NCLEX: Respiratory disorders

Respiratory disorders: Common respiratory disorders

Focus topic: Respiratory disorders

Below are several common respiratory disorders, along with their causes, pathophysiology, signs and symptoms, diagnostic test findings, treatments, and nursing interventions.

Respiratory disorders: Acute respiratory distress syndrome

Focus topic: Respiratory disorders

A form of pulmonary edema that leads to ARF, acute respiratory distress syndrome (ARDS) results from increased permeability of the alveolocapillary membrane. Although severe ARDS may be fatal, recovering patients may have little or no permanent lung damage.

What causes it
ARDS may result from:
• aspiration of gastric contents
• sepsis (primarily gram-negative)
• trauma (such as lung contusion, head injury, and long-bone fracture with fat emboli)
• oxygen toxicity
• viral, bacterial, or fungal pneumonia
• microemboli (fat or air emboli or disseminated intravascular coagulation)
• drug overdose (such as barbiturates and opioids)
• blood transfusion
• smoke or chemical inhalation (such as nitrous oxide, chlorine, ammonia, and organophosphate)
• hydrocarbon or paraquat ingestion
• pancreatitis, uremia, or miliary TB (rare)
• near drowning.

Pathophysiology
In ARDS, fluid accumulates in the lung interstitium, alveolar spaces, and small airways, causing the lung to stiffen. This impairs ventilation and reduces oxygenation of pulmonary capillary blood.

What to look for
Assess your patient for the following signs and symptoms:
• rapid, shallow breathing; dyspnea; and hypoxemia
• tachycardia
• intercostal and suprasternal retractions, crackles, and rhonchi
• restlessness, apprehension, mental sluggishness, and motor dysfunction.

What tests tell you
• ABG values on room air show decreased PaO2 (less than 60 mm Hg) and PaCO2 (less than 35 mm Hg). As ARDS becomes more severe, ABG values show respiratory acidosis, with PaCO2 values elevated above 45 mm Hg. The patient’s PaO2 decreases despite oxygen therapy.
• Noninvasive cardiac output monitoring can help determine the patient’s fluid volume status and heart function.
• Pulmonary artery catheterization helps identify the cause of pulmonary edema by evaluating pulmonary artery wedge pressure and allows collection of pulmonary artery blood, which shows decreased oxygen saturation, a sign of tissue hypoxia. It also measures pulmonary artery pressure as well as cardiac output by thermo dilution t echniques.
• Serial chest X-rays initially show bilateral infiltrates. In later stages, the X-rays have a ground-glass appearance and, as hypoxemia becomes irreversible, shows “whiteouts” in both lung fields.
• Other tests may be done to detect infections, drug ingestion, or pancreatitis.

How it’s treated
Treatment aims to correct the underlying cause of ARDS to prevent its progression toward potentially fatal complications. Supportive medical care includes humidified oxygen through a tight-fitting mask, allowing the use of CPAP. When hypoxemia doesn’t respond to these measures, patients require ventilatory support with intubation, volume ventilation, and PEEP. Other supportive measures include fluid restriction, diuretics, and correction of electrolyte and acid-base abnormalities.

 

Just relax…

Patients who receive mechanical ventilation commonly require sedatives and narcotics or neuromuscular blocking agents, such as vecuronium and pancuronium, to minimize anxiety. Decreasing anxiety enhances ventilation by reducing oxygen consumption and carbon dioxide production. If given early, a short course of high-dose steroids may help patients with ARDS that results from fat emboli or chemical injury to the lungs. Fluids and vasopressors maintain the patient’s blood pressure. Nonviral infections require antimicrobial drugs.

Respiratory disorders

What to do
• Carefully monitor your patient and provide supportive care to prepare him for transfer to an intensive care unit (ICU).
• Frequently assess his respiratory status. Watch for retractions on inspiration. Note the rate, rhythm, and depth of respirations, and watch for dyspnea and the use of accessory muscles of respiration. On auscultation, listen for adventitious or diminished breath sounds. Check for pink, frothy sputum, which may indicate pulmonary edema.
• Observe and document the hypoxemic patient’s neurologic status. Assess his LOC and observe for mental sluggishness.
• Maintain a patent airway by suctioning the patient as needed.
• Closely monitor heart rate and rhythm and blood pressure.
• Reposition the patient often and observe for hypotension, increased secretions, or elevated body temperature — all signs of deterioration.
• Evaluate the patient. After successful treatment, he should have normal ABG values; a normal respiratory rate, depth, and pattern; and clear breath sounds.

Respiratory disorders

Respiratory disorders: Acute respiratory failure

Focus topic: Respiratory disorders

When the lungs no longer meet the body’s metabolic needs, ARF results. In patients with essentially normal lung tissue, ARF usually means PaCO2 above 50 mm Hg and PaO2 below 50 mm Hg. These limits, however, don’t apply to patients with COPD, who commonly have a consistently high PaCO2 and low PaO2. In patients with COPD, only acute deterioration in ABG values, with corresponding clinical deterioration, indicates ARF.

What causes it
ARF may develop from any condition that increases the work of breathing and decreases the respiratory drive. Respiratory tract infections, such as bronchitis and pneumonia, are the most common precipitating factors but bronchospasm or accumulated secretions due to cough suppression can also lead to ARF. Other causes of ARF include:
• CNS depression — head trauma or injudicious use of sedatives, narcotics, tranquilizers, or oxygen
• cardiovascular disorders — MI, heart failure, or pulmonary emboli
• airway irritants — smoke or fumes

• endocrine and metabolic disorders — myxedema or metabolic alkalosis
• thoracic abnormalities — chest trauma, pneumothorax, or thoracic or abdominal surgery.

Pathophysiology
Respiratory failure results from impaired gas exchange, when the lungs don’t oxygenate the blood adequately and fail to prevent carbon dioxide retention. Any condition associated with hypoventilation (a reduction in the volume of air moving into and out of the lung), V mismatch (too little ventilation with normal blood flow or too little blood flow with normal ventilation), or intrapulmonary shunting (right-to-left shunting in which blood passes from the heart’s right side to its left without being oxygenated) can cause ARF if left untreated.

What to look for
Patients with ARF experience hypoxemia and acidemia affecting all body organs, especially the central nervous, respiratory, and cardiovascular systems. Although specific symptoms vary with the underlying cause, you should always assess for:
• altered respirations (increased, decreased, or normal rate; shallow, deep, or alternating shallow and deep respirations; possible cyanosis; crackles, rhonchi, wheezes, or diminished breath sounds on chest auscultation)
• altered mentation (restlessness, confusion, loss of concentration, irritability, tremulousness, diminished tendon reflexes, or papilledema)
• cardiac arrhythmias (from myocardial hypoxia)
• tachycardia (occurs early in response to low PaO2)
• pulmonary hypertension (increased pressures on the right side of the heart, elevated jugular veins, enlarged liver, and peripheral edema).

What tests tell you
• Progressive deterioration in ABG levels and pH, when compared with the patient’s baseline values, strongly suggests ARF. (In patients with essentially normal lung tissue, a pH value below 7.35 usually indicates ARF. However, COPD patients display an even greater deviation in pH values, along with deviations in PaCO2 and PaO2.)
• Arterial blood gas levels show a pH value of 7.35 or less, PaO2 of 50 mm Hg or less, and PCO2 of 50 mm Hg or greater.
• Hematocrit and Hb levels are abnormally low, possibly from blood loss, indicating decreased oxygen-carrying capacity.

• The white blood cell (WBC) count is elevated if ARF results from bacterial infection (Gram stain and sputum culture identify pathogens).

Get the picture

Focus topic: Respiratory disorders

  • A chest X-ray shows pulmonary abnormalities, such as emphysema, atelectasis, lesions, pneumothorax, infiltrates, and effusions.
  • An electrocardiogram (ECG) shows arrhythmias, which commonly suggest cor pulmonale and myocardial hypoxia.

How it’s treated
ARF is an emergency requiring immediate action to correct the underlying cause and restore adequate pulmonary gas exchange. If significant respiratory acidosis persists, the patient may require mechanical ventilation through an ET or a tracheostomy tube. If he doesn’t respond to conventional mechanical ventilation, the practitioner may try HFV; prone positioning may also help. Treatment routinely includes antibiotics for infection, bronchodilators and possibly steroids.

What to do
• Closely monitor airway patency and oxygen supply.
• To reverse hypoxemia, administer oxygen at appropriate concentrations to maintain PaO2 at a minimum of 50 mm Hg. Patients with COPD usually require only small amounts of supplemental oxygen. Watch for a positive response, such as improvement in ABG results and the patient’s breathing and color.
• Maintain a patent airway. If the patient is intubated and lethargic, turn him every 1 to 2 hours. Use postural drainage and chest physiotherapy to help clear secretions.
• In an intubated patient, suction the airways as required, after hyperoxygenation. Observe for changes in quantity, consistency, and color of sputum. To prevent aspiration and reduce the risk of ventilator-associated pneumonia, always suction the oropharynx and the area above the cuff of the ET tube before deflating the cuff. Provide humidity to liquefy secretions.
• Observe the patient closely for respiratory arrest. Auscultate for breath sounds. Monitor ABG levels and report any changes immediately.

Fluid situation

Focus topic: Respiratory disorders

  • Monitor serum electrolyte levels and correct imbalances; monitor fluid balance by recording fluid intake and output and daily weight.
  • Check the cardiac monitor for arrhythmias.
  • If the patient requires mechanical ventilation and is unstable, he’ll probably be transferred to an ICU. Arrange for his safe transfer.
  • Evaluate the patient. Make sure that ABG values are returning to normal, with a PaO2 greater than 50 mm Hg, and that the patient can make a normal respiratory effort.

Respiratory disorders

Respiratory disorders: Atelectasis

Focus topic: Respiratory disorders

Atelectasis (collapsed or airless condition of all or part of the lung) may be chronic or acute and commonly occurs to some degree in patients undergoing abdominal or thoracic surgery. The prognosis depends on prompt removal of airway obstruction, relief of hypoxia, and re-expansion of the collapsed lobules or lung.

What causes it
Atelectasis may result from:
• bronchial occlusion by mucus plugs (a common problem in heavy smokers or people with COPD, bronchiectasis, or cystic fibrosis)
• occlusion by foreign bodies
• bronchogenic carcinoma
• inflammatory lung disease
• oxygen toxicity
• pulmonary edema
• any condition that inhibits full lung expansion or makes deep breathing painful, such as abdominal surgical incisions, rib fractures, tight dressings, obesity, and neuromuscular disorders
• prolonged immobility
• mechanical ventilation using constant small tidal volumes without intermittent deep breaths
• CNS depression (as in drug overdose), which eliminates periodic sighing.

Pathophysiology
In atelectasis, incomplete expansion of lobules (clusters of alveoli) or lung segments leads to partial or complete lung collapse. Because parts of the lung are unavailable for gas exchange, unoxygenated blood passes through these areas unchanged, resulting in hypoxemia.

What to look for
Your assessment findings will vary with the cause and degree of hypoxia and may include:
• dyspnea, possibly mild and subsiding without treatment if atelectasis involves only a small area of the lung; severe if massive collapse has occurred
• cyanosis
• anxiety, diaphoresis
• dull sound on percussion if a large portion of the lung has collapsed
• hypoxemia, tachycardia
• substernal or intercostal retraction
• compensatory hyperinflation of unaffected areas of the lung
• mediastinal shift to the affected side
• decreased or absent breath sounds.

What tests tell you
• A chest X-ray shows characteristic horizontal lines in the lower lung zones. Dense shadows accompany segmental or lobar collapse and are commonly associated with hyperinflation of neighboring lung zones during widespread atelectasis. However, extensive areas of “micro-atelectasis” may exist without showing abnormalities on the patient’s chest X-ray.
• When the cause of atelectasis is unknown, bronchoscopy may rule out an obstructing neoplasm or a foreign body.

How it’s treated
Atelectasis is treated with incentive spirometry, chest percussion, postural drainage, and frequent coughing and deep-breathing exercises. If these measures fail, bronchoscopy may help remove secretions. Humidity and bronchodilators can improve mucociliary clearance and dilate airways and are sometimes used with a nebulizer. Atelectasis secondary to an obstructing neoplasm may require surgery or radiation therapy.

What to do
• Take appropriate steps to keep the patient’s airways clear and
relieve hypoxia.
• To prevent atelectasis, encourage the patient to cough, turn, and breathe deeply every 1 to 2 hours as ordered. Teach the patient to splint his incision when coughing. Gently reposition a postoperative patient often and help him walk as soon as possible. Administer adequate analgesics to control pain.
• During mechanical ventilation, make sure tidal volume is maintained at 10 to 15 ml/kg of the patient’s body weight to ensure adequate lung expansion. Use the sigh mechanism on the ventilator, if appropriate, to intermittently increase tidal volume at the rate of three to four sighs per hour.
• Humidify inspired air and encourage adequate fluid intake to mobilize secretions. Loosen and clear secretions with postural drainage and chest percussion.
• Assess breath sounds and ventilatory status frequently and report any changes.
• Evaluate the patient. Secretions should be clear and the patient should show no signs of hypoxia.

Respiratory disorders

Respiratory disorders: Bronchiectasis

Focus topic: Respiratory disorders

An irreversible condition marked by chronic abnormal dilation of bronchi and destruction of bronchial walls, bronchiectasis can occur throughout the tracheobronchial tree or can be confined to one segment or lobe. However, it’s usually bilateral, involving the basilar segments of the lower lobes. It affects people of both sexes and all ages.

What causes it
Bronchiectasis may be caused by such conditions as:
• cystic fibrosis
• immunologic disorders
• recurrent, inadequately treated bacterial respiratory tract infections such as TB
• measles, pneumonia, pertussis, or influenza
• obstruction by a foreign body, tumor, or stenosis associated with recurrent infection
• inhalation of corrosive gas or repeated aspiration of gastric content into the lungs.

Pathophysiology
Bronchiectasis results from repeated damage of bronchial walls and abnormal mucociliary clearance that causes breakdown of supportive tissue adjacent to the airways. This disease has three forms: cylindrical (fusiform), varicose, and saccular (cystic).

Respiratory disorders

What to look for
Initially, bronchiectasis may not produce symptoms. Assess your patient for a chronic cough that produces copious, foul-smelling, mucopurulent secretions, possibly totaling several cupfuls daily (classic symptom). Other characteristic findings include:
• coarse crackles during inspiration over involved lobes or segments
• occasional wheezes
• dyspnea
• weight loss, malaise
• clubbing
• recurrent fever, chills, and other signs of infection.

What tests tell you
• The most reliable diagnostic test, bronchography reveals the location and extent of disease.
• Chest X-rays show peribronchial thickening, areas of atelectasis, and scattered cystic changes.
• Bronchoscopy helps identify the source of secretions or the site of bleeding in hemoptysis.
• Sputum culture and Gram stain identify predominant organisms.
• Complete blood count and WBC differential identify anemia and leukocytosis.
• PFTs detect decreased vital capacity and decreased expiratory flow.
• ABG analysis shows hypoxemia.

How it’s treated
Treatment for bronchiectasis includes:
• antibiotics given by mouth or I.V. for 7 to 10 days or until sputum production decreases
• bronchodilators, with postural drainage and chest percussion, to help remove secretions if the patient has bronchospasm and thick, tenacious sputum
• bronchoscopy used occasionally to aid removal of secretions
• oxygen therapy for hypoxemia
• lobectomy or segmental resection for severe hemoptysis.

What to do
• Provide a warm, quiet, comfortable environment, and urge the patient to rest as much as possible.
• Administer antibiotics as ordered.
• Perform chest physiotherapy several times per day (early morning and bedtime are best); include postural drainage and chest percussion for involved lobes. Have the patient maintain each position for 10 minutes; then perform percussion and tell him to cough.
• Encourage balanced, high-protein meals to promote good health and tissue healing and plenty of fluids to aid expectoration.
• Provide frequent mouth care to remove foul-smelling sputum.
• Evaluate the patient. His secretions should be thin and clear or white.

Respiratory disorders

Respiratory disorders: Chronic obstructive pulmonary disease

Focus topic: Respiratory disorders

COPD is an umbrella term that could refer to emphysema and chronic bronchitis and, more commonly, a combination of these conditions. Asthma was once classified as a type of COPD and shares some of the same characteristics but it’s now considered a distinct chronic inflammatory disorder. The most common chronic lung disease, COPD affects an estimated 30 million Americans, and its incidence is rising. It now ranks fourth among the major causes of death in the United States.

Equal opportunity disease?

Focus topic: Respiratory disorders

The disorder affects more men than women, probably because until recently men were more likely to smoke heavily. However, the rate of COPD among women is increasing. Early COPD may not produce symptoms and may cause only minimal disability in many patients, but it tends to worsen with time.

What causes it
COPD may result from:
• cigarette smoking
• recurrent or chronic respiratory tract infection
• allergies
• familial and hereditary factors such as alpha1-antitrypsin deficiency.

Pathophysiology
Smoking, one of the major causes of COPD, impairs ciliary action and macrophage function and causes inflammation in the airways, increased mucus production, destruction of alveolar septa, and peribronchiolar fibrosis. Early inflammatory changes may reverse if the patient stops smoking before lung disease becomes extensive.
The mucus plugs and narrowed airways trap air, as occurs in chronic bronchitis and emphysema, and the alveoli hyperinflate on expiration. On inspiration, airways enlarge, allowing air to pass beyond the obstruction, but they narrow on expiration, preventing gas flow. Air trapping (also called ball valving) occurs commonly in asthma and chronic bronchitis.

What to look for
The typical COPD patient is asymptomatic until middle age, when the following signs and symptoms may occur:
• reduced ability to exercise or do strenuous work
• productive cough
• dyspnea with minimal exertion.

What tests tell you
For specific diagnostic tests used to determine COPD.

How it’s treated
Treatment for COPD aims to relieve symptoms and prevent complications. Most patients receive beta-agonist bronchodilators (albuterol [Proventil HFA] or salmeterol), anticholinergic bronchodilators (ipratropium [Atrovent]), and corticosteroids (beclomethasone [Beconase AQ]). These drugs are usually given by metered dose inhaler.

What to do
• Administer antibiotics as ordered to treat respiratory tract infections.
• Administer low concentrations of oxygen as ordered.
• Check ABG levels regularly to determine oxygen need and to avoid carbon dioxide narcosis.
• Evaluate the patient. The patient’s chest X-rays, respiratory rate and rhythm, ABG values, and pH should be approaching normal. He should have a PaO2 level above 60 mm Hg. He should also have normal body weight and urine output.

Respiratory disorders

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Respiratory disorders: Tuberculosis

Focus topic: Respiratory disorders

TB is an acute or chronic infection characterized by pulmonary infiltrates and formation of granulomas with caseation, fibrosis, and cavitation. The American Lung Association estimates that active TB afflicts nearly 5 out of every 100,000 people. The prognosis is excellent with correct treatment.

What causes it
Mycobacterium tuberculosis is the major cause of TB. Other strains of mycobacteria may also be involved. Several factors increase the risk of infection, including:
• gastrectomy
• uncontrolled diabetes mellitus
• Hodgkin’s disease
• leukemia
• treatment with corticosteroid therapy or immunosuppressant therapy
• silicosis
• human immunodeficiency virus infection.

Pathophysiology
TB spreads by inhalation of droplet nuclei when infected persons cough or sneeze. Here’s what happens:

On the move

Focus topic: Respiratory disorders

Transmission — An infected person coughs or sneezes, spreading infected droplets. When someone without immunity inhales these droplets, the bacilli are deposited in the lungs.

Rallying the troops

Focus topic: Respiratory disorders

Immune response — The immune system responds by sending leukocytes, and inflammation results. After a few days, macrophages replace the leukocytes. The macrophages then ingest the bacilli, and the lymphatics carry the bacilli off to the lymph nodes.

We have you surrounded…

Focus topic: Respiratory disorders

Tubercle formation — Macrophages that ingest the bacilli fuse to form epithelioid cell tubercles (tiny nodules surrounded by lymphocytes). Within the lesion, caseous necrosis develops and scar tissue encapsulates the tubercle. The organism may be killed in the process.

…come out with your hands up!

Focus topic: Respiratory disorders

Dissemination — If the tubercles and inflamed nodes rupture, the infection contaminates the surrounding tissue and may spread through the blood and lymphatic circulation to distant sites. This process is called hematogenous dissemination.

What to look for
In primary infection, the disease usually doesn’t produce symptoms. However, it may produce nonspecific signs and symptoms such as:
• fatigue
• cough
• anorexia
• weight loss
• night sweats
• low-grade fever.
In reinfection, the patient may experience cough, productive mucopurulent sputum, and chest pain.

What tests tell you
• Chest X-rays show nodular lesions, patchy infiltrates (many in upper lobes), cavity formation, scar tissue, and calcium deposits. However, they may not distinguish active from inactive TB.
• Tuberculin skin tests detect exposure to TB but don’t distinguish the disease from uncomplicated infection. Patients from non–North American countries may test positive for TB by skin test because of the positive antibody titer produced by the bacille Calmette-Guérin live vaccine they received as children.
• Stains and cultures of sputum, CSF, urine, drainage from abscesses, or pleural fluid show heat-sensitive, nonmotile, aerobic, acid-fast bacilli and confirm the diagnosis.

How it’s treated
Antitubercular therapy with daily oral doses of isoniazid, rifampin (Rifadin), and pyrazinamide (and sometimes with ethambutol [Myambutol] or streptomycin) for at least 6 months usually cures TB. After 2 to 4 weeks, the disease is typically no longer infectious, and the patient can resume his normal lifestyle while
continuing to take medication. The patient with atypical mycobacterial disease or drug-resistant TB may require second-line drugs, such as capreomycin (Capastat), streptomycin, cycloserine (Seromycin), amikacin, and quinolones.

What to do
• Isolate the infectious patient in a negative-pressure room until he’s no longer contagious.
• Watch for adverse effects of medications. Pyridoxine (vitamin B6) is sometimes recommended to prevent peripheral neuropathy caused by large doses of isoniazid. If the patient receives ethambutol, watch for optic neuritis; if it develops, discontinue the drug. Observe for hepatitis and purpura in patients receiving rifampin.
• Evaluate the patient. His sputum culture should be negative and secretions should be thin and clear.

Respiratory disorders

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