1

rspiratory system
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INDEX
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RESPIRATORY
Overview of respiratory system examination
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Findings of respiratory system in some common diseases:

Condition Mediastinal Percussion Breath VR/ VF Added sound(s)
shifting sound
Pleural effusion Often no shift Dull VBS↓ ↓ -
(at & below the
level of effusion) Opposite: in case of
massive effusion

Pneumothorax Often no shift Tympanitic VBS↓↓ ↓↓ -

Entire hemithorax
of the afftected Opposite side: in
side case of massive

COPD No shift Hyperresona Early stage Rhonchi- often

(bilateral nt Normal Normal ( airway narrowing)
symmetrical) ONLY if Well established case
hyperinflated
VBS↓ ↓↓

Asthma No shift Normal Rhonchi

(bilateral Inactive/ well ( airway narrowing)
symmetrical) controlled

Normal Normal
Active disease
VBS↓ ↓↓

Consolidation No shift Impaired/ a Crepts (moist sound)

(Over that part of dull a Crepts only
the chest wall
which overlies the VBS↓ ↓↓
pathology)
BBS ↑ Crepts (moist sound)

Collapse No shift Impaired/ VBS↓ ↓↓ -

(Over that part of dull
the chest wall Same side BBS ↑
which overlies the
pathology)
Fibrosis Same side Impaired/ VBS↓ ↓↓ Crepts
(Over that part of dull
the chest wall
which overlies the
pathology)
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Respiratory failure
It is defined as an arterial blood gas (ABG) pO2<60 mm Hg
Types

Causes
Type 1 failure Type 2 failure
Pneumonia Centre failure/ CNS diseases:
Pulmonary edema (LVF)  Brainstem depression: Drug overdose (Opiate/
Pulmonary embolism barbiturate)/Deep coma
Parenchymal Lung disease  Brainstem structural damage: CVA/Head injury/IC-SOL
(ILD) Pump failure/ respiratory diseases: COPD (Most common)
ARDS Neuromuscular diseases:
Acute asthma  MND/ Guillain-Barré syndrome/ Myasthenia gravis
 Muscle fatigue/overworking: ALL causes of Type 1
Respiratory failure
(Increased work of breathing)
Chest wall diseases: Kyphosis &/or Scoliosis

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 (“breaths for the patient”)  Invasive
 Non-invasive: (“helps the patient to  Non-invasive: BiPAP (Bilevel positive
breath”) airway pressure)
CPAP (Continuous positive airway
pressure).

CPAP:
The Continuous Positive Airway Pressure (CPAP) machine gives a predetermined level of pressure.
This continuous air pressure keeps the 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.
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Pulmonary function test (PFT)

Although PFT will be invariably abnormal in ALMOST all lung diseases however MOST of the
diseases can be and are actually diagnosed by other means (tests other than PFT). So PFT is NOT
“routinely done” in lung disease patients.

FEV1 (Forced expiratory volume in 1 second): FEV1 is the volume exhaled during the first second of a
forced expiratory effort after a full inspiration.
FVC (Forced vital capacity): FVC is the TOTAL volume of air that can be forcibly blown out after a
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): extent to which
oxygen passes from the alveoli into the blood. The test involves measuring partial pressure difference
between inspired and expired carbon monoxide. It relies on the strong affinity and large absorption
capacity of red blood cells for carbon monoxide and thus demonstrates gas uptake by the capillaries.
DLCO measures the ability of the lungs to transfer gas from inhaled air to the red blood cells in
pulmonary capillaries.
KCO: Diffusion capacity of the lung per unit volume.

Basic clinical application of PFT in lung diseases

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Acid base balance

Normal ABG values
pH: 7.35-7.45PaO2: 80-100 mm HgPaCO2: 35-40 mm Hg SpO2: 95-100%HCO3-: 22-26 mEq/LBase
excess: -2 to +2.
Classification of acid base disorders

Condition pH PCO2 HCO3-

(N: 7.35-7.45) (N: 35-40 mm Hg) (N: 22-26 mEq/L)
Respiratory acidosis <7.35 >40 >26
Metabolic acidosis <7.35 <35 <22
Respiratory alkalosis >7.45 <35 <22
Metabolic alkalosis >7.45 >40 >26

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
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Respiratory acidosis
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 (MND/MG
4. Acute brainstem damage etc.)
4. Sleep related breathing disease:
a. Obstructive sleep apnoea
b. Obesity hypoventilation syndrome.

Clinical features
1. Features of underlying disease
2. Features due to high CO2 narcosis (Metabolic encephalopathy):
A. Altered sensorium D. Delirium
B. Behaviourial disturbance F. Flapping tremor
C. Confusion/Convulsion/Coma
Investigation: To identify respiratory acidosis: ABG 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
Condition characterized by low HCO3- state either due to overconsumption or excessive loss of
HCO3-.

Anion gap

Normal anion gap: 6-12 mEq/L Anion gap represents unmeasured anions in the body
The unmeasured anions in our body are: Organic and inorganic acids, Serum proteins, SO4, PO4.

Classification and causes

High anion gap metabolic acidosis Normal anion gap metabolic acidosis
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 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
1. ABG: To identify metabolic acidosis (pH↓, HCO3-↓, PCO2↓)

2. Anion gap should be calculated

Treatment
1. Treatment of the underlying cause
2. In selective cases, when HCO3- is too low, NaHCO3 administration
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Respiratory alkalosis
Condition characterized by excess wash out of CO2.
Primary problemHyperventilation.
Causes (4Ps)
1. Physical exercise b. Pneumothorax
2. Pregnancy c. Pulmonary interstitial disease
3. Panic attack d. Pulmonary edema
4. Pulmonary causes*: 5. High altitude.
a. Pulmonary embolism
*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:
✓ Laziness/ light headacheness
✓ Tingling
✓ Perioral numbness/ paresthesia.
Investigation
1. ABG: To identify respiratory alkalosis (pH↑, PCO2↓ , HCO3-↓, PO2↓)

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 oxygeAssisted ventilation: Noninvasive/ invasive.
3. In panic attack:Reassure the patientRebreathing into the bag.

Metabolic alkalosis
Condition characterized by abnormal retention of HCO3-.
Causes
1. ↑Cl- loss/ ↑H+ loss: (Hypochloremic metabolic alkalosis)
a. Severe vomiting
b. Repeated gastric suction.
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.
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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.

Pleural effusion
It is defined as accumulation of abnormal amount of fluid in the pleural space.
Types and causes:
Transudative pleural effusion:
LHF/ CCF
CKD Exudative pleural effusion:
Chronic liver disease Infection in the pleural space: TB.;
Nephrotic syndrome Parapneumonic
Hypothyroid Malignancy: Bronchogenic
/Breast/Lymphoma.
Autoimmune/ connective tissue disorder:
PE

Due to effusion Due to underlying etiology

Chest discomfort/ dull ache in the affected LHF: SOB, PND, Orthopnea.
side. Chronic liver disease: Abdominal swelling,GI
Shortness of breath (SOB). bleeding.
Sharp pleuritic chest pain (if there is an Nephrotic syndrome: Generalized swelling.
underlying acute pleurisy). Bacterial infection: Fever, cough, dyspnea.
TB: Weight loss, loss of appetite, low grade
fever, haemoptysis.
Malignancy: Rapid weight loss, loss of appetite.
A lump with features of primary malignancy.
Connective tissue disorders:
Red eye/ gritty eye.Skin
rash.Arthralgia.Hematuria.

Affected side/Hemithorax Clubbing: Bronchogenic CA.

Inspection- Movement restricted Lymphadenopathy TB. Malignancy (Breast,
Bulging. Lymphoma)
JVP: ↑CCF (Pulsatile); SVC obstruction (Non-
Palpation Expansion restricted. pulsatile)
Shift: To the opposite side, Malignancy (Breast CA, Lymphoma).
in case of massive effusion Jaundice: CLD; Metastatic disease of liver.
Percussion At and below the level of Gallop+ Basal Crepts: LVF
effusion: Dull. GI signs of chronic liver disease may be present
Auscultation VBS↓ + VR/VF ↓ Breast examination may show the lump.
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Investigation
1.Blood:
 Hb/ TC/ DC/ CRP or ESR.
 Urea-creatinine Na+ K+.
 Liver function test.
2.Chest X Ray: It helps
 to diagnose effusion
 in many cases, the underlying etiology: PNEUMONIA/LUNG SUSPICIOUS MASS

3. Diagnostic aspiration of pleural fluid: Often( but not ALWAYS) diagnoses the cause of effusion
Physical character: Hemorrhagic: Malignant effusion Turbid: Infection( Parapneumonic/TB)
Chemical character: Paired serum sample for protein and LDH:
Diagnostic criteria:
▪ Exudative (if it fulfils any 1 criteria):
❖
❖
❖
▪ Transudative: doesn’t fulfil any criteria.
Microbiological character:
 Gram stain, culture sensitivity: MAY BE positive in Parapneumonic effusion
 AFB, Mycobacterial culture: MAY BE positive in TB effusion Diagnostic yield is very low
 GeneXpert TB: may be positive for M.TB DNA
Cytological character:
 Abnormal/ malignant cells: In malignant effusion ( but unable to tell the primary focus of
malignancy)
 Polymorphonuclear predominant: Parapneumonic effusion
 Predominant lymphocytic: TB, Malignant effusion
Markers of TB: Adenosine Deaminase (ADA) level: high in TB effusion

4. Pleural biopsy: Either under radiological evidence/ thoracoscopically

5. Further investigation(s): OFTEN REQUIRED PARTICULARLY IF Fluid result in

INCONCLUSIVE/CONCLUSIVE but further assessment is required to “complete” the diagnosis.
Nature of these tests depend on suspected diagnosis and report of pleural fluid analysis:
Depending on the underlying etiology
Exudative fluid + LYMPHOCYTIC FLUID (but TB not confirmed):
 CECT Chest
 Pleural biopsy
Exudative fluid+ Atypical cells/malignant cells present: Tests to find out the primary focus
 CECT chest+ abdomen
 Biopsy of a suspicious lesion seen in CECT
 Pleural biopsy
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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.
c. In case of recurrent effusion:
 Pleurodesis can be attempted where adhesion is induced between visceral and
parietal pleura by some sclerosing agent like Talc
 Insertion of a long term indwelling pleural catheter.
2. Treating the underlying cause.

Pneumothorax
It is defined as presence of air in the pleural space.
Types:
1. Based on clinical features
Primary (in absense of lung disease)- At risk: Tall, young and thin individuals
Secondary (in presence of underlying lung disease)
At risk:
• COPD • Marfan's syndrome
• Long standing asthma • Langerhans cell histiocytosis
• TB • Lymphangioleiomyomatosis
2. Based on pathophysiology
1. Closed type: Air starts to accumulate, but the punctured area of lung gets sealed off on its own
after a while.
2. Open type: Air freely flows in and out of pleura during inspiration and expiration,
respectively.
3. 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
Dyspnea: 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.
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Chest pain: momentary sharp chest pain may occur (due to tear of the underlying lung tissue).
Sudden collapse/ blackout: In tension penumothorax.
History suggestive of underlying lung disease may be present.

Signs
1. Tachypnea
2. Tachycardia
3. Pulse oxymetry: Low SpO2 (where normal oxygen saturation is 95-100%).
4. Cyanosis: In case of severe hypoxia
5. Hemodynamic instability: Suggestive of tension pneumothorax

Inspection Movement: restricted

Palpation Mediastinal shifting towards the opposite side (usually in case of tension
pneumothorax).
Percussion Tympanitic.

Auscultation Reduced VBS/ VR/ VF.

Added sound 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).
Coin percussion: A metallic sound is heard when the patient is asked to percuss a
coin against another and the stetho is placed at a diametrically opposite point.
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Chest examination: Findings are elictible OVER the affected hemithorax

Investigation:
Chest X Ray (CXR):
a. Confirms diagnosis.An area of lung not traversed by bronchovascular margins.
Collapsed border: Visible.
b. Presence/ absence of tracheal shifting.
1. Other relevant investigations to assess the underlying disease.
Treatment protocol

Persistent Air leak/Pneumo fails to resolve

Indications of cardiothoracic referral: Cardiothoracic referral

1. Persistent air leak (bubbling> 3 days)
2. Second episode of ipsilateral pneumothorax
3. First episode of contralateral pneumothorax 1. Pleurodesis
Post-discharge advice: 2. Pleurectomy/Decortication
1. Avoid air travel for 4-6 weeks.
2. Refrain from deep sea diving for rest of life.

*Size of pneumothorax: Distance between rib margin and collapsed lung border at the level of hilum.
Pneumonia
If Types
it is ≥2 cm, it is suggestive
1.Community acquiredof pneumothorax
pneumonia of 50%
2. Hospital pleural
acquired space 3. Aspiration pneumonia
pneumonia
If it is ≥2 cm, it is suggestive of pneumothorax of 50% pleural space.
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Community acquired pneumonia

Pneumonia occurring outside hospital setting/ within 48 hours of admission in a person who
hasn’t been in hospital in last 14 days.
Organism
Typical: 1. Strepto pneumoniae 2. H. influenza 3. Moraxella 4. Klebsiella
Atypical pneumonia: 1. Mycoplasma 2. Legionella 3. Chlamydia

Clinical features
Symptoms: Followings in different combination
Systemic symptoms:
Appetite loss/Apathy Respiratory symptoms:
Bodyache/weakness Breathlessness: if a significant part of lung
Chill +/-rigor parenchyma is affected
Drowsiness/Delirium Chest pain: pleuritic
Cough- Often with purulent/ mucopurulent
sputum
Hemoptysis: blood stained sputum
Signs: Severity/degree of signs depend on extent/severity of Pneumonia
Altered sensorium Chest: Over the “Pneumonic zone” of chest
Breathing- rapid (tachypnoea) 1. Signs of consolidation:
Cyanosis a. Impaired percussion c. VR/ VF: ↑
Decreased O2 saturation b. BBS d. crepitation

or
2. Signs of reduced air entry:
a.VBS: ↓ b.VR/ VF: ↓ c.crepitation:

3. Pleural rub +/-

Investigation
1. Blood: 3. Chest X Ray-confirms diagnosis
a.Hb, TC, DC, ESR/ CRP
b.Na+ K+ Urea creatinine 4. Special tests: specially when non resolving
c.Blood C/S CT chest
d.Procalcitonin: sensitive marker of bacterial Bronchoscopy- to obtain samples for
infection microbiological
e.ABG: if the patient is hypoxic diagnosis
2. Sputum: Gram stain and culture-sensitivity
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Treatment
Supportive treatment (particularly in critically ill patients)
A. Airway protection: frequent suction
Intubate if required Anbiotic: Empirical therapy with:
A: admit (Co-amoxiclav + Macrolide) or Levofloxacin
B. Breathing: Oxygen if hypoxic OR
Assisted ventilation: if Resp Pip-Taz/ 4TH gen. Cephalosporin/
failure Carbapenem
✓ Non-invasive (in critically ill patients)
✓ Invasive
B: Blood parameters monitoring: Antipyretic
B: Bed rest Nebulization, if required
C. Circulation: IV fluid Mucolytic agent

D: Diet
D: DVT prevention
D. Drug:

Complications of pneumonia 4. Non-resolving pneumonia:

1. Septicemia a. Wrong diagnosis
2. Respiratory failure b. Wrong choice of antibiotic
3. Lung abscess c. Unusual/ resistant organism
d. Underlying pulmonary disease
(malignancy/ bronchiectasis).

Hospital acquired pneumonia

Pneumonia occurring after 48 hours of hospital admission.
Common organismPseudomonasStaph. aureusAcinetobacter.
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
Colistimethate
Aspiration pneumonia
Pneumonia secondary to aspiration of gastric content/ oropharyngeal secretion.
Which people are at risk of aspiration pneumonia?
1. Impaired cough reflex-Semi/unconscious 2. Neuromuscular diseases involving
patients esophagus
• Alcohol • Motor neurone disease
• Brain damage • Myasthemia gravis
• Coma • Bulbar pulsy
• Drug overdose (eg. sedative)
• Epilepsy
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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 or Pip-Taz

Lung cavity
Pulmonary cavities, which are most of the time radiologically diagnosed, are gas-filled areas
of the lung in the c center of a nodule, mass or area of consolidation
C: Cancer
Bronchogenic Ca: most frequently Sq.CC
Cavitatory pulmonary metastasis
A: Autoimmune -Wegener's granulomatosis/Rheumatoid nodules
V: Vascular-Pulmonary Embolus
I: Infection (bacterial/fungal) TB/Abscess
T:Trauma – Pneumatocoele
Y: Young asymptomatic individuals- (often) pulmonary sequestration/Bronchogenic cyst
Investigations
1. CxR
1. CECT Chest
2. Relevant others- as per suspected cause
Treatment
Treatment of the underlying causes/disease. Certain conditions do not require any treatment.

Swine flu-management (H1NI Rx)

Antipyretics: Paracetamol
Analgesics: NSAIDs
Antiviral: Oseltamivir or Zanamivir
Indications:
1. Initial presentation with severe illness or whose condition begins to deteriorate
2. patients with underlying medical comorbidities that increase the risk of more severe
disease
3. Pregnant women
4. Pre or post-exposure prophylactic antiviral for “high risk” individuals
Bedrest: if very sick
Cough suppressants
Diet: Nutritious diet
Early recognition of complication: particularly viral Pneumonia and treat it promptly if required
Ventilatory support
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Fluid: adequate hydration- oral fluid or if required IV fluid
Future risk prevention: Vaccine

Bronchogenic Carcinoma
Malignancy of bronchial/ bronchiolar epithelium.
Risk factors
1. Cigarette smoking: Asbestos (usually causes adenocarcinoma
a. Initiator: Polyaromatic hydrocarbon of lung
b. Promoter: Phenol derivatives 3. Environmental toxins
2. Occupational exposure:

Pathophysiology
Intrathoracic effects of bronchogenic CA Extra-thoracic effects of bronchogenic CA
Metastasis to:
Paraneoplastic syndromes.

Structures affected Effects

Airway  Obstruction Narrowing

Parenchyma  CollapseConsolidationCavitation
PleuraPericardium Effusion
Ribs Erosion Irritation of intercostal nerves (ICN)
Lymph node Hilar/ mediastinal/ supraclavicular lymphadenopathy
✓

Mediastinal
structures 2 tubes:EsophagusTrachea.
2 nerves:Sympathetic trunkRecurrent laryngeal nerve.
2 great vessels:Superior vena cavaSubclavian artery.
Extra-thoracic Metastasis: BrainBoneLiver
effects 1. Paraneoplastic syndromes.
.

Clinical features: WIDELY VARIABLE: any 1 or more than 1 of these

Symptoms:
Category Symptoms
Respiratory  Breathlessness
complaints  Productive cough
 Chest pain: dull in nature in erosion of ribs
sharp shooting in nature in irritation of IC nerves
 Hemoptysis.
Due to compression  Dysphagia
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 Stridor
 Hoarseness of voice (due to injury to recurrent laryngeal nerve
 Explosive nature of cough (also termed as ‘bovine cough’: due
to RLN palsy)
 Symptoms of SVC obstruction.
Due to extrathoracic  Bone pain
effect  Increased intracranial tension (ICT) due to brain metastasis:
✓ Headache
✓ Vomiting
✓ Convulsion.

Signs:
1. Pallor: may be present 4. Signs of SVC obstruction
2. Clubbing may be positive 5. Supraclavicular lymphadenopathy.
3. Jaundice may be present (liver metastasis)
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 Hormone Effect
(most commonly seen ACTH Cushing syndrome
in small cell lung PTHrP Hypercalcemia
carcinoma) ADH SIADH
Gonadotropin Gynecomastia
CNS  Lambert–Eaton myasthenic syndrome
 Subacute cerebellar degeneration.
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Hematological  DIC
 Anemia.

CVS  Non-infective endocarditis

 Migratory thrombophlebitis.

Renal Nephrotic/ nephritic syndrome

Investigation
1.Confirmation of diagnosis: Tissue diag +
metastasis
1. Chest X Ray To evaluate various effect of tumor:
2. CECT of chest and abdomen Blood:
3. PET scan (in selected cases) Hb, TC, DC, ESR/ CRP.
4.Histopathological confirmation by: with Na+ K+ Urea Creatinine: Hyponatremia due
IHC to SIADH
✓ Bronchoscopic biopsy LFT : deranged due to Liver metastasis
✓ CT guided lung biopsy Serum Ca++ level:may be elevated
✓ Lymph node biopsy Bone metastasis
✓ Cytological examination of pleural Secretion of PTHrP by
fluid the tumor
CT/ MRI of brain
3.Assessment of physical function: Bone scan (if bone metastasis is suspected).
A.ECG B.Echocardiogram C.Pulmonary function test
Treatment: MDT approach
Treatment depends on Treatment options:
1. Staging of tumor 1. Surgery
2. Overall fitness of patient. 2. Chemotherapy
3. Radiotherapy

Therapeutic classification and treatment of choice:

Group Feature Treatment of choice
Small cell lung CA More aggressive ▪ Chemotherapy: Carboplatin/ Cisplatin
Limited role of ▪ Radiotherapy
surgery
Non-small cell lung Less aggressive ▪ Surgery:
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.
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SVC Obstruction
Occlusion of SVC due to extraluminal/ intraluminal compression.
Cause
1. Malignancy: 2. Benign:
a. Bronchogenic CA a. Thymoma
b. Lymphoma b. Retrosternal goitre
c. Clot/ thrombus.
Clinical features
Symptoms:
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 (Pemberton’s sign).
3. Superficial venous prominence over the chest wall with direction of filling from above
downwards may be seen.
InvestigationCT chestHistopathological confirmation the underlying disease/ condition
Treatment
1. Supportive treatment:Oxygen 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
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 nerve  Pain/ paresthesia along the ulnar border of arm and
root forearm
 Wasting of hypothenar muscles.

Compression of sympathetic Horner’s syndrome

trunk Symptom Cause
Miosis Due to involvement of dilator pupillae
Anhydrosis of Due to involvement of vasomotor fibers to
same side of face face
Partial ptosis Due to paralysis of Muller’s muscle
Loss of ---
ciliospinal reflex
Enophthalmos Due to paralysis of Orbitalis muscle
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Acute respiratory distress syndrome (ARDS)

It is an acute complication of a wide variety of underlying diseases and it is characterized by non-
cardiogenic pulmonary edema.

Causes: A. Acute pancreatitis R: RBC transfusion (massive) D: DIC/ Drug overdose S:

Septicemia
A: Aspiration Pneumonitis
Clinical features
1. Rapidly progressing breathlessness 4. Often patient is hemodynamically
2. An underlying illness/ condition must unstable
be present 5. Usually bilateral crepitations are
3. Often tachypnea/ tachycardia/ low present.
SpO2 is present
Investigation:
1. ABG 4. Relevant tests to assess underlying
2. Chest Xray condition
3. HRCT (if pt’s condition permits)
Treatment
Airway protection: Often require intubation Circulation: IV fluid and vasopressors
Breathing: invasive ventilation Drugs for underlying conditions

Bronchiectasis
It is defined as chronic infection of airways leading to abnormal, permanent dilation of bronchi/
bronchioles.
Causes
1. Infection:Post infective causes: 3. Impaired mucociliary clearance:
a. TB. a. Cystic fibrosis
b. Necrotizing pneumonia b. Primary ciliary dyskinesia
c. Whooping cough pneumonia c. Kartagener’s syndrome
2. Immune related: 4. Insult to the bronchus:
Immunodeficiency: Primary and a) Obstruction (Foreign body/ Lymph
secondary. node etc.)
Hyperimmune reaction:ABPA 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).
 25
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.

Investigations:
Initial investigations
1. Hb, TC, DC, CRP/ ESR. 4. CXR:changes suggestive of
2. Sputum: Gram stain and culture bronchiectasis.
sensitivity. 5. HRCT: Confirms the diagnosis.
3. Blood culture: During infective
exacerbations.

Treatment
1. Antibiotic therapy: 2 types: 4. Surgery: Removal of the bronchiectatic
Short term (during exacerbation). area.
Long term (for prophylaxis). 5. Vaccine:
2. Bronchodilators (in case of airway a. Influenza vaccine: Yearly.
obstruction). b. Pneumococcal vaccine: Single dose.
3. Clearance of airway secretion(Bronchial
toileting)
 Postural drainage
 Chest physiotherapy
 Special breathing exercise
 Cough assist device

Interstitial Lung Disease (ILD)/ Intersitital Pneumonitis/DPLD

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
Cryptogenic fibrosing alveolitis (Usual interstitial pneumonia/UIP)
Non-specific interstitial pneumonia (NIP)
Acute interstitial pneumonia
Desquamative interstitial pneumonia
Lymphoid interstitial pneumonia
Cryptogenic organizing pneumonia
Respiratory bronchiolitis associated interstitial lung disease (RB-ILD).
 26

Causes: 1. Idiopathic 2. Iatrogenic (Amiodarone) 3. Infection 4. Immunological (Connective tissue

disease).

Symptoms
Breathlessness: Onset, severity and progression depend on the underlying disease.
Chronic productive/ dry cough
Systemic: Fever/Arthralgia/Weight loss may occur
Swelling (due to RVF)

Signs: If breathless: Tachypnea/Low SpO2/Cyanosis

Clubbing: particularly in UIP.
Chest: Signs of reduced air entry:VBS↓, VR↓, VF↓
Crepitation: Fine inspiratory crepitation

Investigation
Chest X Ray:Reticular pattern is seen.
HRCT:Honey comb / ground glass appearance.
PFT:Restrictive parenchymal defect
Lung biopsy If radiological appearance is inconclusive,
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.
 27

COPD (Chronic obstructive pulmonary disease)

It’s a chronic progressive disease characterized by fixed/irreversible airway obstruction +/- alveolar
damage.
Etiology:
Cigarette smoking(10 pack Years- 50% smokers develop COPD)
Contributory factors: 1. Outdoor air pollutant 2. Occupational pollutant 3. .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: abnormal permanent dilation of alveoli with destruction of their walls without any fibrosis.

Pathophysiological changes:

Symptoms:

Breathlessness: Chronic, slowly progressive leading to reduced exercise tolerance.

No diurnal variation/ no seasonal variation (Asthma) and no orthopnea/ PND
Chronic cough: Often productive; mucoid/ mucopurulent. May be dry also. Volume of sputum
increases and becomes more purulent during infective exacerbation.
Edema/Swelling: When RVF develops.
 28
Signs
1. Depeneding on severity of hypoxia: Added sounds: Rhonchi/ wheeze(due to
Tachypnea +/- Tachycardia. bronchospasm).
Pulse oxymetry: Reduced oxygen A localized area with crepitation may be
saturation. present (due to infection of underlying
Cyanosis may be evident. parenchyma).
2. Oedema (in RVF). CVS:
3. Raised JVP (in RVF). Signs of PAH: Accentuated P2 +/- Palpable P2.
Mid-systolic murmur due to
4. Respiratory system: functional PS
Inspection: Hyperinflated: Barrel shaped chest. Signs of RV enlargement: Left parasternal
Palpation: No shifting. heave
Percussion: Hyper-resonant at both sides.
Auscultation: Signs of A/Entry- reduced
VBS/ VR/ VF

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.

Investigation
Blood: FBC: Polycythemia (hypoxia stimulates Erythropoietin production, leading to polycythemia).
ABG: To document the baseline gas status
Sputum: Gram stain+ culture sensitivity.
Spirometry:

Pre and post-bronchodilator challenge FEV1: No evidence of reversibility.

CXR:
a. Prominent bronchovascular markings.
b. Hyperinflated lung.
c. Always look for any pneumothorax.
Treatment
Principles of treatment:
A-Aviod smoking (Smoking cessation) D-Drug (Pharmacotherapy) D- Domiciliary
B- Breathing exercise (Pulmonary O2 therapy
rehabilitation) E- Exacebation Rx
C- Chest Physiotherapy E- Emerging Treatment

Smoking cessation Nicotine replacement therapy (in different forms)- a.Nicotine patch b.Chewing
gum
c.Drugs (Bupropion/
Varenicline)
 29

Pulmonary rehabilitation 1. Special breathing techniques. 2. Graded physical exercises. 3. Cough

assist device 4. Physio

Pharmacotherapy
Inhalers:
Anticholinergic (anitmuscarinic) β2-agonist:
Corticosteroid:
Short acting: Ipratropium. Short acting: Levo-salbutamol.
Fluticasone/ Budesonide
Long acting: Tiotropium Long acting: Salmeterol/ Formoterol/Indacaterol
Beclomethasone

Oral:
1.Xanthine:Aminophylline/Theophylline/Acebr 3.Corticosteroid: Short term use during
ophylline Exacerbation
2.PDE-4 inhibitor: Roflumilast 4.Antibiotics: Short term use during
Exacerbation

Vaccination 1.Influenza vaccine: Yearly 2. Pneumococcal vaccine: Single dose + Booster after 5
years

Stepwise treatment approach

 30
Domiciliary long term Oxygen therapy
Criteria:
ABG: PaO2< 50 mm Hg, when done in a stable state and at least twice, at least 3 weeks apart.
ABG: PaO2: 55-60 mm Hg, with evidence of PAH/ RVF/ Polycythemia.
Duration of long term oxygen therapy: At least 15 hours a day.

Emerging Treatment: Surgery: Various options are: 1. Bullectomy 2. Lung volume reduction
surgery.

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) – Encephalopathy: “abcde”
4. Systemic manifestations of infection: Appetite loss; Bodyache; Chill +/- Rigor Drowsiness/ Elevated
temp
Signs Apathy Delirium

1. Hypoxic: 1.Tachypnoea +/-Tachycardia2.Pulse oximetry: Low SpO2 3.Cyanosis)

2. Hypercapnoeic: 1.Flapping tremor 2 .GCS: low/falling
3. 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.

Respiratory system 1.Signs of COPD are present 2.Widespread rhonchi and localized crepts may be
present.
Investigation Same as COPD.
Treatment
Airway protection : Frequent oropharyngeal suction; Intubation if required.
Breathing: Controlled oxygen: Ideally via venturi mask PARTICULARLY IF Pco2 High. If patient is
hypercapnoeic during acute stage, a saturation of 88-92% should be acceptable, so that the hypoxia is
not overcorrected.
Assisted ventilation may be required: Non-invasive (BiPAP)/ Invasive.
Circulatory support with IV fluids.
Drugs:
Antibiotics: Oral/ IV, depending on patient’s ability to swallow a tablet and severity of infection
Usually a 7-10 days course is given.
Empirical antibiotic: Coamoxiclav + Macrolide
 31
Severe infection/Critically ill: Carbapenem
Aminophylline infusion: ONLY if in spite of optimum medical therapy patient remains symptomatic.
Max 24-48 hours.
Bronchodilator: Nebulization with Levosalbutamol + Budesonide+ Ipratropium: initial few days then
switch to inhalers
Corticosteroid: Oral/ IV short course steroid: usually Prednisolone/ Hydrocortisone: 5- 10 days
Diet: Nutritous diet
DVT prophylaxis
Exercise: Chest Physiotherapy/Breathing exercise
Further treatment plan: appropriate long term inhalers

Bronchial asthma
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:
Indoor allergen: Dust/ mites/ fungus Drugs: Aspirin/ β-blocker
(aspergillus) Physical exercise
Outdoor allergen: Dust/ smoke Chemical: Perfume/ tobacco smoke
Occupational: Isocyanate/ flour

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.
 32
Sign
a. Examination may be entirely normal in asymptomatic intervals

b. During an active spell of asthma:

1. If hypoxic: Tachypnoea+ Tachycardia +/- Pulse oximetry: Low SpO2 ± Cyanosis
2. Respiratory system:
 Movement/ expansion may be restricted.
 Signs of reduced air entry: Reduced VBS, VR, VF.
 Added sound: Diffuse polyphonic wheeze may be present.
Investigation
Preliminary investigations:

1. Spirometry:
2. Bronchodilator reversibility: +Ve: Pre-bronchodilator FEV1 increases by 15%/200 ml following
bronchodilator challenge with inhaled short acting β2 agonist.
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.
4. Atopic/Allergic Tendency: Estimation of serum IgE.

Treatment
A-Avoid any suspected allergen (if any)
B- Breathing Exercise
C: Chest Physiotherapy
D-Drug (Pharmacotherapy)

Inhalers:
Anticholinergic (anitmuscarinic) β2-agonist:
Corticosteroid:
 33
Short acting: Ipratropium. Short acting: Levo-salbutamol.
Fluticasone/ Budesonide
Long acting: Tiotropium Long acting: Salmeterol/ Formoterol/Indacaterol
Beclomethasone

✓ Reliever: Short acting β2 agonist/Short acting Antimuscarinic

✓ Preventer: Long acting β2 agonist, Inhaler corticosteroid
Oral:
Xanthine: Leukotriene antagonist: Montelukast,
Aminophylline/Theophylline/Acebrophylline Zafirlukast
Mast cell stabilizer: Sodium cromoglycate Corticosteroid
Anti-IgE agent: Omalizumab

[SABA/LABA: Short/long acting β2 agonist, ICS: Inhaled corticosteroid, MX:xanthine, LTA:

Leukotriene antagonist

Treatment outcomes Well controlled asthma:It is defined as:

1.No symptoms (or ≤1 per week) 3.No nocturnal symptoms
2.No reliever use (or ≤1 per week) 4.No restriction of activity of daily living.
 34

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.
2. Wheeze
3. Often productive cough.

Signs:
1. Tachypnoea+/-Tachycardia
2. Low SpO2 ± Cyanosis
3. Signs of reduced air entry
Clinical features: Symptoms: 4. Widespread wheeze
1. Worsening dyspnea

Investigation:
Blood: 1. Sputum: Gram stain and culture sensitivity
Hb, TC, DC, CRP 2. Chest X Ray
ABG: Usually hypoxia with type 1 respiratory 3. ECG
failure 4. ECHO (In selected patients)
Blood culture: If patient is febrile

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.
MgSO4- A single dose of IV MgSO4
Diet: Nutritious diet
DVT prophylaxis
E-Exercise: Chest Physiotherapy/Breathing exercise
F-Further treatment plan: appropriate long term inhalers
 35

Points Moderate Severe Life threatening

Peak expiratory flow 50-75% 33-50% <33%
rate (% of predicted)
Features: Increasing symptoms Increasing symptoms - Silent chest
- Cyanosed
Absence of severe/ Respiratory rate
- Tachy/brady-
life threatening >30/min
arrhythmia
features Heart rate >110/min
- Hypotension
- Confusion/ coma
- pO2 <60 mm Hg
- Saturation <92%
- pCO2: Normal/ near
normal.
 36

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).

Vascular stasis Hypercoagulable state

Prolonged bed ridden state/ immobility • Pregnancy
Lower limb fracture • Active cancer
Post operative state • Protein C/ Protein S/ Antithrombin 3
Long distance flight deficiency
• Leiden's disease (Factor 5 deficiency)
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. 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
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.
 37
Treatment
1.Anticoagulation: Initially Heparin (Unfractionated/ Low molecular weight/ Fondaparinux) +
Warfarin
Heparin stopped and Warfarin continued once target INR is achieved.

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.

Pulmonary arterial hypertension (PAH)

It is a condition characterized by pulmonary arterial pressure >20 mm Hg.
Causes
1. Primary/Idiopathic
2. Secondary:
 Cardiac: Chronic LEFT heart diseases
 Chronic Lung disease: COPD/ILD/Bronchiectasis
 Clot: Acute or chronic Pulmonary Thromboembolic disease
 Connective tissue disease: Scleroderma/SLE/RA
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.
 38
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: PG analogue: Iloprost
✓ Nifedipine Endothelin receptor
PDE-5 inhibitors: Sildenafil/Tadalafil. antagonists:Bosentan

C. Cause: Treat the underlying cause.

Cor pulmonale
It is a clinical condition characterized by right ventricular enlargement (RVE) from acute/ chronic
lung pathology.
Etiology
1.Airway and Parenchymal disease: COPD/ ILD/Bronchiectasis
2.Pulmonary arterial disease: Acute or Chronic Pulmonary Thomboembolic disease
3.Thoracic cage disease: Kypho/scoliosis

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. it is diffuse in nature.
Left parasternal heave
PSM due to a functional TR
Visible/ palpable epigastric pulsation.
4. Symptoms and signs of RVF:
 Symptoms: Swelling.
 Signs: a. Raised JVP b. Bilateral edema c. Soft tender hepatomegaly.
Investigation
1. To assess the underlying disease
2. To assess the RV: a. ECG b. ECHO.
 39
Treatment
1. Treatment of the underlying disease
2. For RVF:
a. Salt and fluid restriction
b. Diuretics.
Extrinsic allergic alveolitis/ Hypersensitivity pneumonitis
It is an inflammatory condition characterized by alveolar/ parenchymal inflammation usually due
to a hypersensitivity reaction against organic antigens.
Common antigens
1. Fungus: a. Actinomycetes b. 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 4. ABG: Hypoxic
2. HRCT 5. Detection of serum precipitins against the
3. Blood: CBC organic antigens
Treatment
1. Supportive:
a. Oxygen: If the patient is hypoxic
b. Systemic corticosteroid.

Cryptogenic organizing pneumonia

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:
Fever/Malaise/ Loss of appetite.
Signs
1. Tachypnea, low SpO2 ± cyanosis
2. Signs of consolidation/ reduced air
entry
3. Crepitations usually present.
 40
Investigations

1. Chest X Ray:
a. Often peripheral consolidation is
seen
b. Fleeting consolidation (if previous
X Rays are available)

2. HRCT: Often confirms the diagnosis

3. Lung Biopsy: 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.
 41

Sarcoidosis

It is an immunologically mediated multisystem disease characterized by non-caseating granulomatous

inflammation.
Involvement and clinical features

1.Constitutional: Fever/Malaise/Arthralgia/Weight loss

2. Pulmonary: Asymptomatic
Cough: persistent dry cough; seldom productive
SOB
3.Extrapulmonaty
a. Derm: Erythema Nodosum
b. CNS: 7th nerve palsy
c. CVS: Arrhythmia
Investigations
1.Pulmonary:
a. Chest X Ray
b. HRCT (If CXR is abnormal) Both will show reticulonodular pattern ± lymphadenopathy.
c. Biopsy: Histopathological confirmation by biopsy from: a. Lymph node b. 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
1. Coricosteroid
2. Immunnosuppressive

Coin lesion/ Solitary pulmonary nodule

SPN, a radiological entity is defined as a well defined round or oval pulmonary parenchymal lesion
≤ 3 cm in diameter. It is surrounded by pulmonary parenchyma and/or visceral pleura.
Coin lesion refers to a round or oval, well-circumscribed solitary pulmonary lesion. It is typically 1-5
cm in diameter and calcification may or may not be present.Typically but not always the patient is
asymptomatic
 42

Cancer- Brochogenic Ca; Solitary Pulmonay metastasis

Artefact-Nipple shadow; cutaneous lesion-Wart/Mole
Vascular- Hamartoma/Arteriovenous malformation/Vasculitis:Wegner’s Granulomatosis
Infective/Inflammatory- ‘round’ Pneumonia/lung abscess/rheumatoid nodule
TB
Young asymptomatic individual- Congential Cysts

C/F- often asymptomatic even if it’s a pathological lesion. Manifestations, if present depend on the
underlying cause-pts may develop Cough/Sputum/SOB/Fever/Wt loss.O/E- Clubbing/Signs of
Peumonia ets may be present.

Investigations

1. CxR- Nodule often gets diagnosed incidentally

2. Further tests, IF ANY depends on the suspected cause-
a. CECT (Many patients need follow up serial CTs to keep an eye on the nodule- as per Fleischner
Society guideline)

b. Biopsy from the lesion

c. Bronchoscopy with Bronchial wash/Bronchoalveolar lavage from the suspected lobe- for
microbiological diagnosis
Many patients need follow up serial CTs to keep an eye on the nodule- as per Fleischner Society
guideline
Treatment

1. Malignant nodule/High risk nodules- Excision 3. Infection: Antibiotic

2. Benign/Low risk nodule- wait and watch 4. TB: ATD

Hemothorax
Blood in the pleural space.

Causes
1. Trauma- Accidental/Deliberate/ Iatrogenic- Intercostal drain/central venous catheter/
thoracostomy tube placement (Penetrating injuries of the lungs, heart, great vessels. Blunt chest
trauma can occasionally result in hemothorax by laceration of internal vessels)
2. Nontraumatic
Neoplasia (primary or metastatic)
Bleeding disorders
Tuberculosis
Nonpulmonary intrathoracic vascular pathology-aortic aneurysm or aneurysm of the internal
mammary artery
 43

C/F-vary widely, depending on the amount and rapidity of bleeding

Chest pain
Dyspnea
Tachypnea
Diminished ipsilateral breath sounds+ dull percussion note.
If substantial blood loss has occurred- hypotension and tachycardia

Investigations
FBC/CBC
CxR
USG Chest with diagnostic fluid aspiration - hematocrit value > 50% of that of the blood hematocrit
confirms hemothorax
CT Chest

Treatment
Tube thoracostomy drainage/Intercostal drain
Video-assisted thoracoscopic surgery (VATS)
Thoracotomy is the procedure of choice for surgical exploration of the chest when massive
hemothorax or persistent bleeding is present.
Foetid sputum
Foul smelling sputum is called foetid sputum
Causes- Usually occurs if a foci of suppurative infection in the lungs- particularly with anaerobic
organism-

1. Abscess 4. Bronchiectasis
2. Aspiration Pneumonia 5. Cavity communicating with a major
3. Bacterial Pneumonia bronchus
C/F- such pts may have ≥ 1 of these manifestations

1. Productive cough- sputum- often Profuse/ often purulent/ foetid

2. Fever
3. SOB
4. Hemoptysis
5. Constitutional manifestations of infection- appetite loss/malaise/bodyache….
Investigations-
1. FBC/CRP- TC high/CRP high 4. Blood culture
2. CxR- often shows the underlying pathology 5. Special test- CT Chest/Bronchoscopy
3. Sputum- G.S/C.S/ZN Stain/Myco TB
culture/XpertTB
Rx- 1. Antibiotic 2. Chest physio 3. Specific Rx, if any of underlying cause
 44
Related SN- Purulent sputum- Exactly same, just add/modify
Purulent sputum= pus like sputum composed of white blood cells, cellular debris, dead tissue,
serous fluid, and viscous liquid (mucus).
Cause-1-5 + 6.Exacerbation COPD/Asthma 7. LRTI
Pulmonary encephalopathy
= CO2 narcosis/Hypercapnoeic respiratory failure/type 2 respiratory failure….see notes
Alpha 1 antitrypsin deficiency (AATD)
AATD is a genetic condition that predisposes to COPD and liver disease (cirrhosis and
hepatocellular carcinoma)

Pathophysiology:
Alpha1- AT is a member of the protease inhibitor superfamily of proteins. The genetic defect
(mutations) responsible for the disease alters the configuration of the alpha1- AT molecule and
prevents its release from hepatocytes. As a result, serum level of alpha1- AT is decreased, leading
to low alveolar concentrations, where the alpha1 AT serves as protection against proteases. The
resulting protease excess in alveoli destroys alveolar walls and causes emphysema. The
accumulation of excess alpha1-antitrypsin in hepatocytes leads to destruction of these cells and
ultimately, chronic liver disease.

C/F:
1. Asymptomatic till significant clinical damage occurs
2. Lung: Dyspnoea +/- cough +/-sputum production +/- wheeze: AATD pts frequently develop
dyspnea many years earlier than smokers with emphysema and normal alpha1- AT levels. By
the time dyspnea becomes the dominant manifestation and a diagnosis is established, most
patients will have severe emphysema.
3. Liver: f/o cirrhosis and chronic hepatitis
The presentation of disease depends on the type of mutation associated with AATD however,
most of the symptoms are limited to the respiratory system as clinically appreciable liver disease
appear mush later.

Signs: Mild emphysema generally have no abnormal findings on physical examination.

Mod- severe emphysema: ≥ 1 of the followings:
Tachypnea
Pursed-lip breathing
Hyperinflation: barrel shaped chest + increased percussion note
Decreased breath sound + wheeze

Young patients with “unexplained” liver disease with or without respiratory symptoms- look
for AATD
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Investigations:

Definitive tests: To diagnose the condition

Serum alpha1-antitrypsin level: typically low
Alpha1-antitrypsin phenotype: Phenotyping is required to confirm AATD

Supportive tests: To assess organ damage

Pulmonary function tests LFT
CxR USG liver
HRCT

Treatment:
1. Supportive: a. Rx of Emphysema b. Rx of Liver disease

2. Definitive: Replacing enzymes: alpha1-antitrypsin protein concentrates