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Respiratory Failure and Acute Respiratory Distress Syndrome

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University of Toronto Scarborough
Biological Sciences
Stephen Reid

Chapter 68: Respiratory Failure and Acute Respiratory Distress Syndrome ACUTE RESPIRATORY FAILURE  Respiratory failure results when gas exchange, which involves the transfer of oxygen (O ) and carbon dioxide (CO ) between the atmosphere and the blood, is inadequate. 2 2  Respiratory failure is not a disease; it is a condition that occurs as a result of one or more diseases involving the lungs or other body systems.  Respiratory failure can be classified as hypoxemic or hypercapnic. o Hypoxemic respiratory failure:  Commonly defined as a PaO <60 2m Hg when the patient is receiving an inspired O concentration >60%. 2  Disorders that interfere with O 2ransfer into the blood include pneumonia, pulmonary edema, pulmonary emboli, heart failure, shock, and alveolar injury related to inhalation of toxic gases and lung damage related to alveolar stress/ventilator-induced lung injury.  Four physiologic mechanisms may cause hypoxemia and subsequent hypoxemic respiratory failure: (1) mismatch between ventilation and perfusion, commonly referred to as V/Q mismatch; (2) shunt; (3) diffusion limitation; and (4) hypoventilation.  Hypoxemic respiratory failure frequently is caused by a combination of two or more of these mechanisms. o Hypercapnic respiratory failure:  Also referred to as ventilatory failure since the primary problem is insufficient CO 2emoval.  Commonly defined as a PaCO >45 mm Hg in combination with acidemia 2 (arterial pH <7.35).  Disorders that compromise CO rem2val include drug overdoses with central nervous system (CNS) depressants, neuromuscular diseases, acute asthma, and trauma or diseases involving the spinal cord and its role in lung ventilation.  Hypercapnic respiratory failure results from an imbalance between ventilatory supply and ventilatory demand. Ventilatory supply is the maximum ventilation that the patient can sustain without developing respiratory muscle fatigue, and ventilatory demand is the amount of ventilation needed to keep the PaCO wi2hin normal limits.  Though PaO an2 PaCO deter2ine the definition of respiratory failure, the major threat of respiratory failure is the inability of the lungs to meet the oxygen demands of the tissues. This may occur as a result of inadequate tissue O2delivery or because the tissues are unable to use the O2delivered to them.  Manifestations of respiratory failure: o Are related to the extent of change in PaO or2PaCO , th2 rapidity of change (acute versus chronic), and the ability to compensate to overcome this change. o Clinical manifestations are variable and it is important to monitor trends in ABGs and/or pulse oximetry to evaluate the extent of change. o A change in mental status is frequently the initial indication of respiratory failure. o Tachycardia and mild hypertension can also be early signs of respiratory failure. o A severe morning headache may suggest that hypercapnia may have occurred during the night, increasing cerebral blood flow by vasodilation and causing a morning headache. o Cyanosis is an unreliable indicator of hypoxemia and is a late sign of respiratory failure because it does not occur until hypoxemia is severe (PaO ≤25 mm Hg). o Hypoxemia occurs when the amount of O in arte2ial blood is less than the normal value, and hypoxia occurs when the PaO fall2 sufficiently to cause signs and symptoms of inadequate oxygenation. o Hypoxemia can lead to hypoxia if not corrected, and if hypoxia or hypoxemia is severe, the cells shift from aerobic to anaerobic metabolism. Clinical Manifestations  Clinical findings include a rapid, shallow breathing pattern or a respiratory rate that is slower than normal. A change from a rapid rate to a slower rate in a patient in acute respiratory distress such as that seen with acute asthma suggests extreme progression of respiratory muscle fatigue and increased probability of respiratory arrest.  The position that the patient assumes is an indication of the effort associated with breathing. o The patient may be able to lie down (mild distress), be able to lie down but prefer to sit (moderate distress), or be unable to breathe unless sitting upright (severe distress). The patient may require pillows to breathe when attempting to lie flat and this is termed orthopnea. o A common position is to sit with the arms propped on the overbed table.  Pursed-lip breathing may be used.  The patient may speak in sentences (mild or no distress), phrases (moderate distress), or words (severe distress).  There may be a change in the inspiratory (I) to expiratory (E) ratio. Normally, the I:E ratio is 1:2, but in patients in respiratory distress, the ratio may increase to 1:3 or 1:4.  There may be retractions of the intercostal spaces or the supraclavicular area and use of the accessory muscles during inspiration or expiration. Use of the accessory muscles signifies moderate distress.  Paradoxic breathing indicates severe distress and results from maximal use of the accessory muscles of respiration.  Breath sounds: o Crackles and rhonchi may indicate pulmonary edema and COPD. o Absent or diminished breath sounds may indicate atelectasis or pleural effusion. o The presence of bronchial breath sounds over the lung periphery often results from lung consolidation that is seen with pneumonia. o A pleural friction rub may also be heard in the presence of pneumonia that has involved the pleura. Diagnostic Studies  ABGs are done to obtain oxygenation (PaO ) and2ventilation (PaCO ) statu2, as well as information related to acid-base balance.  A chest x-ray is done to help identify possible causes of respiratory failure.  Other diagnostic studies include a complete blood cell count, serum electrolytes, urinalysis, and electrocardiogram. o Cultures of the sputum and blood are obtained as necessary to determine sources of possible infection. o For the patient in severe respiratory failure requiring endotracheal intubation, end- tidal CO 2EtCO ) 2ay be used to assess tube placement within the trachea immediately following intubation. o In severe respiratory failure, a pulmonary artery catheter may be inserted to measure heart pressures and cardiac output, as well as mixed venous oxygen saturation (SvO 2. Nursing and Collaborative Management: Acute Respiratory Failure  The overall goals for the patient in acute respiratory failure include: (1) ABG values within the patient’s baseline, (2) breath sounds within the patient’s baseline, (3) no dyspnea or breathing patterns within the patient’s baseline, and (4) effective cough and ability to clear secretions.  Prevention involves a thorough physical assessment and history to identify the patient at risk for respiratory failure and, then, the initiation of appropriate nursing interventions (coughing, deep breathing, incentive spirometry, and ambulation as appropriate).  The major goals of care for acute respiratory failure include maintaining adequate oxygenation and ventilation. o The primary goal of O therapy is to correct hypoxemia. 2 o The type of O de2ivery system chosen for the patient in acute respiratory failure should (1) be tolerated by the patient, and (2) maintain PaO a2 55 to 60 mm Hg or more and SaO at290% or more at the lowest O conce2tration possible. o Additional risks of O th2rapy are specific to the patient with chronic hypercapnia as this may blunt the response of chemoreceptors in the medulla, a condition termed CO n2rcosis. o Retained pulmonary secretions may cause or exacerbate acute respiratory failure and can be mobilized through effective coughing, adequate hydration and humidification, chest physical therapy (chest physiotherapy), and tracheal suctioning. o If secretions are obstructing the airway, the patient should be encouraged to cough.  Augmented coughing is performed by placing the palm of the hand or hands on the abdomen below the xiphoid process. As the patient ends a deep inspiration and begins the expiration, the hands should be moved forcefully downward, increasing abdominal pressure and facilitating the cough. This measure helps increase expiratory flow and thereby facilitates secretion clearance.  Huff coughing is a series of coughs performed while saying the word “huff.” The huff cough is effective in clearing only the central airways, but it may assist in moving secretions upward.  The staged cough is performed by having the patient sit in a chair, breathe three or four times in and out through the mouth, and cough while bending forward and pressing a pillow inward against the diaphragm. o Positioning the patient either by elevating the head of the bed at least 45 degrees or by using a reclining chair or chair bed may help maximize thoracic expansion, thereby decreasing dyspnea and improving secretion mobilization. o Lateral or side-lying positioning may be used in patients with disease involving only one lung and this position is termed good lung down. o Adequate fluid intake (2 to 3 L/day) is necessary to keep secretions thin and easy to expel.  Assessment for signs of fluid overload (e.g., crackles, dyspnea, increased central venous pressure) at regular intervals is paramount.  Aerosols of sterile normal saline, administered by a nebulizer, may be used to liquefy secretions.  Mucolytic agents such as nebulized acetylcysteine mixed with a bronchodilator may be used to thin secretions but, as a side effect, may also cause airway erythema and bronchospasm. o Chest physical therapy is indicated in patients who produce more than 30 ml of sputum per day or have evidence of severe atelectasis or pulmonary infiltrates. o If the patient is unable to expectorate secretions, nasopharyngeal, oropharyngeal, or nasotracheal suctioning is indicated.  Suctioning through an artificial airway, such as endotracheal or tracheostomy tubes, may also be performed.  A mini-tracheostomy (or mini-trach) may be used to suction patients who have difficulty mobilizing secretions. Contraindications for a mini-trach include an absent gag reflex, history of aspiration, and the need for long-term mechanical ventilation. o If intensive measures fail to improve ventilation and oxygenation, positive pressure ventilation (PPV) may be provided invasively through orotracheal or nasotracheal intubation or noninvasively through a nasal or face mask. o Noninvasive PPV may be used as a treatment for patients with acute or chronic respiratory failure.  With NIPPV it is possible to decrease the work of breathing without the need for endotracheal intubation.  Bilevel positive airway pressure (BiPAP) is a form of NIPPV in which different positive pressure levels are set for inspiration and expiration.  Continuous positive airway pressure (CPAP) is another form of NIPPV in which a constant positive pressure is delivered to the airway during inspiration and expiration.  NIPPV is most useful in managing chronic respiratory failure in patients with chest wall and neuromuscular disease.  Goals of drug therapy for patients in acute respiratory failure include (1) relief of bronchospasm, (2) reduction of airway inflammation and pulmonary congestion, (3) treatment of pulmonary infection, and (4) reduction of severe anxiety and restlessness. o Short-acting bronchodilators, such as metaproterenol and albuterol, are frequently administered to reverse bronchospasm using either a handheld
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