Acute pulmonary failure
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Acute pulmonary failure occurs when abnormal gas exchange results from dysfunction of the respiratory system that threatens life. Risk factors include smoking, infections, lung disease, and neurological or muscular disorders. Symptoms include altered mental status, cyanosis, respiratory distress, and abnormal blood gases. Treatment focuses on stabilizing the patient, treating the underlying cause, and supporting respiratory function through oxygen, ventilation, suctioning, and positioning. Nursing care aims to maintain the airway, enhance gas exchange and nutrition, prevent complications, and provide education to the patient.
Acute pulmonary failure
- 1. Acute pulmonary Failure Definition Acute respiratory failure occurs when dysfunction of the respiratory system results in abnormal gas exchange that is potentially life-threatening. Each element of this definition is important to understand. The term acute implies a relatively sudden onset (from hours to days) and a substantial change from the patient’s baseline condition. Dysfunction of the respiratory system indicates that the abnormal gas exchange may be caused by abnormalities in any element of the respiratory system (e.g., a central nervous system abnormality affecting the regulation of breathing or a musculoskeletal thoracic abnormality affecting ventilation; Chapter 83), in addition to abnormalities of the lung itself. The term respiration refers, in a broad sense, to the delivery of oxygen (O2) to metabolically active tissues for energy usage and the removal of carbon dioxide (CO2) from these tissues (Table 104-1). Respiratory failure is a failure of the process of delivering O2 to the tissues and/or removing CO2 from the tissues. Abnormalities in the periphery (e.g., cyanide poisoning, pathologic distribution of organ blood flow in sepsis) can also lead to tissue hypoxia; although these conditions represent forms of respiratory failure in the broadest terms, this chapter focuses on respiratory failure resulting from dysfunction of the lungs, chest wall, and control of respiration. Risk Factors Strong Factor cigarette smoking young age old age pulmonary infection chronic lung disease airway obstruction alveolar abnormalities perfusion abnormalities cardiac failure peripheral nerve abnormalities muscle system abnormalities opiate and sedative medications toxic fumes and gases traumatic spinal injury traumatic thoracic injury central nervous system disorders acute vascular occlusion pneumothorax hypercoagulable states
- 2. PA Clinical Signs and Symptoms of Acute Respiratory Failure Clinical manifestations of respiratory distress reflect signs and symptoms of hypoxemia, hypercapnia, or the increased work of breathing necessary. These include Altered mental status (agitation, somnolence) Peripheral or central cyanosis or decreased oxygen saturation on pulse oximetry Manifestations of a "stress response" including tachycardia, hypertension, and diaphoresis Evidence of increased respiratory work of breathing including accessory muscle use, nasal flaring, intercostal indrawing, suprasternal or supraclavicular retractions, tachypnea Evidence of diaphragmatic fatigue (abdominal paradox) Abnormal arterial blood gas results ARF : CXR Findings Clear CXR with hypoxemia and normocapnia.- Pulmonary embolus, R to L shunt, Shock Diffusely white (opacified) CXR with hypoxemia and normocapnia - ARDS, NCPE, CHF, pulmonary fibrosis Localized infiltrate - pneumonia, atelectasis, infarct Clear CXR with hypercapnia - COPD, asthma, overdose, neuromuscular weakness Management of Acute Respiratory Failure The management of acute respiratory failure can be divided into an urgent resuscitation phase followed by a phase of ongoing care. The goal of the urgent resuscitation phase is to stabilize the patient as much as possible and to prevent any further life-threatening deterioration. Once these goals are accomplished the focus should then shift towards diagnosis of the underlying process, and then the institution of therapy targeted at reversing the primary etiology of the ARF. DX: 1st Tests To Order Test Result pulseoximetry SpO2 <80% arterial blood gases pH<7.38; PaO2 <60 mmHg (or <50 mmHg in chronic lung disease) on room air; PaCO2 >50 mmHg on room air Other Tests to Consider Test Result CBC elevated white blood cell count screening for hypercoagulable states variable serum bicarbonate (HCO3) may be elevated ECG
- 3. variable CXR diffuse or patchy infiltrates; pneumothorax; pulmonary effusion; hyperinflation; asymmetric opacification of lung fields; asymmetric lucency of lung fields pulmonary function tests PEFR <35% to 50% of predicted; FEV <35% to 50% of predicted; FVC <50% to 70% of predicted; FEV1 <50% of predicted; NIF above -25 cm H2O chest CT pulmonary embolism; chronic lung disease; infection; parenchymal disease; bronchiectasis ventilation/perfusion lung scan pulmonary embolism Emerging Tests Test Result transcutaneous CO2 monitoring reduced PaCO2 cardiothoracic ultrasound evidence of effusion, pneumothorax, consolidation, or abscess Meds: Pharmacotherapy for cardiogenic pulmonary edema and acute exacerbations of chronic obstructive pulmonary disease (COPD) is discussed here. The goals of therapy in cardiogenic pulmonary edema are to achieve a pulmonary capillary wedge pressure of 15-18 mm Hg and a cardiac index greater than 2.2 L/min/m2 while maintaining adequate blood pressure and organ perfusion. These goals may have to be modified for some patients. Diuretics, nitrates, analgesics, and inotropes are used in the treatment of acute pulmonary edema. Nursing interventions for Nursing Priorities Maintain airway patency. Assist with measures to facilitate gas exchange. Enhance nutritional intake. Prevent complications, slow progression of condition. Provide information about disease process/prognosis and treatment regimen. Ineffective Airway Clearance May be related to Bronchospasm Increased production of secretions; retained secretions; thick, viscous secretions Decreased energy/fatigue Possibly evidenced by Statement of difficulty breathing Changes in depth/rate of respirations, use of accessory muscles Abnormal breath sounds, e.g., wheezes, rhonchi, crackles Cough (persistent), with/without sputum production Auscultate breath sounds. Note adventitious Some degree of bronchospasm is present with
- 4. breath sounds, e.g., wheezes, crackles, rhonchi. obstructions in airway and may/may not be manifested in adventitious breath sounds, e.g., scattered, moist crackles (bronchitis); faint sounds, with expiratory wheezes (emphysema); or absent breath sounds (severe asthma). Assess/ monitor respiratory rate. Note inspiratory/ expiratory ratio. Tachypnea is usually present to some degree and may be pronounced on admission or during stress/ concurrent acute infectious process. Respirations may be shallow and rapid, with prolonged expiration in comparison to inspiration. Note presence/ degree of dyspnea, e.g., reports of “air hunger,” restlessness, anxiety, respiratory distress, use of accessory muscles. Use 0–10 scale or American Thoracic Society’s “Grade of Breathlessness Scale” to rate breathing difficulty. Ascertain precipitating factors when possible. Differentiate acute episode from exacerbation of chronic dyspnea. Respiratory dysfunction is variable depending on the underlying process, e.g., infection, allergic reaction, and the stage of chronicity in a patient with established COPD. Note: Using a 0–10 scale to rate dyspnea aids in quantifying and tracking changes in respiratory distress. Rapid onset of acute dyspnea may reflect pulmonary embolus. Assist patient to assume position of comfort, e.g., elevate head of bed, have patient lean on overbed table or sit on edge of bed. Elevation of the head of the bed facilitates respiratory function by use of gravity; however, patient in severe distress will seek the position that most eases breathing. Supporting arms/legs with table, pillows, and so on helps reduce muscle fatigue and can aid chest expansion. Keep environmental pollution to a minimum, e.g., dust, smoke, and feather pillows, according to individual situation. Precipitators of allergic type of respiratory reactions that can trigger/ exacerbate onset of acute episode. Encourage/ assist with abdominal or pursed-lip breathing exercises. Provides patient with some means to cope with/ control dyspnea and reduce air-trapping.
- 5. Observe characteristics of cough, e.g., persistent, hacking, moist. Assist with measures to improve effectiveness of cough effort. Cough can be persistent but ineffective, especially if patient is elderly, acutely ill, or debilitated. Coughing is most effective in an upright or in a head-down position after chest percussion. Increase fluid intake to 3000 mL/day within cardiac tolerance. Provide warm/ tepid liquids. Recommend intakeof fluids between, instead of during, meals. Hydration helps decrease the viscosity of secretions, facilitating expectoration. Using warm liquids may decrease bronchospasm. Fluids during meals can increase gastric distension and pressure on the diaphragm. Monitor/ graph serial ABGs, pulse oximetry, chest x-ray. Establishes baseline for monitoring progression/ regression of disease process and complications. Note: Pulse oximetry readings detect changes in saturation as they are happening, helping to identify trends before patient is symptomatic. However, studies have shown that the accuracy of pulse oximetry may be questioned if patient has severe peripheral vasoconstriction. 2. Impaired Gas Exchange May be related to Altered oxygen supply (obstruction of airways by secretions, bronchospasm; air-trapping) Alveoli destruction Possibly evidenced by Dyspnea Confusion, restlessness Inability to move secretions Abnormal ABG values (hypoxia and hypercapnia) Changes in vital signs Reduced tolerance for activity Assess respiratory rate, depth. Note use of accessory muscles, pursed-lip breathing, inability to speak/ converse. Useful in evaluating the degree of respiratory distress and/or chronicity of the disease process. Elevate head of bed, assist patient to assume position to ease work of Oxygen delivery may be improved by upright position and breathing exercises to decrease airway collapse, dyspnea,
- 6. breathing. Include periods of time in prone position as tolerated. Encourage deep-slow or pursed-lip breathing as individually needed/ tolerated. and work of breathing. Note: Recent research supports use of prone position to increase Pao2. Assess/ routinely monitor skin and mucous membrane color. Cyanosis may be peripheral (noted in nailbeds) or central (noted around lips/or earlobes). Duskiness and central cyanosis indicate advanced hypoxemia. Encourage expectoration of sputum; suction when indicated. Thick, tenacious, copious secretions are a major source of impaired gas exchange in small airways. Deep suctioning may be required when cough is ineffective for expectoration of secretions. Auscultate breath sounds, noting areas of decreased airflow and/or adventitious sounds. Breath sounds may be faint because of decreased airflow or areas of consolidation. Presence of wheezes may indicate bronchospasm/ retained secretions. Scattered moist crackles may indicate interstitial fluid/ cardiac decompensation. Palpate for fremitus. Decrease of vibratory tremors suggests fluid collection or air-trapping. Monitor level of consciousness/ mental status. Investigate changes. Restlessness and anxiety are common manifestations of hypoxia. Worsening ABGs accompanied by confusion/ somnolence are indicative of cerebral dysfunction due to hypoxemia. Evaluate level of activity tolerance. Provide calm, quiet environment. Limit patient’s activity or encourage bed/chair rest during acute phase. Have patient resume activity gradually and increase as individually tolerated. During severe/ acute/ refractory respiratory distress, patient may be totally unable to perform basic self-care activities because of hypoxemia and dyspnea. Rest interspersed with care activities remains an important part of treatment regimen. An exercise program is aimed at increasing endurance and strength without causing severe dyspnea and can enhance sense of well-being.
- 7. Evaluate sleep patterns, note reports of difficulties and whether patient feels well rested. Provide quiet environment, group care/ monitoring activities to allow periods of uninterrupted sleep; limit stimulants, e.g., caffeine; encourage position of comfort. Multiple external stimuli and presence of dyspnea may prevent relaxation and inhibit sleep. Monitor vital signs and cardiac rhythm. Tachycardia, dysrhythmias, and changes in BP can reflect effect of systemic hypoxemia on cardiac function. 3. Nutrition: imbalanced, less than body requirements May be related to Dyspnea; sputum production Medication side effects; anorexia, nausea/vomiting Fatigue Possibly evidenced by Weight loss; loss of muscle mass, poor muscle tone Reported altered taste sensation; aversion to eating, lack of interest in food Assess dietary habits, recent food intake. Note degree of difficulty with eating. Evaluate weight and body size (mass). Patient in acute respiratory distress is often anorectic because of dyspnea, sputum production, and medications. In addition, many COPD patients habitually eat poorly, even though respiratory insufficiency creates a hypermetabolic state with increased caloric needs. As a result, patient often is admitted with some degree of malnutrition. People who have emphysema are often thin with wasted musculature. Auscultate bowel sounds. Diminished/ hypoactive bowel sounds may reflect decreased gastric motility and constipation (common complication) related to limited fluid intake, poor food choices, decreased activity, and hypoxemia. Give frequent oral care, remove expectorated secretions promptly, provide specific container for disposal of secretions and tissues. Noxious tastes, smells, and sights are prime deterrents to appetite and can produce nausea and vomiting with increased respiratory difficulty.
- 8. Encourage a rest period of 1 hr before and after meals. Provide frequent small feedings. Helps reduce fatigue during mealtime, and provides opportunity to increase total caloric intake. Avoid gas-producing foods and carbonated beverages. Can produce abdominal distension, which hampers abdominal breathing and diaphragmatic movement and can increase dyspnea. Avoid very hot or very cold foods. Extremes in temperature can precipitate/ aggravate coughing spasms. Weigh as indicated. Useful in determining caloric needs, setting weight goal, and evaluating adequacy of nutritional plan. Note: Weight loss may continue initially, despite adequate intake, as edema is resolving. Administer supplemental oxygen during meals as indicated. Decreases dyspnea and increases energy for eating, enhancing intake. 4. Risk for Infection Risk factors may include Inadequate primary defenses (decreased ciliary action, stasis of secretions) Inadequate acquired immunity (tissue destruction, increased environmental exposure) Chronic disease process Malnutrition Monitor temperature. Fever may be present because of infection and/or dehydration. Review importance of breathing exercises, effective cough, frequent position changes, and adequate fluid intake. These activities promote mobilization and expectoration of secretions to reduce risk of developing pulmonary infection. Observe color, character, odor of sputum. Odorous, yellow, or greenish secretions suggest the presence of pulmonary infection. Demonstrate and assist patient in disposal of tissues and sputum. Stress proper handwashing (nurse and patient), and use gloves when handling/ disposing of Prevents spread of fluid-borne pathogens.
- 9. tissues, sputum containers. Monitor visitors; provide masks as indicated. Reduces potential for exposure to infectious illnesses, e.g., upper respiratory infection (URI). Encourage balance between activity and rest. Reduces oxygen consumption/ demand imbalance, and improves patient’s resistance to infection, promoting healing. Discuss need for adequate nutritional intake. Malnutrition can affect general well-being and lower resistance to infection. Recommend rinsing mouth with water and spitting, not swallowing, or use of spacer on mouthpiece of inhaled corticosteroids. Reduces localized immunosuppressive effect of drug and risk of oral candidiasis. Obtain sputum specimen by deep coughing or suctioning for Gram’s stain, culture/ sensitivity. Done to identify causative organism and susceptibility to various antimicrobials. Administer antimicrobials as indicated. May be given for specific organisms identified by culture and sensitivity, or be given prophylactically because of high risk. 6. Knowledge Deficit May be related to Lack of information/unfamiliarity with information resources Information misinterpretation Lack of recall/cognitive limitation Possibly evidenced by Request for information Statement of concerns/misconception Inaccurate follow-through of instructions Development of preventable complications Other Possible Nursing Diagnoses 1. Self-Care deficit, specify—intolerance to activity, decreased strength/endurance, depression, severe anxiety.
- 10. 2. Home Maintenance, ineffective—intolerance to activity, inadequate support system, insufficient finances, unfamiliarity with neighborhood resources. 3. Infection, risk for—decreased ciliary action, stasis of secretions, tissue destruction, increased environmental exposure,chronic disease process, malnutrition. Pathophysiology Respiratory failure can arise from an abnormality in any of the components of the respiratory system, including the airways, alveoli, central nervous system (CNS), peripheral nervous system, respiratory muscles, and chest wall. Patients who have hypoperfusion secondary to cardiogenic, hypovolemic, or septic shock often present with respiratory failure. Ventilatory capacity is the maximal spontaneous ventilation that can be maintained without development of respiratory muscle fatigue. Ventilatory demand is the spontaneous minute ventilation that results in a stable Pa CO2. Normally, ventilatory capacity greatly exceeds ventilatory demand. Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both). Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller. Ventilatory demand is augmented by an increase in minute ventilation and/or an increase in the work of breathing