Cardiac Dysrhytmias

7/28/2019 Cardiac Dysrhytmias

1/24

Cardiac Dysrhytmias

A 54-year-old man (90 kg, 181 cm, body mass index [BMI] 27.7 kg per m2) presented for

wide local excision of a melanoma on his thigh, along with intraoperative lymphatic mapping

and sentinel lymph node biopsy. He had no medical allergies, took no medicines, and

reported excellent exercise tolerance (he walks his treadmill at 5 mph and 15% grade for 30to 60 minutes nearly every day). His preoperative examination was significant only for sinus

bradycardia with a rate of 54 bpm. His heart and lung examination findings were normal. His

laboratory values (the surgeon ordered a complete blood count, electrolytes, blood urea

nitrogen [BUN], creatinine, and lactic dehydrogenase) and electrocardiogram (ECG)

demonstrated no abnormalities.

Anesthetic induction was carried out with fentanyl 200 g, propofol 200 mg, and

cisatracurium 14 mg. His trachea was intubated with a 7 Fr endotracheal tube, and anesthesia

was maintained with desflurane 5.8% in 50% oxygen per air. Cefazolin (1 gm) was given.

Shortly after anesthetic induction, but before incision, his sinus rate fell into the 40s and he

developed isorrhythmic atrioventricular dissociation (see Fig. 18.1). His blood pressure

(which had been 120/50 mmHg) fell to 80/30. A decision was made to insert atransesophageal pacemaker (TAPSCOPE, Cardiocommand, Inc, Tampa, FL), and pacing was

begun at 60 bpm. When the pacing rate was increased to 90 bpm, the patient developed a

second degree, Mobitz type I (Wenckebach) block (see Fig. 18.2).

After completion of his surgery, he admitted to feeling occasional pounding in his chest

and neck, especially at night. A subsequent Holter monitor revealed significant sinus

bradycardia with ventricular escapes. A permanent pacemaker was suggested to increase his

overall heart rate, because his postoperative echocardiogram showed moderate aortic

regurgitation in a structurally normal valve.

What Is the Importance of Cardiac Dysrhythmias?

Cardiac dysrhythmia (also arrhythmia) comprises any abnormality or perturbation in the

normal activation sequence of the myocardium. Cardiac dysrhythmias can produce too slow a

ventricular rate (bradydysrhythmia) or too fast a ventricular rate (tachydysrhythmia). These

abnormalities frequently occur in the perioperative period. Although some are benign and

require only watchful waiting or assurance of no biochemical derangements, others result

from developing or ongoing malignant process(es). Some dysrhythmias represent a harbinger

of a more serious condition (e.g., bradycardia that develops in the face of arterial hypoxemia).

According to Atlee, the first recorded death during anesthesia, that of Hannah Greener in

1848,1 was most likely because of ventricular fibrillation (VF) (a malignant cardiac

dysrhythmia) resulting from the sensitizing action of chloroform.2

Although lethal cardiac dysrhythmias remain a rare occurrence, any abnormal cardiac rhythm

represents a potentially unstable condition. Some dysrhythmias are dangerous because theyprovoke inappropriate medical intervention (such as the treatment of benign premature

ventricular contractions with antiarrhythmic agents as documented in the Cardiac Arrhythmia

Suppression Trial [CAST] study3), whereas other abnormal rhythms can threaten

cardiovascular homeostasis. Both bradydysrhythmias and tachydysrhythmias can produce an

imbalance between myocardial oxygen supply (by reducing cardiac output or shortening

diastole) and demand (by increasing rate), and some dysrhythmias can progress to life-

threatening situations (e.g., supraventricular tachycardia producing myocardial ischemia,

leading to ventricular tachycardia [VT] and death).

A cardiac dysrhythmia should always be considered in the differential diagnosis of any

sudden hemodynamic imbalance. For example, an abrupt reduction in blood pressure

associated with little change in heart rate might result from an atrioventricular(atrioventricular [AV])


2/24

P.256nodal junctional rhythm, and the hemodynamics in this case might be furthercompromised by the sympathetic discharge associated with an isorhythmic AVdissociation. Sometimes, merely reducing the depth of the inhalation anestheticagent, or the substitution of another balanced anesthetic technique, may end the

dysrhythmia and improve blood pressure.

FIGURE 18.1 Isorhythmic atrioventricular nodal dissociation. As noted in the text, this 54-

year-old man with outstanding exercise tolerance and preexisting sinus bradycardia

developed an accelerated idioventricular rhythm that overtook his sinus node pacemaker,

resulting in the rhythm strip shown here. The PP interval at complexes 3 to 4 (1,395 ms)

represents a rate of 43 bpm. The idioventricular escape interval was 1,250 ms (rate = 48

bpm). Note that QRS complex 8 is fusion beat, wherein the wide complex behavior of the

ventricular escape was overtaken (and, therefore, narrowed) by the sinus event (P wave) that

can be seen immediately preceding it.This chapter focuses on the origins, recognition, and treatment of the common

atrial and ventricular perioperative dysrhythmias. His-Purkinje system (HPS)conduction blockade (heart block) will be discussed as well. The authors haveassumed that that the reader has basic electrocardiographic knowledge.

FIGURE 18.2 Second degree atrioventricular Mobitz type I block (Wenckebach) during

transesophageal pacing. An esophageal stethoscope with two stainless steel rings for atrial

pacing was introduced to 36 cm (from the lips). Initially, atrial capture was obtained with an

indicated output of 8 mA and a rate of 60 bpm. When the pacing rate was increased to 90

bpm, Wenckebach block developed. The two top traces are electrocardiogram (ECG) leads II

and V5, respectively, and the bottom trace is the pulse oximeter plethysmogram. The

numbers (added) are shown below the pacing artifacts, which are large signals, initially

downward, and cause considerable distortion of the ECG baseline. The smaller, upwarddeflections are the QRS complexes. QRS complexes are absent after pacing artifacts 3, 6, 9,

and 11. Note that the interval from the pacing stimulus to the QRS lengthens in sequences 1-

3, 4-6, and 7-9. Because there are P-wave deflections at pacing stimulus 3 and 11, the lack of

a QRS indicates AV block. There is no P-wave deflection after pacing stimulus 6 and 9, and

therefore these QRS failures might have resulted from failure to obtain atrial capture with the

transesophageal pacing device.

What Are the Basic Facts About Bradydysrhythmias, and How Are They Managed?

SINUS NODE DYSFUNCTION

The sinoatrial (SA) node and the atrium are intimately involved in the initiation of a cardiac

cycle, and therefore any failure of these tissues can result in bradycardia. Conditions that lead

to failure of heart beat initiation include: Sinus node arrest (no spontaneous depolarization)

Sinus node exit block (SA node depolarizes but electric signal is not propagated

within the region of the SA node)

Atrial tissue failure (the propagating depolarization fails to reach the AV node)

Often, without electrophysiologic study, differentiation of these conditions is difficult if not

impossible. Abnormal electrolytes, preoperative -blocker use, and many of the

intraoperative drugs have the potential to aggravate bradycardia and bradycardia-dependent

arrhythmias.4

Probably the most common bradycardia results from the slowing of the sinus node, as in ourcase summary. In the operating room, it can be caused by drugs, especially dexmedetomidine


3/24

and vagotonic agents such as fentanyl, sufentanil, and remifentanil. In a retrospective analysis

of 6,663 electronically recorded cases of neuraxial anesthesia, Lesser et al. found that a

baseline heart rate


4/24

FIGURE 18.4 Third-degree atrioventricular block. This 12-lead electrocardiogram (ECG)

was obtained from an asymptomatic 83-year-old man. It shows a sinus rhythm with a rate of

77 bpm (note that P waves, marked by downward arrows, are hidden in the QRS complexes

as well as the T waves). The ventricular rate is 43 bpm and the QRS complexes are 150 ms in

duration and in a left bundle branch pattern. There is no relation between any P wave (arrowson the rhythm strip lead II) and an ensuing QRS. Also present on this ECG is left atrial

enlargement. The patient underwent placement of a permanent pacemaker followed by

uneventful parotidectomy.

Whether treatment (pharmacologic or pacing) becomes necessary depends upon the patient's

hemodynamic stability and medical condition. Pharmacologic therapy can include atropine,

ephedrine, or epinephrine. Some practitioners might also consider glycopyrrolate, but it is

indicated only for vagally induced bradycardia.10 Use of these chronotropic drugs can

sometimes lead to uncontrolled sinus tachycardia.11

PACING

In this setting, temporary cardiac pacing also can be considered. Pacing may be carried out

through transcutaneous, transvenous, transthoracic (introduction of pacing wire[s] directlyinto the thorax), and transesophageal modalities. Transcutaneous and ventricular-only

transvenous pacing, even if feasible, may exacerbate hemodynamic problems in patients with

cardiomyopathy, as these pacing modalities do not preserve AV synchrony (i.e., they produce

only ventricular or global myocardial activation). Although perioperative temporary pacing

has been completely reviewed elsewhere,12 a few important aspects will be discussed.

Transvenous

Transvenous cardiac pacing provides the most reliable means of temporary pacing, albeit at

the expense of the time required to arrange the equipment, establish central access, and

determine the appropriate position of the ventricular catheter to provide ventricular capture.

Flow-directed catheters and a right internal jugular approach afford the shortest insertion

times.13 The reported incidence of successful capture in urgent situations without fluoroscopy

ranges from 30% to 90%.14 Also, temporary pacing in the patient with a permanently placed

pacemaker or implantable cardioverter-defibrillator (ICD) may be contraindicated without

reprogramming, because the temporary pacing equipment can interfere with the permanent

cardiac generator.

Most transvenous, flow-directed pacing catheters offer only ventricular pacing. The

pulmonary artery AV pacing catheter, described by Zaidan in 1983,15 allows for AV

sequential pacing through electrodes attached to the outside of the catheter, as well as routine

pulmonary artery catheter functions. Combination of the two functions into one catheter

eliminates the need for separate insertion of temporary transvenous pacing electrodes.

However, several potential disadvantages exist with this catheter: Varying success in initiating and maintaining capture15

External electrode displacement from the catheter16 and

Relatively high cost when compared with standard pulmonary artery catheters

The Paceport PAC provides ventricular pacing with a separate bipolar pacing lead (Chandler

probe), which

P.259

allows more stable ventricular pacing as well as pulmonary artery catheter function.17 This

catheter has been used for successful resuscitation in cardiac arrest during closed chest

cardiac massage when transcutaneous and simple bipolar pacing had failed. A newer AVPaceport PAC adds another lumen to allow placement of another pacing lead for atrial


5/24

pacing. The atrial wire can also be used to diagnose supraventricular tachydysrhythmias

(supraventricular and ventricular tachycardia [SVT]) by atrial electrograms and to overdrive

pace of atrial flutter (AFL) and reentrant SVT.18

Transcutaneous

Transcutaneous pacing, first described by Zoll,19 is readily available and can be rapidly

implemented in emergency situations. Capture rate is variable, and the technique often causespain in awake patients, but usually is tolerated until temporary transvenous pacing can be

instituted. It may be effective even when endocardial pacing fails.20 It is now considered by

many to be the method of choice for prophylactic and emergent applications.21

Transesophageal

Esophageal pacing is the newest technique available, and it has been shown to be quite

reliable.22,23,24,25 Esophageal pacing is relatively noninvasive, well tolerated even in most

awake patients, and it appears to be devoid of serious complications. It is contraindicated in

the patient with atrial disease (e.g., atrial fibrillation (AF) or flutter), AV nodal disease, or

any patient with a permanently implanted cardiac generator, because the electric output from

the esophageal pacemaker can inhibit the output from the permanent device. This modality is

useful for heart rate support of cardiac output, overdrive suppression of reentrant SVT, andfor diagnostic atrial electrograms. Ventricular capture must be excluded before attempts are

made at rapid atrial pacing for overdrive suppression to prevent potential VT or VF. Some

surgical positions (e.g., prone) can increase the chance of unintentional ventricular capture,

and esophageal atrial pacing should be followed very carefully.26 Typically, the pacing

stimulus is delivered using a modified esophageal stethoscope, with the distal end of

esophageal stethoscope inserted to a depth of 30 to 40 cm from the teeth. Capture should be

confirmed using the peripheral pulse (i.e., from the pulse oximeter plethysmogram or an

invasive hemodynamic monitor), because the pacing stimulus often is large relative to the

QRS and frequently fools the electrocardiographic counting algorithm on the monitor. Atrial

capture is obtained in virtually all patients using an indicated output of 8 to 20 mA; the output

should be set to two to three times the threshold for capture. Thresholds are not influenced by

weight, age, atrial size, or previous cardiac surgery.25 Because there is no sensing element

involved, esophageal pacing is AOO


6/24

ventricular depolarization, inscribing a QRS complex often identical to that of the normal

sinus beat. APCs frequently reset the sinus node timing, so the interval from the APC to the

next true P wave might be less than fully compensatory.29 Frequently, the P wave from the

APC remains hidden in the prior T wave. If a P wave is present, it usually differs in

morphology from the normal sinus P wave, because it originates from a site different from

the SA node. Because the distance from this aberrant atrial focus might be different from thatof the SA node to the AV node, the PR interval also might be different from that of a sinus

event. Although these morphologic features can help differentiate APCs from premature

ventricular complexes (PVCs), none of these features is absolutely reliable. For instance, as

noted in the preceding text, the aberrant P wave may fall upon the preceding T wave and

becomes difficult to identify. The post-extrasystolic pause may appear fully compensated if

there is a delay in the sinus node discharge of the following beat. When aberrant ventricular

conduction occurs, the QRS complex may appear widened.

If the HPS is, in fact, redepolarized before complete repolarization of the conduction system

or ventricular tissue, a bizarre, wide complex QRS can be inscribed on the surface ECG.

Most commonly, this QRS will appear in a right bundle branch patternthis event is termed

the Ashman Phenomenon.30

P.260

FIGURE 18.5 An atrial premature contraction (PAC) resets the sinus node. In this strip, the

top trace is lead V5, the middle trace is the pulse oximeter plethysmogram, and the bottom

trace is from a noninvasive arterial pressure device (Tensys Corporation, San Diego, CA).

This strip was obtained from an awake, normal 30-year-old woman with a sinus rate of 44

bpm (interval of 1,365 ms) and PR interval of 200 ms. It shows a PAC (the third QRS

complex on the top trace) preceded by a P wave that is morphologically different from the

remaining P waves. The next true sinus event (fifth complex) takes place 1,390 ms from the

abnormal P wave, and the remainder of the sinus events follow this new timing cycle. The

fourth QRS most likely represents an AV junctional escape beat (narrow complex, similaraxis as remaining QRS events) that did not reset the sinus node timer. Owing to the profound

sinus bradycardia, there was sufficient time after each QRS for complete ventricular

repolarization.

A few simple criteria often help distinguish a wide complex QRS inscribed by an aberrantly

conducted APC from a PVC. Generally, the initial deflection of an aberrantly conducted QRS

is identical in direction to the sinus-induced QRS, and its configuration is similar to the right

bundle branch block (RBBB) pattern with a duration 0.14 seconds.

Hemodynamic SignificanceIn most cases, APCs are completely asymptomatic. When they occur frequently in the

conscious patient, they may cause palpitations or an unpleasant feeling of irregular heart

beats. APCs very early in the hyperexcitable phase of the cardiac cycle may precipitate

tachyarrhythmias, in particular AF.31

Prevalence

Occasional APCs are very common, even in patients without underlying heart disease. In

normal subjects, stress, physical exhaustion, heavy smoking, alcohol, and caffeine may

induce APCs. The frequency of APCs increases with increasing age and in the presence of

structural heart disease. The incidence of APCs is higher in patients with diseases of the

mitral valve such as mitral stenosis and mitral valve prolapse, ischemic heart disease, and

congestive heart failure. Noncardiac medical conditions associated with APCs include acuteand chronic pulmonary diseases, chronic renal failure, and metabolic abnormalities.


7/24

Management

In asymptomatic cases, no treatment is required for occasional APCs. For patients with

frequent symptomatic APCs, management begins with simple reassurance, along with

identification and avoidance of precipitating factors such as stress or excess caffeine. If these

measures fail to alleviate symptoms, drug therapy can be started with -blockers, 32 which

may also help prevent APCs from triggering other more serious tachyarrhythmias such as AF. PAROXYSMAL REENTRANT SUPRAVENTRICULAR TACHYCARDIA

Paroxysmal reentrant supraventricular tachycardias are characterized by abrupt onset and

regularity. The pathophysiology of these arrhythmias involves two tissues that have different

conduction velocities and refractory periods (slow and fast pathways). The impulse travels

down one

P.261pathway while the second is in the refractory period, then travels up the second,thereby perpetuating the arrhythmia. The most common paroxysmal reentrantsupraventricular tachycardia is AV nodal reentrant tachycardia, which involvesreentry within the AV node. AV nodal reentrant tachycardia usually demonstrates

a regular, narrow complex tachycardia of 160 to 180 bpm. It is generally benignunless structural heart disease is present. Patients typically present withpalpitations and shortness of breath.

FIGURE 18.6 Atrial fibrillation. This 12-lead electrocardiogram (ECG) was obtained from a

72-year-old woman. It demonstrates an irregularly irregular rhythm without any clear relation

between small deflections that might be called P waves and the following QRS complexes. In

fact, this ECG was misdiagnosed by both the ECG machine and a number of physicians, who

believed this patient to be in sinus rhythm with APCs. Also seen is a leftward axis (-35

degrees), poor R wave progression, left ventricular hypertrophy, and T waves consistent with

strain.

ManagementVagal maneuvers, such as Valsalva maneuver or carotid massage (after ensuring there is no

carotid bruit) usually terminate the tachycardia. Adenosine can be used with good success

rates. AV nodal blocking agents, such as -blockers and calcium channel blockers, often are

effective in terminating and preventing the recurrence of AV nodal reentrant tachycardia.

Patients with refractory AV nodal reentrant tachycardia or those who do wish to take

medication can undergo catheter ablation.

ATRIAL FIBRILLATION AND ATRIAL FLUTTER

AF is the most common sustained atrial arrhythmia encountered in anesthesia practice. 33 AF

represents loss of the sinus node as the primary cardiac pacemaker, being replaced by totally

disorganized atrial activity with rapid fibrillatory waves with varying morphology and an

irregularly irregular ventricular rhythm on the ECG (see Fig. 18.6). The QRS complex isusually narrow but may be wide in cases of coexisting bundle branch blocks or aberrant

conduction. With QRS complexes of varying amplitudes and total irregularity of the arterial

pulse, this rhythm has often been classically referred to as delirium cordis. This arrhythmia

has important clinical implications because patients with AF have increased risk for

morbidity and mortality. AF can often lead to symptoms impairing patients' functional status

and quality of life.

AFL is sometimes seen with AF. It is characterized by more regular atrial activity, with a

saw-tooth pattern on ECG, and the ventricular response is generally regular because of a 2:1,

3:1, or greater atrial-to-ventricular conduction pattern (see Fig. 18.7). Sustained AFL is less

common than AF, and AFL generally degenerates to AF. The evaluation and management of

AFL is identical to that of AF and will be discussed in the subsequent text.

Epidemiology


8/24

The overall prevalence of AF is estimated to be one percent of the total population. The

prevalence increases with advancing agefrom 0.1% for people younger than 55 years to 9%

in those older than 80 years34 Prevalence is higher

P.262in men than in women, and higher in whites than African Americans. The risk of

AF increases with cardiovascular diseases such as hypertension, ischemic heartdisease, valvular heart disease, and sick sinus syndrome.35

FIGURE 18.7 Atrial flutter with a variable ventricular response. This 12-lead

electrocardiogram (ECG) was obtained from a 58-year-old man on postoperative day 3

following a right thoracotomy with right upper lobectomy. Note the notching of the baseline,

primarily showing in lead II. The variable block in this setting has produced the irregularly

irregular ventricular rhythm. Left ventricular hypertrophy is present with considerable T-

wave flattening. (Courtesy of Daniel Lenihan, MD, FACC.)

Classification

AF has been classified based upon its morphology and appearance on ECG. The baseline

undulations may be clearly distinct and visible (coarse AF), intermediate (medium AF), orbarely discernable (fine AF). To the extreme, there may be no perceptible undulation of the

baseline. There is no consistent correlation of these different types of AF with either the

severity of AF or its associated underlying cardiac conditions. Currently, the American

College of Cardiology/American Heart Association/European Society of Cardiology

(ACC/AHA/ESC) classifies AF into four types as follows:36

PAROXYSMAL: Sudden AF that spontaneously reverts; that is, the abnormal rhythm

self-terminates in < 7 days (usually


9/24


10/24

patients with rheumatic heart disease found a prevalence of 70% in those with mitral stenosis,

mitral regurgitation, and tricuspid regurgitation. Patients with mitral stenosis and mitral

regurgitation had a 52% prevalence of AF, whereas isolated mitral stenosis had a 29%

prevalence.43

Cardiomyopathy and congestive heart failure are found in up to 30% of AF patients.44 AF has

been reported in 10% to 28% of patients with hypertrophic cardiomyopathy.45 Surprisingly,stable coronary artery disease remains an uncommon cause of AF. In the Coronary Artery

Surgical Study involving 18,000 patients with chronic, stable coronary artery disease

documented by angiography, AF was present in only 0.6%.46 In acute severe ischemia,

however, AF can be precipitated by hypoperfusion of the left atrium, especially during an

acute inferior wall myocardial infarction (MI);47,48 AF has been shown to occur transiently in

6% to 10% of patients with an acute MI. The development of AF during an MI portends a

worse prognosis due to comorbidities such as older age and heart failure.

Hyperthyroidism appears to be a significant precipitating factor in AF. In one population-

based study involving 40,000 patients with clinical hyperthyroidism, 8% had AF.49 In patients

older than 60 years, AF occurred in 10% to 20%, but in patients younger than 40 years, the

risk was < 1%. The underlying pathophysiology usually includes a hyperdynamic circulationsecondary to increased sympathetic stimulation, hypersensitivity of -receptors, and dilated

cardiomyopathy. Hyperthyroidism should always be suspected in cases of AF in the absence

of cardiac causes. Subclinical hyperthyroidism, defined by a low serum thyroid-stimulating

hormone (TSH) concentration with a normal serum thyroid hormone level, appears to

increase the risk of AF fivefold.50 Spontaneous reversion to sinus rhythm often occurs within

6 weeks in patients who achieve a euthyroid state. Patients older than 60 years often

demonstrate an age-related decline in the frequency of spontaneous reversal. 51

Chronic lung disease, especially chronic obstructive pulmonary disease and obstructive sleep

apnea, appears to produce right ventricular dysfunction as a result of chronic hypoxia and

pulmonary hypertension. Longstanding pulmonary hypertension ultimately causes

chronically elevated atrial pressures and dilation, leading to AF. Patients with untreated

obstructive sleep apnea have a higher frequency of AF recurrence if it remains untreated. 52

Assessment and Evaluation

Assessment of patients with AF should include a history and physical examination, ECG,

chest radiograph, echocardiogram, and thyroid function tests. Further investigation, when

indicated, includes Holter monitoring, exercise stress testing, and electrophysiologic studies.

The intent of these studies is to define symptoms, the clinical type, the frequency and

duration of AF episodes, as well as any precipitating causes. Searching for reversible

precipitating factorssuch as the recent use of caffeine, alcohol, or marijuanais important,

as episodes of AF incited by these causes will usually abate once the factors are removed. In

older patients, coexisting medical problems should be ruled out, such as untreatedhyperthyroidism and chronic lung disease. Patients with structural heart disease usually

develop AF from underlying cardiac conditions, such as mitral stenosis from rheumatic heart

disease, hypertension, ischemic heart disease, and cardiomyopathy.

The physical examination should focus on findings associated with the conditions mentioned

in the preceding text. Electrocardiography will verify the presence of AF, as well as other

abnormalities such as prior MI, left ventricular hypertrophy, bundle branch block, or

preexcitation. A chest radiograph can aid in assessment of lungs and cardiac silhouette.

Transthoracic echocardiography can be used to evaluate atrial size, ventricular function, and

valvular heart disease. It may also identify a thrombus in the left atrium, although sensitivity

is superior with transesophageal echocardiography (TEE) for identification of thrombi in the

left atrium or left atrial appendage. Exercise stress testing might be indicated to investigateexercise-induced AF or detect underlying ischemic heart disease. Holter monitoring will help


11/24

document intermittent AF, poor rate control, or other associated arrhythmias. Finally,

electrophysiologic studies may be needed to identify the focus of AF that may be amenable to

possible catheter ablation.

Management

The principle objectives in the management of AF include ventricular rate control and

prevention of thromboembolic complications. In any patient, a logical approach includes thefollowing questions:

Is the patient hemodynamically stable or unstable?

Has the duration of AF been more than 48 hours?

Is AF associated with a preexcitation syndrome such as Wolff-Parkinson-White

(WPW) syndrome?

Does the patient have ongoing ischemia, cardiomyopathy, or congestive heart failure?

For unstable patients with a rapid ventricular response resulting in deteriorating

hemodynamics, emergent cardioversion is indicated. Primary indications for urgentcardioversion include significant arterial hypotension and poor perfusion of vital organs,

particularly in patients with severe underlying cardiopulmonary and cerebrovascular disease.

Manifestations of life-threatening conditions brought on by acute AF include congestive heart

failure and coronary or cerebral ischemia. AF in patients with an underlying preexcitation

syndrome may result in extremely rapid ventricular rates and severe hypotension, which also

requires urgent cardioversion. Following cardioversion, atrial contraction may be impaired by

the stunning effect of electric discharge, and therefore the risk of thrombus formation remains

high. As a result, these patients should remain on anticoagulation therapy for at least 1 month.

P.265

In cases of stable AF, the practice guidelines of the ACC/AHA/ESC recommend rate control

and chronic anticoagulation for most patients. For patients with preserved left ventricularfunction, -blockers (e.g., atenolol) or calcium channel blockers (e.g., diltiazem) are

recommended. -blockers remain the preferred choice in patients with ischemic heart disease,

and calcium channel blockers may be preferable in patients with lung disease. Digoxin should

be considered for patients with a history of heart failure or in elderly patients with poor

exercise tolerance.

Even with a well controlled ventricular rate, chronic AF is associated with increased

thromboembolic strokes ranging from 3% to 5% per year.53 The risk of stroke increases with

advancing age >70 years and in the presence of underlying diseases such as congestive heart

failure, hypertension, diabetes, rheumatic heart disease, valvular disease, and history of prior

thromboembolic events.54 In most cases, chronic anticoagulation is achieved with warfarin.

Aspirin can be substituted when a contraindication to warfarin exists, but has lesseffectiveness for preventing thromboembolic complications.55

In stable patients who present with new onset AF of


12/24

should take place immediately before cardioversion to rule out the presence of intracardiac

thrombi. TEE studies in patients with AF longer than 48 hours showed the presence of left

atrial appendage thrombus in approximately 15% of patients with AF. The Assessment of

Cardioversion Using Transesophageal Echocardiography trial randomized more than 1,200

patients to either TEE arm (TEE and cardioversion and 4 weeks of warfarin therapy) or

through a conventional approach (3 weeks of therapeutic anticoagulation followed by electriccardioversion and 4 weeks of warfarin therapy). The rate of embolic events were similar in

the groups, but patients in the TEE arm had a shorter duration of AF and higher cardioversion

success rates, with less bleeding.58

After successful cardioversion, more than 70% of patients without maintenance

antiarrhythmic therapy will experience recurrence of AF.59 Amiodarone is generally believed

to be the most effective agent for this purpose, followed by sotalol and flecainide. 60

Unfortunately, long-term prophylactic therapy can be associated with significant side effects.

Patients with AF who have an accessory AV pathway with a pre-excitation syndrome (e.g.,

WPW syndrome) can present with a ventricular rate exceeding 250 bpm, associated with a

widened QRS complex due to abnormal conduction over their accessory pathway. This

pattern may lead to the erroneous diagnosis of VT. Appropriate drug therapy for thesepatients can include procainamide or ibutilide (although reported to terminate AF in the

presence of WPW, this is an unlabeled indication for ibutilide.10)

Electric cardioversion can also be used. Drugs that slow normal AV conduction without

slowing the accessory pathway (e.g., -blockers, digoxin, or calcium channel blockers) are

contraindicated. Adenosine and lidocaine are ineffective and are also contraindicated,

because their use will delay appropriate therapy. Once the rhythm is stabilized, patients with

WPW and AF should be evaluated for catheter ablation of the accessory pathway.

Finally, caution is warranted in the acute treatment of patients with significant

cardiomyopathy or history of congestive heart failure when using calcium channel blockers.

These drugs can further depress myocardial function, which could aggravate the cardiac

failure. In these patients, IV amiodarone and digitalis (or -blocker in the patient with stable

cardiomyopathy) are the preferred drugs for rate control. Sotalol is contraindicated in patients

with impaired left ventricular function.

Intraoperative Atrial Fibrillation

The acute intraoperative onset of AF during general anesthesia should be considered a serious

cardiac event with potentially life-threatening consequences. As with any intraoperative

arrhythmia, mechanical irritation of the atria should be identified and eliminated. For

instance, the insertion of a guide wire during the placement of a central venous catheter has

been associated with both atrial and ventricular dysrhythmias, including APCs, PVCs, AF,

and VT. Sympathetic or parasympathetic discharge, which can occur during manipulation of

the trachea (intubation or tractions), heart, or brainstem, or during peritoneal traction, canresult in AF. Once these surgical manipulations are recognized and discontinued, the

arrhythmia usually resolves. In cases of severe hemodynamic deterioration caused by AF,

immediate cardioversion is indicated.

Even in the stable patient, the onset of new AF should be carefully investigated and properly

managed. Any underlying cardiac diseases that may have precipitated the AF, such as

myocardial ischemia and congestive heart failure should be identified and treated. An arterial

blood gas should be obtained to rule out hypoxemia, hypercarbia, acidosis, or alkalosis. Other

laboratory tests should include an electrolyte panel. Specifically, serum potassium and serum

magnesium should be obtained, as hypokalemia and hypomagnesemia are common in the

perioperative period and may contribute to the AF. These electrolyte abnormalities are also

common in patients who have been on diuretic therapy. If patients have been on digoxin


13/24

preoperatively, a digoxin level determination may be needed to confirm a therapeutic level or

rule out toxic levels. Placement of a central venous pressure

P.266

catheter may help guide fluid management and optimize volume status in patients with AF.

Without effective atrial contractions, no definite A waves can be detected on central venous

pressure monitoring. In more critically ill patients, pulmonary artery catheter placementmight be useful to assess pulmonary artery pressure, cardiac output, and mixed venous

oxygen saturation. Some patients may require inotropes, vasodilators, or changes in their

fluid therapy. New onset AF can also be evaluated using intraoperative TEE, which offers

valuable data in the management of the patient with coexisting ischemic heart disease and

congestive heart failure.

Postoperative Atrial Fibrillation

Some surgical procedures, such as coronary artery revascularization, as well as disease

comorbidities seem associated with higher rates of postoperative AF. AF has been reported in

approximately 35% of patients following coronary artery bypass surgery.61 In one study of

patients undergoing thoracic noncardiac surgery, a retrospective analysis of 2,588 patients

revealed a 12.3% incidence of postoperative AF, with risk factors such as age >50 years,history of congestive heart failure, male gender, history of arrhythmias or peripheral vascular

disease, and intraoperative transfusion.62 Studies have shown that the perioperative use of -

blockers may reduce AF incidence.63 To decrease the frequency of postoperative AF,

amiodarone for 1 week has also been given. Patients who experience transient AF after

thoracic surgery may also respond to calcium channel blocking drugs such as diltiazem or

verapamil for rate control.64 Usually, in the absence of prior AF history, acute postoperative

AF generally resolves without long-term treatment. However, these patients have higher

mortality rates, longer hospital stays, and, as a result, higher mean hospital charges. When AF

lasts longer than 48 hours, anticoagulation therapy becomes necessary.

Even in other types of surgery, acute AF may occur in the immediate postoperative period.

Upon emergence from general anesthesia, a variety of factors may contribute to severe

sympathetic stimulation and generalized vasoconstriction in the postanesthesia recovery unit:

Withdrawal from anesthetic drugs

Inadequate postoperative analgesia

Hypoxia and hypercapnia due to inadequate ventilation from residual paralysis or

narcotization

Severe shivering from postoperative hypothermia, and discomfort from a distended

urinary bladder

Whether these changes result from sudden shifts in vascular volume due to factors such as thewithdrawal of vasodilating anesthetic agent(s), increased sympathetic tone accompanying

emergence and extubation, or pulmonary vascular changes due to changes in oxygen tension,

acute AF during emergence frequently heralds the impending presence of acute pulmonary

edema. Meticulous management and monitoring of all cardiac and pulmonary parameters, as

well as careful attention to assure that the patient is pain-free and warm, remain the

imperative factors to prevent this serious postoperative complication.

How Are Ventricular Dysrhythmias Evaluated and Managed?

Ventricular dysrhythmias commonly present during the perioperative period. The severity of

these dysrhythmias range from PVCs, which usually represent a benign condition, to

nonsustained VT, to sustained VT, and finally VF and death.

PREMATURE VENTRICULAR COMPLEXES


14/24

PVCs originate from spontaneous depolarization of ventricular tissue, and they occur earlier

in the cardiac cycle than normal ventricular depolarization conducted along the HPS bundle.

Typically, a PVC appears on the surface ECG as a bizarre, wide complex QRS with an ST

segment in the opposite direction of the QRS deflection. Usually, no P wave precedes a PVC,

and, if the heart is in sinus rhythm, the atrial cycle is rarely disrupted. As a result, the next

atrial depolarization fails to conduct to the ventricle, and the PVC is followed by a fullcompensatory pause. As noted earlier, however, a ventricular depolarization initiated by the

HPS during the repolarization period can result in a bizarre, wide complex QRS that might

appear as a PVC (the Ashman Phenomenon).30

Two successive PVCs are called a couplet. Three or more successive PVCs are referred to as

VT. PVCs have been found in more than 50% of normal male volunteers, and they have

minimal prognostic significance if the left ventricular ejection fraction (LVEF) is preserved.

In patients with depressed LVEF, frequent PVCs are associated with increased mortality. 65 In

clinical practice, the occurrence of PVCs is particularly worrisome when it follows an acute

or extending MI. Therefore, in patients who present with frequent PVCs, structural heart

disease (i.e., cardiomyopathy) should be ruled out.

The need to treat PVCs depends on the severity of associated symptoms, the degree ofresulting hemodynamic compromise, and the presence of underlying cardiac disease. Certain

features of PVCs warrant intervention. Treatment should be considered for PVC frequency

>6 per minute, steadily increasing frequency, multifocal appearance, or frequent appearance

of successive PVCs. PVCs that occur early in the cardiac cycle are also ominous because they

may result in the R on T phenomenon, precipitating VT or VF.

Management

Asymptomatic PVCs, especially in a patient without evidence of cardiac disease, carry no

increased risk of sudden cardiac death.66 Therefore, they require no specific therapy apart

from careful observation and monitoring. For a patient presenting with PVCs associated

P.267

with mild symptoms, such as palpitations and fatigue, therapy should be directed at

alleviating these symptoms. Initial treatment includes reassurance and avoidance of

precipitating factors including excessive caffeine or alcohol, physical overexertion, and

environmental stress. If the patient does not improve despite these simple measures, low dose

-blockade can be started.

Patients who have well-documented structural heart disease, low LVEF, and frequent PVCs

are subject to the increased risk of sudden death. These patients should be carefully

investigated by 24-hour Holter ECG monitoring to detect recurrent episodes of nonsustained

VT. In the patient with an ischemic cardiomyopathy (LVEF


15/24

antibiotic, her QTc was 450 ms, afterward it was 515 ms. She underwent preoperative

chemotherapy with paclitaxel. Immediately following her segmental mastectomy and axillary

dissection with general anesthesia, she experienced her first episode of TdP at extubation.

Her underlying rhythm is sinus at 80 bpm (P waves are marked with the bars). The top trace

is electrocardiogram (ECG) lead II and the bottom trace is the invasive arterial pressure.

Treatment consisted of electric cardioversion and phenytoin, because her electrolytes werewithin normal range. (Courtesy of Joseph Swafford, MD, FACC.)

Classification

VT is classified as sustained or nonsustained. Sustained VT is defined as a run of VT lasting

longer than 30 seconds or resulting in severe hemodynamic collapse requiring emergency

termination. Nonsustained VT is defined as VT lasting 140 ms is present with VT and < 140 ms in SVT with

aberrant conduction.

The QRS morphology in SVT with aberrant conduction usually follows a RBBB

pattern. On the other hand, because of its ventricular origin, the QRS morphology in

VT often assumes a more bizarre appearance, typically resembling a ventricular beat

originating from a ventricular pacemaker.


16/24

In a patient with a history of ischemic heart disease, especially with low LVEF, and

without previous history of paroxysmal tachycardia, a wide complex tachycardia is

more likely to be VT instead of SVT with aberrant conduction.71

Pathophysiology

The ventricular substrate most favorable to the genesis of VT consists of an area of abnormalmyocardium next to an area of healthy myocardium, such as areas of myocardial fibrosis

following a myocardial infarct, or areas of distended myocardium due to congestive heart

failure. This juxtaposition creates a setting whereby slowed conduction, unidirectional block,

reentry, and perpetuation of reentrant circuits will precipitate VT.72,73 On the other hand, a

homogeneous, completely healed, fibrotic scar from an old infarct is much less likely to cause

reentry and VT.

Evaluation

Because VT can deteriorate to VF and sudden cardiac arrest, reversible conditions that

precipitate or sustain VT should be investigated, identified, and rapidly corrected. These

causes include electrolyte imbalances (especially potassium, magnesium and calcium), drug

toxicities, and serious cardiac disease such as acute coronary ischemia and congestive heartfailure. Even after the acute episode of VT has reverted to sinus rhythm, a comprehensive

investigation including a careful history, physical examination, and cardiac workup is

indicated. Although a 12-lead ECG is usually adequate to differentiate VT from SVT with

aberrant conduction, 24-hour Holter monitoring may be prudent to document the frequency

of VT episodes and their association with potential precipitating factors. Signal-averaged

ECG is useful to identify patients at high risk for developing VT.74 In patients with substrates

predisposing to VT, the conduction of the cardiac impulse is slowed by areas of abnormal

myocardium affected by necrosis, fibrosis, and inflammation. These areas produce small

electric potentials (late potentials) that arrive later than the normally conducted action

potential. These ventricular late potentials are on the order of microvolts, too small to be

detected on the surface ECG, although they can be identified with signal-averaged ECG

while the patient is in sinus rhythm. Exercise testing can help detect coronary artery disease

and may be useful to induce catecholamine-sensitive VT.75 An echocardiogram will help

detect structural heart diseases. Finally, electrophysiologic studies constitute the most reliable

method of confirming the diagnosis of VT.76 They also allow documentation of the

hemodynamic consequences of the VT, and identification of patients at high risk for

occurrence of VF who would require an ICD.77

Because the VTs comprise a very heterogeneous group of arrhythmias, each particular type of

VT will be discussed individually, including etiology, associated diseases, and treatment.

UNSTABLE VENTRICULAR TACHYCARDIA

The degree of hemodynamic compromise induced by VT depends not only on the rapidity ofthe ventricular rate, but also on the presence and severity of underlying cardiac diseases and

left ventricular function.78,79 The word unstable confers serious signs and symptoms of

hemodynamic deterioration, such as mental status change, dyspnea, or angina. Signs include

rles, rhonchi, pulmonary edema, hypotension, and acute ECG changes consistent with

ischemia. In this setting, unstable VT requires immediate therapy with synchronized

cardioversion to restore normal cardiac rhythm. In addition to supplemental oxygen,

continuous ECG monitoring and oxygen saturation by pulse oximetry should be instituted.

Intravenous access should be secured, and equipment for endotracheal intubation should be

ready, as further patient deterioration may be imminent.

STABLE VENTRICULAR TACHYCARDIA

In the hemodynamically stable patient with VT, an attempt should be made to differentiatemonomorphic from polymorphic VT. In monomorphic VT, the QRS complexes are wide,


17/24

regular, and stable, with a uniform configuration appearing almost identical in shape. The

morphology does not change from one beat to another. Monomorphic VT can be further

divided into two types, depending on the presence or absence of underlying heart disease.

P.269

In the patient with monomorphic VT and underlying structural heart diseases, the most

common pathologies include ischemic coronary artery disease and dilated cardiomyopathy.In the ischemic heart, the origin of VT typically involves an extensive fibrotic scar following

a MI. The juxtaposition of scar tissue and healthy myocardium serves as an anatomic basis

for slowed conduction and reentry. The risk is highest in the first months following an acute

MI. Even when the infarct is well healed and the ischemia is well controlled, these patients

still carry a significant risk for occurrence of VT many years later.80

Many patients with VT have underlying, nonischemic, dilated cardiomyopathy. This

heterogeneous group includes patients with decompensated valvular heart disease, alcoholic

and nutritional cardiomyopathies, hypertensive cardiomyopathy, chemotherapy-induced

cardiomyopathy, and viral myocarditis. Here again, the presence of patchy areas of dilated

myocardium next to healthy myocardial tissue serves as substrates for conduction blocks and

reentry. Monomorphic VT in the patient without underlying heart disease (idiopathic VT)carries a better prognosis than VT in the presence of structural disease. Examination of the

QRS morphology and its axis offers clues to the site of VT origin and the treatment of choice.

Monomorphic VT presenting with RBBB configuration and a superior axis usually originates

from the apex of the left ventricle. It often responds to verapamil, and, for this reason, is

referred to as verapamil-sensitive VT. It occurs most commonly in adolescents and young

adults with no detectable structural heart disease. It can be induced by atrial pacing and can

be readily terminated by verapamil, which also is effective in preventing recurrence. Because

of its relatively narrow QRS complexes and its favorable response to verapamil, this type of

VT has often been misdiagnosed as supraventricular tachycardia with aberrant conduction.

Monomorphic VT with left bundle branch block (LBBB) morphology and an inferior axis is

referred to as adenosine-sensitive VT. It is usually precipitated by excessive caffeine,

strenuous exercise, and psychologic stress. It usually affects young to middle-aged adults. An

exercise stress test or infusion of a catecholamine such as isoproterenol will induce this

arrhythmia and an adenosine infusion can be used to abolish it. After the acute episode, -

blockers are the drug of choice for maintenance therapy to prevent recurrences.

POLYMORPHIC VENTRICULAR TACHYCARDIA

In polymorphic VT, the morphology of the QRS complexes changes from one QRS complex

to the next. Polymorphic VT can be subdivided into two types: Those with a normal baseline

QT interval and those with a prolonged QT interval. These QT intervals may be obtained

from the patient's 12-lead ECG recorded before the onset of current VT. 81

Polymorphic VT with normal baseline QT interval remains the most common presentation ofVT following acute myocardial ischemia secondary to coronary artery stenosis or coronary

artery spasm. In many instances, the conventional history of angina on exertion or obvious

ST abnormalities may not be present before the attack of VT. 82 Treatment is directed

primarily towards relieving myocardial ischemia with nitroglycerin, -blockers, or calcium

channel blockers. In the acute setting, electric cardioversion (unstable hemodynamics) or

amiodarone therapy (stable hemodynamics) should be employed. Amiodarone administration

is indicated following electric cardioversion. For chronic refractory cases, coronary

revascularization may be required.83

Polymorphic VT with a prolonged baseline QT interval often presents as TdP, in which the

initial deflection of the QRS complexes follow a periodic pattern of change from an upward

or positive direction to a downward or negative direction. This condition can either becongenital or acquired,84 and a prolonged QTc (QT interval corrected for heart rate, see the


18/24

subsequent text) portends an increased incidence of sudden cardiac death. 85 In the congenital

type, mutations in seven different genes designated as LQT 1 to 7 have been identified. These

genotypes usually express their clinical manifestations through two principal phenotypes: the

Romano-Ward syndrome and the Jervell-Lange-Nielsen syndrome. The former is more

common, transmitted through an autosomal dominant mechanism, and involves only the

heart. The latter is more rare, transmitted through an autosomal recessive mechanism, and isassociated with congenital sensorineural deafness.86 Excessive adrenergic stimulation caused

by physical exertion or emotional stress may precipitate VT, with resultant syncope or

cardiac arrest. blockade, aiming to reduce sympathetic stimulation of the myocardium, is

the treatment of choice. Left stellate ganglion sympathectomy for refractory cases has been

done with variable success. The rationale behind this treatment is the belief that VT is caused

by unbalanced predominance of the left sympathetic system over the right.

In the acquired type, TdP can be precipitated by severe electrolyte abnormalities such as

hypomagnesemia and hypokalemia. A large number of classes of drugs also known to cause

prolongation of the QT interval include antiarrhythmic agents, antihistamines, antibiotics, and

tricyclic antidepressants. Class IA antiarrhythmic drugs such as quinidine, procainamide, and

disopyramide and class III drugs such as sotalol, dofetilide, and amiodarone have been mostoften implicated. Furthermore, the risk of TdP increases dramatically in the setting of

combined effects of hypokalemia, hypomagnesemia, and antiarrhythmic drugs. Finally, other

significant contributing factors to the occurrence of TdP include congestive heart failure and

stroke.

Depending on the severity of the hemodynamic compromise, the modalities of treatment may

include urgent cardioversion or ventricular overdrive pacing. In more stable patients,

intravenous magnesium is the drug of first choice. It has the advantages of being effective in

both reverting the TdP and preventing its recurrence. Other effective modalities of treatment

include -blockers, overdrive pacing, and implantation of an ICD.70,87

P.270

Measurement of the QT interval can be difficult, and ECG-interpreted QT intervals can be

incorrect.88 Using the standard Bazett formula to correct for the normal shortening of the QT

interval with increasing heart rate,

QTc = QT(measured)/square root of RR interval [in seconds]

normal intervals are


19/24

not indicated in this situation because it carries a high risk of precipitatingrefractory VF in the setting of digitalis toxicity.

FIGURE 18.10 Evaluation of the QT interval. This strip was produced on a 12-lead

electrocardiogram (ECG) from a 64-year-old woman with pneumonia. She had multiple

myeloma and had undergone considerable chemotherapy exposures, including twoautologous stem cell transplants. Because of a heart rate of 108 bpm (RR interval 555 ms)

and a wandering baseline, the ECG machine incorrectly identified the QT interval as 323 ms

with a QTc of 433 ms (below the upper limit of normal 450 ms for women). In fact, the QT

interval is 390 ms, resulting in a QTc of 523 ms (see text for Bazett correction formula). This

woman experienced torsade de pointes approximately 10 minutes after this ECG was

obtained.

KEY POINTS

Sinus node dysfunction and atrioventricular blocks are commonly seen in anesthesia

practice. Whether treatment (either pharmacologic or pacing) becomes necessary

depends upon the patient's hemodynamic stability and medical condition. Pacing may

be carried out through transcutaneous, transvenous, transthoracic (introduction ofpacing wire[s] directly into the thorax), and transesophageal modalities.

Premature atrial contractions are common, benign, and usually require no treatment.

In the patient with frequent premature atrial contractions, it is necessary to exclude

underlying causes, including stress, physical exhaustion, heavy smoking, alcohol and

caffeine, and the presence of structural heart disease (mitral stenosis, mitral valve

prolapse, ischemic heart disease, and congestive heart failure), as well as noncardiac

medical conditions such as acute and chronic pulmonary diseases, chronic renal

failure, and metabolic abnormalities.

Paroxysmal supraventricular tachycardia (the most common form is AV nodal

reentrant tachycardia) usually presents as a regular, narrow complex tachycardia of160 to 180 bpm. It is generally benign unless structural heart disease is present. Vagal

maneuvers can terminate the tachycardia. Medical therapy with adenosine, -blockers,

or calcium channel blockers may be used.

AF is the most common arrhythmia. The prevalence increases with advancing age, is

higher in men than women, and is higher in whites than African Americans. The risk

of AF increases with cardiovascular diseases such as hypertension, ischemic heart

disease, valvular heart disease, and sick sinus syndrome. Lone AF refers to people

younger than 60 years without clinical or echocardiographic evidence of

cardiopulmonary diseases or hypertension.

Evaluation of new onset AF should include search for reversible precipitating factors

(e.g., recent use of caffeine, alcohol, or marijuana) and coexisting medical problems

(e.g., untreated hyperthyroidism or chronic lung disease). Structural heart diseases

such as mitral stenosis, hypertension, ischemic heart disease, and cardiomyopathy

should be ruled out.

Chronic AF is associated with increased thromboembolic strokes, ranging from 3% to

5% per year. The risk of stroke increases with advancing age >70 years and with the

presence of underlying diseases such as congestive heart failure, hypertension,

diabetes,

P.271


20/24

rheumatic heart disease, valvular disease, and history of prior thromboembolic

events.54 In most cases, chronic anticoagulation is achieved with warfarin. Rate

control with AV nodal blocking agents (digoxin, -blockers, and calcium channel

blockers) are generally effective.

When evaluating a wide complex tachycardia, VT is far more common than asupraventricular tachycardia with aberrant conduction. When in doubt, always assume

the dysrhythmia represents VT, and not SVT with aberrant conduction, especially in

patients with ischemic heart disease.

REFERENCES

1. Snow J. On chloroform and other anaesthetics. London: John Churchill; 1858.

2. Atlee JL III, Dennis DM: Cardiac dysrhythmias. In: Gravenstein N, Kirby RR, eds.

Complications in anesthesiology, 2nd ed. Philadelphia: Lippincott-Raven; 1996:281-315.

3. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. Preliminary report:

Effect of encainide and flecainide on mortality in a randomized trial of arrhythmia

suppression after myocardial infarction. N Engl J Med. 1989;321:406.4. Atlee JL, III, Pattison CZ, Mathews EL, et al. Evaluation of transesophageal atrial pacing

stethoscope in adult surgical patients under general anesthesia. Pacing Clin Electrophysiol.

1992;15(10 Pt 1):1515.

5. Lesser JB, Sanborn KV, Valskys R, et al. Severe bradycardia during spinal and epidural

anesthesia recorded by an anesthesia information management system. Anesthesiology.

2003;99:859.

6. Liu S, Paul GE, Carpenter RL, et al. Prolonged PR interval is a risk factor for bradycardia

during spinal anesthesia. Reg Anesth. 1995;20:41.

7. Mymin D, Mathewson FA, Tate RB, et al. The natural history of primary first-degree

atrioventricular heart block. N Engl J Med. 1986;315:1183.

8. Bernards CM, Hymas NJ. Progression of first degree heart block to high-grade second

degree block during spinal anaesthesia. Can J Anaesth. 1992;39:173.

9. Hayward R, Domanic N, Enderby GE, et al. Anaesthesia in first degree atrioventricular

block. Anaesthesia. 1982;37:1190.

10. Thompson Micromedix. Micromedix(R) Healthcare Series, Vol. 119. Greenwood

Village: Thompson Micromedix; 2006.

11. Smith I, Monk TG, White PF. Comparison of transesophageal atrial pacing with

anticholinergic drugs for the treatment of intraoperative bradycardia. Anesth Analg.

1994;78:245.

12. Rozner MA, Trankina MF. Cardiac pacing and electroversion. In: Kaplan JA, Reich DL,

Lake CL, et al. eds. Kaplan's cardiac anesthesia, 5th ed. Philadelphia: WB Saunders/ElsevierScience; 2006.

13. Lang R, David D, Klein HO, et al. The use of the balloon-tipped floating catheter in

temporary transvenous cardiac pacing. Pacing Clin Electrophysiol. 1981;4:491.

14. Syverud SA, Dalsey WC, Hedges JR, et al. Radiologic assessment of transvenous

pacemaker placement during CPR. Ann Emerg Med. 1986;15:131.

15. Zaidan JR, Freniere S. Use of a pacing pulmonary artery catheter during cardiac surgery.

Ann Thorac Surg. 1983;35:633.

16. Heiselman DE, Maxwell JS, Petno V. Electrode displacement from a multipurpose Swan-

Ganz catheter. Pacing Clin Electrophysiol. 1986;9(1 Pt 1):134.

17. Colardyn F, Vandenbogaerde J, De Niel C, et al. Ventricular pacing via a Swan Ganz

catheter: A new mode of pacemaker therapy. Acta Cardiol. 1986;41:23.


21/24

18. Trankina MF. Pacemakers and automatic implantable cardiac defibrillators. Semin

Anesth. 1993;12:165.

19. Zoll PM. Resuscitation of the heart in ventricular standstill by external electric

stimulation. N Engl J Med. 1952;247:768.

20. Estes NA III, Deering TF, Manolis AS, et al. External cardiac programmed stimulation

for noninvasive termination of sustained supraventricular and ventricular tachycardia. Am JCardiol. 63:177, 1989.

21. Zoll PM. Noninvasive cardiac stimulation revisited. Pacing Clin Electrophysiol.

1990;13(12 Pt 2):2014.

22. Luck JC, Markel ML. Clinical applications of external pacing: A renaissance? Pacing

Clin Electrophysiol. 1991;14:1299.

23. Pattison CZ, Atlee JL III, Mathews EL, et al. Atrial pacing thresholds measured in

anesthetized patients with the use of an esophageal stethoscope modified for pacing.

Anesthesiology. 1991;74:854.

24. Backofen JE, Schauble JF, Rogers MC. Transesophageal pacing for bradycardia.


25. Atlee JL III, Pattison CZ, Mathews EL, et al. Transesophageal atrial pacing forintraoperative sinus bradycardia or AV junctional rhythm: Feasibility as prophylaxis in 200

anesthetized adults and hemodynamic effects/of treatment. J Cardiothorac Vasc Anesth.

1993;7:436.

26. Trankina MF, Black S, Mahla ME. Cardiac pacing using a pacing esophageal stethoscope

in patients undergoing posterior fossa craniotomy in the three quarter prone position. J

Neurosurg Anesthesiol. 1994;6:340.

27. Roth JV, Brody JD, Denham EJ. Positioning the pacing esophageal stethoscope for

transesophageal atrial pacing without P-wave recording: Implications for transesophageal

ventricular pacing. Anesth Analg. 1996;83:48.

28. Burack B, Furman S. Transesophageal cardiac pacing. Am J Cardiol. 1969;23:469.

29. Wu D. Supraventricular tachycardias. JAMA. 1983;249:3357.

30. Kennedy LB, Leefe W, Leslie BR. The Ashman phenomenon. J La State Med Soc.

2004;156:159.

31. Josephson ME, Kastor JA. Supraventricular tachycardia: Mechanisms and management.

Ann Intern Med. 1977;87:346.

32. Venditti FJ Jr, Garan H, Ruskin JN. Electrophysiologic effects of beta blockers in

ventricular arrhythmias. Am J Cardiol. 1987;60:3D.

33. Chugh SS, Blackshear JL, Shen WK, et al. Epidemiology and natural history of atrial

fibrillation: Clinical implications. J Am Coll Cardiol. 2001;37:371.

34. Furberg CD, Psaty BM, Manolio TA, et al. Prevalence of atrial fibrillation in elderly

subjects (the Cardiovascular Health Study). Am J Cardiol. 1994;74:236.35. Psaty BM, Manolio TA, Kuller LH, et al. Incidence of and risk factors for atrial

fibrillation in older adults. Circulation. 1997;96:2455.

36. Fuster V, Ryden LE, Asinger RW, et al. ACC/AHA/ESC guidelines for the management

of patients with atrial fibrillation: Executive summary. A report of the American College of

Cardiology/American Heart Association Task Force on Practice Guidelines and the European

Society of Cardiology Committee for Practice Guidelines and Policy Conferences

(Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation):

Developed in Collaboration with the North American Society of Pacing and

Electrophysiology. J Am Coll Cardiol. 2001;38:1231.

37. Haissaguerre M, Jais P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by

ectopic beats originating in the pulmonary veins. N Engl J Med. 1998;339:659.P.272


22/24

38. Moe GK, Abildskov JA. Atrial fibrillation as a self-sustaining arrhythmia independent of

focal discharge. Am Heart J. 1959;58:59.

39. Tsang TS, Gersh BJ, Appleton CP, et al. Left ventricular diastolic dysfunction as a

predictor of the first diagnosed nonvalvular atrial fibrillation in 840 elderly men and women.

J Am Coll Cardiol. 2002;40:1636.

40. Vaziri SM, Larson MG, Benjamin EJ, et al. Echocardiographic predictors ofnonrheumatic atrial fibrillation. The Framingham heart study. Circulation. 1994;89:724.

41. Kochiadakis GE, Skalidis EI, Kalebubas MD, et al. Effect of acute atrial fibrillation on

phasic coronary blood flow pattern and flow reserve in humans. Eur Heart J. 2002;23:734.

42. Clark DM, Plumb VJ, Epstein AE, et al. Hemodynamic effects of an irregular sequence of

ventricular cycle lengths during atrial fibrillation. J Am Coll Cardiol. 1997;3:1039.

43. Diker E, Aydogdu S, Ozdemir M, et al. Prevalence and predictors of atrial fibrillation in

rheumatic valvular heart disease. Am J Cardiol. 1996;77:96.

44. Stevenson WG, Stevenson LW, Middlekauff HR, et al. Improving survival for patients

with atrial fibrillation and advanced heart failure. J Am Coll Cardiol. 1996;28:1458.

45. Robinson K, Frenneaux MP, Stockins B, et al. Atrial fibrillation in hypertrophic

cardiomyopathy: A longitudinal study. J Am Coll Cardiol. 1990;15:1279.46. Cameron A, Schwartz MJ, Kronmal RA, et al. Prevalence and significance of atrial

fibrillation in coronary artery disease (CASS Registry). Am J Cardiol. 1988;61:714.

47. Crenshaw BS, Ward SR, Granger CB, et al. Atrial fibrillation in the setting of acute

myocardial infarction: The GUSTOI experience. Global Utilization of Streptokinase and TPA

for Occluded Coronary Arteries. J Am Coll Cardiol. 1997;30:406.

48. Wong CK, White HD, Wilcox RG, et al. New atrial fibrillation after acute myocardial

infarction independently predicts death: The GUSTO-III experience. Am Heart J.

2000;140:878.

49. Frost L, Vestergaard P, Mosekilde L. Hyperthyroidism and risk of atrial fibrillation or

flutter: A population-based study. Arch Intern Med. 2004;164:1675.

50. Auer J, Scheibner P, Mische T, et al. Subclinical hyperthyroidism as a risk factor for

atrial fibrillation. Am Heart J. 2001;142:838.

51. Woeber KA. Thyrotoxicosis and the heart. N Engl J Med. 1992;327:94.

52. Kanagala R, Murali NS, Friedman PA, et al. Obstructive sleep apnea and the recurrence

of atrial fibrillation. Circulation. 2003;107:2589.

53. Frost L, Engholm G, Johnsen S, et al. Incident stroke after discharge from the hospital

with a diagnosis of atrial fibrillation. Am J Med. 2000;108:36.

54. Atrial Fibrillation Investigators. Risk factors for stroke and efficacy of antithrombotic

therapy in atrial fibrillation. Analysis of pooled data from five randomized controlled trials.

Arch Intern Med. 1994;154:1449.

55. Go AS, Fang MC, Singer DE. Antithrombotic therapy for stroke prevention in atrialfibrillation. Prog Cardiovasc Dis. 2005;48:108.

56. Nichol G, McAlister F, Pham B, et al. Meta-analysis of randomised controlled trials of

the effectiveness of antiarrhythmic agents at promoting sinus rhythm in patients with atrial

fibrillation. Heart. 2002;87:535.

57. Gallagher MM, Guo XH, Poloniecki JD, et al. Initial energy setting, outcome and

efficiency in direct current cardioversion of atrial fibrillation and flutter. J Am Coll Cardiol.

2001;38:1498.

58. Tong AT, Roudaut R, Ozkan M, et al. Transesophageal echocardiography improves risk

assessment of thrombolysis of prosthetic valve thrombosis: Results of the International PRO-

TEE Registry. J Am Coll Cardiol. 2004;43:77.

59. Pritchett EL. Management of atrial fibrillation. N Engl J Med. 1992;326:1264.


23/24

60. Roy D, Talajic M, Dorian P, et al. Canadian Trial of Atrial Fibrillation Investigators.

Amiodarone to prevent recurrence of atrial fibrillation. N Engl J Med. 2000;342:913.

61. Maisel WH, Rawn JD, Stevenson WG. Atrial fibrillation after cardiac surgery. Ann Intern

Med. 2001;135:1061.

62. Vaporciyan AA, Correa AM, Rice DC, et al. Risk factors associated with atrial

fibrillation after noncardiac thoracic surgery: Analysis of 2588 patients. J Thorac CardiovascSurg. 2004;127:779.

63. Crystal E, Connolly SJ, Sleik K, et al. Interventions on prevention of postoperative atrial

fibrillation in patients undergoing heart surgery: A meta-analysis. Circulation. 2002;106:75.

64. Sedrakyan A, Treasure T, Browne J, et al. Pharmacologic prophylaxis for postoperative

atrial tachyarrhythmia in general thoracic surgery: Evidence from randomized clinical trials. J

Thorac Cardiovasc Surg. 2005;129:997.

65. Bigger JT Jr. Relation between left ventricular dysfunction and ventricular arrhythmias

after myocardial infarction. Am J Cardiol. 1986;57:8B.

66. Kennedy HL, Whitlock JA, Sprague MK, et al. Long-term follow-up of asymptomatic

healthy subjects with frequent and complex ventricular ectopy. N Engl J Med. 1985;312:193.

67. Buxton AE, Lee KL, Fisher JD, et al. Multicenter Unsustained Tachycardia TrialInvestigators. A randomized study of the prevention of sudden death in patients with

coronary artery disease. N Engl J Med. 1999;341:1882.

68. Cleland JG, Ghosh J, Freemantle N, et al. Clinical trials update and cumulative meta-

analyses from the American College of Cardiology: WATCH, SCD-HeFT, DINAMIT,

CASINO, INSPIRE, STRATUS-US, RIO-lipids and cardiac resynchronisation therapy in

heart failure. Eur J Heart Fail. 2004;6:501.

69. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-

defibrillator for congestive heart failure. N Engl J Med. 2005;352:225.

70. Khan IA. Long QT syndrome: Diagnosis and management. Am Heart J. 2002;143:7.

71. Akhtar M, Shenasa M, Jazayeri M, et al. Wide QRS complex tachycardia. Reappraisal of

a common clinical problem. Ann Intern Med. 1988;109:905.

72. Josephson ME, Horowitz LN, Farshidi A. Continuous local electrical activity. A

mechanism of recurrent ventricular tachycardia. Circulation. 1978;57:659.

73. de Bakker JM, van Capelle FJ, Janse MJ, et al. Reentry as a cause of ventricular

tachycardia in patients with chronic ischemic heart disease: Electrophysiologic and anatomic

correlation. Circulation. 1988;77:589.

74. Gomes JA, Winters SL, Ip J, et al. Identification of patients with high risk of arrhythmic

mortality. Role of ambulatory monitoring, signal-averaged ECG, and heart rate variability.

Cardiol Clin. 1993;11:55.

75. Stevenson WG, Brugada P, Waldecker B, et al. Clinical, angiographic, and

electrophysiologic findings in patients with aborted sudden death as compared with patientswith sustained ventricular tachycardia after myocardial infarction. Circulation. 1985;71:1146.

76. Volgman AS, Zheutlin TA, Mattioni TA, et al. Reproducibility of programmed electrical

stimulation responses in patients with ventricular tachycardia or fibrillation associated with

coronary artery disease. Am J Cardiol. 1992;70:758.

P.273

77. Moss AJ, Hall WJ, Cannom DS, et al. Multicenter Automatic Defibrillator Implantation

Trial Investigators. Improved survival with an implanted defibrillator in patients with

coronary disease at high risk for ventricular arrhythmia. N Engl J Med. 1996;335:1933.

78. Hamer AW, Rubin SA, Peter T, et al. Factors that predict syncope during ventricular

tachycardia in patients. Am Heart J. 1984;107(5 Pt 1):997.

79. Lima JA, Weiss JL, Guzman PA, et al. Incomplete filling and incoordinate contraction asmechanisms of hypotension during ventricular tachycardia in man. Circulation. 1983;68:928.


24/24

80. Mukharji J, Rude RE, Poole WK, et al. Risk factors for sudden death after acute

myocardial infarction: Two-year follow-up. Am J Cardiol. 1984;54:31.

81. Nguyen PT, Scheinman MM, Seger J. Polymorphous ventricular tachycardia: Clinical

characterization, therapy, and the QT interval. Circulation. 1986;74:340.

82. Wolfe CL, Nibley C, Bhandari A, et al. Polymorphous ventricular tachycardia associated

with acute myocardial infarction. Circulation. 1991;84:1543.83. Eisenberg SJ, Scheinman MM, Dullet NK, et al. Sudden cardiac death and polymorphous

ventricular tachycardia in patients with normal QT intervals and normal systolic cardiac

function. Am J Cardiol. 1995;75:687.

84. Khan IA. Clinical and therapeutic aspects of congenital and acquired long QT syndrome.

Am J Med. 2002;112:58.

85. Straus SM, Kors JA, De Bruin ML, et al. Prolonged QTc interval and risk of sudden

cardiac death in a population of older adults. J Am Coll Cardiol. 2006;47:362.

86. Chiang CE, Roden DM. The long QT syndromes: Genetic basis and clinical implications.

J Am Coll Cardiol. 2000;36:1.

87. Passman R, Kadish A. Polymorphic ventricular tachycardia, long Q-T syndrome, and

torsades de pointes. Med Clin North Am. 2001;85:321.88. Charbit B, Samain E, Merckx P, et al. QT interval measurement: Evaluation of automatic

QTc measurement and new simple method to calculate and interpret corrected QT interval.


89. Yildirim H, Adanir T, Atay A, et al. The effects of sevoflurane, isoflurane and desflurane

on QT interval of the ECG. Eur J Anaesthesiol. 2004;21:566.

90. Owczuk R, Sawicka W, Wujtewicz MA, et al. Influence of spinal anesthesia on corrected

QT interval. Reg Anesth Pain Med. 2005;30:548.

91. Paventi S, Santevecchi A, Ranieri R. Effects of sevoflurane versus propofol on QT

interval. Minerva Anestesiol. 2001;67:637.

92. Morris SN, Zipes DP. His bundle electrocardiography during bidirectional tachycardia.

Circulation. 1973;48:32.

93. Kelly RA, Smith TW. Recognition and management of digitalis toxicity. Am J Cardiol.

1992;69:108G.

Documents

Cardiac Dysrhytmias