ARDS and Pulmonary Embolism: Comprehensive Study Notes

ARDS (Acute Respiratory Distress Syndrome) and PE Study Notes

ARDS: Overview

• ARDS is a sudden and progressive form of acute respiratory failure.

• The alveolar capillary membrane becomes damaged and more permeable to intravascular fluid.

• Alveoli fill with fluid, leading to impaired gas exchange.

Predisposing Conditions of ARDS

• Common causes

  • Direct Lung Injury

  • Indirect Lung Injury

• Aspiration of gastric contents or other substances

• Sepsis (especially gram-negative infection)

• Bacterial or viral pneumonia

• Severe massive trauma

• Near drowning

• Severe traumatic brain injury (TBI)

• Sepsis is the most common indirect cause

• Shock states (hypovolemic, cardiogenic, septic)

Pathophysiologic Phases of ARDS

• Injury or exudative phase

• Reparative or proliferative phase

• Fibrotic or fibroproliferative phase

Injury or Exudative Phase

• Usually occurs 24–72 hours after initial insult (direct or indirect injury).

• Lasts 7–10 days.

• Interstitial edema occurs from peri-bronchial and perivascular interstitial space engorgement.

• Fluid surrounding alveoli crosses the alveolar membrane into the alveolar space.

• V/Q mismatch and intrapulmonary shunt occur; blood in alveolar capillaries cannot be oxygenated.

Stages of Edema Formation in ARDS

• Normal alveolus and pulmonary capillary (A)

• Interstitial edema with increased fluid flow into interstitial space (B)

• Alveolar edema when fluid crosses the blood–gas barrier (C)

ARDS: Injury and Exudative Phase – Key Events

• Neutrophils are attracted to the site and release mediators, causing changes in the lungs.

• ↑ Pulmonary capillary membrane permeability.

• Destruction of elastin and collagen.

• Formation of pulmonary microemboli.

• Pulmonary artery vasoconstriction.

Types of Alveolar Cells

• Type I alveolar cells (Type I): occupy most of the alveolar surface and are involved in gas exchange.

• Type II alveolar cells (Type II): secrete pulmonary surfactant and reabsorb sodium and water, preventing fluid buildup.

• Alveolus contains macrophages and capillaries with red blood cells.

ARDS: Injury/Exudative Phase – Additional Details

• Alveolar cells (Type I and II) are damaged.

• Surfactant dysfunction → surfactant production decreases or becomes inactivated.

• Surfactant dysfunction leads to atelectasis (collapse of alveoli).

• Hyaline membranes line the alveoli; composed of necrotic cells, protein, and fibrin.

• Hyaline membranes contribute to atelectasis and fibrosis.

ARDS: Injury/Exudative Phase – Gas Exchange and Compliance

• Severe V/Q mismatch and shunting result in refractory hypoxemia (unresponsive to increasing O2 concentrations).

• Diffusion limitation caused by hyaline membranes.

• Lungs become less compliant due to decreased surfactant, pulmonary edema, and atelectasis.

• Increased airway pressures are required to inflate “stiff” lungs.

• Mechanical ventilation becomes essential.

ARDS: Injury/Exudative Phase – Breathing Dynamics

• ↑ Work of breathing and ↑ respiratory rate (stimulated by hypoxia).

• ↓ Tidal volume.

• Respiratory alkalosis from increased CO2 removal (note: text also mentions hypoventilation with ↓ CO2; there is a potential inconsistency in the source material).

• Result: hypoxemia and potential ↓ tissue perfusion.

ARDS: Injury/Exudative Phase – Edema and Shunting

• Interstitial and alveolar edema (noncardiogenic pulmonary edema).

• Atelectasis leading to V/Q mismatch.

• Shunting of pulmonary capillary blood.

• Hypoxemia unresponsive to increasing O2 (refractory hypoxemia).

ARDS: Reparative/Proliferative Phase

• Occurs 1–2 weeks after initial lung injury.

• Influx of neutrophils, monocytes, and lymphocytes.

• Fibroblast proliferation.

• Pulmonary vasculature destroyed; lung becomes dense and fibrous, with ↓ lung compliance.

• Hypoxemia continues due to thickened alveolar membrane, V/Q mismatch, diffusion limitation, and shunting.

• Fluid in the lungs and secretions increase airway resistance.

• If reparative phase persists, widespread fibrosis results; if reparative phase stops, lesions may resolve.

ARDS: Fibrotic or Fibroproliferative Phase (Chronic/Late Phase)

• Can occur anytime between 24 hours to 2–3 weeks after initial injury.

• Lung is remodeled with collagenous and fibrous tissue.

• Decreased lung compliance due to diffuse scarring, interstitial fibrosis, and alveolar duct fibrosis.

• ↓ lung compliance and ↓ gas exchange surface area.

• Pulmonary hypertension develops due to vascular destruction and fibrosis.

ARDS: Clinical Progression

• Progression varies among patients.

• Some survive the acute phase; pulmonary edema may resolve; complete recovery within a week or two.

• Survival is poorer for those who progress to the fibrotic phase, often requiring several weeks or long-term mechanical ventilation.

• Unclear why some injured lungs repair/recover while others do not.

• Factors influencing course: nature of initial injury, extent/severity of comorbid conditions, and pulmonary complications (e.g., pneumothorax or oxygen toxicity).

ARDS: Early Clinical Manifestations

• Initial presentation is often subtle: dyspnea, tachypnea, cough, restlessness.

• Chest auscultation may be normal or show fine, scattered crackles.

• ABGs: mild hypoxemia and respiratory alkalosis due to hyperventilation.

• Chest X-ray: normal or show diffusely scattered, minimal interstitial infiltrates.

ARDS: Late Clinical Manifestations

• Worsening symptoms with fluid accumulation and decreased lung compliance.

• Respiratory distress, increased work of breathing, tachypnea, intercostal and suprasternal retractions.

• Tachycardia, diaphoresis, changes in mental status, cyanosis, pallor.

• Lung auscultation: scattered to diffuse crackles; chest X-ray 72+ hours after injury shows diffuse bilateral interstitial and alveolar infiltrates.

• ABGs reflect changes in oxygenation and ventilation; refractory hypoxemia remains hallmark.

Imaging

• Chest X-ray progression: from minimal infiltrates to diffuse bilateral interstitial/alveolar infiltrates in ARDS; see illustrative images (Normal CXR vs. ARDS on the provided page).

Abbreviations and Oxygenation Indices

• FiO2 (Fraction of Inspired Oxygen): the percentage of oxygen in the inspired gas.

  • Room air typically contains 21% oxygen, FiO2 ≈ 0.21.

• PaO2 (Partial Pressure of Oxygen): measurement of oxygen pressure in arterial blood; normal ~ 80\text{ mmHg} \le PaO_2 \le 100\text{ mmHg}.

PaO2 / FiO2 (P/F) Ratio

• Definition: \text{P/F ratio} = \frac{PaO2}{FiO2}

• Healthy example: PaO2 = 90 mmHg, FiO2 = 0.21 → \frac{PaO2}{FiO2} = \frac{90}{0.21} \approx 429 (i.e., > 400).

• Severity thresholds (per slide):

  • Normal lung function: P/F > 400

  • Mild ARDS: P/F < 300

  • Moderate ARDS: P/F < 200

  • Severe ARDS: P/F < 100

• If FiO2 is increased with no corresponding rise in PaO2 (refractory hypoxemia), the P/F ratio decreases.

• With PEEP or CPAP ≥ 5 cm H2O, P/F ratio thresholds help define ARDS severity (per presentation).

Practice Question (Example)

• Case: 26-year-old woman with ARDS after near-drowning, 4 days ago; mechanically ventilated; FiO2 = 0.90; PEEP = 15 cm H2O; VT = 350 mL; RR = 12/min; peak pressure = 35 cm H2O; PaO2 = 83 mmHg.

• Calculation of P/F Ratio:

  • P/F ratio = PaO2 / FiO2

  • In this case, P/F ratio = 83 mmHg / 0.90 = 92.2

• Interpretation of P/F Ratio:

  • With a P/F ratio of 92.2, this indicates severe ARDS (as per Berlin definition: P/F < 100).

  • The patient’s high FiO2 requirement and significant positive end-expiratory pressure indicate substantial hypoxemia.

ARDS: Clinical Diagnosis and Management (Summary)

• ARDS features: profound respiratory distress, hypoxemia, diffuse alveolar damage, noncardiogenic edema, refractory hypoxemia, and progressive lung stiffness.

• Management often requires endotracheal intubation and positive-pressure ventilation; chest X-ray tends toward a “whiteout.”

• Complications: hypoxemia, hypercapnia, metabolic acidosis, organ dysfunction.

ARDS: Complications

• Abnormal lung function persists or worsens.

• Ventilator-associated pneumonia.

• Barotrauma from ventilation.

• GI ulcers.

• Venous thromboembolism (VTE).

• Acute kidney injury (AKI); consideration of CRRT.

• Psychological issues.

Nursing and Interprofessional Management of ARDS

• ARDS is a severe form of acute respiratory failure; nursing care parallels that for acute respiratory failure.

• Core elements: assessment, planning, implementation (and ongoing re-evaluation).

• Multidisciplinary approach including respiratory therapy, nursing, medicine, and nutrition.

Respiratory Therapy: Oxygen Administration

• Use high-flow systems to maximize O2 delivery.

• SpO2 continuously monitored.

• Nasal cannula (NC) or simple mask may be ineffective for ARDS; use the lowest FiO2 that achieves PaO2 ≥ 60 mmHg.

Mechanical Ventilation: Lung-Sparing Strategies

• Low tidal volume ventilation: VT = 4 \text{ to } 8\ \text{mL/kg}

• Goal: reduce mortality and risk of volutrauma (volutrauma).

• Permissive hypercapnia: allow CO2 to rise slowly; keep pH between 7.30 and 7.45; PaCO2 may rise to ~60 mmHg.

Mechanical Ventilation: PEEP and Oxygenation

• PEEP (positive end-expiratory pressure): typically = 5 cm H2O to begin; helps keep alveoli open.

• Increase PEEP in 3–5 cm H2O increments until oxygenation adequate with FiO2 of ~60% (FiO2 ≈ 0.60).

• Higher PEEP levels may be required to achieve adequate oxygenation, but can cause hemodynamic compromise:

  • ↓ venous return, preload, cardiac output, and BP.

  • Hyperinflation and compression of pulmonary capillary bed, reducing BP.

  • Risk of barotrauma.

Mechanical Ventilation: Positioning

• Fluid can pool in dependent lung regions; dependent compression worsens atelectasis in supine position.

• Prone positioning reduces mediastinal and cardiac pressure on the lungs, improves recruitment, and may reduce oxygen needs for some cases.

• Prone position can reduce the need for higher FiO2 or PEEP in some patients.

Continuous Lateral Rotation (CLR)

• Example: Continuous Lateral Rotation Therapy bed systems aid repositioning, percussion, and vibration to improve drainage and oxygenation.

Extracorporeal Membrane Oxygenation (ECMO)

• ECMO is used in specialized ICUs for refractory hypoxemia or hypercapnia when conventional ventilation fails.

• Functionally similar to dialysis: adds oxygen and removes CO2 from the blood.

Analgesia and Sedation in ARDS

• Essential for intubated patients to minimize discomfort, reduce work of breathing, and prevent ventilator dyssynchrony.

• Analgesia: IVP or continuous infusion.

• Neuromuscular blocking agents may be used (e.g., vecuronium, pancuronium).

Hemodynamic Monitoring in ARDS

• Monitor with EKG, arterial blood pressure, MAP, SpO2.

• If cardiac output is decreased, manage with IV fluids, drugs, or both.

Fluid Balance and Nutrition

• Pulmonary permeability increase can cause pulmonary edema, yet patients may be intravascularly volume depleted.

• Monitor hemodynamic parameters and urine output; daily weight.

• Nutrition: Maintain protein and energy stores to support recovery and healing.

Evaluation and Goals of Care in ARDS

• Maintain adequate oxygenation/ventilation with decreasing O2 requirements.

• Achieve hemodynamic stability; no abnormal breath sounds; effective cough and sputum clearance.

• ABG goals: PaO2 and PaCO2 within normal ranges or at baseline; weight maintenance; normal serum albumin and protein.

Pulmonary Embolism (PE)

(Content summarized from pages 532–537 in the provided transcript)

What is PE?

• Blockage of 1 or more pulmonary arteries by a thrombus, fat or air embolus, or tumor tissue.

• Most commonly arises from deep vein thrombosis (DVT) in the legs.

• Other sites: femoral or iliac veins, right heart (atrial fibrillation), pelvic veins (especially after childbirth).

• Less common causes: fat emboli (fractured long bones), air emboli (improper IV therapy).

PE Clinical Manifestations

• Signs and symptoms are varied and nonspecific; diagnosis can be challenging.

• Small emboli may go undetected; symptoms may be gradual or sudden.

• Dyspnea is the most common presenting symptom.

• May have mild to moderate hypoxemia; other manifestations include tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, tachycardia, syncope.

PE Complications

• 10% die within the first hour with a massive PE.

• Anticoagulation treatment reduces mortality.

• Pulmonary infarction (death of lung tissue).

• Pulmonary hypertension (recurrent PEs).

PE Diagnostics

• D-dimer: measures cross-linked fibrin fragments.

• Spiral (helical) CT scan with IV contrast to visualize the pulmonary vessels.

• V/Q scan: Ventilation-perfusion scanning (perfusion with IV radiotracer; ventilation with radioactive gas).

PE Treatment

• Supplemental oxygen if hypoxemic.

• Encourage coughing and deep breathing.

• Immediate anticoagulation: Low-molecular-weight heparin (Lovenox) or oral anticoagulation (Warfarin).

• Pulmonary embolectomy in selected cases.

• Inferior vena cava (IVC) filter in certain patients.

• Prevention: DVT prevention strategies.

PE Key Takeaways

• Early recognition and anticoagulation significantly impact outcomes.

• Hemodynamic and gas-exchange support are critical in acute management.