Exam #2: Respiratory Failure And ARDS Flashcards
Acute Respiratory Failure results from
- Insufficiency O2 transferred to blood: Hypoxia
2. Inadequate CO2 removal: Hypercapnia
Classification of Respiratory Failure:
- Hypoxemic aka Oxygenation Failure (Pao2 <60 mm Hg on inspired O2 concentration >60%)
- Hypercapnic aka Ventilatory Failure (PaCO2 above normal (>48 mm Hg) and Acidemia (pH <7.35))
Hypoxemic Respiratory Failure can be caused by
- Mismatch between ventilation (V) and perfusion (Q) - (V/Q mismatch) should be 1:1 (1 mL of air for each 1 mL of blood flow to lungs)
- Shunt
- Diffusion limitation
- Alveolar hypoventilation
Hypoxemic Respiratory Failure: V/Q mismatch can be caused by
- COPD
- Pneumonia
- Asthma
- Atelectasis
- Result of pain
- Pulmonary embolus
Range of V/Q Relationships
Look at slide 7!
Hypoxemic Respiratory Failure: Shunt
- Anatomic shunt
- Intrapulmonary shunt
*Read notes
Hypoxemic Respiratory Failure: Fluid in the alveoli
ARDS, pneumonia
*Read notes
Causes of Hypoxemic Respiratory Failure: Diffuse limitations include
- R/t alveoli being scarred:
- Severe COPD
- Recurrent pulmonary emboli
- Pulmonary fibrosis
- ARDS
- Interstitial lung disease - Hypoxemia present during exercise
*Read notes
Diffuse limitation occurs when
gas exchange across the alveolar-capillary membrane is compromised by a process that thickens, damages, or destroys the alveolar membrane or affects blood flow through the pulmonary capillaries (Fig. 67-5).
Causes of Hypoxemic Respiratory Failure: Alveolar Hypoventalation
- Restrictive lung disease
- CNS disease (stroke, brain infarct)
- Chest wall dysfunction
- Neuromuscular disease
Hypoxemic Respiratory Failure: Interrelationship of mechanisms
Combination of two or more physiologic mechanisms:
- V/Q mismatch
- Shunt
- Diffusion limitation
- Alveolar hypoventilation
*Read notes!!
Hypercapnia Respiratory Failure
- CO2 levels cannot be maintained within normal limits due to:
- An increase in CO2 production or
- A decrease in alveolar ventilation
- Acute or chronic
*Read notes
What can cause hypercapnic respiratory failure?
- Airway and alveoli abnormalities
- Central nervous system abnormalities
- Chest wall abnormalities
- Neuromuscular conditions
Causes of Hypercapnic Respiratory Failure: Airways and alveoli abnormalities
- Asthma
- COPD
- Cystic fibrosis
Causes of Hypercapnic Respiratory Failure: Central Nervous System Abnormalities
- Drug overdose
- Brainstem infarction
- Spinal cord injuries
*Read notes
Causes of Hypercapnic Respiratory Failure: Chest wall abnormalities
- Flail chest (fractures prevent the rib cage from expanding normally because of pain, mechanical restriction and muscle spasm)
- Kyphoscoliosis (compresses the lungs and prevents normal expansion of the chest wall)
- Severe obesity
Causes of Hypercapnic Respiratory Failure: Neuromuscular conditions
- Muscular dystrophy
- Guillain-Barré syndrome
- Multiple sclerosis
- Exposure to toxins
- Muscle wasting
*Read notes
Respiratory Failure: The major threat is inability of the lungs to meet the O2 needs of tissues:
- Inadequate O2 delivery to tissues or
- Tissues cannot use O2 delivered to them:
- Septic shock
- Acid-base alterations
*Read notes
Respiratory Failure Characteristics of Clinical Manifestations
- Sudden or gradual onset
- A sudden decrease in PaO2 or rapid rise in PaCO2 implies a serious condition
- When compensatory mechanisms fail, respiratory failure occurs
- Signs may be specific or nonspecific
- Mental status changes often occur early
*Read notes!!
Respiratory Failure: Early Signs
- Tachycardia
- Tachypnea
- Mild HTN
*read notes
Respiratory Failure: Late sign
Cyanosis
*read notes
Consequences of Hypoxemia and hypoxia
- Cells shift from aerobic to anaerobic metabolism (Metabolic acidosis and cell death)
- Decreased cardiac output
- Impaired renal function
- GI tissue ischemia
*Read notes
Specific Clinical Manifestations of Respiratory Failure
- Rapid, shallow breathing pattern
- Tripod position
- Pursed-lip breathing
- Dyspnea
- Retractions
- Paradoxic breathing
- Diaphoresis
*Read notes!
Clinical Manifestations of Respiratory Failure:: Abnormal breath sounds
- Crackles
- Loud crackles
- Absent or diminished
- Bronchial
- Pleural friction rub
*read notes
Respiratory Failure: Diagnostic Studies
- Physical assessment
- Chest x-ray
- ABG analysis**
- Pulse oximetry
- CBC (look at hgb and hct), serum electrolytes, urinalysis (baseline)
- ECG
- Sputum/blood cultures (pneumonia?)
- CT scan (tells you what’s in those lungs, structural problems, etc)
- V/Q lung scan
- End-tidal CO2 (ETCO2) (how much CO2 you’re retaining)
- Pulmonary artery catheter (severe cases): CVP, PA pressures, CO, SV, Scvo2/Svo2
*read notes on slides 25 and 26
Acute Respiratory Failure Nursing Assessment: Health information includes
- Health history
- Medications
- Surgery
Acute Respiratory Failure Nursing Assessment: Functional health patterns
- Health perception–health management
- Nutritional-metabolic
- Activity-exercise
- Sleep-rest
- Cognitive-perceptual
- Coping–stress tolerance
Acute Respiratory Failure Nursing Assessment: Physical assessment includes
- General
- Integumentary (dusky colored)
- Respiratory
- Cardiovascular (increased HR, Dysrhythmias)
- Gastrointestinal (delayed emptying)
- Neurologic
+ lab findings (ABGs!! pH, PO2, PCO2)
Acute Respiratory Failure: Nursing Diagnosis
- Impaired gas exchange related to alveolar hypoventilation, intrapulmonary shunting, V/Q mismatch, and diffusion impairment
- Ineffective airway clearance related to excessive secretions, decreased level of consciousness, presence of an artificial airway, neuromuscular dysfunction, and pain
- Ineffective breathing pattern related to neuromuscular impairment of respirations, pain, anxiety, decreased level of consciousness, respiratory muscle fatigue, and bronchospasm
Acute Respiratory Failure Planning: Overall goals
- Independent maintenance of airway
- Effective cough and ability to clear secretions
- Normal ABG values or values within patient’s baseline
- Absence of dyspnea or recovery to baseline breathing patterns for patient
- Breath sounds within patient’s baseline
Acute Respiratory Failure: Prevention
- Thorough history and physical assessment to identify at-risk patients
- Early recognition of respiratory distress
Acute Respiratory Failure: Respiratory Therapy includes
- Oxygen therapy
- Mobilization of secretions
Acute Respiratory Failure Treatment: Oxygen Therapy
Delivery system should:
- Be tolerated by the patient
- Maintain PaO2 at 55 to 60 mm Hg or more and SaO2 at 90% or more at the lowest O2 concentration possible ***
*Read notes
Acute Respiratory Failure Treatment: Mobilization of secretions can be done through
- Effective coughing
- Adequate hydration and humidification
- Chest physiotherapy
- Airway suctioning
- Patient positioning
- Ambulation
Tripod position
Increases chest and lung expansion
How is an augmented cough done?
- Perform augmented coughing by placing one or both hands on the anterolateral base of the lungs (Fig. 67-7).
- As the patient ends a deep inspiration and begins the expiration, move your hands forcefully upward, increasing abdominal pressure and facilitating the cough.
Huff cough
- Serious of coughs performed while saying “huff”
- Effective in clearing central airways
Staged cough
- Sit leaning forward
- Take three deep breaths through mouth and cough
Acute Respiratory Failure Treatment: Hydration and Humidification includes what methods
- Adequate fluid intake (2-3L/day)
- IV hydration
- Humidification devices
- O2 via aerosol mask
- Mucolytic drugs (i.e mucomyst to thin secretions)
Acute Respiratory Failure Treatment: Chest Physiotherapy
- Postural drainage
- Percussion
- Vibration
What does FiO2 measure?
Measured from ventilator.
What does it measure though?
Acute Respiratory Failure Treatment: Airway Suctioning
- Nasopharyngeal
- Oropharyngeal
- Nasotracheal
Respiratory Therapy includes
- Positive pressure ventilation (PPV)
- Noninvasive PPV
- BiPAP
- CPAP
*Read notes
Bilevel positive airway pressure(BiPAP)
is a form of NIPPV in which different positive pressure levels are set for inspiration and expiration (Fig. 67-8).
Continuous positive airway pressure (CPAP)
Continuous positive airway pressure (CPAP) is another form of NIPPV in which a constant positive pressure is delivered to the airway during inspiration and expiration.
Non-invasive PPV is not appropriate for what patients?
Not appropriate for patients who have excessive secretions, decreased level of consciousness, high O2 requirements, facial trauma, or hemodynamic instability.
Acute Respiratory Failure Drug Therapy
- Relief of bronchospasm = Bronchodilators
- Reduction of airway inflammation = Corticosteroids
- Reduction of pulmonary congestion = Diuretics, nitrates if heart failure present
- Treatment of pulmonary infections = IV antibiotics
- Reduction of severe anxiety, pain, and agitation = Benzodiazepines and Opioids
Acute Respiratory Failure: Medical Supportive Therapy includes
- Treat the underlying cause
- Maintain adequate cardiac output and hemoglobin concentration
*Read notes
Acute Respiratory Failure: Nutritional Therapy
- Maintain protein and energy stores
- Enteral or parenteral nutrition
- Nutritional supplements
*Read notes!
Acute Respiratory Failure: Expected Outcomes
- Maintain a patent airway with effective removal of secretions
- Achieve normal or baseline respiratory rate and rhythm, and breath sounds
- Maintain adequate oxygenation as indicated by normal or baseline ABGs
- Experience normal hemodynamic status
Acute Respiratory Distress Syndrome
- Sudden progressive form of acute respiratory failure
- Alveolar capillary membrane becomes damaged and more permeable to intravascular fluid -> Alveoli fill with fluid
Stages of Edema Formation in ARDS
Slide48
ARDS results in
- Severe dyspnea
- Hypoxia
- Decreased lung compliance
- Diffuse pulmonary infiltrates
ARDS Etiology and Pathophysiology: Lung Injury
- Develops from a variety of direct or indirect lung injuries
- Most common cause is sepsis
- Exact cause for damage to alveolar-capillary membrane not known
- Pathophysiologic changes of ARDS thought to be due to stimulation of inflammatory and immune systems
Slide 51 has diagram and Read through slides
ARDs Etiology and Pathophysiology: Immune response
- Neutrophils are attracted and release mediators, producing changes in lungs including:
- ↑ Pulmonary capillary membrane permeability
- Destruction of elastin and collagen
- Formation of pulmonary microemboli
- Pulmonary artery vasoconstriction
The physiologic changes in ARDS are divided into three phases
- Injury or educative phase
- Reparative or proliferative phase
- Fibrotic phase
ARDs Etiology and Pathophysiology: What happens during the Injury or Exudative Phase?
- 1–7 days after initial lung injury or host insult
- Neutrophils adhere to pulmonary microcirculation leading to:
- Damage to vascular endothelium
- ↑ Capillary permeability
ARDS Etiology and Pathophysiology: What is the result of injury or exudative phase?
- Engorgement of peribronchial and perivascular interstitial space
- Fluid crosses into alveolar space
- Intrapulmonary shunt develops as alveoli fill with fluid, and blood passing through cannot be oxygenated
- Alveolar cells type 1 and 2 are damaged
- Hyaline membranes line alveoli
- Interstitial and alveolar edema and atelectasis
- Severe V/Q mismatch and shunting of pulmonary capillary blood result in refractory hypoxemia (unresponsive to increasing O2 concentrations)
- Lungs become less compliant (higher airway pressures must be generated)
Injury/Exudative Phase: Alveolar cells type 1 and 2 are damaged
Surfactant dysfunction -> atelectasis
Injury/Exudative Phase: Hyaline membranes line alveoli
- Contribute to fibrosis and atelectasis
- Leads to decreased gas exchange capability and lung compliance
Injury/Exudative Phase can lead to what findings?
- ↑ Work of breathing (WOB)
- ↑ Respiratory rate
- ↓ Tidal volume:
- Produces respiratory alkalosis from increase in CO2 removal
- ↓ CO2 and tissue perfusion
*Read notes
Reparative Proliferative Phase: What happens during this phase?
- 1–2 weeks after initial lung injury
- Influx of neutrophils, monocytes, and lymphocytes
- Fibroblast proliferation
- Lung becomes dense and fibrous
- Lung compliance continues to ↓
- Worsening hypoxemia
Reparative or Proliferative Phase: Worsening hypoxemia
Thickened alveolar membrane -> diffuse limitation and shunting
What happens if the reparative phase persists?
Widespread fibrosis results
If reparative phase is stopped,
Lesions will resolve
Fibrotic or Chronic/Late Phase
- 2–3 weeks after initial lung injury
- Lung is completely remodeled by collagenous and fibrous tissues
What findings can be seen in a patient in the fibrotic or chronic/late phase of ARDs?
- ↓ Lung compliance
- ↓ Area for gas exchange: Hypoxemia continues
- Pulmonary hypertension: Results from pulmonary vascular destruction and fibrosis
Progression of ARDS: People who survive the acute phase of lung injury
- Pulmonary edema resolves
- Makes a complete recovery
Survival changes for those who enter the fibrotic phase
- Poor
- Requires long-term mechanical ventilation
ARDS: Early Clinical Manifestations include
- Dyspnea, tachypnea, cough, restlessness
- Chest auscultation may be normal or may reveal fine, scattered crackles
- Edema (may not show until 30% increase in fluid content in lungs)
ARDS: Early Clinical Lab Findings
- ABGs: Mild hypoxemia and respiratory alkalosis caused by hyperventilation
- CXR may be normal or reveal scattered interstitial infiltrates
ARDS: Characteristics of Late Clinical Manifestations
- Symptoms worsen with increased fluid accumulation and decreased lung compliance
- Pulmonary function tests reveal decreased compliance, lung volumes, and functional residual capacity (FRC)
Late Clinical Manifestations for ARDS include
- Tachycardia, diaphoresis, changes in mental status, cyanosis, and pallor
- Diffuse crackles and coarse crackles
- Hypoxemia despite increased FIO2
- Increasing WOB despite initial findings of normal PaO2 or SaO2
Clinical Manifestations: As ARDS progresses, profound respiratory distress requires
Endotracheal intubation and PPV
ARDS: Chest x-rays are termed
- Whiteout or white lung because of consolidation and widespread infiltrates throughout lungs
- Leaves few recognizable air spaces
ARDS: Complications of Treatment include
- Ventilator-associated pneumonia
- Barotrauma
- Volutrauma
- High risk for stress ulcers
- Renal failure
ARDS Complications of Treatment: Strategies for prevention of Ventilator associated pneumonia
- Strict infection control measures
- Ventilation protocol bundle:
- Elevate HOB 30 to 45 degrees
- Daily “sedation holidays”
- Venous thromboembolism prophylaxis
- Daily oral care with chlorhexidine
ARDS Complications of Treatment: Barotrauma
- Rupture of overdistended alveoli during mechanical ventilation
- Can lead to Interstitial emphysema, pneumothorax and subcutaneous emphysema, etc.
XUTE Respiratory Distress Syndrome Clinical Network (ARDSNet)
Ventilate with smaller tidal volumes
Higher Paco2 - permissive hypercapnia
ARS Complications of Treatment: Volutrama
- Occurs when large tidal volumes are used to ventilate noncompliant lungs -> Alveolar fracture (damage or tears in the alveoli) and movement of fluids and proteins into alveolar spaces
- Smaller tidal volumes or pressure-control ventilation is now standard in ARDS
ARDS Complications of Treatment: Stress Ulcers
Bleeding from stress ulcers occurs in 30% of patients with ARDS on mechanical ventilation
PEEP and its affect on CO
Look it up
How to manage stress ulcers associated with ARDS treatment?
- Correction of predisposing conditions
- Prophylactic antiulcer drugs (Proton pump inhibitors)
- Early initiation of enteral nutrition
ARDS Complications of Treatment: Renal Failure
- Occurs from decreased renal perfusion and subsequent decreased delivery of O2 to kidneys: From hypotension, hypoxia, or hypercapnia
- May also be caused by nephrotoxic drugs used to treat ARDS-related infections
ARDS: Nursing Assessment includes
- History of lung disease
- Exposures to lung toxins
- Tobacco, alcohol, or drug use
- Related hospitalizations
- Thoracic or spinal cord trauma
- Severe obesity
- Use of O2, inhalers, nebulizers, OTC drugs, immunosuppressant therapy
- Previous intubation
- Thoracic or abdominal surgery
- Exercise
- Immunizations
ARDS Nursing Assessment of Symptoms include
- Eating habits, change in appetite
- Weight gain/loss
- Fatigue
- Dizziness
- Dyspnea, wheezing, cough, sputum, palpitations, swollen feet
- Changes in sleep pattern, use of CPAP
- Shallow, increasing respiratory rate progressing to decreased rate
- Use of accessory muscles
- Asymmetric chest expansion
- Abnormal breath sounds
- Pleural friction rub
- Tachycardia progressing to bradycardia
- Hypertension progressing to hypotension
- Pulsus paradoxus, JVD, pedal edema
- Abdominal distention, ascites
- Somnolence, confusion, delirium
ARDS Nursing Assessment: Changes in labs
- Decreased tidal volume, FVC
- Abnormal x-ray
- Abnormal central venous or pulmonary artery pressures
- Initial increased CO: As hypoxemia, hypercapnia, and acidosis become more severe, CO will decrease
- Changes in pH, PaCO2, PaO2, SaO2
ARDS: Nursing Diagnoses can include
- Ineffective airway clearance
- Ineffective breathing pattern
- Risk for imbalanced fluid volume
- Anxiety
- Impaired gas exchange
- Imbalanced nutrition: less than body requirements
*Read notes for reasons
ARDS: Following recovery, overall goals include
- PaO2 within normal limits for age or at baseline on room air
- SaO2 >90%
- Resolution of precipitating factor(s) for ARDS
- Clear lungs on auscultation
Respiratory Therapy: Goals of Oxygen Administration
Primary goal is to correct hypoxemia:
- Initially nasal cannula or face mask with high-flow systems used to maximize O2 delivery
- SpO2 continuously monitored
Respiratory Therapy for ARDs: Modest to severe ARDS and refractory hypoxemia requires what treatments?
Need intubation with mechanical ventilation to maintain the PaO2 at acceptable levels
Respiratory Therapy for ARDS: Positive Pressure Ventilation
- PEEP at 5 cm H2O compensates for loss of glottic function: Opens collapsed alveoli
- Apply PEEP at 3 to 5 cm H2O increments
- Higher levels of PEEP may be used in patients with ARDS
Respiratory Therapy: Problems with PPV
- Can compromise venous return to right side of the heart: decreases preload, CO and BP
- Higher levels of PEEP can hyperinflate the alveoli = barotrauma or volutrauma.
*Read notes
Respiratory Therapy for ARDS: Alternative modes of mechanical ventilation and respiratory therapies if hypoxemia persists
- Airway pressure release ventilation
- Pressure control inverse ratio ventilation
- High-frequency ventilation
- Permissive hypercapnia
Respiratory Therapy for ARDS: Positioning Strategies
-Turn from supine to prone position “proning”: May be sufficient to reduce inspired O2 or PEEP
- When in supine position mediastinal and heart contents place more pressure on lungs than when in prone
- Predisposes patient to atelectasis
- Fluid pools in dependent regions of lung
Respiratory Therapy for ARDS: Other positioning Strategies include
- Continuous lateral rotation therapy
2. Kinetic Therapy
ARDS Positioning Strategies: Continuous lateral rotation therapy
- Continuous, slow side-to-side turning <40 degrees
- 18 of every 24 hours
ARDS Positioning Strategies: Kinetic therapy
Patient rotated side-to-side >40 degrees
ARDS Medical Supportive Therapy: Maintenance of CO and tissue perfusion
- Hemodynamic monitoring via a central venous or pulmonary artery catheter:
- Monitor CO and BP
- Sample blood for ABGs
ARDS Medical Supportive Therapy: Nutrition/fluid balance
- Enteral or parenteral feedings are started
- Monitor hemodynamic parameters
(e. g., CVP, stroke volume variation) - Monitor daily weight, intake and output
*Read notes
ARDS Evaluation:
Add last three slides
