Bongard Frederic , Darryl Sue. Diagnosis and Treatment Critical Care

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pulmonary artery, and pulmonary capillary wedge pressures.

Since the latter value is a rough estimate of the left ventricu-

lar end-diastolic pressure, pulmonary capillary wedge pres-

sure can provide valuable information regarding the

necessity for volume expansion or diuresis. The right-sided

heart catheters are equipped with a temperature-measuring

thermistor that allows determination of cardiac output by

thermodilution.

Right-sided heart catheterization should be considered at

any point during the course of an acute myocardial infarc-

tion when a question exists regarding fluid volume status.

For example, a patient with acute myocardial infarction and

possible pneumonia may have a lung examination that could

represent pulmonary edema, pneumonia, or both. On the

other hand, treatment of hypotension in the presence of sus-

pected right ventricular infarction usually can commence

without right-sided heart catheter guidance. Patients with an

acute inferior infarction who experience hypotension and

have clear lungs and no S

gallop should receive 500–1000

mL normal saline to see if volume expansion will increase the

blood pressure without causing rales. However, should fur-

ther volume supplementation seem necessary or should

incipient left-sided heart failure be present or suspected,

right-sided heart catheterization would be invaluable in

determining the true volume status of the patient.

For patients in whom hypotension persists for more than

an hour despite use of vasopressors, right-sided heart

catheterization is strongly advised.

4. Cardiac catheterization—Cardiac catheterization

after acute STEMI generally is reserved for patients who

develop instability. The routine use of cardiac catheterization

after acute myocardial infarction for the purpose of elective

angioplasty or bypass surgery has not found justification in

randomized trials of elective revascularization after acute

STEMI. Rather, patients who have an uncomplicated

myocardial infarction (no recurrent chest pain) can safely

undergo stress testing (usually with a low-level exercise pro-

tocol) prior to hospital discharge to identify those at high

risk for reinfarction or death who should undergo further

study.

Cardiac catheterization before hospital discharge is indi-

cated in two classes of patients: (1) patients who develop

chest pain after acute myocardial infarction, which is thought

to be ischemic in nature, and (2) patients who have chest

pain or evidence of ischemia on electrocardiography or

myocardial perfusion scintigraphy during low-level exercise

stress testing. These patients have “failed” medical therapy by

virtue of having chest pain in the hospital (presumably while

on adequate medication) and are likely to be best served by

undergoing coronary angioplasty or coronary bypass graft-

ing if their anatomy is found to be suitable by angiography.

Differential Diagnosis

The differential diagnosis of myocardial infarction is essen-

tially the same as that of angina pectoris (see above).

Treatment

Treatment may be divided into immediate and later phases.

Immediate therapy is empirical and is initiated after obtain-

ing the history, performing a physical examination, and

examining the ECG.

A. Initial Outpatient Treatment—Sublingual nitroglycerin

tablets or nitroglycerin spray should be self-administered if

the patient has either drug. Otherwise, sublingual nitroglyc-

erin should be administered by paramedics or by personnel

in the emergency department. A sublingual nitroglycerin

tablet (usually 0.3 mg) can be administered every 3–5 min-

utes (if pain persists) for an initial total of three to five

tablets. Repeat doses of nitroglycerin can be administered

once blood pressure monitoring is available and the patient

has no significant side effects such as dizziness or severe

headaches.

B. Immediate Hospital Therapy—Initial therapy of a

patient in the hospital suspected of having myocardial

infarction consists of nitroglycerin as indicated earlier.

Oxygen therapy, usually 2 L/min by nasal cannula, is fre-

quently begun empirically and adjusted based on pulse

oximetry. One aspirin tablet (325 mg) should be chewed and

swallowed by the patient to reduce subsequent morbidity

and improve chances for survival. For aspirin-allergic

patients or patients already taking prophylactic aspirin, oral

clopidogrel, 75 mg, may be substituted.

1. Reperfusion—All patients with STEMI must be consid-

ered for an early strategy for reperfusion at the time of initial

contact. The choice of strategy depends on duration of

symptoms, availability of resources, and relative risks of the

patient and the treatments.

Fibinolysis (ie, thrombolytic therapy) and an invasive

strategy (eg, angioplasty with stent) are the two options.

There is no preference for either strategy if presentation time

is less than 3 hours and there is no delay for an invasive strat-

egy. Otherwise, an invasive strategy generally is preferred if

the procedure can be performed within 60–90 minutes, the

patient is at high risk of complications from STEMI (eg, car-

diogenic shock or pulmonary edema), thrombolysis is con-

traindicated because of increased bleeding risk, or STEMI

diagnosis is in doubt. Thrombolytic therapy is preferred if an

invasive strategy is not an option or there is a potential delay

of angioplasty of more than 1 hour from hospital arrival to

onset of the procedure.

a. Thrombolytic therapy—If the patient has a classic his-

tory for acute myocardial infarction and has more than 1

mm of ST-segment elevation in two contiguous leads [eg, in

two inferior leads (II, III, or aVF), or in leads I and aVL, or in

two contiguous chest or V leads], thrombolytic therapy

should be an option. The presence of a left bundle branch

block not known to be old is also an indication for throm-

bolytic therapy.

Tenecteplase, intravenous streptokinase, or anisoylated

plasminogen streptokinase activator complex (anistreplase;

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APSAC) can be administered if the patient does not have one

or more of the following contraindications: active internal

bleeding; history of stroke; intracranial or intraspinal surgery

or trauma within 2 months; intracranial neoplasm, arteri-

ovenous malformation, or aneurysm; known bleeding

diathesis; or severe uncontrolled hypertension. Age over 75

has been used as a contraindication to thrombolytic therapy,

but this remains controversial.

Following thrombolysis, patients receive heparin, either

unfractionated heparin titrated to the activated partial thrombo-

plastin time or, preferably, low-molecular-weight heparin

(LMWH). In comparison trials, LMWH was associated with

improved survival and a lower rate of recurrent myocardial

infarction and restenosis compared with unfractionated heparin.

b. Primary angioplasty—Facilities with an available

catheterization laboratory may opt for urgent coronary

angiography and percutaneous angioplasty (usually with

stenting). If the patient can be brought to the angiographic

laboratory in an expeditious manner, the angiographer may

initiate a glycoprotein IIb/IIIa inhibitor, which binds to the

platelet glycoprotein IIb/IIIa receptor and inhibits platelet

aggregation, to reduce the incidence of subsequent myocar-

dial infarction and death.

Whether angioplasty or thrombolytic treatment is chosen

as the therapy for acute STEMI, the administration of aspirin

and intravenous beta blockade should not be delayed.

2. Beta-adrenergic blockade—β-adrenergic blockade with

intravenous metoprolol should be accomplished as soon as

possible after the diagnosis of acute myocardial infarction has

been established by history and electrocardiography.

Intravenous beta blockade can be initiated provided the patient

has an initial heart rate over 50 beats/min, a systolic blood pres-

sure over 90 mm Hg, rales less than one-third the way up the

back, a PR interval less than 0.28 s, and no other contraindica-

tions (eg, asthma). Metoprolol should be administered intra-

venously in 5-mg increments more than 2 minutes apart to a

total dose of 15 mg (or more if greater control of the heart rate

is desired). Following intravenous loading of β-blockers, oral

metoprolol, 50 mg twice daily, or oral atenolol, 50 mg once

daily, should be initiated.

3. Intravenous nitroglycerin—Intravenous nitroglycerin

frequently was administered to all patients with known or

suspected myocardial infarction in the hope of reducing mor-

bidity and mortality. Large trials of patients with STEMI have

failed to justify the enthusiasm for the routine use of this

agent in asymptomatic patients with acute myocardial infarc-

tion. Current recommendations for intravenous nitroglycerin

include relief of ischemic pain and reduction of systolic

blood pressure. A dose of 0.5 μg/kg per minute (35 μg/min

for an average-sized patient) can be initiated and the rate of

administration increased until pain relief or a reduction in

systolic blood pressure to less than 90–100 mm Hg is seen.

The rate of administration should not be increased further if

the patient develops dizziness or other evidence of decreased

organ perfusion. If long-term nitrate therapy is desired, long-

acting nitrates such as isosorbide dinitrate or isosorbide

mononitrate should be started within 24 hours. The continu-

ous administration of intravenous nitroglycerin can rapidly

lead to “nitrate tolerance” and loss of anti-ischemic effect.

4. Morphine sulfate—Morphine beginning with 2 mg

intravenously should be administered if nitroglycerin does

not provide prompt relief of pain. Incremental doses of mor-

phine can be administered to a total that is usually less than

20 mg. Much lower doses may be effective. As morphine

doses exceed 10–15 mg, the possibility of respiratory depres-

sion must be considered.

5. Antiarrhythmic therapy—Patients with acute myocar-

dial infarction who have hemodynamically unstable ventricu-

lar arrhythmias (eg, ventricular fibrillation or ventricular

tachycardia) lasting for more than 30 seconds or causing

hemodynamic collapse or hypotension should be electrically

cardioverted. Sustained monomorphic ventricular tachycardia

not associated with symptoms or hypotension (blood pressure

< 90 mm Hg) should be treated with one of the following.

a. Lidocaine—An intravenous bolus of lidocaine

(1–1.5 mg/kg) is given, followed by supplemental boluses of

0.5–0.75 mg/kg every 5–10 minutes to a maximum loading

dose of 3 mg/kg. Loading is followed by an intravenous infu-

sion of lidocaine at a rate of 2–4 mg/min. Nursing staff must

be alert to changes in the patient’s mental status (eg, somno-

lence, disorientation, or dysesthesias) that may signal lido-

caine toxicity. The elderly are particularly susceptible.

b. Amiodarone—Give 150 mg intravenously over 10 min-

utes, followed by an infusion of 1 mg/min for 6 hours and

then a maintenance infusion of 0.5 mg/min.

c. Procainamide—Give a loading dose by intravenous

infusion of 12–17 mg/kg at a rate of 20–30 mg/min, followed

by an infusion of 1–4 mg/min.

The acute administration of antiarrhythmics allows time

to diagnose and correct electrolyte abnormalities such as

hypokalemia and hypomagnesemia, correct hypoxemia, and

allow anti-ischemic therapy (beta blockade) to be intensified.

6. Sedation—Sedatives such as intravenous or oral benzodi-

azepines may be useful in reducing the level of anxiety

engendered by the ICU setting.

C. Additional Care in the ICU—

1. General measures—The patient should be placed at

complete bed rest during the first 24 hours. Thereafter, in sta-

ble uncomplicated patients, the patient should be encouraged

to sit up in bed, dangling the legs over the side several times a

day, and then spend increasing amounts of time sitting in a

chair or ambulating with assistance. The patient should be

provided with a clear-liquid diet for the first 8–12 hours of

hospitalization for acute myocardial infarction. Stool soften-

ers are useful to prevent straining during defecation.

Subcutaneous heparin, 5000 units twice daily, should be

considered—if no contraindication exists—to prevent deep

venous thrombosis and pulmonary embolism. Additional

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509

supportive measures for patients in the coronary care unit

include daily monitoring of serum electrolytes (including

serum Mg

) for at least 72 hours. In patients with normal

renal function, potassium supplements should be adminis-

tered to keep the serum K

greater than 4.5 meq/L, and mag-

nesium should be given intravenously to maintain serum

levels at greater than 2.0 mg/dL. These maneuvers will

reduce the incidence of ventricular arrhythmias in a safe and

physiologic manner. While prophylactic Mg

administra-

tion does not reduce mortality overall, there is some sugges-

tion that high-risk groups (nonreperfused patients) may

benefit. Magnesium sulfate [10 g (40 mmol) in 100–200 mL

W administered over 2–3 hours] usually will increase the

steady-state serum levels of Mg

about 0.3–0.4 mg/dL in

patients with normal renal function. Hyperglycemia is a risk

factor for poor outcome in acute myocardial infarction; tight

glycemic control may decrease complications.

2. Aspirin—One aspirin tablet per day (eg, enteric-coated

aspirin, 160–325 mg) should be administered to all patients

after myocardial infarction unless there are contraindications.

Regardless of whether thrombolytic therapy has been given or

not, prophylactic aspirin therapy has reduced the

post–myocardial infarction mortality rate by 23%. For aspirin-

allergic patients, clopidogrel, 75 mg/day, can be substituted.

3. Beta-adrenergic blockade—Any of the following—

propranolol, 180 mg daily in divided doses; timolol, 10 mg

twice daily; metoprolol, 100 mg twice daily; or atenolol, 100 mg

once daily—should be administered after acute myocardial

infarction to prevent sudden death in patients who can toler-

ate this class of drugs. The criteria used to define patients eli-

gible for prophylactic β-adrenergic blockade are similar to

those applicable in the immediate post–myocardial infarc-

tion period: systolic blood pressure greater than 90–100 mm

Hg, heart rate greater than 50 beats/min, no rales, PR inter-

val less than 0.28 s, and no contraindications (eg, asthma or

“brittle” diabetes).

Randomized trials of over 50,000 patients in the United

States and Europe have consistently demonstrated a 25–35%

decrease in post–myocardial infarction sudden death with the

prophylactic use of beta blockade. Of particular interest is the

observation that if a patient can tolerate beta blockade after

acute myocardial infarction, the greatest benefit accrues to

those in whom some of the most serious concerns against beta

blockade are raised. Specifically, a patient who has had heart

block, sudden death (eg, ventricular fibrillation or ventricular

tachycardia), or heart failure after myocardial infarction and

can tolerate beta blockade subsequently (ie, if heart failure

clears with one or two doses of diuretics) gains the greatest

cardioprotective effect from beta blockade. For example,

assuming a pool of patients with prior congestive heart failure

who subsequently stabilize, it is estimated that prophylactic

treatment with β-blockers of only 26 patients is required to

save one life. Carvedilol, a nonselective β- and α-blocker has

been approved by the Food and Drug Administration (FDA)

for post-MI patients with LV dysfunction.

4. Antihypertensive agents—Patients with hypertension

have an obvious need for lowering systolic blood pressure. A

goal for systolic blood pressure of approximately 120 mm Hg

or less would be desirable, although any evidence of cerebral

hypoperfusion may frustrate this goal in some patients.

While most antihypertensive drugs are potentially suitable

for treatment of hypertension in patients with acute myocar-

dial infarction, preference should be given to agents likely to

treat both hypertension and the underlying coronary artery

disease. For example, β-blockers would seem an ideal antihy-

pertensive choice because they reduce the work of the heart

(by lowering both heart rate and blood pressure) as well as

providing a cardioprotective effect that reduces the incidence

of sudden death following acute myocardial infarction.

ACE inhibitors may be useful for the treatment of hyper-

tension and should be strongly considered if the patient has

any element of congestive heart failure (eg, rales, car-

diomegaly, or known reduction of ejection fraction) in con-

junction with an acute myocardial infarction. Survival

benefit in the post–myocardial infarction setting has been

demonstrated for a host of ACE inhibitors, with greater

improvement in survival being observed in the patients with

the greatest reductions in ejection fraction. For patients

intolerant of ACE inhibitors, the angiotensin II receptor

blocking agents (eg, losartan, valsartan, candesartan, and

others) are suitable alternatives.

The calcium channel blockers diltiazem and verapamil are

reasonable alternatives to β-adrenergic blockade in patients

with brittle diabetes or bronchospastic lung disease. Both

agents have a modest bradycardic effect in addition to their

antihypertensive effects. It should be remembered that these

agents should be reserved for patients with preserved left ven-

tricular function because these drugs increase mortality sub-

stantially in patients with ejection fractions under 0.40.

5. Diltiazem—In patients with acute myocardial infarction

who do not develop Q waves on the ECG (acute non-Q-wave

myocardial infarction or subendocardial myocardial infarc-

tion), strong consideration should be given to administering

diltiazem in a dose of 60 mg four times daily or 90 mg every

8 hours. At these doses, this agent has been shown to prevent

reinfarction in the month following an acute non-Q-wave

myocardial infarction.

Complications

A. Arrhythmias—

1. Atrial fibrillation—This disorder, characterized by a

narrow QRS complex and an irregular rhythm, is frequently

associated with extensive damage to the myocardium. If

rapid atrial fibrillation is associated with symptomatic

hypotension or with chest pain, conservative measures

should be abandoned, and synchronized electrical cardiover-

sion should be performed immediately.

Typically, initial therapy would consist of digoxin given

intravenously in a dose of 0.25–0.5 mg to slow the ventricular

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response and improve left ventricular function. Subsequent

doses of 0.125–0.25 mg of intravenous digoxin can be given

up to a total of 1–1.5 mg over the initial 24 hours after

myocardial infarction. Oral digoxin, usually 0.125–0.25

mg/day, is administered for maintenance therapy. The goal of

digoxin therapy is to reduce the ventricular rate to less than

90–100 beats/min.

Concomitant therapy with either β-adrenergic blockers

or the calcium channel blocking agent diltiazem will achieve

acceptable heart rate control in a shorter period of time than

with digoxin alone. For example, 5 mg intravenous metopro-

lol can be administered every 5 minutes to achieve prompt

control of rapid atrial fibrillation while digoxin therapy is

being initiated. An oral maintenance dose of metoprolol, 50

mg twice daily, can be initiated once the resting heart rate is

controlled with the intravenous preparation. Intravenous dilti-

azem, a loading dose of 20 mg (or 0.25 mg/kg) over 2 minutes,

can be given and repeated in 15 minutes. A maintenance infu-

sion of 10–15 mg/h can be prescribed for 24 hours if necessary.

Heparin should be given in the absence of contraindications.

2. Ventricular premature beats—Prophylactic aboli-

tion of asymptomatic ventricular ectopy after myocardial

infarction results in a marked increase in mortality rate. The

results of the Cardiac Arrhythmia Suppression Trial (CAST)

have documented conclusively that routine use of antiar-

rhythmic therapy for asymptomatic ventricular ectopy is

contraindicated. It is worth noting, however, that the pro-

phylactic use of β-adrenergic blockade has been associated

with a decrease in the frequency of ventricular ectopy. Since

β-blockers prolong survival after a myocardial infarction,

they should be considered the primary form of nonspecific

antiectopy therapy.

Isolated ventricular premature beats need not be treated,

but repetitive forms of ventricular ectopy such as couplets

and ventricular tachycardia (ie, more than three ventricular

premature beats in a row) are indications for prophylactic

lidocaine if they are associated with hypotension (see above).

If longer-term antiarrhythmic therapy is believed necessary,

intravenous procainamide (2–4 mg/min) or oral sustained-

release procainamide (750 mg every 6 hours) would be

potentially beneficial. Alternative agents include quinidine

sulfate (200 mg every 6 hours) and sustained-release quini-

dine gluconate (324 mg every 8 hours), as well as tocainide,

mexiletine, and amiodarone.

B. Heart Failure—Heart failure complicating acute

myocardial infarction will increase the mortality rate from

2–3% to as high as 50% per year. A primary goal of ther-

apy for acute myocardial infarction is to prevent the pro-

gression of uncomplicated myocardial infarction to

reinfarction with development of heart failure. The admin-

istration of intravenous, cutaneous, or oral nitrates, as well

as β-adrenergic blockade therapy and thrombolytic therapy,

is directed toward this goal.

If congestive heart failure develops after myocardial

infarction, initial therapy may include the following.

1. Diuretics—Rales and S

gallop sometimes are eradicated

by a single intravenous dose of furosemide (20–40 mg intra-

venously in patients who have not previously received this

agent). Larger doses of intravenous furosemide may be used

as the initial diuretic dose if the patient is known to have

been receiving diuretic therapy in the past.

2. Vasodilators—ACE inhibitors are first-line therapy for

the treatment of congestive heart failure in acute myocardial

infarction. In addition to their beneficial hemodynamic

effects, these agents improve survival by altering favorably

the “remodeling” of the left ventricle that occurs with

myocardial infarction. Captopril can be initiated in dosages

of 12.5 mg every 8 hours and then increased to 100 mg every

8 hours. Dose escalation can occur daily (or more frequently)

if no orthostatic symptoms are noted. Corresponding doses

of enalapril range from 2.5–10 mg twice daily—and for

lisinopril, 5 mg once daily initially, titrated upward to 10–20

mg/day. Ramipril is another ACE inhibitor with proof of effi-

cacy and survival benefit in the treatment of congestive heart

failure complicating acute myocardial infarction.

Cough and elevation of the serum creatinine can limit

the use of ACE inhibitors. Some clinicians have substituted

angiotensin II receptor antagonists such as losartan and

valsartan for ACE inhibitors. Clinical trials in chronic heart

failure would support this practice, although the ACE

inhibitors remain the vasodilators of choice for prolonga-

tion of life with heart failure and depressed left ventricular

function. Another alternative therapy for heart failure with

proven survival benefits is the combination of the

vasodilator hydralazine with isosorbide dinitrate.

Hydralazine can be started at 25 mg orally with the dose

increased every 3–6 hours to a target of 100 mg every 8 hours.

Isosorbide dinitrate can be initiated at 20 mg three times

daily and increased with each dose to a target of 60 mg

three times daily.

A serum sodium level of less than 135 meq/L developing

during the course of acute myocardial infarction or chronic

congestive heart failure suggests that the patient’s blood pres-

sure is critically dependent on various compensatory mech-

anisms designed to support blood pressure, such as

production of antidiuretic hormone and angiotensin. In

such patients, heart failure therapy with ACE inhibitors may

result in substantial or profound hypotension.

3. Digoxin—Digoxin is frequently administered to patients

with heart failure who do not respond to one or two doses of

intravenous furosemide. Since digoxin may increase myocar-

dial O

consumption and may aggravate ventricular arrhyth-

mias, it should be given orally at a dose of 0.125–0.25 mg

daily. The administration of a “loading dose” of digoxin is

unnecessary unless rapid atrial fibrillation coexists with

heart failure and rapid control of ventricular rate is desired.

C. Cardiogenic Shock—The mortality rate for cardiogenic

shock complicating acute myocardial infarction still remains

over 50%. Treatment may include the following.

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511

1. Increase intravascular fluid volume—Vol ume

expansion with 250–500 mL of normal saline may be used as

the first treatment for cardiogenic shock if no evidence of left

ventricular failure is present (ie, no rales and absent S

gal-

lop). If no clear response is seen (ie, blood pressure does not

increase), more fluid may be administered, but consideration

of pressor agents or right-sided heart catheterization (or

both) should be high on the list of subsequent priorities.

2. Vasoactive and inotropic agents—Intravenous

dopamine in the range of 5–25 μg/kg per minute may be given

to raise the systolic blood pressure to more than 90 mm Hg or

to otherwise maintain organ perfusion. Intravenous dobuta-

mine given in doses of 2.5–25 μg/kg per minute is frequently

helpful in cardiogenic shock. This agent is particularly useful

because it is both a vasodilator and an inotropic agent. Despite

its vasodilator properties, in patients with a markedly reduced

cardiac output, dobutamine infusions frequently result in an

increase in blood pressure as a result of increased cardiac

output.

If either of these agents is required for more than a few

minutes to an hour, placement of a pulmonary artery

catheter is warranted so that the dose of each agent can be

adjusted to meet hemodynamic goals. The simultaneous

administration of dopamine (6–7 μg/kg per minute initially)

and dobutamine (3–4 μg/kg per minute initially) may be

useful in increasing both the blood pressure and the cardiac

output in patients with acute myocardial infarction and

severely compromised hemodynamics. These dosages are an

empirical starting point. A right-sided heart catheter is

required for rational adjustment of these two pressor agents.

Milrinone has a hemodynamic profile similar to that of

dobutamine, but it is much more costly. This phosphodi-

esterase inhibitor does not demonstrate the rapid tachyphy-

laxis seen with β-adrenergic agonists. If long-term high-dose

catecholamine support is required to maintain cardiac out-

put, milrinone may be a suitable alternative.

3. Intraaortic balloon pump—The intraaortic balloon

pump should be considered if acute ischemia is suspected as

the primary cause of cardiogenic shock. If a patient has con-

tinued chest pain after myocardial infarction and develops

cardiogenic shock, intraaortic balloon pumping may provide

a bridge to surgical therapy of shock. The intraaortic balloon

is inflated in the descending aorta during diastole, thereby

increasing coronary perfusion pressure. By deflating during

systole, it “unloads” the left ventricle.

D. Heart Block

1. Inferior myocardial infarction and heart block—

Heart block frequently occurs along with acute inferior wall

myocardial infarction during which the blood supply to the

AV node has been compromised either by ischemia or by

infarction. However, temporary pacing is not necessarily

indicated if the heart block is Mobitz I (Wenckebach) and the

patient’s blood pressure and clinical status are stable.

Atropine is very useful for increasing the heart rate in

patients with symptomatic bradycardia. An increase in heart

rate and blood pressure is seen frequently after a 1-mg intra-

venous bolus of atropine sulfate. Atropine can be repeated

once or twice if necessary. However, serious side effects (eg,

dry mouth, blurred vision, and even psychosis) preclude its

continued use. Therefore, the development of heart block

with hemodynamic compromise (ie, fall in blood pressure,

decrease in mentation, or other evidence of peripheral

hypoperfusion) should lead to serious consideration of a

transvenous temporary pacemaker.

2. Temporary transcutaneous pacing—Transcutaneous

pacing may be very helpful as a temporary expedient. The

technique is very painful to the patient and should be

replaced by transvenous pacemaker placement in high-risk

patients likely to require pacing. Transcutaneous pacing is

indicated for symptomatic bradycardia (heart rate < 50

beats/min) or bradycardia with hypotension (systolic blood

pressure < 80 mm Hg) unresponsive to drug therapy, Mobitz

type II second-degree AV block, third-degree heart block and

bilateral bundle branch block (BBB)(ie, alternating BBB),

new BBB or fascicular block, and right or left BBB with first

degree AV block.

3. Temporary transvenous pacing—Temporary transve-

nous pacing in the acute myocardial infarction patient is

indicated for the following conditions: asystole, symptomatic

bradycardia unresponsive to medications and type I second-

degree AV block, bilateral BBB, a new BBB or fascicular block

and first-degree AV block, and Mobitz type II second-degree

AV bl o c k .

4. Permanent pacing after acute myocardial infarc-

tion—Consideration for permanent pacemaker implanta-

tion should take place in the presence of persistent Mobitz

type II second-degree AV block or complete heart block after

myocardial infarction, transient second- or third-degree AV

block plus BBB, and symptomatic AV block at any level.

E. Right Ventricular Infarction—Right ventricular myocar-

dial infarction complicates roughly one-third of all acute

inferior wall myocardial infarctions. The right ventricle is a

very thin-walled structure that is poorly adapted to acute

demands of either pressure or volume. The diagnosis of

this entity can be made through echocardiography,

radionuclide ventriculography, cardiac catheterization, or

electrocardiography.

1. Diagnosis—ST-segment elevation in the right-sided elec-

trocardiographic chest leads is the most sensitive test for

detecting an acute right ventricular infarction. Lead V

R is

the most sensitive and most specific lead. However, all elec-

trocardiographic criteria begin to dissipate within hours of

an acute right ventricular infarction, and the hemodynamic

consequences may be more apparent than changes on the

ECG. Right ventricular infarction should be suspected in all

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patients with acute inferior wall myocardial infarction with

hypotension, especially if there is evidence that left ventricular

function is preserved. The hallmarks of a hemodynamically

significant right ventricular infarction include the presence

of elevated neck veins with clear lungs but evidence of poor

cardiac output.

2. Treatment

Since right ventricular infarction is a common complication

in patients with acute inferior wall myocardial infarction,

initial doses of nitroglycerin should be given cautiously to

these patients. This is so because right ventricular output

may decrease markedly in response to systemic venodilation

by nitroglycerin. These patients also may be particularly sen-

sitive to diuretics such as furosemide.

To increase blood pressure and cardiac output in the face

of a known or suspected acute right ventricular myocardial

infarction, initial therapy should consist of intravenous flu-

ids, provided there is no evidence of pulmonary congestion

or a left ventricular S

gallop. Patients who fail to respond to

fluid infusion with an increase in blood pressure and

improved systemic perfusion should be treated next with

intravenous dobutamine, preferably with a pulmonary artery

catheter to help guide therapy.

F. Other Complications

1. Pericarditis—Pericarditis is a common complication of

myocardial infarction. If the infarction process involves the

epicardium of the left ventricle, irritation of the pericardium

may occur. The patient typically complains of chest pain

exacerbated by respiration and supine posture; the patient

frequently feels more comfortable sitting upright. The

appearance of a three-component friction rub representing

the left ventricular epicardium rubbing against an inflamed

pericardium confirms the diagnosis.

Treatment is generally straightforward. An asymptomatic

friction rub heard on routine daily examinations need not be

treated. Symptomatic episodes of pericarditis can be treated

with either aspirin, 325 mg every 4–6 hours, or nonsteroidal

anti-inflammatory agents. Rarely, corticosteroids are required

to control post–myocardial infarction pericarditis pain.

Most episodes of pericarditis are self-limited and require

no more than symptomatic therapy. If a question regarding a

patient’s symptoms arises, an echocardiogram that demon-

strates an increase in pericardial fluid may be helpful in

establishing the diagnosis of pericarditis.

Thrombolytic therapy and heparin (except for subcuta-

neous heparin for prevention of deep venous thrombosis)

should be terminated if pericarditis is suspected or diag-

nosed after myocardial infarction. Rarely, post–myocardial

infarction pericarditis leads to a pericardial effusion sizable

enough to cause hemodynamic compromise. The hallmarks

of a significant pericardial effusion include an increase in

heart rate, an increase in the magnitude of paradoxic pulses,

a decrease in the systolic pressure, a decrease in the systemic

pulse pressure, elevated neck veins, and, in advanced stages,

evidence of low cardiac output (eg, cool extremities,

decreased mentation, and decreased urine output). Should a

hemodynamically significant pericardial effusion be sus-

pected, urgent echocardiography should be performed to

confirm the diagnosis and to localize the effusion. While the

echocardiogram is being performed, cardiac catheterization

laboratory personnel should be preparing to perform peri-

cardiocentesis if necessary.

2. Papillary muscle rupture and ventricular septal

rupture—These are rare but life-threatening complications

of acute myocardial infarction. A murmur consistent with

acute mitral regurgitation may be heard in up to 50% of

patients with acute myocardial infarction during the first

24–48 hours after the event. However, these mitral regurgi-

tant murmurs usually represent transient papillary muscle

ischemia and disappear with time or remain hemodynami-

cally unimportant.

Papillary muscle rupture or an acute ventricular septal

rupture should be suspected in patients who develop sudden

hypotension or evidence of severe heart failure. The hallmark

of both lesions is a loud systolic murmur, often with a thrill

palpable over the left chest. The diagnosis of these lesions can

be confirmed by echocardiography. Alternatively, since these

lesions are usually associated with heart failure and a low car-

diac output, a pulmonary artery catheter should be placed to

help guide subsequent management. The presence of high

(near systemic) O

saturation in a right atrial blood sample

confirms the diagnosis of ventricular septal rupture (with

left-to-right shunting of blood). The presence of a large v

wave in the pulmonary capillary wedge pressure tracing may

lend support to the diagnosis of left ventricular papillary

muscle rupture.

Both these conditions are acute emergencies. Conservative

measures usually are insufficient to allow survival.

Consideration should be given to urgent cardiac catheteriza-

tion with anticipation of emergent open-heart surgery.

Antman EM et al: ACC/AHA guidelines for the management of

patients with ST-elevation myocardial infarction. A report of

the American College of Cardiology/American Heart

Association Task Force on Practice Guidelines (Committee to

Revise the 1999 Guidelines for the Management of Patients with

Acute Myocardial Infarction). J Am Coll Cardiol

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with acute myocardial infarction complicated by cardiogenic

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lower mortality only among high-risk patients with ST- and

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infarction: A report from the SHOCK registry. J Am Coll

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Mehta SR et al: Impact of right ventricular involvement on mortal-

ity and morbidity in patients with inferior myocardial infarction.

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12907014]

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receiving low-molecular-weight heparin versus unfractionated

heparin in ST-elevation myocardial infarction treated with fibri-

nolytics in the CLARITY-TIMI 28 trial. Circulation

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Sura AC, Kelemen MD: Early management of ST-segment elevation

myocardial infarction. Cardiol Clin 2006;24:37–51. [PMID:

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514

Primary cardiovascular disease is the most common single

indication for ICU care and monitoring. Many patients with

other diseases requiring intensive care develop secondary

cardiovascular complications. Moreover, cardiac surgery

patients remain the most common group of surgical patients

requiring intensive care and monitoring. Many of the ICU

concerns relevant to cardiac surgical patients are covered in

other sections of this text, but certain aspects are unique to

this common subset of patients. The following sections cover

these unique problems and include aneurysm and dissection

of the great vessels, postoperative arrhythmias, perioperative

coagulopathy, complications of artificial circulation, and

postoperative low-output states.

ANEURYSMS, DISSECTIONS, & TRANSECTIONS

OF THE GREAT VESSELS

ESSENTIALS OF DIAGNOSIS



Chest pain.



Differential peripheral pulses.



Aortic insufficiency.



Widened mediastinum on chest x-ray.



Cardiovascular collapse.



End-organ ischemic symptoms.

General Considerations

Disease of the great vessels often presents dramatically and

is often lethal if not managed expeditiously. Timely surgical

correction or, when appropriate, medical therapy may be

lifesaving. However, despite considerable progress in surgi-

cal approaches and medical therapies, a minority of patients

still faces the specter of complications: potential paraplegia,

pre- or postoperative mortality, end-organ injury, delayed

recovery from surgical incisions, or subsequent surgery from

disease progression after initial medical or surgical therapy.

Terminology is frequently confusing owing, in part, to the

nature of the pathology and because of various classification

schemes. Aortic dissections, transections, and aneurysms are

related but distinct entities. Aortic dissections and transec-

tions predispose to false (pseudo) aneurysms, and

aneurysms predispose to dissections, but because of thera-

peutic and prognostic considerations, it is desirable and

usually possible to determine which came first. These three

entities frequently present simultaneously as a combined

lesion, but the relative contribution of each component of

the disease should be considered separately—while appreci-

ating their interrelationships.

Aneurysms of the great vessels (ie, aorta, innominate

artery, carotid artery, ductus arteriosus, and subclavian

artery) are pathologically either true aneurysms composed of

all three layers of the vascular wall or false aneurysms con-

taining only adventitia and periaortic fibrous tissue. True

aneurysms result from transmural degeneration of the struc-

tural components of the vessel (eg, Marfan’s syndrome,

residual ductus arteriosus tissue, ectatic vein grafts, and aor-

tic disease associated with obstructive lung disease) or from

a localized degeneration of vascular layers (eg, atherosclero-

sis and vasculitis). False aneurysms usually are due to prior

dissection, trauma, prior great vessel surgery, or rarely,

tumor. Descriptively, both true and false aneurysms are

either saccular or fusiform (Figure 23–1). Classification of

great vessel aneurysms based on location and extent is help-

ful for diagnosis, prognosis, and therapy. Aneurysms that

involve the arch are more technically complex than those iso-

lated to the ascending or descending aorta. Because they usu-

ally require circulatory arrest for repair, they have an

increased potential for neurologic injury. Repair of

aneurysms that traverse the diaphragm are more prone to

cause paraplegia because of their proximity to the arterial

supply of the anterior spinal artery. Aneurysms that involve

the aortic root are likely to require coronary reimplantation

Cardiothoracic Surgery

Edward D. Verrier, MD

Craig R. Hampton, MD



CARDIOTHORACIC SURGERY

515

and valve resuspension or replacement. Hence they have

increased risk for myocardial ischemia and the potential

complications associated with valvular surgery. Extensive

aneurysms of the entire aorta may require a staged approach

with initial replacement of the ascending aorta, followed by

the arch, and subsequently by the descending thoracic and

abdominal portions.

Aneurysms presumably cause symptoms by expansion,

compression of local structures, distal embolism of con-

tained material, secondary dissection, and either contained

or free rupture. The frequency of these complications

increases exponentially with aneurysm size.

Etiology

A. Aortic Transection—Aortic transection occurs most

commonly after significant blunt trauma and generally

occurs at points of relative aortic fixation—in descending

order of frequency, near the ligamentum arteriosus, at the

diaphragmatic hiatus, at the ascending aorta, and at the

abdominal aorta. Shearing stress from rapid deceleration has

been regarded as the primary biomechanism of this injury,

but recent evidence suggests that lateral-impact collision

forces with simultaneous acceleration of the victim and

increased hydrostatic pressure within the aorta also may be

important mechanisms. In survivable cases, tenuous vascular

integrity is maintained by the adventitia. Early symptomatic

presentation usually is exsanguinating rupture or distal dis-

section, whereas late presentation is in the form of a

pseudoaneurysm. Aortic transection occasionally is due to

penetrating violent injury or to iatrogenic trauma during

cardiac or other surgery.

B. Aortic Dissection—Aortic and other great vessel dissec-

tions represent pathologic separation of the vessel layers,

thereby creating a true lumen and a false one. Since aortic tis-

sue is intrinsically stable, there is usually associated pathology

such as disease of the intima or media (eg, atherosclerosis,

cystic medial necrosis, or Marfan’s syndrome), increased wall

tension (eg, preexisting aneurysm or hypertension), or

trauma (blunt or sharp). Indeed, the two conditions most

frequently associated with aortic dissection are hypertension

(about 80%) and Marfan’s syndrome. Mechanistically, rup-

ture of the vasa vasorum is probably the most important

inciting event. It is not clear whether spontaneous bleeding

into the aortic wall (ie, intramural hematoma) may cause

aortic dissection. Dissections are usually complex anatomi-

cally and dynamic in presentation. Once the intimal tear

occurs, there is progressive separation of the adventitia and

the intima. This separation typically propagates distally but

occasionally may extend proximally. As the separation

extends, branch vessels may be themselves dissected,

occluded, or completely unaffected depending on the loca-

tion and extent of the aortic dissection. Ultimately, the dis-

section reaches an equilibrium between the vessel’s intrinsic

resistance and shear forces that promote propagation. The

dissection then either reenters the true lumen via a second or

third tear in the intima or creates a blind pouch. These

“neostructures” then may remain permanently patent

because of continued flow down the false channel, or they

may thrombose owing to stasis. These dynamics of aortic

dissection are a function of the balance between tissue

strength and continued shear forces. Shear forces, in turn, are

determined by blood pressure, change in blood pressure with

time (dP/dT), size and location of the intimal tear, and blood

vessel diameter.

Two classification schemes are used commonly, based on

the location and extent of dissection—the Stanford and

DeBakey classifications. A Stanford type A dissection begins

in the ascending or transverse aorta with variable amounts of

aortic involvement. Type B dissections begin distal to the

takeoff of the last great vessel, usually the left subclavian

artery. By comparison, a type I DeBakey lesion is analogous

to an extensive Stanford type A dissection. Both begin in the

ascending aorta and extend across the arch and down the

descending aorta. A DeBakey type II dissection involves only

the ascending aorta, whereas a type III DeBakey lesion is

analogous to a Stanford type B dissection.

These classification schemes are vital to management and

prognosis, with particular emphasis on identifying involve-

ment of the ascending aorta. Type A dissections have an 80%

mortality within 48 hours without surgical treatment,

whereas selected type B dissections frequently can be man-

aged medically with only a 10% mortality at 30 days. These

vastly different outcomes are based primarily on the proxim-

ity of type A dissections to vital structures, including the

heart, coronary arteries, aortic valve, and carotid vessels.

Myocardial infarction, acute aortic insufficiency, intrapericar-

dial rupture causing tamponade, and stroke are all frequent

consequences of proximal dissections. In addition, progres-

sion of a type A dissection may result in all the complications

normally associated with a type B dissection such as intratho-

racic rupture, paraplegia, visceral ischemia, extremity ischemia,



Figure 23–1. Types of thoracic aortic aneurysms.

A. Fusiform. B. Saccular. (Reproduced, with permission,

from Way LW (ed), Current Surgical Diagnosis & Treatment,

10th ed. Originally published by Appleton & Lange.



CHAPTER 23

516

and intraabdominal rupture. Fortunately, many of the struc-

tures affected by type B dissections are either paired

(eg, renal), tolerate ischemia for long periods of time (eg,

extremities), or have collateral pathways (eg, GI tract) for

blood supply.

Other changes related to the dissection process include

(1) lability of the blood pressure to fluid shifts, cardiac

decompensation, baroreceptor involvement, and underlying

etiology, (2) coagulopathy from massive blood exposure to

tissue, (3) metabolic derangements from hypoperfusion,

(4) respiratory compromise from systemic inflammation

and local airway compression, (5) any variety of neurologic,

renal, GI, cardiac, and extremity complications, and (6) pro-

gression to chronic pseudoaneurysm or, rarely, stenosis or

obstruction of the aortic lumen. The surgical risks and

adverse effects of therapy multiply with extent and acuity of

the disease process.

Clinical Features

A. Symptoms and Signs—Any patient with significant

chest pain should be assumed to have an aortic catastrophe

until another cause is established. Discrepancies in periph-

eral pulses and blood pressures occur frequently, particularly

in the presence of aortic valve insufficiency. Changes in pulse

contour or distribution may help to localize the extent of a

dissection or transection. Patients with recent or remote

trauma, a family history of Marfan’s syndrome, hyperten-

sion, or prior surgery of the aorta are at increased risk.

Dissections in particular—and sometimes aneurysms—

have myriad presentations, making them a diagnostic chal-

lenge. By far the most common symptom accompanying

aneurysms, transections, and dissections is chest pain, usu-

ally sharp and, less frequently, tearing or ripping, with radia-

tion to the back or abdomen.

Aneurysms may present with pressure symptoms related

to the recurrent laryngeal nerve, great veins, trachea, esoph-

agus, or chest wall. Significantly, aneurysms may be asymp-

tomatic until they rupture and present with circulatory

collapse.

Any number of end organs may become ischemic tem-

porarily or permanently with their own characteristic symp-

toms. Temporary neurologic findings are particularly

common, but any vascular organ can present with initial or

subsequent ischemia.

B. Electrocardiography—Because primary coronary artery

disease is more common than significant aortic disease, a

normal ECG with normal cardiac enzymes should heighten

the suspicion of dissection or aneurysm as a cause of chest

pain. However, if a type A dissection extends into a coronary

(more commonly the right coronary) artery, an ECG cannot

make this distinction. Moreover, electrocardiographic find-

ings occur in about 70% of dissection patients, including

nonspecific ST-segment–T-wave changes, left ventricular

hypertrophy, ischemia, myocardial infarction with old Q

waves, or myocardial infarction with new Q waves.

C. Imaging Studies—A normal chest x-ray is helpful but does

not exclude disease. Overlying structures may compromise

aortic visibility. Tortuosity of the aorta may falsely suggest

enlargement. Aortic transections and dissections may be pres-

ent in an aorta of normal caliber. However, the majority of

cases will show mediastinal widening that mandates further

investigation. To evaluate mediastinal widening, a posteroan-

terior chest x-ray should be obtained because anteroposterior

views are frequently misleading. If available, prior films should

be examined. Other radiographic findings, in decreasing order

of frequency, are abnormal aortic or cardiac contour, displace-

ment or calcification of the aorta, and pleural effusion.

Many patients will have more than one special imaging

study to determine the presence and extent of disease. All the

examinations mentioned below have sensitivities and speci-

ficities greater than 90% when performed and interpreted

properly. Probably the most important consideration is to

establish in advance which approach will be used based on

resources and expertise because diagnosis must be rapid.

In the past, angiography was standard for evaluating aor-

tic disease, and it still has many advantages over other tech-

niques. Angiography has sensitivity and specificity similar to

those of other examinations, provides an assessment of flow

to vessels from both the true and false lumens, permits coro-

nary angiography to be obtained simultaneously in selected

patients, allows evaluation of aortic insufficiency, and fre-

quently establishes the etiology of the disease. Disadvantages

include its invasive nature, the possibility of iatrogenic

catheter injury, peripheral access problems secondary to dis-

sections or underlying obstructive disease, contrast load,

occasional inadequate visualization of a nonperfused false

channel, and nonvisualization of surrounding structures.

Furthermore, angiography is more time-consuming than

other diagnostic techniques (see below), and delay in diagno-

sis may contribute to further morbidity and mortality. With

these considerations, echocardiography and CT scanning are

the diagnostic tests of choice.

CT scanning and MRI provide similar views. CT scanning

is more widely available than MRI and usually can be

obtained rapidly, but it requires contrast material adminis-

tration. The sensitivity and specificity of these modalities are

excellent, and both provide information about surrounding

structures.

Echocardiography—particularly transesophageal echo-

cardiography—has emerged as a valuable technique in the

diagnosis of aortic disease and is considered by many to be

the preferred diagnostic modality. For adequate visualiza-

tion, a biplane transesophageal probe is required. Expertise

in evaluating the images is crucial. The technique is limited

by the presence of intervening structures, particularly those

containing air, and distance of the probe from the vessel.

Differential Diagnosis

Pericarditis, myocardial infarction, and primary aortic insuf-

ficiency are common cardiac diseases that can have similar

presentations. Similarly, pain from esophageal diseases such