Acute respiratory distress syndrome (ARDS) is a severe lung condition caused by diffuse damage to the alveoli, which results in reduced oxygen exchange and respiratory failure. It has an annual incidence of 75 per 100,000 people in the US and a high mortality rate of 40-60%. ARDS is managed through lung-protective mechanical ventilation with low tidal volumes, application of PEEP, prone positioning, and conservative fluid management. Outcomes are predicted by factors like chronic liver disease, non-pulmonary organ dysfunction, and sepsis, with long-term survivors often having impaired quality of life. Nursing care focuses on supporting respiratory function and managing complications through techniques like airway clearance and treatment of anxiety.

1. ACUTE RESPIRATORY
DISTRESS SYNDROME
COMPILED BY :
MR. ASHISH H. ROY
(NURSING TUTOR)

2. ANATOMY AND PHYSIOLOGY

3. DEFINITION OF ARDS
 Severe, acute lung injury involving diffuse alveolar damage, increased
micro-vascular permeability and non carcinogenic pulmonary edema
 Acute refractory hypoxemia
 Annual incidence 75/100,000 in the US
 High mortality- 40%-60%
 First described in 1967

4. CRITERIA OF ARDS
ARDS
Criteria
Acute
onset of
respiratory
failure
PCWP <18
or absence
of left atrial
HTN
PaO2/FiO2
< 200
Bilateral
infiltrate on
CXR or with
pleural
effusion

6. MORTALITY
 40-60%
 Deaths due to:
 multi-organ failure
 sepsis
 Mortality may be decreasing in recent years
 better Ventilatory strategies
 earlier diagnosis and treatment

7. CAUSES OR RISK FACTORS
Direct
lung
injury
Aspiration of
gastric
contents
Viral/
bacterial
pneumonia
Chest
trauma
Embolism:
fat,air,amnioti
c fluid Inhalation of
toxic
substances
Near
drowning
Radiation
pneumonitis

8. CAUSES CONTINUED…

9. MECHANISM OF INJURY
MODS, SIRS,
Direct injury
Activation of
inflammatory
mediators
Damage to
endothelium
Micro emboli,
vasoconstriction
Increased
permeability,
edema
Destruction of
elastin,
collagen
Destruction of
alveoli
Surfactant
dysfunction

10. Pulmonary
edema
Impaired
gas
exchange
Bronchocon
striction
Outward
migration from
capillaries
Release of
inflammatory
mediatory
Damage to Ty-II
cells
Injury to capillary
membrane
WoB
Hyalin
membrane
formation
Further
decreased
compliance
Atelectasis
Alveolar
compliance
Surfectant
prouction
Permiabiity
Vascular
narrowing
PHTN
ARDS

13. Patho-physiology
Abnormal
gas
exchange
Abn. O2
delivery
/consumpti
on
•Hypoxemia
Cardiopul
monary
interaction
s
•A = Pulmonary
hypertension resulting
in increased RV after
load
•B = Application of high
PEEP resulting in
decreased preload
•A+B = Decreased
cardiac output
Multiple
organ
involveme
nt

14. Phases of ARDS

15. Phases Contd…
Rapid onset of
respiratory failure after
trigger
Diffuse alveolar
damage with
inflammatory cell
infiltration
Hyaline membrane
formation
capillary injury
Protein-rich edema
fluid in alveoli
disruption of alveolar
epithelium
Injury/Acute
exudative phase

18. MANAGEMENT
 Respiratory therapy
 Metabolic management
 Positioning strategies
 Maintenance of cardiac output
 Fluid electrolyte management
 Infection control
 Maintenance of nutritional and fluid balance
 GI ulcer/DVT prophylaxis

19. Respiratory therapy

20. MECHANICAL VENTILATION
 Lung protective strategy
 Higher levels of PEEP required(10-20)mm H2O to attain FiO2 of 60 or less
 Treatment strategy is one of low volume and high frequency
ventilation(ARDSnet protocol)
 If fails alternative modalities
 to be tried

22. Permissive Hypercapnoea
 Low tidal volume (6ml/kg) to prevent over-distention
 Increase respiratory rate to avoid very high level of hypercapnoea
 PaCO2 allowed to rise
 Usually well tolerated
 May be beneficial
 Potential Problems: tissue acidosis, autonomic dysregulation, CNS effect,
and circulatory effects

23. PRONE VENTILATION
 Ventilatory Strategies other than Lung Protective Strategy.
 - Prone Ventilation
 - Liquid Ventilation
 - High Frequency Ventilation
 - Extracorporeal Gas Exchange
 Hemodynamic Management – Fluids, Vasopressors.
 Selective Pulmonary vasodilators.
 Surfactant replacement therapy.

 Anti-inflammatory Strategies.
 a) Corticosteroids.
 b) Cycloxygenase inhibitors.
 Antioxidants
 Anticoagulants.

24. Prone Position
 Effect on gas exchange
 Improves oxygenation – allows decrease Fio2; PEEP

 response rate – 50-70%
 Proposed mechanism – how it improves oxygenation
 1) Increase in FRC
 2) Improved ventilation of previously dependent regions.

26. HIGH FREQUENCY VENTILATION
 Utilizes small volume (<VD) and high RR (100 b/min)
 Avoids over distention (Vili).
 Alveolar recruitment.
 Enhances gas mixing, improves V/Q.
 APPLIC.
 Neonatal RDS.
 ARDS.
 BPF.
 COMPLIC.

 Shear at interface of lung.
 Air trapping.

27. PARTIAL LIQUID VENTILATION
 In ARDS there is increased surface tension which can be eliminated by
filling the lungs with liquid (PFC).
Perflurocarbon:
 Colourless, clear, odourless, inert, high vapour pressure
 Insoluble in water or lipids
 Most Commonly used – perflubron (Perfluoro octy bromide) (Liquivent)
 Bromide radiopaque

28. EXTRACORPOREAL MEMBRANE
OXYGENATION
 Adaptation of conventional cardiopulmonary bypass technique.
 Oxygenate blood and remove CO2 extra corporally.

29. HEMODYNAMIC MANAGEMENT
 Controversial
 Restriction of Fluid
 Benefit Vs detrimental effects

 Obs. Studies Show

 Negative fluid balance is associated with improved survival
 .
 Net positive balance <1 lt. in first 36 hrs. a/w improved survival decrease length
of ventilation, ICU stay and hospitalization.

30. Fluid restriction-pros and cons

31. Hemodynamic management
 Correct Volume deficit

 Promote oxygen delivery
 Adequate volume CVP – 8-12 mmHg
 Transfuse < 10 gm/dl
 Reduce oxygen demand :
 a) Sedation : Analgesia
 b) Treat Hyperpyrexia
 c) Early institution of mech. vent.
 3. Vasopressors
 4. Inotropes

32. PULMONARY VASCULAR CHANGES IN
ARDS/ALI
 Reduced pulmonary vasoconstriction in hypoxic shunt areas, along with
vasoconstriction in well ventilated areas.
 PAH (Pulm. Vasoconst. ; Thromboembolism; Interstitial edema)
 - PAH aggravates edema by increasing inflow pressure.
 - So role of pulm. vasodilators
 Selective Pulmonary Vasodilators :
 Inhaled Nitric oxide (iNo)
 iv almitrine with/without iNo.
 Aerosolized prostacyclins.

33. SURFACTANT REPLACEMENT THERAPY
 In ARDs there is deficiency and fn abn. of surfactant
 Decrease production (injury to type-2 pneumocytes)
 Inhibitors of surfactant fn (TNF- a, reactive oxygen sp. Peroxynitrite,
neutrophil elastases)
 Alteration/Destruction caused by substances in alveolar space (plasma,
fibrinogen, fibrin, alb; Hb)
 Impaired surfactant fn 1) Atelactasis / collapse
 2) Increase edema formation
 In experimental ALI models surfactant replacement.
 Improved lungs fn., compliance, oxygenation.

34. Complications

35. Predictors of outcome
 Factors whose presence can be used to predict the risk of death at the
time of diagnosis of acute lung injury and the acute respiratory distress
syndrome include
 a)chronic liver disease
 b)non-pulmonary organ dysfunction,
 c)sepsis,
 d)advanced age.

36. ARDSnet and Long-term outcome
 120pts randomized to low Vt or high Vt
 a) 25%mortality w/ low tidal volume
 b) 45% mortality w/ high tidal volume
 Standardized tested showed health-related quality of life lower than normal

37. NURSING MANAGEMENT

38.  Ineffective breathing pattern r/t neuro
 muscular impairment of respirations,
 pain, anxiety, decreased level of
 consciousness, respiratory muscle fatigue,
 and bronchospasm as evidenced by
 resp.rate<12 or >24/min, altered I:E
 ratio, irregular breathing pattern, use of accessory muscle

39.  Impaired gas exchange r/t alveolar hypoventilation, ventilation-perfusion
mismatch, and diffusion impairment as evidenced by hypoxemia and / or
hypercapnoea
 Ineffective airway clearance related to
 excessive secretions, decreased level of
 consciousness, presence of an artificial airway,
 neuro muscular dysfunction and pain as
 evidenced by difficulty in expectorating
 sputum, presence of crackles, ineffective or
 absent cough

40.  Impaired tissue perfusion r/t hypoxia, decreased cardiac output secondary
to PEEP, fluid volume deficit
 Risk for injury r/t artificial ventilation, emboli formation.

41.  Risk for fluid volume imbalance r/t sodium and water retention
 Imbalanced nutrition :less than body requirements r/t poor appetite, SoB,
presence of artificial airway, decreased energy, increased calorie
requirement as evidenced by weight loss, weakness, muscle wasting

42.  Anxiety/ fear r/t effects of hypoxemia, situational crisis, fear of death
possibly evidenced by increased tension, restlessness,simpathetic
stimulation

43. BIBLIOGRAPHY
 Lewis.Heitkemper; Medical surgical nursing-assessment and management
of clinical problems;7th ;Mosby Elsevier;1812-18
 Braunwald; Harrison's principle of internal medicine;16th ;McGraw Hill;1523-
31
 Kumar and Abbas; Robbins Basic Pathology ;8th ;Saunders Elsevier; 481-83
 Marilynn E Doenges; Nurses Pocket guide Diagnoses, prioritized
interventions, and rationales;FA Davis 2006
 Xiaoming Jia et al ;Risk factors for ARDS in Patients receiving mechanical
ventilation for >48 hrs;CHEST;April 2008:133;4;853-860

44.  R Phillip Dellinger et al; Surviving sepsis campaign: International guidelines
for management of severe sepsis and septic shock :2008;CRITICAL ARE
MEDICINE;36;1:296-318
 John J Marini; Propagation Prevention: a complementary mechanism for
"lung Protective ventilation in ARDS;CRITICAL CARE MEDIINE2008;36;12:3252-
57
 Dougulas J.E Schuerer;Extra corporeal membrane Oxygenation-Current
clinical practice ,coding and reimbursement; CHEST 2008;134;1:179-184

45. THANKYOU FOR YOUR ACTIVE
LISTENING AND ATTENTION..
IF ANY QUERY REGARDING THE TOPIC
KINDLY ASK….
The End.