Professional Documents
Culture Documents
Arrhythmias 7
Fabio Guarracino and Rubia Baldassarri
7.1 Introduction
The perioperative period is defined as the length of time between the preoperative
assessment and 36–48 h after surgery. Perioperative arrhythmias are one of the most
common cardiac complications in noncardiac surgery. In addition, the arrhythmic
events are a major cause of perioperative morbidity and mortality.
Although most of the perioperative arrhythmic events occur in patients undergo-
ing lung surgery with more or less extensive resection of the parenchyma (lobec-
tomy, pneumonectomy), disturbances of the heart rhythm can occur in any surgical
setting.
Early detection of perioperative cardiac arrhythmias is fundamental. In fact,
although the majority of the arrhythmic events are either self-limited or well toler-
ated in critically ill patients, malignant arrhythmias may cause severe cardiac dys-
function in some cases and can even lead to cardiac arrest (Table 7.1).
The arrhythmic events can also lead to severe haemodynamic alteration and
increase the perioperative risk of the patients scheduled for noncardiac surgery.
The availability of systems for the continuous monitoring of the electrocardio-
gram (EKG) has allowed for real-time evaluation of any arrhythmic event occurring
in either the operating room or the postoperative care units.
Prior to this, the true incidence of perioperative cardiac arrhythmias has long
been underestimated. It should be considered that the evaluation of the heart rhythm
was based on periodic EKGs recorded at more or less regular intervals of time [1].
In addition, the application of the Holter technique, which provides continuous
recording of the heart rhythm, has allowed for the detection of arrhythmic events
that occur outside of both the operating room and the intensive care units where the
Table 7.1 Cardiac Site Supraventricular: origin above the AV node (atrial
arrhythmias: classification or nodal)
Supraventricular premature beats
Paroxysmal supraventricular tachycardia (PSVT)
Atrial fibrillation (AF)
Atrial flutter
Wolff-Parkinson-White (WPW)
Ventricular: origin under the AV node
Ventricular premature beats (VBPs)
Ventricular tachycardia (VT)
Ventricular fibrillation (VF)
Heart rate Tachyarrhythmia (>100 b/min)
Bradyarrhythmia (<50 b/min)
patients are under EKG monitoring. The data emerging from the recent literature
report an incidence of perioperative arrhythmias of 10–30 % in cardiothoracic sur-
gery versus 4–20 % in noncardiac surgery [2] (Table 7.2). Although cardiac
arrhythmias can occur in healthy patients under stress conditions, such as surgery,
temporary haemodynamic impairment and electrolyte disturbance, in most cases,
the arrhythmic event is the expression of an underlying cardiac disease that may
also be undiagnosed. For example, the majority of the hyperkinetic arrhythmias,
such as atrial fibrillation (AF) and ventricular tachycardia (VT), are associated
with a pre-existing cardiopulmonary disease. In the recent guidelines [2] for the
perioperative management of cardiac patients undergoing noncardiac surgery, con-
tinuous EKG monitoring is highly recommended in all patients undergoing surgery
(class IC). Still, according to the mentioned guidelines, EKG monitoring should
start before either the induction of general anaesthesia or the performance of a
peripheral block [3]. The early detection of arrhythmic events should be aimed at
the evaluation of both the severity of the arrhythmia and the associated haemody-
namic implications. The early detection and treatment of malignant, life-threaten-
ing arrhythmias are mandatory in surgical patients, especially those at high risk.
An adequate haemodynamic support is required in cases of arrhythmias inducing
severe cardiovascular dysfunction. The identification of the aetiological
7 Management of Perioperative Arrhythmias 113
7.2 Diagnosis
hypertrophic), myocardial scar and myocardial structural alterations [5, 6]. The
most common ventricular arrhythmias are the ventricular premature beats (VPBs)
and the VT.
VT can be classified according to:
• The site of origin: from the right ventricle (RV) or the left ventricle (LV). The VT
arising from the RV outflow tract (RVOT) is the most common idiopathic VT [7].
• The structural characteristics: monomorphic, polymorphic, sustained and
non-sustained.
• The response to pharmacologic agents and catecholamines.
7.3.1 Diagnosis
7.3.2 Treatment
Perioperative supraventricular arrhythmias are quite common and are more frequent
than ventricular arrhythmias in patients undergoing noncardiac surgery. In most
cases, the withdrawal of the trigger (perioperative respiratory failure, electrolyte
alterations) is sufficient to terminate the arrhythmic event.
116 F. Guarracino and R. Baldassarri
The association between perioperative neurologic events such as stroke and supra-
ventricular tachyarrhythmias (ST) has been well documented [16]. Despite the increas-
ing number of patients undergoing noncardiac surgery, studies of the incidence and
complications of perioperative AF (POAF) in a large surgical population are still lack-
ing [17]. POAF is the most common perioperative arrhythmia in noncardiac surgery
patients [18, 19]. The cardiac arrhythmias occurring in noncardiac surgery strictly
depend on the patients’ clinical conditions and the type of surgery [1]. Approximately
10–20 % of the patients who undergo noncardiac thoracic surgery experience POAF,
and this is dependent on the type of surgery and the patients’ characteristics (age, ther-
apy with beta-blockers, cardiac valve disease and heart failure) [20–23].
New-onset POAF in noncardiac surgery patients has been associated with an
increased risk of perioperative neurologic complications leading to an increased
perioperative risk [24, 25].
7.4.1 Treatment
According to the current guidelines, the treatment of POAF should be aimed at the
control of the ventricular heart rate. The use of beta-blockers and calcium channels
blockers is recommended as the treatment of choice by the ESC guidelines on AF
management [26].
The use of amiodarone is recommended in patients with heart failure, while
digoxin is not helpful in surgical patients because of the increased perioperative
adrenergic stress.
When surgery can be delayed, select patients with paroxysmal supraventricular
tachycardia (PST) and AF can benefit from transcatheter radiofrequency ablation
to remove the aetiological pattern of the arrhythmia.
According to the guidelines, supraventricular PBs do not require any therapy,
and STs generally respond to vagal manoeuvres. In these cases, adenosine is effec-
tive to terminate the ST. The prophylactic use of beta-blockers, amiodarone and
calcium channel blockers should be used in patients with recurrent ST.
AF with haemodynamic instability requires immediate electrical cardioversion.
In the case of new-onset AF in patients undergoing noncardiac surgery, the use of
beta-blockers appears to be associated with a high incidence of cardioversion to
sinus rhythm [27].
7.5 Bradyarrhythmias
Patients with definitive cardiac pacing and/or ICD can safely undergo surgery, but
require a careful management of the devices.
It is well known that the electrical stimulation induced by the use of the unipolar
electrocautery can alter the function of the PM either suppressing or reprogramming
the intracardiac device.
Some precautions can be taken to reduce the interferences with the PM/ICD
function during surgery:
• Using bipolar electrocautery far from the site of the intracardiac device; employ-
ing brief bursts at the lowest amplitude possible.
• Setting the PM in the asynchronous or non-sensing mode in those patients who
are PM dependent; in the operating setting, this can easily be done by positioning
a magnet on the skin over the PM.
The same precautions should be taken in patients with ICD: the device should be
deactivated before surgery and immediately switched on in the postoperative period.
Additionally, an external defibrillator should always be available in the operating
room when patients with ICD are submitted to noncardiac surgery.
In the case of elective surgery, the identification of the type of the device
implanted and the evaluation of its effective functioning should always be per-
formed before surgery.
In addition, the patients’ clinical history should be investigated to understand
why and when the device has been implanted.
7.7.3 Preoperative
Most anaesthetic agents can be safely used in patients with LQTS. Propofol can be
safely used either for the induction or maintenance of general anaesthesia because
it has minimal effects on the QT interval. It should be considered that all of the vola-
tile agents affect ventricular repolarization. Among them, isoflurane can be safely
used for the maintenance of general anaesthesia [38, 45, 46]. Muscle relaxation can
be safely induced by rocuronium, vecuronium and atracurium, and the opioids
remifentanil and fentanyl are safe [38, 45, 47]. The use of anticholinesterase is not
recommended. Ketamine and thiopental sodium should not be used because of sym-
pathomimetic activity and the effect on the QT interval, respectively [46].
Regardless of the anaesthetic agent used, the aim of anaesthesiological manage-
ment should be the achievement of an adequate anaesthesiological plan, especially
prior to endotracheal intubation. The association between an adequate preoperative
sedation and deep anaesthesia, the use of intraoperative opioids and the topic admin-
istration of local anaesthetics on the laryngeal mucosa should minimize the risk of
arrhythmogenic events induced by endotracheal intubation.
During general anaesthesia, electrolyte disturbances and hypothermia should be
avoided.
Continuous ECG monitoring should be performed during general anaesthesia
and prolonged until the first postoperative hours. Patients at high risk for TdP should
receive intravenous administration of short half-life beta-blockers (esmolol) under
ECG monitoring [48]. An external defibrillator for transcutaneous pacing/defibrilla-
tion should be available for high-risk patients, and everything should be ready for
the emergency insertion of a temporary pacemaker.
Another important recommendation concerns the use of high peak pressures and
a long inspiratory/expiratory ratio during mechanical ventilation that, mimicking a
Valsalva manoeuvre, can prolong the QT interval.
7 Management of Perioperative Arrhythmias 121
Recovery from general anaesthesia should take place in a calm environment, and
ECG monitoring should be continued in the postoperative hours, especially in
patients without ICD.
Postoperative analgesia can be achieved with opioids such as morphine.
Ondansetron seems to be the drug of choice for the prevention and treatment of
postoperative nausea and vomiting [38, 45, 46].
Conclusion
The management of perioperative arrhythmias is a challenge for anaesthesiolo-
gists. The preoperative patient evaluation is aimed at the performance of periopera-
tive risk stratification. The detection of pre-existing cardiac diseases, of a history of
receiving therapy for arrhythmias and of new-onset arrhythmias, as well as the
early detection of intraoperative adverse arrhythmic events with continuous ECG
monitoring, should be aimed at the selection of patients at high risk of developing
severe perioperative arrhythmias who will require postoperative intensive care.
Although most of the perioperative arrhythmias are benignant and self-limit-
ing, the anaesthesiologist should know the recommendations for the manage-
ment of the perioperative arrhythmias in patients undergoing noncardiac surgery.
Because of the increasing number of patients with intracardiac devices who are
enrolled for noncardiac surgery, the implementation of the previously reported
precautions is fundamental to avoid perioperative arrhythmic adverse events.
References
1. Alati GL, Allaria B, Berlot G, Gullo A, Luzziani A, Martinelli G, Torelli L (1997) Springer-
Verlag, Milan
2. Melduni RM, Koshino Y, Shen WK (2012) Management of arrhythmias in the perioperative
setting. Clin Geriatr Med 28(4):729–743
3. Kristensen SD, Knuuti J, Saraste A, Anker S, Bøtker HE, De Hert S, Ford I, Juanatey JR,
Gorenek B, Heyndrickx GR, Hoeft A, Huber K, Iung B, Kjeldsen KP, Longrois D, Luescher
TF, Pierard L, Pocock S, Price S, Roffi M, Sirnes PA, Uva MS, Voudris V, Funck-Brentano C,
Authors Task Force Members (2014) 2014 ESC/ESA Guidelines on non-cardiac surgery:
cardiovascular assessment and management: The Joint Task Force on non-cardiac surgery:
122 F. Guarracino and R. Baldassarri
21. Passman RS, Gingold DS, Amar D et al (2005) Prediction rule for atrial fibrillation after major
noncardiac thoracic surgery. Ann Thorac Surg 79:1698–1703
22. Vaporciyan AA, Correa AM, Rice DC et al (2004) Risk factors associated with atrial fibrilla-
tion after noncardiac thoracic surgery: analysis of 2588 patients. J Thorac Cardiovasc Surg
127:779–786
23. Onaitis M, D’Amico T, Zhao Y, O’Brien S, Harpole D (2010) Risk factors for atrial fibrillation
after lung cancer surgery: analysis of the Society of Thoracic Surgeons general thoracic sur-
gery database. Ann Thorac Surg 90(2):368–374
24. Kamel H, Elkind MS, Bhave PD, Navi BB, Okin PM, Iadecola C, Devereux RB, Fink ME
(2013) Paroxysmal supraventricular tachycardia and the risk of ischemic stroke. Stroke
44(6):1550–1554. doi:10.1161/STROKEAHA.113.001118, Epub 2013 Apr 30
25. Gialdini G, Nearing K, Bhave PD, Bonuccelli U, Iadecola C, Healey JS, Kamel H (2014)
Perioperative atrial fibrillation and the long-term risk of ischemic stroke. JAMA
312(6):616–622
26. Camm AJ, Lip GY, De Caterina R, Savelieva I, Atar D, Hohnloser SH et al (2012) 2012
focussed update of the ESC Guidelines for the management of atrial fibrillation: an update of
the 2010 ESC Guidelines for the management of atrial fibrillation. Developed with the special
contribution of the European Heart Rhythm Association. Eur Heart J 33:2719–2747
27. Balser JR, Martinez EA, Winters BD, Perdue PW, Clarke AW, Huang WZ et al (1998) Beta-
adrenergic blockade accelerates conversion of post-operative supraventricular tachyarrhyth-
mias. Anesthesiology 89:1052–1059
28. Brugada P, Brugada J (1992) Right bundle branch block, persistent ST segment elevation and
sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter
report. J Am Coll Cardiol 20:1391–1396
29. Refaat MM, Hotait M, London B (2015) Genetics of sudden cardiac death. Curr Cardiol Rep
17(7):606
30. Wilde AA, Antzelevitch C, Borggrefe M, Brugada J, Brugada R, Brugada P, Corrado D, Hauer
RN, Kass RS, Nademanee K, Priori SG, Towbin JA, Study Group on the Molecular Basis of
Arrhythmias of the European Society of Cardiology (2002) Proposed diagnostic criteria for the
Brugada syndrome: consensus report. Circulation 106(19):2514–2519
31. Antzelevitch C, Brugada P, Borggrefe M, Brugada J, Brugada R, Corrado D, Gussak I,
LeMarec H, Nademanee K, Perez Riera AR, Shimizu W, Schulze-Bahr E, Tan H, Wilde A
(2005) Brugada syndrome: report of the second consensus conference: endorsed by the
Heart Rhythm Society and the European Heart Rhythm Association. Circulation
111(5):659–670
32. Minoura Y, Kobayashi Y, Antzelevitchet C (2013) Drug-induced Brugada syndrome.
J Arrhythmia 29:88–95
33. Yap YG, Behr ER, Camm AJ (2009) Drug-induced Brugada syndrome. Europace
11(8):989–994
34. Delise P, Allocca G, Marras E, Sitta N, Sciarra L (2010) Sindrome di Brugada: diagnosi e
stratificazione del rischio. G Ital Cardiol 11(10 Suppl 1):107S–113S
35. Hanna EB, Glancy DL (2015) ST-segment elevation: differential diagnosis, caveats. Cleve
Clin J Med 82(6):373–384
36. Martella G, De Persis C, Bonsi P, Natoli S, Cuomo D, Bernardi G, Calabresi P, Pisani A (2005)
Inhibition of persistent sodium current fraction and voltage-gated L-type calcium current by
propofol in cortical neurons: implications for its antiepileptic activity. Epilepsia
46(5):624–635
37. Flamée P, De Asmundis C, Bhutia JT, Conte G, Beckers S, Umbrain V, Verborgh C, Chierchia
GB, Van Malderen S, Casado-Arroyo R, Sarkozy A, Brugada P, Poelaert J (2013) Safe single-
dose administration of propofol in patients with established Brugada syndrome: a retrospective
database analysis. Pacing Clin Electrophysiol 36(12):1516–1521
38. Owczuk R, Wujtewicz MA, Zienciuk-Krajka A, Lasińska-Kowara M, Piankowski A,
Wujtewicz M (2012) The influence of anesthesia on cardiac repolarization. Minerva Anestesiol
78(4):483–495
124 F. Guarracino and R. Baldassarri
39. Antzelevitch C (2005) Role of transmural dispersion of repolarization in the genesis of drug-
induced torsades de pointes. Heart Rhythm 2(Suppl 2):S9–S15
40. Perry MD, Ng CA, Mann SA, Sadrieh A, Imtiaz M, Hill AP, Vandenberg JI (2015) Getting to
the heart of hERG K(+) channel gating. J Physiol 593(12):2575–2585
41. Antzelevitch C (2008) Drug-induced spatial dispersion of repolarization. Cardiol
J 15:100–121
42. Wisely NA, Shipton EA (2002) Long QT syndrome and anaesthesia. Eur J Anaesthesiol
19(12):853–859
43. Chang DJ, Kweon TD, Nam SB, Lee JS, Shin CS, Park CH et al (2008) Effects of fentanyl
pretreatment on the QTc interval during propofol induction. Anaesthesia 63:1056–1060
44. Ay B, Fak AS, Toprak A, Göğüş YF, Oktay A (2003) QT dispersion increases during intuba-
tion in patients with coronary artery disease. J Electrocardiol 36:99–104
45. Kies SJ, Pabelick CM, Hurley HA, White RD, Ackerman MJ (2005) Anesthesia for patients
with congenital long QT syndrome. Anesthesiology 102(1):204–210
46. Staikou C, Stamelos M, Stavroulakis E (2014) Impact of anaesthetic drugs and adjuvants on
ECG markers of torsadogenicity. Br J Anaesth 112(2):217–230
47. Cafiero T, Di Minno RM, Di Iorio C (2011) QT interval and QT dispersion during the induc-
tion of anesthesia and tracheal intubation: a comparison of remifentanil and fentanyl. Minerva
Anestesiol 77:160–165
48. Mikuni I, Torres CG, Bakshi T, Tampo A, Carlson BE, Bienengraeber MW, Kwok WM (2015)
Enhanced effects of isoflurane on the long QT syndrome 1-associated A341V mutant.
Anesthesiology 122(4):806–820