Education

2. C.NITHYA KALYANI
M.Sc. Nursing 1st Year
GCON,CUDDLORE

6. INDRODUCTION
The body 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 failure develops.

7. INDRODUCTION
Respiratory failure is a broad ,non-specific clinical diagnosis indicating that the
respiratory
System is unable to supply the O2 necessary to maintain or cannot eliminate
sufficient CO2
ACUTE RESPIRATOR 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 a defined as a pao2 value of less than 60 mmhg while
breathing air or paco2 of more than 50mmhg
 Respiratory failure is inadequate gas exchange by the respiratory system with
result that levels of arterial oxygen ,carbon dioxide or both cannot be
maintained their normal range .
 A drop in blood oxygenation is known as hypoxemia .
 A rise in arterial carbon dioxide level is called hypercapnia ,

9. INCIDENCE
 360,000 cases per year
 137 cases per 100,000 population
 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

10. CLASSIFICATION OF RESPIRATORY
FAILURE
RESPIRATORY FAILURE
HYPOXEMIC
(Oxygenation failure)
PaO2<60mmhg on
60% oxygen
HYPERCAPNIC
(ventilator failure)
PaCO2 >45mmhg
And pH<7.35
Acute
(Minutes
To hours)
Chronic
(several
Days or longer)
Acute
(Minutes
To hours
Chronic
(several
Days or long

11. CLASSIFICATION OF RESPIRATORY
FAILURE
 Type I or hypoxemic (paoa2 <60 mmhg ) : failure of oxygen exchange
 Type II or hypercapnic (paco2 >45 mmhg ) : failure to exchanges or
remove carbon dioxide .
 Type III respiratory failure : peri - operative respiratory failure .
 Type IV respiratory failure (shock): secondary cardiovascular instability .

12. TYPE I - HYPOXEMIC RESPIRATORY
FAILURE
 It is characterized by a pao2 off less than 60 mmhg .
 This is the most common of respiratory failure, and it can be associated
with virtually all acute diseases of the lung which generally involve fluid
filling or collapses of alveolar units .
 Some examples of type I respiratory failure are pulmonary edema
,pneumonia ,and pulmonary hemorrhage

13. TYPE –II HYPERCAPNIC REDPIRATORY
FAILURE
 It is characterized by a pac;o2 of more than 00 mmhg .
 Hypoxemia is common in patient with hypercapnic respiratory
failure who are breathing room air .
 Common etiologies includes drug overdose , neuromuscular
diseases ,chest wall abnormalities ,and severe airway disorder .
E.g. asthma ,COPD

14. TYPE III – PERIOPERATIVE RESPIRATORY
FAILURE
 RESIDYAL anesthesia effects ,post-operative pain and
abnormal mechanics contribute to decreasing FRC and
progressive collapse of dependent lungs .
 This is generally a subject of type I failure but is sometimes
considered separately because it is so common.
 Causes of peri-operative atelectasis includes : decreased
functional residual capacity anesthesia , upper abdominal
incision ,airway secretions ,supine /obese /ascites .
 Effective means of preventing or treating atelectasis include
incentive spirometry

15. TYPE IV – SHOCK RESPIRATORY FAILURE
 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. ACUTE RESPIRATORY FAILURE
CLASSICIFICATION
1. Hypoxemic respiratory 2.Acute ventilator
failure
failure . Pao2 decreased
Pao2 low (<60mmhg) . Paco2 increased
Paco2 normal or low . PA_ao2 normal
PA_ao2 increased . PH decreased

17. TYPE OF RESPIRATORY FAILURE
ACUTE RESPIRATORY FAILURE
CHRONIC RESPIRATORY FAILURE

18. 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

19. 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
Eg : acute exacerbation of advanced COPD

20. HYPOXEMIC RESPIRATORY FAILURE
Hypoxemic respiratory failure is characterized by a
pao2 of less than 60mm hg normal or low paco2
This is the most common form of respiratory ,and it
can be associated with virtually all acute diseases of the
lung ,which generally involve fluid filling or collapse of
alveolar units

21. FACTORS AFFECTS HYPOXEMIC
RESPIRATORY FAILURE
v/q mismatch
shunt
Diffusion limitation
Alveolar
hypoventilation
Increase co2
Decrease po2

22. VENTILAION PERFUSION
MISMATCH(V/Q)
An imbalance between alveolar ventilation and
pulmonary capillary blood flow
Normal v/q =1 (1ml air /1ml of blood )

23. SHUNT
 In medicine a shunt is a small hole or a small passage which
moves or allows movement of fluid from one part of the body to
another .
TWO TYPE OF SHUNTS
 ANATOMIC SHUNT
 PHYSIOLOGIC SHUNT

24. ANATOMIC SHUNT
When a portion of blood bypass the lungs through an
anatomic channel
In healthy individuals
1) a portion of the bronchial circulation’s (blood
supply to the conducting zone of airways ) venous
blood drains into the pulmonary vein
2)a portion of the coronary circulation’s venous blood
drains through the veins into the left ventricle

25. Congenital abnormalities
 1) intra – cardiac shunt [e.g. tetralogy of fallot ,ventricular
septal defect + pulmonary artery stenosis ]
 2)intra –pulmonary fistulas [direct communication between a
branch of the pulmonary artery and a pulmonary vein ]

26. PHYSIOLOGIC SHUNT
In disease states ,a portion of the cardiac output
goes through the regular pulmonary vasculature but
does not come into contact with alveolar air due to
filling of the alveolar spaces with fluid (e.g
pneumonia ,drowning ,pulmonary edema )

27. SHUNT
extra pulmonary shunt
response to PEEP not response to PEEP
ARDS right to left shunt
severe pulmonary edema pulmonary AVM
Intra pulmonary shunt

28. DIFFUSION LIMITATIONS
 Gas exchange is comprised
by a process that thickness or
Destroys membrane
1. Pulmonary fibrosis
2. ARDS
A classic sign of diffusion limitation
is hypoxemia during exercise but not at rest .

29. ALVEOLAR HYPOVENTILATION
Alveolar hypoventilation is a rare disorder in which a
person does not take enough breath per minute .mainly
due to hypercapnic respiratory failure but can cause
hypoxemia .
Increased pco2 with decreased po2
Restrictive lung disease
CNS disease
Neuromuscular diseases.

30. HYPERCAPNIC RESPIRATORY FAILURE
This is characterized by a paco2 of more than 50
mmhg . Hypoxemia is a common in patients with
hypercapnic respiratory failure who are breathing in
room air . The pH depends on the level of
bicarbonate ,which in turn ,is dependent on the
duration of hypercapnia .

31. FACTERS THAT AFFECTS HYPERCAPNIC
FAILURE
1) Abnormalities of the airways alveolar flow obstruction
and air trapping ;asthma ,COPD ,and cystic fibrosis .
2) Abnormalities of the CNS suppress drive to breath
3) Drugs e.g. narcotics
4) Head injury and spinal cord injury

32. RISK FACTORS FOR RESPIRATORY FAILURE
People who have diseases or conditions that affect the
muscles,nerve,bones,or tissue that support breathing
are at risk for respiratory failure .
People who have lung diseases or conditions also are at
risk for respiratory failure

34. ETIOLOGY OF HYPOXEMIC
RESPIRATORY FAILURE
Chronic bronchitis and emphysema
Pneumonia ,asthma
Pulmonary edema ,bronchiectasis
Pulmonary fibrosis
Asthma
Pneumothorax
Pulmonary embolism
Pulmonary arterial hypertension
Pneumoconiosis
Granulomatous lung disease

35. ETIOLOGY OF HYPERCAPNIC
RESPIRATORY FAILURE
 In acute ventilator failure ,the respiratory load placed on the
lungs, to exchange co2 is impaired by;
 1) problem of resistance to moving air in and out of lung ,
 2)the ability of lung to expand and contact (elastic recoil)and
 3)conditions that increase the productions of co2 or decrease
the surface available for exchange of gases .

36. PATHOPHYSIOLOGY OF HYPOXEMIC
RESPIRATORY FAILURE

37. hydrostatic pressures in the pulmonary vessels creates imbalance in starling forces
Increase in fluid filtration into interstitial spaces of lungs that exceeds the lymphatic capacity to drain the fluid away.
Increasing volumes of fluids leak the alveolar space
The lymphatic system attempts to compensate by draining excess interstitial fluid into the vascular system through the hilar lymph
nods
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

38. PATHOPHYSIOLOGY OF HYPOCAPNIC
RESPIRATORY FAILURE

39. PATHOPHYSIOLOGY OF HYPOCAPNIC RESPIRATORY FAILURE
In obstructive type respiratory failure ,the residual pressure in the chest impairs inhalation and increase
the workload of 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 alveoli tends to collapse
No oxygenation or blood flow to the alveoli occurs
Leads to true intra pulmonary shunt and decreased lung complaisance
Leads to hypoxia

40. CLINICAL FEATURE OF HYPOXEMIC
RESPIRATORY FAILURE
 Hypoxemia as alveolar membrane is thickened by fluid that
impaired the gas exchange
 Dyspnea ,tachypnea
 Weak and thread tachycardia
 Hypertension
 Orthopnea at less than 90 degrees
 Coughing as to attempt to rid the fluid of 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

41. CLINICAL FEATURES OF HYPOXEMIC
RESPIRATORE
 Patient may be anxious and restless from hypoxemia
 Chest auscultation reveals crackles ,wheeze ,and presence of s3
sound spo2 is less than 85%
 Arterial pao2 revels less than 50%
 Respiratory alkalosis because of tachypnea
 Pressure in pulmonary artery pulmonary wedge
 Pressure will increase
 Chest x-ray shows area of white out where fluid has replaced air
filled lung tissues
 Right ventricular failure may be noted

42. CLINICAL FEATURE OF HYPERCAPNIC
RESPIRATORY FAILURE
 Altered respiratory rate and patterns
 Breaths are shallow due to spasm of the airway
 Client become confused ,less conversant, and are difficult to
arouse
 Pulses paradoxes
 Pulse oxymetry shows steadily decrease in spo2
 ABG analysis shows falling pao2 and rising paco2

43. 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 ,inhalation injury and some interstitial lung diseases

44. DIAGNOSTIC EVALUATION
Physical findings
Hypotension usually with sings of poor perfusion
suggests severe sepsis
Hypertension usually with sings of poor perfusion
suggests pulmonary edema.
Wheezing suggests airway obstruction ,
bronchospasm, secretions, pulmonary edema

45. DIAGNOSTIC EVALUATION
 LABORATORY TESTS
ABG analysis
Quantifies level of gas exchange abnormality .
Identifies type and chronicity of respiratory failure
COMPLETE BLOOD COUNTS
Anemia may cause cardiogenic pulmonary edema leukocytosis ,or leukopenia
suggestive of infection
MICROBIOLOGY
Respiratory culture :sputum /tracheal aspirate blood ,urine and body fluid (e.g
pleural) culture

46. DIAGNOSTIC EVALUATION
DIAGNOSTIC INVESTICATIONS
 Chest radiography : identify chest wall ,pleural and lung parenchymal with
opacities present
 ELECTROCARDIOGRAM: identify arrhythmias ,ischemia, and ventricular
dysfunction
 ECHOCARDIOGRAPHY :identify right and left ventricular dysfunction
 PULMONARY FUNCTION TESTS /BED SIDE SPIROMETRY: identify
obstruction ,restriction .may be difficult to perform if critically ill.
 BRONCHOSCOPY :obtain biopsies ,bronchoscopy may not be safe for
critically ill patient

47. MANAGEMENT OF THE PATIENT
RESPIRATORY FAILURE
Cardiac monitoring ,vitals sign and spo2
monitoring
Underlying causes identification and treating
O2 therapy
Position
Mobilization of secretions
correct hypoxia by positive pressure ventilation

48. O2 THERAPHY
oxygen therapy is the administration of
oxygen at concentrations greater than
that in room air to treat
or prevent hypoxemia
Mechanism of action: reverses
hypoxemia

49. O2 THERAPHY
If seconds to v/q mismatch 1-3Lor 24% - if secondary to v/Q
match 1-3L or 24%-32 by mask 32%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
concentrations possible
O2 at high concentrations for longer than 48 hours causes o2
toxicity

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

51. 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

52. PREVENTION OF OXYGEN TOXICITY
 If high concentrations of oxygen are necessary ,it is important to
minimize the duration of administration and reduces its concentration as
soon as possible
 Often ,positive end expiratory pressure (PEEP)or continuous positive air
way pressure (CPAP) is used with oxygen therapy to reverse or prevent
micro atelectasis ,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

53. POSITION OF THE PATIENT
The patient should be stay upright position
Positioning -45 degree or recliner chair or bed

54. MOBILIZATION OF SECRETIONS
 Effective coughing :assist in cough
 Positioning :head of bed 45 degree 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
 Air way suctioning

55. POSITIVE PRESSURE VENTILATION
(PPV)
Invasively through oro or nasotracheal intubation
Non invasively (NIPPV) through mask
Used for acute and chronic respiratory failure
BiPAP –different levels of pressure for inspiration and expiration
CPAP- for sleep apnea.
Used best in chronic respiratory failure in patients with chest
wall neuromuscular disease, also with HF and COPD.

56. POSITIVE PRESSURE VENTILATION
(PPV)
The provision of air under pressure by a mechanical
respirator ,a machine designed to improve the
exchange of air between the lungs and the atmosphere.

57. NON INVASIVE PPV

58. NON INVASIVE PPV

59. EMERGENCY MAMAGEMENT OF
HYPOXEMIC RESPIRATORY FAILURE
RESPIRATORY FAILURE
Secure air way
Supplemental oxygen as needed
Treat underlying condition
Invasive mechanical
Ventilation Non invasive
Mechanical ventilation
Need for endotracheal
Intubation or tracheostomy
YES
NO
FAILS

60. MAMAGEMENT OF HYPOXEMIC
RESPIRATORY FAILURE
REDUCE PRELOAD
 Treating the underlying causes .
 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 &after load
 Opioid analgesics :morphine iv is an excellent adjunct .causes arterial
dilatation ,which reduces systemic vascular resistance and may increase
cardiac output

61. MAMAGEMENT OF HYPOXEMIC
RESPIRATORY FAILURE
 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.

62. MAMAGEMENT OF HYPOXEMIC
RESPIRATORY FAILURE
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 urine output

63. MAMAGEMENT OF HYPERCAPNIC
RESPIRATORY FAILURE
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 ipratropium
,theophylline ,and corticosteroids
If infection is cause then broad spectrum antibiotics are used
.E.G vancomycin

64. MAMAGEMENT OF HYPERCAPNIC
RESPIRATORY FAILURE
Maintain oxygenation
 Oxygen by mask may be adequate to support oxygenation .
 Using forms of NPPV such as CPAP reduce the workload of
 breathing by decrease the force needed to overcome the
pressure
in the chest
 Manage the underlying problem
 Maintain ventilation

65. MECHANICAL VENTILATOR INDICATION IN
HYPERCAPNIC RESPIRATORY FAILURE
Mechanical ventilation
Correct hypoxemia
Correct respiratory acidosis
Assistance for neutral and muscle dysfunction
Enhance ventilation
Optimize cardiac function
Meet increased metabolic demand
Hyperventilation may be used as a short term
adjunct
To treat to acutely elevated ICP

66. GERONTOLOGIC CONSIDERATIONS
 Physiologic aging results in
 Ventilator capacity
 Alveolar dilation
 Larger air spaces
 Loss of surface area
 Diminished elastic recoil
 Decreased respiratory muscle strength
 Chest wall compliance
 Life long smoking
 Poor nutritional status

67. COMPLICATIONS
 Pulmonary emboli
 Barotrauma
 Pulmonary fibrosis
 Infection ,sepsis
 ARDS,pneumonia
 Cardiac arrhythmias ,hypotension, acute MI
 Renal failure
 Hemorrhage
 Malnutrition

68. NURSING MANAGEMENT
Theory of application
 Florence nightingale’s environmental theory can be applied in
condition
 The theory is focused on the environment . The environment is
viewed as all the conditions and influences the effect the 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

69. NURSING MANAGEMENT
Nursing assessment
History of smoking ,family history
,occupational history
Respiratory rate ,depth and characteristics
ABG analysis
Ineffective breathing pattern
Deficient knowledge

70. NURSING DIAGNOSIS
Impaired gas exchange related to capacity 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 the lungs
Impaired spontaneous ventilation related to imbalance between
ventilator capacity and ventilator demand evidence by SPO2
and ABG findings
Ineffective breathing pattern related to underlying disease
process and artificial airway and ventilator system abnormal
ABG findings and respiratory rate

71. NURSING DIAGNOSIS
 Ineffective airway clearance related to increased mucus production
associated with continuous positive –pressure mechanical ventilation
evidence by wheezes and crackles sound in lungs
 Risk for trauma and infection related to endotracheal intubation or
tracheotomy
 Impaired physical mobility related to ventilator dependency
 Impaired verbal communication related to endotracheal tube and
attachment to ventilator
 Defensive coping and powerlessness related to ventilator dependency

72. NURSING INTERVENTION
 Patients with acute respiratory failure should be closely observed for
potential deterioration
 Monitoring may involve intermittent /continual pulse oximetry.
 Any change in physiological signs should be reported promptly to the
senior practitioner
 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

73. NURSING DIAGNOSIS
 Administer diuretics, anticoagulants or corticosteroids as prescribed
 Prepare the client for intubation and mechanical ventilation using PEEP
 Nutrition 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 than carbohydrates

74. SUMMARY
So today we discussed definition,
Classification ,etiology factors
,pathophysiology,clinincal features
,diagnostic studies ,medical management
,nursing management ,and complications
of acute respiratory failure

75. CONCLUSSION
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