This document provides information about acute respiratory distress syndrome (ARDS), including its pathophysiology, clinical manifestations, diagnosis, treatment, nursing care, and complications. ARDS is a respiratory failure condition caused by lung injury and results in increased permeability of the alveolar-capillary membrane. It progresses through exudative, proliferative, and fibrotic phases. Treatment involves supportive care, mechanical ventilation, positioning strategies, and managing complications such as nosocomial pneumonia and renal failure.
3. Acute respiratory distress syndrome
(ARDS) is a sudden, progressive form of
respiratory failure characterized by severe
dyspnea, refractory hypoxemia, and diffuse
bilateral infiltrates.
ACUTE RESPIRATORY
DISTRESS SYNDROME (ARDS)
4. • It follows acute and massive lung injury
that results from a variety of clinical
states, often occurring in previously
healthy people.
5. The syndrome was first described in 1967,
and has been referred to by several terms,
including shock lung, wet lung, post-
traumatic lung, congestive atelectasis,
capillary leak syndrome, and adult hyaline
membrane disease.
17. Insult (direct and indirect)
Activation of inflammatory cells and
mediators (serotonin, histamine,
bradykinin)
Damage to alveolar capillary
membrane
Increased permeability of alveolar
capillary membrane
Influx of protein rich edema fluid
and inflammatory cells into air filled
spaces. Dysfunction of surfactant.
Loss of lung tissue
18. Lung injury
Release of Vasoactive substances
(serotonin, histamine, bradykinin)
Damaged Type II alveolar cell
Surfactant production
Alveolocapillary
membrane
permeability
Vascular
narrowing &
obstruction
Alveolar
Compliance and recoil
Bronchoconstriction
Outward migration
of blood cells &
fluids from capillaries
Atelectasis
Pulmonary Edema
Hyaline membrane
formation
Lung
compliance
Impairment in
gas exchange
ARDS
Pulmonary
hypertension
19. Phases
Three distinct stages (or phases) of the syndrome including:
Exudative stage
Proliferative (or fibroproliferative) stage
Fibrotic stage
20. 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.
21. 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.
22. 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.
28. IF PNEUMONIA IS CAUSING ARDS THEN CLIENT MAY HAVE
Cough Fever
29. Late signs & symptoms
• Severe difficulty in breathing i.e., labored, rapid
breathing.
• Shortness of breath.
• Tachycardia
• Thick frothy sputum
• Metabolic acidosis
• Cyanosis (blue skin, lips and nails)
• Abnormal breath sounds, like crackles
• Decreased PaCo2 with respiratory alkalosis.
• Decreased PaO2
30.
31. Complete history
On physical examination-Auscultation reveals
abnormal breath sounds- wheezing, crackles.
The first tests done are :
Arterial blood gas analysis
Blood tests
Chest x-ray
Bronchoscopy
Sputum cultures and analysis
Other tests are :
Chest CT Scan
Echocardiogram
33. • Persons with ARDS are hospitalized and
require treatment in an intensive care unit.
• No specific therapy for ARDS exists.
• Supportive measures :
Supplemental oxygen
Mechanical VENTILATION
34. • Positioning strategies
Turn the patient from supine to prone.
Another position is lateral rotation
therapy
• Fluid therapy
35. 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 in prone is more than supine
position )
36. Lateral rotation therapy
To stimulate postural drainage and help
mobilised the secretion.
The lateral movement of bed is done for
18-24 hours slowly.
37. 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.
38. Respiratory therapy
• Primary goal is o2 therapy is correct hypoxemia .
• O2 administered by mask.
• Spo2 continuously mointored .
• O2 administration is give patient the lowest
concerntration 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
38
43. Management of complication
• Hospital acquired pneumonia – it occur in 68% of
patient with ARDS in which include
Infection
Contaminated medical equipments
Aspiration
Prolonged ventilation
Respiratory tract infection
Main control on infection, sterile techniques ,elevate
the bed to prevent aspiration.
43
45. NURSING DIAGNOSIS
Ineffective breathing pattern related to decreased lung
compliance, decreased energy as characterized by dyspnea,
abnormal ABGs, cyanoisis & use of accessory muscles.
Impaired gas exchange related to diffusion defect as
characterized by hypoxia (restlessness, irritability & fear of
suffocation), hypercapnia, tachycardia & cyanosis.
Risk for decreased Cardiac output related to positive
pressure ventilation.
46. Ineffective protection related to positive pressure
ventilation, decreased pulmonary compliance & increased
secretions as characterized by crepitus, altered chest
excursion, abnormal ABGs & restlessness
Impaired physical mobility related to monitoring devices,
mechanical ventilation & medications as characterized by
imposed restrictions of movement, decreased muscle
strength & limited range of motion.
Risk for impaired skin integrity related to prolonged bed
rest, prolonged intubation & immobility.
Knowledge deficit related to health condition, treatment
modalities & hospitalization as characterized by increased
frequency of questions posed by patient.
