PERIOPERATIVE CARDIAC

ARRHYTHMIAS
Prof. Vithal Dhulkhed

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 Miles Vaughan Williams
centenary -2018

• Pioneering work on
beta-blockers, which
have saved countless
lives since.
• His index of anti-
arrhythmic drugs –
established in 1970 –
is still used today British cardiac pharmacologist and academic
He was born in Bangalore, India

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 Incidence
 Cardiac arrhythmias are a signifcant cause of morbidity
and mortality in the periop period.*
 Growing knowledge of molecular targets provides
options for therapy advances*
 In general anesthesia, dysrhythmias were observed in
70.2%, of which only 1.6% required treatment 2. the
incidence of atrial fibrillation (AF) varies from low to 12%
to 33% ***.

*Thompson et al , Journal of Anaesthesia 93 (1): 86-94 (2004) *

*Atlee JL - Anesthesiology, 1997;86:1397-424
***Amar D .Curr Opin Anaesthesiol, 2007;20:43-47

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• Ventricular arrhythmias affect about 10%,
most are simple. Malignant ventricular
arrhythmias (fibrillation or tachycardia) occurr
in 3%.*
• Stress response and inflammatory response
sepsis specially in lower resp tract, M Isch,
pulm edema, electrolyte imbalance,might be
the causes in first 4 days post op **

•*Batra et al Ann R Coll Surg Engl 2001; 83: 174–6.

•*Walsh et al. Colorect Dis 2006: 8: 212–216.
•**Bruins et al Circulation 1997; 96: 3542–8.
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 Mortality 20–50% with new onset arrhythmias.
 The arrhythmia itself is rarely the cause of
death. Instead, most patients died from another
underlying complication thought to have
triggered the arrhythmia.

Ann R Coll Surg Engl 2007; 89: 91–95

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 New-onset arrhythmias
following major non-cardiothoracic surgery

Rates of arrhythmias in prospective cohort series

Series (first author) T

Totals

Polanczyk Goldman Brathwaite Batra Valentine Bender Walsh

Total patients 4181 916 462 226 211 206 51 6253

Atrial fibrillation 276
171 17 31 20 21 9 7
(4.41%)
Atrial flutter 59
51 5 0 0 3 0
(0.94%)
Paroxysmal atrial
tachycardia 14 4 0 1 0 0 19 (0.3%)
Multifocal atrial
tachycardia 10 3 1 7 0 0 21 (0.4%)
PSVT 156 6 15 0 16 4 197 (3%)
Ventricular ectopics – – 18 – 1 19 (0.3%)
Ventricular tachycardia – – 7 – 1 8 (0.13%)
Ventricular fibrillation – – 1 – 0 1 (0.02%)
Any dysrhythmia 490
317 35 47 29 21 28 13
(7.84%)

Walsh et al.Ann R Coll Surg Engl 2007; 89: 91–95

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 Risk factors for arrhythmias in the perioperative period

Acute anaesthetic factors Acute surgical factors

Anaesthesia-induced cardiac Pain
Depression, certain drugs , inhalational Trauma
anesthetics, Anemia
S.choline, dropoeridol, powerful Local and systemic inflammation
antiemetics (elevated
Inotropes, digoxin, antiarrhythmics IL-6 and CRP)
( refer to literature) Mediastinal manipulation
Hypervolaemia acute atrial stretch open cardiac surgery, valvular
Auto-PEEP surgery, thoracotomy, or other
Shock Use of drugs like vasopressors intrathoracic surgery.
Pulmonary artery catheter/misplaced
central line
Local anaesthetic toxicity

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Ferreira .http://pier.acponline.org/physicians/diseases/periopr877/periopr877.html
 Chronic medical factors
Acute medical factors Ageing (fibrosis and inflammation)
Hypoxia ASA Class III or IV
Hypovolaemia Atrial distension HF, valvular disease
Electrolyte disturbances IHD H/O arrhythmia
Acute myocardial infarction Chronic hypoxia, e.g. COPD, OSA
Metabolic/respiratory acidosis Hypertension obesity asthma
Pneumonia Persistent tachycardia-induced atrial
Sepsis remodeling
Pulmonary embolism Accessory pathways
Hypoglycemia/hyperglycemia Congenital heart disease
Hypothermia/hyperthermia Scarring post-cardiac surgery
Myocarditis/pericarditis Pulmonary hypertension
Pneumothorax Hyper/hypothyroidism
Malignancy,history of SVA

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 Anesthetic agents Surgery types
(volatile or (ocular - cranial interventions,
intravenous agents, peritoneal traction)
neuromuscular Comorbidities (cardiac,
blockers, opioids) endocrine, others)
Local anesthetics Laryngoscopy, intubation,
Hypotermia other irritating factors
Anesthesia depth Alternative drugs
(adrenaline…)
Artifact

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 Congenital Heart Disease
 JET and SVT were the most common postoperative
arrhythmias.
 Lower age, lower body weight, higher Aristotle Basic
Score, longer CPB time, longer crossclamp time, and
 Use of DHCA are risk factors for postoperative
arrhythmias.

J Thorac Cardiovasc Surg 2007;133:900-4

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Arrhythmia in the preoperative setting should
prompt investigation into underlying
cardiopulmonary disease, ongoing myocardial
ischemia or MI, drug toxicity, or metabolic
derangements, depending on the nature and
acuity of the arrhythmia and the patient’s
history

AHA guidelines 2014

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 Case Scenario
A 62-y-old man H/O CAD & cardiomyopathy, LVEF - 40%,
moderate AS, scheduled for hip arthroplasty.
 Large-bore IV access, radial artery invasive BP
After induction and intubation, HR 110 ,BP to 207/110 .
 Stabilized with Labetalol 30 mg IV. Then BP drops to 70/41 responds to
volume boluses,   ephedrine,  phenylephrine.
Again tachycardia and BP 200/115
5-lead ECG shows ST-T elevation in leads I-aVL-V5.
labetalol 10 mg IV is given,
 ECG shows wide, polymorphic QRS complexes at 140/min,
BP falls to 0, EtCO2 to 12 mm Hg.

Horvath et al https://emedicine.medscape.com/article/2500081-overview
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CPR instituted. 200-J
asynchronous biphasic shock
 VF noticed, Epinephrine  1 mg IV , 200 J
shock , CPR continued,
ABG - mixed met and resp acidosis ,BE –8,
3rd shock, epinephrine, amio 300 mg IV,
Result- sinus rhythm
with ST elevation
Now BP -100/62, and HR 92. The
incision was closed
The patient transferred to the cath lab, where a
90% stenosis of LAD detected A stent was
placed,
The patient recovered with no neurologic
complications.

AHA Guidelines Update for CPR and Emergency Cardiovascular Care. Circulation. 2015 Nov 3. 132 (18 Suppl 2):S444-6

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 Basic science
Cardiac ion channels Na K Ca and adrenergic
receptors are the drug targets*

Virtually all drugs that modulate the heart

rhythm work through the adrenergic
receptor/second-messenger systems,through
one or more of the ion channel classes

*Priori et al Circulation 1999; 99: 518±28

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 A critical feature of arrhythmia management
 Cardiac action potential has 5 phases the current responsible for impulse initiation
in the atria and ventricles differs from that of the SA and AV nodes.

Drugs targetting Phase 0

Atria / Ventricle AV node / SA node
INa ch suppression ICaL ch suppression PR prolonged
Prolong QRS and P No action on ventricles
Phase 1,2,3
Maintained by ICA-in terminated by IK-out
Class 2 and 4 drugs target ICA-in APD and QT
-ve inotropic, therapeutic or arrhythmogenic
Phase 4
Here spontaneous depolarization
Adenosine acts on it’s A1 receptor
Here adenosine has no action Increases IK-out causes
hyperpolarisation; reduced pacing
Inhibits Ica-in by reducing cAMP

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 HCN
NCX

05/27/2020 HCN Hyper polarisation activated cyclic neucleotide gated INaf channels 19
NCX- involve spon release of Ca from SR
EXCITATION CONTRACTION COUPLING

Structures
participating in ECC

1. Sarcolemma

2. Transverse Tubules

3. Sarcoplasmic
Reticulum

4. Microfilaments

SERCA (sarcoendoplasmic
reticulum calcium ATPase)
Vaughan Williams scheme

Receptor Class2 Drugs

Na+, K+ channels IA Procainamide, quinidine, amiodarone

Na+ channels IB Lidocaine, phenytoin, *mexiletine, *tocainide
Beta adrenoceptors II Esmolol, amiodarone, propranolol, atenolol,
*sotalol
K+ channels III Bretylium, ibutilide, *sotalol, *dofetilide
Ca2+ channels IV Verapamil, diltiazem, amiodarone

Problems in Anaesthesia. Lippincott-Raven, Philadelphia, 1998; Vol 10(2): 199The American Heart
Association Guidelines 2000 f Circulation 2000; 102: I158±65

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Drugs class II, IV reduce inward Ca2+ current,
abbreviate AP plateau, shorten the QT;
clinical potential to act as negative inotropes.

Agents with class IA or III activity block

outward K+ current, prolonging AP and the QT
This has therapeutic or arrhythmogenic
effect
AP -action potential
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During phase 4 Nodal cells spontaneously
depolarize (`pace'), and activation of the
adenosine A1 receptor triggers IK out that
hyperpolarize the nodal cell and oppose pacing.

Adenosine also slows nodal conduction by

inhibiting ICa in through reducing cyclic AMP.

Belardinelli et al Am J Physiol 1983; 244: H737±47

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 The response of common SVT to i.v. adenosine

SVT Mechanism Adenosine response

AV nodal re-entry Re-entry within AV node Termination
AV reciprocating tachycardias Re-entry involving AV node and Termination
accessory pathway (WPW)
(orthodromic and antidromic)
Intra-atrial re-entry Re-entry in the atrium Transiently slows
ventricular response
Atrial ¯utter/®brillation Re-entry in the atrium Transiently slows
ventricular response
Other atrial tachycardias 1 Abnormal automaticity 1 Transient suppression
2 cAMP-mediated triggered of tachycardia
activity 2 Termination

Adapted from Balser JR. Perioperative management of arrhythmias. In: Barash PG, Fleisher LA, Prough DS, eds. Problems in Anaesthesia.
Lippincott-Raven,Philadelphia, 1998; Vol 10(2): 201)
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 Re-entry, automaticity and arrhythmias
 Reentry : anatomic – WPW ; functional- disparities
in repolarisation or conductance in normal and
ischemic areas or refractory period differences in
epi and endocardial layers

 Automaticity: due to abnormal depolarisation

during phase 2,3,4.
IK-out ch blockers Class 1a and ,3 are
effecive, more successful in fibrillation. May
provoke Ventricular arrhymias in 2-10%
 If Serum K is low TdP may be induced
 Acquired (druge ffect) or congenital (Ch mutations)
long QT syndrome
 Silent mutation may be unmasked

Lukas et al.Circulation 1993; 88: 2903±15

05/27/2020 Mason JW et al N Engl J Med 1993; 329: 452±8 Roden et al Clin Electrophysiol 25
1998; 21:1029
NORMAL CARDIAC CONDUCTION SYSTEM
 Supraventricular arrhythmias

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 Management Plan
• The management of arrhythmias will involve
initially recognising a problem, diagnosing an
arrhythmia and assessing its physiological
effect on the patient.
• The ALS protocol has algorithms for the
treatment of bradycardia (heart rate < 40 bpm)
and tachycardia (heart rate > 150 bpm). If the
patient does not have a pulse, the arrest
protocol should be followed
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 Supraventricular arrhythmias
• Adverse physiological phenomena can precipitate SVT
• Rapid assessment of aetiologies and correctable
causes except in emergency
• Narrow Complex Tachycardia -Extreme hemodynamic
instability- cardioversion
• Response may be transient .Brief period of sinus
rhythm buys time for proper evaluation treatment
• Less urgent –adenosine 6-12
• Usually AV node not involved in periop situation

*Thompson et al.Journal of Anaesthesia 93 (1): 86-94 (2004)

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• In underlying structural heart disease during
induction, arrhytmias secondary to
hypotension,autonomic imbalance, airway
stimulation .*
• During cardiac surgery various manipulations
precipitate SVT. In critical CAD , AV stenosis,
CPB has to be ready .
• If refractory institute CPB to avoid M Isch

*Waldo et al. Med Clin North Am 1984; 68: 1153±70

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 • Ventricular rate control is the mainstay of therapy
for SVT requiring immediate cardioversion.
• Drugs: AV blockers in Class II ; esmolol easily
treatable, avoid in severe LV dysfunction,
• CCB ,Verapamil and diltiazam may be used latter is
better.*
• With CCF digitalis ( slow action), diltiazem ,
amiodarone recommended for SVT.**

*Walsh rt al. J Am Coll Cardiol 1984; 3: 1044±50

The American Heart Association : the tachycardia algorithms. Circulation 2000; 102: I158±65
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 • In WPW syndrome avoid AVB,Adenosine,Beta
blocker,CCB,Digitalis use procainamide may be
flecanide or amiodarone consult cardiology*
• For intraoperative patients who are stable and
rate controlled in SVT, the wisdom of chemical
cardioversion is questionable.**Spontneous
remission rate is quite high in emergence or in
upto 24 hours
• K ch blockers most efficaceous. QT can be
prolonged
*The American Heart Association the tachycardia algorithms. Circulation 2000; 102: I158±65
**Galve E er al, J Am Coll Cardiol 1996; 27:1079±82
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 • In stable SVT with DC cardioversion risk of VF,
asystole and stroke can be there
• when elective DC cardioversion is considered, it
may be prudent to first establish a therapeutic level
of an antiarrhythmic agent that maintains sinus
rhythm (i.e. procainamide, amiodarone) in order to
minimize the risk of SVT recurrence.

*Thompson et al. British Journal of Anaesthesia 93 (1): 86-94 (2004)

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 Atrial fibrillation

• Rate control strategy to be used as discussed

earlier.
• in post operative period risk of
thromboembolism in persists for more than
48 hours.
• Risk has to be stratified according to CHADS 2
score if appropriate anticoagulation therapy as
soon as it is safe to administer.
Man et al.Heart 2007;93:45-7
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 Ventricular arrhythmias

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 Premature ventricular contraction

ventricular tachycardia

ventricular fibrillation

Torsade de pointes

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 Ventricular arrhythmias
• Ventricular arrhythmias can be subdivided
according to
• morphology - monomorphic vs polymorphic
• duration -sustained vs non-sustained (NSVT).
• NSVT: 3 or more PVC > 100 beats /min for
30 s or less without haemodynamic
compromise. Occur in absence of cardiac
disease. May not require therapy

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 • In structural heart disease predict life
threatening arrhythmias .*
• Prefer amiodarone .Antiarrhytmics except
amiodarone worsen survival**
• If good ventricular function do not require
therapy. They signal reversible causes which
are to be treated.
• Post cardiac surgery 2% develop sustained VT

*Kuchar et al.J Am Coll Cardiol 1987; 9: 531-8

**Singh et al N Engl J Med 1995; 333: 77±82

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 • low CO post CABG (requiring pressor support) -an independent predictor
of life-threatening VT/VF within 72 h post op.*
• Graft dysfunction can be a cause.
• 50% incidence after AVR**
• Recurrent NSVT may affect IABP,pacemaker function suppress with
lignocaine orbeta blockade
• Beta blockade or lignocaine Mg 2g ( as a routine) beneficial ***
• EP guided prophylactic ICD placement has survival benefit with low EF
before elective cardiac surgery

*Topol et al Am J Cardiol 1986; 57: 57-9

**Michel et al Acta Cardiol 1992; 47: 145±56

***Thompson et al Br Journal of Anaesthesia 93 (1): 86-94 (2004)

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 Sustained VT
• Monomorphic:formation of a re-entrant
pathway around scar tissue in myocardium
• Procainamide or amiodarone more effective
than lignocaine *

*The American Heart Association, the tachycardia algorithms. Circulation 2000; 102: I158-65

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 polymorphic VT
• If QT normal, VT can occur in M Isch,
structural ht disease, or idiopathic. VF may
precipitate.
• If QT is prolonged focus on its reversal.( TDP)
• It may be inherited
• Usually antiarrhytmics (IA,III) or many other
drugs can cause this.

(www.Torsades.org/druglist.cfm)
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 torsades de pointes
• Management
• i.v. magnesium sulfate (2-4 g), repleting
potassium, and manoeuvres aimed at
increasing HR (atropine, isoprenolol or
temporary atrial or ventricular pacing).
Haemodynamic collapse - asynchronous DC
shocks.

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From: Nicorandil Successfully Abolished Intraoperative Torsade de Pointes 
Anesthes. 1998;88(6):1669-1671.

Preinduction of anesthesia (QT, 0.44 s; QTc, 0.50 s

PVC, prolonged QT (QT, 0.50 s; QTc, 0.57 s).

Torsade de pointes (TdP) terminated spontaneously after

nicorandil (4 mg/h) (QT, 0.54 s; QTc, 0.60 s).
.

• Intraoperative TdP in 70 yr lady with ataxia for cerbello pontine angle

tumor isoflurane discontinued,did not respond to lidocaine, Mg.
Hemodynamically stable.Nicorandil terminated She had long QTc.0.69s
Preop QTc was normal
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Date of download: 11/1/2018 Copyright © 2018 American Society of Anesthesiologists. All rights reserved.
 • When antiarrhythmic therapy is deemed
necessary, prefer lidocaine or
phenytoin,devoid of K+-channel blocking
properties and no effect On QT.*
• In unclear situation empirical Mg or lignocaine
• If refractory try amiodarone having minimal
effect on QT
• Avoid more than one antiarrhytmics

*Priori SG et al in Cardiac Arrhythmia: Mechanisms, Diagnosis, and Management. Baltimore:

Williams and Wilkins, 1995; 951±63
05/27/2020 48
 Drug for acute management of unstable VT
and VF
• Rapid defibrillation and correction of reversible
aetiologies
• Amiodarone is useful. amiodarone has non-
competitive alpha- and beta-blocking effects, so
that rapid i.v. loading may exacerbate
haemodynamic instability in severe LV
dysfunction,Consider pressors and IABP .
Slowing the rate of infusion

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Installe et al J Thorac Cardiovasc Surg 1981; 81: 302±8
 Droperidol black box warning
• Issued by the US FDA in Decembe
• Cases of QT prolongation and/or torsade de
pointes have been reported in patients receiving
INAPSINE at doses at or below recommended
doses. Some cases have occurred in patients with
no known risk factors for QT prolongation and
some cases have been fatal.

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 Risk for development of prolonged QT
syndrome-examples
• congestive heart failure, bradycardia, use of
antidiuretic, cardiac hypertrophy, hypokalemia,
hypomagnesemia, or administration of other
drugs known to increase the QT interval
• Other risk factors may include
• age over 65 years, alcohol abuse, and use of
agents such as benzodiazepines, volatile
anaesthetics, and i.v. opiates

prolonged QT interval (i.e., QTc greater than 440 msec for males or 450 msec for females)
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 Newer antiarrhythmics
• Vernakalant atrial specific K channels Ikur,IK- ACh)
blocker has minimal effects on the ventricles and is
being studied for the management of atrial fibrillation
• For ranolazine is ventricle specific ,a late INa inhibitor.
• Currently under investigation.
Drugs targetting late INa channels,the ryanodine
receptors, the NCX ch, cardiac-specific KATP channels
activated by ATP depletion during ischemia.
•  

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 I.V. pacemakers and implantable
cardioverter de®brillators

• ICD insertion is a class IIa indication for patients with EF <30%

for whom it is at least 1 month since MI and 3 months since CA
revascularization*
• Electromagnetic interference (EMI) from electrocautery or
cardioversion inhibits output, activation of rate responsive
sensor-increase in HR
• Injury of myocardium at Lead tip and failure to sense **

*(ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines).

Circulation 2002; 106: 2145±61
**ACC/AHA
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Guideline Update . Anesth Analg 2002; 94: 1052±64 53
 Interventions to Decrease Risk
• Administer β-blocking before cardiac surgery and prophylactic amiodarone in
select patients.
• Add statins preoperatively
• preoperative discontinuation of long-term oral anticoagulation therapy
• Be alert for reflex vagal stimulation
• ICD device-consult cardiology
• A transvenous pacemaker in special situation
• During open cardiac procedures, minimize mechanical and procedural risks for
arrhythmias, and place temporary epicardial pacing wires.
• Consider atrial overdrive pacing at risk of A Fib.
• Continue telemetry monitoring for at least 2- 4 days in high risk patients
• Use positive inotropic drugs judiciously
• Inform patients about the effectiveness of preoperative arrhythmia prophylaxis
• Educate patients postoperatively

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• Patients with a preoperative history of AF who
are clinically stable generally do not require
modification of medical management or
special evaluation in the perioperative period,
other than adjustment of anticoagulation
(Section 6.2.7).
• AHA guidelines 2014

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 Occult Wolff-Parkinson-White syndrome
• A young man presented with a rapid,
narrow-complex atrial fibrillation.
• IV metoprolol and diltiazem for rate
control
• He developed intermittent ventricular
preexcitation on ECG and experienced
Vfib, -successfully defibrillated
• A subsequent ECG in sinus rhythm
revealed WPW pattern. A left lateral
accessory pathway was successfully
ablated.

Pacing Clin Electrophysiol. 2008 Jun;31(6):776-9

Sinus Tachycardia due to hyperthyroidism

• A 26 y female for laminectomy and excision of spinal

tumor hyperthyroid, irregular treatment
• Although advised did not take morning dose of
carbimazole as well as propranolol
• After induction developed tachycardia,Incr BP
• There was no effective response to deepening
anaesthesia and metaprolol
• Carbimazol through RT 40 min later HR settled to 80-
90
 Multifocal Atrial Tachycardia (MAT)
• 82y F, diabetes, HTN left
hip hemiarthroplasty,
• On Aminophylline
• After SA BP 80/60
• IV ephedrine
• ECG-MAT , IV infusion of
phenylephrine and procainamide
was given
• Conversion of MAT to sinus rhythm
was successfully achieved.
• Ephedrine can amplify the action
of aminophylline HR>100, at least 3 distinct P waves, irregular P-
P intervals-isoelectric baseline between Ps)

Korean J Anesthesiol 2010 December 59(Suppl): S77-S81

 SVT and Propofol

• A 68-yr-old man 80 kg presented to the ED with a 4 h history-

chest pain, and palpitations. H/O MI on oral enalapril 20 mg
daily for hypertension.
• HR 160 suggesting SVT-Adenosine 6mg IV- result-transient
AFL ,no effect with carotid sinus massage.
• Cardioversion planned, Selick’s, propofol 100 rhythm reverted
to Sinus
• Thrombolysed ,streptokinase
British Journal of Anaesthesia 88 (6): 874±5 (2002)
 AF with concealed Sick Sinus Syndrome
• 83-y-F height: 168 cm, weight: 56 kg
• For second transurethral resection
of a bladder tumor , HTN diabetes
on Amlo and , Candelotan( ARB) for
high blood pressure. H/O stroke
ECG Afib with Ventricular Rate 59
• Echo LVH and LAE
• After Induction HR 27 no effective
response to ephedrine Ext Pacing
.Cardiology consult.permanent
pacemaker inserted

Korean Journal of Anesthesiology VOL. 68, NO. 4, August 2015

 Atrioventricular Nodal Reentrant
Tachycardia in Transplanted Heart
• 18-year-old male 10 years
after heart transplantation,
palpitations (170) without
syncope.
• right carotid sinus massage,
terminated to sinus rhythm
• electrophysiology study
where AVNRT was induced
and successful
radiofrequency catheter
ablation
retrograde P´ waves
Gonsorcik et al., J Clin Exp Cardiolog 2016, 7:7
 A case of Atrial Fibrillation
• 81-y -lady with a 30 y H/O
permanent AF, DM and diverticular
- sudden onset palpitations
• On warfarin for AF, bisoprolol,
metformin.
• Echo RA 5.5 cm LVEF of 50%.
fast AF with a vent rate of approximately 138/min.

• Monitored on telemetry. AF strict rate control with

bisoprolol and digoxin which reduced her ventricular rate
to between 80 - 110 for the next 48 h. subtherapeutic INR
treated by increased warfarin with LMWH.
•  Underwent laparotomy

Alexander Liu, and Edward Nicol BMJ Case Reports

2011;2011:bcr.10.2011.4982
From: Successful Resuscitation from Prolonged Ventricular Fibrillation Using a Portable Percutaneous Cardiopulmonary
Support System Anesthes. 2003;99(5):1227-1229.

the portable cardiopulmonary support system..

• 58-yr M-pt, 82-kg, rt shoulder surgery.
• H/O CABG, angina at exertion /rest on NTG , ACEI,
RBBB- LAHB old AW MI
• Bracheal block with Bupivacaine and mepivacine
• He had seizure treated by propofol then later
Pulseless VT and asystole - ACLS protocol started
• Bolus 20% intralipid then infusion- shock
-adrenaline 15 sec later heart rhythm noted
• Angio revealed block of RCA pt inserted AICD

Rosenblatt et al.   Anesthesiology 2006; 105: 217–8

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