Anesthesia and Arrhythmias
Causes and Treatment
William A. Shapiro, M.D.
UCSF Department of Anesthesia
November 24, 2004
E-mail: shapirob@anesthesia.ucsf.edu
Introduction
One challenge an anesthesiologist continually faces is to provide a surgical environment with
minimal disturbance in cardiac rhythm. To optimize intraoperative management of arrhythmias,
anesthesiologists must be skilled in interpreting the 12-lead ECG, have a good understanding of
the basic principles of electrocardiogram (ECG) rhythm analysis,1 2 and a working knowledge of
the available antiarrhythmic agents.3
Transient alterations in cardiac rhythm occur often during anesthesia and surgery.4 5,6 7 A
study reporting on the incidence of nonfatal complications in 112,000 anesthetics listed
arrhythmias as the most common intraoperative complication.8 For patients without cardiac or
pulmonary disease, the hemodynamic consequences of changes in heart rate or rhythm are minor.
The overall incidence of serious intraoperative arrhythmias is approximately 1%.8 9
Many surgical patients have some degree of cardiac and/or pulmonary disease limiting their
cardiopulmonary reserve. Therefore, delays in identifying a new rhythm in these patients, or
poor choice of antiarrhythmic therapy when treatment is required, may result in irreversible
myocardial damage and patient morbidity.
Simulating critical incidents during surgery can be useful as a teaching model to improve
performance skills in recognition and treatment of intraoperative arrhythmias.10 11 These studies
have identified two important lessons pertaining to managing changes in intraoperative cardiac
rhythm: First, the more experienced anesthesiologist will recognize changes in cardiac rhythm
earlier, and Second, current knowledge of treatment regimen’s (e.g., ACLS protocols) requires
review periodically.
GENERAL CONSIDERATIONS
Systemic oxygen transport depends on delivery of inspired air to the alveoli, gas exchange
across the alveolar-capillary membrane, and transport of oxygen saturated hemoglobin to
different organs of the body. To ensure adequate oxygen delivery, cardiac output is maintained
by a heart which beats approximately 70 times per minute, that is, 4200 times per hour or
approximately 100,000 times per day. During normal activity, including periods of exercise,
stress, quiet relaxation, and sleep, the heart is an organ of remarkable consistency and regularity;
it responds to changing requirements by increasing or decreasing its rate, rarely dropping or
adding extra beats.
Normal heart rates at birth vary in the range of 120-150 beats/minute and fall slowly with age
such that at 70 years of age the average heart rates vary between 60 and 80 beats per
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minute. Sinus arrhythmia (variation of sinus rate with varying autonomic influence, most
notably secondary to changing autonomic tone with the respiratory cycle) is a normal response
during the majority of a person's lifetime. Lesser variation in heart rate with respiration is noted
immediately after birth and then again in later years. With increasing age there is a tendency
toward occasional premature atrial or ventricular beats interrupting sinus rhythm. In spite of the
increased frequency of single atrial or ventricular extrasystoles with advancing age, sustained
arrhythmias almost never occur.
THE PREOPERATIVE ECG
The incidence of an abnormality discovered on a preoperative ECG is approximately 10% by
age 40 and 25% by age 60.12 For asymptomatic patients, the incidence of ECG abnormalities is
lower. In older adults especially, a preoperative ECG may reveal previously unappreciated
abnormalities which may have an impact on anesthetic care. Recommendations regarding the
need for a preoperative ECG has been addressed by a Task Force of the American College of
Cardiology and the American Heart Association.13 Roizen (an anesthesiologist) offers 12 specific
conditions in which he says a patient will benefit from a preoperative ECG, ie, produce an
alteration in anesthetic plan or informed consent.14 He further identifies 10 ECG findings on a
preoperative ECG which will have anesthetic implications. The cost-benefit analysis of a
preoperative ECGs is also discussed. Clearly, recommendations suggesting when to obtain a
preoperative ECG will continue to undergo periodic review.
Patients Who Benefit From a Preoperative ECG14
1.
2.
3.
4.
5.
6.
Chest pain without any etiology
Angina or anginal equivalents
A history of CHF
A history of high blood pressure
A history of diabetes
A history of arrhythmias
7.
8.
9.
10.
11.
12.
Shortness of breath
Myocardial infarction
A history of smoking
Impending vascular surgery
Exercise producing SOB or angina
Men > 40 yrs, Women > 50 yrs
ECG Abnormalities That May Alter Management14
1.
2.
3.
4.
5.
Atrial flutter or fibrillation
1st-, 2nd-, or 3rd-degree heart block
ST segment abnormalities
PAC’s or PVC’s
Wolf-Parkinson-White syndrome
6.
7.
8.
9.
10.
LVH or RVH
Myocardial infarction
Prolonged QT segment
Tall peaked T waves
Small QRS voltage
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INTRAOPERATIVE ECG LEAD SYSTEM
A reliable ECG arrhythmia detection system must show clear P-waves as well as the QRS
complex. Arrhythmias are either present or absent, their detection is not generally as subtle as
identifying ST segments changes produced by myocardial ischemia. The challenge involved in
arrhythmia detection is twofold: first, identification of the arrhythmia, and second, determination
of the cause of the arrhythmia. Only after identification of the arrhythmia and its most likely
cause can appropriate therapy be instituted.
MECHANISMS VERSUS CAUSES OF ARRHYTHMIAS
Mechanisms describe how arrhythmias occur. Knowing how does not always explain why an
arrhythmia occurs. Intraoperatively, the answer to why may be more salient to the reversal of a
disturbance in cardiac rhythm. If, for example, a change in cardiac rhythm immediately follows
an intraoperative event, quickly identifying the precipitating event will allow more prompt
treatment of the arrhythmia than determining its mechanism. Moreover, eliminating or altering
the cause often terminates the arrhythmia regardless of the mechanism producing it. Thus,
attention to intraoperative temporal relationships is the foundation to the management of
arrhythmias—providing a basis for treatment, particularly of “new”, transient, arrhythmias likely
due to intraoperative stresses and dynamics.
Mechanisms of Cardiac Arrhythmias
The majority of clinically significant arrhythmias observed outside the operating room are
attributed to three basic mechanisms. In order of decreasing frequency, they are reentry,
abnormal automaticity, and triggered rhythms caused by delayed-after depolarizations. Reentry
accounts for over 90% of the clinical supraventricular tachycardias and over 50% of the clinical
ventricular tachycardia occurring outside the operating room.
Although the mechanisms producing intraoperative arrhythmias are believed to be similar,
the frequency with which each mechanism produces arrhythmias is different. That is, most
changes in intraoperative cardiac rhythm appear to result from alterations in autonomic tone due
to anesthetic agents or surgical manipulations which produce fluctuations in automaticity at both
the sinus node and the AV node, which in turn generate disturbances in cardiac rhythm.
Mechanisms of Cardiac Arrhythmias
1. Reentry
2. Automaticity
a. Altered normal automaticity
b. Abnormal automaticity
3. Triggered rhythms
from delayed after depolarizations (DAD's)
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Causes of Intraoperative Cardiac Arrhythmias
Most intraoperative arrhythmias result from medication used for iv sedation, local anesthesia
(particularly when combined with epinephrine), anesthetic agents, or anesthetic or surgical
manipulations, pain, or anxiety, all of which alter the balance between sympathetic and
parasympathetic tone. All anesthetic agents (inhalation and intravenous), muscle relaxants and
muscle relaxant antagonists independently affect cardiac rate and rhythm. Sinus tachycardia and
bradycardia are common (often predictable) responses to these agents or surgical stimulation.
Certain agents (e.g., nitrous oxide, succinylcholine) are associated with junctional rhythms, and
the volatile anesthetics, particularly halothane, are associated with premature ventricular
contractions during periods of stimulation or elevated PaCO2.
Intraoperative Causes of Cardiac Arrhythmias
1. Anesthetic agents
(including those used for conscious sedation)
2. Anesthetic manipulations, ie- laryngoscopy
3. Surgical stimulation
4. Physiologic responses
pain, vagal reflex, baroreceptor reflex
cerebral pressure response (Cushing Reflex)
5. Pathologic processes
hypoxia, fever, sepsis, hypovolemia,
myocardial ischemia, CNS disease,
acid-base or electrolyte imbalances,
anaphylaxis, drug/blood reaction, etc.
Other common causes of changes in intraoperative cardiac rate and rhythm include
laryngoscopy, intubation of the trachea, and surgical traction of visceral structures. When any of
these intraoperative manipulations causes a change in cardiac rate or rhythm, the easiest, quickest
and, often, most reliable way to return the heart rate and rhythm to baseline is to stop the
stimulating event.
Myocardial Ischemia
Changes in impulse formation and conduction properties of the heart are commonly
associated with myocardial ischemia and infarction. Myocardial ischemia may produce lifethreatening arrhythmias. Intraoperatively, whenever arrhythmias are due to inadequate
myocardial perfusion, attention must be directed at improving myocardial oxygen delivery or
decreasing myocardial work and oxygen consumption. Treating only the arrhythmias without
eliminating myocardial ischemia will have disastrous results and, if attention is misdirected for
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any length of time, periods of prolonged ischemia undoubtedly will lead to more serious and
persistent arrhythmias and worsening heart failure.
Hypoxia
Hypoxia always will produce myocardial ischemia and can induce all cardiac arrhythmias.
Consequently, analysis and treatment of arrhythmias or acute changes in cardiac rhythm must
begin by eliminating hypoxia. Whenever a change in cardiac rhythm occurs, the adequacy of
inspired oxygen concentration and distal oxygen saturation must be verified immediately. Pulse
oximetry is a reliable monitor of adequacy of distal tissue oxygen delivery and can be used to
distinguish whether hypoxia is the cause of a new cardiac rhythm. When necessary, an arterial
blood sample should be analyzed to determine arterial oxygenation. Because its effects are
severe, hypoxia must be treated immediately.
TREATMENT: INTRAOPERATIVE CONSIDERATIONS
Studies of the treatment of intraoperative arrhythmias are few. Results from clinical research
conducted in controlled settings, particularly coronary care units and cardiac electrophysiologic
laboratories, have defined the mechanisms of arrhythmias and delineated our current guidelines
for use of antiarrhythmic agents.15 Intraoperatively, clinical trial and error appear to confirm that
the therapies used to terminate various cardiac arrhythmias encountered outside the operating
room work equally well to treat the same arrhythmias during anesthesia and surgery.
Neonates, Infants, And Children
Arrhythmias and their hemodynamic consequences occurring during surgery are different in
children than in adults.16 In children, especially neonates, sinus bradycardia (heart rate less than
100 beats/minute) is a potentially dangerous intraoperative arrhythmia. This decrease in heart
rate must be assumed secondary to hypoxia until proven otherwise. In fact, in a Closed Claims
study comparing adult and pediatric insurance claims, bradycardia (64%) more commonly
preceded respiratory arrest than cyanosis (49%) in children.17 Other common causes of
bradycardia in children include drugs, laryngoscopy, pleural, peritoneal or eye muscle stretching.
Repeated intravenous injections of succinylcholine also may produce bradycardia. Occasionally,
this bradycardia is slow enough to require treatment with atropine. Some clinicians always
precede succinylcholine with atropine or mix them and administer them together.
Ventricular premature contractions and junctional rhythms may be seen with inhalation
anesthesia, especially halothane.
Adults
“Normal” events such as laryngoscopy, surgical stimulation, intubation, or extubation
frequently result in changes in heart rate. The interaction between the patient's preoperative
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cardiac condition, anesthetic agents, surgical manipulations, neuromuscular blocking agents, and
their reversal agents all combine to produce short transient periods of cardiac rhythm changes.
Common “vagal” events producing bradycardia include laryngoscopy, eye muscle manipulation,
and pleural or peritoneal stretching. Almost every drug used in anesthesia has autonomic effects
influencing heart rate, independent of its interaction with other drugs or surgery. Junctional
rhythms are frequently seen but as long as adequate blood pressure is maintained, treatment is
not necessary. Transient AV block (type I or II second degree) is occasionally seen but rarely
needs treatment. The new onset of AV block requiring a pacemaker during surgery is essentially
nonexistent, its presence should suggest a search for other causes (i.e., hypoxia).
Perhaps surprisingly, the frequency and types of arrhythmias observed during regional
anesthesia tend to be similar to those seen during general anesthesia. Spinal and epidural
anesthesia, even when performed in healthy patients can result in cardiac arrest.18
Sinus Tachycardia
Treatment:
Ensure adequate sedation
Use additional local anesthesia (if indicated)
Correct the underlying cause
Beta Blocker, either esmolol or propanolol
Sinus Bradycardia
Treatment:
Decide if treatment is required.
Discontinue vagal stimulation if possible.
Administer ephedrine, atropine, glycopyrrolate
or isuprel infusion intravenously.
Initiate cardiac pacing.
Atrial Fibrillation
Treatment:
To slow ventricular rate:
digitalis, a beta blocker, or
a calcium channel blocker.
To terminate atrial fibrillation: cardioversion (usually requires
relatively high energy levels > 100 joules).
To prevent subsequent bouts of atrial fibrillation: iv procainamide.
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Ventricular Tachycardia and/or Fibrillation
Treatment:
Stable VT (VF is never stable): lidocaine 100 mg or amiodarone 150 mg
Cardioversion may be required
Pulseless VT or VF: Cardioversion/defibrillation up to 360 joules
To prevent subsequent bouts of VT or VF: IV amiodarone or lidocaine
Junctional Rhythms
Treatment:
Junctional bradycardia (escape rhythm):
—Discontinue vagal stimulation;
—IV atropine, ephedrine, isuprel or cardiac pacing.
Accelerated junctional rhythm (isorhythmic AV dissociation)
—Small doses of a beta blocker.
AV node re-entry tachycardia
—IV adenosine, verapamil, or beta blocker.
Heart Block
1st degree AV block: no treatment required.
2nd degree AV block:
—Type I: no treatment if ventricular rate is acceptable.
atropine or isuprel if sinus or ventricular rate is slow.
—Type II: iv atropine or isuprel may be used, but without
delay to establishing ventricular pacing.
rd
3 degree AV block: ventricular pacing, transvenous or
transcutaneous.
Transcutaneous pacing for all emergencies requiring a pacemaker.
Treatment:
Electrical Management of Arrhythmias
The decision to cardiovert is a clear one when an arrhythmia results in a pulseless patient.
Such patients require immediate electrical management, usually in conjunction with
cardiopulmonary resuscitation (ACLS protocol). All pulseless tachycardias should be
defibrillated immediately and severe bradycardia or asystole should be paced.
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FINAL REMARKS
Successful management of intraoperative arrhythmias also requires a good working
relationship between anesthesiologist and surgeon. Working together is the only method that
offers the best outcome. Staying out of trouble is always preferred to getting out of trouble.
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