3. Factors precipitate arrhythmias
May include:
• Ischemia, hypoxia, electrolytes disturbance,
excessive catecholamines exposure , drug
toxicity.
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4. Mechanisms of arrhythmias
1. Disturbances in impulse formation.
– Vagal stimulation or β- receptor blocking drugs slow
normal pacemaker .
– Acceleration of pacemaker by hypokalemia or β-
adrenoceptor stimulants.
– Development of ectopic pacemakers.
2. Disturbances in impulse conduction.
– May result from block ( nodal block or bundle branch
block).
– Reentry : circus movement in which one impulse reenters
and excites areas of the heart more than ones.
– Some forms of reentry are anatomical in shape as in Wolff-
Parkinson –White syndrome.
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8. Class 1 : Na+ channel blockers
• Local anaesthetic effect
• -ve inotropic action
– Class 1( A ): prolongs duration of action potential
& refractory period.
• Have K+ channel blocking effect
• Antimuscarinic & hypotensive effects.
– Class1(B):Shorten the duration of action potential
& refractory period.
– Class1(C) : No effect on the duration of action or
refractory period.
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13. • Lidocaine
Ventricular arrhythmia: 1-1.5 mg/kg IV bolus (2-3 min);
may repeat doses of 0.5-0.75 mg/kg in 5-10 minutes
up to a total of 3 mg/kg;
continuous infusion: 1-4 mg/minute.
Intratracheal: 2 to 2.5 times the recommended I.V. dose; dilute
in 10 ml NS/ distilled water.
Prevention of ventricular fibrillation: Initial bolus: 0.5
mg/kg; repeat every 5-10 minutes to a total dose of
2 mg/kg.
Refractory ventricular fibrillation: Repeat 1.5 mg/kg bolus
may be given 3-5 minutes after initial dose.
E.T. (loading dose only): 2 to 2.5 times IV dose
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17. Class 11 : β-adrenoceptor blockers
Effective in atrial & ventricular arrhythmias
associated with increase in sympathetic activity .
Reduce the incidence of sudden arrhythmic death
after myocardial infarction.
• Propranolol
• Metoprolol ( β1 selective)
• Esmolol
Very short acting used for intraop & acute
arrhythmias
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18. • Esmolol
Beta-1 Selective Blocker.
SVT or gradual control of postop tachycardia/hypertension:
500 mcg/kg IV loading dose over 1 minute, f/b 50
mcg/kg/minute over 4 minutes.
If ineffective, repeat load of 500 mcg/kg, followed by 100
mcg/kg/min.
If needed, may repeat process of loading dose plus increase
infusion by another 50 mcg/kg/min (up to max of 200
mcg/kg/min).
Titration interval: max q4 min.
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19. Esmolol contd..
Intraop tachycardia and/or hypertension
(immediate control):
Initial bolus: 80 mg IV (~1 mg/kg) over 30 seconds,
f/b 150 mcg/kg/minute infusion, if necessary.
Adjust infusion rate as needed to maintain desired
heart rate and/or blood pressure, up to 300
mcg/kg/minute.
For control of postoperative hypertension, as many
as one-third of patients may require higher doses
(250-300 mcg/kg/minute) to control bp.
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21. • Metoprolol
Post MI (early tx): 5 mg IV bolus x 3 doses q2 minutes.
In patients who tolerate full 15 mg dose, oral 50mg po
q6h should be started 15 min after last IV dose x 48
hours.
Unstable angina: 5 mg IV bolus x3 q2min f/b 2 to 5 mg
hourly titrated to min HR of 55 to 60 BPM or min
systolic BP of 80 . May switch to oral dosing (50 to
100mg po q6h) after IV bolus therapy.
Supraventricular tachycardias(PAT, A-fib/flutter): 5 to 15
mg (usually 5 mg) over 2.5 min at 7.5min intervals-
usually a high response rate.
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23. • Amiodarone
First Rapid: 150 mg over the FIRST - 10 minutes (15
mg/min).
3 ml of Cordarone I.V. (150 mg) to 100 ml D 5 W. Infuse 100 ml
over 10 minutes.
Followed by Slow: 360 mg over the NEXT 6 hours (1
mg/min).
18 ml of Cordarone I.V. (900 mg) to 500 ml D 5 W (conc = 1.8
mg/ml).
Maintenance infusion: 540 mg over 18 hours (0.5
mg/min).
After the first 24 hours, the maintenance infusion rate of
0.5 mg/min (720 mg/24 hours).
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24. Class1V : Ca++ channel blockers
• e.g. Verapamil, Diltiazem
• Their main site of action is A.V.N & S.A.N.
• Effective only in atrial arrhythmias
• Second drugs of choice for the treatment of
paroxysmal supraventricular tachycardia
• Not effective in Wolff Parkinson White
syndrome.
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26. • Verapamil
PSVT: 2.5 to 5 mg IV (2 min). May repeat dose of 5-
10mg 15-30 minutes after 1st dose. Alternative
initial choice in stable patients.
Decrease dose by 30-50% in hepatic insufficiency.
Adverse reactions: Severe hypotension;
bradycardia; ventricular standstill in digitalized
patients; asystole; respiratory failure.
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27. • Diltiazem
Direct Intravenous Single Injections: 0.25 mg/kg actual
body weight bolus (2 min).
If inadequate response, second dose administered after 15
minutes, 0.35 mg/kg actual body weight (2 min).
Continuous Intravenous Infusion: The recommended
initial infusion rate 10 mg/h. Some patients may
maintain response to an initial rate of 5 mg/h. The
infusion rate may be increased in 5 mg/h increments
up to 15 mg/h.
Maintained for up to 24 hours.
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28. Miscellaneous drugs.
• Adenosine
– Binds to specific G protein – coupled adenosine
receptors (A1&A2)opening K+ channel
hyperpolarization influx of calcium.
– Very rapid onset of action .
– Short half-life (seconds)
– Given as a rapid I.V. bolus injection for acute
termination of re-entrant supraventricular
tachycardia (paroxysmal attack).
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29. Adenosine contd..
PSVT: Initial 6 mg rapid bolus (1-2 seconds). If not
effective within 1-2 minutes, 12 mg may be given; may
repeat 12 mg bolus if needed;
maximum single dose: 12 mg. (Each I.V. Bolus followed with NS
flush).
Pharmacologic stress agent (Adenoscan®): Continuous
I.V. infusion: 140 mcg/kg/minute for 6 minutes using
syringe or columetric infusion pump (total dose: 0.84
mg/kg).
Thallium-201 is injected at midpoint (3 minutes) of infusion.
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30. – Adverse effects- Bronchospasm, Chest pain,
Shortness of breath, Flushing, A-V block,
Hypotension.
– Contraindications- Bronchial asthma, A-V block.
– Drug interactions-
Less effective with adenosine receptor blockers (Caffeine
or theophylline).
More effective with uptake inhibitors as dipyridamole.
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31. • Magnesium
Used in:
Digitalis induced arrhythmias
Torsade de pointes
Sinus tachycardia
Patients in cardiac arrest associated with torsades de
pointes- 1-2 g magnesium sulfate in 10 mL of 5%
dextrose solution (5-20 min).
Patients with torsades de pointes not in cardiac arrest-
1-2 g magnesium sulfate in 50 mL 5% dextrose
solution (60 min).
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32. • Digoxin
– Loading dose:
CHF: 8-12 mcg/kg in divided doses (q4-8h) over 12 to 24 hours. EKG 6 hours
after each dose to assess potential toxicity (AV block, sinus bradycardia, atrial
or nodal ectopic beats, ventricular arrhythmias); Other: vision changes,
confusion.
Renal insufficiency 6 to 10 mcg/kg IBW.
A-fib: 10 to 15 mcg/kg IBW given as above. (If given IVPush-admin over at
least 5 min).
PSVT: (For patients not on digoxin): 0.25 to 0.5 mg IV. May follow with 0.125
to 0.25 mg IV q2-6h until 0.75 to 1.5 mg is given over 24hrs. [Loading: 10 to
15 mcg/kg IBW in divided doses (q4-8h) over 12-24hrs.] Digoxin is considered
to be a 3rd line drug in stable patients who fail to respond to
adenosine/verapamil/esmolol. Not preferred drug for PSVT because it is not
rapidly effective (may take up to 60 minutes).
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33. Digoxin contd..
Maintenance dose: Digoxin clearance= [CRCL + 40] x 1.44 (add
20 instead of 40 if pt has CHF).
Predicted Css= (Dose) (0.65 to 0.8)/ Digoxin clearance.
Alternatively, maint dose= Loading dose x [0.14 x crcl / 500 ].
Monitoring: Obtain blood samples at least 4 hrs after IV dose and
6-8hrs after oral dose.
Serum levels: 0.5 to 2.0 ng/ml. Obtain first level within 24 hours of
digitalization. Monitor BUN and serum creatinine q2days (qd if
unstable). Monitor apical pulse daily.
Onset/peak: IV: 5-30min/ 1-4hrs Oral: 1-2hrs/ 2-8 hrs.
Time to steady state: 5-7 days (average) ESRD: 15-20 days.
Half-life: 38-48 hrs. (anephric: 4-6 days).
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34. Digoxin contd..
Factors that increase likelihood of digoxin toxicity:
Hypokalemia, hypomagnesaemia, hypothyroidism,
renal dysfunction, interacting drugs (eg quinidine,
verapamil).
Adverse reactions: sinus bradyarrhythmias; AV
block; N/V/D; yellow vision and hallucinations;
supra and ventricular arrhythmias.
Contraindications: V-fibrillation; hypokalemia;
WPW syndrome with wide complex.
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38. • Beck was the first physician to use DC
defibrillation on a human to treat ventricular
fibrillation on a 14-year-old during cardiac
surgery in 1947.
• Fifteen years later, Lown applied synchronized
DC shocks to the heart to convert atrial
fibrillation and ventricular tachycardia to
normal sinus rhythm
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39. Cardioversion
• DC electrical discharge is synchronized with the R
or S wave of the QRS complex.
• Synchronization in the early part of the QRS
complex avoids energy delivery near the apex of
the T wave in the surface ECG, which coincides
with a vulnerable period for induction of
ventricular fibrillation.
• The peak of the T wave represents the terminal
portion of the refractory state when adjacent
heart fibers are in differing states of
repolarization.
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40. Basic principles
• Transient delivery of electrical current causes a
momentary depolarization of most cardiac cells
allowing the sinus node to resume normal
pacemaker activity.
• In the presence of reentrant-induced arrhythmia,
such as paroxysmal supraventricular tachycardia
(PSVT) and ventricular tachycardia (VT), electrical
cardioversion interrupts the self-perpetuating
circuit and restores a sinus rhythm.
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41. External cardioversion
– narrow or wide QRS complex tachycardia (ventricular rate
>150) who is unstable (eg, chest pain, pulmonary edema,
lightheadedness, hypotension) should be immediately
treated with synchronized electrical cardioversion.
– Synchronized electrical cardioversion may also be used to
treat stable VT that does not respond to a trial of iv
medications.
– It is also recommended for the treatment of the following:
• Supraventricular tachycardia due to reentry
• Atrial fibrillation
• Atrial flutter
• Atrial tachycardia
• Monomorphic VT with pulses
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42. Internal cardioversion
– Internal cardioversion for atrial fibrillation is used
in patients who are resistant to external
cardioversion or inadvertently induced during an
electrophysiologic study. Cardioversion should
occur before placement of an atrial defibrillator.
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43. • Contraindications
– digitalis toxicity–associated tachycardia.
– sinus tachycardia caused by various clinical
conditions.
– multifocal atrial tachycardia.
– patients who are not anticoagulated should not
undergo cardioversion without a transesophageal
echo to r/o left atrial thrombus.
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44. • Complications
– Most anaesthetic complications following elective
cardioversion are related to cardiovascular depression.
– Moderate or deep sedation aspiration pneumonia.
– Other fast or slow arrhythmias.
– Ventricular fibrillation, death due to synchronisation
failure of a defibrillator, elevation of cardiac enzyme
levels(although this is mainly from skeletal muscle
damage), rhabdomyolysis and renal failure, systemic
embolisation and severe bradycardia.
– It is advisable to remove the oxygen source from patient
prior to cardioversion or defibrillation as there have been
reports of burns.
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46. Procedure
• ACLS guidelines should be followed as
indicated.
• The key components- intravenous access,
airway management equipment, sedative
drugs, and a cardioverter/defibrillator
monitoring device.
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48. • Sedation- short-acting agent such as
midazolam or propofol.
• In addition, an opioid such as fentanyl.
• Reversal agents, such as flumazenil and
naloxone, should be available.
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50. • The defibrillator should be placed in the
synchronized mode, which permits a search
for a large R or S wave.
• The delivered energy selected. Most
monophasic and biphasic models can deliver
up to 360 Joules.
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51. • Two options exist for placement of paddles on the
chest wall.
1. Anterolateral- single paddle is placed on the left fourth
or fifth intercostal space on the midaxillary line; the
other paddle is placed just to the right of the sternal
edge on the second or third intercostal space.
2. Anteroposterior- single paddle is placed to the right of
the sternum, and the other paddle is placed between the
tip of the left scapula and the spine.
• Since the skin can conduct away a significant portion of
the current, conductive gel or pre-gelled pads are used
to ensure good contact. Under ideal circumstances, 10-
30% of total current reaches the heart.
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53. • The paddles should be placed firmly against
the chest wall to avoid arcing and skin burns.
• Pacemakers and ICDs should be at least 10 cm
from direct contact with paddles and be
interrogated for any malfunction after
cardioversion.
– The anteroposterior approach is preferred in
patients with implantable devices to avoid
shunting current to the implantable device and
damaging the system.
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54. PM/ICD checklist in case of
cardioversion.
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55. • Energy requirements for atrial fibrillation are 100-200 J initially and
360 J for subsequent shocks.
• Biphasic shocks require a typical energy level of 75 J for correction
of atrial fibrillation.
• Atrial flutter and PSVT require less energy: 50 J initially, then 100 J if
needed.
• Cardioversion of VT involves shocks of 50-100 J initially, then 200 J if
unsuccessful.
• Pediatric patients with PSVT or VT who are not hemodynamically
stable, an initial synchronized shock of 0.5 J/kg is recommended. In
subsequent attempts, the energy is increased.
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56. Internal cardioversion
• Three temporary catheters are inserted in the venous system and
positioned under fluoroscopic guidance.
• Two catheters of large surface area are used for shock delivery;
• Third quadripolar catheter is used for R-wave synchronization &
temporary ventricular postshock pacing.
• The first defibrillation catheter is advanced into the distal coronary
sinus; the second is positioned in the right atrium appendix/ lateral
wall of the right atrium. These catheters are connected to an
external defibrillator that delivers biphasic shocks.
• The quadripolar catheter is placed in the apex of the right ventricle
and is also connected to an external pacemaker.
• A right atrium-to-coronary sinus cardioversion vector was
successfully used with mean of energy of 5.6 +/- 4.7 J (0.4-35) in
one study.
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