Acute Respiratory Distress Syndrome (ARDS): An Overview

Acute respiratory distress syndrome (ARDS) is a critical medical condition characterized by severe lung inflammation, impaired oxygen exchange, and life-threatening respiratory failure.

This syndrome can develop as a result of various underlying factors, such as pneumonia, sepsis, or trauma, and it poses a significant challenge to healthcare professionals due to its high mortality rate and complex management.

This guide breaks down the key aspects of ARDS, including its causes, symptoms, diagnosis, and treatment options, in order to shed light on this critical medical condition.

What is ARDS?

Acute respiratory distress syndrome (ARDS) is a severe lung condition causing widespread inflammation and damage. It typically occurs in critically ill or injured patients, often as a response to infection or trauma. ARDS leads to fluid accumulation in the lungs, severely impairing oxygen exchange and breathing.

Causes

ARDS is triggered by various factors, often linked to severe illness or injury. Common causes include:

• Infections: Severe pneumonia or systemic infections (sepsis) can lead to ARDS.
• Inhalation of Harmful Substances: Inhaling smoke, chemicals, or vomit can damage the lungs.
• Trauma: Serious injuries, such as those from car accidents or falls, can initiate ARDS.
• Medical Procedures: Complications from surgeries or blood transfusions.
• Chronic Health Conditions: Conditions like pancreatitis or severe inflammatory diseases.

Note: These triggers cause widespread inflammation in the lungs, leading to fluid accumulation and respiratory failure.

Symptoms

The symptoms of ARDS typically develop rapidly and include:

• Severe Shortness of Breath: This is often the most prominent symptom, caused by insufficient oxygen in the blood.
• Labored and Rapid Breathing: To compensate for low oxygen levels, breathing becomes fast and difficult.
• Low Blood Oxygen Levels: Despite receiving oxygen therapy, blood oxygen levels may remain dangerously low.
• Cough: Some patients might experience a mild cough.
• Fatigue and Weakness: Due to the lack of oxygen and the body’s response to inflammation.
• Confusion and Agitation: Caused by low oxygen levels affecting the brain.
• Fever: In cases where ARDS is triggered by an infection.

Note: These symptoms warrant immediate medical attention, as ARDS is a life-threatening condition.

Diagnosis

Diagnosing ARDS involves several steps:

• Medical History and Physical Exam: Doctors assess symptoms, medical history, and perform a physical examination, focusing on the heart and lungs.
• Blood Tests: These tests check for infection, inflammation, and oxygen levels in the blood.
• Chest X-ray: This imaging test helps identify any abnormalities or fluid in the lungs.
• CT Scan: A more detailed imaging test can provide a clearer picture of the lungs and potential damage.
• Arterial Blood Gas (ABG) Test: This measures oxygen and carbon dioxide levels in the blood, indicating how well the lungs are functioning.
• Echocardiogram: To rule out heart-related causes of symptoms.
• Bronchoscopy: Occasionally used to view the airways and check for other lung conditions.

Note: No single test confirms ARDS; instead, doctors diagnose it based on a combination of clinical findings and tests while ruling out other possible causes of symptoms.

Treatment

Treatment for ARDS focuses on supporting lung function and addressing the underlying cause. Key aspects include:

• Mechanical Ventilation: To help with breathing, a ventilator delivers oxygen and supports lung function. Settings are carefully adjusted to minimize lung injury.
• Oxygen Therapy: Supplemental oxygen is provided to increase blood oxygen levels.
• Prone Positioning: Placing patients on their stomachs (prone position) can improve oxygenation.
• Fluid Management: Careful control of fluid balance is crucial to prevent fluid overload while ensuring adequate organ function.
• Medications: These may include antibiotics for infections, corticosteroids to reduce inflammation, or sedatives for ventilated patients.
• Treatment of Underlying Causes: Addressing the initial cause of ARDS, such as treating infections or injuries.
• Supportive Care: Includes nutritional support and measures to prevent complications like blood clots and bedsores.

The approach is often multidisciplinary, involving critical care specialists, pulmonologists, and other healthcare professionals.

Recovery can be lengthy and may require rehabilitation.

What is the ARDSnet protocol?

The ARDSnet protocol refers to a set of guidelines developed by the ARDS Network, a group of U.S. research centers focused on studying acute respiratory distress syndrome (ARDS).

This protocol is primarily known for its recommendations on mechanical ventilation strategies for ARDS patients. Key aspects include:

• Low Tidal Volume Ventilation: The protocol recommends using lower tidal volumes (about 6 ml/kg of predicted body weight) instead of traditional higher volumes. This approach aims to reduce lung injury caused by the ventilator (ventilator-induced lung injury or VILI).
• Limiting Plateau Pressure: Keeping the plateau pressure (the pressure in the lungs at the end of an inhalation) below 30 cm H2O to minimize lung stress and damage.
• Oxygenation and Ventilation Goals: Setting specific targets for blood oxygen levels (PaO2) and carbon dioxide levels (PaCO2) to ensure adequate oxygenation without overventilating.
• Fluid Management: The protocol also includes guidelines for conservative fluid management to prevent fluid overload while maintaining sufficient organ perfusion.
• Prone Positioning and Other Strategies: Recommendations for prone positioning, neuromuscular blockade in early ARDS, and other supportive care measures.

Note: The ARDSnet protocol, particularly its low tidal volume ventilation strategy, has been shown to reduce mortality in ARDS patients and is considered a cornerstone of modern ARDS management.

ARDS Practice Questions

1. What is acute respiratory distress syndrome (ARDS) characterized by?
ARDS is characterized by rapid-onset, severe inflammation in the lungs, leading to fluid accumulation and significant breathing difficulties.

2. What are the clinical hallmarks of ARDS?
Hypoxemia, bilateral radiographic opacities, and diffuse alveolar damage.

3. What should a respiratory therapist monitor in patients with ARDS?
Cardiovascular compromise (decreased carbon dioxide), changes in blood pressure, decreased pulse intensity, oxygen saturation, mental status changes, and laboratory values.

4. What can be seen in the chest imaging of patients with ARDS?
Bilateral opacities that are not fully explained by effusions, lobar/lung collapse, or nodules.

5. What is the origin of edema in ARDS?
Respiratory failure that is not fully explained by cardiac failure or fluid overload. If no risk factors are present, echocardiography can be used to exclude hydrostatic edema.

6. What are the most common risk factors for ARDS?
Severe sepsis, pneumonia, aspiration, trauma (including pulmonary contusion), multiple transfusions, pancreatitis, near-drowning, medical prescription overdose, hyper transfusion, burns, infections, post-resuscitation, and cardiopulmonary bypass.

7. What are the signs and symptoms of ARDS?
This disease has a rapid onset, occurring 12-48 hours after insult/injury, respiratory distress, and multi-organ dysfunction syndrome.

8. How do you diagnose ARDS?
Diagnosis happens simultaneously with interventions, chest x-ray, CT scan of the chest with or without contrast, CBC count, comprehensive metabolic panel, CE, lactate, and urine drug testing. The medical history is important to consider (i.e., what occurred within 48 hours), type of work, drug use, medications, and the patient’s past medical history.

9. What can be observed on the chest x-ray of a patient with ARDS?
It is indistinguishable from those of cardiogenic pulmonary edema. Bilateral opacities consistent with pulmonary edema with diffuse bilateral infiltrates (i.e., white-out). Bilateral infiltrates may be patchy or asymmetric and may include pleural effusions.

10. What are some treatment methods for ARDS?
Oxygen therapy, prone positioning, administration of Nitric oxide and steroids, inverse ratio ventilation, and high-frequency oscillatory ventilation.

11. What are the pathologic or structural changes with ARDS?
Interstitial and intra-alveolar edema and hemorrhage, alveolar consolidation, intra-alveolar hyaline membrane, and pulmonary surfactant deficiency or abnormality atelectasis

12. What is another name for ARDS?
“Shock Lung Syndrome”

13. What etiologic factors can produce ARDS?
These include aspiration, disseminated intravascular coagulation, drug overdose, fat or air emboli, fluid overload, infection, inhalation of toxins and irritants, immunologic reaction, massive blood transfusion, oxygen toxicity, and pulmonary ischemia. Also, radiation-induced lung injury, shock, systemic reactions to processes initiated outside the lungs, thoracic trauma (i.e., pneumothorax), and uremia.

14. What are the clinical manifestations of ARDS?
Atelectasis, alveolar consolidation, and increased alveolar-capillary membrane thickness.

15. What clinical data can be obtained at the bedside of patients with ARDS?
Patients manifest increased RR (respiratory rate), HR (heart rate), BP (blood pressure, and CO (carbon monoxide). The chest has a dull percussion note, bronchial breath sounds, and crackles.

16. What are the typical ABG results for a patient with ARDS?
Mild to moderate-acute alveolar hyperventilation with hypoxemia. In severe cases, acute ventilatory failure with hypoxemia.

17. What are the general radiologic findings for ARDS?
Increased opacity

18. What are the ideal ventilator settings for ARDS patients?
Low tidal volumes (4-6 mL/kg) and high respiratory rates (as high as 35 bpm).

19. Which white blood cell is most commonly implicated in the inflammatory process of ARDS?
Neutrophils

20. What is the mortality rate for ARDS?
The mortality rate for ARDS is not definite and depends on the severity of the condition. Mortality correlates with the driving pressure, the difference between plateau and positive end-expiratory pressure (PEEP).

21. What clinical features are seen in both ARDS and CHF patients?
They both have diffused alveolar and interstitial infiltrates on a chest radiograph.

22. What time frame does ARDS typically occur?
Between one and three days.

23. What is not a common finding in the exudative phase of ARDS?
Bradypnea

24. What mode of mechanical ventilation is designed to optimize ventilation by recruiting alveolar units while minimizing ventilator-induced barotrauma in patients with ARDS?
Airway pressure release ventilation (APRV)

25. What organ plays a major role in the induction and modulation of the systemic inflammatory response?
Liver

26. What is a secondary risk factor for ARDS?
Sepsis

27. What treatment is not recommended for patients with ARDS?
The routine use of extracorporeal membrane oxygenation (ECMO) is not recommended.

28. What mode of mechanical ventilation is designed to optimize ventilation by reducing alveolar collapse while using small tidal volumes in patients with ARDS?
High-frequency ventilation (HFV)

29. What can be observed in the physical size of the lungs of patients suffering from ARDS?
The lungs are reduced by 20-30% of their normal size.

30. What is the indication that inhaled nitric oxide may be useful for patients with ARDS?
Severe elevation of the pulmonary vascular resistance.

31. What mechanisms ultimately lead to ARDS regardless of the etiology?
Disruption of the endothelial and epithelial barriers.

32. What assessment tool is most useful in distinguishing ARDS from CHF?
Swan-Ganz catheter

33. What is considered an experimental therapy for patients with ARDS?
Inhaled nitric oxide (NO)

34. What tidal volume range is recommended for patients with ARDS?
4-6 mL/kg

35. What parameter is important in determining the optimal level of PEEP for a patient with ARDS?
Oxygen delivery

36. What frequent assessments should be completed by a respiratory therapist in the treatment of a patient with ARDS?
Arterial blood gas, hemodynamic parameters, and evaluation of the effectiveness of treatment.

37. What ventilatory strategy has been found to be useful for avoiding barotrauma in the treatment of patients with ARDS?
Permissive hypercapnia

38. What drug therapy is available for ARDS?
Antibiotics, diuretics, and sedation in mechanically ventilated patients.

39. What parameters are important in the management of patients with ARDS?
Keep hemoglobin saturation above 90%, ensure adequate urine output, and keep the mean arterial pressure above 60 mmHg.

40. What lung protective strategies can be used during mechanical ventilation?
Low tidal volume (i.e., 4-6 mL/kg) and low to moderately high PEEP (i.e., 5-20 cmH20) to keep alveoli open and diminish the negative effects of high-pressure settings.

41. What is the benefit of prone positioning when treating ARDS?
It produces transient improvement of gas exchange.

42. What is the maximal inspiratory pressure that should be targeted when using pressure control ventilation in patients with ARDS?
30-35 cmH2O

43. What benefit has not been associated with the use of PEEP when treating ARDS?
Improved venous return

44. What complication has been associated with the use of PEEP in patients with ARDS?
Reduced cardiac output

45. What is the name of the period that follows the exudative phase of ARDS?
Fibroproliferative

46. What test provides useful information in making the diagnosis of ARDS for patients with inconclusive results on traditional tests?
Examination of bronchoalveolar lavage fluid.

47. What is the difference between acute lung injury (ALI) and acute respiratory distress syndrome (ARDS)?
Acute lung injury is when the P/F ratio is 200-300. The alveoli fill with fluid resulting in severe dyspnea, hypoxemia refractory to supplemental oxygen, reduced lung compliance, and diffuse pulmonary infiltrates. On the other hand, ARDS is a sudden and progressive form of acute respiratory failure in which the alveolar-capillary interface becomes damaged and more permeable to intravascular fluid. The P/F ratio for ARDS is less than 200.

48. What are the most common causes of ARDS?
ARDS is caused by aspiration of gastric contents or other substances, viral or bacterial pneumonia, sepsis, and severe massive trauma. Other cause includes chest trauma, embolism, near-drowning, oxygen toxicity, DIC (disseminated intravascular coagulation), pancreatitis, severe head injury, and shock.

49. What are pulmonary insults that can cause ARDS?
These are inhaled or aspirated noxious agents that induce the inflammatory response in the lung and result in alveolar collapse and endothelial damage, which leads to hyaline membrane formation.

50. What are the most important causes of ARDS?
Pneumonia, aspiration, sepsis, and trauma.

51. What is the result of both pulmonary and systematic causes of ARDS?
Increased permeability of the alveolar-capillary membrane leading to pulmonary edema.

52. What is the result of a lung scan in patients with ARDS?
There will be a ventilation/perfusion (V/Q) mismatch.

53. What causes arterial hypoxemia in ARDS?
Shunting and mixing of unoxygenated blood.

54. What manifestation can be seen in the blood oxygen level of patients with ARDS?
Severe arterial hypoxemia

55. Does ARDS result in increased or decreased compliance?
Decreased compliance

56. In ARDS, will the lungs increase or decrease in stiffness?
ARDS causes increased lung stiffness.

57. What is the typical onset time of ARDS after a triggering event?
Within 72 hours or 7 days after a triggering event.

58. What are the severity levels of ARDS?
ARDS is classified as mild, 200-300 mmHg; moderate, 100-200 mmHg; and severe, less than 100 mmHg, based on the PaO2/FiO2 ratio.

59. What is the summary of the clinical assessment of ARDS?
Hyperventilation, respiratory alkalosis, dyspnea, hypoxemia, metabolic acidosis, respiratory acidosis, hypotension, decreased carbon dioxide, and death.

60. What is not required as a component in the diagnosis of ARDS?
Heart failure

61. What is the basic pathogenesis of ARDS?
Initiation (includes triggering/injuring event), amplification, and injury.

62. What happens in the initiation phase of the pathogenesis of ARDS?
A precipitating event and inflammatory response.

63. What is the amplification phase of the pathogenesis of ARDS?
Immune cells (e.g., neutrophils) are recruited and activated, then migrate into the pulmonary parenchyma.

64. What is the injury phase of the pathogenesis of ARDS?
Immune cells (e.g., neutrophils) release damaging substances that injure the lung tissue.

65. What are the clinical presentations of ARDS?
Decreased pulmonary compliance, increased work of breathing, fatigue, decreased tidal volume, and diminished gas exchange.

66. What happens to the lung parenchyma as ARDS worsens?
End-stage fibrosis, remodeling of lung architecture, and “honeycomb lung.”

67. What lung field does ARDS affect?
ARDS typically affects most lung fields.

68. How does oxygen therapy affect patients with ARDS?
Hypoxemia may occur despite oxygen administration because of the shunting and mixing of unoxygenated blood.

69. What are the clinical phases of ARDS?
Phase 1 (acute injury), Phase 2 (latent phase), Phase 3 (acute respiratory failure), and Phase 4 (severe abnormalities).

70. What happens in Phase 1 of ARDS?
Phase 1, or the “acute injury” phase, is characterized by edema and thickening of the alveolar-capillary membrane. The chest x-ray will be normal. Early changes in this phase result in dyspnea and tachypnea. Intervention for this is to provide oxygen therapy and support.

71. What happens in Phase 2 of ARDS?
Phase 2, or the “latent phase”, happens 6-38 hours after the injury. The manifestation of increasing edema, right-to-left pulmonary shunting, V/Q mismatch, hyperventilation that leads to hypocapnia, and increased work of breathing can be observed. Patchy infiltrates form from pulmonary edema is an early stage change of this phase. It can be intervened through mechanical ventilation and prevention of complications.

72. What happens in Phase 3 of ARDS?
Phase 3, or the “acute respiratory failure” phase, involves inflammatory damage of type II alveolar cells, which results in the inhibition of surfactant production. This inhibition causes decreased compliance that leads to increased work of breathing such as tachypnea, dyspnea, high-pitched, and diffuse crackles. Phase 3 occurs over 2-10 days with an early-stage change of progressive hypoxemia that can be managed by maintaining oxygenation and supporting the failing lung until it can heal.

73. What happens in Phase 4 of ARDS?
Phase 4, or the “severe abnormalities phase,” is considered a chronic phase with characteristics of late effects that develop over time. It includes fibrin deposition resulting in fibrosis, permanent alveolar damage, severe hypoxemia that is unresponsive to therapy, and metabolic and respiratory acidosis. Phase 4 occurs after 10 days and can lead to pulmonary fibrosis pneumonia. At this stage, ARDS may be irreversible.

74. How should you treat ARDS?
While there is no known cure for ARDS, treatment involves managing the symptoms.

75. What does “alveolar recruitment” mean?
It involves the opening of closed alveoli (i.e., recruiting more alveoli to hold air).

76. Does ARDS affect all parts of the lung?
No, even in this condition, there are patches of normal lung.

77. What can affect ARDS symptoms?
Position; patients should be turned periodically to improve oxygenation.

78. What is the prognosis for acute respiratory failure with ARDSnet?
26-44% mortality

79. What is a characteristic of ARDS?
Severe hypoxemia that can rapidly lead to acute respiratory failure.

80. Is ARDS difficult to diagnose, and if not promptly treated, can it be fatal?
Yes, diagnosing this disease is difficult and can be fatal within 48 hours of onset.

81. What mortality rate is highest for patients with ARDS?
Patients 65 years and older with coexisting organ failure.

82. What are the lasting effects that can occur from severe cases of ARDS?
Persistent pulmonary fibrosis, symptoms of restrictive lung diseases with decreased expansion, increased work of breathing (WOB), and inadequate ventilation.

83. The acute phase of ARDS may cause a rapid onset of what?
There is a rapid onset of severe dyspnea that occurs 12-48 hours after the initial injury.

84. What is a characteristic of ARDS when dealing with supplemental oxygen?
ARDS causes arterial hypoxemia that doesn’t respond to supplemental oxygen.

85. What are some other signs and symptoms of ARDS?
Rapid, shallow breathing; intercostal retractions; rhonchi and crackles; tachycardia; decreased urine output; respiratory alkalosis; cyanosis; altered mental status due to low oxygen levels and hypotension.

Final Thoughts

Acute respiratory distress syndrome (ARDS) is a serious, life-threatening condition characterized by rapid-onset lung inflammation and fluid accumulation, leading to severe breathing difficulties.

It arises from various causes, including infections, trauma, and inhalation of harmful substances. The symptoms, such as severe shortness of breath and low oxygen levels, necessitate prompt medical attention.

Diagnosis involves a combination of medical history, physical examination, imaging tests, and bloodwork.

Treatment centers on supporting lung function through mechanical ventilation, oxygen therapy, and addressing the underlying cause.

ARDS requires a comprehensive, multidisciplinary approach for management, emphasizing the critical nature of this condition and the complexity of its treatment.