Acute Respiratory Distress Syndrome (ARDS)

Acute Respiratory Distress Syndrome (ARDS)

• ARDS is an acute event that typically develops over 4 to 48 hours.
• It is noncardiogenic pulmonary edema due to alveolar injury from an inflammatory process that can be pulmonary or systemic.
• The pathogenesis and pathophysiology begins with acute lung injury, triggering an inflammatory-immune response.
• Mediators are released leading to increased capillary membrane permeability and decreased airway diameter
• Alveolar flooding with loss of surfactant occurs, with increased airway resistance and decreased lung compliance.
• This increases the work of breathing, leading to alveolar hypoventilation and intrapulmonary shunting.
• Alveolar collapse happens including pulmonary vasoconstriction, microemboli formation, and pulmonary hypertension occurs
• This causes alveolar dead space and decreased cardiac output, resulting in hypoxemia.
• Risk factors include pneumonia and ventilator-induced lung injury, especially from PEEP usage.
• The resulting pathophysiology is a diffuse alveolar damage.
• Inflammatory triggers release cellular and chemical mediators, causing injury to the alveolar capillary membrane and structural lung damage.
• Ventilation-perfusion mismatching occurs which causes alveoli to collapse due to inflammatory infiltrate, blood, fluid, and surfactant dysfunction.
• Small airways narrow due to interstitial fluid and bronchial obstruction.
• Lung compliance decreases significantly, reducing functional residual capacity and causing severe hypoxemia.
• Blood is pumped through nonventilated, nonfunctioning areas of the lung, causing shunting.

Assessment & Diagnostic Tests

• Plasma brain natriuretic peptide (BNP) levels, echocardiography, and pulmonary artery catheterization are included for potential ARDS.
• BNP levels are helpful in distinguishing ARDS from hemodynamic pulmonary edema.
• ABG monitoring helps to identify respiratory failure.
• Chest x-ray findings are similar to cardiogenic pulmonary edema, showing bilateral infiltrates that worsen quickly.
• Transthoracic echocardiography may be used if the BNP is not conclusive.
• Pulmonary artery catheterization is a definitive method to distinguish between hemodynamic (heart failure) and permeability pulmonary edema (ARDS).
• Clinical and research modalities include ventilation parameters, imaging, gas exchange, coagulation biomarkers and inflammatory biomarkers

Clinical Manifestations

• Intercostal retractions and crackles may be present when fluid leaks into the alveolar interstitial space.
• Closely resembles severe hemodynamic pulmonary edema.
• The acute phase involves rapid onset of severe dyspnea, typically 12 to 48 hours after the initial event.
• Arterial hypoxemia (PaO2 in ABG) does not respond to supplemental oxygen.
• Acute lung injury progresses into fibrosing alveolitis with persistent, severe hypoxemia.
• Increased alveolar dead space and decreased pulmonary compliance ("stiff lungs," difficult to ventilate) is expected.
• A patient is considered in recovery if hypoxemia gradually resolves, chest x-ray improves, and lungs become more compliant.

Medical Management

• Identification and treatment of initial conditions is key in medical management
• Aggressive, supportive care is also provided to compensate for severe respiratory dysfunction.
• Interventions will include intubation and mechanical ventilation, circulatory support, adequate fluid volume, and nutritional support.
• Supplemental oxygen is less effective for initial hypoxemia, intubation and mechanical ventilation are instituted.
• Oxygen concentrations, ventilator settings, and modes are determined by the status of the patient and are based on arterial blood gas analysis, pulse oximetry, and bedside pulmonary function testing.
• PEEP is employed to improve oxygenation, increase functional residual capacity, and reverse alveolar collapse by maintaining open alveoli. This improves arterial oxygenation and lessens the severity of ventilation-perfusion imbalance.
• PEEP may reduce FiO2 requirements, and the goal is to achieve a PaO2 greater than 60 mm Hg or an oxygen saturation level of more than 90% at the lowest possible FiO2.

Monitoring

• Monitor for systemic hypotension which may occur in ARDS due to hypovolemia from fluid leakage into interstitial spaces and depressed cardiac output from high PEEP.
• Treatment for hypovolemia includes a fluid challenge, closely monitor for further overload.
• Inotropic or vasopressor agents may be required.
• Pulmonary artery pressure catheters monitor fluid status and the potentially severe, progressive pulmonary hypertension in ARDS.
• Extracorporeal life support replaces endogenous alveolar gaseous exchange, extracorporeal gas exchange (ECMO) or extracorporeal carbon dioxide removal, reduces ventilatory settings, reducing the risk of ventilator-induced lung injury
• ECMO is a limited and costly resource, it carries complications like bleeding, vascular damage, and interhospital transfer risks.

Pharmacologic and Nutritional Therapies

• ARDS has no specific pharmacologic treatments, only supportive care.
• Pharmacologic treatments may include surfactant replacement therapy, pulmonary antihypertensive agents, and antisepsis agents.
• Patients with ARDS need 35 to 45 kcal/kg/day to meet caloric requirements.
• Enteral feeding is the first consideration, with parenteral nutrition also required at times.

Nursing Management

• Close monitoring in the intensive care unit is necessary, patient conditions can quickly become life-threatening.
• Respiratory support includes oxygen therapy, nebulizer therapy, chest physiotherapy, endotracheal intubation or tracheostomy, mechanical ventilation, suctioning, and bronchoscopy.
• Frequent Assessment: Assess vital signs, temperature, BP, P, RR, SpO2 to determine the effectiveness of treatment
• Positioning the patient in High Fowler's, turning left or right, and can improve ventilation and perfusion and enhance secretion drainage.
• Changes in position: Closely monitor the patient for deterioration in oxygenation with changes in position and prone position may sometimes improve oxygenation.
• Promote bedrest: Bed rest may reduce oxygen consumption and oxygen needs, and providing assistance in self-care activities is also necessary if they have limited energy Psychological Support: Offer support to patients with anxiety, may be agitated, and increased dyspnea to limit anxiety to prevent increases in oxygen consumption.

Management of Intubation and Mechanical Ventilation with PEEP

• PEEP may cause anxiety which causes patients to "fight" the ventilator, assist by providing psychological support
• Address underlying problems like pain, a new pneumothorax etc
• Check for tube blockage by kinking or retained secretions
• Monitor oxygenation and ventilation levels.

Sedatives

• They may be given to decrease oxygen demand and anxiety.
• Typical medications can include lorazepam, midzolam, dexmedetomidine, propofol or barbiturates.

Paralytics

• Paralytic agents may be administered to paralyze the patient, especially with PEEP, agents may be used to help the patient to be ventilated easier.
• Neuromuscular blocking agents include pancuronium, vecuronium, atracurium, and rocuronium.
• When administering paralytics, they patient will appear to be unconscious, loses motor function, is unable to verbally communicate or visually communicate
• The patient will be awake, so reassure them medications are temporary
• Always administer with adequate sedation and pain management.
• Paralytics are very risky medications because they require full support to use

While Using Paralytic Agents

• Check the ventilator to ensure all connections are secure.
• Monitor vital signs, especially RR and SpO2 because the patient can experience apnea.
• Provide eye care as blinking will be suppressed.
• Prevent DVT as the patient will essentially be immobilized.
• Perform routine passive ROM exercise and skin care to prevent breakdown
• Pain management

Respiratory Failure (RF)

• Respiratory failure (RF) isn't a primary illness but a consequence of underlying issues interfering with the ability to breathe.
• The lungs inability to deliver Oxygen into the blood, and it's inability to eliminate the blood of CO2.
• Oxygenation failure occurs, referring to an inability to get oxygen, acute cause is commonly pneumonia while chronic is pulmonary fibrosis
• Ventilatory failure, which refers to not being able to eliminate CO2, with acute cause of pulmonary fibrosis, and chronic being a neuromuscular disease.

Classifications of Respiratory Failure

• Acute respiratory failure is a decrease in arterial oxygen tension (PaO2) to less than 60 mm Hg (hypoxemia), accompanied by an increase in arterial carbon dioxide tension (PaCO2) to greater than 50 mm Hg (hypercapnia), and an arterial pH of less than 7.35.
• Type I respiratory failure involves low oxygen, and normal or low carbon dioxide levels.
• Type II respiratory failure involves low oxygen, with HIGH carbon dioxide.

Chronic respiratory failure

• Deterioration of the lungs exchange function over a long period of time, often after an episode of acute respiratory failure.
• Lack of severe symptoms + chronic respiratory acidosis can indicate it being a chronic respiratory failure.
• Patients with chronic respiratory failure can tolerate this development.
• Can quickly shift to acute failure if they develop things like COPD, exacerbation or infection with worsening exchange

Chronic Respiratory Failure

• Two common causes of chronic respiratory failure are COPD, and various neuromuscular diseases.
• Results in a gradually worsening hypoxia and hypercapnia with increasing tolerance
• Patients with COPD can also develop infections or exacerbation of their condition in addition to their existing respiratory failure

Pathophysiology acute failure

• Impaired ventilation or perfusion mechanisms in the lungs.
• Ventilatory failure mechanisms include:
  • Central Nervous problems like drug overdose, head trauma and sleep apnea
  • Neuromuscular dysfunction like myasthenia gravis
  • Musculoskeletal dysfunction like chest trauma, kypho, malnutrition
• Oxygen failure mechanisms leading to acute RF:
  • pneumonia
  • distress syndrome
  • heart failure
  • COPD
  • pulmonary failure
  • restrictive lung disease
• Anesthetic agents can also interfere with breathing

Acute Respiratory Failure - Types

• Type 1 (Hypoxemic): PO2 < 60 mmHg on room air and it usually seen in patients with acute pulmonary edema or acute lung injury
• Type 2 (Hypercapnic/ Ventilatory): PCO2 > 50 mmHg (if not a chronic CO2 retainer). This can be seen in patients with breathing issues due to decreased O2 or decreased ventilation
• Type 3 (Peri-operative): Generally subset of type 1 where breathing problems can occur post operation
• Type 4 (Shock): Occurs due to secondary cardiovascular issues/instability

Respiratory Failure (Type 1)

• There are multiple potential factors that can cause "Type 1" failure
• Shunting, where blood passes parts of systems but no oxygen is happening, or lung hemorrhaging happening
• Intracardia: genetic related defects that creates right to left shunt
• Intrapulmonary: AVM formation, pnemonia, edema, etc

Respiratory Failure (Type 1) - Diffusion limitation

• Small cells exist between the capillary and lungs.
• Limit due to fluid in lungs, 100% o2 can help fix this
• Severe underlying problems tend to be the cause, pulmonary function test should be done to ensure this is the case before other procedures
• Severe problems can include, recurrent PE, pulmonary fibrosis, or exhaustion induced hypoxemia

Therapies

• Oxygen therapy
• Diuresis
• PEEP
• Ventilation or pressure monitoring

Respiratory Failure-Clinical Manifestations

• Early signs of respiratory failure include restlessness, fatigue, headache, dyspnea, tachycardia, and increased blood pressure.
• Progression of hypoxemia leads to confusion, lethargy, tachycardia, tachypnea, central cyanosis, diaphoresis, and ultimately respiratory arrest.

Respiratory Failure Clinical Manifestations Chart:

• CNS/ Generally: Headache, visual disturbances, anxiety, confusion, memory loss, sweaty, clammy, fatigue, cyanotic
• Pulmonary: Cough, chest pains, sputum production, stridor, dyspnea
• Cardiac: Fast HR/pulse, chest pain
• SpO2/ABG: <90%, respiratory acidosis
• Mental status: Confusion, agitation or convulsions, poor GCS
• Breathing pattern: Observe chest movements, Purse-lip breathing prolonged expiratory phase, Use of accessory muscle, nasal flaring, retraction intercostal muscle
• Talking style: Interrupted speech Answer with nonverbal communication
• Position: High Fowler's position

Management Principles for Respiratory Failure

– To prevent progression of the underlying diseases – To reverse and prevent hypoxemia – To control PaCO2 and respiratory acidosis – To closely monitor CNS and CVS – Intubation can restore ventilation

Acute Respiratory Failure – Medical Management

• Objectives of treatment are to correct the underlying cause and to restore adequate gas exchange in the lung.
• Interventions:
  • Urgent resuscitation
  • Oxygenation
  • Airway control
  • Bronchodilators/ Steroids
  • Stabilization of the circulation
  • Ventilator management
  • Ongoing investigation
  • A therapeutic plan for the diagnosis is needed
• Intubation and mechanical ventilation may be required to maintain adequate ventilation and oxygenation while the underlying cause is corrected.

Respiratory Failure Assessment:

– Accurate throughout history – Fever check and cough check for sputum production – Onset of SOB or chest pain for PE – Physical examination: respiratory system

Respiratory Failure Assessments:

• Spirometry: Tidal Volume • ABG analysis: PaO2, Paco2, pH, • CBC: RBC, WBC, Platelet • chest x-ray, • sputum/blood analysis, • Serum electrolytes, • Urinalysis • ECG: identify arrhythmias, ischemia, ventricular dysfunction • Lung function test: identify obstruction/ restriction; assess TV & VC, and monitor PEF rate • lung scan

Nursing Management Acute Failure

• Check LOC and treat the underlying issues related to it
• Assess vitals signs
• Assess ABG and report
• Assess for accessory function
• Assess the breathing

Nursing Management of Acute Respiratory Failure

– Assist in and maintain intubation. – Ensure open ventilation and perform suctioning – Provide skin care: bed bath, rotating properly – Provide mouth care and do ROM to strengthen muscles

Respiratory Failure Medical Interventions

– Support Airways – O2 – Breathe deep and cough – Suctioning – Medications – Relief – Relax patient with pain killers – Chest Phsyio

Respiratory Failure- Further interventions

• Treat patients for conditions that can cause failure and maintain cardio and hemo pressure and ensure nutritional status.

• Help Non invasive function if its not bad
• Try and wean off
• If it gets worse, go to ICU and Invasive control

Respiratory Failure: Education

• Stop smoking
• Vaccinate against influenza and other problems
• Regular exercises/ consults
• Medication compliance