Ch 32: Acute Respiratory Distress Syndrome (ARDS) Flashcards
(225 cards)
What is a sudden and progressive form of acute respiratory failure (ARF) in which the alveolar-capillary membrane becomes damaged and more permeable to intravascular fluid?
acute respiratory distress syndrome (ARDS)
Severe V/Q mismatch and shunting of pulmonary capillary blood result in hypoxemia unresponsive to increasing O2 concentrations.
refractory hypoxemia
reflects the ratio of the patient’s Pa02 to the FIO2 that the patient is receiving
Pa02/FIO2 ratio
As a result of delivering a lower-than-normal low tidal volume ventilation to the patient with ARDS, the PaCO2 level will slowly rise above normal limits.
permissive hypercapnia
A 64-year-old male is admitted to the ICU with a diagnosis of necrotizing pancreatitis. Over the past 12 hours, he has become increasingly hypoxic despite receiving high-flow oxygen via a non-rebreather mask. Chest auscultation reveals crackles bilaterally, and his PaO2/FiO2 ratio is 180. The provider suspects the development of ARDS.
Which of the following best explains the patient’s current condition?
A. Direct injury from the aspiration of gastric contents
B. Indirect injury from systemic inflammatory response
C. Complication of chronic obstructive pulmonary disease
D. Inflammatory infiltration of alveoli caused by a fungal infection
B. Indirect injury from systemic inflammatory response
Rationale: Necrotizing pancreatitis is an example of an indirect injury that can lead to ARDS. The systemic inflammatory response releases mediators into the bloodstream, which then affect the lungs, causing increased capillary permeability and fluid accumulation in the alveoli.
Which patient is at the highest risk for developing ARDS?
A. A 55-year-old with COPD exacerbation
B. A 39-year-old who underwent an elective cholecystectomy
C. A 70-year-old with sepsis from a perforated bowel
D. A 29-year-old recovering from a fractured tibia
C. A 70-year-old with sepsis from a perforated bowel
Rationale: Sepsis from a perforated bowel represents both an indirect injury and systemic infection, placing the patient at the highest risk for ARDS. Sepsis is the most common cause of ARDS, especially when coupled with MODS or abdominal catastrophes like perforation.
What is the most common cause of ARDS?
sepsis
A nurse is caring for a patient who developed ARDS following the aspiration of gastric contents. Which mechanism best explains how this direct lung injury contributes to the development of ARDS?
A. Fluid shifts from the interstitial to intravascular space
B. Surfactant production increases, leading to alveolar hyperinflation
C. The inflammatory response damages alveolar-capillary membranes
D. Alveolar macrophages eliminate the aspirated particles rapidly
C. The inflammatory response damages alveolar-capillary membranes
Rationale: In direct lung injury like aspiration, pathogens or irritants contact lung tissue directly, triggering an inflammatory response. This leads to increased permeability of the alveolar-capillary membrane, allowing fluid and proteins to leak into alveoli—hallmarks of ARDS.
A 60-year-old man with a history of diverticulitis is admitted for a suspected bowel perforation. He becomes febrile, hypotensive, and tachypneic. Labs reveal elevated WBCs and lactic acid levels. Chest x-ray shows bilateral infiltrates.
Which complication is most concerning for this patient?
A. Pulmonary embolism
B. Hospital-acquired pneumonia
C. Atelectasis
D. Acute respiratory distress syndrome
D. Acute respiratory distress syndrome
Rationale: This patient has signs of sepsis from bowel perforation, a common indirect cause of ARDS. Bilateral infiltrates, hypoxia, and the systemic inflammatory state suggest progression toward ARDS, which is more critical and time-sensitive than the other options listed.
Which of the following best describes why the lungs are particularly vulnerable to the effects of circulating inflammatory mediators in systemic illness?
A. The lungs act as a filtration system for blood-borne pathogens and mediators
B. The lungs have a slow metabolic rate, causing delayed immune response
C. The lungs are isolated from systemic circulation under normal conditions
D. Inflammatory mediators selectively bypass pulmonary tissue
A. The lungs act as a filtration system for blood-borne pathogens and mediators
Rationale: The lungs receive the entire cardiac output and act as a natural filter for circulating debris and mediators. This makes them a prime target in systemic inflammation, like in sepsis or MODS, often resulting in ARDS.
A nurse is educating a new ICU nurse on the causes of ARDS. Which of the following examples should the nurse include as a direct cause of ARDS?
A. Sepsis due to urinary tract infection
B. Multiple long bone fractures
C. Aspiration of gastric contents
D. Pancreatitis
C. Aspiration of gastric contents
Rationale: Aspiration is a direct insult to the lung parenchyma. It causes inflammation and fluid accumulation in the alveoli almost immediately. The other options are considered indirect causes that result in systemic inflammation impacting the lungs.
Which best explains why patients with multiple risk factors for ARDS are significantly more likely to develop the syndrome?
A. They are more likely to receive high levels of oxygen therapy
B. The immune system overcompensates, enhancing surfactant levels
C. The accumulation of risk factors intensifies the inflammatory response
D. Coexisting conditions restrict lung expansion, leading to infection
C. The accumulation of risk factors intensifies the inflammatory response
Rationale: Patients with multiple risk factors (e.g., trauma + sepsis + blood transfusions) have heightened and sustained inflammatory responses, significantly increasing the risk of alveolar-capillary damage and development of ARDS.
Which of the following are considered indirect causes of ARDS? (Select all that apply)
A. Near-drowning
B. Sepsis
C. Pancreatitis
D. Smoke inhalation
E. Multiple blood transfusions
B. Sepsis
C. Pancreatitis
E. Multiple blood transfusions
Indirect causes of ARDS originate outside the lungs but affect them via systemic inflammation. These include sepsis, pancreatitis, and multiple transfusions. Near-drowning and smoke inhalation are direct causes since the lungs are immediately impacted.
A 48-year-old female was admitted to the ICU with septic shock. After 24 hours on mechanical ventilation, she is showing signs of worsening oxygenation despite increased FiO₂, bilateral crackles, and a PaO₂/FiO₂ ratio of 150. The healthcare provider suspects she is in the early stage of ARDS.
Which of the following describes the primary pathological event occurring in this stage?
A. Formation of fibrotic scar tissue in alveolar spaces
B. Proliferation of type II alveolar cells and fibroblasts
C. Damage to the alveolar-capillary membrane causing fluid leakage
D. Chronic remodeling of lung parenchyma with collagen deposition
C. Damage to the alveolar-capillary membrane causing fluid leakage
Rationale: In the injury or exudative phase, which occurs within the first 1–7 days (often within 24–48 hours), inflammation increases capillary permeability, causing fluid to leak into the alveoli. This leads to non-cardiogenic pulmonary edema and impaired gas exchange—hallmark features of early ARDS.
A patient is in the reparative (proliferative) phase of ARDS. Which of the following clinical or pathophysiological findings is most consistent with this stage?
A. Restoration of normal lung architecture with minimal residual damage
B. Increased fibroblast activity and thickening of the alveolar membrane
C. Rapid resolution of pulmonary edema and complete normalization of compliance
D. Immediate improvement in oxygenation due to new capillary formation
B. Increased fibroblast activity and thickening of the alveolar membrane
Rationale: During the proliferative phase, inflammatory mediators begin to subside, but fibroblasts and other repair cells proliferate. This can lead to thickened alveolar membranes, worsening lung compliance, and persistent hypoxemia. This phase typically occurs 7 to 14 days after the initial injury.
Which statement best describes the fibrotic phase of ARDS?
A. It is a reversible phase where alveolar edema clears rapidly
B. It is characterized by development of hyaline membranes and alveolar collapse
C. It leads to long-term lung dysfunction due to scarring and fibrosis
D. It occurs before the proliferative phase and marks the onset of inflammation
C. It leads to long-term lung dysfunction due to scarring and fibrosis
Rationale: The fibrotic or fibroproliferative phase is the final stage of ARDS. If lung repair is incomplete, fibrosis and scarring replace healthy tissue. This results in permanent damage, reduced lung compliance, and long-term respiratory issues. It can lead to chronic ARDS or death.
Which finding best indicates that a patient has entered the injury or exudative phase of ARDS?
A. Hypoxemia unresponsive to increasing oxygen levels
B. Development of respiratory acidosis and bradycardia
C. Normal chest X-ray with mild respiratory distress
D. Productive cough with yellow sputum
A. Hypoxemia unresponsive to increasing oxygen levels
Rationale: Refractory hypoxemia is a hallmark of the exudative phase of ARDS. Despite increased oxygen delivery, gas exchange is severely impaired due to alveolar filling, surfactant dysfunction, and V/Q mismatch.
A patient with sepsis is developing ARDS. The nurse notes a rapid respiratory rate and decreased tidal volume. Which acid-base imbalance is expected at this early stage?
A. Metabolic acidosis
B. Respiratory alkalosis
C. Respiratory acidosis
D. Metabolic alkalosis
B. Respiratory alkalosis
Rationale: In the early phase of ARDS, stimulation of juxtacapillary (J) receptors triggers hyperventilation, causing CO₂ loss and leading to respiratory alkalosis.
What is the primary role of surfactant in the alveoli?
A. Promotes mucus clearance and humidifies air
B. Destroys bacteria that enter the lung
C. Reduces surface tension to prevent alveolar collapse
D. Enhances carbon dioxide transport across membranes
C. Reduces surface tension to prevent alveolar collapse
Rationale: Surfactant, produced by alveolar type II cells, maintains alveolar stability by reducing surface tension. In ARDS, surfactant is decreased or dysfunctional, leading to atelectasis.
A 56-year-old male admitted with pancreatitis is now hypoxic with bilateral infiltrates on CXR. Despite receiving 100% FiO₂, his PaO₂ remains low. What is the underlying mechanism of this hypoxemia?
A. Central hypoventilation
B. Recurrent pulmonary embolism
C. Pulmonary shunt and V/Q mismatch
D. Bronchoconstriction from asthma exacerbation
C. Pulmonary shunt and V/Q mismatch
Rationale: In the exudative phase, fluid-filled alveoli prevent gas exchange despite perfusion, causing shunting. V/Q mismatch further worsens oxygenation, leading to refractory hypoxemia.
Which structural lung damage contributes to decreased lung compliance in the injury phase of ARDS?
A. Damage to type II alveolar cells and loss of surfactant
B. Pleural effusion and rib fractures
C. Enlargement of alveoli and bronchodilation
D. Bronchial wall thickening and airway edema
A. Damage to type II alveolar cells and loss of surfactant
Rationale: Type II alveolar cells produce surfactant. When damaged, surfactant levels drop, leading to increased alveolar surface tension, collapse (atelectasis), and stiff lungs.
Which complication in the injury phase of ARDS contributes most to increased work of breathing (WOB)?
A. Elevated pH
B. Bronchodilation
C. Reduced lung compliance
D. Hyperkalemia
C. Reduced lung compliance
Rationale: The stiff, non-compliant lungs in ARDS make inhalation more difficult. The patient must generate higher airway pressures, increasing work of breathing significantly.
Which hemodynamic response occurs early in the exudative phase as a compensatory mechanism for hypoxemia?
A. Decreased cardiac output
B. Pulmonary hypertension
C. Increased cardiac output
D. Bradycardia
C. Increased cardiac output
Rationale: To compensate for tissue hypoxia, the body initially increases cardiac output to deliver more oxygenated blood, even though pulmonary oxygenation is impaired.
What causes diffusion impairment in ARDS during the injury phase?
A. Pulmonary emboli obstructing the capillaries
B. Formation of thick hyaline membranes
C. Increased alveolar surface area
D. Alveolar overdistension from hyperinflation
B. Formation of thick hyaline membranes
Rationale: Hyaline membranes form from necrotic debris, fibrin, and protein. These thicken the alveolar-capillary barrier, hindering gas diffusion and worsening hypoxemia.