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nursing 272: final semester > Unit 2: Acute Respiratory Distress Syndrome (ARDS) > Flashcards

Unit 2: Acute Respiratory Distress Syndrome (ARDS) Flashcards

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1
Q

Epidemiology: Acute Respiratory Distress Syndrome

A
  • high mortality rate
  • life-threatening
  • death d/t multiple organ dysfunction bought on by hypoxia and/or infection
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2
Q

Most Common cause of ARDS

A

sepsis

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3
Q

Direct Causes of ARDS

A

damage or disruption of the respiratory system

  • aspiration
  • chest trauma
  • pneumonia (infectious or aspiration)
  • pulmonary contusion
  • inhalation injury (smoke; toxins)
  • pulmonary embolus
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4
Q

Indirect Causes of ARDS

A

processes or disorders that occur outside the respiratory system but have deleterious effect on the lungs

  • sepsis, shock
  • pancreatitis
  • multiple blood-transfusions; transfusion-related acute lung injury (TRALI)
  • cardiopulmonary bypass
  • drug/alcohol overdose
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5
Q

How is ARDS Defined?

A
  • acute onset of less than 7 days
  • refractory hypoxemia
  • bilateral infiltrates ruling out cardiac pulmonary edema as the cause
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6
Q

ARDS Severity

A

based on PaO2/FIO2 ratio

  • Mild ARDS
  • Moderate ARDS
  • Severe ARDS
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7
Q

Mild ARDS

A

PaO2/FIO2 ratio: 200-300 on ventilator settings that include positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) >5 cm H2O

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8
Q

Moderate ARDS

A

PaO2/FIO2: 100-200 on ventilator settings that include positive end-expiratory pressure (PEEP) >5 cm H2O

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9
Q

Severe ARDS

A

PaO2/PIO2: less than 100 on ventilator settings that include PEEP >5 cm H20
-if patient has a PaO2 of 70 mmHg while receiving 70% (0.7) FIO2, the ratio (PaO2/FIO2) is 100, which is diagnostic for severe ARDS

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10
Q

ARDS Severity: PaO2/FIO2 ratio

A

ratio of the partial pressure of oxygen over the fraction of inspired oxygen
-divide fraction

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11
Q

How to determine PaO2/PIO2 ratio

A

divide PaO2 by FIO2
-Normal Average PaO2: 90 mm Hg
(normal is 80 to 100)
-Breathing room air, FIO2 is 21% (or 0.21)
>Equation: 90/.21 or a PaO2/FIO2 ratio of approximately 428

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11
Q

How to determine PaO2/PIO2 ratio

A

divide PaO2 by FIO2
-Normal Average PaO2: 90 mm Hg
(normal is 80 to 100)
-Breathing room air, FIO2 is 21% (or 0.21)
>Equation: 90/.21 or a PaO2/FIO2 ratio of approximately 428

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12
Q

Normal PaO2 Level

A

80 to 100 mmHg

-Average: 90 mmHg

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13
Q

Breathing room air (RA), What is the normal FIO2 level?

A

21% (0.21)

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14
Q

3 Phases of ARDS

A
  • Exudative
  • Proliferative
  • Fibrotic
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15
Q

Exudative Phase

A
  • occurs within 24 to 48 hours after injury
  • there is a disruption of the alveolar-capillary membrane (ACM) as a result of the activation and release of inflammatory mediators
  • ACM becomes dilated d/t inflammatory mediators; allows fluid to move from capillaries into interstitial space and alveoli
  • Disruption of ACM allows protein to move from the vascular space; loss of protein from vascular space lessens the oncotic forces, worsening the movement of fluid into the alveoli
  • The alveolar and interstitial edema results in a severe V/Q mismatch (ventilation/perfusion; inadequate ventilation occurring in the face of adequate perfusion or blood flow) which results in hypoxemia; blood is shunted past the fluid-filled alveoli w/o being oxygenated
  • there is damage to the alveolar cells that produce surfactant; at risk for atelectasis
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16
Q

Surfactant

A

responsible for maintaining alveolar surface tension
-alveolar surface tension keeps the alveoli from fully collapsing at the end of expiration
-if alveolar surface tension is lost, then the alveoli collapse; atelectasis
>there is damage to cells that produce surfactant in the exudative phase of ARDS

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17
Q

Clinical Manifestations Shown During the Exudative Phase

A

-Hyperventilation and Tachycardia as a compensatory response to hypoxemia
-ABGs reveal Respiratory Alkalosis d.t hyperventilation
-Cardiac Output increases; attempt to increase blood flow through the lungs
-Chest x-ray reveals the increased alveolar fluid as bilateral infiltrates (pulmonary edema)
>there would be no evidence of increased left atrial or ventricular pressure, which indicates left heart failure (noncardiogenic pulmonary edema)

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18
Q

Proliferative Phase

A

neutrophils and other inflammatory mediators cross the damaged alveolar-capillary membrane (ACM) and release toxic mediators that further damage both the alveolar and capillary endothelium

  • diffusion defects
  • V/Q mismatch worsens
  • pulmonary hypertension b/c of locally occurring vasoconstriction in the lung caused by hypoxemia; right sided heart failure d/t increase in PVR or high vascular pressures in the lung
  • widespread fibrotic changes; lungs become stiff and non-compliant; increases work of breathing
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19
Q

Clinical Manifestations Shown in Proliferative Stage

A
  • Hypercarbia (High CO2) and worsening hypoxemia
  • PaCO2 begins to rise despite hyperventilation
  • Refractory hypoxemia (in spite of increasing oxygen delivery (DO2) to the patient, the hypoxemia does not improve and will eventually worsen)
  • Lung compliance continues to deteriorate; increasing work of breathing
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20
Q

Fibrotic Phase

A
  • diffuse and fibrotic scarring, results in impaired gas exchange and compliance
  • pulmonary hypertension worsens
  • accompanying right sided heart failure worsens
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21
Q

Clinical Manifestations Shown in the Fibrotic Stage

A
  • decreased left-heart preload d/t the right heart failure and reduced capacity of the right ventricle to deliver blood to the lungs and on the left side of the heart
  • decreased BP
  • decreased CO
  • severe V/Q mismatch, diffusion defects, and intrapulmonary shunting result in refractory hypoxemia
  • severe tissue hypoxia and lactic acidosis
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22
Q

Refractory Hypoxemia

A

in spite of increasing oxygen delivery to the patient, the hypoxemia does not improve and will eventually worsen

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23
Q

Connection Check: The pulmonary edema associated with ARDS is caused by?
A. increased permeability of the ACM
B. right ventricular failure w/ pulmonary hypertension
C. left ventricular failure d/t poor oxygenation
D. fluid overload r/t resuscitation in the first phase

A

A. Increased permeability of the ACM

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24
Q

Diagnosis: Imaging Studies

A

> Chest x-ray

  • to identify bilateral infiltrates in the early stages that are the hallmark sign of ARDS
  • “ground-glass appearance”
  • “snow screen effect” or whiteout effect on chest x-ray
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25
Q

Diagnosis: Laboratory Testing

A
  • ABGs
  • Complete blood count (CBC) w/ differential
  • Sputum
  • Blood
  • Urine cultures
  • Coagulation Studies
  • Electrolyte panels
  • Liver Function Tests
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26
Q

Laboratory Tests: Arterial Blood Gases (ABGs)

A

initially show hypoxemia and hypocapnia as alveolar compromise develops

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27
Q

Laboratory Tests: CBC w/ differential

A

to determine if cause is infection

-abnormally high WBC (above 10,000)

28
Q

Laboratory Tests: Sputum, Blood, Urine Cultures

A

to determine the source of any infection

29
Q

Laboratory Tests: Comprehensive metabolic panels (CMP), Coagulation Studies, and Liver and Renal Function Tests

A
  • used to determine cause of ARDS

- used to determine if hypoxia from the disease process is affecting other body systems

30
Q

Treatment for Acute Respiratory Distress Syndrome

A
  • Mechanical Ventilation
  • Positioning
  • Medications
  • Hydration
  • Nutrition
31
Q

Mechanical Ventilation

A
  • primary treatment for the refractory hypoxemia
  • initiated as lung compliance decreases, work of breathing increases, and oxygenation continues to be refractory regardless of interventions

> Uses several modes of ventilation:

  • Most common: conventional ventilation using reduced tidal volumes and PEEP
  • High-frequency oscillating ventilation and airway pressure-release ventilation (APRV)
  • Partial liquid ventilation
  • High-flow nasal cannula (HFNCs)
  • Extracorporeal membrane oxygenation (ECMO)
32
Q

Treatment: Positioning

A

-prone position

33
Q

Prone Positioning

A

proning while on mechanical ventilation may improve oxygenation through increased recruitment of collapsed posterior alveolar units and reduction in the V/Q mismatch
-via gravity; blood flow is directed on the better-aerated anterior portion of the lungs

34
Q

Benefits for the use of Prone Positioning

A
  • dorsal lung re-expansion w/ improved oxygenation
  • aiding in secretion and extravascular water distribution, which decreases stress on the soft tissues of the lung
  • improved lung recruitment; opens more alveoli, improving oxygenation
  • reducing the need for higher PEEP an FIO2, decreasing ventilator-induced lung injury (VILI)
  • overall effects reduce mortality
35
Q

When to Implement Prone Positioning

A
  • Within 72 hours of diagnosis
  • Up to 20 hours per day in prone position is recommended
  • Accomplished by manually turning the patient in bed or by using a mechanical device that can turn the patient as needed and place the patient in the Trendelenburg or reverse Trendelenburg as needed
36
Q

Contraindications for Prone Positioning

A
  • spine instability
  • conditions that increase intracranial pressure
  • pregnancy- possible concerns
  • abdominal wounds- possible concerns
  • unstable peripheral fractures or rib fractures
  • need for frequent airway access
37
Q

Nursing Considerations When using Prone Positioning

A
  • any change in baseline oxygenation parameters after proning should be case for a new ABG determiniation
  • eye and facial skin care; eye lubricant and padding areas of the face
  • sedation d/t patient anxiety during process
  • enteral feedings stopped at least 1 hour before proning; parenteral feeding considered
  • tubes free of compromise during proning procedure and evaluated frequently during process
  • have a plan in place for a rapid return to the supine position in case of hemodynamic compromise or cardiac arrest
  • educate family on process; pros and cons; answer all questions r/t treatment modality
38
Q

Treatment: Medications

A
  • Antibiotics if caused of ARDS is infection; broad-spectrum initially, then narrow spectrum after pathogen identified
  • Corticosteroids to decrease inflammatory response; controversial
  • Neuromuscular Blocking agents or paralytics when mechanically ventilated
39
Q

Why use Neuromuscular Agents or Paralytics?

A
  • sometimes used for mechanically ventilated patients
  • neuromuscular agents reduce risk of barotrauma b/c of controlled patient-ventilator synchrony; patient cannot take a breath out of sync w/ the ventilator
  • reduce oxygen demand by limiting muscle movement
  • if neuromuscular agents are used, patient must receive pain and sedative medication to ensure optimum comfort during treatment
40
Q

Treatment: Hydration

A
  • necessary to maintain circulatory volume
  • helps avoid issues with thick, dry secretions that may be difficult to clear and potentially cause plugged airways
  • if too much fluid is given, ARDS can worsen b/c of increased permeability of the ACM
  • If an insufficient amount is administered, preload and blood pressure may decrease; results in decreased perfusion to the brain and vital organs
  • urine output and hemodynamic volume status should be carefully monitored via central venous or PA catheter
41
Q

Treatment: Nutrition

A

ARDS is associated with proinflammatory, hypermetabolic state

  • without adequate nutrition, malnutrition, loss of body mass, and reduced respiratory muscle strength can result
  • Enteral (nasogastric tube feedings through GI tract), or Parenteral (IV nutrition via a peripheral or central venous catheter) initiated within 48 to 72 hours of the initiation of mechanical ventilation
42
Q

Enteral Nutrition

A

preferred method unless contraindicated b/c of GI issues

  • ex: nasogastric tube feeding through GI tract
  • risks: aspiration
  • nursing: feeding tube properly placed, HOB elevated, tube feeding turned off during times when patient is supine
43
Q

Complications

A
  • Barotrauma
  • Renal Failure/ Multisystem organ-dysfunction syndrome
  • Ventilator associated pneumonia (VAP)
44
Q

Complications: Barotrauma

A

ARDS results in stiffening of the lungs and loss of compliance (elasticity) requiring careful application of tidal volume and PEEP to maximize oxygenation w/o causing barotrauma
-patient is at risk for alveolar or lung rupture; resulting in pneumomediastinum (air in mediastinal space), or pneumothorax (air in pleural space), causing further hypoxemia

45
Q

Complications: Renal failure/Multisystem Organ-Dysfunction Syndrome

A
  • renal failure d/t hypotension and use of nephrotoxic medications to treat infection
  • renal failure may indicate the progression of ARDS to multisystem organ-dysfunction syndrome (MODS)
  • MODS results from prolonged refractory hypoxemia, hemodynamic instability, and the inflammation associated w/ sepsis
46
Q

Complications: Ventilator Associated Pneumonia (VAP)

A
  • any patient on mechanical ventilation is at risk
  • when an artificial airway is in place, normal mechanisms to protect patient from pneumonia is compromised
  • development of fever, leukocytosis (high WBC), increased respiratory effort, and purulent secretions
  • sputum cultures will indicated infection
47
Q

Hallmark Signs of VAP

A
  • fever
  • leukocytosis (high WBC)
  • increased respiratory effort
  • purulent secretions
48
Q

Preventions for Ventilator-Associated Pneumonia (VAP)

A
  • Mouth care q 2 hours
  • Brush teeth q 12 hours w/ chlorhexidine
  • HOB elevated at 30 degrees at all times to prevent gastric aspiration
  • Suctioning routinely and PRN
  • Conventional endotracheal tubes (ETTs) should be replaced w/ ETTs with subglottic secretion drainage; these have an extra port above the inflated cuff that is connected to low continuous suctioning; prevents secretions that sit above the cuff from becoming infected with bacteria and then oozing down around the cuff into the airway, infecting the airway
  • ventilator circuit changed per hospital protocol; avoid water build up in circuit
  • sterile water should be used for the humidification of the air being delivered to the patient
49
Q

Nursing Management: Assessment and Analysis

A

clinical manifestations d/t refractory hypoxemia, pulmonary edema, and lung parenchymal changes

  • first indication: increased work of breathing; dyspnea, tachypnea, accessory muscle use
  • crackles upon auscultation associated w/ pulmonary edema
  • later, breath sounds diminished or absent b/c of fibrotic lung changes and atelectasis
  • anxiety and agitation from hypoxemia
  • SpO2 continually decreases despite increasing FIO2 levels
  • Initially ABGs reveal respiratory alkalosis d/t hyperventilation
  • later respiratory acidosis develops
50
Q

Nursing Diagnoses

A
  • Impaired gas exchange r/t disrupted pulmonary function e/b increased work of breathing, refractory hypoxemia, and increased oxygen demand
  • Anxiety r/t hypoxemia, lack of cerebral perfusion, and loss of personal control
  • Imbalanced nutrition, less than body requirements r/t increased metabolic demand (body in a hypermetabolic state)
51
Q

Nursing Assessments: What will you assess as the nurse?

A
  • Hemodynamic monitoring: vital signs, SpO2/pulse oximetry, central venous pressure (CVP) or pulmonary artery (PA) pressure monitoring
  • Neurological Assessment: LOC and pupillary assessment must be done q 1 to 2 hours
  • Respiratory Assessment
  • Urine Output
  • Mechanical Ventilation
  • ECG
  • Laboratory tests: ABGs, Serum Lactate, Liver/Renal function tests, Blood and Sputum cultures
  • Skin assessment
  • Chest x-ray
52
Q

Assessment: Vital Signs

A
  • HR increases b/c of hypoxemia
  • Respiratory rate increases in attempt to increase oxygenation
  • BP decreases b/c of right sided heart failure
53
Q

Assessment: SpO2/Pulse Oximetry

A

may be low b/c of V/Q mismatch and intrapulmonary shunting

54
Q

Assessment: Central Venous Pressure (CVP) or Pulmonary Artery (PA) pressure monitoring

A

variable

  • decreased b/c of decreased venous return r/t increased intrathoracic pressure
  • increased d/t increased vasoconstriction in the lungs
54
Q

Assessment: Central Venous Pressure (CVP) or Pulmonary Artery (PA) pressure monitoring

A

variable

  • decreased b/c of decreased venous return r/t increased intrathoracic pressure
  • increased d/t increased vasoconstriction in the lungs
55
Q

Neurological Assessment

A

LOC and Pupillary assessment done q 1 to 2 hours

  • at risk for neurological compromise d/t refractory hypoxemia and potential increase in PaCO2, that can result in cerebral vasodilation
  • frequently checked if heavily sedated and chemically paralyzed or has a decreased ability to communicate d/t intubation ad mechanical ventilation
56
Q

Respiratory Assessment

A
  • crackles auscultated b/c of fluid buildup in the alveoli d/t increased capillary permeability
  • later may be diminished b/c of atelectasis and fibrotic changes in the lungs
57
Q

Assessment: Urine Output

A

decreased urine output = early sign of poor oxygen delivery to the tissues and shock

58
Q

Assessment: Mechanical Ventilation

A
  • frequent monitoring of airway pressure on ventilator
  • increases in airway pressure may = presence of secretions or worsening lung compliance
  • decreases in airway pressure may = a leak in system
59
Q

Assessment: Monitor ECG

A

hypoxemia can lead to cardiac dysrhythmias

60
Q

Assessment: ABG monitoring

A
  • Initially, hypoxemia and respiratory alkalosis secondary to poor gas exchange and hyperventilation
  • Later, respiratory acidosis b/c of increased PaCO2 and the permissive hypercapnia of low-tidal-volume ventilation
  • Later, metabolic acidosis b/c of worsening hypoxemia and decreased oxygen delivery to the tissues; transition to anaerobic metabolism
61
Q

Assessment: Serum Lactate Level

A

increased serum lactate confirms anaerobic metabolism

62
Q

Assessment: Liver/Renal Function Tests

A

abnormal renal and liver values indicate the progression of ARDS to MODS

63
Q

Assessment: Blood/Sputum Cultures/CBC

A
  • positive cultures may indicate cause of ARDS
  • later, positive cultures b/c of complications associated with critical illness, such as indwelling lines and catheters or VAP
  • a CBC showing increased BC count = infection
64
Q

Skin Assessment

A

increased risk for skin breakdown d/t immobility and hypoxemia/hypoxia

65
Q

Assessment: Chest x-ray

A

daily to monitor the progression or improvement of ARDS

66
Q

Nursing Actions: What actions should you take as the nurse for ARDS

A

-Airway suctioning when indicated by the presence of secretions to ensure the ETT is clear

-Medication administration:
>Paralytic agents, analgesics, sedative meds: comfort
>Inotropic/vasoactive agents: inotropic to augment CO; vasoactive meds to support BP
>Antibiotics

-Positioning/Activity:
>prone positing (proning)
>elevate HOB
>frequent position changes
>ROM exercises
-Infection protection/prevention
>hand washing
>monitoring and care of central IV lines
>Foley catheter care 
>diligent mouth care
67
Q

Nursing Teachings

A

disease process

nursing 272: final semester (79 decks)

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