PANCE Blueprint Pulmonary (9%)

Acute respiratory distress syndrome (Lecture)

Patient will present as → a patient brought to the emergency room with acute onset of dyspnea and tachypnea. He has a long history of alcoholism and was involved in a motor vehicle accident two days ago. He is hypoxic with crackles auscultated bilaterally and frothy pink sputum. Chest radiography reveals diffuse bilateral infiltrates, which spare the costophrenic angle and air bronchograms. There is no cardiomegaly or pleural effusion noted. Oxygen saturation is 70%.

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Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by fluid collecting in the lungs, depriving organs of oxygen

  • The underlying abnormality in ARDS is ⇑ permeability of alveolar-capillary membranes ⇒ development of protein-rich pulmonary edema (non-cardiogenic pulmonary edema)
  • ARDS can occur in those who are critically ill or who have significant injuries

Three clinical settings account for 75% of ARDS cases:

  • Sepsis syndrome (most common cause)
  • Severe multiple trauma
  • Aspiration of gastric contents (alcoholics), toxic inhalation, near-drowning

People with ARDS have severe shortness of breath and often are unable to breathe on their own without support from a ventilator

  • Rapid onset of profound dyspnea occurring 12-24 hours after the precipitating event
  • Tachypnea, pink frothy sputum, crackles

Acute respiratory distress syndrome (ARDS) vs. Hyaline membrane disease/newborn respiratory distress syndrome (RDS) 

  • Hyaline membrane disease/respiratory distress syndrome in preterm infants (RDS) is often due to young gestational age, immature type II alveolar cells, and lack of alveolar surfactant, resulting in inadequate alveolar surface tension during expansion, which results in atelectasis, reduced gas exchange, severe hypoxia, and acidosis.
    • Hyaline membrane disease and RDS are two names for the same thing!
  • Acute respiratory distress syndrome (ARDS) in newborns and children is distinct from RDS/Hyaline membrane disease and involves diagnostic criteria (Montreux standard). Unlike RDS, ARDS of newborns and children is not based on a lack of alveolar surfactant.
  • These diagnostic criteria for ARDS of newborns and children include:
    • Acute exacerbation (within 1 week) after clinical or possible injury
    • Not caused by RDS, transient tachypnea of the newborn (TTN), congenital malformations, atelectasis, local effusions
    • Congenital heart disease that can be explained by pulmonary edema
    • Oxygenation index (OI) value ≥4
The diagnosis of ARDS requires symptoms developing within 1 week, bilateral diffuse infiltrates on chest x-ray, symptoms not being explained by congestive heart failure, and a ratio of PaO2 to FiO2 of less than 300.
  • Chest radiograph shows air bronchograms and bilaterally fluffy infiltrate
  • Normal BNP, pulmonary wedge pressure, left ventricle function, and echocardiogram
ARDSSevere

Severe ARDS. The person is intubated with an orogastric (OG) tube in place.

Treatment involves identifying and managing underlying precipitation and secondary conditions

  • Tracheal intubation with the lowest level PEEP to maintain PaO2 > 60 mmHg or SaO2 > 90
  • Lung-protective (low–tidal-volume) ventilation is the cornerstone6 mL/kg predicted body weight with plateau pressure <30 cmH2O and permissive hypercapnia (ARDSNet) — the only therapy with a proven mortality benefit
  • Prone positioning (≥16 hours/day) for moderate-to-severe ARDS (PaO2/FiO2 <150) improves survival (PROSEVA)
  • Titrate PEEP to oxygenation, use a conservative fluid strategy, and treat the underlying cause
  • ARDS is often fatal. The risk increases with age and the severity of illness
osmosis Osmosis
Picmonic
Acute Respiratory Distress Syndrome (ARDS) Assessment

IM_NUR_ARDSAssessment_V1.2_

ARDS is a sudden and progressive failure of the respiratory system in which the alveolar-capillary membrane becomes damaged. Damage to this membrane makes it more permeable to fluid, which can lead to difficulty breathing, atelectasis, and hypoxemia that is unresponsive to oxygen therapy. Patients who develop ARDS are typically afflicted by another illness or injury such as COPD, pneumonia, tuberculosis, aspiration, sepsis, shock, or fluid overload. Patients with this condition may also develop pulmonary hypertension, which is a late indicator of decreased lung compliance.

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Acute Respiratory Distress Syndrome (ARDS) Interventions

Patients with ARDS are at an increased risk for developing renal failure and stress ulcers. Close monitoring of patients for these conditions is essential. Hemodynamic monitoring should also be an important component of care, as these patients may experience hypotension, hypoxemia, and hypercapnia, which can cause negative consequences if left untreated.

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Neonatal respiratory distress syndrome (NRDS)

IM_NUR_Neonatal_respiratory_distress_syndrome_V1.3_

Neonatal respiratory distress syndrome (NRDS) is a condition related to fetal lung immaturity in premature infants (<37 weeks gestational age) and a lack of surfactant. Infants with NRDS will exhibit signs of respiratory distress including tachypnea, nasal flaring, intercostal/substernal retractions, and audible grunting upon expiration. Interventions used to treat NRDS include administration of exogenous surfactant, oxygen therapy, and mechanical ventilation. It is important to note that infants with NRDS should not receive bottle or gavage feedings, as these may increase their respiratory rate and risk of aspiration. Instead, total parenteral nutrition (TPN) is used to provide the infant with adequate nutrients.

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Question 1
A 45-year-old man develops acute hypoxemic respiratory failure 24 hours after emergency surgery for perforated diverticulitis. He is intubated and mechanically ventilated. Chest radiograph shows new diffuse bilateral infiltrates, bedside echocardiography shows normal left ventricular function, and his PaO2/FiO2 ratio is 150 on adequate PEEP. Which of the following is the most likely diagnosis?
A
Acute respiratory distress syndrome
Hint:
Correct — this presentation meets the Berlin criteria for ARDS.
B
Cardiogenic pulmonary edema
Hint:
Normal left ventricular function and the absence of volume overload argue against cardiogenic pulmonary edema.
C
Hospital-acquired pneumonia
Hint:
Pneumonia would typically produce a focal infiltrate; diffuse bilateral infiltrates with a low PaO2/FiO2 ratio after sepsis indicate ARDS.
D
Pulmonary embolism
Hint:
Pulmonary embolism usually shows a relatively clear chest radiograph rather than diffuse bilateral infiltrates.
E
Spontaneous pneumothorax
Hint:
A pneumothorax produces a hyperlucent hemithorax with absent lung markings, not diffuse bilateral infiltrates.
Question 1 Explanation: 
This patient meets the Berlin criteria for acute respiratory distress syndrome: acute onset within one week of a known insult (sepsis/major surgery), bilateral infiltrates not fully explained by effusion or lobar collapse, respiratory failure not fully explained by cardiac failure or fluid overload (normal LV function), and a PaO2/FiO2 ratio ≤ 300 mmHg on PEEP ≥ 5 cmH2O (150 = moderate ARDS). Sepsis is the most common precipitant.
Question 2
A 36-year-old male who is hospitalized because of severe injuries from a motor vehicle accident develops rapid onset of profound dyspnea. Initial chest x-ray shows a normal heart size with diffuse bilateral infiltrates. Follow-up chest xray shows confluent bilateral infiltrates that spare the costophrenic angles. Which of the following is the best clinical intervention for this patient?
A
Tracheal intubation
B
Bilateral chest tube insertion
Hint:
Chest tube insertion is not indicated in a patient with ARDS.
C
Type-specific packed cells
Hint:
Fluids are the preferred treatment initially for hypovolemia. Type-specific packed cells are given when the patient's blood type is identified. Until then O negative packed cells are administered.
D
Colloid solutions
Hint:
Use of crystalloid solutions are preferred to avoid pulmonary edema.
E
Provide supplemental oxygen
Hint:
Marked hypoxemia is refractory to treatment with supplemental oxygen in ARDS.
Question 2 Explanation: 
Tracheal intubation with lowest level of PEEP is required to maintain the PaO2 above 60 mmHg or SaO2 above 90% in a patient with ARDS.
Question 3
A 58-year-old woman is in the intensive care unit with acute respiratory distress syndrome (ARDS) following severe pancreatitis. She is intubated and mechanically ventilated, her PaO2/FiO2 ratio is 140, and a chest radiograph shows diffuse bilateral infiltrates. Which of the following ventilator strategies is most likely to reduce her mortality?
A
High tidal volume ventilation (12 mL/kg predicted body weight)
Hint:
High tidal volumes cause ventilator-induced lung injury and increase mortality.
B
Low tidal volume ventilation (6 mL/kg predicted body weight)
Hint:
Correct — 6 mL/kg predicted body weight is the ARDSNet lung-protective strategy with a proven mortality benefit.
C
Routine high-frequency oscillatory ventilation
Hint:
High-frequency oscillatory ventilation has not shown a mortality benefit and is not routine (OSCAR/OSCILLATE trials).
D
Zero positive end-expiratory pressure (ZEEP)
Hint:
PEEP, not zero PEEP, is used to maintain alveolar recruitment and oxygenation in ARDS.
Question 3 Explanation: 
In ARDS, low-tidal-volume (lung-protective) ventilation — 6 mL/kg of predicted body weight targeting a plateau pressure < 30 cmH2O with permissive hypercapnia — is the only ventilator strategy proven to reduce mortality (ARDSNet/ARMA, NEJM 2000). High tidal volumes cause ventilator-induced lung injury; PEEP (not zero PEEP) maintains oxygenation; and routine high-frequency oscillatory ventilation has not demonstrated benefit.
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References: Merck Manual · UpToDate

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