Asthma and Chronic Obstructive Pulmonary Disease
Asthma
- Cough, wheezing, chest tightness, often worse at night
- Physical examination:Prolonged expiratory phaseor bilateral wheezing, tachypnea, tachycardia, hypoxia
- Reversible with bronchodilators
Chronic Obstructive Pulmonary Disease
- Smoker with chronic productive cough complains of dyspnea
- Increased sputum production, bilateral wheezing, rales, and rhonchi
Obstructive lung disease is classified into two categories: asthma and chronic obstructive pulmonary disease (COPD). Patients with asthma have disease that is episodic and reversible to a significant degree. Between acute attacks these patients may have relatively normal lung function. However, patients who have persistent inflammation may develop over time permanent changes that contribute to a decline in functional capacity. Patients with COPD, have significant fixed airway obstruction that remains at baseline even when the patient’s illness is under optimal control. In addition to the concept of reversibility, there are other characteristics that distinguish these two groups. Asthmatic patients tend to be younger and more likely to have allergic triggers and conditions. A family history is common. Patients with COPD usually have a long history of cigarette smoking and more significant permanent lung injury and chest remodeling. Associated right heart failure does not occur in asthma but is common in advanced cases of COPD.
Many conditions commonly associated with asthma and COPD exacerbations are listed in Table 33–1. Some of these conditions are treatable, and the clinician should ask about them specifically while taking the patient’s history.
| Infection (especially upper respiratory tract viral infections) |
| Drugs (aspirin, nonsteroidal anti-inflammatory agents, food coloring, β-blockers) |
| Exercise |
| Emotional stress |
| Inhaled irritants (eg, air pollution, cigarette smoke) |
| Occupational exposure to dusts, gases, etc |
| Aeroallergens (pollens, grasses, molds, animal dander) |
| Gastroesophageal reflux disease |
| Weather changes (especially cold) |
| Menses (catamenial asthma) |
There are two varieties of COPD: chronic bronchitis and emphysema. Chronic bronchitis is characterized by chronic cough and sputum production and is almost invariably associated with prolonged and heavy cigarette smoking. Such patients usually have increased lung volumes and a barrel-shaped chest with increased lung markings on chest X-ray. In advanced cases they may have cyanosis and peripheral edema due to right heart failure. Patients with emphysema on the other hand are typically thin without cyanosis and breathe through pursed lips. Accessory muscle use is more prominent. The chest X-ray usually shows a paucity of lung markings reflecting tissue destruction. Some patients with emphysema have genetic factors (α1-antitrypsin deficiency) as the basis of their illness, but most have a long history of cigarette smoking.
Most asthmatic patients present with exacerbations of known disease with shortness of breath and cough. They frequently complain of tightness in the chest. Those with significant chest pain, fever, or purulent sputum may have associated pneumonia. Acute attacks are frequently precipitated by upper respiratory infection, exercise, or inhaled allergens.
Most patients are wheezing and coughing with respiratory distress. Tremor and tachycardia are common due to a combination of sympathomimetic therapy and the stress of the illness. Mild degrees of hypoxia are common. Dehydration due to inadequate oral intake or vomiting is almost always present. Tachypnea and sometimes fever increase insensible losses. Thick and tenacious secretions tend to cause mucous plugging and significantly contribute to impaired gas exchange. Patients with moderate distress typically prefer to sit up and frequently are agitated, tachycardic, and tachypneic with accessory muscle use. Patients with severe distress may be hypoxic even with supplemental oxygen or have marked abnormalities of vital signs. Those with alteration of mental status, CO2 retention, or who begin to tire are in danger of respiratory arrest.
COPD is a chronic disease and baseline functional limitations are characteristic of the illness. The presentation of an acute exacerbation is increased shortness of breath, wheezing, and cough that becomes progressively worse over several days. An increase in sputum production is frequently seen, especially in patients with chronic bronchitis. Activity tolerance becomes more limited in these patients. Most are dyspneic at rest when they present to the emergency department.
Patients with emphysema have diminished breath sounds due to the loss of lung parenchyma. Patients with advanced disease are usually thin and appear uncomfortable even at baseline with obvious use of accessory muscles. These patients may be described as “pink puffers” because they are generally not cyanotic or significantly hypoxic and breathe through pursed lips.
In addition to wheezing and prolonged expiration, patients with chronic bronchitis usually have a few course rales and prominent rhonchi. Heart tones are usually distant because of a barrel shape to the chest and the loss of pulmonary parenchyma that transmits sound. They frequently are moderately obese. Peripheral edema may be due to right heart failure associated with advanced disease. Patients with chronic bronchitis are not as uncomfortable in appearance as those with emphysema and frequently have minimal symptoms in the face of pronounced CO2 retention and hypoxia. These patients are sometimes referred to as “blue bloaters,” because of the frequent occurrence of cyanosis and edema.
In addition to standard medical history, the use of oxygen at home is important. Patients who have required ICU care or intubation are at greater risk for severe disease. Continued smoking contributes more than any other factor to the increased risk of illness and death.
Pulse oximetry usually gives better information regarding oxygenation than do blood gases because it is available in real time. An accurate reading depends on good blood flow and a thin body part to attach the device. When a good arterial waveform is visible on the monitor the readings are very accurate and reliable.
The assessment of alveolar ventilation and respiratory acidosis are best evaluated with blood gas analysis. Many patients with COPD but particularly those on home oxygen have a chronic respiratory acidosis (elevated pco2) with metabolic compensation (increased total CO2, or bicarbonate). A low pH is indicative of acute decompensation. Comparing values from previous measurements is helpful in assessing the significance of these abnormalities.
Most patients with mild asthma will not need a chest X-ray unless pneumonia or pneumothorax is suspected. Patients with COPD or advanced age are more likely to have important findings on chest X-ray. Congestive heart failure, pleural effusions along with lung cancer, and associated complications are important diagnoses that may be made or suspected with plain images of the chest. If pulmonary embolism (PE) is suspected, then CT scanning with contrast is necessary.
Peak expiratory flow (PEF) measurements are a practical way of following the severity of illness and response to therapy in patients with asthma. The values should be compared with predicted peak flow values, which are based on age, sex, and height.
Most patients with significant respiratory distress or abnormal vital signs should be placed on a cardiac monitor and the cardiac rhythm determined. The electrocardiogram provides additional information where the rhythm is not easily determined from a single lead monitor or if cardiac ischemia is suspected.
Some patients with COPD are polycythemic due to chronic hypoxia. Metabolic compensation from chronic CO2 retention is usually evident from venous electrolytes in the form of an elevated bicarbonate as reflected in the total CO2.
Sputum examination is primarily useful in selected patients when adequate specimens are available and pneumonia is suspected. They also can be useful in the diagnostic evaluation when atypical pathogens such as mycobacteria or Legionella species are suspected.
Theophylline is no longer commonly used. Patients who do take theophylline may be toxic and drug levels are indicated if toxicity is suspected.
Most patients with COPD present with a long history of previous exacerbations similar to the present episode. The diagnostic challenge is usually in the identification or exclusion of associated conditions including congestive heart failure, PE, pneumothorax, and cancer of the lung. Most patients are elderly and at risk for all these illnesses. In many cases, the reason for dyspnea may be multifactorial. Patients with fever may have pneumonia or another type of infection. If chest pain is present, associated cardiac disease must be considered. Other pulmonary pathology such as pneumothorax may be present. It cannot be stressed too strongly that many patients who present with wheezing actually have acute heart failure as the primary reason for dyspnea. Impressively elevated blood pressure is a valuable clue to the presence of associated acute heart failure.
Respiratory syncytial virus infection is a significant cause of wheezing and respiratory distress in young children. Rapid testing for these infections helps to identify these patients but usually does not change therapy. The test is used to determine the need for respiratory isolation if the patient requires hospitalization. Most children may be given a diagnosis of reactive airway disease and treated in a similar manner. Foreign body aspiration typically presents with the acute onset of wheezing and respiratory distress in a crawler or young toddler.
Asthma by definition should be largely reversible with treatment. Patients with COPD have fixed obstruction but do have episodes when symptoms are exaggerated and can be improved with therapy.
Most patients with mild asthma can be treated with nasal cannula oxygen at 2–4 L/min. Patients whose saturations fall below 90% require higher concentrations by mask. Patients who are anxious, hypoxic, and struggling to breathe should receive high concentrations of oxygen as necessary to achieve adequate oxygen saturations. A nonrebreather mask with an oxygen reservoir can be used to deliver nearly a 100% inspired oxygen concentration if necessary.
Some patients with advanced COPD, especially those maintained on oxygen at home, may develop CO2 narcosis if high concentrations of oxygen are used. Such patients develop an altered mental status when their hypoxic ventilatory drive is removed, CO2 levels rise, and a respiratory acidosis develops. Most of the time, this is seen when a patient not short of breath is treated with oxygen for another reason such as chest pain.
Patients are usually in need of intravenous fluids. This is particularly true of asthmatics and an aspect of treatment that is frequently neglected. Young adults with asthma and without cardiac disease should receive 1–2 L of normal saline over the first hour or two and at 500 cc/h thereafter. Children should be treated with 20 cc/kg of saline as a bolus.
Patients with COPD are usually older and may have associated cardiac disease; therefore, caution is indicated in these patients to avoid fluid overload. A fluid bolus of 250–500 cc of saline is typically appropriate in an elderly patient or someone with known heart disease.
If patients begin to tire or show signs that failure of ventilation is developing, they should be supported mechanically.
The technology of noninvasive treatment with Bilevel (BiPAP) support has improved over the last several years. Many patients who otherwise would require intubation can be supported noninvasively and avoid the risks of an artificial airway. An initial setting of 10 cm H2O of inspiratory pressure and 5 cm H2O of expiratory pressure is usually an appropriate initial setting for BiPAP support for either asthma or COPD.
If a patient cannot manage their airway either because of confusion, lethargy, or agitation, then they will require an artificial airway (see Chapter 7). Patients may also require intubation because of excessive secretions or a need for frequent suctioning. Controlled rapid sequence intubation is preferable to crash intubation which may be required if the patient suddenly deteriorates. Larger endotracheal tubes facilitate suctioning and bronchoscopy and should be used if possible. Low tidal volume ventilation (Table 33–2) helps to decrease overdistention, air trapping, and resultant barotrauma. Measurement of blood gases is important in guiding therapy when positive pressure support of any kind is used.
These medications are the mainstay of treatment for asthma and COPD. The ones most commonly used are the short-acting β2-selective agents. These agents cause rapid relaxation of bronchial smooth muscles, resulting in bronchodilation, and reducing airflow obstruction. Albuterol, levalbuterol (the R-isomer of albuterol), and metaproterenol are used most often. Inhalation, through metered-dose inhalers (MDIs) or nebulizers, has been shown to be faster and to deliver higher concentrations of medication to the lungs with fewer systemic side effects than oral preparations. However, MDIs require coordination and a cooperative, alert patient who can hold his or her breath for 5–10 seconds. Therefore, passive nebulized β2-agonists are more often used in moderate and severe exacerbations. For mild disease, albuterol MDI dosing is 4–6 puffs every 20 minutes (up to 4 hours), and nebulized solutions should be given at 2.5 mg every 20–30 minutes. Patients who are severely ill may receive 5 mg every 20–30 minutes or a continuous treatment for an hour or more. Attention to monitoring the patient for tachycardia and for signs of respiratory failure should be continued and not neglected in patients on continuous treatment.
Ipratropium nebulized solution, 0.5 mg every 20–30 minutes, can be used. This is frequently mixed with albuterol and given every 20–30 minutes. Hospitalized patients may be scheduled every 4–6 hours.
Steroids are well known to inhibit both inflammatory cell recruitment and the release of inflammatory mediators into the airways. Many patients with moderate to severe obstructive airway disease take chronic steroids. Although steroids do not initially change emergency department management, these medications are crucial to reduce the rate of relapse in moderate to severe exacerbations. They can also be helpful in mild attacks if the patient is not responding well to initial bronchodilator treatments. Consider steroids if the patient is taking oral or inhaled steroids, has had prolonged symptoms, or recently completed a steroid taper. Patients who are severely ill should receive steroids. Steroid doses for adults are prednisone, 40–60 mg orally, or methylprednisolone, 60–125 mg intramuscularly or intravenously. Dosing for children includes prednisone, 2 mg/kg orally, or methylprednisolone 0.5–2 mg/kg intravenously. Discharge the patient to home with a steroid burst (adults: prednisone, 40 mg/d; children: 1 mg/kg, for 3–5 days) or taper (10–14 days) depending on severity.
Antibiotics are typically not indicated for mild asthma unless evidence of infection is present on physical examination or chest X-ray. Patients with an acute exacerbation of COPD, presenting with worsening dyspnea and increased cough and sputum production, usually benefit from antibiotics. Patients who have associated pneumonia should be treated with antibiotics. (See Pneumonia and Bronchitis, below.)
| Tidal Volume | 6 mL per kilogram of predicted, not actual, body weight |
| Predicted Body Weight in Men = 50.0 + 0.91 (height in centimeters − 152.4) | |
| Predicted Body Weight in Women = 45.5 + 0.91 (height in centimeters − 152.4) | |
| Initial Respiratory Rate | 18 to 22 breaths per minute |
| Partial pressure of carbon dioxide pco2 | Less than 80 mm Hg |
| Plateau airway pressure | 30 cm of water or less |
| Target arterial oxyhemoglobin saturation | Greater than 90% |
Magnesium has a direct relaxing effect on bronchial smooth muscle and also helps to stabilize many inflammatory mediators. For patients with severe asthma, magnesium (in conjunction with ongoing treatment) may help improve airway obstruction and avoid intubation. The dosing is 2–3 g intravenously, infused at 1 g/min, with close monitoring of blood pressure. The infusion should stop if hypotension, respiratory depression, or decreased deep tendon reflexes occurs.
Theophylline (oral) or aminophylline (intravenous) are moderately effective bronchodilators. However, toxicity, particularly vomiting and resulting dehydration, is a particular problem. These medications are no longer recommended for the treatment of acute exacerbations of asthma or COPD.
Ketamine has been shown to be a significant bronchodilator and can be used to facilitate intubation of severely agitated patients with refractory disease (status asthmaticus). Usual anesthetic induction dose is 1–2 mg/kg intravenously or 4 mg/kg intramuscularly.
Asthma patients who demonstrate a good response (PEF > 70% of predicted) and whose symptoms have resolved can be discharged home. Those with an incomplete response to treatment (PEF, 50–70% of predicted), with improved symptoms, and no hypoxia can be discharged if close follow-up and correct use of inhalers can be demonstrated. Most patients that have returned to the emergency department within 3 days should be admitted for continued treatment in the hospital.
Acute exacerbations of COPD are more difficult and resolve slower than acute exacerbations of asthma. Most patients with COPD will require admission. Some patients will have significant comorbidities such as pneumonia or associated heart failure. Some are severely ill and require ICU care. Many patients are elderly and social issues such as the availability of home health care, and assistance with the activities of daily living make treatment outside the hospital impractical.
Pulmonary Vascular Diseases
- Acute onset of dyspnea, pleuritic chest pain, tachypnea, tachycardia
- Hypoxemia with widened A-a gradient
- Pulmonary angiogram is gold standard
A variety of clinical conditions may cause clots to form in the venous system that when dislodged will cause pulmonary emboli (Table 33–3). Venous thrombosis may result from a generalized hypercoagulable state, venous endothelial injury, or local stasis (Virchow triad). Clots that cause clinically significant pulmonary emboli form most commonly in the iliofemoral and pelvic venous beds. Pulmonary embolization, from veins of the upper extremities or distal lower extremities, is unusual and rarely clinically significant.
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When embolization occurs, the manifestations depend on the size of the embolism, the patient’s underlying cardiorespiratory status, and whether subsequent infarction of pulmonary tissue occurs. With small to medium sized emboli, obstruction of a localized portion of the pulmonary vascular tree causes local atelectasis with resulting ventilation–perfusion (V/Q) abnormalities and hypoxemia. Reflex hyperventilation with resultant hypocapnia and tachycardia also occurs. With massive embolization (obstructing over 60% of the vascular bed), acute pulmonary hypertension, right heart strain, systemic hypotension, and shock may also occur. Pulmonary emboli may also present with sudden cardiovascular collapse and death.
The illness often begins abruptly, and a predisposing underlying condition is almost always present. Dyspnea and chest pain are the usual presenting symptoms. Tachycardia and hypoxia are the most common clinical signs. Fever, hypotension, cyanosis, pleural friction rub, and pulmonary consolidation may be the result of PE but are usually the result of other illnesses when they occur.
The chest X-ray is abnormal in most patients with pulmonary embolization with infarction but the abnormalities are often nonspecific (eg, atelectasis, pleural effusions, small infiltrates). The Westermark sign (dilated pulmonary vasculature proximal to embolus with oligemia distal) and Hampton’s Hump (a pleural-based density with a rounded border facing the hilum) are more suggestive though uncommon findings with pulmonary emboli.
The electrocardiogram is often abnormal, usually demonstrating tachycardia or diffuse nonspecific ST-T abnormalities. The classic finding of acute right heart strain (S1/Q3/T3; T-wave inversion in leads V1–V3) is more specific but somewhat uncommon.
A clinically significant PE is usually but not always associated with hypoxemia (oxygen saturation < 90%; Po2 < 80 mm Hg). Hyperventilation and hypocapnia are also common findings. An arterial puncture is required to measure the arterial Pco2 and calculate an alveolar-arterial oxygen gradient (A-a gradient). The value of the A-a gradient over the more easily measured oxygen saturation by pulse oximetry is minimal. Most of the time the additional time, discomfort and expense is not justified by any additional discriminatory ability of the A-a gradient.
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