MEDICAL DIAGNOSIS

Respiratory Failure

DEFINITION

Inadequate gas exchange by the respiratory system, with the result that arterial oxygen and/or carbon dioxide levels cannot be maintained within their normal ranges. Respiratory failure can arise from an abnormality in any of the components of the respiratory system,

PATHOPHYSIOLOGY

including the airways, alveoli, CNS, peripheral nervous system, respiratory muscles, and chest wall. Hypoventilation, V/Q mismatch, and shunt are the most common pathophysiologic causes of acute respiratory failure. Hypoventilation Hyperventilation is usually occurs from depression of the CNS from drugs or neuromuscular diseases affecting respiratory muscles. Hypoventilation is characterized by hypercapnia and hypoxemia. The relationship between PaCO2 and alveolar ventilation is hyperbolic. As ventilation decreases below 4-6 L/min, PaCO2 rises precipitously. Hypoventilation can be differentiated from other causes of hypoxemia by the presence of a normal alveolar-arterial PO2 gradient. V/Q mismatch V/Q mismatch is the most common cause of hypoxemia. V/Q units may vary from low to high ratios in the presence of a disease process. The low V/Q units contribute to hypoxemia and hypercapnia in contrast to high V/Q units, which waste ventilation but do not affect gas exchange unless quite severe. The low V/Q ratio may occur either from a decrease in ventilation secondary to airway or interstitial lung disease or from overperfusion in the presence of normal ventilation. The overperfusion may occur in case of pulmonary embolism, where the blood is diverted to normally ventilated units from regions of lungs that have blood flow obstruction secondary to embolism. Administration of 100% oxygen eliminates all of the low V/Q units, thus leading to correction of hypoxemia. Hypoxemia increases minute ventilation by chemoreceptor stimulation, but the PaCO2 level generally is not affected. Shunt Shunt is defined as the persistence of hypoxemia despite 100% oxygen inhalation. The deoxygenated blood (mixed venous blood) bypasses the ventilated alveoli and mixes with oxygenated blood that has flowed through the ventilated alveoli, consequently leading to a reduction in arterial blood content. The shunt is calculated by the following equation: QS/QT = (CCO2 CaO2)/CCO2 CvO2) QS/QT is the shunt fraction, CCO2 (capillary oxygen content) is calculated from ideal alveolar PO2, CaO2 (arterial oxygen content) is derived from PaO2 using the oxygen dissociation curve, and CVO2 (mixed venous oxygen content) can be assumed or measured by drawing mixed venous blood from pulmonary arterial catheter. Anatomical shunt exists in normal lungs because of the bronchial and thebesian circulations, accounting for 2-3% of shunt. A normal right-to-left shunt may occur from atrial septal defect, ventricular septal defect, patent ductus arteriosus, or arteriovenous malformation in the lung. Shunt as a cause of hypoxemia is observed primarily in pneumonia, atelectasis, and severe pulmonary edema of either cardiac or noncardiac

origin. Hypercapnia generally does not develop unless the shunt is excessive (>60%). When compared with V/Q mismatch, hypoxemia produced by shunt is difficult to correct by oxygen administration. Almost all lung diseases including asthma, chronic obstructive pulmonary disease (COPD), AIDS-related pneumonia, other pneumonias and lung infections, and cystic fibrosis may eventually lead to respiratory failure particularly if the diseases are inadequately treated. These patients find it very hard to breathe and the result is low oxygen and high carbon dioxide blood levels. People whose normal lungs have been injured, such as from exposure to noxious gases, steam, or heat during a fire, can subsequently go into respiratory failure The clinical features of respiratory failure vary widely in individual patients because so many different conditions can lead to this disorder. There are no physical signs unique to respiratory failure. At extremely low arterial oxygen (PaO2) levels, patients have rapid heart rates, rapid breathing rates, and they are confused, sweaty, and cyanotic (blue). Chronically low arterial oxygen makes patients irritable, and elevated carbon dioxide produces headaches and sleepiness. Difficult, rapid, or labored breathing (dyspnea) is a consistent symptom in the awake patient. The way to diagnose respiratory failure, therefore, is to measure oxygen (PaO2) and carbon dioxide (PaCO2) in the arterial blood. Depending on age, a PaO2 less than 60 mm Hg or PaCO2 greater than 45 mm Hg generally mean that the patient is in respiratory failure. Cardiac serologic markers Troponin, Creatine kinase- MB fraction (CK- MB) B-type natriuretic peptide (BNP) Microbiology Respiratory cultures: sputum/tracheal aspirate/broncheoalveolar lavage (BAL) Blood, urine and body fluid (e.g. pleural) cultures Chest radiography Identify chest wall, pleural and lung parenchymal, pathology and distinguish disorders that cause primarily V/Q mismatch (clear lungs) vs. Shunt(intra- pulmonary shunt with opacities present) Electrocardiogram Identify arrhythmias, ischemia, ventricular dysfunction Echocardiography Identify right and/or left ventricular dysfunction Pulmonary function tests/bedside spirometry Identify obstruction, restriction, gas diffusion abnormalities May be difficult to perform if critically ill Bronchoscopy Obtain biopsies, brushings and BAL for histology, cytology and microbiology Results may not be available quickly enough to avert respiratory failure Bronchoscopy may not be safe in the if critically ill Oxygenation is the basic therapy for acute respiratory failure due to lung disease. Oxygen-enriched air is usually given to the patient by nasal prongs, oxygen mask, or by placing an air tube into the trachea (windpipe). Since prolonged high oxygen levels can be toxic, the concentration of oxygen must be carefully controlled for both short- and long-term treatment. Assisted ventilation with mechanical devices may be the first priority for neuromuscular disease patients going into respiratory failure. Additional treatments employ ventilation which helps to keep the lungs inflated at low lung volumes (positive end-expiratory pressure, PEEP), and fluid and nutritional management. Bronchodilatory drugs cause relaxation of the smooth muscles in the airways, improving airway calibre. They may be administered using a variety of routes, in particular inhaled in the form of aerosol sprays or nebulisers. Inhaled bronchodilators are an essential component in the treatment of asthma and obstructive airways disease. Peak expiratory flow rate measurements taken pre and post dose are usually recorded to assess effectiveness. Other medications particularly anti-inflammatory drugs such as steroids may be required. Antimicrobial, antiviral or antifungal therapy is usually initiated if the cause of respiratory failure is considered to be of infective origin. Again, these drugs may be administered using a variety of routes and time periods.

ETIOLOGY & EDPIDEMOLOGY

CLINICAL MANIFESTATION

DIAGNOSTIC TESTS

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

NURSING MANAGEMENT

Patients with acute respiratory failure should be closely observed for potential deterioration. Respiratory assessment should occur on a frequent/continual basis. Monitoring may involve intermittent/continual pulse oximetry and regular peak expiratory flow rate measurement but should always include basic respiratory rate monitoring and general assessment. Physiological track and trigger warning systems are widely used to identify patients on general wards at risk of clinical deterioration. These systems provide a framework to access higher levels of care. Patients at risk of developing acute respiratory failure are an ideal group for these systems and their use should be encouraged. Any changes in physiological signs should be reported promptly to the senior practitioner. Anxiety Patients will most likely be frightened and anxious as a result of dyspnea. While undertaking assessments and during subsequent care it is very important to try to alleviate these anxieties and provide reassurance. Simple techniques, such as patient positioning, may reduce symptoms by maximizing lung expansion. Patients may advise which position they feel offers some relief. Communication skills, such as asking closed questions during assessment, may be used if patients are breathless to a point where they cannot answer in sentences. Pulmonary secretions Many processes leading to acute respiratory failure are associated with an increase in pulmonary secretions. Tissues or receptacles for sputum should be provided to assist patients to void secretions independently. If their ability to void is limited, assistance may be required in the form of o ropharyngeal/nasopharyngeal suction. These procedures should not be undertaken without appropriate training. Sputum and other samples may be required for microbiological screening this should be performed according to local guidelines. Pain management Pain, particularly associated with abdominal or thoracic surgery or injury, can limit chest expansion. If patients are experiencing pain, relief should be provided and future control optimised. Expert advice may be necessary because of the respiratory depressant effects of some analgesics. Liaison with multidisciplinary specialists such as acute or chronic pain specialists may be required. Oxygen therapy The majority of patients in acute respiratory failure will need oxygen supplementation. Before starting oxygen therapy, it is important to explain the reasons for this to them, their relatives and carers, and check their understanding (Jevon and Ewens, 2001). Unless in a medical emergency situation, the oxygen flow rate or percentage and duration of therapy should be prescribed. Nurses are best placed to select the most appropriate delivery system for a particular patient. The system chosen should aim to deliver therapy with maximum effectiveness and optimise patient independence. The detrimental effects of oxygen therapy, such as the dehydration of mucosa, should be observed for and appropriate therapies such as gas humidification introduced where necessary. Tissue damage from a delivery device may occur in particular, oxygen masks cause soreness behind the ears after longer-term use and nasal cannulas cause irritation to the nostrils. Small adaptations to the device, such as adding gauze padding, may prevent or alleviate this. Other medication If aerosol-inhaled medications are prescribed, effective delivery will only occur through patient compliance. Therapeutic effectiveness can be improved by providing education on inhaler technique. It is imperative that appropriate devices are chosen and patients technique is adequate (Bennett, 2003). When administering nebulizers, patients should be sat upright (as tolerated), be encouraged to take normal breaths and avoid talking in order to maximize drug delivery (Bennett, 2003). Nebulised medication may be administered using air flow or oxygen and nurses should ensure the type of gas used to deliver the drug is prescribed. Certain concentrations of oxygen may be contraindicated in certain patients. Practitioners should also bear in mind that patients may be dependent on a certain oxygen flow before nebulisation and interrupting this may be contraindicated. Attempts should be made to minimize oxygen consumption (Smyth, 2005). This can be achieved by minimizing patient exertion. They should be assisted with activities of daily living such as meeting hygiene

needs, and all essential items, such as sputum pots, drinks and nurse call bells, should be within easy reach. Patients will also require time to catch their breath following exertion, so activities should be planned with this in mind.

Knowledge deficit related to condition evidenced by verbalization. NURSING DIAGNOSIS Hypoxemia, pulmonary hypertension COMPLICATIONS

MEDICAL DIAGNOSIS

ADULT RESPIRATORY DISTRESS SYNDROME Also referred to as acute respiratory distress syndrome, is a form of acute respiratory failure caused by extensive lung injury following a variety of catastrophic events such as shock, severe infection, and burns. ARDS can occur in individuals with or without previous lung disease. ARDS is a massive inflammatory response by the ling that increases permeability of the alveolar membrane, with resultant fluid movement into the interstitial and alveolar space. This leads to the development of noncardiogenic pulmonary edema, which decreases lung complicance and impairs oxygen transport. There are three phases: 1. Phase one Exudative : happens about 24 hours after the initial insult and consist of damage to the capillary endothelium and leakage of fluid into the pulmonary interstitium. Microemboli also develop and cause a futher increase in pulmonary artery pressure. Inflammatory stage response accompany the pulmonary parenchymal damage , leading to the release of toxic mediators , the activation of compliment , the mobilization of macrophages and the release of vasoactive substances from mast cells. There is future damage to the basal membrane, interstitial space, around the alveoli and increase the distance around the capillary membrane. Phase Two proliferative: begins about 7-10 days later. At this time type one and type 2 alveolar cells are damaged. As a result there is decreased surfactant production, alveolar collapse, and atelectasis, leading to future impairment in gas exchange. Hypoxemia is present because of decreased surfactant production, intrapulmonary shunting and V/Q mismatch. Phase 3- Fibrotic: 2-3 weeks. There is irreversible decomposition of fibrin into the lungs, resulting in pulmonary fibrosis , future decrease in lung compliance and worsening hypoxemia . the end result is significant V/Q imbalance and profound arterial hypoxemia. Oxygen toxicity Breathing in (aspiration) of the stomach contents when regurgitated, or salt water or fresh water from nearly drowning. Inhaling smoke, as in a fire; toxic materials in the air, such as ammonia or hydrocarbons; or too much oxygen, which itself can injure the lungs. Infection by a virus or bacterium, or sepsis, a widespread infection that gets into the blood.

DEFINITION PATHOPHYSIOLOGY

2.

3.

ETIOLOGY & EDPIDEMOLOGY

Massive trauma, with severe injury to any part of the body. Shock with persistently low blood pressure may not in itself cause ARDS, but it can be an important factor. A blood clotting disorder called disseminated intravascular coagulation, in which blood clots form in vessels throughout the body, including the lungs. A large amount of fat entering the circulation and traveling to the lungs, where it lodges in small blood vessels, injuring the cells lining the vessel walls. An overdose of a narcotic drug, a sedative, or, rarely, aspirin. Inflammation of the pancreas (pancreatitis), when blood proteins, called enzymes, pass to the lungs and injure lung cells. Severe burn injury. Injury of the brain, or bleeding into the brain, from any cause may be a factor in ARDS for reasons that are not clear. Convulsions also may cause some cases.

CLINICAL MANIFESTATION

Increased respiratory rate, cough, respiratory acidosis, crackles, tachypnea, , hypoxemia, refractory hypoxemia, defused bilateral infiltrates, severe dyspnea, thick frothy sputum, hemoptysis, decreased compliance. Chest x ray (interstitial edema), ABG analysis (resp. acidosis) Administer O2, antioxidants to reverse O2 toxicity, homodynamic agents, to improve cardiac out put, high fowlers position, prophylactic antibiotics, anti-inflammatory agents, surfactant, and mechanical ventilation.

DIAGNOSTIC TESTS

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

NURSING MANAGEMENT NURSING DIAGNOSIS

Place client in high fowlers position, give emotional support, educate client about progression of disease, adequate perfusion, monitor and record VS, I/O, lad studies, pulse oximetry, allow rest periods. Anxiety related to implications of condition and critical care setting Powerlessness related to condition and treatments (ventilator, monitoring) Lung fibrosis, cardiac dysrhythmias caused by hypoxemia, oxygen toxicity , renal failure, thrombocytopenia, gastrointestinal bleeding secondary to stress ulcer, sepsis from invasive line , and disseminated intravascular coagulation.

COMPLICATIONS

Cystic fibrosis MEDICAL DIAGNOSIS Cystic fibrosis (CF) is an inherited disease characterized by an abnormality in the glands that produce sweat and mucus. It is a chronic and progressive disease. Cystic fibrosis is life-threatening and causes severe lung damage and nutritional deficiencies. The protein created by this gene is anchored to the outer membrane of cells in the sweat glands, lungs, pancreas, and other affected organs. The protein spans this membrane and acts as a channel connecting the inner part of the cell (cytoplasm) to the surrounding fluid. This channel is primarily responsible for controlling the movement of chloride from inside to outside of the cell; however, in the sweat ducts it facilitates the movement of chloride from the sweat into the cytoplasm. When the CFTR protein does not work, chloride is trapped inside the cells in the airway and outside in the skin. Because chloride is negatively charged, positively charged ions cross into the cell because they are affected by the electrical attraction of the

DEFINITION PATHOPHYSIOLOGY

chloride ions. Sodium is the most common ion in the extracellular space and the combination of sodium and chloride creates the salt, which is lost in high amounts in the sweat of individuals with CF. This lost salt forms the basis for the sweat test ETIOLOGY & EDPIDEMOLOGY An inherited condition, cystic fibrosis affects the cells that produce mucus, sweat, saliva and digestive juices. Normally, these secretions are thin and slippery, but in cystic fibrosis, a defective gene causes them to become thick and sticky. Instead of acting as a lubricant, the secretions plug up tubes, ducts and passageways, especially in the pancreas and lungs. Respiratory failure is the most dangerous consequence of cystic fibrosis. Also, the secretions block pancreatic enzymes that help digest fats and proteins, and they prevent your body from absorbing key vitamins. In cystic fibrosis, a defective gene alters a protein that regulates the normal movement of salt (sodium chloride) in and out of cells. This results in thick, sticky secretions in the respiratory and digestive tracts, as well as in the reproductive system. It also causes increased salt in sweat. The affected gene, which is inherited from a child's parents, is a recessive gene. With recessive genes, children need to inherit two copies of the gene, one from each parent, in order to have the disease. If children inherit only one copy, they won't develop cystic fibrosis, but will be carriers and possibly pass the gene to their own children. If two people who carry the defective gene conceive a child, there's a 25 percent chance the child will have cystic fibrosis, a 50 percent chance the child will be a carrier of the cystic fibrosis gene, and a 25 percent chance the child will neither have the disease nor be a carrier. People who carry the cystic fibrosis gene are healthy and have no symptoms they may be carriers and not know it.

The greatest risk factor for cystic fibrosis is a family history of the disease. If both you and your partner come from families with cystic fibrosis, then each of your children has a one in four chance of having cystic fibrosis. Your risk is also greater if you're of Northern European ancestry. In that case, you have a one in 29 chance of carrying the gene. Among other ethnic groups in the United States, Hispanics have a one in 46 chance of carrying the gene, blacks have a one in 65 chance and Asian-Americans a one in 90 chance.

CLINICAL MANIFESTATION

The following are the most common symptoms for cystic fibrosis. However, individuals may experience symptoms differently. Symptoms may include: Abnormalities in the glands that produce sweat and mucus This may cause a loss of salt. A loss of salt may cause an upset in the balance of minerals in the blood, abnormal heart rhythms, and, possibly, shock. Thick mucus that accumulates in the lungs and intestines This may cause malnutrition, poor growth, frequent respiratory infections, breathing difficulties, and/or lung disease. Other medical problems, such as: sinusitis, nasal polyps, clubbing of fingers and toes - a condition marked by the ends of the fingers and toes become enlarged; more prevalent in the fingers, pneumothorax - the presence of air or gas in the pleural cavity causing the lung to collapse, hemoptysis - coughing blood, cor pulmonale - enlargement of right side of heart, abdominal pain, gas in the intestines, rectal prolapsed, liver

disease, diabetes, pancreatitis, gallstones. Infants born with CF usually show symptoms within the first year. Some children, though, may not show symptoms until later in life. The following signs are suspicious of CF, and infants having these signs may be tested for CF: diarrhea that does not go away, foul-smelling stools, greasy stools, frequent episodes of wheezing, frequent episodes of pneumonia, persistent cough, skin tastes like salt, poor growth

DIAGNOSTIC TESTS

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

Prenatal and genetic tests are performed to identify fetal disease and carrier status. Failure to thrive and frequent upper respiratory infections often lead to diagnostic testing to confirm the CF diagnosis. Quantitative sweat electrolyte test. Genotyping, Serum electrolytes, chest x-ray, arterial blood gases, pulmonary function tests, semen analysis, nasal potential difference measurement of the nasal mucosa, pulmonary function tests, bronchoalveolar lavage, and sputum microbiology. The major goals of treatment are to improve pulmonary, GI, and pancreatic status. These goals are achieved through a combination of medications, nutrition, and exercise regimens. If antibiotics are given to prevent and treat pneumonia, the physician and pharmacist monitor therapeutic blood levels of the antibiotics to determine the peak and trough levels. To help prevent the recurrence of pneumonia, chest physiotherapy (CPT) is performed in the home or hospital four times a day before meals to avoid emesis or after an aerosol treatment. A ThAIRapy vest, a device that provides high-frequency chest wall oscillations to loosen secretions, may also be used to maintain calorie counts on daily meal plans; supplement nutritional needs with high-calorie feedings. A patient may also have nasogastric feedings to which pancreatic enzymes are added to ensure the digestion and absorption of fats, protein, and carbohydrates. The physician may also prescribe total parenteral nutrition and fat-soluble vitamins (A, D, E, and K). Regular exercise, including mobility and muscle-strengthening exercises should be encouraged on a regular basis. Exercises help maintain physical wellness and supplement the patients airway clearance strategies by helping to loosen pulmonary secretions. Some patients develop right-sided heart failure, and if this occurs, most of them die within a year. They may require the use of home portable oxygen therapy and receive dioxin and/or diuretics. As the disease progresses toward the terminal phase, hemoptysis is present and cyanosis is markedly apparent. Educate to reinforce the importance of regular CPT and expectoration of the mucus. Encourage increased fluid intake to loosen the secretions, and provide frequent mouth care before meals. Teach the parents not to offer cough suppressants, which can lead to obstruction, lung collapse, and infection. Support the childs or adolescents body image concerns; compliment the patient on her or his strengths. Encourage the child to develop in as many areas as possible. Very often, other CF patients become a significant support group as the child matures. The child is always dramatically affected when another peer with CF dies. Plan group discussions with the patients and have a psychiatric nurse clinical specialist serve as facilitator of this grief work for both patients and staff. In addition, siblings often worry that they may contract the disease or they may exhibit feelings of jealousy of the attention given to the sibling with CF. A referral to a social worker or the Cystic Fibrosis Foundation may be needed. Counsel couples on the risk that subsequent pregnancies may result in a child with CF, since there is a one in four chance with any pregnancy that a child could have CF if both parents are carriers. Discuss the role of amniocentesis and the difficult issues surrounding terminating a pregnancy if CF is confirmed prenatally. Ineffective airway clearance related to excess tenacious mucus. Altered nutrition less than body requirement related to impaired digestive process and absorption of nutrients. Respiratory complications Frequent complications of cystic fibrosis are chronic respiratory infections, including pneumonia, bronchitis, chronic sinusitis and bronchiectasis an abnormal dilation of the walls of the bronchial tubes that makes it more difficult to clear your airways. Asthma can result from chronic inflammation of the bronchial lining. Nutritional complications Cystic fibrosis makes you prone to chronic diarrhea and severe nutritional deficiencies. That's because thick secretions obstruct the ducts in your pancreas, preventing enzymes that digest fats and proteins from

NURSING MANAGEMENT

NURSING MANAGEMENT (Nursing Diagnoses)

COMPLICATIONS

reaching your intestines. These secretions also prevent your body from absorbing the fat-soluble vitamins A, D, E and K. Reproductive complications Cystic fibrosis also affects the reproductive system. Because thick secretions often block the tube connecting the testes and prostate gland (vas deferens), many men with cystic fibrosis are infertile. Although women with cystic fibrosis may be less fertile than other women, it's possible for them to conceive and to have successful pregnancies.

MEDICAL DIAGNOSIS

Bronchiectasis An extreme form of onstructive bronchitis, causes permanent, abnormal dilation and distortion of bronchi and bronchioles All the causative conditions impair airway clearance mechanisms and host defenses, resulting in an inability to clear secretions, which, in turn, predisposes patients to chronic infection and inflammation. As a result of frequent infections, most commonly with Haemophilus influenzae (35%), Pseudomonas aeruginosa (31%), Moraxella catarrhalis (20%), Staphylococcus aureus (14%), and Streptococcus pneumoniae (13%), airways become inspissated with viscous mucous containing inflammatory mediators and pathogens and slowly become dilated, scarred, and distorted. Histologically, bronchial walls are thickened by edema, inflammation, and neovascularization. Destruction of surrounding interstitium and alveoli causes fibrosis, emphysema, or both. Superinfection with multidrug-resistant organisms, including Mycobacterium tuberculosis, and mycobacteria other than M. tuberculosis can cause recurrent exacerbations and worsen airflow limitation on pulmonary function tests. Pulmonary hypertension and right-sided heart failure may ensue because functional lung tissue decreases. Develops when bronchial wall are weakened by chronic inflammatory changes in the bronchial mucosa and occurs most often recurrent inflammatory conditions .conditions which cause the narrowing of the lumen of the bronchioles i.e tuberculosis, adenoviral infections, & pneumonia. May vary according to etiologic agent.main manifestation including, coughing, and purulent sputum production in large amount. Fever , Hemoptysis, nasal stuffiness, and drainage from sinusitis. Client complains of fatigue. Clubbing of nails present. Diagnosis may be confirmed by performing chest radiograph, bronchogram, or computer tomography (CT) scan. Antibiotics, chest therapy, hydration, bronchodilators, and oxygen are prescribed . In severe cases surgical resection in the pathologic process is well localized in one lobe or two adjacent lobes & when no contraindications exist.

DEFINITION PATHOPHYSIOLOGY

ETIOLOGY & EDPIDEMOLOGY

CLINICAL MANIFESTATION

DIAGNOSTIC TESTS

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

NURSING MANAGEMENT

Note signs of dyspnea, orthopnea, decreased breath sounds, evaluate mental status for confusion and restlessness due to hypoxia, and hypercapnea record baseline oximetry and level of inspired O2. note color

of sputum or hemoptysis.

(Nursing Diagnoses)

COMPLICATIONS

Imbalanced Nutrition: Less than body requirements, related to malnutrition caused by bronchiectasis Impaired gas exchange related to damage to the bronchial walls caused by bronchiectasis Ineffective airway clearance related to abnormal mucosa clearance and stagnated sputum in bronchi Advanced bronchiectasis may produce chronic malnutrition and amyloidosis, right ventricular failure, and cor pulonale

Dypnea, nasal flaring, pursed lip breathing, use of accessory muscles, wheezing cyanosis,

Bronchial asthma MEDICAL DIAGNOSIS

DEFINITION

Bronchial asthma is a chronic relapsing inflammatory disorder with increased responsiveness of tracheobroncheal tree to various stimuli, resulting in paroxysmal contraction of bronchial airways.

PATHOPHYSIOLOGY

During an asthma episode, inflamed airways react to environmental triggers such as smoke, dust, or pollen. The airways narrow and produce excess mucus, making it difficult to breathe. In essence, asthma is the result of an immune response in the bronchial airways. The airways of asthma patients are "hypersensitive" to certain triggers, also known as stimuli. In response to exposure to these triggers, the bronchi (large airways) contract into spasm (an "asthma attack"). Inflammation soon follows, leading to a further narrowing of the airways and excessive mucus production, which leads to coughing and other breathing difficulties. Bronchospasm may resolve spontaneously in 1 2 hours, or in about 50% of subjects, may become part of a 'late' response, where this initial insult is followed 312 hours later with further bronchoconstriction and inflammation. The normal caliber of the bronchus is maintained by a balanced functioning of these systems, which both operate reflexively. The parasympathetic reflex loop consists of afferent nerve endings which originate under the inner lining of the bronchus. Whenever these afferent nerve endings are stimulated (for example, by dust, cold air or fumes) impulses travel to the brain-stem vagal center, then down the vagal efferent pathway to again reach the bronchial small airways. Acetylcholine is released from the efferent nerve endings. This acetylcholine results in the excessive formation of inositol 1,4,5-trisphosphate (IP3) in bronchial smooth muscle cells which leads to muscle shortening and this initiates bronchoconstriction.

ETIOLOGY & EDPIDEMOLOGY

Inherited disorder. Environmental factors interact with inherited factors to produce disease. Symptoms can occur spontaneously or can be triggered by respiratory infections, exercise, cold air, tobacco smoke or other pollutants, stress or anxiety, or by food allergies or drug allergies.

Dypnea, nasal flaring, pursed lip breathing, use of accessory muscles, wheezing cyanosis, CLINICAL MANIFESTATION Spirometery, pulse oximetry, ABG, chest x ray DIAGNOSTIC TESTS Prevention of chronic asthma, maintain patent airway, administer beta2- agonists, nebulize atropine, IV corticosteroids, supplemental oxygen, end tracheal intubation,. bronchodilators such as inhaled Alupent or Vanceril. Acute severe asthma may require hospitalization, oxygen, and intravenous medications. Reinforce pursed lip breathing, monitor and record color, amt, and consistency of sputum, high fowlers position. Ineffective breathing pattern related to impaired exhalation evidenced by dyspnea use of accessory muscles and wheezing. Ineffective airway clearance related to increased production of secretions.

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

NURSING MANAGEMENT

NURSING MANAGEMENT (Nursing Diagnoses)

Apart from chronicity, usually no complications.

COMPLICATIONS

Pneumothorax, emphysema, or areas of consolidation or pulmonary collapse may occur in very

advanced cases.

10

MEDICAL DIAGNOSIS

Atelectasis Atelectasis is a medical condition in which the lungs are not fully inflated. It may affect part or all of one lung. It is a condition where the alveoli are deflated, as distinct from pulmonary consolidation. There is a collapse of lung tissue, preventing the respiratory exchange of carbon dioxide and oxygen.

DEFINITION

PATHOPHYSIOLOGY

Obstructive atelectasis Following obstruction of a bronchus, the circulating blood absorbs the gas in the peripheral alveoli, leading to retraction of the lung and an airless state within a few hours. In the early stages, blood perfuses the airless lung; this results in ventilation-perfusion mismatch and arterial hypoxemia. A filling of the alveolar spaces with secretions and cells may occur, thereby preventing complete collapse of the atelectatic lung. The uninvolved surrounding lung tissue distends, displacing the surrounding structures. The heart and mediastinum shift toward the atelectatic area, the diaphragm is elevated, and the chest wall flattens. Nonobstructive atelectasis The loss of contact between the visceral and parietal pleurae is the primary cause of nonobstructive atelectasis. A pleural effusion or pneumothorax causes relaxation or passive atelectasis. Pleural effusions affect the lower lobes more commonly than pneumothorax, which affects the upper lobes. A large pleuralbased lung mass may cause compression atelectasis by decreasing lung volumes. Adhesive atelectasis is caused by a lack of surfactant. The surfactant has phospholipid dipalmitoyl phosphatidylcholine, which prevents lung collapse by reducing the surface tension of the alveoli. Lack of production or inactivation of surfactant, which may occur in ARDS, radiation pneumonitis, and blunt trauma to the lung, cause alveolar instability and collapse. Middle lobe syndrome (recurrent atelectasis and/or bronchiectasis involving the right middle lobe and/or lingula) has recently been reported as the pulmonary manifestation of primary Sjgren syndrome. Scarring of the lung parenchyma leads to cicatrization atelectasis. Replacement atelectasis is caused by filling of the entire lobe by a tumor such as bronchoalveolar carcinoma. Platelike atelectasis Also called discoid or subsegmental atelectasis, this type is seen most commonly on chest radiographs. Platelike atelectasis probably occurs because of obstruction of a small bronchus and is observed in states of hypoventilation, pulmonary embolism, or lower respiratory tract infection. Small areas of atelectasis occur because of inadequate regional ventilation and abnormalities in surfactant formation from hypoxia, ischemia, hyperoxia, and exposure to various toxins. A mild-to-severe gas exchange abnormality may occur because of ventilation-perfusion mismatch and intrapulmonary shunt. Postoperative atelectasis Atelectasis is a common pulmonary complication in patients following thoracic and upper abdominal procedures. General anesthesia and surgical manipulation lead to atelectasis by causing diaphragmatic dysfunction and diminished surfactant activity. The atelectasis is typically basilar and segmental in distribution. The most common cause is post-surgical atelectasis, characterized by splinting, restricted breathing after abdominal surgery. Smokers and the elderly are at an increased risk. Outside of this context, atelectasis implies some blockage of a bronchiole or bronchus, which can be within the airway (foreign body, mucus plug), from the wall (tumor, usually squamous cell carcinoma) or compressing from the outside (tumor, lymph node, tubercle). Another cause is poor surfactant spreading during inspiration, causing an increase in surface tension which tends to collapse smaller alveoli. Atelectasis may also occur during suction, as along

ETIOLOGY & EDPIDEMOLOGY

11

with sputum, air is withdrawn from the lungs. Another cause of Atelectasis is a Pulmonary embolism (PE). Atelectasis may be an acute or chronic condition. Acute atelectasis is a common postoperative complication, especially after chest or abdominal surgery. Acute atelectasis may also occur with an injury, usually to the chest (such as that caused by a car accident, a fall, or a stabbing). Atelectasis following surgery or injury, sometimes described as massive, involves most alveoli in one or more regions of the lungs. Chronic atelectasis may take one of two formsmiddle lobe syndrome or rounded atelectasis. In middle lobe syndrome, the middle lobe of the right lung contracts, usually because of pressure on the bronchus from enlarged lymph glands and occasionally a tumor. The blocked, contracted lung may develop pneumonia that fails to resolve completely and leads to chronic inflammation, scarring, and bronchiectasis.

CLINICAL MANIFESTATION

Some client is asymptomatic. If significant, hypoxia is present; however dyspnea, tachycardia, and cyanosis In severe cases the following is present over the affected area: -A dull percussion note -A decrease in tactile fremitus. -decrease chest movement on the involved side -A tracheal shift toward the side of the atelectasis may occur. Symptoms may not be present if the atelectasis is minor and the patient has previously healthy lungs. Dyspnea is common when the atelectasis is severe, cough, but not prominent, chest pain, breathing difficulty, low oxygen saturation, pleural effusion (transdate type), cyanosis (late sign), increased heart rate.

DIAGNOSTIC TESTS

ABG, chest radiography (airless area over region of atelectisis area.) Diagnosed through physical examination when auscultation of the lungs reveal bronchial or diminished breathe sounds and crackles over the involved area. Generally its detected on a chest radiograph. Chest physiotherapy, lung expansion therapy, artificial surfactant, analgesics, bronchodilators, antieffective agents, surgical excision or insertion of drainage tube, bronchoscopy.

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

NURSING MANAGEMENT

Elevate for dyspnea, decreased chest wall expansion, diaphoresis, tachypnea, tachycardia and pleuritic chest pain. Auscultate for abnormal breath sounds. Pulse oximetry and hypoxemia, instruct & monitor the use of incentive spirometry. Localized airway obstruction related to mucus plugging. Nursing care focuses on preventing atelectasis, especially when the client is at risk because of failure to aerate the lungs properly. Postoperative deep breathing and coughing can prevent atelectasis. If atelectasis occurs, the nurse encourages the client to take deep breaths and coughs at frequent intervals and instructs the client in the use of an incentive spiromter. Complications arising from underlying disorder Hypoxemia Secondary infection of the atelectatic lung Bronchiectasis in the atelectatic of the chronically infected lung

NURSING MANAGEMENT (Nursing Diagnoses)

COMPLICATIONS

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Pleural effusion MEDICAL DIAGNOSIS Is an accumulation of fluid in the pleural spaces. Two types transcudate and exudate DEFINITION PATHOPHYSIOLOGY Pleural effusion is an indicator of a pathologic process that may be of primary pulmonary origin or of an origin related to another organ system or to systemic disease. It may occur in the setting of acute or chronic disease and is not a diagnosis in itself. Normal pleural fluid has the following characteristics: clear ultrafiltrate of plasma, pH 7.60-7.64, protein content less than 2% (1-2 g/dL), fewer than 1000 WBCs per cubic millimeter, glucose content similar to that of plasma, lactate dehydrogenase (LDH) level less than 50% of plasma and sodium, and potassium and calcium concentration similar to that of the interstitial fluid. The principal function of pleural fluid is to provide a frictionless surface between the two pleurae in response to changes in lung volume with respiration. The following mechanisms play a role in the formation of pleural effusion:

Altered permeability of the pleural membranes (eg, inflammatory process, neoplastic disease, pulmonary embolus) Reduction in intravascular oncotic pressure (eg, hypoalbuminemia, hepatic cirrhosis) Increased capillary permeability or vascular disruption (eg, trauma, neoplastic disease, inflammatory process, infection, pulmonary infarction, drug hypersensitivity, uremia, pancreatitis) Increased capillary hydrostatic pressure in the systemic and/or pulmonary circulation (eg, congestive heart failure, superior vena caval syndrome) Reduction of pressure in pleural space; lung unable to expand (eg, extensive atelectasis, mesothelioma) Inability of the lung to expand (eg, extensive atelectasis, mesothelioma) Decreased lymphatic drainage or complete blockage, including thoracic duct obstruction or rupture (eg, malignancy, trauma) Increased fluid in peritoneal cavity, with migration across the diaphragm via the lymphatics (eg, hepatic cirrhosis, peritoneal dialysis) Movement of fluid from pulmonary edema across the visceral pleura Persistent increase in pleural fluid oncotic pressure from an existing pleural effusion, causing accumulation of further fluid Iatrogenic causes (eg, central line misplacement)

ETIOLOGY & EDPIDEMOLOGY

CLINICAL

Transcudate: congestive heart failure, cirrhosis, peritoneal dialysis, pericarditis. Exudates; TB, trauma, lung cancer, respiratory infection, heart surgery complications, pneumonia, metastatic disease. Or Conditions that interferes with either secretion or drainage of pleural fluid leads to effusion. It can be grouped into 4 groups: Increased systemic hydrostatic pressure.(e.g., heart failure.) Reduced capillary oncotic pressure ( e.g. Liver or renal failure.) Increased capillary permeability ( e.g. Infections of trauma) Impaired lymphatic function ( e.g. Lymphatic obstruction caused by tumor) Depends on the amount of fluid present& severity of lung compression. There may be dyspnea , primarily on exertion, and a dry non productie cough cause by bronchial irritation or mediastinal shift.

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MANIFESTATION

Tactile fremitus may be decreased or absent , percussion note dull or flat Thoractcentesis is used to remove excess pleural fluid.the removed fluid is assess to determine weather whether it is transudate or exudates. Differenciating the fliud type helps extablish a specific diagnosis.other test include white blood cell, malignant cells, bacteria, Glucose, ph, LDH. Two features of human parietal pleura explain its role in the formation and removal of pleural liquid and protein in the normal state: the proximity of the microvessels to the pleural surface and the presence of stomata situated between mesothelial cells. For pleural fluid to accumulate in disease, there must be increased production from increased hydrostatic pressure, decreased oncotic or pleural pressure, increased microvascular permeability, or peritoneal-pleural movement. The rate of formation must overwhelm lymphatic clearance, which may be decreased by hydrostatic forces or blocked by malignant infiltration. Assess patient for respiratory changes and chest pain during inspiration. Auscultate lungs for decreased breath sounds or a pleural rub. Perform chest percussion and assess for alterations in tactile fremitus. Monitor pulse oximetry. Help client into a position that maximizes ventilation, typically high Fowler's position. Teach client deep-breathing and effective coughing techniques. Show client how to splint his chest during coughing and how to perform incentive spirometry. Provide supplemental oxygen, as ordered. If client requires thoracentesis or insertion of a chest tube, gather the equipment and explain the procedure. Provide emotional support; administer analgesics, as ordered; and assist with positioning. Prepare to receive specimen tubes as the physician removes fluid. If your patient has a chest tube inserted, monitor the amount and type of fluid drained. Maintain the fluid level in the suction control chamber and watch for bubbling in the water seal chamber. If the bubbling stops, evaluate whether the lung has completely reexpanded or if the drainage tube has become occluded. Complete a respiratory assessment after each procedure and as needed. Increased dyspnea, decreased or absent breath sounds, and increased pain on inspiration could indicate further effusion or development of a pneumothorax.

DIAGNOSTIC TESTS

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

NURSING MANAGEMENT

Ineffective breathing pattern related to decreased lung expansion. NURSING MANAGEMENT (Nursing Diagnoses) Delaying antimicrobial therapy for parapneumonic and other effusions, when antimicrobial therapy is indicated, potentially increases the risk of developing empyema, pulmonary fibrosis, and sepsis.

COMPLICATIONS

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Pleuritis MEDICAL DIAGNOSIS Pleurisy is inflammation of the linings around the lungs the pleura. There are two layers of pleura: one covering the lung termed the visceral pleura and the other covering the inner wall of the chest the parietal pleura. These two layers are lubricated by pleural fluid. The pleural space normally contains 0.10.2 ml/kg body weight of fluid, filtered from systemic capillaries down a small pressure gradient. Fluid drains into the systemic circulation via a delicate network of lymphatics and eventually enters the mediastinal lymph nodes. Fluid may accumulate in the pleural space by a number of mechanisms: increased pulmonary capillary pressure, decreased (more negative) intrapleural pressure (e.g. atelectasis), decreased plasma oncotic pressure (e.g. hypoalbuminaemia), increased pleural membrane permeability and obstructed lymphatic flow (e.g. pleural malignancy or infection). Pleurisy can be caused by any of the following conditions Infections: bacterial (including those that cause tuberculosis), fungus, parasites, or viruses Inhaled chemicals or toxic substances: exposure to some cleaning agents like ammonia Collagen vascular diseases: lupus, rheumatoid arthritis Cancers: for example, the spread of lung cancer or breast cancer to the pleura Tumors of the pleura: mesothelioma or sarcoma Congestion: heart failure Pulmonary embolism: blood clot inside the blood vessels to the lungs. These clots sometimes severely reduce blood and oxygen to portions of the lung and can result in death to that portion of lung tissue (termed lung infarction). This, too, can cause pleurisy. Obstruction of lymph channels: as a result of centrally located lung tumors Trauma: rib fractures or irritation from chest tubes used to drain air or fluid from the pleural cavity in the chest Certain drugs: drugs that can cause lupus-like syndromes (such as Hydralazine, Procan, Dilantin, and others) Abdominal processes: such as pancreatitis, cirrhosis of the liver Lung infarction: lung tissue death due to lack of oxygen from poor blood supply

DEFINITION

PATHOPHYSIOLOGY

ETIOLOGY & EDPIDEMOLOGY

CLINICAL MANIFESTATION

Pain in the chest that is aggravated by breathing Shortness of breath "Stabbing" sensation The most common symptom of pleurisy is pain that is generally aggravated by inspiration (breathing in). Although the lungs themselves do not contain any pain nerves, the pleura contains abundant nerve endings. When extra fluid accumulates in the space between the layers of pleura, the pain usually is a less severe form of pleurisy. With very large amounts of fluid accumulation, the expansion of the lungs can be limited, and shortness of breath can worsen. Chest x-ray A chest x-ray takes a picture of the heart and lungs. It may show air or fluid in the pleural space. It also may show what's causing the pleurisy for example, pneumonia, a fractured rib, or a lung tumor.

DIAGNOSTIC TESTS

15

Sometimes an x-ray is taken while lying on the painful side. This may show fluid that did not appear on the standard x-ray taken while standing. Ultrasound Ultrasonography uses sound waves to create pictures of the lungs. It may show where fluid is located in the chest. It also can show some tumors. Magnetic resonance imaging (MRI) Magnetic resonance imaging (MRI), also called nuclear magnetic resonance (NMR) scanning, uses powerful magnets and radio waves to show pleural effusions and tumors. Blood tests: Blood tests can detect bacterial or viral infection, pneumonia, rheumatic fever, a pulmonary embolism, or lupus. Arterial blood gas In arterial blood gas sampling, a small amount of blood is taken from an artery, usually in the wrist. The blood is then checked for oxygen and carbon dioxide levels. This test shows how well the lungs are taking in oxygen

Treatment has several goals: MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

Remove the fluid, air, or blood from the pleural space Relieve symptoms Treat the underlying condition

Procedures: If large amounts of fluid, air, or blood are not removed from the pleural space, they may put pressure on the lung and cause it to collapse. The surgical procedures used to drain fluid, air, or blood from the pleural space are as follows:

During thoracentesis, a needle or a thin, hollow, plastic tube is inserted through the ribs in the back of the chest into the chest wall. A syringe is attached to draw fluid out of the chest. This procedure can remove more than 6 cups (1.5 liters) of fluid at a time. When larger amounts of fluid must be removed, a chest tube may be inserted through the chest wall. The doctor injects a local painkiller into the area of the chest wall outside where the fluid is. A plastic tube is then inserted into the chest between two ribs. The tube is connected to a box that suctions the fluid out. A chest x-ray is taken to check the tube's position. A chest tube also is used to drain blood and air from the pleural space. This can take several days. The tube is left in place, and the patient usually stays in the hospital during this time. Sometimes the fluid contains thick pus or blood clots, or it may have formed a hard skin or peel. This makes it harder to drain the fluid. To help break up the pus or blood clots, the doctor may use the chest tube to put certain medicines into the pleural space. These medicines are called fibrinolytics. If the pus or blood clots still don't drain out, surgery may be necessary.

Medications A couple of medications are used to relieve pleurisy symptoms:

Paracetamol (acetaminophen) or anti-inflammatory agents to control pain and decrease inflammation. Only indomethacin (brand name Indocin) has been studied with respect to relief of pleurisy. Codeine-based cough syrups to control a cough

There may be a role for the use of corticosteroids (for tuberculous pleurisy), tacrolimus (Prograf) and methotrexate (Trexall, Rheumatrex) in the treatment of pleurisy. Further studies are needed before they are used routinely.

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NURSING MANAGEMENT

Monitor resp. observe breathing patterns, oximetry, high fowlers position to facilitate chest expansion, encourage deep breathing every 1-2 hrs, help patient splint chest with pillows to cough, administer analgesic drugs, provide receptacle for collection of sputum, recommend rest periods. Lifestyle changes: The following may be helpful in the management of pleurisy:

Lying on the painful side may be more comfortable Breathing deeply and coughing to clear mucus as the pain eases. Otherwise, pneumonia may develop. Getting plenty of rest

Assess respiratory function. NURSING MANAGEMENT (Nursing Diagnoses) - Administer analgesic as ordered. - Teach patient to support ribcage when coughing. - Help reposition to alleviate pain, such as lying on the affected side. - Assess level of anxiety and provide reassurances of safety

Pleural effusion (excessive pleural fluid, which forces the pleura apart and collects in the lower parts). COMPLICATIONS - The effusion may compress and partially collapse the lung. - Pleural adhesion (inflamed patches of the pleura become permanently stuck together).

Emphysema MEDICAL DIAGNOSIS Empyema is the presence of pus in a body cavity, especially the pleural cavity. Empyema is the accumulation of pus and necrotic tissue in the pleural space. Normally, this space contains a small amount of extracellular fluid that lubricates the pleural surfaces. Accumulation of pus in the lung cavity, usually as a result of infection. Most commonly the pleural space surrounding the lungs.

DEFINITION

17

Empyema in the pleural cavity is sometimes called empyema thoracis, or empyema of the chest.

PATHOPHYSIOLOGY

In normal breathing, air is drawn in through the bronchi and into the alveoli, which are tiny sacs surrounded by capillaries. Alveoli absorb oxygen and then transfer it into the blood. When toxicants, such as cigarette smoke, are breathed into the lungs, the harmful particles become trapped in the alveoli, causing a localized inflammatory response. Chemicals released during the inflammatory response (e.g., elastase) can eventually cause the alveolar septum to disintegrate. This condition, known as septal rupture, leads to significant deformation of the lung architecture. These deformations result in a large decrease of alveoli surface area used for gas exchange. To accommodate the decreased surface area, thoracic cage expansion (barrel chest) and diaphragm contraction (flattening) take place. Expiration increasingly depends on the thoracic cage and abdominal muscle action, particularly in the end expiratory phase. Due to decreased ventilation, the ability to exude carbon dioxide is significantly impaired. In the more serious cases, oxygen uptake is also impaired. As the alveoli continue to break down, hyperventilation is unable to compensate for the progressively shrinking surface area, and the body is not able to maintain high enough oxygen levels in the blood. The body's last resort is vasoconstricting appropriate vessels. This leads to pulmonary hypertension, which places increased strain on the right side of the heart, the side responsible for pumping deoxygenated blood to the lungs. The heart muscle thickens in order to pump more blood. This condition is often accompanied by the appearance of jugular venous distension. Eventually, as the heart continues to fail, it becomes larger and blood backs up in the liver

Empyema results as a complication of bacterial infections such as pneumonia and lung abscess. ETIOLOGY & EDPIDEMOLOGY Empyema may be caused by bacteria such as Streptococcus pneumonia, Staphylococcus aureus, or Haemophilus influenza type b. The infected fluid may be build up to a quantity of a pint or more, which puts pressure on the lungs, causing shortness of breath and pain. The infected fluid can build up to a quantity of a pint or more. Empyema thoracis may be caused by a number of different organisms, fungi, and amebas, in connection with pneumonia, chest wounds, chest surgery, lung abscesses, or a ruptured esophagus. Pelvic empyema in women is most often caused by Bacteroides strains or Pseudomonas aeruginosa.

CLINICAL MANIFESTATION

Physical findings include tachypnea, and decreased breath sounds; percussion over the effused area, detects dullness, which doesn't change with breathing. The signs and symptoms of empyema vary somewhat according to the location of the infection and its severity. Ultrasound confirms the size and location of the pocket of pus and the presence of fibrin aggregates. The symptoms of the empyema may be included: fever & cough, coma, malaise, fatigue, sweating, weight loss, chest pain, general discomfort, shortness of breath.

Chest x ray, arterial blood gas, sputum specimen, pulmonary function test DIAGNOSTIC TESTS The goal of treatment is to cure the infection and remove the collection of pus from the lung. A chest tube is

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MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

inserted to drain the pus from the pleural space. Ultrasound has been used to evaluate empyema. Some evidence suggests that intrapleural fibrinolytic drugs may be useful, especially in children. Intravenous antibiotics may be given. If this is insufficient, surgical decortication of the pleura may be required. Mechanical ventilation, bronchodilators, corticosteroids, beta agonists, methylxanthines H.F position.

NURSING MANAGEMENT

Give O2 at 2L because with emphysema excessive exogenous O2 diminishes the respiratory drive and results in breathing and CO2 retention (CO2 narcosis). Normally CO2 stimulates breathing. With emphysema there is chronic CO2 and as a result low O2 stimulates breathing Teach diaphragmatic and pursed-lip breathing to extend exhalation and keep alveoli open Impaired gas exchange related to decreased ventilation and mucus plugs.

NURSING MANAGEMENT (Nursing Diagnoses)

COMPLICATIONS

The list of complications that have been mentioned in various sources for Emphysema includes: Finger clubbing Recurrent chest infections Heart failure Right-sided heart failure Often individuals who are unfortunate enough to contract this disease have a very short life expectancy often 0-3 years at most

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Acute Bronchitis MEDICAL DIAGNOSIS Bronchitis is a respiratory disease in which the mucous membrane in the lungs' bronchial passages becomes inflamed. As the irritated membrane swells and grows thicker, it narrows or shuts off the tiny airways in the lungs, resulting in coughing spells accompanied by thick phlegm and breathlessness. The disease comes in two forms: acute (lasting less than 6 weeks) and chronic (reoccurring frequently for more than two years). In addition, people with asthma also experience an inflammation of the lining of the bronchial tubes called asthmatic bronchitis. Acute bronchitis is responsible for the hacking cough and phlegm production that sometimes accompany anupper respiratory infection. In most cases the infection is viral in origin, but sometimes it's caused by bacteria. Respiratory viruses are the most common causes of acute bronchitis. The most common viruses include influenza A and B, parainfluenza, respiratory syncytial virus, and coronavirus, although an etiologic agent is identified only in a minority of cases. During an episode of acute bronchitis, the cells of the bronchial-lining tissue are irritated and the mucous membrane becomes hyperemic and edematous, diminishing bronchial mucociliary function. Consequently, the air passages become clogged by debris and irritation increases. In response, copious secretion of mucus develops, which causes the characteristic cough of bronchitis. For instance, with mycoplasmal pneumonia, bronchial irritation results from the attachment of the organism (Mycoplasma pneumoniae) to the respiratory mucosa, with eventual sloughing of affected cells. Acute bronchitis usually lasts approximately 10 days. If the inflammation extends downward to the ends of the bronchial tree, into the small bronchi (bronchioles), and then into the air sacs, bronchopneumonia results. Chronic bronchitis is a condition associated with excessive tracheobronchial mucus production sufficient to cause cough with expectoration for at least 3 months for more than 2 consecutive years. The alveolar epithelium is both the target and the initiator of inflammation in chronic bronchitis. Acute bronchitis is generally caused by lung infections; approximately 90% of these infections are viral inorigin, 10% bacterial. Chronic bronchitis may be caused by one or several factors. Repeated attacks of acute bronchitis, which weaken and irritate bronchial airways over time, can result in chronic bronchitis, Industrial pollution is another culprit

DEFINITION

PATHOPHYSIOLOGY

ETIOLOGY & EDPIDEMOLOGY

A cough that is frequent and produces mucus CLINICAL MANIFESTATION A lack of energy A wheezing sound when breathing, which may or may not be present A fever, which may or may not be present cultures of respiratory secretions for influenza virus, M pneumoniae, and Bordetella pertussis when these organisms are suspected. Obtain a throat swab. Obtain a CBC count with differential. Blood culture may sometimes be helpful if bacterial superinfection is suspected. Sputum cytology may be helpful if the cough is persistent

DIAGNOSTIC TESTS

Culture and Gram stain of sputum is often performed Chest radiography should be performed in those patients whose physical examination findings suggest pneumonia. Bronchoscopy may be needed to exclude foreign body aspiration, tuberculosis, tumors, and other

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chronic diseases of the tracheobronchial tree and lungs.

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

Medical therapy generally targets symptoms and includes use of analgesics and antipyretics. These agents are used to control fever, myalgias, and arthralgias. Acetaminophen (Tylenol, Aspirin-Free Anacin, Feverall) Treatment of choice for pain in patients who are unable to take aspirin or NSAIDs. Ibuprofen (Ibuprin, Advil, Motrin) Usual treatment of choice for mild-to-moderate pain if no contraindications exist. Inhibits inflammatory reactions and pain, probably by decreasing activity of cyclooxygenase, which inhibits prostaglandin synthesis. Corticosteroids, systemic These agents are used for short courses (3-10 d) to gain prompt control of inadequately controlled acute asthmatic episodes. Systemic corticosteroids also are used for long-term prevention of symptoms in severe persistent asthma, as well as for suppression, control, and reversal of inflammation.

NURSING MANAGEMENT

1. 2. 3. 4. 5.

6.

7.

Encourage mobilization of secretion through ambulation, coughing, and deep breathing. Ensure adequate fluid intake to liquefy secretions and prevent dehydration caused by fever and tachypnea. Encourage rest, avoidance of bronchial irritant, and a good diet to facilitate recovery. Instruct the patient to complete the full course of prescribed antibiotics and explain the effect of meals on drug absorption. Caution the patient on using over-the-counter cough suppressants, antihistamines, and decongestants, which may cause drying and retention of secretions. However, cough preparations containing the mucolytic guaifenesin may be appropriate. Advise the patient that a dry cough may persist after bronchitis because of irritation of airways. Suggest avoiding dry environments and using a humidifier at bedside. Encourage smoking cessation. Teach the patient to recognize and immediately report early signs and symptoms of acute bronchitis.

Abnormal breathing sounds related to ineffective cough NURSING MANAGEMENT (Nursing Diagnoses)

COMPLICATIONS

Complications occur in approximately 10% of patients with acute bronchitis and include the following: o Bacterial superinfection o Lower respiratory tract infection and pneumonia: Less than 5% of patients with bronchitis develop pneumonia. The incidence of subsequent pneumonia, however, remains unaffected by the use of antibiotics. o Chronic bronchitis: Repeated episodes of acute bronchitis may lead to chronic bronchitis. o Reactive airway disease: Acute bronchitis may lead to reactive airway disease. o Hemoptysis

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Lung abscess MEDICAL DIAGNOSIS Lung abscess is necrosis of the pulmonary tissue and formation of cavities (more than 2 cm) containing necrotic debris or fluid caused by microbial infection. This pus-filled cavity is often caused by aspiration, which may occur during altered consciousness. Alcoholism is the most common condition predisposing to lung abscesses

DEFINITION

PATHOPHYSIOLOGY

Most frequently, the lung abscess arises as a complication of aspiration pneumonia caused by mouth anaerobes. The patients who develop lung abscess are predisposed to aspiration and commonly have periodontal disease. A bacterial inoculum from the gingival crevice reaches the lower airways, and infection is initiated because the bacteria are not cleared by the patient's host defense mechanism. This results in aspiration pneumonitis and progression to tissue necrosis 7-14 days later, resulting in formation of lung abscess. Other mechanisms for lung abscess formation include bacteremia or tricuspid valve endocarditis, causing septic emboli (usually multiple) to the lung. Lemierre syndrome, an acute oropharyngeal infection followed by septic thrombophlebitis of the internal jugular vein, is a rare cause of lung abscesses. The oral anaerobe F necrophorum is the most common pathogen. Conditions contributing to lung abscess Aspiration of oropharyngeal or gastric secretion Septic emboli Necrotizing pneumonia Vasculitis: Wegener's granulomatosis Necrotizing tumors: 8% to 18% are due to neoplasms across all age groups, higher in older people; primary squamous carcinoma of the lung is the commonest. Organisms In the post-antibiotic era pattern of frequency is changing. In older studies anaerobes were found in up to 90% cases but they are much less frequent now. Anaerobic bacteria: Peptostreptococcus, Bacteroides, Fusobacterium species, Microaerophilic streptococcus : Streptococcus milleri Aerobic bacteria: Staphylococcus, Klebsiella, Haemophilus, Pseudomonas,Nocardia, Escheria coli, Streptococcus, Mycobacteria Fungi: Candida, Aspergillus Parasites:Entamoeba histolytica Onset of symptoms is often gradual, but in necrotizing staphylococcal or gram-negative bacillary pneumonias patients can be acutely ill. Cough, fever with shivering and night sweats are often present. Cough can be productive with foul smelling purulent sputum (70%) or less frequently with blood (i.e. hemoptysis in one third cases). Affected individuals may also complain of chest pain, shortness of breath, lethargy and other features of chronic illness. Patients are generally cachectic at presentation. Finger clubbing is present in one third of patients. Dental decay is common especially in alcoholics and children. On examination of chest there will be features of consolidation such as localised dullness on percussion, bronchial breath sound etc.

ETIOLOGY & EDPIDEMOLOGY

CLINICAL MANIFESTATION

Chest Xray and other imaging studies DIAGNOSTIC TESTS Abscess is often unilateral and single involving posterior segments of the upper lobes and the apical segments of the lower lobes as these areas are gravity dependent when lying down. Presence of air-fluid levels implies rupture into the bronchial tree or rarely growth of gas forming organism. Laboratory studies

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Raised inflammatory markers (high ESR, CRP) are usual but not specific. Examination of sputum is important in any pulmonary infections and here often reveals mixed flora. Transtracheal of Transbronchial (via bronchoscopy) aspirates can also be cultured. Fibre optic bronchoscopy is often performed to exclude obstructive lesion; it also helps in bronchial drainage of pus.

Antibiotic therapy MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

Standard treatment of an anaerobic lung infection is clindamycin (600 mg IV q8h followed by 150300 mg PO qid). This regimen has been shown to be superior over parenteral penicillin in published trials. Several anaerobes may produce beta-lactamase (eg, various species of Bacteroides and Fusobacterium) and therefore develop resistance to penicillin. Although metronidazole is an effective drug against anaerobic bacteria, the experience with metronidazole in treating lung abscess has been rather disappointing because these infections are generally polymicrobial. A failure rate of 50% has been reported. In hospitalized patients who have aspirated and developed a lung abscess, antibiotic therapy should include coverage against S aureus and Enterobacter and Pseudomonas species. Ampicillin plus sulbactam is well tolerated and as effective as clindamycin with or without a cephalosporin in the treatment of aspiration pneumonia and lung abscess. Moxifloxacin is clinically effective and as safe as ampicillin plus sulbactam in the treatment of aspiration pneumonia and lung abscess.

Duration of therapy

Although the duration of therapy is not well established, most clinicians generally prescribe antibiotic therapy for 4-6 weeks. Expert opinion suggests that antibiotic treatment should be continued until the chest radiograph has shown either the resolution of lung abscess or the presence of a small stable lesion. The rationale for extended treatment maintains that risk of relapse exists with a shorter antibiotic regimen.

NURSING MANAGEMENT

Antibiotic administration as indicated Chest physiotherapy Ensure proper nutritional intake Emotional support Impaired gas exchange related to mismatch between ventilation and perfusion as a result of a thoracotomy

NURSING MANAGEMENT (Nursing Diagnoses)

COMPLICATIONS

Complications of pulmonary abscess o Rupture into pleural space causing empyema o Pleural fibrosis o Trapped lung o Respiratory failure o Bronchopleural fistula o Pleural cutaneous fistula In a patient with coexisting empyema and lung abscess, draining the empyema while continuing prolonged antibiotic therapy is often necessary.

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Pneumothorax MEDICAL DIAGNOSIS Presence of air in pleural cavity: the presence of air or gas in the pleural cavity surrounding the lungs, causing pain and difficulty in breathing. This creates positive intrapleural pressure and prevents proper lung inflation. If this accumulation is of a sufficient size, the lung parenchyma may collapse. The lungs are located inside the chest cavity, which is a hollow space. Air is drawn into the lungs by the diaphragm (a powerful abdominal muscle). The pleural cavity is the region between the chest wall and the lungs. If air enters the pleural cavity, either from the outside (open pneumothorax) or from the lung (closed pneumothorax), the lung collapses and it becomes mechanically impossible for the injured person to breathe, even with an open airway. If a piece of tissue forms a one-way valve that allows air to enter the pleural cavity from the lung but not to escape, overpressure can build up with every breath; this is known as tension pneumothorax. It may lead to severe shortness of breath as well as circulatory collapse, both life-threatening conditions. This condition requires urgent intervention.

DEFINITION PATHOPHYSIOLOGY

It most commonly arises: ETIOLOGY & EDPIDEMOLOGY

Spontaneously (most commonly in tall slim young males and in Marfan syndrome) Following a penetrating chest wound Following Barotrauma to the lungs

It may also be due to:

Chronic lung pathologies including emphysema, asthma Acute infections Chronic infections, such as tuberculosis Lung damage caused by cystic fibrosis Cancer Rare diseases that are unique to women such as Catamenial pneumothorax (due to endometriosis in the chest cavity) and lymphangioleiomyomatosis (LAM).

Pneumothoraces are divided into tension and non-tension pneumathoraces. A tension pneumothorax is a medical emergency as air accumulates in the pleural space with each breath. The increase in intrathoracic pressure results in massive shifts of the mediastinum away from the affected lung compressing intrathoracic vessels. A non-tension pneumothorax by contrast is of lesser concern because there is no ongoing accumulation of air and hence no increasing pressure on the organs within the chest. The accumulation of blood in the thoracic cavity (hemothorax) exacerbates the problem, creating a hemopneumothorax.

Signs and symptoms of a pneumothorax usually include: CLINICAL MANIFESTATION

Sudden, sharp chest pain on the same side as the affected lung this pain doesn't occur in the center of your chest under the breast bone Shortness of breath, which may be more or less severe, depending on how much of your lung is collapsed A feeling of tightness in your chest

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A rapid heart rate If only a small amount of air enters the space between your lungs and your chest wall (pleural space), you may have few signs or symptoms. However, even a slightly collapsed lung is likely to cause some chest pain and some shortness of breath that slowly improves over a few hours to a day or so, even if there is no reduction in the size of the collapse.

DIAGNOSTIC TESTS

Thoracic CT: Studies show that CT is more sensitive than x-ray in detecting thoracic injuries, lung contusion, hemothorax, and pneumothorax. Early CT may influence therapeutic management. Chest x-ray: Reveals air and/or fluid accumulation in the pleural space; may show shift of mediastinal structures (heart). ABGs: Variable depending on degree of compromised lung function, altered breathing mechanics, and ability to compensate. PaCO2 occasionally elevated. PaO2 may be normal or decreased; oxygen saturation usually decreased. Thoracentesis: Presence of blood/serosanguineous fluid indicates hemothorax. Hb: May be decreased, indicating blood loss. Signs and symptoms of a pneumothorax usually include:

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

Sudden, sharp chest pain on the same side as the affected lung this pain doesn't occur in the center of your chest under the breast bone Shortness of breath, which may be more or less severe, depending on how much of your lung is collapsed A feeling of tightness in your chest A rapid heart rate If only a small amount of air enters the space between your lungs and your chest wall (pleural space), you may have few signs or symptoms. However, even a slightly collapsed lung is likely to cause some chest pain and some shortness of breath that slowly improves over a few hours to a day or so, even if there is no reduction in the size of the collapse.

NURSING MANAGEMENT

1.Promote/maintain lung re-expansion for adequate oxygenation/ventilation. 2. Minimize/prevent complications. 3. Reduce discomfort/pain. 4. Provide information about disease process, treatment regimen, and prognosis. Impaired gas exchange related to diagnosis

NURSING MANAGEMENT (Nursing Diagnoses) Possible complications from a spontaneous or traumatic pneumothorax include: COMPLICATIONS Recurrence. Persistent air leak. Complications of a tension pneumothorax are more serious and include: Low blood oxygen levels (hypoxemia).

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Cardiac arrest Respiratory failure Shock

Chronic Obstructive Pulmonary Disease MEDICAL DIAGNOSIS Chronic obstructive pulmonary disease (COPD) refers to chronic bronchitis and emphysema, a pair of two commonly co-existing diseases of the lungs in which the airways become narrowed. This leads to a limitation of the flow of air to and from the lungs causing shortness of breath. In contrast to asthma, the limitation of airflow is poorly reversible and usually gets progressively worse over time. The inflammatory process is a driving aspect in the pathophysiology of COPD. Chronic inflammation of the cells lining the bronchial tree plays a major role. Smoking and, seldom, other inhaled irritants, perpetuates an ongoing inflammatory response that results in airway narrowing and hyperactivity. Airways become edematous, excessive mucus production occurs and cilia function weakly. Patients face increasing difficulty clearing secretions with disease progression. Accordingly, they develop a chronic productive cough, wheezing and dyspnea. The basic pathophysiologic process in COPD consists of increased resistance to airflow, loss of elastic recoil and decreased expiratory flow rate. The alveolar walls frequently break because of the increased resistance of air flows. The hyper inflated lungs flatten the curvature of the diaphragm and enlarge the rib cage. The altered configuration of the chest cavity places the respiratory muscles, including the diaphragm, at a mechanical disadvantage and impairs their force-generating capacity. Consequently, the metabolic work of breathing increases and the sensation of dyspnea heightens.

DEFINITION

PATHOPHYSIOLOGY

ETIOLOGY & EDPIDEMOLOGY

Cigarette smoking is by far the most serious and common risk factors for COPD, but there are other risk factors that make it more likely that a person will develop the disease. These risk factors fall into two categories: host factors and environmental exposures. Host factors include; a history of frequent or severe childhood respiratory infection, a personal or family history of asthma or COPD (so-called familial clustering), a personal history of airway hyperactivity (a defining feature of asthma) , a genetic predisposition to emphysema, most notably a hereditary deficiency of the blood protein alpha-1 antitrypsin, which, when combined with cigarette smoke, can result in precocious COPD, not infrequently in the third or fourth decade of life. Environmental factors include; exposure to side stream (passive) tobacco smoke, exposure to tobacco smoke in utero, exposure to chemicals and dust on the job, including vapors, irritants, and fumes.

CLINICAL MANIFESTATION

DIAGNOSTIC TESTS

Symptoms of COPD include; increase or decrease in sputum production, sputum color change to yellow, green, or reddish, increase in shortness of breath, coughing, and wheezing, General feeling of ill health, Ankle swelling ,Forgetfulness, confusion, speech slurring ,Trouble sleeping, Unexplained increase or decrease in weight Increased, persistent fatigue, Lack of sexual drive ,Increased morning headaches, dizzy spells, restlessness The diagnosis of COPD should be considered in anyone who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease such as regular tobacco smoking. The

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diagnosis of COPD is confirmed by spirometry, a test that measures breathing. Spirometry measures the forced expiratory volume in one second (FEV 1). Spirometry also measures the forced vital capacity (FVC) which is the greatest volume of air that can be breathed out in a whole large breath. An x-ray of the chest may show an over-expanded lung (hyperinflation) and can be useful to help exclude other lung diseases. Complete pulmonary function tests with measurements of lung volumes and gas transfer may also show hyperinflation and can discriminate between COPD with emphysema and COPD without emphysema. A high-resolution computed tomography scan of the chest may show the distribution of emphysema throughout the lungs and can also be useful to exclude other lung diseases. A blood sample taken from an artery can be tested for blood gas levels which may show low oxygen levels (hypoxemia) and/or high carbon dioxide levels (respiratory acidosis). A blood sample taken from a vein may show a high blood count (reactive polythycaemia), a reaction to long-term hypoxemia.

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

Three types of medications generally are prescribed for patients with COPD. Bronchodilators help patients breathe more easily by relaxing smooth muscle around the bronchial tubes. Common inhaled long-acting beta agonists include: Serevent (salmeterol) , Foradil (formoterol), Common inhaled short-acting beta agonists include: Proventil, Ventolin, HFA (albuterol). Anticholinergics: These bronchodilators relax and open airways. They are prescribed to help patients take fuller breaths and are generally administered through inhalers. Theophylline: This third-line, long-acting drug relaxes and opens airways and is administered orally or intravenously. Anti-inflammatory drugs, also called steroids, help reduce and prevent swelling inside the lungs' airways and decrease mucus production. They may be swallowed or administered through an inhaler.

NURSING MANAGEMENT

Regular monitoring of clients respiratory rate and pattern, pulse oximetry, ABG results, and manifestations of hypoxia or hypercapnia. Administer low flow oxygen therpy (1-3 L/min or 24% to 31 % Fio2) as needed via nasal prongs or a high flow venture mask. Assist the client into high fowler position. Administer Bronchodilators if ordered. Monitor lung sounds every 4-8 hours and before and after episodes. Teach the client to maintain adequate hydration by drinking at least 8-10 glasses of water per day.. Teach and supervise effective coughing technique. Advise client to avoid conditions that increase O2 demands, e.g. Smoking. Instruct client in energy conserving techniques, provide a high caloric, protein rich diet to promote health and healing and to increase energy and conserve energy by giving frequent small meals ( e.g. six meals a day ). Avoid gas producing foods such as beans and cabbage Impaired gas exchange related to decreased ventilation and mucus plugs Ineffective airway clearance related to excessive secretions and ineffective coughing Activity intolerance related to inadequate oxygenation and dyspnea evidenced by decreased arterial blood gas and verbalization of fatigue. Inbalance nutrition less than body requirement related to reduced appetite , decrease energy level and dyspnea/ Heart failure, pulmonary hypertension, cor pulmonale, polycthemia, secondary polycythemia, death, breathlessness, cough, abnormal sputum

NURSING MANAGEMENT (Nursing Diagnoses)

COMPLICATIONS

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Pneumonia MEDICAL DIAGNOSIS An inflammation of the lungs caused by an infection. DEFINITION PATHOPHYSIOLOGY The invading organism causes symptoms, in part, by provoking an overly exuberant immune response in the lungs. The small blood vessels in the lungs (capillaries) become leaky, and protein-rich fluid seeps into the alveoli. This results in a less functional area for oxygen-carbon dioxide exchange. The patient becomes relatively oxygen deprived, while retaining potentially damaging carbon dioxide. The patient breathes faster and faster, in an effort to bring in more oxygen and blow off more carbon dioxide. Mucus production is increased, and the leaky capillaries may tinge the mucus with blood. Mucus plugs actually further decrease the efficiency of gas exchange in the lung. The alveoli fill further with fluid and debris from the large number of white blood cells being produced to fight the infection. Consolidation, a feature of bacterial pneumonias, occurs when the alveoli, which are normally hollow air spaces within the lung, instead become solid, due to quantities of fluid and debris. Viral pneumonias, and mycoplasma pneumonias, do not result in consolidation. These types of pneumonia primarily infect the walls of the alveoli and the parenchyma of the lung. Pneumonia is a very common, serious illness and affects about 1 out of 100 people each year. It is caused by many different organisms and can range in seriousness from mild to life-threatening illness. There are different categories of pneumonia. here are different categories of pneumonia. Two of these types are hospital-acquired and communityacquired. Common types of community-acquired pneumonia are pneumococcal pneumonia and Mycoplasma pneumonia. In some people, particularly the elderly and those who are debilitated, pneumonia may follow influenza. Hospital-acquired pneumonia tends to be more serious because defense mechanisms against infection are often impaired. Some of the specific pneumonia-related disorders include: aspiration pneumonia, pneumonia in immunocompromised host and viral pneumonia Cough (with mucus-like, greenish, or pus-like sputum chills with shaking ), fever, easy fatigue, chest pain (sharp or stabbing increased by deep breathing or increased by coughing), headache, loss of appetite, nausea and vomiting, general discomfort, uneasiness, or ill feeling (malaise), joint stiffness (rare), muscular stiffness (rare), rales Additional symptoms that may be associated with this disease: shortness of breath, clammy skin, nasal flaring, coughing up blood, tacypnea, apnea, anxiety, stress, and tension, abdominal pain . Crackles are heard when listening to the chest with a stethoscope (auscultation). Tests include: chest X-ray, sputum gram stain, CBC, arterial blood gases. This disease may also alter the results of the following tests: thoracic CT, routine sputum culture, pulmonary ventilation/perfusion scan, pleural fluid culture, lung needle biopsy . The goal of treatment is to cure the infection with antibiotics. If the pneumonia is caused by a virus, antibiotics will not be effective. Supportive therapy includes oxygen and respiratory treatments to remove secretions

ETIOLOGY & EDPIDEMOLOGY

CLINICAL MANIFESTATION

DIAGNOSTIC TESTS

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

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NURSING MANAGEMENT

Pt will need to have breath sounds monitored q 4 to determine if pneumonia is progressing. O2 sats should be done regularly ( at least q4during acute phase) to make sure that patient is getting adequate perfusion. Make sure to give all scheduled antibiotics on schedule so that therapeutic ranges are maintained. Any s/s of infection must be monitored and reported to MD. Impaired gas exchange related to effects of alveolar-capillary membrane changes.

NURSING MANAGEMENT (Nursing Diagnoses)

Ineffective airway clearance related to effects of infection, excessive tracheobronchial secretions, fatigue and decreased energy, chest discomfort and muscle weakness. Pneumonia complications may include:

COMPLICATIONS

Bacteria in your bloodstream. Pneumonia can be life-threatening when inflammation from the disease fills the air sacs in your lungs and interferes with your ability to breathe. In some cases the infection may invade your bloodstream (bacteremia). It can then spread quickly to other organs. Fluid accumulation and infection around your lungs. Sometimes fluid accumulates between the thin, transparent membrane (pleura) covering your lungs and the membrane that lines the inner surface of your chest wall a condition known as pleural effusion. Normally, the pleurae are smooth, allowing your lungs to slide easily along your chest wall when you breathe in and out. But when the pleurae around your lungs become inflamed (pleurisy) often as a result of pneumonia fluid can accumulate and may become infected (empyema). Lung abscess. A cavity containing pus (abscess) that forms within the area affected by pneumonia is another potential complication. Acute respiratory distress syndrome (ARDS). The pneumonia involves most areas of both lungs, making breathing difficult and depriving your body of oxygen. Underlying lung disease of any kind, but especially COPD, makes you more susceptible to ARDS.

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Pulmonary edema MEDICAL DIAGNOSIS Pulmonary edema is a condition caused by excess fluid in the lungs. This fluid collects in the numerous air sacs in the lungs, making it difficult to breathe.

DEFINITION

PATHOPHYSIOLOGY

ETIOLOGY & EDPIDEMOLOGY

By definition, pulmonary edema is simply excess fluid in the lung. The distribution of the fluid dictates the clinical significance of the edema. As far as a mechanism of edema formation, microvascular hydrostatic pressure remains the predominant Starling force. The lung interstitium is a major factor in determining both the amount of edema formed as well as the distribution. Increased permeability edema, with a more peripheral distribution of fluid as seen in the adult respiratory distress syndrome, may well be the result of interstitial matrix and basement membrane changes rather than simply more holes in the endothelial membrane. The significance of the edema, again, depends on its distribution, with perihilar interstitial fluid being much less significant than alveolar flooding. The relevance of the measurement of lung water, therefore, is dependent as much on where the water resides as on the absolute amount. Pulmonary edema is usually caused by heart failure. As the heart fails, pressure in the veins going through the lungs starts to rise. As the heart fails, pressure in the veins going through the lungs starts to rise. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs. This fluid interrupts normal oxygen movement through the lungs, resulting in shortness of breath. Pulmonary edema may be caused by damage directly to the lung, such as that caused by poisonous gas or severe infection, as a side effect of medications, or the result of major trauma. Lung damage with a buildup of body fluid is also seen in kidney failure. Exercising at very high altitudes can also cause pulmonary edema Pulmonary edema may also be a complication of a heart attack, leaking or narrowed heart valves (mitral or aortic valves), or any disease of the heart that results in weakening or stiffening of the heart muscle (cardiomyopathy).

CLINICAL MANIFESTATION

Breathing difficulty ,shortness of breath, shallow breathing, rapid breathing, shortness of breath worse on lying down, wheezing, cyanosis, anxiety, restlessness, cough, dry cough, pink-stained sputum cough, bubbling sounds when breathing, weak pulse, pounding pulse, lung crackling sounds (rales) in stethoscope, swollen hands, swollen ankles, hypotension, enlarged veins, visible veins The health care provider will perform a physical exam and use a stethoscope to listen to the lungs and heart. The following may be detected:

DIAGNOSTIC TESTS

Crackles in the lungs, called rales Abnormal heart sounds Increased heart rate (tachycardia) Pale or blue skin color (pallor or cyanosis)

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Rapid breathing (tachypnea)

Possible tests include:

Complete blood count (CBC) to check for anemia and reduced red cell count Other blood tests to measure blood chemistries and kidney function Blood oxygen levels (oximetry or arterial blood gases) -- low in patients with pulmonary edema Chest x-ray may reveal fluid in or around the lung space or an enlarged heart Electrocardiogram (ECG) to detect abnormal heart rhythm or evidence of a heart attack Ultrasound of the heart (echocardiogram) to see if there is a weak heart muscle, leaky or narrow heart valves, or fluid surrounding the heart

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

Medical treatment for Pulmonary Edema is considered an emergency If possible, find and treat the underlying cause of Pulmonary Edema O2 via nasal cannula or mask Intubation and mechanical ventilation may be necessary If intubated, pulmonary toilet, respiratory medication treatments Furosemide (Lasix) increases urine output and works quickly to remove excess fluid from the body Morphine Sulfate decreases anxiety and work load of breathing. Dobutamine dilates the peripheral vessels to decrease work load of left ventricle Aspirin helps decrease blood viscosity for easy oxygen delivery. If required, titrate inotropic and Vasoactive medications to maintain contractility, preload and afterload parameters

NURSING MANAGEMENT

Monitor for symptoms of heart failure/decreased cardiac output Monitor vital signs Observe for confusion, restlessness, agitation (may be sign of decrease cardiac output) Monitor for chest pain, discomfort (note severity, radiation and duration) If chest pain present (have patient lie down, give O2, medicate for pain and notify physician) Cardiac monitor for dysrhythmias If patient has a Pulmonary Artery Catheter, monitor for increased PAWP, SVR and a decreased cardiac output O2 per physicians order If patient intubated, pulmonary toilet, suction, med-neb treatments Monitor intake and output (kidney perfusion may be compromised if cardiac output low) Note results of EKG, chest X-ray and other diagnostic tests Monitor labs work such as ABG, CBC, electrolytes (blood work should be routine) Place patient in semi-fowlers or upright position Activity/Rest balance (gradually increase activity) If eating, diet should be sodium restricted, low cholesterol (limit caffeine) Serve smaller more frequent meals Monitor bowel and bladder function (stool softeners prn) Minimize environmental stimuli (decrease anxiety for patient and family) Daily weight Refer appropriately (heart failure programs, cardiac rehab, support groups)

NURSING MANAGEMENT (Nursing Diagnoses)

Decreased urine output related to inadequate fluid intake Alteration in Comfort: Pain Altered Breathing Pattern Ineffective Airway Impaired Gas Exchange

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COMPLICATIONS

Altered Tissue Perfusion: (peripheral, cardiac) Anxiety Ineffective Coping Knowledge Deficit Impaired Nutrition Potential for Skin Breakdown

If pulmonary edema continues, it can raise pressure in the pulmonary artery and eventually the right ventricle begins to fail. The right ventricle has a much thinner wall of muscle than does the left side. The increased pressure backs up into the right atrium and then into various parts of your body, where it can cause:

Leg swelling (edema) Abdominal swelling (ascites) Buildup of fluid in the membranes that surround your lungs (pleural effusion) Congestion and swelling of the liver When not treated, acute pulmonary edema can be fatal. In some instances it may be fatal even if you receive treatment.

Pneumoconiosis (occupational lung disease) MEDICAL DIAGNOSIS Any chronic lung disease where deposition of large amounts of dust or other particulate matter in the lungs, causing a tissue reaction, usually in workers in certain occupations and in residents of areas with excessive particulates in the air; there are many types, including anthracosis, asbestosis, bituminosis, and silicosis. Alveolar macrophages engulf the dust, release cytokines that stimulate inflammation, and collect in lung interstitium around bronchioles and alveoli (coal macules). Coal nodules develop as collagen accumulates, and focal emphysema develops as bronchiole walls weaken and dilate. Fibrosis can occur but is usually limited to areas adjacent to coal macules. Distortion of lung architecture, airflow obstruction, and functional impairment are usually mild but can be highly destructive in some patients.

DEFINITION PATHOPHYSIOLOGY

Two forms of CWP are described:

Simple, with individual coal macules Complicated, with coalescence of macules and PMF

Patients with simple CWP develop PMF at a rate of about 1 to 2%. In PMF, nodules coalesce to form black, rubbery parenchymal masses usually in the upper posterior fields. The masses may encroach on and destroy vascular supply and airways or may cavitate. PMF can develop and progress even after exposure to coal dust

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has ceased. Despite the similarity of coal-induced PMF and conglomerate silicosis, the development of PMF in coal workers is unrelated to the silica content of the coal.

Complications: An association between CWP and features of rheumatoid arthritis (RA) is well-described. It is unclear whether CWP predisposes miners to developing RA, whether RA takes on a unique form in patients with CWP, or whether RA alters the response of miners to coal dust. Multiple rounded nodules in the lung appearing over a relatively short time (Caplan's syndrome) represent an immunopathologic response related to rheumatoid diathesis. Histologically, they resemble rheumatoid nodules but have a peripheral region of more acute inflammation. Patients with CWP are at a slightly increased risk of developing active TB and non-TB mycobacterial infections. Weak associations have been reported between CWP and progressive systemic sclerosis and stomach cancer.

ETIOLOGY & EDPIDEMOLOGY

Risk factors for pneumoconiosis include:

Asthma Chronic obstructive pulmonary disease Smoking

CLINICAL MANIFESTATION

Initial symptoms of pneumoconiosis include a cough, wheezing, and difficulty breathing during exertion. Symptoms of severe pneumoconiosis include shortness of breath at rest, leg swelling, and chest pain. Tests that may be used to evaluate pneumoconiosis include:

DIAGNOSTIC TESTS

Chest x-ray:

o o

Normal chest x-ray Signs of chronic lung disease or fibrosis may be present

Arterial blood gas Pulse oximetry Pulmonary function tests:

o o

Before and after treatment with bronchodilator medication

Bronchoscopy Using a flexible fiberoptic scope to look at the air passageways

Lung biopsy Thoracoscopy

Using a fiberoptic scope to examine the outside of the lung and the inside of the chest wall

MEDICAL/SURGICAL

There is no cure for pneumoconiosis.

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MANAGEMENT INCLUDING PHARMACOLOGICAL

Treatment for pneumoconiosis may include:

Antibiotics for bronchitis Bronchodilator medications for wheezing:

o o o o

Albuterol Proventil

Inhaled corticosteroid medications Azmacort Beclovent

Pneumoconiosis clinical trials

NURSING MANAGEMENT

Educate client about safety if they work in hardzous environments Provide for rest and reduce energy expenditure (r/t) impaired breathing and ventilation abilities

Ineffective airway clearance related to disease symptom NURSING MANAGEMENT (Nursing Diagnoses) Complications may include: COMPLICATIONS

Cor pulmonale (failure of the right side of the heart) Pulmonary tuberculosis

Pulmonary embolism/pulmonary infarction MEDICAL DIAGNOSIS A Pulmonary Embolism is a sudden lodgment of a blood clot in a pulmonary artery that causes an obstruction of blood supply to lung tissue. Once a thrombus separates from its site of origin, it travels through the circulation to the inferior vena cava. From the inferior vena cave, it then passes through the right ventricle which pumps the thrombus into the pulmonary arteries where it finally lodges. Once a Pulmonary embolism has lodged in an artery, a disruption of both pulmonary hemodynamics and gas exchange occurs A pulmonary embolism is most often caused by blood clots from veins in the legs (Deep Vein Thrombosis DVT) or in the pelvis or hip area. They can also be caused by air bubbles, fat droplets, amniotic fluid or tumor cells that clump and obstruct pulmonary vessels. Although anyone can develop blood clots and subsequent pulmonary embolism together known as venous thromboembolism (VTE) the following factors increase your risk:

DEFINITION PATHOPHYSIOLOGY

ETIOLOGY & EDPIDEMOLOGY

Inactivity. You're not likely to develop a blood clot after an evening on the couch with a good book, but prolonged sitting in a cramped position during lengthy plane or car trips ups your risk. Inactivity slows the current of blood flow, which contributes to the formation of clots.

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Prolonged bed rest. Being confined to bed for an extended period after surgery, a heart attack, leg fracture or any serious illness makes you far more vulnerable to blood clots. Although pulmonary embolism is a leading cause of hospital deaths, it's also a serious problem for nursing home residents, who are likely to have a number of risk factors for DVT, as well as for people immobilized at home. Certain surgical procedures. Especially likely to cause blood clots are hip, pelvic and knee surgeries as well as some obstetric or gynecologic procedures. Some medical conditions. Certain cancers, especially pancreatic, ovarian and lung cancers can increase levels of substances that help blood clot, and chemotherapy further increases the risk. Women with a history of breast cancer who are taking tamoxifen or raloxifene also are at risk. High blood pressure and cardiovascular disease make clot formation more likely, as does having an inflammatory bowel disease such as ulcerative colitis or Crohn's disease. Being overweight. Researchers aren't certain why weighing more than normal increases the risk of blood clots, but one theory links the formation of clots to leptin, a hormone produced by fat cells in the body. People who are overweight have more leptin-producing cells than slender people do, and so may be more prone to develop clots. Another theory is that the fat in obese women contains estrogen, which contributes to clot formation. Pacemakers or venous catheters. Having a pacemaker or catheter a soft, flexible tube in a central vein makes the formation of clots more likely in that vein. Pregnancy and childbirth. Pulmonary embolism is the leading cause of death in pregnancy. Some women who have pregnancy-related venous thromboembolism also have an inherited clotting disorder. Supplemental estrogen. The estrogen in birth control and in hormone replacement therapy can increase clotting factors in your blood, especially if you smoke or are overweight. Family history. Having a personal or family history of venous thromboembolism increases the risk of blood clots. Smoking. For reasons that aren't well understood, tobacco use predisposes some people to blood clot formation, especially when combined with other risk factors

CLINICAL MANIFESTATION

Cough (sudden onset) Bloody sputum Shortness of breath (sudden onset) Splinting of ribs with breathing Chest pain (under the breast bone described as sharp, stabbing, burning) Tachycardia Tachyapnea Wheezing Cool clammy skin (may be sweaty) Bluish skin discoloration Nasal flaring Pelvis/Leg pain (DVT) Swelling of leg (DVT) Hypotension Weak pulse Anxiety/Nervousness Lightheadedness/Dizziness

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DIAGNOSTIC TESTS

Physical Exam (Pulmonary Hemodynamics if Pulmonary Artery Catheter in place) Chest X-ray Pulmonary ventilation/perfusion scan Pulmonary Angiogram Doppler Ultrasound (to rule out DVT) Venogram (to rule out DVT) Elevated Troponin Level (which indicates right ventricular micro-infarction) Elevated pro-B-type peptide Level (which indicates right ventricular overload)

MEDICAL/SURGICAL MANAGEMENT INCLUDING PHARMACOLOGICAL

Anticoagulation - When acute Pulmonary Embolism is suspected, anticoagulation should be started immediately (Heparin 80 unit/kg bolus followed by 18 units/kg/hr). Target of activated partial thromboplastin should be between 60-8- seconds (Patient should eventually be weaned of IV Heparin and oral Warfarin (Coumadin) should be started). Inferior Vena Caval Filters Filters can be inserted percutaneously to prevent further Pulmonary Embolism, but they do not stop an already activated thrombolic process. They are indicated for recurrent Pulmonary Embolism and for cases when anticoagulation is contraindicated. Because these filters are retrievable, they can be used on a temporary basis. Thrombolysis Recombinant Tissue Plasminogen (rt-PA) is a treatment option for lysing Pulmonary Embolism. If ordered it should be given as a 100mg IV infusion over 2 hours. (This treatment is somewhat controversial due to the fact that most patients with Pulmonary Embolism also have increased systemic arterial pressure and/or moderate to severe right ventricular dysfunction). Other medications include Streptokinase and Urokinase. Embolectomy When thrombolysis is contraindicated, a catheter (angio procedure that delivers high velocity jet saline that blasts the clot) can be attempted or surgical embolectomy can be considered Avoid leaving IV catheters in place for long periods of time If SOB, HOB should be in semi-fowlers position to assist with air distribution O2 as prescribed (monitor for signs of hypoxia) Pulse Oximetry Administer Opioids for sever pain Administer anticoagulation as prescribed and monitor for untoward bleeding (gums, bruising) Encourage verbalization of fear and anxiety Respiratory toilet to include: Nebulizer treatments Incentive spirometry Postural drainage (vibration and percussion) Alteration in Comfort: Pain Altered Breathing Pattern Ineffective Airway Impaired Gas Exchange Altered Tissue Perfusion: (peripheral, cardiac) Anxiety Ineffective Coping Knowledge Deficit Impaired Nutrition Potential for Skin Breakdown

NURSING MANAGEMENT

NURSING MANAGEMENT (Nursing Diagnoses)

Pulmonary embolism can lead to several serious complications, including: COMPLICATIONS

High blood pressure in your lungs (pulmonary hypertension). Heart damage

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