SECTION IX. Respiratory System
A Adult Respiratory Distress Syndrome
DEFINITION
The term acute respiratory failure is often used synonymously with acute (formerly adult) respiratory distress syndrome (ARDS). Although ARDS may be caused by or associated with a variety of clinical conditions, most patients with this disease demonstrate similar clinical and pathologic features regardless of the cause of lung injury. Common features include the following: (1) a history of a preceding noxious event that served as a trigger for the subsequent development of ARDS; (2) an interval from hours to days of relatively normal lung function after the insult; and (3) the rapid onset and progression over several hours of dyspnea, severe hypoxia, diffuse bilateral pulmonary infiltration, and stiffening and noncompliance of the lungs.
INCIDENCE AND OUTCOME
Risk factors for the development of ARDS appear to be additive. The incidence of occurrence is 25% with the presence of one risk factor, 42% with the presence of two, and 85% with the presence of three. The mortality rate for ARDS remains high, ranging from 50% to 70% and often exceeds 90% when gram-negative septic shock precedes ARDS development.
ETIOLOGY
Events and risk factors associated with the development of ARDS include the following: (1) shock (septic, cardiogenic, or hypovolemic); (2) trauma; (3) pulmonary infection (e.g., with Pneumocystis carinii (jiroveci) or Escherichia coli); (4) disease states that result in the release of inflammatory mediators (e.g., extrapulmonary infections, disseminated intravascular coagulation, anaphylaxis, coronary bypass grafting, and transfusion reactions); (5) exposure to various agents (e.g., narcotics, barbiturates, and O 2); (6) diseases of the central nervous system; (7) aspiration (e.g., of gastric contents or as in drowning); and (8) metabolic events (e.g., pancreatitis and uremia).
PATHOPHYSIOLOGY
The pathophysiology of ARDS is centered around severe damage and inflammation to the alveolocapillary membrane. Irrespective of the cause of acute respiratory failure, the lung’s structural response to injury and subsequent repair occurs in a similar fashion. Although the exact mechanisms of this response and repair remain unclear, research has focused on the release of cytokines and membrane-bound phospholipids from the capillary endothelium and the activation of leukocytes and macrophages (via the complement system) within the lungs.
CLINICAL MANIFESTATIONS AND DIAGNOSIS
The clinical presentation includes patients who are dyspneic, hypoxic, and hypovolemic and require intubation and mechanical ventilation. Recovery of lung function is unpredictable. Milder cases resolve quickly, whereas others progress to fibrosis and death.
TREATMENT
Because lung infections (e.g., P. carinii [jiroveci] pneumonia) mimic ARDS, antibiotic therapy often is initiated before the cause of respiratory failure is known. Maintenance of tissue oxygenation and replacement of lost intravascular fluids are the main goals of therapy. Preservation of end-organ perfusion is of utmost importance. Treatment is supportive and includes correction of hypoxia, preload and afterload reduction, and inotropic support as indicated.
ANESTHETIC CONSIDERATIONS
Anesthetic preparation includes evaluation of the patient’s respiratory, cardiac, and renal status. Ventilator settings should be noted and special attention devoted to peak inspiratory pressures and PEEP levels. If the anesthesia ventilator cannot accommodate these settings, then arrangements must be made to bring the patient’s ventilator into the operating room. The nature of lung sounds and amount of secretions should be noted. The presence of excess secretions should alert the anesthesia provider to the potential risk of airway obstruction. The degree of barotrauma from prolonged mechanical ventilation with high levels of PEEP can be assessed by the presence of chest tubes and subcutaneous emphysema secondary to pneumothorax. The effectiveness of therapy with bronchodilators should be assessed, because the use of these drugs may be initiated preoperatively and continued intraoperatively if effective. An arterial line should be placed preoperatively and arterial blood gas (ABG) analysis performed. If possible, lactic acid values should be determined.
Volume status should be evaluated closely because patients with ARDS often are hypovolemic. Invasive monitoring via central venous lines and pulmonary artery catheters often is available, and cardiac filling pressures along with CO values should be assessed. Patients requiring inotropic support may arrive for surgery with infusions of dopamine or dobutamine. For all procedures, renal function should be monitored with a bladder catheter. Antibiotic therapy should be continued intraoperatively, and continuation of steroid preparations should be considered if patients were receiving these medications preoperatively.
Because patients with ARDS often are hemodynamically unstable, careful titration of anesthetic agents and adjunct agents is necessary. Owing to the multisystemic involvement characteristic of ARDS, drug metabolism and elimination should be carefully considered.
Transport should be carefully planned so that complications are minimized and safe arrival in the intensive care unit is ensured. Patients should undergo pulse oximetry, ECG, and blood pressure transport monitoring (by arterial line or noninvasively) before departure from the operating room. Breath sounds should be continually assessed with a precordial stethoscope. A full tank of O 2 and PEEP adapter valves should be available for transport. The potential need for emergency medications and a defibrillator should be considered. If the patient’s ventilator needs to be returned to the intensive care unit, plans should be made so that it arrives there before the patient does. Finally, if possible, another member of the anesthesia team should accompany the patient during transport. Pulmonary dysfunction is the most common cause of postoperative complications after the administration of general anesthesia. To minimize pulmonary derangement, the anesthesia provider must identify those patients who are at risk for the development of pulmonary impairment and must have a thorough understanding of the preexisting lung dysfunction.
B Aspiration Pneumonia
DEFINITION
Two entirely separate clinical aspiration disorders existed. One followed the aspiration of solid food and produced a picture of laryngeal or bronchial obstruction, whereas the other resulted from direct acid injury to the lung and produced the “asthma-like” syndrome. Pulmonary aspiration occurs when the gastric contents escape from the stomach into the pharynx, and then enter the lungs. This results from preexisting disease, airway manipulation, and the inevitable compromise in protective reflexes that accompanies the anesthetized state. Aspirates are commonly categorized as contaminated, acidic, alkaline, particulate, and nonparticulate. Less than half of all aspirations lead to pneumonia. Pneumonia occurs most often in patients with aspiration of infected material or who are immunocompromised.
INCIDENCE AND OUTCOME
While the incidence of regurgitation is estimated to be frequent (as high as 15%), pulmonary aspiration complicates only about 1 in 3000 anesthetics. This incidence is roughly doubled for cesarean section surgery and emergency surgery. Fortunately, the majority of aspiration incidents require little or no treatment.
ETIOLOGY
Although vomiting and gastroesophageal reflux are common clinical events, aspiration usually occurs only when normal protective reflexes (swallowing, coughing, gagging) fail. Three broad categories of failure include the following: (1) depression of reflex protection; (2) alteration in anatomic structures; and (3) iatrogenic disorder. Reflex responses to aspiration are automatically blunted with depression of consciousness. The most common setting for depression of reflex protection occurs during anesthesia induction and emergence.
Three aspiration syndromes have been identified: (1) chemical pneumonitis (Mendelson’s syndrome); (2) mechanical obstruction; and (3) bacterial infection. Because acute chemical pneumonitis poses the greatest difficulty to anesthesia providers, the pathophysiology, presentation, and anesthetic implications of Mendelson’s syndrome are discussed. The triphasic sequence of (1) immediate respiratory distress combined with bronchospasm, cyanosis, tachycardia, and dyspnea followed by (2) partial recovery and (3) a final phase of gradual return of function is characteristic of Mendelson’s syndrome. This acute chemical pneumonitis is caused by the irritative action of hydrochloric acid, alkaline aspirates, or particulate materials, which are damaging to the lungs.
PATHOPHYSIOLOGY
The pathophysiology of aspiration pneumonitis is typically characterized by four stages: (1) The aspirated substance causes immediate damage to the lung parenchyma, resulting in tissue necrosis. (2) Atelectasis results within minutes, due to a parasympathetic response that leads to airway closure and a decrease in lung compliance. (3) One to two hours after the injury, there is an intense inflammatory reaction characterized by pulmonary edema and hemorrhage. Inflammatory cytokines play a central role in this, including interleukin-8 and tumor necrosis factor alpha (TNF-α) released by alveolar macrophages. Neutrophils also play a key role in this phase by releasing oxygen radicals and proteases. (4) Later, secondary injuries result from fibrin deposits and necrosis of alveolar cells by 24 hours after the insult.
CLINICAL MANIFESTATIONS AND DIAGNOSIS
Arterial hypoxemia, the hallmark sign of aspiration pneumonitis, is frequently the first sign of aspiration. Since the majority of aspiration incidents are asymptomatic or mildly symptomatic, unexplained hypoxemia occurring in otherwise healthy patients postoperatively may frequently be a vague sign of silent aspiration. Other signs to alert the anesthetist to the possibility of aspiration include tachypnea, dyspnea, tachycardia, hypertension, and cyanosis.
ANESTHETIC CONSIDERATIONS
Preoperative Management
When dealing with aspiration, “an ounce of prevention is worth a pound of cure.” Avoiding the use of general anesthesia is the most effective means of preventing aspiration. However, regional and local sedation anesthesia is unrealistic for many procedures and in certain patient populations. When the use of general anesthesia is unavoidable, taking the following steps may help minimize the risk of aspiration, or at least limit its consequences.
• Adhere to Nil per os (NPO) policy.
• Use pharmacologic prophylaxis for aspiration. Agents such as gastrokinetics, histamine blockers, anticholinergics, antacids, proton pump inhibitors, and antiemetics are all used alone or in various combinations to raise gastric pH and lower volume (see the table on p. 182).
• Consider the application of cricoid pressure.
• Other nonpharmacologic mechanisms such as elevating the patient’s head may offer limited benefit.
| Medication Type | Common Examples | Recommendation |
|---|---|---|
| Gastrointestinal stimulants | Metoclopramide | No routine use∗ |
| Gastric acid secretion blockers | Cimetidine | No routine use∗ |
| Famotidine | ||
| Omeprazole | ||
| Lansoprazole | ||
| Antacids | Sodium citrate | No routine use∗ |
| Sodium bicarbonate | ||
| Magnesium trisilicate | ||
| Antiemetics | Droperidol | No routine use∗ |
| Ondansetron | ||
| Anticholinergics | Atropine | No use† |
| Scopolamine | ||
| Glycopyrrolate | ||
| Combinations of the medications above | No routine use∗ | |
| ∗The routine preoperative use of these medications to decrease aspiration risk in patients with no apparent increased risk is not recommended. | ||
| †The use of anticholinergics to decrease aspiration risk is not recommended. | ||
Data from American Society of Anesthesiologists. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to healthy patients undergoing elective surgery, Anesthesiology 90:896-905, 1999. | ||
Intraoperative Management
If intubation is not expected to be difficult, a rapid-sequence induction (rather than awake endotracheal intubation) is indicated in the patient with aspiration risk. There is little evidence that “modified” rapid sequence technique (which allows for gentle mask ventilation) would worsen aspiration incidence, and this approach may be preferable in patients at risk for rapid oxygen desaturation. As difficult intubation itself is a risk factor for aspiration, there should be a low threshold for performing awake intubation in a patient with aspiration risk who may also pose airway challenges. Endotracheal intubation is considered the optimal approach for airway isolation, however regurgitated material can seep around the ETT cuff, particularly if it is not lubricated. Preventative measures in the anesthetic plan include assuring that the patient is fully awake before extubation, is manifesting protective reflexes, minimize any residual neuromuscular blockade, avoid narcosis, and empty the stomach.
If vomiting or aspiration occurs during induction, immediate treatment includes tilting of the patient’s head downward or to the side, rapid suctioning of the mouth and pharynx, and intubation. There is little benefit in performing tracheal or bronchial suctioning in most cases, and bronchoscopy should be reserved for those patients who are suspected of having aspirated solid material. If aspiration is severe, surgery may be postponed. ABG analysis should be performed for determination of the extent of hypoxemia. Early application of PEEP is recommended for improving pulmonary function and combating atelectasis. Oxygenation should be supported with supplemental oxygen only to the minimum extent necessary.
TREATMENT OF ASPIRATION PNEUMONITIS
• Suction mouth and pharynx.
• Use deeper suctioning only for particulate material.
• Administer oxygen, only to the extent needed.
• Administer lidocaine to inhibit neutrophil response.
• Steroids have questionable benefit.
• Intubate as needed to support oxygenation.
• Use bronchodilator, PEEP to support ventilation.
• Administer antibiotics only if indicated or for fever or ↑ WBC >48 hours.
C Asthma
DEFINITION
Asthma is a chronic inflammatory disorder of the airways characterized by increased responsiveness of the tracheobronchial tree to a variety of stimuli. Many cells and cellular elements play a role—in particular, mast cells, eosinophils, T lymphocytes, neutrophils, and epithelial cells. In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment.
Various subtypes of asthma exist. The most important consideration is the identification of exacerbating factors whenever possible. A well-known system classifies asthmas as either extrinsic or intrinsic. Although this system is conceptually helpful, its two groups are not mutually exclusive. Extrinsic asthma (or allergic asthma) most commonly affects children and young adults and involves infectious, environmental, psychological, or physical factors, whereas intrinsic asthma (or idiosyncratic asthma) usually develops in middle age without specifically identifiable attack-provoking stimuli. The term atopy, which refers to a hereditary, IgE-mediated, clinical hypersensitive state, is often used when extrinsic asthma is described.
INCIDENCE AND OUTCOME
Up to 15 million persons in the United States have asthma. It is the most common chronic disease of childhood, affecting an estimated 4.8 million children. People with asthma collectively have more than 100 million days of restricted activity and 470,000 hospitalizations annually. More than 5000 people die of asthma each year.
PATHOGENESIS AND PATHOPHYSIOLOGY
Asthma is a heterogeneous clinical syndrome characterized by episodes in which airways are hyperresponsive, interspersed with symptom-free periods. Bronchoconstriction is a factor long associated with the asthmatic symptom complex, but asthma is much more than bronchoconstriction. Airway inflammation and a nonspecific hyperirritability of the tracheobronchial tree are now recognized as being central to the pathogenesis of even mild cases of asthma. Permanent changes in airway anatomy, referred to as airway remodeling, magnify the inflammatory response.
Allergic asthma (atopic or immunologic disease) is triggered by antigens that provoke a T-lymphocyte–generated, IgE-mediated immune response. It is often associated with a personal or familial history of allergic disease. Potent biochemical mediators released from proinflammatory and airway epithelial cells promote vasoconstriction, increased smooth muscle tone, enhanced mucous secretion, submucosal edema, increased vascular permeability, and inflammatory cell chemotaxis. Leukotrienes have been identified as especially potent spasmogenic and proinflammatory substances. Released molecules that are toxic to the airway epithelium cause patchy desquamation, which exposes cholinergic nerve endings and compounds the bronchoconstrictive and hyperresponsive response.
The asthmatic diathesis creates airways that are inflamed, edematous, and hypersensitive to irritant stimuli, and the degree of airway hyperresponsiveness and bronchoconstriction appears to parallel the extent of inflammation. When airway reactivity is high, asthmatic symptoms are generally more severe and unrelenting, and the amount of therapy required to control the episode is greater.
The mechanisms underlying idiosyncratic asthma (nonimmunologic disease) are less clearly defined. Nonimmunologic asthma occurs in patients with no history of allergy and normal serum IgE. These patients typically develop asthmatic symptoms in response to some provocative or noxious stimulus such as cold air, airway instrumentation or irritation, climate changes, or an upper respiratory illness. Recent upper respiratory infection may precipitate bronchospasm in any patient, but the risk is higher in patients with a history of asthma.
The mechanism of exercise-induced asthma is unknown. Regardless of the mechanism, most symptoms last less than 1 hour and are usually quickly reversed with administration of β 2-adrenergic receptor agonists. Occupational asthma develops when irritants directly stimulate vagal nerve endings in the airway epithelium. Infection-induced asthma with acute inflammation of the bronchi may be caused by viral, bacterial, or mycoplasmal infections. Aspirin-induced asthma occurs when, in some predisposed persons, cyclooxygenase promotes an increase in leukotriene levels via the arachidonic acid pathway, thereby triggering the asthma attack. This peculiar response can occur with the use of other nonsteroidal antiinflammatory agents. The aspirin-induced asthma variant is not IgE mediated or allergic in nature; furthermore, it is clinically associated with nasal polyps.
CLINICAL MANIFESTATIONS
Key hallmarks of asthma in the awake patient include the following:
• Wheezing
• Dyspnea (may parallel the severity of expiratory airflow obstruction)
• Cough (productive or nonproductive; frequently at night or early morning)
• Labored respirations with accessory muscle use
• Tachypnea (a respiratory rate >30 breaths per minute and a heart rate of 120 suggests severe bronchospasm)
• Chest tightness
• Prolonged expiratory phase of respiration
• Fatigue
Typically attacks are short-lived, lasting minutes to hours. Between attacks, the asthmatic patient may be entirely symptom free; however, underlying airway remodeling is still evident. Severe obstruction persisting for days or weeks is known as status asthmaticus. Use of accessory muscles of respiration and the increased work of breathing associated with a protracted asthmatic episode can result in respiratory muscle fatigue and respiratory failure. During exacerbations, pulmonary function tests may reflect acute expiratory airflow obstruction (↓ forced expiratory flow [FEF] 25%-75%; ↓ FEV 1/FVC). Viscid mucous secretion may compound the airway narrowing and produce airway collapse.
The asthmatic episode produces not only airflow obstruction, but also gas exchange abnormalities. The resulting low ventilation/perfusion (V/Q) state produces arterial O 2 desaturation. Hypoxemia is common, but in most patients with acute bronchospasm, CO 2 elimination is relatively well preserved until V/Q abnormalities are severe. An increased arterial CO 2 tension may indicate impending respiratory failure in the acutely ill asthmatic patient. Chronic asthma may eventually lead to irreversible lung destruction, loss of lung elasticity, pulmonary hypertension (PH), and lung hyperinflation.
Anesthetized Patients
In anesthetized patients, prominent manifestations of the asthmatic episode are wheezing, mucous hypersecretion, high inspiratory pressures, a blunted expiratory CO 2 waveform, and hypoxemia. Mechanical ventilation and positive airway pressure are associated with a higher incidence of air trapping and lung hyperinflation, and the associated barotrauma can result in a pneumothorax. Additionally, alveolar overdistention may lead to decreased venous return and diminution of CO. The combination of impaired ventilation and hypoxia can precipitate increased pulmonary vascular resistance, enhanced right ventricular afterload, and finally hemodynamic collapse.
The onset of an asthmatic episode may occur abruptly in surgical patients. Airway manipulation, acute exposure to allergens, or the stress of surgery can provoke wheezing in a patient who was previously asymptomatic. Wheezing often suggests potentially reversible bronchoconstriction, but the extent or degree of wheezing is a notoriously poor indicator of the degree of airway obstruction. Care must be taken to differentiate wheezing of asthmatic origin from other causes of wheezing such as pneumothorax, endotracheal tube obstruction, endobronchial intubation, anaphylaxis, pulmonary edema, and pulmonary aspiration.
ANESTHETIC CONSIDERATIONS
Several important anesthetic considerations and risk reduction strategies have been reported (see the following box).
Risk Reduction Strategies for Anesthetization of Patients with Asthma
Preoperative
Encourage cessation of cigarette smoking for at least 8 weeks.
Aggressively treat airflow obstruction.
Administer antibiotics and delay surgery if respiratory infection is present.
Begin patient education regarding lung-expansion maneuvers.
Intraoperative
Limit duration of surgery to less than 3 hours.
Use regional anesthesia when possible.
Avoid the use of long-acting neuromuscular blocking agents.
Use laparoscopic procedures when possible.
Substitute a less ambitious procedure for upper abdominal or thoracic surgery when possible.
Postoperative
Encourage deep-breathing exercises or incentive spirometry.
Use continuous positive airway pressure.
Use intercostal nerve blocks and local anesthesia infiltration of incisional area for pain when appropriate.
D Chronic Obstructive Pulmonary Disease
DEFINITION
Chronic obstructive pulmonary disease (COPD) is a “disorder characterized by abnormal tests of expiratory flow that does not change markedly over periods of several months of observation.” Asthma, chronic bronchitis, and emphysema are all common obstructive diseases characterized by decreased air flow through the tracheobronchial tree and small airways.
The terms chronic obstructive pulmonary disease and chronic obstructive lung disease are widely used as synonyms for the combination of chronic bronchitis and emphysema. Because of the prevalence of cigarette smoking, the combination of these two entities is encountered much more commonly than either of the two in its “pure” form. As a rule, the combination of chronic bronchitis and emphysema is seen in those who smoke heavily, and the disease process takes 30 years or longer to manifest. Differential diagnosis of COPD compared with other common lung disorders is described in the following table.
| Diagnosis | Suggestive Features∗ |
|---|---|
| COPD | Onset in midlife; symptoms slowly progressive; long-term smoking history; dyspnea during exercise; largely irreversible airflow limitation |
| Asthma | Onset early in life (often childhood); symptoms vary from day to day; symptoms occur at night or in early morning; allergy, rhinitis, or eczema also present; family history of asthma; largely reversible airflow limitation |
| Congestive heart failure | Fine basilar crackles on auscultation; chest radiograph shows dilated heart, pulmonary edema; pulmonary function tests indicate volume restriction, not airflow limitation |
| Bronchiectasis | Large volumes of purulent sputum; commonly associated with bacterial infection; coarse crackles or clubbing on auscultation; chest radiograph or CT scan shows bronchial dilation, bronchial wall thickening |
| Tuberculosis | Onset at all ages; chest radiograph shows lung infiltrate or nodular lesions; microbiologic confirmation; high local prevalence of tuberculosis |
| Obliterative bronchiolitis | Onset at younger age, in nonsmokers; may have history of rheumatoid arthritis or fume exposure; CT scan taken on expiration shows hypodense areas |
| Diffuse panbronchiolitis | Most patients are male and nonsmokers; almost all have chronic sinusitis; chest radiograph and HRCT scan show diffuse small centrilobular nodular opacities and hyperinflation |
| COPD, Chronic obstructive pulmonary disease; CT, computed tomography; HRCT, high-resolution computed tomography. | |
| ∗These features tend to be characteristic of the respective diseases but do not occur in every case. For example, a person who has never smoked can develop COPD (especially in developing countries, where other risk factors may be more important than cigarette smoking); asthma can develop in adult and even elderly patients. | |
From Rable KF, Hurd S, Anzueto A et al: Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease, AM J Respir Crit Care Med 176:532-555, 2007. | |
INCIDENCE AND OUTCOME
COPD affects an estimated 15 to 20 million Americans and is the fifth leading cause of death in the United States, accounting for approximately 60,000 deaths each year. Chronic bronchitis and emphysema are the most common causes of COPD.
ETIOLOGY
The principal factor that predisposes a patient to the development of COPD is cigarette smoking. Environmental pollution appears to have some role, but its effects are minor compared with those of cigarette smoking. Additionally, emphysema may develop in some patients because of a genetic predisposition to an imbalance between protease and antiprotease activities in the lungs.
PATHOPHYSIOLOGY
The dominant feature of the natural history of COPD is progressive air flow obstruction, as reflected by a decrease in forced expiratory volume in 1 second (FEV 1). Three causes of decreases in FEV 1 are as follows:
1. A decrease in the intrinsic size of bronchial lumina
2. An increase in the collapsibility of bronchial walls (this cause is the most difficult to quantify)
3. A decrease in elastic recoil of the lungs
CLINICAL MANIFESTATIONS AND DIAGNOSIS
The clinical presentation of COPD varies markedly, and crippling changes for one person may be a minor incapacity for another. Chronic productive cough and progressive exercise limitation are the hallmarks of COPD. The clinical and functional changes are noted in the following tables.
ANESTHETIC MANAGEMENT
Preoperative Evaluation
The surgical site and the preoperative status of the patient are critical factors in determining the incidence of postoperative complications. Multiple factors are predictive of postoperative respiratory difficulties, but no preoperative pulmonary function test establishes absolute contraindications to surgery. The preoperative evaluation of patients with COPD should determine the severity of the disease and identify treatments for reducing inflammation, improving secretion clearance, treating underlying infection, and increasing airway caliber that can ensure the best surgical outcome. Supplemental administration of O 2 usually is recommended if the Pa o2 is less than 60 mm Hg, if the hematocrit is greater than 55%, or if evidence of cor pulmonale is present.
Bronchodilators should be used if the patient exhibits some degree of airway obstruction and are listed in the following table.
| Drug | Formulation | Delivery Device | Adult Dosage |
|---|---|---|---|
| Short-Acting Beta 2 Agonists | |||
| Albuterol generic Proventil (Schering-Plough) | 90 mcg base/inhalation | MDI | 2 inhalations q4-6h PRN |
| Albuterol sulfate | |||
ProAir HFA (Teva) Proventil HFA (Schering-Plough) Related posts: Stay updated, free articles. Join our Telegram channel
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