Study Notes on Acute Respiratory Distress Syndrome (ARDS)
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) OVERVIEW
ARDS is a form of respiratory failure characterized by:
Non-cardiogenic pulmonary edema
Refractory hypoxia
Pathophysiological characteristics of ARDS include:
Inflammation of lung tissue
Damage to pulmonary capillaries
Injury to alveoli, leading to impaired gas exchange.
Arterial Blood Gases (ABGs) typically show:
Rise in PaCO2 (partial pressure of carbon dioxide in arterial blood)
Decreased PaO2 (partial pressure of oxygen in arterial blood)
PATHOPHYSIOLOGY
ARDS can be caused by either direct or indirect lung injury:
Direct Injury:
Lung tissue is damaged initially, causing a local inflammatory response.
This response leads to:
Damage to alveolar-capillary membrane
Increased permeability, resulting in fluid leakage into the alveoli, which causes ARDS.
Indirect Injury:
A systemic inflammatory response occurs elsewhere in the body (e.g., Sepsis).
Inflammatory mediators circulate to the lungs, resulting in:
Alveolar-capillary damage and the onset of ARDS.
In both cases, inflammatory mediators elevate the permeability of the alveolar-capillary membranes, causing a leakage of protein-rich fluid into the alveoli, leading to:
Non-cardiogenic pulmonary edema
Decreased surfactant production due to damage to type II alveolar cells, resulting in:
Alveolar collapse (atelectasis)
Decreased lung compliance
Continued inflammation results in:
Formation of fibrin and cellular debris creating hyaline membranes
Severe ventilation-perfusion mismatch and refractory hypoxemia.
ETIOLOGY / RISK FACTORS
Direct Lung Injury can be due to:
Pneumonia
Aspiration of gastric contents
Inhalation injuries
Near drowning
Indirect Lung Injury can occur from:
Sepsis
Major burns
Drug overdoses
Pancreatitis
CLINICAL MANIFESTATIONS
Early Symptoms:
Dyspnea (difficulty breathing)
Tachypnea (rapid breathing)
Progressive Respiratory Distress:
Increased respiratory rate
Intercostal retractions and use of accessory muscles of respiration
Tachycardia due to oxygen demand increase
Development of crackles and rhonchi later in the progression
Potential for cyanosis
Altered mental status including agitation, confusion, and lethargy as respiratory failure advances.
Signs of Hypoxia:
Early Signs:
Neuro: Restlessness, anxiety, confusion
Respiratory: Tachypnea, dyspnea, use of accessory muscles, deep and labored breaths, mild to low SaO2 (oxygen saturation)
Cardiovascular (CV): Tachycardia, hypertension (HTN)
Skin: Pallor
Late Signs:
Neuro: Lethargy, stupor, decreased level of consciousness (LOC)
Respiratory: Bradypnea (slow breathing), shallow respirations, periods of apnea, low SaO2
CV: Bradycardia, hypotension, arrhythmias (related to ischemia and acidosis)
Skin: Cyanosis
Presence of metabolic acidosis.
DIAGNOSTICS
Berlin Criteria for ARDS diagnosis include:
Timing: ARDS condition precipitated by an acute event with symptoms developing within the last week.
Chest Imaging: Evidence of bilateral opacities on imaging (CXR or CT).
Edema Origin:
Primarily or exclusively non-cardiogenic.
Hypoxemia Severity Based on the P:F Ratio:
Mild: P:F ratio 200-300
Moderate: P:F ratio < 200
Severe: P:F ratio < 100 *Where P:F ratio is calculated by dividing the PaO2 by the FiO2 (fraction of inspired oxygen) as a decimal when on a ventilator with PEEP > 5 cm H2O.
Other diagnostics:
ABG analysis to determine oxygen levels
Blood tests (CBC, chemistries, cultures) to identify underlying causes
Sputum culture to identify infections contributing to ARDS.
COLLABORATIVE INTERVENTIONS
PHARMACOTHERAPY
No definitive drug therapy exists for ARDS, however, the following treatments may be employed:
Bronchodilators
Corticosteroids (considered for moderate to severe ARDS)
Antibiotics (if infection is present)
Paralytics in cases of ventilator asynchrony
Diuretics
Prophylaxis for Deep Venous Thrombosis (DVT) and gastrointestinal (GI) complications
Inhaled nitric oxide and prostacyclin to enhance pulmonary vasodilation, reducing pulmonary vascular resistance (PVR) and improving oxygenation.
VENTILATORY SUPPORT
The cornerstone of ARDS management involves mechanical ventilation strategies that may be either invasive or non-invasive.
**Non-Invasive Ventilatory Support:
**
High Flow Nasal Cannulas
Deliver heated, humidified oxygen-air blend up to 100% FiO2 with distinct features:
The flow rate does not determine FiO2 (e.g., 50 L/min may deliver either 50% or 100% FiO2 depending on setting).
Flow and oxygen concentration are set separately.
Fit snugly in nares to minimize ambient air entrainment and allow for precise FiO2 delivery.
Provide low levels of positive pressure preventing atelectasis.
Biphasic Positive Airway Pressure (BiPAP):
Delivers:
Higher positive pressure during inspiration (IPAP) and lower pressure during expiration (EPAP).
Sample settings: IPAP = 10 mmHg, EPAP = 5 mmHg, and FiO2 = 50%.
Advantages include prevention of atelectasis, CO2 flushing, reduced work of breathing (WOB), ability to deliver FiO2 up to 100%, and delaying intubation.
Disadvantages include:
High risk for aspiration if the patient vomits.
Potential leaks with patient movement.
Discomfort and risk of pressure injuries.
Contraindications:
Absolute: Cardiopulmonary arrest, inability to maintain patent airway, severe agitation/coma, facial trauma, severe refractory hypotension.
Relative: Altered level of consciousness (ALOC), vomiting, copious secretions, recent upper GI or respiratory surgery, right ventricular failure, mild hypotension.
Invasive Ventilatory Support:
Possible indications for endotracheal (ET) intubation include:
Altered mental status requiring airway protection
Anticipated airway obstruction
Copious secretions not amenable to suctioning
High-risk aspiration cases
Severe respiratory distress, bradypnea, apnea, code blue situations, or general anesthesia.
Preparation for Intubation
Supplies Needed:
Oxygen, ventilator, Ambu-bag for pre-intubation ventilation
Endotracheal (ET) tube (sizes 6 to 8 mm for adults)
Laryngoscope
End-tidal CO2 detector (yellow indicator confirms correct placement)
Tape or ET holder for stabilization
Nursing Responsibilities:
Positioning patient at the top of the bed
Hyperextending the neck using towels
Set up for suctioning to visualize vocal cords during insertion
Administer Rapid Sequence Intubation (RSI) with sedation (e.g., Propofol) and paralytic agent (e.g., Succinylcholine).
Preoxygenate the patient (to mitigate transient hypoxemia)
Limit intubation attempts to no more than 30 seconds.
Monitor vital signs during intubation.
Nursing Responsibilities After Intubation:
Assess pilot balloon inflation, stabilize ET tube, and measure at lip line.
Conduct respiratory assessment (lung sounds, chest rise, air emerging from tube).
Obtain chest X-ray to confirm tube position (should be 1-2 cm above the carina).
Employ soft restraints as necessary and potentially place a nasogastric tube (NGT).
Initiate sedation for comfort.
Ventilator Settings:
Tidal Volume (TV): Air delivered per breath, typically 8 to 10 mL/kg of ideal weight, approximately 400-500 mL in an average adult.
Respiratory Rate (RR): Generally set at 12 to 16, adjustable based on PaCO2 levels.
Fraction of Inspired Oxygen (FiO2): Adjustable between 21% to 100%, starting at a minimum of 30% and titrated to maintain PaO2 between 60 and 100 mmHg to avoid oxygen toxicity.
Positive End Expiratory Pressure (PEEP): Typically starts at 5 cmH20, can be increased for ARDS management, keeping alveoli open; excessive PEEP may induce barotrauma or pneumothorax.
I:E Ratio: Standard ratio is usually 1:2 (duration of inspiration to expiration).
Ventilator Strategies for Patients with ARDS:
Lung-Protective Ventilation:
Recommendations to prevent:
Barotrauma from high pressures
Volutrauma from large tidal volumes
Atelectrauma from cyclical collapse and reopening of alveoli.
Ventilator Recommendations include:
Use low tidal volumes (4 to 8 mL/kg of ideal body weight against the norm of 6 to 8 mL/kg)
Respiratory rate up to 35 to compensate for low tidal volume
Maintain goal PaO2 between 55 and 80 mmHg.
SpO2 target between 88% to 95%.
Maintain pH levels between 7.30 and 7.45.
Reverse inspiratory-to-expiratory ratios as necessary.
PEEP can extend up to 24 cmH2O under specific treatment conditions.
VENTILATOR MODES
Assist-Control Mandatory Ventilation (ACMV):
Patients can initiate breaths with each being fully supported at:
Volume Control:
Preset tidal volume and respiratory rate.
Delivers full preset tidal volume regardless of patient spontaneity.
Pressure Control:
Preset respiratory rate and inspiratory pressure,
Delivers based on reaching a set pressure leading to variable tidal volumes dependent on compliance.
Utilized initially in ARDS when lung protection is critical.
Pressure Regulated Volume Control (PRVC):
Combines volume control with pressure protection to guarantee volume while preventing excessive pressure.
Airway Pressure Release Ventilation (APRV):
Features very long inspiratory times, high continuous pressure (similar to CPAP), with brief release phases for expiration.
Conceptualized as CPAP with intermittent release.
WEANING MODES
Synchronous Intermittent Mandatory Ventilation (SIMV):
Contains mandatory breaths (fully supported) interspersed with spontaneous breaths devoid of support.
Continuous Positive Airway Pressure (CPAP):
Requires spontaneous breathing without mandatory breaths, providing constant pressure to maintain airway patency.
Pressure Support Ventilation (PSV):
Covers scenarios where the patient initiates breaths with the ventilator boosting pressure during inspiration, significantly easing effort.
COMPLICATIONS OF MECHANICAL VENTILATION
Barotrauma/Pneumothorax:
Ventilator-assisted Pneumonia (VAP):
Potential sources of infection include:
Aspiration of gastric contents
Contaminated intubation procedure
Biofilm development along the endotracheal tube
Accumulated secretions.
Cardiovascular (CV) Effects:
Vena cava compression secondary to increased intrathoracic pressure may diminish preload and ultimately lower cardiac output (CO).
GI Effects:
Gastric distention attributable to excess air from intubation or PEEP and stress-induced gastric ulcers resulting from increased secretions.
VENTILATOR ALARMS
Regularly assess the patient prior to troubleshooting the ventilator. Look for signs such as:
Respiratory distress
Oxygen saturation
Chest rise
Breath sounds
Tube placement.
Low-Pressure Alarm (Low Tidal Volume)
Meaning: Indicates a loss of pressure in the ventilator circuit, generally due to an air leak or tubing disconnection.
Possible Causes & Interventions:
Disconnection of ventilator tubing:
Reestablish connections.
ET tube displacement:
Assess depth and tube placement, checking for breath sounds; notify respiratory therapist/MD if displaced.
Self-extubation:
Immediately call for help, supply oxygen or utilize a bag-valve-mask, prepare for reintubation if necessary.
Cuff leak:
Respiratory therapist may reinflate cuff or reintubate if cuff is ruptured.
Air leak/damaged tubing:
Replace tubing as required.
High-Pressure Alarm
Meaning: Indicates increased airway resistance or an obstruction disrupting normal airflow.
Possible Causes & Interventions:
Patient biting the tube:
Insert a bite block, adjusting sedation as needed.
Coughing due to secretions:
Suction as needed; adjust sedation if cough is non-secretive.
Kinked ventilator tubing:
Inspect and resolve obstructions.
Excess secretions:
Perform suctioning.
Mucus plug:
Immediate suction required.
Decreased lung compliance (e.g., worsening ARDS):
Notify the provider; ventilator settings might require adjustment.
Pneumothorax:
High-pressure alarm ominously appears with reduced breath sounds; notify the provider and prepare for chest tube placement.
Patient fighting the ventilator (dyssynchrony):
Provide reassurance, encourage slow breathing, assess pain/anxiety/hypoxia, adjust sedation or ventilator settings as necessary.
NURSING CARE
Ventilator-associated Pneumonia Prevention Methods:
VAP Prevention Bundle:
Suctioning as warranted (often q2-4 hrs).
Endotracheal (Tracheal) Suctioning Done through a closed (in-line) system to clear secretions from the trachea and bronchi.
Subglottis Suctioning should clear pooled secretions above the endotracheal tube cuff to avoid microaspiration and VAP.
Oropharyngeal Suctioning should address oral secretions.
Oral Care:
Administer chlorhexidine typically twice daily as determined by facility policy.
Elevate Head of Bed (HOB):
Position at 30-45° to reduce aspiration risk.
Daily Spontaneous Awakening Trial (SAT):
Lighten sedation to evaluate neurologic status.
Daily Spontaneous Breathing Trial (SBT):
Monitor readiness for extubation via ABGs and vital signs during SBT in pressure support mode.
Strict Hand Hygiene:
Rotate/Repositioning:
Every 2 hours to assist with lung expansion and secretion mobilization.
GI & DVT Prophylaxis:
Implement measures to prevent stress ulcers and thromboembolic complications extending hospital stays.
Monitor Descriptions of Secretions:
Assess color, consistency, and odor.
Perform Chest Physiotherapy:
To facilitate secretions clearance.
Monitor Kidney Function:
Conduct sequential studies as indicated.
Consider Prone Positioning:
As prescribed for improved oxygenation.
NUTRITION MANAGEMENT
Initiate nutrition 12 to 24 hours post-intubation contingent on hemodynamic stability.
Calculate caloric requirements with a feeding formula determined by a dietician (e.g., Glucerna for diabetics, Jevity for standard nutrition, Nepro for renal patients).
RN responsibility involves tube insertion as ordered, utilizing options such as OG, NG, or post-pyloric tubes which reduce aspiration risk.
Begin feedings slowly, progressing gradually while monitoring tolerance. Flush with water every 6 hours.
SEDATION FOR INTUBATED PATIENTS
Propofol:
Class: Sedative Hypnotic
Indications: Rapid and easily adjustable sedation (onset within 30 seconds).
Nursing Considerations:
Watch for respiratory depression, hypotension, and hypertriglyceridemia.
Monitor blood pressure and triglycerides (hold for TG ≥ 500).
Replace tubing every 12 hours.
Dosing:
Start at 5 mcg/kg/min, titrate to effect at increments of 5 mcg/kg/min, up to 50-70 mcg/kg/min, reducing after effective sedation found. Lower doses may be required for elderly patients.
Dexmedetomidine (Precedex):
Class: Alpha-2 Agonist
Indications: Light sedation during ventilator weaning; maintains arousability without respiratory depression (can be used without mechanical ventilation).
Nursing Considerations: Good for SBT, may induce hypotension and bradycardia.
Fentanyl:
Class: Opioid analgesic
Indication: For pain-driven agitation.
Midazolam:
Class: Benzodiazepine
Indication: For deep sedation when other agents are inadequate.
Nursing Considerations: Beware of drug accumulation in renal/hepatic pathologies.
MONITORING PATIENTS ON SEDATION
Maintain RASS (Richmond Agitation-Sedation Scale) goals as ordered, typically between 0 and -2 for intubated patients.
Document RASS scores every 1-2 hours.
PRONATION THERAPY
Utilized for moderate to severe ARDS:
Enhances oxygenation through various mechanisms:
Alleviates mechanical pressure from the heart and abdominal viscera on lungs.
Promotes even blood and air distribution within the lungs.
Aids in the mobilization and drainage of secretions.
Facilitates oxygenation of dorsal lung areas (potentially more surface area available).
Patients are typically pronated for 12 to 16 hours, entailing considerable effort but capable of reducing mortality and ventilatory duration.
WEANING FROM VENTILATOR
Conduct SAT/SBT (sedation vacations) usually during day shifts.
Evaluate SAT safety to discern if a mechanically ventilated patient is prime for potential sedation duration halting. Criteria for failure necessitating continuous sedation infusion includes:
Requirement for excessive sedatives hindering safety in a spontaneous awakening trial.