Bongard Frederic , Darryl Sue. Diagnosis and Treatment Critical Care

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CARDIAC PROBLEMS IN CRITICAL CARE

487

follow. Class Ic and class III antiarrhythmic agents such as

flecainide and amiodarone also can be helpful for medical

management of patients with bypass tracts. The develop-

ment of transvenous radiofrequency ablation of bypass

tracts obviates the need for long-term pharmacologic ther-

apy for most patients and has largely replaced surgical abla-

tion. AV nodal reentry arrhythmias without bypass tracts

and atrial flutter are also treated effectively with transvenous

ablation techniques.

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Atrial Tachycardia

Atrial tachycardia is an automatic rhythm (repetitive single

focus) and does not depend on the AV node and reentry to

continue. Atrial tachycardia is less common than AV nodal

reentrant rhythms and usually has a regular ventricular rate

of 140–220 beats/min, although AV block may cause the ven-

tricular rate to be considerably slower. The P waves have uni-

form morphology and relationship to the QRS complex.

Although calcium channel blockers, beta-blockers, and

digoxin usually will not terminate these atrial arrhythmias,

they will decrease the ventricular response rate by slowing AV

nodal conduction and therefore can effectively improve

hemodynamics. Slowing of the ventricular rate may be help-

ful in identifying underlying atrial activity on the ECG so

that a distinction can be made between atrial tachycardia, AV

nodal reentry, atrial flutter, and atrial fibrillation. After the

ventricular rate is controlled, conversion to sinus rhythm can

be attempted with class Ia, Ic, or III antiarrhythmic agents or

electrical cardioversion. Radiofrequency ablation can be con-

sidered in selected patients when the focus of the arrhythmia

can be localized and the arrhythmia occurs frequently.



Atrial Flutter

Atrial flutter is a macroreentrant arrhythmia and in many

ways behaves like atrial tachycardia. Atrial flutter always

should be considered when a patient presents with supraven-

tricular tachycardia with a rate of approximately 150

beats/min. The atrial flutter rate usually is approximately 300

beats/min, but because of normal delays in conduction

through the AV node, the ventricular response rate is slower

than the atrial rate, with only every other (2:1 AV block) or

every third (3:1 AV block) beat effectively conducted to the

ventricle. Increasing the degree of AV nodal block with drugs

(adenosine) or by carotid massage brings out the underlying

flutter waves on the ECG and establishes the diagnosis.

Drugs that increase AV nodal block usually—though not

always—can control the ventricular rate at rest, but conver-

sion to sinus rhythm usually requires either antiarrhythmic

drugs or, more commonly, electrical cardioversion. Ibutilide,

sotalol, or amiodarone can be tried. In general, atrial flutter

is more resistant to pharmacologic conversion than AV nodal

reentrant tachycardia. However, unlike atrial fibrillation and

atrial tachycardia, atrial flutter can be converted using fairly

small amounts of electrical energy, usually less than 50 J.

Atrial flutter also can be converted to sinus rhythm with

overdrive pacing using a transvenous right atrial pacemaker

electrode or an esophageal pacemaker electrode. Atrial flutter

is a rhythm that is amenable to radiofrequency ablation, with

success rates approaching those for other supraventricular

tachycardias. Given the difficulty of treating atrial flutter and

converting it with medical therapy, ablation provides effec-

tive long-term treatment.

A subset of patients with atrial tachyarrhythmia may

develop bradycardia after electrical cardioversion or drug

therapy. Patients with tachy-brady syndrome pose a particu-

lar problem in designing therapy and may require temporary

pacing if cardioversion is attempted. They also may require a

permanent pacemaker to generate an adequate ventricular

rate when receiving necessary drug therapy to control the

tachyarrhythmias.

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Atrial Fibrillation

Atrial fibrillation is a chaotic arrhythmia probably owing to

multiple reentry circuits within the atria that results in loss

of atrial contraction and an irregular, often rapid ventricu-

lar rate. Because of the rapid but unpredictable bombard-

ment of the AV node by the atrial fibrillatory impulses and

variable penetration of the impulses through the AV node to

the ventricle, the ventricular rate is highly variable. An irreg-

ularly irregular ventricular rate with the absence of P waves

is the hallmark of atrial fibrillation and makes it easily dis-

tinguishable from the other more organized and regular

atrial arrhythmias. Patients with acute atrial fibrillation may

develop hypotension, myocardial ischemia, decreased perfu-

sion of vital organs, and acute congestive heart failure.

Those with chronic atrial fibrillation have an increased risk

of atrial mural thrombus formation, usually in the left atrial

appendage, with the risk of subsequent systemic emboliza-

tion. Atrial fibrillation is very common in patients with

mitral stenosis, lung disease, sepsis, and hyperthyroidism, as

well as in any form of heart disease or after cardiac surgery.

Therapy is directed at slowing the ventricular rate initially,

followed, in appropriate patients, by conversion of atrial fibril-

lation to sinus rhythm. Slowing of the ventricular rate can be

achieved with β-adrenergic blockers, calcium channel block-

ers, or digoxin, all of which increase the AV nodal refractory

period. Control of the ventricular rate is particularly impor-

tant in patients with ischemia and chest pain, congestive heart

failure, mitral stenosis, and hypotension. Intravenous diltiazem

can be given at a dose of 5–10 mg followed by a continuous infu-

sion. Alternatively, intravenous digoxin is effective when given at

a dosage of 0.125–0.25 mg every 4–6 hours until the desired rate

is achieved or until 1–1.5 mg has been given. In some patients,

combinations of these drugs are necessary, but excessive AV

nodal blockade should be avoided. The goal of rate control is to

lower the ventricular rate to about 80–100 beats/min.

Ibutilide, an intravenous short-acting class III antiar-

rhythmic agent, can be used to convert atrial fibrillation to

normal sinus rhythm. When given before direct current (DC)

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cardioversion, it increases the likelihood of success. It has

proarrhythmic effects, including torsade de pointes, that

necessitate close monitoring during its infusion and for sev-

eral hours thereafter. Intravenous magnesium is given fre-

quently prior to ibutilide to reduce this risk. Combined use

with amiodarone may increase heart block or arrhythmias.

Sotalol, a class III antiarrhythmic with β-adrenergic blocking

properties, also can be used. These agents can be continued to

help maintain normal sinus rhythm. Long-term use of sotalol

and amiodarone, however, may result in bradycardia, which

may be prolonged with amiodarone because of the 32-day

half-life.

Today, conversion to sinus rhythm is only rarely

attempted using class Ia antiarrhythmic drugs such as

quinidine or procainamide. Before administering class Ia

drugs, the ventricular response rate must be well controlled

because acceleration of the ventricular rate may occur when

these drugs are given. This problem is also seen with atrial

flutter and atrial tachycardia. It also should be noted that

the administration of quinidine may result in nearly a dou-

bling of the serum digoxin level. Thus, a patient with atrial

fibrillation whose ventricular rate is controlled with

digoxin and who has no evidence of digoxin toxicity may

develop digoxin toxicity when quinidine is given.

Procainamide therefore may be a better short-term choice

in the critically ill patient receiving digoxin. Neither quini-

dine nor procainamide is well tolerated as a long-term oral

medication, and both also have significant proarrhythmic

effects. They are being replaced by the newer class agents

Ic agents flecainide and propafenone, which can be used

safely in patients without coronary disease, left ventricular

hypertrophy, or left ventricular dysfunction, and by the

class III agent dofetilide. The latter is safe in patients with

left ventricular dysfunction but does require initial in-

patient monitoring for excessive QT-interval prolongation.

Sotalol is also effective, but it too carries a risk of QT-

interval prolongation and torsades de pointes, necessitating

initial monitoring for safest administration. Amiodarone is

probably the most effective medication for maintaining

sinus rhythm, but its myriad of potentially dangerous side

effects indicate the need for caution in using it to treat an

arrhythmia that is not lethal.

Electrical cardioversion of atrial fibrillation to sinus

rhythm is effective at least acutely but generally requires higher

amounts of electrical energy than other atrial arrhythmias,

often more than 200 J. Newer biphasic defibrillators have a

higher success rate and require less energy. In a hemodynam-

ically unstable patient with rapid atrial fibrillation, electrical

cardioversion is the appropriate first treatment. Patients with

acute myocardial infarction, hypertrophic cardiomyopathy,

severe systolic left ventricular dysfunction, critical aortic

stenosis, or recent major surgery are patients who would

benefit from rapid restoration of normal sinus rhythm but

who might not tolerate the hypotensive episode or further

hypotension caused by the antiarrhythmic agents used to

chemically treat the atrial fibrillation.

Atrial fibrillation poses a risk of embolization because the

noncontracting atria are potential sites for thrombus forma-

tion, and the risk of embolization increases with cardiover-

sion. The greatest risk of embolization is associated with

atrial enlargement and atrial fibrillation of long duration.

Therefore, patients who have had atrial fibrillation for more

than 2–3 days should be anticoagulated for 3–4 weeks before

conversion is attempted. Alternatively, it has been shown to

be safe to undertake cardioversion if a transesophageal

echocardiogram performed while the patient is on anticoag-

ulation demonstrates no atrial thrombi and anticoagulation

is continued for 4 weeks after cardioversion. This approach

allows fairly prompt cardioversion of patients in whom the

duration of atrial fibrillation is unknown and avoids leaving

the patient in atrial fibrillation for several additional weeks.

Patients without mitral stenosis who develop acute atrial fib-

rillation can be cardioverted within the first few days without

anticoagulation.

Patients with atrial fibrillation who cannot be converted

to sinus rhythm are managed by controlling their ventricular

rates. Anticoagulation with warfarin should be considered

in patients with chronic atrial fibrillation because of the

increased frequency of embolic strokes even in the absence

of intrinsic heart disease. Patients at higher risk for embolic

events include the elderly; those with ischemic, valvular, or

hypertensive heart disease; diabetics; and patients with a

history of stroke or TIA. Aspirin may be an alternative in

otherwise healthy younger patients with lone atrial fibrilla-

tion or in those with contraindications to anticoagulation

with warfarin.



Multifocal Atrial Tachycardia

Multifocal atrial tachycardia is an atrial arrhythmia that can

be confused with atrial fibrillation, but it is managed quite

differently. This arrhythmia generally is seen in patients with

severe lung disease and respiratory failure. The hallmark of

this atrial tachycardia is an irregular ventricular rate but with

multiple atrial foci (P waves with different morphologic

appearances). Atrial fibrillation also has an irregular ventric-

ular response, but P waves are absent.

Treatment of the underlying lung disease and respiratory

failure usually corrects the arrhythmia. Once the precipitat-

ing pulmonary process resolves, sinus rhythm often returns.

Multifocal atrial tachycardia responds poorly to digoxin,

with neither slowing of the ventricular rate nor conversion to

sinus rhythm. Verapamil may be effective sometimes in slow-

ing ventricular rate and decreasing the frequency of ectopic

atrial beats.

VENTRICULAR ARRHYTHMIAS

Management of ventricular arrhythmias in the ICU is often

more complicated than management of atrial arrhythmias

because the treatment is sometimes worse than the disease,

and because these arrhythmias may be poorly tolerated by

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CARDIAC PROBLEMS IN CRITICAL CARE

489

critically ill patients. Rapid ventricular arrhythmias (eg, ven-

tricular tachycardia) require immediate treatment, particu-

larly in patients who have severe underlying cardiac disease.

Almost all antiarrhythmic agents used for the treatment of

ventricular arrhythmias may facilitate arrhythmias (proar-

rhythmic effect) and have a variety of other unpleasant or

life-threatening side effects. Therefore, treatment of ventric-

ular arrhythmias should be limited to those known to cause

hemodynamic compromise or those that occur in the setting

of underlying myocardial disease. In general, the more malig-

nant the arrhythmia appears—that is, the more rapid the

rate, the longer the duration of the arrhythmia, the more fre-

quent the occurrence, and the greater the hemodynamic

compromise (eg, hypotension or syncope)—the more

important it is to treat. In addition, the presence of ventricu-

lar tachycardia always should raise the question of ischemia

with underlying coronary artery disease.

The nuances of evaluation and management of sudden

cardiac death and nonsustained and sustained ventricular

tachycardia in the presence or absence of ventricular dys-

function are beyond the scope of this text. However, develop-

ment of significant ventricular arrhythmia justifies and

necessitates consultation with an electrophysiologist to

determine whether medical therapy is indicated, to assess

drug efficacy, and to consider more definitive treatment,

including implantable defibrillators and transvenous abla-

tion. The development of sudden cardiac death and sus-

tained ventricular tachycardia in patients without known

cardiac disease should result in a careful search for cardiac

disease, particularly ischemia. Cardiac catheterization with

coronary arteriography may be indicated.



Ventricular Ectopy (Premature Ventricular

Contractions)

Treatment of asymptomatic ventricular ectopy (ie, premature

ventricular contractions [PVCs]) is usually not indicated, par-

ticularly in light of many studies demonstrating both the lack

of efficacy and potential catastrophic side effects resulting

from treatment of non-life-threatening ventricular arrhyth-

mias in certain populations. Ventricular ectopy is often benign

and requires no treatment. However, development of PVCs

may be a clue to the presence of digoxin toxicity or electrolyte

or other metabolic imbalance—particularly hypokalemia but

also hypomagnesemia, alkalosis, hyperkalemia, hypoxemia,

and ischemia. Correcting these abnormalities often eliminates

the PVCs. High catecholamine states, including treatment in

an ICU, recent surgery, and prolonged pain, can result in

PVCs. Beta-adrenergic blockade may help to reduce the fre-

quency of PVCs in these patients.

Unifocal PVCs, bigeminy, and couplets (paired PVCs)

usually do not require treatment even in a patient with

myocardial ischemia. Antiarrhythmic therapy should be

reserved for patients with sustained or nonsustained ventric-

ular tachycardia accompanied by hemodynamic compro-

mise. However, the indications for short-term therapy of

PVCs are less rigorous than the indications for long-term

antiarrhythmic treatment, and short-term therapy to sup-

press PVCs may be appropriate while a patient is medically

unstable in the ICU. In patients with congestive heart failure

and ventricular ectopy, PVCs may not generate an adequate

stroke volume, and frequent PVCs may result in a reduced

cardiac output. Suppression of the ectopy therefore may be

indicated to increase cardiac output. This goal often can be

achieved with administration of intravenous lidocaine.

Procainamide and quinidine are alternatives that are essen-

tially no longer used. Their long- and short-term toxicity

generally outweighs any perceived benefit.

Lidocaine toxicity is seen most often in elderly patients

and those with decreased liver function or congestive heart

failure, and the proarrhythmic effects of lidocaine are mini-

mal. Both quinidine and procainamide can cause torsade de

pointes and worsening of ventricular arrhythmias; use of

these agents calls for close monitoring and careful consider-

ation of indications for therapy. The use of beta-blockers,

particularly in a patient who has evidence of a high-

catecholamine state (eg, tachycardia, agitation, and hyper-

tension), may result in a reduction in PVCs, heart rate, and

blood pressure.



Ventricular Tachycardia

Ventricular tachycardia is defined as three or more consecu-

tive ventricular beats and is most commonly a reentrant type

of tachycardia. Nonsustained ventricular tachycardia lasts for

less than 30 seconds and terminates spontaneously, in con-

trast to sustained ventricular tachycardia. Myocardial

ischemia is the most common situation in which ventricular

tachycardia is seen, but valvular heart disease, myocarditis,

and other forms of heart disease also predispose to this

arrhythmia. Patients with prolonged QT intervals with or

without administration of quinidine or another drug that

prolongs the QT interval (such as a tricyclic antidepressant)

may have a form of ventricular tachycardia known as torsade

de pointes. This arrhythmia presents as ventricular tachycar-

dia marked by a pattern of multiform ventricular beats with

the axis shifting with each beat, yielding an undulating QRS

pattern (Figure 21–6). Rapid ventricular tachycardia often

deteriorates into ventricular fibrillation.

In the presence of underlying cardiac disease, ventricular

tachycardia often deserves therapy. Nonsustained ventricular

tachycardia in the setting of acute ischemia or infarction

justifies antiarrhythmic suppression at least over the first

24–48 hours. A similar arrhythmia in a healthy 20-year-old

postoperative patient might be observed without therapy, or

the patient might be given a β-adrenergic blocker to decrease

the effects of excess catecholamines. Electrolyte imbalances

(particularly hypokalemia, hypomagnesemia, and alkalosis)

and hypoxemia increase ventricular irritability and therefore

may predispose to ventricular arrhythmias. In addition,

there is evidence that magnesium administration may

decrease or prevent ventricular arrhythmias even in the

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Figure 21–6. Four-channel ECG demonstrating torsade de pointes. This multiform ventricular tachycardia changes its axis with changing height and

direction of the QRS complex shifting over the episode. The arrhythmia was initiated by a premature ventricular contraction during a period of high-

degree heart block. Note that not all the P waves are conducted to the ventricle and that the ventricular rate is quite slow.

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CARDIAC PROBLEMS IN CRITICAL CARE

491

absence of hypomagnesemia. Digoxin toxicity, alcohol with-

drawal, and ischemia also must be considered in ICU

patients who develop ventricular arrhythmias.

As a general rule, patients with sustained ventricular

tachycardia that produces hemodynamic instability with

syncope, obtundation, hypotension, congestive heart failure,

or chest pain should be electrically cardioverted immediately

using 100–200 J. Persistent myocardial ischemia or hypoten-

sion that occurs while trying various pharmacologic agents

puts the patient at risk of further deterioration and ventric-

ular fibrillation. As the ventricle becomes more ischemic, sta-

bilization becomes more difficult, and intractable ventricular

fibrillation and death may ensue.

Pharmacologic conversion of ventricular tachycardia can

be used in patients with ventricular tachycardia who are tol-

erating this rhythm without chest pain, hypotension, or con-

gestive heart failure. Initial therapy is lidocaine administered

by an intravenous bolus of 1–2 mg/kg, followed by an intra-

venous infusion of 1–4 mg/min. Procainamide can be given

intravenously as a loading dose (500–1000 mg given at a rate of

50 mg/min), followed by an intravenous infusion (2–4 mg/min)

as an alternative if lidocaine fails. Intravenous amiodarone is an

effective alternative that is being used more frequently, and it is

now recommended as the initial antiarrhythmic medication for

refractory ventricular arrhythmia in Advanced Cardiac Life

Support (ACLS). Amiodarone has a fairly complicated load-

ing schedule: 150 mg is given over 10 minutes followed by 1

mg/min for 6 hours and then 0.5 mg/min for 18 hours.

Loading of amiodarone can be repeated if ventricular tachy-

cardia recurs. Bretylium, another class III antiarrhythmic

agent, is no longer available. Overdrive pacing to suppress

ventricular arrhythmias is helpful in occasional patients.

Patients with torsade de pointes or polymorphic ventricu-

lar tachycardia with a long QT interval are treated differently.

Antiarrhythmic drugs that prolong the QT interval should

not be given including class Ia (eg, quinidine or pro-

cainamide), class Ic (eg, flecainide or propafenone), and some

class III agents (eg, amiodarone or sotalol). These drugs

should be stopped if the arrhythmia occurs during their use.

Isoproterenol or ventricular overdrive pacing may be helpful

in suppressing the initiating ectopic beats and shortening the

QT interval; this is unlike other ventricular arrhythmias in

which β-adrenergic agonists may exacerbate the arrhythmia.

Indications for implantable defibrillators in the treatment

of ventricular arrhythmias are changing rapidly. They are not

generally placed in the acute setting for the management of

ICU-related ventricular arrhythmias. Patients with reduced

left ventricular function after myocardial infarction or owing

to cardiomyopathy, patients with complex ventricular

arrhythmias and depressed left ventricular function, and

patients at high risk for sudden arrhythmic death owing to

underlying heart disease are appropriate candidates. The

presence of an implantable cardiac defibrillator in an ICU

patient can complicate management of the arrhythmias,

including pacemaker-mediated tachycardia; inappropriate

shocks in an ICU setting in the presence of a variety of atrial

tachycardias could lead to inappropriate therapies. In an

emergency when there are incessant inappropriate

implantable cardiac defibrillator shocks, placement of a mag-

net over the implantable cardiac defibrillator usually will

inhibit the defibrillator from delivering therapy. Patients

with implantable cardiac defibrillators and increasing

arrhythmias in the ICU should have their device interrogated

by an electrophysiologist to determine the extent and type of

arrhythmia and to potentially modify the programming of

the device to better control the rhythm.

HEART BLOCK

Heart block occurs when one or more segments of the car-

diac conduction system transmit impulses at an inadequate

rate. Heart block can be divided into (1) sinus node prob-

lems including sinus arrest, sinus node Wenckebach, and

some forms of sinus bradycardia; (2) AV nodal block includ-

ing first-degree AV block, and second-degree Mobitz type I

block (Wenckebach); and (3) infranodal block including

bundle branch block, Mobitz type II AV block, and third-

degree heart block. Both Mobitz type II block and third-

degree heart block also can occur in the AV node, but they

are more commonly manifestations of infranodal disease. In

addition to degeneration caused by aging of the conduction

system, heart block can be induced iatrogenically with med-

ications or may be due to myocardial ischemia or infarction;

metabolic abnormalities; enhanced vagal tone from tracheal

irritation, suction, or intubation; abdominal distention; or

severe vomiting. Heart block sometimes can be confused

with other cardiac dysrhythmias.

It is important to determine whether the arrhythmia is

due to an inadequate impulse formation or poor conduction

from the atrium to the ventricles (default) or to a fast nodal

or ventricular rate relative to the atrial rate (usurpation).

Accelerated idioventricular rhythms, junctional tachycardia,

and isorhythmic dissociation are not due to heart block but

rather result from an acceleration of AV nodal or infranodal

pacemakers. Since there is no heart block, speeding of the

atrial rate will entrain the ventricles normally.

Heart block is managed differently depending on whether

the ventricular rate is adequate or there is clinically significant

bradycardia. Treatment of heart block should focus on several

issues: (1) identification of reversible causes, (2) the hemody-

namic consequences of the arrhythmia, (3) the potential to

progress or recur, and (4) the patient’s underlying medical

condition. For example, the management of patients with

second-degree heart block secondary to the combined use of

a calcium blocker and a β-adrenergic blocker for hyperten-

sion is different from management of a similar degree of heart

block owing to intrinsic conduction system disease. Time, cal-

cium, and perhaps isoproterenol may obviate the need for

even temporary pacing support in the former, but permanent

pacing probably will be required for the latter.

External cardiac pacing may be used for short periods of

time, permitting stabilization with adequate ventricular rates

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and decreasing the urgency of the need for temporary trans-

venous pacing. Temporary transvenous pacing should be

used in patients who are hemodynamically compromised by

heart block. Indications for both temporary and permanent

pacing in coronary artery disease are discussed in Chapter 22.



Heart Block & Conduction Disturbances

Sinus Bradyarrhythmias

The name sick sinus syndrome has been given to a variety of

bradyarrhythmias arising in the sinus node including sinus

arrest and symptomatic sinus bradycardia. When seen in

association with alternating bradycardia and supraventricu-

lar tachycardia, the term tachy-brady syndrome is sometimes

used. Many patients with sinus bradyarrhythmias have

intrinsic heart disease, but digoxin, beta-blockers, calcium

channel blockers, and other drugs may precipitate bradycar-

dia with syncope, hypotension, and heart failure. In patients

with drug-related bradyarrhythmias, discontinuation of the

drug is necessary; in others with symptomatic bradycardia, a

pacemaker may be necessary. As described earlier, treatment

of supraventricular tachycardia associated with alternating

bradycardia may require drug treatment of the tachycardia

(eg, digoxin and beta-blockers) and a pacemaker (because of

drug-induced bradycardia).

AV Block

Temporary or permanent alteration of conduction through

the AV node or bundle of His is classified as AV block.

Patients with prolonged PR intervals (>210 ms) have first-

degree AV block; this can be due to intrinsic conduction sys-

tem disease, increased vagal tone, or more commonly,

cardiac medications or ischemia. First-degree AV block is

usually benign. Second-degree AV block is diagnosed when

atrial impulses are conducted intermittently through to the

ventricles. In Mobitz type I second-degree AV block

(Wenckebach block), the PR interval lengthens on successive

beats prior to a nonconducted atrial beat (P wave without a

following QRS complex). The electrocardiographic pattern

that emerges is grouped beating in which the number of ven-

tricular complexes is equal to the number of P waves

minus 1. This rhythm is usually due to increased vagal tone

and is seen often in conjunction with reversible ischemia of

the AV node. Treatment of symptomatic or severe bradycar-

dia with Mobitz type I block is begun with atropine.

Isoproterenol and dopamine may be tried; a temporary pace-

maker is necessary occasionally if the ventricular response is

inadequate and prolonged.

Mobitz type II second-degree AV block is usually due to

disease in the infranodal conduction system. The PR interval

is constant in conducted beats. The QRS interval is usually

mildly prolonged secondary to the infranodal conducting

system disease. In the nonconducted or blocked beats, a P

wave is seen without a QRS interval. This form of block may

occur in a pattern or may occur randomly. Several P waves

without accompanying ventricular beats may be seen (3:1 or

4:1 block). A temporary pacemaker is often necessary with

this type of block because of the higher likelihood of pro-

gression to complete AV block, and the escape pacemaker

with type II block, which originates in the ventricle, may not

generate an adequate ventricular rate.

During complete heart block (ie, third-degree AV block),

no atrial impulses are conducted to the ventricles because of

usually infranodal or severe AV nodal conduction system dis-

ease. There is no relationship between P waves and the QRS

interval (AV dissociation). The prolonged QRS interval indi-

cates that ventricular activation is initiated by a ventricular

pacemaker (automatic focus). Ventricular rates of 25–40

beats/min are seen with these ventricular escape rhythms

and usually are inadequate to maintain acceptable cardiac

output and blood pressure. Temporary and often permanent

pacing is required in adults with type II second-degree heart

and third-degree heart block.



Malfunction of Permanent Artificial

Pacemakers

Permanent pacemakers are used to support cardiac electrical

activity and maintain adequate heart rate by providing elec-

trical stimulation to the cardiac chambers. Pacemaker leads

are placed transvenously, although occasionally they may be

placed epicardially in association with other cardiac surgery.

Pacemakers have become increasingly more complex and

sophisticated in the last 10–15 years. In addition to the famil-

iar single-lead pacemakers, which sense and pace in the ven-

tricular chamber, pacemakers now are often dual-chamber,

sensing and pacing in both the atrium and the ventricle, and

sometimes they have an additional left ventricular lead for

cardiac resynchronization to treat congestive heart failure.

Pacemakers can be programmed to interrupt arrhythmias by

overdrive pacing or by administering ectopic beats.

Pacemakers can have rate-responsive features that allow the

heart rate to increase in response to increased physiologic

demand. When the pacemaker’s rate-responsive sensor is

minute ventilation (measured by transthoracic impedance),

inappropriate tachycardia may be observed during mechani-

cal ventilation.

Because of these added features, assessing pacemaker

function has become extremely complex and requires knowl-

edge of the type of pacemaker, understanding of the algo-

rithms the pacemaker uses, and information about the mode

in which the pacemaker is functioning. For example, for a

rate-responsive pacemaker, knowing the rate at which the

pacemaker should be inhibited involves not only knowing its

backup settings but the ramp used to adjust the pacing rate

and the stimulus to which it is responding.

In a critically ill patient, the major concerns about perma-

nent pacemaker function are (1) that the electrical impulse

from the pacemaker results in stimulation and electrical acti-

vation in the heart, (2) that the pacemaker is providing an

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CARDIAC PROBLEMS IN CRITICAL CARE

493

adequate heart rate to meet the patient’s needs, and (3) that

the pacemaker is sensing the intrinsic cardiac activity and

not competing with it. A properly functioning pacemaker is

able to sense the intrinsic electrical activity of the heart so

that the pacemaker-generated rhythm and intrinsic rhythm

are not competing with each other. Failure to sense the

intrinsic rhythm raises the possibility of pacemaker-induced

arrhythmia; for example, ventricular tachycardia may result

from a pacemaker-triggered QRS interval occurring on a T

wave from the intrinsic rhythm.

In general, in the absence of battery failure, pacemaker

failure is almost always due either to lead malfunction from

wire fracture, loss of insulation, or fibrosis at the endocardial

contact site or to dislodgment in the cardiac chamber or dis-

connection at the connection between the pacemaker and

the pacemaker lead. Lead malfunctions produce problems

with both sensing and capturing, but often the malfunction

is intermittent, occurring when the lead is moved in a partic-

ular way, making detection difficult. Interrogation of the

pacemaker using the programming device provided by the

manufacturer will produce information about the pace-

maker’s settings as well as lead impedance, thresholds, ampli-

tude of sensed electrical activity, and strength of the battery.

This information often can differentiate lead malfunction

from component malfunction. Unfortunately, the older the

pacemaker, the less information can be derived from the pro-

grammer, and the older the pacemaker, the more likely it is

that malfunction will occur.

Programmability of the pacemaker, the ability to change

the rate of pacing or the relationship of ventricular to atrial

activation, allows manipulation of the patient’s hemodynam-

ics. For example, in a febrile or septic patient or one with

heart failure, increasing the ventricular rate may be needed to

increase cardiac output. In patients who develop atrial tach-

yarrhythmias, changing the pacemaker function to ignore the

atrial activity sometimes can allow much better rate control.

Blomstrom-Lundqvist C et al: ACC/AHA/ESC guidelines for the

management of patients with supraventricular arrhythmias:

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 (Writing Committee to Develop

Guidelines for the Management of Patients with Supraventricular

Arrhythmias). Developed in collaboration with NASPE-Heart

Rhythm Society. J Am Coll Cardiol 2003;42: 1493–531. [PMID:

14563598]

Delacrétaz E: Supraventricular tachycardia. N Engl J Med 2006;354:

1039–51. [PMID: 16525141]

Fuster V et al: ACC/AHA/ESC 2006 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

Guildines. Developed in collaboration with the European Heart

Rhythm Association and the Heart Rhythm Society. Circulation

2006;114:e257–354. [PMID: 17695733]

Gregoratos G et al: ACC/AHA/NASPE 2002 guideline update for

implantation of cardiac pacemakers and antiarrhythmia

devices: Summary article. A report of the American College of

Cardiology/American Heart Association Task Force on Practice

Guidelines (ACC/AHA/NASPE Committee to Update the 1998

Pacemaker Guidelines). J Am Coll Cardiol 2002;40:1703–19.

[PMID: 12427427]

Holdgate A, Foo A: Adenosine versus intravenous calcium channel

antagonists for the treatment of supraventricular tachycardia in

adults. Cochrane Database Syst Rev 2006;4:CD005154. [PMID

17054240]

Jarcho JA: Biventricular pacing. N Engl J Med 2006;355:288–94.

[PMID: 16855269]

Naccarelli GV et al: Old and new antiarrhythmic drugs for con-

verting and maintaining sinus rhythm in atrial fibrillation:

Comparative efficacy and results of trials. Am J Cardiol 2003;91:

15–26D. [PMID: 12670638]

Trappe HJ, Brandts B, Weismueller P: Arrhythmias in the intensive

care patient. Curr Opin Crit Care 2003;9:345–55. [PMID:

14508146]

Zimetbaum P: Amiodarone for atrial fibrillation. N Engl J Med 2007;

356:935–41. [PMID: 17329700]

Zipes DP et al: ACC/AHA/ESC 2006 guidelines for management

of patients with ventricular arrhythmias and the prevention of

sudden cardiac death. A report of the American College of

Cardiology/American Heart Association Task Force and the

European Society of Cardiology Committee for Practice

Guidelines (Writing Committee to Develop Guidelines for

Management of Patients with Ventricular Arrhythmias and the

Prevention of Sudden Cardiac Death). Developed in Collaboration

with the European Heart Rhythm Association and the Heart

Rhythm Society. Circulation 2006;114:e385–484. [PMID:

16935995]

CARDIAC PROBLEMS DURING PREGNANCY

Pregnant patients with cardiac disorders may pose difficult

management problems. One always must consider the

impact of therapy on both the patient and the fetus. It is

often possible to pick a medication that will achieve the

desired clinical effect without injuring the fetus. However,

when the issue of fetal injury secondary to medication arises,

the risks need to be defined and the patient advised.

Knowledge of which medications cross the placenta and have

known teratogenic effects is mandatory. Ultimately, it is the

patient and physician who need to make the decision about

fetal risks to be accepted or avoided.

Common cardiac problems that occur in pregnant

women and may lead to admission to the ICU include valvu-

lar heart disease, arrhythmias, congestive heart failure, and

pulmonary hypertension.



Valvular Heart Disease During Pregnancy

Valvular heart disease may be unsuspected in a woman of

childbearing age who has been previously healthy.

Rheumatic heart disease resulting in mitral stenosis is seen

with increased frequency in regions that have large Hispanic

and Asian populations.

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494

Clinical Features

Women with mitral stenosis often are asymptomatic until the

normal increase in blood volume and cardiac output occurring

during pregnancy leads to elevated left atrial pressures and pul-

monary venous hypertension. Tachycardia or atrial fibrillation

is seen often in the acute presentation. These patients present

with signs and symptoms mimicking asthma and, if heart dis-

ease is unsuspected, become progressively worse owing to

drug-induced tachycardia from treatment with β-adrenergic

agonists. Atrial fibrillation also may result in atrial thrombus

formation, so the initial presentation may be a stroke.

The rapid heart rate does not allow time for atrial emptying,

and left atrial pressures therefore rise, resulting in pulmonary

edema. The presence of a diastolic murmur and opening snap

consistent with mitral stenosis and an echocardiogram showing

decreased mitral valve area and increased right ventricular pres-

sure should lead to appropriate management.

Treatment

When mitral stenosis is the dominant cardiac lesion, β-

adrenergic blockers should be used to slow the heart rate and

allow more time for ventricular filling. In general, cardiose-

lective β-adrenergic blockers such as atenolol are preferred

because they cross the placental barrier less effectively than

noncardioselective beta-blockers such as propranolol. If

atrial fibrillation rather than sinus tachycardia is present,

digoxin also can be used to slow the ventricular rate.

Although calcium channel blockers such as diltiazem and

verapamil also will slow heart rate, their effects on the fetus

need to be considered. In pregnant patients with tight mitral

stenosis and especially those with atrial fibrillation, anticoag-

ulation is important to reduce the risk of a stroke. Depending

on the stage of pregnancy, unfractionated heparin or low-

molecular-weight heparin may be most appropriate.

Returning the patient to normal sinus rhythm may

improve cardiac function by allowing better rate control, and

restored atrial contraction will aid in left ventricular filling.

Cardioversion must be done with the patient fully anticoag-

ulated—with plans to continue anticoagulation—and it is

necessary to demonstrate that atrial thrombi are not present

by transesophageal echocardiography. Finally, in patients

with severe mitral stenosis who continue to have severe con-

gestive heart failure symptoms despite medical therapy, per-

cutaneous valvuloplasty can be considered. Patients should

be chosen based on appropriate valve morphology and the

absence of significant mitral regurgitation. Fetal age and via-

bility should be considered in the timing of the intervention,

and neonatologists and obstetricians should be involved in

weighing the risk and benefit to the fetus.

In patients with other types of valvular heart disease,

management is directed toward maximizing the patient’s

cardiac output. However, some of the unloading agents used

to treat left ventricular dysfunction and left-sided valvular

regurgitation may decrease blood supply to the placenta and

therefore to the fetus. Thus the risks of treatment must be

weighed carefully. Fetal monitoring can be used to help assess

the impact of therapy.



Arrhythmias During Pregnancy

Atrial and ventricular arrhythmias are often benign.

However, sustained rapid atrial or ventricular tachycardia

has the potential to impair uterine blood flow resulting in

compromised fetal oxygenation. Late in pregnancy, when

systemic venous return is limited by compression of the infe-

rior vena cava by the enlarged uterus, a tachyarrhythmia may

result in profound hypotension and syncope. Therefore,

pregnant women who complain of dizziness or syncope must

be evaluated and monitored carefully, usually in an inpatient

setting. Because of toxic side effects and potential effects on

the fetus, antiarrhythmic drugs should be used only for doc-

umented sustained arrhythmias, with drugs and dosages

chosen to minimize effects on the fetus. Beta-blockers and

digoxin generally are safe in pregnancy.



Congenital Heart Disease and Pulmonary

Hypertension During Pregnancy

Pregnancy in patients with cyanotic congenital heart disease

is associated with a high incidence of fetal loss as well as

maternal death. Pulmonary hypertension, atrial tach-

yarrhythmias, inability to increase cardiac output with

increased demand, and hypoxemia all result in inadequate

cardiac output to the mother and the fetus. Postpartum,

acute exacerbation of pulmonary hypertension and sudden

death occur frequently. Treatment during the pregnancy is

supportive, including restricting activity, avoiding volume

overload, and treating polycythemia. A controlled elective

delivery using an epidural block or cesarean section to mini-

mize myocardial demand should be considered. Inhaled nitric

oxide or intravenous prostacyclin can be used to help manage

the worsening pulmonary hypertension seen after delivery in

patients with Eisenmenger’s syndrome with cyanosis.

Elkayam U, Bitar F: Valvular heart disease and pregnancy: I. Native

valves. J Am Coll Cardiol 2005;46:223–30. [PMID: 16022946]

Elkayam U, Bitar F: Valvular heart disease and pregnancy: II.

Prosthetic valves. J Am Coll Cardiol 2005;46:403–10. [PMID:

16053950]

Elkayam U et al: Pregnancy-associated cardiomyopathy: Clinical

characteristics and a comparison between early and late presen-

tation. Circulation 2005;111:2050–5. [PMID: 15851613]

van Mook WN, Peeters L: Severe cardiac disease in pregnancy: II.

Impact of congenital and acquired cardiac diseases during preg-

nancy. Curr Opin Crit Care 2005;11:435–48. [PMID 16175030]

TOXIC EFFECTS OF CARDIAC DRUGS

Cardiac medications have changed the treatment of patients

with heart disease dramatically, improving the quality and

duration of life, but these drugs have side effects both major



CARDIAC PROBLEMS IN CRITICAL CARE

495

and minor. Some of the toxic effects are extensions of a

drug’s therapeutic effects, whereas others are idiopathic or

autoimmune in nature. In some patients, toxicity may

develop only when metabolic changes occur that result in

decreased clearance of the drug, but reactions may occur

unpredictably even when drugs levels are in the therapeutic

range. Thus drug levels that produce a desirable drug effect in

one patient may produce a life-threatening side effect in

another. Toxicity also may develop when several drugs inter-

act. Both the toxic and the therapeutic effects of drugs, their

interaction with other drugs, and drug metabolism should be

understood and considered in making treatment decisions

and in evaluating patients receiving cardiac medications.

Discussed below are some of the more common and

important side effects of frequently used cardiac medica-

tions. The key to treating critically ill patients with cardiac

drugs is always to consider the possible or likely side effects

and interactions of the drugs, especially when the patient has

unexplained problems.



Digoxin

Pharmacology

Digoxin is a glycoside that inhibits Na

-K

ATPase and

thereby changes the intracellular Na

concentration. By alter-

ing the amount of Na

available for the Na

-Ca

exchanger,

the net effect of digoxin is to increase the intracellular cal-

cium. Similarly, the effect of digoxin on Na

-K

ATPase also

alters the transmembrane potential of other cells and there-

fore affects cell excitability, conduction velocity, and refrac-

tory periods. Various cell types are affected differently; this

accounts for the differing effects of digoxin on atrial, AV

nodal, and ventricular tissue. Digoxin, like other cardiac gly-

cosides, also has neurally mediated effects that alter auto-

nomic balance and sympathetic output.

In appropriate doses, digoxin functions as an inotropic

agent, increasing contractility. Its clinically important elec-

trophysiologic effect is to block the AV node, thereby

decreasing the ventricular response rate in atrial fibrillation

and inhibiting reentrant supraventricular tachycardia.

Digoxin has a fairly long half-life of 36–48 hours. It also has

a relatively narrow therapeutic range. Digoxin is cleared pri-

marily by the kidneys with, perhaps, some clearance through

the GI tract.

In critically ill patients, rapidly changing renal function

and the requirement for multiple other drugs make the

development of digoxin toxicity more frequent. Electrolyte

abnormalities such as hypokalemia, hypomagnesemia, and

hypercalcemia enhance digoxin toxicity. Serum levels of

digoxin are affected by a variety of drugs. Quinidine alters

the renal clearance and volume of distribution of digoxin.

Therapeutic levels of quinidine double digoxin serum con-

centrations. Therefore, the dose of digoxin should be

reduced by half when instituting quinidine therapy.

Amiodarone, verapamil, and propafenone have similar

effects on renal clearance of digoxin and digoxin serum level,

although the magnitude of the effect is smaller. Periodic

determination of drug levels with appropriate dose reduc-

tion or cessation can avoid the worse complications.

Toxicity

Digoxin serum levels generally are considered therapeutic in

the range of 0.8–2 ng/mL, which, unfortunately, overlaps with

the range in which toxicity may be seen. Toxicity is rare in

patients with serum levels under 1.4 ng/mL but is seen with

increased frequency when serum levels exceed 2 ng/mL. The

positive inotropic effect of digoxin increases in a dose-related

manner, and this effect persists even in the face of high drug

levels. The toxic effects of digoxin can be broken down into

systemic and electrolyte effects and mild and severe arrhyth-

mias. With mild toxicity, the patient may develop nausea,

visual disturbances, and decreased appetite. At higher serum

levels of digoxin, as the Na

-K

ATPase is poisoned, hyper-

kalemia develops that may lead to cardiac arrest. Arrhythmias

seen at low levels of toxicity reflect the effect of digoxin on

automaticity, resulting in paroxysmal atrial tachycardia, junc-

tional tachycardia, and ventricular ectopy (particularly

bigeminy). Because digoxin increases AV nodal block, the

atrial tachycardias are associated with heart block.

Treatment

Treatment depends on the severity of toxic manifestations.

Withholding digoxin and correcting hypoxemia, hypokalemia,

and the acid-base disturbances that exacerbate digoxin toxi-

city usually correct arrhythmias over time. Marked bradycar-

dia in the setting of atrial fibrillation can be treated with

atropine in mild cases and temporary pacing in more severe

situations. Lidocaine or phenytoin often can control the less

serious ventricular arrhythmias. Electrical cardioversion may

be necessary acutely to treat sustained ventricular tachycar-

dia from digoxin toxicity when drugs and other measures

have failed, but there is an increased risk of arrhythmic com-

plications because of increased ventricular automaticity

caused by digoxin. Using less electrical energy (fewer joules)

may decrease the risk.

In cases of severe digoxin toxicity that include the devel-

opment of hyperkalemia, severe bradyarrhythmia, recurrent

ventricular tachycardia, or ventricular fibrillation, digoxin

immune Fab (ovine) can be lifesaving. This preparation is a

sheep antibody fragment that has a high affinity for digoxin,

rapidly binding to the drug and reversing its effect. The Fab

fragments have a lower molecular weight than complete anti-

bodies and thus have a greater rate and volume of distribu-

tion. The Fab-digoxin complexes are excreted in the urine,

thus enhancing renal clearance of the drug. Digoxin anti-

body is indicated in the setting of life-threatening digoxin

toxicity or when the ingestion of large amounts of digoxin

makes the development of toxic side effects likely. The dosage

of digoxin immune Fab depends on the digoxin level and the



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496

estimated volume of distribution. However, if the desired

effect is not achieved with the calculated dose, treatment

with the maximum dose is indicated in life-threatening situ-

ations. Side effects from digoxin immune Fab are minimal.

The drug is expensive, and its use therefore is reserved for

patients with severe life-threatening digoxin toxicity. In most

patients, prevention of digoxin toxicity is preferable and

achievable with forethought. For example, for elderly

patients or critically ill patients in the ICU with acute renal

failure or cardiogenic shock, digoxin should not be given as a

standing order for more than 1 day without careful review

and adjustment if necessary.



Antiarrhythmic Drugs

Lidocaine

Because lidocaine is metabolized by the liver, hypotension,

right-sided heart failure, and liver failure may result in

decreased clearance of this drug. Lidocaine has minimal

proarrhythmic and myocardial depressant effects. Its side

effects are primarily neurologic consisting of acute onset of

agitation, tremulousness, psychosis, and seizures.

Withdrawal of the drug and time are the treatments. If indi-

cated, another antiarrhythmic agent can be used when lido-

caine is discontinued.

Procainamide and Quinidine

Procainamide, used for treatment of both atrial and ventric-

ular arrhythmias, is cleared by the kidneys. Both the drug

and its by-product, N-acetyl procainamide (NAPA), accu-

mulate in patients with renal failure. Procainamide is a

myocardial depressant and can cause hypotension. It also can

cause QT-interval prolongation with the development of

polymorphic ventricular tachycardia similar to the effects of

quinidine. Unlike quinidine, procainamide does not alter

serum digoxin levels. A number of noncardiac side effects are

caused by procainamide, the most important being agranu-

locytosis and the development of a lupus-like syndrome.

Agranulocytosis is reversible, but the patient may present

with sepsis. The lupus-like syndrome is generally a late devel-

opment in the course of prolonged administration with man-

ifestations such as fever, pleuropericarditis, and arthralgias.

There are serum antihistone antibodies associated with this

drug-induced syndrome as well. This side effect may be seen

more frequently in patients who metabolize the drug slowly

(slow acetylators). The syndrome is reversible with discontin-

uation of the drug.

Quinidine should not be used as a routine drug in the

ICU and virtually never should be started as a new agent.

Quinidine, a class Ia agent whose indications are similar to

those of procainamide, has less myocardial depressant effects

but is only available orally. Its proarrhythmic effects are well

known, with QT-interval prolongation resulting in ventricu-

lar tachycardia and syncope. GI side effects are frequent, and

the development of nausea and diarrhea often limits its use.

Neurologic side effects include tinnitus, hearing loss, and

confusion. Autoimmune thrombocytopenia or hemolytic

anemia occasionally develops unexpectedly, resulting in

hemorrhage or death. Quinidine-induced thrombocytopenia

is treated as autoimmune thrombocytopenia.

If polymorphic ventricular tachycardia (torsade de

pointes) develops during treatment with quinidine or pro-

cainamide, the drug should be stopped, and other class Ia and

Ic agents should be avoided. Beta-adrenergic agonists such as

isoproterenol can be used to speed up the heart rate and

shorten the QT interval. Overdrive pacing with a transvenous

pacing wire also can be used in patients with recurrent ven-

tricular tachycardia until the offending drug is cleared or

metabolized. When monitoring the QT interval during

administration of quinidine or procainamide, the drug

should be discontinued if the QT interval exceeds 500 ms.

Flecainide

Flecainide is a class Ic antiarrhythmic agent that is well toler-

ated, with minimal noncardiac side effects. It is proarrhyth-

mic, however, and can cause significant and sustained

ventricular tachycardia that is resistant to other antiarrhyth-

mic agents. Flecainide slows conduction throughout the con-

ducting system, which can result in bradycardia as well as

heart block. It is poorly tolerated by patients with depressed

left ventricular function and should not be used for those

patients.

Amiodarone

Amiodarone is a powerful antiarrhythmic agent with mini-

mal proarrhythmic effects. However, it has a number of car-

diac and noncardiac side effects that are magnified by its long

half-life. Resulting toxicities can last from days to months

depending on the duration of therapy and the dose.

Amiodarone slows conduction throughout the heart, result-

ing in bradycardia and heart block, which may require per-

manent pacing. GI side effects include nausea and decreased

appetite resulting in weight loss and necessitating dose

reduction or termination of therapy. Either hypo- or hyper-

thyroidism can result from amiodarone’s effect on iodine

metabolism. Deposits in the skin can result in darkening of

skin especially in sun-exposed areas. Intracytoplasmic lamel-

lar deposits can occur in several parts of the eyes, most com-

monly causing corneal epithelial opacities in more than 70%

of patients and lens opacities in 50–60%. Neither impairs

visual acuity, and amiodarone treatment can be continued.

Pulmonary fibrosis is a frightening and potentially life-

threatening complication that can further compromise

patients who already have significant cardiac impairment.

Baseline and follow-up pulmonary function tests are manda-

tory to monitor the development of pulmonary involvement.

Amiodarone interacts with and changes the metabolism of a

myriad of drugs. Its interactions with digoxin, β-adrenergic

blockers, calcium channel blockers, and warfarin should be

monitored carefully.