ARDS: Acute Respiratory Distress Syndrome

• Acute Respiratory Distress Syndrome (ARDS) is a severe lung condition marked by rapid and widespread lung inflammation.
• ARDS can quickly lead to acute respiratory failure.

Characteristics of ARDS

• Acute onset of symptoms usually within a week of a known respiratory insult.
• Bilateral opacities are visible on chest imaging, unexplained by effusions or nodules.
• Respiratory failure is indicated by severe hypoxemia.
• Fluid accumulation in the lungs is not due to heart failure but non-cardiogenic pulmonary edema.

Pathophysiological Mechanisms of ARDS

• ARDS is initiated by direct or indirect injury to the alveolar-capillary membrane, caused by pneumonia, sepsis, trauma, or aspiration.
• The injury causes an intense inflammatory response, releasing pro-inflammatory cytokines like TNF-α, IL-1, and IL-6, and recruiting neutrophils to the lungs.
• Inflammatory mediators increase alveolar-capillary barrier permeability, causing protein-rich fluid to leak into alveolar spaces, leading to non-cardiogenic pulmonary edema.
• Fluid accumulation and surfactant loss lead to alveolar collapse (atelectasis), reducing available surface area for gas exchange.
• Fluid-filled alveoli impair oxygenation and ventilation, causing severe hypoxemia and hypercapnia.
• Inflammatory process leads to lung tissue fibrosis and remodeling, impairing lung function and compliance.

Phases of ARDS

• Exudative Phase (Days 1-7): Diffuse alveolar damage, capillary permeability increases and protein-rich edema fluid accumulates.
• Proliferative Phase (Days 7-21): Type II alveolar cells, fibroblasts, and myofibroblasts proliferate, forming granulation tissue and initiating lung repair.
• Fibrotic Phase (After 3 Weeks): Extensive fibrosis and lung tissue remodeling occurs, leading to long-term respiratory impairment and reduced compliance.

Exudative Phase (Inflammatory Phase) - Days 1 to 7:

• Pathophysiology sees injury to alveolar-capillary membrane, increased permeability, and leakage of bad stuff into alveoli.
• Surfactant dysfunction leads to alveolar collapse (atelectasis).
• Non-cardiogenic pulmonary edema develops.
• Clinical findings include refractory hypoxemia, tachypnea, dyspnea, respiratory distress and bilateral infiltrates on chest X-rays.
• Management will see mechanical ventilation with low tidal volumes, PEEP to prevent alveolar collapse and general supportive care.

Proliferative Phase - Days 7 to 21

• Pathophysiology decreases inflammatory response because of fibroblast proliferation.
• Type II alveolar cells are trying to fix surfactant and epithelial integrity.
• Fibrosis begins, which causes stiff lungs and decreases compliance.
• Clinical findings show persistent hypoxemia but there is some better gas exchange.
• Worsening lung compliance increases breathing workload.
• Hypercarbia is caused by poor ventilation.
• Management continues lung-protective ventilation, optimizes PEEP, monitors for secondary infections and VAP and considers prone positioning and sedation.

Fibrotic Phase (Chronic/Late Phase) - After 3 Weeks

• Pathophysiology shows lung tissue scarring, leading to lung disease.
• Decreased lung compliance leads to more required mechanical inflation.
• Pulmonary hypertension may develop due to vascular remodeling.
• Clinical Findings show persistent hypoxia and hypercapnia, increased pneumothorax risk and multi-organ involvement from prolonged hypoxia.
• Management includes supportive care, pulmonary rehabilitation, tracheostomy for ventilator use and monitoring for secondary complications.

Summary of ARDS

• ARDS results from direct or indirect lung injury, causing an intense inflammatory response, alveolar collapse, increased alveolar-capillary permeability, and impaired gas exchange.
• Progresses through exudative, proliferative, and fibrotic phases, potentially causing long-term consequences for the lung.

Assessment of Patient Progress

• Improvement in arterial blood gases (ABGs) indicates better oxygenation.
• Reduction in the need for high levels of ventilation suggests improvement.
• Improvements in respiratory rate, effort, and overall breathing can indicate progress.
• Follow-up chest X-rays or CT scans showing reduced opacities or fluid in the lungs is a positive sign.

Complications of ARDS

• Barotrauma: Lung damage caused by by high pressures from mechanical ventilation.
• Ventilator-Associated Pneumonia (VAP): Increased risk of infection from prolonged mechanical ventilation.
• Pulmonary Fibrosis: Long-term lung tissue scarring that leads to chronic respiratory issues.
• Multi-Organ Dysfunction Syndrome (MODS): Severe ARDS causes other organ failure due to systemic inflammation and bad oxygenation.

ARDS Management Strategies

• Low tidal volume ventilation (6 mL/kg) reduces ventilator-induced lung injury.
• Positive End-Expiratory Pressure (PEEP) keeps alveoli open.
• Prone positioning improves oxygenation.
• Fluid management uses a conservative approach to reduce pulmonary edema.
• Extracorporeal Membrane Oxygenation (ECMO) is used in severe cases.

Physiological Effects of PEEP

• PEEP increases the amount of air remaining in the lungs, keeping alveoli open.
• PEEP enhances gas exchange and increases partial pressure of oxygen by preventing alveolar collapse.
• PEEP decreases the effort required to breathe by keeping alveoli open and reducing resistance to airflow.

Benefits of PEEP

• Prevents alveoli collapse, effective in conditions like ARDS.
• Improves oxygenation and decreases the need for high levels of supplemental oxygen.
• Improves lung compliance by keeping alveoli open.

Risks of PEEP

• High levels of PEEP cause alveoli to stretch, leading to lung injury or pneumothorax.
• PEEP increases intrathoracic pressure, which reduces blood flow to the heart and decreases cardiac output.
• Excessive PEEP can cause lung injury because of overinflation of the alveoli.

Prone Positioning

• Prone positioning involves placing a patient face down instead of on their back to improve oxygenation in patients with ARDS.
• Improves V/Q matching and reduces shunt, enhancing oxygenation.
• Recruits dorsal lung regions and reduces ventilator-induced lung injury.

Risks of Prone Positioning

• Increased risk of pressure ulcers.
• Tubes and lines can get dislodged.
• Blood pressure and cardiac output can be affected.
• Airway management can get more challenging.

Nursing Management of Prone Patients

• Regularly assess skin and pressure points to prevent sores.
• Continuously monitor vital signs, oxygenation, and hemodynamic status.
• Ensure the endotracheal tube and other lines are secure and properly placed.
• Coordinate care with the healthcare team and respond to complications promptly.

VAP (Ventilator-Associated Pneumonia) Prevention Strategies

• Hand Hygiene: Strict adherence to hand hygiene protocols.
• Oral Care: Regular oral care with antiseptic to reduce bad bacteria.
• Head of Bed Elevation: Elevating to 30-45 degrees reduces the risk of aspiration.
• Subglottic Suctioning: Using endotracheal tubes with subglottic suction ports removes secretions.
• Sedation Management: Implement protocols to minimize sedation and enable early weaning from mechanical ventilation.
• Daily Assessment: Conduct daily assessments for readiness to extubate and implement spontaneous breathing trials.

Ventilator Waveforms

• Used during mechanical ventilation.
• They show pressure, volume, and flow over time.
• Provide information about the patient's respiratory mechanics and interaction with the ventilator.
• Pressure-Time Waveform: Illustrates the pressure in the airway over time.
• Volume-Time Waveform: Displays the volume of air delivered to the patient.
• Flow-Time Waveform: Shows the flow of air in and out of the lungs.

Interpretation of Ventilator Waveforms

• Changes in waveforms can indicate lung compliance or airway resistance.
• Waveforms can help identify patient-ventilator asynchrony.
• Waveforms provide real-time feedback on ventilation effectiveness to helps guide adjustments.

Ventilator-Associated Pneumonia (VAP)

• VAP is a serious infection that happens >48 hours after being intubated and put on mechanical ventilation.
• This leads to increased rates of people getting sick, dying and bad healthcare costs.

Pathophysiology of VAP

• VAP happens because of respiratory tract colonization and subsequent infection.
• Bacteria from the oropharynx or stomach enter the lower respiratory tract via the endotracheal tube, called aspiration of secretions.
• Biofilm Formation sees Pathogens that form biofilms, creating antibiotic resistance.
• Mechanical ventilation drops the ability to cough, this causes impaired lung defense, allowing bacteria accumulation.
• Microaspiration leakage around the endotracheal tube cuff introduces bacteria.

Common Causative Organisms of VAP

• Early-Onset VAP (within 4 days) is less likely to be drug-resistant, including Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.
• Late-Onset VAP (after 4 days) is often multidrug-resistant, including Pseudomonas aeruginosa, Acinetobacter baumannii, Klebsiella pneumoniae, Escherichia coli and Staphylococcus aureus (especially MRSA).

VAP Diagnosis & Biomarkers

• Diagnosis is based on clinical, radiological, and microbiological findings:
• Clinical includes Fever, Leukocytosis or leukopenia, Increased respiratory secretions and Worsening oxygenation.
• Imaging includes Chest X-ray for New/ progressive infiltrates and CT Scan for visualization.
• Testing includes Endotracheal aspirate culture, Bronchoalveolar lavage (BAL), Protected specimen brush (PSB) culture and Blood cultures. Biomarkers include Procalcitonin for bacterial infection, C-reactive protein to track inflammation and Soluble Triggering Receptor Expressed on Myeloid Cells-1 (sTREM-1) to differentiate types of VAP.

VAP Prevention Strategies

• Prevention should include bundle measures.
• Guidelines include Head of Bed Elevation, Daily Sedation Interruption & Extubation Assessment, Oral Care with Chlorhexidine, Subglottic Secretion Drainage and Hygiene Control.
• Extra measures include Use of ventilation when possible, Digestive Decontamination and Minimize antibiotic overuse.

VAP Treatment

• Empiric Antibiotic Therapy depends on MDR pathogens:
• Low-Risk get Ceftriaxone OR Ampicillin-Sulbactam OR Levofloxacin or Moxifloxacin and no MDR Risk.
• High-Risk patients get ẞ-lactam with Anti-Pseudomonal, Fluoroquinolone/Aminoglycoside and MRSA Coverage.
• Duration: 7 days needed, prolonged for slow infections.
• De-Escalation Strategy means to Adjust antibiotics, and Switch from shots to therapy when you get results.

Multi-Drug Resistant Pathogens

• Treatment for the Pathogens are MRSA-Requires Vancomycin, Pseudomonas aeruginosa needs dual therapy and Acinetobacter needs Colistin.

VAP Complications & Prognosis

• Complications: Sepsis, Lung Abscess, Empyema and ARDS.
• Prognosis: 20-50% Mortality Rate, depends on the pt and early treatment.

Key VAP Takeaways

• VAP is dangerous and kills quick
• Prevention is key.
• Early good antibiotics are needed
• MDR messes up treatment
• Use a shorter 7 day treatment.

Weaning from Ventilation

• Ventilation intolerance refers to someone who can't breathe in their own after the machine is removed.
• This leads to more risks and mortality rates in ICUs.
• Weaning attempts requires these criterias:

Criteria for Weaning Readiness

• Stable heart
• Hemodynamically stable
• Managed oxygen
• Managed ventilation
• Fix or improving disease

Weaning with Adequate Respiratory Mechanics

• Breathing Index
• Inspiratory Pressure
• Oxygenation and GAs
• 90% with 40%
• Within Range

Weaning that causes intolerance

• The causes for this intolerance shows:

Respiratory Causes

□ Respiratory muscle gets tired □ Airway resistance Inadequate gas exchange □ Traps air in lungs

Cardiovascular Causes

□ Heart failure cause increased issues Myocardial cause cardiac overload

Neuromuscular Causes

Weakness from extended machine usage Neuropathy or myopathy Can't cough good and clear secretions

Psychological & Metabolic Causes

Anxiety or panic Electrolyte imbalances Malnutrition

Signs of Bad Weaning

• Must stop if they show any signs:

Respiratory Signs

• Breaths increase for 5 mins
• Gases increase lots

Cardiovascular Signs

• Sudden bad beats
• Systolic gets bad
• Signs of chest change

Neurological Signs

• Get confused
• Level drops

Weaning Strategies

• Treat Identify/Treat underlying cause
• Fix oxygenation and unit ventilation
• Fix heart & infection issue
• Support Strategies
• Trials of T-pieces
• Reducing breathing effort
• decrease the ventilator

Rehabilitation & Strengthening

: Get to reduce ICU-acquired weakness Use Diaphragmatic training for endurance

Psychological Support

: Reduce anxiety and management Minimize sleep disturbances

Weaning Monitors:

• Asses for ventilary waning
• Check for - Dyspnea, apprehension, or agitation Decreasing oxygen saturation level
• Cyanosis or pallor, diaphoresis
• Increased pressure
• Diminished sounds
• Decreased LOC
• bad values