Bongard Frederic , Darryl Sue. Diagnosis and Treatment Critical Care

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are 2.4 L/min/m

, which sustains systemic blood pressure at

greater than 40 mm Hg.

Determinants of tissue metabolic demand include tissue

activity (primarily skeletal and cardiac muscle), temperature,

tissue mass, and preexisting metabolic debt. Certain organs are

intrinsically more susceptible to inadequate flows. Brain and

spinal cord, heart, liver, kidneys, GI tract, skeletal muscle, and

skin tolerate warm ischemia for periods varying between a few

minutes and many hours. Metabolic activity of cardiac muscle

can be markedly decreased with hyperkalemic or other forms of

arrest. Skeletal muscle relaxants vastly decrease the metabolic

demands of skeletal muscle. Barbiturates may decrease CNS

metabolic demands. In addition to minimizing contraction of

cardiac and skeletal muscle, hypothermia is often added to

extend the period of safe hypoperfusion. Systemic hypothermia

further attenuates metabolic demands and may be used during

certain cardiac surgical procedures (eg, coronary artery bypass

grafting) to minimize the sequelae of bypass or circulation

arrest. The routine use of systemic hypothermia during cardiac

surgery remains controversial. The length of time that decreased

or arrested circulation is tolerated varies inversely with temper-

ature, with CNS protection being the limiting factor. At core

temperatures near or below 18°C, circulatory arrest may be well

tolerated for periods exceeding 1 hour in extreme circum-

stances. However, the safety of the CNS is not guaranteed owing

to temperature variations and undesirable metabolic activity.

Following cardiopulmonary bypass, patients usually are

anemic because they have gained significant extracellular and

intracellular fluid. The combined effects of anesthesia, sur-

gery, and cardiopulmonary bypass produce hypothermia and

coagulopathy. The latter is caused by factor loss and activa-

tion, hemodilution, and residual heparin and protamine.

Ongoing effects are due to reperfusion of tissues inadequately

protected or congested during cardiopulmonary bypass. In

addition, a number of drugs, anesthetics, blood products, and

ongoing insults from cardiac instability make the period

immediately following cardiopulmonary bypass unique.

All organs are potential sites of dysfunction, and each

should be examined as it becomes accessible to evaluation.

Cardiovascular and renal complications are evident almost

immediately. Neurologic function frequently is slow to return

secondary to anesthetics, particularly in the elderly, but is

probably the most sensitive measure of the adverse effects of

cardiopulmonary bypass. Indeed, much of the impetus for

off-pump techniques was directed toward minimizing the

neurologic sequelae that occur frequently after bypass. Short-

term memory loss, focal defects, choreoathetoid motions,

paraplegia, confusion, worsening of previous neurologic

deficits, seizures, and visual changes occur frequently and are

presumably due to edema, microemboli, hypoperfusion,

residual anesthetics, and drugs and the systemic effects of car-

diopulmonary bypass. GI function usually returns within

24 hours, and persistent GI complaints are rare. The extrem-

ities may be hypoperfused individually or in concert and

occasionally are sufficiently ischemic to result in tissue

(usually muscle) loss.

A. Circuit-Related Complications—Circuit-related compli-

cations are infrequent following cardiac surgery but are seri-

ous when they occur. Full knowledge of the type, location,

and variations of the cannulas used during bypass or ventric-

ular support is essential to evaluate subsequent problems.

Complications include aortic dissection from ascending aor-

tic cannulation; arterial occlusion from peripheral cannula-

tion; congestion of the upper body, lower body, or both from

venous cannulation mishaps; and obstruction, leakage, and

cavitation of indwelling cannulas owing to kinking, disrupted

connections, or excessive pump flows. Monitoring lines are

frequently placed in unusual locations, particularly in

patients with congenital disease and in those with ventricular

assist devices. Familiarity with their care and use is essential.

Certain bypass components are related more frequently

than others to adverse effects. Oxygenators are either of the

membrane or bubble type, with a trend nowadays toward

membrane oxygenators because of a perception that they are

associated with fewer deleterious effects because a “mem-

brane” separates blood from air. Roller pumps or centrifugal

pumps are used for total cardiopulmonary bypass.

Centrifugal pumps are used more commonly because there

is less blood component trauma and less chance of massive

air embolism. Care providers of patients with ventricular

assist devices should familiarize themselves with the

anatomy, connections, components, and monitoring associ-

ated with individual patient situations. The complications in

these patients secondary to circuit failure are characteristi-

cally immediate and severe. A familiarity with typical oper-

ative circuits also provides excellent background for

diagnosis of related problems.

B. Coagulation Parameters—Profound heparin anticoagu-

lation is required for cardiopulmonary bypass. Protamine is

used intraoperatively to reverse the heparin effect.

Inadequate anticoagulation results in consumption coagu-

lopathy; with inadequate protamine, rebound heparinization

may occur. Significant protamine reactions are infrequent

but may result in hypotension, coagulopathy, pulmonary

hypertension, and massive pulmonary edema.

C. Crossclamp Time and Hypothermia—Crossclamp time

primarily applies to cardiac procedures, but any organ that

was isolated from systemic cardiopulmonary bypass support

should be considered at special risk. With current organ pro-

tection techniques, crossclamp time does not always repre-

sent ischemia and may in fact be beneficial, but the

circumstances and length of altered organ perfusion should

be considered.

The degree of hypothermia and the length of decreased

or absent systemic perfusion should be established to raise

the index of suspicion for complications of these interven-

tions. At the extremes of age, systemic effects are common, as

outlined below. The extent of rewarming is variable, and

ongoing temperature changes have significant effects.

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528

D. Fluid and Drug Administration—To monitor the course

of the operation and to assist with postoperative fluid

management, both perfusion and anesthesia records

should be evaluated. Intake and output fluids—including

blood loss, hemoconcentrators, urine output, red blood

cell scavenger, acute blood donations, cardioplegia, chest

tube autotransfusion, rapid infusers, and priming solu-

tions—should be considered carefully.

Inotropes, pressors, vasodilators, inhaled and intravenous

anesthetics, paralyzing agents, antiarrhythmics, anticoagu-

lants, and antibiotics are a routine part of cardiopulmonary

bypass and have altered effects, kinetics, and distribution vol-

umes in the bypass circuit itself and in cold, artificially per-

fused organs. As in all critically ill patients, effects of current

and past drugs should be considered as the cause of a variety

of complications.

E. Surgical Details—The specifics of the operative proce-

dure, particularly in unusual cases, are essential to under-

standing ongoing problems. Complex aortic procedures,

congenital disease, valvular disease, and noncardiac surgery

requiring cardiopulmonary bypass frequently have unique

complications secondary to old and new anatomy and

physiology.

Diagnosis

A. Peripheral Perfusion—Alterations in generalized or local

perfusion can result from prior cardiopulmonary bypass or

ongoing cardiac support with assist devices. Peripheral

pulses should be examined immediately following operation

or device placement so that the severity of subsequent

changes can be appreciated fully. Peripheral perfusion is fre-

quently decreased immediately following cardiopulmonary

bypass owing to vasoconstriction from hypothermia but

should return to normal when normothermia is reached.

A general evaluation of all major tissue beds should be

performed early. Examination of the circulation, including

peripheral pulses, ankle/brachial pressure indices, duplex

examinations of vascular beds with abnormal perfusion,

ophthalmologic examination, and angiography, should be

pursued early when localized changes are noted.

Cardiovascular parameters, including filling pressures, out-

puts, vascular resistances, and oxygen saturations, should be

reviewed. Pulmonary function may change dramatically with

reperfusion, and blood gases—particularly Pa

levels—

increase rapidly with rewarming and inactivation of muscle

relaxants. Renal function is normally quite brisk owing to

excess fluid and mannitol administration surrounding the

period of cardiopulmonary bypass. Low urine output may

indicate renal hypoperfusion. Neurologic dysfunction is

present in almost all patients to a mild degree when evalu-

ated by psychometric testing. Single and multifocal CNS

defects result most commonly from thromboembolism and

hemorrhage. Watershed defects frequently are due to inade-

quate local or generalized flows. More severe psychometric

defects, seizures, blindness, and choreoathetoid movements

may result from air embolus, microparticulate emboli,

hypoxia, profound anemia, or hypoperfusion. Paraplegia

from regional hypoperfusion, aortic dissection, or embolism

is rarely seen with full cardiopulmonary bypass but may

occur in up to 40% of patients with complex thoracoabdom-

inal procedures with or without artificial support. GI and

hepatic symptoms, including abdominal pain, ileus, ascites,

and GI bleeding, may represent prior or ongoing venous

congestion or arterial hypoperfusion.

B. Hypothermia—Numerous local temperatures are meas-

ured during bypass. Core temperature should be evaluated

postoperatively, and other localized temperatures (ie, axillary

and rectal) should be correlated.

C. Coagulopathy—Coagulopathy and hemolysis usually are

most evident during or immediately after cardiopulmonary

bypass, respectively, and both may herald a complicated

post–cardiopulmonary bypass course. Examine for diffuse

bleeding, blood-tinged urine, evidence of abnormal throm-

bosis, or abnormal laboratory values.

D. Edema—Differential edema and severe generalized

edema should be noted and potential reversible mechanical

causes (venous obstruction) evaluated. Accurate pre- and

postoperative weights are essential for evaluating fluid accu-

mulations and losses, which may represent 10–20 L in

extreme cases.

E. Laboratory Studies—Coagulation studies, free hemoglo-

bin, amylase, liver function tests, and arterial blood gases

may delineate secondary adverse effects of cardiopulmonary

bypass on tissue beds.

F. Imaging Studies—A chest x-ray should be examined

postoperatively for retained foreign bodies, catheter position,

ventricular support cannula positions, chest tubes, valves,

pulmonary parenchymal and pleural abnormalities, medi-

astinal contour, aortic calcification and evidence of displace-

ment, endotracheal tube position, and if applicable,

intraaortic balloon pump placement.

G. Mechanical Problems—In patients with ongoing ven-

tricular support, erratic pump flows or increased tubing

motion may herald cannula obstruction or pump failure. Air

in the circuit is always an emergency, and although rare, it

should be excluded. Left- and right-sided chamber pressures

are vitally interdependent in patients being maintained on

ventricular assist devices because the normal physiologic

homeostatic mechanisms do not apply. Filling, arterial, and

line pressures require constant vigilance.

Differential Diagnosis

Secondary organ changes owing to congenital, valvular, and

coronary disease are frequently superimposed on—and

magnified by—the effects of cardiopulmonary bypass. An

appreciation of the preexisting and subsequent anatomy and

physiology is essential. Sepsis, either preexisting or new,

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CARDIOTHORACIC SURGERY

529

mimics almost all the inflammatory, organ failure, and

embolic effects of cardiopulmonary bypass, as do many ana-

phylactic or cardiovascular drug reactions and hemolysis.

Superimposed myocardial infarction during cardiopul-

monary bypass may have profound systemic effects.

Treatment

A. Minimize Support Period—Decreasing the level and

time of artificial circulation is the most direct treatment but

is rarely feasible. Changing the type of support device will be

possible occasionally, and many available pulsatile support

devices are tolerated for long periods of time. As mentioned

earlier, improvements in the biocompatibility of the bypass

circuit blunt the systemic coagulation and inflammation

abnormalities and may improve clinical endpoints. Despite

these “equipment” improvements, they are only partially

effective, and optimal therapy in the future probably will

combine multiple strategies for optimal outcomes.

B. Restore Perfusion—Organs with documented inade-

quate flow should have perfusion restored by moving cannu-

las, administering vasodilators locally, performing peripheral

bypass grafts where appropriate, or performing thromboem-

bolectomy.

C. Correct Hypothermia—Correction of hypothermia should

be ongoing with warmed intravenous fluids, radiant heat,

and heated ventilatory gases. However, the efficacy of all

these maneuvers is very limited, and in cases of extreme

hypothermia, consideration should be given to direct blood

rewarming with a partial bypass circuit and heat exchanger.

During rewarming, fluid requirements may be substan-

tial secondary to vasodilation and ongoing losses. The sig-

nificant cellular and extracellular edema that accumulates

demands vigorous diuresis as soon as feasible to prevent the

increased cardiovascular burden of increasing preload as

fluid is mobilized. Robust urine output of 300–500 mL/h

may be necessary to keep pace with fluid administration and

mobilization.

D. Correct Coagulopathies—Coagulopathies frequently cor-

rect spontaneously with rewarming, but the occasional

patient with ongoing fibrinolysis, significant factor deficits,

or ongoing bleeding needs specific therapy as outlined in the

section on coagulation.

E. Organ Dysfunction—Patients who develop myocardial

dysfunction, neurologic or ophthalmologic deficits, acute

respiratory distress syndrome (ARDS), pancreatitis, general-

ized inflammatory states, renal failure, and extremity

ischemia temporally related to cardiopulmonary bypass are

treated in fashion similar to what is available for these mal-

adies caused by other insults. Cardiopulmonary bypass

should not be assumed to be the cause of these deficits until

other primary causes are excluded.

Griepp RB: Cerebral protection during aortic arch surgery. J Thorac

Cardiovasc Surg 2001;121:425–27. [PMID: 11241074]

Hessel EA: Abdominal organ injury after cardiac surgery. Semin

Cardiothorac Vasc Anesth 2004;8:243–63. [PMID: 15375483]

Nussmeier NA: A review of risk factors for adverse neurologic out-

come after cardiac surgery. J Extra Corpor Technol 2002;34:4–10.

[PMID: 11911628]

Sellke FW, del Nido PJ, Swanson SJ (eds): Sabiston & Spencer

Surgery of the Chest, 7th ed. Philadelphia: Elsevier Saunders,

2005.



Postoperative Low-Output States

ESSENTIALS OF DIAGNOSIS



Diaphoresis.



Cyanosis or pallor.



Poor peripheral perfusion.



Thready pulse; tachycardia or bradycardia.



Tachypnea.



Venous congestion.



Pulmonary rales.



New or increased murmurs.



Mental status changes.



Anxiety.



Low urine output.

General Considerations

Cardiac insufficiency may complicate the course of postop-

erative cardiac surgical patients. Intrinsic myocardial dys-

function, valvular disease, and congenital anomalies

frequently coexist with extrinsic cardiac factors and compli-

cate the diagnosis and therapy of shock in this group of

patients. Rapid diagnosis and reversal of decreased cardiac

output are essential to avoid secondary organ damage.

Etiology

A. Intrinsic Factors—The preoperative cardiac and vascular

anatomy, rhythm, ventricular function (diastolic and sys-

tolic), vascular resistances, valvular gradients and insufficien-

cies, coronary anatomy, and prior interventions should be

reviewed and correlated. This cannot be overemphasized,

particularly in patients with cardiomyopathy, acute coronary

insufficiency, valvular heart disease, congenital cardiac

lesions, pulmonary hypertension, ventricular outflow

obstruction, or ventricular failure.

B. Cardiomyopathy—Cardiomyopathy is conveniently clas-

sified by etiology as ischemic or nonischemic and by type as

dilated or nondilated. Dilated cardiomyopathy is character-

ized by loss of muscle mass or function that is compensated

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530

for by moving residual myocardial function farther along the

Starling curve, that is, by increasing myofibril length. Resting

cardiac output is preserved, but systolic reserve is limited,

and compliance is decreased. These cardiomyopathies fre-

quently are associated with ventricular dilatation, areas of

dyskinesis, mitral incompetence, cardiac rhythm distur-

bances, pulmonary hypertension, and secondary right ven-

tricular failure. Hypertrophic disease usually is nondilated

and causes decreased diastolic function with small chamber

size, increased left ventricular mass, functional outflow

obstruction, and elevated filling pressures. Many patients

with cardiomyopathy undergo revascularization, arrhythmia

surgery, valvular replacement, or eventual transplant.

C. Acute Coronary Insufficiency—Preoperative acute coro-

nary insufficiency frequently necessitates emergent revascu-

larization. This may be complicated by reperfusion injury,

residual ischemia, and myocardial infarction with secondary

mitral regurgitation, ventricular rupture, or ventricular sep-

tal defect. Reperfusion injury results in decreased ventricular

compliance, decreased systolic and diastolic function, and

rhythm disturbances (eg, atrial fibrillation and flutter, pre-

mature atrial contractions, ventricular fibrillation, ventricu-

lar tachycardia, and heart block). Residual ischemia causes

similar derangements that may fluctuate with the level of

ischemia. Acute papillary muscle rupture with severe mitral

regurgitation, ventricular free wall rupture, and ischemic

ventricular septal defects can occur pre- or postoperatively.

These events usually are associated with large transmural

infarcts and usually present acutely with severe compromise.

D. Valvular Heart Disease—Valvular heart diseases fre-

quently leave residua that predispose to poor cardiac func-

tion despite correction of the valvular lesion. Aortic stenosis

leads to left ventricular hypertrophy and severely reduced

ventricular compliance early in its course. Ventricular dilata-

tion and reduced systolic function are frequent late conse-

quences. Associated coronary artery disease or left

ventricular outflow tract obstruction also may contribute to

poor hemodynamics in patients with aortic stenosis. Aortic

insufficiency classically evolves into a dilated, hypokinetic

left ventricle with decreased compliance. Aortic valve disease

of both types is often complicated by pulmonary hyperten-

sion and right-sided heart failure. With mitral valve disease,

left ventricular dynamics may be near normal (eg, rheumatic

mitral stenosis) or severely depressed (eg, ischemic mitral

regurgitation). Mitral stenosis frequently coexists with a nor-

mally functioning ventricle preoperatively; however, with

relief of inflow obstruction, ventricular overload may occur.

Mitral regurgitation is often associated with decreased left

ventricular function and dilatation preoperatively. Function

may worsen in the early postoperative period because of an

acute increase in afterload and anatomic changes. Left ven-

tricular function is usually less compromised following

mitral valve commissurotomy or repair, but prosthetic

mitral valve replacement changes ventricular dynamics sig-

nificantly and in many cases severely impairs left ventricular

function. Other confounding factors include left ventricular

outflow obstruction following mitral valve repair or replace-

ment, pulmonary hypertension, right ventricular failure, and

tricuspid regurgitation.

E. Congenital Lesions—Congenital lesions are beyond the

scope of this discussion, but an assessment of preoperative

and postoperative anatomy and function is essential to treat-

ment. Specifically, both the systemic status and the pul-

monary (if present) ventricle’s functional state should be

assessed, preoperative and residual shunts quantitated, vas-

cular resistances determined, outflow and inflow obstruc-

tions documented, and associated pulmonary and vascular

changes considered. Ventricular function may be compro-

mised for a variety of reasons. Patients with a right ventricle

as a systemic chamber have minimal reserve function and are

a subset of the cardiomyopathies mentioned earlier.

Congenital lesions may be associated with coronary compro-

mise and secondary loss of ventricular function (eg, tricus-

pid atresia with intact ventricular septum). In patients

without a pulmonary ventricle (eg, postoperative Fontan

patients), supranormal systemic ventricular function, low

systemic-sided filling pressures, and low pulmonary vascular

resistance all must be maintained to promote passive pul-

monary flow. Patients with left ventricular outflow obstruc-

tion (eg, coarctation or aortic stenosis) frequently have

significant left ventricular hypertrophy and dysfunction.

Shunts at multiple levels are also common. Residual shunts

following correction of congenital anomalies may be benefi-

cial by permitting decompression of high filling pressures and

maintenance of cardiac output (eg, following Fontan repair)

or may cause significant compromise owing to ventricular

overload or arterial desaturation. In view of these complexi-

ties and their interrelationships, a detailed understanding of

the function of each ventricle, the volume load presented to

each chamber, and the configuration of outflow and inflow is

essential to proper management.

F. Arrhythmias—Arrhythmias may complicate the postop-

erative course and produce low-output states.

Supraventricular rhythms, including atrial fibrillation and

flutter, occur in up to 30% of open-heart surgery patients

and are particularly detrimental in the presence of decreased

ventricular compliance or marginal functional reserve.

Metabolic derangements, atrial ischemia, atrial dilatation,

and sympathetic activity all contribute to supraventricular

arrhythmias. Similarly, ventricular arrhythmias are com-

mon, particularly in dilated cardiomyopathies, hypertrophic

disease, and ischemia. Finally, bradycardias and conduction

disturbances are common, particularly at the extremes of age.

G. Pulmonary Disease—Pulmonary and pulmonary vascu-

lar disease may be superimposed on any of the preceding

lesions. Chronic left ventricular failure compromises lung

compliance, airflow, and oxygenation. Pulmonary vascular

resistance is frequently elevated and may or may not be

reversible.Vascular rings and slings may directly compromise

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CARDIOTHORACIC SURGERY

531

pulmonary blood flow or gas exchange. Additionally, some

conditions may be associated with decreased lung parenchyma

or vasculature (eg, endocardial cushion defects, tetralogy of

Fallot, and pulmonary atresia).

H. Extrinsic Factors—Pericardial tamponade, tension pneu-

mothorax, inadequate or excessive resuscitation, and circu-

lating myocardial depressants all should be considered

during evaluation of inadequate cardiac output.

Resuscitation is frequently inadequate during the early post-

operative course. Patients with ongoing blood loss, decreased

ventricular compliance, perioperative infarcts, significant

organ damage, or complicated cardiopulmonary bypass

courses have particularly high fluid requirements, as do those

who are rewarming following hypothermic bypass or circu-

latory arrest. Overzealous fluid administration also can result

in acute cardiac insufficiency, especially in patients with

exceptionally low ejection fractions. This delicate balance

between inadequate and excessive fluid administration pro-

vides the basis for invasive hemodynamic monitoring in

patients with complex problems.

1. Tamponade—Tamponade may result from both early

bleeding and late pericardial fluid accumulation. Localized

collections can result in atypical but equally dangerous pre-

sentations. The causes of tamponade are reviewed in the sec-

tions on postoperative hemorrhage and postpericardiotomy

syndrome.

2. Tension pneumothorax—Tension pneumothorax

should be excluded in any patient with hemodynamic com-

promise. Myocardial depressants are frequently active peri-

operatively. Calcium channel blockers, β-blockers,

antiarrhythmics, and anesthetic agents all contribute to

decreased myocardial performance. Endogenous substances

such as interleukin 6 (IL-6) also may play a role in patients

with long cardiopulmonary bypass runs or systemic injury

from prolonged hypoperfusion.

Clinical Features

A. Symptoms and Signs—Invasive hemodynamic moni-

toring with pulmonary artery catheters is valuable to assess

cardiopulmonary physiology and guide therapy.

Confounding problems specific to cardiac surgery patients

are due to the frequent presence of endotracheal tubes, resid-

ual anesthetic agents, and continued “normal” residual

effects of cardiopulmonary bypass. Ongoing hemorrhage,

pulmonary insufficiency, metabolic derangements, volume

shifts, and temperature changes all contribute to variable

cardiac performance.

B. Imaging Studies—Chest radiographs should be

obtained early and evaluated for evidence of enlarging car-

diac silhouette (eg, tamponade), pulmonary venous conges-

tion (eg, congestive heart failure and tamponade), pleural

fluid (eg, ongoing bleeding), mediastinal shift, and extrapul-

monary air (eg, tension pneumothorax). Chest radiographs

need to be evaluated in comparison with previously obtained

films to highlight changes and permit correlation with a

changing clinical course.

C. Echocardiography—Surface or transesophageal echocar-

diography can be invaluable in specific clinical circumstances.

Surface echo is usually performed initially. If necessary, trans-

esophageal studies can be added to provide additional infor-

mation about posterior structures, particularly the mitral

valve and thoracic aorta. Echocardiography is useful in the

evaluation of tamponade because it can display diffuse or

localized fluid collections as well as shift and paradoxical

motion of the ventricular septum, which suggest hemody-

namic compromise. In addition, echo can confirm poor ven-

tricular function, which occurs with cardiomyopathy or global

ischemia. It visualizes localized wall motion abnormalities

owing to new or recurrent local ischemia. Ventricular filling

and insufficient or excess volume resuscitation also can be

evaluated. Echo is also helpful in evaluating left ventricular

outflow obstruction, seen frequently present in patients with

hypertrophic cardiomyopathies and after mitral or aortic valve

repair or replacement. New or residual valvular disease, dissec-

tion of the aorta, and septal defects also can be visualized.

D. Electrocardiography—Electrocardiographic tracings

should be compared with preoperative and earlier postoper-

ative examinations for evidence of ischemia, rhythm and rate

disturbances, or diffuse changes sometimes seen with peri-

cardial hematoma and pericarditis.

E. Hemodynamic Monitoring—Cardiac output, central

venous pressure, and pulmonary artery and pulmonary wedge

pressures, as determined with a thermodilution pulmonary

artery catheter, are invaluable for assessment of cardiovascular

status at the bedside. Indeed, these data are often the earliest

and easiest to obtain, further underscoring their importance.

A cardiac index of less than 2.0 L/min/m

always requires

prompt evaluation and correction. Even higher indices may be

inadequate in specific situations. Inaccurate output measure-

ments can occur if incorrect calibration constants are used or

tricuspid regurgitation is present. If measured values appear

inappropriate to the clinical situation, their validity should be

confirmed by venous O

saturation measurement or echocar-

diography (see below). Central pressures should be evaluated

early in the course of low-output states.

F. Oxyhemoglobin Saturation—Venous oxyhemoglobin

saturation can be measured intermittently by transcatheter

aspiration or continuously by fiberoptic pulmonary artery

catheters. Central venous (right atrial) oxygen saturations

typically are measured, and resting values are usually 75%.

Assuming a 100% arterial saturation, this represents unload-

ing of one-fourth of the available oxygen. Venous desatura-

tion usually indicates inadequate tissue perfusion whether or

not the cardiac index is depressed. Oxygen content calcula-

tions from specific chambers also can be used to determine

intracardiac shunts and flows.

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CHAPTER 23

532

Differential Diagnosis

Intravascular volume changes, including hypovolemia,

ongoing bleeding, and overload with impaired right or left

ventricular function, all can result in acute cardiovascular

insufficiency. Extrinsic factors (eg, pericardial tamponade,

tension pneumothorax, or hemothorax) and intrinsic cardiac

compromise (eg, ventricular free wall rupture, acute ventric-

ular septal defect, papillary muscle rupture, prosthetic valve

dehiscence or thrombosis, coronary ischemia, and arrhyth-

mias) also can be confused with low-output syndromes.

Systemic hypoxia, hypocalcemia, acidosis, sepsis, and organ

ischemia occasionally can present initially as a low-output

state in the postoperative period. Malfunctioning arterial

catheters and electronic monitors occasionally prompt a

search for the cause of hypotension in a normal patient.

Treatment

A. Supportive Measures—As with any critically ill patient,

the first objective is to maintain adequate oxygen delivery

and pH control by optimizing ventilation. If the cause of the

low-output state is not easily identifiable and remedied, then

early reintubation, while the patient is still hemodynamically

resuscitatable, is preferable to subsequent emergent interven-

tion. If an endotracheal tube is already in place, its function

and position should be confirmed rapidly by assessing breath

sounds, ventilatory settings and pressures, and inspired O

Pulse oximetry and blood gas analysis should be obtained as

quickly as possible, as well as electrolytes and hematocrit.

Reversible causes (eg, respiratory disorders and electrolyte

imbalance) should be corrected promptly.

During evaluation for specific causes, the circulation should

be supported aggressively, and this is best accomplished by a

systematic approach to appraisal of the hemodynamic status of

the patient. As mentioned earlier, adequate oxygenation and

ventilation must be ensured. Preload then should be optimized.

The virtues of prompt administration of fluids, when appro-

priate, cannot be overemphasized. Inadequate volume admin-

istration is common in patients who are rewarming following

a period of hypothermia, who are being treated with vasodila-

tors, or who have poor left or right ventricular compliance. In

these circumstances, prompt fluid administration is all that is

required for full restoration of cardiovascular stability. In addi-

tion, patients with tamponade frequently respond to fluids

while preparations for definitive therapy are being made.

Conversely, in the patient who has gradually become volume-

overloaded, with subsequent impairment of ventricular per-

formance, it is important to treat with inotropes and afterload

reduction instead of with additional volume. Patients with very

poor ventricular function are prone to both hyper- and hypo-

volemia. Occasionally, some of the classic signs of hypov-

olemia, such as increased creatinine and decreased cardiac

output, are the result of excessive fluid administration and sub-

sequent ventricular impairment.

Heart rate and rhythm disturbances then should be

assessed and treated as outlined in Chapter 22. Contractility

may be enhanced with inotropic agents, with particular atten-

tion to right ventricular status. Lastly, afterload may be reduced

with vasodilators to further improve cardiac output and sys-

temic perfusion. Although most inotropes are described else-

where in the text, a few warrant further comment.

There are a number of inotropic drugs that are used com-

monly to support the failing heart—including dopamine,

dobutamine, epinephrine, and phosphodiesterase inhibitors

(eg, milrinone). While these agents are all effective for improv-

ing the contractile state of the myocardium and have variable

effects on heart rate and afterload, their effects are exerted pri-

marily on the left ventricle. More recently, the importance of

adequate right ventricular function to cardiovascular success

has been appreciated, as well as the sensitivity of the right ven-

tricle to increased afterload, which is manifested as cardiovas-

cular failure. Accordingly, pharmacologic agents that provide

physiologic benefit to the right ventricle—in the context of

perioperative low cardiac output syndrome—including phos-

phodiesterase III inhibitors (eg, amrinone and milrinone),

inhaled nitric oxide (NO), and the increasingly used agent

recombinent human B-type natriuretic peptide (BNP, ie,

nesiritide [Natrecor]) have received attention.

The phosphodiesterase III inhibitors have been termed

inodilators because of their ability to improve myocardial

contractility while simultaneously causing vascular smooth

muscle relaxation. As a result, these agents have consistently

been shown to improve cardiac index and decrease systemic

vascular resistance (SVR) and pulmonary vascular resistance

(PVR). Furthermore, they cause little or no increase in

myocardial oxygen consumption and have almost no effect

on systemic blood pressure and heart rate. Moreover, these

agents may act synergistically with β

-adrenergic agonists

(eg, epinephrine). Amrinone and its newer derivative, milri-

none, are the most common drugs used in this class. As a

result of these beneficial effects on the myocardium and the

pulmonary and systemic vasculature, these agents are playing

an increasing role in the management of perioperative low

cardiac output syndrome.

Nitric oxide (NO), formerly known as endothelium-derived

relaxing factor (EDRF), has emerged as a critical regulator of

vascular tone and reactivity in both normal and pathologic

processes. Exogenous (ie, inhaled) NO retains the biologic

properties of endogenous NO and is the only known agent that

specifically dilates the pulmonary vasculature. Accordingly, it

has been used with success when pulmonary hypertension is

the primary physiologic disturbance When it is used, continu-

ous monitoring of its lethal by-product (nitrogen dioxide) is

necessary. Furthermore, therapy with inhaled NO mandates

mechanical ventilation and is very expensive—thus it is infre-

quently a first-line agent. The role of NO in the treatment of

perioperative low cardiac output syndrome is limited at this

time, but NO offers specific physiologic benefits that may pro-

vide the basis for increased use of NO in this setting.



CARDIOTHORACIC SURGERY

533

BNP, or nesiritide, is a promising new agent in cardiovas-

cular medicine. It has been approved for use in heart failure

but may assist with management of cardiac surgery patients.

Like endogenous BNP, nesiritide has widespread favorable

effects, including vasodilatation (thus reducing peripheral

and pulmonary vascular resistance), natriuresis, increased

glomerular filtration rate, symphathoinhibition, and inhibi-

tion of the renin-aldosterone system. Although there is lim-

ited experience published to date, these pharmacologic

properties make it an attractive adjunct to postoperative

management of cardiac surgery patients, particularly, per-

haps, those with current congestive heart failure, renal insuf-

ficiency, or pulmonary hypertension.

In patients who continue to have low-output states

despite these strategies, intraaortic balloon counterpulsation

should be added. In appropriate patients who fail to respond

to intraaortic balloon counterpulsation, more extensive ven-

tricular support should be considered.

B. Correction of Arrhythmias—Most patients will have

continuous electrocardiographic monitoring, and the rate

and rhythm should be established and corrected as appropri-

ate. Rate abnormalities may have profound hemodynamic

consequences, and a rate of 80–100 beats/min should be the

goal. Temporary atrial, ventricular, and ground wires are fre-

quently available and can be used to correct bradycardias

with atrial, ventricular, or sequential AV pacing. In emergent

settings, simple single-chamber ventricular pacing should be

instituted first to restore cardiac function immediately. Then,

if atrial wires are available, sequential AV pacing can be insti-

tuted to optimize cardiac function. Electrical cardioversion

of hemodynamically significant arrhythmias is preferable to

long periods of low cardiac output and is performed easily,

particularly in intubated and ventilated patients. In extu-

bated patients, brief intravenous anesthesia is sometimes

appropriate for cardioversion of atrial fibrillation, atrial flut-

ter, or sustained slow ventricular tachycardia. This is not

indicated in patients who are significantly compromised.

C. Surgical Evaluation of Pericardial Tamponade—

Ventilation, rhythm, blood pressure, and fluid status should

be established within the first few minutes of evaluation.

Classically, cardiac tamponade is suggested by hemodynamic

instability in a patient with significant bleeding that recently

decreased or stopped. Further evidence includes elevated

filling pressures (possibly left-right equilibration), mediasti-

nal widening on serial chest radiographs, and increasing

tachycardia (compensatory). If not diagnosed rapidly, pulse-

less electrical activity may result. Despite full evaluation,

tamponade frequently cannot be excluded conclusively, and

mediastinal exploration, either in the ICU or in the operat-

ing room, is required. If time permits, echocardiography may

be performed at the bedside to determine the presence or

absence of pericardial tamponade. Any patient with cardio-

vascular collapse in the early period following cardiac sur-

gery should be considered to have tamponade and should be

explored surgically if they are not responding to appropriate

therapy—even if other examinations are inconclusive or are

negative. Tension pneumothorax can occur in any critically

ill patient and should be treated on the basis of ventilator

pressure changes, physical examination, and chest x-ray.

D. Other Modalities—Occasional patients will be incom-

pletely revascularized or may have vein or arterial conduit

spasm. If serial ECGs are suggestive of ischemia, vascular

antispasmodics (ideally calcium channel blockers) should be

administered and consideration given to echocardiography

to document localized wall motion abnormalities, angiogra-

phy to definitively establish localized vascular lesions, or

early reoperation to treat acute graft occlusion.

Baskett RJ et al: The intraaortic balloon pump in cardiac surgery.

Ann Thorac Surg 2002;74:1276–87. [PMID: 12400798]

Feneck RO et al: Comparison of the hemodynamic effects of mil-

rinone with dobutamine in patients after cardiac surgery.

European Minrinone Multicenter Trial Group. J Cardiothorac

Vasc Anesth 2001;15:306–15. [PMID: 11426360]

Fonarow GC: B-type natriuretic peptide: Spectrum of application.

Nesiritide for heart failure. Heart Fail Rev 2003;8:321–25.

[PMID: 14574051]

Gorman JH et al: Circulatory management of the unstable cardiac

patient. Semin Thorac Cardiovasc Surg 2000;12:316–25.

[PMID: 11154727]

Moazami N et al: Nesiritide (BNP) in the management of postop-

erative cardiac patients. Ann Thorac Surg 2003;75:1974–6.

[PMID: 12822655]



534



Status Asthmaticus

ESSENTIALS OF DIAGNOSIS



Usually unremitting asthma, rapidly increasing in severity,

but may present with sudden and severe obstruction

without warning.



Poor and decreasing response to β-adrenergic agonist

therapy.



May develop hypercapnic respiratory failure.



Severe hyperinflation.



Evidence of respiratory (inspiratory) muscle fatigue.

General Considerations

Status asthmaticus is very severe asthma that is unremitting

and poorly responsive to usual therapy. Studies have empha-

sized the differences between chronic stable asthma and sta-

tus asthmaticus in terms of pathophysiology, prognosis,

management, and response to treatment. Importantly, there

has been increased awareness of mortality and morbidity

from severe asthma, recognition of the key role of inflamma-

tion in the mechanism of severe asthma, changes in the mode

of delivery of agents for treating asthma, and revised concepts

in management of patients requiring mechanical ventilation.

Many patients with asthma will have episodic attacks that

are treated easily and rapidly. These mild exacerbations call

for changes in management because even episodic asthma is

undesirable, but the important feature of such cases is that

the patient responds and returns to baseline in a short time.

These attacks are distinguished from status asthmaticus,

which is characterized by slow and inadequate response to

treatment and a poor outlook for resolution of attacks. The

recognition of severe acute asthma in some cases may be dif-

ficult when the patient is assessed against a background of

chronic but stable asthma.

Pathophysiology and Pathogenesis

Asthma prevalence is increasing throughout the world, and

asthma mortality is a matter of great concern. Airway

obstruction is the major feature of this disorder, and

asthma is both an acute reversible obstructive disease and a

chronic pulmonary disease leading to permanent airway

obstruction. Failure to control asthma symptoms is associ-

ated with a more rapidly progressive decline in lung func-

tion and loss of reversibility. This is the basis for consensus

recommendations for chronic asthma management, which

can be summarized as follows: (1) There is a key role for anti-

inflammatory therapy (eg, corticosteroids), (2) regular

β-adrenergic agonist use as the sole therapy for asthma is

ineffective and potentially harmful, and (3) the goal of

asthma treatment is to keep the patient completely

symptom-free at all times. Despite widespread dissemination

of these recommendations, optimal management of asthma

is far from an achieved objective, and many asthmatics have

moderate to severe exacerbations requiring hospitaliza-

tion—with some requiring ICU management.

Airway obstruction in asthma results from three mecha-

nisms: enhanced bronchial smooth muscle contraction

(increased tone and response to stimuli), bronchial mucosal

inflammation and edema, and plugging of the bronchi by

secretions and inflammatory debris. The response to therapy

depends on the relative contributions of each of these mech-

anisms. For example, bronchodilators relax bronchial

smooth muscles but have little or no effect on reducing air-

way obstruction caused by inflammation or debris.

Corticosteroids have no direct effect on bronchial smooth

muscle but reduce inflammation in the bronchial walls.

The baseline amount of inflammation and airway nar-

rowing is a major determinant of the severity of exacerba-

tions once an asthma exacerbation is triggered.

Exacerbations may be triggered by allergens in susceptible

individuals, by cold air or irritants such as dust, by aspirin, or

by respiratory infections, especially viral infections. These

insults cause release of mast cell products such as histamine,

Pulmonary Disease

Darryl Y. Sue, MD

Janine R. E. Vintch, MD



PULMONARY DISEASE

535

inflammatory mediators (eg, leukotrienes and prostaglandins),

and substances that attract and activate leukocytes, especially

eosinophils. An identifiable precipitating cause for an exacer-

bation often cannot be identified. Bronchial smooth muscle

contraction and bronchospasm usually occur early, with

mucosal edema, increased mucous gland secretions, and

inflammatory cell infiltration following rapidly. The propor-

tion of airway obstruction owing to bronchospasm and that

owing to edema, inflammation, and mucus plugging is

highly variable between patients.

Eosinophilic infiltration of the bronchial mucosa in

asthma plays a key role, but neutrophils and T-lymphocytes

also have been implicated. Eosinophils may be attracted by

platelet-activating factor produced by a variety of cells, and

there is increased local production of interleukin 5 (IL-5), an

activator of eosinophils.

A number of studies have suggested an association

between regular use of β-adrenergic agonists and fatal or

near-fatal asthma events. Proposed mechanisms are (1) pro-

motion of airway hyperresponsiveness by these drugs

because they are so effective that the patients are more apt

to undergo prolonged exposure to allergens or irritants,

(2) heavy use of β-adrenergic agonists results in

hypokalemia and cardiac arrhythmias, and (3) some other

effects of β-agonists that remain undetermined. Recent stud-

ies have linked long-acting β-adrenergic agonists to worsening

asthma and increased mortality, yet there are very clear data

demonstrating benefits of these agents. Some studies have

shown that concomitant inhaled corticosteroids may protect

against adverse effects of long-acting β-agonists, but this has

not been settled. Furthermore, it is likely that some patients

are more susceptible to adverse effects of β-agonists poten-

tially because of polymorphisms of the β-adrenergic receptor

resulting in greater downregulation with repeated stimuli.

Status asthmaticus is characterized by poor responsive-

ness to bronchodilator therapy; a rapid, unremitting, and

often progressive course; and slow recovery to a baseline.

Patients who die with status asthmaticus are often found to

have severe mucus impaction of airways and marked inflam-

matory infiltration of the bronchial walls, suggesting a

greater role of airway mucosal inflammation over bronchial

smooth muscle contraction. In some patients with status

asthmaticus, hypoxemia persists much longer than airway

narrowing (as measured by peak flow or forced expiratory

capacity in 1 second [FEV

]), suggesting that persistent

blockage of small airways with mucus prolongs ventilation-

perfusion mismatching. It is not known why an asthmatic

with exacerbation sometimes may develop a self-terminated

bronchoconstrictor response and at other times generate a

persistent unremitting response (status asthmaticus) with

airway edema and inflammation.

A small number of patients with fatal or near-fatal asthma

appear to have rapid onset of symptoms with little airway

inflammation. These patients experience very severe bron-

chospasm that may lead to death within minute or hours.

Identification of such patients before they have a fatal or

near-fatal episode is difficult, but evidence suggests that

these patients may have reduced perception of increased

airway resistance combined with decreased hypoxic ventila-

tory drive.

Most patients with asthma exacerbations can be treated

successfully before they develop severe respiratory failure.

Respiratory failure in status asthmaticus comes about from

two major mechanisms. First, the diffuse and variable

bronchial obstruction causes ventilation-perfusion mismatch-

ing with resulting hypoxemia and, if the patient fails to

increase alveolar ventilation appropriately, hypercapnia.

Second is respiratory muscle fatigue, which somewhat para-

doxically is more marked for the inspiratory than for the expi-

ratory muscles. Because airway obstruction in asthmatics is

intrathoracic, airway narrowing is more marked during the

expiratory phase, increasing expiratory work of breathing and

lengthening the time needed for adequate exhalation.

However, because respiratory drive is increased in asthma as a

result of hypoxemia, hypercapnia, and other factors, the respi-

ratory rate increases and expiratory time shortens. This com-

bination of greater expiratory airway obstruction and

shorter expiratory time results in hyperinflation (air trap-

ping). Hyperinflation puts an additional burden on the

inspiratory muscles because these muscles are shorter than

normal prior to contraction and thus are unable to generate

as much tension for as long a time. Respiratory failure devel-

ops because the patient becomes unable to compensate for

the pathophysiologic changes. The result is fatigue of inspira-

tory muscles, worsening hypercapnia and respiratory acidosis,

and usually a need for intubation and mechanical ventilation.

Clinical Features

A. Symptoms and Signs—The severity of an asthma exac-

erbation should be judged in order to make decisions about

management. Early (30–60 minutes) response to therapy is

the key piece of information, but other information may be

helpful including prolonged duration of attacks, history of

hospitalization for asthma, prior or current use of systemic

corticosteroids, poor response to bronchodilators, increas-

ingly more frequent or increased dosages of medications,

recent or repeated emergency room or office visits for acute

asthma, and a history of requiring mechanical ventilation for

asthma. Increasing severity of asthma may be manifested by

less diurnal variation in asthma severity, diminished peak

flow both before and after bronchodilators, and inability to

sleep. A minority of asthmatics present with status asthmati-

cus after very short duration of symptoms. Some investiga-

tors have suggested that these patients presenting with a

hyperacute attack may have a variety of asthma marked by

sudden severe airway closure, perhaps from a neural mecha-

nism rather than from airway inflammation. Because preg-

nancy has a variable effect on women with stable chronic

asthma, including causing marked worsening in some indi-

viduals, pregnancy in women with childbearing potential

should be considered as a factor for asthma worsening.



CHAPTER 24

536

The physical examination is helpful for identifying signs

of severe airway obstruction (eg, absence of wheezing, use of

accessory muscles of respiration, intercostal retractions, and

pulsus paradoxus) or signs of impending respiratory muscle

fatigue (eg, paradoxical abdominal wall movement), but

these signs are insensitive or unreliable when used by them-

selves to assess severity. A number of studies have attempted

to assess the value of other signs, such as tachycardia, tachyp-

nea, cyanosis, and hypotension, singly or in combination, but

these have not proved to be of discriminating value. A key

role of physical examination is to exclude other acute respi-

ratory problems that may be mistaken for asthma, such as

pulmonary edema, pulmonary embolism, anaphylaxis or

angioedema, pneumothorax, pneumonia, and upper or cen-

tral airway obstruction owing to tumor, foreign body, or

epiglottitis.

B. Laboratory Findings—Ninety percent of patients with

acute asthma will have hypoxemia of mild to moderate

degree, and hypoxemia is not a particularly discriminating

variable for asthma severity. Most asthmatics (80%) present-

ing with an acute episode have mild respiratory alkalosis.

Only a small proportion have normal or elevated P

, and

there is an association between severe airway obstruction and

hypercapnia in asthma. Nonetheless, although hypercapnia is

of concern in status asthmaticus, hypercapnia is not consis-

tently linked with prolonged severe asthma or the need for

mechanical ventilation. Metabolic acidosis owing to an

increase in blood lactate in patients presenting with acute

asthma, especially in association with hypoxemia, may be

seen. Although pulse oximetry gives an estimate of arterial

oxygenation, an arterial blood gas determination of pH and

is mandatory for any asthmatic admitted from the

emergency department or being considered for admission to

the ICU.

Serum sodium and potassium should be measured

because of the association of hyponatremia with pulmonary

diseases and respiratory failure and the observation that

aggressive β-adrenergic agonist use can result in severe

hypokalemia. Although magnesium has been used as a bron-

chodilator and hypokalemia and hypomagnesemia are

closely related, hypomagnesemia has not been associated

with asthma exacerbations.

C. Imaging Studies—Chest radiographs during acute

asthma almost always show hyperinflation, with low, flat

hemidiaphragms and an increased anteroposterior diameter.

They are not helpful in assessment of the severity of asthma,

precipitating factors, or complications. However, some inves-

tigators have claimed that chest radiographs provide impor-

tant diagnostic information in asthmatics who are admitted

to the hospital in that the choice of therapy is altered by the

findings on the radiograph. Features to be sought include the

presence of pneumothorax, infiltrates suggestive of bacterial

or viral pneumonia, findings suggestive of allergic bron-

chopulmonary aspergillosis (eg, fleeting infiltrates or cylin-

dric bronchiectasis), and lobar or segmental atelectasis

suggesting mucous impaction of large airways. Because pul-

monary edema may present with acute onset of dyspnea and

wheezing, cardiomegaly and features of congestive heart fail-

ure should be excluded.

D. Spirometry—Spirometry can be very helpful in the assess-

ment of status asthmaticus both initially and in following

treatment. The objective response to therapy after the first

1–2 hours provides much meaningful information. Peak flow

or FEV

should be measured on initial presentation to the

emergency room and then hourly with treatment until a deci-

sion is made to hospitalize. The frequency of spirometry

thereafter depends on clinical assessment, but the response to

additional treatment with bronchodilators and, after suffi-

cient time has elapsed, to corticosteroids may be of additional

value in planning treatment and observation. The FEV

peak flow may be compared with predicted values for the

patient’s age, sex, and size, but improvement in the measured

values over time is the most helpful indicator. In one study,

good response to treatment at 30 minutes was the single vari-

able most highly correlated with favorable patient outcome.

Differential Diagnosis

Features suggesting status asthmaticus, including acute onset

of shortness of breath, cough, wheezing, and progression to

respiratory failure, may be seen to varying degrees in conges-

tive heart failure, upper airway obstruction, exacerbation of

chronic bronchitis or emphysema, spontaneous pneumotho-

rax, anaphylaxis, acute pulmonary embolism, and foreign-

body aspiration. Upper airway obstruction is characterized

by inspiratory wheezing or stridor, sometimes loudest over

the trachea in the neck. Asthmatics who had prior endotra-

cheal intubation—especially for long duration—or tra-

cheostomy should be suspected of having extrathoracic

airway obstruction. A small but significant number of

patients mistakenly diagnosed as having asthma instead have

vocal cord dysfunction syndrome. In this syndrome, the

vocal cords adduct inappropriately during exhalation,

increasing expiratory resistance and causing expiratory

wheezing and hyperinflation. Vocal cord dysfunction may go

unidentified for years until direct visualization of the vocal

cords during the respiratory cycle makes the diagnosis. On

some occasions, patients who are intubated for severe asthma

have sudden and complete relief of obstruction and wheez-

ing, and these patients should be suspected of vocal cord dys-

function syndrome.

Treatment

Status asthmaticus is treated with bronchodilators (titrated to

patient response), corticosteroids, and oxygen, with endotra-

cheal intubation and mechanical ventilation if necessary. The

aim of treatment is to relieve the airway obstruction by relax-

ing bronchial smooth muscles and reversing inflammation

while supporting respiratory function. Support of respira-

tory function depends on the severity of the asthma and the