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ARDS, Respiratory Failure

Dr. Manu Mohan K

Dept. of Pulmonary Medicine

ARDS

• Severe dyspnea of rapid onset

• Hypoxemia

• Diffuse pulmonary infiltrates

• Respiratory failure

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Etiology

3Harrison’s Principles of Internal

Medicine 17th ed.

Clinical features

• Diagnostic criteria for ALI and ARDS• Oxygenation

ALI – PaO2/FiO2 < 300mm of Hg

ARDS - PaO2/FiO2 < 200mm of Hg• Onset

Acute• Chest radiograph

Bilateral alveolar or interstitial infiltrates

4Harrison’s Principles of Internal

Medicine 17th ed.

• Absence of left atrial hypertension

PCWP < 18 mm of Hg or no clinical evidence of increased left atrial pressure

Harrison’s Principles of Internal Medicine 17th ed. 5

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Clinical course and pathophysiology

• Exudative

• Proliferative

• Fibrotic

Harrison’s Principles of Internal Medicine 17th ed. 8

Exudative phase

• First 7 days

• Alveolar and interstitial edema

• Hyaline membrane whorls

• Atelectasis

• Decreased lung compliance

Harrison’s Principles of Internal Medicine 17th ed. 9

Proliferative Phase

• 7 to 21 days

• Early pulmonary fibrosis

• Proliferation of Type 2 pneumocytes

Harrison’s Principles of Internal Medicine 17th ed. 10

Fibrotic stage

• 3 to 4 weeks

• Extensive alveolar duct and interstitial fibrosis

• Emphysema and bullae

• Pulmonary hypertension

Harrison’s Principles of Internal Medicine 17th ed. 11

Treatment

• General

• Mechanical ventilation

Ventilator induced lung injury

Prevention of alveolar collapse

PEEP

Inverse ratio ventilation

Prone position ventilationHarrison’s Principles of Internal

Medicine 17th ed. 12

• Other strategies of mechanical ventilation

High frequency ventilation

Extracorporeal membrane oxygenation

Partial liquid ventilation

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General support during ventilation

• Fluid management

Maintaining low left atrial filling pressure

• Glucocorticoids

• Other therapies

Surfactant replacement

Nitric oxide inhalation

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Complications of Mechanical ventilation

• Pulmonary complications

• Barotrauma

• Nosocomial pneumonia

• Oxygen toxicity

• Tracheal stenosis

• Deconditioning of respiratory muscles

Harrison’s Principles of Internal Medicine 17th ed. 15

• Hypotension

• GI - Stress ulcer and mild cholestasis

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Prognosis

• Mortality 41-65%

• >80 % deaths due to nonpulmonary complications

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• Functional recovery

Recover maximum lung function in 6 months

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Respiratory failure

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Respiratory failure

• When lungs cannot fulfill their primary function of maintaining adequate gas exchange at rest, or during exercise

• This results in an inability to maintain normal blood gases, so that the Po2 (less than 60) is low with or without Hypercarbia (more than 50).

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• Two types of respiratory failure

• Type I and Type II

• Type I - Hypoxemia without Hypercarbia

• Type II- Hypoxemia with Hypercarbia

• It can be acute or chronic

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• Type I respiratory failure causes

• Chronic bronchitis and emphysema

• Pneumonia

• Pulmonary edema

• Pulmonary fibrosis

• Asthma

• Pneumothorax

• Pulmonary embolism

• Bronchiectasis

• Obesity

• ARDS

• Cyanotic heart disease

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Type II Hypercarbic Respiratory failure causes

• COPD

• Asthma

• Drug overdose

• Poisoning

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• Myasthenia Gravis• Polyneuropathy• Poliomyelitis• Sleep apnea syndrome• Pulmonary edema• ARDS• Tetanus• Foreign body

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Mechanism

• Oxygenation failure and ventilatory failure

• Type I respiratory failure

Ventilation perfusion mismatch is marked

Control of ventilation is intact

So excess CO2 is exerted by normal areas of lung

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• Type II

Ventilatory failure marked

PaCO2 rises due to alveolar hypoventilation, PaO2 falls.

Clinical features

• Clinical evidence of hypoxemia

• Central cyanosis best assessed by examining the oral mucous membrane.

• Not useful in anemia

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• CNS effects- irritability impaired intellectual function and clouding of consciousness

• Progress to convulsion, coma and death

• Persistent hypoxemia can lead to secondary polycythemia

Clinical evidence of hypercapnia

• CNS effects- irritability, confusion, somnolence and coma, tremor, myoclonic jerks, asterixis, even seizures, headache, papilledema.

• Warm flushed skin with bounding pulse.

• Tachycardia and sweating

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• Gastric dilatation, paralytic ileus

• Head ache on waking up common in chronic hypercapnia due to progressive increase in CO2retention during sleep.

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DIAGNOSIS

• ABG• It is important to measure arterial pH and

assess degree on compensation. • In acute respiratory failure 10mm of Hg

increase in CO2 increases HCO3 by 1meq/L pH increase by 0.08 units. In Chronic 10mm Hg increase in CO2 increase pH by 0.03 and HCO3 by 3.5meq/L

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Management

• Type I

• Treatment of primary cause

• Correction of arterial hypoxemia highest priority

• The goal should be to increase saturation of oxygen to at least 85-90% without risk of oxygen toxicity.

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• High Fi02 for short period can be used. The use of PEEP, change in position, sedation and paralysis may help in lowering Fi02

• Fever, agitation, overfeeding, vigorous respiratory activity and sepsis increases the oxygen demand.

General indication of ventilation

• Inadequate oxygenation despite an increasing Fi02

• Increased PaCO2 associated with decreased mental status or increasing fatigue.

• Failure to control secretions

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Methods

• Non invasive mechanical ventilation

• Mechanical ventilation

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Mechanical ventilation• Indications

• PaO2 less than 60 mm Hg despite FiO2 > 0.6 with hypercapnia

• Rapid increase in CO2 causing uncompensated

• Respiratory acidosis

• Tachypnea > 35 breaths per minute

• Clinical judgment on impending exhaustion of the patient

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Complications

• Barotrauma

• GIT bleeding

• Nosocomial Pneumonia

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• LTOT - long term oxygen therapy

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