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Common lung diseases

The lungs are susceptible to an eclectic arrangement of diseases ranging from congenital anomalies (some of which are incompatible with life) to infectious disorders and malignancies. It is important that the astute healthcare professional is able to clinically examine and appropriately investigate patients with pulmonary disorders, as some of these conditions can become life-threatening if they are left unattended. This article will focus on common clinical disorders of the lungs. There will be an emphasis on common chief complaints, clinical examination, and investigations of the respiratory system, and discussion of common pathologies.

Key facts
Common complaints

Chest pain: pleuritic, costonchondritis, cardiac

Coughing: normal reflex, chemical irritant, drug-induced

Dyspnea: exercise-induced, psychogenic, cardiogenic source, respiratory source

Hemoptysis: pneumonia, lung abscess, congestive cardiac failure

Common disorders

Pneumonia: CAP, HCAP, HAP, aspiration, pneumonia in immunocompromised patients 

Tuberculosis: latent TB, disseminated TB

Pulmonary embolism: small to medium acute embolism, massive acute embolism, small and chronic/recurrent emboli

Pneumothorax: spontaneous, primary, secondary, tertiary

Common chief (presenting) complaints related to the lungs

Patients visit the emergency department for countless reasons. These range from the weird and wonderful to the common garden variety concerns. As it pertains to the respiratory system, here is a brief list of reasons why patients seek professional assistance for concerning symptoms:

  • Chest pain
  • Coughing
  • Hemoptysis (coughing up blood)
  • Shortness of breath

Chest pain

There are several causes of chest pain ranging from a simple cutaneous irritation to the pain of a myocardial infarction. It is important for the physician to identify the source of the chest pain in order to adequately treat serious conditions. One of the common causes of chest pain related to the lungs is known as pleurisy. This is a sharp sensation associated with respiration or coughing. Patients with an infection or infarction of the lungs may complain of this sensation. Acute obstruction of the pulmonary veins by an embolus often presents with ischemic cardiac pain.

Chest pain associated with movement is more likely to be of musculoskeletal origin. Cardiac chest pain is a crushing sensation lasting more than 15 minutes and typically relieved with nitroglycerin. Some patients may also experience radiation of the pain up the left side of the neck and down the left upper limb.


Coughing is actually a protective physiological mechanism designed to guard the airway. Receptors that facilitate this reflex are located in the mucosa of the caudal part of the upper respiratory tract (i.e. larynx, pharynx, and trachea) and bronchi. Exposure to irritants such as smoke, changes in the ambient temperature, drugs such as angiotensin-converting enzyme inhibitors, excessive mucus from a respiratory tract irritation, and aspiration of liquids or food particles are known triggers of the natural cough reflex. The aim of the reflex is to provide an expulsive mechanism to clear the airway and prevent obstruction.

Anatomy of the respiratory system (anterior view)

Pathological coughing may occur as chronic persistent or acute transient symptoms of the underlying disease. Further classification of a cough refers to whether or not it is from a cardiovascular, respiratory, mechanical (i.e. foreign body obstruction), psychogenic (in panic disorders), or metabolic (lactic acidosis, salicylate poisoning, diabetic ketoacidosis) causes. A cough may be further characterized as a wet vs a dry cough. The former is usually associated with sputum production or suggests that there is a build-up of mucous within the airway; while the latter suggests that there is no associated hypersecretion.


Coughing up blood is likely to cause anyone to run to the nearest emergency room. However, this bleeding may originate from the gastrointestinal tract, cardiovascular system, or upper aerodigestive tract. Hemoptysis refers specifically to coughing up blood in the sputum; and is different from vomiting blood, which is hematemesis. The etiology of hemoptysis may be obscure at times and requires diligent investigation to identify the source of the bleeding. An encapsulated organism known as Streptococcus pneumoniae – which is the causative agent behind Pneumococcal pneumonia – may result in overt hemoptysis; but is also associated with a ‘rusty’- colored sputum. 

However, these symptoms are not unique to Pneumococcal pneumonia as patients with lung abscesses and other suppurative lung infections may also have these symptoms. Recurrent streaking of blood in sputum is usually suggestive of a bronchial malignancy or tuberculosis. A history of unintentional weight loss and nights sweats usually supports both etiologies and further investigation (plain film, computed tomography of the chest, sputum culture, or Mantoux testing) should be conducted. The most concerning underlying cause of hemoptysis is a pulmonary embolism, as this is acutely life-threatening.

Shortness of breath

Breathlessness is also referred to as being short of breath or dyspnea. It has a variety of benign and clinically urgent etiologies that can be identified with a thorough history and examination. Patients often describe it as an unsettling desire to breathe. This presentation may result from physical exercise in an unfit individual, but would rapidly resolve after a period of rest without leaving any deficits. Anxiety disorder is another cause of shortness of breath that can be identified with a thorough psychiatric history.

The healthcare professional should explore the patient history for the presence of chest pain, diaphoresis, nausea, or palpitations as these findings are suggestive of a cardiogenic source of dyspnea (i.e. decompensated heart failure or a myocardial infarction). An antecedent or concurrent history of stridor, wheezing, coughing, or hemoptysis is strongly indicative of a respiratory source of the dyspnea. Some patients with pre-existing conditions such as bronchial asthma, left heart failure, or chronic obstructive pulmonary disorders may have periodic episodes of breathlessness. The patient and caregivers should be educated regarding potential triggers that may cause them to decompensate and when to seek medical attention.

Summary of Common Presenting Complaints

Common presenting complaints
Chest pain Pleuritic, costochondritis, cardiac
Coughing Normal reflex, chemical irritant, drug-induced
Shortness of breath Exercise-induced, psychogenic, cardiogenic source, respiratory source
Hemoptysis Pneumonia, lung abscess, congestive cardiac failure

Common lung diseases

The list of disorders affecting the lungs is expansive and difficult to cover in one sitting. Also, what is considered as common varies by geographical and socioeconomic stratification. The list generated here is based on diseases that are commonly encountered globally and those that can be acutely life-threatening. It focuses on some non-neoplastic disorders of the lung parenchyma (and not the airway proper) and is not intended to be an exhaustive list of all pulmonary disorders.


Pathogens must overcome a host of defense mechanisms in order to gain access to the lung parenchyma. The mucous secretions, cilia, lymphoid tissue, and resident macrophages all work synergistically to prevent microbes from settling in the lungs. Unfortunately, these mechanisms are not full-proof. Consequently, either viral, bacterial, fungal, or parasitic organisms can gain access to the parenchyma, leading to pneumonia. While the treatment of pneumonia depends on identification of the underlying pathogen, it is sometimes difficult to isolate the organism from the available specimen.

Lung (histological slide)

A crude way of determining the probable infectious organism is by determining when and where the patient fell ill. These pneumonia syndromes serve as a guide for clinicians to provide empirical treatment until culture studies are complete. These syndromes include:

  • Community-acquired pneumonia (CAP) occurs in an otherwise healthy individual who was infected in the general environment. Bacterial agents commonly associated with community-acquired pneumonia include (but is not limited to) S. pneumoniae, H. influenzae, M.  catarrhalis, S. aureus, and K. pneumoniae. 
  • Hospital-acquired pneumonia (HAP), otherwise called nosocomial pneumonia, occurs within 2 days of being admitted to the hospital. There is a predilection for elderly patients and those who have been receiving ventilator support (i.e. ventilator-associated pneumonia). A mixture of gram-positive (S. aureus, S. pneumonia) and gram-negative (E. coli, Pseudomonas species, K. pneumoniae) bacteria are commonly associated with this disorder. Patients with hospital-acquired pneumonia are also at risk of contracting antibiotic-resistant organisms such as methicillin-resistant Staphylococcus aureus (MRSA); which is associated with a higher mortality rate compared to pneumonia resulting from other microbes.
  • Healthcare-associated pneumonia (HCAP) differs from hospital-acquired pneumonia in that these patients would have been admitted to the hospital for more than 2 days within the last 3 months. Alternatively, individuals who received hemodialysis, nursing facility residents, or recently received intravenous antibiotics or chemotherapy are also considered as healthcare-associated pneumonia patients. The offending organisms are similar to those found in hospital-acquired pneumonia.
  • Aspiration pneumonia or aspiration pneumonitis results from the accidental passage of foreign substances into the airway. This phenomenon is often seen in patients who are unable to protect their airway from fluids being swallowed or regurgitated. Most commonly, gastric fluid is aspirated into the airway; resulting in the offending organisms being the anaerobes found in the gastric flora. 
  • Pneumonia in the immunocompromised patient is caused by agents that would not normally result in an infection in a non-immunocompromised individual. These patients may have a defect in the defensive pathway of the respiratory tract either due to drug use (chemotherapy) or disease processes (e.g. leukemia, HIV). Viral (herpes virus, influenza virus), fungal (Pneumocystis jirovecii, Candida albicans), and bacterial (listed above) agents of varying degrees of virulence are able to cause an infection in some immunocompromised individuals.

Pneumonia chest X-ray

Pneumonia can also be classified anatomically according to the pattern of infection observed on plain film radiographs. A lobar pneumonia is one in which an entire lobe of the lung (either unilateral or bilateral) is opaque. In contrast, lobular pneumonia refers to one in which only a segment of a lobe is affected. Interstitial pneumonia refers to diffuse opacification of the lung field in keeping with the disease of the supportive tissue of the lung (i.e. alveolar walls). This is also referred to as atypical pneumonia as the patient does not have the overt signs of pneumonia and the offending organism may be viral. Bronchopulmonary pneumonia is a condition in which the bronchioles and adjacent alveoli are infected. Consequently, the plain film shows patchy opacification throughout the lung fields. 


The incidence of tuberculosis has declined significantly due to the implementation of the Bacillus Calmette–Guérin (BCG) vaccine given between birth and 6 weeks of age. Unfortunately, it is still a significant contributor to the global mortality rate as it is the second most common cause of death resulting from an infectious agent. This potentially fatal bacterial pulmonary disease is caused by the Mycobacterium tuberculosis pathogen that can easily be passed from one individual to another through airborne respiratory droplets. Globally, the mycobacterial infection is more commonly observed among those of low socioeconomic status and among those living with HIV. This distribution also supports the pathogenesis of the infection as the microbes are spread through unpasteurized cow’s milk (M. bovis) or from person to person living in close contact with each other (M. tuberculosis).

Anatomy of the bronchioles and alveoli (anterior view)

The aerosolized mycobacterium them enters the alveoli, at which point the local macrophages are activated. The macrophages become Langhan’s and epithelioid cells that then form a granuloma around the affected area. This wall prevents further spread of the bacteria to unaffected lung tissue. As a result, tuberculosis can exist for years in a latent phase (latent tuberculosis). When multiple granulomas coalesce, they form a yellow, caseous nodule in the peripheral lung field known as a Ghon focus. If the mycobacterium spreads to the hilar lymph nodes then an identical pathological process ensues. Together, the main granuloma and the regional lymphadenopathy is called the primary complex of Ranke. The mycobacterium may spread hematogenously or via the lymphatic system, leading to extra-pulmonary disease that affects every organ system within the body.

Pulmonary tuberculosis: Necrotizing granuloma

Pulmonary embolism

The endothelial lining of the blood vessels is equipped with numerous mechanisms that inhibit the coagulation cascade within the vascular lumen. The German physician Rudolf Virchow described three factors that result in a prothrombotic state. Virchow’s triad speaks to the presence of venous stasis, endothelial injury, and a hypercoagulable state as predisposing factors that may result in the formation of a thrombus within the venous system. These thrombi often form in the deep venous systems and are subsequently referred to as deep vein thrombosis. While that is locally problematic, systemic complications arise when the thrombi embolize (i.e. venous thromboembolism) and migrate to the pulmonary arteries via the right heart

The resulting pulmonary embolism can present in three general patterns depending on the size of the embolus. In the acute setting, a small to medium sized pulmonary embolus may occlude a segmental artery; thus initiating the hypoxia, ischemia, infarction cascade. The patient may experience pleuritic-type chest pain that may limit respiration. The possibility exists that the patient may also experience hemoptysis. On examination, these patients are often tachycardic and mildly febrile, with stony-dull percussion in the presence of an effusion. A pleural rub and crackles may also be auscultated. Plain film radiographs may reveal a raised hemidiaphragm ipsilateral to the infarct and a pleural effusion. The only electrocardiographic change noted is sinus tachycardia and the arterial blood gas study may reveal reduced or normal values for the partial pressures of carbon dioxide and oxygen.

A massive pulmonary embolus in the acute setting is life-threatening. There is a significant reduction in the cardiac output and possibly acute right heart failure. Patients may complain of a central crushing chest pain, dyspnea, and syncope or collapse. Clinical findings in keeping with a massive pulmonary embolism include:

  • Profound hypotension 
  • Underlying tachycardia
  • Elevated jugular venous pressure
  • Loud P2
  • Presence of an S3  gallop rhythm
  • Reduced urine output
  • Decreased blood oxygen saturation

There are usually no changes to the plain chest radiograph in the acute setting. However, the electrocardiograph may demonstrate a right bundle-branch block with inverted T-waves, deep S-waves in lead I, Q-waves and inverted T-waves in lead III, right axis deviation, peaked P-waves in lead II, and sinus tachycardia. Arterial blood gas studies show metabolic acidosis with significantly reduced partial pressures of carbon dioxide and oxygen. 

A small recurrent embolism occurring over time will have a cumulative destructive effect on the lungs and heart. This chronic pulmonary embolism obstructs the microvascular circulation of the lungs leading to increased pulmonary arterial pressure, right ventricular hypertrophy and subsequent dilatation, tricuspid regurgitation, right atrial hypertrophy and dilation, and subsequent right heart failure. Patients usually complain of shortness of breath on exertion and features of right heart failure (i.e. hepatomegaly, elevated JVP, decreased cardiac output, etc). Later on, in the disease process, the physician may detect a right parasternal heave, loud P2, and other features of right heart failure on clinical examination. A plain chest radiograph shows enlarged right ventricle and pulmonary trunk. This right ventricular enlargement along with the accompanying right heart strain can also be detected on electrocardiography. The arterial blood gas study may be normal at rest but if repeated following formal exercise, the partial pressure of oxygen will be reduced.


The thoracic cavity is a closed space under negative pressure that houses the lungs and mediastinum. Therefore, if there is an injury to the chest wall that allows communication with the external environment, then air will be pulled into the cavity. Additionally, spontaneous injury to the lung can also result in leakage and accumulation of air into the pleural space. In both cases, the resulting disorder is known as a pneumothorax. This disorder can occur spontaneously or secondary to a lung injury. Spontaneous primary pneumothorax tends to occur in tall individuals with a history of smoking and a predisposition to developing apical blebs (thin-walled air-filled sacs beneath the pleural membrane). The blebs may rupture with increased intrathoracic pressures such as Valsalva maneuvers or changes in atmospheric pressure (pilots and deep-sea divers). Iatrogenic, accidental, or malicious injury to the chest wall often results in a traumatic pneumothorax. These injuries may be associated with blood (hemopneumothorax), pus (empyema), or lymphatic fluid (chylothorax) within the pleural space. Additionally, the lung parenchyma may be compromised by an underlying infection or disease process that results in rupture of the lung parenchyma and leakage of air into the thorax. This is referred to as a secondary pneumothorax.

 If, after a rupture, the communication between the airway and thorax is sealed and the pleural pressure is still negative, then the leaked air may be reabsorbed. This is a simple or closed pneumothorax where the following reabsorption of air will cause the lungs to re-expand and no intervention is required. However, there are instances where there is continuous leakage of air into the chest cavity resulting in a mediastinal shift and subsequent kinking of the venae cavae. These cases are referred to as tension pneumothoraces and can be acutely life-threatening. This should be a clinical diagnosis with signs of:

  • Use of accessory respiratory muscles
  • Tracheal deviation away from the affected side
  • Displaced apex beat away from the affected side
  • Reduced tactile vocal fremitus on the affected side
  • Hyper-resonant percussion note on the affected side
  • Reduced vocal resonance on the affected side
  • Reduced breath sounds on the affected side

There is not enough time for radiological investigations as the patient may expire on the way to the radiology suite. These patients require urgent needle decompression by introducing a 14 to 16 gauge (referring to the internal diameter of the needle) needle into the second intercostal space in the midclavicular line on the affected side. A sudden gush of air and restoration of the patient’s vital signs is indicative of adequate placement of the needle. This procedure should then be followed by placement of a thoracostomy tube in the 3rd to 4th intercostal space between the middle and anterior axillary lines under sterile conditions. The tube should then be connected to an underwater seal to prevent air from entering the chest cavity via this route. Placement of the tube can then be confirmed with a plain film chest radiograph.

Summary of disorders of the lungs

The table below contains a quick summary of the common pulmonary disorders and their subtypes.

Common disorders of the lungs
Pneumonia CAP, HCAP, HAP, aspiration, pneumonia in the immunocompromised patient
Tuberculosis Latent TB, disseminated TB
Pulmonary embolism Small to medium acute embolism, massive acute embolism, small and chronic/recurrent emboli
Pneumothorax Spontaneous, primary, secondary, tertiary

Clinical examination of the lungs

Examination of the respiratory system should follow the general template of clinical examinations, which is inspection, palpation, percussion, and auscultation. After explaining the procedure to the patient and obtaining informed consent, ask the patient to remove their clothing on the upper half of the body. The patient should be placed in the supine position if this can be tolerated. Some patients may experience difficulty breathing while lying flat based on the underlying cause of their respiratory problem. As such, the examination should be adapted to accommodate the patient. This examination also requires the clinician to examine both the anterior and posterior thorax to create a complete clinical picture.  This format is most suitable for a stable patient where an individual who is in acute distress may require more immediate attention. Please note that clinical findings must be supplemented by a thorough history and appropriate investigations in order to make and confirm a diagnosis. 


This part of the examination process begins as the patient enters the office. Make note of whether or not the patient is visibly distressed, has labored breathing, or speaks in broken sentences or words only due to respiratory problems. Once the patient is prepared as described above, look for the use of accessory muscles of respiration (contraction of sternocleidomastoid), nasal flaring, tracheal tugging, subcostal flaring or intercostal recessions. These are all early signs of acute airway obstruction that require urgent attention. Assess the respiratory rate by counting the number of breaths over a 60 second period. In a healthy adult, the normal respiratory rate ranges from 12 – 20 breaths per minute.

Also look at the shape of the patient’s chest as some individuals with chronic obstructive pulmonary disorders have a widened or barrel-shaped chest. In this case, the anteroposterior diameter of the chest is greater than the lateral diameter. The sternum may be abnormally elevated or depressed (pectus carinatum or excavatum, respectively). Pay close attention to whether or not the patient has lordotic (abnormal inward curvature of the spine) or kyphotic (abnormal convex curvature of the spine) deformities, as they may also impact the respiratory system based on their severity. 

Pectus excavatum

The clinician should observe the breathing movements of the chest and abdomen while stooping at the foot of the bed. At rest, females tend to use their intercostal muscles more than their diaphragm to aid respiration. On the other hand, males utilize the diaphragm more than their intercostals. As a result, males have more abdominal respiratory movements, while females have more thoracic respiratory movements. However, patients with severe respiratory compromise may display paradoxical breathing movements such that the abdomen moves inward and the thoracic cage go outward during inspiration. While standing at the foot of the bed, the clinician should also note whether or not the patient Is overweight or if they appear wasted. Obesity is associated with obstructive sleep apnoea and obesity hypoventilation syndrome, while excessive, unintentional weight loss has been associated with non-benign processes. Furthermore, bedside adjuncts such as metered dose inhalers face mask for the administration of oxygen, or an incentive spirometer can also clue the physician in on the possible diagnosis.

Ask the patient to position both upper limbs such that each limb is flexed at the shoulders and extended at the elbows and wrists. Observe the hands for frequent back and forth motions referred to as flapping tremors or asterixis. Another way to elicit asterixis is by asking the patient to squeeze the middle and index fingers together for 30 seconds or more. Patients with a flapping tremor would be unable to maintain their grip for that long. This clinical sign is indicative of carbon dioxide retention and impending respiratory failure as a result of pulmonary or hepatic dysfunction.

While the patient’s arms are stretched out, use the opportunity to examine the hands. Pallor of the palms and nailbeds is suggestive of anemia; while bluish discoloration of the nail beds suggests peripheral cyanosis. Patients with a long history of smoking may also have brownish discoloration of the nails and sides of the distal phalanges resulting from the tar found in cigarettes. Also, assess the fingers for evidence of clubbing. This phenomenon occurs in stages (i.e. grades 1 to 4) and is characterized by loss of the nail bed angle, increased fluctuance of the nail bed, and increased anteroposterior diameter of the distal phalanges of the digits. These changes are most often with bronchiectasis, interstitial lung disease, lung malignancies, and cardiac abnormalities. 

Check the conjunctival mucous membranes for pallor, and the buccal membranes and subglossal mucosa for bluish color change suggesting central cyanosis. Position the patient’s bed and ask them to turn their head to the side opposite to where the examining physician is standing. Inspect the neck for the elevation of the jugular venous pressure; which is a double inward pulsation occurring between the heads of the sternocleidomastoid muscle. This clinical change can result from obstruction of the superior vena caval pathway by an adjacent lung tumor, or by right heart failure secondary to pulmonary hypertension. Another key feature to look for in the neck is for visibly enlarged cervical or supraclavicular lymph nodes as they are commonly enlarged in patients with lung malignancies. 

Internal jugular vein (lateral-right view)


Palpation of the lymph nodes is a part of the examination of the peripheries. Palpate the epitrochlear, axillary, cervical, and supraclavicular nodes. This allows detection of enlarged lymph nodes that are not readily visible. With regards to the thorax, palpation involves checking the trachea, location of the apex beat, chest expansion, and tactile vocal fremitus. The abbreviation TACT can be used to remember the sequence. 

The trachea can become deviated in cases of lung collapse, a space-occupying lesion, or a pneumothorax. The technique to check for tracheal centrality can be uncomfortable so be sure to explain this to the patient. Ask the patient to look straight ahead then gently rest the index finger of the right hand in the suprasternal notch and feel for the trachea. It is normal to have a slight deviation in some individuals; however, gross deviation suggests an underlying pathology. In patients with a pneumothorax (simple or tension), hemothorax, a large pleural effusion, or a lung tumor would result in tracheal deviation away from the affected side. On the other hand, the trachea can deviate to the affected side in cases of lung collapse, fibrosis of the upper lobe, or a pneumonectomy.

Anatomy of the trachea (anterior view)


Localizing the apex beat is a relatively simple task that is also done in the cardiovascular examination. Both hands are placed on the anterior chest wall to detect the cardiac impulse. Under normal circumstances, the apex beat can be localized in the left fifth intercostal space, in the midclavicular line. Deviation of the apex beat in conjunction with tracheal shift suggests an overall mediastinal shift. However, an isolated shift in the apex beat with a central trachea supports a cardiac pathology instead of a pulmonary disorder. 

Firmly press the palmar aspect of each examining hand to the upper part of the patient’s anterior chest. Observe for equal rise and fall of both hands with inspiration and expiration. This provides a crude assessment of the patient’s chest expansion of the upper lung fields. The lower lung fields can be assessed by placing the hands slightly lower down on the anterior chest wall, extending the fingers around the sides of the chest, and approximating the thumbs in the midline. As the patient respires, there should be symmetrical movement of the thumbs away from the midline. If the chest expansion is reduced on both sides then the underlying etiology is likely due to extensive pulmonary fibrosis or severe chronic obstructive pulmonary disorder. Conversely, if only one side is affected then the likely cause is an ipsilateral lobar or lung collapse, pleural effusion, or pneumothorax.

Another useful technique in the respiratory examination is testing for tactile vocal fremitus. This test is performed by resting the ulnar border of the hand within an intercostal space and asking the patient to say a monotonous word like “ninety-nine” or “one, one, one”. The principle behind the test is that sound generated within the larynx is transmitted into the trachea, bronchi, lung parenchyma, and then the chest wall. Since the normal lung contains a mixture of solid lung parenchyma and air-filled airways, the vibrations are readily perceivable. Vibrations are transmitted well through dense material but poorly through air. Therefore vocal fremitus is reduced in conditions that result in air trapping, such as emphysema, asthma, and airway obstruction. The opposite occurs with consolidation or inflammation where the lung density increases.


The goal of this examination is to appreciate the loudness and pitch of the percussion as well as the subsequent vibrations. Percussion is done over each lung zone (upper, middle, and lower) on both sides of the chest. It is also important to ensure that identical areas on both sides are being percussed, as this examination relies on comparing the findings on one side with the other. Apply the volar aspect of the left hand on the patient’s chest. With the digits slightly separated, firmly press the left middle digit in the intercostal space. Hit the center of the middle phalanx of the left middle finger with the tip of the right middle finger. Be sure to briskly remove the left finger to avoid dampening the sound generated by percussing. Using the same technique, percuss the lung apices in the supraclavicular fossa.

The findings from this technique are described as being resonant, hyper-resonant, dull, and stony dull. Normal, healthy lungs are resonant; while solid, dense structures are dull. Hyper-inflated lungs such as those of an asthmatic patient or one with a pneumothorax are hyper-resonant (louder than normal). Inflamed and consolidated lungs are dull (similar to percussing the liver); while those of a patient with a hemothorax and pleural effusion are stony dull


Low-frequency sounds are transmitted to the chest wall and can be readily detected with the bell of the stethoscope, while the diaphragm picks up high-pitched sounds. The physician should test for vocal resonance, which complements tactile vocal fremitus. During auscultation, ask the patient to say “one, one, one” or “ninety-nine”, while listening to the quality and volume of the sound as it resonates. In an individual with healthy lungs, low-pitched sounds are more readily appreciated than high-pitched sounds. Therefore, the numbers are easily heard over consolidations but are diminished over collapsed lung segments or an effusion. Also, ask the patient to whisper the same numbers as above. This will not be easily heard over normal lungs but is significantly increased over consolidated areas of lung parenchyma. The phenomenon is known as whispering pectoriloquy.

Continue auscultating the chest by applying the diaphragm to the chest wall and listen to identical areas on each side of the thorax. Ask the patient to breathe in and out deeply through the mouth and alternate from left to right while working from the apex to the base of each lung. Also listen laterally in an effort to detect any changes in normal breath sounds or any added breath sounds. Breath sounds are described as being vesicular or bronchial. Vesicular breath sounds are rustling in nature, while bronchial breath sounds are hollow and high-pitched. Breath sounds tend to be louder in the apex during inspiration and loud in the base during mid-expiration. There is a rapid decrease in the breath sound during expiration. Pathological causes of diminished breath sounds include pleural effusions, pneumothorax, obesity, or hyperinflation.

There are additional breath sounds that can be appreciated in pathological processes. These sounds include but are not limited to crackles and wheezes. Wheezes are musical sounds generated by uninterrupted passage of air within a partially obstructed airway. While it is most commonly associated with asthma, wheezing can also occur as a result of cardiac failure. Crackles, on the other hand, are non-musical and occur due to collapsing peripheral airways. They can occur at any point during the respiratory cycle. When they occur in the early phase, it is indicative of small airway disease such as bronchiolitis. Crackles during the middle of inspiration suggest pulmonary edema; while those occurring in late respiration can be fine, medium or coarse crackles. Late fine crackles suggest pulmonary fibrosis, medium ones indicate pulmonary edema, and coarse crackles are in-keeping with lung abscesses, pneumonia, or tuberculosis. Coarse crackles heard in both inspiration and expiration suggests bronchiectasis.


While there is a lot of detail to recall, here is a summary of the sequence of events involved in the respiratory examination:

  • Assessment of the patient begins from the first encounter. Look at the patient’s overall appearance and disposition.
  • Position and inspect the patient appropriately; assessing the respiratory and pulse rates.
  • Assess the patient for peripheral cyanosis, clubbing, and asterixis.
  • Examine JVP and lymph nodes.
  • Palpate for trachea centrality, apex localization, chest expansion, and tactile vocal fremitus.
  • Follow up with percussion.
  • Auscultation includes assessing vocal resonance, breath sounds, and listening for added sounds.
  • Repeat the above steps on the posterior thoracic wall as well. 
  • A clinical diagnosis is dependent on a collection of clinical signs and not just a particular sign. 

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