1932, Dr. Albert Hyman designed the first artificial pacemaker, though it was not widely used. In 1950, Canadian engineer John Hopps developed a portable pacemaker using vacuum tubes. In 1958, Dr. Åke Senning and engineer Rune Elmqvist implanted the first fully functional pacemaker in a patient in Sweden. Advancements (1960s-1990s) Lithium-ion batteries replaced older mercury-zinc batteries, increasing longevity. The first demand pacemakers, which only activate when needed 1932, Dr. Albert Hyman designed the first artificial pacemaker, though it was not widely used. In 1950, Canadian engineer John Hopps developed a portable pacemaker using vacuum tubes. In 1958, Dr. Åke Senning and engineer Rune Elmqvist implanted the first fully functional pacemaker in a patient in Sweden. Advancements (1960s-1990s) Lithium-ion batteries replaced older mercury-zinc batteries, increasing longevity. The first demand pacemakers, which only activate when needed 1932, Dr. Albert Hyman designed the first artificial pacemaker, though it was not widely used. In 1950, Canadian engineer John Hopps developed a portable pacemaker using vacuum tubes. In 1958, Dr. Åke Senning and engineer Rune Elmqvist implanted the first fully functional pacemaker in a patient in Sweden. Advancements (1960s-1990s) Lithium-ion batteries replaced older mercury-zinc batteries, increasing longevity. The first demand pacemakers, which only activate when needed 1932, Dr. Albert Hyman designed the first artificial pacemaker, though it was not widely used. In 1950, Canadian engineer John Hopps developed a portable pacemaker using vacuum tubes. In 1958, Dr. Åke Senning and engineer Rune Elmqvist implanted the first fully functional pacemaker in a patient in Sweden. Advancements (1960s-1990s) Lithium-ion batteries replaced older mercury-zinc batteries, increasing longevity. The first demand pacemakers, which only activate when needed 1932, Dr. Albert Hyman designed the first artificial pacemaker, though it was not widely used. In 1950, Canadian engineer John Hopps developed a portable pacemaker using vacuum tubes. In 1958, Dr. Åke Senning and engineer Rune Elmqvist implanted the first fully functional pacemaker in a patient in Sweden. Advancements (1960s-1990s) Lithium-ion batteries replaced older mercury-zinc batteries, increasing longevity. The first demand pacemakers, which only activate when needed 1932, Dr. Albert Hyman designed the first artificial pacemaker, though it was not widely used. In 1950, Canadian engineer John Hopps developed a portable pacemaker using vacuum tubes. In 1958, Dr. Åke Senning and engineer Rune Elmqvist implanted the first fully functional pacemaker in a patient in Sweden. Advancements (1960s-1990s) Lithium-ion batteries replaced older mercury-zinc batteries, increasing longevity. The first demand pacemakers, which only activate when needed 1932, Dr. Albert Hyman designed the first artificial pacemaker, though it was not widely used. In 1950, Canadian e

1. PACEMAKER AND ANAESTHESIA
CHAIRPERSON – Dr HV AIRANI
MODERATOR - Dr DHARANISH
PRESENTER - Dr VANDHANA S

2. SLIDE TITLE
• Cardiac implanted electronic devices (CIEDs) are implanted
cardiac rhythm management devices.
• They are used to treat problems with rhythm and heart failure.
• Treat near fatal conditions (such as extreme bradycardia,
‑
ventricular fibrillation and pulseless ventricular tachycardia).

4. TYPES OF CIED’S
• Pacemakers - problem with conduction system
Temporary and permanent
• Implantable Cardioverter defibrillators - Treatment of
life threatening arrhythmias
‑
• Cardiac resynchronization therapy devices – Treating heart
failure
• two types
CRT pacers
CRT defibrillators

5. Temporary pacing
• Transcutaneous pacing via multifunction pads attached to
Defibrillator machines set on Pacer Mode.
• Transvenous pacing via a pacing wire that is inserted thru an
introducer in a central large vein into the right ventricle, then
attached to a pacer box (pulse generator box) via a pacing
cable.
• Epicardial pacing (post cardiac surgery) via epicardial pacing
wires inserted into the endocardium during cardiac surgery that
are attached to a pacer box (pulse generator box) via a
pacing cable.

6. Indications of permanent pacemaker lmplantation
1) Acquired AV block:
A) Third degree AV block
• Bradycardia with symptoms
• After drug treatment that cause symptomatic bradycardia
• Postoperative AV block not expected to resolve
• Neuromuscular disease with AV block
• Escape rhythm <40 bpm or asystole > 3s
B) Second degree AV block
• Permanent or intermittent symptomatic bradycardia

7. 2) After Myocardial infarction:
• Persistent second degree or third degree block
• Infranodal AV block with LBBB
• Symptomatic second or third degree block
3) Bifascicular or Trifascicular block:
• Intermittent complete heart block with symptoms
• Type II second degree AV block
• Alternating bundle branch block

8. 4) Sinus node dysfunction:
• Sinus node dysfunction with symptoms as a result of long term
drug therapy
• Symptomatic chronotropic incompetence
5) Hypertensive carotid sinus and neurocardiac syndromes:
• Recurrent syncope associated with carotid sinus stimulation
• Asystole of >3s duration in absence of any medication

9. History of Pacemaker
• 1932 -Albert Hyman -Concept of artificial pacemaker, magneto-
generator to power up electrode.
• 1950 -John Hopps -1st transcutaneous pacemaker. Vaccum
tube technology and direct AC power supply is used.
• 1958 Earl Bakken 1st wearable transistorized pacemaker.
• 1958, 8th
October- Ake Senning, Dr. Rune Elmquist
1st implanted (trans-venous) pacemaker.
• 1959 W.M. Chardack, Wilson Greatbatch
1st successful long term implantable pacemaker.
• 1970 Introduction of Li-Iodide battery technology.
• 1980 Introduction of rate responsive pacing.

10. EVOLUTION OF PACEMAKERS

11. • Arne Larsson (1915–2001) became the first to receive an
implantable pacemaker (1958).
• He had a total of 26 devices during his life

12. Important Definitions
• Pulse Generator - It includes the energy source (battery) and
electric circuits for pacing and sensory function.
Mercury–Zinc batteries that were used in the early days had a
short useful life (2-3 yrs).
• Currently Lithium-iodine batteries are being used which have
longer shelf life (5-10 yrs) and high energy density.

13. • Leads - These are insulated wires connecting the pulse
generator.
• Electrode - It is an exposed metal end of the lead in contact
with the endocardium or epicardium.

14. TYPES OF PACING
• Unipolar Pacing - There is one
electrode, the cathode (negative
pole) or active lead.
• Current flows from the cathode,
stimulates the heart and returns
to anode (positive pole) on the
casing of pulse generator via the
myocardium and adjacent tissue
to complete the circuit.
• Unipolar sensing is more likely
to pick up extracardiac signals
and myopotentials.

15. • Bipolar Leads - They consist
of two separate electrodes,
anode
(positive pole) and cathode
(negative pole), both located
within the chamber that is
being paced.
• As the electrodes are very
close, the possibility of
extraneous noise disturbance
is less and the signals are
sharp.

17. Endocardial Pacing
• It is also called as transvenous pacing which implies that the
leads/ electrodes system has been passed through a vein to
the right atrium or right ventricle.
• It can be unipolar or bipolar.

18. Epicardial Pacing
• This type of pacing is accomplished by inserting the electrode
through the epicardium into the myocardium.
• This can also be unipolar or bipolar.

19. TYPES OF PERMANENT PACEMAKERS
• Single chamber pacemaker
‑
• Dual chamber pacemakers
‑
• Biventricular pacemakers
• Leadless systems have a self contained system which includes
‑
both the pulse generator and the electrode within a single unit
that is placed into the RV via a transvenous approach.

20. Single chamber pacemaker
‑
• Has a pulse generator with a single lead implanted in the right
ventricle.

21. Dual chamber pacemakers
‑
• Have a pulse generator with two leads, one implanted in the
right atrium and the other in the RV

22. Biventricular pacemakers
• Have a pulse generator with three leads implanted in the right
atrium, RV and coronary sinus which allows pacing of the left
ventricle.

24. Pacing Threshold
• This is the minimum amount of energy required to consistently
cause depolarization and therefore contraction of the heart.
• Pacing threshold is measured in terms of both amplitude and
duration for which it is applied to the myocardium.
• The amplitude is programmed in volts (V) or in milliampers in
some devices, and the duration is measured in milliseconds.

25. FACTORS AFFECTING PACING THRESHOLD
• Increase Decrease
• 1-4 weeks after implantation -Increased catecholamines
• Myocardial ischaemia/infaction -Stress, anxiety
• Hypothermia, hypothyroidism -Sympathomimetic drugs
• Hyperkalaemia, acidosis/alkalosis -Anticholinergics
• Antiarrythmics (class Ic,3) -Glucocorticoides
• Antiarrythmics ( class IA/B,2) -Hyperthyroidism
• Severe hypoxia/hypoglycaemia -Hypermetabolic status
• Inhalation-local anaesthetics

26. R Wave Sensitivity
• It is the measure of minimal voltage of intrinsic R wave,
necessary to activate the sensing circuit of the pulse generator
and thus inhibit or trigger the pacing circuit.
• The R wave sensitivity of about 3mV on an external pulse
generator will maintain ventricle inhibited pacing.

27. Resistance
• It can be defined as impedance to the flow of current.
• In the pacemaker system it amounts to a combination of resistance in
lead, resistance through the patient’s tissue and polarization that
takes place when voltage and current are delivered into the tissues.
• Abrupt changes in the impedance may indicate problem with the
lead system.
• Very high resistance can indicate a conductor fracture or poor
connection to the pacemaker.
• A very low resistance indicates an insulation failure.

28. Runaway Pacemaker
• It is the acceleration in paced rates due to aging of the
pacemaker or damage produced by leakage of the tissue
fluids into the pulse generator.
• Treatment with antiarrhythmic drugs or cardioversion may be
ineffective in such cases.
• It is necessary to change the pacemaker to an asynchronous
mode, or reprogram it to lower outputs.
• If the patient is haemodynamically unstable temporary pacing
should be done followed by changing of pulse generator.

29. Types of Pacing Modes
Asynchronous: (AOO, VOO, and DOO)
• It is the simple form of fixed rate pacemaker which discharges
at a preset rate irrespective of the inherent heart rate.
• It can be used safely in cases with no ventricular activity.
• However, the problems associated with asynchronous
pacemaker are that it competes with the patient’s intrinsic
rhythm and results in induction of tachyarrythmias.
• Continuous pacing wastes energy and also decreases the half-
life of the battery.

30. Single Chamber Atrial Pacing (AAI, AAT)
• In this system atrium is paced and the impulse passes down the
conducting pathways, thus maintaining atrioventricular
synchrony.
• A single pacing lead with electrode is positioned in the right
• atrial appendage, which senses the intrinsic P wave and causes
inhibition or triggering of the pacemaker.
• This is useful in patients with sinus arrest and sinus bradycardia
provided atrioventricular conduction is adequate.
• It is inappropriate for chronic atrial fibrillation and long
ventricular pauses.

31. Single Chamber Ventricular Pacing (VVI, VVT)
• VVI is the most widely used form of pacing in which ventricle is
sensed and paced.
• It senses the intrinsic R wave and thus inhibits the pacemaker
function.
• This type of pacemaker is indicated in a patient with complete
heart block with chronic atrial flutter, atrial fibrillation and long
ventricular pauses.
• Single chamber ventricular pacing is not recommended for
patients with sinus node disease, as these patients are more
likely to develop the pacemaker syndrome.

32. Dual Chamber AV Sequential Pacing
• Two leads that can be unipolar or bipolar are used, one for the
right atrial appendage and the other for right ventricular apex.
• The atrium is stimulated first to contract, then after an adjustable
PR interval ventricle is stimulated to contract.
• These pacemakers preserve the normal atrioventricular contraction
sequence, and are indicated in patients with AV block, carotid
sinus syncope, and sinus node disease.
• In DDD system, both the atrium and ventricle can be sensed and
paced.

33. • The advantages of dual chamber pacemaker are that they are
similar to sinus rhythm and are beneficial in patients, where atrial
contraction is important for ventricular filling (aortic stenosis).
• The disadvantage of dual chamber pacing is the development of
a pacemaker-mediated tachycardia (PMT) due to ventriculo atrial
(VA) conduction in which ventricular conduction is conducted back
to the atrium and sensed by the atrial circuit, which triggers a
ventricular depolarization leading to PMT.
• This problem can be overcome by careful programming of the
pacemaker.

35. Rate responsive pacing
• When the need for oxygenated blood increases, the
pacemaker ensures that the heart rate increases to provide
additional cardiac output.

36. Variety of Rate Response Sensors
• Activity sensors that detect physical movement and increase the
rate according to the level of activity.
• Minute ventilation sensors that measure the change in
respiration rate and tidal volume via transthoracic impedance
readings.

37. PACEMAKER NOMENCLATURE
• A ‘three’ letter NBG code was first proposed in 1974 and was
‑
universally accepted.
• Subsequently, a five letter code was proposed and is the
‑
mode currently used and accepted.
• O – None; A – Atrium; V – Ventricle; D – Dual; I – Inhibited; T
– Triggered; R – Rate modulation
Position I
Pacing
chamber(s)
Position II
Sensing
chamber(s)
Position III
Response(s)
to sensing
Position IV
Programmability
Position V
Multisite
pacing
O O O O O
A A I R A
V V T V
D ( A+V ) D(A+V ) D (I+T) D (A+V)
O – None; A – Atrium; V – Ventricle; D – Dual; I – Inhibited; T – Triggered;
R – Rate modulation

38. • However, most clinicians in their day to day communication
‑ ‑
continue to use the three letter model.
‑
• Asynchronous: (AOO, VOO, and DOO)
• Single Chamber Atrial Pacing (AAI, AAT)
• Single Chamber Ventricular Pacing (VVI, VVT)
• Dual Chamber AV Sequential Pacing (DDD, DVI, DDI, and VDD)

39. Pacemaker Syndrome
• Some individuals, particularly those with intact retrograde VA
conduction, may not tolerate ventricular pacing and may
develop a variety of clinical signs and symptoms resulting from
deleterious haemodynamics induced by ventricular pacing
termed as pacemaker syndrome.

40. • These include hypotension,
• syncope
• vertigo
• light-headedness
• fatigue
• exercise intolerance
• malaise
• weakness, lethargy
• dyspnoea and
• induction of congestive heart failure

41. • Cough
• Awareness of beat-to-beat variation of cardiac response from
spontaneous to paced beats
• Neck pulsation or pressure sensation in the chest, neck, or head
• Headache and
• Chest pain are the other symptoms.

42. • The pathophysiology of pacemaker syndrome results from a
complex interaction of haemodynamic, neurohumoral and
vascular changes induced by the loss of AV synchrony.
• Patients with retrograde VA conduction are in a state of
constant AV dys-synchrony.
• Retrograde VA conduction is present in about 15% of patients
with complete antegrade AV block and in about 67% of
patients with intact antegrade AV conduction paced for sinus
node disease.

43. Pacemaker Failure
• It may be due to generator failure, lead failure, or failure to
capture.
• Failure to capture owing to a defect at the level of
myocardium (i.e. the generator continues to fire but no
myocardial depolarization takes place) remains the most
difficult problem to treat.

44. Haemodynamic Changes During Pacing
• In single chamber pacemaker, atrial pacing increases the
cardiac output by about 26% in comparison to ventricular
pacing, as atrial contraction contributes 15 to 25% of preload
to ventricles.
• Also atrial systole increases the coronary blood flow and
decreases the coronary resistance.
• The new AV sequential pacing results in 35 % increase in
cardiac output in comparison to the single chamber pacing.

45. • While matching pacemaker to a patient, several factors need
to be taken into consideration such as
• patient’s age,
• Symptoms
• cardiac rhythm
• presence of underlying heart disease
• ventricular function
• response of sinus node to activity (chronotropic response)
• BPEG have issued guidelines on the recommended pacing
modes for all types of bradyarrhythmias requiring pacing.

46. British pacing and electrophysiology group
recommended pacemaker modes
OPTIMAL ALTERNATE INAPPROPRIATE
Sinus node disease AAIR AAI VVI, VDD
Atrioventricular block DDD VDD AAI, DDI
Sinus node disease with
atrioventricular block
DDDR, DDIR DDD, DDI AAI, VVI
Chronic atrial fibrillation with
atrioventricular block
VVIR VVI AAI, VVI, VDD
Carotid sinus syncope DDI DDD, VVI AAI, VDD
Malignant vasovagal syndrome DDI DDD AAI, VVI, VDD

47. FACTORS AFFECTING
PACEMAKER PERFORMANCE
.

48. Physiological changes
• During the first two weeks, there is an initial sharp increase in
the pacing threshold i.e. up to ten times the acute level because
of the tissue reaction around the electrode tip.
• Then it decreases to two to three times the acute level because
of the scar formation.
• In chronic state, it reaches the initial level in 80% of patients.
• But this has become far less of a problem with the introduction
of steroid-eluting leads and other refinements in the lead
technology.

49. Potassium
• Its equilibrium across the cell membrane determines the resting
membrane potential (RMP).
• In certain clinical situations, the RMP becomes less negative and
approaches the membrane’s threshold potential so that less current
density at the electrode tissue interface is required to initiate an
action potential, making capture by the pacemaker easier.
• If the RMP becomes more negative, an increased current density
would be required to raise the RMP to the membrane threshold
potential, making it more difficult for the pacemaker to initiate
myocardial contraction.

50. INCREASED SERUM POTASSIUM LEVELS
• An acute increase in extracellular potassium concentration as in
patients
 with myocardial ischaemia,
 rapid potassium
 replacement in chronic hypokalaemic patients or
 use of depolarising muscle relaxants in patients with burns,
trauma or neuromuscular disease may
• increase the RMP to less negative value, thus making the
capture easier

51. DECREASED SERUM POTASSIUM LEVELS
• In patients on diuretic therapy or
• those undergoing hyperventilation such as neurosurgical
patients
• leads to more negative RMP making the pacemaker capture
difficult.

52. OTHER FACTORS
• Myocardial Infarction - Its scar tissue is unresponsive to electrical
stimulation and may cause loss of pacemaker capture.
• Antiarrhythmic Drug Therapy- Class Ia (quinidine,
procainamide), Ib (lidocaine, diphenylhydrantoine), and Ic
(flecainide, encainide, propafenone) drugs have been found to
increase the pacing threshold.
• Acid Base Status -Alkalosis and acidosis both cause increase in
pacing threshold.
• Hypoxia - It causes increase in pacing threshold.

53. Anesthesia for Cardiac Pacemaker Insertion
• Most pacemakers are inserted under conscious sedation in the
cardiac catheterization laboratory or under monitored anesthesia
care in the operating room.
• Routine anesthetic monitoring is employed.
• Drugs such as atropine and isoproterenol should be available
should a decrease in heart rate compromise hemodynamics before
the new pacemaker is functional.
• An artificial cardiac pacemaker can be inserted intravenously
using endocardial leads or via a subcostal incision or median
sternotomy (after cardiac surgery) using epicardial or myocardial
leads

54. Permanently Implanted Cardioverter-
Defibrillators
• The ICD system consists of a pulse generator and leads for
dysrhythmia detection and current delivery.
• In addition to internal defibrillation, an ICD can deliver
antitachycardia or antibradycardia pacing and synchronized
cardioversion.

55. • The pulse generator is a small computer powered by a lithium
battery that is sealed within a titanium case.
• The transvenous leads consist of pacing and sensing electrodes
and one or two defibrillation coils.
• The defibrillation circuit is completed by the titanium case of the
pulse generator, which acts as a defibrillation electrode.
• The pulse generator is usually implanted into a subcutaneous
pocket.
• The position of the pulse generator is important because the
position affects the defibrillation wave front.
• The left pectoral region is the ideal location for the pulse
generator.

56. Working principle
• The ICD uses a specialized lead in the right ventricle that senses
ventricular depolarization. It amplifies, filters, and rectifies the
signal and then compares it with the programmed sensing
thresholds and the R-R interval algorithms.
• If the device detects VF, the capacitor charges, a secondary
algorithm is fulfilled by signal analysis to confirm the rhythm, and
then the shock is delivered.
• This secondary confirmatory process prevents inappropriate
shocks in response to self-terminating events or spurious signals.

57. • The process takes approximately 10 to 15 seconds from
dysrhythmia detection to shock delivery.
• During this time the patient may experience presyncope or
syncope

58. CODING SYSTEM
• A defibrillator coding system exists similar to the one used for pacemakers.
• The first letter is the chamber shocked (O, none; A, atrium; V, ventricle; D,
dual).
• The second letter indicates the antitachycardia pacing chamber (O, none;
A, atrium; V, ventricle; D, dual).
• The third position indicates the tachycardia detection mechanism (E,
electrogram; H, hemodynamic).
• The fourth position denotes the antibradycardia pacing chamber(O, none;
A, atrium; V, ventricle; D, dual).

59. Cardiac Resynchronization Devices
• Cardiac resynchronization therapy (CRT) using biatrial or
biventricular pacing is being employed in heart failure patients
with electromechanical asynchrony and intraventricular
conduction block.
• As CHF progresses, ventricular electrical dyssynchrony can result
in mechanical dyssynchrony.
• As a result, left ventricular contraction becomes increasingly
inefficient and cardiac output decreases.

61. • Cardiac resynchronization therapy uses three pacing leads:
right atrial, right ventricular, and a coronary sinus lead.
• By adjusting the timing of each lead, AV synchrony is optimized.
• Cardiac resynchronization therapy is now a mainstay of
treatment in patients who have left ventricular dysfunction
(ejection fraction ≤ 35%), QRS prolongation (≥120 ms), and
moderate to severe heart failure symptoms (NYHA III, IV).

62. PREOPERATIVE EVALUATION
• Determining whether a patient has a CIED should be based on
the following:
• A focused history including, but not limited to, the patient
interview, medical records review, and review of available
chest x-rays, electrocardiograms, or any available monitor or
rhythm strip information;
• A focused physical examination (i.e., checking for scars and
palpating for device).

63. • Defining the type of device is accomplished by
• Obtaining the manufacturer’s identification card from the patient
or other source,
• Ordering chest x-rays if no other data are available,
• Referring to supplemental resources (e.g., manufacturer’s
databases, pacemaker clinic records, and consultation with a
cardiologist).

66. • CIED dependence for pacemaking function may be determined by
one or more of the following:
• A verbal history or an indication in the medical record that the
patient has experienced a bradyarrhythmia that has caused
syncope or other symptoms requiring CIED implantation,
• A history of successful atrioventricular nodal ablation that resulted
in CIED placement, or
• A CIED evaluation that shows no evidence of spontaneous
ventricular activity when the pacemaking function of the CIED is
programmed to VVI pacing mode at the lowest programmable rate.

67. • CIED function is ideally assessed by a comprehensive evaluation
of the device.
• If a comprehensive evaluation is not possible, then, at a minimum,
confirm whether pacing impulses are present and create a paced
beat.
• Consultation with a cardiologist or CIED service may be
necessary.
• Contacting the manufacturer for perioperative recommendations
may be a consideration.

68. Pacemaker Evaluation
• Most of the information about the pacemaker, such as type of
pacemaker (fixed rate or demand rate), time since implanted,
pacemaker rate at the time of implantation, and half-life of the
pacemaker battery can be taken from the manufacture’s book
kept with the patient.
• Ten percent decrease in the rate from the time of implantation
indicates power source depletion.
• In patients with VVI generator, if intrinsic heart rate is greater
than pacemaker set rate, evaluation of pacemaker function can be
done by slowing down the heart rate by carotid sinus massage,
while the patient’s ECG is continuously monitored.

69. Effect of the Magnet Application on
Pacemaker Function
• Magnet application is an extremely important function.
• The magnet is placed over the pulse generator to trigger the
reed switch present in the pulse generator resulting in a non-
sensing asynchronous mode with a fixed pacing rate.
• Newer pacemakers do not require this, are not responsive to
magnet.

70. Pre operative preparations
• Planned procedures should include a determination of whether
EMI is likely to occur for either conventional pacemakers or
ICDs.
• If EMI is likely to occur, the conventional pacing function of a
CIED should be altered by changing to an asynchronous pacing
mode in pacemaker-dependent patients and suspending
special algorithms, including rate-adaptive functions.
• These alterations may be accomplished by programming or
applying a magnet when applicable.

71. .
• In addition, an ICD’s antitachyarrhythmia functions should be suspended
if present.
• For the ICD patient who depends on pacing function for control of
bradyarrhythmia, these functions should be altered by programming as
noted above.
• Consultation with a cardiologist or pacemaker ICD service may be
necessary.
• For all CIEDs, consider advising the individual performing the procedure
to use a bipolar electrocautery system or an ultrasonic scalpel when
applicable.
• Temporary pacing and defibrillation equipment should be immediately
available before, during, and after a procedure.

72. • Finally, the Task Force believes that anesthetic techniques do
not influence CIED function.
• However, anesthetic-induced physiologic changes (i.e., cardiac
rate, rhythm, or ischemia) in the patient may induce unexpected
CIED responses or adversely affect the CIED-patient
interaction.

73. Intraoperative Management
• The primary activities associated with intraoperative
management of a CIED include the following:
(1) Monitoring the operation of the device;
(2) preventing potential CIED dysfunction; and
(3) performing emergency defibrillation, cardioversion, or heart
rate support.

74. • Intraoperative monitoring includes -
• Continuous electrocardiography
• Monitoring of the peripheral pulse –
 palpation of the pulse,
 auscultation of heart sounds,
 monitoring of a tracing of intra-arterial pressure,
 ultrasound peripheral pulse monitoring, or
 pulse plethysmography or oximetry

75. IMPLICATIONS IN GENERAL ANAESTHESIA
• Skeletal myopotentials, electroconvulsive therapy,
succinylcholine fasciculation, myoclonic movements, or direct
muscle stimulation can inappropriately inhibit or trigger
stimulation, depending on the programmed pacing modes.
• Etomidate and ketamine should be avoided as these cause
myoclonic movements.
• Pacemaker function should be verified, before and after
initiating mechanical ventilation, as there may be dislodgement
of pacemaker leads by positive pressure ventilation, or nitrous
oxide entrapment in the pacemaker pocket.

76. • In patients with rate responsive pacemakers, rate responsive mode
should be deactivated before surgery.
• If this is not possible for some reason, the mode of rate response
must be known so that conditions causing changes in paced heart
rate can be avoided.
• Shivering and fasciculations should be avoided if the pacemaker
is ‘activity’ rate responsive.
• Ventilation (respiratory rate and tidal volume) should be kept
controlled and constant in case of ‘minute ventilation’ rate
responsive.
• Temperature must be kept constant in ‘temperature’ rate
responsive pacemakers.

77. • Anaesthetic agents have no effect on the function of CIEDs in
the perioperative period.
• However, in patients with bradycardia, avoiding high doses of
fentanyl or dexmedetomidine may be prudent to prevent PPM
dependence.
• In patients with long QT syndrome, drugs which cause QT
prolongation such as methadone, haloperidol, ondansetron and
high doses of inhalation agents are best avoided due to the
theoretical risk of polymorphic ventricular tachycardia.

78. MANAGEMENT DURING SPINAL ANAESTHESIA
• Care to be taken to avoid hypotension which might lead to
tachycardia.
• Main aim is to maintain haemodynamic stability.
• Correct hypotension and drugs like atropine should be readily
available.

79. Managing Potential Sources of EMI
Procedures using
• electrocautery,
• radiofrequency ablation,
• lithotripsy,
• MRI, or
• radiation therapy
may damage CIEDs or interfere with CIED function, potentially
resulting in severe adverse outcomes.

80. Electrocautery
(1) Assuring that the cautery tool and current return pad are
positioned so the current pathway does not pass through or
near the CIED pulse generator and leads;
(2) Avoiding proximity of the cautery’s electrical field to the pulse
generator or leads;
(3) Using short, intermittent, and irregular bursts at the lowest
feasible energy levels; and
(4) Using a bipolar electrocautery system or an ultrasonic
(harmonic) scalpel if possible.

81. Radiofrequency (RF) Ablation
• Avoid direct contact between the ablation catheter and the
CIED and leads and
• Should keep the RF ablation current path as far away from the
pulse generator and lead system as possible.

82. Lithotripsy
(1) avoiding focus of the lithotripsy beam near the pulse
generator and
(2) Disabling atrial pacing if the lithotripsy system triggers on the
R-wave.

83. Electroconvulsive Therapy
• Associated with significant cardiac risks.
• Transient electrocardiographic changes (e.g., increased P-wave
amplitude, altered QRS shape, and Twave and ST-T
abnormalities) may result from ECT, and
• Additional cardiac complications (e.g., arrhythmia or ischemia)
• May occur in patients with preexisting cardiac disease.

84. • Finally, physiologic stresses after ECT, such as
• a period of bradycardia and
• reduced blood pressure followed by
• tachycardia and a rise in blood pressure,
• may account for cardiac failure in the extended postoperative
period (i.e., several hours or days after ECT) among patients
with marginal cardiac function.

85. Managing EMI from Electroconvulsive
Therapy
• Although transient or long-term myocardial and nervous system
effects may be associated with ECT, the Task Force believes that
such therapies may be administered to CIED patients without
significant damage to a disabled CIED.
• All CIEDs should undergo a comprehensive interrogation before the
procedure(s).
• ICD functions should be disabled for shock therapy during ECT;
however, be prepared to treat ventricular arrhythmias that occur
secondary to the hemodynamic effects of ECT.

86. • CIED-dependent patients may require a temporary pacing
system to preserve cardiac rate and rhythm during shock
therapy.
• Also, the CIED may require programming to asynchronous
activity to avoid myopotential inhibition of the device in
pacemaker-dependent patients

87. Emergency Defibrillation or Cardioversion
• In this case, the primary concern is to minimize the current
flowing through the pulse generator and lead system.
• Case reports suggest that optimal positioning of the
defibrillation or cardioversion pads or paddles may be an
important factor in the prevention of adverse CIED-related
outcomes

88. • Before attempting emergency defibrillation or cardioversion of
the patient with an ICD and magnet-disabled therapies, all
sources of EMI should be terminated and the magnet removed
to reenable antitachycardia therapies.
• The patient should then be observed for appropriate CIED
therapy.
• For the patient with an ICD and antiarrhythmic therapies that
have been disabled by programming, consider reenabling
therapies through programming.
• If the above activities fail to restore ICD function, proceed with
emergency external defibrillation or cardioversion.

89. • If a life-threatening arrhythmia occurs, follow ACLS guidelines for
energy level and for paddle placement.
• If possible, attempt to minimize the current flowing through the pulse
generator and lead system by
(1) positioning the defibrillation or cardioversion pads or paddles as
far as possible from the pulse generator
(2) positioning defibrillation or cardioversion pads or paddles
perpendicular to the major axis of the CIED pulse generator and
leads to the extent possible by placing them in an anterior-posterior
location

90. • A clinically- appropriate energy output should always be used
regardless of the presence of a CIED, and the paddles should
be positioned as best as can be done in an emergency.

91. EMERGENCY SURGERY
• In an emergency, time may be inadequate to evaluate the CIED.
• Patients who are undergoing supraumbilical surgeries are at a
higher risk for EMI from the ECU if monopolar cautery use is
needed.
• Application of a magnet would be ideal if time permits.
• An ECG paper recording pre and post magnet application will
‑ ‑
allow us to know if the desired response is achieved.

92. • Application of transcutaneous pacing/defibrillator pads is
essential along with a standby external defibrillator with
pacing capabilities.
• Continuous ECG, pulse oximetry monitoring and additionally an
arterial line if indicated are essential.

93. Postoperative Management
• Primarily consists of interrogating and restoring CIED function.
• Cardiac rate and rhythm should be monitored continuously
throughout the immediate postoperative period.
• Back-up pacing capability and cardioversion-defibrillation
equipment should be immediately available at all times.

94. • The CIED first should be interrogated to assess postoperative
device functions.
• If interrogation determines that CIED settings are
inappropriate, then the device should be reprogrammed to
appropriate settings.
• For an ICD, all antitachyarrhythmic therapies should be
restored.
• Consultation with a cardiologist or pacemaker-ICD service may
be necessary.

95. Conclusion
• Patients with implanted pacemakers can be managed safely
for surgery and other non-surgical procedures.
• It requires thorough understanding about indication of
pacemaker insertion, various modes of pacing, and
programming of pacemaker.
• Anaesthetic management should beplanned preoperatively
according to patient’s medical status.
• Careful monitoring of ECG, pulse oximetry and arterial blood
pressure should be done.

96. • While using electocautery, precaution for minimal EMI should be
taken.
• Magnet should not be placed over pacemaker in the OT in
presence of electocautery.
• Rate responsive pacemakers should have rate responsive mode
disabled before surgery.
• Provision of temporary pacing should be available in the OT to
deal with emergency situation of pacemaker malfunction.
• Pacemaker should be rechecked after the procedure.

97. REFERENCE
• Stoelting’s Anesthesia and Co-existing Disease
• Rastogi et al. Patients with Pacemakers & Defibrillators Annals of
Cardiac Anaesthesia 2005; 8: 21–32.
• Practice Advisory for the Perioperative Management of Patients
with Cardiac Implantable Electronic Devices: Pacemakers and
Implantable Cardioverter-Defibrillatorsthe American Society of
Anesthesiologists, Inc. LippincottWilliams & Wilkins. Anesthesiology
2011; 114: 247–61.
• Chakravarthy M, Prabhakumar D, George A. Anaesthetic
consideration in patients with cardiac implantable electronic
devices scheduled for surgery. Indian J Anaesth 2017;61:736-43.

98. THANK YOU