Acute Respiratory Failure

2. General Objectives: At the end of the class, students will acquire knowledge about
Acute Respiratory Failure.
Specific Objective: At the end of this class, students will be able:-
 To introduce the acute respiratory failure
 To define acute respiratory failure
 To describe the classifications of acute respiratory failure.
 To enumerate the types of acute respiratory failure
 To state the risk factors of acute respiratory failure.
 To enlist the aetiology of acute respiratory failure.
 To explain the pathophysiology of acute respiratory failure
 To state the clinical features of acute respiratory failure
 To enlist the diagnostic evaluation of acute respiratory failure
 To describe the management of acute respiratory failure
 To list the complications of acute respiratory failure
 To explain the nursing management of acute respiratory failure
 To summarize the topic

6. INTRODUCTION:
• The body relies primarily on the central nervous
system, the pulmonary system, the heart and
the vascular system to accomplish effective
respiration. Respiratory failure occurs when one or
more of these system or organ fails to maintain
optimal functioning.
• If the respiratory failure occurs so rapidly that the
compensatory mechanisms cannot accommodate or if
the compensatory mechanisms overwhelmed the
acute respiratory failuredevelops.

7. INTRODUCTION:
Respiratory failure is a broad, non-specific clinical diagnosis
indicating that the respiratory system is unable to supply the
O2 necessary to maintain metabolism or cannot eliminate
sufficient Co2.
Acute respiratory failure occurs when: pulmonary system
is no longer able to meet the metabolic demands of the body.
Respiratory failure is a syndrome in which the respiratory
system fails in one or both of its gas exchange functions that
is Oxygenation and Carbon dioxide elimination. May be
classified as either hypoxemic or hyper capnic.

8. DEFINITION:
Respiratory failure is defined as a PaO2 value of less than 60
mm Hg while breathing air or a PaCO2 of more than 50mm
Hg.
Respiratory failure is inadequate gas exchange by the
respiratory system, with the result that levels of arterial
oxygen, carbon dioxide or both cannot be maintained within
their normal ranges.
A drop in blood oxygenation is known as hypoxemia.
A rise in arterial carbon dioxide levels is
called hypercapnia.

9. INCIDENCE
The problem in US
1. 360,000 cases per year
2. 137 cases per 100,000 population
3. With 36% failing to survive the hospitalization
The problem in India: not known but respiratory failure is a
common occurrence either as a complication of other
diseases or as a terminal event

11. CLASSIFICATION OF RESPIRATORY FAILURE
 Type I or Hypoxemic (PaO2 <60 mm hg ): Failure of
oxygen exchange
 Type II or Hypercapnic (PaCO2 >45 mm hg): Failure
to exchange or remove carbon dioxide.
 Type III Respiratory Failure: Peri-operative
respiratory failure.
 Type IV Respiratory Failure (Shock): secondary to
cardiovascular instability.

12. CLASSIFICATION OF RESPIRATORY FAILURE
Hypoxemic respiratory failure (type I):
 It is characterized by a PaO2 of less than 60 mm Hg.
 This is the most common form of respiratory failure, and
it can be associated with virtually all acute diseases of the
lung which generally involve fluid filling or collapse of
alveolar units.
 Some examples of type I respiratory failure are
pulmonary edema, pneumonia, and pulmonary
hemorrhage.

13. CLASSIFICATION OF RESPIRATORY FAILURE
Hypercapnic respiratory failure (type II):
 It is characterized by a PaCO2 of more than 50 mm Hg.
 Hypoxemia is common in patients with hypercapnic
respiratory failure who are breathing room air.
 Common etiologies include drug overdose,
neuromuscular disease, chest wall abnormalities, and
severe airway disorders. eg, asthma, COPD.

14. CLASSIFICATION OF RESPIRATORY FAILURE
Perioperative respiratory failure (Type iii):
 Residual anesthesia effects, post-operative pain, and
abnormal mechanics contribute to decreasing FRC and
progressive collapse of dependent lung units.
 This is generally a subset of type I failure but is
sometimes considered separately because it is so
common.
 Causes of Peri-operative atelectasis includes: Decreased
functional residual capacity (FRC), Anaesthesia, Upper
abdominal incision, Airway secretions, Supine/Obese/
Ascites.
 Effective means of preventing or treating atelectasis
include incentive spirometry.

15. CLASSIFICATION OF RESPIRATORY FAILURE
Shock Respiratory Failure (Type iv):
 It describes patients who are intubated and ventilated in
the process of resuscitation for shock.
 Goal of ventilation is to stabilize gas exchange and to
unload the respiratory muscles, lowering their oxygen
consumption.
 Respiratory failure can also due to shock.

16. 1.Hypoxemic
Respiratory Failure
PaO2 low (<60mmHg
(8.0 kPa))
PaCO2 normal orlow
PA-aO2increased
2. Acute
Ventilatory Failure
PaO2 decreased
PaCO2 increased
PA-aO2 normal
pH decreased
Acute respiratory failure may be classified as:

17. TYPES OF RESPIRATORY FAILURE
 Acute Respiratory Failure
 Chronic Respiratory Failure:
Acute Respiratory Failure
 Acute hypercapnic respiratory failure develops over
minutes to hours.
 Acute respiratory failure can develop quickly and may
require emergency treatment.
 Acute respiratory failure usually is treated in an intensive
care unit

18. TYPES OF RESPIRATORY FAILURE
Chronic Respiratory Failure
 Chronic respiratory failure develops over several days or
longer.
 Chronic respiratory failure develops more slowly and lasts
longer.
 Chronic respiratory failure can be treated at home or at a
long-term care centre.
 E.g.: acute exacerbation of advanced COPD

19. HYPOXEMIC RESPIRATORY FAILURE
Hypoxemic respiratory failure (type I) is characterized
by a PaO2 of less than 60 mm Hg with a normal or low
PaCO2.
This is the most common form of respiratory failure,
and it can be associated with virtually all acute
diseases of the lung, which generally involve fluid
filling or collapse of alveolarunits.

20. Factors that affects Hypoxemic Respiratory Failure
 V/Q Mismatch
 Shunt
 Diffusion Limitation
 Alveolar Hypoventilation:
Increase CO2
Decrease PO2

23. Shunt
 In medicine, a shunt is a hole or a small passage which
moves, or allows movement of fluid from one part of the
body to another. There are 2 Types: Anatomical or
physiological. PO2 is elevated and PaCO2 is normal.
1. Anatomic- passes through an anatomic channel of the heart
and does not pass through the lungs exercise.
 e.g. ventricular septal defect. (The hole that occurs in the
wall of the heart that separates the heart's lower chambers
(septum) and allows blood to pass from the left to the right
side of the heart)

27. Shunt
Intrapulmonary shunt- blood flows through pulmonary
capillaries without participating in gas exchange ex: alveoli
filled with fluid.
 Patients with shunts are more hypoxemic than those with
VQ mismatch and they may require mechanical ventilators.

31. Diffusion Limitations
 Gas exchange is compromised
by a process that thickens or
destroys the membrane.
1. Pulmonary fibrosis
2. ARDS(Acute respiratory
distress syndrome)
A classic sign of diffusion
limitation is hypoxemia during
exercise but not at rest.

32. Alveolar Hypoventilation
 Alveolar hypoventilation is a rare disorder in which a
person does not take enough breaths per minute. Mainly
due to hypercapnic respiratory failure but can cause
hypoxemia.
 Increased pCO2 with decreased PO2
 Restrictive lung disease
 CNS diseases
 Neuromuscular diseases.

33. This is characterized by a PaCO2 of more than 50 mm
Hg. Hypoxemia is common with
hypercapnic respiratory failure
in patients
who are breathing
room air.The pH depends on the level of bicarbonate,
which, in turn, is dependent on the duration of
hypercapnia.
VENTILATORY/ HYPOCAPNIC
RESPIRATOTY FAILURE

34. Factors that affects Hypercapnic Ventilatory Failure.
1. Abnormalities of the airways and alveoliair flow
obstruction and air trapping; Asthma, COPD, and cystic
fibrosis.
2. Abnormalities of the CNS- suppresses drive to breath
3. Drugs e.g. narcotics,
4. Head injury and spinal cord injury

35. RISK FACTOR FOR RESPIRATORY FAILURE
• People who have diseases or conditions that affect the
muscles, nerves, bones, or tissues that support
breathing are at risk for respiratory failure.
• People who have lung diseases or conditions also are
at risk for respiratory failure.

36. The most common cause for hypoxemic respiratory
failure in ICU patients is perfusion of non-ventilated
alveoli(shunting).

37. Etiology of Hypoxemic Respiratory Failure
Chronic bronchitis and emphysema (COPD)
Pneumonia, Asthma
Pulmonary edema. Bronchiectasis
Pulmonary fibrosis
Asthma
Pneumothorax
Pulmonary embolism
Pulmonary arterial hypertension
Pneumoconiosis
Granulomatous lung diseases
Cyanotic congenital heart disease
Adult respiratory distress syndrome
Fat embolism syndrome
Kyphoscoliosis, Obesity

38. In acute Ventilatory failure, the respiratory loadplaced
on the lungs to exchange CO2 is impaired by;
1. Problem of resistance to moving air in and out ofthe
lung,
2. The ability of lung to expand andcontact(elastic
recoil), and
3. Conditions that increase the productions of CO2 or
decrease the surface available for exchange ofgases.
Etiology of Hypocapnic Respiratory Failure

39. Pathophysiology of Hypoxemic Respiratory Failure

40. ↑ed hydrostatic pressures in the pulmonary vessels
Creates Imbalance in Starling Forces,
↓
Increase in fluid filtration into interstitial spaces of lungs that
exceeds the lympatis capacity to drain the fluid away
↓
Increasing volumes of fluids leak into the alveolar space
↓
The lymphatic system attempts to compensate by draining excess
interstitial fluid into the vascular system through the hilar lymph
nodes
↓
If the pathway becomes overwhelmed, fluid moves from pleural
interstitial to into the alveolar walls
↓
If the alveolar epithelium is damaged, the fluid begins to accumulate
in the alveoli.
↓
Alveolar edema is serious late manifestation in the progression of
fluid imbalance.

41. Pathophysiology of Hypocapnic Respiratory
Failure

42. In obstructive type respiratory failure, the residual pressure in
the chest impairs inhalation and increase the workloadof
breathing.
↓
When end expiratory alveolar volume remains above their critical
closing point, the alveoli remain open and functioning,
↓
Allowing oxygen to diffuse in bloodstream
↓
If alveolar volume falls below the closing point, the alveolitends
to collapse
↓
No oxygenation or blood flow to the alveolioccurs,
↓
Leads to true intra pulmonary shunt (perfusion without
oxygenation) and decreased lung compliance
↓
Leads to hypoxia

43. Clinical Features Of Hypoxemic Respiratory Failure
Hypoxemia as alveolar membrane is thickened by fluid that
impaired the gas exchange
Dyspnea, Tachypnea
Weak and thread tachycardia
Hypertension(if cardiogenic)
Orthopnea at less than 90 degrees
Coughing as to attempt to rid the fluidof chest
Sputum is thin and frothy because it is combined with water
Pink tinged sputum if small capillaries break
Patient may be anxious and restless from hypoxemia

44. Clinical Features of Hypoxemic Respiratory Failure
Patient may be anxious and restless from hypoxemia
Chest auscultation reveals crackles, wheezes, and presence of
S3 sound and SPO2 is less than 85%
Arterial PaO2 revels less than 50%
Respiratory alkalosis because of Tachypnea
Pressure in Pulmonary artery and Pulmonary wedge
Pressure(PAWP)will Increase
Chest X-Rays showsAreas of “white-out” where fluid has
replaced air filled lung tissues
Right ventricular failure may be noted

45. Altered respiratory rate and patterns
Breaths are shallow due to spasm of theairway
Client become confused, less conversant, and are
difficult to arouse
Pulsus paradoxes
Pulse oxymetry shows steadily decrease inSpO2
ABG analysis shows falling PaO2 and rising PaCO2
Clinical Features of Hypocapnic Respiratory
Failure

46. DIAGNOSTIC EVALUATION:
History of:
• Sepsis suggested by fever, chills
• Pneumonia suggested by cough, sputum production, chest
pain
• Pulmonary embolus suggested by sudden onset of
shortness of breath or chest pain.
• COPD exacerbation suggested by history of heavy
smoking, cough, sputum production pulmonary edema
suggested by chest pain, and orthopnea.
• Non-cardiogenic edema suggested by the presence of risk
factors including sepsis, trauma, aspiration, and blood
transfusions.
• Additional exposure to toxins history may help diagnose
asthma, aspiration, inhalational injury and some
interstitial lung diseases.

47. DIAGNOSTIC EVALUATION:
Physical Findings:
• Hypotension usually with signs of poor perfusion
suggests severe sepsis.
• Hypertension usually with signs of poor perfusion
suggests pulmonary edema.
• Wheezing suggests airway obstruction: Bronchospasm,
Secretions, Pulmonary edema.

48. DIAGNOSTIC EVALUATION:
Laboratory Tests:
ABG Analysis:
Quantifies level of gas exchange abnormality.
Identifies type and chronicity of respiratory failure
Complete blood count:
Anemia may cause cardiogenic pulmonary edema
Leukocytosis, or leukopenia suggestive of infection
Microbiology:
Respiratory cultures: sputum/tracheal aspirate
Blood, urine and body fluid (e.g. pleural) cultures

49. DIAGNOSTIC EVALUATION:
Diagnostic Investigations:
• Chest radiography: Identify chest wall, pleural and lung
parenchymal with opacities present.
• Electrocardiogram - Identify arrhythmias, ischemia, and
ventricular dysfunction.
• Echocardiography - Identify right and/or left ventricular
dysfunction.
• Pulmonary function tests/bedside spirometry: Identify
obstruction, restriction. May be difficult to perform if
critically ill.
• Bronchoscopy: Obtain biopsies. Bronchoscopy may not
be safe for critically ill patient.

50. MANAGEMENT OF THE PATIENT WITH
RESPIRATORY FAILURE
• Cardiac monitoring, Vitals sign and Spo2 monitoring.
•Underlying causes identification and treatment.
• O2 therapy
• Position
• Mobilization of secretions
• Correct hypoxia by Positive pressure ventilation(PPV)

51. O2 Therapy
Oxygen therapy is the administration
of oxygen at concentrations greater
than that in room air to treat or
prevent hypoxemia (not enough
oxygen in the blood).
• Mechanism of action:–
Reverses hypoxemia

52. O2 Therapy
 If secondary to V/Q mismatch- 1-3L or 24%-If secondary
to V/Q mismatch- 1-3L or 24%- 32% by mask32% by
mask
 If secondary to intrapulmonary shunt- positive pressure
ventilation-PPV
May be via ET tube
Tight fitting mask
Goal is PaO2 of 55-60 with SaO2 at 90% or more at
lowest O2 concentration possible
O2 at high concentrations for longer than 48 hours causes
O2 toxicity

53. Oxygen toxicity
 Oxygen toxicity may occur when too high a
concentration of oxygen (greater than 50%) is
administered for an extended period (longer than 48
hours).
 It is caused by overproduction of oxygen free radicals,
which are byproducts of cell metabolism. If oxygen
toxicity is untreated, these radicals can severely damage
or kill cells.

54. Signs and symptoms of oxygen toxicity
 Signs and symptoms of oxygen toxicity include:
 Sub sternal discomfort
 Paresthesia's
 Dyspnea
 Restlessness, fatigue
 Malaise
 Progressive respiratory difficulty, and alveolar infiltrates
evident on chest x- rays.

55. Prevention of oxygen toxicity
 If high concentrations of oxygen are necessary, it is
important to minimize the duration of administration
and reduce its concentration as soon as possible.
 Often, positive end expiratory pressure (PEEP) or
continuous positive airway pressure (CPAP) is used
with oxygen therapy to reverse or prevent
microatelectasis, thus allowing a lower percentage of
oxygen to be used.
 The level of PEEP that allows the best oxygenation
without hemodynamic compromise is known as
“best PEEP”.

57. Mobilization of secretions
• Effective coughing: assist
in cough
• Positioning: Head of bed
45 degrees or recliner chair
or bed (“Good lung
down”)
• Hydration - fluid intake 2-3
L/day
• Humidification: aerosol
treatments (mucolytic
agents )
• Chest PT: postural
drainage, percussion and
vibration
• Airway suctioning

58. POSITIVE PRESSURE VENTILATION(PPV)
 Invasively through oro or nasotracheal intubation.
 Noninvasively( NIPPV) through mask
Used for acute and chronic respiratory failure
 BiPAP- different levels of pressure for inspiration and
expiration- (IPAP) higher for inspiration, (EPAP) lower
for expiration
CPAP- for sleep apnea.
Used best in chronic respiratory failure in patients with
chest wall and neuromuscular disease, also with HF and
COPD.

62. Emergency management of Hypoxemic Respiratory
Failure:

63. • Reduce preload:
Treating the underlying cause.
Upright position.
Diuretics: First-line therapy generally includes a loop
diuretic such as furosemide, which inhibits sodium chloride
reabsorption in the ascending loop of Henle.
Nitrates (nitroglycerin): Nitrates reduce myocardial oxygen
demand by lowering preload & afterload.
Opioid Analgesics: Morphine IV is an excellent adjunct.
Causes arterial dilatation, which reduces systemic vascular
resistance and may increase cardiac output.
Management of Hypoxemic Respiratory Failure:

64. • Antihypertensive such as nitroprusside: Reduce after load.
• Corticosteroids: Effective in accelerating recovery from
acute COPD exacerbations & are an important anti-
inflammatory therapy in asthma.
• Beta 2 Agonists: These agents act to decrease muscle tone
in both small and large airways in the lungs. Includes beta-
adrenergics, methylxanthines & anticholinergics.
• Anticholinergics: Antagonize the action of acetylcholine
with muscarinic receptor on bronchial smooth muscle.
Management of Hypoxemic Respiratory
Failure:

65. Support perfusion:
Inotropic agents: The left
ventricle is supported by
using isotropic medication such
as dobutamine, dopamine,
dobutamine & digoxin.
An intra aortic balloon pump
(IABP)
Monitor urinr Output.
Management of Hypoxemic Respiratory
Failure:

66. Reverse Bronchospasms:
• Several forms of bronchodilators are used to treat
obstructions to airflow in client with COPD and asthma.
• These agents include beta2 selective agonists
(albuterol), ipratropium, theophyllin, and
corticosteroids.
• If infection is cause then broad spectrum antibiotics
are used. E.g: vancomycin
Management of Hypocapnic Respiratory Failure:

67. Maintain oxygenation:
• Oxygen by mask may be adequate to support oxygenation.
• Using forms of NPPV such as CPAP reduces the workload
of breathing by decreasing the force needed to overcome
the pressure in the chest.
• Manage the underlying problem.
• Maintain ventilation.
Management of Hypocapnic Respiratory Failure:

68. Mechanical ventilator Indication in Hypocapnic
Respiratory Failure:

69. GERONTOLOGIC CONSIDERATIONS
Physiologic aging results in
 ↓ Ventilatory capacity
 Alveolar dilation
 Larger air spaces
 Loss of surface area
 Diminished elastic recoil
 Decreased respiratory muscle strength
 ↓ Chest wall compliance
Lifelong smoking
Poor nutritional status
Less available physiologic reserve: Cardiovascular,
Respiratory and Autonomic nervous system

70. COMPLICATIONS
• Pulmonary Emboli
• Barotrauma
• Pulmonary Fibrosis
• Infection, Sepsis
• ARDS, Pneumonia
• Cardiac arrhythmias, hypotension, Acute MI
• Renal failure
• Hemorrhage
• Malnutrition

71. NURSING MANAGEMENT
THEORY APPLICATION
 Florence Nightingale’s environmental theory can be
applied in this condition.
 The theory is focused on the environment. The
environment is viewed as all the conditions and influences
the effect the life and development of an organism and
capable of preventing, supporting or contributing to
disease or death.
 Following problems can be found in patient with acute
respiratory failure.

72. NURSING MANAGEMENT
Nursing Assessment
• History of smoking, family history, occupational history
• Respiratory rate, depth and characteristics
• ABG analysis
• Ineffective breathing pattern
• Deficient knowledge

73. • Impaired gas exchange related to capillary membrane
obstruction from fluid evidence by decreased PaO2 and SiO2
• Excessive fluid volume related to excess preload
evidence by weight gain, peripheral edema, and
wheezes and crackles sounds in thelungs.
• Impaired spontaneous ventilation related to imbalance
between Ventilatory capacity and Ventilatory demand
evidence by SPO2 and ABG findings.
• Ineffective breathing pattern related to underlying
diseases process and artificial airway and ventilator
system abnormal ABG findings and respiratory rate .
NURSING DIAGNOSIS

74. • Ineffective airway clearance related to increased mucus
production associated with continuous positive-pressure
mechanical ventilation evidence by wheezes and crackles
sounds in lungs.
• Risk for trauma and infection related to endotracheal
intubation or tracheotomy.
• Impaired physical mobility related to ventilatordependency.
• Impaired verbal communication related to endotracheal tube
and attachment to ventilator
• Defensive coping and powerlessness related to ventilator
Dependency.

75. Nursing Intervention
• Patients with acute respiratory failure should be closely
observed for potential deterioration.
• Monitoring may involve intermittent/continual pulse
oximetry.
• Any changes in physiological signs should be reported
promptly to the senior practitioner.
• Pulmonary secretions: oropharyngeal/nasopharyngeal
suction helps to clear secretions.
• Identify and treat cause of the acute respiratory distress
syndrome
• Administer oxygen as prescribed.
• Position client in high fowler’s position.
• Restrict fluid intake as prescribed.
• Provide respiratory treatment as prescribed.

76. Nursing Intervention
• Administer diuretics, anticoagulants or corticosteroids as
prescribed.
• Prepare the client for intubation and mechanical
ventilation using PEEP.
• Nutritional Support
• Nutritional support is critical for the patient with ARDS
as metabolic demand is high, caloric needs will be
increased.
• Adequate calories and protein should be provided.
• During acute phase, enteral or parenteral nutrition
formulas have been developed that provide a large
amount of fat calories rather than carbohydrates

77. SUMMARY
So, today we discussed definition, classification, etiology
factors, pathophysiology, clinical features, diagnostic
studies, medical management, nursing management, and
complications of acute respiratory failure.

78. CONCLUSION:
Respiratory failure is a syndrome of inadequate gas
exchange due to dysfunction of one or more essential
components of the respiratory system Issues involved in
timely recognition of & response to clinical deterioration
remain complex, yet patient safety relies on nurses’ timely
assessments and actions.

79. REFERENCES:
Book:
• Brunner and Suddharth‟s Textbook of Medical Surgical
Nursing, 11th Edition, New Delhi, Wolters Kluwer (India)
Pvt. Ltd. 3rd Edition , page no:183-187.
• Black, J.M., Hawks, J.H., & Annabelle, M.K. (2005).
Medical-Surgical Nursing-clinical management for
positive outcomes. (6th ed.). P 1631
• Chintamani, Lewis, Heitkemper, Dirksen, O’Brien and
Bucher. (2011).
• Lewis’s Medical Surgical Nursing: Assessment and
Management of Clinical Problems. (7th Ed.). Mosby. P
595.
• Manual of medical & surgical Nursing Care/Nursing
Intervention and collaborative management/Mosby/5th
Edition/Page 191-195.

80. REFERENCES:
Book:
• Lippincott/Manual of Nursing practice/8th edition/page
no: 416 – 417.
• Hinkle LJ, Cheever HK. Brunner & Sudharth's textbook
of medical surgical nursing. 13th Edition. I volume .New
Delhi: Wolters Kluwer Publications; 2014.Pp 545-47.
• NCP Nursing Care Plan for Acute Respiratory Failure
[Internet]. [cited 2018 Mar 6]. Available from:
http://nursethought.blogspot.in/2011/03/ncp-nursing-
care-plan-foracute_18.html

81. REFERENCES:
Internet
• https://medlineplus.gov/respiratoryfailure.html
• https://www2.slideshare.net/mahesh0926/acute-
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• https://www.healthline.com/health/acute-respiratory-
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• http://www.authorstream.com/Presentation/monikajo
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