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34—PULMONARY EMBOLISM
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289
negative, the probability of pulmonary embolism is only 0.93%, a risk regarded to be lower than
the risk of further testing.
PERC negative is 0.1.)
36–42
(e corresponding LR for combined low clinical probability and
37,39,40,42
Clinicians appropriately applying the PERC rule to low probability
patients can safely reduce the number of diagnostic tests performed (both D-dimer measurements
and computed tomography), shorten the time patients spend in emergency departments, and
reduce hospitalizations.
43,44
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
References
https://t.me/medicina_free
1. Ryu JH, Olson EJ, Pellikka PA. Clinical recognition of pulmonary embolism: problem of unrecognized
and asymptomatic cases. Mayo Clin Proc. 1998;73(9):873–879.
2. Morgenthaler TI, Ryu JH. Clinical characteristics of fatal pulmonary embolism in a referral hospital.
Mayo Clin Proc. 1995;70(5):417–424.
3. Hoellerich VL, Wigton RS. Diagnosing pulmonary embolism using clinical findings. Arch Intern Med.
1986;146(9):1699–1704.
4. Hull RD, Raskob GE, Carter CJ, etal. Pulmonary embolism in outpatients with pleuritic chest pain. Arch
Intern Med. 1988;148(4):838–844.
5. Kline JA, Nelson RD, Jackson RE, Courtney DM. Criteria for the safe use of D-dimer testing in emer-
gency department patients with suspected pulmonary embolism: a multicenter US study. Ann Emerg
Med. 2002;39(2):144–152.
6. Miniati M, Monti S, Bottai M. A structured clinical model for predicting the probability of pulmonary
embolism. Am J Med. 2003;114(3):173–179.
7. Miniati M, Bottai M, Monti S. Comparison of 3 clinical models for predicting the probability of pulmo-
nary embolism. Medicine. 2005;84(2):107–114.
8. Wicki J, Perneger TV, Junod AF, Bounameaux H, Perrier A. Assessing clinical probability of pulmonary
embolism in the emergency ward: a simple score. Arch Intern Med. 2001;161(1):92–97.
9. Stein PD, Beemath A, Matta F, etal. Clinical characteristics of patients with acute pulmonary embolism:
data from PIOPED II. Am J Med. 2007;120(10):871–879.
10. Tsimogianni AM, Rovina N, Porfyridis I, etal. Clinical prediction of pulmonary embolism in respiratory
emergencies. romb Res. 2011;127(5):411–417.
11. Stein PD, Willis III PW, DeMets DL. History and physical examination in acute pulmonary embolism
in patients without preexisting cardiac or pulmonary disease. Am J Cardiol. 1981;47(2):218–223.
12. Bell WR, Simon TL, DeMets DL. e clinical features of submassive and massive pulmonary emboli.
Am J Med. 1977;62(3):355–360.
13. Sutton GC, Honey M, Gibson RV. Clinical diagnosis of acute massive pulmonary embolism. Lancet.
1969;1(7589):271–273.
14. Wells PS, Anderson DR, Rodger M, etal. Derivation of a simple clinical model to categorize patients
probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer. romb
Haemost. 2000;83(3):416–420.
15. Le Gal G, Righini M, Roy PM, etal. Prediction of pulmonary embolism in the emergency department:
the revised Geneva score. Ann Intern Med. 2006;144(3):165–171.
16. Kline JA, Corredor DM, Hogg MM, Hernandez J, Jones AE. Normalization of vital signs does not
reduce the probability of acute pulmonary embolism in symptomatic emergency department patients.
Acad Emerg Med. 2012;19(1):11–17.
17. Di
Marca S, Cilia C, Campagna A, et al. Comparison of Wells and revised Geneva rule to assess
pretest
probability of pulmonary embolism in high-risk hospitalized elderly adults.
2015;63(6):1091–1097.
18. Hendriksen JM, Lucassen WA, Erkens PM, etal. Ruling out pulmonary embolism in primary care: com-
parison of the diagnostic performance of “gestalt” and the Wells rule. Ann Fam Med. 2016;14(3):227–234.
19. Chen
20. Le Gal G, Testuz A, Righini M, Bounameaux H, Perrier A. Reproduction of chest pain by palpation:
21. Stein PD, Henry JW, Gopalakrishnan D, Relyea B. Asymmetry of calves in the assessment of patients
22. Chagnon I, Bounameaux H, Aujesky D, etal. Comparison of two clinical prediction rules and implicit
23. Wells PS, Anderson DR, Rodger M, etal. Excluding pulmonary embolism at the bedside without diag-
24. Wolf SJ, McCubbin TR, Feldhaus KM, Faragher JP, Adcock DM. Prospective validation of Wells Criteria
JY, Chao TH, Guo YL, et al. A simplified clinical model to predict pulmonary embolism in
patients with acute dyspnea. Int Heart J. 2006;47(2):259–271.
diagnostic accuracy in suspected pulmonary embolism. BMJ. 2005;330(7489):452–453.
with suspected acute pulmonary embolism. Chest. 1995;107(4):936–939.
assessment among patients with suspected pulmonary embolism. Am J Med. 2002;113(4):269–275.
nostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and D-dimer. Ann Intern Med. 2001;135(2):98–107.
in the evaluation of patients with suspected pulmonary embolism. Ann Emerg Med. 2004;44(5):503–510.
J Am Geriatr Soc.
290.e1
25. Anderson DR, Kovacs MJ, Dennie C, etal. Use of spiral computed tomography contrast angiography
https://t.me/medicina_free
and ultrasonography to exclude the diagnosis of pulmonary embolism in the emergency department.
J Emerg Med. 2005;29(4):399–404.
26. Calisir C, Yavas US, Ozkan IR, etal. Performance of the Wells and revised Geneva scores for predicting
pulmonary embolism. Eur J Emerg Med. 2008;16(1):49–52.
27. Klok FA, Kruisman E, Spaan J, etal. Comparison of the revised Geneva score with the Wells rule for
assessing clinical probability of pulmonary embolism. J romb Haemost. 2008;6(1):40–44.
28. Wong DD, Ramaseshan G, Mendelson RM. Comparison of the Wells and revised Geneva scores for the
diagnosis of pulmonary embolism: an Australian experience. Int Med J. 2011;41(3):258–263.
29. Penaloza A, Verschuren F, Meyer G, etal. Comparison of the unstructured clinician gestalt, the Wells
score, and the revised Geneva score to estimate pretest probability for suspected pulmonary embolism.
Ann Emerg Med. 2013;62(2) 117-124.e2.
30. Penaloza A, Melot C, Motte S. Comparison of the Wells score with the simplified revised Geneva score
for assessing pretest probability of pulmonary embolism. romb Res. 2011;127(2):81–84.
31. Yap KS, Kalff V, Turlakow A, Kelly MJ. A prospective reassessment of the utility of the Wells score in
identifying pulmonary embolism. Med J Aust. 2007;187(6):333–336.
32. Robert-Ebadi H, Mostaguir K, Hovens MM, etal. Assessing clinical probability of pulmonary embo-
lism: prospective validation of the simplified Geneva score. J romb Haemost. 2017;15(9):1764–1769.
33. Stein PD, Goldhaber SZ, Henry JW, Miller AC. Arterial blood gas analysis in the assessment of sus-
pected acute pulmonary embolism. Chest. 1996;109(1):78–81.
34. Leclercq MGL, Lutisan JG, van Marvijk Kooy M, etal. Ruling out clinical suspected pulmonary embo-
J
lism by assessment of clinical probability and D-dimer levels: a management study. romb Haemost.
2003;89:97–103.
35. Kruip
36. Kline JA, Mitchell AM, Kabrhel C, Richman PB, Courtney DM. Clinical criteria to prevent unneces-
37. Buchanan I, Teeples T, Carlson M, Steenblik J, Bledsoe J, Madsen T. Pulmonary embolism testing among
38. Crane
39. Kline JA, Courtney DM, Kabrhel C, etal. Prospective multicenter evaluation of the pulmonary embolism
40. Penaloza A, Soulié C, Moumneh T, etal. Pulmonary embolism rule-out criteria (PERC) rule in European
41. eunissen J, Scholing C, van Hasselt WE, van der Maten J, Ter Avest E. A retrospective analysis of the
42. Wolf
43. Freund Y, Cachanado M, Aubry A, etal. Effect of the pulmonary embolism rule-out criteria on subse-
44. Raja
45. Klok FA, Mos IC, Nijkeuter M, etal. Simplification of the revised Geneva score for assessing clinical
MJHA, Leclercq MGL, van der Heul C, Prins MH, Büller HR. Diagnostic strategies for
excluding
2003;138(12):941–951.
sary diagnostic testing in emergency department patients with suspected pulmonary embolism. J romb
Haemost. 2004;2(8):1247–1255.
emergency
Med. 2017;24(11):1369–1376.
out
2018;25(3):185–190.
rule-out criteria. J romb Haemost. 2008;6(5):772–780.
patients with low implicit clinical probability (PERCEPIC): a multicentre, prospective, observational
study. Lancet Haematol. 2017;4(12):e615–e621.
combined use of PERC rule and Wells score to exclude pulmonary embolism in the emergency department. Emerg Med J. 2016;33(10):696–701.
embolism
department. Am J Emerg Med. 2008;26(2):181–185.
quent thromboembolic events among low-risk emergency department patients: the PROPER randomized clinical trial. JAMA. 2018;319(6):559–566.
embolism: best practice advice from the Clinical Guidelines Committee of the American College of
Physicians. Ann Intern Med. 2015;163(9):701–711.
probability of pulmonary embolism. Arch Intern Med. 2008;168(19):2131–2136.
pulmonary embolism in clinical outcome studies: a systematic review.
department patients who are pulmonary embolism rule-out criteria negative.
S, Jaconelli T, Eragat M. Retrospective validation of the pulmonary embolism rule-
criteria rule in ‘PE unlikely’ patients with suspected pulmonary embolism.
SJ, McCubbin TR, Nordenholz KE, Naviaux NW, Haukoos JS. Assessment of the pulmonary
rule-out criteria rule for evaluation of suspected pulmonary embolism in the emergency
AS, Greenberg JO, Qaseem A, et al. Evaluation of patients with suspected acute pulmonary
Ann
Eur
Intern Med
Acad Emerg
Emerg Med
.
.
290.e2
CHAPTER
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35
Pleural Effusion
KEY TEACHING POINTS
• In patients with dyspnea, the following findings increase probability of pleural effusion:
abnormal auscultatory percussion, asymmetric chest expansion, diminished vocal
resonance, reduced tactile fremitus, diminished breath sound intensity, and percussion
dullness.
• The presence of normal breath sound intensity or normal resonance during percussion
significantly decreases the possibility of underlying pleural effusion. Indeed, the diagnosis
of pleural effusion is one of the main reasons students should still learn how to percuss
the chest.
Introduction
I.
Although ancient Greek physicians routinely recognized and treated empyema, the modern diagnostic signs of pleural effusion date to two physicians: Auenbrugger, who described the pathologic
dullness and diminished chest expansion of effusions1; and Laennec, who described the uniform
absence of breath sounds and, in some patients, the appearance of bronchial breath sounds and
abnormal
clinicians to approach patients with chronic respiratory complaints and confidently distinguish
empyema from tuberculosis.
pneumonia, and cancer.
II.
Accumulation of pleural fluid, if large enough, expands the hemithorax (and collapses the underlying
flattening or even bulging of the normally concave intercostal spaces. Because pleura fluid reduces
transmission
involved side. All patients have diminished breath sounds, especially in the lower chest, from the
combined effects of reduced flow rates (the underlying lung is collapsed) and diminished transmission of the low-frequency vesicular breath sounds through the fluid.
stethoscope) may produce either of two distinct findings: (1) diminished or absent vocal resonance (the patient’s voice is muted compared to the uninvolved sign) or (2) “abnormal” vocal resonance with egophony, bronchophony, whispered pectoriloquy, and often, bronchial breath sounds.
Chapter 30 discusses further these paradoxical findings (in the section on vocal resonance).
vocal resonance.
e most common causes of pleural effusions in the United States are congestive heart failure,
The Findings
lung), which may create the appearance of an asymmetrically enlarged hemithorax with
of low frequency vibrations (see
Nonetheless, testing of vocal resonance (i.e., sound of the patient’s voice through the clinician’s
2
e
introduction of percussion into 19
3
4
Fig.
),
30.2
tactile fremitus is diminished on the
th
century
medicine allowed
291
292
PLEURAL EFFUSION
Diminished or absent breath sounds
Dullness by conventional percussion
Normal
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7—SELECTED PULMONARY DISORDERS
III. Clinical Significance
Several findings increase the probability of pleural effusion: abnormal auscultatory percussion
(likelihood ratio [LR] = 8.3, EBM Box 35.1), asymmetric chest expansion (LR = 8.1), diminished vocal resonance (LR = 6.5), reduced tactile fremitus (LR = 5.7), diminished or absent
breath sounds (LR = 5.2), and asymmetric percussion dullness (LR = 4.8). Findings that decrease
the probability of pleural effusion include normal breath sound intensity (LR = 0.1), normal
percussion resonance (LR = 0.1), normal tactile fremitus (LR = 0.2), symmetric chest expansion
(LR = 0.3), and normal vocal resonance (LR = 0.3).
In two studies of patients in the intensive care unit, most of whom were mechanically ventilated, the absence of breath sounds over a region of the chest increased the probability of underlying pleural fluid (sensitivity of 34% to 42%, specificity of 84% to 90%, LR = 3).
EBM BOX 35.1 Pleural Effusion*
Finding (Reference)
Inspection
Asymmetric chest expansion
Palpation
Reduced tactile fremitus
†
8
8
Percussion
Dullness by conventional percussion
Abnormal auscultatory percussion
(method of Guarino)
7,8
Auscultation
Diminished or absent breath sounds
Diminished vocal resonance
8
Crackles
Pleural rub
*Diagnostic standard: for pleural effusion, chest radiograph.
†
Definition of findings: for abnormal auscultatory percussion, the method of Guarino7 (see the section on
auscultatory percussion in Chapter 29); for diminished vocal resonance intensity, reduction or absence of
transmitted sounds from the patient’s voice when reciting numbers, as detected by a stethoscope on the
patient’s posterior chest;8 for all other findings, see Chapters 28 to 30.
‡
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
NS, Not significant.
8
8
Sensitivity
(%)
74 91 8.1 0.3
82 86 5.7 0.2
8
89 81 4.8 0.1
58–96 85–95 8.3 NS
8
88 83 5.2 0.1
76 88 6.5 0.3
44 38 NS 1.5
5 99 NS NS
Specificity
(%)
5,6
Likelihood Ratio‡
if Finding Is
Present Absent
LRs
Absence of dullness by
conventional percussion
breath sound intensity
Symmetric chest expansion
0.1 0.2 0.5 12510
Normal tactile fremitus
Normal vocal resonance
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
Probability
Decrease Increase
+45%+30%+15%–15%–30%–45%
LRs
Abnormal auscultatory
percussion
Asymmetric chest expansion
Diminished vocal resonance
Reduced tactile fremitus
References
https://t.me/medicina_free
1. Auenbrugger L. On Percussion of the Chest Being a Translation of Auenbrugger's Original Treatise Entitled
“Inventum Novum ex Percussione oracis Humani, ut Signo Abstrusos Interni Pectoris Morbos Detegendi”
(Facsimile Edition by Johns Hopkins Press). e Johns Hopkins Press; 1761:1936.
2. Laënnec RTH. A Treatise on the Diseases of the Chest, and on Mediate Auscultation (Facsimile Edition by
Classics of Medicine Library). T and G Underwood; 1821.
3. McGee S. Percussion and physical diagnosis: separating myth f rom science. Dis Mon. 1995;41(10):643–692.
4. Feller-Kopman D, Light R. Pleural disease. N Engl J Med. 2018;378(8):740–751.
5. Lichtenstein D, Goldstein I, Mourgeon E, Cluzel P, Grenier P, Rouby JJ. Comparative diagnostic per-
formance of auscultation, chest radiography, and lung ultrasonography in acute respiratory distress syndrome. Anesthesiology. 2004;10(1):9–15.
6. Inglis AJ, Nalos M, Sue KH, etal. Bedside lung ultrasound, mobile radiography and physical examina-
tion: a comparative analysis of diagnostic tools in the critically ill. Crit Care Resusc. 2016;18(2):124.
7. Guarino JR, Guarino JC. Auscultatory percussion: a simple method to detect pleural effusion. J Gen
Intern Med. 1994;9(2):71–74.
8. Kalantri S, Joshi R, Lokhande T, etal. Accuracy and reliability of physical signs in the diagnosis of pleural
effusion. Respir Med. 2007;101(3):431–438.
292.e1
CHAPTER
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36
Inspection of the Neck Veins
KEY TEACHING POINTS
• In patients with dyspnea, ascites, or edema, determination of venous pressure at the
bedside is essential. If venous pressure is elevated, the patient has cardiopulmonary
disease; if venous pressure is normal, liver or kidney disease is likely.
• Bedside estimates of venous pressure are accurate when compared to measured values.
• In patients with chest pain or dyspnea, elevated neck veins increase probability of
elevated left heart pressure and depressed ejection fraction.
• The most important feature that distinguishes the internal jugular venous waveform from
arterial movements is its conspicuous inward movement (arterial movements have a
conspicuous outward movement).
• Kussmaul sign and the positive abdominojugular test often appear together. They appear
in constrictive pericarditis and right ventricular infarction and in some patients with severe
heart failure. In heart failure, Kussmaul sign is associated with an unfavorable prognosis.
Introduction
I.
Clinicians should inspect the neck veins for the following reasons: (1) to detect elevated central
venous pressure (CVP) and (2) to detect specific abnormalities of venous waveforms, which are
characteristic of certain arrhythmias and some valvular, pericardial, and myocardial disorders.
Clinicians first associated conspicuous neck veins with heart disease approximately 3 centuries
1,2
ago.
In the late 1800s Sir James Mackenzie described venous waveforms of arrhythmias and
various heart disorders, using a mechanical polygraph applied over the patient’s neck or liver. His
labels for the venous waveforms—A, C, and V waves—are still used today.
estimate venous pressure at the bedside routinely in the 1920s, after the introduction of the glass
manometer and after Starling’s experiments linking venous pressure to cardiac output.
II.
Venous Pressure
A.
DEFINITIONS
1. Central Venous Pressure
Central venous pressure (CVP) is the mean vena caval or right atrial pressure, which, in the
absence of tricuspid stenosis, equals the right ventricular end-diastolic pressure. Disorders that
increase diastolic pressures of the right side of the heart—left heart disease, lung disease, primary
pulmonary hypertension, and pulmonic stenosis—all increase the CVP and make the neck veins
abnormally conspicuous. CVP is expressed in millimeters of mercury (mm Hg) or centimeters
(cm) of water above atmospheric pressure (1.36 cm water = 1.0 mm Hg).
3,4
Clinician began to
5
295
296
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8—THE HEART
Estimations of CVP are most helpful in patients with ascites or edema, in whom an elevated
CVP indicates heart or lung disease and a normal CVP suggests alternative diagnoses, such
as chronic liver disease. Despite the prevailing opinion, the CVP is normal in patients with
liver disease (without associated cardiopulmonary disease); the edema in patients with isolated
liver disease results from hypoalbuminemia and the weight of ascites compressing veins to
the legs.
6–9
2. Physiologic Zero Point
Physiologists have long assumed that a location in the cardiovascular system (presumed to be the
right atrium in humans) tightly regulates venous pressure so that it remains the same even when
the person changes position.
5,10–12
All measurements of the CVP—whether by clinicians inspecting neck veins or by catheters in intensive care units—attempt to identify the pressure at this zero
point (e.g., if a manometer connected to a systemic vein supports a column of saline 8 cm above
the zero point, with the top of the manometer open to atmosphere, the recorded pressure in that
vein is 8 cm water). Estimates of CVP are related to the zero point because interpretation of
this value does not need to consider the hydrostatic effects of different patient positions, and any
abnormal value thus indicates disease.
3. External Reference Point
Clinicians require some external reference point to reliably locate the level of the zero point. Of
the many such reference points that have been proposed over the last century,5 only two are commonly used today: the sternal angle and the phlebostatic axis.
a. Sternal Angle
In 1930 Sir omas Lewis, a pupil of Mackenzie, proposed a simple bedside method for measuring venous pressure designed to replace the manometer, which he found too burdensome for
general use.13 He observed that the top of the jugular veins of normal persons (and the top of the
fluid in the manometer) always came to lie within 1 to 2 cm of vertical distance from the sternal
angle, whether the person was supine, semiupright, or upright (an observation since confirmed
by others).14 If the top level of the neck veins was more than 3 cm above the sternal angle, Lewis
concluded the venous pressure was elevated.
Others have modified this method, stating that the CVP equals the vertical distance between
the top of the neck veins and a point 5 cm below the sternal angle (Fig. 36.1).15 is variation is
commonly called the method of Lewis, although Lewis himself never made such a claim.
b. Phlebostatic Axis
e phlebostatic axis is the midpoint between the anterior and posterior surfaces of the chest at
the level of the fourth intercostal space. is reference point, the most common landmark used in
intensive care units and cardiac catheterization laboratories, was originally proposed in the 1940s,
when studies showed that using it as the zero point minimized variation in venous pressure of
normal persons as they changed position between 0 and 90 degrees.
c. Relative Merits of Sternal Angle and Phlebostatic Axis
Obviously, the measurement of venous pressure is only as good as the reference point used. e
phlebostatic axis locates a point in the right atrium several centimeters posterior to the point
identified by the method of Lewis (i.e., the zero point using the phlebostatic axis is 9 to 10 cm
posterior to the sternal angle; that using the method of Lewis is 5 cm below the sternal angle).
is means that clinicians using the phlebostatic axis will estimate the CVP to be several cm of
water higher than those using the method of Lewis, even if these clinicians completely agree on
the location of the neck veins.
11
16,17
36—INSPECTION OF THE NECK VEINS
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2 cm
Fig. 36.1 Measurement of venous pressure. The clinician should vary the patient’s position until the top of
the neck veins become visible. In this patient, who has normal central venous pressure (CVP), the neck veins
are fully distended when supine and completely collapsed when upright. A semiupright position, therefore,
is used to estimate pressure. In this position, the top of the neck veins is 2 cm above the sternal angle, and
according to the method of Lewis, the patient’s CVP is 2+5 = 7 cm water.
e sternal angle is a better reference point for bedside examination, simply because clinicians can
reproducibly locate it more easily than the phlebostatic axis. Even using standard patient positions
and flexible right-angle triangles or laser levels, experienced observers trying to locate a point similar
to the phlebostatic axis disagreed by several centimeters in both horizontal and vertical directions.
297
18,19
B.
ELEVATED VENOUS PRESSURE
1.
Technique
To measure the patient’s venous pressure, the clinician should examine the veins on the right side
of the patient’s neck, because these veins have a direct route to the heart. Veins in the left side
of the neck reach the heart by crossing the mediastinum, where the normal aorta may compress
them, causing left jugular venous pressure to be sometimes elevated even when CVP and right
venous pressure are normal.
e patient should be positioned at whichever angle between the supine and upright position
best reveals the top of the neck veins (see Fig. 36.1). e top of the neck veins is indicated by
the point above which the subcutaneous conduit of the external jugular vein disappears or above
which the pulsating waveforms of the internal jugular vein become imperceptible.
2.
External vs. Internal Jugular Veins
Either the external or internal jugular veins may be used to estimate pressure, because measurements
in both are similar.
jugular vein because the external jugular vein contains valves that purportedly interfere with the
development of a hydrostatic column necessary to measure pressure. is teaching is erroneous
for two reasons: (1) e internal jugular vein also contains valves, a fact known to anatomists for
centuries.
23–25
ese valves are essential during cardiopulmonary resuscitation, preventing blood
from flowing backward during chest compression26; (2) Valves in the jugular veins do not interfere
with pressure measurements because flow is normally toward the heart. In fact, valves probably act
like a transducer membrane (e.g., the diaphragm of a speaker), which amplify right atrial pressure
pulsations and make the venous waveforms easier to see.
20,21
22
Traditionally
clinicians have been taught to use only the internal
23
298
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8—THE HEART
3. Definition of Elevated CVP
After locating the top of the external or internal jugular veins, the clinician should measure the
vertical distance between the top of the veins and one of the external reference points discussed
above (see Fig. 36.1). e venous pressure is abnormally elevated if (1) the top of the neck veins
are more than 3 cm above the sternal angle, (2) the CVP exceeds 8 cm water using the method of
Lewis (i.e., >3 cm above the sternal angle + 5 cm), or (3) the CVP is greater than 12 cm water
using the phlebostatic axis.
C. BEDSIDE ESTIMATES OF VENOUS PRESSURE VS. CATHETER
MEASUREMENTS
1. Diagnostic Accuracy*
In studies employing a standardized reference point, bedside estimates of CVP are within 4 cm
water of catheter measurements 85% of the time.
22,30,31
According to these studies, the finding
of an elevated CVP (i.e., top of neck veins >3 cm water above sternal angle or >8 cm water
using method of Lewis) greatly increases the probability that catheter measurements are elevated
(likelihood ratio [LR] = 8.9, EBM Box 36.1). e finding of a normal CVP on examination
(< 8 cm using the method of Lewis) decreases significantly the probability of a measured CVP
> 12 cm water (LR = 0.2; see EBM Box 36.1). If disease is defined instead as measured CVP >
8 cm, the finding of normal venous pressure on examination is slightly less compelling (LR = 0.3),
indicating that some patients with normal venous pressure on examination have modestly elevated
measured values (between 8 and 12 cm water†).
is tendency to slightly underestimate the measured values, which is elucidated further in the
following section, explains why estimates made during expiration are slightly more accurate than
are those made during inspiration: during expiration, the neck veins move upward in the neck,
increasing the bedside estimate and minimizing the error.
22
2. Why Clinicians Underestimate Measured Values
Of the many reasons why clinicians tend to underestimate the measured values of CVP, the most
important one is that the vertical distance between the sternal angle and physiologic zero point
varies as the patient shifts position (see Fig. 36.2).
sure are always made while the patient is lying supine, whether the venous pressure is high or
low. Bedside estimates of the venous pressure, however, must be made in the semiupright or
upright positions if the venous pressure is high, because only these positions reveal the top of the
distended neck veins. Fig. 36.2 shows that the semiupright position increases the vertical distance
between the right atrium and sternal angle by approximately 3 cm, compared with the supine
position, which effectively lowers the bedside estimate by the same amount. e significance of
this is that patients with a mildly elevated CVP by catheter measurements (i.e., 8 to 12 cm), whose
neck veins are interpretable only in more upright positions, may have bedside estimates that are
normal (i.e., <8 cm water).
In support of this, even catheter measurements using the sternal angle as reference point are
approximately 3 cm lower when the patient is in the semiupright position than when the patient
is supine.
*
Studies that test the diagnostic accuracy of bedside estimates of CVP are difficult to summarize because they
†
For purposes of comparison, “measured pressure” here is in centimeters water using the method of Lewis.
48–50
often fail to standardize which external reference point was used.
Most catheterization laboratories measure pressure in mm Hg using the phlebostatic axis as the reference
point.
5,47
Catheter measurements of the venous pres-
27–29
.
Соседние файлы в папке Библиотека им академика М.И. Перельмана