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150
Chest wall movements:
Abdominal wall movements:
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4—VITAL SIGNS
Outward
Inward
Normal
Asynchronous
Paradoxical
Fig. 19.2 Respiratory abdominal movements. Chest movements are depicted in the first row. “I” denotes
inspiration and “E,” expiration. Upward sloping lines on the drawing indicate outward body wall movements;
downward sloping lines, inward movements. In normal persons, the abdominal and chest wall movements are
completely in sync. In asynchronous breathing, only expiratory abdominal movements are abnormal. In paradoxical abdominal movements, both inspiratory and expiratory abdominal movements are abnormal. See text.
IE
b. Clinical Significance
In patients with chronic airflow obstruction, asynchronous breathing correlates with lower forced
expiratory volumes and a much poorer prognosis.
tion who develop acute respiratory symptoms, the presence of an asynchronous breathing pattern
predicts subsequent hospital death or the need for artificial ventilation with a sensitivity of 64%,
specificity of 80%, and positive LR of 3.2 (negative LR not significant).
c. Pathogenesis
e outward abdominal movement during expiration probably reflects the strong action of chest
wall accessory muscles during expiration, which push the flattened diaphragm temporarily downward, and thus the abdomen abruptly outward.
2.
Paradoxical Abdominal Movements
a. Finding
Paradoxical abdominal movements are completely out of sync with those of the chest wall. During
inspiration the abdomen moves in as the chest wall moves out; during expiration, the abdomen
moves out as chest moves in.
b. Clinical Significance
61,66–68
Paradoxical abdominal movements are a sign of bilateral diaphragm weakness. Most of
these patients also complain of severe orthopnea. In one study of patients with dyspnea and
65
Among patients with chronic airflow obstruc-
64
62,64
19—RESPIRATORY RATE AND ABNORMAL BREATHING PATTERNS
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151
neuromuscular
weakness with a sensitivity of 95%, specificity of 70%, and positive LR = 3.2 (in this study, the
definition of paradoxical movements was any inspiratory inward abdominal movement, and the
definition of diaphragm weakness was a maximal transdiaphragmatic pressure ≤30 cm H2O; the
normal sniff transdiaphragmatic pressure is >98 cm H2O).
c. Pathogenesis
If the diaphragm is totally paralyzed, the inspiratory outward movement of the chest wall will
draw the diaphragm upward, and thus the abdomen inward. e weight of the abdominal viscera
probably also plays a role, because paradoxical movements are most obvious in affected patients
who are positioned supine and are often absent when the patient is upright.
A
mimic of paradoxic abdominal movements is seen in patients with tetraplegia. In these
patients, respiratory motion relies entirely on the diaphragm: as it descends during inspiration,
pushing the abdominal wall out, the paralyzed chest wall may be drawn inward. e chest and
abdomen are completely out of sync in these patients, but in contrast to the paradoxical abdominal
movements of diaphragm weakness, the abdominal wall of tetraplegic patients moves outward
disease, the finding of paradoxical abdominal movements detected diaphragm
66
66
during inspiration, not inward.
V.
Orthopnea, Trepopnea, Platypnea, and Bendopnea
ese terms describe tachypnea (and dyspnea) that appears abruptly in particular positions: when
the patient is supine (orthopnea), lying on one side (trepopnea), upright (platypnea), or bending over (bendopnea). ese findings are often first diagnosed during observation of the patient’s
respirations at the bedside.
A.
ORTHOPNEA
1.
Finding
Orthopnea describes dyspnea that appears when the patient lies down but is relieved when the
patient sits up (from the Greek words ortho meaning straight or vertical, and pnea meaning to
breathe).
2.
Clinical Significance
Orthopnea occurs in a variety of disorders, including massive ascites, bilateral diaphragm paralysis,
pleural effusion, morbid obesity, and severe pneumonia, although its most important clinical association is congestive heart failure.
pulmonary disease, the finding of orthopnea distinguished between those patients with abnormally low ejection fraction (less than 50%) and those with normal ejection fraction with a sensitivity of 97%, specificity of 64%, positive LR = 2.7, and negative LR = 0.04.
in patients with lung disease, the presence of orthopnea has limited value (i.e., occurs in both lung
and heart disease), but the absence of orthopnea is more compelling, decreasing the probability of
associated left ventricular dysfunction (LR = 0.04).
3. Pathogenesis
In patients with orthopnea, lung compliance and vital capacity decrease significantly after moving from the upright to supine position. is explains in part why dyspnea worsens in the supine
position and why orthopnea is a finding common to so many different clinical conditions.
Nonetheless, orthopnea cannot be entirely caused by postural changes in lung mechanics, for
several reasons. First, orthopnea is uncommon in other disorders with similar reductions of vital
capacity and compliance (e.g., interstitial fibrosis). Second, in patients with congestive heart
66,67,69
In one study of patients with known chronic obstructive
70
is suggests that,
69,71,72
152
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4—VITAL SIGNS
failure, orthopnea correlates poorly with the pulmonary artery wedge pressure, which should have
some relation to interstitial edema and pulmonary mechanics.73 Finally, elevation of the head
alone brings prompt relief to some orthopneic patients. It was once believed that elevation of the
head relieved dyspnea because it reduced intracranial venous pressure and thus improved cerebral
perfusion, although this hypothesis has been experimentally disproved.
69
B. TREPOPNEA
1. Finding
Trepopnea† (from Greek trepo meaning twist or turn) describes dyspnea that is worse in one lateral decubitus position and relieved in the other.
2. Clinical Significance
ere are three principal causes of trepopnea.
a. Unilateral Parenchymal Lung Disease
76,77
Affected patients usually prefer to position their healthy lung down, which improves oxygenation
because blood preferentially flows to the lower lung.
b. Congestive Heart Failure from Dilated Cardiomyopathy
74,75,78
Patients usually prefer to have their right side down. Whether this is due to positional changes in
lung mechanics (e.g., left lung atelectasis from cardiomegaly), right ventricular preload, or airway
compression is unclear. e preference for the right side down in heart failure may contribute to
the right-sided predilection of pleural effusions in these patients.
79
c. Mediastinal or Endobronchial Tumor
Tumors may compress the airways or central blood vessels in one position but not the other.
A clue to this diagnosis is a localized wheeze that appears in the position causing symptoms.
80–82
80
d. Other Causes
Rare reports of trepopnea include a patient with position-dependent right-to-left intracardiac
shunting83 and a patient with unilateral diaphragmatic paralysis.84 e patient with hemidiaphragm paralysis (on the right side) had left-sided trepopnea, possibly because this position
increased the weight of abdominal viscera against the only functioning half of the diaphragm.
84
C. PLATYPNEA
1. Finding
Platypnea (from the Greek platus, meaning “flat”) is the opposite of orthopnea: patients experience worse dyspnea when upright (sitting or standing) and relief after lying down (a related term,
orthodeoxia, describes a similar deterioration of oxygen saturation in the upright position). is
rare syndrome was first described in 1949, and the term platypnea was first coined in 1969.
85,86
†
In 1937, Drs. Wood and Wolferth first described trepopnea in patients with congestive heart failure.74 In
searching for a name for the finding, a patent lawyer suggested to them rolling relief, which they translated
into rotopnea, until a Dr. Kern pointed out that roto was a Latin root and the pure Greek term trepopnea
would be better.
75
19—RESPIRATORY RATE AND ABNORMAL BREATHING PATTERNS
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2. Clinical Significance
153
Platypnea occurs in patients with right-to-left shunting of blood through intracardiac or intrapulmonary shunts.
87
a. Right-to-Left Shunting of Blood through a Patent Foramen Ovale or Atrial Septal
Defect
ese patients often first develop the finding after undergoing pneumonectomy or developing
a pulmonary embolus or pericardial effusion, which for unclear reasons promotes right-to-left
shunting in the upright position.
88–93
b. Right-To-Left Shunting of Blood through Intrapulmonary Shunts
Right-to-left shunting of blood through intrapulmonary shunts located in the bases of the lungs
occurs in the hepatopulmonary syndrome, a complication of chronic liver disease (see Chapter 8)94
and hereditary hemorrhagic telangiectasia.95 In these patients, the upright position causes more
blood to flow to the bases, thus aggravating the right-to-left shunting of blood and the patient’s
hypoxemia. In one series of 110 patients with chronic liver disease, the symptom of platypnea
detected hepatopulmonary syndrome with a sensitivity of 66%, specificity of 94%, positive LR =
10.6, and negative LR = 0.4 (see Chapter 8).
96
D. BENDOPNEA
1. Finding
Bendopnea describes shortness of breath that develops when a seated patient bends over. Chapter 48
describes a specific bedside test for bendopnea.
2. Clinical Significance
In patients with heart failure, a positive bendopnea test increases probability that the patient’s
pulmonary capillary wedge pressure is 22 mm Hg or more (LR = 3.2).97 e pathogenesis and
clinical significance of this finding are fully discussed in Chapter 48.
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
References
https://t.me/medicina_free
1. Stokes W. An Introduction to the Use of the Stethoscope (Facsimile Edition by the Classics of Cardiology
Library). Maclachlin and Stewart; 1825.
2. Geddes LA. Perspectives in physiological monitoring. Med Instrum. 1976;10(2):91–97.
3. Osler W. e Principles and Practice of Medicine (Facsimile by Classics of Medicine Library). D. Appleton and
Co.; 1892.
4. Krieger B, Feinerman D, Zaron A, Bizousky F. Continuous noninvasive monitoring of respiratory rate in
critically ill patients. Chest. 1986;90(5):632–634.
5. Kory RC. Routine measurement of respiratory rate: an expensive tribute to tradition. JAMA.
1957;165(5):448–450.
6. Bianchi W, Dugas AF, Hsieh YH, etal. Revitalizing a vital sign: improving detection of tachypnea at
primary triage. Ann Emerg Med. 2013;61(1):37–43.
7. Granholm A, Pedersen NE, Lippert A, Petersen LF, Rasmussen LS. Respiratory rates mea-
sured by a standardised clinical approach, ward staff, and a wireless device. Acta Anaesthesiol Scand.
2016;60(10):1444–1452.
8. Semler MW, Stover DG, Copland AP, etal. Flash mob research: a single-day, multicenter, resident-
directed study of respiratory rate. Chest. 2013;143(6):1740–1744.
9. Hooker EA, O’Brien DJ, Danzl DF, Barefoot JAC, Brown JE. Respiratory rates in emergency depart-
ment patients. J Emerg Med. 1989;7(2):129–132.
10. McFadden JP, Price RC, Eastwood HD, Briggs RS. Raised respiratory rate in elderly patients: a valuable
physical sign. Br Med J. 1982;284(6316):626–627.
11. Quetelet LAJ. A treatise on Man and the Development of his Faculties (1969 Facsimile by Scholars Facsimiles
and sReprints). William and Robert Chambers; 1842.
12. Mulroy MF. Monitoring opioids. Reg Anesth. 1996;21(6S):89–93. (suppl).
13. Hoffman JR, Schriger DL, Luo JS. e empiric use of naloxone in patients with altered mental status: a
reappraisal. Ann Emerg Med. 1991;20(3):246–252.
14. Duron VP, Rutigliano S, Machan JT, Dupuy DE, Mazzaglia PJ. Computed tomographic diagnosis of
pneumatosis intestinalis: clinical measures predictive of the need for surgical intervention. Arch Surg.
2011;146(5):506–510.
15. Umapathi BA, Friel CM, Stukenborg GJ, Hedric k T L. Estimating the risk of bowel ischemia requiring sur-
gery in patients with tomographic evidence of pneumatosis intestinalis. Am J Surg. 2016;212(4):762–768.
16. Tobin MJ, Perez W, Guenther SM, et al. e pattern of breathing during successful and unsuccessful
trials of weaning from mechanical ventilation. Am Rev Respir Dis. 1986;134(6):1111–1118.
17. Fieselmann JF, Hendryx MS, Helms CM, Wakefield DS. Respiratory rate predicts cardiopulmonary
arrest for internal medicine inpatients. J Gen Intern Med. 1993;8(7):354–360.
18. Churpek MM, Yuen TC, Huber MT, Park SY, Hall JB, Edelson DP. Predicting cardiac arrest on the
19. Heckerling PS. e need for chest roentgenograms in adults with acute respiratory illness: clinical pre-
dictors. Arch Intern Med. 1986;146(7):1321–1324.
20. Gennis P, Gallagher J, Falvo C, Baker S, an W. Clinical criteria for the detection of pneumonia
in adults: guidelines for ordering chest roentgenograms in the emergency department. J Emerg Med.
1989;7(3):263–268.
21. Mehr DR, Binder EF, Kruse RL, Zweig SC, Madsen RW, D’Agostino RB. Clinical findings associated
with radiographic pneumonia in nursing home residents. J Fam Pract. 2001;50(11):931–937.
22. Nolt BR, Gonzales R, Maselli J, Aagaard E, Camargo Jr CA, Metlay JP. Vital-sign abnormalities as
predictors of pneumonia in adults with acute cough illness. Am J Emerg Med. 2007;25(6):631–636.
23. Conte HA, Chen YT, Mehal W, Scinto JD, Quagliarello VJ. A prognostic rule for elderly patients admit-
ted with community-acquired pneumonia. Am J Med. 1999;106(1):20–28.
24. Community-acquired pneumonia in adults in British hospitals in 1982–1983: a survey of aetiology, mor-
tality, prognostic factors and outcome. e British oracic Society and the Public Health Laboratory
Service. Q J Med. 1987;62(239):195–220.
25. Farr BM, Sloman AJ, Fisch MJ. Predicting death in patients hospitalized for community-acquired pneu-
monia. Ann Intern Med. 1991;115(6):428–436.
154.e1
26. Brancati FL, Chow JW, Wagener MM, Vacarello SJ, Yu VL. Is pneumonia really the old man's friend?
https://t.me/medicina_free
Two-year prognosis after community-acquired pneumonia. Lancet. 1993;342(8862):30–33.
27. Ewig S, Kleinfeld T, Bauer T, Seifert K, Schäfer H, Göke N. Comparative validation of prognostic rules
for community-acquired pneumonia in an elderly population. Eur Respir J. 1999;14(2):370–375.
28. Jeon K, Yoo H, Jeong BH, etal. Functional status and mortality prediction in community-acquired pneu-
monia. Respirology. 2017;22(7):1400–1406.
29. Kolditz M, Bauer TT, König T, Rohde G, Ewig S. 3-day mortality in hospitalised community-acquired
pneumonia: frequency and risk factors. Eur Respir J. 2016;47(5):1572–1574.
30. Li HY, Guo Q, Song WD, etal. CUR-65 score for community-acquired pneumonia predicted mortality
better than CURB-65 score in low-mortality rate settings. Am J Med Sci. 2015;350(3):186–190.
31. Liu JL, Xu F, Zhou H, etal. Expanded CURB-65: a new score system predicts severity of community-
acquired pneumonia with superior efficiency. Sci Rep. 2016;6:22911.
32. Zhang ZX, Yong Y, Tan WC, Shen L, Ng HS, Fong KY. Prognostic factors for mortality due to pneu-
N
monia among adults from different age groups in Singapore and mortality predictions based on PSI and
CURB-65. Singapore Med J. 2018;59(4):190–198.
33. Gravelyn
1980;244(10):1123–1125.
34. Cohen CA, Zagelbaum G, Gross D, Roussos C, Macklem PT. Clinical manifestations of inspiratory
muscle fatigue. Am J Med. 1982;73(3):308–316.
35. Mower WR, Sachs C, Nicklin EL, Safa P, Baraff LJ. A comparison of pulse oximetry and respiratory rate
in patient screening. Respir Med. 1996;90(10):593–599.
36. Webb P. Periodic breathing during sleep. J Appl Physiol. 1974;37(6):899–903.
37. Altschule MD, Iglauer A. e effect of position on periodic breathing in chronic cardiac decompensation.
N Engl J Med. 1958;259(22):1064–1066.
38. Mortara A, Sleight P, Pinna GD, et al. Association between hemodynamic impairment and Cheyne-
Stokes respiration and periodic breathing in chronic stable congestive heart failure secondary to ischemic
or idiopathic dilated cardiomyopathy. Am J Cardiol. 1999;84(8):900–904.
39. Sternbach GL. John Cheyne and William Stokes: periodic respiration. J Emerg Med. 1985;3(3):233–236.
40. Morse
1974;66(4):345–346.
41. Lange RL, Hecht HH. e mechanism of Cheyne-Stokes respiration. J Clin Invest. 1962;41(1):42–52.
42. Franklin KA, Sandström E, Johansson G, Bâlfors EM. Hemodynamics, cerebral circulation, and oxygen
saturation in Cheyne-Stokes respiration. J Appl Physiol (1985). 1997;83(4):1184–1191.
43. McGee SR. Cheyne-Stokes breathing and reduced ejection fraction. Am J Med. 2013;126(6):536–540.
44. Tobin MJ, Snyder JV. Cheyne-Stokes respiration revisited: controversies and implications. Crit Care Med.
1984;12(10):882–887.
45. Dowell AR, Buckley E, Cohen R, Whalen RE, Sieker HO. Cheyne-Stokes respiration. A review of clini-
cal manifestations and critique of physiological mechanisms. Arch Intern Med. 1971;127(4):712–726.
46. Harrison TR, King CE, Calhoun JA, Harrison WG. Congestive heart failure: XX. Cheyne-Stokes respi-
ration as the cause of paroxysmal dyspnea at the onset of sleep. Arch Intern Med. 1934;53(6):891–910.
47. Rees PJ, Clark TJH. Paroxysmal nocturnal dyspnea and periodic respiration. Lancet. 1979;2(8156-8157):
1315–1317.
48. Brown HW, Plum F. e neurologic basis of Cheyne-Stokes respiration. Am J Med. 1961;30(6):849–860.
49. Lanfranchi PA, Braghiroli A, Bosimini E, etal. Prognostic value of nocturnal Cheyne-Stokes respiration
in chronic heart failure. Circulation. 1999;99(11):1435–1440.
50. Koehler U, Kesper K, Timmesfeld N, Grimm W. Cheyne-Stokes respiration in patients with heart fail-
ure. Int J Cardiol. 2016;203:775–778.
51. Karp HR, Sieker HO, Heyman A. Cerebral circulation and function in Cheyne-Stokes respiration. Am J
Med. 1961;30:861–870.
52. Javaheri
1999;341(13):949–954.
53. Minagar A, Weiner WJ. Adolf Kussmaul and his respiratory sign. J Med Biogr. 2001;9(3):181–183.
54. English M, Waruiru C, Amkoye E, etal. Deep breathing in children with severe malaria: indicator of
metabolic acidosis and poor outcome. Am J Trop Med Hyg. 1996;55(5):521–524.
TR, Weg JG. Respiratory rate as an indicator of acute respiratory dysfunction.
SR, Chandrasekhar AJ, Cugell DW. Editorial: Cheyne-Stokes respiration redefined.
S. A mechanism of central sleep apnea in patients with heart failure.
Engl J Med.
JAMA.
Chest.
154.e2
55. Bhaskaran K, Ebonyi AO, Walther B, Walther M. Predictors of hyperlactataemia among children pre-
https://t.me/medicina_free
senting with malaria in a low transmission area in the Gambia. Malar J. 2013;12:423.
56. Newton CR, Valim C, Krishna S, etal. e prognostic value of measures of acid/base balance in pedi-
57. Poole SR, Chetham M, Anderson M. Grunting respirations in infants and children. Pediatr Emerg Care.
58. Grinman S, Whitelaw WA. Pattern of breathing in a case of generalized respiratory muscle weakness.
59. Barach
60. Knelson JH, Howatt WF, DeMutyh GR. e physiologic significance of grunting respiration. Pediatrics.
61. Loh L, Goldman M, Davis NJ. e assessment of diaphragm function. Medicine. 1977;56(2):165–169.
62. Goldman
63. Sharp JT, Goldberg NB, Druz WS, Danon J. Relative contributions of rib cage and abdomen to breathing
64. Gilbert R, Ashtosh K, Auchinocloss JH, Rana S, Peppi D. Prospective study of controlled oxygen ther-
65. Ashutosh K, Gilbert R, Auchincloss JH, Peppi D. Asynchronous breathing movements in patients with
66. Mier-Jedrzejowicz A, Brophy C, Moxham J, Green M. Assessment of diaphragm weakness. Am Rev
67. Chan CK, Loke J, Virgulto JA, Mohsenin V, Ferranti R, Lammertse T. Bilateral diaphragmatic paralysis:
68. Newsom Davis J, Goldman M, Loh L, Casson M. Diaphragm function and alveolar hypoventilation.
69. Calhoun JA, Cullen GE, Harrison TR, Wilkins WL, Tims MM. Studies in congestive heart failure. XIV.
70. Zema MJ, Masters AP, Margouleff D. Dyspnea: the heart or the lungs? Differentiation at bedside by use
71. Sharp JT, Rakowski D, Keefer D. e effect of body position change on lung compliance in normal sub-
72. Nava S, Larovere MT, Fanfulla F, Navalesi P, Delmastro M, Mortara A. Orthopnea and inspiratory effort
73. Chakko S, Woska D, Martinez H, etal. Clinical, radiographic, and hemodynamic correlations in chronic
74. Wood FC, Wolferth CC. e tolerance of certain cardiac patients for various recumbent positions (tre-
75. Wood FC. Trepopnea. Arch Intern Med. 1959;104:966–973.
76. Zack
77. Remolina C, Khan AU, Santiago TV, Edelman NH. Positional hypoxemia in unilateral lung disease.
78. Fujita M, Miyamoto S, Tambara K, Budgell B. Trepopnea in patients with chronic heart failure. Int J
79. de Aruajo BS, Reichert R, Eifer DA, etal. Trepopnea may explain right-sided pleural effusion in patients
80. Acosta J, Khan F, Chitkara R. Trepopnea resulting from large aneurysm of sinus of Valsalva and descend-
falciparum malaria, compared with other clinical and laboratory parameters.
atric
2005;41(7):948–957.
1995;11(3):158–161.
Chest. 1983;84(6):770–772.
AL. Physiologic advantages of grunting, groaning, and pursed-lip breathing: adaptive symp
related to the development of continuous positive pressure breathing.
toms
1973;49(8):666–673.
1969;44(3):393–400.
MD, Williams AJ, Soo Hoo G, Trang TT, Gaultier C. Asynchronous thoracoabdominal
movements in chronic airflow obstruction (CAO). Active expiration during spontaneous breathing in
sleep and wakefulness. Adv Exp Med Biol. 1995;393:95–100.
in normal subjects. J Appl Physiol. 1975;39(4):608–618.
apy: poor prognosis of patients with asynchronous breathing. Chest. 1977;71(4):456–462.
chronic obstructive pulmonary disease. Chest. 1975;67(5):553–557.
Respir Dis. 1988;137(4):877–883.
clinical spectrum, prognosis, and diagnostic approach. Arch Phys Med Rehabil. 1988;69(11):976–979.
Q J Med. 1976;45(177):87–100.
Orthopnea: its relation to ventilation, vital capacity, oxygen saturation and acid-base condition of arterial
and jugular blood. J Clin Invest. 1931;10(4):833–855.
of the simple valsalva maneuver. Chest. 1984;85(1):59–64.
jects and in patients with congestive heart failure. J Clin Invest. 1959;38(4):659–667.
in chronic heart failure patients. Respir Med. 2003;97(6):647–653.
congestive heart failure: conflicting results may lead to inappropriate care.Am J Med. 1991;90(3):353–359.
popnea). Am J Med Sci. 1937;193(3):354–378.
MB, Pontoppidan H, Kazemi H. e effect of lateral positions on gas exchange in pulmonary
disease. A prospective evaluation. Am Rev Respir Dis. 1974;110(1):49–55.
N Engl J Med. 1981;304(9):523–525.
Cardiol. 2002;84(2-3):115–118.
with decompensated heart failure. Am J Emerg Med. 2012;30(6):925–931.
ing aorta. Heart Lung. 1982;11(4):342–344.
Bull
Infect Dis
Clin
NY Acad Med
.
.
154.e3
81. Mahler DA, Snyder PE, Virgulto JA, Loke J. Positional dyspnea and oxygen desaturation related to
https://t.me/medicina_free
carcinoma of the lung: up with the good lung. Chest. 1983;83(5):826–827.
82. Tsunezuka Y, Sato H, Tsukioka T, Shimizu H. Trepopnea due to recurrent lung cancer. Respiration.
2000;67(1):98–100.
83. Wolf D, Benz A, Hardt SE, Katus HA, Mereles D. Case reports. Trepopnea associated with paroxysmal
severe tricuspid regurgitation triggered at left lateral decubitus position. Echocardiography. 2010;27(8):
E77–E79.
84. Aslam F, Kolpakchi A, Muscher D, Lu L. Unilateral diaphragmatic paralysis in a diabetic patient: a case
of trepopnea. J Gen Intern Med. 2010;26(5):555–558.
85. Altman M, Robin ED. Platypnea (diffuse zone 1 phenomenon?). N Engl J Med. 1969;281(24):1347–1348.
86. Robin ED, McCauley RF. An analysis of platypnea-orthodeoxia syndrome, including a “new” therapeutic
approach. Chest. 1997;112(6):1449–1451.
87. Agrawal A, Palkar A, Talwar A. e multiple dimensions of platypnea-orthodeoxia syndrome: a review.
Respir Med. 2017;129:31–38.
88. LaBresh KA, Pietro DA, Coates EO, Khuri SF, Folland ED, Parisi AF. Platypnea syndrome after left
pneumonectomy. Chest. 1981;79(5):605–607.
89. Seward JB, Hayes DL, Smith HC, etal. Platypnea-orthodeoxia: clinical profile, diagnostic workup, man-
agement, and report of seven cases. Mayo Clin Proc. 1984;59(4):221–231.
90. Wright RS, Simari RD, Orszulak TA, Edwards WD, Gleich GJ, Reeder GS. Eosinophilic endomyocar-
dial disease presenting as cyanosis, platypnea, and orthodeoxia. Ann Intern Med. 1992;117(6):482–483.
91. Adolph EA, Lacy WO, Hermoni YI, Wexler LF, Javaheri S. Reversible orthodeoxia and platypnea due to
right-to-left intracardiac shunting related to pericardial effusion. Ann Intern Med. 1992;116(2):138–139.
92. Begin R. Platypnea after pneumonectomy. N Engl J Med. 1975;293(7):342–343.
93. Hussain SF, Mekan SF. Platypnea-orthodeoxia: report of two cases and review of the literature. South
Med J. 2004;97(7):657–662.
94. Robin ED, Laman D, Horn BR, eodore J. Platypnea related to orthodeoxia caused by true vascular
lung shunts. N Engl J Med. 1976;294(17):941–943.
95. Kumar N, Kraemer RR, Murthy RK, Hartig JR. Platypnea-orthodeoxia syndrome as a presentation of
hereditary hemorrhagic telangiectasia. Circulation. 2012;126(22):2645–2647.
96. Younis I, Sarwar S, Butt Z, Tanveer S, Qaadir A, Jadoon NA. Clinical characteristics, predictors, and
survival among patients with hepatopulmonary syndrome. Ann Hepatol. 2015;14(3):354–360.
97. ibodeau JT, Turer AT, Gualano SK, etal. Characterization of a novel symptom of advanced heart
failure: bendopnea. JACC Heart Fail. 2014;2(1):24–31.
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CHAPTER
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20
Pulse Oximetry
KEY TEACHING POINTS
• Pulse oximetry rapidly measures the patient’s arterial oxygen saturation, a finding that is
more sensitive than cyanosis and one that provides vital information independent of the
patient’s respiratory rate.
• Abnormally low oxygen saturation readings predict mortality in hospitalized patients,
detect hepatopulmonary syndrome in patients with chronic liver disease, and increase
probability of pneumonia in patients with cough and fever.
• Limitations of oximetry are its failure to detect hypercapnia and problems of poor oxygen
delivery (anemia, low cardiac output). Oximetry readings are not accurate in patients with
carbon monoxide poisoning or methemoglobinemia.
Introduction
I.
Pulse oximetry measures the arterial oxygen saturation rapidly and conveniently. It is regarded
the fifth vital sign,
physical sign, because it requires special equipment. Measurement of oxygen saturation, however,
is no different from the other vital signs whose measurement requires a thermometer, sphygmomanometer, or stopwatch.
Takuo Aoyagi of Japan discovered the basic principle of pulse oximetry—pulsatile transmis
sion of light through tissue depends on the patient’s arterial saturation—in the mid-1970s.
first pulse oximeters were successfully marketed in the 1980s.
II.
The Finding
Measurements are obtained by using a self-adhesive or clip-type probe attached to the patient’s
finger, nose, forehead, or earlobe.
and then displays an average value based on the previous 3 to 6 seconds, a value that is updated
about every second.
studies show that, between oxygen saturation levels of 70% and 100%, pulse oximeters are only
accurate within 5% (i.e., ±2 standard deviations) of measurements made by in vitro arterial blood
gas analysis using co-oximetry).
e most common causes of inadequate oximeter signals are poor perfusion (due to cold or
hypotension) and motion artifact. e clinician can sometimes correct these problems and thus
improve the signal by warming or rubbing the patient’s hand, repositioning the probe, or resting
the patient’s hand on a soft surface.
ing measurements with the clip probe attached to the lobule or pinna of the patient’s ear.
1,2
although some clinicians argue that pulse oximetry is a diagnostic test, not a
6
Although the digital display of pulse oximeters creates a sense of precision,
4
5
e oximeter makes several hundred measurements each second
4,7,8
6
If inadequate signals persist, the clinician should try obtain-
3
-
e
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4—VITAL SIGNS
In patients with hemiparesis, the results of pulse oximetry on the right and left sides of the
body are the same.
9
III. Clinical Significance
A. ADVANTAGES OF PULSE OXIMETRY
As a sign of low oxygen levels, pulse oximetry is superior to the physical sign of cyanosis, because
of oximetry is more sensitive and because readings do not depend on the patient’s hemoglobin
level (see Chapter 9). Consequently, pulse oximetry has become indispensable in the monitoring of patients in emergency departments, recovery and operating rooms, pulmonary clinics, and
intensive care units, where measurements often reveal unsuspected oxygen desaturation, leading
to changes in diagnosis and treatment. Oxygen therapy prolongs survival of some hypoxemic
patients, such as patients chronically hypoxemic from lung disease.
apy benefits patients with acute hypoxemia as well.
In hospitalized patients, an O2 saturation of less than 90% predicts hospital mortality (like-
lihood ratio [LR] = 4.5, EBM Box 20.1). As a diagnostic sign, an O2 saturation of less than
96% increases probability of hepatopulmonary syndrome in patients with chronic liver disease
EBM BOX 20.1 Oxygen Saturation by Pulse Oximetry*
Finding (reference)
Predicting hospital mortality in hospitalized patients
Oxygen saturation
12,13
<90%
Detecting hepatopulmonary syndrome in patients with chronic liver disease
Oxygen <96%
Detecting pneumonia in outpatients with cough and fever
Oxygen <95%
14,15
16–19
Sensitivity
(%)
21–39 87–97 4.5 0.8
28–39 91–94 4.3 0.7
32–52 80–99 3.0 0.7
Specificity
(%)
10,11
Presumably, oxygen ther-
Likelihood Ratio† if Finding Is
Present Absent
*Diagnostic standard: for hepatopulmonary syndrome, triad of cirrhosis, intrapulmonary shunting by
contrast echocardiography, and arterial alveolar to arterial oxygen gradient >20 mm Hg; for pneumonia,
chest radiography.
†
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
LRs
0.1 0.2 0.5 12510
PULSE OXIMETRY
Probability
Decrease Increase
sat <90%, predicting mortality
O
2
if hospitalized
O
sat <96%, detecting
2
hepatopulmonary syndrome
O
sat <95%, detecting pneumonia
2
if cough and fever
+45%+30%+15%–15%–30%–45%
LRs
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