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NUR 2063 Essentials of Pathophysiology (NUR2063) / Pathophysiology Final Rasmussen Univers, Exams of Nursing

NUR 2063 Essentials of Pathophysiology (NUR2063) / Pathophysiology Final Rasmussen University /NUR 2063 Essentials of Pathophysiology (NUR2063) / Pathophysiology Final Rasmussen University /NUR 2063 Essentials of Pathophysiology (NUR2063) / Pathophysiology Final Rasmussen University

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Download NUR 2063 Essentials of Pathophysiology (NUR2063) / Pathophysiology Final Rasmussen Univers and more Exams Nursing in PDF only on Docsity! pg. 1 1 Exam 1 Chapter 26: Nursing Assessment: Respiratory System STRUCTURES AND FUNCTIONS OF RESPIRATORY SYSTEM • The primary purpose of the respiratory system is gas exchange, which involves the transfer of oxygen and carbon dioxide between the atmosphere and the blood. • The upper respiratory tract includes the nose, pharynx, adenoids, tonsils, epiglottis, larynx, and trachea. • The nose warms, cleanses, and humidifies air before it enters lungs. • Vibrational sounds originating in the larynx lead to vocalization. • The lower respiratory tract consists of the bronchi, bronchioles, alveolar ducts, and alveoli. • Gas exchange takes place in the bronchioles. • The prior passages are the anatomic dead space, since they are only conducting passageways. • Surfactant is a lipoprotein that helps to keep the alveoli open. • Contraction of the diaphragm, the major muscle of respiration, results in decreased intrathoracic pressure, allowing air to enter the lungs. Physiology of Respiration • Ventilation involves inspiration (movement of air into the lungs) and expiration (movement of air out of the lungs). • Inspiration is an active process, involving muscle contraction. • Expiration is a passive process. When elastic recoil is reduced, expiration becomes a more active, labored process. • In adults, a normal tidal volume (Vt), or volume of air exchanged with each breath, is about 500 ml. • When compliance, or a measure of the ease of lung expansion, is decreased, the lungs are more difficult to inflate. • Arterial blood gases (ABGs) are measured to determine oxygenation status and acid-base balance. ABG analysis includes measurement of the PaO2, PaCO2, acidity (pH), and bicarbonate (HCO3 –) in arterial blood. • Arterial oxygen saturation can be monitored continuously using a pulse oximetry probe on the finger, toe, ear, or bridge of the nose. Control of Respiration • The respiratory center in the brainstem medulla responds to chemical and mechanical signals from the body. • A chemoreceptor is a receptor that responds to a change in the chemical composition (PaCO2 and pH) of the fluid around it. • Mechanical receptors are stimulated by a variety of physiologic factors, such as irritants, muscle stretching, and alveolar wall distortion. • The respiratory defense mechanisms include filtration of air, the mucociliary clearance system, the cough reflex, reflex bronchoconstriction, and alveolar macrophages. GERONTOLOGIC CONSIDERATIONS: EFFECTS OF AGING ON RESPIRATORY SYSTEM • Age-related changes in the respiratory system can be divided into alterations in structure, defense mechanisms, and respiratory control. • There is much variability in the extent of these changes in persons of the same age. The elderly patient who has a significant smoking history, is obese, and is diagnosed with a chronic illness is at greatest risk of adverse outcomes. ASSESSMENT OF RESPIRATORY SYSTEM • Use judgment in determining whether all or part of the history and physical examination will be completed based on problems presented by the patient and the degree of respiratory distress. If respiratory distress is severe, only obtain pertinent information and defer a thorough assessment until the patient’s pg. 2 2 condition stabilizes. • A health history for the respiratory system consists of assessment of past health history, medications, surgery or other treatments, family health history, psychosocial history, and a review of systems using functional health patterns. pg. 5 5 rhinitis. • During the cold season, advise patients with a chronic illness or a compromised immune status regarding measures to decrease the risk of acquiring a cold. • In contrast to acute viral rhinitis, the onset of influenza is typically abrupt with systemic symptoms of cough, fever, and myalgia often accompanied by a headache and sore throat. • Supportive care is directed at preventing pneumonia and other secondary infections and providing relief of symptoms. • Antivirals such as amantadine (Symmetrel) or rimantadine (Flumadine) are used to prevent and treat influenza. Zanamivir (Relenza) and oseltamivir (Tamiflu) are used to prevent and treat influenza A and B. • To combat the likelihood of developing influenza, there are two types of flu vaccines available: inactivated; and live, attenuated. • The nurse should advocate the use of inactivated influenza vaccination in all patients greater than 50 years of age, who are at high risk during routine office visits, or who are hospitalized at the time of discharge. • Sinusitis develops when the exit from the sinuses is narrowed or blocked by inflammation or swelling of the mucosa. Accumulating secretions provide a rich medium for growth of bacteria, viruses, and fungi, all of which may cause infection. • Acute sinusitis usually results from an upper respiratory infection, allergic rhinitis, swimming, or dental manipulation. Symptoms include significant pain over the affected sinus, purulent nasal drainage, nasal obstruction, congestion, fever, and malaise. • Chronic sinusitis lasts longer than 3 weeks and is a persistent infection usually associated with allergies and nasal polyps. Although there may be facial or dental pain, nasal congestion, and increased drainage, severe pain and purulent drainage are often absent. • Treatment of sinusitis includes supportive care, antibiotics, and the use of ancillary medications to relieve symptoms, including oral or topical decongestants, nasal corticosteroids, and antihistamines. • Nasal polyps can cause obstruction and speech distortion, necessitating surgical removal. PROBLEMS OF PHARYNX • Acute pharyngitis is an acute inflammation of the pharyngeal walls that may include the tonsils, palate, and uvula. • Symptoms range in severity from complaints of a ―scratchy throat‖ to pain so severe that swallowing is difficult. Both viral and strep infections appear as a red and edematous pharynx, with or without patchy yellow exudates so appearance is not always diagnostic. • The goals of nursing management for acute pharyngitis are infection control, symptomatic relief, and prevention of secondary complications. • Since a peritonsillar abscess—a complication of acute pharyngitis—may threaten the airway, needle aspiration, drainage, or surgery is indicated. PROBLEMS OF TRACHEA AND LARYNX • Airway obstruction is a medical emergency. Interventions to reestablish a patent airway include the obstructed airway (Heimlich) maneuver, cricothyroidotomy, endotracheal intubation, and tracheostomy. • A tracheostomy is the stoma that results from a tracheotomy, or a surgical incision into the trachea for the purpose of establishing an airway. • Indications for a tracheostomy are to (1) bypass an upper airway obstruction, (2) facilitate removal of secretions, (3) permit long-term mechanical ventilation, and (4) permit oral intake and speech in the patient who requires long-term mechanical ventilation. • A wide variety of tracheostomy tubes are available. While the nurse must provide care specific to the type of tube present, general nursing care for any tracheostomy patient revolves around the diagnoses of ineffective airway clearance, risk for aspiration, impaired verbal communication, and ineffective self-care management. LARYNGEAL POLYPS • Polyps on the vocal cords develop as a result of vocal abuse or irritation. pg. 6 6 • The most common symptom is hoarseness. • They are treated conservatively with voice rest and adequate hydration. Surgical removal may be indicated for large polyps, which may cause dyspnea. HEAD AND NECK CANCER pg. 7 7 • This category of tumors arises from the mucosal surfaces of the paranasal sinuses; oral cavity; or nasopharynx, oropharynx, and larynx. • Early signs and symptoms of head and neck cancer vary with the tumor location. Late stages have easily detectable signs and symptoms, including pain, dysphagia, decreased mobility of the tongue, airway obstruction, and cranial nerve neuropathies. • Choice of treatment for head and neck cancer is based on medical history, extent of disease, cosmetic considerations, urgency of treatment, and patient choice. • Approximately one third of patients with head and neck cancers have highly confined lesions that are stages I or II at diagnosis. Such patients can undergo radiation therapy or surgery with the goal of cure. • Advanced lesions are treated by a total laryngectomy in which the entire larynx and preepiglottic region is removed and a permanent tracheostomy performed. • After radical neck surgery, the patient may be unable to take in nutrients through the normal route of ingestion because of swelling, the location of sutures, or difficulty with swallowing. Parenteral fluids will be given for the first 24 to 48 hours. • Nursing care revolves around the diagnoses of ineffective airway clearance, risk for aspiration, risk for infection, imbalanced nutrition: less than body requirements, pain, impaired verbal communication, and anxiety. Chapter 28: Nursing Management: Lower Respiratory Problems LOWER RESPIRATORY TRACT INFECTIONS ACUTE BRONCHITIS • Acute bronchitis is an inflammation of the bronchi that usually occurs with a viral upper respiratory infection or in conjunction with chronic obstructive pulmonary disease (COPD). • It is a self-limiting condition; treatment is supportive. PERTUSSIS • It is a highly contagious infection of the lower respiratory tract. Although immunization is available, incidence rates are rising possibly because of waning immunity. • Pertussis is characterized by a cough that has a ―whooping‖ sound. • Treatment consists of antibiotics and supportive care. PNEUMONIA • Pneumonia is an acute inflammation of the lung parenchyma. • It can be classified according to the causative microorganism, such as bacteria, viruses, Mycoplasma, fungi, parasites, and chemicals. • Organisms can reach the lung by three methods: aspiration, inhalation, and homogenous spread from an infection elsewhere in the body. • A clinically effective way to classify pneumonia: • Community-acquired pneumonia is a lower respiratory tract infection of the lung parenchyma with onset in the community or during the first 2 days of hospitalization. • Hospital-acquired pneumonia is pneumonia occurring 48 hours or longer after hospital admission and not incubating at the time of hospitalization. • Aspiration pneumonia refers to the sequelae occurring from abnormal entry of secretions or substances into the lower airway. • Opportunistic pneumonia occurs in certain patients with altered immune responses who are highly susceptible to respiratory infections. pg. 10 10 • CT scanning is the single most effective noninvasive technique for evaluating lung cancer. Biopsy is necessary for a definitive diagnosis. • Staging of non–small cell lung cancer is performed according to the TNM staging system. Staging of small cell lung cancer by TNM has not been useful because the cancer is very aggressive and always considered systemic. • Treatment options are dependent upon the stage of disease. pg. 11 11 • Surgical resection is the treatment of choice in non–small cell lung cancer stages I and II, because the disease is potentially curable with resection. • Radiation therapy may be used as adjuvant therapy after resection or with the intent to cure if the patient is unable to tolerate surgical resection caused by co-morbidities. • Chemotherapy and targeted therapy may be used in the treatment of nonresectable tumors or as adjuvant therapy to surgery in non–small cell lung cancer. • The overall goals of nursing management of a patient with lung cancer will include effective breathing patterns, adequate airway clearance, adequate oxygenation of tissues, minimal to no pain, and a realist ic attitude toward treatment and prognosis. OTHER TYPES OF LUNG TUMORS • Secondary lung tumors are rare, accounting for only 5% of lung masses. They include chondromas, hamartomas, leiomyomas, and mesotheliomas. • The lungs are a common site for secondary metastases for a number of cancers. CHEST TRAUMA AND THORACIC INJURIES PNEUMOTHORAX • Pneumothorax is air in the pleural space resulting in a partial or complete collapse of the lung. There are several types: • Closed pneumothorax has no associated external wound. The most common form is a spontaneous pneumothorax, which is accumulation of air in the pleural space without an apparent antecedent event. • Open pneumothorax occurs when air enters the pleural space through an opening in the chest wall. Examples include stab or gunshot wounds and surgical thoracotomy. • A tension pneumothorax may be open or closed; there is a rapid accumulation of air in the pleural space causing severely high intrapleural pressures with resultant tension on the heart and great vessels. • Hemothorax is an accumulation of blood in the intrapleural space. Chylothorax is lymphatic fluid in the pleural space caused by a leak in the thoracic duct. Causes of both include trauma, surgical procedures, and malignancy. • reatment depends on the severity of the pneumothorax and the nature of the underlying disease. FRACTURED RIBS • Rib fractures are the most common type of chest injury resulting from blunt trauma. • Clinical manifestations include pain at the site, especially with inspiration and coughing. • The main treatment goal is to decrease pain to promote effective breathing. Patients also need to be taught deep breathing, coughing, and use of incentive spirometry. FLAIL CHEST • Flail chest results from multiple rib fractures, causing an unstable chest wall. The diagnosis of flail chest is made on the basis of fracture of two or more ribs, in two or more separate locations, causing an unstable segment. • Initial therapy consists of airway management, adequate ventilation, supplemental oxygen therapy, careful administration of intravenous (IV) solutions, and pain control. • The definitive therapy is to reexpand the lung and ensure adequate oxygenation. CHEST TUBES AND PLEURAL DRAINAGE • The purpose of chest tubes and pleural drainage is to remove the air and fluid from the pleural space and to restore normal intrapleural pressure so that the lungs can reexpand. • Chest tube malposition is the most common complication. • Routine monitoring is done by the nurse to evaluate if the chest drainage is successful by observing for tidaling in the water-seal chamber, listening for breath sounds over the lung fields, and measuring the amount of fluid drainage. CHEST SURGERY pg. 12 12 • A thoracotomy, or the surgical opening into the thoracic cavity, is considered major surgery because the incision is large, cutting into bone, muscle, and cartilage. The two types of thoracic incisions are median sternotomy, performed by splitting the sternum, and lateral thoracotomy. • Video-assisted thoracic surgery (VATS) is a minimally invasive thoracoscopic surgical procedure that in many cases can avoid the impact of a full thoracotomy. pg. 15 15 cardiopulmonary support if indicated. PULMONARY HYPERTENSION • Pulmonary hypertension can occur as a primary disease (primary pulmonary hypertension) or as a secondary complication of a respiratory, cardiac, autoimmune, hepatic, or connective tissue disorder (secondary pulmonary hypertension [SPH]). • Primary pulmonary hypertension is a severe and progressive disease. It is characterized by mean pulmonary arterial pressure greater than 25 mm Hg at rest (normal 12-16 mm Hg) or greater than 30 mm Hg with exercise in the absence of a demonstrable cause. • Primary pulmonary hypertension is a diagnosis of exclusion. All other conditions must be ruled out. • Although there is no cure for primary pulmonary, treatment can relieve symptoms, increase quality of life, and prolong life. • SPH occurs when a primary disease causes a chronic increase in pulmonary artery pressures. Secondary pulmonary hypertension can develop as a result of parenchymal lung disease, left ventricular dysfunction, intracardiac shunts, chronic pulmonary thromboembolism, or systemic connective tissue disease. COR PULMONALE • Cor pulmonale is enlargement of the right ventricle resulting from diseases of the lung, thorax, or pulmonary circulation. Pulmonary hypertension is usually a preexisting condition in the individual with cor pulmonale. • The most common cause of cor pulmonale is COPD. • The primary management of cor pulmonale is directed at treating the underlying pulmonary problem that precipitated the heart problem. LUNG TRANSPLANTATION • There are four types of transplant procedures available: single lung transplant, bilateral lung transplant, heart-lung transplant, and transplant of lobes from living related donor. • Lung transplant recipients are at high risk for bacterial, viral, fungal, and protozoal infections. Infections are the leading cause of death in the early period after the transplant. • Immunosuppressive therapy usually includes a three-drug regimen of cyclosporine or tacrolimus, azathioprine (Imuran) or mycophenolate mofetil (CellCept), and prednisone. Chapter 29: Nursing Management: Obstructive Pulmonary Diseases ASTHMA • Asthma is a chronic inflammatory disorder of the airways that results in recurrent episodes of airflow obstruction that it is usually reversible. • The primary pathophysiologic process in asthma is persistent but variable inflammation of the airways. The airflow is limited because the inflammation results in bronchoconstriction, airway hyperresponsiveness (hyperreactivity), and edema of the airways. • Although the exact mechanisms that cause asthma remain unknown, often exposure to a trigger, such as an pg. 16 16 allergen or irritant, initiates the inflammatory cascade. Respiratory infections are also precipitating factors of an acute asthma attack. • Common allergens include tree or weed pollen, dust mites, molds, animals, feathers, and cockroaches. • Asthma that is induced or exacerbated after physical exertion is called exercise-induced asthma. • Various air pollutants, cigarette or wood smoke, vehicle exhaust, elevated ozone levels, sulfur dioxide, pg. 17 17 and nitrogen dioxide can trigger asthma attacks. • Occupational asthma occurs after exposure to agents of the workplace. These agents are diverse and include wood dusts, laundry detergents, metal salts, chemicals, paints, solvents, and plastics. • The characteristic clinical manifestations of asthma are wheezing, cough, dyspnea, and chest tightness, particularly at night or early in the morning. Expiration may be prolonged. Examination of the patient during an acute attack usually reveals signs of hypoxemia. • Asthma can be classified as mild intermittent, mild persistent, moderate persistent, or severe persistent, based upon current impairment of the patient and their risk for exacerbations. • Severe acute asthma can result in complications such as rib fractures, pneumothorax, pneumomediastinum, atelectasis, and pneumonia. • A diagnosis of asthma is usually made based upon the presence of various indicators (e.g., clinical manifestations, health history, pulmonary function tests, and peak flow variability). • The goal of asthma treatment is to achieve and maintain control of the disease. Established guidelines give direction on the classification of severity of asthma at initial diagnosis and help determine which types of medications are best suited to control the asthma symptoms. • A stepwise approach to drug therapy is based initially on the asthma severity and then on level of control. Persistent asthma requires daily long-term therapy in addition to appropriate medications to manage acute symptoms. • Medications are divided into two general classifications: (1) long-term–control medications to achieve and maintain control of persistent asthma, and (2) quick-relief medications to treat symptoms and exacerbations. • Because chronic inflammation is a primary component of asthma, corticosteroids are more effective in improving asthma control than any other long-term drug. Inhaled (ICS) agents, such as Flovent and Pulmicort, are first-line therapy for patients with persistent asthma. • Orally administered corticosteroids are indicated for acute exacerbations of asthma. Maintenance doses of oral corticosteroids may be necessary to control asthma in a minority of patients with severe chronic asthma. • Short-acting inhaled β2-adrenergic agonists, including Proventil, are the most effective drugs for relieving acute bronchospasm. They are also used for acute exacerbations of asthma. • Mast cell stabilizers, including Cromolyn, have weak antiinflammatory effects and are less effective than low-dose ICS. They are not used to treat acute bronchospasm but can be effective in exercise-induced asthma. • The use of leukotriene modifiers can be used successfully as add-on therapy to reduce (not substitute for) the doses of inhaled corticosteroids. • Methylxanthine (theophylline) preparations are less effective long-term control bronchodilators as compared with β2-adrenergic agonists and carry a high incidence of side effects. • Anticholinergic agents (e.g., ipratropium [Atrovent], tiotropium [Spiriva]) block the bronchoconstricting influence of parasympathetic nervous system. • The overall goals are that the patient with asthma will have asthma control as evidenced by minimal symptoms during the day and night, acceptable activity levels (including exercise and other physical activity), maintenance greater than 80% of personal best peak expiratory flow rate (PEFR) or forced expiratory volume in 1 second (FEV1), few or no adverse effects of therapy, no recurrent exacerbations of asthma, and adequate knowledge to participate in and carry out management. • Education remains the cornerstone of asthma management. Your role in preventing asthma attacks or decreasing the severity focuses primarily on teaching the patient and caregiver. • One of the major factors determining success in asthma management is the correct administration of drugs. • Inhalation devices include metered-dose inhalers, dry powder inhalers, and nebulizers. • Teaching should include information about medications, including the name, purpose, dosage, method of administration, schedule, side effects, appropriate action if side effects occur, how to properly use and clean devices, and consequences for breathing if not taking medications as prescribed. • Several nonprescription combination drugs are available over the counter. An important teaching responsibility is to warn the patient about the dangers associated with nonprescription combination drugs. pg. 20 20 O2 be humidified when administered, either by humidification or nebulization. • Three different surgical procedures have been used in severe COPD. • Lung volume reduction surgery is used to reduce the size of the lungs by removing about 30% of the most diseased lung tissue so the remaining healthy lung tissue can perform better. pg. 21 21 • A bullectomy is used for certain patients and can result in improved lung function and reduction in dyspnea. • In appropriately selected patients with very advanced COPD, lung transplantation improves functional capacity and enhances quality of life. • Airway clearance techniques include breathing retraining, effective cough techniques, and chest physiotherapy. • Pursed-lip breathing is a technique that is used to prolong exhalation and thereby prevent bronchiolar collapse and air trapping. • Effective coughing conserves energy, reduces fatigue, and facilitates removal of secretions. Huff coughing is an effective technique that the patient can be easily taught. • Chest physiotherapy consists of percussion, vibration, and postural drainage. • Weight loss and malnutrition are commonly seen in the patient with severe emphysematous COPD. The patient with COPD should try to keep body mass index (BMI) between 21-25 kg/m2. • The patient with COPD will require acute intervention for complications such as exacerbations of COPD, pneumonia, cor pulmonale, and acute respiratory failure. • Pulmonary rehabilitation should be considered for all patients with symptomatic COPD or having functional limitations. The overall goal is to increase the quality of life. • Walking is by far the best physical exercise for the COPD patient. Also, adequate sleep is extremely important. OXYGEN THERAPY • O2 therapy is frequently used in the treatment of COPD and other problems associated with hypoxemia. Long-term O2 therapy improves survival, exercise capacity, cognitive performance, and sleep in hypoxemic patients. • Goals for O2 therapy are to reduce the work of breathing, maintain the PaO2, and/or reduce the workload on the heart, keeping the SaO2 >90% during rest, sleep, and exertion, or PaO2 >60 mm Hg. • O2 delivery systems are classified as low- or high-flow systems. Most methods of O2 administration are low-flow devices that deliver O2 in concentrations that vary with the person’s respiratory pattern. • Dry O2 has an irritating effect on mucous membranes and dries secretions. Therefore it is important that O2 be humidified when administered, either by humidification or nebulization. • Medical complications associated with oxygen therapy include CO2 narcosis, oxygen toxicity, infection, and absorption atelectasis. The risk of combustion related injury is also a possibility requiring specific precautions for patient safety. CYSTIC FIBROSIS • Cystic fibrosis (CF) is an autosomal-recessive, multisystem disease characterized by altered function of the exocrine glands primarily involving the lungs, pancreas, and sweat glands. • Initially, CF is an obstructive lung disease caused by the overall obstruction of the airways with mucus. Later, CF also progresses to a restrictive lung disease because of the fibrosis, lung destruction, and thoracic wall changes. • The major objectives of therapy in CF are to promote clearance of secretions, control infection in the lungs, and provide adequate nutrition. • Nursing care for the patient with CF revolves around the diagnoses of ineffective airway clearance, impaired gas exchange, ineffective breathing patterns, imbalanced nutrition, and ineffective coping, BRONCHIECTASIS • Bronchiectasis is characterized by permanent, abnormal dilation of one or more large bronchi. The pathophysiologic change that results in dilation is destruction of the elastic and muscular structures supporting the bronchial wall. • The hallmark of bronchiectasis is persistent or recurrent cough with production of large amounts of purulent sputum that may exceed 500 ml/day. • Bronchiectasis is difficult to treat. Therapy is aimed at treating acute flare-ups and preventing decline in lung function. • Antibiotics are the mainstay of treatment and are often given empirically, but attempts are made to culture the sputum. Long-term suppressive therapy with antibiotics is reserved for those patients who have symptoms that recur a few days after stopping antibiotics. pg. 22 22 • An important nursing goal is to promote drainage and removal of bronchial mucus. Rest, good nutrition, and adequate hydration are also important. pg. 25 25 • Erythrocyte sedimentation rate (ESR, or ―sed rate‖) measures the sedimentation or settling of RBCs and is used as a nonspecific measure of many diseases, especially inflammatory conditions. • The laboratory tests used in evaluating iron metabolism and differentiating anemias include measuring serum levels of iron, total iron-binding capacity (TIBC), serum ferritin, and transferrin saturation. • Radiologic studies for the hematology system involve primarily the use of computed tomography (CT) or magnetic resonance imaging (MRI) for evaluating the spleen, liver, and lymph nodes. • Bone marrow examination is important in the evaluation of many hematologic disorders. The examination of the marrow may involve aspiration only or aspiration with biopsy. After a bone marrow aspiration and biopsy, the site must be assessed frequently on the day of the procedure and for several days thereafter. Clients can experience some discomfort or pain and can require a mild analgesic. • Lymph node biopsy involves obtaining lymph tissue for histologic examination to determine the diagnosis, and to help for planning therapy. • Testing for specific genetic or chromosomal variations in hematologic conditions is often helpful in assisting in diagnosis and staging. These results also help to determine the treatment options and prognosis. Chapter 68: Nursing Management: Respiratory Failure and Acute Respiratory Distress Syndrome ACUTE RESPIRATORY FAILURE • Respiratory failure results when gas exchange, which involves the transfer of oxygen (O2) and carbon dioxide (CO2) between the atmosphere and the blood, is inadequate. • 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. The major threat of respiratory failure is the inability of the lungs to meet the oxygen demands of the tissues. • Respiratory failure can be classified as hypoxemic or hypercapnic. • Hypoxemic respiratory failure is commonly defined as a PaO2 ≤60 mm Hg when the patient is receiving an inspired O2 concentration ≥60%. 1 •Disorders that interfere with O2 transfer 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. 2 •Four physiologic mechanisms may cause hypoxemia and subsequent hypoxemic respiratory failure: V/Q mismatch; shunt; diffusion limitation; and hypoventilation. 1 o In hypercapnic respiratory failure, or ventilatory failure, the primary problem is insufficient CO2 removal. 1 ♣ It is commonly defined as a PaCO2 >45 mm Hg in combination with acidemia (arterial pH <7.35). 2 ♣ Disorders that compromise CO2 removal include drug overdoses with central nervous system (CNS) depressants, neuromuscular diseases, acute asthma, chronic obstructive pulmonary disease (COPD) exacerbations, and trauma or diseases involving the spinal cord and its role in lung ventilation. 1 • The manifestations of respiratory failure are related to the extent of change in PaO2 or PaCO2, the rapidity of change (acute versus chronic), and the ability to compensate to overcome this change. • A change in mental status is frequently the initial indication of respiratory failure. • Other early signs include tachycardia, tachypnea, and mild hypertension. • A severe morning headache may suggest nighttime hypercapnia. • Hypoxemia occurs when the amount of O2 in arterial blood is less than the normal value, and hypoxia occurs when the PaO2 falls sufficiently to cause signs and symptoms of inadequate oxygenation. • Hypoxemia can lead to hypoxia if not corrected. • Cyanosis is an unreliable indicator of hypoxemia and is a late sign of respiratory failure. Specific Clinical Manifestations • The patient may have a rapid, shallow breathing pattern or a respiratory rate that is slower than normal. A change from a rapid rate to a slower rate suggests progression of respiratory muscle fatigue and increased probability of respiratory arrest. • Other signs that give indicators of the efforts associated with breathing include: pg. 26 26 • The position that the patient assumes • The ability of the patient to speak • Use of pursed-lip breathing • A change in the inspiratory (I) to expiratory (E) ratio. • Presence of muscle retractions of the intercostal spaces or the supraclavicular area and use of the accessory pg. 27 27 muscles during inspiration or expiration • Breath sounds: • Crackles and rhonchi may indicate pulmonary edema and COPD. • Absent or diminished breath sounds may indicate atelectasis or pleural effusion. • Bronchial breath sounds over the lung periphery often result from lung consolidation that is seen with pneumonia. • A pleural friction rub may also be heard in the presence of pneumonia that has involved the pleura. Diagnostic Studies • Arterial blood gases (ABGs) are obtained to learn oxygenation (PaO2) and ventilation (PaCO2) status, 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, sputum and blood cultures, urinalysis, and electrocardiogram. NURSING AND COLLABORATIVE MANAGEMENT: ACUTE RESPIRATORY FAILURE • The overall goals for the patient in acute respiratory failure include normal ABG values or values within the patient’s baseline, normal breath sounds or within the patient’s baseline, no dyspnea or breathing patterns within the patient’s baseline, and 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. • The major goals of care for acute respiratory failure include maintaining adequate oxygenation and ventilation. • The appropriate O2 delivery system is chosen with the therapeutic goal of correcting hypoxemia. • 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), proper patient positioning, tracheal suctioning, and ambulation when possible. • If intensive measures fail to improve ventilation and oxygenation, positive pressure ventilation (PPV) is provided invasively through orotracheal or nasotracheal intubation or noninvasively through a nasal or face mask. • Noninvasive PPV is also used as a treatment for patients with acute or chronic respiratory failure, particularly patients with chronic respiratory failure from chest wall and neuromuscular disease. • Goals of drug therapy for patients in acute respiratory failure include relief of bronchospasm, reduction of airway inflammation and pulmonary congestion, treatment of pulmonary infection, and reduction of severe anxiety and restlessness. • Short-acting bronchodilators are given to reverse bronchospasms. • Corticosteroids are used in conjunction with bronchodilating agents when bronchospasm and inflammation are present. • Diuretics and nitroglycerin are given to decrease the pulmonary congestion caused by heart failure. • If atrial fibrillation is present, calcium channel blockers and β-adrenergic blockers are used to decrease heart rate and improve cardiac output. • IV antibiotics are given if infection is present. • Sedation and analgesia are used to decrease anxiety, agitation, and pain. • Patients who are asynchronous with mechanical ventilation may require neuromuscular blockade. • Decreased cardiac output is treated by administration of IV fluids, medications, or both. • A hemoglobin concentration of ≥9 g/dl (90 g/L) typically ensures adequate O2 saturation of the hemoglobin. • Maintenance of protein and energy stores is especially important. Ideally, enteral or parenteral nutrition is started within 24 hours in malnourished patients and within 3 days in well-nourished patients. GERONTOLOGIC CONSIDERATONS: RESPIRATORY FAILURE • Multiple factors contribute to an increased risk of respiratory failure in older adults, including the reduction in ventilatory capacity, decreased respiratory muscle strength, and delayed responses in respiratory rate and depth to pg. 30 30 Exam 2 Chapter 36: Nursing Management: Dysrhythmias RHYTHM IDENTIFICATION AND TREATMENT The ability to recognize normal and abnormal cardiac rhythms, called dysrhythmias, is an essential nursing skill. • Four properties of cardiac cells (automaticity, excitability, conductivity, and contractility) enable the conduction system to initiate an electrical impulse, transmit it through the cardiac tissue, and stimulate the myocardial tissue to contract. • The autonomic nervous system plays an important role in the rate of impulse formation, the speed of conduction, and the strength of cardiac contraction. Electrocardiogram Monitoring • The electrocardiogram (ECG) is a graphic tracing of the electrical impulses produced in the heart. • ECG waveforms are produced by the movement of charged ions across the semipermeable membranes of myocardial cells. • There are 12 recording leads in the standard ECG. Changes in a 12-lead ECG may occur with damage such as ischemia or infarction, electrolyte imbalance, dysrhythmias, or drug toxicity. • Continuous ECG monitoring is done using a combination of leads II, V1, and MCL1. • Telemetry monitoring involves the observation of a patient’s HR and rhythm to help rapidly diagnose dysrhythmias, ischemia, or infarction. • Normal sinus rhythm originates in the SA node and follows the normal conduction pattern of the cardiac cycle. • The P wave represents the depolarization of the atria (passage of an electrical impulse through the atria), causing atrial contraction. • The PR interval represents the time period for the impulse to spread through the atria, AV node, bundle of His, and Purkinje fibers. • The QRS complex represents depolarization of the ventricles (ventricular contraction), and the QRS interval represents the time it takes for depolarization. • The ST segment represents the time between ventricular depolarization and repolarization. This segment should be flat or isoelectric and represents the absence of any electrical activity between these two events. • The T wave represents repolarization of the ventricles. • The QT interval represents the total time for depolarization and repolarization of the ventricles. • Dysrhythmias result from disorders of impulse formation, conduction of impulses or both. Evaluation of Dysrhythmias • Dysrhythmias result from various abnormalities and disease states, and the cause of a dysrhythmia influences the treatment. • Noninvasive diagnostic tests used to evaluate cardiac dysrhythmias and the effectiveness of antidysrhythmia drug therapy include Holter monitoring, event monitoring (or loop recorder), exercise treadmill testing, and signal- averaged ECG. • An electrophysiologic study (EPS) identifies different mechanisms of tachydysrhythmias, heart blocks, bradydysrhythmias, and causes of syncope. Types of Dysrhythmias • Sinus bradycardia has a normal sinus rhythm, but the SA node fires at a rate less than 60 beats/min. It may be a normal clinical condition. Treatment is only indicated in those with symptoms. • Sinus tachycardia has a normal sinus rhythm, but the SA node fires at a rate 101-200 beats/min because of vagal inhibition or sympathetic stimulation. • It is associated with stressors such as exercise, fever, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, myocardial ischemia, heart failure (HF), hyperthyroidism, anxiety, and fear. It can also be an effect of certain drugs. • Treatment is based on the underlying cause. • Premature atrial contraction (PAC) is a contraction originating from an ectopic focus in the atrium in a location other than the sinus node. In healthy persons, isolated PACs are not significant. In persons with heart disease, frequent PACs may warn of or initiate more serious dysrhythmias. • Paroxysmal supraventricular tachycardia (PSVT) is a dysrhythmia originating in an ectopic focus anywhere pg. 31 31 above the bifurcation of the bundle of His. • Prolonged PSVT with HR greater than 180 beats/min may decrease cardiac output (CO), resulting in hypotension, dyspnea, and angina. • o Treatments for PSVT includes vagal stimulation and IV adenosine. • Atrial flutter is an atrial tachydysrhythmia identified by recurring, regular, sawtooth-shaped flutter waves that pg. 32 32 originate from a single ectopic focus in the right atrium. • High ventricular rates (over 100/min) and the loss of the atrial ―kick‖ (atrial contraction reflected by a sinus P wave) can decrease CO and cause serious consequences such as chest pain and HF. • Patients with atrial flutter are at increased risk of stroke. • Radiofrequency catheter ablation is the treatment of choice. • Atrial fibrillation is characterized by a total disorganization of atrial electrical activity caused by multiple ectopic foci resulting in loss of effective atrial contraction. • Atrial fibrillation usually occurs in the patient with underlying heart disease, such as coronary artery disease (CAD), rheumatic heart disease, and cardiomyopathy. • Atrial fibrillation often results in a decrease in CO and poses an increased risk of cardiovascular accident (CVA) because of clot formation, necessitating anticoagulation therapy. • For patients with drug-refractory atrial fibrillation or who do not respond to electrical conversion, radiofrequency catheter ablation and the Maze procedure are options. • Junctionaldysrhythmias refer to dysrhythmias that originate in the area of the AV node, in which the AV node becomes the pacemaker of the heart. Junctional dysrhythmias include junctional premature beats, junctional escape rhythm, accelerated junctional rhythm, and junctional tachycardia. These dysrhythmias are treated according to the type, patient’s tolerance of the rhythm, and patient’s clinical condition. • In first-degree AV block, every impulse is conducted to the ventricles, but the duration of AV conduction is prolonged. First-degree AV block is usually not serious but can be a precursor of higher degrees of AV block. Patients with first-degree AV block are asymptomatic. There is no treatment. • In second-degree AV block, type I (Mobitz I or Wenckebach heart block), there is a gradual lengthening of the PR interval until an atrial impulse is nonconducted and a QRS complex is blocked (missing). • Type I AV block is usually a result of myocardial ischemia or infarction. It is almost always transient and is usually well tolerated. However, it may be a warning signal of a more serious AV conduction disturbance. • If the patient is symptomatic, atropine is used to increase HR, or a temporary pacemaker may be needed. • Second-degree AV block, type II (Mobitz II heart block), involves a P wave that is nonconducted without progressive antecedent PR lengthening. This almost always occurs when a block in one of the bundle branches is present. • Type II AV block often progresses to third-degree AV block and is associated with a poor prognosis. • Temporary treatment before the insertion of a permanent pacemaker may be necessary if the patient becomes symptomatic and involves the use of a temporary transvenous or transcutaneous pacemaker. • In third-degree AV block, or complete heart block, no impulses from the atria are conducted to the ventricles. • It almost always results in reduced CO with subsequent ischemia, HF, and shock. • For symptomatic patients, a transcutaneous pacemaker is used until a temporary transvenous pacemaker can be inserted followed by a permanent pacemaker. • Premature ventricular contraction (PVC) is the premature occurrence of a QRS complex, which is wide and distorted in shape compared with a QRS complex initiated from the normal conduction pathway. • PVCs are usually a benign finding in the patient with a healthy heart. In heart disease, depending on frequency, PVCs may reduce the CO and precipitate angina and HF. • Treatment is often based on the cause of the PVCs (e.g., oxygen therapy for hypoxia, electrolyte replacement). Drugs that can be considered include -adrenergic blockers, procainamide, amiodarone, or lidocaine (Xylocaine). • Ventricular tachycardia (VT) is a run of three or more PVCs. It occurs when an ectopic focus or foci fire repetitively and the ventricle takes control as the pacemaker. • VT is a life-threatening dysrhythmia because of decreased CO and the possibility of deterioration to ventricular fibrillation, which is a lethal dysrhythmia. • VT is associated with myocardial infarction (MI), CAD, significant electrolyte imbalances, cardiomyopathy, mitral valve prolapse, long QT syndrome, digitalis toxicity, and central nervous system disorders. • VT can be stable (patient has a pulse) or unstable (patient is pulseless). pg. 35 35 • ST-segment elevation and pathologic Q wave may be seen on the ECG of a patient with MI. • Patient-monitoring guidelines for patients with suspected ACS include continuous, multilead ECG, and ST- segment monitoring. SYNCOPE pg. 36 36 • Syncope is a brief lapse in consciousness accompanied by a loss in postural tone (fainting). • The causes of syncope are categorized as cardiovascular or noncardiovascular: • Common cardiovascular causes of syncope include vasovagal syncope and primary cardiac dysrhythmias. • Noncardiovascular causes can include hypoglycemia, hysteria, seizure, stroke, and transient ischemic attack. • Various diagnostic tests are used to determine the cause of syncope, including echocardiography, stress testing, EPS, head-up tilt-test, Holter monitors, and event/loop recorders. Chapter 32: Nursing Assessment: Cardiovascular System Structures and Functions of CARDIOVASCULAR SYSTEM Heart • The heart: • Has four chambers: the right and left atrium and ventricles. • Is composed of three layers: endocardium, myocardium, and epicardium. • Is surrounded by a fibroserous sac called the pericardium. • Has four valves, which maintain the one-way flow of blood. • The right side of the heart receives venous blood from the body (via the vena cava) and pumps it to the lungs where it is oxygenated. Blood returns to the left side of the heart (via the pulmonary veins) and is pumped to the body via the aorta. • The coronary circulation provides blood to the myocardium. The right and left coronary arteries are the first branches of the aorta. • The conduction system consists of specialized cells that create and transport electrical impulses. These electrical impulses initiate depolarization of the myocardium and ultimately a cardiac contraction. • Each electrical impulse starts at the SA node (located in the right atrium), travels to the AV node (located at the atrioventricular junction), through the bundle of His, down the right and left bundle branches (located in the ventricular septum), and terminating in the Purkinje fibers. • The electrical activity of the heart is recorded on the electrocardiogram (ECG). • Contraction of the myocardium, or systole, results in ejection of blood from the ventricles. Relaxation of the myocardium, or diastole, allows for filling of the ventricles. • Cardiac output (CO) is the amount of blood pumped by each ventricle in 1 minute. It is calculated by multiplying the amount of blood ejected from the ventricle with each heartbeat (stroke volume [SV]) by the heart rate (HR) per minute: CO = SV HR. • Factors affecting SV are preload, afterload, and contractility. Preload is the volume of blood in the ventricles at the end of diastole, and afterload represents the peripheral resistance against which the left ventricle must pump. Regulation of Cardiovascular System • Stimulation of the sympathetic nervous system increases HR, speed of conduction through the AV node, and force of atrial and ventricular contractions, whereas stimulation of the parasympathetic nervous system decreases HR. • Stimulation of baroreceptors and chemoreceptors, located in the aortic arch and carotid sinus, can initiate changes in HR and arterial pressure. • Normal BP is systolic BP less than 120 mm Hg and diastolic BP less than 80 mm Hg. • The two main factors influencing BP are cardiac output (CO) and systemic vascular resistance (SVR), which is the force opposing the movement of blood. • BP can be measured by invasive techniques (catheter inserted in an artery) and noninvasive techniques (using a sphygmomanometer and a stethoscope, or an automated noninvasive device). • A mean arterial pressure (MAP) of greater than 60 is necessary to sustain the vita l organs of an average person under most conditions. Assessment OFCARDIOVASCULAR SYSTEM Past Health History • A health history for the cardiac system consists of assessment of past health history, medications, surgery or other treatments, family health history, psychosocial history, risk factor identification, and a review of systems using functional health patterns. pg. 37 37 • Obtain a thorough history of the present illness. Explore and document common signs of cardiac problems (e.g., pain, dyspnea). Describe the course of the patient’s illness, including when it began, the type of symptoms, and factors that alleviate or aggravate these symptoms. Physical Examination pg. 40 40 of all cases of hypertension. • Secondary hypertension: elevated BP with a specific cause; accounts for 5% to 10% of hypertension in adults. Pathophysiology of Primary Hypertension • The hemodynamic hallmark of hypertension is persistently increased SVR. • This persistent elevation in SVR may come about in various ways. Abnormalities of any of the mechanisms involved in the maintenance of normal BP, including sodium intake, the renin-angiotensin-aldosterone mechanism, and sympathetic nervous system (SNS) stimulation, can result in the development of hypertension. • Abnormalities of glucose, insulin, and lipoprotein metabolism are common in primary hypertension. • Contributing factors to the development of hypertension include cardiovascular risk factors combined with socioeconomic conditions and gender and ethnic differences. Clinical Manifestations • Often called the ―silent killer‖ because it is frequently asymptomatic until it becomes severe and target organ disease occurs. • Target organ diseases occur in the heart (hypertensive heart disease), brain (cerebrovascular disease), peripheral vasculature (peripheral vascular disease), kidney (nephrosclerosis), and eyes (retinal damage). • It is one of the leading causes of end-stage renal disease, especially among African Americans. • Damage to retinal vessels provides an indication of concurrent vessel damage in the heart, brain, and kidney. Manifestations of severe retinal damage include blurring of vision, retinal hemorrhage, and loss of vision. • There is a direct relationship between hypertension and cardiovascular disease (CVD). Hypertension is a major risk factor for coronary artery disease (CAD), stroke, and cerebral atherosclerosis. • Sustained high BP increases the cardiac workload and produces left ventricular hypertrophy (LVH). Progressive LVH, especially in association with CAD, is associated with the development of heart failure. DIAGNOSTIC STUDIES • Basic laboratory studies are performed to (1) identify or rule out causes of secondary hypertension, (2) evaluate target organ disease, (3) determine overall cardiovascular risk, or (4) establish baseline levels before initiating therapy. • Routine urinalysis, BUN, serum creatinine, and creatinine clearance levels are used to screen for renal involvement and to provide baseline information about kidney function. • Lipid profile provides information about additional risk factors that predispose to atherosclerosis and cardiovascular disease. • ECG and echocardiography provide information about the cardiac status. • Ambulatory blood pressure monitoring (ABPM) may be used to measure BP at preset intervals over a 24-hour period. Collaborative Care • The goal for treating primary hypertension is BP <140/90 mm Hg. A goal of <130/80 mm Hg is recommended for patients who are high risk for CAD as well as for patients with preexisting CAD. A goal of <120/80 mm Hg may be considered for some patients. • Lifestyle modifications are indicated for all patients with prehypertension and hypertension. These include weight reduction, using the DASH eating plan, dietary restriction of sodium, restricted alcohol intake, avoidance of tobacco products, participating in physical activity, and reducing psychosocial risk factors that contribute to the risk of developing CVD. Drug Therapy • Drugs currently available for treating hypertension work by (1) decreasing the volume of circulating blood, and/or (2) reducing SVR. • Diuretics promote sodium and water excretion, reduce plasma volume, and reduce the vascular response to catecholamines. • Adrenergic-inhibiting agents act by diminishing the SNS effects that increase BP. Adrenergic inhibitors include drugs that act centrally on the vasomotor center and peripherally to inhibit norepinephrine release or to block the adrenergic receptors on blood vessels. • Direct vasodilators decrease the BP by relaxing vascular smooth muscle and reducing SVR. pg. 41 41 • Calcium channel blockers increase sodium excretion and cause arteriolar vasodilation by preventing the movement of extracellular calcium into cells. • Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II and reduce angiotensin II (A-II)–mediated vasoconstriction and sodium and water retention. • A-II receptor blockers (ARBs) prevent angiotensin II from binding to its receptors in the walls of the pg. 42 42 blood vessels. • Most patients who are hypertensive will require two or more antihypertensive medications to achieve their BP goals. • Side effects and adverse effects of antihypertensive drugs may be so severe or undesirable that the patient does not comply with therapy. Patient and family teaching related to drug therapy is needed to identify and minimize side effects and to cope with therapeutic effects. • Resistant hypertension is the failure to reach goal BP in patients who are adhering to full doses of an appropriate three-drug therapy regimen that includes a diuretic. NURSING MANAGEMENT: PRIMARY HYPERTENSION • The primary nursing responsibilities for long-term management of hypertension are to assist the patient in reducing BP and complying with the treatment plan. • Nursing actions include patient and caregiver teaching, detection and reporting of adverse treatment effects, compliance assessment and enhancement, and evaluation of therapeutic effectiveness. • Patient and family teaching includes the following: (1) nutritional therapy, (2) drug therapy, (3) lifestyle modification, and (4) home monitoring of BP (if appropriate). Blood Pressure Measurement • Accurate BP measurements are important; an important role of the nurse is to provide patient and family teaching regarding measuring BP at home. • Orthostatic hypotension is defined as a decrease of 20 mm Hg or more in SBP, a decrease of 10 mm Hg or more in DBP, and/or an increase of 20 beats/min or more in pulse from supine to standing. • Orthostatic (or postural) changes in BP and pulse should be measured in older adults, in people taking antihypertensive drugs, and in patients who report symptoms consistent with reduced BP upon standing (e.g., light-headedness, dizziness, syncope). GERONTOLOGIC CONSIDERATIONS: HYPERTENSION • The prevalence of hypertension increases with age. The lifetime risk of developing hypertension is approximately 90% for middle-age (age 55-65) and older (age >65) normotensive men and women. • In some older people, there is a wide gap between the first Korotkoff sound and subsequent beats (auscultatory gap). Failure to inflate the cuff high enough may result in underestimating the SBP. • Older adults are sensitive to BP changes and may by resistant to the effects of ACE inhibitors and ARBs. • Orthostatic hypotension occurs often in older adults because of impaired baroreceptor reflex mechanisms, volume depletion, and chronic disease states, such as decreased renal and hepatic function or electrolyte imbalance. HYPERTENSIVE CRISIS • Hypertensive crisis is a term used to indicate either a hypertensive urgency or emergency. This is determined by the degree of target organ damage and how quickly the BP must be lowered. • Hypertensive urgency develops over days to weeks; the BP is severely elevated but there is no clinical evidence of target organ damage. • Hypertensive urgencies usually do not require IV medications but can be managed with oral agents. • If a patient with hypertensive urgency is not hospitalized, outpt F/U should be arranged within 24 hours. • Hypertensive emergencies require hospitalization with intensive care monitoring and the intravenous (IV) administration of antihypertensive drugs, including vasodilators, adrenergic inhibitors, and the ACE inhibitor enalaprilat. The rate of drug administration is titrated according to the level of MAP or BP. • Regular, ongoing assessment (e.g., ECG monitoring, vital signs, urinary output, level of consciousness, visual changes) is essential to evaluate the patient with severe hypertension. Chapter 34: Nursing Management: Coronary Artery Disease and Acute Coronary Syndrome CORONARYARTERY DISEASE • Coronary artery disease (CAD) is a type of blood vessel disorder included in the general category of atherosclerosis. Atherosclerosis is characterized by the deposit of cholesterol and lipids within the intimal wall of an artery. • CAD is a progressive disease that develops in stages; when it becomes symptomatic, the disease process is usually well advanced. pg. 45 45 • Smoking and tobacco use may precipitate coronary artery spasms. Prinzmetal’s angina may also be seen in patients with a history of migraine headaches and Raynaud’s phenomenon. • The pain may be relieved by moderate exercise or it may disappear spontaneously. Calcium channel blockers and/or nitrates are used to control the angina. ACUTE CORONARY SYNDROME pg. 46 46 • Acute coronary syndrome (ACS) develops when ischemia is prolonged and not immediately reversible. ACS encompasses the spectrum of unstable angina, non–ST-segment-elevation myocardial infarction (NSTEMI), and ST-segment-elevation myocardial infarction (STEMI). • Unstable angina (UA) is chest pain that is new in onset, occurs at rest, or has a worsening pattern. UA is unpredictable and represents an emergency. MYOCARDIAL INFARCTION • Myocardial infarction (MI) occurs as a result of sustained ischemia, causing irreversible myocardial cell death. Contractile function of the heart stops in the infarcted area(s). • The acute MI process takes time, evolving over a period of up to 12 hours. • Infarctions are described based on the location of damage. • Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration is the hallmark of an MI. The pain is usually described as a heaviness, pressure, tightness, burning, constriction, or crushing. • Complications after MI • Dysrhythmias are the most common complication and the most common cause of death in patients in the prehospital period. • Other complications include heart failure, cardiogenic shock, papillary muscle dysfunction or rupture, ventricular aneurysm, and pericarditis. • Primary diagnostic studies used to determine whether a person has UA or an MI includes an ECG and serum cardiac markers. COLLABORATIVE CARE: ACUTE CORONARY SYNDROME • Rapid diagnosis and treatment for a patient with ACS is necessary to preserve cardiac function. • For patients with STEMI or NSTEMI with positive cardiac markers, reperfusion therapy is the recommended treatment of choice. This can include emergent PCI or fibrinolytic (thrombolytic) therapy. • Cardiac catheterization is used to locate and assess blockage and implement treatment modalities if needed. • Fibrinolytic therapy aims to stop infarction process by dissolving the thrombus in the coronary artery to reperfuse the myocardium. • Coronary revascularization with coronary artery bypass graft (CABG) surgery is recommended for patients who fail medical management, have left main coronary artery or three-vessel disease, are not candidates for PCI, have failed PCI with ongoing chest pain, or have diabetes. • Minimally invasive direct CABG surgery can be used for patients requiring one or two bypasses in one or two coronary arteries on the anterior surface of the heart. • Off-pump coronary artery bypass procedure uses full or partial sternotomy to enable access to all coronary vessels. • Transmyocardial laser revascularization is an indirect revascularization procedure used for patients with advanced CAD who are not candidates for traditional bypass surgery and who have persistent angina after maximum medical therapy. Drug Therapy • Initial management of the patient with chest pain includes aspirin, IV nitroglycerin, systemic anticoagulation, morphine sulfate for pain unrelieved by nitroglycerin, and oxygen. • IV antiplatelet agents may also be used if PCI is anticipated. • β-Adrenergic blockers are administered IV initially or orally within 24 hours if there are no contraindications. • ACE inhibitors, calcium channel blockers, angiotensin receptor blockers, and long-acting nitrates are also used in select situations. • Stool softeners are given to facilitate and promote the comfort of bowel evacuation (opioid constipation). NURSING MANAGEMENT: CHRONIC STABLE ANGINA AND ACUTE CORONARY SYNDROME • The following nursing measures should be instituted for a patient experiencing angina: (1) administer supplemental oxygen and position patient in upright position unless contraindicated, (2) determine vital signs, (3) obtain a 12-lead ECG, (4) provide prompt pain relief first with a nitrate followed by an opioid analgesic if needed, and (5) auscultate heart sounds. • Teaching for a patient with angina should include information regarding ACS, managing angina, risk factor reduction, and medication. pg. 47 47 Nursing Implementation: Acute Coronary Syndrome • Initial treatment of a patient with ACS includes pain assessment & relief, physiologic monitoring, promotion of rest & comfort, alleviation of stress & anxiety, & understanding of the patient’s emotional & behavioral reactions. • Nitroglycerin, morphine sulfate, and supplemental oxygen should be provided as needed to eliminate or reduce chest pain. pg. 50 50 • Heart failure (HF) is an abnormal clinical syndrome involving impaired cardiac pumping and/or filling. • HF is characterized by ventricular dysfunction, reduced exercise tolerance, diminished quality of life, and shortened life expectancy. • Risk factors include coronary artery disease (CAD) and advancing age. Hypertension, diabetes, cigarette smoking, obesity, and high serum cholesterol also contribute to the development of HF. • Heart failure is classified as systolic or diastolic failure. • oSystolic failure results from an inability of the heart to pump blood effectively. • oDiastolic failure is an impaired ability of the ventricles to relax and fill during diastole. Clinical Manifestations: Acute Decompensated Heart Failure and Chronic Heart Failure • • HF can have an abrupt onset as with acute myocardial infarction or it can be an insidious process resulting from slow, progressive changes. • • Compensatory mechanisms are activated to maintain adequate cardiac output (CO). Several counter regulatory processes are activated, including the production of hormones from the heart muscle to promote vasodilation. • • Cardiac compensation occurs when compensatory mechanisms succeed in maintaining an adequate CO that is needed for tissue perfusion. • • Cardiac decompensation occurs when these mechanisms can no longer maintain adequate CO and inadequate tissue perfusion results. • • Over time, ventricular remodeling, dilation, and hypertrophy develop and lead to chronic HF. • • The most common form of HF is left-sided failure from left ventricular dysfunction. Blood backs up into the left atrium and into the pulmonary veins, causing pulmonary congestion and edema. • • Acute decompensated heart failure (ADHF) typically manifests as pulmonary edema, an acute, life-threatening situation. • • Clinical manifestations of chronic HF depend on the patient’s age and the underlying type and extent of heart disease. Common symptoms include fatigue, cough, dyspnea, tachycardia, edema, and limitations of usual activities of daily living (ADLs). • • Pleural effusion, atrial fibrillation, thrombus formation, renal insufficiency, and hepatomegaly are all complications of HF. Diagnostic Studies • • To determine the underlying etiology of HF, a thorough history, physical examination, chest x-ray, electrocardiogram (ECG), laboratory data (e.g., cardiac enzymes, b-type natriuretic peptide [BNP], serum chemistries, liver function studies, thyroid function studies, complete blood count), hemodynamic assessment, echocardiogram, stress testing and cardiac catheterization may be done. Collaborative Care: Acute Decompensated Heart Failure • • The goals of therapy for ADHF are to improve patient symptoms, reverse ventricular remodeling, improve quality of life, and decrease mortality and morbidity. • • Treatment strategies should include the following: • o Decreasing intravascular volume with the use of diuretics or ultrafiltration, • o Decreasing venous return (preload) to reduce the amount of volume returned to the left ventricle (LV) during diastole. • o Decreasing afterload (the resistance against which the LV must pump) to improve CO and decrease pulmonary congestion. • o Gas exchange is improved by the administration of intravenous (IV) morphine sulfate and supplemental oxygen. • o Inotropic therapy and hemodynamic monitoring may be needed in patients who do not respond to conventional pharmacotherapy. • o Reduction of anxiety is an important nursing function, since anxiety may increase the sympathetic nervous system (SNS) response and further increase myocardial workload. pg. 51 51 Collaborative Care: Chronic Heart Failure • • The main goal in the treatment of chronic HF is to treat the underlying cause and contributing factors, maximize CO, provide treatment to alleviate symptoms, improve ventricular function, improve quality of life, preserve target organ function, and improve mortality and morbidity. • • Administration of oxygen improves saturation and assists greatly in meeting tissue oxygen needs and pg. 52 52 helps relieve dyspnea and fatigue. • • Physical and emotional rest allows the patient to conserve energy and decreases the need for additional oxygen. The degree of rest recommended depends on the severity of HF. • • Nonpharmacologic therapies, including cardiac resynchronization therapy, biventricular pacing, intraaortic balloon pump, and ventricular assist devices, are an integral part of the management of HF patients. • • Drug therapy is a critical part of the care of patients with HF: • o Diuretics are used in HF to mobilize edematous fluid, reduce pulmonary venous pressure, and reduce preload. • o Vasodilator drugs have been shown to improve survival in HF by increasing venous capacity, improving EF through improved ventricular contraction, slowing the process of ventricular dysfunction, and decreasing heart size. • o Angiotensin-converting enzyme (ACE) inhibitors are the primary drug of choice in chronic HF patients with systolic dysfunction. • o Angiotensin II receptor blockers may be used in patients who are ACE inhibitor intolerant. • o -Adrenergic blockers in combination with ACE inhibitors and diuretics have improved survival of patients with HF. • o Digitalis glycosides remain the mainstay in the treatment of HF; however, they have not been shown to prolong life. • • Diet education and weight management are critical to the patient’s control of chronic HF. • o The edema of chronic HF is often treated by dietary restriction of sodium. • o Fluid restrictions are not commonly prescribed for the patient with mild to moderate HF. In moderate to severe HF, fluid restrictions are usually implemented. • o Patients should weigh themselves daily. If a patient experiences a weight gain of 3 lb over 2 days or 3 to 5 lb over a week, the primary care provider should be called. NURSING MANAGEMENT: HEART FAILURE • • The overall goals for the patient with HF include a decrease in symptoms, an increase in exercise tolerance, compliance with the medical regimen, and no complications related to HF. • • Treatment or control of underlying heart disease is key to preventing episodes of ADHF. • • Nursing care of the patient with ADHF revolves around the nursing diagnoses of decreased CO, impaired gas exchange, excess fluid volume, and activity intolerance. Ambulatory and Home Care • • Effective home health nursing can prevent or limit hospitalizations of the HF patient. • • Preventive care should focus on slowing the progression of the disease. Teaching must include information on medications, diet, and exercise regimens. • • Important nursing responsibilities in the care of a patient with HF include (1) teaching the patient about the physiologic changes that have occurred, (2) assisting the patient to adapt to both the physiologic and psychologic changes, and (3) integrating the patient and the patient’s family or support system in the overall care plan. • o Many patients with HF are at high risk for anxiety and depression. • o Patients should be taught to evaluate the action of the prescribed drugs and to recognize the manifestations of drug toxicity. 1 ♣ Patients should be taught how to take their pulse rate and to know under what circumstances drugs, especially digitalis and -adrenergic blockers, should be withheld and a health care provider consulted. 2 ♣ It may be appropriate to instruct patients in home BP monitoring. 3 ♣ Patients should be taught the symptoms of hypokalemia and hyperkalemia if diuretics that deplete or spare potassium are being taken. • o The physical therapist, occupational therapist, or you should instruct the patient in energy- conserving and energy-efficient behaviors after an evaluation of daily activities has been done. pg. 55 55 • • Acute pericarditis most often is idiopathic but can be caused by uremia, viral or bacterial infection, acute myocardial infarction (MI), cardiac surgery, tuberculosis, neoplasm, inflammation caused by radiation to the chest, and trauma. • • Pericarditis in the acute MI patient may be described as two distinct syndromes: (1) acute pericarditis pg. 56 56 (occurs within the initial 48-72 hours after an MI), and (2) Dressler syndrome (late pericarditis that appears 4-6 weeks after an MI). • • Clinical manifestations include the following: • o Progressive, frequently severe chest pain that is sharp and pleuritic in nature and worse with deep inspiration and when lying supine. The pain is relieved by sitting up and leaning forward. It can be referred to the shoulder and upper back. • o The hallmark finding in acute pericarditis is a pericardial friction rub. • • Complications include pericardial effusion and cardiac tamponade. • • Collaborative care includes the following: • o Antibiotics • o Pain and inflammation are usually treated with nonsteroidal antiinflammatory drugs (NSAIDs) or high-dose salicylates; corticosteroids may be an option in some patients. • o Colchicine, an antiinflammatory agent used for gout, may be considered for patients who have recurrent pericarditis. • o Pericardiocentesis is usually performed if accompanied by acute cardiac tamponade, purulent pericarditis, and a high suspicion of a neoplasm. • • The management of the patient’s pain and anxiety during acute pericarditis is a primary nursing consideration. Pain relief measures include maintaining bed rest with the head of the bed elevated to 45 degrees and providing an overbed table for support, and antiinflammatory medications. CHRONIC CONSTRICTIVE PERICARDITIS • • Chronic constrictive pericarditis results from scarring with consequent loss of elasticity of the pericardial sac. The end result is that the pericardium impairs the ability of the atria and ventricles to stretch adequately during diastole. • • Clinical manifestations mimic HF and cor pulmonale. Jugular venous distention (JVD) and a pericardial knock, a loud early diastolic sound often heard along the left sternal border, are the most common. • • Treatment of choice for chronic constrictive pericarditis is a pericardiectomy. MYOCARDITIS • • Myocarditis is a focal or diffuse inflammation of the myocardium caused by viruses, bacteria, fungi, radiation therapy, and pharmacologic and chemical factors. • • Clinical manifestations include the following: • o Fever, fatigue, malaise, myalgias, pharyngitis, dyspnea, lymphadenopathy, and nausea and vomiting are early systemic manifestations of the viral illness. • o Early cardiac signs appear 7 to 10 days after viral infection and include pleuritic chest pain with a pericardial friction rub and effusion. • o Late cardiac signs relate to the development of HF and may include an S3 heart sound, crackles, JVD, syncope, peripheral edema, and angina. • • Treatment for myocarditis consists of managing the associated cardiac symptoms. • o Drug therapy includes the use of digoxin, angiotensin-converting enzyme (ACE) inhibitors, -blockers, and diuretics. • o Vasodilators may be used if hypotension is not present. • o Anticoagulation therapy is used in those who are at risk for thrombus formation. • o Immunosuppressive therapy to reduce myocardial inflammation and to prevent irreversible myocardial damage may be considered. • o Oxygen therapy, bed rest, and restricted activity • o Intraaortic balloon pump therapy and ventricular assist devices • • Nursing interventions focus on assessment for the signs and symptoms of HF and include assessing the level of anxiety, instituting measures to decrease anxiety, and keeping the patient and caregiver informed about therapeutic measures. • • Most patients with myocarditis recover spontaneously, although some may develop dilated pg. 57 57 cardiomyopathy (CMP). If severe HF occurs, the patient may require heart transplantation. RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE • • Rheumatic fever (RF) is an inflammatory disease of the heart that occurs as a complication following group A streptococcal pharyngitis. pg. 60 60 • • Mitral valve prolapse (MVP) is an abnormality of the mitral valve leaflets and the papillary muscles or chordae that allows the leaflets to prolapse, or buckle, back into the left atrium during systole. The etiology of MVP is unknown. • • In many patients, MVP found by echocardiography is not accompanied by any other clinical manifestations of cardiac disease, and the significance of the finding is unclear. AORTIC VALVE STENOSIS • • In older patients, aortic stenosis is a result of rheumatic fever or senile fibrocalcific degeneration that may have an etiology similar to coronary artery disease. • • Aortic stenosis results in left ventricular hypertrophy and increased myocardial oxygen consumption. As the disease progresses, cardiac output (CO) is reduced, leading to decreased tissue perfusion, pulmonary hypertension, and HF. • • Clinical manifestations include a systolic murmur and the classic triad of angina, syncope, and exertional dyspnea. AORTIC VALVE REGURGITATION • • Acute aortic regurgitation (AR) is caused by IE, trauma, or aortic dissection. • • Chronic AR is generally the result of rheumatic heart disease, a congenital bicuspid aortic valve, syphilis, or chronic rheumatic conditions. • • Clinical manifestations of acute AR include severe dyspnea, chest pain, and hypotension indicating left ventricular failure and cardiogenic shock that constitute a medical emergency. • • Clinical manifestations of chronic AR include exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea after considerable myocardial dysfunction has occurred. TRICUSPID AND PULMONIC VALVE DISEASE • • Diseases of the tricuspid and pulmonic valves are uncommon, with stenosis occurring more frequently than regurgitation. Pulmonary stenosis is almost always congenital. • • Tricuspid stenosis occurs almost exclusively in patients with rheumatic mitral stenosis, in IV drug abusers, or in patients treated with a dopamine agonist. It results in right atrial enlargement and elevated systemic venous pressures. COLLABORATIVE CARE OF VALVULAR HEART DISEASE • • Collaborative care of valvular heart disease includes the prevention of recurrent RF and IE and the prevention of exacerbations of HF, acute pulmonary edema, and thromboembolism. • • Anticoagulant therapy is used to prevent and treat systemic or pulmonary embolization. • • An alternative treatment for stenotic valvular heart disease is percutaneous transluminal balloon valvuloplasty to split open the fused commissures. • • Surgical intervention is based on the clinical state of the patient and depends on the valves involved, the pathology and severity of the disease, and the patient’s clinical condition. • o Valve repair, including a valvulotomy, valvuloplasty, or annuloplasty, is typically the surgical procedure of choice. • o Valve replacement may be required; a wide variety of prosthetic valves, both mechanical and biologic, are available. • • The overall goals for a patient with valve disease include normal cardiac function, improved activity intolerance, and an understanding of health maintenance measures. • o Prophylactic antibiotic therapy is necessary to prevent IE and, if the valve disease was caused by RF, ongoing prophylaxis is necessary. • o Patients on anticoagulation therapy after valve replacement surgery must have the international normalized ratio (INR) checked regularly. • o You must teach the patient to seek medical care if any manifestations of infection or HF, any signs of bleeding, and any planned invasive or dental procedures are planned. pg. 61 61 CARDIOMYOPATHY • • CMP constitutes a group of diseases that directly affect the structural or functional ability of the myocardium. • • CMP is classified as primary (refers to those conditions in which the etiology of the heart disease is pg. 62 62 unknown) or secondary (the cause of the myocardial disease is known and is a result of another disease process). DILATED CARDIOMYOPATHY • • Dilated CMP is characterized by a diffuse inflammation and rapid degeneration of myocardial fibers that result in ventricular dilation, impairment of systolic function, atrial enlargement, and stasis of blood in the left ventricle. • • Clinical manifestations develop acutely after an infectious process or insidiously over a period. Most people eventually develop HF. • • Interventions focus on controlling HF by enhancing myocardial contractility and decreasing afterload. The goal of therapy is to keep the patient at an optimal level of function and out of the hospital. • o Drug therapy is the mainstay of treatment. • o Nutritional therapy and cardiac rehabilitation may help alleviate symptoms and improve quality of life. • o Cardiac resynchronization therapy, ICDs, and ventricular assist devices may be considered in appropriate patients. HYPERTROPHIC CARDIOMYOPATHY • • Hypertrophic CMP is asymmetric left ventricular hypertrophy without ventricular dilation. The end result is impaired ventricular filling as the ventricle becomes noncompliant and unable to relax. • • Patients with hypertrophic CMP may be asymptomatic or may have exertional dyspnea, fatigue, angina, syncope, and dysrhythmias. • • Goals of intervention are to improve ventricular filling by reducing ventricular contractility and relieving left ventricular outflow obstruction. • o Drug therapy for hypertrophic CMP includes -adrenergic blockers or calcium channel blockers. Digitalis preparations are contraindicated unless they are used to treat atrial fibrillation, and antidysrhythmics are used as needed. • o For patients at risk for sudden cardiac death (SCD), the implantation of a cardioverter- defibrillator is recommended. • o Atrioventricular pacing can be beneficial for patients with hypertrophic CMP and outflow obstruction. • o Some patients may be candidates for a ventriculomyotomy and myectomy. • • Nursing interventions for hypertrophic CMP focus on relieving symptoms, observing for and preventing complications, and providing emotional and psychologic support. RESTRICTIVE CARDIOMYOPATHY • • Restrictive CMP, the least common CMP, impairs diastolic filling and stretch, although systolic function remains unaffected. • • The specific etiology of restrictive CMP is unknown. • • Clinical manifestations include fatigue, exercise intolerance, and dyspnea. Currently no specific treatment for restrictive CMP exists, and interventions are aimed at improving diastolic filling and the underlying disease process. • o Treatment includes conventional therapy for HF and dysrhythmias. • o Heart transplant may also be a consideration. • o Nursing care is similar to the care of a patient with HF. Chapter 38: Nursing Management: Vascular Disorders pg. 65 65 pressure and deep pain sensations. • o Physical findings include thin, shiny, and taut skin with loss of hair on the lower legs; diminished or absent pedal, popliteal, or femoral pulses; elevation pallor; and reactive hyperemia when the limb is in a dependent position. pg. 66 66 • • Complications of PAD include nonhealing ulcers over bony prominences on the toes, feet, and lower leg, and gangrene. Amputation may be required if blood flow is not restored. • • Various tests are used to diagnose PAD, including Doppler ultrasound with segmental blood pressures, calculating the ankle-brachial index (ABI), and angiography. • • The overall goals for the patient with lower-extremity PAD include adequate tissue perfusion, relief of pain, increased exercise tolerance, and intact, healthy skin on extremities. • o The first treatment goal for patients with PAD is to aggressively modify all cardiovascular risk factors. All tobacco use and products must be stopped. • o Drug therapy includes antiplatelet agents and angiotensin-converting enzyme (ACE) inhibitors. Two drugs approved to treat intermittent claudication are cilostazol (Pletal) and pentoxifylline (Trental). • o The primary nonpharmacologic treatment for claudication is a formal exercise-training program with walking being the most effective exercise. • o Interventional radiologic procedures for PAD include percutaneous transluminal balloon angioplasty with stenting. • o The most common surgical procedure for PAD is a peripheral arterial bypass operation with autogenous vein or synthetic graft material to bypass or carry blood around the lesion. • o All patients with PAD should be taught the importance of meticulous foot care. • • Critical limb ischemia is a chronic condition characterized by ischemic rest pain, arterial leg ulcers, and/or gangrene of the leg caused by advanced PAD. ACUTE ARTERIAL ISCHEMIC DISORDERS • • Acute arterial ischemia is a sudden interruption in the arterial blood supply to a tissue, organ, or extremity that, if untreated, results in tissue death. • • Common causes include embolism, thrombosis, or trauma. • • Specific manifestations depend on the area affected of the body. Signs and symptoms of an acute arterial ischemia usually have an abrupt onset and include the six Ps: pain, pallor, pulselessness, paresthesia, paralysis, and poikilothermia. • • Treatment options include anticoagulation, thrombolysis, embolectomy, surgical revascularization, or amputation. Thromboangiitis Obliterans • • Thromboangiitis obliterans (Buerger’s disease) is a somewhat rare nonatherosclerotic, segmental, recurrent inflammatory vaso-occlusive disorder of the small and medium-sized arteries, veins, and nerves of the upper and lower extremities. • • Patients may have intermittent claudication of the feet, hands, or arms. As the disease progresses, rest pain and ischemic ulcerations develop. • • There are no laboratory or diagnostic tests specific to Buerger’s disease. • • Treatment includes complete cessation of tobacco use in every form. Conservative management includes the use of antibiotics to treat any infected ulcers and analgesics to manage the ischemic pain. • • Surgical options include revascularization, implantation of a spinal cord stimulator, and sympathectomy. Raynaud’s Phenomenon • • Raynaud’s phenomenon is an episodic vasospastic disorder of small cutaneous arteries, most frequently involving the fingers and toes. The exact etiology is unknown. • • Clinical symptoms include vasospasm-induced color changes of the fingers, toes, ears, and nose (white, blue, and red). An episode usually lasts only minutes but in severe cases may persist for several hours. • • Symptoms usually are precipitated by exposure to cold, emotional upsets, caffeine, and tobacco use. • • There is no diagnostic test; diagnosis is based on persistent symptoms for at least 2 years. • • Patient teaching should be directed toward prevention of recurrent episodes; temperature extremes and all tobacco products should be avoided. • • Calcium channel blockers are the first-line drug therapy. pg. 67 67 Venous Thrombosis • • Phlebitis is the inflammation of a superficial vein without the presence of a thrombus. • • Venous thrombosis is the most common disorder of the veins and involves the formation of a thrombus (clot) in association with inflammation of the vein. Venous thromboembolism (VTE) represents the spectrum of pg. 70 70 Chronic Venous Insufficiency and VENOUS Leg Ulcers • • Chronic venous insufficiency (CVI) is a condition in which the valves in the deep veins are damaged, which results in retrograde venous blood flow, pooling of blood in the legs, and swelling and can lead to venous leg ulcers. • • Causes of CVI include VTE, vein incompetence, deep vein obstruction, congenital venous malformation, and AV fistula. • • Clinical manifestations include the skin of the lower leg appearing leathery, with a characteristic brownish or ―brawny‖ appearance; edema and eczema, and pruritus. • • Venous ulcers classically are located above the medial malleolus. The wound margins are irregularly shaped, and the tissue is typically a ruddy color. Ulcer drainage may be extensive. Pain is present and may be worse when the leg is in a dependent position. • • Compression is essential to the management of CVI, venous ulcer healing, and prevention of ulcer recurrence. • o Options include elastic wraps, custom-fitted graduated compression stockings, elastic tubular support bandages, a Velcro wrap, sequential compression devices, a paste bandage with an elastic wrap, and multilayer (three or four) bandage systems. • o Moist environment dressings are the basis of wound care and include transparent film dressings, hydrocolloids, hydrogels, foams, impregnated gauze, and combination dressings. • o Nutritional status and intake should be evaluated. • o Wounds need to be monitored for signs of infection. The usual treatment for infection is sharp debridement, wound excision, and systemic antibiotics. • • Alternative treatments may include coverage with a split-thickness skin graft, cultured epithelial autograft, allograft, or bioengineered skin. • • Long-term management of venous leg ulcers should focus on teaching the patient about self-care measures because the incidence of recurrence is high. • o Proper foot and leg care is essential to avoid additional trauma to the skin. • o The patient with CVI should avoid standing or sitting with the feet dependent for long periods. • o Venous ulcer patients are instructed to elevate their legs above the level of the heart to reduce edema. • o Once an ulcer is healed, a daily walking program is encouraged. • o Prescription graduated compression stockings should be worn daily and replaced every 4 to 6 months to reduce the occurrence of CVI. • Chapter 67: Nursing Management: Shock, Systemic Inflammatory Response Syndrome, and Multiple Organ Dysfunction Syndrome SHOCK • • Shock is a syndrome characterized by decreased tissue perfusion and impaired cellular metabolism resulting in an imbalance between the supply of and demand for oxygen and nutrients. • • The four main categories of shock are cardiogenic, hypovolemic, distributive (includes septic, anaphylactic, and neurogenic shock), and obstructive. Cardiogenic Shock • • Cardiogenic shock occurs when either systolic or diastolic dysfunction of the pumping action of the heart results in reduced cardiac output (CO). • • Causes of cardiogenic shock include acute myocardial infarction (AMI), cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary hypertension, and myocardial depression from metabolic problems. pg. 71 71 • • Clinical manifestations include tachycardia, hypotension, a narrowed pulse pressure, tachypnea, pulmonary congestion, cyanosis, pallor, cool and clammy skin, diaphoresis, decreased capillary refill time, anxiety, confusion, and agitation. Hypovolemic Shock pg. 72 72 • • Hypovolemic shock occurs when there is a loss of intravascular fluid volume. • • Absolute hypovolemia results when fluid is lost through hemorrhage, gastrointestinal (GI) loss (e.g., vomiting, diarrhea), fistula drainage, diabetes insipidus, or diuresis. • • Relative hypovolemia results when fluid volume moves out of the vascular space into extravascular space, such as with sepsis and burns. • • Clinical manifestations depend on the extent of injury or insult, age, and general state of health and may include anxiety; an increase in heart rate, CO, and respiratory rate and depth; and a decrease in stroke volume, pulmonary artery wedge pressure (PAWP), and urine output. Neurogenic Shock • • Neurogenic shock is a hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks, or in response to spinal anesthesia. • • Clinical manifestations include hypotension, bradycardia, temperature dysregulation (resulting in heat loss), dry skin, and poikilothermia. Anaphylactic Shock • • Anaphylactic shock is an acute and life-threatening hypersensitivity (allergic) reaction to a sensitizing substance (e.g., drug, chemical, vaccine, food, insect venom). • • Immediate reaction causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability resulting in fluid leaks from the vascular space into the interstitial space. • • Clinical manifestations can include anxiety, confusion, dizziness, chest pain, incontinence, swelling of the lips and tongue, wheezing, stridor, flushing, pruritus, urticaria, and angioedema. Septic Shock • • Sepsis is a systemic inflammatory response to a documented or suspected infection. Severe sepsis is sepsis complicated by organ dysfunction. • • Septic shock is the presence of sepsis with hypotension despite fluid resuscitation along with the presence of inadequate tissue perfusion. • • In severe sepsis and septic shock, the body’s response to infection is exaggerated, resulting in an increase in inflammation and coagulation, and a decrease in fibrinolysis. • • Septic shock has three major pathophysiologic effects: vasodilation, maldistribution of blood flow, and myocardial depression. • • Patients often have hypotension, respiratory failure, alteration in neurologic status, decreased urine output, and GI dysfunction. Stages of Shock • • The initial stage of shock that occurs at a cellular level is usually not clinically apparent. • • The compensatory stage is clinically apparent and involves neural, hormonal, and biochemical compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis. • • The progressive stage of shock begins as compensatory mechanisms fail and aggressive interventions are necessary to prevent the development of multiple-organ dysfunction system (MODS). • • In the irreversible stage, decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism. The patient will demonstrate profound hypotension and hypoxemia, as well as organ failure; at this stage, recovery is unlikely. Diagnostic Studies • • There is no specific diagnostic study to determine shock. The diagnosis depends on the history and physical. • • Studies that assist in diagnosis include a serum lactate, base deficit, 12-lead ECG, continuous cardiac monitoring, chest x-ray, continuous pulse oximetry, and hemodynamic monitoring. pg. 75 75 • • Further assessment focuses on the assessment of tissue perfusion and includes evaluation of vital signs, peripheral pulses, level of consciousness, capillary refill, skin (e.g., temperature, color, moisture), and urine output. Planning pg. 76 76 • • The overall goals for a patient in shock include (1) evidence of adequate tissue perfusion, (2) restoration of normal BP, (3) return/recovery of organ function, and (4) avoidance of complications from prolonged states of hypoperfusion. Nursing Implementation • • Your role in shock involves (1) monitoring the patient’s ongoing physical and emotional status, (2) identifying trends to detect changes in the patient’s condition, (3) planning and implementing nursing interventions and therapy, (4) evaluating the patient’s response to therapy, (5) providing emotional support to the patient and caregiver, and (6) collaborating with other members of the health team to coordinate care. • • The patient in shock requires frequent assessment of heart rate/rhythm, BP, CVP, and pulmonary artery (PA) pressures; neurologic status; respiratory status, urine output, and temperature; capillary refill; skin for temperature, pallor, flushing, cyanosis, diaphoresis, or piloerection; and bowel sounds and abdominal distention. • • Rehabilitation of the patient who is recovering from shock necessitates correction of the precipitating cause and prevention or early treatment of complications. SYSTEMIC INFLAMMATORY RESPONSE SYNDROME AND MULTIPLE ORGAN DYSFUNCTION SYNDROME • • Systemic inflammatory response syndrome (SIRS) is a systemic inflammatory response to a variety of insults, including infection (referred to as ―sepsis‖), ischemia, infarction, and injury. • • SIRS is characterized by generalized inflammation in organs remote from the initial insult and can be triggered by mechanical tissue trauma (e.g., burns, crush injuries), abscess formation, ischemic or necrotic tissue (e.g., pancreatitis, myocardial infarction), microbial invasion, and global and regional perfusion deficits. • • MODS results from SIRS and is the failure of two or more organ systems such that homeostasis cannot be maintained without intervention. • o The respiratory system is often the first system to show signs of dysfunction in SIRS and MODS, often culminating in acute respiratory distress syndrome (ARDS). • o Cardiovascular changes, neurologic dysfunction, acute renal failure, DIC, GI dysfunction, and liver dysfunction are common. Nursing and Collaborative Management: SIRS and MODS • • The prognosis for the patient with MODS is poor; the most important goal is to prevent the progression of SIRS to MODS. • • A critical component of your role is vigilant assessment and ongoing monitoring to detect early signs of deterioration or organ dysfunction. • • Collaborative care for patients with MODS focuses on (1) prevention and treatment of infection, (2) maintenance of tissue oxygenation, (3) nutritional and metabolic support, and (4) appropriate support of individual failing organs. pg. 77 77 Exam 3 Chapter 30: Nursing Assessment: Hematologic System STRUCTURESAND FUNCTIONS OF HEMATOLOGIC SYSTEM • Hematology is the study of blood and blood-forming tissues. This includes the bone marrow, blood, spleen, and lymph system. • Blood cell production (hematopoiesis) occurs within the bone marrow. Bone marrow is the soft material that fills the central core of bones. • Blood is a type of connective tissue that performs three major functions: transportation, regulation, and protection. There are two major components of blood: plasma and blood cells. • Plasma is composed primarily of water, but it also contains proteins, electrolytes, gases, nutrients, and waste. • There are three types of blood cells: erythrocytes (RBCs), leukocytes (WBCs), and thrombocytes (platelets). • Erythrocytes are primarily composed of a large molecule called hemoglobin. Hemoglobin, a complex protein-iron compound composed of heme (an iron compound) and globin (a simple protein), functions to bind with oxygen and carbon dioxide. • Leukocytes (WBCs) appear white when separated from blood. There are five different types of leukocytes, each of which has a different function. • Granulocytes: The primary function of the granulocytes is phagocytosis, a process by which WBCs ingest or engulf any unwanted organism and then digest and kill it. The neutrophil is the most common type of granulocyte. • Lymphocytes: The main function of lymphocytes is related to the immune response. Lymphocytes form the basis of the cellular and humoral immune responses. • o Monocytes: Monocytes are phagocytic cells. They can ingest small or large masses of matter, such as bacteria, dead cells, tissue debris, and old or defective RBCs. • The primary function of thrombocytes, or platelets, is to initiate the clotting process by producing an initial platelet plug in the early phases of the clotting process. • Hemostasis is a term used to describe the blood clotting process. This process is important in minimizing blood loss when various body structures are injured. • Four components contribute to normal hemostasis: vascular response, platelet plug formation, the development of the fibrin clot on the platelet plug by plasma clotting factors, and the ultimate lysis of the clot. • The spleen, which is located in the upper left quadrant of the abdomen, has four major functions: hematopoietic, filtration, immunologic, and storage. • The lymph system—consisting of lymph fluid, lymphatic capillaries, ducts, and lymph nodes—carries fluid from the interstitial spaces to the blood. GERONTOLOGIC CONSIDERATIONS: EFFECTS OFAGING ON HEMATOLOGIC SYSTEM • Hemoglobin levels begin to decrease in both men and women after middle age. The osmotic fragility of RBCs is increased in the older person. • The total WBC count and differential are generally not affected by aging. However, a decrease in humoral antibody response and decrease in T-cell function may occur. ASSESSMENT OF HEMATOLOGIC SYSTEM • A health history for the hematopoietic system consists of biographic and demographic data, current health, past health history, past and current use of medications, surgical history, herbal preparations and nutritional supplements, family health history, and review of systems using functional health patterns. • A complete physical examination is necessary to accurately examine all systems that affect or are affected by the hematologic system, depending on the nature of the patient’s problem, including an assessment of lymph nodes, liver, spleen, and skin. pg. 80 80 • The symptoms of thalassemia major are managed with blood transfusions or exchange transfusions in conjunction with intravenous (IV) deferoxamine to reduce the iron overloading (hemochromatosis) that occurs with chronic transfusion therapy. MEGALOBLASTIC ANEMIAS pg. 81 81 • Megaloblastic anemias are a group of disorders caused by impaired deoxyribonucleic acid (DNA) synthesis and characterized by the presence of large RBCs. • Macrocytic (large) RBCs are easily destroyed because they have fragile cell membranes. • Two common forms of megaloblastic anemia are cobalamin deficiency and folic acid deficiency. • o Cobalamin (vitamin B12) deficiency is most commonly caused by pernicious anemia, which results in poor cobalamin absorption through the gastrointestinal (GI) tract. Parenteral or intranasal administration of cobalamin is the treatment of choice. • o Folic acid (folate) is required for DNA synthesis leading to RBC formation and maturation and therefore can lead to megaloblastic anemia. Folic acid deficiency is treated by replacement therapy. ANEMIA OF CHRONIC DISEASE • Chronic inflammatory, autoimmune, infectious, or malignant diseases can lead to an underproduction of RBCs and mild shortening of RBC survival. • The best treatment of anemia of chronic disease is correction of the underlying disorder. APLASTIC ANEMIA • Aplastic anemia is a disease in which the patient has peripheral blood pancytopenia (decrease of all blood cell types) and hypocellular bone marrow. • Management of aplastic anemia is based on identifying and removing the causative agent (when possible) and providing supportive care until the pancytopenia reverses. ANEMIA CAUSED BYBLOOD LOSS ACUTE BLOOD LOSS • Acute blood loss occurs as a result of sudden hemorrhage; this can be a result of trauma, complications of surgery, and conditions or diseases that disrupt vascular integrity. • Collaborative care is initially concerned with replacing blood volume to prevent shock and identifying the source of the hemorrhage and stopping the blood loss. CHRONIC BLOOD LOSS • The sources of chronic blood loss are similar to those of iron-deficiency anemia (e.g., bleeding ulcer, hemorrhoids, menstrual and postmenopausal blood loss). • Management of chronic blood loss anemia involves identifying the source and stopping the bleeding. Supplemental iron may be required. ANEMIA CAUSED BY INCREASED ERYTHROCYTE DESTRUCTION SICKLE CELL DISEASE • Sickle cell disease is a group of inherited, autosomal recessive disorders characterized by the presence of an abnormal form of Hb in the erythrocyte. • The major pathophysiologic event of this disease is the sickling of RBCs. Sickling episodes are most commonly triggered by low oxygen tension in the blood. • With repeated episodes of sickling, there is gradual involvement of all body systems, especially the spleen, lungs, kidneys, and brain. • Collaborative care for a patient with sickle cell disease is directed toward alleviating the symptoms from the complications of the disease and minimizing end target-organ damage. There is no specific treatment for the disease. ACQUIRED HEMOLYTIC ANEMIA • Extrinsic causes of hemolysis can be separated into three categories: (1) physical factors, (2) immune pg. 82 82 reactions, and (3) infectious agents and toxins. • Physical destruction of RBCs results from the exertion of extreme force on the cells. • Antibodies may destroy RBCs by the mechanisms involved in antigen-antibody reactions. • Infectious agents foster hemolysis in four ways: (1) by invading the RBC and destroying its contents, (2) by releasing hemolytic substances, (3) by generating an antigen-antibody reaction, and (4) by contributing to pg. 85 85 • Neutropenia is a clinical consequence that occurs with a variety of conditions or diseases. It can also be an expected effect, a side effect, or an unintentional effect of taking certain drugs. • Occasionally the cause of the neutropenia can be easily treated (e.g., nutritional deficiencies). However, neutropenia can also be a side effect that must be tolerated as a necessary step in therapy (e.g., chemotherapy, radiation therapy). In some situations the neutropenia resolves when the primary disease is treated (e.g., tuberculosis). • You need to monitor the neutropenic patient for signs and symptoms of infection and early septic shock. MYELODYSPLASTIC SYNDROME • Myelodysplastic syndrome (MDS) is a group of related hematologic disorders characterized by a change in the quantity and quality of bone marrow elements. Although it can occur in all age groups, the highest prevalence is in people over 60 years of age. • Supportive treatment consists of hematologic monitoring, antibiotic therapy, or transfusions with blood products. The overall goal is to improve hematopoiesis and ensure age-related quality of life. LEUKEMIA • Leukemia is the general term used to describe a group of malignant disorders affecting the blood and blood-forming tissues of the bone marrow, lymph system, and spleen. • Classification of leukemia can be done based on acute versus chronic and on the type of WBC involved, whether it is of myelogenous origin or of lymphocytic origin. • o The onset of acute myelogenous leukemia (AML) is often abrupt and dramatic. AML is characterized by uncontrolled proliferation of myeloblasts, the precursors of granulocytes. • o Acute lymphocytic leukemia (ALL) is the most common type of leukemia in children. • o Chronic myelogenous leukemia (CML) is caused by excessive development of mature neoplastic granuloctyes in the bone marrow, which move into the peripheral blood in massive numbers and ultimately infiltrate the liver and spleen. The natural history of CML is a chronic stable phase, followed by the development of a more acute, aggressive phase referred to as the ―blastic phase.‖ • o Chronic lymphocytic leukemia (CLL) is characterized by the production and accumulation of functionally inactive but long-lived, small, mature-appearing lymphocytes. The lymphocytes infiltrate the bone marrow, spleen, and liver, and lymph node enlargement is present throughout the body. • o Hairy cell leukemia is a chronic disease of lymphoproliferation predominantly involving B lymphocytes that infiltrate the bone marrow and spleen. Cells have a ―hairy‖ appearance under the microscope. • Once a diagnosis of leukemia has been made, collaborative care is focused on the initial goal of attaining remission. In some cases, such as non-symptomatic patients with CLL, watchful waiting with active supportive care may be appropriate. • Cytotoxic chemotherapy is the mainstay of the treatment for leukemia. Hematopoietic stem cell transplantation is another type of therapy used for patients with different forms of leukemia. • The overall nursing goals are that the patient with leukemia will (1) understand and cooperate with the treatment plan; (2) experience minimal side effects and complications associated with both the disease and its treatment; and (3) feel hopeful and supported during the periods of treatment, relapse, or remission. LYMPHOMAS • Lymphomas are malignant neoplasms originating in the bone marrow and lymphatic structures resulting in the proliferation of lymphocytes. There are two major types of lymphoma: Hodgkin’s lymphoma and non- Hodgkin’s lymphoma (NHL). HODGKIN’S LYMPHOMA • Hodgkin’s lymphoma, also called Hodgkin’s disease, is a malignant condition characterized by proliferation of abnormal giant, multinucleated cells, called Reed-Sternberg cells, which are located in lymph nodes. pg. 86 86 • Although the cause of Hodgkin’s lymphoma remains unknown, the main interacting factors include infection with Epstein-Barr virus, genetic predisposition, and exposure to occupational toxins. The incidence of Hodgkin’s lymphoma is increased among human immunodeficiency virus–infected patients. • The nursing care for Hodgkin’s lymphoma is largely based on managing problems related to the disease (e.g., pain caused by tumor), pancytopenia, and other side effects of therapy. pg. 87 87 NON-HODGKIN’S LYMPHOMAS • NHLs are a heterogeneous group of malignant neoplasms of primarily B- or T-cell origin affecting all ages. A variety of clinical presentations and courses are recognized from indolent (slowly developing) to rapidly progressive disease. • NHLs can originate outside the lymph nodes, the method of spread can be unpredictable, and the majority of patients have widely disseminated disease at the time of diagnosis. • Treatment for NHL involves chemotherapy and sometimes radiation therapy. Nursing care is largely based on managing problems related to the disease (e.g., pain caused by the tumor, spinal cord compression, tumor lysis syndrome), pancytopenia, and other side effects of therapy. MULTIPLE MYELOMA • Multiple myeloma, or plasma cell myeloma, is a condition in which neoplastic plasma cells infiltrate the bone marrow and destroy bone. • Multiple myeloma develops slowly and insidiously. The patient often does not manifest symptoms until the disease is advanced. • Multiple myeloma is seldom cured, but treatment can relieve symptoms, produce remission, and prolong life. Chemotherapy is usually the first treatment recommended for multiple myeloma. • Maintaining adequate hydration is a primary nursing consideration to minimize problems from hypercalcemia. Because of the potential for pathologic fractures, care must be taken when moving and ambulating the patient. DISORDERS OF THE SPLEEN • The spleen can be affected by many illnesses, which can cause varying degrees of splenomegaly, or enlargement of the spleen. • With splenomegaly, there is an increased filtering and sequestering capacity, lowering the number of circulating blood cells. • Splenomegaly is generally well tolerated; there may be complaints of abdominal pain and early satiety. An enlarged spleen is easily palpable on physical examination. • A splenectomy may be indicated for the evaluation or treatment of splenomegaly; it may also be performed if the spleen ruptures from trauma. BLOOD COMPONENT THERAPY • Blood component therapy is frequently used in managing hematologic diseases. However, blood component therapy only temporarily supports the patient until the underlying problem is resolved. • When the blood or blood components have been obtained from the blood bank, positive identification of the donor blood and recipient must be made. Improper product-to-patient identification causes 90% of hemolytic transfusion reactions. • The blood should be administered as soon as it is brought to the patient. It should not be refrigerated on the nursing unit. • Autotransfusion, or autologous transfusion, consists of removing whole blood from a person and transfusing that blood back into the same person. The problems of incompatibility, allergic reactions, and transmission of disease can be avoided. • A blood transfusion reaction is an adverse reaction to blood transfusion therapy that can range in severity from mild symptoms to a life-threatening condition. Blood transfusion reactions can be classified as acute or delayed. Acute Transfusion Reactions • The most common cause of hemolytic reactions is transfusion of ABO-incompatible blood. • Febrile reactions are most commonly caused by leukocyte incompatibility. Many individuals who receive five or more transfusions develop circulating antibodies to the small amount of WBCs in the blood product. • Allergic reactions result from the recipient’s sensitivity to plasma proteins of the donor’s blood. These pg. 90 90 axons innervate the skeletal muscles. Brain 1 The brain consists of the cerebral hemispheres, cerebellum, and brainstem. 2 The cerebrum is composed of the right and left hemispheres. Both hemispheres can be further dividedinto four major lobes, each with specific functions. pg. 91 91 1 o The frontal lobe controls higher cognitive function, memory retention, voluntary eye movements, voluntary motor movement, and expressive speech 2 o The temporal lobe contains Wernicke’s area, which is responsible for receptive speech and for integration of somatic, visual, and auditory data. 3 o The parietal lobe is composed of the sensory cortex, controlling and interpreting spatial information. 4 o Processing of sight takes place in the occipital lobe. 1 The basal ganglia, thalamus, hypothalamus, and limbic system are also located in the cerebrum. 2 The brainstem includes the midbrain, pons, and medulla. The vital centers concerned with respiratory, vasomotor, and cardiac function are located in the medulla. 3 The cerebellum coordinates voluntary movement and to maintain trunk stability and equilibrium. 4 Cerebrospinal fluid (CSF) circulates within the subarachnoid space that surrounds the brain, brainstem, and spinal cord. This fluid provides cushioning for the brain and spinal cord, allows fluid shifts from the cranial cavity to the spinal cavity, and carries nutrients. Peripheral Nervous System 1 The PNS includes all the neuronal structures that lie outside the CNS. It consists of the spinal and cranial nerves, their associated ganglia (groupings of cell bodies), and portions of the ANS. 2 The spinal nerve contains a pair of dorsal (afferent) sensory nerve fibers and ventral (efferent) motor fibers, which innervate a specific region of the neck, trunk, or limbs. This combined motor-sensory nerve is called a spinal nerve. 3 The cranial nerves (CNs) are the 12 paired nerves composed of cell bodies with fibers that exit from the cranial cavity. Unlike the spinal nerves, which always have both afferent sensory and efferent motor fibers, some CNs have only afferent and some only efferent fibers; others have both. 4 The ANS governs involuntary functions of cardiac muscle, smooth (involuntary) muscle, and glands. The ANS is divided into two components: sympathetic and parasympathetic nervous systems. Protective Structures 1 The blood-brain barrier is a physiologic barrier between blood capillaries and brain tissue. The structure of brain capillaries differs from that of other capillaries. Some substances that normally pass readily into most tissues are prevented from entering brain tissue. 2 The meninges are three layers of protective membranes that surround the brain and spinal cord. 1 The skeletal system provides protection and support to the nervous system. The bony skull protects the brain from external trauma; the vertebral column protects the spinal cord, supports the head, and provides flexibility. GERONTOLOGIC CONSIDERATIONS: EFFECTS OF AGING ON NERVOUS SYSTEM 1 There are a number of changes in the nervous system associated with aging that affect the nervous system, including a loss of neurons occurring in certain areas of the brainstem, cerebellum, and cerebral cortex. 2 These changes place the older adult at risk for a number of changes in muscle strength, memory, vision, hearing, taste, smell, reaction time, and functional ability. Assessment OFNERVOUS SYSTEM Subjective Data 1 The mode of onset and the course of the illness are especially important aspects of the history. Often the nature of a neurologic disease process can be described by these facts alone. You should obtain all pertinent data in the history of the present illness, especially data related to the characteristics and progression of the symptoms. 2 Additional health history information consists of assessment of past health history, medications, surgery or other treatments, family health history, psychosocial history, risk factor identification, and a review of systems using functional health patterns. 3 Special attention should be given to obtaining a careful medication history, especially the use of sedatives, pg. 92 92 opioids, tranquilizers, and mood-elevating drugs. Objective Data 1 The physical examination assesses six categories of functions: mental status, function of CNs, motor function, cerebellar function, sensory function, and reflex function. pg. 95 95 cytotoxic, and interstitial. More than one type may occur in the same patient. • The clinical manifestations of increased ICP can take many forms, depending on the cause, location, and rate at which the pressure increase occurs. The earlier the condition is recognized and treated, the better the patient outcome. • Complications of ICP include changes in the level of consciousness, changes in vital signs, dilation of pupils, decline in motor function, headache, and vomiting. • The major complications of uncontrolled increased ICP are inadequate cerebral perfusion and cerebral herniation. • ICP monitoring is used to guide clinical care when the patient is at risk for or has elevations in ICP. It may be used in patients with a variety of neurologic insults, including hemorrhage, stroke, tumor, infection, or traumatic brain injury. • The ―gold standard‖ for monitoring ICP is the ventriculostomy, in which a specialized catheter is inserted into the right lateral ventricle and coupled to an external transducer. Other devices now allow for an indirect assessment of cerebral oxygenation and perfusion. • With the ventricular catheter and certain fiberoptic systems, it is possible to control ICP by removing CSF. The level of the ICP at which to initiate drainage, amount of fluid to be drained, height of the system, and frequency of drainage are ordered by the physician. • The goals of collaborative care are to identify and treat the underlying cause of increased ICP and to support brain function. • o Maintenance of a patent airway is critical in supporting brain function in the patient with increased ICP and is a primary nursing responsibility. • o Drug therapy plays an important part in the management of increased ICP. An osmotic diuretic, corticosteroids, and barbiturates may be prescribed. • o Metabolic demands, such as fever and pain, which contribute to increased ICP, must be controlled. • o All patients must have their nutritional needs met, regardless of their state of consciousness or health. • The Glasgow Coma Scale is a quick, practical, and standardized system for assessing the degree of impaired consciousness that should be used during nursing assessment. Other components of the neurologic assessment include cranial nerve assessment; pupil evaluation for size, shape, movement, and reactivity; and motor and sensory testing. • The overall nursing goals are that the patient with increased ICP will maintain a patent airway, have ICP within normal limits, demonstrate normal fluid and electrolyte balance, and have no complications resulting from immobility and decreased level of consciousness. • Nursing care for the patient with increased ICP revolves around the diagnoses of decreased intracranial adaptive capacity, risk for ineffective cerebral perfusion, and risk for disuse syndrome. • The patient with increased ICP and a decreased level of consciousness needs protection from self-injury. Confusion, agitation, and the possibility of seizures increase the risk for injury. HEAD INJURY • Head injury is a broad term used to describe any trauma to the scalp, skull, or brain. • Scalp lacerations are an easily recognized type of external head trauma. Because the scalp contains many blood vessels with poor constrictive abilities, the major complications associated with scalp laceration are blood loss and infection. • Skull fractures frequently occur with head trauma. There are several ways to describe skull fractures: (1) linear or depressed; (2) simple, comminuted, or compound; and (3) closed or open. • o The manifestations may vary depending on the location of the fracture. • o The major potential complications associated with fractures are intracranial infections and hematoma, as well as meningeal and brain tissue damage. pg. 96 96 • Head trauma, or brain injuries, are categorized in a variety of ways: • o In diffuse or generalized injury (e.g., concussion, diffuse axonal) damage to the brain cannot be localized to one particular area of the brain, whereas a focal or localized injury (e.g., contusion, hematoma) occurs in a specific area of the brain. • o Injury can be classified as minor (GCS 13-15), moderate (GCS 9-12), and severe (GCS 3-8). pg. 97 97 • A concussion is a sudden transient mechanical head injury with disruption of neural activity and a change in the level of consciousness (LOC) and is considered a minor head injury. • A contusion, a major head injury, is the bruising of the brain tissue within a focal area. A contusion may contain areas of hemorrhage, infarction, necrosis, and edema and frequently occurs at a fracture site. • Bleeding complications associated with head injuries may include an epidural hematoma, a subdural hematoma, and intracerebral hematoma. • CT scan is considered the best diagnostic test to evaluate for craniocerebral trauma because it allows rapid diagnosis and intervention in the acute setting. Magnetic resonance imaging (MRI), positron emission tomography (PET), and evoked potential studies may also be used. • The most important aspects of nursing assessment are noting the GCS score, assessing and monitoring the neurologic status, and determining whether a CSF leak has occurred. • The overall nursing goals are that the patient with an acute head injury will maintain adequate cerebral oxygenation and perfusion; remain normothermic; achieve control of pain and discomfort; be free from infection; and attain maximal cognitive, motor, and sensory function. • Management at the injury scene can have a significant impact on the outcome of the head injury. The general goal of acute nursing management of the head-injured patient is to maintain cerebral oxygenation and perfusion and prevent secondary cerebral ischemia. • The major focus of nursing care for the brain-injured patient relates to increased ICP. However, there may be other specific problems that require nursing intervention, such as hyperthermia, pain, and impaired physical mobility. • Once the condition has stabilized, the patient is usually transferred for acute rehabilitation management to prepare the patient for reentry into the community. Many of the principles of nursing management of the patient with a stroke are appropriate. BRAIN TUMORS • Brain tumors can occur in any part of the brain or spinal cord. Tumors of the brain may be primary, arising from tissues within the brain, or secondary, resulting from a metastasis from a malignant neoplasm elsewhere in the body. • Brain tumors are generally classified according to the tissue from which they arise. The most common primary brain tumors originate in astrocytes and these tumors are called gliomas. • Unless treated, all brain tumors eventually cause death from increasing tumor volume leading to increased ICP. Brain tumors rarely metastasize outside the central nervous system (CNS) because they are contained by structural (meninges) and physiologic (blood-brain) barriers. • A wide range of possible clinical manifestations, depending on the location and size of the tumor, are possible. Headache is a common problem and seizures are common in gliomas and brain metastases. • An extensive history and a comprehensive neurologic examination must be done in the workup of a patient with a suspected brain tumor. A new onset seizure disorder may be the first indication of a brain tumor. • Surgical removal is the preferred treatment for brain tumors. Radiation therapy is commonly used as a follow-up measure after surgery. The effectiveness of chemotherapy has been limited by difficulty getting drugs across the blood-brain barrier, tumor cell heterogeneity, and tumor cell drug resistance. • The overall nursing goals are that the patient with a brain tumor will maintain normal ICP, maximize neurologic functioning, achieve control of pain and discomfort, and be aware of the long-term implications with respect to prognosis and cognitive and physical functioning. CRANIAL SURGERY • The cause or indication for cranial surgery may be related to a brain tumor, CNS infection (e.g., abscess), vascular abnormalities, craniocerebral trauma, seizure disorder, or intractable pain. • Depending on the location of the pathologic condition, a craniotomy may be frontal, parietal, occipital, temporal, or a combination of any of these. • Stereotactic surgery uses precision apparatus (often computer guided) to assist the surgeon to precisely
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