What does ARDS stand for? What is ARDS in medical terms? These are common questions of students and those interested who are interested in the medical field.
ARDS stands for Acute Respiratory Distress Syndrome and this article provides an overview of the ARDS guidelines and most of the other important information regarding this topic. Not to mention, it has practice questions that can help you master this topic as well. So if you’re ready, let’s go ahead and dive right in.
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What is ARDS?
ARDS, or Acute Respiratory Distress Syndrome, is a condition that is characterized by fluid in the alveoli that causes refractory hypoxemia, decreased lung compliance, and severe oxygen insufficiency.
What Causes ARDS?
There are both direct and indirect causes of ARDS. In general, here are the most common causes:
- Lung Injury
- Drug overdose
- Fluid overload
ARDS Signs and Symptoms
The signs and symptoms of ARDS can begin to show within hours or days of the initial onset. Here are some examples:
- Severe hypoxemia
- Shortness of breath
- Muscle weakness and fatigue
How to Diagnose ARDS?
- Chest x-ray
- Arterial Blood Gas (ABG)
- Pulmonary Function Tests (PFT)
- Hemodynamic monitoring
The chest radiograph of a patient with ARDS will show bilateral opacities or infiltrates and the image will resemble a ground-glass appearance.
The patient’s ABG results would reveal severe hypoxemia, also known as refractory hypoxemia. Their pulmonary measurements would reveal decreased lung volumes and capacities.
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ARDS Practice Questions:
1. What is Acute Respiratory Distress Syndrome (ARDS)?
An acute respiratory failure following systemic or pulmonary insult, diffuse, non-cardiogenic, profound hypoxia and inflammatory lung injury leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated tissue.
2. What are the clinical hallmarks of ARDS?
Hypoxemia and bilateral radiographic opacities. The pathological hallmark is diffuse alveolar damage.
3. What should the Respiratory Therapist monitor and be alert for in ARDS patients?
Cardiovascular compromise (decreased carbon dioxide), changes in blood pressure, decreased pulse intensity, oxygen saturation, mental status changes, laboratory values (Hgb)
4. What can be seen in the ARDS chest imaging?
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 not fully explained by cardiac failure or fluid overload. If no risk factors present, echocardiography can be used to exclude hydrostatic edema.
6. What is the oxygenation status for patients with ARDS?
For mild cases, it is < 200. In moderate cases, 100-200 and in severe case, < 100 with >/= 5cm H2O PEEP.
7. What are the most common risk factors for ARDS?
They are severe sepsis (> 40% with 50% mortality), pneumonia, aspiration (> 30%), trauma (> 34%) including pulmonary contusion, multiple transfusions, pancreatitis, near-drowning, medical prescription overdose, hyper transfusion, burns, infections, post-resuscitation, and cardiopulmonary bypass.
8. What is the pathophysiology of ARDS?
Healthy lungs can regulate the movement of fluid around the pulmonary parenchyma. The injury causes the release of pro-inflammatory cytokines, recruits neutrophils, release toxic mediators that ultimately damage the capillary endothelium and alveolar epithelium. This increase allows proteins to escape and change the oncotic gradient overwhelming the lymphatic system.
9. 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.
10. 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
11. What can be observed on a chest x-ray in ARDS?
It is indistinguishable from those of cardiogenic pulmonary edema. Bilateral opacities consistent with pulmonary edema with diffuse bilateral infiltrates (“white out”). Bilateral infiltrates may be patchy or asymmetric and may include pleural effusions.
12. How can you treat ARDS patients?
Treatment modalities for ARDS include mechanical ventilation, fluid management by keeping fluids to a minimum as dry lungs are better working lungs, nutritional support (enteral preferred), sedation and paralysis, DVT (deep vein thrombosis), and, ulcer, nosocomial pneumonia prophylaxis. In addition to these, supportive care in ICU, adequate oxygenation with avoidance of complications, drug therapy, and permissive hypercapnia
13. What are some other treatments for ARDS?
These are prone positioning, administration of Nitric oxide and steroids, inverse ratio ventilation, and high-frequency oscillatory ventilation.
14. What are some ways to limit ventilator-associated lung injury from happening?
Use of lung protective strategies with a target tidal volume.
15. 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
16. What is another name for ARDS?
“Shock Lung Syndrome”
17. What are the etiologic factors that may 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 and uremia.
18. What are the clinical manifestations of ARDS?
Atelectasis, alveolar consolidation, and increased alveolar-capillary membrane thickness.
19. What are the clinical data obtained at the bedside?
Patients manifest increased RR (respiratory rate), HR (heartbeat per minute), BP (blood pressure, and CO (carbon monoxide). The chest has a dull percussion note, bronchial breath sounds, and crackles.
20. What are the clinical data obtained from the laboratory?
Expiratory maneuver: PEFR, FEF50%, FEF200-1200, FEV1%, rest low; lung volumes: low; ABG: Mild to moderate-acute alveolar hyperventilation with hypoxemia and for severe, acute ventilatory failure with hypoxemia.
21. What will be the radiologic findings for?
22. What is the ideal ventilator settings for ARDS patients?
Low tidal volumes (4-8ml/kg) and high respiratory rates (as high as 35bpm)
23. Which white blood cell is most commonly implicated in the inflammatory process of ARDS?
24. What is the mortality rate of patients with ARDS?
The mortality rate of patients with ARDS is not definite. It ranges from the severity of the condition. In a study conducted, a mild condition mortality rate was reported to be 35%, 40% for those with
They both have diffused alveolar and interstitial infiltrates in chest radiograph.
26. What time frame does ARDS typically occur?
Between one and three days.
27. What is not a common finding in the exudative phase of ARDS?
28. 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)
29. What is recommended in terms of fluid management of patients with ARDS?
30. What organ plays a major role in the induction and modulation of the systemic inflammatory response?
31. What is considered
32. What treatment is not recommended for patients with ARDS?
The routine use of extracorporeal membrane oxygenation (ECMO) is not recommended.
33. 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)
34. What can be observed on the physical size of the lungs of patients suffering from ARDS?
The lungs of a patient with ARDS are effectively reduced
35. What is the indication that the use of inhaled nitric oxide may be useful for patients with ARDS?
Severe elevation of pulmonary vascular resistance
36. What mechanisms ultimately lead to ARDS regardless of the etiology?
Disruption of the endothelial and epithelial barriers
37. What assessment tool is most useful in distinguishing ARDS from CHF?
38. What is considered an experimental therapy used for patients with ARDS?
Although promising, inhaled NO (nitric oxide) remains an experimental therapy for patients with ARDS.
39. What range is now recommended for tidal volumes in a patient with ARDS who is being mechanically ventilated?
5 to 7 ml/kg
40. According to the Starling and Apos’s equation, which forces influence the movement of fluid from the bloodstream to the interstitium?
Microvascular hydrostatic pressure and interstitial osmotic pressure.
41. What parameter is important in determining the optimal level of PEEP in a patient with ARDS?
DO2 or oxygen delivery.
42. What are frequent assessments should be completed by the Respiratory Therapist?
Arterial blood gas, hemodynamic parameters, and evaluation of the effectiveness of treatment.
43. What ventilatory strategy has been found to be useful for avoiding barotrauma in the treatment of patients with ARDS?
44. What drug therapy is available for ARDS?
Antibiotic therapy: sepsis-related ARDS or suspected underlying infection; diuretic: increases renal excretion of H20 then decreases pulmonary interstitial and alveolar edema; and, mechanically ventilated patient: may need sedation. The gold standard has yet to be developed.
45. What parameters are important in the management of patients with ARDS?
Keep hemoglobin saturation above 90%. Ensure adequate urine output. Keep mean arterial pressure above 60 mm Hg.
46. What are some lung protective strategies when it comes to mechanical ventilation?
Low tidal volume (6 mL/kg) and low to moderately high PEEP (positive end-expiratory pressure) (5-20 cm H20) to keep alveoli open and diminish the negative effects of high-pressure settings.
47. What is the benefit of prone-positioning for patients with ARDS?
It produces a transient improvement in gas exchange. Prone positioning is for patients who require high Fi02 levels and should be considered early in the treatment. Complication includes pressure ulcers, corneal abrasions, and brachial nerve injury through overextension of shoulders.
48. What is the maximal inspiratory pressure that should be targeted when using pressure control ventilation in patients with ARDS?
30 to 35 cm H2O
49. What benefit has not been associated with the use of PEEP in a patient with ARDS?
Improved venous return.
50. What complication has been associated with the use of PEEP in patients with ARDS?
Reduced cardiac output
51. What is the name of the period that follows the exudative phase in ARDS?
52. What test provides useful information in making the diagnosis of ARDS for patients with inconclusive results on traditional tests?
Examination of bronchoalveolar lavage fluid
53. 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 to 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 is less than 200.
54. What are the 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.
55. What are pulmonary insults that can cause ARDS?
These are inhaled or aspirated noxious agents that
56. What are the most important causes of ARDS?
Pneumonia, aspiration, sepsis, and trauma.
57. What are systemic insults that can cause ARDS?
They are disorders that induce an overwhelming inflammatory response and a result in an alveolar collapse.
58. What is the result of both pulmonary and systematic causes of ARDS?
Increased permeability of
59. What insults involve neutrophil recruitment?
Pulmonary insults and systemic insults.
60. What will be the result of the lung scan of patients with ARDS?
There will be a V/Q (ventilation/perfusion) mismatch.
61. What causes arterial hypoxemia in ARDS?
Shunting and mixing of unoxygenated blood.
62. What manifestation can be seen in the blood oxygen level of patients with ARDS?
Severe arterial hypoxemia will be seen.
63. In acute respiratory distress syndrome, will the lungs have increased or decreased compliance?
64. In ARDS, will the lungs increase or decrease in stiffness?
Increased lung stiffness.
65. When assessing ventilation/oxygenation with blood analysis, what type of blood do you need?
66. What causes a shift in the oxygen dissociation curve?
A right shift of the oxygen dissociation curve is targeted for ARDS patients as this decreases the oxygen affinity of hemoglobin which allows more oxygen to be available to the tissues. To cause this shift, remember “CADET, face right!” where C stands for carbon dioxide (leading to acid formation), A for acid, D for 2,3-DPG (diphosphoglycerate), E for exercise (leading to carbon dioxide) and T for temperature.
67. What are some causes of hypercapnia?
Decreased minute ventilation, increased dead air space and increased CO2 production.
68. What common cardiac arrhythmias may cause hypoxemia?
A-fib, a-flutter and multifocal atrial tachycardia
69. What is the typical onset time of ARDS after a triggering event?
Most within 72 hours or 7 days after a triggering event.
70. What are the levels of severity of ARDS and what are their criteria?
ARDS are classified as mild, 200-300 mmHg; moderate, 100-200 mmHg; and severe, < 100 mmHg. Criteria are based on PaO2
71. What is the summary of the clinical assessment of ARDS?
Hyperventilation, respiratory alkalosis, dyspnea and hypoxemia, metabolic acidosis, respiratory acidosis, further hypoxemia, hypotension, decreased CO (carbon dioxide) and death
72. What is not required as a component in the diagnosis of ARDS?
73. What is the basic pathogenesis of ARDS?
Initiation (includes triggering/injuring event), amplification and injury
74. What is the initiation phase of the pathogenesis of ARDS?
Precipitating event and inflammatory response (involves endotoxin, TNF, IL-1, other cytokines)
75. 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.
76. What is the injury phase of the pathogenesis of ARDS?
Immune cells (e.g. neutrophils) release damaging substances that injure the lung tissue.
77. What is the pathogenesis of ARDS?
Injury/trigger; cytokine and inflammatory mediator release; PMN (polymorphonuclear leukocyte) injury (via reactive O2 species and proteases) to alveoli and capillaries; pulmonary edema; and increased RV (right ventricle) pressure, impaired gas exchange, decreased lung compliance; with chronic disease, hyaline membrane and fibrous scar formation
78. What are the clinical presentations of ARDS?
Decreased pulmonary compliance –> increased work of breathing –> fatigue and decreased tidal volume –> diminished gas exchange
79. What is the Berlin Definition criterion for acute respiratory distress syndrome?
It defines the clinical features of ARDS (acute respiratory distress syndrome). Patients suffer from respiratory failure within one week of insult with acute symptoms. The bilateral opacities are consistent with pulmonary edema. It is non-cardiogenic pulmonary edema where symptoms are not fully explained by heart failure or fluid overload. The PaO2/FiO2 ratio is < 300.
80. What criteria should you consider when diagnosing ARDS?
Remember that ARDS is non-cardiogenic. Consider these criteria: exclusion of cardiogenic pulmonary edema (e.g. HTN emergency), occurrence of acute lung injury or history of systemic and pulmonary risk factors, acute onset of respiratory distress, exclusion of other causes of hypoxemic respiratory rate (e.g. volume overload) and severe, refractory hypoxemia, Berlin definition, laboratory tests and CXR (chest x-ray) for bilateral infiltrates involvement.
81. What happens to the lung parenchyma as ARDS worsens?
End-stage fibrosis, remodeling of lung architecture and “honeycomb lung”
82. What lung field does ARDS effect?
It involves most lung fields. But remember, patches of normal lung still remain.
83. How will the
Diffuse, bilateral infiltrates and lower > upper.
84. What will be the results when 100% oxygen is administered to a patient with ARDS?
The SpO2 will be low. Hypoxemia may occur despite oxygen administration because of the shunting and mixing of unoxygenated blood.
85. What are the clinical phases of acute respiratory distress syndrome?
Phase 1 is the acute injury. Phase 2 is the latent phase. Phase 3 is the acute respiratory failure. And, Phase 4 is the severe abnormalities.
86. What happens in Phase 1 of ARDS?
Phase 1 or the “acute injury”, edema and thickening of the alveolar-capillary membrane are evident. The chest x-ray will be normal. Early changes in this phase result in dyspnea and tachypnea. Intervention for this is to provide support and oxygen.
87. What happens in Phase 2 of ARDS?
Phase 2 or the “latent phase”, happens on 6-38 hours after injury. The manifestation of increasing edema, right-to-left pulmonary shunting, V/Q (ventilation/perfusion) 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.
88. What happens in Phase 3 of ARDS?
Phase 3 or the “acute respiratory failure”, involves inflammatory damage of type II alveolar cells which result 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 support failing lung until it can heal.
89. What happens in Phase 4 of ARDS?
Phase 4 or the “severe abnormalities” is considered a chronic phase with characteristics of late effects that develop over time, fibrin deposition resulting to 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 (acute respiratory distress syndrome) may be irreversible.
90. What is the standard medical treatment for acute respiratory distress syndrome?
As of this time, there is no standard medical treatment available for this disease.
91. How should you treat ARDS?
While it is true that there is no known cure for this disease, treatment is centered on managing the symptoms. Patients are treated on the underlying etiology of ARDS (acute respiratory distress syndrome) in order for the lungs to recover. Aggressive supportive care is essential to ensure that there is enough oxygen in the blood to prevent further damage to the lungs. Vasodilators are used to improve gas exchange and right heart function by manipulating the pulmonary blood flow. Nutritional support is needed for prevention of cumulative caloric deficits, malnutrition, and loss of lean body mass and deterioration of respiratory muscle. This is important as metabolic demand is so high that caloric needs will be increased, enteral nutrition is preferred. Administration of heparin to prevent DVT (deep vein thrombosis) and H2 blockers for ulcers are also important.
92. What benefit do corticosteroids have in ARDS patients?
There is no proven benefit.
93. What is the definition of acute respiratory failure?
Acute respiratory failure is a respiratory dysfunction resulting in abnormal oxygen or CO2 levels that is severe enough to threaten the function of vital organs.
94. What is the ABG criteria for respiratory failure?
ABG criteria for respiratory failure are as follows: for hypoxemia, PaO2 < 50 mmHg, and SpO2 < 85% or PaO2 drop of > 10 mmHg; hypercapnia, PaCO2 > 50 mmHg or increase > 10 mmHg above baseline. Remember that the normal PaO2 = 80-100 and the normal PaCO2 = 35-45.
95. What are the two classifications of respiratory failure?
Hypoxemic respiratory failure and hypercapnic respiratory failure.
96. What is the characteristic of hypoxemic respiratory failure?
It is a failure of oxygenation. There is low oxygen, diffusion impairment, VQ mismatch, shunting, hypoventilation, and loss of functional alveoli.
97. What is PEEP?
PEEP stands for
98. What does “alveolar recruitment” mean?
It is the opening of closed alveoli or “recruiting more alveoli to hold air”.
99. What is the ARDSnet protocol?
ARDSnet protocol is a very specific set of vent settings to use for acute respiratory distress syndrome. The tidal volume is calculated based on the ideal body weight (6-7cc / kg).
100. Does ARDS affect all parts of the lung?
No, even in this condition, there are patches of normal lung. This is why careful handling is a must when patients are vent as the pressure will go to the normal tissue first, risking damage.
101. What can affect ARDS symptoms?
Position can affect ARDS (acute respiratory syndrome) symptoms. Patients should be turned periodically to improve oxygenation.
102. What is the prognosis for acute respiratory failure with ARDSnet?
103. What is the psychological component to ARDS?
Seventy-nine percent of patients remember adverse events and 30% will develop post-traumatic stress disorder (PTSD).
104. What is a characteristic of ARDS?
Acute respiratory distress syndrome (ARDS) is a form of pulmonary inflammation/edema characterized by severe hypoxemia that can rapidly lead to acute respiratory failure.
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105. Is ARDS difficult to diagnose, and if not promptly treated, can ARDS be fatal?
Yes, diagnosing this disease is difficult and can be fatal within 48 hours of onset.
65 years and older patients with coexisting organ failure. The rate increases with the number of failing organs.
107. What lasting effects can survivors of severe cases of ARDS?
Persistent pulmonary fibrosis or scarring in lungs, symptoms of restrictive lung diseases with decreased expansion, increased work of breathing (WOB), and inadequate ventilation
108. What causes ARDS?
ARDS is caused by direct or indirect lung injury. A direct injury such as gastric aspiration, bacterial/fungal/viral pneumonia, pulmonary contusion (bruise to lung caused by trauma), near drowning and prolonged inhalation of high oxygen/smoke/toxic substances. The indirect injury includes sepsis, shock, non-thoracic trauma, drug overdose, prolonged hypotension, cardiopulmonary bypass, acute pancreatitis, hematologic disorders (disseminated intravascular coagulation (DIC), multiple blood transfusions), fat embolism, head injury
109. In the acute phase of ARDS, what is there a rapid onset of?
There is a rapid onset of severe dyspnea which occurs 12-48 hours after initial injury.
110. What is a characteristic of acute respiratory distress syndrome when dealing with supplemental oxygen?
Arterial hypoxemia that doesn’t respond to supplemental oxygen
111. What are 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.
112. What is systemic inflammatory response syndrome (SIRS)?
Systemic inflammatory response syndrome is a clinical syndrome characterized by systemic inflammation and widespread tissue injury. The cause of this syndrome is broad and includes infectious and noninfectious conditions, surgical procedures, trauma, medication,
As always, be sure to go through the practice questions a few times so that your brain can truly learn this information. Thank you so much for reading and as always, breathe easy my friend.
The following are the sources that were used while doing research for this article:
- Faarc, Kacmarek Robert PhD Rrt, et al. Egan’s Fundamentals of Respiratory Care. 12th ed., Mosby, 2020. [Link]
- Rrt, Des Terry Jardins MEd, and Burton George Md Facp Fccp Faarc. Clinical Manifestations and Assessment of Respiratory Disease. 8th ed., Mosby, 2019. [Link]
- Diamond, Matthew. “Acute Respiratory Distress Syndrome (ARDS) – StatPearls – NCBI Bookshelf.” National Center for Biotechnology Information, 2 July 2020, www.ncbi.nlm.nih.gov/books/NBK436002.
- “Acute Respiratory Distress Syndrome.” PubMed Central (PMC), 8 Sept. 2020, www.ncbi.nlm.nih.gov/pmc/articles/PMC6709677.
- “Current Concepts of ARDS: A Narrative Review.” PubMed Central (PMC), 1 Jan. 2017, www.ncbi.nlm.nih.gov/pmc/articles/PMC5297699.
- “Acute Respiratory Distress Syndrome: An Update and Review.” PubMed Central (PMC), 1 June 2018, www.ncbi.nlm.nih.gov/pmc/articles/PMC6032183.
- “Guidelines on the Management of Acute Respiratory Distress Syndrome.” PubMed Central (PMC), 8 Sept. 2020, www.ncbi.nlm.nih.gov/pmc/articles/PMC6561387.
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