The document defines acute respiratory failure as abnormal gas exchange resulting from dysfunction of the respiratory system that is potentially life-threatening. It can be caused by issues in the lungs, chest wall, or central nervous system control of breathing. Signs include altered mental status, cyanosis, increased work of breathing, and abnormal blood gases. Diagnostic tests may include blood gases, chest x-ray, and pulmonary function tests. Risk factors include smoking, age, infection, and chronic lung disease. Treatment involves addressing the underlying cause, supplemental oxygen, bronchodilators, diuretics, and vasodilators. Nursing care focuses on monitoring respiratory status, clearing secretions, managing oxygen needs, and patient education.

1. ACUTE
PULMONARY
FAILURE
Prepared By:
BSN, Level IV
Sarah Jane A. Cristobal

2. DEFINITION
Acute respiratory failure occurs when
dysfunction of the respiratory system results in
abnormal gas exchange that is potentially life-
threatening. Each element of this definition is
important to understand. The term acute implies
a relatively sudden onset (from hours to days)
and a substantial change from the patient’s
baseline condition.

3. DEFINITION
Dysfunction of the respiratory system
indicates that the abnormal gas exchange may
be caused by abnormalities in any element of
the respiratory system (e.g., a central nervous
system abnormality affecting the regulation of
breathing or a musculoskeletal thoracic
abnormality affecting ventilation), in addition to
abnormalities of the lung itself.

4. DEFINITION
The term respiration refers, in a broad
sense, to the delivery of oxygen (O2) to
metabolically active tissues for energy usage
and the removal of carbon dioxide (CO2) from
these tissues. Respiratory failure is a failure of
the process of delivering O2 to the tissues
and/or removing CO2 from the tissues.

5. DEFINITION
Abnormalities in the periphery (e.g.,
cyanide poisoning, pathologic distribution of
organ blood flow in sepsis) can also lead to
tissue hypoxia; although these conditions
represent forms of respiratory failure in the
broadest terms, this chapter focuses on
respiratory failure resulting from dysfunction of
the lungs, chest wall, and control of respiration.

6. PHYSICAL
ASSESSMENT
Clinical manifestations of respiratory distress reflect
signs and symptoms of hypoxemia, hypercapnia, or
the increased work of breathing necessary. These
include:
• Altered mental status (agitation, somnolence)
• Peripheral or central cyanosis or decreased oxygen
saturation on pulse oximetry
Manifestations of a "stress response" including
tachycardia, hypertension, and diaphoresis

7. PHYSICAL
ASSESSMENT
• Evidence of increased respiratory work of
breathing including accessory muscle use, nasal
flaring, intercostal indrawing, suprasternal or
supraclavicular retractions, tachypnea
• Evidence of diaphragmatic fatigue (abdominal
paradox)
• Abnormal arterial blood gas results

8. PHYSICAL
ASSESSMENT
• ARF : CXR Findings
• Clear CXR with hypoxemia and normocapnia.-
Pulmonary embolus, R to L shunt, Shock
• Diffusely white (opacified) CXR with hypoxemia and
normocapnia - ARDS, NCPE, CHF, pulmonary
fibrosis
• Localized infiltrate - pneumonia, atelectasis, infarct
• Clear CXR with hypercapnia - COPD, asthma,
overdose, neuromuscular weakness

9. DIAGNOSTIC
EXAMINATIONS
First Tests To Order:
• pulseoximetry
SpO2 <80%
• arterial blood gases
pH<7.38; PaO2 <60 mmHg (or <50
mmHg in chronic lung disease) on
room air; PaCO2 >50 mmHg on room
air

10. DIAGNOSTIC
EXAMINATIONS
• CBC
elevated white blood cell count
screening for hypercoagulable states
Variable
serum bicarbonate (HCO3)
may be elevated

11. DIAGNOSTIC
EXAMINATIONS
• CXR
diffuse or patchy infiltrates; pneumothorax;
pulmonary effusion; hyperinflation; asymmetric
opacification of lung fields; asymmetric
lucency of lung fields
pulmonary function tests
PEFR <35% to 50% of predicted; FEV <35%
to 50% of predicted; FVC <50% to 70% of
predicted; FEV1 <50% of predicted; NIF above
-25 cm H2O

12. DIAGNOSTIC
EXAMINATIONS
• chest CT
pulmonary embolism; chronic lung disease;
infection; parenchymal disease;
bronchiectasis
ventilation/perfusion lung scan
pulmonary embolism

13. DIAGNOSTIC
EXAMINATIONS
• ECG
Variable
• transcutaneous CO2 monitoring
reduced PaCO2
• cardiothoracic ultrasound
evidence of effusion, pneumothorax,
consolidation, or abscess

14. RISK FACTORS
• cigarette smoking
• young age
• old age
• pulmonary infection
• chronic lung disease
• airway obstruction
• alveolar abnormalities

15. RISK FACTORS
• perfusion abnormalities
• cardiac failure
• peripheral nerve abnormalities
• muscle system abnormalities
• opiate and sedative medications
• toxic fumes and gases

16. RISK FACTORS
• traumatic spinal injury
• traumatic thoracic injury
• central nervous system disorders
• acute vascular occlusion
• pneumothorax
• hypercoagulable states

17. Respiratory failure can arise from an
abnormality in any of the components of the
respiratory system, including the airways, alveoli,
central nervous system (CNS), peripheral nervous
system, respiratory muscles, and chest wall.
Patients who have hypoperfusion secondary to
cardiogenic, hypovolemic, or septic shock often
present with respiratory failure.

18. Ventilatory capacity is the maximal
spontaneous ventilation that can be maintained
without development of respiratory muscle fatigue.
Ventilatory demand is the spontaneous minute
ventilation that results in a stable Pa CO2.

19. Normally, ventilatory capacity greatly exceeds
ventilatory demand. Respiratory failure may result
from either a reduction in ventilatory capacity or an
increase in ventilatory demand (or both). Ventilatory
capacity can be decreased by a disease process
involving any of the functional components of the
respiratory system and its controller. Ventilatory
demand is augmented by an increase in minute
ventilation and/or an increase in the work of breathing

21. The management of acute respiratory
failure can be divided into an urgent resuscitation
phase followed by a phase of ongoing care. The
goal of the urgent resuscitation phase is to stabilize
the patient as much as possible and to prevent any
further life-threatening deterioration. Once these
goals are accomplished the focus should then shift
towards diagnosis of the underlying process, and
then the institution of therapy targeted at reversing
the primary etiology of the ARF.

22. MEDICATIONS
Pharmacotherapy for cardiogenic
pulmonary edema and acute exacerbations of
chronic obstructive pulmonary disease (COPD)
is discussed here.

23. MEDICATIONS
The goals of therapy in cardiogenic
pulmonary edema are to achieve a pulmonary
capillary wedge pressure of 15-18 mm Hg and a
cardiac index greater than 2.2 L/min/m2 while
maintaining adequate blood pressure and organ
perfusion.

24. MEDICATIONS
These goals may have to be modified
for some patients. Diuretics, nitrates, analgesics,
and inotropes are used in the treatment of acute
pulmonary edema.

25. MEDICATIONS
• First-line therapy generally includes a loop diuretic such
as furosemide, which inhibits sodium chloride
reabsorption in the ascending loop of Henle.
• Furosemide (Lasix)
This allows both superior potency and a
higher peak concentration despite an increased
incidence of adverse effects, particularly ototoxicity

26. MEDICATIONS
• Metolazone (Zaroxolyn)
Has been used as adjunctive therapy in
patients initially refractory to furosemide. It has been
demonstrated to be synergistic with loop diuretics in
treating refractory patients and causes a greater loss
of potassium. Metolazone is a potent thiazide-related
diuretic that sometimes is used in combination with
furosemide for more aggressive diuresis. It is also
used for initiating diuresis in patients with a degree of
renal dysfunction.
•

27. MEDICATIONS
Nitrates reduce myocardial oxygen
demand by lowering preload and after load. In
severely hypertensive patients, nitroprusside
causes more arterial dilatation than
nitroglycerin. Nevertheless, in view of the
possibility of thiocyanate toxicity and the
coronary steal phenomenon associated with
nitroprusside, IV nitroglycerin may be the initial
therapy of choice for afterload reduction.
•

28. MEDICATIONS
• Nitroglycerin sublingual (Nitro-Bid, NitroMist,
Nitrostat, Nitrolingual)
Sublingual nitroglycerin tablets and spray are
particularly useful in the patient who
presents with acute pulmonary edema with
a systolic blood pressure of at least 100
mm Hg. As with sublingual nitroglycerin
tablets, the onset of action of nitroglycerin
spray is 1-3 minutes, with a half-life of 5
minutes. Administration of the spray may be
easier, and it can be stored for as long as 4
years.

29. MEDICATIONS
• Nitroprusside sodium (Nitropress)
Nitroprusside produces vasodilation of
venous and arterial circulation. At higher
dosages, it may exacerbate myocardial
ischemia by increasing heart rate. It is easily
titratable.

30. MEDICATIONS
Morphine IV is an excellent adjunct in
the management of acute pulmonary edema. In
addition to anxiolysis and analgesia, its most
important effect is venodilation, which reduces
preload. It also causes arterial dilatation, which
reduces systemic vascular resistance and may
increase cardiac output.

31. MEDICATIONS
• Morphine sulfate (Duramorph, Astramorph)
Morphine sulfate is the drug of choice
for narcotic analgesia because of its reliable and
predictable effects, safety profile, and ease of
reversibility with naloxone. Morphine sulfate
administered IV may be dosed in a number of
ways and commonly is titrated until the desired
effect is obtained.

32. MEDICATIONS
• Dopamine
Dopamine is a positive inotropic agent that
stimulates both adrenergic and dopaminergic
receptors. Its hemodynamic effects depend on the
dose. Lower doses stimulate mainly dopaminergic
receptors that produce renal and mesenteric
vasodilation; higher doses produce cardiac stimulation
and renal vasodilation. Doses of 2-10 µg/kg/min can
lead to tachycardia, ischemia, and dysrhythmias.
Doses higher than 10 µg/kg/min cause
vasoconstriction, which increases afterload.

33. MEDICATIONS
• Norepinephrine (Levophed)
Used in protracted hypotension after
adequate fluid replacement. It stimulates beta1- and
alpha-adrenergic receptors, which leads to
increased cardiac muscle contractility and heart
rate, as well as vasoconstriction. As a result,
norepinephrine increases systemic blood pressure
and cardiac output. Adjust and maintain infusion to
stabilize blood pressure (eg, 80-100 mm Hg
systolic) sufficiently to perf

34. MEDICATIONS
• Dobutamine
Dobutamine produces vasodilation and
increases the inotropic state. At higher dosages, it
may cause increased heart rates, thus exacerbating
myocardial ischemia. It is a strong inotropic agent
with minimal chronotropic effect and no
vasoconstriction.

35. MEDICATIONS
Bronchodilators are an important
component of treatment in respiratory failure
caused by obstructive lung disease. These
agents act to decrease muscle tone in both
small and large airways in the lungs. This
category includes beta-adrenergics,
methylxanthines, and anticholinergics.

36. MEDICATIONS
• Terbutaline (Brethaire, Bricanyl)
Terbutaline acts directly on beta2
receptors to relax bronchial smooth muscle,
relieving bronchospasm and reducing airway
resistance.

37. MEDICATIONS
• Albuterol (Proventil)
Albuterol is a beta-agonist useful in the
treatment of bronchospasm. It selectively
stimulates beta2-adrenergic receptors of the
lungs. Bronchodilation results from relaxation of
bronchial smooth muscle, which relieves
bronchospasm and reduces airway resistance.

38. NURSING
DIAGNOSIS
1. Ineffective Airway Clearance May be related to
Bronchospasm, Increased production of secretions; retained
secretions; thick, viscous secretion
Possibly evidenced by
 Statement of difficulty breathing
 Changes in depth/rate of respirations, use of accessory
muscles
 Abnormal breath sounds, e.g., wheezes, rhonchi, crackles
 Cough (persistent), with/without sputum production

39. NURSING
DIAGNOSIS
2. Impaired Gas Exchange May be related to Altered oxygen
supply (obstruction of airways by secretions, bronchospasm;
air-trapping) Alveoli destruction
Possibly evidenced by
 Dyspnea
 Confusion, restlessness
 Inability to move secretions
 Abnormal ABG values (hypoxia and hypercapnia)
 Changes in vital signs
 Reduced tolerance for activity

40. NURSING
DIAGNOSIS
3. Nutrition: imbalanced, less than body requirements May be
related to Dyspnea; sputum production, Medication side
effects; anorexia, nausea/vomiting , Fatigue
Possibly evidenced by
 Weight loss;
 loss of muscle mass,
 poor muscle tone
 Reported altered taste sensation;
 aversion to eating,
 lack of interest in food

41. NURSING
DIAGNOSIS
4. Knowledge Deficit May be related to Lack of
information/unfamiliarity with information resources,
Information misinterpretation, Lack of recall/cognitive
limitation
Possibly evidenced by
Request for information
Statement of concerns/misconception
Inaccurate follow-through of instructions
Development of preventable complications

42. NURSING
DIAGNOSIS
5. Self-Care deficit, specify—intolerance to activity,
decreased strength/endurance, depression,
severe anxiety.
6. Home Maintenance, ineffective—intolerance to
activity, inadequate support system, insufficient
finances, unfamiliarity with neighborhood
resources.

43. NURSING
DIAGNOSIS
7. Infection, risk for—decreased ciliary action,
stasis of secretions, tissue destruction,
increased environmental exposure, chronic
disease process, malnutrition.

44. NURSING
INTERVENTIONS
• Auscultate breath sounds. Note adventitious breath
sounds, e.g., wheezes, crackles, rhonchi.
• Assess/ monitor respiratory rate. Note inspiratory/
expiratory ratio.
• Note presence/ degree of dyspnea, e.g., reports of “air
hunger,” restlessness, anxiety, respiratory distress, use of
accessory muscles. Use 0–10 scale or American Thoracic
Society’s “Grade of Breathlessness Scale” to rate
breathing difficulty. Ascertain precipitating factors when
possible. Differentiate acute episode from exacerbation of
chronic dyspnea.

45. NURSING
INTERVENTIONS
• Assist patient to assume position of comfort, e.g.,
elevate head of bed, have patient lean on overbed
table or sit on edge of bed.
• Keep environmental pollution to a minimum, e.g.,
dust, smoke, and feather pillows, according to
individual situation.
• Encourage/ assist with abdominal or pursed-lip
breathing exercises.

46. NURSING
INTERVENTIONS
• Observe characteristics of cough, e.g., persistent,
hacking, moist. Assist with measures to improve
effectiveness of cough effort.
• Increase fluid intake to 3000 mL/day within cardiac
tolerance. Provide warm/ tepid liquids. Recommend
intakeof fluids between, instead of during, meals.
• Monitor/ graph serial ABGs, pulse oximetry, chest x-ray.

47. NURSING
INTERVENTIONS
• Assess respiratory rate, depth. Note use of accessory
muscles, pursed-lip breathing, inability to speak/
converse.
• Elevate head of bed, assist patient to assume
position to ease work of breathing. Include periods of
time in prone position as tolerated. Encourage deep-
slow or pursed-lip breathing as individually needed/
tolerated.
• Assess/ routinely monitor skin and mucous
membrane color.

48. NURSING
INTERVENTIONS
• Expectoration of sputum; suction when
indicated.
• Auscultate breath sounds, noting areas of
decreased airflow and/or adventitious sounds.
• Palpate for fremitus.
• Monitor level of consciousness/ mental status.
Investigate changes.

49. NURSING
INTERVENTIONS
• Assess dietary habits, recent food intake.
Note degree of difficulty with eating.
Evaluate weight and body size (mass).
• Auscultate bowel sounds.
• Give frequent oral care, remove
expectorated secretions promptly, provide
specific container for disposal of
secretions and tissues.

50. NURSING
INTERVENTIONS
• Encourage a rest period of 1 hr before and after
meals. Provide frequent small feedings.
• Avoid gas-producing foods and carbonated
beverages.
• Avoid very hot or very cold foods.
• Weigh as indicated.
• Administer supplemental oxygen during meals
as indicated.

51. THANK YOU
FOR
LISTENING…