PERI OPERATIVE ARRYHTHMIAS

.,

dr. Juzny Alkatiri, SpPD, SpJP

 Most frequent peri operative cardiac
abnormality with high incidence
 Can occur in a patient with or without
cardiac disease
 During cardiac or non cardiac surgeries
 During general or regional anesthesia
 Perioperative : 44%
 Age > 50 y.o.
 Unstable coronary
syndrome
 Prior angina
 Recent-/post-MCI
 Heart failure (EF<35%)
 Previous arrhythmias
 Severe valvular disease
 Cerebrovascular disease
 Diabetes Mellitus
 Hypertension
 Smoker
 Chronic pulmonary
disease
 Hematologic disorders:
 Anemia
 Polycythemia
 thrombocytopenia
Conduction System:

S.A Node
Inter Nodal Pathway
AV Node
HIS Bundle
- Right Bundle Branch
- Left Bundle Branch
- Purkinje System
 Injuryor damage (pathology) to the cardiac
conduction systems.
 Re-entry
 Automaticity
 Mutations in ion channels
 Ectopic foci/ irritable foci
 Due to lack of atrial transport mechanism
Inadequate atrial contraction →
Inadequate ventricular filling occurs when
there is obstruction between atrium and
ventricles, hypertrophied ventricle,
sudden stress

 BradyArrhythmia
Dangerous in patients with low fixed
stroke volume – depend on the heart rate
for cardiac output
 Tachy arrhythmias
Less time for diastolic filling
Increased Myocardial O2 consumption

 Abnormal ventricular arrhythmia

Less effective ventricular contraction
leads to decreased cardiac output
Yes……….when it produces
haemodynamic changes
1. Anaesthetic agents
 Halogenated hydro carbons like Halothane,
Enflurane
 Drugs blocking reuptake of catecholamine
e.g. Ketamine
 Others like Atropine, Suxamethonium etc
2. Drugs
 Digoxin, Tricyclic antidepressants
3. Electrolyte abnormalities
 Potassium, Sodium, Calcium, Magnesium
4. ABG abnormalities
 Hypo or Hypercarbia
 Acidosis and Alkalosis – Potassium related
 Profound Hypoxemia – Bradycardia, Ventricular
arrhythmias, asystole
5. Temperature changes
 Hypothermia – Decreases conduction velocity in
all areas of conduction system
 Hyperthermia – Catecholamine induced
arrhythmias
6. Laryngoscopy and intubation
 Endotracheal intubation is most common cause of
arrhythmias during surgery
 Can also occur at time of extubation
7. Reflexes
 Vagal stimulation → Sinus Bradycardia
 Reflexes arise from pharynx, larynx, abdominal &
thoracic organs
 Direct pressure on vagus during carotid surgery
 Specific reflexes like ocular cardiac reflex
8. Autonomic disturbances
9. Pre existing cardiac diseases
Cardiomyopathy, Myocarditis, CAD, Ventricular
hypertrophy,
Low cardiac output states

10. Pre existing arrhythmias

11. Central venous cannulation
12. Surgical manipulation of cardiac structures
13. Physical factors
 High atrial pressure – Atrial arrhythmias
 High arterial pressure – Ventricular arrhythmias
14. Surgical site
15. Increased catecholamine levels
 Exogenous - Inotropes, Adrenaline
 Endogenous release due to pain, hypoxia, light anesthesia,
Hypercarbia
16. Intracranial pathology
17. Endocrine disorders
 Phaeochromoctoma, Thyrotoxicosis, Diabetes, Adreno cortical
excess
 High grade AV block
 Symptomatic ventricular arrhythmias
 Supraventricular arrhythmias with ventricular
rates > 100 at rest
 Symptomatic bradycardia
 Newly recognized ventricular tachycardia
Anti hypertensive agents

Drugs used for the treatment of myocardial

ischemia (anti angina agents)

Pharmacological treatment of heart failure

Anti arrhythmic drugs

 Sinus Tachycardia
 Sinus Bradycardia
 Sinus Arrhythmias
 Premature Atrial Complex (PAC)
 Paroxysmal Supra-ventricular Tachycardia
(PSVT)
 Atrial Flutter
 Atrial Fibrillation
 Premature Junctional Complex (PJC)
 Junctional Escape Complex and Junctional
Rhythm
 Premature ventricular complex (PVC)
 Ventricular Tachycardia
 Ventricular Fibrillation
 Ventricular Asystole
Arrhythmia recognized

(1) Haemodynamic Disturbances?

(2) Treatment Required ?
(3) How urgently ?

Rule out Pseudo arrhythmias

 Due to
 Electrocautery
 ECG lead disconnections
 Movement of lead wires
 Muscle artifact
 What is the heart rate ?
 Is the rhythm regular ?
 Is there one P wave for each QRS ?
 Is QRS complex normal ?
 Is the rhythm dangerous ?
 Does the rhythm require treatment ?
• Normal sequence of conduction, originating in the sinus node

•EKG Characteristics: Regular narrow-complex rhythm

Rate 60-100 bpm
Each QRS complex is proceeded by a P wave
P wave is upright in lead II & downgoing in lead aVR
 Alternate periods of
slower and faster
rates
 Rate increases with
inspiration and
decreases with
expiration
 Common in children
 ECG - normal
pattern
 Treatment - None
 Most common arrhythmia occuring intra
operatively
 Occurs due to increase in rate of discharge of
impulses from S.A.node
 Etiology – Inadequate anesthesia and light
plane, anxiety, pain, fever, hypovolemia,
hypoxia, hypercarbia,drug effect, heart
failure
• Awake patient ( + Hypertension)
• Hypovolemia
• Hypoxia
• Hyperthyroidism

http://www.emedu.org/
Significance
- can precipitate heart failure, angina

Treatment
 Treat underlying cause
 Beta blockers – Esmolol, Metaprolol
 Areaof ‘automaticity’ develops in AV node
 Bothretrograde and ante grade transmission
occurs

ECG criteria
 Rate – 100 – 180/min
 Rhythm- regular atrial and ventricular firing
 PR- not measurable or will be short
 P wave - obscured, may arise before, after or
with QRS
 QRS complex - narrow
• Abnormal rhythm after weaning from CPB
• May be poorly tolerated
• Amiodarone

http://www.emedu.org/
Supraventricular tachycardia

• Abnormal rhythm after weaning from CPB

• May be poorly tolerated
• Amiodarone, adenosine
http://www.emedu.org/
• Abnormal rhythm after weaning from CPB
• May be poorly tolerated
• Amiodarone

http://www.emedu.org/
Diagnosis Unknown → Vagal stimulation
Adenosine
↓
Preserved heart function
 Beta blockers
 Calcium channel blockers
 Amiodarone
 NO DC CONVERSION

Impaired heart function

 Amiodarone
 NO DC CONVERSION
http://www.emedu.org/
 Re entry phenomenon – impulse arise and
recycle repeatedly in AV node because of
unidirectional block in Purkinje fibers
 Rate – exceeds upper limit of sinus tachycardia
(120bpm ); seldom150 bpm up to 250bpm
 Rhythm – regular
 Narrow complex tachycardia
 P waves – seldom seen
Diagnosis Unknown → Vagal stimulation
Adenosine
↓
Preserved heart function
 Beta blockers
 Calcium channel blockers
 Amiodarone
 NO DC CONVERSION

Impaired heart function

 Amiodarone
 NO DC CONVERSION
Atrial level
 Areas of automaticity originate irregularly
and rapidly at different points in atria
 Rate- >100bpm
 Rhythm- irregular atrial firing
 PR- variable
 P wave- 3 or more that differ in polarity,
shape and size
 QRS complex- narrow
• Valve surgery (+++): Mitral, tricuspid
• COPD and advanced Pulmonary hypertension

http://www.emedu.org/
Preserved heart Impaired heart
function function

 Beta blockers  Amiodarone

 Calcium channel  Diltiazem
blockers  NODC
 Amiodarone cardioversion
 Atrial impulses faster than SA node impulses
 Atrial fibrillation  impulse takes multiple,
chaotic, random pathways through atria
 Atrial flutter  impulse takes a circular
course around atria
 Impulse formation is by ‘re entry’
phenomenon
ECG Atrial Fibrillation Atrial Flutter
Rate Wide ranging ventricular Atrial rate 220 to 350bpm
response to atrial rate of Ventricular response rarely
300 to 400bpm >150bpm

Rhythm Irregularly irregular Regular

Set ratio to atrial rhythm
e.g, 2 to 1

P waves Chaotic atrial fibrillatory No true P waves

waves only “saw tooth” pattern

PR/QRS Cannot be Cannot be

measured/Normal measured/Normal
Macroreentry Microreentry

Atrial Flutter Atrial Fibrillation

• Valvular heart disease (+++ mitral valve)
• Manipulation of right atrium (canulation)
• Electrolyte disturbances
• Hypovolemia
• Hyperthyroidism

http://www.emedu.org/
Atrial fibrillation / Flutter

• Valvular heart disease (+++ mitral valve)

• Manipulation of right atrium (canulation)
• Electrolyte disturbances
• Hypovolemia
• Hyperthyroidism
http://www.emedu.org/
Atrial fibrillation / Flutter

• Valvular heart disease (+++ mitral valve)

• Manipulation of right atrium (canulation)
• Electrolyte disturbances
• Hypovolemia
• Hyperthyroidism
http://www.emedu.org/
Normal Heart Impaired Heart

•Diltiazem or another •Digoxin or

calcium channel blocker •Diltiazem or
•Metaprolol or another •Amiodarone
beta blocker
Normal Heart Impaired Heart

•DC cardioversion or •DC cardioversion or

•Amiodarone •Amiodarone
•Provide •Provide
anticoagulation anticoagulation
Ventricle level
 Results from ectopic pacemaker activity from
either ventricle
 Wide, bizarre QRS complex
 Unifocal- PVCs from same focus; coupling
interval is normal
 Multifocal- coupling interval and QRS morphology
vary
 Ventricular bigeminy-
every other beat is a
PVC
 Ventricular
trigeminy- 2 normal
beats and a PVC or 1
normal beat and 2
PVCs
• Bigeminism
• Paired
• Triplet
• Polymorphic
• Ischemic
• Ventricle irritation

http://www.emedu.org/
 Usually not needed

If hemodynamically unstable
 Digitalis
 Beta blockers
 Verapamil
 Heart rate: Chaotic, random and
asynchronous
 Rhythm: Irregular
 Mechanism: Multiple wavelets of reentry
 Recognition:
 No discrete QRS complexes
 Treatment:
 Defibrillation
• Mechanical arrest
• Great O2 consumption +++
• Before CPB: critical ischemia (Left main, severe CAD)
• During CPB: poor myocardial protection
• On weaning from CPB: Reperfusion
• After CPB: Myocardial ischemia, electrolyte disturbances
 Heartrate: Variable
 Rhythm: Irregular
 Mechanism:
 Reentry
 Triggered activity
 Recognition:
 Wide QRS with phasic variation
 Torsades de pointes
• Mechanical arrest or severe hypotension
• Great O2 consumption +++
• Before CPB: critical ischemia (Left main, severe CAD)
• After CPB: Myocardial ischemia, electrolyte disturbances
• electroshock

http://www.emedu.org/
 Pharmacologic therapy:
 Potassium
 Magnesium
 Isoproterenol
 Possibly class Ib drugs (lidocaine) to decrease
refractoriness/shorten length of action potential
 Overdrive ventricular pacing
 Defibrillation
• Beta-blockers
• Calcium Channel blockers
Katrina Kardos, MD
PGY-3
Albany Medical Center
1st Degree AV block

 Rate – bradycardia or tachycardia

 Rhythm – sinus, regular
 PR – prolonged, > 0.20 sec, fixed
 P wave – size & shape normal, each P wave have
1 QRS complex
 QRS complex – narrow: ≤0.10 sec in absence of
intraventricular conduction defect
Key- PR interval > 0.20 sec
• Beta blockers
• Frequent in elderly
• AV node (valve surgery, MI)

http://www.emedu.org/
• Beta blockers
• Frequent in elderly
• AV node (valve surgery, MI)

http://www.emedu.org/
 Siteof pathology is AV node
 Impulse conduction is increasingly slowed at AV
node – causing increasing PR interval
 Occurs till one sinus impulse is completely
blocked and a QRS complex fails to follow
 Rhythm : Irregular
 Rate : Usually slow but can be normal
 P wave : Sinus P wave present ;
some not followed by QRS complexes
 PR : Progressively lengthens
 QRS : Normal
– Lesion to conduction tissues (AVR, MVR, TVR)
Mobitz I
Intervention sequence
 Atropine 0.5 to 1mg i.v
 Transcutaneous pacing if available

If signs and symptoms are severe

 Dopamine 5 to 20 μg/kg/min
 Epinephrine 2 to 10 μg/min
 Isoproterenol 2 to 10 μg/min
 Infra nodal block – site of block most often
below AV node
 Impulse conduction is normal through the
node
 Etiology : Acute coronary syndrome – left
coronary
 Atrial rate- usually 60 to 100 bpm
 Ventricular rate- slower than atrial rate
 Rhythm- Atrial- regular; Ventricular- irregular
 PR- constant, no progressive prolongation
 P wave- some P waves will not be followed by QRS
complex or Two, three, or four P waves before each
QRS
 QRS complex- narrow implies high block; wide
implies low block

Key - No progressive prolongation of P wave

Mobitz II atrioventricular block
 Prepare for Tran venous pacer
 Atropine is seldom effective
 Transcutaneous pacing

If signs and symptoms are severe, unresponsive

 Dopamine 5 to 20 μg/kg/min
 Epinephrine 2 to 10 μg/min
 Isoproterenol 2 to 10 μg/min
 Injury to cardiac conduction system producing
complete block of impulses
 Block can occur at AV node or Bundle of His or
Bundle branches
 Impulses completely independent from ventricular
rate
 Rhythm- Atrial&Ventricular- regular, independent
 PR- no relationship between P and R wave
 Rhythm : Regular
 Rate : 40 – 60 if block in His bundle;
 30 – 40 if block involves bundle branches
 P wave : Sinus P wave present; bear no relationship
to QRS; can be found hidden in QRS complexes and T
waves
 PR : Varies greatly
 QRS : Normal if block in His bundle; wide if block
involves bundle branches
http://www.emedu.org/
Atrioventricular dissociation secondary to complete heart block
 Prepare for Tran venous pacer
 Transcutaneous pacing

If signs and symptoms are severe, unresponsive

 Dopamine 5 to 20 μg/kg/min
 Epinephrine 2 to 10 μg/min
 Isoproterenol 2 to 10 μg/min

Never treat third degree block plus

ventricular escape beats with Lidocaine
RBBB
• Preoperative: Normal (10%), RVH
• New RBBB
– poor RV myocardial protection (imperfect retrograde cardioplegia)
– incomplete revascularization to RCA
– Technical problem with graft (Kink, Twist) to RCA
– Air embolism in the RCA ostium (+++ valve surgery)
– Lesion to conduction tissues (tricuspid)

http://www.emedu.org/
LBBB
• Preoperative: HTA, LVH, CHF, Ischemia
• New LBBB
– MI
– poor myocardial protection Risk of complete
– incomplete revascularization
– Technical problem with graft (Kink, Twist) heart bloc with
– Air embolism Swan Ganz KT
– Lesion to conduction tissues (AVR, MVR)

http://www.emedu.org/
Sodium channel blocker
• Sodium channel (++)
• Diisopyramide, Quinidine, Procainamide
• Blocks K+ Efflux (+)
• Lidocaine, Mexiletine, Tocainide
• Sodium channel (+++)
• Flecainide, Encainide, Propafenone
Anti adrenergic
• β blocker

K+ channel Efflux blockers also Na+ blockers

• Amiodarone
• Sotalol
Ca++ channel blockers
• Verapamil & Diltiazem

Autonomic Effects
• Vagus stimulation
• Digoxin
• Adenosine receptor activation
• Adenosine
 Dosis Kadar Meta Eks Indikasi Efek samping
puncak b
KINIDIN 3 X 200 mg 60 – 90’ H G/H AF, SVT
PROKAINAMID 3X (250000 45 – 70’ H G VES, SVT Lupus like
– 500) mg syndrome,
leukopeni
DIISOPIRAMID 3X 100 mg 60 – 120’ H G VES, SVT Mulut kering,
konstipasi,
penglihatan
kabur
LIDOKAIN 1 MG/ KG H VT (pasca hipotensi
bb =1mg/ miokard infark)
jam
PROPAFENON 3 x(150 - 60 – 180’ VES
300) mg

Hipotensi / Sinkop
Kardiovaskular
•SA block
•QRS – Interval •AV block
•Torsades de Poentes
•Long QT • ↑ ventrikuler rate (efek anti
kolinergik)
Cinchonism

•Demam
•Tinitus
•Penglihatn kabur
•Diplopia
•Sakit kepala
•Delirium
•Prikosis
•Gangguan GIT
Farmakokinetik indikasi Efek samping
T1/2 Dosis VT, AF Pro aritmik,
Hipotensi, gangguan fungsi: hati,
25 – 60 jam Loading 600 tiroid, paru & mata
s/d 800 mg/
hari
Maintenance
300mg/ hari

Sotalol
Farmakokinetik indikasi Efek samping
T1/2 Dosis SVT, VT Gagal jantung
11 jam 800 s/d 320
mg/hari
Sinus Bradicardy
1. Ephedrine
2. Aminophylline
3. Atropine (I.V.)

Heart Block
1. Atropine (I.V.)
2. Temporary Pacemaker
3. Permanent Pacemaker
.,
Drugs IV bolus IV infusion Oral dose Cautions

Heparin 5,000 units APTT 2-3 X

Warfarin INR 2-3

Propanolol 1 mg / 5 min 2-3 mg / hr 10-80 mg / 6- Bradycardia,
Max 5 mg 8 hr hypotension, or
bronchospasm
Metoprolol 5 mg / 5 min 25-100 mg
Max 15 mg twice a day
Atenolol 5 mg / 10 min 50-200 mg /
Max 10 mg day
Diltiazem 0.25 mg / kg 5-15 mg / hr 180-360 mg/d Bradycardia,
Verapamil 0.15 mg / kg 5 mg / hr 120-480 mg/d hypotension

N Engl J Med 1997; 336: 1429-34

Drugs IV bolus IV infusion Oral dose Cautions

Disopyramide 150-300 mg Heart failure,

Twice a day renal failure
Propafenone 1-2.5 mg / kg 2 mg / min 150-300 mg Bronchospasm
3X a day
Amiodarone 150 mg 1000 mg / 200 – 400 mg Pulmonary
day / day fibrosis,
cirrhosis, thyroid
abnormalities
Sotalol 0.2-1.5 mg / 0.15 mg / 80 – 240 mg Hypotension,
kg kg / hr Twice a day renal failure

N Engl J Med 1997; 336: 1429-34