TA

Acute Respiratory Failure and Acute Respiratory Distress Syndrome

ACUTE RESPIRATORY FAILURE (ARF)

  • Definition: Acute respiratory failure is not classified as a disease but rather a condition that arises due to one or more diseases affecting the lungs or other body systems.

GAS EXCHANGE INSUFFICIENCIES

  • Insufficient Gas Exchange: Leads to various complications:

    • Inadequate transfer of oxygen (O2) to the blood, causing Hypoxemia.

    • Inadequate removal of carbon dioxide (CO2), resulting in Hypercapnia.

CLASSIFICATION OF RESPIRATORY FAILURE

  • Types:

    • Hypoxemic Respiratory Failure: Defined as an oxygenation failure.

    • Hypercapnic Respiratory Failure: Also referred to as ventilatory failure.

    • Combined Hypoxemic and Hypercapnic Respiratory Failure.

DIAGNOSTIC CRITERIA FOR ARF

  • Acute Respiratory Failure Criteria:

    • PaO2 of 60 mm Hg or less while on 60% FiO2 (fraction of inspired oxygen).

    • PaCO2 greater than 50 mm Hg.

    • A pH of less than 7.25.

PATHOPHYSIOLOGY OF ARF

  • Positive Feedback Mechanism: Continuous hypoxemia and hypercapnia lead to:

    • Increased pulmonary vascular resistance.

    • Right ventricular failure (Cor Pulmonale).

    • Impaired left ventricular function, resulting in reduced cardiac output.

    • Cardiogenic pulmonary edema due to increased pressures.

    • Diaphragmatic fatigue caused by increased work of breathing.

HYPOXEMIC RESPIRATORY FAILURE

  • Definition: Also termed oxygenation failure.

    • Characterized by PaO2 < 60 mm Hg on inspired O2 concentration > 60% or < 50 mm Hg on room air.

Etiology and Pathophysiology

  • Causes include:

    • Ventilation-Perfusion (V/Q) Mismatch: Common in conditions such as:

    • COPD (Chronic Obstructive Pulmonary Disease)

    • Pneumonia

    • Asthma

    • Atelectasis (lung collapse)

    • Pulmonary embolus

    • Shunt: Can be classified as:

    • Anatomic shunt (blood bypasses the lungs).

    • Intrapulmonary shunt (blood passes through unventilated areas of the lung).

    • Diffusion Limitation: Impaired transfer in conditions like severe COPD, recurrent pulmonary emboli, and ARDS (Acute Respiratory Distress Syndrome).

    • Alveolar Hypoventilation: Due to restrictive lung disease, CNS disease, chest wall dysfunction, or neuromuscular disease.

HYPERCAPNIC RESPIRATORY FAILURE

  • Definition: Also known as ventilatory failure.

    • Characterized by PaCO2 above normal (> 50 mm Hg) and acidemia (pH < 7.25).

Etiology and Pathophysiology

  • Imbalance: Affected by both ventilatory supply and demand.

  • Abnormalities:

    • Airways and Alveoli: Conditions leading to obstruction and impaired airflow (e.g., asthma, COPD, cystic fibrosis).

    • Central Nervous System (CNS) Abnormalities: Drug overdose, brainstem infarction, and spinal cord injuries affect the respiratory drive.

    • Chest Wall Abnormalities: Such as flail chest, kyphoscoliosis, severe obesity, fractures, and muscle spasms.

    • Neuromuscular Conditions: Including muscular dystrophy, Guillain-Barré syndrome, multiple sclerosis, and exposure to toxins.

CLINICAL MANIFESTATIONS

  • Signs and Symptoms of ARF:

    • Hypoxemia: Classic symptom includes dyspnea.

    • Additional symptoms include: Cyanosis, restlessness, confusion, anxiety, tachypnea, tachycardia, hypertension, cardiac dysrhythmias, tremors.

    • Hypercapnia: Symptoms including dyspnea, headache. Accompanied by peripheral and conjunctival hyperemia, hypertension, tachycardia, impaired consciousness, and asterixis.

    • Consequences of persistent hypoxemia may lead to:

    • Metabolic acidosis and cell death.

    • Decreased cardiac output and impaired renal function.

Specific Clinical Symptoms

  • Examples:

    • Rapid, shallow breathing patterns, orthopnea.

    • Use of tripod position for breathing difficulty.

    • Pursed-lip breathing to increase expiratory phase and prevent collapse.

    • Retractions during breathing efforts and observable changes in inspiratory:expiratory (I:E) ratio.

ASSESSMENT OF ARF

  • Diagnosis Confirmation:

    • Arterial Blood Gases (ABGs) confirm ARF.

    • Chest X-ray and sputum culture are used for imaging and sample collection.

    • Pulmonary Function Tests (PFTs), angio/ventilation-perfusion scanning, CT scans, ECG, echocardiography, thoracentesis, toxicology screen, CBC, electrolytes, urinalysis are also critical in assessment.

MANAGEMENT OF ARF

  • Treatment Goals:

    • Correct or compensate for gas exchange abnormalities.

    • Mechanical Ventilation as necessary.

    • Administer oxygen therapy, targeting SaO2 > 90%.

    • Continuous pulse oximetry monitoring.

    • Utilize reversal agents for narcotic or benzodiazepine overdose.

    • Administer corticosteroids or bronchodilators for bronchospasm alleviation.

In-Depth Nursing and Collaborative Management

  • Overall Goals Include:

    • ABG values within patient's baseline range.

    • Breath sounds maintained within baseline.

    • Absence of dyspnea or normalization of breathing patterns based on the individual’s baseline.

    • Independent maintenance of airway and effective coughing capabilities with secretion clearance.

Respiratory Therapy Components

  • Oxygen Therapy: Delivery systems should be patient-tolerated and maintain PaO2 at least 55 to 60 mm Hg and SaO2 at or above 90% with minimal O2 concentration.

  • Mobilization of Secretions: Involves hydration and humidification, chest physical therapy techniques, airway suctioning, effective coughing exercises, and proper patient positioning to facilitate secretion clearance.

  • Techniques such as augmented cough and huff coughing assist in clearing central airways effectively.

Care for Hydration and Humidification

  • Ensure adequate fluid intake possibly through IV hydration.

  • Utilize humidification devices or aerosol masks for oxygen delivery.

Chest Physical Therapy

  • Techniques to improve secretion clearance include:

    • Postural drainage.

    • Percussion and vibration.

Airway Suctioning Techniques

  • May be performed nasopharyngeally, oropharyngeally, or nasotracheally, depending on necessity.

Positive Pressure Ventilation

  • Types:

    • Non-invasive Positive Pressure Ventilation (NPPV), including BIPAP and CPAP, as well as High-Flow Nasal Cannula.

Medical Supportive Therapy

  • Focuses on treating the underlying cause, maintaining adequate cardiac output and hemoglobin concentration, as well as addressing any comorbid conditions.

Drug Therapy

  • Includes bronchodilators to relieve bronchospasm, corticosteroids for airway inflammation, diuretics, nitrates if heart failure is present, IV antibiotics for pulmonary infections, and medications to manage anxiety, pain, and agitation (such as benzodiazepines and opioids).

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

  • Mortality and Clinical Manifestation: ARDS is characterized by high mortality rates and occurs as a clinical syndrome due to direct or indirect lung injury. Key pathological changes involve increased lung edema and impaired gas exchange.

Pathophysiology of ARDS

  • The condition presents as a sudden and progressive form of acute respiratory failure. The alveolar-capillary interface becomes damaged, enhancing permeability to intravascular fluid, thus leading to fluid filling in the alveoli.

  • Causes: Most commonly stems from sepsis occurring 1 to 7 days after direct lung injury or host insult.

    • Increased membrane permeability, and fluids transition from vascular space into interstitial and alveolar spaces leading to pulmonary edema and inflammatory responses, reducing lung compliance and increasing airway resistance.

IV: Results of ARDS

  • Clinical Manifestations: Include severe dyspnea and hypoxia, decreased lung compliance, diffuse pulmonary infiltrates.

    • ARDS accounts for approximately 150,000 cases annually with a 50% mortality rate.

Phases of ARDS Development

  • Injury Phase: Normal blood flow to the lungs is disrupted, leading to aggregates of platelets and the release of inflammatory mediators.

  • Exudative Phase: Alveolar cells become damaged, surfactant dysfunction occurs resulting in atelectasis, and hyaline membranes form and line the alveoli contributing to atelectasis and potential fibrosis.

  • Proliferative Phase: Repair processes begin but may lead to fibrotic changes in lung architecture.

Clinical Presentation of ARDS

  • Early Signs: Tachypnea, dyspnea, usage of accessory muscles for breathing, severe hypoxia that is unresponsive to oxygen therapy, and crackles/rhonchi.

  • Diagnostic Criteria: Must show PaO2/FIO2 ratio ≤200, bilateral infiltrates present without cardiogenic cause.

  • Late Signs: Symptoms exacerbate with fluid accumulation leading to decreased lung compliance, abnormal pulmonary function tests, and potential deteriorating respiratory distress requiring intubation and mechanical ventilation.

Recognition through Imaging

  • Chest X-Ray: May initially be normal but could show whiteout patterns indicating severe consolidation and fluid infiltrates, dramatically reducing recognizable air spaces.

Complications of ARDS Treatment

  • Ventilator-Associated Pneumonia: A significant risk alongside barotrauma and volutrauma during mechanical ventilation.

    • Prevention involves the use of smaller tidal volumes when ventilating noncompliant lungs and being cautious of higher pressures.

  • Renal Failure: Can stem from decreased renal tissue oxygenation, often exacerbated by nephrotoxic drugs.

  • Barotrauma: Rupture of overdistended alveoli during mechanical ventilation, necessitating smaller tidal volumes and permissive hypercapnia.

Nursing Assessment for ARDS

  • Key indicators include headache, chest pain, anxiety, restlessness, skin color changes, and respiration difficulties. Detectable heart rate variations, hypertension leading to hypotension, and abnormal lung sounds are vital observations.

  • Assessment Techniques: Employing bronchoalveolar lavage, serum lactate levels, evaluating lung compliance and airway resistance, regular ABG analyses, and monitoring dynamic changes on chest X-rays.

Management of ARDS

  • Supportive Treatment: Centers around oxygenation/ventilation, maintaining a stable circulation/perfusion, managing fluids/electrolytes, ensuring patient mobility/safety, maintaining skin integrity, supporting nutrition, providing comfort/pain control, and engaging in thorough psychosocial metrics as well as discharge planning.

  • Respiratory Therapy Details:

    • Utilize high-flow oxygen systems to maximize delivery and continually monitor blood oxygen levels, adjusting concentrations to maintain PaO2 > 60 mm Hg.

  • Risks of Oxygen Therapy: Oxygen toxicity rises if FiO2 exceeds 60% for longer than 48 hours, which often necessitates intubation.

  • Mechanical Ventilation Techniques: With mechanical ventilation under PEEP at 5 cm H2O, compromised lung compliance can be improved.

    • Strategically employing PEEP may maintain adequate PaO2 but requires monitoring to prevent impacts on venous return and cardiac output.

  • Positioning Strategies: Transitioning patients from supine to prone can alleviate pulmonary pressure and reduce the incidence of atelectasis due to fluid pooling. Immediate repositioning is essential for emergency health responses like CPR.

Other Positioning Strategies

  • Implement continuous lateral rotation therapy and kinetic therapy as additional supportive strategies to prevent complications.

Pharmacotherapy for ARDS

  • Include antibiotics, bronchodilators, and mucolytics to improve lung function. Ensure administration of exogenous surfactants where applicable and apply corticosteroids to manage inflammation while monitoring for the prevention of systemic inflammatory response syndrome.

  • Mechanical Ventilation Support: Focus on lung-protective strategies employing low tidal volumes (<6 mL/kg), adequate PEEP, and limiting plateau pressures to a maximum of 30 cm H2O.