Unit 2: Acute Respiratory Distress Syndrome (ARDS) Flashcards
Epidemiology: Acute Respiratory Distress Syndrome
- high mortality rate
- life-threatening
- death d/t multiple organ dysfunction bought on by hypoxia and/or infection
Most Common cause of ARDS
sepsis
Direct Causes of ARDS
damage or disruption of the respiratory system
- aspiration
- chest trauma
- pneumonia (infectious or aspiration)
- pulmonary contusion
- inhalation injury (smoke; toxins)
- pulmonary embolus
Indirect Causes of ARDS
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
How is ARDS Defined?
- acute onset of less than 7 days
- refractory hypoxemia
- bilateral infiltrates ruling out cardiac pulmonary edema as the cause
ARDS Severity
based on PaO2/FIO2 ratio
- Mild ARDS
- Moderate ARDS
- Severe ARDS
Mild ARDS
PaO2/FIO2 ratio: 200-300 on ventilator settings that include positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) >5 cm H2O
Moderate ARDS
PaO2/FIO2: 100-200 on ventilator settings that include positive end-expiratory pressure (PEEP) >5 cm H2O
Severe ARDS
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
ARDS Severity: PaO2/FIO2 ratio
ratio of the partial pressure of oxygen over the fraction of inspired oxygen
-divide fraction
How to determine PaO2/PIO2 ratio
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
How to determine PaO2/PIO2 ratio
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
Normal PaO2 Level
80 to 100 mmHg
-Average: 90 mmHg
Breathing room air (RA), What is the normal FIO2 level?
21% (0.21)
3 Phases of ARDS
- Exudative
- Proliferative
- Fibrotic
Exudative Phase
- 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
Surfactant
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
Clinical Manifestations Shown During the Exudative Phase
-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)
Proliferative Phase
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
Clinical Manifestations Shown in Proliferative Stage
- 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
Fibrotic Phase
- diffuse and fibrotic scarring, results in impaired gas exchange and compliance
- pulmonary hypertension worsens
- accompanying right sided heart failure worsens
Clinical Manifestations Shown in the Fibrotic Stage
- 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
Refractory Hypoxemia
in spite of increasing oxygen delivery to the patient, the hypoxemia does not improve and will eventually worsen
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. Increased permeability of the ACM
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
Diagnosis: Laboratory Testing
- ABGs
- Complete blood count (CBC) w/ differential
- Sputum
- Blood
- Urine cultures
- Coagulation Studies
- Electrolyte panels
- Liver Function Tests
Laboratory Tests: Arterial Blood Gases (ABGs)
initially show hypoxemia and hypocapnia as alveolar compromise develops
Laboratory Tests: CBC w/ differential
to determine if cause is infection
-abnormally high WBC (above 10,000)
Laboratory Tests: Sputum, Blood, Urine Cultures
to determine the source of any infection
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
Treatment for Acute Respiratory Distress Syndrome
- Mechanical Ventilation
- Positioning
- Medications
- Hydration
- Nutrition
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)
Treatment: Positioning
-prone position
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
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
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
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
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
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
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
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
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
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
Complications
- Barotrauma
- Renal Failure/ Multisystem organ-dysfunction syndrome
- Ventilator associated pneumonia (VAP)
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
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
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
Hallmark Signs of VAP
- fever
- leukocytosis (high WBC)
- increased respiratory effort
- purulent secretions
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
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
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)
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
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
Assessment: SpO2/Pulse Oximetry
may be low b/c of V/Q mismatch and intrapulmonary shunting
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
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
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
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
Assessment: Urine Output
decreased urine output = early sign of poor oxygen delivery to the tissues and shock
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
Assessment: Monitor ECG
hypoxemia can lead to cardiac dysrhythmias
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
Assessment: Serum Lactate Level
increased serum lactate confirms anaerobic metabolism
Assessment: Liver/Renal Function Tests
abnormal renal and liver values indicate the progression of ARDS to MODS
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
Skin Assessment
increased risk for skin breakdown d/t immobility and hypoxemia/hypoxia
Assessment: Chest x-ray
daily to monitor the progression or improvement of ARDS
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
-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
Nursing Teachings
disease process
