe for both
treatment and diagnosis
• However, adenosine should not be given for
unstable or irregular or polymorphic wide
complex tachycardias
• • It may cause degeneration of the
arrhythmia to VF
87. • If the wide-complex tachycardia proves to be
SVT with aberrancy
• transiently slowed or converted by
adenosine to sinus rhythm
• If due to VT there will be no effect on rhythm
(except in rare cases of idiopathic VT)
• When adenosine is given for undifferentiated
wide complex tachycardia
• Defibrillator should be available
88. For patients who are stable with
likely VT
• IV antiarrhythmic drugs or elective
cardioversion is the preferred treatment
strategy
• Amiodarone
• Procainamide
• Sotalol
• Procainamide and sotalol should be avoided
in patients with prolonged QT, CHF
89. Wide-complex irregular
rhythm
• Should be considered preexcited atrial
fibrillation
• Expert consultation is advised
• Avoid AV nodal blocking agents
• adenosine, calcium channel blockers,
digoxin, and possibly β-blockers
90. Polymorphic (Irregular) VT
• First step
• Stop medications known to prolong the QT
interval
• Correct electrolyte imbalance
• Acute precipitants: drug overdose or
poisoning
91. Prolong QT interval (Torsades de
pointes)
• The management of torsades de pointes
differs markedly from other forms of VT, and
includes
• i.v. magnesium sulfate (2±4 g),
• repleting potassium,
• and manoeuvres aimed at increasing the heart
rate (atropine, isoprenolol or temporary atrial
or ventricular pacing).
• Haemodynamic collapse with torsades
requires asynchronous DC counter shocks