Acute Respiratory Failure PDF

## Acute Respiratory Failure ### Definition of Acute respiratory failure - A sudden and life-threatening deterioration in pulmonary gas exchange, resulting in carbon dioxide retention and inadequate oxygenation. - It is a major cause of morbidity and mortality in the intensive care units. ### Acu...

## Acute Respiratory Failure ### Definition of Acute respiratory failure - A sudden and life-threatening deterioration in pulmonary gas exchange, resulting in carbon dioxide retention and inadequate oxygenation. - It is a major cause of morbidity and mortality in the intensive care units. ### Acute respiratory failure (ARF) is defined as: - A fall in arterial oxygen tension (PaO2) to less than 50 mm Hg (hypoxemia) and - A rise in arterial carbon dioxide tension (PaCO2) to greater than 50 mm Hg (hypercapnia), with an arterial pH of less than 7.35. - In ARF, the ventilation and perfusion mechanisms in the lung are impaired. ### Classification of Acute respiratory failure #### A) Acute hypoxemic respiratory failure (type I): - Type I failure is a direct defect in oxygenation. #### B) Acute hypercapnic respiratory failure (type II): - Type II failure is a direct defect in ventilation. #### C) Combined hypoxemic and hypercapnic respiratory failure (type I and type II). ## Types of Respiratory Failure ### **Acute Hypoxemic Respiratory Failure (Type I)** - PH→↑ - Paco2↓-PaCO2 - Alkaloses - Type I is the result of abnormal oxygen transport secondary to pulmonary parenchymal disease, with increased alveolar ventilation resulting in a low PaCO2. ### **Acute Hypercapnic Respiratory Failure (Type II)** - PH↓ - PaCO2 ↑-PaO2 ↓ - Acidosis - Type II is the result of inadequate alveolar ventilation and is characterized by marked elevation of carbon dioxide with relative preservation of oxygenation. - Hypoxemia results from reduced alveolar pressure of oxygen (PaO2) and is proportionate to hypercapnia. ## Pathophysiology of Acute respiratory failure - Hypoxemia is the result of impaired gas exchange and is the hallmark of acute respiratory failure. - Hypercapnia may be present, depending on the underlying cause of the problem. - The main causes of hypoxemia are: - Alveolar hypoventilation - Ventilation/perfusion (V/Q) mismatching - Intrapulmonary shunting - Diffusion impairment ## Type II Respiratory Failure - Type II respiratory failure usually results from alveolar hypoventilation, which may or may not be accompanied by V/Q mismatching and intrapulmonary shunting. ### A) Alveolar Hypoventilation - Alveolar hypoventilation occurs when the amount of oxygen being brought into the alveoli is insufficient to meet the metabolic needs of the body. - This can be the result of increasing metabolic oxygen needs or decreasing ventilation. - Hypoxemia caused by alveolar hypoventilation is associated with hypercapnia and commonly results from extrapulmonary disorders. ### B) Ventilation/Perfusion (V/Q) Mismatching - V/Q mismatching occurs when ventilation and blood flow are mismatched in various regions of the lung in excess of what is normal. - Blood passes through alveoli that are under ventilated for the given amount of perfusion, leaving these areas with a lower-than-normal amount of oxygen. - V/Q mismatching is the most common cause of hypoxemia and is usually the result of alveoli that are partially collapsed or partially filled with fluid. ### C) Intrapulmonary Shunting - Occurs when blood reaches the arterial system without participating in gas exchange. - The extreme form of V/Q mismatching, intrapulmonary shunting occurs when blood reaches the arterial system without participating in gas exchange. - The mixing of deoxygenated (shunted) blood and oxygenated blood lowers the average level of oxygen present in the blood. - Intrapulmonary shunting occurs when blood passes through a portion of a lung that is not ventilated - This may be the result of (1) alveolar collapse secondary to atelectasis or (2) alveolar flooding with pus, blood, or fluid. - Hypercapnia generally does not develop unless the shunt is excessive (> 60%). - When compared with V/Q mismatch, hypoxemia produced by shunt is difficult to correct by oxygen administration. - The distinction between V/Q mismatch and shunt can be made by assessing the response to oxygen supplementation or calculating the shunt fraction following inhalation of 100% oxygen. - In most patients with hypoxemic respiratory failure, these 2 mechanisms coexist. ### D) Diffusion impairment - Another rare but potential cause of impaired oxygenation in the critically ill patient is diffusion defect. - Gas exchange between the alveoli and the pulmonary capillaries occurs across the alveolar capillary membrane, which is normally a thin structure, freely permeable to carbon dioxide and oxygen. - Gas exchange is compromised by a process that thickens or destroys the membrane e.g. pulmonary fibrosis, ARDS. - A classic sign of diffusion limitation is hypoxemia during exercise but not at rest. ## Causes of Acute Respiratory Failure: ### A. Intrinsic Lung/Airway Diseases - Large Airway Obstruction: Foreign bodies, Obstructive sleep apnea - Bronchial Diseases: Chronic bronchitis, acute bronchiolitis, Asthma - Parenchymal Diseases: Pulmonary emphysema, severe pneumonia - Acute lung injury from various causes (acute respiratory distress syndrome) - Cardiovascular Disease: Cardiac pulmonaryedema ### B. Extra pulmonary Disorders - Diseases of the Pleura and the Chest Wall: Pneumothorax, Pleural effusion, Obesity, Traumatic injury to the chest wall, flail chest. - Disorders of the Respiratory Muscles and the Neuromuscular Junction: muscular dystrophies, Botulism, Muscle-paralyzing drugs. - Disorders of the Peripheral Nerves and Spinal Cord: Poliomyelitis, Guillain-Barré syndrome, Spinal cord trauma - Disorders of the Central Nervous System: Sedative and narcotic drug overdose, Head trauma, cerebral hypoxia, Cerebrovascular accident, Sleep apnea syndrome. ## Assessment of Acute Respiratory Failure: ### 1 History: - A complete medical and social history should be obtained from the patient or a family member to determine the patient's baseline respiratory status on admission. ### History and Symptoms Profile #### Pulmonary Symptoms - Dyspnea - Sputum - Cough - Hemoptysis - Wheeze - Chest pain (e.g., pleuritic) - Orthopnea, paroxysmal nocturnal apnea - Snoring, sleep disturbances, daytime drowsiness - Sinus problems #### Risk Factors related to respiratory system - Smoking history: type (cigarettes, cigar, pipe); amount per day; duration (years) - Childhood respiratory diseases/symptoms - Family history of respiratory disease - Environmental exposures: location (e.g., home, work, region); type (e.g., asbestos, silica, gases, aerosols); duration - Obesity or nutritional depletion. - Previous History: Pulmonary problems - Immunizations - Number of hospitalizations. #### Extrapulmonary Symptoms - Night sweats - Headaches on awakening - Weight changes - Fluid retention - Nasal stuffiness, discharge - Fatigue ### 2 Physical Findings: #### Hypoxemia: - The classic symptoms are dyspnea, cyanosis, restlessness, confusion, anxiety, delirium, tachypnea, tachycardia, hypertension, cardiac dysrhythmia and tremor. - Peripheral cyanosis of the skin, lips, or nail beds suggests the presence of profound arterial hypoxemia, usually with a PaO2 less than 10 mm Hg. #### Hypercapnia: - The cardinal symptoms of hypercapnia are dyspnea and headache. - Other clinical manifestations include peripheral and conjunctival hyperemia, hypertension, tachycardia, tachypnea, impaired consciousness, papilledema, and asterixis. - Uncorrected carbon dioxide narcosis leads to diminished alertness, disorientation, increased intracranial pressure, and ultimately unconsciousness. - Other physical findings on examination may include use of accessory muscles of respiration, intercostal or supraclavicular retraction, and paradoxical abdominal movement if diaphragmatic weakness or fatigue is present. ### 3 Diagnostic Studies: - Because the signs and symptoms of acute respiratory failure are nonspecific and insensitive, the physician must request an ABG analysis to determine the exact level of PaO2, PaCO2, and blood pH in cases of suspected (ARF). Only determination of the blood gases and pH can confirm the diagnosis. - Other diagnostic tests necessary to determine the etiology of acute hypoxemic respiratory failure include: - Serum electrolytes - Urine analysis - ECG - CT - Sputum examination - Bronchogram - CBC - Chest radiography - Pulmonary function test - Bronchoscopy - Echocardiography - Pulmonary angiography ## Management of Acute Respiratory Failure - Treatment of acute respiratory failure focus on immediate intervention to correct or compensate for the gas exchange abnormality and identify the cause. - Therapy is directed toward correcting the cause and alleviating the hypoxia and hypercapnia. - If alveolar ventilation is inadequate to maintain PaO2 or PaCO2 levels related to respiratory or neurological failure, endotracheal intubation and mechanical ventilation may be lifesaving. - The initial assessment and the decision to initiate mechanical ventilation should be performed rapidly to minimize the life-threatening. Complications associated with extended hypoxemia (t.g., cardiac dysrhythmias, anoxic encephalopathy). ## Nursing diagnosis for patient with acute respiratory failure 1. Impaired Gas Exchange related to alveolar hypoventilation. 2. Impaired Gas Exchange related to ventilation/ perfusion mismatching or Intrapulmonary shunting. 3. Ineffective airway clearance related to excessive secretion or abnormal viscosity of mucus. 4. Ineffective Breathing Pattern related to musculoskeletal fatigue or neuromuscular impairment. 5. Imbalanced Nutrition: Less than Body Requirements related to lack of exogenous Nutrients or increased metabolic demand. 6. Impaired Verbal Communication 7. High risk for Aspiration ## Nursing interventions for patient with acute respiratory failure: 1. **Monitoring**: Initiate continuous pulse oximetry or monitor SpO2 every hour. Assess sputum for color, consistency, and amount. Asses for clinical manifestations of pneumonia. 2. **Positioning**: - Place patient in semi-Fowler's position or in a chair at bedside for best use of ventilatory muscles and to facilitate diaphragmatic descent. - Position patient to optimize ventilation/perfusion matching. For patient with unilateral lung disease, position with the good lung down because gravity will improve perfusion to this area, and this will best match ventilation with perfusion. - For patient with bilateral lung disease, position with right lung down because right lung is larger than left lung and affords a greater area for ventilation and perfusion, or Change position every 2 hours, favoring positions that improve oxygenation. - Avoid any position that seriously compromises oxygenation status. 3. **Oxygenation**: - Administer supplemental oxygen via appropriate oxygen delivery device-to increase driving pressure of oxygen in alveoli to maintain SpO2 greater than 90%. - If supplemental oxygen alone is not effective, administer continuous positive airway pressure (CPAP) or mechanical ventilation with positive end-expiratory pressure (PEEP) to open collapsed alveoli and increase surface area for gas exchange. 4. **Prevent hypoventilation**: - Position patient in high-Fowler's position or semi-Fowler's position to promote diaphragmatic descent and maximal inhalation. - Assist with deep-breathing exercises and incentive spirometry. 5. **Assist physician to initiation of mechanical Ventilation as indicated.** 6. **Perform procedures only as needed and provide adequate rest and recovery time in between to prevent desaturation.** 7. **Chest physiotherapy**: - Provide for maximal thoracic expansion by repositioning, deep breathing, splinting. - Maintain adequate hydration by administering oral and intravenous fluids (as ordered) to thin secretions and facilitate airway clearance. - Provide humidification to airways via oxygen-delivery device or artificial airway to thin secretions and facilitate airway clearance. - Administer inhalation therapy every 4 hours to facilitate expectoration of sputum. - Assist with directed coughing exercises to facilitate expectoration of secretions. Suction as necessary to assist with secretion removal. - Consider chest physiotherapy (postural drainage and chest percussion) 3 to 4 times per day in a patient with large amounts of sputum to assist with expulsion of retained secretions. - Allow rest periods between coughing sessions, chest physiotherapy, suctioning, or any other demanding activities to promote energy conservation. 8. **Nutrition**: - Collaborate with physician and dietitian to ensure that at least 50% of diet's non-protein caloric source is in form of fat versus carbohydrates to prevent excess carbon dioxide production. - Monitor patient's caloric intake and weight daily to ensure adequacy of nutritional interventions. - Monitor patient for signs of nutritional deficiencies to facilitate evaluation of extent of nutritional deficit. - Provide patient with oral care before eating to ensure optimal consumption of diet. - Assessment of parenteral and enteral nutrition as needed. 9. **Pain**: Analgesics, to treat pain if present. Treat pain if present, to prevent hypoventilation. Pain management to avoid hypoventilation and atelectasis. 10. **Communication**: Assess patient's ability to comprehend, speak, read, and write. Maintain an uncluttered environment and decrease external distractions that could hinder communication. 11. **Collaborate with physician regarding administration of drugs.** - Sedatives, to decrease ventilator asynchrony. - Neuromuscular blocking agents, to prevent ventilator asynchrony and decrease oxygen demand. - Bronchodilators, to treat of prevent bronchospasm and facilitate expectoration of mucus. - Mucolytics and expectorants, to enhance mobilization and removal of secretions. - Antibiotics, to treat infection. - Reversal agents (opiate antagonists, e.g., naloxone) are used in the case of impaired central respiratory drive, and inhaled bronchodilators and systemic corticosteroids are used in the case of underlying bronchospasm.