Pulmonary Diseases and Disorders, Exams of Nursing

Download Pulmonary Diseases and Disorders and more Exams Nursing in PDF only on Docsity! 1 N5315 Advanced Pathophysiology Pulmonary I. Pulmonary Disease- General Comments a. Pulmonary diseases are often classified into 2 broad categories. i. Restrictive versus Obstructive is the first classification of pulmonary disorders. 1. Restrictive disorders refer to the inability of the person to breathe in adequate amounts of air. Typically, these individuals have low lung volumes on pulmonary function tests. Lung volumes are essentially the amount of air the lungs contain at a given time during ventilation. Disease examples include aspiration, pulmonary fibrosis, atelectasis, bronchiectasis, bronchiolitis, and pulmonary edema. 2. Obstructive disorders refer to the inability of the person to completely exhale air which has been inhaled. Typically, on PFTs these individuals will have high lung volumes because they are retaining air in the lungs. Disease examples include asthma and COPD. ii. Infectious versus Non-infectious is the second classification for pulmonary disorders. 1. Infectious examples include Pneumonia and Tuberculosis. 2. Non-infectious examples include pulmonary fibrosis, lung cancer, and pulmonary HTN. b. Overview of Pulmonary Disease States i. Acute Respiratory Failure is classified into two main types. a. Hypoxemia respiratory failure is defined as a PaO2 of ≤50mmHg. This is typically due to inadequate diffusion of oxygen from the alveoli to the capillary. Disorders which may impair diffusion include pulmonary edema, pulmonary embolus, and pneumonia. b. Hypercapnic respiratory failure is defined as a PaCO2 ≥ 50mmhg. This is typically due to inadequate alveolar ventilation. Causes of hypercapnia include depression of the respiratory center by medications (opioids, benzodiazepines), abnormalities of the spinal cord conducting systems, disorders of the medulla, diseases of the neuromuscular junction, chest wall abnormalities, obstruction of large airways, or COPD. c. Acute respiratory failure may result from direct injury to the lungs or may simply be triggered by an injury or dysfunction to one or more body systems or organs. It may also occur as a post-operative complication secondary to anesthesia or narcotics. 2 d. In either case, the main dysfunction is an impairment in diffusion which results in low oxygen levels or the accumulation of CO2. e. Most pulmonary diseases can cause respiratory failure, as can brain and spinal cord injuries. ii. A Pneumothorax is the presence of air or gas in the pleural space. The air in the thoracic cavity may press on the lung and cause it to collapse completely, or it may be a small amount of air that does not cause any difficulties. The two main types are spontaneous pneumothorax and secondary pneumothorax. 1. A spontaneous pneumothorax occurs in young (20-40), tall thin males. They may also occur as a result of bleb rupture in persons who have emphysema. Smoking increases the risk of spontaneous pneumothorax. The bleb ruptures are usually in the apexes and may occur during exercise, while at rest or while asleep. The rupture allows air into the pleural space. In some individuals there is a genetic component and a family history of this diagnosis. 2. A secondary pneumothorax is caused by trauma. A tension pneumothorax occurs when air becomes trapped in the thoracic cavity and cannot escape. The site of the injury on the pleural membrane acts as a one-way value and only lets air into the thoracic cavity. In this instance the person may experience a complete lung collapse. If this occurs the individual will have a deviated trachea, shortness of breath, and hypotension. 3. Clinical manifestations of a pneumothorax include sudden pleural pain, tachypnea, dyspnea, decreased breath sounds, and hyperresonance to percussion. iii. Pulmonary Edema is the accumulation of water in the pulmonary alveolar sacs. This prevents the proper exchange of gases and leads to dyspnea, chest pain, and hypoxia. Often individuals will also have orthopnea or paroxysmal nocturnal dyspnea. 1. The most common cause is left-sided heart failure. In left-sided heart failure the backup of blood to the lungs increases capillary hydrostatic pressure which pushes fluid out into the alveolar sacs. Other causes include ARDS, inhalation of toxic gases, increased pulmonary venous pressure and damaged alveolar capillaries. ARDS or inhalation of toxic gases causes capillary injury which leads to the movement of fluid into the alveolar space. 2. Post-obstructive pulmonary edema or re-expansion pulmonary edema occurs after relieving airway obstruction. Inspiration against an occluded airway creates excessive intrathoracic negative pressure which leads to increased venous return to the right side of the heart and a decreased outflow of blood from the left side of the heart. This creates increased pulmonary blood volume and pressure which causes the pulmonary edema. 5 same as in adults. Acute episodes are characterized by coughing, wheezing, and dyspnea. Exacerbations are usually triggered by viral infections. In infants and toddlers, the most common viral infection to trigger asthma is RSV. Children will have runny noses, low grade fevers, expiratory wheezing, faint breath sounds and sometimes a barrel chest. In severe cases they may have retractions, nasal flaring and accessory muscle use. i. COPD- results in the obstruction of airflow and is preventable and treatable. The obstruction in airflow is typically not reversible and is progressive. Risk factors for the development of COPD include the use of tobacco products, occupational dusts and chemicals and indoor air pollutants. There are two main types - emphysema and chronic bronchitis. The treatment guidelines (GOLD) do not define these entities separately as they believe that they do not fully describe the pathological processes which occur when these terms are used. 1. There are genetic susceptibilities which have been identified which predispose one to the development of COPD. An inherited mutation in the alpha 1 antitrypsin gene causes emphysema to develop at an early age, even in persons who do not use tobacco products. This deficiency should be considered in anyone who has emphysema before the age of 40 and in persons who do not smoke. 2. The pathologic hallmarks of Emphysema are the dilation of the airways and the destruction of the alveolar walls. Both of these defects cause a decrease in the elastic recoil. As a result, air is trapped in the lungs and cannot be completely exhaled. As the amount of air trapped increases, the thoracic cavity changes shape to accommodate for the increased lung volumes (amount of air) and becomes the shape of a barrel. Alveolar destruction results in the formation of bullae in the lung tissue, which are pockets of air and do not assist with gas exchange. All of this causes hypoxemia, hypoventilation and hypercapnia. These patients tend to have pursed lipped breathing and use the tripod position to help improve their breathing. They tend to have a high metabolic rate because they have shallow, rapid breaths and burn a lot of calories. As a result, these individuals tend to be thin. On examination they will have hyper-resonant sound with percussion. 3. Chronic Bronchitis is a condition marked by the presence of a productive cough which occurs over the course of a minimum of three consecutive months for two sequential years. The mucus- secreting cells in the airways undergo a hyperplasia and secrete excessive amounts of mucus. This mucus can be hard to clear due to its viscosity and impaired ciliary function. It may plug the airway and impair oxygenation. The hyperplasia of these cells is typically triggered by a chronic irritant such as smoking. The pathological process initially impairs the larger airways but then it 6 progresses to involve all airways. The airways become narrow, causing obstruction and air retention. As a result, the thorax expands, the person has hypoxemia, low tidal volumes, hypercapnia, and hypoventilates. a. These people experience poor exercise tolerance, wheezing, and dyspnea. They will have signs of obstruction on pulmonary function testing. The main sign is a decreased FEV1. The hypoxemia causes polycythemia and cyanosis. This may lead to pulmonary HTN and cor pulmonale. ii. Pneumonia is an inflammatory and/or infectious process which results in the accumulation of inflammatory exudate in the alveolar sacs. Causes include bacterial, viral, or fungal organisms or it may simply be caused by aspiration. Elderly have the highest incidence and mortality from pneumonia. Risk factors include advanced age, suppressed immune system, underlying lung disease (COPD), alcohol abuse, decreased level of consciousness, chest trauma, dysphagia, smoking, intubation, malnutrition, immobility, cardiac or liver disease, and residing in a nursing home. 1. Community-Acquired Pneumonia is a pneumonia which occurs outside of the healthcare system. a. Common bacterial causes include the following organisms: i. Streptococcus Pneumoniae is the most common cause of PNA. It is seen more frequently in the elderly and debilitated patients such as those who are malnourished or have cardiopulmonary diseases. ii. Staphylococcus Aureus often arises as a complication from influenza or a viral pneumonia. This is seen mainly in the elderly, debilitated hospitalized patients and those persons with chronic lung disease. iii. Streptococcus Pyogenes occurs as a complication of a viral infection such as influenza or measles. iv. Klebsiella Pneumoniae is common in hospitalized debilitated patients, diabetics, or alcoholics. Elderly infected with this bacteria have a high mortality. v. Haemophilus Influenzae is commonly seen in infants and children. It occurs commonly in those adults with COPD. b. Healthcare-Associated Pneumonia is a PNA which is diagnosed in any individual who has had contact with the healthcare system. Persons who have developed pneumonia and received infusion therapy or dialysis or have resided in a nursing home within 90 days, on tube feedings, or receiving home wound care are said to have a healthcare- associated pneumonia. 7 c. Hospital-Acquired Pneumonia is one which is diagnosed 48 hours after being admitted to the hospital. Common causes include gram-negative bacteria such as Klebsiella, Pseudomonas aeruginosa, and Escherichia Coli. These organisms are also common ones implicated in healthcare- associated pneumonia too. Ventilator associated pneumonia occurs in persons who have been on the ventilator and develop pneumonia. 2. Pathophysiology a. Pneumonia develops from the aspiration of oral secretions into the lower respiratory tract or through the inhalation of a microorganism in the air which is present from a sneeze, cough or a person talking. Endotracheal tubes become colonized with bacteria. Once bacteria reach the alveoli, macrophages trigger the immune and inflammatory cascades. 3. Clinical Manifestations a. CAP has an acute onset. One minute the person is feeling fine and then all of a sudden they feel bad. Unlike PCP in a person who is immunocompromised. PCP presents insidiously. This is important to remember. This helps us to distinguish between CAP and PCP. b. Symptoms include dyspnea, fever, cough, chills, malaise, pleuritic chest pain, pulmonary rales, tactile fremitus, egophony and whispered pectoriloquy. iii. Tuberculosis is a pulmonary infection which occurs worldwide and most commonly in disadvantaged populations. It is caused by the mycobacterium tuberculosis and is spread via air droplets containing the organism. 1. Crowded institutional living, homeless, substance abuse and lack of access to care contributes to the spread of the disease. 2. Multidrug resistant tuberculosis has become a problem and is defined as TB which is resistant to both isoniazid and rifampin. Extensive drug resistant TB is the term used when the mycobacterium is resistant to fluoroquinolones and at least one of three injectable second line drugs: amikacin, kanamycin, or capreomycin. The resistance to drugs has been attributed to mutations in the RNA and is more prevalent in persons who have received inconsistent treatment. 3. In primary infection, macrophages engulf the mycobacterium and form a granuloma called a tubercle. This triggers the inflammatory cascade, which causes the center of the lesion to necrose and eventually calcify. This infection is usually asymptomatic and usually does not cause active disease. 4. In secondary infection, the tubercle has activated and the infection has spread to additional sites within the lung. Individuals with 10 constriction of the pulmonary artery. Additionally, there are changes in the precapillary pulmonary arteries which make them resistant to vasodilation. There are increased levels of calcium which causes vasoconstriction, phosphodiesterases which increase cellular proliferation, increased serotonin levels which cause vasoconstriction all of which add to the pathogenesis of this disorder. The higher pressure in the pulmonary artery causes the right ventricle to work harder. It must push against the increased pressure. The right ventricle will compensate for the increased work load by enlarging and will eventually fail, causing cor pulmonale. v. On CXR one will see an enlarged right ventricle and pulmonary artery. Non-specific manifestations include fatigue, chest pain, tachypnea, dyspnea on exertion, palpitations and cough. They will have signs of right sided heart failure as well. d. Cor Pulmonale i. This condition is secondary to pulmonary artery hypertension. The right ventricle in normal physiology is not made to push against high pressures. In the setting of PAH, it must push against the higher pulmonary artery pressure and eventually fails. The person will have symptoms of right sided heart failure. II. Childhood Disorders a. Croup i. This is an upper respiratory infection which may be caused by a virus or bacteria that leads to inflammation and obstruction. Viral croup causes a subglottic edema which can lead to obstruction. ii. Clinical manifestations start with rhinorrhea, sore throat, and low-grade fever. They then develop a seal like, barking cough, hoarse voice and inspiratory stridor. Most cases resolve spontaneously; however, if they have upper airway obstruction, this must be treated. b. Cystic Fibrosis i. This is an autosomal recessive disorder which results from a defective gene on chromosome 7. It is more common in Caucasians and the median age of diagnosis is 4 months old. The average life span is 30 years old. i. CF affects the airways, gastrointestinal tract and reproductive tract. The cystic fibrosis transmembrane conductance regulator gene mutation results in the production of an abnormal protein called the cystic fibrosis transmembrane conductance regulator protein. This protein makes the chloride channel on the surface of many epithelial cells, especially those which line the airways, bile ducts, the pancreas, sweat ducts, paranasal sinuses and the vas deferens. Chloride intracellular balance is maintained in these cells by the chloride channels. The mutation results in a failure of the chloride channels. When the chloride channels fail, they are unable to secrete chloride out of the cell and the cell increases absorption of sodium. ↑ Na+ intracellularly → water moves intracellularly → less water on the epithelial surface tissues → increased viscosity of secretions from these tissues. ii. Effects in lungs 11 1. Occlusion of airways, chronic inflammation, decrease in elastic recoil (difficulty with exhalation), and increased susceptibility to infections. iii. Effects in the pancreas 1. Viscous secretions disable the pancreas’ ability to release pancreatic enzymes into the gut to assist with digestion iv. Effects of the Reproductive System 1. Causes infertility v. In the sweat glands the process is opposite and the Cl- and Na+ are secreted extracellularly and into the sweat; therefore, these persons have a high concentration of Na in their sweat. vi. Clinical manifestations include persistent cough, wheezing, excessive sputum production, recurrent pneumonia, clubbing, development of barrel chest, pulmonary rales. vii. Persons with CF are at an increased risk of pulmonary infections, particularly with pseudomonas. N5315 Advanced Pathophysiology Shock I. Shock States a. The basic pathological reasons for shock are related to a decrease in cardiac output, a decrease in circulating volume or a widespread vasodilation. Regardless, the volume available in the vasculature system is not enough to maintain homeostasis. Shock will lead to hypotension, decreased organ perfusion, tissue and cellular hypoxia, anaerobic metabolism, and the production of lactic acid. b. One basic rule to remember is that one needs a minimum of a systolic BP of 90mmHg to maintain adequate perfusion to the body. II. Common pathological characteristics of all shock states a. There is a lack of cellular oxygen available. This is due to a lack of perfusion to the cells and/or increased cellular consumption. Cells are therefore unable to use oxygen normally. In shock states the cells extract more oxygen from hemoglobin and this decreases available oxygen even more. Eventually the cells will turn to anaerobic metabolism which results in the production of lactic acid. Hence lactic acid levels are used clinically as a marker of perfusion. Additionally, SVO2 levels are a reflection of oxygen extraction from the cells. Low levels mean that more oxygen is being extracted. Normal levels with an elevated lactic acid is an ominous sign. Anaerobic metabolism uses ATP faster and eventually the cell is using more ATP than it can replace. The lack of ATP leads to a failure in the 12 sodium potassium pump. Sodium accumulates inside the cell and potassium exits the cell. The action potentials of neurons and myocardial cells are immediately affected. Myocardial depressant factor is released and this suppresses myocardial contraction. The increased intracellular sodium content draws water into the cells from the interstitial space and causes cellular edema. This leaves the interstitial space draw and it dry water from the vascular space and swells. This decreases intravascular volume. Albumin is consumed for energy and this decreases oncotic pressure and further decreases intravascular volume. b. Impaired glucose delivery and use results from impaired perfusion. During shock the body releases cortisol, growth hormone and catecholamines which contribute to the development of hyperglycemia and insulin resistance, tachycardia, increased SVT and increased cardiac contractility. During shock states cells shift to glycogenolysis, gluconeogenesis and lipolysis to generate fuel for survival. c. Impairment of protein metabolism and the deletion of protein stores results in organ failure. Gluconeogenesis causes proteins to be metabolized for fuel and when this happens they are not available to help maintain the cellular structure, function, repair and replication. The metabolism of protein leads to the production of ammonia and urea. Ammonia is toxic to cells. Albumin is the first protein to be consumed. III. Types of Shock a. Hypovolemic shock results from a decrease in circulating volume secondary to loss. Volume loss may occur from hemorrhage, burns, vomiting or diarrhea. Simple dehydration from not drinking may lead to shock. i. The loss of volume leads to fluid shifting as I described earlier; however, early compensatory mechanisms offset the effect of the volume loss. These early compensatory mechanisms include 1. A vasoconstriction and tachycardia from a release of catecholamines. 2. The low intravascular volume leads to a decrease in hydrostatic pressure, which in turn allows fluid from the interstitium to enter the intravascular space. 3. The liver and spleen release stored RBCs. 4. The kidneys release renin. 5. All of these mechanisms cause extreme vasoconstriction and increase vascular resistance. ii. If fluid loss is too great or continues, the above mechanisms will fail and the processes described earlier will kick in.