Page 452 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

322 PART 3: Cardiovascular Disorders

. This can be dem- for the evaluation of critically ill patients—non-invasiveness, potential
until a new steady state is reached at a higher Pa CO 2
onstrated numerically by the alveolar dead-space fraction (AVDSf) to elucidate competing diagnoses (such as myocardial infarction or
as follows: pericardial disease), and rapid availability, echocardiography is insen-
sitive, and should not be used to exclude PE. In prospective trials of
AVDSf = (Pa CO 2 – P ET CO )/Pa CO 2 unselected patients, sensitivities of between 29% and 52% are reported
2
When combined with a negative D-dimer value, as will be discussed for various echocardiographic criteria of right ventricular strain or
shortly, an AVDSf of less than 0.15 has been shown to exclude PE in dysfunction or tricuspid regurgitation. 35,36 Many patients with PE have
hospitalized patients with a sensitivity of 97.8% and a negative predictive normal echocardiograms.
value of 98%. In calculating the AVDSf, however, one must take care When echocardiography exhibits right ventricular dysfunction, it reli-
16
to ensure a properly calibrated blood gas analyzer, as even small changes ably predicts an increased risk of mortality from pulmonary embolism.
measurements will cause large differences in AVDSf. Strong One study examined 126 patients with PE with echocardiography on
https://kat.cr/user/tahir99/
in Pa CO 2
is noted the day of diagnosis, and found moderate RV dysfunction to impart
consideration of PE is warranted whenever a rising arterial P CO 2
in the setting of relatively constant CO production. a sixfold increased risk of in-hospital death compared to normal RV
2 function. Even in patients assessed to be hemodynamically stable at
37
Pulmonary Artery Catheter: The most obvious clues from the pulmonary presentation, right ventricular dysfunction portends a worse prognosis;
artery catheter (PAC) are the elevations in right atrial, right ventricu- one study found that 10% of such patients develop shock and 5% died in
lar, and Pa pressures and concomitant fall in Q ˙ t that occur with PE. the hospital, compared to a 0% mortality amongst patients with normal
Concomitant with reduced Q ˙ t, one observes widening of the arterial (A) RV function. In another series of hemodynamically stable patients,
38
to venous (V) oxygen content difference (Fick principle) and a decre- recurrent embolism was strongly associated with baseline echocar-
) or the central venous
39
ment in the mixed venous oxygen saturation (Sv O 2 diographic abnormalities in right ventricular wall motion. A word
oxygen saturation. A final clue from the PAC may lie in the difference of caution is prudent, however, in that the classic echocardiographic
between the Pa diastolic pressure and the pulmonary artery occlusion findings of PE are nonspecific, being common to a number of causes of
pressure (Paop), though rising pericardial constraint may blunt a fall in acute right ventricular pressure overload such as the acute respira-
Paop. Normally, flow through the pulmonary circulation is pulsatile, tory distress syndrome, other forms of severe hypoxemia, or status
26
so that by the end of diastole, there is no more flow from the Pa to left asthmaticus (see Chaps. 52 and 55).
atrium. Without flow, there can be no pressure gradient from the Pa to
left atrium. Thus the end-diastolic Pa pressure and the Paop are nearly
equal. When there is obstruction of the pulmonary vascular bed, how- DIAGNOSIS
remains. A discrepancy between the Pa diastolic pressure and Paop may ■ SPECIAL PROBLEMS IN THE ICU
ever, flow is not completed by the end of diastole and a pressure gradient
provide a clue to Pa obstruction. 31 The typical critically ill patient is unable to complain of the usual symp-
Unfortunately, such pulmonary arterial changes are both nonspecific toms of PE, has numerous explanations for tachycardia and tachypnea,
and insensitive, so that only rarely do such changes indicate PE. For is hemodynamically unstable, and is a poor candidate for transport for
example, cardiac dysfunction (systolic or diastolic) causes a rise in right radiographic studies. For that reason, it is important to have a clear
heart pressures and a fall in Q ˙ t, any cause of low Q ˙ t will result in a sense of the probability of PE in any given patient. Such a judgment is
widened A-V oxygen content difference; and any cause of acute lung complex, and validated algorithms for determining prior probability in
injury or global hypoxic vasoconstriction may raise the Pa diastolic to critically ill patients are not available. The clinician must synthesize the
Paop gradient. A further layer of complexity is added by observations patient’s risk factors and cardiopulmonary physiology to arrive at a risk
that in randomized trials, PAC use results in a small but significant determination. In the following sections, the contribution of various
increase in the risk of PE compared to central venous catheters. 32,33 tests in evaluating suspected PE is discussed. An approach to diagnosis
Given the limitation of the PAC as a diagnostic tool and the risk of actu- is summarized in Figure 39-5.
Echocardiography: Intensivist-performed, goal-directed echocardiog- ■ RISK FACTORS
ally causing PE, it cannot be advocated for the diagnosis of PE.
raphy occasionally points to PE as the cause of cardiopulmonary Since the symptoms, signs, and laboratory findings of PE are usu-
failure (Chap. 29). Similarly, a formal study requested for evaluation ally nonspecific, to wait for a patient with classic, unmistakable clues
of a low flow state may unexpectedly reveal findings strongly sugges- before pursuing a diagnosis risks missing the majority of patients with
34
tive of PE. These include a dilated, thin-walled, poorly contracting this potentially lethal disease. However, since nonspecific indicators of
right ventricle, bowing of the interventricular septum to the left, or potential PE are ubiquitous, indiscriminant pursuit of the diagnosis is
McConnell’s sign. Very rarely, echocardiography may demonstrate a prohibitively costly and dangerous. Most patients with PE have identifi-
thrombus in the right atrium or right ventricle (Table 39-2), clinching able risk factors (Table 39-3). Absence of risk factors for VTE should
the diagnosis of PE. While its attractions include portability—especially lead the physician to seek alternative explanations for the patient’s
findings. On the other hand, when numerous risk factors are present,
the diagnosis should be more seriously considered.
Given the nonspecific presentation of most patients with PE, a clinical
TABLE 39-2 Echocardiographic Signs of Pulmonary Embolism risk prediction tool has been developed to help stratify patients with a
possible diagnosis of PE and to identify a low-risk group of patients for
Dilated, thin-walled right ventricle whom further testing is unnecessary. Known as the Wells criteria, the
40
Poorly contracting right ventricle most often cited prediction rule is shown in Table 39-4, and for stable
Tricuspid regurgitation patients, it appears safe to withhold anticoagulation when the score is
≤4.0 and the D-dimer test is negative. The Wells criteria have not been
Pulmonary hypertension estimated from the tricuspid regurgitation jet
tested in critically ill populations, but the assessment of a patient’s global
Leftward shifting of the interventricular septum risk for PE based on patient historical factors, clinical presentation,
Pulmonary artery dilation and differential diagnosis remains a necessary step. Because PE lacks
a perfect diagnostic test, the clinician must synthesize both pretest
Visualized thrombus in RA, RV, or Pa
probability and test results in order to select the most rational therapy
Loss of respirophasic variation in IVC diameter
for each patient.

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