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Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by rapid onset of severe breathing difficulties, low oxygen levels in the blood, and diffuse fluid buildup in the lungs. It consists of three phases - exudative, proliferative, and fibrotic. The exudative phase involves fluid accumulation in the lungs over 7 days, while the proliferative phase sees inflammation and scarring over 2 weeks. Some patients may progress to long-term ventilation if they enter the fibrotic phase. Treatment focuses on treating the underlying cause, providing oxygen, and supporting breathing with mechanical ventilation. Mortality is high and associated with factors like age, sepsis, and preexisting organ dysfunction.

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Pooja Shashidharan
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170 views24 pages

Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by rapid onset of severe breathing difficulties, low oxygen levels in the blood, and diffuse fluid buildup in the lungs. It consists of three phases - exudative, proliferative, and fibrotic. The exudative phase involves fluid accumulation in the lungs over 7 days, while the proliferative phase sees inflammation and scarring over 2 weeks. Some patients may progress to long-term ventilation if they enter the fibrotic phase. Treatment focuses on treating the underlying cause, providing oxygen, and supporting breathing with mechanical ventilation. Mortality is high and associated with factors like age, sepsis, and preexisting organ dysfunction.

Uploaded by

Pooja Shashidharan
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd

Acute respiratory distress

syndrome
(ARDS)
DEFINITION
• Acute respiratory distress syndrome is a
clinical syndrome of severe dyspnoea of rapid
onset, hypoxaemia and diffuse pulmonary
infiltrates leading to respiratory failure.
CAUSES
DIAGNOSTIC CRITERIA
PATHOPHYSIOLOGY
• ARDS consists of three phases:
A. Exudative phase:
• This phase lasts for about seven days.
• Injury involving alveolar capillary endothelial cells
and type I pneumocytes cause exudation of highly
proteinaceous fluid into the interstitial and alveolar
spaces.
• The oncotic pressure is normal.
• B. Proliferative phase:
• This phase lasts for about two weeks (8th-21st
days)
• This phase is characterised by prominent
interstitial inflammation and early
fibrosis
• C. Fibrotic phase:
• Many ARDS patients recover lung
function four weeks after initial lung injury.
• Some will enter a fibrotic phase that may
require long term support on mechanical
ventilation
• Secondary effects include loss of surfactant and
impaired surfactant production.
• The net effect is alveolar collapse and reduced lung
compliance, most marked in dependent regions of
the lung (mainly dorsal in supine patients).
The affected airspaces become fluid-filled and can
no longer contribute to ventilation, resulting in
hypoxaemia and hypercapnia (due to inadequate
ventilation
in some areas of the lung): that is, ventilation–
perfusion mismatch
CLINICAL FEATURES
• Tachypnoea followed by
• dyspnoea,
• cyanosis,
• extensive
crackles over both lung fields.
INVESTIGATIONS
• Investigations
1. ABG analysis: Demonstrates hypoxaemia.

2. Chest X-ray: Diffuse, extensive alveolar


shadowing bilaterally and more peripherally.
• 3. Haemodynamic measurements: Pulmonary
capillary wedge pressure < 18 mm Hg;
• Pcwp > 18 mm Hg suggests hydrostatic
pulmonary oedema.

4. Investigations to determine specific cause


DIFFERENTIAL DIAGNOSIS
 cardiogenic pulmonary edema,(most common)
 diffuse pneumonia, and
 alveolar hemorrhage.
Less common diagnoses:
acute interstitial lung diseases ,
acute immunologic injury (e.g., hypersensitivity
pneumonitis; ),
toxin injury (e.g., radiation pneumonitis)
and neurogenic pulmonary edema
TREATMENT
• 1. Treat the cause
2. Oxygen inhalation
3. Respiratory support with Mechanical
Ventilation
• Set PEEP to minimize Fio2 and optimize Pao2.
• PEEP helps in the redistribution of capillary
blood flow resulting in improved V/Q
matching and the recruitment of previously
collapsed alveoli and prevention of their
collapse during exhalation
• Oxygenation can also be improved by
increasing mean airway pressure with inverse
ratio ventilation(Inspiration: Expiration ratio >
1:1).
• Prone position ventilation can also be tried
• Sedation and muscle paralysis to prevent the
patient from fighting the ventilator and oxygen
utilisation.
• If cardiac output cannot be preserved, inotropic
agents, vasodilators or both can be used.
• Cyclo-oxygenase inhibitors, protease inhibitors,
antioxidant therapy, antitumour necrosis factor
orinterleukin-1 receptor antagonists are being
evaluated
• Nitric oxide inhalation (reduces pulmonary artery
pressure and improves oxygenation)
• Current evidence does not support the use of
high-dose glucocorticoids in the care of ARDS
patients.
PROGNOSIS
• Mortality in ARDS is largely attributable to
nonpulmonary causes, with sepsis and
nonpulmonary organ failure accounting for
>80% of deaths.
• FACTORS ASSOCIATED WITH INCREASED
MORTALITY
 Advanced age
 Sepsis
 Preexisting organ dysfunction from chronic
medical illness—chronic liver disease,cirrhosis,
chronic alcohol abuse, chronic
immunosuppression, sepsis, chronic renal
disease.
 ARDS arising from direct lung
injury (including pneumonia, pulmonary
contusion, and aspiration)
 An early (within 24 h of presentation)
elevation in pulmonary dead space (>0.60)
and severe arterial hypoxemia (Pao2/Fio2,
<100 mmHg)

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