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Acute Respiratory Distress Syndrome (ARDS)

A severe lung condition primarily characterized by refractory hypoxemia.

What is the hallmark feature of ARDS?

Refractory hypoxemia.

What does refractory hypoxemia mean?

Blood oxygen levels remain low or worsen despite aggressive or maximal oxygen delivery.

What happens to tissue when refractory hypoxemia persists?

Tissue hypoxia develops because inadequate oxygen reaches the body's cells.

What type of injury always precedes ARDS?

Lung injury, which may be direct or indirect.

What are the 4 basic steps in the development of ARDS?

1) Insult/injury or widespread inflammation → 2) alveoli rapidly fill with inflammatory fluid → 3) oxygen fails to cross the injured membrane → 4) the patient compensates by breathing faster and harder.

What is the "insult" in ARDS development?

The lungs are injured directly or widespread inflammation is triggered indirectly.

What is the "flood" in ARDS development?

Alveoli rapidly fill with inflammatory fluid.

What is the "barrier" in ARDS development?

The injured alveolar membrane prevents oxygen from effectively moving into the blood.

What is the "compensation" in ARDS development?

The patient breathes faster and harder in an attempt to maintain oxygenation.

What are the two categories of ARDS lung injury?

Direct lung injury and indirect lung injury.

What is a direct lung injury?

An injury that directly affects lung tissue.

What is the most common cause of direct lung injury leading to ARDS?

Pneumonia and aspiration of gastric contents, especially large food particles.

What are less common causes of direct lung injury?

Pulmonary contusion, fat emboli, near-drowning, inhalation injury, and reperfusion injury.

What types of water are specifically associated with near-drowning as a direct ARDS trigger in the notes?

Salt or chlorinated water.

What is an example of inhalation injury that can cause ARDS?

Inhalation injury from fires or toxic chemicals.

What is an example of reperfusion injury that can cause ARDS?

Injury after lung transplant or pulmonary embolectomy.

What is an indirect lung injury?

A systemic process triggers inflammation or injury that subsequently damages the lungs.

What are the most common causes of indirect lung injury?

Sepsis and severe trauma with shock.

What are less common causes of indirect lung injury?

Cardiopulmonary bypass, drug overdose, acute pancreatitis, and massive blood product transfusions causing TRALI.

What does TRALI stand for?

Transfusion-Related Acute Lung Injury.

Why should patients with ARDS risk factors be monitored closely?

They are at risk of developing ARDS.

What are the early physical findings of ARDS?

Dyspnea, tachypnea, increased work of breathing, pallor, diaphoresis, and tachycardia.

What does tachypnea mean?

Rapid breathing.

What findings indicate increased work of breathing in early ARDS?

Accessory muscle use and nasal flaring.

What happens to respiratory distress in late ARDS?

Respiratory distress worsens while the patient becomes fatigued.

What happens to respiratory rate in late ARDS?

Respiratory rate decreases as respiratory muscle fatigue develops.

What happens to work of breathing in late ARDS?

The apparent work of breathing may decrease because the patient is becoming exhausted and unable to compensate.

What happens to oxygen saturation in late ARDS?

It plummets.

Why can altered mental status occur in late ARDS?

Worsening hypoxia decreases oxygen delivery to the brain.

What cardiac complication can develop in late ARDS?

Right-sided heart failure, which can lead to hypotension.

What pulse oximetry finding is typical of ARDS?

O2 saturation less than 90% despite significant and increasing oxygen requirements.

What ABG pattern is expected in early ARDS?

Respiratory alkalosis with high pH and low PaCO2.

Why does early ARDS cause respiratory alkalosis?

Tachypnea causes the patient to "blow off" more CO2.

What PaO2 may be seen in early ARDS?

PaO2 is often less than 80 mmHg.

What ABG pattern develops in late ARDS?

Respiratory acidosis with low pH and high PaCO2.

Why does late ARDS cause respiratory acidosis?

Respiratory muscle fatigue causes breathing to become slower and shallower, resulting in CO2 retention.

What PaO2 is characteristic of late ARDS?

PaO2 drops below 60 mmHg and continues to decline despite escalating oxygen support.

What does a lactic acid level greater than 2 mmol/L indicate?

Lactic acidosis resulting from cellular hypoxia and anaerobic metabolism.

Why does lactic acid increase in severe ARDS?

Cellular hypoxia forces cells to rely more on anaerobic metabolism, producing lactate.

What can happen when lactic acidosis combines with respiratory acidosis?

The pH can fall severely, often below 7.2.

What is the classic chest X-ray finding in ARDS?

Diffuse bilateral opacities, often described as a "white-out" appearance.

What does the bilateral "white-out" appearance indicate?

Both lungs are affected by diffuse lung injury and fluid/inflammatory changes.

What are the three phases of ARDS?

Exudative, proliferative, and fibrotic phases.

What occurs during the exudative phase?

Diffuse alveolar damage causes increased permeability, inflammation, surfactant dysfunction, hyaline membrane formation, V/Q mismatch, and pulmonary hypertension.

When does the exudative phase occur?

Within approximately 24–72 hours through about 7–10 days after injury.

Which pneumocytes are damaged during the exudative phase?

Type I pneumocytes, Type II pneumocytes, and the alveolar-capillary membrane are affected.

What is the role of Type I pneumocytes?

They provide structural support for the alveolar surface and participate in gas exchange.

What is the role of Type II pneumocytes?

They produce surfactant.

What happens when Type I pneumocytes are damaged?

The alveolar barrier becomes leaky, allowing protein-rich fluid to enter the alveoli and surrounding tissue.

Why does protein-rich fluid entering the alveoli cause refractory hypoxemia?

The fluid creates a barrier to oxygen diffusion from the alveoli into the capillaries.

What inflammatory response occurs during the exudative phase?

Proinflammatory mediators such as TNF-α and interleukins are released, while neutrophils invade lung tissue and release cytokines and chemokines.

What happens to Type II pneumocytes during ARDS?

They become damaged, resulting in decreased surfactant production.

Why is decreased surfactant dangerous?

It increases alveolar surface tension and promotes alveolar collapse, causing atelectasis.

What is a hyaline membrane?

A thick, waxy layer on alveolar walls formed from inflammatory cells, cellular debris, and collapsed alveolar material.

Why are hyaline membranes harmful?

They further trap fluid and debris and interfere with oxygen exchange.

How do surfactant loss and hyaline membrane formation affect V/Q matching?

They cause widespread atelectasis and fluid-filled spaces, worsening V/Q mismatch and intrapulmonary shunting.

What happens to pulmonary blood vessels in response to severe hypoxemia/V/Q abnormalities?

They constrict, contributing to pulmonary arterial hypertension.

Why is pulmonary hypertension dangerous in ARDS?

It places significant strain on the right side of the heart and can contribute to right-sided heart failure.

What occurs during the proliferative phase of ARDS?

Inflammation subsides, fluid is reabsorbed, and new Type I and Type II pneumocytes regenerate to repair the alveolar lining and restore surfactant.

When does the proliferative phase occur?

Approximately day 8 through day 21.

What is another way to remember the proliferative phase?

The "repair and cleanup" phase.

What happens to many patients during the proliferative phase?

They improve and can often be weaned from mechanical ventilation with minimal scarring.

What occurs during the fibrotic phase?

Lung tissue is replaced with dense fibrous scar tissue, causing permanent lung damage.

When does the fibrotic phase typically occur?

Approximately 3–4 weeks after the initial injury.

How common is progression to the fibrotic phase according to the notes?

Only a small number of patients progress to this irreversible phase.

What complications can result from the fibrotic phase?

Permanent lung damage, chronic pulmonary hypertension, and often the need for long-term mechanical ventilation.

What is the prognosis associated with the fibrotic phase?

Extremely poor prognosis.

What assessment finding represents impaired gas exchange in ARDS?

Tachypnea.

Why does ARDS cause tachypnea?

Impaired gas exchange causes the patient to increase respiratory rate in an attempt to compensate for inadequate oxygenation.

Why does ARDS cause extreme work of breathing?

Edema and inflammation make the lungs stiff and difficult to inflate because lung compliance is reduced.

What physical findings reflect reduced lung compliance?

Nasal flaring, accessory muscle use, and respiratory exhaustion.

What does reduced lung compliance mean?

The lungs become stiff and require greater effort to expand.

What finding reflects V/Q mismatch in ARDS?

Refractory oxygenation in which oxygen saturation improves only modestly despite major increases in oxygen delivery.

What findings reflect systemic hypoxia in ARDS?

Tachycardia, confusion, reduced urine output, unstable blood pressure, and altered mental status.

What does the Berlin definition diagnose?

ARDS based on acute hypoxemia, impaired P/F ratio, bilateral infiltrates, and evidence that the pulmonary edema is not primarily cardiac in origin.

What does the "A" in the ARDS Berlin mnemonic represent?

Acute hypoxemia, with O2 saturation less than 90% within one week of a lung insult.

What does the "R" in the ARDS Berlin mnemonic represent?

Ratio of P/F less than 300, indicating significant impairment of oxygen exchange.

What does the "D" in the ARDS Berlin mnemonic represent?

Diffuse bilateral infiltrates on chest X-ray.

What does the "S" in the ARDS Berlin mnemonic represent?

Swan-Ganz catheter showing a PAWP less than 18 mmHg, indicating the lung problem is not due to a primary cardiac problem.

What does PAWP stand for?

Pulmonary artery wedge pressure.

Why is PAWP less than 18 mmHg important in ARDS?

It supports the idea that the pulmonary edema is not primarily caused by a cardiac problem.

What is the P/F ratio?

The PaO2 divided by FiO2; it measures the severity of impaired oxygenation.

How is the P/F ratio calculated?

PaO2 from the ABG ÷ FiO2 expressed as a decimal.

What is a normal P/F ratio?

Greater than 400 in a healthy person breathing room air.

What FiO2 is room air?

0.21, or 21%.

What P/F ratio is a key criterion for ARDS?

Less than 300.

What P/F ratio indicates mild ARDS?

200–300 mmHg.

What P/F ratio indicates moderate ARDS?

100–200 mmHg.

What P/F ratio indicates severe ARDS?

Less than 100 mmHg.

What is the cornerstone of ARDS management?

Lung-protective mechanical ventilation.

Why is low tidal volume used in ARDS?

To prevent overdistension and barotrauma of stiff, noncompliant lungs.

Why is the respiratory rate increased when low tidal volumes are used?

To compensate for the lower tidal volume and help prevent CO2 retention.

What is PEEP?

Positive end-expiratory pressure applied at the end of exhalation to prevent alveolar collapse.

How does PEEP improve oxygenation?

It keeps alveoli open and recruits previously collapsed alveoli, improving oxygen exchange.

Why should FiO2 ideally be maintained below 60% when possible?

To reduce oxygen toxicity and avoid worsening lung injury.

What lower oxygen saturation target may be accepted in ARDS?

Approximately 88%, according to the notes.

Why may neuromuscular blocking agents be used in severe ARDS?

To improve ventilator synchrony and reduce oxygen consumption.

What is ECMO?

Extracorporeal membrane oxygenation, which can bypass the lungs and directly oxygenate blood in severe cases unresponsive to conventional therapy.

When may ECMO be considered?

In the most severe ARDS cases that do not respond to conventional therapies.