PULMONARY & EMERGENCY MEDICINE

Approach to pulmonary function testing

SHAPES OF FLOW VOLUME CURVES

• Small airway obstruction = characteristic coving curve on expiratory limb of curve
• Restrictive lung disease = when shape is normal but size is small
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Medicine

– V/Q mismatch
ƒ If ratio is >1 → shock, pulmonary HTN
ƒ If ratio is <1 → airway diseases (asthma,
COPD), parenchymal diseases (pneumonia,
ILD )
– Shunt formation (mixed blood amount should
be atleast >40% for shunting)
ƒ V/Q ratio = 0

Anatomical Shunt vs physiological shunt

• Anatomical
– EX: cyanotic congenital heart disease
– Physiological is a pathological process that
causes shunting at microscopic level
– Ex:- B/L Diffuse process
ƒ Alveolar filling process
○ Fluid: pulmonary edema → could be
cardiogenic (ARDS) or non Cardiogenic
○ Pus: B/L extensive pneumonia
• Large airway obstruction = Flattening of ○ Blood: Diffuse alveolar haemorrhage
inspiratory limb of curve (Suggests variable
ƒ U/L total collapse
/ dynamic extra thoracic large airway
obstruction) ○ Tension Pneumothorax
○ Massive effusion on 1 side
• Variable / dynamic intra thoracic large airway
obstruction = Entire expiratory limb Flattening ○ Right endobronchial intubation

• Fixed obstruction = Flattening of both ƒ Hepato pulmonary syndrome (Cirrhosis,

end stage liver disease, severe Portal
expiratory & inspiratory limb of curve
HTN)

APPROACH TO RESPIRATORY Types 2 respiratory failure

FAILURE
Also known as hypercapnic respiratory failure
Q
•
Types 1 respiratory failure
Q
•
• Primary problem - ↑ PaCO2 + ↓ PaO2 + Normal
– Also known as hypoxemic respiratory failure
Q

A-a gradient
– Primary problem - ↓ PaO2 + ↓ PaCO2 + ↑ A-a
• Causes
gradient
– Causes: – Alveolar hypoventilation

– Diffusion limitation – Minute ventilation = tidal volume × RR

ƒ ILD – Low minute ventilation = ex:- neuromuscular

disorders such as:- GBS , myasthenia crisis,
ƒ Emphysema etc → because of this, patient is unable to
breath properly
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Cerebellum Quick Revision Notes

ƒ Low RR causes are: CNS problems – Type 4 respiratory failure

such as drug toxicity, severe alcohol
Primary problem – shock / heart arrest
Q
•
intoxication, Traumatic brain injury, brain
stem compression, raised intra cranial
Mixed Type 1 & Type 2 respiratory
pressure, etc.
failure
Type 3 respiratory failure • Problem - ↑ PaCo2 + ↓ PaO2 + ↑ A-a gradient
Primary problem – post operative atelectasis
Q
•

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ENVIRONMENTAL EMERGENCIES • Heat stroke : Severe form

– Temperature >40.5 °C
– Alter mental status
– Low BP
– No Sweating
– Treatment: IV fluids, active cooling (ice
packs), active internal cooling (cold saline)
Q

– Stop active cooling if patient starts Shivering

• Common features of Heat exhaustion & stroke
1. Altitude related problems
– Tachycardia
• Acute mountain sickness
– Increase respiratory rate
– Complains: fatigue, exercise intolerance, +/-
mild headache (treatment: Acetazolamide) • Exertional Heat stroke

• High altitude pulmonary edema: cough, – Seen in athletes, soldiers

Haemoptysis, dyspnoea (treatment: rapid – Sweating
descent)
Q

– Severe electrolyte imbalance (ex:

• High altitude cerebral edema severe headache, hyperkalaemia)
alter mental status, coma (treatment: rapid – Rhabdomyolysis
descent)
– If patient unable to descent rapidly: give 4. Cold related problems
hyperbaric bags + Dexamethasone + O2, +/-
Nifidipine (in case of Pulmonary edema) • Hypothermia related issues
– Mild <35°c
2. Diving related problems ƒ Features: Shivering, tachypnea, Tachycardia,
• Barotrauma hypertension, increase urine output
due to increased renal blood flow, clear
– Tympanic membrane rupture → Deafness consciousness
– Pneumothorax – Moderate : <32°c
• Decompression sickness – also known as caisson ƒ Features :- no Shivering, bradypnea,
disease (due to formation of N2 bubble in blood)
Q

bradycardia ,hypotension , variable urine

– Clinical features: arthralgia, altered mental output , alter mental status , EEG & ECG
status, dyspnea, hypotension changes ( form J wave)
– Treatment: hyperbaric O2 therapy – Severe: <28°c

3. Heat related problems ƒ Features: coma, respiratory arrest,

apnea, ventricular arrhythmia, no urine
• Heat cramps output
• Heat exhaustion: Mild form – Treatment: rewarming → passive or active
Q

– Temperature <40.5 °C ƒ Passive rewarming: blankets

– Clear consciousness ƒ Active rewarming: external = special
– BP Normal warming blankets, internal = thoracic >
abdominal lavage with warm fluids (40-
– Sweating 42°C)
– Treatment: conservative, hydrate the patient ƒ Rate of rewarming: 0.5-2 °C / hour

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Cerebellum Quick Revision Notes

– Best site to measure core body temperature:- Beta blockers/ CCBs

Pulmonary artery < distal esophagus < rectal Bradycardia , hypotension Q
Glucagon
temperature , pulmonary edema , acute
heart failure
• Freezing injuries: frostbite
TCAs
– Usual sites of Frostbite: sacral areas / distal
Q
Cardiac effects – wide QRS , IV NaHCO 3
extremities ventricular tachyarrhythmia

– Clinical features: numbness, chunk of wood LAs 20% IV intra Lipid- given in
Ex: Lignocaine , bupivacaine case of cardiac irritations
sensation → immediately do rewarming (37-
40°C) , if pain present during rewarming,
Q
Opioids
reduce the temperature, & if pain is severe Pin point pupil, Bradypnea, IV naloxone
Q

alter mental status, coma,

– give analgesics → because patient will Hypothermia
develops vesicle, blisters & become cyanotic
Benzodiazepines Flumazenil ( increase risk of
– Grade of cyanosis: Bradypnea , alter mental
seizures)
Q

status, coma, Hypothermia

ƒ I = No cyanosis during rewarming
ƒ II = cyanosis up to the distal phalangeal
joint
ƒ III = cyanosis extend
metacarpophalangeal joint
ƒ IV = cyanosis extend up to proximal
metacarpophalangeal joint
– Perform MRA – if patient presents within 24
hours
ƒ If it shows significant Vascular occlusion
= rTPA (recombinant tissue plasminogen
activator)
– Perform Bone scan if patient presents after
24 hours
ƒ Perform amputation
Methemoglobinemia
• Chocolate cyanosis
• Treatment:- IV methylene
(chocolate colour blood)
blue ( contraindicated in
up to • High anion gap Metabolic G6PD deficiency – use IV
acidosis because of Ascorbic acid)
hypoperfusion of
• Precipitants :- well water ,
tissues , low SpO2 (real
drug intake (dapsone etc..)
SpO2 measured by co-
oximeter), Normal PaO 2
Iron (oral Fe)
• Produce free radical via
Fenton reaction
Treatment:- IV deferoxamine
• Cardiopulmonary failure ,
hepato cellular necrosis,
gastric outlet obstruction
CO
• Cherry red discoloration
• When person is exposed

TOXICOLOGY to fire, automobile

Toxin
APAP → NAPQI → hepatic
failure because of severe
zone 3 central lobular
necrosis + renal failure +
Lactic acidosis
Treatment:- IV fluids > liver
transplantation
Digoxin
Main problem :-
xanthochromia
Main side effect:- Brady &
tachy arrhythmia
Antidote
Q
N acetyl cysteine ( oral or IV)
• Most common side effect of
oral is nausea & vomiting
Safe in pregnancy, safe for
• Fomepizole (alternative :- IV
liver failure only , not safe
for renal failure
Q
Digibind
Treatment:- for bradycardia
atropine → for ventricular
arrhythmia = lignocaine
exhaust
Treatment:- hyperbaric oxygen
therapy
• High anion gap Metabolic
acidosis, falsely elevated
SpO2
Ethylene glycol / methanol
Alter mental status, coma,
renal failure, high anion
gap Metabolic acidosis
Q
ethanol)
with increase osmolal gap,
blindness
OPC
Cholinergic crisis :-
DUMBELS = Diarrhea,
urination, myosis, IV atropine , pralidoxime
bronchorrhea, bradycardia,
Bronchospasm, emesis,
lacrimation, salivation

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Cyanide ƒ Catatonic rigidity / Lead pipe rigidity

• Smell- bitter almonds ƒ Treatment: bromocriptine +/- IV dantrolene
• Cause :- fires
100% O2 , IV hydroxocobalamin – Malignant hyperthermia is a genetic defect,
• C/f: high anion gap / IV sodium thiosulfate
Metabolic acidosis,
fuel to RYR gene mutation, Autosomal
altered mental status, dominant
normal SpO2 & PaO2 ƒ Due to use of anaesthetic agents &
paralytic agents
Extrapyramidal toxidrome
ƒ Most common cause in world =
• Because of D2 receptor blockers succinylcholine
• Patient develops acute dystonic reactions , ƒ Extreme hyperthermia
oculogyric crisis ƒ Rigidity (mortis like rigidity)
• Treatment :- central anticholinergic = Benzhexol ƒ Massive elevation of end tidal CO2 in OT
/ trihexyphenidyl , Benztropine, antihistamines
ƒ Treatment: Dantrolene
Q

drug = promethazine, diphenhydramine

– Common features of all toxidrome:-
• Treatment for Drug induced parkinsonism =
ƒ Fever
central anticholinergic
ƒ Tachycardia
• Akathisia (constant feeling of restlessness) =
beta blockers + clonazepam ƒ Tachypnea
ƒ Alter mental status
Hyperthermic toxidrome ƒ Hypertension
• Ex:
GIT contamination process
– Sympathomimetic toxidrome = use of • Can be done with activated charcoal = 1g/kg -
MDMA, cocaine , amphetamine 50g/kg, whole bowel irrigation by polyethylene
glycol
ƒ Patient will have mydriasis, extreme
hypertension • Contraindication of activated charcoal:

ƒ Treatment: alpha blocker → beta blockers – Altered mental status/ low GCS score
– Late presentation (after 1-2 hours of
– Serotonin syndrome caused by SSRIs, SNRI
ingestion of toxin)
ƒ Patient will have rigidity , extremities
– Any evidence of presence of bowel obstruction
clonus, ocular clonus
– Toxins → alcohol , petroleum products , boric
ƒ Treatment: cyproheptadine
acid, inorganic ions , heavy metals
– Anticholinergic toxidrome due to datura or
• Indication of whole bowel irrigation
belladonna toxicity
ƒ L = Lithium
ƒ Dry patient, urinary retention, constipation
severe delirium ƒ I = iron

ƒ Treatment:- physostigmine ƒ M = metals

– Neuroleptic Malignant syndrome due to ƒ P = body packers

consumption of Dopamine receptor blockers ƒ S = sustain release preparation
present after 24 hours

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Cerebellum Quick Revision Notes

Enhanced elimination REVERSAL OF

• Urinary alkalization: give IV NaHCO3 & ANTICOAGULATION
maintain urinary pH of ≥ 6.5 – 7 → increase
Anticoagulant Reversal
elimination of salicylate like substances (it is
Warfarin INR >2 + bleeding → treatment – IV
present with high anion gap Metabolic acidosis
vitamin K + 4 FPCC
& mixed respiratory alkalosis), methotrexate,
phenobarbitone , chlorpropamide UFH Protamine sulphate
LMWH Protamine sulphate (but no Efficacy,
• IV intra Lipid → used for local anaesthetic
give Andexanet alpha)
toxicity
Fondaparinux Andexanet alpha
• Renal replacement therapy - to eliminate toxin
Dabigatran Idarucizumab
via dialysis
FXai Andexanet alpha
– Low Vd & less protein binding
– Drugs which are eliminated by renal SHOCK
replacement therapy
Q

• Hypoperfusion to tissues / MAP <65 mmHg

ƒ B = Barbiturates (not benzodiazepines)
ƒ L = lithium
ƒ I = Isoniazid
ƒ S = salicylate
ƒ T = theophylline, aminophylline
ƒ M = methanol, metformin, methotrexate
ƒ E = ethylene glycol
ƒ D = Depakote, Dabigatran
ƒ C = carbamazepine
– Drugs that can not be eliminated by this
therapy:-
ƒ Benzodiazepines
ƒ Sulphonylurea
ƒ Beta blockers (except atenolol) , CCB
ƒ Phenytoin
ƒ Warfarin, heparin
ƒ Amiodarone, digoxin

ƒ TCAs , SSRI

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Features Hypovolemic Cardiogenic Distributive Obstructive

Pulmonary/RV Mechanical
Hemodynamics
Preload (PCWP) ↓ ↑ ↓ ↓ ↑
Pump function N ↓ ↑ /Variable ↓ ↓
Afterload (SVR) ↑ ↑ ↓ ↑ ↑
Q
Tissue perfusion ↓ ↓ ↑ ↓ ↓
(MvO2)
Clinical Features
JVP ↓ ↑ ↓ ↑
Extremities Cold Cold Warm Cold
Fluid responsive Yes No Yes Variable/ no
LV function N ↓↓ N N
Q
Initial treatment Fluids +/- blood Inotropes +/- • Septic = • Tamponade = urgent pericardiocentesis
products MCs, Ab, Iv fluid, • Tension Pneumothorax = needle
NA, Dopamine vasopressin thoracostomy, chest drain
Atropine Sync.
• Anaphylaxis • RVMI = IV fluids +/- inotropes
Q

DCC
= adrenaline • Pulmonary embolism = thrombolysis
(1mg = :1000) (alteplase) + anticoagulation

• Hypovolemic shock
• MvO2 or SvO2 measured best at pulmonary
– Hemorrhagic = road traffic accident , surgery artery by Swan ganz catheter/ white heart
catheter/ pulmonary artery catheter
– Non Hemorrhagic = vomiting , Diarrhea,
acute pancreatitis Massive transfusion
• Most common cause : cardiac surgery > trauma
• Cardiogenic shock
• Old Definition:- >10 U PRBC / 24 hours
– Cardiomyopathic shock = poor pump function
Now : >4 U PRBC / 1 hour
Q
•
– Arrythmogenic shock • Complications :-
• Distributive shock – due to citrate overload → hypocalcaemia,
Metabolic alkalosis
Q

– Septic shock
– Hypokalaemia > hyperkalaemia (in case of
– Non Septic shock = neurogenic shock due to renal failure , neonates + old PRBC )
spinal cord trauma , anaphylactic shock – Hypothermia

• Pulmonary RV = due to pulmonary embolism, – Dilutional Thrombocytopenia (PRBC : FFP :

platelets = 1:1:1)
acute RVF
– Persistent hemodynamic instability
• Mechanical obstructive = due to tension
– Blunt abdominal trauma + eFAST positive +
Pneumothorax, tamponade
unstable patient

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Cerebellum Quick Revision Notes

– High risk scores → ABC ≥ 2 , RABT ≥ 2 , CARDIAC ARREST

shock index >1

• Treatment of Septic shock patient

– qSOFA score ≥ 2 = indicates high risk

Q

ƒ RR ≥ 22/min

ƒ SBP ≤ 100 mmHg

ƒ Alter mental status ( GCS <15)

– SOFA

ƒ GCS

ƒ PaO2 / FaO2 ratio

ƒ MAP & dose of vasopressors

ƒ Total bilirubin

ƒ S. creatinine , urine output

ƒ Platelets

Sepsis + hypotension
Collect alteast 2 sets of blood
culture from different sites
(CBC , BMP , lactate)

IV fluids + antibiotics (within <1 hour)

Not responding

Septic shock

CPR
1. Circulation
Vasopressors ( NA +/- vasopressin +/- Dopamine)
• Good Chest compression :- rate = 110-120/ min,
– If Adjunctive therapy: CIRCI (critical depth = 2-2.5 inches (5-6 c ) → uninterrupted
illness related corticosteroid insufficiency) Chest compression
Q

→ add hydrocortisone (also in refractory

shock = 50mg / QID)

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2. Airway • Clinical examination:

• Basic: Oropharyngeal , Nasopharyngeal airway – >24 hours :- status myoclonus

• Advanced: LMA, Endotracheal intubation – >72 hours :- absent pupil reflex & Corneal
reflex
3. Breathing: • Serological markers
• Rescue breath (30:2 → chest compression: – NSE → increased → poor prognosis
breath)
• In Advanced airway, compression is: 10/min PNEUMONIA
Drugs used in cardiac arrest
• Adrenaline
– used in both Shockable & non shockable
rhythm
– Dose :- 1:1000 IV 1 mg
– Repeat Every 3-5 minutes
• Anti arrhythmia drugs like amiodarone,
lignocaine
– Used in shockable rhythm (after 3rd shock)
– Dose: 300 mg amiodarone, 1:1.5 mg/kg for
lignocaine
– Half Dose of this can be repeated once
• Not used drugs: atropine, vasopressin

Outcomes of CPR
• Successful → indicated by ETCO2 >40 mmHg
– Check brain response of the patient:- if
patient follows the command, outcome is
good
– If patient dose not follow the commands, Community acquired pneumonia
improve brain condition by using Targeted
• 65% Idiopathic, 25% viral cause, 15%
temperature management for 24 hours
bacterial cause (most common typical bacteria
(also known as therapeutic Hypothermia
previously). - pneumococcus, atypical – Mycoplasma →
infiltrates, chlamydia, legionella).
• Not successful → dead people
• Features:- fever , productive cough, shortness
• To assess neurological outcome:- of breath, haemoptysis
– CT (in 1st 24 hours) / MRI (after 24 hours)
• Examination:- crepitation ,bronchial breath
– Electrophysiology:- EEG (after 24 hours, if sound , bronchophony / egophony
there is persistent myoclonic seizures, & >72
hours = burst suppression pattern, N20 SSEP • Investigation :- increased CRP / ESR , x- ray
(>24 hours :- B/L absent = death) :- consolidation, infiltration

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Cerebellum Quick Revision Notes
• Treatment:- CURB 65 score
– C = confusion
– U = BUN >7mmol/L (in India:- ≥40 mg% )
– R = RR ≥30/min
– B = BP :- SBP < 90 or DBP ≤60
– 65 = age >65
– Score :-
ƒ 0-1 = treat as out patient → look for risk
factors :- if no risk - give Azithromycin
/ Doxycycline, if risk factors present
(example:- any comorbidities such
as CKD , heart failure, lung diseases ,
took antibiotics in last 90 days) give
beta lactam (Amoxicillin- clavulanic
acid, 3rd generation cephalosporin –
cefexime) + Azithromycin / Doxycycline
or respiratory (3rd & 4th generation)
Fluoroquinolones = levofloxacin,
moxifloxacin
ƒ 2 = as short impatient → give beta
lactam + Azithromycin/ Doxycycline or
respiratory Fluoroquinolones
ƒ ≥ 3 = admit patient +/- ICU → beta
lactam + Azithromycin/ respiratory
Fluoroquinolones, if patient have
penicillin allergy = give Aztreonam
Community acquired MRSA
• Can Produce Panton valentine leukocidin
• History of post influenza pneumonia,
pneumatoceles
• IE / iv drug users who are is on renal replacement
therapy + have a central venous catheter
• Treatment:- Vancomycin (nephrotoxic) /
Linezolid (cause bone marrow suppression, Lactic
acidosis, peripheral neuropathy) + clindamycin
(increase risk of Clostridium difficile colitis)
Q
Pseudomonas aeruginosa
• It is a typical hospital acquired organism
• History of Bronchiectasis, cystic fibrosis
* For Making Notes
• Treatment:- beta lactam → cefepime ,
piperacillin & tazobactam , meropenem
• Duration of therapy :- 5-12 days + patient
should be stable + afebrile for ≥ 48 hours
• Most common complication:- Para pneumonic
effusion → if it gets more complicated, do
drainage (loculated effusion is one of the
Indications of chest drain
Q
– Signs of complicated Para pneumonia
effusion :-
ƒ pH of Pleural fluid <7.2 ( normal is 7.4-
7.6)
ƒ Glucose <40 mg %
ƒ Gram stain +
ƒ Pleural fluid Culture +
ƒ Frank pus – Emphyema
– Clue for complicated Para pneumonia effusion:-
non resolution of Clinical illness
Hospital acquired pneumonia &
Ventilation acquired pneumonia
• HAP = Pneumonia occur after 48 hours of
hospitalization
• VAP = Pneumonia occur after 48 hours of
Endotracheal intubation
• Look for MDR risk
– Infection occurs after 5 days of hospitalization
– Patient in Septic shock at the time of
presentation
– ARDS
– Already on Renal replacement therapy
– If no risk factors → monotherapy +
piperacillin and tazobactam , cefepime ,
meropenem
– If risk factors present → triple therapy
(piperacillin & tazobactam, cefepime,
meropenem + Aminoglycosides , Fluoroquinolones
+ Vancomycin)
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Lung abscess • Halo sign Seen → can be converted into

crescent sign
• Risk factors
• Other investigation:- blood test = 1,3 beta D
– Aspiration due to any cause (low GCS)
glucan +, S. Galactomannan +
Q

• Features
• Differential diagnosis of 1,3 beta D Glycan:
– High grade fever Aspergillus , candida, Pneumocystis carinii
pneumonia, Histoplasmosis, Coccidioidomycosis
– Foul smelling sputum +/- postural variation
of sputum • Serum Galactomannan can be false positive in
case of patient taking Amoxicillin- clavulanic
– D/D for thick wall cavity with air fluid level
acid, piperacillin and tazobactam
= SCC of the lung
Treatment:- voriconazole
Q
•
• Treatment :- antibiotic regimen:-
– Ampicillin – sulbactam Allergic broncho pulmonary
– Piperacillin and tazobactam Aspergillosis
– Meropenem • Patient have hypersensitivity reaction
– Moxifloxacin/ levofloxacin + Metronidazole • Features:- history of bronchial asthma > cystic
– Clindamycin fibrosis , worsening of asthma symptoms
• Blood parameters :- elevated eosinophils ,
ASPERGILLUS LUNG DISEASE elevated IgE (>1000), history of coughing of
brown to black flakes of sputum
Q

• Chest x-ray → infiltration + Mucus plugging

(finger in glove appearance) +/- central or
peroximal Bronchiectasis

• To confirm ABPA, blood test – Aspergillus

specific Ab or skin prick test +

• Treatment: corticosteroid (Prednisolone or

dexamethasone) +/- itraconazole or voriconazole
Aspergilloma
• Patient have normal immunity PLEURAL DISORDERS
Light’s criteria
Q

• Features:- Asymptomatic •

• Complication:- massive Hemoptysis – Efficient protein / serum protein: Efficient

protein is > 0.5
• Monod sign Seen
– Efficient LDH / serum LDH: Efficient LDH
• Treatment: surgery > 0.6
– Efficient LDH > 2/3 of serum LDH
Invasive pulmonary Aspergillosis
(Immunosuppressive patient) – Any one of these is present, indicates
exudate
• Features:- fever, shortness of breath ,
hemoptysis , hemodynamic instability
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Cerebellum Quick Revision Notes

Etiology Appear WBC RBC pH Glucose Comments

B/L ,
Normal (<1000) cardiomegaly
CHF Clear , straw
, mainly N N N in chest X-ray,
Cirrhosis Yellow colour
lymphocytes Cirrhosis,
portal HTN
Uncomplicated Increased, mainly N / mildly N / Mildly No chest Drain
Turbid Variable
parapneumonic neutrophil reduced reduced requires
Complicated Increased,
Turbid Variable <7.2 <40 mg% Chest drain
parapneumonic mainly neutrophil
Very high (25000
Emphyema Purulent Variable Very low Very low Chest Drain
to 1 lakh)
Gold standard
Increased, mainly Mildly Mildly
Tuberculosis Serosanguinous Variable Diagnosis:
lymphocytes reduced reduced
Pleural biopsy
Mildly Mildly
Malignancy Bloody effusion Increased Increased Cytology
reduced reduced
70 %
Pulmonary
Bloody effusion Increased Increased N N exudate, 30%
embolism
transudate
RA:-
Rheumatoid Mildly extremely low
Turbid Increased N RF + , serology
arthritis/ SLE Reduced SLE:- Mildly
reduced
Left sided
Serosanguinous Variable / effusion,
Pancreatitis Increased N N
or turbid Increased increased
Q
amylase
Left sided
Esophageal Turbid to effusion,
Increased Variable Reduced Reduced
rupture purulent increased
Q
amylase

Other causes – Diagnosis: effusion hematocrit / blood

• Urinothorax: transudate hematocrit > 0.5

– To diagnose, efficient/ creatinine > 1 = • Chylothorax: exudate

confirm Urinothorax
– Diagnosis: Triglyceride ≥100 mg% or >55 & if
• Peritoneal related Pleural effusion:- commonly chylomicrons are detectable in Pleural fluid
Q

have right sided effusion

• Cardiac causes: post CABG, Dressler’s
– Diagnosis: efficient/ serum glucose = >1 syndrome → both have left sided effusion
• Hemothorax: exudate

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Medicine

• Drugs: have high eosinophils

Q Aspirin hypersensitivity

– B = bromocriptine

– A = amiodarone

– M = methotrexate, methysergide

– +/- nitrofurantoin Bronchial asthma Nasal polyps

• Pleurodesis:- obliteration of Pleural
– EGPA known as Churg Strauss syndrome
– Agents of Chemical Pleurodesis Triad:- Bronchial asthma

ƒ TALC (Increase success)

ƒ Tetracycline

ƒ Bleomycin

Tension Pneumothorax
Eosinophilia Vasculitis
• It is a Clinical diagnosis

• Complaints: Pleuritic chest pain , shortness of Diagnosis Definition of Sign of severe

breath, reduce air entry , Hyper resonant note control exacerbation
on percussion • Is a • Symptoms ≤ • Severe
• Signs :- hemodynamic instability , low BP , spirometry 2 weeks shortness of
based • Reliever use breath
evidence of trachea & mediastinal shift
diagnosis is ≤ 2 times • PEFR cut-off:
• Treatment:- immediate needle thoracostomy • FEV1/FVC / week ≤50-60
→ chest drainage (at 2nd ICS in MCL, 5th ICS <0.7 • Nocturnal • Pulsus
MAC → preferred)
Q
awaking ≤ 2 paradoxus
• In X-ray → Hyperleucency, no Broncho / month • HR >120/min /
Vascular markings, trachea shifted to left side, Use Broncho • Exacerbation increased RR
right heart border is flat means mediastinum dilator ≤ 1 /year >30/ min
also shifted • Recheck • Normal lung • SpO2 <90%,
ratio after function normal PaCO2 ,
Bronchial asthma 15 minutes • Good quality increased PaO2
→if it’s ≥ 0.7 of life Cyanosis
• Symptoms:- shortness of breath, cough , •
wheeze • Satisfaction / altered
mental status/
• Asthma plus syndrome:- Bronchial
bradycardia /
– Atopy → allergic rhinitis & Conjunctivitis + asthma
hypotension
atopic Dermatitis + family history + high IgE • Abdominal
& eosinophils paradox / silent
– ABPA → worsening asthma chest

– AERD → over activation of LOX → increased

leukotriene receptor → Triad
Q

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Cerebellum Quick Revision Notes

Reversibility Th2 type release

IL4 IL5 IL 13

• Class • eosinophils • Increased

switching blocked by Mucus
Variability Hyper mepolizumab, production
• block IgE by
reslizumab,
Responsiveness Omlaizumab
Benralizumab

• Treatment of bronchial asthma: MART

– IL-4 & IL -13 blocked together by Dupilumab
(maintenance & reliever therapy)
– TSLP is a protein which stimulates pulmonary
– Preferred reliever :- LABA + low dose ICS
Q
dendritic cells → block by Tezepelumab
– Biological: effective if asthma is Th2 type

• Treatment of acute exacerbation of bronchial asthma

– Give O2 → target : 90-92%
– Use Broncho dilators → SABA (Salbutamol/ levo salbutamol) +/- SAMA (ipratropium bromide)
Q

– Systemic corticosteroid → prednisolone or IV methylprednisolone

– Adjunctive therapy:- MgSO4 +/- IPPV

COPD
Diagnosis Assess severity Treatment
Post Broncho dilator Gold 1:- ≥ 80% - mild ABCD assessment
FEV1 / FVC < 0.7 Gold 2:- 50-70% - • Use MMRC scale ≥2 = symptom burden is high
moderate • Grade of MMRC:-
Gold 3:- 30-49% - 0:- shortness of breath only with mild exercise
severe
Gold 4:- <30% - very 1:- SOB after hurry on level ground or walking on slight uphill
severe 2:- SOB while walking at normal speed
3:- patient able to walk <100 m , develop SOB within few minutes
4:- home bound patient
• Quality of life :- COPD assessment tool ≥ 10 → poor quality of life
• Risk :- look for number of exacerbation /year → ≥ 2/ year or ≥ 1/
year → require exacerbation
Q
• Treatment:- LAMA +/- LABA +/- ICS
(LAMA: Tiotropium, glycopyrrolate, aclidinium, umeclidinium)
(LABA: formeterol, salmeterol) (ultra long acting drugs:-
vilanterol, indacaterol, olodaterol)
Improve quality of life →
• Stop smoking by giving nicotinic replacement therapy, varanicline,
bupropion
• *Long term ONotes
For Making 2
therapy to those having long term resting hypoxemia
• Lung volume reduction surgery
 117
Medicine

Diagnosis Assess severity Treatment

Treatment of AECOPD
• Increase in symptoms + no relief with usual treatment
• target O2 :- 88-92%
• BD :- SAMA +/- SABA
• Systemic corticosteroid
• If infections present, give Macrolides
• PPV:- NIPPV > IPPV (indication for BPAP = pH ≤ 7.35 / PaCO2 ≥ 45
mmHg
• Reduce exacerbation rare:- Roflumilast, chronic Azithromycin
therapy × 1 year

• Most common cause for exacerbation:-

Emphysema infection
• Irreversible dilatation of the terminal • Complications :- high risk Pseudomonas colonization,
respiratory airways → increased static high amyloidosis
compliance , protease- anti protease imbalance
Etiology Clinical Evaluation
• Characteristics: exercise desaturation due to
Tb :- Sputum or
diffusion limitation , low DLCO , V/Q mismatch
, significant hyperinflation in chest X-ray, Chronic cough, BAL analysis
Chronic infections
avascular regions in lung → transform into bullae persistent ABPA :- IgE ,
( MC is TB, ABPA)
infiltration eosinophils, skin
• It is a clinical diagnosis → > 3 months / year for
more than 2 years → shunt formation ↔ blue prick test
blotter = cyanosis & heart failure risk + edema Refractory
sinusitis +
Bronchiectasis infertility +
1° ciliary
• It is an irreversible disease, permanent situs inversus
dyskinesia
dilatation of medial sized bronchus = Kartagener
Q
syndrome
(Dynein mutation)
Chronic &
IgG , IgM, IgA,
Immunodeficiency recurrent
IgF
infections
RA , Sjogren, Arthralgia + other RF , ANCA ,
ANCA issues ANA, ACPA
MC pulmonary
Colonoscopy ,
IBD manifestation =
• Clinical features: chronic productive cough +/- Q biopsy
Bronchiectasis
hemoptysis
Young , lower
• Most common cause :- TB Alpha 1 AT lobe Emphysema Alpha 1 AT
• Most common site :- lower lobe deficiency & lower lobe levels + Genetics
• Diagnosis:- IOC :- HRCT
Q Bronchiectasis
Right middle lobe
• Treatment:- supportive – chest physiotherapy,
Anatomic syndrome – in CT
Broncho dilators , drainage
children

* For Making Notes

118
Cerebellum Quick Revision Notes

• William Campbell syndrome:- cartilage defect lumacaftor , Tezacaftor , Elexacaftor (in

→ affects 3rd to 6th order bronchi
• Mounier Kuhn syndrome :- smooth muscle &
elastin defect
• Causes of Right middle lobe & left Lingular
lobe bronchiectasis
– In Elderly female → known as Lady windermere
disease due to MAC infection
F508 Deletion, do this triple therapy)
• DNAase therapy (dornase alpha)
• Most common cause of exacerbation:- infection
(Staphylococcus aureus)
• In 1-10 years :- Colonization due to MSSA >
H. Influenza
• >10-15 years :- due to MRSA , Pseudomonas
aeruginosa, BCC , stenotrophomonas
Q

Cystic fibrosis
• Defect in CFTR gene on Chromosome 7, AR Indications for Lung transplantation in
pattern
Q
cystic fibrosis patients
• MC mutation:- F508 Deletion → comes under • Severely declined lung function → FEV1 <30% ,
type 2 trafficking effect rapidly decrease in FEV1, evidence of Pulmonary
Q

HTN , walking capacity <400 m

Manifestations Features
Rhino - pulmonary Sinusitis , Bronchiectasis
GI Meconium ileus , rectal prolapse ,
EVALUATION OF HEMOPTYSIS
young adults, DIOS
Non massive
GU Infertility , Male :- absence vas ,
• Most common cause is bronchitis
female :- thick cervical secretion
Metabolic Hyponatremia, hypochloremia, • Look at chest X-ray → normal = check risk
factors for cancer such as old age & heavy
Metabolic alkalosis , hypokalemia
smoking → if risk factors present = do CT
Other Aquagenic wrinkling, stones ( Gall
chest, if no risk factors → look for bronchitis
bladder, kidney)
• If bronchitis is present = conservative
Diagnosis treatment for 1-2 weeks → no response → do
CT chest, if bronchitis is not present:- observe
Sweat chloride testing >60
for 4-6 weeks → no improvement→ CT chest

• Chest x-ray abnormal →

– Mass lesion / parenchymal disease → CT
chest

– Infiltrates → antibiotic trial for 1-2 weeks

Genetic testing abnormal
→ no response → CT chest → flexible
2 mutations nasal potential
difference bronchoscopy
should be +

• Immuno reactive trypsinogen Massive

• Treatment • Most common cause is Bronchiectasis (source –
bronchial artery)
• Supportive +/- disease modifying therapies
→ potentiators = ivacaftor , correctors = • >400 ml of blood in cough in 1 day or >150 ml

* For Making Notes

 119
Medicine

blood in single episode – Make patient lie in Lateral decubitus (bad

Q

lung down)
• Treatment :-
– Endotracheal intubation
– Patient dies due to asphyxia
– +/- urgent rigid bronchoscopy
– ABC + correct coagulopathy
– +/- angio embolization

APPROACH TO ILD
Known causes Unknown causes Rare but well defined ILD’s
Smoking → Granulomatous ILD • Pulmonary infiltrates eosinophilia
• DIP • Sarcoidosis Causes
Q
• RB- ILD • Lofgren syndrome Triad :-
1. AEP
• Pulmonary Langerhans cell B/L hilar lymphadenopathy BAL eos ≥30
histiocytosis (tennis racket shaped 2. CEP
birbeck granules
Q
3. HES
Drug induced ILD’s
Arthritis, Erythema 4.ABPA
• methotrexate
Fever nodosum
• amiodarone 5. Loeffler syndrome → transpulmonary
• nitrophenytoin • Herford waldenstrom syndrome
Q
passage of helminths
• Bleomycin Uveitis Paratoid Enlargement 6.TPE = trapping of microfilia
• Busulfan
• cyclophosphamide 7. EGPA

CTD related ILD’s BA

Fever 7th CN palsy
• NSIP – most common pattern

exception:- RA • +/- pituitary involvement = CDI

Occupational ILD’s
• Inorganic = known as
pneumoconiosis
• Organic → Hypersensitivity
pneumonitis → Thermophilic
actinomycosis ( farmer’s lung ,
Bagassosis , mushroom workers
lung)
→ Byssinosis = increase risk of COPD
→ other = grain dust , toxic chemicals
• +/- skin = lupus pernio
• +/- renal involvement = DTA , NDI , stones Eosinophilia Vasculitis
• Cardiac involvement = RCMP , conduction
• Lymphangioleiomyomatosis
blocks
– Defect in TSC gene
• Liver involvement = Granulomatous
– Female > male
hepatitis, neurosarcoidosis
– Pregnancy is contraindicated
• Other = elevation of serum ACE level
• IOC :- biopsy ( EBUS guided biopsy) from – C/F :- recurrent chylous effusion
LN of lung with recurrent Pneumothorax
– CT :- Swiss cheese appearance
• TOC :- corticosteroid
• Pulmonary Alveolar proteinosis
Non Granulomatous ILD’s
– Defective clearance of surfactant
• IIP:-
– C/F:- Cough , gummy sputum
Types :-
– CT:- crazy paving appearance
• IPF :- at > 50 years →C/F = chronic cough,
– Treatment:- lung lavage
SOB
On examination: Dry fine end inspiratory
crackles , +/- clubbing, on HRCT = bibasal
subpleural fibrosis +/- Honeycombing +/-
traction Bronchiectasis
Treatment:- TKI :- Nintedanib , TG Beta # :-
pirfenidone ,
• NSIP * For Making Notes
• COP (BOOP)
• AIP
Diagnose of exclusion
120
Cerebellum Quick Revision Notes

Hypersensitivity pneumonitis (type 3 (acute), • CT features :- mosaic pattern, centrilobular

4 (chronic) hypersensitivity reaction) nodules
• Treatment :- short course steroid

Pneumoconiosis
Q
Silicosis (most common) Asbestosis CWP Berylliosis
Fibrogenicity +++++ ++ Least + ++
Pleural
- ++ - -
involvement
LAN + - + +
ILD +++ + (lower lobe) + +
COPD ++ - + -
Bronchogenic
+ + - +
cancer
Malignant
- + - -
Mesothelioma
• Anthracosis
Occupational exposure
Increase TB risk , acute • Normal x-ray,
to beryllium, non
condition can mimic PAP In biopsy, ferruginous asymptomatic
Comments caseating granuloma ,
(Pulmonary Alveolar bodies seen patient, dust cells
dihelium lymphocyte
proteinases) present in LN
proliferation test +
biopsy

Caplan syndrome – Hormonal Imbalance:- Pregnancy , Early Post

partum period , OCPs
• Due to pneumoconiosis → develops RA → RA
nodules in upper lobe – Other:- Cancers, thrombophilia → most
common is factors 5 leiden mutation, most
Most commonly associated with Silicosis
Q
•
common acquired thrombophilia is anti
phospholipid syndrome
VENOUS THROMBOEMBOLISM – Most common reason for upper limb DVT:
• Virchow’s Triad central venous catheter
Stasis of blood flow – Work up:
ƒ Suspicious VTE

Endothelial Injury hypercoagulopathy

• Risk factors:
– Immobilization ≥ 3 days within 3 months or
long flight travels (6-8 hours) Q

* For Making Notes

 121
Medicine

• Treatment of VTE:- Anti coagulation (heparin - ƒ Idiopathic pulmonary

warfarin < DOACs artery HTN
BMPR2 Mutation
Q

• Deep vein thrombosis ƒ Familial pulmonary

artery HTN
• Pulmonary embolism:-
– Unexplained SOB +/- pleuritic chest pain
– Unstable pulmonary embolism treatment:- ƒ Associated pulmonary artery HTN → crest
systemic thrombolysis, IVC filters given syndrome
when anticoagulants are contraindicated ƒ Others
– Duration of anticoagulation therapy :- 3-6 ○ MPAP 20
months
○ Normal PVR >3 wu
– Saddle pulmonary embolism
○ Normal pulmonary capillary
– ECG :- most common – sinus Tachycardia
ƒ Treatment:- vaso dilators
– Other :- RV dysfunction → T Inversion in V1-
ƒ Test:- vaso reactivity testing → + → CCB ,
V4, S1Q3T3
Q

If (-) → combo = ambrisentan + Tadalafil

– Echocardiogram: RV dysfunction + prostanoids
ƒ Prostacyclin receptor agonist is a prodrug
PULMONARY HTN
ƒ Prostacyclin antagonist:- epoprostenol ,
MPAP ≥ 20 mmHg
Q
• treprostinil, iloprost
• Gold standard:- swan ganz catheter or
pulmonary artery catheter
• 5 Types of Pulmonary HTN according to WHO
– Type 1 :- pulmonary artery HTN → problem
is in the small pulmonary arterioles

* For Making Notes

Telegram - @nextprepladdernotes
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 Chapter - 10 Respiratory System

BRONCHIAL ASTHMA Mechanism

→ Inhibit PDE (thereby ↑ cAMP)
→ Adenosine A1 receptor antagonistQ

Adverse effects
Due to PDE inhibition Due to ADEnosine A1 an-
tagonismQ
Nausea, Vomiting, Diarrhea Arrhythmias
Headache Diuresis
Arrhythmias Epileptic seizures
1. Bronchodilators
→ Theophylline is metabolized by microsomal enzymes,
A. Sympathomimetics so prone to drug interactions
b2 Agonists • Enzyme inducers (like smoking) decrease the effect,
therefore smokers require higher doses
• Enzyme inhibitors (like ciprofloxacin, clarithromycin
and erythromycin) can result in toxicity (seizures,
arrhythmias etc.)Q

Salmeterol → Slow acting → Only used for prophylaxis

2.Drugs affecting LTs
Formoterol → Fast acting → Used for acute attacks also
Adverse Effects of b2 Agonists
T - Tachycardia
T - Tremors (Most common side effect)
T - Tolerance (Mainly with long-acting beta 2 agonists)
T - T wave changes (Because of hypokalaemia)
These drugs can cause hyperglycaemia (but never
hypoglycemia)
A. Steroids

B. Parasympatholytics → DOC for prophylaxis

→ Also used in acute attack along with bronchodilators
M3 Blockers
Function in acute attack of asthma is to ↑ the
• Ipratropium
sensitivity of b2 agonists.
• Tiotropium
→ Preferred by inhalational route
→ Given by inhalational route
– MC side effect is oropharyngeal candidiasis
C. Phosphodiesterase Inhibitors – Topical Nystatin or clotrimazole is used to treat
• Include theophylline and aminophylline candidiasis

• Given orally or by intravenous route (not available by – Gargling after every dose will prevent this
inhalational route) adverse effect
 67
Pharmacology
B. LOX inhibitors 4. Omalizumab
– Zileuton → Monoclonal antibody against IgEQ

C. LT Receptor antagonists → Only used for prophylaxis

– Zafirlukast → Given subcutaneously

– Montelukast
GINA (GLOBAL INITIATIVE FOR
3. Mast Cell Stabilizers ASTHMA) GUIDELINES
– Sodium Cromoglycate • Drug of choice for treatment of acute attack
of asthma (rescue therapy) is combination of
– Nedocromil
inhalational formoterol and low dose inhaled
→ Only used for prophylaxisQ corticosteroids.Q
→ Given by inhalational route • Drug of choice for maintenance therapy in asthma
is also the same combination (Formoterol + Low
dose ICS).Q

Previous Years Questions

Q1. A patient was taking theophylline for bronchial Q2. A patient with COPD was given intravenous
asthma. After starting another drug, symptoms of aminophylline therapy following which the patient
theophylline toxicity started appearing. Which is the developed diuresis. This is due to action on which
likely drug started? effector?
A. Erythromycin A. Adenosine receptors
B. Phenytoin B. Beta 2 adrenergic receptors
C. Griseofulvin C. IL-10
D. Rifampicin D. Histone deacetylase

Answers
1. - A
2. - A
 Physiology Revision 5 05 31

PHYSIOLOGY REVISION 5 ----- Active space -----

Respiratory physiology 00:00:15

Airway generations :
Weibel model (23 generations).
Trachea bronchi bronchioles terminal bronchioles
(0) (16)
alveolar sacs alveolar ducts respiratory bronchioles
(23)

Conducting airways (1-16) :

First 16 generations.
Contain cilia ciliary movement d/t Dynein clears sputum.
• Dynein absent in Kartagener’s syndrome.
• Ciliary immotility : Cystic fibrosis.
Has 2 stem cells : Basal cells & Clara cells (for lung regeneration & repair).
Have smooth muscle.

Agents that modify Bronchial smooth muscle activity:

Bronchoconstriction Bronchodilation
Parasympathetic system : ACh, Methacholine. Sympathetic system : 2 ag-
Histamine. onists.
Leukotriene (most potent). NO(Nitric oxide).

Alveolar airways (17-23) :

2 types of pneumocytes :
• Type I : Large, flat, occupies more surface area, less numerous.
• Type II : Small, more numerous, produce surfactants (stored as lamellar
bodies), act as stem cells.
Composition of surfactants
Surfactant lipids Surfactant proteins
Major : Lecithin/dipalmitoyl phosphatidyl choline (DPPC) SP-A.
Minor : Sphingomyelin. SP-B.
L/S ratio is used to assess fetal lung maturity (normal SP-C.
is ≥ 2). SP-D.

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 32 05 Physiology

----- Active space -----

Functions of surfactants :
• Reduce surface tension prevents alveolar collapse.
• SP-A & SP-D : Role in lung immunity.

Production of surfactant :

Accelerated by Inhibited by
Cortisol (steroids). Insulin (inhibits cortisol) thus Infants of diabetic mothers
T3, T4. are more prone to Hyaline membrane disease.
Long term inhalation of 100% O2.
Occlusion of main bronchus.
Occlusion of one pulmonary artery.
Smoking.

Mechanics of breathing 00:12:15

Boyle’s Law : P ∝ 1/V

1. Intrapleural pressure : 2. Intra alveolar pressure :

+ 1 mm Hg
-2.5 mm Hg -2.5 mm Hg Expiration
Inspiration Expiration

0 mm Hg
Inspiration

-6 mm Hg - 1 mm Hg

3. Transpulmonary pressure = Alveolar pressure - Intrapleural pressure.

(TAP : T = A - P).

Lung compliance:
Hys ation

V
Ins resis
tion
i r
Exp
te
pira

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 Physiology Revision 5 05 33

Hysteresis : Difference b/w the pressure volume curves during inspiration & ----- Active space -----
expiration. It happens d/t surface tension forces.

Compliance : Slope of the curve.

= V/ P = 200 mL/cm H2O.

Note : For a given change in pressure, change in volume is more during expiration.

Lung Compliance in air filled Vs saline filled lung :

Saline filled Air filled

Volume

Pressure
In saline filled lungs no air-fluid interface no surface tension no
hysteresis.

Equilibrium volume(FRC) : The volume at

which the 2 opposing forces (expanding
force & collapsing force) are at equilibrium.

Minimal volume : The volume of air remaining

in the lungs after complete collapse.

Compliance of chest wall (A), lung (B)

and combined compliance (C).
1

Compliance in various diseases :

• compliance : Hyperinflation. Seen in COPD.
• compliance : Stiff lung. Seen in restrictive lung diseases (pulmonary
fibrosis, interstitial lung disease).

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 34 05 Physiology

----- Active space -----

Spirometry :

Dynamic measurements : Flow volume curve.

B
A : TLC.
B : Peak expiratory flow rate (PEFR).
C : RV.
A B : Effort dependent part (air from A C
trachea & bronchi).
6 4 2 0
B C : Effort independent part (air from
medium & small airways) - affected in COPD.

FEV1, FVC and FEV1/FVC ratio can be measured

from the graph.

Note :
Dog leg pattern/scooped
out pattern : Seen in COPD.

Miniature version of normal

graph : Seen in restrictive
lung diseases.

Flow volume curves

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 Physiology Revision 5 05 35

Spirometry cannot measure : These can be measured using : ----- Active space -----
1. RV. 1. Helium dilution technique.
2. FRC. 2. Nitrogen washout technique.
3. TLC. 3. Body plethysmography (most practical).

Ventilation : 00:38:30

Tidal volume (VT) = 500 mL.

Dead space (VD) = 150 mL (air in conducting airways).
Alveolar ventilation (VA) = 350 mL.
VA/min = (VT-VD) x Respiratory rate(12).
= 4.2 L/min.
VD/VT = 30% (% of air which goes unexchanged).

Dead space ventilation : Not used for gas exchange.

3 types :
1. Anatomical dead space (ADS).
2. Alveolar dead space (Alv DS).
3. Total dead space (ADS + Alv DS) : Physiological dead space.

Measurement of ADS : Single breath N2 method/Fowler method.

Measurement of physiological dead space : Bohr’s equation.

PACO2 : Alveolar CO2.

PECO2 : Expired CO2.
VD : Physiological dead space.
VT : Tidal volume. Bohr’s equation

Perfusion :

Pulmonary circulation (~5.5L/min) is unique as its response to hypoxia is pulmo-

nary vasoconstriction.
Mechanism :
Hypoxia Inhibits outward K+ current K+ accumulation inside cell

Vasoconstriction Opens Ca2+ channel Depolarisation

causing Ca2+ influx

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 36 05 Physiology

----- Active space -----

Lung zones :
PA : Alveolar pressure.
Pa : Arterial pressure.
PV : Venous pressure.
Blood flow distribution in the lung
Blood flow Pressure Driving
blood flow
Minimal (d/t compression of PA ≥ Pa > PV
blood vessels).
Intermittent blood flow Pa > PA > PV
(Waterfall effect).
Middle
Highest(Continuous blood flow) Pa > PV > PA

Ventilation perfusion ratio (V/Q) :

Alveolar ventilation(V) : 4.2 L/min.

Pulmonary blood flow(Q) : 5.5 L/min.
V/Q = 0.8 (in middle). It is more at apex (3.3) & less at base (0.6).

V/Q = 0 (V=0) V/Q = Infinity (Q=0)

Shunt blood (physiological). Anatomical dead space.
Foreign body causing airflow obstruction. Pulmonary embolism.

Diffusion of gases 00:53:32

Fick’s law governs the diffusion of gases in lung.

Vgas : Diffusion of gas.

A : Area.
P1-P2 : Pressure difference.
T : Thickness.
CO : Gas of choice for measuring diffusion capac

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 Physiology Revision 5 05 37

Normal value of DLCO (Diffusion Capacity of Lungs for CO2) = 25 mL/min/mm Hg. ----- Active space -----

DLCO DLCO
• membrane area : Emphysema. • Polycythemia.
• thickness : Pulmonary fibrosis. • Exercise.
• Anemia.

Oxygen dissociation curve : X

t
shif
It is a sigmoid curve.

al
t

rm
P50 : Partial pressure at which % Lef

ift
No

sh
ht
saturation of Hb with O2 is 50%.
Rig
P50 = 27 mm Hg.

P50

Left/upward shift (Haldane effect) Right/downward shift (Bohr effect)

Loading of O2 leading to unloading of Release of O2/ Unloading at
CO2. Causes : tissue. Causes :
• Hypocarbia. • Hypoxia.
• Alkalosis. • Hypercarbia.
• Fetal Hb. • Acidosis.
• CO poisoning. • 2,3 DPG.
• Stored blood. • High altitude.

CO2 transport :

AE : Anion exchanger.

Chloride shift is aka

Hamburger phenomenon : Buffered
For each HCO3- that exits, a by HCO3-
Cl- enters. Cl- shift

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 38 05 Physiology

----- Active space -----

Regulation of respiration 01:07:39

Neural control :

Brain area Function

Pre Botzinger complex Pacemaker : Initiates respiration.
Pneumotaxic center Limits inspiration (inhibits apneustic
center). Controls respiratory rate.
Apneustic center Prolongs inspiration.
Dorsal Respiratory Generates RAMP signal for smooth
Group (DRG) rise in tidal volume during inspiration.
Ventral Respiratory Controls forceful expiration during
Group (VRG) exercise.
(Mnemonic - DIVE : D Inspiration, V Expiration)

Chemical control :

Central chemoreceptors Peripheral chemoreceptors

Location Ventral surface of medulla. Carotid & aortic bodies.
Sensitive to pCO2 in blood (As CO2 can pO2(Hypoxia)
cross BBB & generate H+ Have oxygen sensors
ions) (glomus cells).
Direct stimulation by Rise in H+ ions in CSF. -

Common stimuli to both chemoreceptors : Rise in H+ ions.

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 Physiology Revision 5 05 39

Asphyxia : Rise in pCO2 & H+, fall in pO2. ----- Active space -----

Chemoreceptor activation
Hyperventilation

pCO2 H+ pO2

Pulmonary reflexes :

Reflex Stimulus Receptor Afferent Effect

Hering-Breuer Overstretch Pulmonary Large • Inhibits
inflation reflex. of lung. stretch myelinated inspiration.
(Prevent injury) (TV = 1500 receptors (slow vagal fibres. • duration of
mL) adapting)
expiration.
Hering-Breuer Deflation. Pulmonary Large • Inhibits
deflation stretch myelinated expiration.
reflex.(Prevent receptors (slow vagal fibres. • duration of
collapse) adapting).
expiration
The paradoxical Lung Pulmonary Increase in lung
reflex of head. inflation. stretch inflation.
receptors. Responsible for first
breath of newborn.
J receptor Pulmonary Juxtapulmonary Unmyelinated • Rapid
reflex. edema, receptors vagal C fibres. breathing.
pulmonary • Bradycardia.
congestion. • Hypotension.

Physiology Revision • 1.0 • Marrow 6.5 • 2023

 40 05 Physiology

----- Active space ----- Periodic breathing patterns

Cheyne Stokes Biot's breathing Kussmaul's breathing Apneustic spasm
breathing (acidotic breathing)

Seen in : Seen in : Seen in : Seen in :

1. Sleep (normal). 1. Injury to Diabetics. Midpontine lesion
2. CCF. Medulla. with vagus cut.
3. Uremia. 2. Meningitis.

Types of hypoxia 01:24:24

Features Hypoxic Anemic Stagnant Histotoxic

hypoxia hypoxia hypoxia hypoxia
Due to Low arterial Reduced O2 Decreased Decreased ability
pO2 content of blood flow of cells to use
blood to tissues oxygen
Arterial pO2 Decreased Normal Normal Normal
Arterial Hb Normal Decreased Normal Normal
content
Peripheral Stimulated Not stimulated Stimulated Stimulated
chemoreceptor (As dissolved O2
stimulation is normal)
Example High altitude CO poisoning Ischemia Cyanide poisoning

Environmental physiology 01:27:13

High altitude :
Acclimatisation : Physiological compensatory response to high altitude.
High altitude is a low pressure state.
Hypoxia in high altitude

ventilation EPO RBC Angiogenesis diffusion of O2 utility

(earliest) production ( vascularity) gases by cells (cellular
acclimatisation)

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 Physiology Revision 5 05 41

Deep sea : ----- Active space -----

High pressure state Gases are compressed.
Decompression sickness/Caisson’s disease/Dysbarism/Diver’s palsy :
Seen during rapid ascent to sea level N2 gets decompressed & released out
as bubbles.
Clinical features :
• N2 narcosis.
• Bends (pain in joints).
• Chokes.
• Air embolism death.
Rx : Slow ascent slow decompression no bubbles.

Space physiology :

It is a state of microgravity.

Positive G Negative G
When an individual is subjected to When an individual is subjected to
positive G, blood is pushed toward the negative G, blood is pushed toward the
lowermost part of the body. head end.
Venous pooling in lower limbs. Venous return : CO.
Cerebral pressure : Unconsciousness. Congestion of head & neck vessels.
Blood flow to eye : Black out. Hyperemia of eye : Red out.

Physiology Revision • 1.0 • Marrow 6.5 • 2023