Respiratory System

FOUR
CHAPTER

15

Patient Assessment:
Respiratory System
OBJECTIVES
Based on the content in this chapter, the reader should be able to:
1 Describe the components of the history for respiratory assessment.
2 Explain the use of inspection, palpation, percussion, and auscultation for
respiratory assessment.
3 Explain the components of an arterial blood gas and the normal values for
each component.
4 Compare and contrast the arterial oxygen saturation and the partial pressure
of oxygen dissolved in arterial blood.
5 Compare and contrast the causes, signs, and symptoms of respiratory
acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis.
6 Analyze examples of an arterial blood gas result.
7 Discuss the purpose of pulse oximetry, end-tidal carbon dioxide monitoring,
and mixed venous oxygen saturation monitoring.
8 Discuss the purpose of respiratory diagnostic studies and associated nursing
implications.

207

Morton_Chap15.indd 207

2/4/2012 3:12:16 PM

commonly include dyspnea, chest pain, sputum
production (Table 15-1), and cough. Because smoking has a significant impact on the patient’s respiratory health, the patient’s use of tobacco should
be quantified by amount and how long the patient
has smoked. Elements of the respiratory history are
summarized in Box 15-1. A pulmonary illness often
results in the production (or a change in the production) of sputum.

Viral infection
Carcinoma
Pulmonary infarct

Physical Examination

A

comprehensive pulmonary assessment allows
the nurse to establish the patient’s baseline status
and provides a framework for rapidly detecting
changes in the patient’s condition.

High-quality physical assessments often provide
information that can lead to the detection of complications or changes in the patient’s condition before
information from laboratory and diagnostic studies
is available.

B O X 1 5 - 1 Respiratory Health History
History of the Present Illness
Complete analysis of the following signs and symptoms
(using the NOPQRST format; see Chapter 12, Box 12-1):
• Dyspnea, dyspnea on exertion

over-the-counter drugs, vitamins, herbs, and
supplements: oxygen, bronchodilators, antitussives,
expectorants, mucolytics, anti-infectives, antihistamines, methylxanthine agents, anti-inflammatory
agents
• Allergies and reactions to medications, foods, contrast dye, latex, or other materials
• Transfusions, including type and date
Family History
• Health status or cause of death of parents and
siblings: tuberculosis, cystic fibrosis, emphysema,
asthma, malignancy
Personal and Social History
• Tobacco, alcohol, and substance use
• Environment: exposure to asbestos, chemicals, coal
dust, allergens; type of heating and ventilation system
• Diet
• Sleep patterns: use of pillows
• Exercise
Review of Other Systems
• HEENT: strep throat, sinus infections, ear infection,
deviated nasal septum, tonsillitis
• Cardiac: heart failure, dysrhythmias, coronary artery
disease (CAD), valvular disease, hypertension
• Gastrointestinal: weight loss, nausea, vomiting
• Neuromuscular: Guillain–Barré syndrome, myasthenia gravis, amyotrophic lateral sclerosis, weakness
• Musculoskeletal: scoliosis, kyphosis

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Patient Assessment: Respiratory System C H A P T E R 1 5

abnormal chest expansion are listed in Box 15-3.
Asynchronous respiratory effort often precedes
the need for ventilatory support.

BOX 15-2

• Clubbing of the fingers (see Chapter 30, Fig. 30-2)
is seen in many patients with respiratory and cardiovascular diseases, especially chronic hypoxia.

Palpation
In addition to observing expansion of the chest
wall, the nurse palpates chest expansion by positioning the thumbs on the patient’s back, at the
level of the 10th rib, and observing the divergence
of the thumbs caused by the patient’s breathing.
Expansion of the chest wall should be symmetrical
(see Box 15-3).
To assess tactile fremitus (the ability to feel sound
on the chest wall), the nurse asks the patient to say
“ninety-nine” while palpating the posterior surfaces of the chest wall. Tactile fremitus is slightly
increased by the presence of solid substances, such
as the consolidation of a lung due to pneumonia,
pulmonary edema, or pulmonary hemorrhage.
Conditions that result in greater air volume in the
lung (eg, emphysema) are associated with decreased
or absent tactile fremitus, because air does not conduct sound well.
The nurse palpates for subcutaneous emphysema by moving the fingers in a gentle rolling
motion across the chest and neck to feel pockets of
air underneath the skin. Subcutaneous emphysema
may result from a pneumothorax or small pockets
of alveoli that have burst with increased pulmonary pressure, (eg, PEEP). In severe cases, the subcutaneous emphysema may spread throughout the

• Alignment of spine
Head and Neck

• Nasal flaring
• Pursed-lip breathing
• Mouth breathing versus nasal breathing
• Use of neck and shoulders
• Tracheal position
• Central cyanosis
Extremities

• Clubbing
• Edema
• Peripheral cyanosis

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210

P A R T F O U R Respiratory System

TA B L E 1 5- 2 Respiration Patterns
Type

Description

Normal

12–20 breaths/min and

compensation for acidosis (eg,
salicylate overdose)

Kussmaul’s
respiration

Rapid, deep, labored

Associated with diabetic ketoacidosis

Hypoventilation

Decreased rate, decreased
depth, irregular pattern

Usually associated with overdose of
narcotics or anesthetics

Cheyne–Stokes
respiration

Regular pattern
characterized by
alternating periods of
deep, rapid breathing
followed by periods of
apnea
Irregular pattern
characterized by varying
depth and rate of


Unilateral diminished expansion
• Atelectasis
• Endotracheal or nasotracheal tube positioned in
right mainstream bronchi
• Collapsed lung
• Pulmonary embolus
• Lobar pneumonia
• Pleural effusion
• Pneumothorax
• Rib fracture
Asynchronous expansion
• Flail chest

Morton_Chap15.indd 210

Clinical Significance

A more extreme expression of Biot’s
respirations; indicates respiratory
compromise and elevated ICP
Seen in chronic obstructive pulmonary
disease (COPD) when air is trapped
in the lungs during forced expiration

Percussion
Percussion of the chest normally produces a resonant or hollow note. In diseases in which there is
increased air in the chest or lungs (eg, pneumothorax, emphysema), percussion notes may be hyperresonant. A flat percussion note is more likely to
be heard if a large pleural effusion is present in the
lung beneath the examining hand. A dull percussion

Expiratory sounds last
longer than inspiratory
ones.

Soft

Relatively low

Over most of both lungs

Intermediate

Intermediate

Loud

Relatively high

Often in the first and second
interspaces anteriorly and
between the scapulae
Over the manubrium, if
heard at all

Inspiratory and expiratory
sounds are about
equal.

Very loud


voice is heard faintly and indistinctly through the
stethoscope. The increased transmission of voice
sounds indicates the presence of fluid in the lungs.
Adventitious sounds are additional breath sounds
heard with auscultation and include discontinuous
sounds, continuous sounds, and friction rubs:
• Discontinuous sounds are brief, nonmusical,
intermittent sounds and include fine and coarse
crackles. When assessing crackles, the nurse notes
their loudness, pitch, duration, amount, location,
and timing in the respiratory cycle. Fine crackles are
soft, high-pitched, very brief popping sounds that
occur most commonly during inspiration. These
result from fluid in the airways or alveoli, or from
the opening of collapsed alveoli. Restrictive pulmonary disease results in fine crackles during late
inspiration, whereas obstructive pulmonary disease
results in fine crackles during early inspiration.
Crackles become coarser as the air moves through
larger fluid accumulations, such as in bronchitis or
pneumonia. Crackles that clear with coughing are
not associated with significant pulmonary disease.
• Continuous sounds include wheezes and rhonchi. Wheezes are high-pitched musical sounds

Morton_Chap15.indd 211

that have a shrill quality. They are caused by the
movement of air through a narrowed or partially
obstructed airway, such as in asthma, chronic
obstructive pulmonary disease (COPD), or bronchitis. Rhonchi are deep, low-pitched rumbling
noises. The presence of rhonchi indicates the presence of secretions in the large airways, such as


P A R T F O U R Respiratory System

BOX 15-4

Measuring pH in the Blood

Normal Arterial Blood Gas (ABG)
Values

The normal blood pH is 7.35 to 7.45. Box 15-5
reviews terms used in acid–base balance. An acid–
base disorder may be either respiratory or metabolic in origin (Table 15-4). If the respiratory system
is responsible, serum carbon dioxide levels are
affected, and if the metabolic system is responsible,
serum bicarbonate levels are affected (see Table
15-4). Occasionally, patients present with both respiratory and metabolic disorders that together cause
an acidemia or alkalemia. When this occurs, the
ABG reflects a mixed respiratory and metabolic acidosis. Examples of ABG values in mixed disorders
are given in Box 15-6.

PaO2: 80 to 100 mm Hg
SaO2: 93% to 99%
pH: 7.35 to 7.45
PaCO2: 35 to 45 mm Hg
HCO3: 22 to 26 mEq/L

and extent of pulmonary gas exchange and acid–base
status. Normal ABG values are given in Box 15-4.


correct the primary disorder. By using the rules for
defining compensation in Box 15-8, it is possible to
determine the compensatory status of the patient’s
ABGs.

The Older Patient. PaO2 tends to decrease with
age. For patients who are 60 to 80 years of age, a
PaO2 of 60 to 80 mm Hg is normal.1

The relationship between PaO2 and SaO2 is depicted
by the oxyhemoglobin dissociation curve (Fig. 15-1).
At a PaO2 greater than 60 mm Hg, large changes in
the PaO2 result in only small changes in the SaO2.
However, at a PaO2 of less than 60 mm Hg, the curve
drops sharply, signifying that a small decrease in PaO2
is associated with a large decrease in SaO2. Factors
such as pH, carbon dioxide concentration, temperature, and levels of 2,3-diphosphoglycerate (2,3-DPG)
influence hemoglobin’s affinity for oxygen and can
cause the curve to shift to the left or to the right (see
Fig. 15-1). When the curve shifts to the right, there is
a reduced capacity for hemoglobin to hold onto oxygen, resulting in more oxygen released to the tissues.
When the curve shifts to the left, there is an increased
capacity for hemoglobin to hold oxygen, resulting in
less oxygen released to the tissues.

100
Shift to the right
Acidosis ( pH)
PaCO2
Temperature


sociation curve is a graphic depiction
of the relationship between oxyhemoglobin saturation (the percentage of
hemoglobin combined with oxygen, or
the SaO2) and the arterial oxygen tension (PaO2) to which it is exposed.

2/4/2012 3:12:21 PM


Patient Assessment: Respiratory System C H A P T E R 1 5

BOX 15-5

Acid–Base Terminology

Acid: A substance that can donate hydrogen ions (H+).
Example: H2CO3 (an acid) → H+ + HCO3
Base: A substance that can accept hydrogen ions (H+).
Example: HCO3 (a base) + H+ → H2CO3
Acidemia: Acid condition of the blood in which the
pH is less than 7.35
Alkalemia: Alkaline condition of the blood in which
the pH is greater than 7.45
Acidosis: The process causing acidemia
Alkalosis: The process causing alkalemia

BOX 15-6

213


High cord injury
Pneumothorax
Hypoventilation
Bronchial obstruction and atelectasis
Severe pulmonary infections
Heart failure and pulmonary edema
Massive pulmonary embolus
Myasthenia gravis
Multiple sclerosis
Excessive elimination of CO2 by the lungs
Anxiety and nervousness
Fear
Pain
Hyperventilation
Fever
Thyrotoxicosis
CNS lesions
Salicylates
Gram-negative septicemia
Pregnancy
Increased acids
Renal failure
Ketoacidosis
Anaerobic metabolism
Starvation
Salicylate intoxication
Loss of base
Diarrhea
Intestinal fistulas


Headache
Tachycardia
Confusion
Lethargy
Dysrhythmias
Respiratory distress
Drowsiness
Decreased responsiveness

Light-headedness
Confusion
Decreased concentration
Paresthesias
Tetanic spasms in the arms and legs
Cardiac dysrhythmias
Palpitations
Sweating
Dry mouth
Blurred vision
Headache
Confusion
Restlessness
Lethargy
Weakness
Stupor/coma
Kussmaul’s respirations
Nausea and vomiting
Dysrhythmias
Warm, flushed skin
Tetany

complete, partial, or uncompensated?

PaO2
SaO2
pH
PaCO2
HCO3

85 mm Hg
90%
7.49
40
29 mEq/L

Normal
Low
Alkalemia
Normal
Increased (metabolic
cause)

Conclusion: Metabolic alkalosis with a low saturation
(uncompensated)

Examples
Sample blood gas

PaO2
SaO2
Ph

HCO3 is also abnormal. There is no indication that the
opposite system has tried to correct for the other.
In the example below, the patient’s pH is alkalotic
as a result of the low (below the normal range of 35 to
45 mm Hg) CO2 concentration. The renal system value
(HCO3) has not moved out its normal range (22 to 26
mEq/L) to compensate for the primary respiratory
disorder.
PaO2
pH
PaCO2
HCO3

94 mm Hg
7.52
25 mm Hg
24 mEq/L

Normal
Alkalotic
Decreased
Normal

Partially compensated: pH is abnormal, and both the
CO2 and HCO3 are also abnormal; this indicates that
one system has attempted to correct for the other but
has not been completely successful.
In the example below, the patient’s pH remains alkalotic as a result of the low CO2 concentration. The renal
system value (HCO3) has moved out its normal range
(22 to 26 mEq/L) to compensate for the primary respiratory disorder but has not been able to bring the pH

In the example below, the patient’s pH is normal
but is tending toward alkalosis (greater than 7.40). The
primary abnormality is respiratory because the PaCO2
is low (decreased acid concentration). The bicarbonate value of 18 mEq/L reflects decreased concentration
of base and is associated with acidosis, not alkalosis.
In this case, the decreased bicarbonate has completely
compensated for the respiratory alkalosis.
PaO2
pH

94 mm Hg
7.44

PaCO2
HcO3

25 mm Hg
18 mEq/L

Normal
Normal, tending toward
alkalosis
Decreased, primary problem
Decreased, compensatory
response

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Patient Assessment: Respiratory System C H A P T E R 1 5

2. The second phase is the expiratory upstroke, which
represents the exhalation of carbon dioxide from
the lungs. Any process that delays the delivery
of carbon dioxide from the patient’s lungs to the
detector (eg, COPD, bronchospasm, kinked ventilator tubing) prolongs the expiratory upstroke.
3. The third phase, the plateau phase, begins as carbon dioxide elimination rapidly continues and
indicates the exhalation of alveolar gases. The
End-tidal carbon dioxide
(ET CO2 ) level

mm Hg

Plateau phase

32
0
Expiration starts;
Inspiration starts;
indicated by CO2 rise
indicated by CO2 fall
(expiratory upstroke
(inspiratory downstroke
phase)
phase)
Baseline
phase

F I G U R E 1 5 - 2 Capnogram tracing.

Morton_Chap15.indd 215

in SvO2 often occurs before other hemodynamic
changes and therefore is an excellent clinical tool
in the assessment and management of critically ill
patients. Elevated SvO2 values are associated with
increased delivery of oxygen or with decreased
demand (see Table 15-5).

Respiratory Diagnostic Studies
Pulmonary function tests measure the ability of the
chest and lungs to move air into and out of the alveoli. Pulmonary function tests include volume measurements, capacity measurements, and dynamic
measurements (Table 15-6):
• Volume measurements show the amount of air
contained in the lungs during various parts of the
respiratory cycle.
• Capacity measurements quantify part of the pulmonary cycle.
• Dynamic measurements provide data about airway resistance and the energy expended in breathing (work of breathing).
These measurements are influenced by exercise, disease, age, gender, body size, and posture.
Other diagnostic studies that are often used to
evaluate the respiratory system are summarized in
Table 15-7.

2/4/2012 3:12:22 PM


216

P A R T F O U R Respiratory System

TA B L E 1 5- 5 Possible Causes of Abnormalities in Mixed Venous Oxygen Saturation (SvO2)
Abnormality


Remarks

Tidal volume

VT

Tidal volume may vary with
severe disease.

Inspiratory reserve
volume
Expiratory reserve
volume

IRV

Normal
Values

Volume Measurements

Residual volume

ERV

Volume of air inhaled and exhaled
with each breath
Maximum volume of air that can be
inhaled after a normal inhalation


Total lung capacity

TLC

Volume of air in lungs after a
maximum inspiration and equal to
the sum of all four volumes (VT,
IRV, ERV, RV)

500 mL
3000 mL

Expiratory reserve volume is
decreased with restrictive
disorders, such as obesity,
ascites, and pregnancy.
Residual volume may be
increased with obstructive
diseases.

1100 mL

1200 mL

Capacity Measurements

Morton_Chap15.indd 216

Decrease in vital capacity


Patient Assessment: Respiratory System C H A P T E R 1 5

217

TA B LE 15- 6 Volume Measurements, Capacity Measurements, and Dynamic Measurements (continued)
Term Used

Symbol Description

Normal
Values

Remarks

Dynamic Measurements

Respiratory rate
(frequency)
Minute volume
(minute ventilation)
Dead space

f

Alveolar ventilation

V˙A

VD

of the VT

4500 mL/min

TA B LE 15- 7 Respiratory Diagnostic Studies
Test and Purpose

Method of Testing

Nursing Implications

X-rays pass through chest wall, making
it possible to visualize structures.
Bones appear as opaque or white;
heart and blood vessels appear as
gray; lungs filled with air appear
black; lungs with fluid appear white.

• Test can be done at the bedside or in the
diagnostic center.
• Nurse may be asked to help position the patient
and ensure that the patient takes a deep breath
during the test.

To test ventilation, the patient inhales
radioactive gas. Diminished areas of
ventilation are visible on the scan.
To test perfusion, a radioisotope
is injected intravenously, enabling
visualization of the blood supply

patient remain in a position with the arms and
shoulders raised (to facilitate needle insertion
between the ribs) and monitors the patient’s
comfort, anxiety, and respiratory status.
• Postprocedure complications may include
pneumothorax, pain, hypotension, and
pulmonary edema.

Chest Radiography

Used to assess anatomical
and physiological
features of the
chest and to detect
pathological processes.
Ventilation–Perfusion
Scanning

A nuclear imaging test
used to evaluate a
suspected alteration
in the ventilation–
perfusion relationship in
the lung.

Bronchoscopy

Used to examine
lung tissue, collect
secretions, determine

sputum from the lungs.

• The nurse instructs the patient not to place
saliva in the container but instead cough up
sputum from the lungs.

A radiopaque contrast material is
injected into one or both arms, the
femoral vein, or a catheter placed
in the pulmonary artery. Positive
test is indicated by impaired flow of
substance through narrowed vessel
or by abrupt cessation of flow.

• The nurse monitors the patient’s pulse, blood
pressure, and breathing during test.
• Possible complications include allergic reaction
to dye, pulmonary embolus, and abnormal
cardiac rhythm.

Continuously rotating x-rays send
images to a computer to create a 3D
composite image.

• Test is done in a diagnostic center.
• The nurse monitors for claustrophobia and
administers a mild sedative if necessary.

Sputum Culture


notes that Mr. J. is using accessory muscles for breathing, and his jugular veins are visibly distended at 45
degrees. Mr. J.’s mucous membranes are pale, and he
has a Glasgow Coma Scale score of 14. On auscultation, the nurse hears coarse crackles in both bases
with some audible expiratory wheezing. During assessment of breath sounds, the nurse is able to clearly hear
whispered sounds through the stethoscope. Arterial
blood gases (ABGs) are PaO2, 68 mm Hg; PaCO2, 49
mm Hg; HCO3, 29 mEq/L; and pH, 7.31.
1. What three findings from Mr. J.’s assessment are
consistent with a diagnosis of heart failure?
2. Describe some of the differences in respiratory
assessment of the older patient.

Morton_Chap15.indd 218

3. What signs of respiratory distress are apparent,
even before auscultating the lungs or obtaining
arterial blood gas (ABG) results?
4. Why is Mr. J. tachypneic?
5. Why is the nurse able to hear whispered sounds
clearly with the stethoscope? What is this condition called?
6. Interpret the ABG results. Is Mr. J.
compensating?

References
1. Miller RD, et al: Chapter 71: Geriatrics: Pulmonary changes.
In Miller’s Anesthesia, 7th edition. Churchill Livingstone,
2009
2. Wilson B, et al: The accuracy of pulse oximetry in emergency department: patients with severe sepsis and septic
shock. BMC Emerg Med 10:9, 2010
3. Respiratory Care. In Best Practices: Evidence-Based Nursing

Bronchial Hygiene Therapy
Hospitalized patients are often not able to deep
breathe, cough, or clear mucus effectively because
of weakness, sedation, pain, or an artificial airway.
Bronchial hygiene therapy (BHT) aims to improve
ventilation and diffusion through secretion mobilization and removal and through improved gas
exchange.
BHT methods include coughing and deep breathing, airway clearance adjunct therapies, chest physiotherapy (CPT), and bronchodilator therapy. BHT
methods are used individually or in combination,
depending on the patient’s needs. Physical assessment, chest radiography, and arterial blood gases
(ABGs) are used to determine the need for BHT, the
appropriate methods to use, and the effectiveness
of these interventions. Incentive spirometry may be

given before any of the BHT methods to promote
mucus removal.

Coughing and Deep Breathing
The objectives of coughing and deep breathing are
to promote lung expansion, mobilize secretions, and
prevent the complications of retained secretions
(atelectasis and pneumonia). Even if crackles or
rhonchi are not auscultated, the nurse encourages
the high risk patient to cough and deep breathe as a
prophylactic measure every hour. These techniques
are effective only if the patient is able to cooperate
and has the strength to cough productively.
The nurse instructs the patient to sit upright,
inhale maximally and cough, and then take a slow,
deep breath and hold it for 2 to 3 seconds. Use

• Oscillating positive expiratory pressure (PEP).
An oscillating PEP device (eg, Acapella valve, Flutter
valve) loosens mucus by producing PEP and oscillatory vibrations in the airways so that the mucus
can then be cleared with a cough. The nurse manually assists the patient’s cough by exerting positive
pressure on the abdominal costal margin during
exhalation, thus increasing the cough’s force.
• High-frequency chest wall oscillation. The
patient wears a vest-like device that uses air pulses
to compress the chest wall, loosening secretions.
High-frequency chest wall oscillation has been
shown to improve mucus removal and pulmonary
function, is well tolerated by surgical patients, and
can be self-administered at home.
• Positive airway pressure (PAP). PAP devices
enable airway recruitment and reduce atelectasis
by delivering pressures between 5 and 20 cm H2O
with variable flow of oxygen during therapy. They
are used in patients when other airway clearance
therapies are not sufficient to reduce or prevent
atelectasis.

Chest Physiotherapy
CPT techniques include postural drainage, chest
percussion and vibration, and patient positioning.
CPT is preceded by bronchodilator therapy and
followed by deep breathing and coughing or other
BHT techniques. Patients with an artificial airway
or an ineffective cough may require suctioning after
CPT. No single method of CPT has been shown to be
superior, and there are many contraindications to

secretions. Percussion involves striking the chest
wall with the hands formed into a cupped shape.
The patient’s position depends on the segment of
lung to be percussed. Vibration involves manually compressing the chest wall while the patient
exhales through pursed lips to increase the velocity
and turbulence of exhaled air to loosen secretions.
Vibration is used instead of percussion if the chest
wall is extremely painful. Critical care unit beds have
options to percuss or vibrate, with variable settings
for high to low frequency of percussion or vibration.
The nurse assesses the patient for tolerance to the
level of therapy.
RED FLAG! Contraindications to percussion
and vibration include fractured ribs, osteoporosis,
chest or abdominal trauma or surgery, pulmonary
hemorrhage or embolus, chest malignancy,
mastectomy, pneumothorax, subcutaneous
emphysema, cervical cord trauma, tuberculosis,
pleural effusions or empyema, and asthma.

Patient Positioning
Turning the patient laterally every 2 hours (at minimum) aids in mobilizing secretions for removal with
cough or suctioning. Changing the patient’s position
affects gas exchange, and positioning the patient
with the “good” lung down improves oxygenation by
improving ventilation to perfusion match.2
RED FLAG! Positioning is altered if the patient
has a lung abscess. In this case, the preferred
position is with the diseased lung down, because
otherwise gravity can cause the abscessed lung’s


F I G U R E 1 6 - 1 Positions used in lung drainage.

Continuous lateral rotation therapy (CLRT),
defined as continuous lateral positioning of less
than 40 degrees for 18 of 24 hours daily, improves
oxygenation and blood flow to the lung tissue in
affected regions and promotes secretion removal
and airway patency.2 Using lateral rotation therapy
beds is more effective than the inconsistent nursing
care of turning every 2 hours at minimum.3 CLRT
beds rotate to less than 40 degrees, while kinetic
therapy beds rotate to 40 degrees or more. The best
evidence-based research involves kinetic therapy
beds. The nurse assesses the patient for tolerance
to position changes when a CLRT or kinetic therapy
bed is in use.
Patients who are ventilated benefit from having
the head of the bed elevated 30 degrees at all times.4
The rationale is to promote lung expansion, prevent the aspiration that can occur in the recumbent
position in intubated patients, and prevent ventilator-associated pneumonia (VAP). Rotation therapy
may also help reduce pneumonia, although it may
not reduce days on the ventilator or the length of

Morton_Chap16.indd 221

hospital stay. For best outcomes, rotation must be
continuous and at the maximum for each side.
Prone positioning is an advanced technique used
with critically ill ventilated patients who have acute

absorptive atelectasis; and carbon dioxide narcosis
(manifested by altered mental status, confusion,
headache, and somnolence).

Several methods of oxygen delivery are available
(Box 16-1). The choice of delivery method depends
on the patient’s condition. Low-flow oxygen devices
are suitable for patients with normal respiratory
patterns, rates, and ventilation volumes. High-flow

BOX 16-1

oxygen devices are suitable for patients with high
oxygen requirements because high-flow devices
deliver up to 100% FiO2 and maintain humidification, which is essential to prevent drying of the nasal
mucosa. The nurse monitors the SaO2 closely for at
least 30 to 60 minutes when switching from a lowflow to a high-flow oxygen delivery device, evaluates
ABGs as needed, and assesses patient tolerance. If
increased distress, desaturation, or both are noted,
more extreme interventions (eg, intubation) may be
necessary.
Oxygen toxicity starts to occur in patients breathing an FiO2 of more than 50% for longer than
24 hours. The FiO2 should be decreased as tolerated
to the lowest possible setting as long as the SaO2
remains greater than 90%. The pathophysiological
changes that occur with oxygen toxicity may progress from capillary leaking to pulmonary edema and
possibly to ALI or ARDS with prolonged high FiO2
continues for several days. Patients on a high FiO2

Oxygen Delivery Methods With Delivered Fraction of Inspired Oxygen (FiO2)

28–32
32–36
36–40
40–44

Facemask

Flow (L/min)
5–6
6–7
7–10

FiO2 (%)
40
50
60

Face Tent

Air is mixed with the oxygen flow in the mask, resulting in variable delivery with humidification (21%
delivered with compressed air and up to 50% delivered with 10 L/min oxygen flow attached). A face tent
is often used for patients who cannot tolerate the
claustrophobic feeling associated with more traditional masks.

Morton_Chap16.indd 222

FiO2 Settinga (%)

4
4

strap on the tracheostomy collar is adjusted to keep the
collar on top of the tracheostomy. With both the T-piece
and tracheostomy collar, the goal is to provide a high
enough flow rate (at least 10 L/min with humidification) to
ensure that there is a minimal amount of entrained room
air. Flow can also be provided by a ventilator.

2/4/2012 3:14:34 PM


Patient Management: Respiratory System C H A P T E R 1 6

223

TA B LE 16- 1 Indications for Chest Tube Placement
Indication

Potential Causes

Hemothorax

Chest trauma, neoplasms, pleural tears, excessive anticoagulation, postthoracic
surgery, post–open lung biopsy

Pneumothorax
Spontaneous (greater than
20%)
Tension
Bronchopleural fistula
Pleural effusion

are used to drain blood or thick pleural drainage.
They are placed at about the fifth to sixth intercostal space (ICS) midaxillary. Smaller tubes (16 to
20 French) are used to remove air and are placed at
the second to third ICS midclavicular.
Chest tubes are attached to a drainage system.
Modern systems are disposable and have three
chambers (Fig. 16-2). The first chamber is the collection receptacle, the second chamber is the water
seal, and the third chamber is suction. The water

Parietal pleura
Visceral
pleura

To suction source
(or air)
From patient
Vent to
room air

Lung
Pleural cavity

20 mm

250 mm
Drainage
collection
chambers

2 mm

in the suction chamber, not the amount of wall
suction, that determines the amount of suction
applied to the chest tube, most commonly −20 cm
H2O. Once the wall suction exceeds the force necessary to “lift” this column of fluid, any additional
suction simply pulls air from a vented cap atop
the chamber up through the water. The amount
of wall suction applied should be sufficient to create a “gently rolling” bubble in the suction control
chamber. Vigorous bubbling results in water loss
through evaporation, changing suction pressure
and increasing the noise level in the patient’s room.
It is important to assess the system for water loss
and to add sterile water as necessary to maintain
the prescribed level of suction.
Dry suction (waterless) systems use a spring
mechanism to control the suction level and can provide levels of suction ranging from −10 to −40 cm
H2O. The amount of negative pressure is dialed in,
again, it is the amount dialed in not the wall suction
which determines the amount of suction. Dry suction systems that can deliver higher levels of suction
may be necessary in patients with large bronchopleural fistulas, hemorrhage, or obesity. They also
afford the patient a quieter environment.
RED FLAG! The chest tube drainage system
should never be raised above the chest, or the
drainage will back up into the chest.

Chest Tube Placement
The patient is placed in Fowler’s or semi-Fowler’s
position for the procedure. Because the parietal
pleura is innervated by the intercostal and phrenic
nerves, chest tube insertion is a painful procedure
and administration of analgesics is indicated. After

respiration or mechanical ventilation breaths.
7. Assess for the air leaks, manifested as constant
bubbling in the water seal chamber. If constant
bubbling is noted, identify the location of the
leak by first turning off the suction. Then,
beginning at the insertion site, briefly occlude
the chest tube or drainage tube below each
connection point until the drainage unit is
reached.
8. Check that all tubing connections are securely
sealed and taped.
9. Ensure water seal chambers are filled to the 2-cm
water line. Relieve negative pressure if the water
level is above the 2-cm water line.
10. Assess the patient for pain, intervene as needed,
and reassess appropriately. Pain management may
include the use of analgesics, a lidocaine patch, or
nonsteroidal anti-inflammatory drugs (NSAIDs).
11. Assess the actual chest tube insertion site for signs
of infection and subcutaneous emphysema.
12. Change the dressing per unit guidelines, when
soiled, and when ordered.

the drainage collection system are securely taped to
prevent air leaks as well as inadvertent disconnection. The proximal portion of the tube is taped to the
chest to prevent traction on the tube and sutures if
the patient moves. A postinsertion chest radiograph
is always ordered to confirm proper positioning.
The lungs are auscultated, and the condition of the
tissue around the insertion site is evaluated for the

is placed on water seal). Premature removal of the
chest tube may cause reaccumulation of the pneumothorax. Before the chest tube is removed, the
patient is premedicated to alleviate pain. The tube is
removed in one quick movement during expiration
to prevent entraining air back into the pleural cavity. Immediately after tube removal, the lung fields
are auscultated for any change in breath sounds,
and an occlusive sterile dressing with petroleum
gauze is applied over the site. A chest radiograph
is obtained to look for the presence of residual air
or fluid.

Pharmacotherapy
Bronchodilators
Bronchodilators dilate the airways by relaxing
bronchial smooth muscle. Bronchodilator therapy
can be delivered through metered-dose inhalers
(MDIs) or nebulization. Patient inhalation ensures
delivery into the lungs. Assessment before, during, and after the therapy is essential and includes
breath sounds, pulse, respiratory rate, and pulmonary function tests to measure improvement in
severity of airway obstruction. ABGs also may be
indicated.
• b2-Adrenergic blockers. Because of their rapid
onset of action, β-adrenergic blockers are the
bronchodilators of choice for the treatment of
acute exacerbation of asthma or severe bronchial constriction. The bronchodilator effects of
β-adrenergic blockers result from stimulation
of β2-adrenergic receptors in the lung bronchial
smooth muscle. These agents may also stimulate
β1-adrenergic receptors in the heart, leading to
undesired cardiac effects. β2-selective drugs are

6 to 12 hours. Corticosteroids may be administered
parenterally, orally, or as aerosols. In acute exacerbations, high-dose parenteral steroids (eg, IV
methylprednisolone) are used and then tapered as
the patient tolerates. Short courses of oral therapy
may be used to prevent the progression of acute
attacks. Long-term oral therapy is associated with
systemic adverse effects and should be avoided if
possible.
• Mast cell stabilizers are thought to stabilize the
cell membrane and prevent the release of mediators from mast cells. These agents are not indicated
for acute exacerbations of asthma. Rather, they are
used prophylactically to prevent acute airway narrowing after exposure to allergens (eg, exercise,
cold air). A 4- to 6-week trial may be required to
determine efficacy in individual patients. The goal
is to reduce the frequency and severity of asthma
attacks and enhance the effects of concomitantly
administered bronchodilator and steroid therapy.
It may be possible to decrease the dose of bronchodilators or corticosteroids in patients who respond
to mast cell stabilizers.
• Leukotriene receptor antagonists may be used
in the management of exercise-induced bronchospasm, asthma, allergic rhinitis, and urticaria.
These agents block the activity of endogenous
inflammatory mediators, particularly leukotrienes, which cause increased vascular permeability,
mucus secretion, airway edema, bronchoconstriction, and other inflammatory cell process activities.
Leukotriene receptor antagonists are administered
once daily and are usually well tolerated. They are

2/4/2012 3:14:35 PM



patients are a poor risk with limited pulmonary
reserve. Bleeding may be extensive following the
surgery, and two chest drains are usually in place
to drain air or blood.
• Lobectomy may be performed as a treatment for
malignant or benign tumors and for infections
such as bronchiectasis, tuberculosis, or fungal
infection.
• Pneumonectomy is performed to remove one lung,
usually because of primary carcinoma or significant infection.
• Lung volume reduction surgery (LVRS) involves
resecting parts of the lung to reduce hyperinflation
(eg, as part of the treatment for emphysema).
• Lung transplantation may involve one lung or
both lungs, and it may be done along with heart
transplantation. To be considered a viable candidate for lung transplantation, a patient must have
minimal comorbidities and advanced lung disease
that is unresponsive to other therapies.

Morton_Chap16.indd 226

CAS E S T U DY

M

r. B. is admitted to the critical care unit for
the diagnosis of pancreatitis. The physician places
a right subclavian central line. Immediately after
the line placement, the nurse notes that Mr. B.
has increasing dyspnea and tachycardia. Further

prevent ventilator-associated pneumonia. Crit Care Med
38(2):706–707, 2010
3. Swadener-Culpepper, L. Continuous lateral rotation therapy.
Critical Care Nurse 30(2):S5–S7, 2010
4. Tolentino-DelosReyes AF, et al.: Am J Crit Care 16(1):20–27,
2007
5. Kopterides P, Siempos I, Armagaidis A, et al.: Prone positioning in hypoxemix respiratory failure: Meta analysis of
randomized controlled trials. J Crit Care 24:89–100, 2009
6. Karch AM (ed): Lippincott’s Nursing Drug Guide, 2007 ed.
Philadelphia, PA: Lippincott Williams & Wilkins, 2007

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to access chapter review
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2/4/2012 3:14:35 PM


CHAPTER

Common Respiratory Disorders

17
OBJECTIVES

Based on the content in this chapter, the reader should be able to:
1 Describe the pathophysiology, assessment, and management of pneumonia in
the critically ill patient.
2 Describe the pathophysiology, assessment, and management of acute

The Older Patient. The incidence of CAP requiring
hospitalization is four times higher in patients older
than 65 years than it is in those 45 to 64 years of
age.3 In addition, the cause of CAP in patients older
than 65 years is frequently a drug-resistant strain of
S. pneumoniae.2
227

Morton_Chap17.indd 227

2/4/2012 3:15:37 PM


228

P A R T F O U R Respiratory System

BOX 17-1

American Thoracic Society (ATS)
Criteria for Diagnosis of Severe
Community-Acquired Pneumonia
(CAP)

Major Criteria

• Need for mechanical ventilation
• Need for vasopressors for greater than 4 hours
(septic shock)
• Acute renal failure (urine output less than 80 mL in

or aspirated foreign material or the uncontrolled
multiplication of microorganisms invading the
lower respiratory tract. This response results in the
accumulation of neutrophils and other proinflammatory cytokines in the peripheral bronchi and alveolar spaces.6 The severity of pneumonia depends on
the amount of material aspirated, the virulence of
the organism, the amount of bacteria in the aspirate, and the host defenses.6
The means by which pathogens enter the lower
respiratory tract include aspiration, inhalation,
hematogenous spread from a distant site, and translocation. Risk factors that predispose a patient to
one of these mechanisms include conditions that
enhance colonization of the oropharynx, conditions

Morton_Chap17.indd 228

favoring aspiration, conditions requiring prolonged
intubation, and host factors.6 The risk for clinically
significant aspiration is increased in patients who
are unable to protect their airways.
Colonization of the oropharynx has been identified
as an independent factor in the development of HAP
and VAP. Gram-positive bacteria and anaerobic bacteria normally live in the oropharynx. When normal
oropharyngeal flora are destroyed, the oropharynx is
susceptible to colonization by pathogenic bacteria.
Pathogenic organisms that have colonized the oropharynx are readily available for aspiration into the
tracheobronchial tree. Gastric colonization may also
lead to retrograde colonization of the oropharynx,
although the role the stomach plays in the development of pneumonia is controversial. The stomach
is normally sterile because of the bactericidal activity of hydrochloric acid. However, when gastric pH
increases above normal (eg, with the use of histamine
type 2 antagonists or antacids), microorganisms are

thromboembolism, drug reactions, pulmonary
hemorrhage, and ARDS.

Diagnostic tests are ordered to determine whether
pneumonia is the cause of the patient’s symptoms
and to identify the pathogen when pneumonia is
present. Table 17-1 summarizes the current ATS

2/4/2012 3:15:39 PM


Common Respiratory Disorders C H A P T E R 1 7

229

Studies in Patients With Severe Community-Acquired Pneumonia (CAP) or Severe
TA B LE 17- 1 Diagnostic
Hospital-Acquired Pneumonia (HAP)
Study

Rationale

Chest radiograph (anterior–posterior and lateral)

Identifies the presence, location, and severity of infiltrates
(multilobar, rapidly spreading, or cavitary infiltrates indicate
severe pneumonia)
Facilitates assessment for pleural effusions
Differentiates pneumonia from other conditions
Isolates the etiologic pathogen in 8%–20% of cases

as bronchoalveolar lavage (BAL) or bronchoscopy
with protected specimen brush (PSB), may be
used in selected circumstances (eg, nonresponse
to antimicrobial therapy, immunosuppression, suspected tuberculosis in the absence of a productive
cough, pneumonia with suspected neoplasm or foreign body, or conditions that require lung biopsy).4
Pneumococcal urinary antigen assay, which returns
results within 15 minutes, is recommended as an
addition to blood culture testing.7 The IDSA recommends HIV testing for people between the ages of
15 and 54 years as well.7

need to modify therapy.4 The duration of therapy
depends on many factors, including the presence
of concurrent illness or bacteremia, the severity of
pneumonia at the onset of antibiotic therapy, the
causative organism, the risk for multidrug resistance, and the rapidity of clinical response.4

Management

Acute Respiratory Failure

Antibiotic Therapy

Acute respiratory failure is a sudden and life-threatening deterioration in pulmonary gas exchange,
resulting in carbon dioxide retention and inadequate
oxygenation. Acute respiratory failure is defined as
an arterial oxygen tension (PaO2) of 50 mm Hg or less,
an arterial carbon dioxide tension (PaCO2) greater
than 50 mm Hg, and an arterial pH less than 7.35.
Patients with advanced COPD and chronic hypercapnia may exhibit an acute increase in PaCO2 to a
high level, a decrease in blood pH, and a significant


BOX 17-2

Causes of Acute Respiratory Failure

Intrinsic Lung and Airway Diseases
Large Airway Obstruction

• Congenital deformities
• Acute laryngitis, epiglottitis
• Foreign bodies
• Intrinsic tumors
• Extrinsic pressure
• Traumatic injury
• Enlarged tonsils and adenoids
• Obstructive sleep apnea
Bronchial Diseases

• Chronic bronchitis
• Asthma
• Acute bronchiolitis
Parenchymal Diseases

• Pulmonary emphysema
• Pulmonary fibrosis and other chronic diffuse infiltrative diseases
• Severe pneumonia
• Acute lung injury (ALI), acute respiratory distress
syndrome (ARDS)
Vascular Disease


• Trauma, including surgery
• Neuromuscular abnormalities
• Allergic disorders: bronchospasm
• Increased oxygen demand: fever, infection
• Inspiratory muscle fatigue

Morton_Chap17.indd 230

• Thoracic wall deformity
• Traumatic injury to the chest wall (flail chest)
• Obesity
Disorders of the Respiratory Muscles and the
Neuromuscular Junction

• Myasthenia gravis and myasthenia-like disorders
• Muscular dystrophies
• Polymyositis
• Botulism
• Muscle-paralyzing drugs
• Severe hypokalemia and hypophosphatemia
Disorders of the Peripheral Nerves and Spinal
Cord

• Poliomyelitis
• Guillain–Barré syndrome
• Spinal cord trauma (quadriplegia)
• Amyotrophic lateral sclerosis
• Tetanus
• Multiple sclerosis
Disorders of the Central Nervous System

hypercapnia.8

2/4/2012 3:15:40 PM


Common Respiratory Disorders C H A P T E R 1 7

• Combined hypoxemic and hypercapnic respiratory failure (type I and type II). The combined
type of acute respiratory failure develops as a consequence of inadequate alveolar ventilation and
abnormal gas transport. Any cause of type I failure
may lead to combined failure, especially if increased
work of breathing and hypercapnia are involved.

Pathophysiology
A vicious positive feedback mechanism characterizes
the deleterious effects of continued hypoxemia and
hypercapnia. Mechanisms of hypoxemia in acute
respiratory failure are summarized in Table 17-2.
Effects of prolonged hypoxemia and hypercapnia
include
•
•
•
•
•
•
•

Increased pulmonary vascular resistance
Right ventricular failure (cor pulmonale)

Other diagnostic tests that may be ordered to aid
in determining the underlying cause may include
chest radiography, sputum examination, pulmonary
function testing, angiography, ventilation–perfusion
scanning, computed tomography (CT), toxicology
screening, complete blood count, serum electrolytes, cytology, urinalysis, bronchogram, bronchoscopy, electrocardiography, echocardiography, and
thoracentesis.8 Table 17-3 summarizes key clinical
findings and diagnostic tests according to the underlying cause of the respiratory failure.

Management
Treatment of acute respiratory failure warrants
immediate intervention to correct or compensate
for the gas exchange abnormality and identify the
cause. Therapy is directed toward correcting the
cause and alleviating the hypoxia and hypercapnia
(see Table 17-3).
If alveolar ventilation is inadequate to maintain
PaO2 or PaCO2 levels (due to respiratory or neurological

TA B LE 17- 2 Mechanisms of Hypoxemia in Acute Respiratory Failure
Mechanism

Comments

Ventilation–perfusion mismatching (“dead space”)

Resultant hypoxemia is reversible with supplemental
oxygen
Oxygen content of inhaled gas is decreased