Nursing Articles: Pulmonary Symptoms

Key components in the evaluation of patients with pulmonary symptoms are the history, physical examination, and, in most cases, a chest x-ray. These components establish the need for subsequent testing, which may include pulmonary function testing and ABG analysis

History

The history can often establish whether symptoms of dyspnea, chest pain, wheezing, stridor, hemoptysis, and cough are likely to be pulmonary in origin. When more than one symptom occurs concurrently, the history should focus on which symptom is primary and whether constitutional symptoms, such as fever, weight loss, and night sweats, are also present. Other important information includes occupational and environmental exposures; family history, travel history, and contact history; previous illnesses and use of prescription, OTC, or illicit drugs; and previous test results (eg, tuberculin skin test, chest x-rays).

Physical Examination

Physical examination starts with assessment of general appearance. Discomfort and anxiety, body habitus, and the effect of talking or movement on symptoms (eg, inability to speak full sentences without pausing to breathe) all can be assessed while greeting the patient and taking a history and may provide useful information relevant to pulmonary status. Next, inspection, auscultation, and chest percussion and palpation are done.

Inspection: Inspection should focus on

Signs of respiratory difficulty and hypoxemia (eg, restlessness, tachypnea, cyanosis, accessory muscle use)
Signs of possible chronic pulmonary disease (eg, clubbing, pedal edema)
Chest wall deformities
Abnormal breathing patterns (eg, Cheyne-Stokes respiration, Kussmal's respirations)
Jugular venous distention

Signs of hypoxemia include cyanosis (bluish discoloration of the lips, face, or nail beds), which signifies low arterial O₂ saturation (< 85%); the absence of cyanosis does not exclude the presence of hypoxemia.

Signs of respiratory difficulty include tachypnea and use of accessory respiratory muscles (sternocleidomastoids, intercostals, scalene) to breathe. Patients with COPD sometimes brace their arms against their legs or the examination table while seated (ie, tripod position) in a subconscious effort to provide more leverage to accessory muscles and thereby enhance respiration. Intercostal retractions (inward movement of the rib interspaces) are common among infants and older patients with severe airflow limitation; paradoxical breathing (inward motion of the abdomen during inspiration) signifies respiratory muscle fatigue or weakness.

Signs of possible chronic pulmonary disease include clubbing, barrel chest (the increased anterior-posterior diameter of the chest present in some patients with emphysema), and pursed lip breathing. Clubbing is enlargement of the fingertips (or toes) due to proliferation of connective tissue between the fingernail and the bone. Diagnosis is based on an increase in the profile angle of the nail as it exits the finger (to > 176°) or on an increase in the phalangeal depth ratio (to > 1—see Fig. 1: Approach to the Patient With Pulmonary Symptoms: Measuring finger clubbing.). “Sponginess” of the nail bed beneath the cuticle also suggests clubbing. Clubbing is most commonly observed in patients with lung cancer but is an important sign of chronic pulmonary disease, such as cystic fibrosis and idiopathic pulmonary fibrosis; it also occurs (but less commonly) in cyanotic heart disease, chronic infection (eg, infective endocarditis), stroke, inflammatory bowel disease, and cirrhosis. Clubbing occasionally occurs with osteoarthropathy and periostitis (primary or hereditary hypertrophic osteoarthropathy); in this instance, clubbing may be accompanied by skin changes, such as hypertrophied skin on the dorsa of the hands (pachydermoperiostosis), seborrhea, and coarse facial features. Digital clubbing can also occur as a benign hereditary abnormality that can be distinguished from pathologic clubbing by the absence of pulmonary symptoms or disease and by the presence of clubbing from an early age (by patient report).

Fig. 1

Measuring finger clubbing.

The ratio of the anteroposterior diameter of the finger at the nail bed (a–b) to that at the distal interphalangeal joint (c–d) is a simple measurement of finger clubbing. It can be obtained readily and reproducibly with calipers. If the ratio is > 1, clubbing is present. Finger clubbing is also characterized by loss of the normal angle at the nail bed.

Chest wall deformities, such as pectus excavatum and kyphoscoliosis, may restrict respirations and exacerbate symptoms of preexisting pulmonary disease.

Abnormal breathing patterns cause fluctuations in respiratory rate so respiratory rate should be assessed and counted for 1 min.

Cheyne-Stokes respiration (periodic breathing) is a cyclic fluctuation of respiratory rate and depth. From periods of brief apnea, patients breathe progressively faster and deeper (hyperpnea), then slower and shallower until they become apneic and repeat the cycle. Cheyne-Stokes respiration is most often caused by heart failure, a neurologic disorder (eg, stroke, advanced dementia), or drugs. The pattern in heart failure has been attributed to delays in cerebral circulation; respiratory centers lag in recognition of systemic acidosis/hypoxia (causing hyperpnea) of alkalosis/hypocapnia (causing apnea).
Biot's respiration is an uncommon variant of Cheyne-Stokes respiration in which irregular periods of apnea alternate with periods in which 4 or 5 deep, equal breaths are taken. It differs from Cheyne-Stokes respiration in that it is characterized by abrupt starts and stops and lacks periodicity. It results from injury to the CNS and occurs in such disorders as meningitis.
Kussmaul's respirations are deep, regular respirations caused by metabolic acidosis.

Jugular venous distention, sometimes observed during inspection, indicates an increase in right atrial and right ventricular pressure. The elevated pressure is usually caused by left ventricular dysfunction, but it may also be due to a pulmonary disorder causing pulmonary hypertension (. The presence of jugular venous distension should prompt a search for other signs of cardiac disorder (eg, a third heart sound [S₃ gallop], dependent edema).

Auscultation: Auscultation is arguably the most important component of the physical examination. All fields of the chest should be listened to, including the flanks, to detect abnormalities associated with each lobe of the lung. Features to listen for include

Character and volume of breath sounds
Presence or absence of vocal sounds
Pleural friction rubs
Ratio of inspiration to expiration (I : E ratio)

Cardiac auscultation, conducted simultaneously with pulmonary auscultation, may reveal signs of pulmonary hypertension, such as a loud pulmonic 2nd heart sound (P₂), and of right heart failure, such as a right ventricular 4th heart sound (S₄) and tricuspid regurgitation.

The character and volume of breath sounds are useful in identifying pulmonary disorders. Vesicular breath sounds are the normal sounds heard over most lung fields. Bronchial breath sounds are slightly louder, harsher, and higher pitched; they normally can be heard over the trachea and over areas of lung consolidation, such as occur with pneumonia. Pulmonary, pleural, and chest wall disorders cause chest pain; examples are

Pneumonia
Pulmonary embolism
Pleuritis
Lung cancer
Rib fractures

COUGH

Cough is an explosive expiratory maneuver that is reflexively or deliberately intended to clear the airways. It is the 5th most common symptom prompting physician visits.

Likely causes of cough (see Table 1: Approach to the Patient With Pulmonary Symptoms: Some Causes of Cough) differ depending on whether the symptom is acute (< 3 wk) or chronic.

In acute cough, the most common causes are

URI (including acute bronchitis)
Postnasal drip
COPD exacerbation
Pneumonia

In chronic cough, the most common causes are

Chronic bronchitis
Postnasal drip
Airway hyperresponsiveness after resolution of a viral or bacterial respiratory infection (ie, postinfection cough)
Gastroesophageal reflux

The causes in children are similar to those in adults, but asthma and foreign body aspiration may be more common.

Very rarely, impacted cerumen or a foreign body in the external auditory canal triggers reflex cough through stimulation of the auricular branch of the vagus nerve. Psychogenic cough is even rarer and is a diagnosis of exclusion.

Some Causes of Cough
Cause	Suggestive Findings	Diagnostic Approach
Acute
URI (including acute bronchitis)	Rhinorrhea Red, swollen nasal mucosa Sore throat Malaise	Clinical evaluation
Pneumonia (viral, bacterial, aspiration, rarely fungal)	Fever Productive cough Dyspnea Pleuritic chest pain Bronchial breath sounds or egophony	Chest x-ray Sputum and blood cultures in seriously ill patients and patients with hospital-acquired pneumonia
Postnasal drip (allergic, viral, or bacterial origin)	Headache Sore throat Nausea Cobblestoning of posterior oropharynx Pale, boggy, swollen nasal mucosa	Clinical evaluation Sometimes response to empiric antihistamine and decongestant therapy CT of the sinuses if diagnosis unclear
COPD exacerbation	Known diagnosis of COPD Poor breath sounds Wheezing Dyspnea Pursed lip breathing Use of accessory muscles Tripod positioning of the arms against the legs or examination table	Chest x-ray
Foreign body*	Sudden onset in a toddler who has no URI or constitutional symptoms	Chest x-ray (inspiratory and expiratory views) Bronchoscopy
Pulmonary embolism*	Pleuritic chest pain Dyspnea Tachycardia	CT angiography Ventilation-perfusion scanning
Heart failure*	Dyspnea Fine crackles on auscultation Extrasystolic heart sound Dependent peripheral edema	Chest x-ray Brain (B-type) natriuretic peptide level
Chronic
Chronic bronchitis (in smokers)	Productive cough on most days of the month or for 3 mo of the year /yr for 2 successive years in a patient with known COPD or smoking history Frequent clearing of the throat Dyspnea	Chest x-ray Pulmonary function testing
Postnasal drip (allergic most likely)	Headache Sore throat Cobblestoning of posterior oropharynx Pale, boggy, swollen nasal mucosa	Clinical evaluation Sometimes response to empiric antihistamine and decongestant therapy Allergy testing
Gastroesophageal reflux	Burning chest or abdominal pain that tends to worsen with consumption of certain foods, activities, or position Sour taste, particularly on awakening Hoarseness Chronic nocturnal or early morning cough	Clinical evaluation Response to empiric H₂-blocker or proton pump inhibitor therapy Sometimes 24-h esophageal pH probe if diagnosis unclear
Asthma (cough variant)	Cough in response to various provoking factors (eg, allergens, cold, exercise) Possibly wheezing and dyspnea	Pulmonary function testing Methacholine challenge Response to empiric bronchodilator therapy
Hyperresponsive airways after resolution of respiratory tract infection	Dry, nonproductive cough that may persist for weeks or months after an acute respiratory tract infection	Typically chest x-ray
ACE inhibitors	Dry, persistent cough that may occur within days or months after initiation of ACE inhibitor therapy	Response to stopping ACE inhibitor
Pertussis	Repeated bouts of ≥ 5 rapidly consecutive forceful coughs during a single expiration, followed by a hurried and deep inspiration (“whoop”) or post-tussive emesis	Cultures of nasopharyngeal specimens
Aspiration	Wet-sounding cough after eating or drinking	Chest x-ray Sometimes modified barium pharyngography Bronchoscopy
Tumor*	Atypical symptoms (eg, weight loss, fever, hemoptysis, night sweats) Lymphadenopathy	Chest x-ray If positive, chest CT and bronchoscopic biopsy
TB or fungal infections*	Atypical symptoms (eg, weight loss, fever, hemoptysis, night sweats) Exposure history Immunocompromise	Chest x-ray Skin testing; if positive, sputum cultures and stains for acid-fast bacilli and fungi Sometimes chest CT or bronchoalveolar lavage
*Indicates rare causes.

Evaluation

History: History of present illness should cover the duration and characteristics of the cough (eg, whether dry or productive of sputum or blood) and whether it is accompanied by dyspnea, chest pain, or both.

Review of symptoms should seek symptoms of possible cause, including runny nose and sore throat (URI, postnasal drip); fever, chills, and pleuritic chest pain (pneumonia); night sweats and weight loss (tumor, TB); heartburn (gastroesophageal reflux); and difficulty swallowing or choking episodes while eating or drinking (aspiration).

Past medical history should note recent respiratory infections (ie, within previous 1 to 2 mo); history of allergies, asthma, COPD, and gastroesophageal reflux disease; risk factors for (or known) TB or HIV infection; and smoking history. Drug history should specifically include use of ACE inhibitors. Patients with chronic cough should be asked about exposure to potential respiratory irritants or allergens and travel to or residence in regions with endemic fungal illness.

Physical examination: Vital signs should be reviewed for the presence of tachypnea and fever.

General examination should look for signs of respiratory distress and chronic illness (eg, wasting, lethargy).

Examination of the nose and throat should focus on appearance of the nasal mucosa (eg, color, congestion) and presence of discharge (external or in posterior pharynx). Ears should be examined for triggers of reflex cough.

The cervical and supraclavicular areas should be inspected and palpated for lymphadenopathy.

A full lung examination is done, particularly including adequacy of air entry and exit; symmetry of breath sounds; and presence of crackles, wheezes, or both. Signs of consolidation (eg, egophony, dullness to percussion) should be sought.

Red flags: The following findings are of particular concern:

Dyspnea
Hemoptysis
Weight loss
Risk factors for TB or HIV infection

Interpretation of findings: Some findings point to particular diagnoses

Other important findings are less specific. For example, the color (eg, yellow, green) and thickness of sputum do not help differentiate bacterial from other causes. Wheezing may occur with several causes. Hemoptysis in small amounts may occur with severe cough of many etiologies, although larger amounts of hemoptysis suggest bronchitis, bronchiectasis, TB, or primary lung cancer. Fever, night sweats, and weight loss may occur with many chronic infections as well as with cancer.

Testing: Patients with red flag findings of dyspnea or hemoptysis and patients in whom suspicion of pneumonia is high should have pulse oximetry and chest x-ray. Those with weight loss or risk factors should have chest x-ray and testing for TB and HIV infection.

For many patients without red flag findings, clinicians can make a diagnosis based on history and physical examination findings and begin treatment without testing. For patients without a clear cause but no red flag findings, many clinicians empirically begin treatment for postnasal drip (eg, antihistamine and decongestant combinations, nasal corticosteroid sprays) or gastroesophageal reflux disease (eg, proton pump inhibitors, H₂ blockers). An adequate response to these interventions usually precludes the need for further evaluation.

Patients with chronic cough in whom presumptive treatment is ineffective should have a chest x-ray. If the x-ray findings are unremarkable, many clinicians sequentially test for asthma (pulmonary function tests with methacholine challenge), sinus disease (sinus CT), and gastroesophageal reflux disease (esophageal pH monitoring). Sputum culture is helpful for patients with a possible indolent infection, such as pertussis, TB, or nontuberculous mycobacterial infection. Sputum cytology is noninvasive and should be done if cancer is suspected and the patient is producing sputum or having hemoptysis. Chest CT and possibly bronchoscopy should be done in patients in whom lung cancer or another bronchial tumor is suspected (eg, patients with a long smoking history, nonspecific constitutional signs) and in patients in whom empiric therapy has failed and who have inconclusive findings on preliminary testing.

Treatment

Treatment is management of the cause.

There is little evidence to support the use of cough suppressants or mucolytic agents. Coughing is an important mechanism for clearing secretions from the airways and can assist in recovery from respiratory infections. Therefore, although patients often expect or request cough suppressants, such treatment should be given with caution and reserved for patients with a URI and for patients receiving therapy for the underlying disorder for whom cough is still troubling.

Antitussives depress the medullary cough center ( dextromethorphan Some Trade Names
BENYLIN DM
DELSYM
DEXALONE
and codeine Some Trade Names
or anesthetize stretch receptors of vagal afferent fibers in bronchi and alveoli ( benzonatate Some Trade Names
TESSALON). Dextromethorphan Some Trade Names
BENYLIN DM
DELSYM
DEXALONE
, a congener of the opioid levorphanol Some Trade Names
LEVO-DROMORAN
is effective as a tablet or syrup at a dose of 15 to 30 mg po 1 to 4 times/day for adults or 0.25 mg/kg po qid for children. Codeine Some Trade Names
No US trade name
has antitussive, analgesic, and sedative effects, but dependence is a potential problem, and nausea, vomiting, constipation, and tolerance are common adverse effects. Usual doses are 10 to 20 mg po q 4 to 6 h as needed for adults and 0.25 to 0.5 mg/kg po qid for children. Other opioids (hydrocodone, hydromorphone Some Trade Names
DILAUDID, methadone Some Trade Names
DOLOPHINE
, morphine Some Trade Names
DURAMORPH
MS CONTIN
MSIR
ROXANOL
have antitussive properties but are avoided because of high potential for dependence and abuse. Benzonatate Some Trade Names
TESSALON
, a congener of tetracaine Some Trade Names
PONTOCAINE NIPHANOID
PONTOCAINE
that is available in liquid-filled capsules, is effective at a dose of 100 to 200 mg po tid.

Expectorants are thought to decrease viscosity and facilitate expectoration (coughing up) of secretions but are of limited benefit. Guaifenesin Some Trade Names
ROBITUSSIN
(200 to 400 mg po q 4 h in syrup or tablet form) is most commonly used because it has no serious adverse effects, but multiple expectorants exist, including bromhexine, ipecac, and saturated solution of K iodide (SSKI). Aerosolized expectorants such as N- acetylcysteine Some Trade Names
MUCOMYST
and DNAse are generally reserved for hospital-based treatment of cough in patients with bronchiectasis or cystic fibrosis. Ensuring adequate hydration may facilitate expectoration, as may inhalation of steam, although neither technique has been rigorously tested.

Topical treatments, such as acacia, licorice, glycerin, honey, and wild cherry cough drops or syrups (demulcents), are locally and perhaps emotionally soothing, but their use is not supported by scientific evidence.

Protussives, which stimulate cough, are indicated for such disorders as cystic fibrosis and bronchiectasis, in which a productive cough is thought to be important for airway clearance and preservation of pulmonary function. DNAse or hypertonic saline is given in conjunction with chest physical therapy and postural drainage to promote cough and expectoration. This approach is beneficial in cystic fibrosis but not in most other causes of chronic cough.

Bronchodilators, such as albuterol Some Trade Names
PROVENTIL
VENTOLIN
and ipratropium Some Trade Names
ATROVENT
or inhaled corticosteroids, can be effective for cough after URI and in cough-variant asthma.

Key Points

Danger signs include respiratory distress, chronic fever, weight loss, and hemoptysis.
Clinical diagnosis is usually adequate.
Remember occult gastroesophageal reflux disease.
Antitussives and expectorants should be used selectively.

Dyspnea

Dyspnea is unpleasant or uncomfortable breathing. It is experienced and described differently by patients depending on the cause.

Pathophysiology

Although dyspnea is a relatively common problem, the pathophysiology of the uncomfortable sensation of breathing is poorly understood. Unlike those for other types of noxious stimuli, there are no specialized dyspnea receptors, although recent MRI studies have identified a few specific areas in the midbrain that may mediate perception of dyspnea.

The experience of dyspnea likely results from a complex interaction between chemoreceptor stimulation, mechanical abnormalities in breathing, and the perception of those abnormalities by the CNS. Some authors have described the imbalance between neurologic stimulation and mechanical changes in the lungs and chest wall as neuromechanical uncoupling.

Etiology

Dyspnea has many pulmonary, cardiac, and other causes, which vary by acuity of onset (see Table 2: Approach to the Patient With Pulmonary Symptoms: Some Causes of Dyspnea).

The most common causes include

Asthma
Pneumonia
COPD
Myocardial ischemia
Deconditioning

The most common cause of dyspnea in patients with chronic pulmonary or cardiac disorders is

Exacerbation of their disease

However, such patients may also acutely develop another condition (eg, a patient with long-standing asthma may have an MI, a patient with chronic heart failure may develop pneumonia).

Table 2

Some Causes of Dyspnea
Cause	Suggestive Findings	Diagnostic Approach*
Acute (within minutes)
*Pulmonary causes*
Pneumothorax	Abrupt onset of sharp chest pain, tachypnea, diminished breath sounds, and hyperresonance to percussion May follow injury or occur spontaneously (especially in tall, thin patients and in patients with COPD)	Chest x-ray
Pulmonary embolism	Abrupt onset of sharp chest pain, tachypnea, and tachycardia Often risk factors for pulmonary embolism (eg, cancer, immobilization, DVT, pregnancy, use of oral contraceptives or other estrogen-containing drugs, recent surgery or hospitalization, family history)	CT angiography or V/Q scanning Doppler or duplex studies of extremities showing positive findings of DVT
Asthma, bronchospasm, or reactive airway disease	Wheezing and poor air exchange that arise spontaneously or after exposure to specific stimuli (eg, allergen, URI, cold, exercise) Possibly pulsus paradoxus Often a preexisting history of reactive airway disease	Clinical evaluation Sometimes pulmonary function testing or bedside peak flow measurement
Foreign body inhalation	Sudden onset of cough or stridor in a patient (typically an infant or young child) without URI or constitutional symptoms	Inspiratory and expiratory chest x-rays Sometimes bronchoscopy
Toxic airway damage (eg, inhalation of chlorine or hydrogen sulfide)	Sudden onset after occupational exposure or inappropriate use of cleaning agents	Inhalation usually obvious by history Chest x-ray Sometimes ABGs and observation to determine severity
*Cardiac causes*
Acute myocardial ischemia or infarction	Substernal chest pressure with or without radiation to the arm or jaw, particularly in patients with risk factors for CAD	ECG Cardiac enzyme testing
Papillary muscle dysfunction or rupture	Sudden onset of chest pain, new or loud holosystolic murmur, and signs of heart failure, particularly in patients with recent MI	Auscultation Echocardiography
Heart failure	Crackles, S₃ gallop, and signs of central or peripheral volume overload (eg, elevated neck veins, peripheral edema) Dyspnea while lying flat (orthopnea) or appearing 1–2 h after falling asleep (paroxysmal nocturnal dyspnea)	Auscultation Chest x-ray BNP measurement Echocardiography
*Other causes*
Diaphragmatic paralysis	Sudden onset after trauma affecting the phrenic nerve Frequent orthopnea	Chest x-ray Fluoroscopic sniff test
Anxiety disorder—hyperventilation	Situational dyspnea often accompanied by psychomotor agitation and paresthesias in the fingers or around the mouth Normal examination findings and pulse oximetry measurements	Clinical evaluation Diagnosis of exclusion
Subacute (within hours or days)
*Pulmonary causes*
Pneumonia	Fever, productive cough, dyspnea, sometimes pleuritic chest pain Focal lung findings, including crackles, decreased breath sounds, and egophony	Chest x-ray Sometimes blood and sputum cultures WBC count
COPD exacerbation	Cough, productive or nonproductive Poor air movement Accessory muscle use or pursed lip breathing	Clinical evaluation Sometimes chest x-ray and ABGs
*Cardiac causes*
Angina or CAD	Substernal chest pressure with or without radiation to the arm or jaw, often provoked by physical exertion, particularly in patients with risk factors for CAD	ECG Cardiac stress testing Cardiac catheterization
Pericardial effusion or tamponade	Muffled heart sounds or enlarged cardiac silhouette in patients with risk factors for pericardial effusion (eg, cancer, pericarditis, SLE) Possibly pulsus paradoxus	Echocardiography
Chronic (hours to years)
*Pulmonary causes*
Obstructive lung disease	Extensive smoking history, barrel chest, and poor air entry and exit	Chest x-ray Pulmonary function testing (at initial evaluation)
Restrictive lung disease	Progressive dyspnea in patients with known occupational exposure or neurologic condition	Chest x-ray Pulmonary function testing (at initial evaluation)
Interstitial lung disease	Fine crackles on auscultation	High-resolution chest CT
Pleural effusion	Pleuritic chest pain and lung field that is dull to percussion with diminished breath sounds Sometimes history of cancer, heart failure, RA, SLE, or acute pneumonia	Chest x-ray Often chest CT and thoracentesis
*Cardiac causes*
Heart failure	Crackles, S₃ gallop, and signs of central or peripheral volume overload (eg, elevated neck veins, peripheral edema) Orthopnea or paroxysmal nocturnal dyspnea	Auscultation Chest x-ray Echocardiography
Stable angina or CAD	Substernal chest pressure with or without radiation to the arm or jaw, often provoked by physical exertion, particularly in patients with risk factors for CAD	ECG Cardiac stress testing Sometimes cardiac catheterization
*Other causes*
Anemia	Dyspnea on exertion progressing to dyspnea at rest Normal lung examination and pulse oximetry measurement Sometimes systolic heart murmur due to increased flow	CBC
Physical deconditioning	Dyspnea only on exertion in patients with sedentary lifestyle	Clinical evaluation
*Most patients should have pulse oximetry and, unless symptoms are clearly a mild exacerbation of known chronic disease, chest x-ray.
BNP = Brain (B-type) natriuretic peptide; CAD = coronary artery disease; DVT = deep venous thrombosis; S₃ = 3rd heart sound; V/Q = ventilation/perfusion.

Evaluation

History: History of present illness should cover the duration, temporal onset (eg, abrupt, insidious), and provoking or exacerbating factors (eg, allergen exposure, cold, exertion, supine position). Severity can be determined by assessing the activity level required to produce dyspnea (ie, dyspnea at rest is more severe than dyspnea only with climbing stairs). For patients with baseline dyspnea, the physician should note how much dyspnea has changed from the patient's usual state.

Review of systems should seek symptoms of possible causes, including chest pain or pressure (pulmonary embolism [PE], myocardial ischemia, pneumonia); dependent edema, orthopnea, and paroxysmal nocturnal dyspnea (heart failure); fever, chills, cough, and sputum production (pneumonia); black, tarry stools or heavy menses (occult bleeding possibly causing anemia); and weight loss or night sweats (cancer or chronic lung infection).

Past medical history should cover disorders known to cause dyspnea, including asthma, COPD, and heart disease, as well as risk factors for the different etiologies:

Smoking history—for cancer, COPD, and heart disease
Family history, hypertension, and high cholesterol levels—for coronary artery disease
Recent immobilization or surgery, recent long-distance travel, cancer or risk factors for or signs of occult cancer, prior or family history of clotting, pregnancy, oral contraceptive use, calf pain, leg swelling, and known deep venous thrombosis—for PE

Occupational exposures (eg, gases, smoke, asbestos) should be investigated.

Physical examination: Vital signs are reviewed for fever, tachycardia, and tachypnea.

Examination focuses on the cardiovascular and pulmonary systems.

A full lung examination is done, particularly including adequacy of air entry and exit, symmetry of breath sounds, and presence of crackles, rhonchi, stridor, and wheezes. Signs of consolidation (eg, egophony, dullness to percussion) should be sought. The cervical, supraclavicular, and inguinal areas should be inspected and palpated for lymphadenopathy.

Neck veins should be inspected for distention, and the legs and presacral area should be palpated for pitting edema (both suggesting heart failure).

Heart sounds should be auscultated with notation of any extra heart sounds, muffled heart sounds, or murmur. Testing for pulsus paradoxus (a > 12 mm Hg drop of systolic BP during inspiration) can be done by inflating a BP cuff to 20 mm Hg above the systolic pressure and then slowly deflating until the first Korotkoff sound is heard only during expiration. As the cuff is further deflated, the point at which the first Korotkoff sound is audible during both inspiration and expiration is recorded. If the difference between the first and second measurement is > 12 mm Hg, then pulsus paradoxus is present.

Conjunctiva should be examined for pallor. Rectal examination and stool guaiac testing should be done.

Red flags: The following findings are of particular concern:

Dyspnea at rest during examination
Decreased level of consciousness or agitation or confusion
Accessory muscle use and poor air excursion
Chest pain
Crackles
Weight loss
Night sweats

Interpretation of findings: The history and physical examination often suggest a cause and guide further testing (see Table 2: Approach to the Patient With Pulmonary Symptoms: Some Causes of Dyspnea). Several findings are of note. Wheezing (see Approach to the Patient With Pulmonary Symptoms: Wheezing) suggests asthma or COPD. Stridor (see Approach to the Patient With Pulmonary Symptoms: Stridor) suggests extrathoracic airway obstruction (eg, foreign body, epiglottitis, vocal cord dysfunction). Crackles suggest left heart failure, interstitial lung disease, or if accompanied by signs of consolidation, pneumonia.

However, the signs and symptoms of life-threatening conditions such as myocardial ischemia and PE can be nonspecific. Furthermore, the severity of symptoms is not always proportional to the severity of the cause (eg, PE in a fit, healthy person may cause only mild dyspnea). Thus, a high degree of suspicion for these common conditions is prudent. It is often appropriate to rule out these conditions before attributing dyspnea to a less serious etiology.

A clinical prediction rule (see Approach to the Cardiac Patient: Clinical Prediction Rule for Diagnosing Pulmonary Embolism and see Approach to the Cardiac Patient: PE testing algorithm) can help estimate the risk for PE. Note that a normal O₂ saturation does not exclude PE.

Hyperventilation syndrome is a diagnosis of exclusion. Because hypoxia may cause tachypnea and agitation, it is unwise to assume every rapidly breathing, anxious young person merely has hyperventilation syndrome.

Testing: Pulse oximetry should be done in all patients, and a chest x-ray should be done as well unless symptoms are clearly caused by a mild or moderate exacerbation of a known condition. For example, patients with asthma or heart failure do not require an x-ray for each flare-up, unless clinical findings suggest another cause or an unusually severe attack. Most adults should have an ECG to detect myocardial ischemia (and serum cardiac marker testing if suspicion is high) unless myocardial ischemia can be excluded clinically.

In patients with severe or deteriorating respiratory status, ABGs should be measured to more precisely quantify hypoxemia, measure PaCO₂, diagnose any acid-base disorders stimulating hyperventilation, and calculate the alveolar-arterial gradient.

Patients who have no clear diagnosis after chest x-ray and ECG and are at moderate or high risk of having PE (from the clinical prediction rule—see Approach to the Cardiac Patient: PE testing algorithm and see Approach to the Cardiac Patient: Clinical Prediction Rule for Diagnosing Pulmonary Embolism) should undergo ventilation/perfusion scanning or CT-angiography. Patients who are at low risk may have D-dimer testing (to detect the presence of clot); a normal D-dimer level effectively rules out PE in a low-risk patient.

Chronic dyspnea may warrant additional tests, such as CT scanning, pulmonary function tests, echocardiography, and bronchoscopy.

Treatment

Treatment is correction of the underlying disorder.

Hypoxemia is treated with supplemental O₂ as needed to maintain SaO₂ > 88% or PaO₂ > 55 mm Hg, as levels above these thresholds provide adequate O₂ delivery to tissues. Levels below these thresholds are on the steep portion of the O₂–Hb dissociation curve, in which small declines in arterial O₂ tension result in large declines in Hb saturation. O₂ saturation should be maintained at > 93% if myocardial or cerebral ischemia is a concern.

Morphine Some Trade Names
DURAMORPH
MS CONTIN
MSIR
ROXANOL
Click for Drug Monograph
0.5 to 5 mg IV helps reduce anxiety and the discomfort of dyspnea in various conditions, including MI, PE, and the dyspnea that commonly accompanies terminal illness. However, opioids can be deleterious in patients with acute airflow limitation (eg, asthma, COPD) because they suppress the ventilatory drive and worsen respiratory acidemia.

Key Points

Pulse oximetry is a key component of the examination.
Low O₂ saturation (< 90%) indicates a significant problem, but normal saturation does not rule one out.
Accessory muscle use, low O₂ saturation, or decreased level of consciousness requires emergency evaluation and hospitalization.
Myocardial ischemia and PE are relatively common, but symptoms and signs can be nonspecific.
Exacerbation of known conditions (eg, asthma, COPD, heart failure) is common, but such patients also may develop new problems.

Hemoptysis

Hemoptysis is coughing up of blood from the respiratory tract. Massive hemoptysis is production of ≥ 600 mL of blood (about a full kidney basin's worth) within 24 h.

Pathophysiology

Most of the lung's blood (95%) circulates through low-pressure pulmonary arteries and ends up in the pulmonary capillary bed, where gas is exchanged. About 5% of the blood supply circulates through high-pressure bronchial arteries, which originate at the aorta and supply major airways and supporting structures. In hemoptysis, the blood generally arises from this bronchial circulation, except when pulmonary arteries are damaged by trauma, by erosion of a granulomatous or calcified lymph node or tumor, or, rarely, by pulmonary arterial catheterization or when pulmonary capillaries are affected by inflammation.

Etiology

Blood-streaked sputum is common in many minor respiratory illnesses, such as URI and viral bronchitis.

The differential diagnosis is broad.

In adults, 70 to 90% of cases are caused by

Bronchitis
Bronchiectasis
TB
Necrotizing pneumonia

Primary lung cancer is an important cause in smokers ≥ 40 yr, but metastatic cancer rarely causes hemoptysis. Cavitary Aspergillus infection is increasingly recognized as a cause but is not as common as cancer.

In children, common causes are

Lower respiratory tract infection
Foreign body aspiration

Massive hemoptysis: The most common causes have changed over time and vary by geographic region but include the following:

Bronchogenic carcinoma
Bronchiectasis
Tuberculous and other pneumonias

Table 3

Evaluation

History: History of present illness should cover the duration and temporal patterns (eg, abrupt onset, cyclical recurrence), provoking factors (eg, allergen exposure, cold, exertion, supine position), and approximate volume of hemoptysis (eg, streaking, teaspoon, cup). Patients may need specific prompting to differentiate between true hemoptysis, pseudohemoptysis (ie, bleeding originating in the nasopharynx that is subsequently coughed up), and hematemesis. A sensation of postnasal drip or any bleeding from the nares without coughing is suggestive of pseudohemoptysis. Concomitant nausea and vomiting with black, brown, or coffee-ground–colored blood is characteristic of hematemesis. Frothy sputum, bright red blood, and (if massive) a sensation of choking are characteristic of true hemoptysis.

Review of systems should seek symptoms suggesting possible causes, including fever and sputum production (pneumonia); night sweats, weight loss, and fatigue (cancer, TB); chest pain and dyspnea (pneumonia, pulmonary embolism); leg pain and leg swelling (pulmonary embolism); hematuria (Goodpasture's syndrome); and bloody nasal discharge (Wegener's granulomatosis).

Patients should be asked about risk factors for causes. These factors include HIV infection, use of immunosuppressants (TB, fungal infection); exposure to TB; long smoking history (cancer); and recent immobilization or surgery, known cancer, prior or family history of clotting, pregnancy, use of estrogen-containing drugs, and recent long-distance travel (pulmonary embolism).

Past medical history should cover known conditions that can cause hemoptysis, including chronic lung disease (COPD, bronchiectasis, TB, cystic fibrosis), cancer, bleeding disorders, heart failure, thoracic aortic aneurysm, and pulmonary-renal syndromes (eg, Goodpasture's syndrome, Wegener's granulomatosis). Exposure to TB is important, particularly in patients with HIV infection or another immunocompromised state.

A history of frequent nosebleeds, easy bruising, or liver disease suggests possible coagulopathy. The drug profile should be reviewed for use of anticoagulants and antiplatelet drugs.

Physical examination: Vital signs are reviewed for fever, tachycardia, tachypnea, and low O₂ saturation. Constitutional signs (eg, cachexia) and level of patient distress (eg, accessory muscle use, pursed lip breathing, agitation, decreased level of consciousness) should also be noted.

A full lung examination is done, particularly including adequacy of air entry and exit, symmetry of breath sounds, and presence of crackles, rhonchi, stridor, and wheezing. Signs of consolidation (eg, egophony, dullness to percussion) should be sought. The cervical and supraclavicular areas should be inspected and palpated for lymphadenopathy (suggesting cancer or TB).

Neck veins should be inspected for distention, and the legs and presacral area should be palpated for pitting edema (suggesting heart failure). Heart sounds should be auscultated with notation of any extra heart sounds or murmur that might support a diagnosis of heart failure and elevated pulmonary pressure.

The abdominal examination should focus on signs of hepatic congestion or masses, which could suggest either cancer or hematemesis from potential esophageal varices.

The skin and mucous membranes should be examined for ecchymoses, petechiae, telangiectasia, gingivitis, or evidence of bleeding from the oral or nasal mucosa.

If the patient can reproduce hemoptysis during examination, the color and amount of blood should be noted.

Red flags: The following findings are of particular concern:

Massive hemoptysis
Back pain
Presence of a pulmonary artery catheter
Malaise, weight loss, fatigue
Extensive smoking history
Dyspnea at rest during examination or absent or decreased breath sounds

Interpretation of findings: The history and physical examination often suggest a diagnosis and guide further testing (see Table 3: Approach to the Patient With Pulmonary Symptoms: Some Causes of Hemoptysis).

Despite the many possibilities, some generalities can be made. A previously healthy person with a normal examination and no risk factors (eg, for TB, pulmonary embolism) who presents with acute-onset cough and fever most likely has hemoptysis from an acute respiratory illness; chronic disorders are much lower on the list of possibilities. However, if risk factors are present, those specific disorders must be strongly suspected. A clinical prediction rule (see Approach to the Cardiac Patient: Clinical Prediction Rule for Diagnosing Pulmonary Embolism and see Approach to the Cardiac Patient: PE testing algorithm) can help estimate the risk for pulmonary embolism. A normal O₂ saturation does not exclude pulmonary embolism.

Patients whose hemoptysis is from a lung disorder (eg, COPD, cystic fibrosis, bronchiectasis) or heart disease (eg, heart failure) typically have a clear history of those disorders. Hemoptysis is not an initial manifestation.

Patients with known immunocompromise should be suspected of having TB or a fungal infection.

Patients with symptoms or signs of chronic illness but no known disorders should be suspected of having cancer or TB, although hemoptysis can be the initial manifestation of lung cancer in a patient who is otherwise asymptomatic.

Several specific findings are of note. Known renal failure or hematuria suggests a pulmonary-renal syndrome (eg, Goodpasture's syndrome, Wegener's granulomatosis). Patients with Wegener's granulomatosis may have nasal mucosal lesions. Visible telangiectasias suggest arteriovenous malformations. Patients with hemoptysis due to a bleeding disorder usually have cutaneous findings (petechiae, purpura, or both) or a history of anticoagulant or antiplatelet drug use. Recurrent hemoptysis coinciding with menses strongly suggests pulmonary endometriosis.

Testing: Patients with massive hemoptysis require treatment and stabilization, usually in an ICU, before testing. Patients with minor hemoptysis can undergo outpatient testing.

Imaging is always done. A chest x-ray is mandatory. Patients with normal results, a consistent history, and nonmassive hemoptysis can undergo empiric treatment for bronchitis. Patients with abnormal results and patients without a supporting history should undergo CT and bronchoscopy. CT may reveal pulmonary lesions that are not apparent on the chest x-ray and can help locate lesions in anticipation of bronchoscopy and biopsy. Ventilation/perfusion scanning or CT angiography can confirm the diagnosis of pulmonary embolism. CT and pulmonary angiography can also detect pulmonary arteriovenous fistulas.

Fiberoptic inspection of the pharynx, larynx, and airways may be indicated along with esophagogastric endoscopy when the etiology is obscure to distinguish hemoptysis from hematemesis and from nasopharyngeal or oropharyngeal bleeding.

Laboratory testing is also done. Patients usually should have a CBC, a platelet count, and measurement of PT and PTT. Anti-factor Xa testing can be used to detect supratherapeutic anticoagulation in patients receiving low mol wt heparin Some Trade Names
HEPFLUSH-10
Click for Drug Monograph
. Urinalysis should be done to look for signs of glomerulonephritis (hematuria, proteinuria, or casts). TB skin testing and sputum culture should be done as the initial tests for active TB, but negative results do not preclude the need to induce sputum or do fiberoptic bronchoscopy to obtain samples for further acid-fast bacillus testing if an alternative diagnosis is not found.

Cryptogenic hemoptysis: The cause of hemoptysis remains unknown in 30 to 40% of cases, but the prognosis for patients with cryptogenic hemoptysis is generally favorable, usually with resolution of bleeding within 6 mo of evaluation.

Treatment

Massive hemoptysis: Initial treatment of massive hemoptysis has two objectives:

Prevent aspiration of blood into the uninvolved lung (which can cause asphyxiation)
Prevent exsanguination from ongoing bleeding

It can be difficult to protect the uninvolved lung because it is often initially unclear which side is bleeding. Once the bleeding side is identified, strategies include positioning the patient with the bleeding lung in a dependent position and selective intubation and obstruction of the bronchus going to the bleeding lung.

Prevention of exsanguination involves reversal of any bleeding diathesis and direct efforts to stop the bleeding. Clotting deficiencies can be reversed with fresh-frozen plasma and factor-specific or platelet transfusions. Laser therapy, cauterization, or direct injection with epinephrine Some Trade Names
ADRENALIN
PRIMATENE MIST
Click for Drug Monograph
or vasopressin Some Trade Names
PITRESSIN
Click for Drug Monograph
can be done bronchoscopically.

Massive hemoptysis is one of the few indications for rigid (as opposed to flexible) bronchoscopy, which provides control of the airway, allows for a larger field of view than flexible bronchoscopy, allows better suctioning, and is more suited to therapeutic interventions, such as laser therapy.

Embolization of a pulmonary segment via bronchial artery catheterization is becoming the preferred method with which to stop massive hemoptysis, with reported success rates of up to 90%. Emergency surgery is indicated for massive hemoptysis not controlled by rigid bronchoscopy or embolization and is generally considered a last resort.

Once a diagnosis is made, further treatment is directed at the cause.

Minor hemoptysis: Treatment of minor hemoptysis is directed at the cause.

Early resection may be indicated for bronchial adenoma or carcinoma. Broncholithiasis (erosion of a calcified lymph node into an adjacent bronchus) may require pulmonary resection if the stone cannot be removed via rigid bronchoscopy. Bleeding secondary to heart failure or mitral stenosis usually responds to specific therapy for heart failure. In rare cases, emergency mitral valvulotomy is necessary for life-threatening hemoptysis due to mitral stenosis.

Bleeding from a pulmonary embolism is rarely massive and almost always stops spontaneously. If emboli recur and bleeding persists, anticoagulation may be contraindicated, and placement of an inferior vena cava filter is the treatment of choice.

Because bleeding from bronchiectatic areas usually results from infection, treatment of the infection with appropriate antibiotics and postural drainage is essential.

Key Points

Hemoptysis needs to be distinguished from hematemesis and nasopharyngeal or oropharyngeal bleeding.
Bronchitis, bronchiectasis, TB, and necrotizing pneumonia or lung abscess are the most common causes in adults.
Lower respiratory tract infection and foreign body aspiration are the most common causes in children.
Patients with massive hemoptysis require treatment and stabilization before testing.
With massive hemoptysis, if the side of bleeding is known, patients should be positioned with the affected lung in the dependent position.
Bronchial artery embolization is the preferred treatment for massive hemoptysis

Table 3

Some Causes of Hemoptysis
Cause	Suggestive Findings	Diagnostic Approach*
Tracheobronchial source
Tumor (bronchogenic, bronchial metastatic, Kaposi's sarcoma)	Night sweats Weight loss History of heavy smoking Risk factors for Kaposi's sarcoma (eg, HIV)	Chest x-ray CT Bronchoscopy
Bronchitis (acute or chronic)	Acute: Productive or nonproductive cough Chronic: Cough on most days of the month or for 3 mo/yr for 2 successive years in patients with known COPD or smoking history	Acute: Clinical evaluation Chronic: Chest x-ray
Bronchiectasis	Chronic cough and mucus production in patients with a history of recurrent infections	High-resolution chest CT Bronchoscopy
Broncholithiasis	Calcified lymph nodes in patients with history of prior granulomatous disease	Chest CT Bronchoscopy
Foreign body (chronic undiagnosed, not acute)	Chronic cough (typically in an infant or young child) without URI symptoms Sometimes fever	Chest x-ray Sometimes bronchoscopy
Pulmonary parenchymal source
Lung abscess	Subacute fever Cough Night sweats Anorexia Weight loss	Chest x-ray or CT showing irregularly shaped cavity with air-fluid levels
Pneumonia	Fever, productive cough, dyspnea, and pleuritic chest pain Decreased breath sounds or egophony Elevated WBC count	Chest x-ray Blood and sputum cultures in hospitalized patients
Active granulomatous disease (tuberculous, fungal, parasitic, syphilitic) or mycetoma (fungus ball)	Fever, cough, night sweats, and weight loss in patients with known exposures Often history of immunosuppression	Chest x-ray Chest CT Microbiologic testing of sputum samples or bronchoscopy washings
Goodpasture's syndrome	Fatigue Weight loss Often hematuria Sometimes edema	Urinalysis Creatinine levels Renal biopsy Antiglomerular basement membrane testing cANCA testing
Wegener's granulomatosis	Often chronic, bloody nasal discharge and nasal ulcerations Often joint pains and skin manifestations (nodules, purpura) Gingival thickening and mulberry gingivitis Saddle nose and nasal septum perforation Sometimes renal insufficiency	Biopsy of any affected area (eg, kidney, skin) with cANCA testing and demonstration of vasculitis in small to medium-sized arteries Bronchoscopy
Lupus pneumonitis	Fever, cough, dyspnea, and pleuritic chest pain in patients with a history of SLE	Chest CT (showing alveolitis) Sometimes bronchoscopy washings (showing lymphocytosis or granulocytosis)
Primary vascular source
Arteriovenous malformation	Presence of mucocutaneous telangiectasia or peripheral cyanosis	CT angiography of the chest Pulmonary angiography
Pulmonary embolism	Abrupt onset of sharp chest pain, increased respiratory rate and heart rate, particularly in patients with known risk factors for pulmonary embolism (see Approach to the Patient With Pulmonary Symptoms: History )	CT angiography or V/Q scanning Doppler or duplex studies of extremities showing positive findings of DVT
Elevated pulmonary venous pressure (especially mitral stenosis, left-sided heart failure)	Crackles Signs of central or peripheral volume overload (eg, elevated neck veins, peripheral edema) Dyspnea while lying flat (orthopnea) or appearing 1–2 h after falling asleep (paroxysmal nocturnal dyspnea)	ECG BNP measurement Echocardiography
Aortic aneurysm with leakage into the pulmonary parenchyma	Back pain	Chest x-ray showing widened mediastinum Chest CT angiography
Pulmonary artery rupture	Recent placement or manipulation of a pulmonary artery catheter	Emergency chest CT angiography or emergency pulmonary angiography
Miscellaneous
Pulmonary endometriosis (catamenial hemoptysis)	Recurrent hemoptysis during menstruation	Clinical evaluation Sometimes therapeutic trial of oral contraceptives
Systemic coagulopathy or use of anticoagulants or thrombolytics	Patients undergoing systemic anticoagulation for treatment of pulmonary embolism, DVT, or atrial fibrillation Patients receiving thrombolytics for treatment of stroke or MI Sometimes a family history	PT/PTT or anti-factor Xa levels Cessation of hemoptysis with correction of coagulation deficit
* All patients with hemoptysis should have chest x-ray and pulse oximetry. BNP = Brain (B-type) natriuretic peptide; cANCA = antineutrophil cytoplasmic antibody; DVT = deep venous thrombosis; V/Q = ventilation/perfusion.

Evaluation

A history of frequent nosebleeds, easy bruising, or liver disease suggests possible coagulopathy. The drug profile should be reviewed for use of anticoagulants and antiplatelet drugs.

The abdominal examination should focus on signs of hepatic congestion or masses, which could suggest either cancer or hematemesis from potential esophageal varices.

The skin and mucous membranes should be examined for ecchymoses, petechiae, telangiectasia, gingivitis, or evidence of bleeding from the oral or nasal mucosa.

If the patient can reproduce hemoptysis during examination, the color and amount of blood should be noted.

Red flags: The following findings are of particular concern:

Massive hemoptysis
Back pain
Presence of a pulmonary artery catheter
Malaise, weight loss, fatigue
Extensive smoking history
Dyspnea at rest during examination or absent or decreased breath sounds

Patients with known immunocompromise should be suspected of having TB or a fungal infection.

Testing: Patients with massive hemoptysis require treatment and stabilization, usually in an ICU, before testing. Patients with minor hemoptysis can undergo outpatient testing.

Treatment

Massive hemoptysis: Initial treatment of massive hemoptysis has two objectives:

Prevent aspiration of blood into the uninvolved lung (which can cause asphyxiation)
Prevent exsanguination from ongoing bleeding

Once a diagnosis is made, further treatment is directed at the cause.

Minor hemoptysis: Treatment of minor hemoptysis is directed at the cause.

Because bleeding from bronchiectatic areas usually results from infection, treatment of the infection with appropriate antibiotics and postural drainage is essential.

Key Points

Hemoptysis needs to be distinguished from hematemesis and nasopharyngeal or oropharyngeal bleeding.
Bronchitis, bronchiectasis, TB, and necrotizing pneumonia or lung abscess are the most common causes in adults.
Lower respiratory tract infection and foreign body aspiration are the most common causes in children.
Patients with massive hemoptysis require treatment and stabilization before testing.
With massive hemoptysis, if the side of bleeding is known, patients should be positioned with the affected lung in the dependent position.
Bronchial artery embolization is the preferred treatment for massive hemoptysis.

Wheezing

Wheezing is a relatively high-pitched whistling noise produced by movement of air through narrowed or compressed small airways. It is a symptom as well as a physical finding.

Pathophysiology

Airflow through a narrowed or compressed segment of a small airway becomes turbulent, causing vibration of airway walls; this vibration produces the sound of wheezing.

Wheezes are more common during expiration because increased intrathoracic pressure during this phase narrows the airways. Wheezing during expiration alone indicates milder obstruction than wheezing during both inspiration and expiration, which suggests more severe airway narrowing.

By contrast, turbulent flow of air through a narrowed segment of the large, extrathoracic airways produces a whistling inspiratory noise (stridor—see Approach to the Patient With Pulmonary Symptoms: Stridor).

Etiology

Small airway narrowing may be caused by bronchoconstriction, mucosal edema, external compression, or partial obstruction by a tumor, foreign body, or thick secretions.

Overall, the most common causes are

Asthma
COPD

But wheezing may occur in other disorders affecting the small airways, including heart failure (cardiac asthma), anaphylaxis, and toxic inhalation. Sometimes, healthy patients manifest wheezing during a bout of acute bronchitis. In children, bronchiolitis and foreign body aspiration are also causes

Some Causes of Wheezing
Cause	Suggestive Findings	Diagnostic Approach*
Acute bronchitis	URI symptoms No known history of lung disease	Clinical evaluation
Allergic reaction	Sudden onset, usually within 30 min of exposure to known or potential allergen Often accompanied by nasal congestion, urticaria, itchy eyes, and sneezing	Clinical evaluation
Asthma	Often known history of asthma Wheezing arising spontaneously or after exposure to specific stimuli (eg, allergen, URI, cold, exercise)	Clinical evaluation Sometimes pulmonary function testing, bedside peak flow measurement, methacholine challenge, or observation of response to empiric bronchodilators
Bronchiolitis	In children < 18 mo (usually during Nov–Apr in the Northern Hemisphere) Usually URI symptoms and tachypnea	Clinical evaluation
COPD exacerbation	Middle-aged or elderly patient Often known history of COPD Extensive smoking history Poor breath sounds Dyspnea Pursed lip breathing Use of accessory muscles	Clinical evaluation Sometimes chest x-ray and ABG measurement
Drugs (eg, ACE inhibitors, aspirin Some Trade Names BUFFERIN ECOTRIN GENACOTE , β-blockers, NSAIDs)	Recent initiation of a new drug, most often in a patient with a history of reactive airway disease	Clinical evaluation
Endobronchial tumors	Fixed and constant inspiratory and expiratory wheezes, especially in a patient with risk factors for or signs of cancer (eg, smoking history, night sweats, weight loss, hemoptysis) May be focal rather than diffuse	Chest x-ray or CT Bronchoscopy
Foreign body	Sudden onset in a young child who has no URI or constitutional symptoms	Chest x-ray or CT Bronchoscopy
GERD with chronic aspiration	Chronic or recurrent wheezing, often with heartburn and nocturnal cough No URI or allergic symptoms	Trial of acid-suppressing drugs Sometimes esophageal pH monitoring
Inhaled irritants	Sudden onset after occupational exposure or inappropriate use of cleaning agents	Clinical evaluation
Left-sided heart failure with pulmonary edema (cardiac asthma)	Crackles and signs of central or peripheral volume overload (eg, distended neck veins, peripheral edema) Dyspnea while lying flat (orthopnea) or appearing 1–2 h after falling asleep (paroxysmal nocturnal dyspnea)	Chest x-ray ECG BNP measurement Echocardiography
*Most patients should have pulse oximetry. Unless symptoms are very mild or are clearly an exacerbation of a known chronic disease, chest x-ray should be done.
BNP = Brain natriuretic peptide; GERD = gastroesophageal reflux disease.

Evaluation

When patients are in significant respiratory distress, evaluation and treatment proceed at the same time.

History: History of present illness should determine whether the wheezing is new or recurrent. If recurrent, patients are asked the previous diagnosis and whether current symptoms are different in nature or severity. Particularly when the diagnosis is unclear, the acuity of onset (eg, abrupt or gradual), temporal patterns (eg, persistent vs intermittent, seasonal variations), and provoking or exacerbating factors (eg, current URI, allergen exposure, cold air, exercise, feeding in infants) are noted. Important associated symptoms include shortness of breath, fever, cough, and sputum production.

Review of systems should seek symptoms and signs of causative disorders, including fever, sore throat, and rhinorrhea (respiratory infection); orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema (heart failure); night sweats, weight loss, and fatigue (cancer); nasal congestion, itching eyes, sneezing, and rash (allergic reaction); and vomiting, heartburn, and swallowing difficulties (gastroesophageal reflux disease with aspiration).

Past medical history should ask about conditions known to cause wheezing, particularly asthma, COPD, and heart failure. Sometimes the patient's drug list may be the only indication of such diagnoses (eg, inhaled bronchodilators and corticosteroids in COPD; diuretics and ACE inhibitors in heart failure). Patients with known disease should be asked about indicators of disease severity, such as previous hospitalization, intubation, or ICU admission. Also, conditions that predispose to heart failure are identified, including atherosclerotic or congenital heart disease and hypertension. Smoking history and exposure to secondhand smoke should be noted.

Physical examination: Vital signs are reviewed for presence of fever, tachycardia, tachypnea, and low O₂ saturation.

Any signs of respiratory distress (eg, accessory muscle use, intercostal retractions, pursed lip breathing, agitation, cyanosis, decreased level of consciousness) should be immediately noted.

Examination focuses on the lungs, particularly adequacy of air entry and exit, symmetry of breath sounds, and localization of wheezing (diffuse vs localized; inspiratory, expiratory, or both). Any signs of consolidation (eg, egophony, dullness to percussion) or crackles should be noted.

The cardiac examination should focus on findings that might indicate heart failure, such as murmurs, a 3rd heart sound (S₃ gallop), and jugular venous distention.

The nose and throat examination should note appearance of the nasal mucosa (eg, color, congestion), swelling of the face or tongue, and signs of rhinitis, sinusitis, or nasal polyps.

The extremities are examined for clubbing and edema, and the skin for signs of allergic reactions (eg, urticaria, rash) or atopy (eg, eczema). The patient's general appearance is noted for constitutional signs, such as the cachexia and barrel chest of severe COPD.

Red flags: The following findings are of particular concern:

Accessory muscle use, clinical signs of tiring, or decreased level of consciousness
Fixed inspiratory and expiratory wheezing
Swelling of the face and tongue (angioedema)

Interpretation of findings: Recurrent wheezing in a patient with a known history of disorders such as asthma, COPD, or heart failure is usually presumed to represent an exacerbation. In patients who have both lung and heart disease, manifestations may be similar (eg, neck vein distention and peripheral edema in cor pulmonale from COPD and in heart failure), and testing is often required. When the cause is known asthma or COPD, a history of cough, postnasal drip, or exposure to allergens or to toxic or irritant gases (eg, cold air, dust, tobacco smoke, perfumes) may suggest a trigger.

Acute (sudden-onset) wheezing in the absence of URI symptoms suggests an allergic reaction or impending anaphylaxis, especially if urticaria or angioedema is present. Fever and URI symptoms suggest infection: acute bronchitis in older children and adults and bronchiolitis in children < 2 yr. Crackles, distended neck veins, and peripheral edema suggest heart failure. Association of wheezing with feeding or vomiting in infants can be a result of gastroesophageal reflux.

Patients with asthma usually have paroxysmal or intermittent bouts of acute wheezing.

Persistent, localized wheezing suggests focal bronchial obstruction by a tumor or foreign body. Persistent wheezing manifesting very early in life suggests a congenital or structural abnormality. Persistent wheezing with sudden onset is consistent with foreign body aspiration, whereas the slowly progressive onset of wheezing may be a sign of extraluminal bronchial compression by a growing tumor or lymph node.

Testing: Testing seeks to assess severity, determine diagnosis, and identify complications.

Pulse oximetry
Chest x-ray (if diagnosis unclear)
Sometimes ABG
Sometimes pulmonary function testing

Severity is assessed by pulse oximetry and, in patients with respiratory distress or clinical signs of tiring, ABG testing. Patients known to have asthma usually have bedside peak flow measurements (or, when available, forced expiratory volume in 1 sec [FEV₁]).

Patients with new-onset or undiagnosed persistent wheezing should have a chest x-ray. X-ray can be deferred in patients with asthma who are having a typical exacerbation and in patients having an obvious allergic reaction. Cardiomegaly, pleural effusion, and fluid in the major fissure suggest heart failure. Hyperinflation and hyperlucency suggest COPD. Segmental or subsegmental atelectasis or infiltrate suggests an obstructing endobronchial lesion. Radiopacity in the airways or focal areas of hyperinflation suggest a foreign body.

If the diagnosis is unclear in patients with recurrent wheezing, pulmonary function testing can confirm airflow limitation and quantify its reversibility and severity. Methacholine challenge testing and exercise testing can confirm airway hyperreactivity in patients for whom the diagnosis of asthma is in question.

Treatment

Definitive treatment of wheezing is treatment of underlying disorders.

Wheezing itself can be relieved with inhaled bronchodilators (eg, albuterol Some Trade Names
PROVENTIL
VENTOLIN
2.5 mg nebulized solution or 180 mg metered dose inhalation). Long-term control of persistent asthmatic wheezing may require inhaled corticosteroids and leukotriene inhibitors.

Intravenous H₂ blockers ( diphenhydramine Some Trade Names
BENADRYL
NYTOL
), corticosteroids ( methylprednisolone Some Trade Names
MEDROL
), and subcutaneous and inhaled racemic epinephrine Some Trade Names
ADRENALIN
PRIMATENE MIST
are indicated in cases of anaphylaxis.

Key Points

Asthma is the most common cause, but not all wheezing is asthma.
Acute onset of wheezing in a patient without a lung disorder may be due to aspiration, allergic reaction, or heart failure.
Reactive airway disease can be confirmed via spirometry.
Inhaled bronchodilators are the mainstay of acute treatment.

Nursing Articles

Labels

Pulmonary Symptoms

History

Physical Examination

COUGH

Dyspnea

Hemoptysis

Evaluation

Wheezing

Evaluation

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