V. ORTHOPNEA, TREPOPNEA, AND PLATYPNEA

154   PART 4 — VITAL SIGNS



why orthopnea is a finding common to so many different clinical conditions.59,61,62 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

failure, orthopnea correlates poorly with the pulmonary artery wedge pressure, which should have some relation to interstitial edema and pulmonary

mechanics.63 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.59

B.  TREPOPNEA

1. Finding

Trepopnea* (from the Greek trepo, meaning twist or turn) describes dysp­

nea that is worse in one lateral decubitus position and relieved in the other.

2.  Clinical Significance

There are three primary causes of trepopnea.

a.  Unilateral Lung Disease66,67

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 Cardiomyopathy64,65,68

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.

c.  Mediastinal or Endobronchial Tumor

Tumors may compress the airways or central blood vessels in one position

but not the other.69–71 A clue to this diagnosis is a localized wheeze that

appears in the position causing symptoms.69

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, described

a similar deterioration of oxygen saturation in the upright position.) This



*In 1937, Drs. Wood and Wolferth first described trepopnea in patients with congestive heart

failure.64 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.65



CHAPTER 18 — RESPIRATORY RATE   155



rare ­syndrome was first described in 1949, and the term platypnea was first

coined in 1969.72,73

2.  Clinical Significance

Platypnea occurs in patients with right-to-left shunting of blood through

intracardiac or intrapulmonary shunts.

a.  Right-to-Left Shunting of Blood through a Patent Foramen Ovale

or Atrial Septal Defect

These 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.74–79

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 7).80 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.

The references for this chapter can be found on www.expertconsult.com.



REFERENCES    155.e1



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34. Rees PJ, Clark TJH. Paroxysmal nocturnal dyspnea and periodic respiration. Lancet.

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35. Lee MC, Klassen AC, Heaney LM, Resch JA. Respiratory rate and pattern disturbances

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43. Javaheri S. A mechanism of central sleep apnea in patients with heart failure. N Engl J

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45. Minagar A, Weiner WJ. Adolf Kussmaul and his respiratory sign. J Med Biograph.

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46. English M, Waruiru C, Amkoye E, et  al. Deep breathing in children with severe

malaria: indicator of metabolic acidosis and poor outcome. Am J Trop Med Hyg.

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47. Poole SR, Chetham M, Anderson M. Grunting respirations in infants and children.

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48. Grinman S, Whitelaw WA. Pattern of breathing in a case of generalized respiratory muscle weakness. Chest. 1983;84(6):770-772.

49. Barach AL. Physiologic advantages of grunting, groaning, and pursed-lip breathing: adaptive symptoms related to the development of continuous positive pressure breathing. Bull

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50. Knelson JH, Howatt WF, DeMutyh GR. The physiologic significance of grunting respiration. Pediatrics. 1969;44:393-400.

51. Loh L, Goldman M, Newsome Davis J. The assessment of diaphragm function. Medicine.

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54. Gilbert R, Ashtosh K, Auchinocloss JH, et al. Prospective study of controlled oxygen therapy: poor prognosis of patients with asynchronous breathing. Chest. 1977;71(4):456-462.

55. Ashutosh K, Gilbert R, Auchincloss JH, Peppi D. Asynchronous breathing movements in

patients with chronic obstructive pulmonary disease. Chest. 1975;67(5):553-557.

56. Mier-Jedrzejowicz A, Brophy C, Moxham J, Green M. Assessment of diaphragm weakness. Am Rev Respir Dis. 1988;137:877-883.

57. Chan CK, Loke J, Virgulto JA, et al. Bilateral diaphragmatic paralysis: clinical spectrum,

prognosis, and diagnostic approach. Arch Phys Med Rehabil. 1988;69:976-979.

58. Newsom Davis J, Goldman M, Loh L, Casson M. Diaphragm function and alveolar

hypoventilation. Q J Med. 1976;45(177):87-100.

59. Calhoun JA, Cullen GE, Harrison TR, et  al. Studies in congestive heart failure. XIV.

Orthopnea: its relation to ventilation, vital capacity, oxygen saturation and acid-base

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60. Zema MJ, Masters AP, Margouleff D. Dyspnea: The heart or the lungs? Differentiation at

bedside by use of the simple Valsalva maneuver. Chest. 1984;85(1):59-64.

61. Sharp JT, Rakowski D, Keefer D. The effect of body position change on lung compliance in normal subjects and in patients with congestive heart failure. J Clin Invest.

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62. Nava S, Larovere MT, Fanfulla F, et al. Orthopnea and inspiratory effort in chronic heart

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63. Chakko S, Woska D, Martinez H, et al. Clinical, radiographic, and hemodynamic correlations in chronic congestive heart failure: conflicting results may lead to inappropriate

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64. Wood FC, Wolferth CC. The tolerance of certain cardiac patients for various recumbent

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65. Wood FC. Trepopnea. Arch Intern Med. 1959;104:966-973.

66. Zack MB, Pontoppidan H, Kazemi H. The effect of lateral positions on gas exchange in

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67. Remolina C, Khan AU, Santiago TV, Edelman NH. Positional hypoxemia in unilateral

lung disease. N Engl J Med. 1981;304(9):523-525.

68. Fujita M, Miyamoto S, Tambara K, Budgell B. Trepopnea in patients with chronic heart

failure. Int J Cardiol. 2002;84:115-118.

69. Acosta J, Khan F, Chitkara R. Trepopnea resulting from large aneurysm of sinus of

Valsalva and descending aorta. Heart Lung. 1982;11(4):342-344.

70. Mahler DA, Snyder PE, Virgulto JA, Loke J. Positional dyspnea and oxygen desaturation

related to carcinoma of the lung: up with the good lung. Chest. 1983;83(5):826-827.

71. Tsunezuka Y, Sato H, Tsukioka T, Shimizu H. Trepopnea due to recurrent lung cancer.

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72. Altman M, Robin ED. Platypnea (diffuse zone 1 phenomenon?) N Engl J Med.

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73. Robin ED, McCauley RF. An analysis of platypnea-orthodeoxia syndrome, including a

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Chest. 1981;79(5):605-607.

75. Seward JB, Hayes DL, Smith HC, et al. Platypnea-orthodeoxia: clinical profile, diagnostic

workup, management, and report of seven cases. Mayo Clin Proc. 1984;59:221-231.

76. Wright RS, Simari RD, Orszulak TA, et al. Eosinophilic endomyocardial disease presenting as cyanosis, platypnea, and orthodeoxia. Ann Intern Med. 1992;117(6):482-483.

77. Adolph EA, Lacy WO, Hermoni YI, et  al. Reversible orthodeoxia and platypnea due

to right-to-left intracardiac shunting related to pericardial effusion. Ann Intern Med.

1992;116(2):138-139.

78. Begin R. Platypnea after pneumonectomy. N Engl J Med. 1975;293(7):342-343.

79. Hussain SF, Mekan SF. Platypnea-orthodeoxia: report of two cases and review of the

literature. South Med J. 2004;97(7):657-662.

80. Robin ED, Laman D, Horn BR, Theodore J. Platypnea related to orthodeoxia caused by

true vascular lung shunts. N Engl J Med. 1976;294(17):941-943.



CHAPTER



19



Pulse Oximetry

I.  INTRODUCTION

Pulse oximetry measures the arterial oxygen saturation rapidly and conveniently. It is regarded as the fifth vital sign,1,2 although some clinicians

argue that pulse oximetry is a diagnostic test, not a 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 transmission of light through tissue depends on the patient’s

arterial saturation—in the mid-1970s.3 The first pulse oximeters were successfully marketed in the 1980s.4



II.  THE FINDING

Measurements are obtained by using a self-adhesive or clip-type probe

attached to the patient’s finger or ear. The oximeter makes several hundred

measurements each second and then displays an average value based on the

previous 3 to 6 seconds, which is updated about every second.5 Although

the digital display of pulse oximeters creates a sense of precision, 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.4,6,7

The most common causes of inadequate oximeter signals are poor perfusion (due to cold or hypotension), excessive ambient light, and motion

artifact. The 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.5 If inadequate

signals persist, the clinician should try obtaining measurements with the

clip probe attached to the lobe or pinna of the patient’s ear.

In patients with hemiparesis, the results of pulse oximetry on the right

and left sides of the body are the same.8



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 oximetry is more sensitive and because readings do not depend on the patient’s hemoglobin level (see Chapter 8).

156



CHAPTER 19 — PULSE OXIMETRY   157



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.9 Oxygen therapy prolongs survival times of some

hypoxemic patients, such as patients chronically hypoxemic from lung

disease.10,11 Presumably, oxygen therapy benefits patients with acute

hypoxemia as well.

In hospitalized patients, an O2 saturation of less than 90% predicts hospital mortality (LR = 4.5; EBM Box 19-1). As a diagnostic sign, an O2

saturation of less than 96% increases the probability of hepatopulmonary



EBM BOX 19-1



Oxygen Saturation by Pulse Oximetry*

Finding

(Reference)



Sensitivity

(%)



Specificity

(%)



Predicting Hospital Mortality in Hospitalized Patients

Oxygen saturation

21-39

87-97

<90%12,13



Likelihood Ratio†

if Finding Is

Present



Absent



4.5



0.8



Detecting Hepatopulmonary Syndrome in Patients with Chronic

Liver Disease

Oxygen saturation

39

94

6.7

<96%14



0.6



Detecting Pneumonia in Outpatients with Cough and Fever

Oxygen saturation

33-52

80-86

3.1

<95%15–18



0.7



*Diagnostic standard: For hepatopulmonary syndrome, triad of cirrhosis, intrapulmonary

shunting by contrast echocardiography, and 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.

Click here to access calculator.

PULSE OXIMETRY

Probability

Decrease

Increase

–45% –30% –15%

+15% +30% +45%

LRs



0.1



0.2



0.5



1



2



5



10



LRs



O2 saturation <96%, detecting

hepatopulmonary syndrome

O2 saturation <90%, predicting mortality

if hospitalized

O2 saturation <95%, detecting pneumonia

if cough and fever



158   PART 4 — VITAL SIGNS



syndrome in patients with chronic liver disease (LR = 6.7), and an O2

saturation of less than 95% increases the probability of pneumonia in

patients with cough and fever (LR = 3.1). The use of pulse oximetry to

diagnose aspiration in patients with stroke (during swallowing) is discussed

in Chapter 58.

B.  LIMITATIONS OF PULSE OXIMETRY4,6,19,20

Because pulse oximetry readings indicate only the degree of oxygen saturation of hemoglobin, they fail to detect problems of poor oxygen delivery

(e.g., anemia, poor cardiac output), hyperoxia, and hypercapnia. Other

limitations of pulse oximetry measurements are discussed in the following

sections.

1.  Dyshemoglobinemias

The pulse oximeter interprets carboxyhemoglobin to be oxyhemoglobin

and therefore seriously underestimates the degree of oxygen desaturation

in patients with carbon monoxide poisoning. In patients with methemoglobinemia, the pulse oximetry readings decrease initially but eventually

plateau at around 85%, despite true oxyhemoglobin levels that continue to

decrease to much lower levels.

2.  Dyes

Methylene blue causes a spurious decrease in oxygen saturation readings. Some colors of nail polish and finger pigments also interfere with

oximetry and should be removed before pulse oximetry monitoring.21–23

Hyperbilirubinemia and jaundice, however, do not affect the pulse oximeter’s accuracy.

3.  Low Perfusion Pressure

In patients with hypotension or peripheral vascular disease, the arterial

pulse may be so weak that the pulse oximeter is unable to pick up the arterial signal, thus making measurements difficult or impossible.

4.  Exaggerated Venous Pulsations

In patients with right-sided heart failure or tricuspid regurgitation, the

oximeter may mistake the venous waveform for the arterial one, leading to

spuriously low oxygen saturation readings.

5.  Excessive Ambient Light

Excessive ambient light (or malposition of the probe allowing ambient

light to reach the sensor) also may interfere with the oximeter’s accuracy,

falsely lowering the value in patients with normal oxygen saturation and,

more important, overestimating it in patients with significant hypoxemia.

The references for this chapter can be found on www.expertconsult.com.



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9. Mower WR, Myers G, Nicklin EL, et al. Pulse oximetry as a fifth vital sign in emergency

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1981;1:681-686.

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1980;93:391-398.

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2005;60:547-553.

13. Caterino JM, Kulchycki LK, Fischer CM, et al. Risk factors for death in elderly emergency

department patients with suspected infection. J Am Geriatr Soc. 2009;57:1184-1190.

14. Arguedas MR, Singh H, Faulk DK, Fallon MB. Utility of pulse oximetry screening for

hepatopulmonary sydrome. Clin Gastroenterol Hepatol. 2007;5:749-759.

15. Gennis P, Gallagher J, Falvo C, et al. Clinical criteria for the detection of pneumonia

in adults: guidelines for ordering chest roentgenograms in the emergency department.

J Emerg Med. 1989;7:263-268.

16. Heckerling PS. The need for chest roentgenograms in adults with acute respiratory illness: clinical predictors. Arch Intern Med. 1986;146:1321-1324.

17. Kyriacou DN, Yarnold PR, Soltysik RC, et al. Derivation of a triage algorithm for chest

radiography of comunity-acquired pneumonia patients in the emergency department.

Acad Emerg Med. 2008;15:40-44.

18. Nolt BR, Gonzales R, Maselli J, et al. Vital-sign abnormalities as predictors of pneumonia

in adults with acute cough illness. Am J Emerg Med. 2007;25:631-636.

19. Schnapp LM, Cohen NH. Pulse oximetry: uses and abuses. Chest. 1990;98:1244-1250.

20. Soubani AO. Noninvasive monitoring of oxygen and carbon dioxide. Am J Emerg Med.

2001;19:141-146.

21. Cote CJ, Goldstein A, Fuchsman WH, Hoaglin DC. The effect of nail polish on pulse

oximetry. Anesth Analg. 1988;67:683-686.

22. Battito MF. The effect of fingerprinting ink on pulse oximetry. Anesth Analg. 1989;69:265.

23. Goucke R. Hazards of henna. Anesth Analg. 1989;69:416.



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