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138 D. Lollar
there was a trend for survival benefit in the less severe group (mortality
26.5% with vasopressin versus 35.7% in norepinephrine group).
• In patients with shock secondary to heart failure, inotropes to support cardiac
functions should only be used when blood pressure is insufficient. In this
case, inotropes should only be started in patients with signs of volume overload and inadequate cardiac function. Guidelines from the American College
of Cardiology and the American Heart Association [J Am College Cardiology
2009; 53(15) e1–e90] do not advise use of any one agent or combination
of agents for this purpose. However, Levy et al. (Crit Care Med 2011;
39: 450–455) published a randomized controlled trial of 30 patients comparing epinephrine to norepinephrine plus dobutamine in patients with
non-ischemic heart failure (cardiac index < 2.2 L/min and mean arterial pressure < 60 mmHg) resistant to dopamine plus dobutamine. While both groups
were able to attain goal hemodynamics (MAP > 65 mmHg), the epinephrine
group had higher rates of arrhythmias and higher lactate levels. Additionally,
the epinephrine group demonstrated decreased microcircular perfusion based
on tonometry of the gastric mucosa.
Chapter 5-(vi)
Dysrhythmias
Jennifer A. Salotto, MD*
* Fellow, Trauma and Acute Care Surgery, Denver Health Medical Center
Take Home Points
• Cardiac arrhythmias occur due to a derangement in electrical impulse
initiation, conduction, or both within the heart.
• In surgical patients, factors including volume overload, manipulation of the
heart, intra-atrial catheters, electrolyte imbalances, and excess sympathetic
tone can predispose to arrhythmia. Underlying structural abnormalities of
the heart, congestive heart failure, and coronary artery disease may also
promote arrhythmia.
• History and electrocardiography are essential in the evaluation of arrhythmia.
• Bradycardias result when impulses fail to generate at the sinoatrial node or
when these impulses are blocked along their path to the ventricles. Common
bradycardias include sinus bradycardia, sinus node dysfunction, and atrioventricular heart block.
• Tachycardias are categorized by the location of the origin of the irregular
impulse — above the atrioventricular node ( supraventricular tachycardia) or
Contact information: Denver Health Medical Center, University of Colorado Health
Sciences Center, 777 Bannock Street, MC 0206, Denver, CO 80204; Tel.: 857-928-4766,
email: Jennifer.salotto@ucdenver.edu
139
140 J. A. Salotto
below the atrioventricular node (ventricular tachycardia). Common supraventricular tachycardias include atrial fibrillation, atrial flutter, and ectopic
supraventricular tachycardia. Ventricular tachycardias include premature
ventricular beats, ventricular tachycardia, and ventricular fibrillation. When
sustained or hemodynamically significant, these entities require urgent intervention as they may lead to sudden death.
• The impact of an arrhythmia will depend upon the ventricular response to the
arrhythmia, the ability to preserve cardiac output, and the degree of underlying
structural or ischemic disease.
• The foundation of therapy for arrhythmias includes antiarrhythmic drugs, car-
dioversion, defibrillation, and permanent implantable pacemaker/defibrillator
devices.
Background
The conduction system of the heart
• The sinoatrial node (SA node) is the physiologic pacemaker of the heart. It
generates the cardiac impulse and displays automaticity.
The sinus node lies at the junction of the superior vena cava and the right
atrium.
The artery supplying the sinus node branches from the right circumfl ex
coronary artery in 60% of people, and from the left circumfl ex coronary
artery in 40% of people.
• After conduction through the atria, electrical signals are transmitted to the
atrioventricular node (AV node). Transmission continues through the interventricular septum via the Bundle of His, the right and left bundle branches,
and then to the Purkinje fibers, which activate the ventricles.
The AV node and the His-Purkinje system are both capable of pacemaker
activity. They can override the SA node if it is suppressed.
The main function of the AV node is to control atrial impulse transmis-
sion to the ventricles, thus regulating the speed of atrial and ventricular
contraction.
• The cardiac conduction system is heavily innervated by the parasympathetic
and sympathetic nervous system. Heart rate and speed of conduction are
determined by the relative degree of input from parasympathetic and sympathetic stimuli.
Dysrhythmias 141
Parasympathetic innervation is supplied by the vagus nerve, which
releases acetylcholine. This neurotransmitter acts on muscarinic receptors to slow sinus node impulse generation and conduction through the
AV node.
Sympathetic stimulation causes epinephrine and norepinephrine to act on
adrenergic receptors. The result is faster conduction and increased impulse
generation by the SA node.
Cardiac electrophysiology and understanding the electrocardiogram
• The P wave on an electrocardiogram (EKG) represents atrial depolarization.
• The PR interval is the time from the beginning of the P wave to the beginning
of the Q wave, the length of which depends on the conduction velocity
through the AV node. A slower conduction means a lengthened interval.
• The QRS complex represents the depolarization of the ventricle.
• The QT interval is the interval from the beginning of the Q wave to the end of the T
wave. The QT interval represents depolarization and repolarization of the ventricle.
• The ST segment is the end of the S wave to the beginning of the T wave. The
T wave represents ventricular repolarization, when the ventricle relaxes and
prepares for another contraction.
Main Body
Arrhythmia in the postoperative period
• Postoperative arrhythmias are very common after both cardiac and non-car-
diac surgery.
• Baseline patient characteristics which can contribute to arrhythmia include
structural abnormalities of the heart (for example, prior scarring after myocardial ischemia), cardiomyopathy, congestive heart failure, and coronary artery
disease.
• Iatrogenic factors which promote arrhythmia include cardiopulmonary
bypass, manipulation or direct injury of the heart, certain drugs, and intraatrial catheters.
• Characteristics of the postoperative state including metabolic and electrolyte
imbalances, hypoxemia, excess sympathetic tone from pain or stress, and
volume overload all predispose the postoperative patient to arrhythmia.
142 J. A. Salotto
The evaluation of a patient with an arrhythmia
• Begin with a thorough history and physical exam.
Ask about family history of arrhythmias or sudden cardiac death, ischemic
or valvular heart disease, and recent medications.
A review of systems should include questions regarding chest pain, short-
ness of breath, a feeling of skipped heartbeats or palpitations, presyncope
(dizziness, lightheadedness, feeling faint), or syncope. These symptoms
may accompany any of the arrhythmias.
Try to determine factors which may precipitate or terminate the symp-
toms. For example, are symptoms relieved with breath-holding or the Valsalva maneuver? This would indicate a problem at or above the AV node
(a supraventricular tachycardia).
• Physical exam
Begin by assessing if the patient is hemodynamically stable or unstable,
and address the fundamentals of airway, breathing and circulation. Ensure
adequate intravenous access.
Assess mentation, ability to protect the airway, pulse rate, blood pressure,
distal perfusion, and consider any underlying ischemia or congestive heart
failure. Ensure that the patient is monitored with telemetry and continuous
pulse oximetry.
The urgency of therapy depends on hemodynamic stability.
If the patient is symptomatic from a bradycardia, call for a transcuta-
neous pacer.
If the patient has lost consciousness and the monitor demonstrates a
wide QRS complex, call for an electrical defi brillator.
If the patient is stable and the monitor demonstrates a rapid, narrow QRS
complex with P waves, consider supraventricular tachycardia as the diagnosis. In this situation, vagal maneuvers should be attempted (see below).
• Progress from simple, less invasive testing to more complex testing. The
first-line in diagnosis is electrocardiography (EKG).
Look for the presence of P waves. If P waves are not visible, suspect atrial
fi brillation. An atrial rate around 300 beats per minute suggests atrial fl utter. In atrioventricular block, there are more P waves than QRS complexes
— the sinoatrial node is fi ring but the signal is not conducting to the ventricles.
Dysrhythmias 143
A wide QRS complex is seen with ventricular tachycardias and also with
supraventricular tachycardias with a bundle-branch block or an accessory
pathway.
• Early in the evaluation of an arrhythmia, be sure to address any underlying
abnormalities which may be triggering the arrhythmia, including ischemia,
hypercarbia, proarrhythmic drugs, electrolyte imbalances, volume overload,
or a catheter which is placed too far into the right atrium.
• Another tool used in the evaluation of an arrhythmia is an echocardiogram.
This will evaluate for functional and structural abnormalities which may predispose to arrhythmia, and is especially recommended for those with
ventricular arrhythmias.
• Finally, invasive electrophysiological testing can give more information.
Cardiologists usually recommend this for those with a history of myocardial
infarction and ventricular tachyarrhythmia prior to ablation, for those with
syncope and impaired LV function or for those with structural heart disease.
Bradyarrhythmias
• Bradyarrhythmias are usually due to SA node dysfunction (failure to initi-
ate an impulse) or an AV conduction block (failure of conduction) which
results in a heart rate less than 60 beats per minute. Bradyarrhythmia can
represent a response to a medication, or it may be physiologic and present
at baseline.
• Common bradyarrhythmias in the postoperative period include sinus brady-
cardia, bradycardia from sinus node dysfunction, and the AV nodal heart
blocks.
• Bradyarrhythmias are commonly asymptomatic, but if cardiac output fails to
meet physiologic demands, symptoms can result. Despite a low heart rate,
cardiac output and oxygen delivery can be preserved if the heart is able to
compensate with an increase in stroke volume.
• Physiologic sinus bradycardia is caused by depressed automaticity in the SA
node. Sinus pauses up to 3 seconds or a heart rate as low as 30 beats per minute can be considered in the normal range if the patient is asymptomatic.
Sinus bradycardia is common in healthy athletes and during sleep. Bradycardia
may be present during periods of hypoxia in patients with obstructive sleep
apnea.
Symptoms include syncope, pre-syncope, fatigue, hypotension, and weak-
ness.
144 J. A. Salotto
• Bradycardia from sinus node dysfunction is often referred to as “sick sinus syn-
drome.” This entity is caused by abnormalities in the sinus node which lead to
disorders in atrial impulse formation and conduction. It may be caused by fibrosis of the SA node, most commonly from inflammation, infection, aging, surgical
trauma, or infarction. Less commonly, sick sinus syndrome may be caused by
infiltrative diseases, increased vagal tone, or collagen vascular diseases.
Extrinsic causes of sick sinus syndrome include medications like beta-
blockers, calcium channel blockers, and digoxin, electrolyte abnormalities, excess intracranial pressure, hypothermia, and hypothyroidism.
An EKG demonstrates bradycardia, sinus pauses, or transient sinus arrest.
Sick sinus syndrome is a common cause for pacemaker implantation.
• Bradycardia from atrioventricular conduction disturbances are commonly
known as atrioventricular block. AV block results from delayed conduction
through the atrioventricular node or through the His bundles. It may be secondary to fibrosis of the pathway, an electrolyte imbalance, an endocrine
disorder, or drugs. The etiology is similar to that causing sinus node dysfunction (fibrosis, inflammation, aging, etc.) A myocardial infarct in the
distribution of the right coronary artery may cause transient AV block.
First degree AV block is slowed conduction through the AV junction. The
PR value is greater than 0.2 seconds, with every P wave followed by a
QRS complex. The ratio of atrial to ventricular contractions is maintained
at 1:1.
Second degree AV block occurs when the atrial rhythm fails to conduct in
a 1:1 ratio, but some transmission is maintained.
Mobitz type I (Wenckebach) will demonstrate a stable PP interval, a
shortening of the RR interval, and progressive prolongation of the PR
interval until one P wave fails to conduct on an EKG.
Mobitz type II will demonstrate a stable PR interval with no predict-
able prolongation of the PR interval and random failure of P wave
conduction on EKG.
Second degree, high grade AV block is any conduction ratio of over 3:1.
Third degree AV block is known as complete heart block, and represents a
complete dissociation between atrial and ventricular activity.
• The treatment of symptomatic bradycardia depends on the presence or
absence of symptoms and hemodynamic stability.
Dysrhythmias 145
No treatment is needed for asymptomatic bradycardia, unless the etiology
is third degree heart block.
Correct electrolytes and withhold any medications which block the AV
node.
For symptomatic bradycardia leading to hypotension, altered mentation,
chest pain, or shock, give atropine 0.5 mg intravenously every 3–5 minutes
up to a total does of 0.04 mg/kg. This should be done in a monitored setting.
Initiate transcutaneous pacing if the arrhythmia is refractory to atropine.
Place pads anteriorly over the apex of the heart and posteriorly be-
tween the spine and the scapula.
Transcutaneous pacing is effective but uncomfortable to the patient.
Initiate transvenous temporary pacing if the patient requires pacing for
longer than a few minutes.
A permanent pacemaker is indicated for ongoing symptomatic SA
dysfunction, severe symptoms related to bradycardia, Mobitz type II
second degree or any third degree heart block, and symptomatic bradycardia with atrial fi brillation. After myocardial infarction, a persistent
second or third degree heart block (especially if symptomatic) or any
AV block associated with a bundle branch block should be treated with
pacemaker.
Tachyarrhythmias
• Tachycardias are categorized by where the irregular impulse originates, either
above the atrioventricular node (supraventricular tachycardia) or below the
atrioventricular node (ventricular tachycardia). Tachyarrhythmia implies a
rhythm that produces a heart rate greater than 100 beats per minute.
• Symptoms may include dyspnea, palpitations, dizziness, chest pain, or
syncope. Hemodynamic compromise may result.
• Supraventricular Tachycardia
In supraventricular tachycardia, an impulse arises above the bundle of His
and leads to a heart rate greater than 100 beats per minute. In postoperative
patients, the most common of these arrhythmias include atrial fi brillation,
atrial fl utter, and ectopic supraventricular tachycardia.
Atrial Fibrillation
146 J. A. Salotto
Atrial fi brillation occurs when an impulse arises above the bundle of
His which results in disorganized atrial activity and a dyssynchrony of
contraction of the atrium and the ventricle. Because contraction is not
coordinated, this causes loss of the “atrial kick” which in turn reduces
cardiac output. In those with poor heart function or little reserve, this
may lead to unstable hemodynamics. Stasis of blood in the heart can
lead to thromboembolic events.
Atrial fi brillation is the most common postoperative arrhythmia. Onset
usually occurs within 4 days of surgery.
The hallmark of atrial fi brillation on EKG is a loss of P-waves. Atrial
activity is rapid and disorganized, with an unpredictable ventricular
response.
Complications of atrial fi brillation include increased costs, longer hos-
pital stays, and an increased risk of thromboembolic events after 24 to
48 hours.
The most important risk factor for the development of atrial fi brilla-
tion after surgery is age over 60 years old. Other risk factors include
male gender, congestive heart failure, and valvular disease. Surgeries
including esophagectomy, pulmonary resection, intra-abdominal surgery, and vascular surgery all carry an increased risk of postoperative
atrial fi brillation.
Most postoperative atrial fi brillation is transient and often requires no
therapy. Of those who do not resolve spontaneously, the majority will resolve with pharmacologic rate or rhythm control during hospitalization.
Therapeutic intervention should be initiated for those with heart
failure, atrial fi brillation lasting over 48 hours, uncontrolled ventricular rates, and a history of prior stroke. Before initiating therapy,
ensure correctable etiologies such as electrolyte imbalance or volume
overload have been addressed.
The pillars of treatment for atrial fi brillation are rate control and
rhythm control.
Rate control slows the ventricular response to atrial fi brillation, allow-
ing for improved ventricular and coronary fi lling and improved cardiac
output. This is a good choice for early (<24 hours) postoperative atrial
fi brillation.
• Beta-blockers
Beta-blockers are safe and effective agents which have direct antiarrhyth-
mic activity on conduction cells and myocardial cells. They counteract the
Dysrhythmias 147
hyperadrenergic state of the postoperative period and have been shown to
accelerate conversion to sinus rhythm in comparison to calcium channel
blockers.
Recommended agents:
Esmolol (500 mcg/kg IV over 1 minute loading dose, then 50 mcg/kg/
minute IV drip).
Metoprolol (5 mg over 3–5 minutes, up to 3 doses, followed by 5 mg
IV every 6 hours).
Contraindications: hypotension, bradycardia, heart block, decompensated
heart failure, asthma.
• Calcium channel blockers (CCBs)
CCBs are recommended as second-line therapy for rate control, or as fi rst-
line in patients who cannot tolerate beta-blockers. They provide a strong
blockade of the calcium channel in the AV node which leads to slowed
impulse conduction.
One study by Siu et al. showed superior time to ventricular rate control
and symptom control with diltiazem when compared to amiodarone or
digoxin.
Recommended agents:
Verapamil (5–10 mg over 3-5 minutes, followed by 2.5–10 mg mainte-
nance dose)
Diltiazem (0.25 mg/kg over 3–5 minutes for maximum of 20 mg, fol-
lowed by 5–15 mg/hour maintenance dose).
May result in hypotension.
• Amiodarone
A good choice for ventricular rate control in atrial fi brillation in those with
heart failure and in those who are hemodynamically unstable.
Must be used under monitoring as side effects may include sinus brady-
cardia, AV block, respiratory dysfunction, and hypotension. For these reasons, not a great fi rst-line agent in stable patients.
Dose: 15 mg/min for 10 minutes, then 1 mg/min for 6 hours; follow with
maintenance dose of 0.5 to 1 mg/minute.
• Digoxin works indirectly by increasing parasympathetic stimulation to the
heart. This may not be enough to counteract the excess sympathetic stimulation found in a surgical patient. It is a good agent to use in heart failure.