Respiratory failure occurs when the respiratory system fails to adequately oxygenate the blood or remove carbon dioxide due to diseases of the lungs, heart, chest wall or neuromuscular system. It is classified as hypoxemic, with low blood oxygen, or hypercapnic, with high blood carbon dioxide. Common causes include pneumonia, pulmonary edema, lung injury and reduced respiratory drive from drug overdose or brain injury. Treatment focuses on oxygen therapy, secretion clearance, ventilation support, treating underlying conditions and preventing further organ damage.

1. RESPIRATORY
FAILURE

2. The major function of the respiratory system
is gas exchange , which involves the transfer
of oxygen and carbon dioxide between the
atmosphere and blood.
Respiratory failure results when one or both
of these gas exchanging functions are
inadequate.
For eg : - insufficient oxygen is transferred to
the blood or inadequate C02 is removed from
the lungs.

3. DEFINITION
•Respiratory failure is a syndrome in which the
respiratory system fails in one or both of its gas
exchange functions: oxygenation and CO2
elimination where either insufficient oxygen is
transferred to the blood or inadequate CO2 is
removed from the lungs and/or both resulting in
hypoxemia and hypercapnia

4. RESPIRATORY FAILURE
•Respiratory failure is not a disease rather is a
condition that occurs as a result of one or more
diseases involving the lungs or other body
systems

5. CLASSIFICATION

6. types

7. HYPOXAEMIC
RESPIRATORY
FAILURE

8. HYPOXAEMIC RESPIRATORY FAILURE
•It is also known as oxygenation failure
because the primary problem is inadequate
oxygen transfer between the alveoli and the
pulmonary capillary bed.
•Hypoxaemic respiratory failure is defined as
a PaO2 of 60 mm of Hg or less when the
patient is receiving an inspired oxygen
concentration of 60% or greater.

9. HYPOXAEMIC RESPIRATORY FAILURE
•It incorporates 2 important concepts
Pa02 is at a level that indicates inadequate
oxygen saturation of haemoglobin
This Pa02 level exists despite
administration of supplemental oxygen at a
percentage that is about 3 times that in
room air.

10. HYPOXAEMIC RESPIRATORY
FAILURE
Disorders that interfere with O2 transfer into the blood
include
•Pneumonia
•Pulmonary edema
•Pulmonary emboli
•Alveolar injury related to inhalation of toxic gases
•Lung damage related to alveolar stress or ventilator
associated lung injury

11. ETIOLOGY&
PATHOPHYSIOLOGY

12. HYPOXAEMIC RESPIRATORY
FAILURE
Disorders that interfere with O2 transfer into the blood
include
•Pneumonia
•Pulmonary edema
•Pulmonary emboli
•Alveolar injury related to inhalation of toxic gases
•Lung damage related to alveolar stress or ventilator
associated lung injury

13. HYPOXAEMIC RESPIRATORY
FAILURE ( Causes)
Respiratory system
•Acute respiratory distress syndrome
•Pneumonia
•Pulmonary artery laceration and haemorrhage
•Massive Pulmonary embolism(thrombus or fat)
•Alveolar injury related to inhalation of toxic gases(eg:
smoke inhalation)
•Lung damage related to alveolar stress or ventilator
associated lung injury

14. HYPOXAEMIC RESPIRATORY
FAILURE
Cardiac system
•Anatomic shunt (eg: VSD)
•Cardiogenic pulmonary edema
•Shock (decreases blood flow through
pulmonary vasculature)

15. HYPOXAEMIC RESPIRATORY
FAILURE ( Pathophysiology)
Mechanisms causing hypoxemia and
respiratory failure are
•Mismatch b/n ventilation and perfusion
•Shunt
•Diffusion limitation and
•Hypoventilation

16. V/Q MATCH
•In the normal lung the volume of blood
perfusing the lungs in each minute is equal to
the amount of fresh gas that reaches the alveoli
each minute
•In a perfectly matched system each portion of
the lung receives 1 ml of air for 1 ml of blood
•It results in a V/Q ratio of 1: 1

18. V/Q MISMATCH-causes
•Increased secretions in the airways (COPD)
and alveoli (pneumonia)
•Bronchospasm (asthma)
•Alveolar collapse/atelectasis
•Pain
•Pulmonary embolism

19. SHUNT
•It occurs when blood exists in the heart without
having participated in gas exchange
•There are two types anatomic and
intrapulmonary
•Anatomic shunt occurs when there is presence
of an anatomic channel in the heart
•Intrapulmonary shunt occurs when blood flows
through the pulmonary capillaries without
participating in gas exchange

20. DIFFUSION LIMITATION
•It occurs when gas exchange across the alveolar
capillary membrane is compromised by a process
that thickens or destroys the membrane.
•It is worsened by disease conditions like severe
emphysema, pulmonary fibrosis, ILD,ARDS where
the alveolar membrane gets thickened and fibrotic ,
slowing down gas transport
•Diffusion limitation causes hypoxemia even during
exercise

22. ALVEOLAR HYPOVENTILATION
•It is a generalised decrease in ventilation that
results in an increase in PaCO2 and decrease in
PaO2
•It is seen in restrictive lung diseases, CNS
diseases, chest wall dysfunction, acute asthma
or neuromuscular diseases

23. HYPERCAPNIC
RESPIRATORY
FAILURE

24. HYPERCAPNIC RESPIRATORY
FAILURE/VENTILATORY FAILURE
It results from an imbalance between ventilatory
supply and ventilatory demand.
Ventilatory supply is the maximum ventilation ( gas
flow in and out the lungs) that patient can sustain
without developing respiratory muscle fatigue.
Ventilatory demand is the amount of ventilation
needed to keep PaC02 within normal limits.

25. HYPERCAPNIC RESPIRATORY
FAILURE/VENTILATORY FAILURE
It is also referred to as ventilatory failure
because the primary problem is insufficient
C02 removal.
It is defined as a PaCO2 >45mmHg in
combination with arterial pH less than 7.35.

26. HYPERCAPNIC RESPIRATORY
FAILURE/VENTILATORY FAILURE
It incorporates three important concepts
PaC02 is higher than normal
There is evidence of body’s inability to
compensate for this increase (acidemia)
The pH is at a level where a further decrease
may lead to severe acid base imbalance.

27. HYPERCAPNIC RESPIRATORY FAI
LURE/VENTILATORY FAILURE
Disorders that compromise lung ventilation
and subsequent CO2 removal include
•Drug overdose with CNS depressants
•Neuromuscular diseases eg:Myasthenia
gravis
•Trauma or diseases involving spinal cord
•Acute asthma

28. ETIOLOGY OR RISK
FACTORS &
PATHOPHYSIOLOGY

29. HYPERCAPNIC RESPIRATORY
FAILURE/VENTILATORY FAILURE
RESPIRATORY SYSTEM
•Asthma
•COPD
•Cystic fibrosis

30. HYPERCAPNIC RESPIRATORY
FAILURE/VENTILATORY FAILURE
CENTRAL NERVOUS SYSTEM
•Brain stem injury/infarct
•Sedative and opioid overdose
•Spinal cord injury
•Severe head injury

31. HYPERCAPNIC RESPIRATORY
FAILURE/VENTILATORY FAILURE
CHEST WALL ABNORMALITIES
•Thoracic trauma (eg: flail chest)
•Kyphoscoliosis
•Pain
•Morbid obesity

32. HYPERCAPNIC RESPIRATORY
FAILURE/VENTILATORY FAILURE
NEUROMUSCULAR SYSTEM DISORDERS
•Myasthenia gravis
•Polyneuropathy
•Toxic ingestion
•Phrenic nerve injury
•GB syndrome
•PM
•Muscular dystrophy
•Multiple sclerosis

33. PREDISPOSING FACTORS
Disorders of airways and alveoli
Disorders of CNS
Disorders of chest wall
Neuromuscular conditions

34. Disorders of airways and alveoli
ARDS
Asthma
COPD
Cystic fibrosis

35. Disorders of airways and alveoli
ARDS: fluid enters the interstitium and alveoli,
impairing gas exchange. This would initially
decrease PaO2 and later increase PaCO2.

36. Disorders of airways and alveoli
Asthma: Bronchospasm, edema of the bronchial
mucosa and plugging of small airways with
secretions greatly reduce airflow.
 Increased work of breathing causing respiratory
muscle fatigue
Decreases PaO2 and increase in PaCO2

37. Disorders of airways and alveoli
COPD: alveoli are destroyed by protease
antiprotease imbalance or respiratory infection or
exacerbation of COPD.
Secretions obstruct airflow
Work of breathing increases and results in
respiratory muscle fatigue
Decreases PaO2 and increase in PaCO2

38. Disorders of airways and alveoli
Cystic fibrosis: It is a progressive genetic disease that causes
persistent lung infections and limit the ability to breathe over
time.
Overtime the airways become clogged with copious,
purulent often greenish coloured sputum
Secretions obstruct airflow
Repeated infections destroy alveoli
Work of breathing increases and results in respiratory
muscle fatigue
Decreases PaO2 and increase in PaCO2

39. Disorders of CNS
Opioid or other drug overdose with CNS
depressants
Respirations are slowed down by drug effect
Insufficient CO2 is excreted and increases
PaCO2

40. Disorders of CNS
Brain stem infarct and head injury
Loss of respiratory drive secondary to brain
stem infarct

41. Disorders of chest wall
Severe soft tissue injury, flail chest, rib fracture,
pain, kyphoscoliosis
They may prevent normal ribcage expansion
resulting in inadequate gas exchange
Changes in the spinal configuration compresses
the lungs and prevents normal expansion of the
chest wall

42. Neuromuscular conditions
Cervical cord injury, phrenic nerve injury
Neural control is lost preventing the use of
diaphragm, resulting in low tidal volume

43. Neuromuscular conditions
GBS, MS, PM,MG,polyneuropathy, effects of NM
blocking agents
Respiratory muscle weakness or paralysis
occurs preventing normal CO2 excretion

44. CLINICAL
MANIFESTATIONS

45. CLINICAL MANIFESTATIONS
May develop suddenly or gradually
Manifestations are related to the extent of
change in PaO2 or PaCO2, the rapidity of
change and the ability to compensate to
overcome the change

46. CLINICAL MANIFESTATIONS-
Hypoxemic –specific
Dyspnoea, tachypnoea
Prolonged expiration (I:E=1:3 or 1:4)
Intercostal muscle retraction
Use of accessory muscles in respiration
Decrease in SpO2(<80%)
Paradoxic chest/abdominal wall movement with
respiratory cycle
Cyanosis

47. CLINICAL MANIFESTATIONS-
Hypoxemic –nonspecific
• Agitation, disorientation, delirium
• Restlessness, confusion, decrease level of consciousness
• Coma
• Tachycardia, hypertension,
• Skin becomes cool, clammy and diaphoretic
• Dysrhythmias
• Hypotension
• Fatigue
• Unable to speak in complete sentences without pausing to breathe

48. CLINICAL MANIFESTATIONS-
Hypercapnic –specific
•Dyspnoea
•Decrease in resp rate or increase rate with
shallow respirations
•Decrease tidal volume and minute
ventilation

49. CLINICAL MANIFESTATIONS-
Hypercapnic –nonspecific
• Morning headache
• Disorientation
• Coma
• Tachycardia, hypotension,
• Dysrhythmias
• Bounding pulse
• Muscle weakness
• Decrease in deep tendon reflexes
• Tremor, seizures
• PLB
• Tripod position

50. DIAGNOSIS
• History collection & physical assessment
• ABG analysis
• Chest X-ray
• Arterial line to monitor BP
• Pulse oximetry
• CBC, S.electrolytes, Urinalysis
• ECG
• Cultures of sputum and blood
• V/Q lung scan or pulmonary angiography
• Hemodynamic parameters-PAP, PAWP, LAP

51. MANAGEMENT
Oxygen therapy
•Supplemental oxygen is administered at 1-3L/min by
nasal canula or 24% to 32% by simple face mask or
venturi mask to correct hypoxaemia
•PPV by ET intubation or NIV mask
•Patients with hypercapnia should receive oxygen
through a low flow oxygen device at 1-2 L/min or
venturi mask at 24% to 28%.
•Closely monitor for changes in mental status,
respiratory rate, and ABG results

52. Mobilization of secretions
•Secretions can be mobilized through
effective coughing, adequate hydration and
humidification, chest physical therapy and
tracheal suctioning

53. Effective coughing and positioning
•The patient is encouraged to cough
•Augmented coughing(quad coughing) is used for
patients with neuromuscular weakness or exhaution.
•It is performed by placing the palm/palms of the hand
on the abdomen below the xiphoid process.
•As the patient ends a deep inspiration and begins the
expiration the hands should be moved forcefully
downward, increasing abdominal pressure and
facilitating the cough.
•This helps to increase expiratory flow and thereby
facilitate secretion clearance.

54. Positioning
•Position the patient either by elevating the
headend of the bed atleast 45 degrees or by
using a reclining chair or chair bed may
help maximize thoracic expansion
•Lateral positions also may be used (good
lung down) as it improves blood supply,
V/Q matching, relieves dyspnoea and helps
in draining out of secretions

55. Hydration and humidification
•Ensure adequate fluid intake of 2-3L/day
to thin and expel the secretions
•IV hydration may be used if oral is
difficult
•Assess for the signs of fluid overload
•Aerosol therapy with sterile NS may be
used to liquefy secretions

56. Chest physical therapy
•It is indicated in patients who produce
more than 30ml of sputum per day or have
evidence of atelectasis or pulmonary
infiltrates.
•If tolerated percussion, vibration and
postural drainage to the affected lung
segments may be given to drain out the
secretions to the larger airways

57. Airway suctioning
•If the patient is unable to expectorate
secretions nasopharyngeal, oropharyngeal or
nasotracheal suctioning is indicated.
•Suctioning through ET or tracheostomy tubes
are also performed

58. Positive pressure ventilation
•PPV may be provided invasively through
oro or nasotracheal intubation or
noninvasively through a nasal or facemask.
• Other means of PPV include NIPPV, BiPAP
or CPAP

59. DRUG MANAGEMENT
Relief of bronchospasm
Short acting bronchodilators eg:
Metaproterenol, Albuterol administered
with nebulizer or MDI with spacer

60. DRUG MANAGEMENT
Reduction of airway inflammation
Corticosteroids in conjunction with
bronchodilators administered IV

61. Reduction of pulmonary congestion
IV diuretics and nitroglycerin
Ca channel blockers and Beta adrenergic
blockers can be administered to decrease
heart rate and improve cardiac output

62. Treatment of pulmonary infections
IV antibiotics eg: Vancomycin,
Ceftriaxone
Serial chest X-rays
Sputum cultures

63. Treatment of anxiety, pain and agitataion
They may result from cerebral hypoxia
Sedation and analgesia with Propofol,
BZDs, Midazolam and opioids

64. SUPPORTIVE THERAPY
Treat the underlying cause
Diagnose and treat rapidly
Monitor the trends using ABGs and other
diagnostic studies

65. Maintain adequate cardiac output
•Monitor BP and MAP
•Administer IV fluids and medications to
treat decreased CO

66. NURSING DIAGNOSIS
•Impaired gas exchange R/T alveolar
hypoventilation, intrapulmonary shunting,
V/Q mismatch and diffusion impairment as
evidenced by hypoxaemia, and/or
hypercapnia

67. •Ineffective airway clearance R/T excessive
secretions, decreased level of
consciousness, presence of an artificial
airway, NM dysfunction, as evidenced by
rhonchi, crackles, ineffective or absent
cough

68. •Ineffective breathing pattern R/T NM
impairment of respirations, pain, anxiety,
respiratory muscle fatigue and
bronchospasm as evidenced by RR<12 or
>24/min, altered I:E ratio, irregular
breathing pattern, use of accessory muscles

69. Differentiation
– Type 1
• Hypoxemic RF
• PaO2 < 60 mmHg with
normal or ↓ PaCO2
• Oxygenation failure
 Associated with acute
diseases of the lung
• Pulmonary edema
(Cardiogenic,
noncardiogenic (ARDS),
pneumonia, pulmonary
hemorrhage, and collapse
– Type 2
• Hypercapnic RF
• PaCO2 > 50 mmHg
• Hypoxemia is common
• Ventilatory failure
 Drug overdose,
neuromuscular disease,
chest wall deformity,
COPD, and Bronchial
asthma