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Respiratory Maladaptations M. DuBois Fennal, PhD, RN, CNS 1/15/15 1 CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) 1/15/15 2 Major obstructive disorders Emphysema, Chronic bronchitis, Definition: A term applied in the clinical setting to refer to pulmonary disorders that hinder expiratory flow (preferred term, chronic airflow limitation). Asthma, Cystic fibrosis (Kidd & Wagner,2001). Chronic Bronchitis, emphysema, asthma (Hudak, Gallo & Martin,1998) Chronic bronchitis, emphysema (Lemone & Burke,2000) 1/15/15 3 ETIOLOGY 1/15/15 Smoking Air pollution Smog Irritating fumes Occupational exposures Infection Heredity Aging 4 INCIDENCE 1/15/15 Approximately fourteen million Americans have COPD. It is the fourth leading cause of death in the United States. Mortality 90,000 deaths in 1996. Mortality is still higher in men than in women in 2002, however, prevalence is increasing in women and decreasing in men. Lost work hours 250 million in 1998. 5 PATHOPHYSIOLOGY 1/15/15 COPD is a slowly developing disease, manifest by obstruction of the airways. Excessive secretions, increase size of airways, loss of alveolar wall elasticity and the loss of the ability of the lungs to recoil may all be found in the pathology of COPD, but may be in lesser combinations. 6 CHRONIC BRONCHITIS 1/15/15 Chronic infection or irritation of the bronchi can lead to bronchitis. Bronchitis is defined as; excessive secretion of bronchial mucus characterized by a productive cough lasting three or months in two consecutive years (Tierney 1998). “BLUE BLOATER” 7 SIGNS AND SYMPTOMS 1/15/15 Shortness of breath Anorexia and weight loss Fever Chronic productive cough 8 CLINICAL PRESENTATION 1/15/15 Bronchospasms Hypoxia Hypoventilation Diminished breath sounds Cyanosis Tachycardia Tachypnea Mucus plugs *May have symptomatology of right sided heart failure. 9 MEDICAL MANAGEMENT 1/15/15 Maintain a patent airway Oxygen, low dose Bronchodilators Prevent infection or additional infection. Improve circulation and perfusion Maintain fluid and electrolyte balance 10 NURSING MANAGEMENT 1/15/15 Airway maintenance Prevention of infection Maintenance of circulation and perfusion. Safety Skin integrity Nutrition Comfort Psychosocial support. 11 EMPHYSEMA 1/15/15 Irreversible destruction of the alveoli and the alveolar walls. Theories under investigation include; neutrophils and macrophages which can release elastase. 12 SIGNS AND SYMPTOMS 1/15/15 Shortness of breath Anorexia and weight loss Fever Chronically productive cough especially in the morning Barrel chest “PINK PUFFER” 13 CLINICAL MANIFESTATIONS 1/15/15 Bronchospasms Hypoxia Hypoventilation Diminished breath sounds Cyanosis Tachycardia Tachypnea Excessive mucus 14 Classification 1/15/15 Panilobular – destruction of bronchioles, alveolar ducts, and alveoli. Centritobular – change in center of secondary lobule, chronic hypoxia, hypercapnia and polycythemia, cyanosis, peripheral edema, respiratory failure. 15 MEDICAL MANAGEMENT 1/15/15 Blood gas determination Chest x-ray Pulmonary studies Allergy test Ventilation perfusion studies CT scan Echocardiogram Oxygenation 16 NURSING MANAGEMENT 1/15/15 Maintenance of airway Maintenance of circulation and perfusion Prevention or treatment of infections. Maintenance of fluid and electrolyte balance. Maintenance of cardiac status 17 CARE OF THE PATIENT WITH COPD 1/15/15 Improve the quality of life or assist to a peaceful death. Oxygen in low doses Intubations and mechanical ventilation as necessary Bronchodilators such as proventil,alupent, brethine, adrenalin, isurprel, theophylline, aminophylline and expectorants such as robitussin. 18 NURSING DIAGNOSIS 1/15/15 Impaired gas exchange Ineffective airway clearance Self-care deficit Activity intolerance Ineffective coping Knowledge deficit Altered nutrition Decisional conflict. 19 PULMONARY EMBOLISM 1/15/15 Definition: Sudden obstruction of one or more of the pulmonary arteries by a thrombus that originates somewhere in the venous system. 20 ETIOLOGY 1/15/15 90% of all pulmonary emboli originate from deep venous thrombosis of the legs. 10% result from stasis, pelvic veins and damaged blood vessels. 21 INCIDENCE 1/15/15 Over 5 million individuals per year in the United States will experience a pulmonary embolism. 250, 000 hospitalizations 50,000 death, 90% within the first 1-2 hours. Incidence is increased in clients with venous stasis, hypercoagulability, vascular disease, heart disease, post-op, the elderly, and on oral contraceptives. 22 PATHOPHYSIOLOGY 1/15/15 When a clot block circulation in a branch of the pulmonary artery, alveoli are ventilated but not perfused, thereby producing areas of mismatched ventilation and perfusion. Decrease pulmonary blood flow and deficient surfactant, leading to atelectasis. May also cause right ventricular failure, pulmonary hypertension, and increase vascular resistance. 23 SIGNS AND SYMPTOMS 1/15/15 Dyspnea Substernal chest pain Rapid weak pulse Shock Syncope Cough with pleuritic pain Sudden death 24 CLINICAL PRESENTATION 1/15/15 Dyspnea at rest Tachycardia Tachypnea Anxious Systemic hypotension Rales Hemoptysis Gallop rhythm Pleural friction rub 25 MEDICAL MANAGEMENT 1/15/15 Electrocardiogram, chest x-ray, ABG’s, Ventilation/perfusion lung scan, pulmonary angiography. Thrombolytic therapy, Anticoagulation therapy Correction of hypoxemia Oxygen Surgery Intubations & mechanical ventilation 26 NURSING MANAGEMENT 1/15/15 Oxygenation Reduction of clotting mechanisms Assessment for complications Sedation Prevention of additional emboli Emotional and psychological support. Safety 27 NURSING DIAGNOSIS 1/15/15 Impaired gas exchange Decrease cardiac output Risk for injury Anxiety Ineffective coping, patient and family. 28 PULMONARY HYPERTENSION 1/15/15 Definition: A condition in which the pulmonary arterial pressure is elevated to an abnormal level. May be a primary disorder, but is usually secondary to another condition 29 ETIOLOGY 1/15/15 Primary, unknown. Secondary, a reduction in the vascular bed. May result from vasoconstriction or wide spread vessel destruction. Initiating factors include: hypoxemia, COPD, sleep apnea, hypoventilation due to obesity. Left ventricular failure, mitral stenosis, and core pulmonale, a condition or right ventricular hypertrophy and failure. 30 INCIDENCE 1/15/15 Seventy-five percent of the cases are caused by core pulmonale. A significant number of cases are caused by multiple pulmonary emboli, lung disease and left sided heart failure. 31 PATHOPHYSIOLOGY 1/15/15 When the pressure in a low-pressure, low-resistance chamber increases, resistance is increased. As resistance increases, the chamber enlarges (right ventricle), because of the increase work load. When the pressure in the pulmonary system becomes too great, the right ventricle fails causing stasis of venous blood in the systemic system. 32 CLINICAL MANIFESTATIONS 1/15/15 Peripheral edema Cyanosis Changes in mental status Dyspnea Increased jugular venous distention Fatigue, ascities, nocturia, weight gain, anorexia and nausea 33 MEDICAL MANAGEMENT 1/15/15 Flow directed catheter, ABG’s, chest xray, hemoglobin and hematocrit. Check history for smoking, COPD, high altitude experiences. Decrease the fluid overload, decrease pulmonary vascular resistance, decrease work load of the heart. Oxygen, bronchodilators, diuretics, echocardiogram 34 NURSING MANGAGEMENT 1/15/15 Continuous assessment to prevent complications. Auscultation of heart sounds Measurement of pulmonary artery pressures Evaluation of laboratory data Evaluation of medications Conservation of energy Interpretation of ABG’s, and dysrhythmias 35 NURSING DIAGNOSIS 1/15/15 Impaired gas exchange Fluid volume excess Anxiety Ineffective coping (patient and family) At risk for injury 36 RESPIRATORY FAILURE 1/15/15 Definition: A Pao2 less than 55 mm Hg, and a PCo2 greater than 50 mm Hg. An imbalance between in supply and demand of O2 The inability of the pulmonary system to maintain adequate gas exchange. 37 ETIOLOGY 1/15/15 Inadequate ventilation impaired gas exchange Ventilation/perfusion mismatch Disease processes Injuries Cardiac and neuromuscular disorders 38 INCIDENCE 1/15/15 Occurs most frequently as a complication of other disease processes, COPD, Pneumonia, pulmonary edema, chest injuries and drug overdose is at the top of the list. Occurs more often in males and more often in older adults. 39 PATHOLOGY 1/15/15 May be acute or chronic Failure of oxygenation is a problem of hypoxemia, such as in ARDS, pulmonary embolus, acute asthmatic attacks, and pneumonia. 40 1/15/15 Failure of ventilation (acute respiratory acidosis) is caused by alveolar hypoventilation, such as with COPD, neuromuscular disorders respiratory muscle fatigue etc. Ventilation failure allows for the build up of high levels of carbon dioxide (hypercapnia) 41 H y p e r c a p n i a SIGNS AND SYMPTOMS D y s p n e a 1/15/15 Hypoxemia Dyspnea Tachypnea Cyanosis Anxiety Dysrhythmias Hypertension Metabolic acidosis 42 CLINICAL MANIFESTATIONS 1/15/15 Dyspnea Tachypnea Tachycardia Cool to cold skin Increase blood pressure Varying states of consciousness 43 MEDICAL MANAGEMENT 1/15/15 Will depend on the cause and the type of failure. Correct the hypoxemia or hypercapnia and treat the underlying cause. Oxygen, intubation, mechanical ventilation, bronchodilators, muscle relaxants i.e. morphine. 44 NURSING MANAGEMENT 1/15/15 Airway management Safety Skin integrity Nutrition Monitor laboratory results and arterial blood gas results, intervene for abnormals. 45 NURSING DIAGNOSIS 1/15/15 Ineffective airway clearance Impaired gas exchange Self-care deficit Activity intolerance Risk for injury Anxiety 46 RESPIRATORY DISTRESS SYNDROME (ARDS) 1/15/15 Definition: characterized by noncardiogenic pulmonary edema, collapsed and fluid filled alveoli and subsequently severe hypoxemia. 47 ETIOLOGY 1/15/15 Occurs in a usually healthy individual after some sort of insult to the body, i.e. sepsis, aspiration, trauma, hemorrhagic shock. The process will usually manifest itself within seventy two hour of a pulmonary insult. 48 INCIDENCE 1/15/15 Highest in individuals who present with shock, sepsis, hypo or hyperthermia, drug overdose, DIC, multiple blood transfusions, cardiopulmonary bypass, eclampsia, burns, pancreatitis, pneumonia, inhalation injury and stress. 200, 000 cases per year, mortality rate of 40% – 90% 49 PATHOPHYSIOLOGY 1/15/15 ARDS may present as mild to severe. In mild no other organs are involved, in severe, multiple organs are involved. Associated with a systemic inflammatory response syndrome (SIRS) (Vollman and Aulbach, 1998). 50 1/15/15 Capillary endothelial cell becomes injured and allows protein and water to leak out into the interstitial and alveolar spaces, producing interstitial edema. Protein destroys surfactant Capillary narrow and finally collapse. 51 1/15/15 Hemorrhage occurs into interstitum Pulmonary edema occurs Blood flow in lungs cease Hyaline membrane develops making the lungs less compliant. Increase PCO2, decrease O2 52 SIGNS AND SYMPTOMS 1/15/15 Tachypnea Cyanosis Grunting respirations Intercostal retractions Extreme agitation 53 Clinical manifestations 1/15/15 Marked dyspnea Restlessness and agitation Cyanosis Bilateral alveolar infiltrates Elevated PaCO2 and decreased PaO2, severe respiratory acidosis, rales, decreased breath sounds, pulmonary friction rub. 54 MEDICAL MANAGEMENT 1/15/15 Admit to critical care Intubations and mechanical ventilation Arterial blood gas and chest x-ray IV access (2) Positive end expiratory pressure (PEEP) or Continuous positive airway pressure (CPAP) 55 NURSING MANAGEMENT 1/15/15 Airway management Control and or support ventilation and gas exchange Restrict fluids Constant assessment Monitor diagnostic studies, cardiac monitor and physical assessment Psychological support 56 COMPLICATIONS 1/15/15 Oxygen toxicity Sepsis Fluid imbalance Injury from tracheotomy and suctioning Complications of PEEP, decrease cardiac output subcutaneous emphysema, pneumothorax, pneumomediastium 57 Nursing Diagnosis 1/15/15 Impaired gas exchange Ineffective airway clearance Potential for aspiration Decrease cardiac output Altered nutrition Potential for infection Sensory-Perceptual alterations Anxiety 58