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Background information

abnormal patterns of breathing 1. sleep apnoea = cessation of airflow for more than 10 seconds more than 10 times a night during sleep causes: obstructive (e.g. obesity with upper narrowing, enlarged tonsils, pharyngeal soft tissue changes in acromegaly or hypothyroidism) 2. Cheyne-Stokes = periods of apnoea alternating with periods of hyperpnoae pathophysiology: delay in medullary chemoreceptor response to blood gas changes causes left ventricular failure brain damage (e.g. trauma, cerebral, haemorrhage) high altitude 3. Kussmaul's (air hunger) = deep rapid respiration due to stimulation of respiratory centre causes: metabolic acidosis (e.g. diabetes mellitus, chronic renal failure) 4. hyperventilation complications: alkalosis and tetany causes: anxiety 5. ataxic (Biot) = irregular in timing and deep causes: brainstem damage 6. apneustic = post-inspiratory pause in breathing causes: brain (pontine) damage 7. paradoxical = the abdomen sucks with respiration (normally, it pouches uotward due to diaphragmatic descent) causes: diaphragmatic paralysis cyanosis 1. refers to blue discoloration of skin and mucous membranes 2. is due to presence of deoxygenated haemoglobin in superficial blood vessels 3. cyanosis does NOT occur in anaemic hypoxia because the total haemoglobin content is low 4. central cyanosis = abnromal amout of deoxygenated haemoglobin in arteries and that blue discoloration is present in parts of body with good circulation such as tongue 5. peripheral cyanosis = occurs when blood supply to a certain part of body is reduced, and the tissue extracts more oxygen from normal from the circulating blood, e.g. lips in cold weather are often blue, but lips are spared 6. presence of central cyanosis should lead one to careful examination of cardiovascular and respiratory systems 7. causes of cyanosis central cyanosis decreased arterial saturation decreased concentration of inspired oxygen: high altitude lung disease: chronic obstructive pulmonary disease with cor pulmoale, massive pulmonary embolism right to left cardiac shunt (cyanotic congenital heart disease) polycythaemia haemoglobin abnromalities (rare): methaemoglobinaemia, sulphaemoglobinaemia peripheral cyanosis

all causes of central cyanosis cause peripheral cyanosis exposure to cold reduced cardiac output: left ventricular failure or shock arterial or venous obstruction

Position: patient sitting over edge of bed undressed to waist General appearance look for the following dyspnoea- shorness of breath normal respiratory rate (16-25) tachypnoea = rapid respiratory rate (>25) are accessory muscles being used (sternomastoids, platysma, strap muscles of neck) - characteristically, the accessory muscles cause elevation of shoulders with inspiration and aid respiration by increasing chest expansion Contraction of the abdominal muscles may occur in expiration in patients with obstructed airways. In some cases, the pattern of breathing is diagnostically helpful Look for pursed lips breathing, which is characteristic of patients with severe chronic obstructive pulmonary disease (COPD). A technique, used by patients with chronic obstructive pulmonary disease, in which air is inhaled slowly through the nose and mouth and exhaled slowly through pursed lips. This manoeuvre reduces the patient's breathlessness, possibly by providing continuous positive airways pressure and helping to prevent airways collapse during expiration????????????????? Careful questioning about:

the timing of onset, severity pattern of dyspnoea

Dyspnoea can be graded from I to IV based on the New York Heart Association classification:

Class I-disease present but no dyspnoea or dyspnoea only on heavy exertion Class II-dyspnoea on moderate exertion Class III-dyspnoea on minimal exertion Class IV-dyspnoea at rest

The duration and variability of the dyspnoea are important. Dyspnoea that worsens progressively over a period of weeks, months or years may be due to pulmonary fibrosis. Cyanosis- cyanosis is the blue discolouration of the skin and mucous membrane due to presence of deoxygenated haemoglobin in blood vessels near the skin.

central cyanosis is best detected by inspecting the tongue - examination of tongue differentiates central from peripheral cyanosis note: severe lung disease may result in significant ventilation-perfusion imbalances may cause reduced arterial oxygen saturation and central cyanosis. (e.g. pneumonia, chronic airflow limitation, pulmonary embolism) Cyanosis becomes evident when the absolute concentration of deoxygenated haemoglobin is 5 g/100 mL of capillary blood. Central cyanosis is therefore a relatively late sign of hypoxaemia. (hypoxaemia

defined as decreased partial pressure of oxygen in blood)In patients with anaemia, cyanosis does not occur until even greater levels of arterial desaturation are reached. character of cough- Coughing is a protective response to irritation of sensory receptors in the submucosa of the upper airways or bronchi. ask patient to cough several times lack of usual explosive beginning may indicate vocal cord paralysis (bovine cough) muffled, wheezy ineffective cough suggests airflow limitation very loose productive cough suggests excessive bronchial secretions due to: chronic bronchitis pneumonia - Pneumonia is an infection of one or both lungs which is usually caused by bacteria, viruses, or fungi. Bronchiectasis- it is the abnormal dilation of bronchioles due to weakening or destruction of muscular and elastic components of the bronchial wall. Involve inflammation leading to edema. dry irritating cough may occur with: Asthma ciliary action inhibited and then mucus thick. carcinoma of bronchus left ventricular failure interstitial lung disease ACE inhibitors The list of possible causes of cough is long and highly varied. Doctors classify coughs into 2 categories, acute and chronic. Many doctors define an acute cough as one that been present for less than 3 weeks. Chronic coughs are those present for more than 8 weeks. Subacute is 3-5 weeks.

Acute coughs can be divided into infectious (caused by an infection) and noninfectious causes. Infectious causes of acute cough include viral upper respiratory infections (the common cold), sinus infections, pneumonia, and whooping cough. Noninfectious causes of cough include flare-ups of the following chronic conditions: chronic bronchitis, emphysema, asthma, and environmental allergies. The easiest way to simplify the causes of chronic cough is to divide them into their locations with respect to the lungs. The categories are environmental irritants, conditions within the lungs, conditions along the passages that transmit air from the lungs to the environment, conditions within the chest cavity but outside of the lungs, and digestive causes. Any environmental substance that irritates the air passages or the lungs is capable of producing a chronic cough with continued exposure. Cigarette smoke is the most common cause of chronic cough. Other cough-producing irritants include dusts, pollens, pet dander, particulate matter, industrial chemicals and pollution, cigar and pipe smoke, and low environmental humidity.

Within the lungs both common and uncommon conditions cause chronic cough. Common causes include asthma, emphysema, and chronic bronchitis. Less common causes of lung-induced chronic cough include cancer, sarcoidosis, diseases of the lung tissue, and congestive heart failure with chronic fluid build-up in the lungs.

The passages that connect the lungs to the external environment are known as the upper respiratory tract. Chronic sinus infections, chronic postnasal drip, diseases of the external ear, infections of the throat, and use of ACE inhibitors for high blood pressure have all been implicated in chronic cough.

An often-overlooked cause of the chronic cough is gastroesophageal reflux (GERD). GERD occurs when acid from the stomach travels up the esophagus. This abnormal condition can cause irritation of the esophagus and larynx resulting in the reflex production of a cough.

Patients' descriptions of their cough may be helpful. A cough associated with inflammation of the epiglottis may have a barking quality. Cough caused by tracheal compression by a tumour may be loud and brassy. Cough associated with recurrent laryngeal nerve palsy has a hollow sound because the vocal cords are unable to close completely; this has been described as a bovine cough. A cough that is worse at night is suggestive of asthma or heart failure, while coughing that comes on immediately after eating or drinking may be due to a tracheo-oesophageal fistula or oesophageal reflux.

sputum volume, colour type (purulent, mucoid, mucopurulent) presence or absence of blood? (hemoptosis) stridor = croaking noise loudest on inspiration resulting from turbulent airflow. causes: (obstruction of larynx, trachea or large bronchus) acute onset (minutes) inhaled foreign body acute epiglottitis anaphylaxis toxic gas inhalation gradual onset (days, weeks) laryngeal and pharyngeal tumours crico-arytenoid rheumatoid arthritis bilateral vocal cord palsy tracheal carcinoma paratracheal compression by lymph nodes post-tracheostomy or intubation granulomata is a sign that requires urgent attention hoarseness causes include: laryngitis laryngeal nerve palsy associated with carcinoma of lung laryngeal carcinoma


The hands

clubbing commonly cause by respiratory disease occasionally, clubbing is associated with hypertrophic pulmonary osteoarthropathy (HPO) = arthropathy in association with lung disease characterised by periosteal inflammation at distal ends of long bones, wrists, ankles, metacarpals and metatarsals

palpate at the wrist joint sweelling and tenderness over wrists and other involved areas note that rarely HPO occurs without clubbing causes include: primary lung carcinoma and pleural mesothelioma

Respiratory Lung carcinoma (usually not small cell carcinoma) Chronic pulmonary suppuration:

Bronchiectasis Lung abscess Emphyema

Idiopathic pulmonary fibrosis staining staining of fingers - sign of cigarette smoking (caused by tar, not nicotine) wasting and weakness compression and infiltration of peripheral lung tumour of lower trunk of brachial plexus results in wasting of small muscles of hand and weakness of finger abduction pulse rate tachycardia, and pulsus paradoxus are important signs of sever asthma the pulse becomes weaker as one inhales and stronger as one exhales. flapping tremor (asterixis) - unreliable sign ask patient to dorsiflex wrists and spread out fingers, with arms outstretched flapping tremor may occur with severe carbon dioxide retention (severe chronic airflow limitation) The face


Horner's syndrome? (constricted pupil, partial ptosis and loss of sweating which can be due to apical lung tumour compressing sympathetic nerves in neck) Horner syndrome (Horners syndrome) refers to a constellation of signs produced when sympathetic innervation to the eye is interrupted. Lesions at any point along the sympathetic pathway may result in Horner syndrome

nose: polpys? (associated with asthma) . A polyp is an abnormal growth of tissue projecting from a mucous membrane engorged turbinates? (various allergic conditions) deviated septum? (nasal obstruction) causing obstruction of the affected nasal passage. The condition can result in poor drainage of the sinuses. Patients can also complain of difficulty breathing easily, headaches, bloody noses, or of sleeping disorders such as snoring or sleep apnea.

mouth and tongue: look for central cyanosis evidence of upper respiratory tract infection (a reddened pharynx and tonsillar enlargement with or without a coating of pus) broken tooth - may predispose to lung abscess or pneumonia sinusitis is indicated by tenderness over the sinuses on palpation facial plethora (an excess of any of the body fluids) or cyanosis may occur if superior vena cava os obstructed (e.g. due to tumour) some patients with obstructive sleep apnoea will be obese with a receding chin, a small pharynx and a short thick neck

LYMPH NODES The trachea

The trachea is felt with the forefinger pushed upwards and backwards from the suprasternal notch. The trachea lies normally in the midline but can be slightly displaced to the right as well. When displaced, the edge rather than its middle will be felt. causes of tracheal displacement: toward the side of the lung lesion upper lobe collapse(due to mediastinal shift) upper lobe fibrosis pneumonectomy( due to mediastinal shift) away from the side of lung lesion (uncommon) massive pleural effusion (LVF is one of the causes) tension pneumothorax(Tension pneumothorax is the accumulation of air under pressure in the pleural space. This condition develops when injured tissue forms a 1-way valve, allowing air to enter the pleural space and preventing the air from escaping naturally.) upper mediastinal masses, such as retrosternal goitre(A retrosternal goitre occurs when the thyroid enlarges downwards into the chest)

tracheal tug (finger resting on trachea feels it move inferiorly with each inspiration) is a sign of gross overexpansion of the chest because of airflow obstruction To assess whether accessory muscles are being used, the finger is placed in the supraclavicular fossa to feel for the scalene. The sternocleidomastoid is felt and the sternal end of the clavivle.

The chest: inspection The chest should be examined anteriorly and posteriorly by inspection, palpation, percussion and auscultation.3 Compare the right and left sides during each part of the examination. Chest excursion shape and symmetry of chest barrel shaped = anteroposterior (AP) diameter is increased compared with lateral diameter causes: hyperinflation due to asthma(, emphysema(Emphysema is a pathological diagnosis defined by permanent enlargement of airspaces distal to the terminal bronchioles. This leads to a dramatic decline in the alveolar surface area available for gas exchange. Furthermore, loss of alveoli leads to airflow limitation by 2 mechanisms. First, loss of the alveolar walls results in a decrease in elastic recoil, which leads to airflow limitation. Second, loss of the alveolar supporting structure leads to airway narrowing, which further limits airflow.) pigeon chest (pectus carinatum) = localised prominence (outward bowing of sternum and costal cartilages) causes: manifestation of chronic childhood illness (due to repeated strong contractions of diaphragm while thorax is still pliable) rickets(Rickets is a softening of bones in children potentially leading to fractures and deformity) funnel chest (pectus excavatum) = developmental defect involving a localised depression of lower end of sternum (figure 4.3); in severe cases, lung capacity may be restricted Harrison's sulcus = linear depression of lower ribs just above costal margins at site of attachment of diaphragm causes: severe asthma in childhood rickets kyphosis = exaggerated forward curvature of spine scoliosis = lateral bowing

kyphoscoliosis: causes: idiopathic (80%) secondary to poliomyelitis (inflammation involving grey matter of cord) associated with Marfan's syndrome (note: severe thoracic kyphoscoliosis may reduce lung capacity and increase work of breathing) lesions of chest wall scars - previous thoracic operations or chest drains for a previous pneumothorax or pleural effusion thoracoplasty (was once performed to remove TB, but no longer is because of effective antituberculosis chemotherapy) invovled removal of large number of ribs on one side to achieve permanent collapse of affected lung erythema and thickening of skin may occur in radiotherapy; there is a sharp demarcation between abnormal and normal skin(indicates treatment of carcinoma, breast cancer and lymphoma) Erythema is redness of the skin, caused by hyperemia of the capillaries in the lower layers of the skin. It occurs with any skin injury, infection, or inflammation (hyperemia describes the increase of blood flow to different tissues in the body)

diffuse swelling of chest wall and neck and upper limbs pathophysiology: air tracking from the lungs causes: pneumothorax rupture of oesopahagus A pancoast tumor, or superior sulcus tumor, is a tumor of the pulmonary apex The growing tumor can cause compression of a brachiocephalic vein, subclavian artery, phrenic nerve, recurrent laryngeal nerve, vagus nerve, or, characteristically, compression of a sympathetic ganglion resulting in a range of symptoms known as Horner's syndrome.

prominent veins: cause: superior vena caval obstruction asymmetry of chest wall movements assess this by inspecting from behind patient, looking down the clavicles during moderate respiration: inspecting upper lobes - diminished movement indicates underlying lung disease the affected side will showed delayed or decreased movement causes of reduced chest wall movements on one side are localised: localised pulmonary fibrosis consolidation collapse pleural effusion pneumothroax causes of bilateral reduced chest wall movements are diffuse: chronic airflow limitation diffuse pulmonary fibrosis Look for paradoxical inward motion of the abdomen during inspiration when the patient is supine (indicating diaphragmatic paralysis).

The chest: palpation

chest expansion place hands firmly on chest wall with fingers extending around sides of chest (fugyre 4.5) as patient takes a big breath in, the thumbs should move symmetrically apart about 5 cm reduced expansion on one side indicates a lesion on that side

note: lower lobe expansion is tested here; upper lobe is tested for on inspection (as above) apex beat (discussed in cardiac section) for respiratory diseases: displacement toward site of lesion - can be caused by: collapse of lower lobe localised pulmonary fibrosis LV hypertrophy displacement away from site of lesion - can be caused by: pleural effusion tension pneumothorax apex beat is often impalpable in a chest which is hyperexpanded secondary to chronic airflow limitation (COPD) as well as in tracheal tug, there is hyperextended chess. vocal fremitus palpate chest wall with palm of hand while patient repeats "99" front and back of chest are each palpated in 2 comparable positions with palms; in this way differences in vibration on chest wall can be detected high pitched voice or thick chest wall may cause absence of vocal fremitus causes of change in vocal fremitus are the same as those for vocal resonance (see later) ribs gently compress chest wall anteroposteriorly and laterally localised pain suggests a rib fracture (may be secondary to trauma or spontaneous as a result of tumour deposition or bone disease)

The chest: percussion

with left hand on chest wall and fingers slightly separated and aligned with ribs, the middle finger is pressed firmly against the chest; pad of right middle finger is used to strike firmly the middle phalanx of middle finger of left hand percussion of symmetrical areas of: anterior (chest) posterior (back) (ask patient to move elbows forward across the front of chest - this rotates the scapulae anteriorly, i.e. moves it out of the way) axillary region (side) supraclavicular fossa Percuss the clavicle directly with the percussing finger. The note is affected by the thickness of the chest wall, as well as by underlying structures.

Percussion note examples Normal lung Resonant Pneumothorax Hyper resonant : emphysema Collapse or consolidation Dull: fibrosis, lung consolidation Stony or very dull: Pleural effusion Abdomen Tympanic

percussion over a solid structure (e.g. liver, consolidated lung) produces a dull note percusion over a fluid filled area (e.g. pleural effusion) produces an extremely dull (stony dull) note percussion over the normal lung produces a resonant note percussion over a hollow structure (e.g. bowel, pneumothorax) produces a hyperresonsant note liver dullness: upper level of liver dullness is determined by percussing down the anterior chest in midclavicular line

normally, upper level of liver dullness is 5th rib in right mid-clavicular line if chest is resonant below this level, it is a sign of hyperinflation usually due to emphysema, asthma cardiac dullness: area of cardiac dullness is uaully present on left side of chest this may decrease in emphysema or asthma

The chest: auscultation

breath sounds introduction see figure 4.7 - one should use the diaphragm of stethoscope to leisten to breath sound in each area, comparing each side remember to listen high up into the axillae remember to use bell of stethoscope to listen to lung ap[ices from above the clavicles quality of breath sounds normal breat sounds(vesicular) are heard with stethoscope over all parts of chest, produced in airways rather than alveoli (although once they had been thought to arise from alveoli (vesicles) and are therefore called vesicular sounds) normal (vesciular) breath sounds are louder and longer on inspiration than on expiration; and there is no gap between the inspiratory and expiratory sounds

This is the sound heard over the chest at a distance from large airways. It is a "soft" sound that has been compared to the sound of wind blowing through the leaves of a tree. This is the most common sound heard in the absence of lung disease.

bronchial breath sounds turbulence in large airways is heard without being filtered by the alveoli, and therefore produce a different quality; they are heard over the trachea normally, but not over the lungs are audible throughout expiration, and often there is a gap between inspiration and expiration are heard over areas of consolidation since solid lung conducts the sound of turbulence in main airways to peripheral areas without filtering

This is the sound heard over large airways. It has a "tubular" quality - it has been compared to the sound of air blowing through a cardboard tube. This sound is abnormal when heard at a distance from large airways.

causes include: lung consolidation (lobar pneumonia) - common localised pulmonary fibrosis - uncommon pleural effusion (above the fluid) - uncommon collapsed lung (e.g. adjacent to a pleural effusion) - uncommon (amphoric sound = when breath sounds over a large cavity have an exaggerated bronchial quality) intensity of breath sounds causes of reduced breath sounds include: chronic airflow limitation (espescially emphysema) pleural effusion pneumothorax pneumonia large neoplasm pulmonary collapse added (adventitious) sounds two types of added sounds: continuous (wheezes) and interrupted (crackles) wheezes

wheeze must be timed in relation to respiratory cycle may be heard in expiration or inspiration or both pathophysiology of wheezes - airway narrowing wheezes tend to be louder on expiration because airway is normally dilated during inspiration, and narrowed during expiration an inspiratory wheeze implies severe airway narrowing pitch of wheeze varies, and is determined by velocity of air jet, accordingly high pitched wheezes are produced in smaller bronchi low pitched wheezes arise from large bronchi causes of wheezes include: asthma (often high pitched) - due to muscle spasm, mucosal oedema, excessive secretions chronic airflow diseases - due to mucosal oedema and excessive secretions carcinoma causing bronchial obstruction - tends to cause a localised wheeze which is monophonic and does not clear with coughing crackles some terms not to use include rales (low pitched crackles) and creptitations (high pitched crackles) crackles are due to collapse of peripheral airways on expiration and sudden opening on inspiration early inspiratory crackles suggests disease of small airways characteristic of chronic airflow limitation are only heard in early inspiration late or paninspiratory crackles suggests disease confined to alveoli may be fine, medium or coarse fine crackles - typically caused by pulmonary fibrosis medium crackles - typically caused by left ventricular failure (due to presence of alveolar fluid) coarse crackes - tend to change with coughing; occur with any disease that leads to retention of secretions; commonly occur in bronchiectasis pleural friction rub when thickened, roughened pleural surfaces rub together, a continuous or intermittent grating sound may be heard suggests pleurisy, which may be secondary to pulmonary infarction or pnuemonia rarely may be caused by: malignany involvement of pleura, spontaneous pneumothorax, pleurodynia (1 - pleuritic pain in chest; 2 - painful affection of tendinous attachments of throacic muscles, usually of one side only) vocal resonanance gives information about lungs' ability to transmit sounds consolidated lung tends to transmit high frequencies so that speech heard through stethoscope takes a bleeting quality (aegophony); when a patient with aegophony says "bee" it sounds like "bay" listen over each part of chest as patient says "99"; over consolidated lung, the numbers will become clearly audible; over normal lung, the sound is muffled whispering pectoriloquy - vocal resonance is increased to such an extent that whispered speech is distinctly heard

The heart

lie patient at 45 degrees measure jugular venous plse for right heart failure examine preacordium; pay close attention to pulmonary component of P2 (which is best heard at 2nd intercostal space on left) and should not be louder than A2; if it is louder, suspect pulmonary

hypertension. There may be signs of right ventricular failure or hypertension. cor pulmonale (also called pulmonary hypertensive heart disease) may be due to : chronic airflow limitation (emphysema) pulmonary fibrosis pulmonary thromboembolism marked obesity sleep apnoea severe kyphoscoliosis
Cor pulmonale or pulmonary heart disease is damage to the right ventricle of the heart as a response to resistance or high blood pressure in the lungs. Chronic cor pulmonale usually results in right ventricular hypertrophy (RVH),

The abdomen

palpate liver for enlargement due to secondary deposits of tumour from lung, or right heart failure Permberton's sign ask patient to lift arms over head look for development of facial plethora, inspiratory stridor (when arm is lift up, thoracic outlet is decreased: thats y increased stridor)pu, non-pulsatile elevation of jugular venous pressure occurs in vena caval obstruction feet inspect for oedema or cyanosis (clues of cor pulmonale) look for evidence of deep vein thrombosisd respiratory rate on exercise and positioning patients complaining of dyspnoea should have their respiratory rate measured at rest, at maximal tolerated exertion and supine if dyspnoea is not accompanied by tachypnoea when a patient climbs stairs, one should consider malingering look for paradoxical inward motion of abdomen during inspiration when patient is uspine (indicating diaphragmatic paralysis) temperature: fever may accompany any acute or chronic chest infection forced expiratory time measure the time taken by a patient to exhale forcefully and completely through an open mouth after taking a maximum inspiration the normal FET is 3 seconds or less; an increased FET indicates airways obstruction note any audible wheeze or cough peak flow meter using the device, ask patient to take a full breath in and to maximally puff suddenly normal values for young men - 600 litres/minute normal values for young women - 400 litres/minute value depends on age, sex and height - consult a table airways obstruction results in reduced and variable PEFR spirometry spirometer graphically records forced expiration and forced vital capacity FEV = volume of air expelled from lungs after maximum inspiration using maximum forced effort FEV1 = volume of air expelled in first second of FEV FVC = total volume of air expelled from lungs after maximum inspiratory effort follwed


Bedside assessment of lung function

by maximum expiration FEV1/FVC is normally at about 80%, but may decline to as little as 60% in old age in obstructive airways disease: airways narrowing occurs hence: FEV1 decreases lots, FVC decreases a bit, FEV/FVC decreases lots (also elastic recoil is decreased, therefore expiration time is increased) obstructive diseases include: asthma, chronic bronchitis, emphysema in restrictive airways disease elastic recoil is increased (i.e. airways collapse more easily) hence: FEV1 decreases a bit (only because VC has decreased), FVC decreases, FEV/FVC increases restrictive diseases include: pulmonary firosis, sarcoidosis, pneumonia, neonatal respiratory distress syndrome flow volume curve: this measures inspiratory and expiratory flow, and therefore FVC and FEV1 and other figures can be calculated Mediastinal displacement none ipsilateral shift Chest wall movement reduced over affected area decreased over affected area Percussion Breath note sounds dull dull bronchial absent or reduced absent over fluid but may be bronchial at upper border absent or reduced normal or reduced Vocal resonance increased absent

COMPARISON OF CHEST SIGNS IN COMMON RESPIRATORY DISORDERS Disorder consolidation collapse Added sounds crackles absent

heart displaced to opposite side; reduced over pleural effusion tracheal only affected area displaced if massive

stony dull

absent, but pleural rub absent over may be found effusion above effusion

tracheal deviation decreased over pneumothorax to opposite side resonant affected area if under tension bronchial decreased normal or none asthma symmetrically decreased interstitial pulmonary fibrosis slightly decreased normal symmetrically

absent wheeze

absent normal or reduced



fine inspiratory crackles over affected lobes normal unaffected by cough or posture

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