Module 2: Respiratory Disorders: Respiratory Failure & Acute Respiratory

Distress Syndrome (ARDS)

Respiratory Failure
Etiology/Pathophysiology
1. Respiratory system as it relates to acute respiratory failure.
a. Major function of the respiratory system is gas exchange
(oxygen and carbon dioxide) between atmosphere and blood.
(Lewis 1800 Fig 68-1)
b. ABG analysis
1) Is the pH normal? (7.4; range 7.35-7.45)
2) Is the PaCO2 normal? (40; range 35-45 mmHg)
3) Is the PaHCO3 normal? (24; range 22-26 mEq/L)
4) Match the PaCO2 or PaHCO3 with the pH.
5) Does the PaCO2 or the PaHCO3 go the opposite
direction of the pH?
6) Are the PaO2 (80-100 mmHg) and the O2 saturation
(95-100%) normal?
c. Example of analysis:
1) Look at the pH. Normal blood pH is 7.4 plus or minus
0.05, forming a normal range of 7.35 to 7.45. If blood
pH falls below 7.35 it is acidotic. If the blood pH rises
above 7.4, it is alkalotic. If it falls into the normal range,
label what side of 7.4 it falls on. Lower than 7.4 is
normal/acidotic, higher than 7.4 is normal/alkalotic.
Label it _____.
2) Look at PaCO2. Normal PaCO2 levels are 35-45 mmHg.
Below is alkalotic, above is acidotic.
Label it ____.
3) Look at PaHCO3 levels. A normal PaHCO3 level is 22-26
mEq/L. If the HCO3 is below 22, the patient is acidotic.
If the HCO3 is above 26, the patient is alkalotic.
Label it _____.
4) Match either the CO2 or the HCO3 with the pH to
determine the acid-base disorder. For example, if the pH
is acidotic, and the CO2 is acidotic, then the acid-base
disturbance is being caused by the respiratory system,
respiratory acidosis. However if the pH is alkalotic and
the HCO3 is alkalotic, the acid-base disturbance is being
caused by the metabolic (or renal) system. Therefore,
metabolic alkalosis.
5) Does either the CO2 or HCO3 go in the opposite
direction of the pH? If so, there is compensation by that
system. For example, the pH is acidotic, the CO2 is
acidotic, and the HCO3 is alkalotic. The CO2 matches
the pH making the primary acid-base disorder

RNSG 2432 19

d.

e.

f.
g.
h.

i.
j.

respiratory acidosis. The HCO3 is opposite of the pH and

would be evidence of compensation from the metabolic
system.
6) Evaluate the PaO2 and the O2 sat. If they are below
normal there is evidence of hypoxemia.
Optional blood gas review sites:
http://www.austincc.edu/adnlev2/rnsg1443online/fluid_electroly
tes_acid_base/abg7a7.html
http://www.m2hnursing.com/ABG/casestudy1.php
Respiratory volume and capacity
1) Tidal volume- amount of air (500ml) moved in and out
of the lungs with each normal breath
2) Inspiratory reserve volume- amount of air (2100-3100
ml) that can be inhaled forcibly over the tidal volume
3) Expiratory reserve volume- air (1000 ml) that can be
forced out over the tidal volume
4) Residual volume- air (110 ml) that remains in the lungs
after forced expiration
5) Vital capacity is the sum of TV + IRV + ERV (4500 ml)
6) Anatomical dead space- air that never reaches the
alveoli still in passageways (150 ml)
Respiratory failure results when one or both of the gas
exchanging systems are inadequate- in the atmosphere (lungalveolus) or blood (pulmonary capillary, vein, artery)
Respiratory failure is not a disease.
Predisposing factors (Lewis 1746 Table 68-2)
1) Airways and alveoli
2) CNS
3) Chest wall
4) Neuromuscular
Respiratory failure is commonly defined in terms of the arterial
blood gases- PaO2 of less than 60 mmHg; PaCO2 of greater
than 45 mmHg and arterial pH of less than 7.35
A PaO2 of 60 mg Hg is minimally adequate to meet oxygen
needs of the bodys tissues

k. Respiratory failure can be classified as hypoxemic or

hypercapic (Lewis 1800 Fig 68-2; Table 68-1) Can be acute (min
to hrs) or chronic (days or longer)
1) Hypoxemic Respiratory Failure:
a) Oxygenation failure- inadequate O2 transfer
between the alveoli and the pulmonary capillary
bed
b) PaO2 of 60 mm Hg or less on 60% O2 (3Xs room
air)
c) Inadequate O2 sat of hemoglobin
d) Common causes: Disorders that interfere with O2
transfer into the blood (respiratory): pneumonia,

20 RNSG 2432

pulmonary edema; lung damage related to alveolar

injury as with a ventilator and (cardiac) low cardiac
output states as heart failure and shock. (Lewis
1800 Table 68-1)
e) Mechanisms that may lead to hypoxemia and
respiratory failure (Lewis 1747Fig 68-3;68-4; 68-5)
1) Mismatch between ventilation and perfusion
(V/Q mismatch)
(a)
Volume of blood perfusing the lungs each
minute is approximately equal to the
amount of gas that reaches the alveoli each
minute (4-5 L). Each portion of the lung
would receive about 1 ml of air for each 1 ml
of blood. 1:1= V/Q ratio of 1.
(b)
Diseases/conditions that alter overall V/Q
mismatch
(1) Ventilation portion blocked: increased
secretions in airways (COPD), secretions in
alveoli (pneumonia); or when
bronchospasm present (asthma) Other:
alveolar collapse (atelectasis) or unrelieved
pain (decreased movement
chest/ventilation, etc)
(2) Perfusion portion blocked: pulmonary
embolus blocking the blood flow causing
the V/Q mismatch
(c) First treat with O2 to reverse hypoxemia &
then treat cause
2) Shunt (Lewis 1747, Fig 68-4)
(a) Occurs when blood leaves the heart without
gas exchange
(b)
Extreme V/Q mismatch
(c)
Two types: anatomic shunt as a
ventricular septal defect where blood
does not pass through the lungs; or
intrapulmonary shunt where the alveoli
fill with fluid (ARDS) and gas can not
exchange
(d)
Mechanical ventilation to force O2 into
lungs
3) Diffusion limitations
(a) Occurs when gas exchange across alveolarcapillary membrane cant occur because
alveoli membrane is thickened (fibrotic) or
destroyed (Lewis 1747 Fig 68-5)
(b)
Caused by pulmonary fibrosis, ARDS
(c)
Classic sign is hypoxemia that is present
during exercise but not at rest

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f. Clinical Manifestations of Hypoxemia (Lewis 1749

Table 68-3)

(1)

(2)

Specific:
a. Respiratory: Dyspnea; tachypnea;
prolonged expiration; intercostal muscle
retraction; use of accessory muscles in
resp;< 80% SpO2; paradoxic chest/abd
wall movement with resp cycle (late);
cyanosis (late)
Nonspecific:
a. Cerebral: agitation, disorientation,
delirium, restless, combative, confusion,
dec LOC, coma (late)
b. Cardiac: tachycardia, hypertension, skin
cool/clammy, dysrhythmias (late),
hypotension (late)
c. Other: fatigue; need to pause to breath
when speaking

g. Treatment of hypoxemia- treat cause, O2 and

mechanical ventilation
2. Hypercapnic Respiratory Failure:
a. Ventilatory failure- insufficient CO2 removal. PaCO2 greater
than 45 mm Hg arterial and pH less than 7.35.
b. There is an imbalance between ventilatory supply (maximum
ventilation without developing respiratory muscle fatigue) and
ventilatory demand (amount of ventilation needed to keep the
PaCO2 within normal limits)
c. Normally supply exceeds demand- so that one can increase
exercise which increases CO2 production without an elevation
PaCO2
d. With preexisting lung disease, as COPD, do not have this ability
and cannot increase lung ventilation in response to exercise or
metabolic demands.
e. When ventilator demand does exceed ventilator supply, the
PaCO2 can no longer be sustained within normal limits and
hypercapnia occurs.
f. Hpercapnia respiratory failure is sometimes called ventilatory
failure because primary problem is the inability of the
respiratory system to ventilate out sufficient CO2 to maintain
normal PaCO2
g. Four categories of causes (Lewis p 1745 Table 68-1)
1) Abnormalities of the airways and alveoli (asthma, COPD,
cystic fibrosis)
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2) Abnormalities of the CNS (overdose depressant drug,

brainstem infart/dysfunction, metabolic causing dec LOC
to interfere swallow/airway block, SCI resp musclesdiaphragm/chest wall muscles)
3) Abnormalities of the chest wall (pain, mechanical
restriction, muscle spasm, kyphoscoliosis, obesity,
weight of chest and abdomen contents limit lung
expansion)
4) Neuromuscular conditions (Resp muscle weakness or
paralysis, Guilain-Barre syndrome, MD, MG, MS.
h. Clinical manifestations (Lewis 1749 Table 68-3)
1) Specific: Respiratory: Dyspnea, Decrease resp rate or
increase rapid rate with shallow resp, Decrease Tidal
volume, Decrease minute ventilation
2) Nonspecific:
a) Cerebral: AM headache, disorientation, progressive
sommolence, coma (late)
b) Cardiac: dyshythmias, hypertension, tachycardia,
bounding pulse
c) Neuromuscular: muscle weakness, decrease deep
tendon reflexes, tremor/seizures (late)
i. Treatment
1) Major goal is maintaining adequate oxygenation and
ventilation
2) Oxygen therapy
3) Mobilization of secretions
4) Positive pressure ventilation (PPV)
5) Drug therapy- relief of bronchospasm, Dec airway
inflammation, pulmonary congestion, treatment of
pulmonary infections, red severe anxiety, pain, agitation
6) Medical teat underlying cause, maintain adeq CO, adeq
hemoglobin concentration.
7) Nutritional therapy- protein and energy stores
Clinical Manifestations/Complications of Respiratory Failure
1. Consequences of hypoxemia
a. Can lead to hypoxia
b. Cells shift from aerobic to anaerobic metabolism> lactic acid
buildup> metabolic acidosis>cell death
c. Heart and CNS affected> others
d. O2 deprived> Brain and renal damage
2. Specific clinical manifestations (see above & Lewis 1804 Table 68-3)
Collaborative Care for Respiratory Failure
1. Diagnostic studies (Lewis p1806 Table 68-5)

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a. H&P, ABGs, Pulse ox, Chest X-ray, CBC, electrolytes, ECG,

hemodynamic monitor/pulmonary function tests
b. V/Q scan- if pulmonary embolism suspected
2. Respiratory Therapy (Lewis p1752 Table 68-5)
a. Oxygen Therapy (PaO2 at least 60mm Hg/SaO2 90%)
b. Mobilization of secretions
1) Effective coughing and positioning (HOB up)
2) Hydration and humidification
3) Chest physical therapy
4) Airway suctioning
c. Positive pressure ventilation- intubation with mech ventilation
3. Artificial Airways (Lewis 1699-1703)
a. Endotracheal tubes (Lewis 1699 Fig 66-16)- oral & nasal
b. Maintaining correct tube placement (Lewis 1699 Fig 66-17)
c. Maintaining proper cuff inflation
d. Monitoring oxygenation and ventilation
e. Maintaining tube placement (Lewis 1701 Fig 66-18)
f. Providing oral care and maintaining skin integrity
g. Fostering comfort and communication
h. Complications of endotracheal intubation
4. Mechanical Ventilation- (Lewis 1703-1713)
a. To assist with breathing; to provide for adequate gas exchange
for tissue perfusion.
b. Criteria to put on ventilator: respiratory rate> 35-45; pCO2 >
45; pO2 <50.
c. Types of ventilators
1) Negative pressure ventilators create subatmosheric
pressure externally to draw chest outward and air into
lungs Example: Iron lung. Not commonly used.(Lewis
1704 Fig 66-20)
2) Positive pressure ventilators (Lewis 1704 Fig 66-21)
forces air into lungs under positive pressure. Must be
connected to an artificial airway- endotrachael tube or
tracheotomy.
d. Settings for Mechanical ventilation (Lewis 1705 Table 66-10)
1) Respiratory rate (f)
2) Tidal Volume (Vt)
3) Oxygen concentration (FIO2)
4) Positive end-expiratory pressure (PEEP)
5) Pressure support
6) I:E ratio
7) Inspiratory flow rate and time
8) Sensitivity
9) High pressure limit
10) Alarm settings- When alarm sounds- always assess the
patient first. The alarm will sound when patient
disconnects from ventilator or with tube, airway, or chest
tube leaks causing low pressure; the alarm sounds when

24 RNSG 2432

high pressure is sensed as by patient coughing, secretions

or mucus in the airway, patient biting the tube, airway
problems, reduced lung compliance as in a
pneumothorax, increased airway resistance, patient
fighting the ventilator, accumulation of water in the tube,
kinking in the tube, or problems with inspiratory or
expiratory valves
e. Modes of mechanical ventilation (Lewis 1706 Table 66-12)
1) Volume ventilation- Predetermined tidal volume is
delivered with each inspiration. Tidal volume is consistent,
airway pressures will vary.
a. AMV-Assisted Mandatory Ventilation: sensitivity set so
when pt initiates a spontaneous breath, a full-volume
breath is delivered
b.SIMV-Synchronized Intermittent Mandatory VentilationIn between mandatory breaths pt can spontaneously
breath at own rate and Tidal Vol
2) Pressure ventilation- Predetermined peak inspiratory
pressure. Tidal volume will vary, airway pressures will be
constant
a. PSV- Pressure support Ventilation: provides an
augmented inspiration(pressure) to a spontaneously
breathing patient.
3) Other ventilator modes:
a. PEEP- Positive End-Expiratory Pressure: positive
pressure maintained at the end of expiration to keep the
alveoli from collapsing, improving functional residual
capacity. Used with other modes on the ventilator.
Improves oxygenation while limiting risk of O2 toxicity.
b. CPAP-Continuous Positive Airway Pressure: similar to
PEEP, pressure in CPAP is delivered continuously. Prevents
airway pressure from falling to zero. Can give by
noinvasive (mask) or ETube. Freq used for sleep apnea.
f. *Complications of Positive Pressure ventilation (Lewis p.
1) Cardiovascular System: decreased CO, inc intrathoracic
pressure
2) Pulmonary System: barotraumas, volutrauma, alveolar
hypoventilation/hyperventilation, ventilator-associated
pneumonia
3) Sodium and water imbalance (dec CO cause dec renal
function- rennin release inc ADH)
4) Neurological system: impaired cerebral blood flow>IICP
5) Gastrointestinal system: stress ulcer/GI bleed, gas,
contipation
6) Musculoskeletal system: decreased muscle tone,
contractractures, footdrop, pressure ulcers from bedrest
7) Psychosocial needs: physical & emotional stress, fight
ventilator (breath against the ventilation breath)

RNSG 2432 25

g. Nursing Care for Ventilator complications:

1) Cardiovascular: monitor BP and arterial pressures, CO,
capillary refill, HR and rythum
2) Pulmonary: monitor trach/endo cuff inflation, ventilator
settings, ABGs
3) Sodium/water: monitor lab and IVs
4) Neurologic: elevate head of bed, keep body in alignment
5) Gastrointestional: set up schedule for BM, admin
laxatives, nutrition- tube feeding
6) Musculoskeletal: passive & active ROM, turn q2hrs, keep
body in alignment
8) Psychosocial: Need for information, regain control, hope
trust. Involve in decision making, medications for
sedation (Proplfor), analgesia (fentanyl), neuromuscular
blocking agents (Nimbex)
h. Machine disconnection or malfunction
i. Nutrition needs when on a ventilator
j. Weaning from positive pressure ventilation and extubation
(Lewis 1712, Table 66-13)
1) Weaning readiness
2) Assessment- be sure to compare with the baseline ABGs
3) Spontaneous Breathing Trials (SBT)- where the individual
is removed from the vent and assessed for ability to
breathe on own (Refer to specific Hospital protocol)
4) Table 66-13 p.1712-readiness/assessment
5. Drug Therapy
a. Relief of bronchospasm, such as albuterol
b. Reduction of airway inflammation, as corticosteroids
c. Reduction of pulmonary congestion, as Lasix
d. Treatment of pulmonary infections, as antibiotics
e. Reduction of severe anxiety, pain, and agitation, as Ativan,
fentanyl
6. Medical Supportive Therapy
a. Treating the underlying cause
b. Maintaining adequate cardiac output
c. Maintaining adequate hemoglobin concentration
7. Nutritional Therapy
a. Enteral nutritional support
b. Parenteral
Nursing Assessment Specific to Respiratory Failure
1. Subjective data (Lewis p.1751 Table 68-4)
b. Health information
c. Functional health patterns
2. Objective data (Lewis p.1751 Table 68-4)
a. General
b. Integumentary
c. Respiratory

26 RNSG 2432

d.
e.
f.
g.

Cardiovascular
Gastrointestinal
Neurologic
Other findings- labs, chest X-ray, wedge pressure changes

Relevant Nursing Problems related to Respiratory Failure (Nursing

Care Plans)
1. Prevention of acute respiratory failure
a. Identify patients at risk
b. Initiation of appropriate nursing interventions- respiratory care,
teaching, hydration, nutrition
2. Nursing Care plans Patient with Acute Respiratory Failure (Lewis p
1807-09)
a. Impaired gas exchange
b. Ineffective airway clearance
c. Ineffective breathing pattern
d. Risk for fluid volume imbalance
e. Imbalanced nutrition: less than body requirements
3. Gerontology considerations
4. Nursing Care Plans- patient Mechanical Ventilation (Lewis 1754-56 NCP
66-1)
5. Suctioning Procedure- patient on mechanical ventilator (Lewis 1701
Table 66-8)
6. Oral care procedures- patient on mechanical ventilator (Lewis 1702
Table 66-9)
Adult Respiratory Distress Syndrome (ARDS)
Etiology/Pathophysiology of ARDS
1. Normal respiratory system as it relates to ARDS.
a. Millions of alveoli provide surface for gas exchange by diffusion
to the pulmonary capillaries.
b. Alveolar walls contain cells that secrete surfactant-containing
fluid. Surfactant reduces the surface tension of the alveolar fluid
to help prevent collapse of the lungs.
c. Intrapulmonary pressure is the pressure within the alveoli. It
rises and falls with respiration.
d. Lung compliance is the ability of the lungs to distend. It depends
on the elasticity of the lung tissue and the flexibility of the rib
cage. Compliance is also decreased by blockage of the
respiratory pathway.
e. Lung elasticity is essential for lung distention during inspiration
and lung recoil during expiration.
2. ARDS is a syndrome where there is sudden and progressive acute
respiratory failure. The alveolar capillary membranes become damaged

RNSG 2432 27

3.
4.
5.
6.
7.

and are more permeable to intravascular fluid resulting in* noncardiac

pulmonary edema and progressive refractory hypoxemia.
Used to be known as Adult Respiratory Distress Syndrome, Shock lung
Causes- ARDS is not primary, but may follow various pulmonary or
systemic conditions.
Sepsis is the most common cause.
Conditions predisposing to ARDS (Lewis p1757 Table 68-6)
a. Direct lung injury- such as aspiration of GI contents, pneumonia
b. Indirect lung injury- such as sepsis, severe massive trauma
Phases of ARDS (Lewis p1756 Fig 68-8 ;p1747 Fig 68-4)
a. Injury or exudates phase
1) Occurs 24-48 hrs post direct or indirect injury
2) This *causes a systemic inflammatory response and
damage to the alveolar-capillary membrane. Increased
capillary permeability
3) Fluid then enters the alveoli, which dilutes and deactivates
surfactant. Surfactant is needed to maintain alveoli
compliance (ability of alveoli membrane to stretch) As
surfactant is lost, the alveoli stiffen and collapse
4) Interstitial and alveolar edema and atelectasisnoncardiogenic pulmonary edema.
5) Intrapulmonary shunt develops because increased alveolar
fluid- no gas exchange
6) Hypoxemia becomes refractory and resistant to
improvement even with supplemental oxygen.
b. Reparative or proliferative phase
1) 1-2 weeks post initial insult
2) Inflammatory response can aide with regeneration of the
lung tissue
3) Fibrin and cell debris from necrotic cells combine to form
hyaline membranes and lungs become fibrotic
4) CO2 cannot diffuse across hyaline membranes; PCO2 rise
leading to respiratory acidosis
5) Phase complete when diseased lung is dense, fibrous
tissue
6) If reparative phase is arrested, the lesions may resolve
c. Fibrotic phase
1) 2-3 weeks post initial lung insult
2) Chronic or late phase
3) Diffuse scarring and fibrosis- decrease lung compliance
4) Decrease surface area for gas exchange- hypoxemia
continues.
5) Pulmonary hypertension results
6) Metabolic acidosis can occur leading to multiple organ
system dysfunction (MOSD) with ensuing death

Clinical Manifestations of ARDS

1. Clinical progression

28 RNSG 2432

a. Insidious onset- symptoms develop 24-48 hrs post initial insult.

b. Course determined by nature of initial injury, extent and
severity of coexisting disease, and pulmonary complications
c. 50% of the individuals who develop ARDS die even with
aggressive treatment.
2. Clinical manifestations
a. Progressive *Refractory hypoxemia (hallmark sign) -not
improved by giving O2.
b. Noncardiac pulmonary edema
c. Early symptoms: labored respirations- dyspnea, tachypnea,
anxiety and restlessness, and dry, non productive cough.
d. Later symptoms: cyanosis, adventitious breath sounds, use of
accessory muscles with retractions and decrease in mental
status.
3. Diagnosis
a. Chest X-ray with bilateral infiltrates (white-out; snow storm
effect)
b. Pulmonary artery wedge of 18 mm Hg or less with no evidence
of heart failure
c. Assess for a predisposing condition for ARDS occurring within
48 hrs of clinical manifestations
Complications of ARDS
1. Hospital-acquired pneumonia
2. Barotrauma
3. Volu-pressure trauma
4. Physiologic stress ulcers
5. Renal failure
Collaborative Care of ARDS
1. Respiratory therapy
a. Oxygen Administration
b. Mechanical ventilation (Lewis 1705)
1) *Main treatment for ARDS
2) To maintain PO2>60 mm Hg and O2 sat >90%
3) To support respiratory function while the underlying
problem is identified and treated
4) May need neuromuscular blocking agents and sedation to
tolerate mechanical ventilation. Neuromuscular blocking
agents paralyze the patient so that he does not fight or
blow against the ventilators efforts.
5) *Also refer to above notes regarding Mechanical
ventilation in Respiratory Failure section.
c. Positioning strategies1) *Proning (Lewis 1761 Fig 68-11) With change to prone,
previously nondependent air-filled alveoli become
dependent, perfusion becomes greater to air-filled alveoli

RNSG 2432 29

opposed to previously fluid-filled dependent alveoli,

thereby improving ventilation-perfusion matching.
2) CLRT continuous lateral rotation therapy (Lewis 1761 Fig
68-12)
2. Medical supportive therapy
a. Maintenance of cardiac output and tissue perfusion--1) Hemodynamic monitoring: arterial catheter for BP and
ABGs; pulmonary artery pressure/wedge pressure; SvO2
and CO monitoring
2) Assess PEEP effect on CO
3) Hemoglobin level 9 or more with O2 sat of 90%
b. Maintenance of nutrition and fluid balance
1) Parenteral or enteral feedings to meet energy demands
2) Monitor fluid status- concern for pulmonary edema
d. Treat underlying cause
Nursing Assessment Specific to ARDS
1. ARDS is a cause of respiratory failure-refer to assessment
2. Assess for clinical progression and clinical manifestations as discussed
above.
Relevant Nursing Problems related to ARDS
1. Nursing Care plans (Similar to Respiratory Failure)
2. Goals for recovery from ARDS:
a. PaO2 within normal limits for age or baseline values on room air
(FIO2 of 21%)
b. SaO2 greater than 90%
c. Patent airway
d. Clear lungs on auscultation

30 RNSG 2432