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Module 2: Respiratory Disorders: Respiratory Failure & Acute Respiratory
Distress Syndrome (ARDS)
Marnie Quick, RN, MSN, CNRN
Respiratory Failure
Etiology/Pathophysiology
1. Normal respiratory system as it relates to respiratory failure.
a. 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?
b. 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 acidbase 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
respiratory acidosis. The HCO3 is opposite of the pH and
RNSG 2432  23
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.
7) For further ABG review and case studies visit:
http://www.maagnursing.com/ABG
c. 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)
2. Respiratory failure
a. Not a disease process, but a sign of severe dysfunction of the
respiratory system.
b. Lungs are unable to oxygenate blood and remove carbon
dioxide.
c. Alveolar ventilation is inadequate to meet the body’s needs.
d. Commonly defined in terms of the arterial blood gases- PO2 of
less than 50 mmHg; PCO2 of greater than 50 mmHg and
arterial pH of less than 7.35
e. Respiratory failure and its affect on acid-base balance:
1) Hypoxemia respiratory failure is a failure of
oxygenation. The PO2 is significantly reduced and the
PCO2 is at or below normal. Metabolic acidosis results
from tissue hypoxia- build up waste products such as
lactic acid
2) Hypercapnia respiratory failure results from
hypoventilation. The PCO2 rises rapidly and respiratory
acidosis develops. The PO2 drops more slowly.
f. Classified as acute or chronic respiratory failure depending on
how fast it develops.
3. Causes of respiratory failure: (p. 1157 Table 36-13 & Fig 36-19)
a. Impaired ventilation
1) Airway obstruction- aspiration, obstruction as foreign
body, laryngospasm, or airway edema.
2) Respiratory disease- asthma, COPD
3) Neurologic causes- spinal cord injury, drug overdose
4) Chest wall injury- flail chest, pneumothorax
b. Impaired diffusion
1) Alveolar disorders- pneumonia, COPD
2) Pulmonary edema- ARDS, heart failure, near-drowning
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c. Ventilation-perfusion mismatch (VQ) (p. 1116 Figure 36-12)
1) Where the ratio of pulmonary alveolar ventilation to
pulmonary capillary perfusion is affected. Example,
pulmonary embolism.
2) A shunt is an extreme mismatch. Inadequate
oxygenated blood being perfused throughout the body
4. COPD is the most common cause of respiratory failure
Common Manifestations/Complications of Respiratory Failure
1. Hypoxemia
a. Dyspnea with retractions, tachypnea to compensate
b. Cardiac output increases to bring oxygen to tissues which
results in tachycardia and hypertension to compensate (this also
keeps CO2 at normal)
c. Neurological symptoms- restlessness, confusion, apprehension,
impaired judgment, confusion, motor impairment
d. Cyanosis
e. Later dsysrhythmias, metabolic acidosis and decreased BP and
CO
f. Hypoxemia is slow to develop and responds well to oxygen
administration (unless gas exchange also impaired).
g. Severe hypoxia PaO2 is less than 40 mmHg
2. Hypercapnia
a. Early signs are dyspnea with retractions and headache
b. Papilledema
c. Drowsiness, coma.
d. Tachycardia, hypertension
e. Systemic vasodilatation, heart failure
f. Respiratory acidosis
g. As hypercapnia worsens with increased CO2 and H+ ion
concentrations, it causes the respiratory center to become
depressed to a point where the respiratory center is not
stimulated, which then causes slowing respirations and reduced
dyspnea.
h. Hypoxia becomes the only active breathing stimulus, so need
ventilatory support with oxygen to prevent respiratory arrest.
3. Underlying disease process symptoms (p.1157 Table)
Therapeutic Interventions for Respiratory Failure
1. Diagnostic tests
a. Arterial blood gases (ABG’s) may show hypoxemia, carbon
dioxide retention, pH changes- acid-base disturbances.
b. Exhaled carbon dioxide (ETCO2) - evaluate alveolar ventilation.
N= 35-45. Elevated when ventilation is inadequate, and
decreased when pulmonary perfusion is impaired.
c. Chest X-ray, EEG, hemodynamic monitoring, sputum for C&S
2. Main treatment is to correct the underlying cause of the respiratory
failure and restore adequate gas exchange in the lung.
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3. Elevate head at least 45 degrees to increase chest expansion and
move fluid from chest into more dependent areas
4. Medications
a. To relieve symptoms and treat underlying cause of respiratory
failure
b. To relieve symptoms
c. Beta-adrenergic or antichloinergic by inhalation- brochodilation
d. Corticosteroids to reduce airway edema by inhalation or IV
d. Antibiotics to treat infection
e. Neuromuscular blockers for individual on ventilator (p. 1159
Box) (Tracrium, Pavulon) To prevent ‘fighting’ against the vent.
f. Medication to control pain/anxiety associated with ventilators.
(Morphine, Versed, Fentanyl)
5. Oxygen therapy
a. Oxygen saturation of 90% without oxygen toxicity
b. A PaO2 of 60 mg Hg is usually adequate to meet oxygen needs
of the body’s tissues
c. O2 by nasal cannula, by tight fitting mask, CPAP (to open closed
alveoli, improve ventilation-perfusion relationship)
6. Airway management- Endotracheal tube (p1159 Figure 36-20; p1160
Table 36-14; p1167 Procedure 36-2) and Tracheotomy
a. Intubation is necessary if upper airway is obstructed or positive
pressure mechanical ventilation is necessary
b. Endotracheal tube extends from mouth or nose to trachea an
has cuff which when inflated obstructs airway, prevent escape of
air: cuffs are low pressure to decrease likelihood of tissue
ischemia
c. If long-term ventilatory support is needed, tracheotomy is done:
associated risks include cuff necrosis and infection
d. Risk of respiratory distress and laryngeal edema post
extubationMust have gag, cough, swallow reflexes
7. Mechanical ventilation- to assist with breathing; to provide for
adequate gas exchange for tissue perfusion. Criteria to put on
ventilator: respiratory rate> 35-45; pCO2 > 45; pO2 <50.
8. Types of ventilators:
a. Negative pressure ventilators create subatmosheric pressure
externally to draw chest outward and air into lungs Example:
Iron lung. Not commonly used.(p. 1160 Fig 36-21)
b. Positive pressure ventilators (p. 1162 Fig 36-22)
1) Forces air into lungs under positive pressure
2) Must be connected to an artificial airway- endotracheal
tube or tracheotomy.
3) Trigger: prompts ventilator to deliver breath
a) Patient’s inspiratory effort: ventilator-assisted
breath
b) Preset time: ventilator-controlled breath
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4)
Cycle: duration of inspiration
a) Preset volume delivered: volume controlled
ventilator.
b) Preset pressure achieved in airway: pressurecycled ventilator
c) Preset inspiratory flow rate: flow-cycled
ventilator
d) Set time interval: time-cycled ventilator.
9. Modes for ventilators (p. 1162 Table 36-15) manner in which the
ventilator delivers breaths to the patient.
a. Controlled mandatory ventilation (CMV) delivers a preset tidal
volume at a preset rate regardless of patient’s inspiratory
efforts. It is used for those patients with no ventilatory effort.
Many anesthesia ventilators operate this way. Paralytic
medication may be given so that the patient does not ‘fight’
(breath against) the ventilator.
b. Synchronized intermittent mandatory ventilation (SIMV) delivers
a preset tidal volume at a set minimum rate that is synchronized
to the patient’s inspiratory effort. Allows the patient to breath
spontaneously between preset rate of ventilator breaths that is
coordinated with patients inspiratory efforts. If the patient
breaths over the minimum rate, the patient’s efforts will
determine the tidal volume. Breaths are synchronized to prevent
‘stacking’ of breaths (one breath on top of another), reducing
competition between patient and ventilator. This is the most
common ventilation currently used.
c. Pressure support ventilation (PSV) Ventilator assisted breaths
are delivered at a preset pressure whenever the patient makes
inspiratory effort; no mandatory breaths given by ventilator.
10. PEEP and CPAP
a. PEEP- Positive end-expiratory pressure. Positive pressure is
maintained at the end of expiration. The pressure at end
expiration keeps alveoli from collapsing. Used with one of the
other modes on the ventilator. Useful in treating ARDS. Causes
decrease in cardiac output.
b. CPAP- Continuous positive airway pressure. Applies positive
pressure to airways of patients during both inspiration and
expiration. Used to help maintain open airways and alveoli and
decreases work of breathing.
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11. Ventilator settings (p. 1163 Table 36-16)
a. Rate- number of breath per minute that the ventilator delivers;
is a number that is combined with mode (ie: ACMV of 12/min.
Usually lower rate with SIMV of 6/min)
b. Tidal volume- amount of air moved in and out of the lungs with
each normal breath. Often expressed in milliliters or liters (700
mL or 0.7 L)
c. Oxygen- FiO2 is fraction of inspired oxygen or oxygen percent;
is the amount of oxygen in the inhaled air from the ventilator; is
expressed as a decimal instead of a percent (FiO2 at .40) Goal
is to maintain an oxygen saturation of greater than 90%. Can
range form .21 (room air) to 1.00 (100% oxygen).
d. Inspiratory-Expiratory ration (I/E ratio) is the ratio of the time
involved in inspiration to the time involved in expiration. Usually
1: 1½ or 1:2.
e. Sighs- larger than normal breaths which inflate more alveoli and
help prevent atelectasis. Usually set at pre-set rate and volume.
f. Alarm sounds when patient disconnects from ventilator or with
tube, airway, or chest tube leaks causing low pressure; the
alarm sounds when 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
12. Complications of mechanical ventilation
a. Ventilation of only one lung from improper placement of
endotracheal tube into mainstream bronchus.
b. Nosocomial pneumonia
c. Barotraumas: alveoli rupture; subcutaneous emphysema (air in
subcutaneous tissue that can be palpated under skin of chest,
face, neck); pneumothorax (chest tube)
d. Cardiovascular effects: decreased cardiac output decreased
venous return to heart and ventricular filling, which can affect
liver and kidney circulation
e. Gastrointestinal effects: stress ulcer- erosive gastritis (histamine
receptor blockers); gastric distension from air leaking around ET
tube (NG tube to drainage); constipation from sedatives/pain
medication.
Nursing Assessment Specific to Respiratory Failure
1. Health history- history of previous respiratory problems, current
symptoms, precipitating factors
2. Physical exam- level of consciousness; vital signs; O2 sat; respiratory
assessment- accessory muscles, lung sounds; cardiac assessment;
evidence of clubbing
28  RNSG 2432
Pertinent Nursing Problems and Interventions
1. Impaired spontaneous ventilation
a. Assess VS, O2 sats, ABG’s, response to O2
b. High Fowlers to allow for full expansion of lungs
c. Conserve energy- ADL’s etc
d. Care of patient on ventilator
1) respiratory therapy monitors ventilator function, work
closely with them
2) evaluate and correct problem if alarms sound (see
above for causes) Never turn off ventilator alarms.
Always assess the patient not just the alarm!
3) assess oxygen saturation, pulmonary assessment
4) assess need for suction Use sterile technique. Inline
suction frequently used with ventilator so that don’t
have to disconnect patient from ventilator.(p. 1167)
5) emotional support as necessary
6) medications to :
Control anxiety: Valium/Ativan/Versed
Control pain: Morphine/Fentanyl
Prevent fighting of ventilator: neuromusclular
blocking agents to induce paralysis and suppress
ability to breath: Tracium/Pavulon
7) means of communication- paper, picture board,
alphabet board to spell out words
8) assess for complications of ventilator (see above)
9) weaning from ventilator- assess progression. Note VS,
O2 sats, ABG’s, etc.
e. Care of the patient with endotracheal and tracheostomy tubes.
(p. 1160 Table 36-14; p. 1167 Procedure 36-2)
2. Ineffective airway clearance
a. Assess respiratory status, VS, fluid balance
b. Suction as necessary
c. Perform percussion, postural drainage
3. Anxiety
a. Monitor
b. Educate regarding equipment- intubation, mechanical
ventilation- especially alarms
c. Allow for rest when possible
d. Family support
4. Home care
a. Discuss factors that precipitated respiratory failure
b. Measures to prevent
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Acute Respiratory Distress Syndrome (ARDS)
Etiology/Pathophysiology
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
and are more permeable to intravascular fluid resulting in noncardiac
pulmonary edema and progressive refractory hypoxemia.
3. Used to be known as Adult Respiratory Distress Syndrome, Shock lung
4. Causes- ARDS is not primary, but may follow various pulmonary or
systemic conditions. (p. 1169 Table 36-17; Fig 36-24)
5. Sepsis is the most common cause.
6. Pathophysiology: Stages (p. 1170-1171 Illustrations)
a. Initiation of ARDS
1) Acute lung injury resulting from an unregulated
systemic inflammatory response, which damages the
alveolar-capillary membrane
b. Onset of Pulmonary edema
1) increased interstitial pressure and damage to alveolar
membrane allow fluid to enter alveoli, which dilutes and
deactivates surfactant
2) surfactant is needed to maintain alveoli compliance
(ability of alveoli membrane to stretch)
c. Alveolar collapse
1) As surfactant is lost, the alveoli stiffen and collapse,
leading to atelectasis.
2) Lungs become less compliant and gas exchange
impaired
3) PO2 and PCO2 levels fall, tachypnea causes more CO2
to be expired
d. End-stage ARDS
1) Fibrin and cell debris from necrotic cells combine to
form hyaline membranes and lungs become fibrotic
2) CO2 cannot diffuse across hyaline membranes; PCO2
rise leading to respiratory acidosis
30  RNSG 2432
3)
Hypoxemia becomes refractory and resistant to
improvement even with supplemental oxygen.
4) Metabolic acidosis occurs leading to multiple organ
system dysfunction with ensuing death
Common Manifestations/Complications of ARDS
1. Symptoms develop 24-48 hrs after initial insult.
2. Early symptoms: labored respirations- dyspnea, tachypnea, anxiety
and restlessness, and dry, non productive cough.
3. Later symptoms: cyanosis, adventitious breath sounds, use of
accessory muscles with retractions and decrease in mental status.
4. Hallmark sign is progressive refractory hypoxemia- not improved by
giving O2. Noncardiac pulmonary edema
5. 50 % of the individuals who develop ARDS die even with aggressive
treatment.
6. If survive may have permanent loss of lung tissue and diminished vital
capacity. May have difficulty exercising or even difficulty performing
ADL’s for the remainder of his life.
Therapeutic Interventions for ARDS
1. Diagnostic tests
a. ABG’s- hypoxemia with PO2 < 60 mmHg; initially show
respiratory alkalosis due to hyperventilation and then
progresses to respiratory acidosis.
b. Chest X-ray- first normal progresses within 24 hrs to complete
‘white out’ or a ‘snow storm’ appearance due to bilateral diffuse
infiltrates.
c. Pulmonary function tests- decreased lung compliance, decrease
vital capacity (lung) and elevated peak inspiratory pressures
d. Hemodynamic monitoring with pulmonary artery catheter
shows the pulmonary capillary wedge pressure (PCWP) as
normal in ARDS as opposed to high in cardiogenic pulmonary
edema. Remember, the PCWP reflects the left side of the heart
and the problem in ARDS is ventilation/perfusion in the lungs
and not the heart.
2. Medications
a. No definite therapy.
b. Antibiotics used if infective process is present
c. Inhaled nitric oxide- improves oxygenation by dilating blood
vessels in nonaffected areas of the lungs.
d. Surfactant therapy- ARDS causes an inactivation of surfactant
and damages alveolar cells that produce it. Surfactant therapy
helps maintain open alveoli, improves compliance and gas
exchange- preventing atelectasis.
e. Non steroidal anti-inflammatory drugs (NSAIDS)
f. Corticosteroids are used late in course to stabilize cellular
membranes and decrease fluid shifts.
g. Mucolytics as mucomyst into the lungs to clear airway by
liquefying thick mucus for easier expectoration
RNSG 2432  31
3. Mechanical ventilation with intubation
a. Mainstay of treatment for ARDS.
b. To maintain PO2>60 mm Hg and O2 sat 90%
c. To support respiratory function while underlying problem is
identified and treated.
d. Use of PEEP to keep alveoli inflated on expiration and allows for
increase of oxygen into the lungs without increasing the FIO2
e. May need neuromuscular blocking agents and sedation to
tolerate mechanical ventilation. Neuromuscular blocking agents
paralyze the client so that he does not ‘fight’ or blow against the
ventilators efforts.
4. Correct underlying condition
5. Fluid replacement to keep intravascular volume. (assess with
hemodynamic monitoring/urine output)
6. Nutrition with a positive protein balance- for healing. Enteral or
parenteral feeding
7. Low-molecular-weight heparin to prevent thrombophlebitis, possible
pulmonary embolus or DIC.
8. ‘Proning’-Prone position may be attempted in individuals on maximal
mechanical ventilation with unresponsive hypoxemia. With position
change to prone, previously nondependent air-filled alveoli become
dependent, perfusion becomes greater to air-filled alveoli opposed to
previously fluid-filled dependent alveoli, thereby improving ventilationperfusion matching.
Nursing Assessment Specific to ARDS
1. Health history- assessing for underlying cause of ARDS.
2. Physical exam- Respiratory and cardiac status-(O2 sats, hemodynamic
monitoring, etc), level of consciousness, assess for complications.
Pertinent Nursing Problems and Interventions for ARDS
1. Decreased cardiac output
a. Ventilator and PEEP causes increase intrathoracic pressure,
which in turn decreases cardiac output.
b. Assess cardiac including PAWP, CVP, CO and respiratory status
including lung sounds, rate
c. Assess urine output (not less than 30 ml/hr)
d. Assess level of consciousness, skin, weight
2. Ineffective airway clearance; impaired tissue perfusion; imbalance
nutrition: less than body requirements; risk for infection
a. Maintain tissue oxygenation and ventilation, assist in the
treatment of the underlying cause, and prevent further organ
system damage
b. Monitor O2 saturation, provide suctioning, encourage coughing,
oral care, sedation as needed to tolerate mechanical ventilation,
and assess for complications of ventilator- especially
barotraumas from PEEP
32  RNSG 2432
c. Monitor effectiveness of treatment plan- vital signs, heart and
lung sounds, EKG rhythm, hemodynamic monitoring, urinary
output, and neurological status
d. Position patient for comfort; prone position; if supine elevate
head of bed; schedule activities to conserve energy
e. Assess nutritional needs
3. Dysfunctional ventilatory weaning response
a. Difficulty adjusting to reduced mechanical ventilation
b. Assess lung sounds; O2 sats; ABG’s
c. High Fowler’s position
d. Keep O2 at bedside
e. Emotional support
f. Limit activities during weaning process
g. Avoid drugs that may depress respirations
4. Home care
a. Need evaluate possible change life style, occupation
b. Avoid respiratory irritants
RNSG 2432  33
34  RNSG 2432