acute repiratory distress syndrome for adult

1. ACUTE RESPIRATORY DISTRESS SYNDROME
PREPARED BY:
RN Arpana Bhusal
BNS

2. Contents
Introduction
Definition
Risk factor
Etiology
Pathophysiology
Phases
Clinical manifestation

3. Content cnt…
Diagnostic evaluation
Management
Medical
Pharmacological
Nursing
Complication
References

5. Introduction
Acute respiratory distress syndrome (ARDS) is a
sudden, progressive form of respiratory failure
characterized by severe dyspnea, refractory
hypoxemia, and diffuse bilateral infiltrates.

6. Introduction
It follows acute and massive lung injury that
results from a variety of clinical states, often
occurring in previously healthy people.

7. ARDS definition is based upon 5 key
clinical features:
1. a risk factor for the development of acute respiratory
distress (e.g., sepsis, trauma, pneumonia, aspiration,
pancreatitis)
2. severe hypoxemia despite a relatively high fraction
of inspired oxygen (FIO2).
3. decreased lung compliance.
4. bilateral pulmonary infiltrates.
5. lack of clinical evidence of cardiogenic pulmonary
edema.
Within one week of known clinical insult or new or
worsening respiratory symptoms.

8. The syndrome was first described in 1967,
and has been referred to by several terms,
including shock lung, wet lung, posttraumatic
lung, congestive atelectasis, capillary leak
syndrome, and adult hyaline membrane
disease

10. RISK FACTORS
Age over 65 years
Chronic lung disease
A history of alcohol misuse or cigarette smoking
ARDS can be a more serious condition for people
who:
Have toxic shock
Are older
Have liver failure
Have a history of alcohol misuse

11. ETIOLOGY
Direct lung injury include:
• Gastric aspiration
• Bacterial, fungal, or viral pneumonia
• Pulmonary contusion
• Near drowning
• Prolonged inhalation of high concentrations of
oxygen, smoke or toxic substances.

12. Indirect injury include:
• Sepsis
• Shock (any cause)
• Drug overdose
• Fat embolism
• Prolonged hypotension
• Non-thoracic trauma
• Cardiopulmonary bypass

13. Indirect injury cnt…
• Head injury
• Acute pancreatitis
• Uremia
• Hematologic disorders, such as disseminated
intravascular coagulation, or multiple blood
transfusions

24. PATHOPHYSIOLOGY

26. Phases
Three distinct stages (or phases) of the syndrome
including:
1. Exudative stage
2. Proliferative (or fibro-proliferative)
stage
3. Fibrotic stage

27. Exudative Stage (0-6 Days)
Characterized by:
Accumulation of excessive fluid in the lungs due to
exudation (leaking of fluids) and acute injury.
Hypoxemia is usually most severe during this phase
of acute injury, as is injury to the endothelium
(lining membrane) and epithelium (surface layer of
cells).
Some individuals quickly recover from this first
stage; many others progress after about a week into
the second stage.

28. Proliferative Stage (7-10 Days)
Connective tissue and other structural elements in
the lungs proliferate in response to the initial
injury, including development of fibroblasts.
The terms "stiff lung" and "shock lung" frequently
used to characterize this stage.
Abnormally enlarged air spaces and fibrotic tissue
(scarring) are increasingly apparent.

29. Fibrotic Stage ( >10-14 Days)
Inflammation resolves.
Oxygenation improves and extubation becomes
possible.
Lung function may continue to improve for as long
as 6 to 12 months after onset of respiratory failure,
depending on the precipitating condition and severity
of the initial injury.
Varying levels of pulmonary fibrotic changes are
possible.

31. EARLY SYMPTOMS
• Restlessness
• Severe dyspnea
• Confusion
• Low blood pressure
• Extreme tiredness
• Change in patient behaviour
Mood swing
Disorientation
Change in LOC

32. LATE SYMPTOMS
• Severe difficulty in breathing i.e., labored, rapid and
shallow breathing.
• Shortness of breath.
• Tachycardia
• Thick frothy sputum
• Metabolic acidosis
• Cyanosis (blue skin, lips and nails)
• Abnormal breath sounds, like crackles, rhonchi
• Decreased PaCo2 with respiratory alkalosis.
• Decreased PaO2
• ↓ urine output

34. Diagnostic evaluation
Complete history
 On physical examination-Auscultation reveals
abnormal breath sounds- wheezing, crackles.
The first tests done are :
 Arterial blood gas analysis
 Blood tests
 Urine test and culture
 Chest x-ray
 Sputum cultures and analysis

35. Diagnosis cnt..
Other tests are :
Chest CT Scan
Echocardiogram
lung biopsy
Bronchoscopy

37. MANAGEMENT

38. Persons with ARDS are hospitalized and require
treatment in an intensive care unit.
No specific therapy for ARDS exists.
1. Medical management
Supportive measures :
Supplemental oxygen
Mechanical VENTILATION

39. Positioning strategies
Fluid therapy
Respiratory therapy
2. Pharmacological management
3. Nursing management

40. Protective Lung Ventilation
During the early stages of ARDS, use mechanical
ventilation to open collapsed alveoli.
The primary goal of ventilation is to support
organ function by providing adequate ventilation
and oxygenation while decreasing the patient’s
work of breathing.
But mechanical ventilation itself can damage the
alveoli, making protective lung ventilation
necessary and believe to reduce the mortality.

41. Positioning strategies
Prone positioning
About two-thirds of patients with ARDS improve their
oxygenation after being placed in a prone position.
Mechanisms that may explain the improvement
include:
1. increased functional residual capacity;
2. change in regional diaphragmatic motion
3. perfusion redistribution;
4. improved clearance of secretions.
(PaO2 level is more in prone than supine position.

42. Lateral rotation therapy
To stimulate postural drainage and help
mobilized the secretion.
The lateral movement of bed is done for
18-24 hours slowly.

43. Fluid management
Distinction between primary ARDS due to
aspiration, pneumonia, or inhalational injury,
which usually can be treated with fluid
restriction,
from secondary ARDS due to remote infection
or inflammation that requires initial fluid and
potential vasoactive drug therapy is central in
directing initial treatments to stabilize the
patient

44. Fluid management cnt…
Give either crystalloids or colloids to replace
the fluids that have leaked from the capillaries
into the alveolar spaces.
Blood transfusions can improve oxygen
delivery but remember they can also cause an
increased inflammatory response and increase
the risk of infection and death.

45. Respiratory therapy
Primary goal is o2 therapy is correct hypoxemia.
O2 administered by mask.
Spo2 continuously monitored .
O2 administration give patient the lowest
concentration that results in Pao2 of 60 mm hg or
greater when the fio2 exceeds 60% for more than
48 hours the risk of o2 toxicity increases.
Mechanical ventilation is provide to client

46. Pharmacological management
Antibiotics
Anti-inflammatory drugs; such as
corticosteroids
Diuretics
Drugs to raise blood pressure
Anti-anxiety
Muscle relaxants
Inhaled drugs (Bronchodilators)

47. Pharma mgmt cnt…
Specific therapy
human recombinant interleukin-1 receptor
antagonist
neutrophil inhibitors
pulmonary- specific vasodilators
surfactant replacement therapy

49. Nursing management
NURSING DIAGNOSIS
1. Ineffective breathing pattern related to
decreased lung compliance, decreased energy as
characterized by dyspnea, abnormal ABGs,
cyanosis & use of accessory muscles.
2. Ineffective tissue perfusion(pulmonary)
related to decreased blood circulation.

50. 3. Risk for decreased Cardiac output related to
positive pressure ventilation.
4. Impaired physical mobility related to
monitoring devices, mechanical ventilation &
medications as characterized by imposed
restrictions of movement, decreased muscle
strength & limited range of motion.

51. 6. Risk for impaired skin integrity related to
prolonged bed rest, prolonged intubation &
immobility.
7. Knowledge deficit related to health condition,
treatment modalities & hospitalization as
characterized by increased frequency of
questions posed by patient.

52.  Correcting breathing pattern
 Assess for hypoxia, headache, restlessness,
apprehension, cyanosis, behavioral changes.
 Monitor vital signs, ECG, oximetery, and
ABG analysis for oxygenation.
 Monitor patients response to IV
fluids/vasopressors

53.  Monitor oxygen therapy used to relieve
hypoxemia.
 Prepare patient for assisted ventilation when
hypoxemia.
 Encourage deep breathing and coughing
exercises after chest physiotherapy.
 Instruct patient to cover nose and mouth while
coughing.

54.  Improving tissue perfusion
 Closely monitor for shock decreasing blood
pressure, tachycardia, cool, clammy skin.
 Monitor prescribed medications given to
preserve right ventricular filling pressure,
increased BP.
 Patient should be kept in bedrest to reduce
oxygen demand and risk of bleeding.

55.  Monitor urinary output hourly, because there
may be reduced renal perfusion and decreased
GFR.
 Consider physician evaluation when these
signs are present, especially if accompanied
by cyanotic nail beds, circumoral pallor, and
increased respiratory rate.

56.  Reducing anxiety
 Correct dyspnea and relief physical
discomfort.
 Explain diagnostic prcedures and the patients
role :correct misconception.
 Listen to patiet concers; attentive listening
relieves anxiety and reduces emotional
distress.
 Speak calmly and slowly.

57. Evaluate patient for sign of hypoxia
thoroughly when anxiety, restlessness, and
agitation of new onset are noted, before
administering as needed sedatives.

58. Rest and sleep
Patient should be kept in bed rest to reduce
oxygen demand.
Encourage use of relaxation techniques and
diversional activities.
Position with head of bed should be slightly
elevated.
Maintain semi-fowler’s position

59. Controlling infection
Recognize early manifestations of respiratory
infection increased dyspnea, fatigue; change in
color, amount, and character of sputum;
nervousness; irritability; low-grade fever.
Obtain sputum for Gram stain and culture and
sensitivity.
Administer prescribed antimicrobials to control
secondary bacterial infections in the bronchial
tree, thus clearing the airways.

60. COMPLICATIONS
Common complications are;
Nosocomial pneumonia:
Barotrauma
 Renal failure

61. COMPLICATIONS cnt…
Other complications are
 stress ulcers,
 Tracheal ulceration,
 Blood clots leading to deep vein thrombosis &
 pulmonary embolism.
Infection –
 catheter related infection
 hospital acquired –pneumonia
 sepsis

62. Respiratory infections-
O2 toxicity
ventilator -associated pneumonia
pulmonary emboli
Acute renal failure
Endotracheal tube intubation complications
laryngeal ulceration
tracheal ulceration

63. Psychological complication
Delirium
Sleep deprivation
Post-traumatic stress syndrome

64. Management of complication
Hospital acquired pneumonia – it occur in 68% of
patient with ARDS in which include
 Infection
 Contaminated medical equipment
 Aspiration
 Prolonged ventilation
 Respiratory tract infection
 Main control on infection, sterile techniques ,elevate
the bed to prevent aspiration.

65. References
Brunner and Suddarth, “Text Book of Medical and
Surgical Nursing”, 12th edition, Wolter Kluwer India
Private Limited
Lewis, Heitkemper Dirksen, “Medical Surgical
Nursing” 6th edition, mosby Publications
Mandal G.N (2016) “A Textbook of Medical Surgical
Nursing”. 5th edition. Kathmandu.Makalu Publication
House.2078/03/11 at 4:30 pm
2019. Mayo Foundation of Medical Foundation and
Research. ARDS.
https://www.mayoclinic.org@2021/06/25 at 3pm.

66. 2019. Mayo Foundation of Medical
Foundation and Research. ARDS.
https://www.mayoclinic.org@2021/06/25 at
3pm.
October 23, 2018. ARDS.
https://www.slideshare.net/PINKEERATHEE
@2021/06/25 at 11AM