`
`Evaluation of the Pulmonary Patient - Pulmonary Disorders - Merck Manuals Professional Edition
`
`\\\ MERCK MANUAL
`
`Brniiveslanal Vere
`
`Professional / Pulmonary Disorders / Approach to the Pulmonary Patient
`
`Evaluation of the
`PulmonaryPatient
`
`By Noah Lechtzin, MD, MHS, Associate Professor of Medicine and
`Director, Adult Cystic Fibrosis Program, Johns Hopkins University
`School of Medicine
`
`Key componentsin the evaluation of patients with pulmonary symptomsare the history, physical
`examination, and, in most cases, a chest x-ray. These componentsestablish the need for
`subsequenttesting, which may include pulmonary function testing and ABG analysis, CT or other
`chest imaging tests, and bronchoscopy.
`
`History
`
`The history can often establish whether symptomsof dyspnea, chest pain, wheezing, stridor,
`hemoptysis, and cougharelikely 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, suchas fever, weight loss, and night sweats, are also present. Other
`important information includes
`
`e Occupational and environmental exposures
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`e Family history, travel history, and contact history
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`e Previous illnesses
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`e Use of prescription, OTC,orillicit drugs
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`e 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
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`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)
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`e Signs of possible chronic pulmonary disease (eg, clubbing, pedal edema)
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`e Chest wall deformities
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`e Abnormal breathing patterns (eg, Cheyne-Stokes respiration, Kussmaul respirations)
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`e jugular venous distention
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`Signs of hypoxemia include cyanosis (bluish discoloration of the lips, face, or nail beds), which
`signifies low arterial oxygen saturation (< 85%); the absence of cyanosis does not exclude the
`presence of hypoxemia.
`
`Signs of respiratory difficulty include tachypnea, use of accessory respiratory muscles
`(sternocleidomastoids, intercostals, scalene) to breathe, intercostal retractions, and paradoxical
`breathing. Patients with COPD sometimesbrace their arms against their legs or the examination
`table while seated(ie, tripod position) in a subconscious effort to provide moreleverage to
`accessory muscles and thereby enhancerespiration. Intercostal retractions (inward movementof
`the rib interspaces) are common amonginfants and older patients with severeairflow 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 enlargementofthe 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 Figure: Measuring finger clubbing.). “Sponginess”of the nail bed beneath the
`cuticle also suggests clubbing, Clubbing is most commonly observedin patients with lung cancer
`but is an importantsign 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
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`distinguished from pathologic clubbing by the absence of pulmonary symptomsor disease and
`by the presence of clubbing from an early age (by patient report).
`
`
`
`Finger Clubbing
`
`© Springer Science+Business Media
`
`Measuringfinger clubbing.
`
`The ratio of the anteroposterior diameterof the finger at the nail bed (a-b) to that at the distal
`interphalangealjoint (c-d) is a simple measurementof finger clubbing.It can be obtained
`readily and reproducibly with calipers.If the ratio is > 1, clubbing is present. Finger clubbingis
`also characterized by loss of the normal angle at the nail bed.
`
`Normalfinger
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`160
`
`Clubbed finger
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`f >180
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`Chest wall deformities, such as pectus excavatum (a sternal depression usually beginning over
`the midportion of the manubrium and progressing inward through the xiphoid process) and
`kyphoscoliosis, may restrict respirations and exacerbate symptomsof preexisting pulmonary
`disease, These abnormalities can usually be observed during careful examination after the
`patient's shirt is removed. Inspection should also include an assessmentof the abdomenand the
`extent of obesity, ascites, or other conditions that could affect abdominal compliance.
`
`Abnormal breathing patterns cause fluctuations in respiratory rate so respiratory rate should
`be assessed and counted for 1 min.
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`e Cheyne-Stokesrespiration (periodic breathing) is a cyclic fluctuation of respiratory rate
`and depth. From periodsof brief apnea, patients breathe progressively faster and deeper
`(hyperpnea), then slower and shallower until they become apneic and repeatthe cycle.
`Cheyne-Stokesrespiration is most often caused by heart failure, a neurologic disorder(eg,
`stroke, advanced dementia), or drugs. The pattern in heart failure has beenattributed to
`delays in cerebral circulation; respiratory centers lag in recognition of systemic
`acidosis/hypoxia (causing hyperpnea)or alkalosis/hypocapnia (causing apnea).
`
`e Biot respiration is an uncommonvariant of Cheyne-Stokesrespiration in which irregular
`periods of apnea alternate with periods in which 4 or 5 deep, equal breaths are taken.It
`differs from Cheyne-Stokesrespiration 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.
`
`e Kussmaulrespirations are deep, regular respirations caused by metabolic acidosis.
`
`Pulmonary hypertension, sometimes observed during inspection, indicates an increasein right
`atrial and usually in right ventricular pressure, The elevated pressureis usually causedbyleft
`ventricular dysfunction, but it may also be due to a pulmonary disorder causing pulmonary
`hypertension. The presenceof jugular venous distension should prompta search for othersigns
`of cardiac disorder(eg, 3rd heart sound [S3] gallop, dependent edema).
`
`Auscultation
`
`Auscultation is arguably the most important componentof the physical examination.All fields of
`the chest should belistened to, including the flanks and the anterior chest, to detect
`abnormalities associated with each lobe of the lung. Featuresto listen for include
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`e Character and volumeof breath sounds
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`e Presence or absence of vocal sounds
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`e Pleural friction rubs
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`e Ratio of inspiration to expiration(I: E ratio)
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`Cardiac auscultation may reveal signs of pulmonary hypertension, such as aloud pulmonic 2nd
`heart sound(P93), and of right heart failure, such as a right ventricular 4th heart sound (S,4) and
`tricuspid regurgitation.
`
`The character and volume of breath soundsare useful in identifying pulmonary disorders.
`Vesicular breath soundsare the normal soundsheard over most lungfields. Bronchial breath
`soundsareslightly louder, harsher, and higher pitched; they normally can be heard over the
`trachea and over areasof lung consolidation, such as occur with pneumonia.
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`Typical breath sounds heard over mostlungfields.
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`Normal Breath Sounds
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`Audio file courtesy of David W. Cugell, MD.
`
`Typical breath sounds heard overthe trachea and areasof lung consolidation.
`
`Normal Bronchial Breath Sounds
`
`Audio file courtesy of David W. Cugell, MD.
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`Crackles
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`Audiofile courtesy of David W. Cugell, MD.
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`Prolonged expiratory phase with wheezing.
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`Wheezing
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`Audio file courtesy of David W. Cugell, MD.
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`Inspiratory stridorin croup.
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`Stridor
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`Audiofile courtesy of David W. Cugell, MD.
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`A leathery soundthat fluctuates with the respiratory cycle.
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`Friction Rub
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`Audio file courtesy of David W. Cugell, MD.
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`Areas of consolidation cause a patient's vocalized "E" to soundlike "A."
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`E to A Change
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`Audio file courtesy of David W. Cugell, MD.
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`Adventitious sounds are abnormal sounds, suchas crackles, rhonchi, wheezes, and stridor.
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`Crackles (previously called rales) are discontinuous adventitious breath sounds. Fine
`crackles are short high-pitched sounds; coarse crackles are longer-lasting low-pitched
`sounds. Crackles have been compared to the soundofcrinkling plastic wrap and can be
`simulated by rubbing strands of hair together between 2 fingers near one’s ear. They occur
`most commonly with atelectasis, alveolarfilling processes (eg, pulmonary edema), and
`interstitial lung disease (eg, pulmonary fibrosis); they signify opening of collapsed airways or
`alveoli.
`
`Rhonchiare low-pitched respiratory sounds that can be heard during inspiration or
`expiration. They occur in various conditions, including chronic bronchitis. The mechanism
`mayrelate to variations in obstruction as airways distend with inhalation and narrow with
`exhalation.
`
`Wheezesare whistling, musical breath soundsthat are worse during expiration than
`inspiration. Wheezing can be a physical finding or a symptom andis usually associated with
`dyspnea.
`
`Stridoris a high-pitched, predominantly inspiratory sound formed by extrathoracic upper
`airway obstruction. It usually can be heard without a stethoscope.Stridor is usually louder
`than wheezing, is predominantly inspiratory, and is heard loudly overthe larynx. It should
`trigger a concernforlife-threatening upper airway obstruction,
`
`Decreased breath soundssignify poor air movementin airways, as occurs with asthma
`and COPD where bronchospasm or other mechanismslimit airflow, Breath sounds may
`also be decreased in the presenceof a pleural effusion, pneumothorax, or obstructing
`endobronchial lesion.
`
`Vocal soundsinvolve auscultation while patients vocalize.
`
`Bronchophonyand whispered pectoriloquy occur whenthe patient's spoken or
`whispered voiceis clearly transmitted through the chest wall. Voice transmission results
`from alveolar consolidation, as occurs with pneumonia.
`
`Egophony(E to A change)is said to occur when, during auscultation, a patient says the
`letter “E” and the examinerhearstheletter “A,” again as occurs with pneumonia.
`
`Friction rubs are grating or creaking soundsthatfluctuate with the respiratory cycle and sound
`like skin rubbing against wetleather. They are a sign of pleural inflammation and are heard in
`patients with pleuritis or empyema and after thoracotomy.
`
`I:E ratio is normally 1:2 but is prolonged to 2 1:3 whenairflow is limited, such as in asthma and
`COPD, even in the absence of wheezing.
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`Percussion and palpation
`
`Percussion is the primary physical maneuver used to detect the presence andlevelof pleural
`effusion. Finding areas of dullness during percussion signifies underlying fluid or, less commonly,
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`consolidation.
`
`Palpation includestactile fremitus (vibration of the chest wall felt while a patient is speaking); it is
`decreasedin pleural effusion and pneumothorax and increased in pulmonary consolidation(eg,
`lobar pneumonias). Point tenderness on palpation maysignal underlying rib fracture or pleural
`inflammation.
`
`In cor pulmonale, a right ventricular impulse at the left lower sternal border may becomeevident
`and may beincreased in amplitude and duration (right ventricular heave).
`
`Last full review/revision August 2016 by Noah Lechtzin, MD, MHS
`
`& MERCK
`
`© 2018 Merck Sharp & DohmeCorp., a subsidiary of Merck & Co,, Inc., Kenilworth, NJ, USA
`
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