Download MBBS Final Year Medicine Notes Respiratory System

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Final Year Medicine Notes Respiratory System

LETUDA'S NOTE
RESPIRATORY SYSTEM
WRITTEN AND COMPILED BY PRITHWIRAJ MAITI
FINAL YEAR MBBS, R.G.KAR MEDICAL COLLEGE
TABLE OF CONTENTS
CHAPTER
PAGE NO
BASIC OVERVIEW
2
PLEURAL EFFUSION
3
PNEUMOTHORAX
7
PULMONARY EMBOLISM
11
BRONCHIECTASIS
14
COPD
16
COR PULMONALE
24
RESPIRATORY FAILURE
26
BRONCHIAL ASTHMA
28
PULMONARY FUNCTION TEST
34
BRONCHOGENIC CA AND ITS COMPLICATIONS
BRONCHOGENIC CARCINOMA
39
SVC OBSTRUCTION
43
PANCOAST TUMOR
45
PNEUMONIA
46
ARDS
51
PAH
53
INTERSTITIAL LUNG DISEASES (ILD)
55
SARCOIDOSIS
59
EXTRINSIC ALLERGIC ALVEOLITIS (HYPERSENSITIVITY PNEUMONITIS)
62
CRYPTOGENIC ORGANISING PNEUMONIA
64
PERICARDIAL DISEASES
ACUTE PERICARDITIS
66
PERICARDIAL EFFUSION
67
CARDIAC TAMPONADE
70
CONSTRICTIVE PERICARDITIS
71
CARDIOMYOPATHIES
72
SPECIAL TOPIC: ACID BASE BALANCE
76

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A basic overview of respiratory system examination
Points to examine in respiratory system:
1. Movement of chest.
2. Mediastinal shifting.
3. Percussion.
4. Auscultation:
a. Breath sounds:
Vesicular breath sound (VBS).
Bronchial breath sound (BBS).
b. Vocal resonance.
c. Any adventitious/ added sound(s).
Findings of respiratory system in some common diseases:
Condition
Mediastinal
Percussion
Breath
VR/ VF
Added sound(s)
shifting
sound
Pleural
Opposite
Dull
VBS
-
effusion
side
Pneumothorax If at all, to
Tympanitic
VBS
-
opposite
COPD
-
Hyper-
VBS
Rhonchi (due to
resonant (if
airway narrowing)
hyperinflation
present)
Asthma
-
Normal
Normal/ Normal/
Rhonchi
VBS
Consolidation
-
Impaired/ dull
BBS
Crepts (wet sound)
Collapse
Same side
Impaired/ dull
BBS
-
Fibrosis
Same side
Impaired/ dull
VBS
Crepts

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Pleural effusion
It is defined as accumulation of abnormal amount of fluid in the pleural space.
Types and causes:
1. Transudative pleural effusion:
a. LHF/ CCF.
b. Chronic liver disease.
c. Nephrotic syndrome.
2. Exudative pleural effusion:
a. Infection in the pleural space:
TB.
b. Malignant effusion:
Bronchogenic CA.
Breast CA.
Lymphoma.
c. Autoimmune/ connective tissue disorder:
Rheumatoid arthritis.
SLE.
d. Acute pancreatitis.
e. Pulmonary embolism/ infarction.
Clinical features:
Due to effusion
Due to underlying etiology
Chest discomfort/
1. LHF: SOB, PND, Orthopnea.
dull ache in the
2. Chronic liver disease: Abdominal swelling,
affected side.
GI bleeding.
Shortness of breath
3. Nephrotic syndrome: Generalized swelling.
(SOB).
4. Bacterial infection: Fever, cough, dyspnea.
Sharp pleuritic
5. TB: Weight loss, loss of appetite, low grade
chest pain (if there
fever, haemoptysis.
is an underlying
6. Malignancy: Rapid weight loss, loss of appetite.
acute pleurisy).
A lump with features of primary malignancy.
7. Connective tissue disorders:
a. Red eye/ gritty eye.
b. SOB.
c. Skin rash.
d. Arthralgia.
e. Hematuria.

---

Signs due to effusion:
Inspection
Affected side:
Movement restricted.
Bulging.
Palpation
Expansion restricted.
Shift: To the opposite side, in case of massive effusion.
Percussion
At and below the level of effusion: Dull.
Auscultation
VBS.
VR/VF .
Signs due to underlying etiology:
Following findings may give clue about underlying etiology:
Findings
Underlying etiology
Clubbing
Bronchogenic CA.
Lymphadenopathy
TB.
JVP
CCF (Pulsatile).
SVC obstruction (Non-pulsatile).
Malignancy (Breast CA, Lymphoma).
Jaundice
Chronic liver disease.
Metastatic disease of liver.
Cardiovascular signs of LVF may be present.
GI signs of chronic liver disease may be present.
Breast examination may show the lump.
Investigation
1. Blood: Hb/ TC/ DC/ CRP or ESR.
2. Urea-creatinine Na+ K+.
3. Liver function test.
4. Chest X Ray:
It helps to diagnose effusion and in many cases, the underlying
etiology.
5. Diagnostic aspiration of pleural fluid.
a. Physical character:
Hemorrhagic: Malignant cause.
Turbid: Infection.

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b. Chemical character:
Paired serum sample for protein and LDH:
Diagnostic criteria:
Exudative (if it fulfils any 1 criteria):
Transudative: If it doesn't fulfil any criteria.
c. Microbiological character:
Gram stain, culture sensitivity.
AFB, Mycobacterial culture: Diagnostic yield is very low.
d. Cytological character:
Abnormal/ malignant cells: In malignant effusion.
Polymorphonuclear predominant: Polymorph. effusion.
Predominant lymphocytic: TB, Malignant effusion.
e. Markers of TB:
Adenosine Deaminase (ADA) level.
Interferon- level.
6. Pleural biopsy:
Either under radiological evidence/ thoracoscopically.
7. Other relevant investigation(s):
Depending on the underlying etiology.
Treatment
1. Treatment of effusion:
a. If it is likely to be a Transudative effusion, then usually treating the
cause is sufficient to get rid of the effusion. In most cases, effusion
doesn't require drainage.
b. In unilateral Exudative effusion, drainage of fluid by inserting an
intercostal chest drain becomes essential under following
circumstances:
Symptomatic effusion.
Moderate to severe effusion even it is asymptomatic.
Empyema.

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c. In case of recurrent effusion:
Pleurodesis can be attempted where adhesion is induced
between visceral and parietal pleura by some sclerosing agent
like TALK/ Bleomycin/ Tetracycline/ Betadine.
Insertion of a long term indwelling pleural catheter.
Treating the underlying cause.

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Pneumothorax
It is defined as presence of air in the pleural space.
Types:
Based on clinical features
Primary (in absense of lung
Secondary (in presence of
disease)
underlying lung disease)
At risk: Tall, young and
At risk:
thin individuals
COPD.
Long standing asthma.
TB.
Marfan's syndrome.
Langerhans cell hiotiocytosis.
Lymphangitis leiomyomatosis.
Based on
pathophysiology
Closed type
Open type
Tension type
Closed type:
Air starts accumulating, but after a certain time, the punctured area of lung
gets sealed off on its own.
Open type:
Air freely flows in and out of pleura during inspiration and expiration,
respectively.

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Tension type:
Here a pulmonary parenchymal flap acts as a one way valve, allowing air to
move in during inspiration but does not allowing it to come out during
expiration, leading to rapidly progressing accumulation of air, leading to
compressive effect (tamponade effect) on heart and hemodynamic instability
(reduced cardiac output).
Clinical features:
Symptoms
1. Dyspnea:
It may be mild/ severe/ rapidly progressing, depending on the amount of
air in the pleural space. At times, it is precipitated following a bout of
severe cough.
2. Chest pain:
A momentary sharp chest pain may occur (due to tear of the underlying
lung tissue).
3. Sudden collapse/ blackout: In tension penumothorax.
4. History suggestive of underlying lung disease may be present.
Signs
1. Tachypnea.
2. Tachycardia.
3. Pulse oxymetry: Low SpO2 (where normal oxygen saturation is 95-96%).
4. Cyanosis: In case of severe hypoxia.
5. Hemodynamic instability: Suggestive of tension pneumothorax.
Chest examination
Inspection
Movement is restricted on the affected side.
Palpation
Mediastinal shifting towards the opposite side (usually in
case of tension pneumothorax).
Percussion
Tympanitic.
Auscultation
Reduced VBS/ VR/ VF.
Added sound
1. Pneumothorax click:
A clicking sound coinciding with each cardiac cycle
due to movement of pleura against the surface of
heart (in case of left sided pneumothorax only).
2. Coin percussion:
A metallic sound is heard when the patient is

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asked to percuss a coin against another and the
stetho is placed at a diametrically opposite point.
Investigation
1. Chest X Ray (CXR):
a. Confirms diagnosis.
b. An area of lung not traversed by bronchovascular margins.
c. Collapsed border: Visible.
d. Presence/ absence of tracheal shifting.
2. Other relevant investigations to assess the underlying disease.
Treatment protocol
Clinical type
Primary type
Secondary type
Symptomatic? / Size of
Symptomatic? / Size of
p eu othorax 2 c ?*
p eu othorax 2 c ?
Yes
No
Yes
No
Needle aspiration
Observe and
ICD
Needle aspiration
follow up by
chest X Ray
Successful?
Successful?
Yes
No
Yes
No
Follow up with
Intercostal chest
Follow up
ICD
repeat X-Ray
drain (ICD)

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*Size of pneumothorax: Distance between rib margin and collapsed lung
border at the level of hilum.
If it is 2 cm, it is suggestive of pneumothorax of 50% pleural space.
Indications of cardiothoracic referral:
1. Persistent air leak (bubbling> 5 days).
2. Second episode of ipsilateral pneumothorax.
3. First episode of contralateral pneumothorax.
Post-discharge advice:
1. Avoid air travel for 4-6 weeks.
2. Refrain from deep sea diving for rest of life.

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Pulmonary Embolism (PE)
It is defined as occlusion of pulmonary artery/ its branches by a variety of
substances.
Types:
Air embolism
Amniotic fluid embolism
Blood clot/ thromboembolism
Cancer cells (RCC)
Fat embolism
Foreign body (in IV drug abusers).
Pulmonary thromboembolism
It is defined as occlusion of pulmonary artery/ its branches by a thrombus
which usually gets dislodged from a deep vein of lower limb.
(It should be noted that venous thrombosis of upper limb is rare.)
Risk factors of PE:
These are actually the risk factors of lower limb deep vein thrombosis (DVT).
Risk factors of DVT
Vascular stasis
Hypercoagulable state
Pregnancy
Prolonged bed ridden state/
immobility
Active cancer
Lower limb fracture
Protein C/ Protein S/ Antithrombin 3
deficiency
Post operative state
Leiden's disease (Factor 5 deficiency)
Long distance flight

---

Clinical features:
Symptoms
1. Dyspnea: Sudden onset. Severity depends on size of thrombus.
2. Pleuritic chest pain: Sudden onset. It occurs due to spread of
inflammation to the adjacent pleura.
3. Hemoptysis: Small amount of hemoptysis may occur.
4. Sudden collapse: In case of a massive PE occluding pulmonary trunk/ one
of the major branches of pulmonary artery.
5. Patient may have pain and swelling in one of the lower limb (due to
DVT).
6. You should always look for symptoms of the underlying factor(s).
Signs
1. Tachypnea.
2. Tachycardia.
3. Pulse oxymetry: Low oxygen saturation.
4. Hemodynamically unstable: In case of a massive PE.
5. Lower limb examination: May show signs of DVT.
6. Respiratory system: Often normal/ unremarkable on examination.
Investigation
1. Estimation of D-Dimer: It is a fibrin degradation product (FDP) which gets
released into bloodstream due to ineffective fibrinolysis. It is a very good
screening test as a negative result virtually excludes PE/DVT but a
positive result does not always confirm the diagnosis as it may also rise
in other conditions (like repeated venepuncture/ septicaemia/ DIC etc.).
2. V/Q Scan: It shows the area of ventilation-perfusion mismatch. It may be
false +Ve in pre-existing lung diseases which can also cause V/Q
mismatch.
3. CT-Pulmonary angiogram: Best test for diagnosing PE.
Associated investigations:
1. Chest X Ray.
2. ECG.
3. Echocardiogram: To assess RV dysfunction.
4. Relevant investigations: If a hypercoagulable state is suspected.

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Treatment
1. Anticoagulation:
Initially heparin (Unfractionated/ Low molecular weight/ Fondaparinux)
+ Warfarin till target INR is achieved.
Note:
The therapeutic range for oral anticoagulant therapy is defined in terms
of an international normalized ratio (INR).
The target INR should be 2-2.5 in case of PE/ DVT.
Duration of therapy:
It depends on the underlying risk factors.
2. Thrombolysis:
It is usually done in patients of PE who are hemodynamically unstable.
Alteplase is the drug of choice.
3. In selected group of patients, insertion of IVC filter may be attempted.

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Bronchiectasis
It is defined as chronic infection of airways leading to abnormal, permanent
dilation of bronchi/ bronchioles.
Causes
1. Post infective causes:
a. TB.
b. Necrotizing pneumonia.
c. Whooping cough pneumonia.
2. Immune related:
a. Immunodeficiency: Primary and secondary.
b. Hyperimmune reaction (Allergic bronchopulmonary aspergillosis).
3. Impaired mucociliary clearance:
a. Cystic fibrosis.
b. Primary ciliary dyskinesia.
c. Kartage er's sy dro e.
4. Insult to the bronchus:
a. Obstruction (Foreign body/ Lymph node etc.).
b. Repeated gastric aspiration.
c. Toxic fumes.
Clinical features:
1. Chronic productive cough: often mucopurulent/ purulent; may be foul
smelling. Volume and appearance of cough suddenly changes during
infective spells/ exacerbations.
2. Breathlessness.
3. Hemoptysis: It may be massive (due to rupture of bronchial artery as
well as erosion of bronchial wall).
Signs:
1. Pulse oximetry: Low oxygen saturation.
2. Clubbing may be present.
3. Respiratory system:
Often coarse crepitations are present, which may be diffuse/ localized
depending upon the extent of distribution of bronchiectasis.

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Investigations:
Initial investigations
1. Hb, TC, DC, CRP/ ESR.
2. Sputum: Gram stain and culture sensitivity.
3. Blood culture: During infective exacerbations.
4. CXR: May show certain changes suggestive of bronchiectasis.
5. High resolution CT scan (HRCT): Confirms the diagnosis.
Special investigations
The nature of special investigation(s) depends on the underlying disease.
Treatment
1. Antibiotic therapy:
It is of 2 types:
a. Short term (during exacerbation).
b. Long term (for prophylaxis).
2. Bronchodilators (in case of airway obstruction).
3. Clearance of airway secretion:
Bronchial toileting
a. Postural drainage.
b. Chest physiotherapy.
c. Special breathing exercise.
d. Cough assist device.
4. Surgery: Removal of the bronchiectatic area.
5. Vaccine:
a. Influenza vaccine: Yearly.
b. Pneumococcal vaccine: Single dose.

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COPD (Chronic obstructive pulmonary disease)
It is defined as a chronic progressive disease of the airway characterized by
fixed irreversible airway obstruction with/ without alveolar damage.
Etiology:
Cigarette smoking.
Contributory factors:
Outdoor air pollutant.
Occupational pollutant.
Indoor air pollutant (biomass fuel).
Types:
1. Chronic bronchitis:
Pathologically characterized by over-secretion of bronchial mucous which
manifests as chronic productive cough lasting most of the days for at
least 3 months in a year for at least 2 consecutive years.
2. Emphysema:
Pathologically characterized by abnormal permanent dilation of alveoli
with destruction of their walls without obvious fibrosis.
Pathophysiological changes:
Changes in
COPD
Airway and
Blood gas
Cardiac effect
alveoli
1. Airway
1. Hypoxia
Chronic hypoxia->
obstruction.
(Low pO2).
Pulmonary
2. Airway collapse.
2. Hypercapnia
vasocontriction to reserve
3. Alveolar dilation.
(High pCO2).
blood flow-> PAH-> RV
enlargement-> RV failure
4. Oversecretion of
mucous.

---

Special note:
In some patients with COPD, there is a tendency to retain CO2 as they
hypoventilate. In these patients, chronically elevated CO2 is no longer
the main stimulus of respiratory centre. In this state, hypoxia becomes
the principal driving force of respiration. Any attempt to completely
correct this hypoxia will therefore take away the main respiratory driving
force.
In the other group of COPD patients, usual y retention of CO2 doesn't
occur.
Symptoms:
In chronic stable COPD patients, the main symptoms are:
Breathlessness:
Chronic, slowly progressive; leading to reduced exercise tolerance. There
is no diurnal variation/ no seasonal variation (Asthma) and no
orthopnea/ PND (CHF).
Chronic cough:
Often productive; mucoid/ mucopurulent. May be dry also.
Volume of this cough increases and becomes more purulent during infective
exacerbation.
Swelling: When RVF develops.
Signs
1. Tachypnea +/- Tachycardia.
2. Pulse oxymetry: Reduced oxygen saturation. If hypoxia is severe, then
cyanosis may be evident.
3. Raised JVP with edema (in RVF).
4. Respiratory system:
a. Inspection: Rate of respiration increased. Expansion of chest may be
restricted.
b. Palpation: No shifting.
c. Percussion: Hyper-resonant at both sides.
d. Auscultation:
Signs of reduced air entry (Reduced VBS/ VR/ VF).
Added sounds:

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Rhonchi/ wheeze may be present (due to
bronchospasm).
A localized area with crepitation may be present (due to
infection of underlying parenchyma).
5. CVS:
a. Signs of PAH: Accentuated P2 +/- Palpable P2. Mid-systolic murmur
due to functional pulmonary stenosis.
b. Signs of RV enlargement: Left parasternal heave. Apical impulse
shifted outwards.
Investigation
1. Spirometry:
1
a. <0.7
b. Pre and post-bronchodilator challenge FEV1: No evidence of
reversibility.
c. Classification of COPD:
Severity
FEV1*
Mild
>80%
Moderate
50-79%
Severe
30-49%
Very severe
<30%
[* These FEV1 values are used to classify COPD in a background of
FEV1/FVC value of <0.7.]
2. CXR:
a. Prominent bronchovascular markings.
b. Hyperinflated lung.
c. Always look for any pneumothorax.
3. Blood:
a. Polycythemia (in response to hypoxia, there is an increased
erythropoietin production, leading to polycythemia).
b. Arterial blood gas (ABG): To document the baseline gas status.
4. Sputum: Gram stain+ culture sensitivity.
Treatment
In a patient of chronic stable COPD
Principles of treatment:
1. Smoking cessation.

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2. Pulmonary rehabilitation.
3. Pharmacotherapy.
4. Long term oxygen therapy.
5. Surgery.
6. Vaccination.
Smoking cessation
Nicotine replacement therapy (in different forms).
Drugs (Bupropion/ Varinicline/ Nortryptiline).
Pulmonary rehabilitation
Special breathing techniques.
Graded physical exercises.
Pharmacotherapy
Inhalers:
2-agonist:
Short acting: Levo-salbutamol.
Long acting: Salmeterol/ Formoterol.
Corticosteroid: Fluticasone/ Beclomethasone/ Budesonide.
Anticholinergic (Muscarinic agonist):
Short acting: Ipratropium.
Long acting: Tiotropium.
Oral:
Methyl xanthine: Aminophylline/ Theophylline.
PDE inhibitor: Roflumilast.

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Stepwise treatment approach
Patient symptomatic
SAMA/ SABA
[as and when required]
FEV1 assessment
50%
<50%
LAMA
ICS + LABA
Still symptomatic
Still symptomatic
Add
Add LAMA
(ICS + LABA)
If required
If required
Add (MX+/Rf)
Add (MX+/Rf)
SAMA: Short acting muscarinic agonist
LAMA: Long acting muscarinic agonist
SABA: Short a ting 2 agonist
LABA: Long a ting 2 agonist
ICS: Inhaled corticosteroid
MX: Methyl Xanthine
Rf: Roflumilast

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Long term Oxygen therapy
Criteria:
1. Arterial blood gas:
paO2< 50 mm Hg, when done in a stable state and at least twice, at least
3 weeks apart.
(Normal value: 95-100 mm Hg)
2. Arterial blood gas:
paO2: (55-60) mm Hg, with evidence of (PAH/ RVF/ Polycythemia/ Any
hypoxic condition).
Duration of long term oxygen therapy: At least 15 hours a day.
Surgery
Various options are:
1. Bullectomy
2. Lung volume reduction surgery.
Vaccination
1. Influenza vaccine: Yearly.
2. Pneumococcal vaccine: Single dose + Booster after 5 years.
Acute exacerbation of COPD
It is an acute emergency characterized by progressive worsening of COPD
symptoms and commonly precipitated by an underlying respiratory infection.
Symptoms
1. Worsening dyspnoea
2. Productive cough: Often increased in volume and more purulent in
appearance (in comparison to regular sputum).
3. In some patients, symptoms of CO2 retention (CO2 Narcosis) may occur.
[CO2 Narcosis Metabolic encephalopathy Hepatic/ uremic in
nature Confusion/ Convulsion/ Coma/ Delirium].

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Signs
1. Tachypnoea
2. Tachycardia
3. Pulse oximetry: Low SpO2 (?Cyanosis)
4. Attitude:
Patient sits up in a tripod position with outstretched hand supporting
upper part of the body and breaths pursed lip. It is an attempt to
prevent the collapsibility of the airway by increasing intra-airway
pressure.
5. Flapping tremor may be present in CO2 narcosis.
Respiratory system
1. Signs of COPD are present
2. Widespread rhonchi and localized crepts may be present.
Investigation
Same as COPD.
Treatment
1. Airway protection:
Frequent oropharyngeal suction, intubation if required.
2. Breathing:
a. Free flow oxygen
b. Controlled oxygen: Ideally via venture mask
c. During acute stage, a target saturation of 88-92% should be
maintained, particularly if pCO2 level is high; so that the hypoxia is
not overcorrected.

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d. Assisted ventilation may be required (non-invasive/ invasive).
3. Circulatory support with IV fluids.
4. Drugs:
Antibiotics
Oral/ IV, depending on patient's a ility to swal ow a ta let and
severity of infection, usually a 7-10 days course is given. The
antibiotics routinely administered in acute exacerbation of COPD are:
Drugs
Description
Aminophylline infusion
Usually given when in spite of maximum
medical therapy, patient remains significantly
symptomatic. Maximum for 24-48 hours.
Bronchodilator
Initially it may be repeated few times every
(Nebulization with
15-30 minutes till the acute stage is over and
Salbutamol +
then every 4-6 hourly, till the patient is stable
Budesonide+
enough to use inhaler.
Ipratropium)
Corticosteroid
It is continued for 5-7 days and is now
(Oral/ IV short course
routinely recommended in acute
steroid: usually
exacerbations of COPD.
Hydrocortisone is given)

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Cor pulmonale
Introduction
It is a clinical condition characterized by right ventricular enlargement (RVE) from
acute/ chronic lung pathology.
Etiology
Etiology of Cor pulmonale
Airway and parenchymal
Pulmonary arterial
Thoracic cage diseases
disease
diseases
Ex: Acute/ chronic
Ex: COPD, Brinchiectasis,
pulmonary
Ex: Kyphosis, Scoliosis,
Interstitial lung diseases.
thromboembolism,
Both.
Idiopathic/ primary PAH.
Clinical features
1. Signs and symptoms of underlying disease
2. Symptoms and signs of PAH:
Symptoms:
Exertional chest pain (also called Right ventricular angina).
Signs:
Loud P2 ? Palpable P2
MSM due to functional PS
EDM due to PR (occurs very lately).
3. Signs of RVE:
Apex: Shifted outwards.
As RV doesn't have an apex, in case of a right ventricular apical
impulse, it is diffuse in nature.

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Left parasternal heave
PSM due to a functional TR
Visible/ palpable epigastric pulsation.
4. Symptoms and signs of RVF:
Symptoms:
Swelling.
Signs:
Raised JVP
Bilateral edema
Soft tender hepatomegaly.
Investigation
1. To assess the underlying disease
2. To assess the RV:
a. ECG
b. ECHO.
Treatment
1. Treatment of the underlying disease
2. For RVF:
a. Salt and fluid restriction
b. Diuretics.

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Respiratory failure
Introduction
It is defined as an arterial blood gas (ABG) value of <60 mm Hg.
Types
Respiratory failure
Type 1 (Hypoxemic)
Type 2 (Hypercapnic)
(pO2 <60 mm Hg +
(pO2 < 60 mm Hg +
pCO2 45 mm Hg)
pCO2 >45 mm Hg)
Causes
Causes of type 1 failure
Causes of type 2 failure
1. Pneumonia
Centre failure/ CNS diseases:
2. Pulmonary edema (LVF)
1. Brainstem depression:
3. Pulmonary embolism
Drug overdose (Opiate/ barbiturate)
4. ARDS
Deep coma.
5. Acute asthma.
2. Brainstem structural damage:
CVA
Head injury
Intracerebral space occupying lesion
(IC-SOL).
Pump failure/ respiratory diseases:
1. COPD (Most common)
2. Neuromuscular diseases:
Motor neuron disease
Guillain-Barr? syndrome
Myasthenia gravis.
3. Chest wall diseases:
Kyphosis
Scoliosis
Both.

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Treatment
Treatment of type 1 failure
Treatment of type 2 failure
1. High flow oxygen
1. Controlled oxygen (in COPD)
2. Assisted ventilation:
2. Assisted ventilation:
Invasive (It breaths for the
Invasive
patient)
Non-invasive: Also called BiPAP
Non-invasive (It gives
(Bilevel positive airway
respiratory support to the
pressure)
patient by recruiting more
alveoli): Also called CPAP
(Continuous positive airway
pressure).
* Star topics: CPAP and BiPAP
CPAP:
The Continuous Positive Airway Pressure (CPAP) machine gives a predetermined
level of pressure. It releases a gust of compressed air through a hose which is
connected to the nose mask. This continuous air pressure keeps the upper airway
open.
BiPAP:
The Bilevel Positive Airway Pressure (BiPAP) machine delivers two levels of
pressure:
Inspiratory Positive Airway Pressure (IPAP) is a high level of pressure,
applied when the patient inhales.
Expiratory Positive Airway Pressure (EPAP) is a low level of pressure exerted
during exhalation.
Advantage of BiPAP over CPAP:
Patients using the CPAP have to exert extra force against the air flow while
exhaling, as the airway pressure remains constant.
With the BiPAP, the airway pressure is set at high and low levels, making it
easier for the patient to breath.

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Bronchial asthma
Introduction
It is a chronic inflammatory disease of airway characterized by reversible airway
obstruction due to hyperactivity of the airway.
Etiology
1. Underlying factors:
Some of the individuals are genetically predisposed to develop airway
hyper-reactivity/ inflammation spontaneously/ when exposed to external
stimulus (allergen).
These individuals are called atopic- often they will have H/O recurrent
allergic rhinitis/ dermatitis/ hay fever and usually having a high serum IgE
level.
2. Triggering factors:
These factors quite often initiate/ precipitate an asthmatic attack. Some of
the common substances are:
a. Indoor allergen: Dust/ mites/ fungus (aspergillus)/ dog.
b. Outdoor allergen: Dust/ smoke.
c. Occupational: Isocyanate/ flour.
d. Drugs: Aspiri / -blocker.
e. Physical exercise.
f. Chemical: Perfume/ tobacco smoke.
Clinical features
Symptoms
1. Breathlessness:
a. May start gradually/ suddenly.
b. Often intermittent, with asymptomatic spells within 2 episodes.
c. Aggravated by exposure to allergen.
d. Shows diurnal variation: increasing symptoms at early morning as
bronchial tone follows a circadian rhythm and is maximum during these
hours.
e. Often shows seasonal variation (aggravates during season changes).

---

2. Wheeze:
Usually intermittent and occurs along with dyspnea.
3. Cough:
a. May be intermittent/ chronic.
b. Usually dry, but may be productive, characteristically thick, white
sputum which becomes purulent and increases in volume during
infective exacerbations.
Sign
Examination may be entirely normal in asymptomatic intervals.
1. Tachypnoea
2. Tachycardia
3. Pulse oximetry: Low SpO2 ? Cyanosis
4. Respiratory system:
Movement/ expansion may be restricted.
Signs of reduced air entry:
Reduced VBS, VR, VF.
Note: In COPD/ Asthma, often VBS will have a prolonged expiratory
phase.
Added sound:
Diffuse polyphonic wheeze may be present.
Investigation
Preliminary investigations:
1
1. Spirometry: <0.7
2. Bronchodilator reversibility: +Ve
Pre-bronchodilator FEV1 increases by 15%/200 ml, following
ro hodilator hal e ge y short a ti g 2 ago ist.
3. Chest X Ray: Often normal.
4. Blood: Hb, TC, DC, ESR/ CRP (Eosinophilia may be present).
5. Sputum: Gram stain and culture sensitivity.

---

Special investigations:
1. Bronchial provocation test:
Helpful if clinically asthma is suspected but spirometry is inconclusive. Here,
bronchoconstriction is provoked with certain substances like Methacholine/
Histamine/ Mannitol and degree of fall of pre-bronchoconstriction FEV1 is
measured.
2. Detection of allergen by skin test.
3. Examination of antibodies against common allergens (also called
precipitins) in the serum.
Evidence of airway inflammation:
1. Sputum eosinophil count
2. Fractional excretion of nitric oxide (NO)
3. Estimation of serum IgE.
Treatment
1. Patient education:
Avoid any suspected allergen (if any)
Protective devices (if feasible)
Show the technique to use inhaler.
2. Pharmacotherapy:
Inhaler:
Relie er: Short a ti g 2 ago ist
Pre e ter: Lo g a ti g 2 ago ist, I haler orti osteroid.
Oral:
Theophylline (Methyl Xanthine)
Mast cell stabilizer (Sodium cromoglycate)
Leukotriene antagonist (Montelukast, Zafirlukast, Zileuton)
Long term oral corticosteroid
Anti-IgE agent (Omalizumab).

---

Step wise treatment approach
Step 1: SABA (as and when required)
Step 2: Low dose ICS/ LTA
Step 3: Medium dose ICS/ (ICS+ LABA)/ Add an oral agent (MX/LTA)
Step 4: High dose ICS/ Increased dose of (ICS+LABA)/ Add an oral agent (MX/LTA)
Step 5: Regular oral steroid
(Add a PPI for gastric protection and a Bisphosphonate for bone protection)
[SABA/LABA: Short/lo g a ti g 2 ago ist, ICS: I haled orti osteroid, MX: Methyl
xanthine, LTA: Leukotriene antagonist]
Treatment outcomes
1. Well controlled asthma:
It is defined as:
I. No sy pto s or 2 per eek
II. No reliever use (or 2 per week)
III. No nocturnal symptoms
IV. No restriction of activity of daily living.

---

2. Acute exacerbation of asthma:
It is an acute emergency presentation of asthma with increasing symptoms
often precipitated by an underlying infection. They are more frequent in
patients with poorly controlled asthma.
Clinical features:
1. Worsening dyspnea
2. Wheeze
3. Often productive cough.
Sign:
1. Tachypnoea
2. Tachycardia
3. Low SpO2 ? Cyanosis
4. Signs of reduced air entry
5. Widespread wheeze.
Investigation:
1. Blood: Hb, TC, DC, CRP
2. ABG: Usually hypoxia with type 1 respiratory failure
3. Blood culture: If patient is febrile
4. Sputum: Gram stain and culture sensitivity
5. Chest X Ray
6. ECG
7. ECHO (In selected patients).
Treatment:
A. Airway:
Protected by frequent suction, intubation if required.
B. Breathing:
High flow oxygen (target saturation > 95%)
Assisted ventilation: Non-invasive (CPAP)/ Invasive.
C. Circulatory support by IV fluid
D. Drugs:
Antibiotic: Short course
Aminophylline infusion:
If patient remains symptomatic after optimal therapy.

---

Bronchodilator:
Nebulization with (Salbutamol + Budesonide+ Ipratropium):
Initially repeated every 15-30 minutes. When acute stage is
over, it is given every 4-6 hours till the patient is stable
enough to use inhaler.
Corticosteroids:
Oral (Prednisolone)/ IV (Hydrocortisone) for 5-7 days.
A single dose of IV MgSO4.
*Star Topic: Grading of asthma*
Points
Moderate
Severe
Life threatening
Peak expiratory flow
50-75%
33-50%
<33%
rate (% of predicted)
Features:
Increasing
Increasing
- No chest sound
symptoms
symptoms
- Cyanosed
Absence of severe/
Respiratory rate
- Tachy/brady-
life threatening
>30/min
arrhythmia
features
Heart rate >110/min - Hypotension
- Confusion/ coma/
exhaustion
- pO2 <60 mm Hg
- Saturation <92%
- pCO2: Normal/
near normal.

---

Pulmonary function test (PFT)
Studies done in PFT
Estimation of
Diffusion
Spirometry
lung volume
study
FEV1
TLC
TLCO/ DLCO
FVC
RV
KCO
FEV1 (Forced expiratory volume in 1 second): FEV1 is the volume exhaled
during the first second of a forced expiratory maneuver started from the
level of total lung capacity.
FVC (Forced vital capacity): FVC is the volume of air that can forcibly be
blown out after full inspiration.
TLC (Total lung capacity): TLC is the maximum volume of air present in the
lungs.
RV (Residual volume): RV is the volume of air remaining in the lungs after a
maximal exhalation.

---

DLCO/TLCO (Diffusing capacity/ Transfer factor of the lungs for carbon
monoxide): DLCO is the carbon monoxide uptake from a single inspiration
in a standard time (usually 10 seconds). The exhaled gas is tested to
determine how much of the tracer gas was absorbed during the breath.
DLCO measures the ability of the lungs to transfer gas from inhaled air to
the red blood cells in pulmonary capillaries.
KCO: Diffusing capacity of the lung per unit volume.
Basic clinical application of PFT in lung diseases
We can clearly differentiate among some common diseases through using the
pulmonary function tests. In this section, we will show how the 3 components of
PFT as discussed above (spirometry, lung volume and diffusion study) can be used
to reach a diagnosis separately.

---

Spirometry
< .7
> .7
1. Obstructive
2. No active airway
airway disease
obstruction
COPD
Normal lung
Asthma with no active
Active asthma
obstruction
Restrictive lung
disease
For group 1:
Bronchodilator reversibility test
COPD:
Active asthma:
Irreversible
Reversible
For group 2:
1. Asthma with no active ostruction: Detect by a bronchial provocation test.
2. Normal lung Vs. Restrictive lung disease:
In normal lung: FVC and FEV1: both values will be high individually.
In restrictive lung disease: FVC and FEV1: both values will be low
individually.

---

Lung volume
Detection of TLC and RV
TLC & RV
TLC and RV: Normal
TLC and RV
COPD
Asthma
Restrictive lung disease

---

Diffusion study
DLCO/ TLCO and KCO
Asthma
COPD
Restrictive lung disease
DLCO and KCO:
DLCO and KCO
DLCO and KCO
DLCO and KCO
Normal
Extra-
Parenchymal
parenchymal
Unexplained
diffusion study
Low DLCO
High DLCO
Interstitial lung
Goodpasture
disease (ILD)
syndrome
Anemia

---

Bronchogenic Carcinoma
Introduction
Malignancy of bronchial/ bronchiolar epithelium.
Risk factors
1. Cigarette smoking:
a. Initiator (Ex: Polyaromatic hydrocarbon: PAH)
b. Promoter (Ex: Phenol derivatives).
2. Occupational exposure:
Ex: Asbestos (usually causes adenocarcinoma of lung).
3. Environmental toxins.
Pathophysiology
Intrathoracic effects of bronchogenic CA
Structures involved
Effects
Airway
Obstruction
Narrowing
Parenchyma
Collapse
Consolidation
Cavitation
Pleura
Effusion
Pericardium
Ribs
Erosion
Irritation of intercostal nerves (ICN)
Lymph node
Hilar/ mediastinal/ supraclavicular lymphadenopathy
may result in compression of the following structures:
2 tubes:
Esophagus
Trachea.
2 nerves:
Sympathetic trunk
Recurrent laryngeal nerve.
2 great vessels:
Superior vena cava
Subclavian artery.

---

Extra-thoracic effects of bronchogenic CA
1. Metastasis to:
Brain
Bone
Liver.
2. Paraneoplastic syndromes.
Clinical features
Symptoms:
Category
Symptoms
Usual complaints
Dyspnea
Productive cough
Chest pain (dull in nature in erosion of ribs/
sharp shooting in nature in irritation of ICN)
Hemoptysis.
Due to compression
Dysphagia (more towards solid food)
Stridor
Hoarseness of voice (due to injury to
recurrent laryngeal nerve: Adductor palsy)
Explosive nature of cough (also termed as
ovi e ough : due to RLN palsy
Symptoms of SVC obstruction.
Due to extrathoracic effect
Bone pain
Increased intracranial tension (ICT) due to
brain metastasis:
Headache
Vomiting
Convulsion.
Signs:
1. Pallor: may be present
2. Clubbing may be positive
3. Jaundice may be present (in case of liver metastasis)
4. Signs of IVC obstruction
5. Supraclavicular lymphadenopathy.

---

System specific signs
System
Signs
Respiratory system
Signs of the following may be present:
Consolidation
Collapse
Cavitation
Pleural effusion.
GIT
Firm to hard hepatomegaly (in case of liver metastasis)
Malignant ascites (in case of peritoneal metastasis).
CNS
Following signs may be present:
Papilledema
Gradual onset hemiparesis
Signs due to Pancoast tumor.
Paraneoplastic syndromes
Distant non-metastatic manifestations of bronchogenic CA which are usually due
to either secretory nature of the tumor or immunologically mediated.
System involvement
Symptoms
Endocrinal (most commonly seen in
Hormone
Effect
small cell lung carcinoma)
ACTH
Cushing syndrome
PTHrP
Hypercalcemia
ADH
SIADH
Gonadotropin
Gynecomastia
CNS
Lambert?Eaton myasthenic syndrome
Subacute cerebellar degeneration.
Hematological
DIC
Anemia.
CVS
Non-infective endocarditis
Migratory thrombophlebitis.
Renal
Nephrotic/ nephritic syndrome

---

Investigation
Confirmation of diagnosis:
1. Chest X Ray
2. Contrast enhanced CT scan (CE-CT) of chest and abdomen
3. PET scan (in selected cases)
4. Histopathological confirmation by:
Bronchoscopic biopsy
CT guided biopsy
Lymph node biopsy
Cytological examination of pleural fluid.
To evaluate and assess various effect of tumor:
1. Blood: Hb, TC, DC, ESR/ CRP.
2. Na+ K+ Urea Creatinine (Hyponatremia due to SIADH may occur)
3. Liver function test (Alkaline phosphatase level may be elevated)
4. Serum Ca++ level (may be elevated in case of bone metastasis/
Paraneoplastic syndrome: secretion of PTHrP by the tumor)
5. CT/ MRI of brain
6. Bone scan (if bone metastasis is suspected).
Assessment of physical function:
1. ECG
2. Echocardiogram (if needed)
3. Pulmonary function test.
Treatment
Treatment depends on:
1. Staging of tumor
2. Overall fitness of patient.
Treatment options:
1. Surgery
2.
1.
Chemotherapy
Down staging of tumor
3.
2.
Radiotherapy
Slow down the progress of tumor
3. Control of symptoms

---

Therapeutic classification and treatment of choice:
Group
Feature
Treatment of choice
Small cell
More aggressive
Chemotherapy: Carboplatin/ Cisplatin
lung CA
Limited role of surgery
Radiotherapy
Non-small
Less aggressive
Surgery:
cell lung CA Often resectable
Options are:
1. Lobectomy
2. Pneumonectomy (removal of a lung).
The choice of surgery depends on the size
of tumor and pre-operative fitness of
patient.
Chemotherapy: Carboplatin/ Cisplatin +
Gemcitabine
Radiotherapy.
Some conditions associated with bronchogenic CA
SVC Obstruction
Introduction
Occlusion of SVC due to extraluminal/ intraluminal compression.
Cause
1. Malignancy:
a. Bronchogenic CA
b. Lymphoma.
2. Benign:
a. Thymoma
b. Retrosternal goitre
c. Clot/ thrombus.
Clinical features
Symptoms:
The following symptoms are commonly seen in SVC obstruction and these occur
because of impaired venous drainage:

---

1. Facial and neck swelling
2. Plethoric appearance (red, flushed) of face
3. Throbbing headache.
Signs:
1. JVP: Raised and non-pulsatile
2. Facial plethora and swelling may increase on lifting both the arms
Pe
erto s sig .
3. Superficial venous prominence over the chest wall with direction of filling
from above downwards may be seen.
Investigation
1. CT chest
2. Histopathological confirmation the underlying disease/ condition
Treatment
1. Supportive treatment:
a. Oxygen
b. Steroid: to reduce the edema surrounding the obstruction.
2. Specific treatment of the underlying cause
3. If the patient is in severe distress, then SVC stenting may be considered.

---

Pancoast tumor
Introduction
It is malignancy situated in the apex of the lung. Because of its location, it
sometimes causes some unusual manifestations. When these manifestations
occur, it is called Pancoast syndrome.
Clinical features
Cause
Symptoms and signs
Compression of C8-T2
Pain/ paresthesia along the ulnar border of arm and
nerve root
forearm
Wasting of hypothenar muscles.
Compression of
Hor er s sy dro e
sympathetic trunk
Symptom
Cause
Miosis
Due to involvement of dilator pupillae
Anhydrosis* of
Due to involvement of vasomotor
same side of face
fibers to face
Partial ptosis
Due to paralysis of Mul er s us le
Loss of ciliospinal
---
reflex^
Enophthalmos~
Due to paralysis of Orbitalis muscle
[*: Decreased sweating, ^: Dilation of the ipsilateral pupil in response to pain
applied to neck, face and upper trunk, ~: Posterior displacement of the eyeball.]

---

Pneumonia
Types
1. Community acquired pneumonia
2. Hospital acquired pneumonia
3. Aspiration pneumonia
Community acquired pneumonia
Introduction
Pneumonia occurring outside hospital setting/ within 48 hours of admission, who
hasn't been in hospital for last 14 days.
Organism
Typical pneumonia:
1. Strep. pneumoniae
2. H. influenzae
3. Moraxella
4. Klebsiella.
Atypical pneumonia:
1. Mycoplasma
2. Legionella
3. Chlamydia.
Clinical features
Symptoms:
1. Systemic symptoms:
a. Fever ? chill and rigor
b. Headache
c. Myalgia
d. Loss of appetite
e. Confusion.
2. Respiratory symptoms:
a. Productive cough

---

b. Often the sputum is purulent/ mucopurulent
c. Shortness of breath (if a significant part of lung parenchyma is
affected)
d. Hemoptysis (blood stained sputum) may occur.
Signs:
1. Tachypnea
2. Tachycardia
3. Pulse oximetry: Low SpO2
4. Respiratory system:
Signs of consolidation:
a. BBS: Unaltered
b. VR/ VF:
c. No shifting.
Signs of reduced air entry:
a. VBS:
b. VR/ VF: .
Localized area with crepitation: Usually present.
Investigation
1. Blood:
a. Hb, TC, DC, ESR/ CRP (Raised inflammatory marker)
b. Na+ K+ Urea creatinine
c. Blood culture and sensitivity
d. Serum pro-calcitonin: Very sensitive marker of bacterial inflammation.
e. Arterial blood gas: Done if the patient is hypoxic.
2. Sputum:
a. Gram stain and culture-sensitivity
b. Chest X Ray (Radiological evidence of resolution always lags behind
clinical picture)
3. Special tests:
In selected cases, special tests like CT chest, bronchoscopy etc. can be
performed.

---

Treatment
Supportive treatment (particularly in critically ill patients)
A. Airway:
Protected by frequent suction and ventilation if required.
B. Breathing:
Oxygen
Assisted ventilation:
Non-invasive
Invasive.
C. Circulation:
IV fluid
Vasopressor (Norepinephrine infusion in septicemic shock).
D. Drug:
Antipyretic
Nebulization, if required
Mucolytic agent.
Antimicrobials
Choice of antibiotic:
Commonly empirical therapy with:
CO-AMOXICLAV + MACROLIDE
OR
LEVOFLOXACIN
OR
3RD/4TH GENERATION CEPHALOSPORIN/ CARBAPENEM (in critically ill patients)
Complications of pneumonia
1. Septicemia
2. Respiratory failure
3. Lung abscess
4. Non-resolving pneumonia:

---

Common causes are:
a. Wrong diagnosis
b. Wrong choice of antibiotic
c. Unusual/ resistant organism
d. Underlying pulmonary disease (malignancy/ bronchiectasis).
Hospital acquired pneumonia
Introduction
Pneumonia occurring after 48 hours of hospital admission.
Common organism
1. Pseudomonas
2. Staph. aureus
3. Acinetobacter.
Clinical features and investigation
Same as community acquired pneumonia.
Treatment
Supportive treatment
Same as community acquired pneumonia.
Antimicrobial
Empirical antibiotic of choice:
PIPERACILLIN + TAZOBACTUM
OR
CARBAPENEM
OR
POLYSTIN
Aspiration pneumonia
Pneumonia secondary to aspiration of gastric content/ oropharyngeal secretion.

---

Which people are at risk of aspiration pneumonia?
Risk of aspiration
Impaired cough reflex
Neuromuscular diseases
involving esophagus
Semi/unconscious patients
Motor neurone disease
Alcohol
Myasthemia gravis
Brain damage
Bulbar pulsy
Coma
Drug overdose (eg. sedative)
Epilepsy
Clinical features
1. Background risk factor(s) of aspiration usually present
2. Often, sudden onset breathlessness with profuse respiratory secretion
3. Signs due to hypoxia
4. Signs of reduced air entry with crepitation.
Investigation
Often suggestive X Ray changes are present in the right lower lobe.
Treatment
Supportive treatment (as in community acquired pneumonia).
Antimicrobial
CO-AMOXICLAV + METRONIDAZOLE

---

Acute respiratory distress syndrome (ARDS)
Introduction
It is an acute complication of a wide variety of underlying diseases and it is
characterized by non-cardiogenic pulmonary edema.
Pathogenesis
Triggering factors:
A. Acute pancreatitis
R: RBC transfusion (massive)
D: DIC/ Drug overdose
S: Septicemia
Release of inflammatory mediators
into lung / distant sites
Reaches pulmonary circulation
ARDS
Clinical features
1. Rapidly progressing breathlessness
2. An underlying illness/ condition must be present
3. Often tachypnea/ tachycardia/ low SpO2 is present
4. Often patient is hemodynamically unstable
5. Usually bilateral crepitations are present.

---

Treatment
A. Airway protection:
Often patient will require intubation
B. Breathing:
Assisted ventilation (often invasive ventilation is required)
C. Circulation:
IV fluid and vasopressors
D. Drugs for underlying conditions.

---

Pulmonary arterial hypertension (PAH)
Introduction
It is a condition characterized by pulmonary arterial pressure >20 mm Hg.
Causes
PAH
Primary/ idiopathic
Secondary PAH
PAH
Clot (acute/ chronic
Cardiac (chronic left
Connective tissue
Chronic lung disease
pulmonary
heart diseases)
diseases
thromboembolism)
COPD
Scleroderma
ILD
SLE
Bronchiectasis
Rheumatoid arthritis
Clinical features
1. Symptoms and signs of underlying disease(s)
2. Symptoms and signs due to PAH:
a. Exertional chest pain (also called right ventricular angina)
b. Shortness of breath
c. Accentuated P2 ? Palpable P2

---

d. MSM in case of a functional PS
e. EDM in case of a functional PR (rare).
3. Signs of RV enlargement:
a. Apical impulse shifted outwards
b. Diffuse apex impulse (in case of a RV apex)
c. Left parasternal heave
d. PSM due to a functional TR
e. Epigastric pulsation.
4. Signs of RV failure:
a. Raised JVP
b. Soft tender hepatomegaly.
Investigations
1. ECG
2. Echo: Assess RV structure/ function and an approximate estimation of
pulmonary arterial pressure
3. RV catheterization
4. Relevant investigations to assess underlying disease(s).
Treatment
A. Anticoagulation agents (Significant PAH leads to a sluggish PA circulation,
predisposing to formation of PA clot)
B. BP lowering agents:
Calcium channel blockers:
Nifedipine
Amlodipine.
PDE-5 inhibitors:
Sildenafil
Tadalafil.
PG analogue:
Iloprost (via inhalation route)
Endothelin receptor antagonists:
Bosentan
Ambrisentan.
C. Cause: Treat the underlying cause.

---

Interstitial Lung Disease (ILD)/
Introduction
It is a group of heterogenous conditions characterized by damage of interstitium
of lung (alveolar epithelium + capillary basement membrane).
In many cases, these diseases also affect interlobular septa.
Types
1. Cryptogenic fibrosing alveolitis (Usual interstitial pneumonia/UIP)
2. Non-specific interstitial pneumonia (NIP)
3. Acute interstitial pneumonia
4. Desquamative interstitial pneumonia
5. Lymphoid interstitial pneumonia
6. Cryptogenic organizing pneumonia
7. Respiratory bronchiolitis associated interstitial lung disease (RB-ILD).
Causes
1. Idiopathic
2. Iatrogenic (Amiodarone)
3. Infection
4. Immunological (Connective tissue disease).

---

Symptoms
1. Shortness of breath:
Onset, severity and progression depend on the underlying disease.
2. Chronic productive/ dry cough
3. Systemic:
a. Fever
b. Arthralgia
c. Weight loss may occur.
4. In the long run: Swelling (due to RVF).
Signs
1. If breathless:
a. Tachypnea
b. Tachycardia
c. Low SpO2 ? Cyanosis
2. Clubbing:
May occur in cases of chronic infection/ inflammation. It is seen particularly
in UIP.
3. Chest:
a. Signs of reduced air entry:
VBS, VR, VF
b. Crepitation:
Fine inspiratory crepitation may be present (during opening up of
alveoli).

---

Investigation
1. Chest X Ray:
Reticular pattern is seen.
Chest X-ray showing bilateral,
predominantly lower zone and
peripheral coarse reticulonodular
shadowing and small lungs
2. High resolution CT scan (HRCT):
Honey comb appearance/ ground glass appearance.
[HRCT showing honeycomb appearance in UIP (left) and extensive ground
glass appearance in NIP (right)]
3. Pulmonary function test:
Pattern: Restrictive parenchymal defect
4. If radiological appearance is inconclusive, then histopathological
confirmation by lung biopsy is recommended.
5. Relevant investigation to diagnose any underlying disease.

---

Treatment
1. Corticosteroid (systemic)
2. Immunosuppressive drugs:
a. Azathioprine
b. N-Acetyl Cysteine (NAC)
c. Pirfenidone.
3. Symptomatic:
a. Long term oxygen therapy
b. Treatment of RHF, if present.
4. Surgery:
Lung transplantation.

---

Sarcoidosis
Introduction
It is an immunologically mediated multisystem disease characterized by non-
caseating granulomatous inflammation.
Involvement and clinical features
Lymph node
involvement
SOB, Cough
(Hilar/
Pulmonary
mediastinal)
involvement
Parenchymal
SOB, Bilateral
ILD
inflammation
crepitations
Mononeuritis
CNS
Facial palsy
multiplex*
Sarcoidosis
Uveitis
Eye
Painful red eye
Episcleritis
Conduction
Extra-pulmonary
Cardiac
abnormality
involvement
Liver dysfunction
Liver
? Chronic liver
Hepatomegaly
disease
Spleen
Splenomegaly
GI
Joints
Arthralgia
Erythema
nodosum
Cutaneous
Skin
manifestations
Lupus pernio~
*Single/ multiple cranial nerve palsy, most common: CN7 palsy. ~Lupus pernio is a
chronic raised indurated (hardened) lesion of the skin, often purplish in color. It

---

resembles frostbite as it is seen on tip of the nose and surrounding cheeks. It is
pathognomonic of sarcoidosis.
Investigations
1. Pulmonary:
a. Chest X Ray
b. HRCT (If CXR is abnormal)
- Both will show reticulonodular pattern ? lymphadenopathy.
c. Histopathological confirmation by biopsy from:
Lymph node
Parenchyma.
- If radiological appearance is inconclusive.
d. Pulmonary function test:
Restrictive lung disease.
2. Other investigations:
a. Hb, TC, DC, CRP/ESR
b. Liver function test
c. Serum Ca++:
Hypercalcemia is quite common due to increased production of 1,25-
(OH)2-cholecalciferol [vitamin D3], which causes increased absorption of
Ca++ from gut.
d. Serum angiotensin converting enzyme (ACE):
Due to activation of macrophages in sarcoidosis and their release of
ACE, serum ACE level is increased. Although serum ACE is a non-specific
marker for sarcoidosis. It is an indicator of disease activity.

---

e. ECG: To look for conductive disturbances.
f. Biopsy of any affected organ.
Treatment
Treatment of
sarcoidosis
Patient is
Patient is
absolutely
symptomatic
asymptomatic
Wait and watch
Immuno-
Corticosteroid
Hydroxy-chloroquine
approach
suppressants
Methotrexate
Particularly for cutaneous
and joint manifestations
Azathioprine
Cyclophosphamide

---

Extrinsic allergic alveolitis/ Hypersensitivity pneumonitis
Introduction
It is an inflammatory condition characterized by alveolar/ parenchymal
inflammation usually due to a hypersensitivity reaction against organic antigens.
Common antigens
1. Fungus:
Actinomycetes
Aspergillus
2. Bird proteins.
Clinical features
1. Breathlessness: acute/ chronic
2. Dry cough
3. On examination: tachypnea, low SpO2, bilateral crepts may be found.
Investigations
1. Chest X Ray
2. HRCT
- Predominantly nodular pattern ? reticulation is seen.
HRCT of the chest in
acute hypersensitivity
pneumonitis showing
widespread centrilobular
nodules.
3. Blood: CBC

---

4. ABG: Hypoxic
5. Detection of serum precipitins against the organic antigens.
Treatment
1. Supportive:
a. Oxygen: If the patient is hypoxic
b. Systemic corticosteroid.

---

Cryptogenic organizing pneumonia
Introduction
It is an atypical type of pneumonia characterized by formation of granulation
tissue inside the alveoli.
Clinical features
Symptoms
1. Shortness of breath
2. Dry/ productive cough
3. Systemic symptoms:
a. Fever
b. Malaise
c. Loss of appetite.
Signs
1. Tachypnea, low SpO2 ? cyanosis
2. Signs of consolidation/ reduced air entry
3. Crepitations usually present.
Investigations
1. Chest X Ray:
a. Often peripheral consolidation is seen
b. Floating consolidation (if previous X Rays are available)
Floating consolidations
This initial chest X-ray (a) at time of viral
illness shows patchy bilateral mid and upper
zone opacities, a second X-ray 1 month later
(b) shows non resolution despite a course of
oral Amoxiclav. The third X-ray 2 months
later (c) shows bilateral basal opacities. A
fourth shows worsening opacities bibasally
another 2 months later (d). HRCT at this
time shows bilateral dense consolidation
with air bronchograms (e). Last chest X-ray
(f) shows marked improvement after 6
weeks of steroids.

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2. HRCT: Often confirms the diagnosis
3. In many cases, histopathological confirmation is required
4. Blood: CBC, ABG, Blood culture
5. Sputum: Gram stain and culture.
Treatment
1. Supportive: Oxygen if required
2. Antibiotic: Often prevent keeping CAP (Community acquired pneumonia) in
mild.
3. Corticosteroid: Many patients need prolonged course of steroids.

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Pericardial diseases
Acute pericarditis
Introduction
Acute inflammation of pericardium.
Etiology
1. Infection: May be viral (more common) or bacterial
2. Post irradiation
3. Immunologically mediated: Connective tissue diseases
4. Inflammatory:
a. Post-MI: If pericarditis occurs within 34 days of AMI, it is called
immediate post MI pericarditis.
b. Dressler's syndrome: It occurs as a delayed complication of MI and it is
also seen in post-CABG patients.
Clinical features
Symptom
Chest pain: Usually sharp, often aggravated on supine position and relieved when
patient sits up and leans forward.
Occasionally, the inflammation spreads to the adjacent pleura causing
pleuropericarditic pain which characteristically aggravates on deep inspiration/
sneezing/ coughing.
Signs
Pericardial rub: Often present and does not disappear on breath holding.
[Upon auscultation, this sound is heard as an extra heart sound of to-and-fro
character, grating in nature, best heard between the apex and sternum.]
Investigation
1. Chest X Ray: Often normal
2. ECG:
a. ST segment elevation with concavity upwards (scooped pattern)
b. Diffuse/ global ST segment elevation (in all leads).

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3. Echocardiogram: To rule out any pericardial effusion.
Treatment
1. In most of the cases: NSAIDS/ Paracetamol
2. In selective cases: Corticosteroid is quite helpful particularly in Dressler's
syndrome.
Pericardial effusion
Introduction
Accumulation of fluid in the pericardial cavity.
Causes
1. Infection: TB
2. Autoimmune diseases/ connective tissue diseases
3. Malignant effusion: Breast/ lung/ lymphoma.
4. Trauma.

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Effects on surrounding structures
Pericardial effusion
Compressive effects
Medially
Laterally
Inferiorly
On the base of
On the heart
On the liver
the left lung
Impaired
Dullness to percussion
Pushed
diastolic filling
over the left
downwards
subscapular area
Clinical features
Symptoms
1. Chest discomfort/ heaviness
2. Swelling of the body
3. In significant effusion, symptoms due to low cardiac output (such as
fatigability, exertional muscle pain etc.) are seen
4. Symptoms due to underlying disease.
Signs
1. Edema
2. JVP
3. CVS: Muffled/ soft heart sound
4. Abdomen:
Hepatomegaly due to portal venous congestion
Liver may be palpable in spite of absence of hepatomegaly due to
pushed down liver
Ascites may be present.
5. Signs due to underlying disease.

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Investigation
1. Chest X Ray: Water-bottle shaped heart
2. ECG: Low amplitude complex
3. Echocardiogram confirms the diagnosis
4. Diagnostic aspiration of pericardial fluid with physical/ biochemical/
cytological/ microbiological character often helps to diagnose the
underlying disease.
Treatment
1. Therapeutic pericardial aspiration (Pericardiocentesis) for symptomatic
relief
2. Specific treatment for underlying cause.

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Cardiac tamponade
Introduction
It is a condition where there is rapid accumulation of fluid in the pericardial cavity
leading to significant compression of the heart.
Cause
Pericardial effusion
Clinical features
Symptoms
Symptoms occur due to severely impaired diastolic filling and subsequently
reduced cardiac output:
1. Sudden collapse/ blackout
2. Chest discomfort
3. Weakness/ fatigability.
Signs
1. JVP
2. Hemodynamic instability: Hypotension with rapid but weak pulse
3. Heart sound: Muffled.
Investigation
1. Urgent chest X Ray
2. Urgent echocardiogram
3. Once the patient is stable, diagnostic pericardiocentesis.
Treatment
1. Immediate pericardiocentesis:
Particularly when the patient is hemodynamically unstable.
2. When the patient is stable, further treatment of the underlying disease.

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Constrictive pericarditis
Introduction
It is a condition characterized by thickening, fibrosis and adhesion between the
pericardial layers which ultimately leads to encasement of the heart.
Etiology
1. TB
2. Post irradiation
Clinical features
Symptoms
1. Swelling
2. Fatigability
3. Exertional muscle pain.
Signs
1. JVP
2. Edema
3. CVS: Pericardial knock may be present: It is a late diastolic abnormal sound
due to sudden vibration caused by the rigid pericardium when it reaches its
elastic limit.
4. Abdomen:
Hepatomegaly
Ascites.
Investigation
1. Chest X Ray
2. ECG
3. Echocardiogram
4. Cardiac MRI.
Treatment
1. Symptomatic treatment with diuretics
2. Pericardiectomy.

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Cardiomyopathies
Dilated cardiomyopathy
Introduction
It is a primary (intrinsic) cardiac muscle disease characterized by abnormal
dilatation/ enlargement of the cardiac chambers.
Etiology
1. Idiopathic: Probably underlying genetic factors are responsible
2. Chronic alcohol abuse: Alcohol acts as a toxin cardiac muscle
3. Long standing diabetes mellitus
4. Infiltration of cardiac muscles:
Ex: Amyloidosis/ Hemochromatosis/ Sarcoidosis.
Pathophysiology
1. Impaired diastolic relaxation
2. Systolic dysfunction.
- Patient develops features of uni/bi-ventricular failure.
Clinical features
Symptoms
1. Shortness of breath/ orthopnea/ PND
2. Swelling.
Signs
1. Signs of LHF:
S3 is usually present
Gallop rhythm (tachycardia + S3/S4) may be audible
Bilateral fine inspiratory crepitations.
2. Signs of RHF:
Edema
JVP
Hepatomegaly.

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Investigations
1. Chest X Ray: Cardiomegaly
2. ECG: Features of chamber enlargement
3. Echocardiogram: Confirms the diagnosis and can assess the degree of
dysfunction.
Treatment
1. Treatment of heart failure
2. Treatment of underlying disease (if any).
Hypertrophic cardiomyopathy
Introduction
It is an intrinsic disease of cardiac muscle characterized by asymmetrical septal
hypertrophy leading to left ventricular outflow tract obstruction.
Clinical features
Symptoms
1. Due to LVOT obstruction:
a. Syncope/ transient blackout
b. Sudden collapse
2. Due to LVF:
SOB/ Orthopnea/ PND.
Signs
1. Apical impulse:
Forceful, well sustained
Double apical impulse (2 systolic impulses) may be felt on palpation.
2. Auscultation:
Signs of LHF may be present
MSM may be present over the aortic area, which accentuates and
decreases in intensity during Valsalva maneuver* and squatting
position, respectively.

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*Valsalva maneuver is performed by moderately forceful attempted exhalation against a closed
airway, usually done by closing one's mouth, pinching one's nose shut while pressing out as if
blowing up a balloon.
Mechanism:
1.
LV outflow
tract
MSM
Valsalva
LV cavity size
obstruction
increases in
Maneuver
becomes more
intensity
prominent
2.
Flow
Total
MSM
Squatting
through LV
peripheral
Afterload
decreases in
position
outflow
resistance
intensity
tract

---

Investigation
1. Chest X Ray
2. ECG
3. Echocardiogram.
Treatment
1. Symptomatic treatment of heart failure
2. Surgical: Septal de-bulking
3. Screening of other family members.

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Special topic: Acid base balance
Normal ABG values
pH: 7.35-7.45
ABG: Arterial blood gas,
PaO2: 80-100 mm Hg
PaCO2: 35-45 mm Hg
Pa: Arterial tension,
SpO2: 96-100%
Sp: Saturation
HCO3-: 22-26 mEq/L
Base excess: -2 to +2.
Classification of acid base disorders
Acid base disorders
pH< 7.35
pH> 7.45
Acidosis
Alkalosis
Due to CO
Due to HCO -
Due to CO2*
Due to HCO -
Respiratory
Metabolic
Respiratory
Metabolic
acidosis
acidosis
alkalosis
alkalosis
Compensatory
Compensatory
Compensatory
Compensatory
mechanism
mechanism
mechanism
mechanism
HCO -
CO
HCO -
CO
Metabolic
Respiratory
Metabolic
Respiratory
alkalosis
alkalosis
acidosis
acidosis
[*Due to hyperventilation, excessive wash out of CO2 causes PaCO2.]

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pH, PCO2 and HCO3- values in different acid base disorders
Condition
pH
PCO2
HCO3-
(N: 7.35-7.45)
(N: 35-45 mm Hg) (N: 22-26 mEq/L)
Respiratory acidosis
<7.35
>45
>22
Metabolic acidosis
<7.35
<35
<22
Respiratory alkalosis
>7.45
<35
<22
Metabolic alkalosis
>7.45
>45
>26
[Red color: From direct mechanism & Green color: From compensatory mechanism]
Steps of ABG
Step 1: pH detection (acidosis/ alkalosis)
Step 2: Primary process identification (respiratory/ metabolic)
Step 3: Compensatory process identification (respiratory/ metabolic)
Step 4: PO2 measurement.
Respiratory acidosis
Introduction
Condition characterized by abnormal CO2 retention.
Causes
Acute
Chronic
1. Acute exacerbation of COPD
1. COPD
2. GB syndrome
2. Thoracic cage disease
3. Myasthenia gravis
3. Neuromuscular junction disease
4. Acute brainstem damage.
(MND/MG etc.)
4. Sleep related breathing disease:
a. Obstructive sleep apnoea
b. Obesity hypoventilation
syndrome.

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Clinical features
1. Features of underlying disease
2. Features due to high CO2: CO2 narcosis (Metabolic encephalopathy):
a. Confusion
b. Convulsion
c. Coma
d. Delirium
e. Flapping tremor.
Investigation
1. To identify respiratory acidosis: ABG
The values will be as below:
pH
PCO2
HCO3- .
In fully compensated cases, pH will return to normal.
Rate of compensation:
In acute respiratory acidosis, rise of HCO3- will be 1 mEq/L for
every 10 mm Hg of CO2.
-= + -
In chronic respiratory acidosis, rise of HCO3- will be 4 mEq/L
for every 10 mm Hg of CO2.
Treatment
1. Treatment of underlying disease
2. Assisted ventilation: Noninvasive/ Invasive.
Metabolic acidosis
Introduction
Condition characterized by low HCO3- state either due to overconsumption or
excessive loss of HCO3-.

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Anion gap
= -
=[ + - + ]
Normal anion gap: 6-12 mEq/L
Anion gap represents unmeasured anions in the body
The unmeasured anions in our body are:
a. Organic and inorganic acids
b. Serum proteins (SO4--, PO4---).
Classification and causes
High anion gap metabolic acidosis
Normal anion gap metabolic acidosis
Overproduction of H+:
Excess loss of HCO3-:
1. Lactic acidosis:
1. Renal loss:
a. Severe hypoxia
Renal tubular acidosis
b. Hypoperfusion:
2. GI loss:
Any shock
a. Severe diarrhoea
Acute pancreatitis
b. Pancreatic fistula
Septicemia
c. Uretero-sigmoidostomy.
2. Ketoacidosis:
a. Diabetic ketoacidosis
*Here, there is a compensatory rise of Cl-
b. Starvation
concentration: hyperchloremic metabolic
c. Alcoholics
acidosis.
Underexcretion of H+:
1. Acute kidney injury
2. Chronic kidney disease.
Clinical features
1. Due to underlying disease
2. Compensatory hyperventilation leading to rapid breathing pattern:
acidotic/ Kussmaul's breathing.
Investigation

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1. ABG: To identify metabolic acidosis (pH, HCO3-, PCO2)
=[ . ? - + ]? .
(?2) is for normal compensation.
2. Anion gap should be calculated.
Treatment
1. Treatment of the underlying cause
2. In selective cases, when HCO3- is too low, NaHCO3 administration.

Respiratory alkalosis
Introduction
Condition characterized by excess wash out of CO2.
Primary problem
Hyperventilation.
Causes (4Ps)
1. Physical exercise
2. Pregnancy
3. Panic attack
4. Pulmonary causes*:
a. Pulmonary embolism
b. Pneumothorax
c. Pulmonary interstitial disease
d. Pulmonary edema
5. High altitude.
*In these pulmonary diseases, because of continuous tachypnea, respiratory
muscles become fatigue and PCO2 level will gradually start to fall.
Clinical features
1. Due to the underlying disease
2. Due to hypocapnia:

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Laziness/ light headacheness
Tingling
Perioral numbness/ paresthesia.
Investigation
1. ABG: To identify respiratory alkalosis (pH, PCO2 , HCO3-, PO2)
Type of respiratory
Fall of HCO3-
Expected HCO3-
alkalosis
Acute
For every
2 mEq/L
Chronic
5 mEq/L
- -PCO
10 mm Hg
in PCO2
level
- -PCO
2. Relevant investigations to assess the underlying condition.
Treatment
1. Treatment of the underlying disease
2. If type 1 respiratory failure occurs, then attempts to correct hypoxia by:
a. High flow oxygen
b. Assisted ventilation: Noninvasive/ invasive.
3. In panic attack:
a. Reassure the patient
b. Rebreathing into the bag.
Metabolic alkalosis
Introduction
Condition characterized by abnormal retention of HCO3-.
Causes
1. Cl- loss/ H+ loss: (Hypochloremic metabolic alkalosis)
a. Severe vomiting
b. Repeated gastric suction.

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2. Abnormal generation of HCO3-:
a. Diuretic use
b. Hypokalemia
c. Mineralocorticoid excess.
3. Post-hypercapnic metabolic alkalosis
If a chronically elevated arterial PCO2 is returned to normal quickly (as if the
patient is intubated and ventilated), then the patient is in the situation of
having an elevated HCO3- (due to renal compensation) without there being
the physiological need for it anymore. The elevated bicarbonate is typically
slow to fall as return to normal requires renal excretion of the excess
bicarbonate.
Clinical features
Due to the underlying disease
Investigation
1. ABG: To identify metabolic alkalosis (pH, HCO3-, PCO2)
=[ . ? - + ]?
?5 is for normal compensation.
2. Investigation to assess the underlying disease.

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