Unit 2: Acute Respiratory Distress Syndrome (ARDS) Flashcards
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
2
Q
Most Common cause of ARDS
A
sepsis
3
Q
Direct Causes of ARDS
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damage or disruption of the respiratory system
- aspiration
- chest trauma
- pneumonia (infectious or aspiration)
- pulmonary contusion
- inhalation injury (smoke; toxins)
- pulmonary embolus
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
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
6
Q
ARDS Severity
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based on PaO2/FIO2 ratio
- Mild ARDS
- Moderate ARDS
- Severe ARDS
7
Q
Mild ARDS
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PaO2/FIO2 ratio: 200-300 on ventilator settings that include positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) >5 cm H2O
8
Q
Moderate ARDS
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PaO2/FIO2: 100-200 on ventilator settings that include positive end-expiratory pressure (PEEP) >5 cm H2O
9
Q
Severe ARDS
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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
10
Q
ARDS Severity: PaO2/FIO2 ratio
A
ratio of the partial pressure of oxygen over the fraction of inspired oxygen
-divide fraction
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
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
12
Q
Normal PaO2 Level
A
80 to 100 mmHg
-Average: 90 mmHg
13
Q
Breathing room air (RA), What is the normal FIO2 level?
A
21% (0.21)
14
Q
3 Phases of ARDS
A
- Exudative
- Proliferative
- Fibrotic
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
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
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)
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
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
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
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
22
Q
Refractory Hypoxemia
A
in spite of increasing oxygen delivery to the patient, the hypoxemia does not improve and will eventually worsen
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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Diagnosis: Imaging Studies
>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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Diagnosis: Laboratory Testing
- ABGs
- Complete blood count (CBC) w/ differential
- Sputum
- Blood
- Urine cultures
- Coagulation Studies
- Electrolyte panels
- Liver Function Tests
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Laboratory Tests: Arterial Blood Gases (ABGs)
initially show hypoxemia and hypocapnia as alveolar compromise develops
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Laboratory Tests: CBC w/ differential
to determine if cause is infection
| -abnormally high WBC (above 10,000)
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Laboratory Tests: Sputum, Blood, Urine Cultures
to determine the source of any infection
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Laboratory Tests: Comprehensive metabolic panels (CMP), Coagulation Studies, and Liver and Renal Function Tests
- used to determine cause of ARDS
| - used to determine if hypoxia from the disease process is affecting other body systems
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Treatment for Acute Respiratory Distress Syndrome
- Mechanical Ventilation
- Positioning
- Medications
- Hydration
- Nutrition
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Mechanical Ventilation
- 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)
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Treatment: Positioning
-prone position
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Prone Positioning
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
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Benefits for the use of Prone Positioning
- 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
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When to Implement Prone Positioning
- 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
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Contraindications for Prone Positioning
- 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
Nursing Considerations When using Prone Positioning
- 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
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Treatment: Medications
- 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
Why use Neuromuscular Agents or Paralytics?
- 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
Treatment: Hydration
- 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
Treatment: Nutrition
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
Enteral Nutrition
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
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Complications
- Barotrauma
- Renal Failure/ Multisystem organ-dysfunction syndrome
- Ventilator associated pneumonia (VAP)
44
Complications: Barotrauma
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
Complications: Renal failure/Multisystem Organ-Dysfunction Syndrome
- 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
Complications: Ventilator Associated Pneumonia (VAP)
- 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
Hallmark Signs of VAP
- fever
- leukocytosis (high WBC)
- increased respiratory effort
- purulent secretions
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Preventions for Ventilator-Associated Pneumonia (VAP)
- 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
Nursing Management: Assessment and Analysis
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
Nursing Diagnoses
- 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)
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Nursing Assessments: What will you assess as the nurse?
- 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
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Assessment: Vital Signs
- HR increases b/c of hypoxemia
- Respiratory rate increases in attempt to increase oxygenation
- BP decreases b/c of right sided heart failure
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Assessment: SpO2/Pulse Oximetry
may be low b/c of V/Q mismatch and intrapulmonary shunting
54
Assessment: Central Venous Pressure (CVP) or Pulmonary Artery (PA) pressure monitoring
variable
- decreased b/c of decreased venous return r/t increased intrathoracic pressure
- increased d/t increased vasoconstriction in the lungs
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Assessment: Central Venous Pressure (CVP) or Pulmonary Artery (PA) pressure monitoring
variable
- decreased b/c of decreased venous return r/t increased intrathoracic pressure
- increased d/t increased vasoconstriction in the lungs
55
Neurological Assessment
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
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Respiratory Assessment
- 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
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Assessment: Urine Output
decreased urine output = early sign of poor oxygen delivery to the tissues and shock
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Assessment: Mechanical Ventilation
- 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
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Assessment: Monitor ECG
hypoxemia can lead to cardiac dysrhythmias
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Assessment: ABG monitoring
- 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
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Assessment: Serum Lactate Level
increased serum lactate confirms anaerobic metabolism
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Assessment: Liver/Renal Function Tests
abnormal renal and liver values indicate the progression of ARDS to MODS
63
Assessment: Blood/Sputum Cultures/CBC
- 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
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Skin Assessment
increased risk for skin breakdown d/t immobility and hypoxemia/hypoxia
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Assessment: Chest x-ray
daily to monitor the progression or improvement of ARDS
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Nursing Actions: What actions should you take as the nurse for ARDS
-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
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-Positioning/Activity:
>prone positing (proning)
>elevate HOB
>frequent position changes
>ROM exercises
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-Infection protection/prevention
>hand washing
>monitoring and care of central IV lines
>Foley catheter care
>diligent mouth care
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Nursing Teachings
disease process
