RESPIRATORY OBJECTIVES (ADN 253 03/2010) 1.

Describe the assessment of the patient with atelectasis and pneumonia with the complication of acute respiratory distress. a. Fever chills or night sweats in a patient who also has respiratory symptoms should alert the nurse for bacterial pneumonia. Clinical manifestations of pneumonia are pleuritictype pain, fatigue, tachypnea, use of accessory muscles for breathing, bradycardia or relative bradycardia, coughing, and purulent sputum. i. Monitor patient for changes in temperature and pulse, amount, odor of secretions, frequency and severity of cough, degree of tachypnea or sob, changes in physical finding, and changes in xray Compare and contrast the pathologies that lead to acute respiratory distress and respiratory insufficiency or failure. a. ARDS Patho: Occurs as a result of an inflammatory trigger that initiates the release of chemical mediators, causing injury to the alveolar capillary membrane. Severe ventilation and perfusion mismatch occurs and the alveoli collapse because of the inflammatory infiltrate, blood, and fluid and surfactant dysfunction. Small airways are narrowed because of fluid and lung compliance decreases. Blood returning to lungs are shunted to nonfunctional alveoli and gas exchange is markedly impaired. b. ARF Patho: Decreased respiratory drive may occur with severe brain injury, multiple sclerosis, sedatives, and metabolic disorders such as hypothyroidism. 2. Chest wall dysfunction due to disease of nerves, spinal cord, muscles, or neuromuscular junction involved in respiration seriously affects ventilation. Guillian-barre, ALS, myestenia gravis and muscular dystrophy are a few causes. Dysfunction of lung parenchyma such as pleural effusion, hemothorax, pneumothorax, pneumonia, PE, pulmonary edema can prevent expansion of lung. Other causes are effects of anesthetic agents, analgesics, sedatives, pain, and mismatch of vent and perfusion after major abdominal, cardiac surgery. Describe the criteria used to define acute respiratory insufficiency and failure a. Failure is a PaO2 less than 50mm HG b. Insuffiency is a PaO2 to fraction of inspired oxygen FiO2 less than 300mmHG c. ARDS is a PaO2 to fraction FiO2 less than 200 mm HG Describe the etiology and progression of ARDS a. Aspiration, drug ingestion and overdose, hematologic disorders (DIC), massive transfusions and cabg, prolong inhalation of oxygen and smoke, localized infection, metabolic disorders (pancreatitis, uremia), shock, trauma, major surgery, fat or air emblism and systemic sepsis b. Progression: rapid onset of severe dyspnea, usually occurring 12-48hrs after initiating event, a characteristic feature is arterial hypoxemia that does not respond to oxygenation. CXR reveals bilateral infiltrates that quickly worsen the lung injury then progresses to fibrosing alveolitis with severe hypoxemia. The patient also has increased alveolar dead space and decreased pulmonary compliance Describe the use of mechanical ventilation for the patient experiencing resp distress. Include the following: negative pressure, positive pressure (pressure cycled, time cycled, volume cycled), features and settings of the ventilator: FIO2, tidal volume, resp rate, sensitivity setting, types of ventilatory control (control, assist control, intermittent ventilation), and positive end-expiratory pressure.

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Negative pressure occurs in normal spontaneous inspiration. The negative pressure in the thorax expands lungs to pull air in and distribute throughout lungs for ventilation. Negative pressure ventilators: exert a negative pressure on external chest. Decreasing the intrathoracic pressure during inspiration allows air to flow into the lung, filling its volume (similar to spontaneous inspiration). It is used mainly in chronic resp failure associated with neuromuscular conditions (ie poliomyelitis, muscular dystrophpy, ALS, Myasthenia Gravis). It is inappropriate for unstable/complex pts who require frequent ventilator changes. Neg-pressure ventilators do n ot require intubation. Iron lung (drinker respirator tank): is a negative-pressure chamber used for ventilation. It was used extensively during polio epidemics and currently used by a few polio survivors and neuromuscular disorders. Body Wrap (pneumo-wrap) and chest cuirass (tortoise shell): portable devices that require a rigid cage or shell to create a negative-pressure chamber around the thorax and abdomen. Due to problems with proper fit and system leaks, these ventilators are only used for carefully selected pts. Positive-Pressure Ventilators inflate lungs by exerting positive pressure on the airway, forcing the alveoli to expand during inspiration. Expiration occurs passively. Endotracheal intubation or tracheostomy is necessary in most cases. 3 types of positive pressure ventilators are classified by the method of ending the inspiratory phase of respiration: Pressure-cycled: when cycled on, it delivers a flow of air (inspiration) until reaching a preset pressure and then cycles off. Expiration occurs passively. Major limitation is that the volume of air/oxygen can vary as the pts airway resistance changes. This results in inconsistent tidal volume delivery, and possibly compromised ventilation. Pressure cyucled vents are intended only for short term. Most common type is IPPB machine Time-cycled ventilators terminate or control inspiration after a set time. The volume of air pt receives is regulated by length of inspiration and flow rate of air. Most ventilators have a rate control determining resp rate, but pure time-cycling is rarely used for adults (mainly in newborns/infants) Volume cycled: most commonly used positive-pressure ventilators. The volume of air delivered with each inspiration is preset. Once the preset volume is delivered to pt, the ventilator cycles off and exhalation occurs passively. From breath to breath, volume of air delivered by vent is relatively constant, ensuring consistent adequate breaths despite varying airway pressures. Features and settings of the ventilator: FIO2: fraction of inspired oxygen. This is the percentage of oxygen in the air entering the lungs. Tidal volume: volume of breath delivered during inspiration. 10 to 15 ml/kg. / Usually set at 6-12 ml/kg (ideal body weight); Resp rate: breaths per min. usually set at 12-16 breaths/min Sensitivity is adjusted so the pt can trigger the ventilator with minimal effort. Usually 2mm Hg negative inspiratory force Types of ventilator control: Control: ventilator completely controls the pts ventilation according to preset tidal volumes and resp rate. Because of problems with synchrony, it is rarely used except in paralyzed or anesthesized pts. Assist control: pts breathing pattern may trigger the ventilator to deliver a preset tidal volume; in the absence of spontaneous breathing, the machine delivers a controlled breath at a preset minimum rate and tidal volume. Intermittent ventilation: provides a combination of mechanically assisted breaths and spontaneous breaths. This allows pt to use their own muscles of ventilation to prevent muscle atrophy. It lowers mean airway pressure, which can assist in preventing barotraumas.

PeeP positive pressure maintained by the ventilator at the end of exhalation (instead of the normal zero pressure) to help increase functional residual capacity and open collapsed alveoli; improves oxygenation with lower FiO2. It is a critical part of treatment of ARDS, Peep usually improves oxygenation. PeeP helps reverse alveolar collapse by keeping the alveoli open resulting in improved arterial oxygenation and a reduction in the severity of the ventilation perfusion imbalance i. The goal is a PaO2 greater than 60mmg or an oxygen saturation above 90% at the lowest FiO2. ARDS should be managed with low tidal volume, with a low or moderately high PEEP. ii. Systemic hypotension may occur due to hypovolemia, leakage of fluid into interstitial spaces and depressed CO due to high levels of PEEP 6. Describe the pathology of COPD: In COPD, airflow limitation is progressive and assoc. with abnormal inflammatory responses of the lungs to noxious particles/gases. Inflammation occurs in airways, parenchyma and pulmonary vasculature. Due to chronic inflammation and the bodys attempts to repair it, narrowing occurs in small peripheral airways. Over time, scar tissue forms and begin to narrow the airway lumen. Airflow obstruction may be caused by parenchymal destruction (seen with emphysema). In addition to inflammation, processes r/t imbalances of proteinases/antiproteinases in lung may be responsible for airflow limitation. When activated, proteinases and other substances are released, damaging parenchyma of the lung. Parenchymal changes occur as a consequence of inflammation/environmental/genetic factors. Early COPD, inflammatory response causes pulmonary vasculature changes characterized by thickening of the vessel wall. Changes result from 1. Exposure to cigarette smoke 2. Use of tobacco products 3. Release of inflammatory mediators. Types of COPD: Chronic Bronchitis is a disease of airways. Presence of cough and sputum production for at least 3 months in each of two consecutive years. Commonly caused by smoke or environmental pollutants. Constant irritation causes mucus secreting glands and goblet cells to increase and decreased ciliary function. Bronchial walls thicken, lumen narrows and mucus plugs the airway. Alveoli damaged and fibrosed leading to altered function of alveolar macrophages. Results: higher risk of resp infection. Emphysema: disease of the airways characterized by impaired o2/co2 exchange resulting from destruction of walls of overdistended alveoli. It is an end stage of a disease that progresses slowly over many years. As alveoli walls are destroyed, alveolar surface area in contact with pulmonary capillaries decrease causing increase in dead space (lung area where no gas exchange can occur) and impaired o2 diffusion (hypoxemia). *end stage of a process that has progressed slowly for years Later stages co2 elimination impaired hypercapnia resp acidosis. As alveolar walls continue to break down, pulmonary capillary bed is reduced in size. Resistance to pulmonary blood flow is increased, forcing right ventricle to maintain higher bp in pulm artery. Hypoxemia increases pulm artery pressure. For this reason, Right sided heart failure is a complication of emphysema. (Congestion, edema, jvd, pain in liver region suggests cardiac failure.) Panlobular type: destruction of resp bronchiole, alveolus. Air spaces are enlarged but little inflammatory disease. Barrel chest, marked dyspnea on exertion and wt loss is common. Expiration becomes active and requires muscular effort. SOB and rigid chest Centrilobular: changes take place in center of secondary lobule. Derangement of ventilation/perfusion. hypoxemia/hypercapnia/polycythemia/ episodes of r-sided heart failure. Central cyanosis/resp failure. Develops peripheral edema treated with diuretics NANDAs: Impaired Gas exchange and airway clearance r/t chronic inhalation of toxins impaired Gas exchange r/t ventilation-perfusion inequality ineffective airway clearance r/t bronchoconstriction, increased mucus production, ineffective cough, bronchopulmonary infection Activity Intolreance r/t fatigue, hypoxemia

7. Describe the principles of water seal drainage for chest tubes including collection of fluids and addition of suction to the system. Water Seal Systems. The traditional water seal system (or wet suction) for chest drainage has three chambers: a collection chamber, a water seal chamber, and a wet suction control chamber. The collection chamber acts as a reservoir for fluid draining from the chest tube. It is graduated to permit easy measurement of drainage. Suction may be added to create negative pressure and promote drainage of fluid and removal of air. The suction control chamber regulates the amount of negative pressure applied to the chest. The amount of suction is determined by the water level. It is usually set at 20-cm H2O; adding more fluid results in more suction. After the suction is turned on, bubbling appears in the suction chamber. A positive-pressure valve is located at the top of the suction chamber that automatically opens with increases in positive pressure within the system. Air is automatically released through a positive-pressure relief valve if the suction tubing is inadvertently clamped or kinked. The water seal chamber has a one-way valve or water seal that prevents air from moving back into the chest when the patient inhales. There is an increase in the water level with inspiration and a return to the baseline level during exhalation; this is referred to as tidaling. Intermittent bubbling in the water seal chamber is normal, but continuous bubbling can indicate an air leak. Bubbling and tidaling do not occur when the tube is placed in the mediastinal space; however, fluid may pulsate with the patient's heartbeat. If the chest tube is connected to gravity drainage only, suction is not used. The pressure is equal to the water seal only. Twochamber chest drainage systems (water seal chamber and collection chamber) are available for use with patients who need only gravity drainage. 8. Describe the NANDA and medical/nursing interventions for the patient with a chest tube to water seal drainage Nursing Diagnosis -Impaired gas exchange related to lung impairment and surgery -Ineffective airway clearance related to lung impairment, anesthesia, and pain -Acute pain related to incision, drainage tubes, and the surgical procedure -Impaired physical mobility of the upper extremities related to thoracic surgery -Risk for imbalanced fluid volume related to the surgical procedure -Imbalanced nutrition, less than body requirements related to dyspnea and anorexia -Deficient knowledge about self-care procedures at home Monitor his vital signsespecially rate, pattern, depth, and ease of respirationsand SpO2 level every 2 hours or as necessary. Assess his breath sounds bilaterally Assess the insertion site for subcutaneous emphysema. Encourage the patient to cough and coach him in deep breathing to promote drainage and lung expansion. Assess for pain using a pain intensity rating scale. Optimal pain management can prevent hypoventilation and complications such as atelectasis and pneumonia. Keep all tubing free from kinks and prevent fluid-filled dependent loops that can interfere with drainage. Make sure that the connections are securely taped and that the chest tube is secured to your patients chest wall. Keep the collection apparatus below the patients chest level. Water in either chamber can evaporate, so you may need to add water The water seal level should fluctuate with respiratory effort; this is called tidaling. If it doesnt, the tubing may be kinked or clamped or the patient may be lying on it. Or, if the lung has reexpanded, the lack of tidaling may be a good sign indicating that no more air is leaking into the pleural space. Measure drainage every 8 hours. Immediately report more than 70 ml/hour of bright red blood or red free-flowing drainage, which could indicate hemorrhage. Also report paradoxical chest movement and tracheal deviation, which could indicate a tension pneumothorax. Frequently reposition the patient and help him ambulate or sit in a chair as ordered. Avoid clamping, striping, milking chest tube.