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304 PART IV Noncoronary Diseases: Diagnosis and Management
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manifestation, cardiac tamponade. Factors that determine the
degree of hemodynamic compromise include the size of the
effusion; its rate of accumulation; and whether the pericardium
A
B
Fig. 29.2 Echocardiogram showing a large circumferential
pericardial effusion. Anterior (A) and posterior (B) aspects of the
effusions are shown. (From Shabetai R. Pericardial disease. In:
Brown DL, ed. Cardiac Intensive Care. Philadelphia: Saunders;
1988:469–475.)
compression of adjacent intrathoracic structures results in hoarseness, hiccough, and nausea.15 Therefore clinicians must maintain
a high index of suspicion for pericardial effusion, particularly in
the intensive care setting, where it is common for many patients
to have undergone percutaneous cardiac procedures that can be
complicated by perforation of coronary arteries, the coronary
sinus, or the cardiac chambers.
On the ECG, pericardial fluid appears as an echolucent
space between the pericardium and the epicardium (Fig. 29.2).
Pericardial effusions are classified according to their onset, size,
distribution, hemodynamic impact, and composition.15 The detection of a pericardial effusion often has important implications
for diagnosis (e.g., acute pericarditis after MI), prognosis (e.g.,
patients with cancer), or both (e.g., acute aortic dissection).
Rapidly accumulating blood in the pericardial space may be
seen in CICU patients with blunt trauma, ascending aortic dissection, cardiac rupture that may complicate MI, or after invasive
cardiac procedures. After cardiac surgery, pericardial effusions are
common but are typically not large and usually resolve without
medication by 1 month; late (>1 week) tamponade is unusual (1
to 2%) and the effusions appear not to be responsive to NSAIDs
or colchicine.
Pericardial effusion should be suspected in patients with any
systemic disorder known to involve the pericardium, elevated
JVP, chest pain consistent with pericarditis or aortic dissection,
unexplained cardiomegaly (especially with a flask-shaped cardiac
silhouette) without pulmonary congestion on chest radiograph,
persistent fever with or without an obvious source of infection,
the presence of an isolated left pleural effusion and a fever, or
hemodynamic deterioration in a patient with another disease
process (or after an invasive cardiac procedure) that can involve
the pericardium.
15
CARDIAC (PERICARDIAL) TAMPONADE
The potential hemodynamic impact of an effusion ranges
from none to mild compromise to the most extreme clinical
is inflamed, scarred, or adherent. Localized pericardial adhesions
or organization of the pericardial fluid can result in localized
tamponade, which is most common after cardiac surgery and
may be difficult to recognize. Diffuse pericardial inflammation
and/or scarring with effusion can result in effusive-constrictive
pericarditis, which has features of both cardiac tamponade and
pericardial constriction.
6
If fluid accumulation is gradual, pericardial pressure remains
low because the pericardium can increase its compliance by
undergoing stretch. However, with continued accumulation of
fluid, the pericardial reserve volume (the difference between
unstressed pericardial volume and cardiac volume that accommodates physiologic changes in ventricular filling) is exceeded
and the intrapericardial pressure eventually increases; once this
becomes high enough to impede cardiac filling, cardiac output
1,2
falls.
Cardiac tamponade is a hemodynamic condition characterized
by equal elevation of atrial (pulmonary capillary wedge and
right atrial) and pericardial pressures, an exaggerated (>10 mm
Hg) inspiratory decrease in aortic systolic pressure (pulsus
paradoxus) and arterial hypotension (Fig. 29.3). The pathophysiology of cardiac tamponade and pulsus paradoxus readily explains
findings on clinical examination, Doppler echocardiography, and
at cardiac catheterization. The primary abnormality is compression of the cardiac chambers owing to increased pericardial
pressure that is exerted throughout the cardiac cycle. While the
pericardium has some degree of elasticity (part of the pericardial
reserve volume), once the elastic limit is reached, the heart must
compete with the intrapericardial fluid for a fixed intrapericardial
volume.2 As the total pericardial volume reaches the stiff portion
of its pressure–volume relation, tamponade rapidly ensues. As
cardiac tamponade progresses, the cardiac chambers become
smaller, transmural chamber pressures (i.e., preload) decrease,
and diastolic chamber compliance and ventricular filling decrease
owing to enhanced ventricular interdependence, which lead to
the characteristic elevation and equalization of diastolic filling
pressures and decreases in stroke volume and blood pressure.
It is important to realize that the clinical presentation and
diagnostic findings associated with tamponade physiology are
not all-or-none phenomena. Rather, the clinical presentation—
echocardiographic and catheterization features present in
tamponade—lie on a spectrum of severity that is dependent as
much on the acuity of presentation and etiology as the patient’s
underlying comorbidities (e.g., ventricular dysfunction, volume
status, valvular disease) and the ability to sustain a compensatory
physiologic response.
Patients with acute tamponade may present with chest pain,
tachypnea, or altered consciousness owing to decreased cardiac
output. On examination, the classic triad of hypotension, elevated
JVP, and diminished heart sounds (one of Beck’s triads) is present
in only a minority of patients.
patients with known tamponade suggested that five features were
present in a majority of patients: dyspnea (87% to 89% sensitive),
tachycardia (77% sensitive), pulsus paradoxus (82% sensitive),
16
A recent systematic review of
CHAPTER 29 Acute Pericardial Disease 305
100
0
0
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90
70
50 20
20
10
Fig. 29.3 Hyperacute cardiac tamponade caused by penetration of a saphenous vein graft during
angioplasty of the graft. The radial arterial tracing shows tachycardia and extreme pulsus paradoxus.
The right atrial and pericardial pressures are equilibrated at a very high level. The volume of blood
in the pericardium was small.
Rt. atrium
Peri
Radial artery
10
elevated JVP (76% sensitive), and cardiomegaly on chest radiograph (89% sensitive), while another review suggests that the
presence of pulsus paradoxus greater than 10 mm Hg in patients
with effusion increases the likelihood of tamponade (likelihood
ratio, 3.3).
17
Echocardiography is the preferred diagnostic modality for
identifying the hallmarks of tamponade physiology, that is, cardiac
chamber collapses (most often right atrial and right ventricular),
exaggerated respiratory variation of cardiac chamber dimensions,
and transvalvular flow velocities and inferior vena cava (IVC)
dilation with reduced respiratory change in dimension (vena
caval plethora; see Videos 29.1 to 29.4). Cardiac chamber collapse
occurs when the intrapericardial pressure exceeds the intracardiac
pressure in a given chamber; the right ventricular (RV) free wall
buckles or invaginates in early diastole when RV pressure is at
a minimum. This is often best visualized in the subcostal view
with an M-mode cursor through the affected chamber wall to
determine timing within the cardiac cycle.
2
Early-diastolic RV
collapse is highly specific for tamponade, although other conditions can reproduce this finding in the absence of a hemodynamically significant effusion.18 At end-diastole when right atrial
pressure is at its nadir, pericardial fluid pressure exceeds right
atrial pressure, resulting in right atrial collapse, often best appreciated in four-chamber imaging (Fig. 29.4). If persistent for longer
than one-third of diastole, the sensitivity, specificity, and positive
predictive values approach 100% in patients with tamponade.19
The degree of invagination has no predictive value for the presence
of tamponade. It is important to note that the absence of any
chamber collapse has a nearly 90% negative predictive value for
clinically significant tamponade.20 Collapse of the left atrium
and the left ventricle are less common; the latter is usually in
the presence of right ventricular pressure and volume overload
or when tamponade is regional (e.g., after cardiac surgery).
Inspiration
L
Fig. 29.4 Echocardiogram showing severe right atrial compres-
sion (arrow) in a patient whose pericardial effusion had caused
cardiac tamponade. L, Left ventricle. (From Shabetai R. Pericardial
disease. In: Brown DL, ed. Cardiac Intensive Care. Philadelphia:
Saunders; 1988:469–475.)
In normal individuals, there is minimal variation in flow
velocity during normal respiration. In tamponade, exaggerated
respiratory variation in transvalvular velocities results from
enhanced ventricular interdependence and suggests the presence
of pulsus paradoxus. With inspiration, tricuspid flow velocity
increases markedly, with a concomitant decrease in mitral flow
velocity. By recent consensus, the percentage of respiratory
variation for mitral and tricuspid inflow is calculated as: 100 ×
(expiration – inspiration)/expiration.6 In tamponade, tricuspid
flow variance usually exceeds 60%, while mitral flow exceeds
306 PART IV Noncoronary Diseases: Diagnosis and Management
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30%. It is important to note that transvalvular flow velocity
should not be the sole criterion used for the diagnosis of tamponade.6 IVC plethora is present in many patients with tamponade.
In one study, up to 92% of patients with an effusion requiring
drainage were found to have dilation and less than 50% inspiratory
decrease in the diameter of the IVC during inspiration, findings
suggestive of elevated central venous pressure.21 While this finding
is highly sensitive, it lacks specificity, as many other conditions
are associated with increased right atrial pressure and have the
same echocardiographic finding.
LOW PRESSURE TAMPONADE
Patients who are severely hypovolemic because of traumatic
hemorrhage, hemodialysis and ultrafiltration, excessive GI losses,
or excessive diuresis may have low pressure tamponade, in which
the intracardiac and pericardial diastolic pressures are only 6 to
12 mm Hg (Fig. 29.5).22 In 143 patients with cardiac tamponade
(equal pericardial and right atrial pressures before pericardiocentesis), 29 had an initial pericardial pressure less than 7 mm
Hg; the spectrum of etiologies and the frequency and severity
of echocardiographic findings were similar to patients with classic
cardiac tamponade.22 However, clinical findings associated with
classic cardiac tamponade—including increased heart rate,
elevated JVP, and pulsus paradoxus—were significantly less
common. As such, clinicians should maintain a high index of
suspicion for tamponade in patients with confounding conditions
that may affect the hemodynamic response to elevated intrapericardial pressure. Treatment consists of intravenous fluid
replacement and pericardiocentesis.
Causes of Tamponade in the CICU
While the majority of cases of tamponade in the CICU are likely
to be related to MI and coronary/cardiac interventions, cases of
EXP. INSP.
Ao
RV
Fig. 29.5 Low-pressure cardiac tamponade. The right ventricular
pressure was only 10 mm Hg, but otherwise the characteristic
hemodynamic abnormalities of severe tamponade were present,
including pulsus paradoxus, which was out of phase between
the right ventricle (RV) and the aorta (Ao), and absence of an
early diastolic dip. EXP, Expiration; INSP, inspiration. (From
Shabetai R. Cardiac tamponade. In: Shabetai R, ed. The Pericar-
dium. Norwell, MA: Kluwer Academic Press; 2003:122–166.)
100
90
80
70
60
50
40
30
20
10
–0
cardiac tamponade owing to a variety of causes may be admitted
to the CICU for monitoring and treatment. After MI, cardiac
tamponade may complicate both early post-MI pericarditis,
Dressler syndrome, and cardiac rupture. While the latter is often
immediately fatal, the rate of intrapericardial hemorrhage may
be slow enough or contained to allow detection (usually by
echocardiography with contrast) and surgical repair of the rupture
and any resultant pseudoaneurysm.
Treatment of Cardiac Tamponade
The 2015 ESC Guidelines treatment recommendations include
targeting the therapy of pericardial effusion to the specific etiology
whenever possible, the use of ASA/NSAID/colchicine when
effusion is associated with systemic inflammation, pericardiocentesis or cardiac surgery for cardiac tamponade or symptomatic
moderate to large effusions that are not responsive to medical
therapy, and for suspicion of unknown bacterial or neoplastic
pericarditis (all IC recommendations).
The choice between pericardiocentesis (see Chapter 44 and
open surgical drainage is based on local preference and experience,
the etiology of the effusion, hemodynamic status of the patient,
and characteristics of the pericardial fluid/contents. Generally,
for a majority of free-flowing or uncomplicated effusions, echoguided percutaneous drainage is preferred in the hands of a
skilled operator. Conversely, the presence of loculated or organized
fluid, hemopericardium, a traumatic etiology of the effusion, or
concern for aortic dissection may be best served with surgical
evacuation of the pericardium.
15
Pericardiocentesis can be performed under fluoroscopic or
echocardiographic guidance. The latter allows the operator to
select the shortest route to the effusion and the puncture site
with the largest collection of fluid. In the largest published series,
the para-apical location was utilized in two-thirds, while the
subxiphoid location was ideal in only 15%.23 An indwelling
pericardial catheter with intermittent or continuous suction is
left in the pericardial space until the rate of fluid return is
negligible (<25 mL/d). Following drainage, whether percutaneous
or surgical, patients should remain on telemetry for at least 24
hours, with a two-dimensional Doppler echocardiogram completed prior to hospital discharge to evaluate for fluid reaccumulation. Early follow-up echocardiography 1 to 2 weeks after discharge
to evaluate for recurrence or early constriction should be considered in the appropriate setting.
Surgical pericardiectomy with drainage, though less commonly
performed than pericardiocentesis, is often preferred when the
pericardial effusion has reaccumulated, is loculated, biopsy of
the pericardium is desired, or the patient has a coagulopathy.
For both chronic and recurrent effusions, the 2015 ESC Guidelines
recommend surgical pericardiectomy only in patients with
symptomatic effusions in whom medical therapy and repeated
pericardiocenteses were not successful.
Patients who are diagnosed with a large pericardial effusion
with minimal or no evidence of hemodynamic compromise may
be treated conservatively with careful hemodynamic monitoring,
serial echocardiographic studies, avoidance of diuretics and
vasodilators (a IIIC recommendation), and therapy aimed at
the underlying cause of the pericardial effusion. Effusions that
15
15
15
CHAPTER 29 Acute Pericardial Disease 307
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progressively enlarge, lead to worsening symptoms suggesting
cardiac tamponade, or that are otherwise refractory to a conservative approach should be treated with pericardial fluid drainage.
There is no role for medical therapy of cardiac tamponade, but
fluid resuscitation may be helpful while preparing for pericardial
drainage. Mechanical ventilation should be avoided whenever
possible.
CONSTRICTIVE PERICARDITIS
Constrictive pericarditis can occur following virtually any cause
of pericarditis but most commonly occurs after idiopathic/viral,
postcardiac surgery, and following radiation therapy. It may
present transiently (i.e., either spontaneous resolution or response
to medical therapy), subacutely, or chronically. Constrictive
pericarditis is seldom an indication for admission to the CICU,
but intensivists might manage patients with transient or subacute
presentations that may clinically resemble cardiac tamponade.
Patients with chronic constriction often present with exertional
dyspnea, lower extremity edema, fatigue, or abdominal distention
and, in rare instances, congestive hepatopathy. Distinguishing
constrictive pericarditis from cardiac tamponade, acute decompensated heart failure, and disorders such as restrictive cardiomyopathy and chronic liver disease is essential, as treatments
are markedly different. The critical pathophysiologic features of
constrictive pericarditis—which are responsible for the physical
examination, hemodynamic, and imaging findings—are enhanced
ventricular interaction (interdependence) and dissociation of
intracardiac and intrathoracic pressures.
The physical exam in constriction is notable for elevated
jugular venous pressure (reported in as many as 93% of patients
with surgically confirmed constrictive pericarditis), hepatomegaly,
splenomegaly, ascites, and edema. The jugular venous waveform
demonstrates prominent x and y descents. The Kussmaul sign
(failure of the JVP to decrease with inspiration) is an examination
finding relatively specific to constriction but does not distinguish
constrictive pericarditis from severe tricuspid valve disease or
right-sided heart failure. In contrast, pulsus paradoxus is rare
and, if present, should raise suspicion for effusive-constrictive
disease (pericardial constriction with a concomitant effusion).
A pericardial knock, an accentuated heart sound that occurs
slightly earlier than an S
approximately 50% of cases.
, is distinctive but reported in only
3
Patients with suspected constrictive pericarditis should undergo
initial evaluation with ECG, chest radiograph, and echocardiography. Unlike patients with cardiomyopathy, B-type natriuretic
peptide (BNP) and N-terminal pro-BNP levels are usually only
mildly elevated in constriction. Two-dimensional Doppler
echocardiography is critical in the diagnosis of constriction and
in differentiating constriction from tamponade, effusiveconstrictive disease, and restrictive cardiomyopathy.
24
The most specific echocardiographic sign of constriction is a
septal bounce with abrupt transient rightward movement of the
interventricular septum. Doppler echocardiography demonstrates
elevated early diastolic tissue Doppler velocities (é) with the
septal e′ often greater than the lateral é tissue velocity (annulus
paradoxus) and an expiratory increase in early mitral inflow
velocity greater than 25% and an expiratory decrease of tricuspid
inflow greater than 40%.6 Computed tomography, magnetic
resonance imaging, and cardiac catheterization are useful to
confirm the diagnosis, particularly in patients with nondiagnostic echocardiographic findings, and to assist in perioperative
management. Delayed enhancement cardiac magnetic resonance
is valuable to assess the extent of pericardial inflammation
and the response to antiinflammatory medications in patients
with increased inflammatory biomarkers or a short duration
(<3 months) of constrictive symptoms.
6
For patients with newly diagnosed constrictive pericarditis
who are hemodynamically stable and do not have evidence of
chronic constriction, a trial of conservative management rather
than pericardiectomy is warranted. Pericardiectomy is the only
definitive treatment option for patients with chronic symptomatic
constrictive pericarditis.
CONCLUSION
While the spectrum of pericardial disease varies from benign to
life threatening, failure to recognize pericardial disease, particularly
in the setting of shock, can have devastating consequences. Often,
a simple ECG and two-dimensional Doppler echocardiography,
in the hands of a skilled clinician, will provide both a diagnosis
and assist in facilitating timely management of patients with
hemodynamic embarrassment due to pericardial disease.
The full reference list for this chapter is available at
ExpertConsult.com.
CHAPTER 29 Acute Pericardial Disease 307.e1
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REFERENCES
1. Hoit BD. Pathophysiology of the pericardium. Prog Cardiovasc
Dis. 2016. Dec 1. pii: S0033-0620(16)30133-5.
2. Spodick DH. Acute cardiac tamponade. N Engl J Med.
2003;349:684–690.
3. Kyto V, Sipila J, Rautava P. Clinical profile and influences on
outcomes in patients hospitalized for acute pericarditis.
Circulation. 2014;130:1601–1606.
4. Throughton RW, Asher CR, Klein AL. Pericarditis. Lancet.
2004;363:717–727.
5. Imazio M, Gaita F, LeWinter M. Evaluation and treatment of
pericarditis: a systematic review. JAMA. 2015;314(14):1498–1506.
6. Klein AL, Abbara S, Agler DA, et al. American Society of
Echocardiography clinical recommendations for multimodality
cardiovascular imaging of patients with pericardial disease:
endorsed by the Society for Cardiovascular Magnetic Resonance
and Society of Cardiovascular Computed Tomography. J Am Soc
Echocardiogr. 2013;26:965–1012.
7. Imazio M, Brucato A, Maestroni S, et al. Prevalence of C-reactive
protein elevation and time course of normalization in acute
pericarditis: implications for the diagnosis, therapy, and
prognosis of pericarditis. Circulation. 2011;123:1092–1097.
8. Imazio M, Demichelis B, Cecchi E, et al. Cardiac troponin I in
acute pericarditis. J Am Coll Cardiol. 2003;42:2144–2148.
9. Imazio M, Demichelis B, Parrini I, et al. Day-hospital treatment
of acute pericarditis: a management program for outpatient
therapy. J Am Coll Cardiol. 2004;43:1042–1046.
10. Imazio M, Bobbio M, Cecchi E, et al. Colchicine in addition to
conventional therapy for acute pericarditis: results of the
COlchicine for acute PEricarditis (COPE) trial. Circulation.
2005;112:2012–2016.
11. Imazio M, Brucato A, Forno D, et al. Efficacy and safety of
colchicine for pericarditis prevention. Systematic review and
meta- analysis. Heart. 2012;98:1078.
12. Alabed S, Cabello JB, Irving GJ, et al. Colchicine for pericarditis.
Cochrane Database Syst Rev. 2014;(8).
13. Imazio M, Brucato A, Belli R, et al. Colchicine for the prevention
of pericarditis: what we know and what we do not known in
2014- systematic review and meta-analysis. J Cardiovasc Med
(Hagerstown). 2014;15:840–846.
14. Schwier N, Tran N. Non-steroidal anti-inflammatory drugs and
aspirin therapy for the treatment of acute and recurrent
idiopathic pericarditis. Pharmaceuticals (Basel). 2016;9:pii: E17.
15. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the
diagnosis and management of pericardial disease. Eur Heart J.
2015;36:2921–2964.
16. Seferovic SM, Ristic AD, Imazio M, et al. Management strategies
in pericardial emergencies. Herz. 2006;31(9):891–900.
17. Roy C, Minor MA, Brookhart MA, et al. Does this patient with a
pericardial effusion have cardiac tamponade? JAMA.
2007;297:1810–1818.
18. Armstrong WF, Schilt BF, Helper DJ, et al. Diastolic collapse of
the right ventricle with cardiac tamponade: an
echocardiographic study. Circulation. 1982;65:1491–1496.
19. Gillam LD, Guyer DE, Gibson TC, et al. Hydrodynamic
compression of the right atrium: a new echocardiographic sign
of cardiac tamponade. Circulation. 1983;68:294–301.
20. Merce J, Sagrista-Sauleda J, Permanyer-Miralda G, et al.
Correlation between clinical and Doppler echocardiographic
findings in patients with moderate and large pericardial effusion:
implications for the diagnosis of cardiac tamponade. Am Heart J.
1999;138:759–764.
21. Himelman RB, Kircher B, Rockey DL, Schiller NB. Inferior vena
cava plethora with blunted respiratory response: a sensitive
echocardiographic sign of cardiac tamponade. J Am Coll Cardiol.
1988;12:1470–1477.
22. Sagrista-Sauleda J, Angel J, Sambola A, et al. Low-pressure
cardiac tamponade: clinical and hemodynamic profile.
Circulation. 2006;114:945–952.
23. Tsang TSM, Enriquez-Sarano M, Freeman WK, et al. Consecutive
1127 therapeutic echocardiographically guided
pericardiocenteses: clinical profile, practice patterns, and
outcomes spanning 21 years. Mayo Clin Proc. 2002;77:429–436.
24. Garcia MJ. Constrictive pericarditis versus restrictive
cardiomyopathy. J Am Coll Cardiol. 2016;67:2061–2076.
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Acute Respiratory Failure
Holly Keyt, Jay I. Peters
OUTLINE
Physiology of Gas Exchange, 308
Pathophysiology of Acute Respiratory Failure, 309
Clinical Assessment, 310
Differential Diagnosis, 311
Management, 314
Mechanical Ventilation, 315
Extracorporeal Membrane Oxygenation, 317
Conclusion, 317
Respiratory failure is defined as the inability to maintain either
the normal delivery of oxygen to tissues or the normal removal
of carbon dioxide from the tissues. From a physiologic perspective,
respiratory failure can be caused by diffuse pulmonary dysfunction
(ventilation/perfusion [V/Q] mismatch or pulmonary shunt),
neurologic dysfunction (depression of the respiratory drive),
cardiac dysfunction (low cardiac output or pulmonary edema),
or a lack of hemoglobin to transport gases. Clinically, this is
seen as arterial hypoxemia leading to tissue hypoxia and/or arterial
hypercapnia. Acute respiratory failure (ARF) may evolve over a
period of minutes to hours to days depending on the clinical
situation. ARF, therefore, is a generic term that encompasses a
heterogeneous spectrum of diseases that eventually end with
the same pathophysiologic outcomes: arterial hypoxemia (usually
with partial pressure of O2 [PaO2] of <60 mm Hg) or hypercapnia
(partial pressure of CO2 [PaCO2] of >45 to 50 mm Hg).
PHYSIOLOGY OF GAS EXCHANGE
In the lung, gas exchange occurs at the capillary-alveolar interface.
Microscopic examination of septal capillaries reveals that they
are significantly thinner on the side that bulges into the air space.
This conformation enhances the diffusion of oxygen from the
air space into the blood and the elimination of carbon dioxide
from the blood into the air space. Equilibration of partial pressures
of gases between the two compartments occurs rapidly. Oxygen
in the blood is carried by hemoglobin. Only a small percentage
is transported as dissolved gas. The following equation describes
the arterial oxygen content (CaO
CO HgbSaO PaO
where CaO2 is the oxygen content of arterial blood in milliliters
of O2 per deciliter of blood; Hgb is the hemoglobin concentration
in grams per deciliter of blood; SaO2 (oxygen saturation) is the
fraction of hemoglobin sites bound by oxygen; and PaO2 is the
arterial partial pressure of oxygen.
a2
13
):
2
003=××+ ×(. )(
Because the amount of dissolved oxygen is small in comparison
to the amount transported by hemoglobin, in most clinical situations, CaO
and the oxygen saturation of the arterial blood, not on PaO2.
Even in severe anemia, the contribution of dissolved oxygen in
the overall CaO2 is negligible despite very high PaO2. This principle
is important clinically in patients with ARF for whom increasing
CaO2 can be accomplished by increasing hemoglobin concentration and SaO2, but not necessarily by increasing PaO2. This follows
from the sigmoid shape of the oxygen-hemoglobin dissociation
curve, in which significantly higher PaO2 is needed to increase
the SaO2 beyond 90% as the curve plateaus.
Carbon dioxide is transported in the blood mostly in the
form of carbonic acid. Only approximately 5% is transported
by binding with hemoglobin. Ten percent is transported as
dissolved gas.1 As the tissues extract an increasing amount of
oxygen from the blood, the deoxygenated hemoglobin increases
its ability to carry carbon dioxide (Haldane effect). Similarly, as
an increasing amount of oxygen becomes available in the arterial
and venous blood, less carbon dioxide may be carried by the
oxidized hemoglobin. This effect has been implicated in the
pathogenesis of worsening hypercapnia after oxygen supplementation in patients with baseline hypercapnia.
To achieve optimal gas exchange, local matching of ventilation
and perfusion has to occur. The interrelationships between
ventilation and blood flow are shown schematically in Fig. 30.1,
in which imbalance (B) is typified by bronchospasm, shunt (C)
is typified by dense pneumonia or severe acute respiratory distress
syndrome (ARDS), and dead space (D) is typified by destruction
of the capillaries in emphysema.
Normally, both ventilation and perfusion exhibit a gradient
from the top to the bottom of the lung. However, the gradient
is more pronounced in blood flow than in ventilation, such that
in the upper portions of the lung there are predominantly high
V/Q areas and in the lower portions of the lung there are low
V/Q areas. The overall V/Q ratio of the normal lung is 0.8.
depends primarily on the hemoglobin concentration
2
2
308
CHAPTER 30 Acute Respiratory Failure 308.e1
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Keywords
acute hypoxemic respiratory failure
oxygen therapy
noninvasive ventilation
mechanical ventilation
extracorporeal membrane oxygenation
CHAPTER 30 Acute Respiratory Failure 309
=−−
V / O
ABCD
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TABLE 30.1 Berlin Definition of Acute
Respiratory Distress Syndrome
Timing Within 1 week of a known clinical insult or
new or worsening respiratory symptoms.
Normal
Fig. 30.1 Schematic representation of various patterns of ventila-
tion (V) and perfusion (Q). A, Normal V/Q ratio in which the PVO
=
40 mm Hg and PCO2 = 46 mm Hg. After equilibration, the
capillary PO2 = 101 mm Hg, PCO2 = 40 mm Hg, and P(A − a)O2
=
0 mm Hg. B, V/Q imbalance caused by airway obstruction
would decrease the PO
mental oxygen. C, A shunt allows mixed venous blood to traverse
the capillary without any gas transfer. D, Dead space, the
ventilated area of the lung that does not participate in gas
exchange. (From Greene KE, Peters JI. Pathophysiology of acute
respiratory failure. Clin Chest Med. 1994;15:1–11.)
V / O
Imbalance
. This could be corrected with supple-
2
Shunt Dead space
Chest imaging (radiograph
or computed
tomography)
Origin of edema Respiratory failure not fully explained by
2
Oxygenation Mild: PaO
CPAP, Continuous positive airway pressure; FIO2, fraction of inspired
oxygen; PaCO2, partial pressure of arterial carbon dioxide; PEEP,
positive end-expiratory pressure.
Bilateral opacities not fully explained by
effusions, lobar/lung collapse, or nodules.
cardiac failure or fluid overload.
Need objective assessment (e.g.,
echocardiography) to exclude hydrostatic
edema if no risk factor present.
/FIO2 ratio of 200–300 mm Hg with
2
PEEP or CPAP ≥5 cm H2O
Moderate: PaO
with PEEP or CPAP ≥5 cm H2O
Severe: PaO
or CPAP ≥
/FIO2 ratio of 100–200 mm Hg
2
/FIO2 < 100 mmg Hg with PEEP
2
5 cm H2O
The overall efficiency of gas exchange can be assessed in terms
of maintenance of normal PaO2 and PaCO2. The assessment can
be performed by calculating the alveolar-arterial partial pressure
oxygen difference (PAO2 – PaO2), which is also known as the A-a
gradient. The mean alveolar oxygen tension (PaO2) is calculated
by using the alveolar gas equation as follows:
PO FIOPBPHO PaCO R
A2 22 2
()
where PB is the barometric pressure of the atmosphere, which
changes with altitude; FIO2 is the fraction of inspired oxygen
(approximately 0.21 in room air); PaCO2 is the partial pressure
of arterial carbon dioxide; and R is the respiratory quotient.
This equation gives an estimation of PaO2, which changes with
altitude (PB), with inspired oxygen concentration, and with
PaCO2. PaO2 not only changes with changes in PAO2 but also
decreases with age in normal individuals. Therefore PAO2-PaO2
increases with age and can be estimated in most adults breathing
room air to be approximately 4 mm Hg for each decade of life
until the maximum of the seventh decade. This estimation is
not valid for patients receiving oxygen supplementation. For
these patients, assessment of efficiency of gas exchange can be
obtained using the ratio of PaO2 to FIO2 (PaO2/FIO2 ratio
normally is >400 mm Hg). Although it is not as accurate as the
PAO2-PaO2 difference, it is useful clinically because most patients
with ARF receive supplemental oxygen at the time that blood
gas analysis is performed. This ratio also forms one of the basic
criteria for the diagnosis of ARDS. By consensus, ARDS is defined
by PaO2/FIO2 ratio less than or equal to 300 mm Hg when
respiratory failure is present and not otherwise explained by
cardiac failure or fluid overload (Table 30.1).3 This ratio is most
helpful when used serially or when the ratio changes significantly
with a therapeutic maneuver.
PATHOPHYSIOLOGY OF ACUTE
RESPIRATORY FAILURE
The three most important pathophysiologic mechanisms that
cause ARF are hypoventilation, V/Q mismatch, and shunt. Diffusion abnormalities, which occur with mild pulmonary edema
or early interstitial lung disease, may cause exercise-induced
hypoxemia but rarely cause clinically significant hypoxemia.
Reduction of inspired PO2 and venous admixture are other
potential but less common causes of hypoxemia.
Hypoventilation can be defined as the inadequate movement
of fresh alveolar gas necessary for maintaining a normal PaCO2.
Pure hypoventilation is a relatively uncommon clinical event.
In most cases, hypoventilation occurs along with other causes
of hypoxemia. When pure hypoventilation does occur, it is usually
caused by depression of the respiratory center by sedative-hypnotic
drugs or by neuromuscular diseases that affect the respiratory
muscles.
The increase in PaCO
hypoventilation invariably affects PaO2 as predicted in the alveolar
gas equation, causing a decrease in PaO2. This results in hypoxemia
with a normal PAO2-PaO2 gradient. In patients on room air, the
PaO2 will fall 5 mm Hg for every 3 mm Hg rise in PaCO2. If the
PAO2-PaO2 gradient is abnormally increased, then other mechanisms may also be involved in the pathogenesis of hypoxemia.
Hypoxemia resulting from pure alveolar hypoventilation usually
responds adequately to increasing FIO2.
By far, the most common cause of clinically important
hypoxemia is V/Q mismatching, which is present as a continuum
from pure shunt (Q, without V) to pure dead space ventilation
(V without Q) and unlimited patterns of V/Q mismatching in
between. In young normal individuals, V/Q ratios range from
0.6 to 3.0 and usually center around 1.0.4 Low V/Q lung units
that accompanies pure alveolar
2
310 PART IV Noncoronary Diseases: Diagnosis and Management
−
()
()
PP
−
22
Ventilation-Perfusion Ratio
ACUTE RESPIRATORY FAILURE
P
and P
(mm Hg)
O
Content (mL/100 mL)
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can result from compromised ventilation, such as obstructed
airways or from partial alveolar filling with pneumonia or
pulmonary edema. High V/Q lung units most often occur with
obstruction of blood flow owing to pulmonary vascular disease
or from a lack of capillaries owing to lung parenchymal destruction, such as that seen in emphysema.
V/Q mismatching causes hypoxemia and hypercapnia. However,
in most cases, an increase in minute ventilation stimulated by
hypercapnia results in normalization of PaCO2 with persistent
hypoxemia. This is possible because the CO2 dissociation curve
is linear, allowing well-ventilated areas to compensate. The O2
dissociation curve is sigmoid shaped; therefore, the increase in
minute ventilation, despite producing higher end-capillary PO2,
results in very modest changes in oxygen saturation, which in
most cases is inadequate to reverse the hypoxemia (Fig. 30.2).
Hypoxemia due to V/Q mismatching is usually correctable by
increasing the FIO2. Local hypoxia in low V/Q areas triggers
reflex hypoxic pulmonary vasoconstriction in an attempt to
correct the V/Q imbalance. This reflex vasoconstriction can be
abolished by a number of vasodilators, including nitroprusside,
nitroglycerin, calcium channel blockers, and inhalational anesthetics. When compensatory mechanisms fail in a patient with severe
lung disease, the body may set a new steady-state PaCO2 and
pH as an adaptive response to conserve the work of breathing.
Right-to-left shunt occurs when there is no ventilation into
a lung unit while perfusion is preserved. It is one of the extreme
ends in the spectrum of V/Q mismatches. In a normal lung, the
amount of shunt present is less than 5%. Shunt in the lung
results from atelectasis, severe pulmonary edema, and air space
consolidation, such as pneumonia. In addition, right-to-left shunt
can also occur as a consequence of arteriovenous malformation
and intracardiac shunts from a patent foramen ovale, patent
ductus arteriosus, or ventricular septal defect. Shunts cause
significant hypoxemia owing to the mixture of oxygenated blood
with shunted, poorly oxygenated venous blood. Hypercapnia is
140
120
100
80
2
CO
60
40
2
O
20
Fig. 30.2 Variations in PO2, PCO2, and O2 content in a gas
exchange lung unit as its ventilation-perfusion ratio is progressively
increased. This lung is assumed to be breathing air, and the
mixed venous blood PO
Hg, respectively. (From West JB. Ventilation-perfusion relationships. Am Rev Respir Dis. 1977;116:919–943.)
.010.005 0.1 1.0
2
21
2
Content
O
2
PO
2
PCO
2
10
and PCO2 are 40 mm Hg and 45 mm
20
19
18
17
16
15
100
usually not present until the shunt is greater than 50%. In contrast
to other mechanisms of respiratory failure, hypoxemia owing
to shunting is not responsive to increases in FIO2. This feature
of shunt can be conveniently used to separate it from other
causes of hypoxemia. Calculation of shunt (Qs/Qt) is easily done
by administering 100% oxygen for 15 minutes and then analyzing
arterial blood gases. Percent shunt can be estimated using a
nomogram or by using the following formula:
Cc Ca
OO
Qs Qt
22
=
Cc Cv
OO
22
100
−
×
In this equation, C denotes content, and the lowercase letters
c, a, and v denote end-capillary, arterial, and venous blood,
respectively. A simplified shunt equation assumes that the Cvo2
is normal and that the shunt is less than 25%. This simplified
shunt equation states that
Qs Qt
=
aAO O
20
When the FIO2 used is less than 1.0, the resulting calculation
is called venous admixture instead of shunt. This reflects the
contribution of severe V/Q mismatching, including very low
V/Q ratios that approach zero, which may act like shunts when
alveoli are not ventilated with 100% oxygen. The hypoxemia of
shunts is remarkably resistant to correction by increasing the
FIO2. Patients with significant shunts may have the same arterial
oxygen saturation when maintained on a relatively toxic FIO2 (near
1.0) or when titrated down to relatively safe FIO2 (0.6 to 0.7).
CLINICAL ASSESSMENT
Patients with ARF commonly have dyspnea. For those with
underlying lung disease, dyspnea may be present chronically.
Therefore, mild changes in the degree of dyspnea may or may
not be perceived. In the presence of significant hypoxemia and
acidosis, patients may have symptoms of central nervous system
depression ranging from irritability to coma. Patients may also
have evidence of the effects of hypoxemia or acidosis on the
cardiovascular system, such as arrhythmias, angina, or myocardial
infarction. Depending on the underlying disease, other symptoms
may also be present. Although they may be important and helpful
in evaluating the underlying process causing the respiratory
failure, they are not that helpful in evaluating the degree of
respiratory dysfunction. For example, the additional symptoms
of cough, sputum production, and fever may suggest pneumonia,
whereas pleuritic chest pain with certain characteristics may
suggest pneumothorax or pulmonary embolism as the cause of
the respiratory distress.
Initial physical examination of patients with ARF should focus
on overall appearance, vital signs, and the ABCs (airway, breathing,
and circulation). In general, patients with ARF have tachypnea,
tachycardia, and variable mental status. The degree of alteration
of mental status may reflect the severity of the respiratory failure.
Confusion or disorientation in the presence of dyspnea and
tachypnea may reflect profound hypoxemia or hypercapnia with
its attendant respiratory acidosis. Pulsus paradoxus, a decrease
in arterial systolic pressure of greater than 10 mm Hg with
CHAPTER 30 Acute Respiratory Failure 311
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TABLE 30.2 Radiographic Approach to Acute Respiratory Failure
Radiograph Clinical Characteristics Responses to Oxygen
“White” Chest Radiograph
Pneumonia Fever, leukocytosis, sputum production + to + + +
Acute respiratory distress syndrome Predisposing risk factors, bilateral infiltrates on imaging + to + +
Cardiogenic edema Paroxysmal nocturnal dyspnea, orthopnea, edema + + + to + + + +
Interstitial lung disease Prior chest radiographic abnormalities + + + to + + + +
“Black” Chest Radiograph
Chronic obstructive pulmonary disease/asthma Reduced flow on bedside spirometry + + to + + + +
Pulmonary emboli Acute dyspnea, pleuritic pain + + + to + + + +
Right-to-left shunt History and physical examination consistent with pulmonary
hypertension
Microatelectasis Postoperative or rib fracture, bronchial breath sounds + + to + + +
a
Range from +, which is shuntlike (Po2 increases 1 mm Hg for 1% rise in FIO2), to + + + +, which is V/Q imbalance (Po2 increases 5 mm Hg for
1% rise in FIO2).
+
a
inspiration, also suggests severe airway obstruction associated with
significant negative intrathoracic pressures. Patients with severe
respiratory distress are usually unable to speak in full sentences.
Likewise, the presence or absence of adventitious breath sounds
may assist the clinician in evaluating the degree and acuity of the
respiratory distress. Crackles suggest alveolar flooding or early
bronchopneumonia, whereas rhonchi often herald an increase in
mucus production or an inability to clear secretions. Wheezing
suggests airway obstruction, whereas wheezes located over the
neck suggest upper airway stridor that may be associated with
respiratory collapse. Decrease in breath sounds may be seen in
patients with chronic obstructive pulmonary disease (COPD) or
those with severe airway obstruction. The absence of wheezing
and breath sounds in a patient with underlying obstructive lung
disease and respiratory distress may suggest impending respiratory collapse as a result of very limited air movement. Absence
of breath sounds may also be associated with pneumothorax.
Subcutaneous emphysema usually indicates pneumomediastinum
with or without accompanying pneumothorax.
Despite advances in noninvasive technologies in oxygenation
assessment, arterial blood gas analysis remains the best and most
accurate test in the initial assessment of patients with ARF. Pulse
oximetry is acceptable as a method for following oxygenation
once it has been calibrated to true blood gas co-oximetry saturation and the arterial PaO
is known. Pulse oximetry (SpO2) carries
2
plus or minus 4% error in measuring oxygen saturation. In
patients with carbon monoxide poisoning, SpO2 does not reflect
true PaO2, and profound hypoxemia may be missed. With
methemoglobinemia, the SpO2 may falsely read the oxygen
saturation at around 85%, irrespective of the true saturation.
Furthermore, pulse oximetry does not give information on PaCO2
and pH, which may be crucial in the differential diagnosis and
management of the patient with ARF. The presence of hypercapnia
is a marker of the severity of disease. Hypercapnia is more likely
to complicate hypoxemic failure when the disease is superimposed
on significant underlying lung or neuromuscular disease.
The presence of hypoxemia, hypercapnia, and respiratory
acidosis can be used to define ARF; however, it is difficult to set
specific levels of PaO2 or PaCO2 because patients with underlying
lung disease may have markedly abnormal baselines. Given these
qualifications, patients with ARF generally have a PaO2 less than
55 mm Hg or a PaCO2 more than 50 mm Hg. The pH is very
helpful in assessing the acuity of the hypoventilation. In cases
of subacute or chronic hypoventilation, the patient usually has
an elevated serum bicarbonate level and a mild depression of
the pH. In acute respiratory acidosis without renal compensation,
the pH drops by 0.08 for each 10 mm Hg rise in PaCO2.
Compensatory bicarbonate retention or wasting by the kidneys
to buffer the pH changes usually takes 2 to 3 days to occur. After
renal compensation, a change of 10 mm Hg of PaCO2 will produce
a 0.03 change in pH in the opposite direction.
The chest radiograph is extremely useful in sorting out the
differential diagnosis of ARF during the initial presentation. The
causes of hypoxemia can be classified based on radiographic
appearance. Table 30.2 shows examples of diseases associated with
“white” chest radiographs showing diffuse or patchy infiltrates
and diseases associated with “black” chest radiographs showing
normal or clear lung fields.
Differential Diagnosis
The clinical classification of ARF based on chest radiographic
appearance provides a convenient algorithm in evaluating
hypoxemic patients. Posteroanterior and lateral radiographs or
computed tomography (CT) of the chest provide better quality
than portable films and can help visualize the retrocardiac space.
Patients having a “white” chest radiograph usually have pneumonia, ARDS, cardiogenic pulmonary edema, or progressive
interstitial lung disease. Patients having a “black” chest radiograph
usually have obstructive lung disease, pulmonary emboli, a
right-to-left shunt, or microatelectasis. Most patients with
hypoxemic respiratory failure have radiographic infiltrates.
The presence of additional compatible history and physical
examination findings often allows the clinician to narrow the
differential diagnosis. With fever, cough, sputum production,
and lobar or patchy infiltrate, pneumonia is a likely possibility.
Pneumonia often presents in an atypical fashion in patients older
than 65 years old.
fever or specific respiratory complaints; confusion or mild
5
Up to 50% of older patients do not have a
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