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CHAPTER
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19
Respiratory Rate and Abnormal
Breathing Patterns
KEY TEACHING POINTS
• Respirations should be observed for at least 60 seconds, not only to increase the
detection of tachypnea but also to uncover unusual breathing patterns, such as CheyneStokes breathing.
• Tachypnea is a valuable diagnostic and prognostic sign in a varisssety of conditions. In
patients with altered mental status, bradypnea (≤12 breaths/min) increases probability of
opiate intoxication.
• In hospitalized patients, Cheyne-Stokes breathing is an accurate sign of left ventricular
dysfunction, especially in patients aged ≤80 years. It is present in one out of three
patients with reduced ejection fraction.
• Abnormal respiratory abdominal movements—abdominal paradox and asynchronous
breathing—are best observed when the patient is supine. These signs indicate respiratory
muscle weakness, either diaphragm paralysis (abdominal paradox) or a patient who is
tiring from the distress of bronchospasm (asynchronous breathing).
• Orthopnea, trepopnea, platypnea, and bendopnea each describe tachypnea that
appears abruptly in particular patient positions. Each has specific diagnostic significance.
RESPIRATORY RATE
I. Introduction
e respiratory rate (i.e., number of breaths per minute) is one of the four traditional vital signs,
the others being heart rate, blood pressure, and temperature. One of the first clinicians to recommend routine measurement of the respiratory rate was Stokes in 1825,1 although routine charting
of this vital sign was infrequent until the late 19th century.
II. Technique
e respiratory rate is usually measured while the clinician is holding the patient’s wrist and
ostensibly counting the pulse, primarily because the respiratory rate may change if attention is
drawn to it. is practice seems reasonable, because the respiratory rate is the only vital sign under
voluntary control.
2,3
143
144
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4—VITAL SIGNS
As routinely recorded in the patient’s hospital record, the respiratory rate is often inaccurate.
4,5
In studies of patients whose actual respiratory rates ranged from 10 to more than 30 breaths/min,
the recorded rates clustered around 16 to 22 breaths/min 75% to 98% of the time.
5–8
ese errors
usually reflect too short a period of observation (i.e., the clinician counting the number of breaths in
15 seconds and multiplying the result times 4); in one study, 15 seconds of observation detected only
23% of tachypneic patients, whereas 60 seconds of observation detected every tachypneic patient.6
Consequently, respirations should be observed for at least 60 seconds, not only to increase accuracy
of the measured rate7 but also to allow detection of unusual breathing patterns, such as CheyneStokes respirations (see later).
III. Finding
A. THE NORMAL RESPIRATORY RATE
e normal respiratory rate averages 20 breaths/min (range 16 to 25 breaths/min), based on careful measurement in persons without fever, heart disease, or lung disease.
cal to that made over 150 years ago by Lambert Quetelet, who was the first to compile and analyze
vital and social statistics.11 Quetelet’s 1835 monumental treatise also provided our current formula
for body mass index, known as the Quetelet index (see Chapter 13). For unclear reasons, many
textbooks, citing no data, mistakenly record the normal rate as 12 to 18 breaths/min.
B. TACHYPNEA
Definitions of tachypnea vary, but the most commonly applied definition, based on the normal
range and clinical studies, is respirations of 25 breaths/min or more.
9,10
is estimate is identi-
9
C. BRADYPNEA
Bradypnea is variably defined as respiratory rates less than 8 to 12 breaths/min. In patients receiving epidural opiate analgesia, respiratory rates less than 8 to 10/min are the best definition of
respiratory depression, a finding heralding respiratory failure.12 In patients with altered mental
status who are evaluated by medics, a respiratory rate of 12 breaths/min or less best identifies those
intoxicated with opiates. (See the section on clinical significance.)
IV. Clinical Significance
A. TACHYPNEA
e finding of tachypnea has both diagnostic and prognostic value. As a diagnostic sign, tachypnea argues modestly for the diagnosis of pneumonia in outpatients with cough and fever (likelihood ratio [LR] = 2.7, see EBM Box 19.1). Tachypnea also increases probability of pneumonia
in hospitalized patients, the abnormal sign sometimes appearing as early as 1 to 2 days before
the diagnosis is apparent by other means.
cysts of gas in the bowel wall on radiologic images), tachypnea increases the probability that the
surgeon will find bowel ischemia or obstruction at laparotomy (LR = 5.9).*
*
In these patients, tachypnea was more accurate than other computed tomography findings, such as portal
venous gas (LR = 3.2), dilated loops of bowel (LR = 1.3), or pneumoperitoneum (LR = NS). In this study
about half of patients with pneumatosis intestinalis had bowel ischemia or obstruction; the other half had
more benign etiologies.
13
10,33
In patients with pneumatosis intestinalis (i.e., small
19—RESPIRATORY RATE AND ABNORMAL BREATHING PATTERNS
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EBM BOX 19.1 Tachypnea*
145
Finding (Reference)
(breaths/min)
Sensitivity
(%)
Specificity
(%)
Likelihood Ratio† if Finding Is
Present Absent
Rate >20
Detecting operative finding
27–29 93–98 5.9 0.8
of intestinal ischemia or
obstruction, in patients with
pneumatosis intestinalis
14,15
Rate >24
Predicting failure of weaning
from the ventilator, in
intubated patients
16
94 68 2.9 NS
Rate >26-27
Predicting cardiopulmonary
arrest, in medical
inpatients
17,18
25–54 82–96 4.3 0.7
Rate >28
Detecting pneumonia, in
patients with cough and
19–22
fever
7–36 80–99 2.7 0.9
Rate >30
Predicting hospital mortality, in
patients with pneumonia
*Diagnostic standard: for failure of weaning, progressive hypoxemia or respiratory acidosis; for
pneumonia, infiltrate on chest radiograph.
†
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
NS, Not significant.
9–85 63–99 2.4 0.9
23–32
TACHYPNEA
Probability
Decrease Increase
+45%+30%+15%–15%–30%–45%
LRs
0.1 0.2 0.5 12510
LRs
Detecting bowel ischemia or
obstruction, in patients with
pneumatosis intestinalis
Predicting cardiopulmonary arrest,
if hospitalized
Predicting weaning failure, if ventilated
Detecting pneumonia, if cough and fever
Predicting mortality, if pneumonia
146
Cycle length
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4—VITAL SIGNS
One characteristic of a vital sign is that it accurately predicts the patient’s prognosis, and
EBM Box 19.1 shows that tachypnea predicts subsequent cardiopulmonary arrest in hospitalized
patients (LR = 4.3), better than does tachycardia or abnormal blood pressure.
17,18
During trials of
weaning from a ventilator, tachypnea is a significant though modest predictor of weaning failure
(LR = 2.9).
16,34
In patients hospitalized with pneumonia, severe tachypnea (i.e., rate >30 breaths/
min) predicts subsequent hospital death (LR = 2.4).
B. TACHYPNEA AND OXYGEN SATURATION
e respiratory rate correlates poorly with the patient’s level of oxygen desaturation (r = 0.16).35
Although this initially seems surprising (i.e., the lower the oxygen level, the more rapid a patient
should breathe), this actually is expected because some hypoxemic patients, by breathing rapidly,
are able to restore a more normal oxygen level (i.e., hyperventilation increases arterial oxygen
levels) and because other patients are hypoxemic simply because they have a primary hypoventilatory disorder. Consequently, the respiratory rate and oxygen saturation are both valuable to the
clinician, each providing information independent of the other.
C. BRADYPNEA
In a study of patients seen by medics for altered mental status, the finding of a respiratory rate of 12
breaths/min or less predicted a positive response to naloxone, thus confirming the clinical impression of
opiate intoxication (sensitivity of 80%, specificity of 95%, positive LR = 15.5, and negative LR = 0.2).
13
ABNORMAL BREATHING PATTERNS
I. Cheyne-Stokes Breathing (Periodic Breathing)
A. INTRODUCTION
Cheyne-Stokes breathing consists of alternating periods of apnea and hyperpnea (Fig. 19.1). Some
authors equate the term periodic breathing with Cheyne-Stokes breathing,
the term periodic breathing for oscillations of tidal volume that lack intervening periods of apnea.
Cheyne-Stokes breathing was described by John Cheyne in 1818 and William Stokes in 1854.
B. THE FINDING
1. The Breathing Pattern
At the end of each apneic period, breathing commences with excursions of the chest that initially are small but gradually increase for several breaths and then diminish until apnea returns.
Fig. 19.1 Cheyne-Stokes respiration. There are alternating cycles of hyperpnea and apnea. During the
hyperpnea phase only the tidal volume oscillates; the respiratory frequency is constant.
36,37
while others reserve
38
39
19—RESPIRATORY RATE AND ABNORMAL BREATHING PATTERNS
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147
e respiratory rate is constant during the hyperpnea phase and does not gradually increase and
then decrease as often surmised.40 Cheyne-Stokes breathing often first appears when the patient
lies down, probably because this position reduces the patient’s functional residual capacity, thus
diminishing the lung’s ability to buffer changes in carbon dioxide.
37,41
(See the section on patho-
genesis later.)
e time between two consecutive peaks of hyperpnea is called the cycle length or period. Each
cycle length is divided into a hyperpnea phase (lasting about 30 seconds on average in patients
with congestive heart failure) and an apnea phase (lasting about 25 seconds on average).
42,43
2. Associated Bedside Observations
Several additional findings appear in patients with Cheyne-Stokes breathing. During the hyperpnea
phase, the patient is alert and sometimes agitated, with dilated pupils, hyperactive muscle stretch
reflexes, and increased muscle tone. During the apnea phase, the patient appears motionless and
asleep with constricted pupils, hypoactive reflexes, and reduced muscle tone.
44,45
e agitation of the
hyperpnea phase can easily startle a patient out of sleep, a symptom that clinicians can mistake for
the paroxysmal nocturnal dyspnea of heart failure caused by transient pulmonary edema.
46,47
C. CLINICAL SIGNIFICANCE
1. Associated Conditions
Cheyne-Stokes breathing affects 30% of patients with stable congestive heart failure.
38,43
e
breathing pattern also appears in many neurologic disorders, including hemorrhage, infarction,
tumors, meningitis, and head trauma involving the brainstem or higher levels of the central nervous system.
altitudes.
44,48
Normal persons often develop Cheyne-Stokes breathing during sleep36 or at high
44
In patients hospitalized on an inpatient medicine service, the finding of Cheyne-Stokes respirations increases the probability left ventricular systolic dysfunction (i.e., ejection fraction less
than 40%; LR = 5.4, EBM Box 19.2). e finding is more accurate in patients under the age of 80
years (LR = 8.1) than in patients over the age of 80 years (LR = 2.7), suggesting that alternative
explanations of Cheyne-Stokes breathing (e.g., central nervous system injury) are more important
in older patients.
43
2. Prognostic Importance
Although Dr. Stokes originally believed that Cheyne-Stokes respirations implied a poor prognosis in patients with heart failure, modern studies demonstrate contradictory results, some showing
that the finding implies worse survival,49 while others showing no independent association with
increased mortality.
43,50
D. PATHOGENESIS
e fundamental problem causing Cheyne-Stokes breathing is enhanced sensitivity to carbon
dioxide. e circulatory delay between the lungs and systemic arteries, caused by poor cardiac
output, also contributes to the waxing and waning of breaths. Cerebral blood flow increases during
hyperpnea and decreases during apnea, perhaps explaining the fluctuations of mental status.
1. Enhanced Sensitivity to Carbon Dioxide
Whether because of congestive heart failure or neurologic disease, patients with Cheyne-Stokes
breathing have 2 to 3 times the normal sensitivity to carbon dioxide.
hyperventilate excessively, eventually driving the carbon dioxide level so low that central apnea
48,52
is causes patients to
42,51
148
LRs
CHEYNE-STOKES BREATHING
n
fraction <40%
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4—VITAL SIGNS
EBM BOX 19.2 Cheyne-Stokes Breathing, Detecting Reduced Ejection
Fraction
Finding (reference)
All adults 33 94 5.4 0.7
Patients aged ≤80 years 32 96 8.1 0.7
Patients aged >80 years 42 84 2.7 NS
*Diagnostic standard: for reduced ejection fraction, <40% by transthoracic echocardiography.
†
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
NS, Not significant.
43,
*
Sensitivity
(%)
Decrease Increase
0.1 0.2 0.5 12510
Specificity
(%)
Probability
Detecting left ventricular ejectio
Likelihood Ratio† if Finding Is
Present Absent
+45%+30%+15%–15%–30%–45%
LRs
results. After they stop breathing, carbon dioxide levels again rise, eliciting another hyperventilatory response and thus perpetuating the alternating cycles of apnea and hyperpnea.
Mountain climbers develop Cheyne-Stokes breathing because hypoxia induces hypersensitiv-
ity to carbon dioxide. In contrast, their native Sherpa guides, who are acclimated to hypoxia, lack
an exaggerated ventilatory response and do not develop Cheyne-Stokes breathing.
44
2. Circulatory Delay between Lungs and Arteries
Ventilation is normally controlled by the medullary respiratory center, which monitors arterial
carbon dioxide levels and directs the lungs to ventilate more if carbon dioxide levels are too high
and less if levels are too low. e medulla signals the lungs almost immediately, the message
traveling via the nervous system. e feedback to the medulla, however, is much slower because it
requires circulation of blood from lungs back to systemic arteries.
In Cheyne-Stokes breathing, the carbon dioxide levels in the alveoli and those of the systemic
arteries are precisely out of sync. During peak hyperpnea, carbon dioxide levels in the alveoli are
very low, yet the medulla is just beginning to sample blood containing high carbon dioxide levels
from the previous apnea phase and thus still directs the lungs to continue breathing deeply.44 e
delay in feedback to the medulla contributes to the gradual waxing and waning of tidal volume.
e length of circulatory delay also governs the cycle length of Cheyne-Stokes breathing, the
two correlating closely (r = 0.8 between cycle length and circulation time from lung to arteries,
p <0.05).
from the observation that carbon dioxide levels in the lungs and arteries are precisely out of sync.
Nonetheless, one study showed poor correlation between cycle length and ejection fraction, indi-
42,51
e cycle length is about 2 times the circulation time, just as would be expected
cating either that ejection fraction is a poor measure of circulation time or that variables other
than cardiac performance govern cycle length.
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149
II. Kussmaul Respiration
Kussmaul respirations are rapid and deep and appear in patients with metabolic acidosis.53 e
unusually deep respirations are distinctive, because other causes of tachypnea, such as heart and
lung disease, reduce vital capacity and thus cause rapid, shallow respirations.
In children with severe malaria, the finding of Kussmaul respirations detects severe metabolic
acidosis with a sensitivity of 19% to 91%, specificity of 81% to 97%, and positive LR = 5.3.
54–56
III. Grunting Respirations
A. DEFINITION
Grunting respirations are short, explosive sounds of low-to-medium pitch produced by vocal cord
closure during expiration. e actual sound is the rush of air that occurs when the glottis opens
and suddenly allows air to escape. Grunting respirations are more common in children,57 although
the finding also has been described in adults as a sign of respiratory muscle fatigue58 and, in the
preantibiotic era, as a cardinal sign of lobar pneumonia, usually appearing after 4 to 6 days of
3,59
illness.
B. PATHOGENESIS
Grunting respirations slow down expiration and allow more time for maximal gas exchange.58 In
animal experiments, artificial mimicking of grunting respirations causes the pO2 to increase by 10%
and the pCO2 to fall by 11%, whether or not the animal has pneumonia.60 Grunting respirations also
produce positive pressure exhalation that may reduce exudation of fluid into the alveoli, based on an
old observation that administration of morphine to patients with pneumonia often reduced grunting
respirations but was sometimes immediately followed by fatal pulmonary edema.
59
IV. Abnormal Abdominal Movements
A. NORMAL ABDOMINAL MOVEMENTS
In the absence of massive gaseous distention, the abdominal viscera are noncompressible and act
like hydraulic coupling fluid that directly transmits movements of the diaphragm to the anterior
abdominal wall.61 Abdominal respiratory movements, therefore, indicate indirectly how the diaphragm is moving. During normal respiration, the chest and abdomen move synchronously: both
out during inspiration and both in during expiration (Fig. 19.2). e chest wall moves more when
the person is upright, and the abdomen moves more when the person is supine.
B. ABNORMAL ABDOMINAL MOVEMENTS
Two abnormal abdominal movements are signs of chronic airflow obstruction or respiratory muscle weakness: asynchronous breathing and paradoxical abdominal movements.
1. Asynchronous Breathing
a. Findings
Asynchronous breathing is an abnormal expiratory movement that sometimes develops in patients
with chronic airflow obstruction. In these patients, the normal smooth inward abdominal movement
during expiration is replaced by an abrupt inward and then outward movement (see Fig. 19.2).
62,63
64,65
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