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 alcohol use disorder 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 (most common cause) and pneumonia
- Severe multiple trauma, pancreatitis, massive transfusion, burns
- Aspiration of gastric contents (e.g., alcohol use disorder), 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 has its own diagnostic criteria (Montreux definition for neonates; PALICC criteria for children). Unlike RDS, ARDS of newborns and children is not based on a lack of alveolar surfactant.
- The neonatal (Montreux) criteria include:
- Acute onset (within 1 week) after a known or suspected clinical insult
- Not caused by RDS, transient tachypnea of the newborn (TTN), congenital malformations, atelectasis, local effusions
- Edema not explained by congenital heart disease
- Oxygenation index (OI) value ≥4
The diagnosis of ARDS (Berlin definition) requires onset within 1 week of a known insult, bilateral opacities on chest x-ray or CT not fully explained by effusions, collapse, or nodules, respiratory failure not fully explained by heart failure or fluid overload, and a PaO2/FiO2 ratio of 300 mmHg or less on PEEP of at least 5 cm H2O.
- Chest radiograph shows air bronchograms and bilaterally fluffy infiltrate
- Echocardiography (with BNP) excludes cardiogenic pulmonary edema: normal heart size and left ventricular function; a wedge pressure (PCWP) is no longer required for diagnosis
- Severity (Berlin): mild PaO2/FiO2 201–300, moderate 101–200, severe 100 or less
- The newer global definition also allows the diagnosis in non-intubated patients on high-flow nasal oxygen (at least 30 L/min) or noninvasive ventilation, using an SpO2/FiO2 of 315 or less, and with lung ultrasound
Severe ARDS. The person is intubated with an orogastric (OG) tube in place. Image: James Heilman, MD, CC BY-SA 4.0, via Wikimedia Commons.
Treatment involves identifying and managing underlying precipitation and secondary conditions
- Oxygen and positive pressure: high-flow nasal oxygen is reasonable first for hypoxemia without hypercapnia, but do not delay intubation in moderate–severe ARDS; target SpO2 88–95% (PaO2 55–80 mmHg)
- Lung-protective (low–tidal-volume) ventilation is the cornerstone — 6 mL/kg predicted body weight (range 4–8) with plateau pressure ≤30 cm H2O and permissive hypercapnia; it reduces mortality
- Prone positioning (≥16 hours/day, started early) for severe ARDS (PaO2/FiO2 <150) also reduces mortality (PROSEVA)
- Set PEEP with a PEEP/FiO2 table (higher PEEP is often used in moderate–severe ARDS) and avoid prolonged high-pressure recruitment maneuvers; use a conservative fluid strategy once shock resolves; treat the underlying cause
- Corticosteroids (dexamethasone or methylprednisolone) are now suggested early (within 14 days) in moderate–severe ARDS; starting after 2 weeks may be harmful, and they are avoided in influenza-related ARDS
- Not routine: neuromuscular blockade (a short course of 48 hours or less only for severe refractory hypoxemia or ventilator dyssynchrony), inhaled nitric oxide (improves oxygenation but not survival), and high-frequency oscillatory ventilation (harmful)
- Refractory severe ARDS: refer early for venovenous ECMO after optimized ventilation and prone positioning
- Mortality is roughly 25–60% and rises with age and severity; survivors often have long-term weakness and cognitive and psychological problems
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 Osmosis |
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Picmonic
Acute Respiratory Distress Syndrome (ARDS) Assessment
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 pneumonia, aspiration, sepsis, shock, trauma, or pancreatitis. Patients with this condition may also develop pulmonary hypertension, which is a late indicator of decreased lung compliance.
Play Video + QuizAcute 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.
Play Video + QuizNeonatal respiratory distress syndrome (NRDS)
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.
Play Video + QuizQuestion 1 |
A 67-year-old woman is admitted to the intensive care unit with acute hypoxemic respiratory failure. Over 48 hours she develops diffuse bilateral infiltrates with a normal heart size, and acute respiratory distress syndrome (ARDS) is diagnosed. Which of the following is the most common cause of ARDS?
Aspiration of gastric contents Hint: A classic direct lung injury and a well-known trigger, but less common overall than sepsis. | |
Near-drowning Hint: A recognized but uncommon direct cause. | |
Pancreatitis Hint: A classic indirect trigger, but less common overall than sepsis. | |
Sepsis | |
Transfusion of blood products Hint: Transfusion-related acute lung injury can cause ARDS, but it is far less common than sepsis. |
Question 1 Explanation:
Sepsis is the most common cause of acute respiratory distress syndrome (ARDS), followed by pneumonia, aspiration of gastric contents, and major trauma. Other triggers include pancreatitis, massive transfusion, burns, inhalation injury, and near-drowning. The insult injures the alveolar-capillary membrane, which becomes leaky and floods the alveoli with protein-rich fluid (noncardiogenic pulmonary edema), usually within hours to a few days and by definition within 1 week.
Question 2 |
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 a PEEP of 8 cm H2O. Which of the following is the most likely diagnosis?
Acute respiratory distress syndrome | |
Cardiogenic pulmonary edema Hint: Normal left ventricular function and the absence of volume overload argue against cardiogenic pulmonary edema. | |
Hospital-acquired pneumonia Hint: Pneumonia typically produces a focal infiltrate; diffuse bilateral infiltrates with a low PaO2/FiO2 ratio after an acute insult point to ARDS. | |
Pulmonary embolism Hint: Pulmonary embolism usually shows a relatively clear chest radiograph rather than diffuse bilateral infiltrates. | |
Spontaneous pneumothorax Hint: A pneumothorax produces a hyperlucent hemithorax with absent lung markings, not diffuse bilateral infiltrates. |
Question 2 Explanation:
This patient meets the Berlin definition of acute respiratory distress syndrome (ARDS): onset within 1 week of a known insult (peritonitis and major surgery), bilateral opacities not fully explained by effusion or collapse, respiratory failure not fully explained by heart failure or fluid overload (echocardiography shows normal left ventricular function), and a PaO2/FiO2 ratio of 300 mmHg or less on PEEP of at least 5 cm H2O. A ratio of 150 is moderate ARDS (mild 201-300, moderate 101-200, severe 100 or less). Echocardiography, often with BNP, is how cardiogenic edema is excluded; a wedge pressure is no longer required. The newer global definition also allows the diagnosis in non-intubated patients on high-flow nasal oxygen of at least 30 L/min.
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?
High tidal volume ventilation (12 mL/kg predicted body weight) Hint: High tidal volumes overstretch the open alveoli, cause ventilator-induced lung injury, and increase mortality. | |
Low tidal volume ventilation (6 mL/kg predicted body weight) | |
Routine high-frequency oscillatory ventilation Hint: Routine high-frequency oscillatory ventilation increased mortality in adults with ARDS and is recommended against. | |
Zero positive end-expiratory pressure (ZEEP) Hint: PEEP, not zero PEEP, keeps alveoli open and maintains oxygenation. |
Question 3 Explanation:
Low tidal volume (lung-protective) ventilation is the cornerstone of ARDS care and reduces mortality: about 6 mL/kg of predicted body weight (range 4-8), plateau pressure 30 cm H2O or less, PEEP set with a PEEP/FiO2 table, a target SpO2 of 88-95%, and permissive hypercapnia. Tidal volume is based on predicted (height-based) body weight, not actual weight. Prone positioning for at least 16 hours a day also reduces mortality when the PaO2/FiO2 ratio stays below 150, so it is the next step if she does not improve. High tidal volumes cause volutrauma, zero PEEP lets alveoli collapse and reopen with every breath, and routine high-frequency oscillation is harmful.
Question 4 |
A 52-year-old man with pneumonia and sepsis has been intubated for acute respiratory distress syndrome (ARDS) for 24 hours. On a tidal volume of 6 mL/kg predicted body weight, PEEP 14 cm H2O, and FiO2 0.80, his plateau pressure is 27 cm H2O and his PaO2/FiO2 ratio is 90. Blood pressure is 112/68 mmHg. Which of the following is the most appropriate next step in management?
High-frequency oscillatory ventilation Hint: Routine high-frequency oscillation increased mortality in adults with ARDS and is recommended against. | |
Increase tidal volume to 10 mL/kg predicted body weight Hint: Larger breaths cause volutrauma and raise mortality; his plateau pressure is already close to the 30 cm H2O limit. | |
Inhaled nitric oxide Hint: Improves oxygenation only briefly and does not improve survival; at most a short rescue bridge. | |
Prone positioning for at least 16 hours a day | |
Venovenous extracorporeal membrane oxygenation Hint: A rescue for refractory severe ARDS after optimized ventilation and prone positioning have been tried; it is not the next step here. |
Question 4 Explanation:
His ARDS remains severe (PaO2/FiO2 below 150) despite correct lung-protective settings, so the next step is early prone positioning for at least 16 hours a day. Proning recruits the dorsal lung and improves ventilation-perfusion matching, and together with low tidal volume ventilation it is one of the two ventilator-side strategies that reduce mortality in ARDS. Venovenous ECMO is reserved for hypoxemia that stays refractory after proning (for example, PaO2/FiO2 below 50 for more than 3 hours or below 80 for more than 6 hours). Inhaled nitric oxide raises the PaO2 briefly without a survival benefit, and high tidal volumes or high-frequency oscillation are harmful.
Question 5 |
A 49-year-old woman with bacterial pneumonia has been intubated for 2 days for acute respiratory distress syndrome (ARDS). On lung-protective ventilation with PEEP 10 cm H2O, her PaO2/FiO2 ratio is 170. Echocardiography shows normal left ventricular function, and testing for influenza is negative. In addition to treating the pneumonia, which of the following therapies is suggested for her ARDS?
Continuous neuromuscular blockade for 7 days Hint: Neuromuscular blockade is not routine in ARDS; a short course of 48 hours or less is reserved for severe refractory hypoxemia or ventilator dyssynchrony. | |
High-frequency oscillatory ventilation Hint: Routine high-frequency oscillation is harmful in adults with ARDS. | |
Inhaled nitric oxide Hint: Improves oxygenation transiently but does not improve survival. | |
Intratracheal surfactant Hint: Surfactant is the treatment for neonatal respiratory distress syndrome, not adult ARDS. | |
Systemic corticosteroids |
Question 5 Explanation:
Systemic corticosteroids (for example, dexamethasone or methylprednisolone) are now suggested early, within 14 days of onset, in moderate to severe ARDS, where they shorten time on the ventilator and probably reduce mortality. Starting them after 2 weeks may be harmful, and they are generally avoided in influenza-related ARDS. Neuromuscular blockade is not routine, inhaled nitric oxide does not improve survival, high-frequency oscillation is harmful, and surfactant helps only the neonatal (surfactant-deficiency) form of respiratory distress syndrome.
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References: Merck Manual · UpToDate