Acute Respiratory Distress Syndrome- NEET PG Medicine

Get ready to elevate your Medicine preparation because today you are going to learn about Acute Respiratory Distress Syndrome, which is an important topic in your Medicine syllabus. 

What is Acute Respiratory Distress Syndrome? It is a condition where fluid gets collected in the air sacs of the lungs and deprives the body of oxygen. In such cases, patients suffer from shortness of breath and are unable to breathe on their own.

Let’s learn more about this syndrome in detail.  

• Cardiogenic pulmonary edema: Increase in left atrial pressure secondary to LVF
  • Edematous fluid is transudate
• acute respiratory distress syndrome is due to non-cardiogenic pulmonary edema

Non-Cardiogenic Pulmonary Edema

• Example, A patient has swine flu or bird flu. As the swine flu virus damages pneumocytes without damaging heart, this will end up in ARDS.
• Collapse of alveoli leads to hypoxia and which in turn leads to damage of Endothelium (damage to gap junctions)
• Leakage of fluids from the pulmonary capillary into alveoli
• ARDS occurs in 10% of ICU patients.
• Sudden onset Respiratory distress
  • Presence of CXR Bilateral infiltrates on chest X-ray. (no cardiac cause found)
  • Reduced pO₂ (demonstrable hypoxia)
  • Normal left atrial pressure (LAP)

Triggers for ARDS
Direct (Most common)	Indirect
Pneumonia (H1N1) Mendelson syndrome Toxic gas inhalation Pulmonary contusion Near drowning	Sepsis Trauma  Multiple bone fracture Flail chest Head injury Burns Multiple blood transfusion /TRALI Acute pancreatitis Post cardiopulmonary bypass

• Mendelson syndrome: Aspiration of stomach acid (Chemical Pneumonitis)

Important information Both pneumonia > sepsis are the leading causes of ARDS Leading cause of death after blood transfusion: TRALI Status asthmaticus (disease of the airway) is not ARDS( disease of alveoli)

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Clinical Presentation 

• Type 1 pneumocytes: cover 90% of surface area (injured during adult ARDS)
• Type 2 pneumocytes: produce surfactant (most abundant cell of alveoli)
• IN ARDS, Type 1 pneumocytes are affected, and Type 2 pneumocytes are not affected.
• Normal surfactant with a reduced surface area of alveoli for gas exchange
• Ventilation and perfusion imbalance (perfusion is secondary to the hypoxia component)
• Hypoxia causes dilatation of all blood vessels in the body except vessels of the pulmonary circuit
• Most vulnerable cells/most damaged cells in ARDS is endothelial cells of alveoli due to hypoxia
• Endothelial cells become leaky resulting in Exudative high-protein pulmonary edema.
• In heart failure: low protein pulmonary edema

FEATURES: (Sudden onset Respiratory Distress)

EXUDATIVE PHASE 0-7 days Respiratory distress starts within 12-36 hours of triggers onset. Intrapulmonary shunting (Blood is getting wasted in the lungs due to alveolar collapse or endothelial injury)  Increase in work of breathing. ↓ pO2, ↑ pCO2 (Refractory hypoxia) Dead space increased. Type 2 Respiratory failure / Respiratory acidosis

PROLIFERATIVE PHASE 7-21 days Able to wean off the ventilator. Proliferation of type 2 pneumocytes Some differentiate into type-1 pneumocytes. Recovery is possible

FIBROTIC PHASE >21 days Require supplemental oxygen for the rest of their life (requirement varies from case to case) It results in pulmonary artery hypertension. Bulla or blebs can also be seen in ARDS

• In the initial phase of ARDS, because of tachypnoea, there will be Respiratory alkalosis (CO₂ washout)
• In acute asthma: type-1 respiratory failure and respiratory alkalosis due to CO₂ washout
• In status asthamaticus: type-2 respiratory failure & Respiratory acidosis due to CO₂ overproduction in lungs
• When PCO₂ is 60mm of Hg, then the compensatory mechanisms begin to fail.

Work –Up in ARDS

CXR 

• In ARDS patient: Bilateral extensive infiltrates
  • Cardiothoracic ratio is normal.
  • Para cardiac area sparing
  • CP angle is normal.
• In cardiogenic pulmonary edema
  • Cardiothoracic ratio is increased.
  • Bat wing edema seen.
  • CP angle is blunted.
• Echo:
  • In ARDS: Ejection fraction is normal, LA pressure is normal.
  • In cardiogenic pulmonary edema:  Decrease ejection fraction and LA pressure increased
• ABG in ARDS: ↓ pO2, ↑ pCO2 (ventilation, perfusion imbalance)

Also Read: EPILEPSY AND Electroencephalography (EEG) : NEET PG Medicine

Keywords: Essentials of Diagnosis

Sudden onset respiratory distress

• Central line insertion:  Pneumothorax
• S. Aureus pneumonia: receiving i.v Vancomycin for 2 days.
  • Pneumatocele rupture resulting in Pneumothorax.
• After multiple bone fractures/ Massive blood transfusion or acute pancreatitis.  

ARDS: BERLIN Criteria 

Sudden onset resp. distress

• CXR: B/L pulmonary infiltrates
• PaO₂ / FiO₂ < 300  (most important diagnostic criteria for ARDS)
• Absence of left atrial Hypertension

GRADING

ARDS	Pa2 / FiO2
Mild Moderate Severe	<300 <200              <100

• Volutrauma can occur in ARDS: Seen in high or normal volume ventilation resulting in Pneumothorax.

Management of ARDS

Low volume ventilation: 6 ml/kg to minimize BAROTRAUMA to the chest. (Normal tidal volume is 12 ml/kg)

• Plateau pressure of ventilator: <30 cm H₂O
• Respiratory rate of ventilator: <35/min
• Prone-position ventilation
  • Risk of extubation
  • CVP line loss
  • Orthopedic injuries
• Extracorporeal membrane oxygenation (ECMO): Patient in whose heart and lungs are too weak for ventilation.

• Limited fluids and diuretics: To maintain normal left atrial pressure.
• Ensure neuromuscular paralysis: Cisatracurium (for effective ventilation)
  • Steroids, surfactant therapy and high-frequency jet ventilation (HFJV) have no role in the treatment.
• Most common cause of death in ARDS: Sepsis (non-pulmonary causes)

Congestive heart failure	ARDS
Transudative pulmonary edema	Exudative pulmonary edema
Hydrostatic pressure increased	Hydrostatic pressure normal
LA pressure increased	LA pressure normal
Low protein pulmonary edema	High protein pulmonary edema
BNP increased	BNP normal

And that is everything you need to know about Acute Respiratory Distress Syndrome to boost your Medicine preparation. For more interesting and informative posts like this keep following our blog!