Cardiac Rhythm Disturbance Temporary Pacemakers Supraventricular Tachyarrhythmia Rapid atrial pacing cardioversion Ventricular Tachyarrhythmias Bradyarrhythmias Temporary Pacemakers Indications for permanent pacemakers Temporary epicardial pacing after cardiac surgery

1. Post Cardiac Surgery

2. Directed by
DR.Karar .A.Ali
department of cardiothoracic surgery
kararbenign@gmail.com

4. Supraventricular Tachyarrhythmias
Supraventricular tachycardias are recognized as the most common
arrhythmia to occur after coronary artery bypass grafting (CABG) with the
reported incidence of 20–40% after CABG surgery (Creswell et al. 1993) and
even higher following valvular surgery (Asher et al. 1998).
AF (Fig. 14.1) and atrial flutter (AFL) (Fig. 14.2) are the most prevalent
supraventricular arrhythmias; however, atrial tachycardias (AT) occurred as
well.
Most cases of AF occur between the second and fourth postoperative days
(Almassi et al. 1997). Although this arrhythmia is usually benign and self-
limiting, it may result in hemodynamic instability, thromboembolic events, a
longer hospital stay, and increased healthcare costs (Hakala et al. 2002;
Lahtinen et al. 2004).

11.  .The mechanism of postoperative AF is not well described and
is probably multifactorial. It is suggested that endogenous
adenosine, inflammation, and oxidative injury may play a
mechanistic role in this arrhythmia
 .The perioperative period is also characterized by acute
ischemic reperfusion injury and delayed inflammatory
response that together result in a net depletion at plasma
antioxidants
 . patients undergoing cardiac surgery often have underlying atrial
enlargement or increased atrial pressures that may predispose to
AF.
 Age-related structural or electrophysiological changes also appear
to lower the threshold for postoperative AF in elderly patients

12.  Other reported predisposing conditions for
development of the postoperative AF included left main
or proximal right coronary artery stenoses, chronic
obstructive pulmonary disease, beta-blocker withdrawal,
history of AF or heart failure, and preoperative
electrocardiographic findings of PR interval of 185 ms or
longer, P-wave duration of 110 ms or longer in lead V1,
and left atrial abnormality

13. Considering the peak incidence of AF in the first
2–3 days after surgery, inflammatory mechanisms
have been suggested. The idea has also been
supported by the efficacy of anti-inflammatory
agents in decreasing the incidence of
postoperative AF

14.  However, there are other electrophysiological explanations
for the higher incidence of AF in this period. Nonuniform atrial
conduction is greatest on postoperative days 2 and 3, and longest atrial
conduction is on day 3 (Ishii et al. 2005).
 Perioperative hypokalemia has been shown to be associated with
postoperative AF partly via changes in atrial conduction and refractoriness
 There are recent evidences indicating that minimally invasive cardiac surgery
or surgery without cardiopulmonary bypass has been associated with lower
incidenceof postoperative AF. In a prospective randomized study, 200
patients were randomly assigned into on-pump CABG and off-pump CABG.
The results of this study clearly indicated that postoperative AF occurs with
lower frequency in patients who underwent off-pump beating heart surgery
compared to those with on-pump CABG(Ascione et al. 2000).

15. Prophylaxis
Several pharmacological and non-pharmacological
strategies have been employed to prevent
postoperative AF after cardiac surgery. Efficacy of
beta-blockers, amiodarone, sotalol, magnesium,
and atrial pacing has been assessed in several
randomized and nonrandomized clinical trials.

16.  Because patients recovering from cardiac surgery often have enhanced sympathetic tone,
the risk of postoperative AF is increased. Beta-blockers antagonize the
effects of catecholamines on the myocardium and are, thus, expected to prevent AF
after cardiac surgery. Multiple clinical trials and three landmark meta-analyses have
shown a significant reduction in postoperative AF by beta-blocker prophylaxis in cardiac
surgery patients (Crystal et al. 2002). Following these remarkable results, updated
American Heart Association/American College of Cardiology Foundation (AHA/
ACCF) 2006/2011 and recent European Society of Cardiology (ESC) 2010 guidelines
recommended beta-blocker prophylaxis to prevent AF in cardiac
surgery patients in the absence of contraindications (Fuster et al. 2011;
Camm et al. 2010).

17. Oral carvedilol, with its unique antioxidant and
antiapoptotic properties, appears to be the most
effective beta-blocker in the prevention of
postoperative AF (Haghjoo et al. 2007).

19. both prophylactic oral and intravenous amiodarone
are effective and safe agents in reducing the incidence
of AF and its related cerebrovascular accident and
postoperative ventricular tachyarrhythmia (Bagshaw
et al. 2006). Currently, preoperative administration of
amiodarone is deemed class IIa indication
for prophylactic therapy in patients at high risk for
postoperative AF in the latest AHA/ACCF and ESC
guidelines for AF management (Fuster et al. 2011;
Camm et al.
2010)

20. 

21. 

27. 

28. Sotalol is a class III antiarrhythmic agent with
potent beta-blocking activity. As
a result, it would be a suitable drug for AF
prevention after cardiac surgeries. Sotalol
has been proven to be an effective agent across all
the clinical trials using this drug
(Pfisterer et al. 1997; Weber et al. 1998). Only
issue is related to its safety profile

29. 

30. 

31.  Hypomagnesemia
 has been suggested as a cause of both supraventricular and
ventricular tachycardias, and it is an independent risk factor
for the development of AF in cardiac surgery patients.
Therefore, it has been hypothesized that magnesium
supplementation may reduce the incidence of AF after heart
surgery. Several clinical trials have examined the use of
intravenous magnesium sulfate for the prevention of AF
after CABG (Fanning et al. 1991; Kaplan et al. 2003). A meta-
analysis of eight identified randomized controlled trials
revealed that the use of intravenous magnesium
supplementation was associated with a significant reduction
in the AF incidence after CABG (Alghamdi et al. 2005).

32. • Hypomagnesemia is common in the cardiac surgical population and
correlates with higher incidence of cardiac arrhythmias and major adverse
cardiac events. However, the role of Mg in preventing postoperative
arrhythmias – especially atrial fibrillation – is controversial. There is
moderate evidence that intravenous Mg therapy, particularly low doses
administered before cardiac surgery, will reduce the postoperative
incidence of atrial fibrillation.
• Hypomagnesemia is also common in hospitalized patients. It is especially
prevalent in the critically ill and correlates with worse clinical outcomes.
Mg has proven effective for treating eclampsia, preeclampsia, and
torsades de pointes. Other therapeutic applications such as adjunctive
therapy in acute asthma exacerbations, acute coronary syndromes, acute
cerebral ischemia, and postoperative pain control are under discussion.
Mg has a low adverse effects profile and multiple theoretical advantages,
including its low cost.

33. 

34. 

35. 

37. 

38. 

39. Management
Considering the self-limited course of the
postoperative AF or AFL, treatment begins with
pharmacological control of the heart rate
Beta-blockers
should be first-line agents for the rate control
because of rapid onset of action and 50%
likelihood of conversion to sinus rhythm. Both
metoprolol and esmolol areavailable in
intravenous (IV) formulation

41. Calcium-channel antagonists are less
effective than beta-blockers and considered as
second-line agents. Calcium-channel
antagonists result in rate control of AF more
rapidly than does digoxin. These latter
agents may be useful when beta-blockers are
contraindicated (i.e., bronchospasm).

42. Conversion of postoperative AF is not needed in the
majority of patients after cardiac surgery because of
high recurrence rate and self-limited nature. However
this approach may be useful in high-risk patients who
are refractory to or intolerant of atrioventricular (AV)
nodal blocking agents.
Conversion of AF, AFL, and AT can be accomplished
using electrical cardioversion, pharmacological
cardioversion, and overdrive pacing (if AFL or AT
present).

43. Pharmacological cardioversion should be
considered in the setting of unstable respiratory
status or other contraindication for anesthesia.
Drugs proven to be useful for cardioversion
include procainamide, amiodarone, propafenone,
ibutilide (VanderLugt et al. 1999), and dofetilide.
Latter two agents carry a risk of torsades de
pointes about 2–4%. This risk is higher in the
setting of bradycardia, female gender,
hypokalemia, and hypomagnesemia.

44. Rapid atrial pacing using epicardial wires
implanted during surgery was proved to be safe
and effective in the conversion of postoperative
AFL and AT. Rapid atrial pacing is highly desirable
in the patients unsuitable for electrical
cardioversion such as patients with chronic
obstructive pulmonary disease.

45.  Gloves always should be worn when handling pacemaker
electrodes to prevent microshock because even small
amounts of electrical current can cause serious
dysrhythmias if they are transmitted to the heart.

46. 

47.  • Supraventricular dysrhythmias (e.g., atrial flutter, reentrant
atrial tachycardia, atrioventricular [AV] nodal reentry
tachycardia, reentrant tachycardias that use an accessory
pathway, such as Wolff-Parkinson-White [WPW] syndrome)
sometimes can be terminated by overdrive atrial pacing
• Atrial fibrillation occasionally terminates with overdrive atrial
pacing, but this is not a reliable therapy for atrial fibrillation.
• • Overdrive atrial pacing is performed most commonly with
epicardial atrial pacing wires placed during cardiac surgery. A
transvenous atrial pacing lead with an active fixation tip to help
keep the lead in the atrium also can be used.
• • Overdrive atrial pacing involves the delivery of short bursts of
rapid pacing stimuli through an epicardial atrial pacing wire or a
transvenous lead in the atrium. The physician or advanced
practice nurse determines the duration and rate of the burst.

48. • One approach to overdrive pacing is to atrial pace the heart
with 20 milliampere (mA) at a rate 20% to 30% faster than
the intrinsic atrial rate for 30 seconds, then stop pacing. An
alternate approach is to initiate atrial pacing at a rate 20
beats/min faster than the intrinsic atrial rate; if 1:1 capture
does not occur after 30 seconds, the paced rate can be
increased by 20 beats/min; repeat every 30 seconds until
1:1 capture is achieved. Continue pacing until the heart rate
decreases from AV block (e.g., 2:1, 3:1) or 1 to 2 minutes of
1:1 pacing have occurred, then stop pacing.6
• Successive bursts usually are performed at gradually
increasing rates (maximal capability of the pulse generator
for overdrive atrial pacing is 800 pulses/min) and may be
delivered for up to 2 minutes

49. • • The atrial pacing wire or atrial pacing lead needs to be accurately identified
with initiation of overdrive pacing because pacing the ventricle at rapid rates may
result in ventricular tachycardia or ventricular fibrillation.
• • Rapid atrial pacing may result in degeneration of the atrial rhythm to atrial
fibrillation with a rapid ventricular response. This pacemaker-induced atrial
fibrillation usually does not sustain itself for more than a few minutes before it
converts to normal sinus rhythm.6
• • If an accessory pathway is present, rapid atrial pacing can result in conduction
to the ventricles over the accessory pathway, leading to ventricular fibrillation.
• • Overdrive suppression of the sinus node may result in periods of bradycardia,
asystole, junctional or ventricular escape rhythms, or polymorphic ventricular
tachycardia on termination of the atrial overdrive pacing and the atrial
tachydysrhythmia.
• • Conversion of an atrial tachydysrhythmia can result in dislodgment of atrial
thrombus and embolization of clots to the pulmonary or systemic circulation.

50. 

51. 

52. 

53. 

55. 

56. 

57. Electrical cardioversion is reserved for patients
exhibiting acute hemodynamic instability. For
elective cardioversion, anterior-posterior paddles
are preferred with the posterior paddle placed at
the lower tip of the scapula.

58. • Technique External cardioversion
• The patient should be adequately sedated with a short-acting agent such as
midazolam or propofol. In addition, an opioid analgesic, such as fentanyl, is
commonly used. Reversal agents, such as flumazenil and naloxone, should be
available.
• The defibrillator should be placed in the synchronized mode, which permits a
search for a large R or S wave. The delivered energy is selected. Most
monophasic and biphasic models can deliver up to 360 joules. Manual button
depression by the operator causes the defibrillator to discharge an electric
current that lasts less than 4 milliseconds and avoids the vulnerable period of
cardiac repolarization when ventricular fibrillation (VF, vfib) can be induced. The
operator should be aware of this brief delay as the cardioverter searches for a
large positive or negative deflection. If the deflections are too small for the
defibrillator to synchronize, the clinician can change the leads or place them
closer to the patient's chest or heart. If the patient develops ventricular
fibrillation, always turn off synchronization to avoid delay in energy delivery.

59.  Energy requirements for atrial fibrillation (AF, afib) are 100-
200 joules initially and 360 joules for subsequent shocks. A
study showed good response to higher energy shocks of 720
joules for the treatment of refractory atrial fibrillation. [11]
Biphasic shocks require a typical energy level of 75 joules for
the correction of atrial fibrillation. Cardioversion of atrial
fibrillation secondary to hyperthyroidism is 90% successful.
[12] Only 25% of patients with atrial fibrillation caused by
severe mitral regurgitation are successfully treated, and half
revert in the first 6 months. Atrial flutter and paroxysmal
supraventricular tachycardia (PSVT) require less energy: 50
joules initially, then 100 joules if needed. Cardioversion of
ventricular tachycardia (VT, vtach) involves shocks of 50-100
joules initially, and then 200 joules if unsuccessful.

60.  Pacemakers and implantable cardioverter-
defibrillators (ICDs) should be at least 10 cm away
from direct contact with the paddles, and these
devices should eventually be interrogated for any
postcardioversion malfunction. The
anteroposterior approach is preferred in patients
with implantable devices to avoid shunting the
current to the implantable device and damaging
the system

61. • Special conditions
• In pediatric patients with PSVT or ventricular
tachycardia who are not hemodynamically stable,
an initial synchronized shock of 0.5 J/kg is
recommended. In subsequent attempts, the
energy is increased.
• During pregnancy, recommendations as for other
adults are applicable.

62. Recently, novel oral anticoagulants
such as dabigatran, rivaroxaban, and apixaban are
shown to be safe and effective in the prevention
of thromboembolic events after cardiac surgery
(Anderson et al. 2015). Duration of
anticoagulation must be based on individual
clinical situation

63. 

64. Ventricular Tachyarrhythmias

65. 

66. 

67. 

68. 

69. 

70. 

71. 

72. 

73. 

74. 

77. 

78. 

79. 

80. 

81. 

82. • Causes of Left Bundle Branch Block
• It is unusual for LBBB to exist in the absence of organic disease. Causes are varied
and include:
• Aortic stenosis
• Ischaemic heart disease
• Hypertension
• Dilated cardiomyopathy
• Anterior MI
• Lenègre-Lev disease: primary degenerative disease (fibrosis) of the conducting
system
• Hyperkalaemia
• Digoxin toxicity
• New LBBB in the context of chest pain was once considered a “STEMI-
equivalent” and part of the criteria for thrombolysis. However, more up-to-date
data suggests that chest pain patients with new LBBB have little increased risk of
acute myocardial infarction at the time of presentation.

83. 

84. 

85. 

87. 

88. Management
Patients with asymptomatic and hemodynamically
stable PVC and even short runs
of nonsustained VT usually do not require any
specific treatment. All reversible
underlying causes should be corrected.
In case of the symptomatic or hemodynamically
significant PVC or nonsustained VT, lidocaine and
overdrive pacing are recommended.

89.  lidocaine (Rx)
• Ventricular Arrhythmias or Pulseless Ventricular Tachycardia (after
defibrillation, attempts, CPR, and vasopressor administration)
• 1-1.5 mg/kg slow IV bolus over 2-3 minutes
• May repeat doses of 0.5-0.75 mg/kg in 5-10 minutes up to 3 mg/kg total
if refractory VF or pulseless VT
• Continuous infusion: 1-4 mg/min IV after return of perfusion
• Administer 0.5 mg/kg bolus and reassess infusion if arrhythmia reappears
during constant infusion
• If IV not feasible may use IO/ET
• Endotracheal (loading dose): 2-3.75 mg/kg (2 to 2.5 recommended IV
dose); dilute in 5-10 mL 0.9% saline or sterile water
• Monitor: ECG

90. • Hemodynamically Stable Monomorphic
Ventricular Tachycardia
• 1-1.5 mg/kg; repeat doses of 0.5-0.75 mg/kg in 5-
10 minutes up to 3 mg/kg total; follow with 1-4
mg/min continuous infusion

91.  For hemodynamically stable sustained VT, IV antiarrhythmic
medication is the first-line treatment approach (Fogel and
Prystowsky 2000). Dosages of common antiarrhythmic
medications are listed in Table 14.3.
 Lidocaine is usually the first-choice drug and can be tried in
dosage recommended in the nonsurgical setting.
 Procainamide is often the second choice. This drug should
be used with caution or not at all in patients with renal
dysfunction.
 In patients with left ventricular dysfunction, amiodarone is a
better choice than other antiarrhythmics.

92. 

93. 

94. In this group of the patients, overdrive ventricular
pacing using epicardial wires placed at the time of
surgery may be attempted.
In patients with hemodynamically unstable
or drug-refractory VT, electrical cardioversion or
defibrillation with energy level of 200–360 J is
recommended.

95. Bradyarrhythmias

96. Incidence and Prognosis
Bradyarrhythmias are a common complication
following cardiac surgery. Permanent pacemaker is
required for sinus node dysfunction (SND) or
atrioventricular block (AVB) in 0.6–4.6% of patients
after CABG (Goldman et al. 1984). Varying degrees of
AVB (Figs. 14.4 and 14.5) are more common after
valve replacement (up to 24%) than other types of
cardiovascular surgery (Jaeger et al. 1994; Brodell et
al. 1991).

97. Bradyarrhythmia due to SND and to lesser extent
AVB is relatively common after orthotopic heart
transplantation and leads to permanent
pacemaker implantation in up to 21% of patients
with SND and 4.5% of patients with AVB (Grant et
al. 1995). Improvement in postoperative
bradyarrhythmia may occur in significant number
of patients. Rate of recovery is less common after
complete AVB than SND (Merin et al. 2009).

98. 

99. 

100. 

101. 

102. • Box 26-1 Causes of Bradycardia
• Noncardiac Causes
• Drugs
• β-blockers
• Calcium channel blockers
• Antiarrhythmic drugs (e.g., amiodarone, ibutilide, flecainide,
lidocaine)
• Digoxin
• Adenosine
• Opiate overdose
• Lithium
• Ivabradine
• Clonidine

103. • Neurogenic
• Reflex-mediated syncope
• Raised intracranial pressure
• Increased ocular pressure (e.g., during eye surgery)
• Neuromuscular disorders (e.g., myotonic dystrophy, Friedreich’s ataxia)
• Guillain-Barré syndrome
• Dysautonomia (e.g., Shy-Drager syndrome)
• Endocrine and Metabolic
• Hypothyroidism
• Acidosis
• Electrolyte abnormalities
• Anorexia nervosa
• Porphyria

104. • Environmental and Infection-related
• Hypothermia
• Lyme disease
• Chagas disease
• Envenomation (e.g., snakebite)
• Diphtheria
• Acute rheumatic fever
• Organophosphate insecticides
• Others
• Physiologic
• Iatrogenic (e.g., following aortic valve replacement or supraventricular
tachycardia ablation)
• Collagen vascular disease (e.g., rheumatoid arthritis, systemic lupus
erythematosus, ankylosing spondylitis)
• Congenital

105. • Cardiac Causes
• Sinus node dysfunction
• Atrioventricular node dysfunction
• Hisian and infra-Hisian block
• Myocardial infarction (especially inferior)
• Myocarditis
• Myocardial infiltration: cardiac sarcoidosis,
hemochromatosis, cardiac amyloidosis, Wegener’s
granulomatosis

107. 

108. 

109. 

110. Pathogenesis
Postoperative bradyarrhythmias can be caused by
incomplete washout of cardioplegia solution,
antiarrhythmic drugs, or their toxicity. In addition,
it may caused by trauma or surgical manipulation
in the area of the AV node or bundle of His.

111. Prophylaxis
In order to reduce the incidence of postoperative
conduction disorder, special attention to the
anatomy of the conduction system, careful
administration of sinus or AV nodal blocking
agents, and complete washout of cardioplegia
solution are warranted

112. Management
According to American College of
Cardiology/American Heart Association guidelines
“permanent pacemaker implantation is indicated for
third-degree and advanced second-degree AVB at
any anatomic level associated with postoperative
AVB that is not expected to resolve after cardiac
surgery” (Tracy et al. 2013).
Generally, it is recommended to implant a permanent
pacemaker if symptomatic complete AVB or SND
persists longer than 5–7 days after cardiac surgery
(Merin et al. 2009).

113. Any decision regarding timing of implantation of a
permanent pacemaker will be impacted by the
stability of the temporary pacing system. Therefore, in
patients with no intrinsic underlying rhythm or those
with failure of temporary pacing leads, permanent
pacing may be performed even sooner. In patients
with resolved or resolving bradyarrhythmias,
electrophysiological study or exercise stress testing is
useful to determine the need for permanent
pacemaker implantation

114. Pacing Wires and
Pacemakers

115.  General comments
1. The use of cold cardioplegic arrest is commonly
associated with temporary sinus node or AV node
dysfunction. Placement of two temporary right atrial and
two right ventricular epicardial pacing wire electrodes is
beneficial in these situations to optimize hemodynamics at
the conclusion of bypass and for several hours in the ICU.
 Pacing wires are also useful in the event that medications
used to control atrial fibrillation precipitate advanced AV
block. They can also be used for overdrive pacing and have
diagnostic utility in delineating unusual
rhythm problems

116. 

117. To assess whether pacing wire placement should be
performed routinely, one study found that 15% of
patients needed pacing to terminate bypass, but less
than 10% of patients required temporary pacing
postoperatively.283 However, it is not always
predictable which patients may require subsequent
pacing, and it is recommended that at least one
ventricular pacing wire (with a skin ground) should be
placed; the risk:benefit ratio of atrial pacing wires
suggests that they should be placed routinely as well.

118. Atrial pacing wires can be used to record atrial
activity in both unipolar and bipolar modes. With
suitably equipped monitors, these recordings can
be obtained simultaneously with standard limb
leads to distinguish among atrial and junctional
arrhythmias and differentiate them from more
life‐threatening ventricular arrhythmias

119.  Therapeutic uses
1. Optimal hemodynamics are achieved at a heart rate of
around 90 bpm in the immediate postoperative period. Use
of temporary pacing wires attached to an
external pulse generator (Figure 11.18) to increase the heart
rate is preferable to the use of positive chronotropic
agents that have other effects on myocardial function.
 Atrial pacing with normal conduction will nearly always
demonstrate superior hemodynamics to AV pacing, which in
turn is superior to ventricular pacing. Since AV delay is often
prolonged after bypass, shortening it artificially using AV
pacing can improve hemodynamics, especially in patients
with impaired ventricular function

120. 

121. 

122. biventricular pacing with leads placed
during surgery will improve LV systolic and diastolic
function compared with RA
or RA–RV pacing in patients with AV block who have
LV dysfunction. Benefit is greatest in patients who
also have a wide QRS complex.
Reentrant rhythms can be terminated by rapid pacing.
Rapid atrial pacing can terminate type I atrial flutter
(flutter rate of less than 350/min) and other
paroxysmal supraventricular tachycardias. Rapid
ventricular pacing can terminate VT

123. 

124. 

125. 

131. 

132. 

133. 

134. 

135. 

136. 

137. 

138. 

139. 

185. 

189. Normal sitting in
VVI

202. TO SET SENSITIVITY (PHYSICIAN ONLY )
Position dial at MOST sensitive setting (1mV)
Adjust pacer rate to 10 less than pt intrinsic rate
Reduce mA to minimum
(to prevent pacer from competing with intrinsic rhythm
Turn the sensitivity dial counterclockwise
(higher mV) until:
VENT. SENSE (orange light) stops flashing and
VENT. PACE (green light) starts flashing
(This is sensitivity threshold)
Adjust the sensitivity indicator to half threshold value
RESET THE mA and RATE TO THEIR
ORIGINAL SETTINGS!

204. ATRIAL PACING: [AAI mode]
Can be used when conduction system of the
heart beyond the SA node is normal.
USES: [the pacer is only stimulating a p wave: the QRS must follow from the
heart!]
Sinus Bradycardia symptomatic
Sick Sinus Syndrome
Sinus Arrythmia
Sinus Rhythm: Higher heart rate to increase
cardiac output (better perfusion)
Junctional Rhythm may work

228. Current external pacemakers, such as the Medtronic
5392 model, can pace in a variety of modes. The DDD
mode senses atrial activity, following which the ventricle
contracts at a preset time interval after the atrial
contraction. This mode reduces the risk of triggering
atrial, junctional, and pacemaker‐induced arrhythmias.
Careful monitoring is necessary in the event that the
pacemaker tracks the atrial signal in atrial
fibrillation/flutter, resulting in a very fast ventricular
response.

229. However, setting an appropriate upper rate limit on
these pacemakers usually prevents this complication.
Occasionally, a pacemaker‐mediated tachycardia can
develop from repetitive retrograde conduction from
premature ventricular complexes, producing atrial
deflections that are sensed and tracked
If atrial activity is absent, either the DDD or DVI mode
can be used. The DVI mode senses only the ventricle, so
if a ventricular beat does not occur, both chambers are
paced. This may lead to competitive atrial activity if the
atrium is beating at a faster rate.

230. 4. Indications
a. Complete heart block
b. Second‐degree heart block to achieve 1:1
conduction
c. First‐degree heart block if 1:1 conduction cannot
be achieved at a faster rate because of a long PR
interval

243. Indications for permanent pacemakers
1. Although the temporary use of epicardial pacing is
not uncommon after surgery, most patients with
preoperative sinus rhythm will achieve a satisfactory
sinus rate within a few days and can receive β‐blockers
for AF prophylaxis.
Conduction abnormalities such as first‐degree block
and bundle branch blocks are the most common
abnormalities noted after CABG, but they have not been
shown to affect long‐term outcome

246. 2. About 1–2% of patients require placement of a
PPM after cardiac surgery. This is more likely in older
patients, those with pulmonary hypertension or a
preexisting left bundle branch block (LBBB), surgery
that involves valve replacements (tricuspid > aortic >
mitral), complex operations requiring a long
cross‐clamp time, and reoperations

247. Tricuspid valve replacement involves suturing in close proximity to the AV
node, and evidence of complete heart block should prompt placement of permanent
epicardial pacing leads

255. 3. The risk of requiring a PPM after TAVR is greater with
self‐expanding valves than balloon‐expandable valves, but
newer designs and higher positioning have reduced the risk to
less than 5%.
Baseline conduction disturbances, especially a right bundle
branch block (RBBB) with first‐degree block, increase the risk
of complete heart block and the need for a PPM.
In fact, a baseline RBBB also increases the risk of high‐grade
AV block and sudden cardiac death after hospital discharge.
A new LBBB leads to deterioration in LV function, increases
the risk of requiring a PPM, and in most studies compromises
intermediate‐term survival

256. 4. If a PPM is being considered in the postoperative
patient, oral anticoagulation with warfarin should be
withheld or given in low doses, with use of IV heparin
for AF or valve thromboprophylaxis, when indicated. If
the patient’s INR is already in therapeutic range, the
dose should be reduced to achieve an INR at the low
therapeutic range if the patient is at high
thromboembolic risk, at which point PPM implantation
can be safely performed. It is preferable to avoid a
heparin bridge, which is associated with more
periprocedural bleeding

257. PPM placement is indicated postoperatively for the following
conditions:
a. Complete heart block
b. Symptomatic or significant sinus node dysfunction
c. Slow ventricular response to AF (usually at rates of less than
50 bpm) that persists despite cessation of potentially
contributory medications, including
β‐blockers, sotalol, amiodarone, CCBs, and digoxin.
d. Tachycardia‐bradycardia syndrome: when medications used
to control a fast response to AF produce a very slow sinus
mechanism upon conversion
e. Advanced second‐degree heart block with a slow
ventricular response

258. The optimal timing for placement of a PPM has not been
determined. In some patients, the indication may be a
transient phenomenon, and waiting a few extra days may
obviate its need. However, it often seems more cost‐effective
to implant a pacemaker after 3–4 days to expedite the
patient’s discharge from the hospital.
A study from the Mayo Clinic showed that 40% of patients
were not pacer‐ dependent at follow‐up, although about 85%
of patients who required implantation for complete heart
block had become pacer‐dependent.300 A follow‐up study
of patients receiving PPMs after TAVR found that only 40% of
patients receiving a PPM within 10 days were
pacer‐dependent at one year