2. INTRODUCTION TO RESPIRATORY SYSTEM
2
Mr sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli
3.
4. Acute respiratory distress syndrome (ARDS) is a
sudden, progressive form of respiratory failure in
which the alveolar capillary becomes damaged
and more permeable to intravascular fluid
characterized by severe dyspnea, refractory
hypoxemia, and diffuse bilateral infiltrates.
ACUTE RESPIRATORY
DISTRESS SYNDROME (ARDS)
13. Injury (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
14. Edema Formation in Acute
Respiratory Distress Syndrome
A, Normal alveolus
and pulmonary
capillary
B, Interstitial oedema
occurs with increased flow
of fluid into the interstitial
space
C, Alveolar oedema
occurs when the fluid
crosses the blood-gas
barrier
15. Lunginjury
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
16. Phases
Three distinct stages (or phases) of the syndrome including:
Exudative stage
Proliferative (or fibroproliferative) stage
Fibrotic stage
17. 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.
18. 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.
• Scarring present .
19. Fibrotic Stage ( >10-14 Days)
and extubation becomes
• Inflammation resolves.
• Oxygenation improves
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.
25. IF PNEUMONIA IS CAUSING ARDS THEN CLIENT MAY HAVE
Cough Fever
26. Late signs & symptoms
• Severe difficulty in breathing i.e. 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
27.
28. 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
30. • 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
Spo2 continuously monitored .
31. • Positioning
Turn the patient from supine to prone.
About two-thirds of patients with ARDS
improve their oxygenation after
being placed in a prone
position.
• Fluid therapy
40. NURSING DIAGNOSIS
Impaired physical mobility related to monitoring devices, mechanical ventilation &
medications as characterized by imposed restrictions of movement, decreased
muscle strength & limited range of motion.
Ineffective breathing pattern related to decreased lung
compliance, as evidenced by dyspnea, abnormal ABGs,
cyanoisis & use of accessory muscles.
Impaired gas exchange related to diffusion defect as
evidenced by hypoxia (restlessness, irritability & fear of
suffocation), hypercapnia, tachycardia & cyanosis.
41. 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.
Editor's Notes
Lung contusion is an injury to the lung tissue without actual structural damage.
Surfactant is released from the lung cells and spreads across the tissue that surrounds alveoli. This substance lowers surface tension, which keeps the alveoli from collapsing after exhalation and makes breathing easy.
The pCO2 determines whether an acidosis is respiratory or metabolic in origin. For a respiratory acidosis, the pCO2 is greater than 40 to 45 due to decreased ventilation. Metabolic acidosis is due to alterations in bicarbonate, so the pCO2 is less than 40.
