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Showing posts with label pulmonary medicine. Show all posts
Showing posts with label pulmonary medicine. Show all posts

Assessment of Patient Fitness for Thoracic Surgery

Thoracic surgery, involving procedures on the lungs, heart, and other structures within the chest cavity, is a major intervention that can pose significant risks. Hence, preoperative assessment of a patient's fitness for thoracic surgery is crucial to determine surgical feasibility, inform patients of potential risks and benefits, and optimize preoperative conditions for a favorable surgical outcome.

Patient Evaluation

  1. History and Physical Examination: Every preoperative evaluation begins with a comprehensive medical history and physical examination. Factors such as age, smoking history, preexisting conditions (like chronic obstructive pulmonary disease (COPD), asthma, cardiovascular disease, or diabetes), and previous surgeries can significantly influence the risk profile.
  2. Pulmonary Function Testing (PFT): PFT is a key part of preoperative assessment for thoracic surgery. It provides vital information about lung function and can predict postoperative pulmonary function. The forced expiratory volume in one second (FEV1) and diffusion capacity of the lung for carbon monoxide (DLCO) are particularly important measures.
  3. Cardiac Evaluation: Cardiovascular disease is a common comorbidity in patients undergoing thoracic surgery. A thorough cardiac evaluation may include an electrocardiogram (ECG), echocardiography, or stress testing. In specific cases, a coronary angiography may be necessary.
  4. Imaging: CT scans of the chest provide crucial information about the disease's location, extent, and potential surgical approach. They also help identify any unforeseen issues, like unexpected metastasis in cases of lung cancer.
  5. Nutritional Status: Malnutrition can lead to delayed wound healing and increase the risk of postoperative complications. Assessing nutritional status, including parameters like BMI and serum albumin levels, is crucial.
  6. Performance Status: Tools like the Eastern Cooperative Oncology Group (ECOG) or Karnofsky Performance Status (KPS) scales help assess a patient's ability to perform everyday tasks, providing insights into their overall health status and resilience.
  7. Exercise Testing: Exercise tests, such as the six-minute walk test or cardiopulmonary exercise testing (CPET), provide objective measures of a patient's aerobic fitness and endurance.

Risk Stratification and Optimization

Assessment data is used to stratify patients into risk categories. High-risk patients may need additional investigations and interventions to optimize their condition before surgery. Smoking cessation, pulmonary rehabilitation, and optimization of any preexisting conditions (like diabetes or hypertension) are key components of preoperative optimization.

Informed Consent

Once fitness for surgery is established, it is crucial to discuss the potential risks and benefits with the patient. This conversation should encompass not only the surgical risks but also the expected postoperative recovery period and the impact on the patient's quality of life.

Assessing patient fitness for thoracic surgery is a comprehensive process, demanding careful consideration of multiple factors, including pulmonary function, cardiac health, and overall performance status. It enables clinicians to identify potential risks, optimize patient condition before surgery, and set realistic expectations, thereby paving the way for successful surgical outcomes. As each patient is unique, the assessment must be personalized and nuanced, balancing the potential benefits of surgery against its risks.

Understanding the Oxygen Dissociation Curve

The oxygen dissociation curve is a graphical representation that delineates the relationship between the partial pressure of oxygen (pO2) in the blood and the oxygen saturation of hemoglobin, the protein in red blood cells responsible for transporting oxygen. This curve is crucial for understanding how oxygen is delivered to body tissues and cells, and how changes in environmental or physiological conditions affect oxygen transportation and availability.

Understanding Hemoglobin and Oxygen Transport

Hemoglobin is a globular, iron-containing protein within red blood cells, uniquely suited for oxygen binding and transportation. Each hemoglobin molecule can bind up to four oxygen molecules, a process called oxygenation. When oxygen binds to hemoglobin, it forms oxyhemoglobin.

When blood flows through the lungs, oxygen molecules bind to the hemoglobin in red blood cells. This oxygen-rich blood then travels to the body's tissues and organs, where the oxygen dissociates from the hemoglobin (hence the term "oxygen dissociation") and is delivered to cells for their metabolic activities.

The Oxygen Dissociation Curve

The oxygen dissociation curve is typically an S-shaped (sigmoidal) curve. The x-axis represents the partial pressure of oxygen in the blood, and the y-axis represents the percentage of hemoglobin saturated with oxygen. The curve's shape is primarily due to the cooperative binding nature of hemoglobin.

When the blood's pO2 is low, such as in the metabolically active tissues, hemoglobin releases its oxygen (a condition favoring oxygen 'dissociation'). Conversely, when the pO2 is high, as in the lungs, hemoglobin binds to oxygen. This relationship between oxygen's partial pressure and its saturation is the essence of the oxygen dissociation curve.

Factors Affecting the Oxygen Dissociation Curve

Several factors can shift the oxygen dissociation curve to the left or right, altering hemoglobin's affinity for oxygen:

  1. Temperature: An increase in body temperature shifts the curve to the right, indicating decreased oxygen affinity. This situation is often seen during fever or heavy exercise.
  2. pH (Bohr Effect): The Bohr effect states that a decrease in pH (indicating an increase in blood acidity) shifts the curve to the right, again, lowering hemoglobin's affinity for oxygen. This effect allows more oxygen to be released in metabolically active tissues that produce more acidic waste products.
  3. Carbon Dioxide (CO2) Levels: High levels of CO2 also shift the curve to the right. CO2 is a byproduct of cellular metabolism and increases in the blood during vigorous exercise or in certain health conditions.
  4. 2,3-Diphosphoglycerate (2,3-DPG): This compound, produced by red blood cells, reduces hemoglobin's affinity for oxygen. Increased levels of 2,3-DPG, as seen in conditions like anemia or high altitude, shift the curve to the right, facilitating oxygen release to tissues.

The oxygen dissociation curve is an integral tool for understanding oxygen transport and delivery in the body. Its sigmoidal shape reflects the cooperative binding of oxygen to hemoglobin, and shifts in the curve due to various physiological or environmental conditions help ensure that tissues receive the oxygen they need. Understanding these concepts is crucial in fields like physiology, medicine, and biomedical research.

Physiological changes in lung at high altitude and pathophysiology of high altitude pulmonary edema

At high altitudes, where the oxygen concentration in the air is lower, the body undergoes several physiological changes to adapt to the reduced oxygen availability. These changes primarily occur in the lungs and cardiovascular system. Here are some of the key physiological changes that take place:

  1. Hyperventilation: At high altitudes, the body increases its respiratory rate and depth of breathing to compensate for the reduced oxygen levels. This hyperventilation helps maintain adequate oxygen uptake and carbon dioxide elimination.
  2. Increased pulmonary blood pressure: In response to low oxygen levels, the blood vessels in the lungs constrict (pulmonary vasoconstriction), causing an increase in pulmonary blood pressure. This redirection of blood flow helps optimize oxygen delivery to the body's tissues.
  3. Increased red blood cell production: The body responds to high-altitude conditions by producing more red blood cells (erythropoiesis). This increase in red blood cells helps enhance the oxygen-carrying capacity of the blood.
  4. Altered gas exchange: The efficiency of gas exchange in the lungs may be impaired at high altitudes due to factors such as reduced oxygen pressure and increased diffusion distance. However, the body's compensatory mechanisms, including hyperventilation and increased red blood cell production, help mitigate the impact of these changes.

Despite these adaptive mechanisms, some individuals may still develop high altitude pulmonary edema (HAPE), which is a potentially life-threatening condition. HAPE is a type of non-cardiogenic pulmonary edema that occurs at high altitudes and is characterized by the accumulation of fluid in the lungs. The exact pathophysiology of HAPE is not completely understood, but several factors contribute to its development:

  1. Increased pulmonary artery pressure: The constriction of blood vessels in the lungs at high altitudes can lead to increased pulmonary artery pressure. This elevated pressure can cause leakage of fluid from the pulmonary capillaries into the lung tissue.
  2. Increased capillary permeability: The increased pulmonary artery pressure and the hypoxic environment at high altitudes can cause damage to the endothelial lining of the pulmonary capillaries. This damage results in increased capillary permeability, allowing fluid to leak into the alveoli.
  3. Inflammation: Hypoxia and other factors at high altitudes can trigger an inflammatory response in the lungs. Inflammatory mediators and increased vascular permeability further contribute to the accumulation of fluid in the alveoli.
  4. Reduced clearance of fluid: The impaired lymphatic drainage from the lungs at high altitudes can hinder the clearance of fluid, exacerbating the accumulation of fluid in the alveoli.

The accumulation of fluid in the lungs leads to impaired gas exchange, causing symptoms such as shortness of breath, cough, wheezing, and fatigue. If left untreated, HAPE can progress rapidly and result in severe respiratory distress and even respiratory failure.

The management of HAPE involves immediate descent to lower altitudes, administration of supplemental oxygen, and the use of medications such as diuretics to reduce fluid accumulation. Prompt medical attention is crucial for the effective treatment of HAPE.

Normal process of respiration, Oxygen uptake in the blood and elimination of CO2 from the body

Respiration is the process by which living organisms take in oxygen from the environment and release carbon dioxide. In humans, respiration involves two main processes: external respiration and internal respiration.

External respiration occurs in the lungs and involves the exchange of gases between the air in the lungs and the bloodstream. When we inhale, air enters the respiratory system and reaches the alveoli, which are tiny air sacs in the lungs. The alveoli are surrounded by a network of capillaries, where the exchange of gases takes place.

Oxygen (O2) from the inhaled air diffuses across the thin walls of the alveoli and enters the bloodstream. It binds to hemoglobin, a protein in red blood cells, forming oxyhemoglobin. This oxygenated blood is then transported to the body's tissues.

Internal respiration occurs at the tissue level, where oxygen is delivered to cells and carbon dioxide (CO2) is produced as a waste product of cellular metabolism. In the tissues, oxygen detaches from hemoglobin and diffuses into the cells, where it is used in the process of cellular respiration to produce energy.

During cellular respiration, glucose and oxygen react to produce carbon dioxide, water, and energy in the form of adenosine triphosphate (ATP). The carbon dioxide generated as a byproduct diffuses out of the cells into the surrounding capillaries.

The oxygen-depleted blood returns to the heart and is pumped to the lungs through the pulmonary artery. In the lungs, carbon dioxide diffuses from the capillaries into the alveoli, and it is then exhaled out of the body during the process of exhalation.

Oxygen uptake in the blood is facilitated by the high affinity of hemoglobin for oxygen. Hemoglobin binds to oxygen in the lungs, and this binding is reversible, allowing for oxygen to be released in the tissues where it is needed. The oxygen-carrying capacity of blood is influenced by factors such as hemoglobin concentration, blood pH, temperature, and partial pressure of oxygen.

The elimination of carbon dioxide occurs through the lungs during exhalation. Carbon dioxide in the bloodstream combines with water to form carbonic acid (H2CO3), which quickly dissociates into bicarbonate ions (HCO3-) and hydrogen ions (H+). The bicarbonate ions are transported back to the lungs through the bloodstream, where they are converted back into carbon dioxide, which is then exhaled.

Hypoxia refers to a condition in which the body or a region of the body is deprived of adequate oxygen supply. There are various forms of hypoxia, including:

  1. Hypoxic hypoxia: This occurs when there is a decrease in the oxygen concentration in the air, such as at high altitudes or in poorly ventilated environments.
  2. Anemic hypoxia: It results from a decrease in the oxygen-carrying capacity of blood due to a decrease in the number of red blood cells or a decrease in the amount of hemoglobin.
  3. Ischemic hypoxia: It happens when there is a reduction in blood flow to tissues, leading to inadequate oxygen supply. It can be caused by conditions such as circulatory disorders or blockages in blood vessels.
  4. Histotoxic hypoxia: This occurs when the cells are unable to utilize oxygen effectively due to the presence of toxins or metabolic poisons, impairing cellular respiration.
  5. Hypoxemic hypoxia: It results from a decrease in the oxygen content of the blood, usually caused by respiratory disorders, such as lung diseases or impaired gas exchange in the lungs.

These forms of hypoxia can have varying degrees of severity and can lead to symptoms ranging from mild breathlessness and fatigue to more severe complications affecting vital organs. Prompt medical attention and appropriate interventions are necessary to address hypoxic conditions and restore oxygen supply to the body's tissues.

Normal Second heart sound (Identify the abnormalities of S2)

The most difficult thing in auscultation is to identify the abnormalities of S2.

Physiology of Second heartsound
Two components for 2nd heart sound are- aortic and pulmonary

Aortic component it is the 1st component and loud one heard in all areas.

Pulmonary component - 2nd component and soft, heard only over pulmonary area.

Normal second heart sound
It is a high pitched sound with normal split - 2 components are separately heard during inspiration and as single component during expiration over the pulmonary area.
Distance between the 2 components during inspiration is 0.04 sec, during expiration is 0.02 sec. Human ear can appreciate, when the distance between the 2 components is 0.03 or more. Normal second heart sound is expressed as - normal in intensity and normal split with respiration.

Things to look for in S2:
A2 heard over aortic area and pulmonary area and the apex.
P2 heard over pulmonary area and 2-4 LICS only and not at the apex.
P2 heard over the apex only in pulmonary artery hypertension and in young.
Best site for S2 in COPD - epigastrium.

Inspection for shape and movement of the chest

Looking from above (standing behind the patient), over the shoulders or the upper part of the chest.If standing or sitting is not possible for the patient, inspect the chest in Iying down position, patient lies absolutely straight in the bed in supine position) inspect from the

  • Top.
  • Foot end of the bed.
  • The sides in profile.
  • Head end.
  • Back (try to turn the patient to any one side).
The following are the points to note :
  1. Any deformity, fullness or depression (i.e. shape of the chest), apical impulse etc.
  2. Back (winging of the scapula, drooping of the shoulder, kyphoscoliosis, gibbus. skin changes).
  3. Whether both the sides of the chest arc moving simultaneously and symmetrically.
  4. Classically  winged scapula is found in paralysis of nerve to serratus anterior (C 6 ,7) and sometimes in facio-scapulo-humeral muscular dystrophy.
  5. Assessment of the expansion of the upper lobes is better achieved by inspection
  6. From behind the patient, looking down at the clavicles during moderate respiration.
  7. Equal on both sides - normal
  8. Reduced movement on one side -  pleural disease ,pulmonary disease
  9. Bilaterally reduced movement - in emphysema.

Assessment of position of Trachea

Trail's sign

Shift of trachea produces prominence of sternal head of sternocleidomastoid on the side to which the trachea is shifted. It is called Trail's sign.

The pretracheal fascia encloses the clavicular head of stemomastoids muscle on both sides. When the trachea is shifted to one side, the pretracheal fascia covering the stemomastoid muscle on that side relaxes, producing the clavicular head more prominent on the side of tracheal deviation.

Causes of tracheal shift

Pleural disease - Shift to opposite side
  • Pleural effusion
  • Pneumothorax
Pulmonary disease-Shift to same side
  • Fibrosis and collapse of lung
Goiter - Shift of trachea to opposite side.

Position of the Trachea and Trail's sign

Shifting of upper border of liver dullness :

To delineate the upper border of liver dullness, you should percuss the anterior chest wall along right MCL from above downwards. Normally the upper border of liver dullness is present in right 5th ICS at MCL
Lowered or obliterated  of liver dullness is noted in 
  • Emphysema.
  • Pneumothorax (right sided).
  • Perforation of abdominal hollow vtscus e.g. perforation of peptic ulcer.
  • Cirrhosis of liver (liver becomes small).
  • Visceroptosis of liver.
Elevated liverdullness :
  • Amoebic or pyogenic liver abscess.
  • Subdiaphragmatie abscess (right).
  • Pleural effusion (right).
  • Basal pneumonia (right).
  • Increased intraabdominal tension due to ascites or pregnancy.
The upper border of liver dullness is present in right 7th and 9th ICS when percussed along
midaxillary and scapular line respectively.

Causes of chestpain in clinical practise

Types of chest pain observed in clinical practise are:
Restrosternal pain
Pleuritic pain
Acut onset chest pain
Chest pain with dyspnea 
Causes of chest pain with circulatory collapse or syncope

  • Acute myocardial infarction.
  • Tension pneumothorax.
  • Pulmonary' thromboemlxilism
  • Dissectlon of aorta.
  • Cardiac tamponade.
  • Acute pancreatitis.
  • Upper gastro intestinal bleeding.

Causes of Retrosternal chest pain

Retrosternal chest pain  causes are given below
  • Ischaemic heart disease.
  • Oesophagitis or diffuse oesophageal spasm.
  • Acute dry percardltis.
  • Acute mediastinitis.
  • Diaphragmatic hernia.
  • Aneurysm of the aorta.
  • Dissecting aneurysm.
  • Psychogenic.
Causes of upper retrosternal Pain
It is a momentary pain which increases in intensity on coughing and subsides when the cough becomes productive. This is seen in acute tracheitis.
Mid or Lower Retrosternal Pain in mediastinal disease
Character resembling cardiac pain, radiate to neck and arms, unrelated to exertion.
This pain is constrictive in character and may be present in:
  • Acute mediastinitis
  • Mediastinal tumour
  • Mediastinal emphysema
  • Reflux esophagitis
  • Achalasia cardia.

Causes of chest pain with breathlessness :

Following are the causes of chest pain with breathlessness
  • Spontaneous pneumothorax.
  • Acute myocardial infarction-Occurs in middle aged or aged persons ,characterised by  retrosternal pain with radiation to left hand, associate with  drenching sweat and shock. Breathlessness with signs of heart failure may occur.
  • Acute pulmonary thromboembolism - Sudden onset of chest pain  with dyspnoea, haemoptysis and circulatory collpase develop. Tachycardia, right ventricular gallop rhythm, loud P2 are the clinical sign present.There is  normal resonant note on percussion over the chest. History of prolonged recumbency or signs of thrombophlebitis may be noted.
  • Dissection of aorta -  Abrupt onset of chest pain with dyspnoea  and will mimick acute myocardial infarction with pain referred to the back. There is discrepancy between carotid pulses difference in BP in two arms, arrhythmia and features of acutely developing aortic regugitation. Dissection  of aorta occur more commonly in  Marfans  syndrome, hypertension, coarctation  and pregnancy
  • Acute dry pleurisy (specially from consolidation) - Dyspnoea is not so common in this situation but chest pain is present. Pleural Friction rub is audible and no sign of pneumothorax can be detected.
  • Massive collapse of the lung -There will be history of aspiration of foreign body .Mediastinalshifting is noted towards the side of collapse. Impaired resonance note on percussion. Breath sound is diminished vesicular or absent.
  • H/O trauma can also produce chest pain with dyspnea. Point of tenderness may be detected. Normal resonant note on percussion.Typical findings of pneumothorax are lacking.
  • Psychogenic condition can also produce chest pian with dyspnea

What are the causes of acute chest pain?

The causes of acute chest pain are the following
  • Ischaemic heart disease (HID), ie. angina pectoris or acute myocardial infarction: aortic stenosis.
  • Acute dry pleurisy due to any cause (tuberculosis, pneumonia commonly)
  • Spontaneous pneumothorax.
  • Diffuse oesophageal spasm (may be food-related) : gastro-oesophageal reflux disease.
  • Acute pulmonary thromboembolism, tracheobronchitis, mediastinilis.
  • Abscess, furuncle on the chest wall/myositis/fibrositis.
  • Trauma to the chest wall, eg. rib fracture.
  • Costoeondritis (Tietzes syndrome)
  • Malignant deposits on the ribs, multiple myeloma.
  • Acute dry percarditis.
  • Intercostal myalgia (Bornholm disease—intercostal muscle involvement by Coxsackie  virus infection).
  • Herpes zoster on the chest wall.
  • Dissection of ascending aorta.
  • Anxiety states /psychogenic  (cardiac neurosis)
  • Abdomina disorders like hiatal hernia ,gall bladder stones, acute  pancreatitis, splenic flexure syndrome

What is Stridor?

Stridor can be laryngeal or tracheal in origin
Laryngeal stridor
High pitched crowing sound better heard during inspiration
Causes of laryngeal stridor are
  • Foreign body
  • Laryngeal spasm
  • Edema
  • Infection
  • Tumor
  • Bilateral vocal cord paralysis.
Tracheal stridor
It is a low pitched sound best heard in inspiration.
Croaking inspiratory sound or continuous sound increased by coughing, associated with inspiratory dyspnoea and indrawing of the suprasternal notch.
Causes of tracheal stridor are
  • Obstruction of the tracheal lumen by tumor or foreign body.

Inspection of respiratory system

Displacement of apical impulse is seen in push and pull of the pleuropulmonary disease
Inspection  for shape and movement of the chest
Crowding of ribs
Patient should be in sitting or standing posture
Crowding of ribs should be made out from the back
Standing behind the patient by sliding the fingers along the lower intercostal spaces on either sides and comparing them
Supraclavicular and Infraclavicular fossa
Supraclavicular and Infraclavicular fossa hollowing is seen following 
  • Fibrosis 
  • Collapse of the lung, 
  • Malnutrition
Unilateral flattening of the chest
It is seen in 
  • Fibrosis 
  • Collapse of lung
Spinal Deformity
Movement of the Chest-It is described in terms of rate, rhythm ,equality and type of breathing.
The skin over the chest wall 
The skin over the chest wall is examined for the following:
  • Engorged veins and subcutaneous nodules seen in sarcoid and malignancy
  • Intercostal scar  are drained pleural effusion, empyema or pneumothorax
  • Discharging sinuses is seen in Tuberculosis
  • Empyema necessitans in which there is an intercostal swelling is seen close to the sternum.
  • Metastatic nodule
  • Swelling due to empyema necessitans.

Presence of Veins over the chest wall
In superior vena caval syndrome look for presence of distended veins over the chest wall 
If the obstruction to SVC occur above the level of azygos vein, collateral venous circulation on the anterior surface of chest wall is less prominent as the intercostal veins drain into the azygos vein.
If the obstruction to SVC is at or below the level of azygos vein, collateral veins on the chest become prominent as these collaterals carry blood caudally to the IVC.
Common causes of intercostal suction
Following are the common causes of intercostalsuction
  • Foreign body wiihin larynx or trachea.
  • Diphtheria.
  • Oedema of the glottis (in anaphylaxis).
  • COPD.
  • Bronchiolitis (in infants and children).
  • Bilateral diaphragmatic palsy.
Observation on inspection of back in respiratory system 

What are the abnormal shape of chest?

Normal chest is symmetrical and elliptical in cross section.The following abnormalities are noted in shape of chest
Flat chest 
The anteroposterior to transverse diameter ratio is 1 : 2
Present in  fibrothorax
Barrel shape chest
The anteroposterior to transverse diameter ratio is 1:1
Seen in physiological states like infancy and old age and in pathological states like COPD (emphysema).
Pectus Carinatum or Pigeon chest
It is the forward protrusion of the sternum and adjacent costal cartilage
It is seen in
  • Childhood respiratory disease like asthma 
  • Rickets
  • Marfan's syndrome 
Pectus excavatum or Funnel chest or cobbler's chest
This is the exaggeration of the normal hollowness over the lower end of the sternum.
It is a developmental defect.
Due to displacement of heart the apex beat is shifted further to the left and the ventilatorv capacity of the lung is restricted
This is found in marfan syndrome.
Thoracic kyphoscoliosis reduce ventilatory capacity of lung
Harrison's sulcus
It is due to the indrawing of ribs to form symmetrical horizontal grooves above the costal margin, along the line of attachment of diaphragm due the hyperinflation of lung,
It is due to the hyperinflation of the lungs and the strong contraction of the diaphragm contraction
  • Occurs in chronic respiratory disease in childhood-Childhood asthma 
  • Rickets 
  • Blocked nasopharynx due to adenoid enlargement
Rachitic and scorbutic rosary
It is the beed like enlargement of costochondral junction in rickets and scurvy
Scorbutic rosary: It is the sharp angulation, with or without beading or rosary formation, of the ribs, arising as a result of backward displacement or pushing in of the sternum,
Scorbutic rosary is painful
Teitz disease
It is characterised by congenital costochondral prominence.
Other abnormalities are
Abnormalities in shape of chest
1.Droopingof shoulder
2.Hollowing of supra/infradavicular fossae is seen in
Bulging of chest wall Seen in  Mass lesion, Empyema
3.Crowding of ribs
Patient should be in sitting or standing posture
Crowding of ribs should be made out from the back
Standing behind the patient by sliding the fingers along the lower intercostal spaces on either sides and comparing them

Normal shape of Chest

  • Normal chest is bilaterally symmetrical without undue elevation or depression,
  • Truncated cone-shaped  with transverse diameter > anteroposterior diameter and vertical is the highest ,elliptical in cross section.
  • The normal anteroposterior to transverse diameter ratio is 5 : 7. 
  • The normal subcostal angle is 90°. 
  • It is more acute in males than in females.
  • Both the sides of the chest move simultaneously and symmetrically
Look for the following in inspection of chest:
Crowding of ribs
Patient should be in sitting or standing posture
Crowding of ribs should be made out from the back
Standing behind the patient by sliding the fingers along the lower intercostal spaces on either sides and comparing them
Supraclavicular and Infraclavicular fossa
Supraclavicular and Infraclavicular fossa hollowing is seen following 
  • Fibrosis 
  • Collapse of the lung, 
  • Malnutrition
Flattening of chest
Unilateral flattening of the chest
It is seen in 
  • Fibrosis 
  • Collapse of lung
The skin over the chest wall is examined for the following:
  • Engorged veins and subcutaneous nodules seen in sarcoid and malignancy
  • Intercostal scar  are drained pleural effusion, empyema or pneumothorax
  • Discharging sinuses is seen in Tuberculosis
  • Empyema necessitans in which there is an intercostal swelling close to the sternum.
  • Features of systemic fungal infection
  • Metastatic nodule
  • Swelling due to empyema necessitans.
Kyphosis (forward bending of the spine) and Scoliosis (lateral bending of the spine).

Drooping of the shoulder

How to detect the drooping of shoulder?
Ask the patient to stand with the face away from the examiner
  • Identify the level difference of the tips of both shouders
  • Distance between the inferior angle of scapula and the midspinal line is noted
  • Note the prominence of the inferior angle of the scapula
  • If any two of the above are positive the patient has a drooped shoulder
  • In drooping the following findings are noted
  • Lower end of scapula is at a lower level
  • Spine - scapular distance is reduced
  • Medial border of scapula is more prominent on the affected side
Causes of drooping
  • Fibrosis
  • Collapse
  • Trapezius paralysis
Mechanism of drooping in Fibrosis
It is due to decreased expansion of the lung producing disuse atrophy of the muscles & irreversible bone changes.
Minimum time for drooping to develop in fibrosis is 6 months
Mechanism of drooping in Collapse
Drooping is due to disuse atrophy,it is partially reversible
This is due to volume loss of the lung
Drooping takes only 6 weeks in collapse whereas it takes 6 months in fibrosis because the lung function is totally lost acutely in collapse and gradually in fibrosis
Drooping correctable on stooping forward is called as pseudodrooping
Causes are
  • Congenital scoliosis 
  • Pleurisy-Due to muscle spasm.
  • Empyema-Due to toxic myositis
Drooping vs Pseudodrooping
Drooping                                                                    Pseudodrooping
Convexity to the opposite side of lung disease        Convexity may to be either side
Not correctable on stoopirfg forwards or walking    Correctable on stooping forwards or walking
Causes of Reversible drooping
  • Pleurisy
  • Empyema
  • Collapse with removal of obstruction
Causes of Irreversible drooping 
  • Fibrosis

Examination of the Respiratory System

Inspection ot upper Respiratory tract
Examination of Oral cavity
  • Oral hygiene
  • Dental caries
  • Oral thrush
  • Tonsils.
Examination of Nose
  • Deviated nasal septum
  • Nasal polyps may be seen in- Wegener's granulomatosis, allergic asthma, ABPAS ,cystic fibrosis.
Examination of Pharynx
  • Postnasal drip
  • Lymphoma deposits.
Inspection of Lower Respiratory Tract
All the findings in the clinical examination should be compared on both sides in the following areas:
  • Supraclavicular area
  • lnfraclavicular area
  • Mammary region
  • Axillary region
  • Infraaxillary region
  • Suprascapular region
  • Interscapular region
  • Infrascapular region.
Assessment of Respiratory System
Physical Examination

  • posture, shape, movement, dimensions of chest,flared nostrils, use of accessory muscles, skin color, and rate, depth, & rhythm of respiration


  • respiratory excursion, masses, tenderness


  • flat, dull, resonant, hyperresonant sounds


  • breath sounds, voice sounds, crackles, wheezes

Observation on inspection of back in respiratory system

Inspection of back (in respiratoty system or CVS) is always done in standing position if the condition of the patient permits.This is to avoid undue obliquity.
One should look for the following

  • Kyphosis (look from sides in profile).
  • Scoliosis.
  • Drooping of the shoulder (signifies apical fibrosis or collapse).
  • Winging of the scapula (long thoracic nerve palsy or spinal deformity).
  • Whether the inferior angle of scapula on both sides are at the same level or not.
  • Interscapular area (spino-scapular distance) you should compare between two sides of chest.
  • Gibbus is an acute angulation in the spine commonly due to caries spine
  • Ankylosing spondylitis (stiff and immobile spine)—may produce restrictive lung disease.
  • Crowding of rib is examined both in the front as well as the back.
  • Skin condition—Scar, sinus, herpes zoster, local oedema, venous prominence, arterial pulsation(Suzman s sign), pigmentation, deformity after thoracic operation,example  thoracoplasty etc. 
  • Movement—Whether both the sides are moving simultaneously and symmetrically, or not

What is hyperventilation?

Hyperventilation means deep rapid breathing as in

  • Acidosis
  • Upper brainstem lesion,
  • Hypoxia
  • Hysteria
  • Salicylate poisoning.

Tachypnea is respiratory rate > 22/min.
Bradypnea is respiratory rate < 10/min.