Respiratory physiology REVISION NOTES PHYSIOLOGY

29-04-2018
Respiratory physiology
TONY SCARIA 2010
KMC
• Takes in 250 mL of O2 &
• gives out 200 mL of CO2
TONY SCARIA 2010
KMC

29-04-2018
• Upper respiratory tract
• Lower respiratory tract
TONY SCARIA 2010
KMC
Weibels classification
• From trachea to alveoli lower respiratory
tract divides 23 times
• Divided in to 23 generations
TONY SCARIA 2010
KMC

29-04-2018
Weibel classification
• Divided in to 23 generations
Conducting zone
• First 16 generations
• From trachea to
terminal bronchioles
• No gas exchange
Respiratory zone
• Remaining 7
generations
• 17 -19 respiratory
bronchioles
• 20-22 alveolar ducts
• 23  alveolar sac
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Cartilage & submucosal glands
only trachea & bronchi
Cilia present up to respiratory
bronchiole
TONY SCARIA 2010
KMC
Goblet cells glands &
hyaline cartilage are
absent in terminal
bronchiole
Smooth muscles
are maximm in
terminal
bronchiole
TONY SCARIA 2010
KMC

29-04-2018
Maximum resistance
in medium sized
bronchi (generation
number 7)
TONY SCARIA 2010
KMC
As we move down the
generation airway length &
diameter decreases
Number & cross sectional
area increases
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
• Alveoli
• 300- 500 million combined surface area of 50 – 100 m2
TONY SCARIA 2010
KMC

29-04-2018
Collateral ventilation in alveoli
• Provide collateral ventilation &
prevent alveolar collapse
TONY SCARIA 2010
KMC
Interalveolar pores of Kohn in
alveolar walls connect adjacent
alveoli
Canals of lambert connect
terminal bronchiole to adjacent
alveoli
TONY SCARIA 2010
KMC

29-04-2018
Bronchial tone
Dilation
• Sympathetic
• Inspiration
• 6pm
• Noncholinergic nonadrenergic
nerves secrete VIP
Constriction
• parasympathetivc
• Expiration
• 6am
• Substance P adenosine
• Irritants chemicals
• cool air exercise
D/T SMOOTH MUSCLE
CONTRACTION
TONY SCARIA 2010
KMC
Glottis
Abductor muscles of larynx
• Pull vocal cord apart early
in inspiration
• Paralysis  inspiratory
stridor
Adductor muscles of larynx
• Closes glottis during
swallowing Px
aspiration
• Paralysis causes aspiration
pneumonia & edema
Both are supplied by vagus
TONY SCARIA 2010
KMC

29-04-2018
Cells in respiratory system
• Clara cells
• Pulmonary neuroendocrine cells
• Alveolar epithelial cells
• Other cells
• Pulmonary alveolar macrophages
• Dust cells
• Plasma cells
• APUD cells
• Mast cells TONY SCARIA 2010
KMC
CLARA CELLS
• NON CILIATED
• COLUMNAR
• STEM CELLS HELP IN REGENERATION OF
CILIATED EPITHELIUM
• PRODUCES SURFACTANT PROTEIN B
• HELPS IN XENOBIOTIC METABOLISM
TONY SCARIA 2010
KMC

29-04-2018
PULMONARY NEUROENDOCRINE CELLS
• ROLE AS CHEMORECEPTORS IN HYPOXIA & HYPERCAPNIA DETECTION
• MODULATE IMMUNE RESPONSE
• SECRETE BIOGENIC AMINES
• DOPAMINE
• SEROTONIN
• GRP
• CALCITONIN
• SUBSTANCE P
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
TYPE 1
• ALVEOLAR GAS
EXCHANGE
• FORM MAIN 0LINING
(90-95 %
• CONTAIN AQAPORIN 5
CHANNEL
TYPE 2
• 5 % OF LINING
• SURFACTANT SYNTHESIS
• IL-8
• IL-1β
• ANTI PROTEASE α 1
ANTITRYPSIN
• REGENERATION OF
ALVEOLAR
EPITHELIUM
TYPE 3
• BRUSHBORDER CELL
• UNKNOWN FUNCTION
TONY SCARIA 2010
KMC
OTHER FUNCTIONS OF LUNG
• FILTERS SMALL EMBOLI
• SECRETES ANGIOTENSIN CONVERTING ENZYME BY ENDOTHELIUM OF
PULMONARY BLOOD VESSELS
• PRODUCES
• LUNG DEFENCE MECHANISM
• BRONCHIAL SECRETION CONTAIN IgA
TONY SCARIA 2010
KMC

29-04-2018
• MAXIMUM AIRWAY RESISTANCE AT
• DIAMETER OF AIRWAY
• MAXIMUM AIRWAY RESISTANCE AT RESIDUAL VOLUME (LOW LONG VOLUME)
• AS THEY ARE FULLY COMPRESSED
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
MECHANICS OF BREATHING
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
• INTRAPLEURAL PRESSURE
• AKA INTRATHORACIC
PRESSURE
• ALWAYS NEGATIVE
• 2-10 ml OF PLEURAL FLUID
TONY SCARIA 2010
KMC
NEGATIVE INTRPLEURAL PRESSURE
IS MAINTAINED BY LYMPHATIC
DRAINAGE
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
INTRAPULMONARY PRESSURE
• PRESENT IN THE ALVEOLI
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
SKEWING IS AIRWAY RESISTANCE
& TISSUE RESISTANCE
TONY SCARIA 2010
KMC

29-04-2018
• TRANSPULMONARY
• INTRAPULMONARY – INTRAPLEURAL
• TRANSTHORACIC
• INTRAPLEURAL – ATMOSPHERIC PRESSURE
• TRANSRESPIRATORY
• INTRAPULMONARY P –ATMOSPHERIC
TONY SCARIA 2010
KMC
TRANSPULMONARY PRESSURE
TONY SCARIA 2010
KMC

29-04-2018
• COSTAL PART OF DIAPHRAGM CONTRACTS DURING VOMITING
• CRURAL PORTION CONTRACTS DURING SWALLOWING
• CENTRAL PART FORMS INFERIOR PART OF PERICARDIUM
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Work of breathing
• Work of breathing (W) = Pressure (P)× Change in volume (ΔV)
• Total work of breathing 0.3- 0.8 kgm/min
• <5% of total O2 consumption) Work of
breathing
Elastic work
(65%)
Tissue
elasticity
(1/3rd)
Surface
tension(2/3rd)
Nonelastc
work (35%)
Tissue
resistance (7
%)
Airway
resistance (28
%)
TONY SCARIA 2010
KMC
Non-elastic resistance work is done
to overcome the nonelastic
resistance. It includes the work
done to overcome:
• Viscous resistance of lungs (7%)
and
• Airway resistance (28%).
It is represented by area AXBYA
AYBCA in . Thus most of the work done (65%) is
used to overcome elastic resistance.
TONY SCARIA 2010
KMC

29-04-2018
• Since in quiet breathing,
expiration is a passive
process so no work is done
during expiration. The
triangle AYBCA in represents
the stored elastic energy
that is present at the end of
inspiration. This stored
energy can compress the
alveolar gas and create
expiratory flow
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
• COMPLIANCE
• DENOTES THE EASE WITH WHICH SOMETHING CAN BE STRETCHED
• MEASURES OF DISTENSIBILITY
• ELASTICITY
• REFERS TO THE TENDENCY TO OPPOSE STRECTH OR ITS ABILITY TO RETURN
TO ITS ORIGINAL CONFIGURATION
• ELASTIC RECOIL IS DEFINED AS ABILITY OF A INFLATED LUNG TO RETURN TO
ITS RESTING VOLUME
• DIRECTLY RELATED TO STIFFNESS & INDIRECTLY RELATED TO COMPLIANCE
• COMPLIANCE IS INVERSELY PROPORTIONAL TP ELASTICITYTONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
DECREASED IN
• PULMONARY
INTERSTITIAL FIBROSIS
• INTERSTIAL LUNG
DISEASE
• ALVEOLAR EDEMA
• DECREASED SURFACTANT
INCREASED IN
• EMPHYSEMA (COPD)
• DURING AN a/c ASTHMA
ATTACK
• AGING
TONY SCARIA 2010
KMC

29-04-2018
RELAXATION VOLUME
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
STATIC
COMPLICANCE
• MEASUREMENT
MADE WITH OUT
TAKING INTO
ACCOUNT OF
DIFFERENT PHASES
OF RESPIRATION
DYNAMIC
COMPLIANCE
• MEASUREMNT
MADE DURING
DIFFERENT PHASES
OF RESPIRATION
PECIFIC
COMPLIANCE
• =COMPLIANCE
/FRC
TONY SCARIA 2010
KMC
STATIC COMPLIANCE
• SLOPE DETERMINES THE
COMPLIANCE
• COMPLIANCE DECREASED
IN CURVE SHIFTS
COMPLIANCE DECREASED ON
STIFFENING OF LUNG WITH FIBROSIS
& CONGESTION
COMPLIANCE INCREASED IN
EMPHYSEMA
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
COMPLIANCE IS MORE DURING
EXPIRATION THAN IN
INSPIRATION
TONY SCARIA 2010
KMC

29-04-2018
INCREASEDCOMPLIANCE
DECREASEDCOMPLIANCE
TONY SCARIA 2010
KMC
IN SALINE INFUSED LUNG
SURFACE TENSION IS NEARLY
ZERO INCREASED COMPLIANCE
 MEASURES ONLY ELASTIC
FORCES
MEASURES ELASTIC FORCES +
SURFACE TENSION
TONY SCARIA 2010
KMC

29-04-2018
HYSTERESIS
• Differences are also obvious
in the curves generated
during inflation and
deflation. This difference is
termed hysteresis, and
notably is not present in the
saline generated curves.
HYSTERESIS
TONY SCARIA 2010
KMC
DYNAMIC COMPLIANCE
TONY SCARIA 2010
KMC

29-04-2018
BOTH DYNAMIC & STATIC
COMPLIANCE DECREASED
• STIFF LUNG BOTH ARE
DECREASED
• PULMONARY EDEM A
• PLEURAL EFFUSION &
PNEUMOTHORAX
IF ONLY DYNAMIC
COMPLIANCE IS DECREASED
• AIRWAY OBSTRUCTION
• ENDOTRACHEAL TUBE
OBSTRCTION
• BRONCHOSPASM
TONY SCARIA 2010
KMC
SURFACTANT
• PRODUCED BY TYPE II PNEUMOCYTES
• MIXTURE OF
• DIPALMITOYL PHOSPHATIDYL CHOLINE
• SURFACTANT PROTEINS – A,B,C & D
• CARBOHYDRATES
• NEUTRAL LIPIDS
DIPALMITOYL PHOSPHATIDYL
CHOLINE  MAIN SURFACE
TENSION LOWERING AGENT
TONY SCARIA 2010
KMC

29-04-2018
SURFACTANT REDUCES SURFACE TENSION T
 LOWER COLLAPSING PRESSURE
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
PREVENT COLLAPSE OF SMALL ALVEOLI INTO
LARGE (ALVEOLAR STABILISATION)
TONY SCARIA 2010
KMC

29-04-2018
SURFACTANT PREVENTS PULMONARY EDEMA
TONY SCARIA 2010
KMC
DEFICIENCY OF SURFACTANT
• IN CIGARETTE SMOKERS
• HYALINE MEMBRANE DISEASE
• 100 % O2 INHALATION
TONY SCARIA 2010
KMC

29-04-2018
• GLUCORTICOIDS PROMOTE SURFACTANT PRODUCTION
TONY SCARIA 2010
KMC
SURFACTANT
• DECREASES HYSTERSIS
• SURFACTANT ALSO DECREASES WORK OF BREATHING
• WITHOUT SURFACTANT  WIDE HYSTERESIS LOOP
TONY SCARIA 2010
KMC

29-04-2018
SURFACTANT PRODUCTION
INCREASED BY
• GLUCORTICOID
• STEROIDS VIA FIBROBLAST
PNEUMOCYTE FACTOR
• OTHERS
• Thyroid
• Prolactin
• Estradiol
• Catechoalmines
SURACTANT PRODUCTION
DECREASED BY
• 100 % oxygen
• Cigarette smoking
• In hyaline membrane ds
TONY SCARIA 2010
KMC
Overproduction of surfactant
• Pulmonary alveolar proteinosis
TONY SCARIA 2010
KMC

29-04-2018
SURFACTANT PROTEIN
• Produced by CLARA cells
• A & D  COLLECTINS
• B& C  SMALL HYDROPHOBIC
PROTEINS
• DEFICIENCY OF SP-C IS A/W
FAMILIAL INTERSTITIAL UNG DS
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
• HYDROPHOBIC TAIL LINES
ALVEOLAR LUMEN
• HDROPHILIC PART BREAKS WATER
LAYER DECRESE SURFACE
TENSION
TONY SCARIA 2010
KMC

29-04-2018
Lung volumes & capacities
TONY SCARIA 2010
KMC
Static lung volumes &
capacities
• Measures size of lung &
amount to which they can
inflate or deflate
• Time factor is not involved
• Expressed in L
Dynamic lung volumes &
capacities
• Measures rate at which
lungs are ventilated
• Time dependant
• Expressed in L or mL/min
TONY SCARIA 2010
KMC

29-04-2018
Spirometry
TONY SCARIA 2010
KMC
Spirometer
Measured by spirometer
• Tidal volume
• Inspiratory reserve
volume
• Expiratory reserve volume
• Vital capacity
Not measured by
spirometer
• Residual volume
• FRC (ERV+RV)
• Total lung capacity (VC+
RC)
TONY SCARIA 2010
KMC

29-04-2018
MEASUREMENTS WHICH CANNOT BE MEASURED
BY SPIROMETER ARE MEASURED BY
• N2 WASH OUT METHOD
• HELIUM DILUTION METHOD
• BODY PLETHYSMOGRAPHY
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
Tidal volume 500mL Amount of air inhaled or exhaled in
one breath in normal breathing
Inspiratory reserve volume 2000 Amount of air in excess of TV that
can be inhaled with maximum
effort
Expiratory reserve volume 1000 Amount of air in excess of of TV
that can be exhaled by maximum
effort
Residual volume 1300 Amount of air remaining in lungs
after maximum expiration
Closing volume Close to RV Lung volume above RV at which
lower dependant parts of lung
begins to close off
TONY SCARIA 2010
KMC

29-04-2018
Total lung capacity 5000 • IRV + TV +ERV+RV
• FRC+IC
VITAL CAPACITY 3500 • ERV+TV+IRV
• TLC-RV
INSPTIRATORY CAPACITY 2500 • TV +IRV
EXPIRATORY CAPACITY 1500 • TV+ ERV
FUNCTIONAL RESIDUAL CAPACITY 2500 • RV+ERV
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Tidal volume (TV).
• It is the volume of air inspired or expired with each breath during
normal quiet breathing.
• It is approximately 500 mL in normal adult male.
TONY SCARIA 2010
KMC
Inspiratory reserve volume (IRV).
• It is the extra volume of air that can be inhaled by a maximum
inspiratory effort over and beyond the normal tidal volume.
• 3000 mL (range 2000–3200 mL) in a normal adult male.
TONY SCARIA 2010
KMC

29-04-2018
ERV
• extra volume of air that can be exhaled by the maximum forceful
expiration
• 1100 ml
TONY SCARIA 2010
KMC
• Residual volume (RV).
• It is the volume of the air that still remains in the lungs after the most
forceful expiration.
• It is about 1200 mL in a normal adult male.
• RV can be calculated from function residual capacity
TONY SCARIA 2010
KMC

29-04-2018
Residual volume
• Cannot be measured by spirometry
• Determined by
• Nitrogen washout technique
• Helium dilution technique
• Underestimate volume of gas in lungs if there are slowly communicating spaces like
bullae
• Body Plethysmography
• Best technique
• Can be used in patients with emphysematous bullae
TONY SCARIA 2010
KMC
Body plethysmography
• In a sealed box
• Repeately panting against a
closed mouth piece
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
Inspiratory capacity.
• This is the maximum volume of the air that can be inspired after
normal tidal expiration.
• IC = TV + IRV
• 3500 mL
• in a normal adult male
TONY SCARIA 2010
KMC

29-04-2018
Expiratory capacity
• maximum volume of air that can be expired after normal tidal
inspiration.
• EC= TV + ERV
• 1600 mL in a normal adult male
TONY SCARIA 2010
KMC
Vital capacity
• Volume of air which can be expired out after maximum inspiration
• VC= TV+IRV+ERV
• VC = EC + IRV
• 4700ml
TONY SCARIA 2010
KMC

29-04-2018
VARIATION OF VITAL CAPACITY WITH
DIFFERENT BODY POSITION
BODY POSITION DECREASE IN VC WITH SITTING POSITION AS
BASELINE
LITHOTOMY 18 %
TRENDELBERG POSITION 15 %
JACK KNIFE POSITION 12.5 %
SUPINE 9 %
TONY SCARIA 2010
KMC
LITHOTOMY POSITION 18%
TONY SCARIA 2010
KMC

29-04-2018
TRENDELENBURG  15 %
TONY SCARIA 2010
KMC
JACK KNIFE POSITION  15 %
TONY SCARIA 2010
KMC

29-04-2018
VC Can be measured as
Forced Vital capcity
• MOST ACCURATE
• Expiration is made forcefully &
quickly
• Airway collapses quickly  less
air is expelled
• FVC is more useful to detect
COPD to detect air trapped in
alveoli
Slow vital capacity
• More than VC
• Expires slowly but completely
• more time for expiring gas
• Airway remain paten during
whole expiration and appear
normal donot detect air trapping
in COPDTONY SCARIA 2010
KMC
• In restrictive lung disease FVC is markedly reduced
TONY SCARIA 2010
KMC

29-04-2018
Functional residual capacity
• Volume of air in the lung at the end of normal expiration
• FRC= RV + ERV
• 2400 ml
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Closing volume
• Closure of small bronchioles aa7 alveoli in dependant portion because
of decreased transpulmonary pressure
TONY SCARIA 2010
KMC
• Closing capacity
• Lung volume at which dependant airway start to close
• CC = RV + CV
• Closing capacity is below FRC
• Closing capacity is the volume at which airway closes functional residual capacity should
be 1 liter more than losing capacity. If it falls below closing capacity premature airway
closure will take place which can lead significant hypoventilation.
• Meausured by Xe gas
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
In lobectomy
• VC RV decreases
•  hypoxia  hypoxic stimulus  rapid shallow breaths  increased
dead space ventilation
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
Dynamic lung volumes
• Measured with reference to time
• FEV1
• FEV1/FVC
• PEFR
TONY SCARIA 2010
KMC

29-04-2018
Dynamic lung volumes
Single breath
•FVC
•FEV
•MMEFR
•PEFR
Multiple breaths
•MV
•MVV
•BR
TONY SCARIA 2010
KMC
FORCED VITAL CAPACITY
• Rapid forceful timed VC
• FEV1  FORCED EXPIRATORY VOLUME IN 1 SEC 80% OF FVC
• FEV2 FORCED EXPIRATORY IN 2 SEC  95 % OF FVC
• FEV3 FORCED EXPIRATORY IN 3 SEC  99-100% OF FVC
TONY SCARIA 2010
KMC

29-04-2018
FEV1
• Detect proximal airway narrowing (such as bronchi close to top of
tree
• Maximum amount of air that can be exhaled in 1st second of
expiration
• Normal = 70 -80 % VC
TONY SCARIA 2010
KMC
• FEV1 is decreased in both obstructive & restrictive lung diseases
• Obstructive lung disease
• FEV1 is decreased out of proportion to FVC (VC is increased )
• Restrictive lung disease
• FEV1 is also decreased as VC is decreased
• fFEV1 decreased in proportion to FVC
TONY SCARIA 2010
KMC

29-04-2018
FEV1/FVC
• Normal > 70 %
• Used to diagnose obstructive lung disease
• Decreased as low as 20 – 30%
• Normal or increased in restrictive lung disease
TONY SCARIA 2010
KMC
FEV 25-75
• Maximal mid expiratory flow rate (MMEFR)
• Small & medium airway ds
• More sensitive measure of small airway disease
• In mild obstructive disease
• FEV1/FVC  normal hence cant be detected by this
• FEV 25 – 75 shows depression  early detection
TONY SCARIA 2010
KMC

29-04-2018
PEFR
• Maximum flow rate which can be generated during a forceful
expiration
• Depends on how quickly he can exhale
• Reflects large airway
• Depends on voluntary effort & muscular strength
• Decreased in obstructive pulmonary disease
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Time volume curve
TONY SCARIA 2010
KMC
Minute ventilation
• Tidal volume * RR
• Volume of air moved in & out by the lungs
• =6L/min
TONY SCARIA 2010
KMC

29-04-2018
Maximum voluntary ventilation
• Maxm volume of air that can be moved in & out
• In 1 min
• 125 – 170L/min
TONY SCARIA 2010
KMC
Breathing reserve
• MVV- MV= BR
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
N2 WASH OUT METHOD
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
• PHASE I
• Pure dead space exhaled
• PHASE II
• Mixture of dead space + alveolar gas
• PHASE III
• Pure alveolar gas
• PHASE IV
• Toward end there is abrupt increase in N2
concentration
• d/t preferential emptying of apex (has higher
concentration of N2 less diluted with O2)
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
Helium dilution method
TONY SCARIA 2010
KMC

29-04-2018
Plethysmography
TONY SCARIA 2010
KMC
• Plethysmography
• Closed box
• Based on boyles law
• On doing plethysmography
• On inspiration against closed glottis  the pressure in the lung decreases &
athat in box increases
• Based on boyles law
TONY SCARIA 2010
KMC

29-04-2018
Mean transmit time
• Very sensitive index of airway obstruction
• Normal  0.5- 0.8 sec
• Increased in obstruction
TONY SCARIA 2010
KMC
Flow volume curve
Effort dependant at high
lung volume
Effort independent at low
lung volume
TONY SCARIA 2010
KMC

29-04-2018
Flow volume loop
Effort independent portion of
curve depressed inward
In restrictive lung ds
low TLC RV
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
• Restrictive ds
• Shift to R side
• mountain like appearance
• Obstructive ds
• Shifts to L side
• Descending limb is curved inwards
TONY SCARIA 2010
KMC
Obstructive lung
disease
•Effort independent
portion of curve
depressed inward
•High TLC & RV
Restrictive lung
disease
•Effort independent
portion of curve not
depressed
•Low TLC & RVTONY SCARIA 2010
KMC

29-04-2018
Obstructive lung disease Restrictive lung disease
Characterised by reduction in air flow Characterised by reduction in ling volume
Shortness of breath in exhaling air Difficulty in taking air inside
COPD asthma bronchiectasis ILD scoliosis obesity
Increase in in TLC RV FRC All volumes & capacities are decreased
Decrease in FEV1 FEV1 decreased (but in less proportion to FVC)
FEV1/FVC decreased FEV1 / FVC  normal or slightly increased
Increase in airway resistance Decreased distensibility (compliance of lung)
Nonelastic work of breathing increased Elastic component of work increased
Most economical & convenient method  slow &
deep breathing
Most economical & coveninrt method  rapid &
shallow breathingTONY SCARIA 2010
KMC
FEV1 decreased
(but in less
proportion to FVC)
Decrease in FEV1
FEV1 / FVC is
normal
FEV1 / FVC is
decreased
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
Special situations in flow volume
loop
TONY SCARIA 2010
KMC

29-04-2018
Special situations in flow volume loop
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Saw toothed appearance in parkinsonism
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Pneumonectomy or lobectomy
• Will have restrictive disease like features
• Decrease in
• Compliance
• TLC
• FRC
• RV
• FVC
• FEV1
• Increase in
• Dead space d/t hyperinflation of remaining lung
• FEV1/FVC
• Remains unchanged
• DLCO
• PaO2
• PaCO2
• Specific compliance
TONY SCARIA 2010
KMC
Ventilation perfusion
TONY SCARIA 2010
KMC

29-04-2018
Ventilation perfusion
• Ventilation is more at base compared to apex
• Perfusion also decreases from base to apex
• Relative change in blood flow is greater than relative change in
ventilation
• v/p ratio is maximum at apex(3.0) & least at base (0.6)
• v/p sat middle is considered to b 0.8
• At zero gravity V/P ratio is uniformly 0.8
TONY SCARIA 2010
KMC
Ventilation perfusion ratio
TONY SCARIA 2010
KMC

29-04-2018
• No flow
• local alveolar capillary pressure in that area of the lung
never rises higher than the alveolar air pressure during
any part of the cardiac cycleZone 1
• Intermittent flow
•only during the peaks of pulmonary arterial pressure
because the systolic pressure is then greater than the
alveolar air pressure, but the diastolic pressure is less
than the alveolar air pressure
Zone 2
• Continous flow
•the alveolar capillary pressure remains greater than
alveolar air pressure during the entire cardiac cycleZone 3TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
• Zone 1 is absent normally
• Seen only in hypotension shock
• Normally, the lungs have only zones 2 and 3 blood flow—zone 2
(intermittent flow) in the apices and zone 3 (continuous flow) in all
the lower areas.
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Poorly perfused apical
alveoli approximates more to
inspired air high PO2 & low
PCO2
Well perfused basal
alveoli becomes equal
to that pulmonary A
low PO2 & high PCO2
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Ventilation perfusion ratio
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Ventilation perfusion special situation
TONY SCARIA 2010
KMC
VP imaging
• Inhaled 133 Xe & injected 99m Tc albumin
TONY SCARIA 2010
KMC

29-04-2018
Dead space
TONY SCARIA 2010
KMC
Anatomical dead space
• respiratory system volume exclusive of alveoli
• No gas exchange occurs
• From Nose to terminal bronchiole
• Equal to 2ml/kg
• Equal to body weight in pounds
• Dead space = 150ml (did not take part in ventilation)
• Measured by N2 wash out method (FOWLERS METHOD)TONY SCARIA 2010
KMC

29-04-2018
Factors which increase anatomical dead space
• Factors which increase or causing dilation of airways
• Nek extension
• Jaw protrusion
• Positive pressure ventilation
• GA
• Emphysema
• Increased age
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Alveolar dead space
• Parallel dead space
• Normally alveolar dead space = 0 ml
• No blood supply  zone 1
TONY SCARIA 2010
KMC
Increased alveolar dead space
• Pulmonary thromboembolism
• Pulmonary HtN
• Less perfusion in supraclavicular
parts in upright posture
• Ventilation of nonvascular air
space
• Emphysema(destruction ob blood
vessels & septa)
TONY SCARIA 2010
KMC

29-04-2018
Total dead space
• total (physiologic) dead space
• volume of gas not equilibrating with
blood; ie, wasted ventilation
• Alveolar+ anatomical
• Normally alveolar = 0ml
• Bohrs equation  total dead space
• VD = VT – (Peco2 × VT)/(Paco2)
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
The volume of anatomical dead
space is measured by
placing a vertical line on the
record from mid-portion of
phase II of expiration (red area
X = blue area Y)
TONY SCARIA 2010
KMC
Alveolar ventilation
TONY SCARIA 2010
KMC

29-04-2018
• Rapid shallow breathing less alveolar ventilation
• Slow deep breathing  more alveolar ventilation
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
More expanded alveoli at
apex
TONY SCARIA 2010
KMC
Gas exchange
TONY SCARIA 2010
KMC

29-04-2018
Alveolar capillary membrane
• 6 layers
• Surfactant
• Alveolar epithelum
• Alveolar epithelial basement membrane
• Interstitial space
• Capillary basement membrane
• Capillary endothelium
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
PaO2 CAN ALSO BE CALCULATED BY
ALVEOLAR GAS EQUATION
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
DIFFUSION
• AVERAGE CAPILLARY TRANSIT TIME THROUGH LUNG IS 0.75 SEC
• DIFFUSION EQUILIBRIUM OF O2 B/W BLOOD & GAS IS 0.25 SEC
TONY SCARIA 2010
KMC
IN LUNG DS DIFFUDION
CAPPACITY OF LUNG FOR O2
IS DECREASED  CAPILALRY
PaO2 DOES NOT
EQUILIBRATE WITH PAO2
TONY SCARIA 2010
KMC

29-04-2018
DIFFUSION OF GASES
• DIFFUSION LIMITED
• PERFUSIONLIMITED
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
Perfusion limited
• Rapid equilibration
• Can be increased by
increasing perfusion
Diffusion limited
• Slow equilibration
• Increased by increasing
area of membrane or
decreasing thickness of
membraneTONY SCARIA 2010
KMC

29-04-2018
PERFUSION LIMITED GASES
• CO2 ,N20
• CAPILLARY PARTIAL PRESSURE RISES
EQUILIBRATES WITH ALVEOLAR
PARTIAL PRESSURE WITH IN 0.25
SECONDS (CAPILLARY TRANSIT TIME IS
0.75 SEC)
• WITH NO ALVEOLAR CAPILLARY
PRESSURE GRADIENT REMAINING
DIFFUSION CEASES
• UPTAKE CAN ONLY BE INCREASED BY
INCREASING CAPILLARY PERFUSIONTONY SCARIA 2010
KMC
DIFFUSION LIMITED
• CO
• CO binds to Hb 10 times faster
than O2
• Partial pressure of CO in capillary
does not rise as partial pressure
does not depend on chemically
bound form
• It depends only on dissolved form
• Its diffusion can be increased by
reducing thickness of membrane &
increasing area of membrane
TONY SCARIA 2010
KMC

29-04-2018
Oxygen is perfusion limited
only under hypoxic
condition it is diffusion
limited
TONY SCARIA 2010
KMC
Diffusion capacity
• Defined as volume of gas that passes through repsiratoy membrane in 1
min when pressure difference is 1 mmHg
• CO is used as an index
• CO is diffusion limited
• DLco = 20 to 30 mL/min/mmHg
• DLo225mL/min/mmHg (1.23 times DLco)
• DLco2 400mL/min/mmHg (20 times than DLo2)
• Increased to 65 during exercise
• Decreased in berylliosis & sarcoidosis
TONY SCARIA 2010
KMC

29-04-2018
Increase blood in alveolar capillary
blood
• Supine position
• Hyperdynamic circulation
• Left to right cardiac shunt
• Bronchial asthma
• Polycythemia
• Obesuty
• Smoking
Decreased DLCO
• Decrease SA
• Emphysema
• V/Q mismatch
• Lung fibrosis
• Pulmonary resection
• Alceoalr capillary membrane ds
• ILD
• Alveolar edema
Normal DLco
• Chronic bronchitis
• Cystic fibrosis
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
• Partial pressure of CO2 is
constant through out 
47mmHg
• Total pressure is 760 mmHg
• When air from upper airway
enters alveoli partial pressure of
O2 still falls d/t high CO2
concentration in alveolar gas
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Alveolar gas equation for PaO2
TONY SCARIA 2010
KMC
O2 CO2
Inspired air 158mmHg 0.3 mmHg
Alveolar air 100 mmHg 40mmHg
Expired air 116mmHg 32mmHg
Venous blood 40 mmHg 46mmHg
Arterial blood 95 mmHg 40mmHg
TONY SCARIA 2010
KMC

29-04-2018
Physiological shunt
• Partial P of O2 in arterial blood is 95-98 mmHg < partial pressure of
O2 in alveolar blood (104 mmHg)
• Reasons
• Bronchial blood flow
• Anastomoses b/w bronchial capillaries & pulmonary capillaries bypassing R ventricle
• Coronary blood flow
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Oxygen transport forms
• 99%
• Sigmoid shaped curveHemoglobin
bound form
• 1 %
• Straight line
• As concentration of dissolved o2 is
directly proportional to partial pressure
Dissolved O2TONY SCARIA 2010
KMC
• 1 gm of Hb contains 3.47mg of iron
• Total iron content in blood is 2.6gm
EACH GRAM OF Hb CARRIES 1.34 ML OF
O2
TONY SCARIA 2010
KMC

29-04-2018
75 % SATURATION
• EXTRACTION RATIO =
CONSUMPTION / SUPPLY
*100
• = 4.6/19.8 = 25 %
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
OXYGEN
DISSOCIATION
CURVE
10mmHg 10 %
15mmHg 20 %
20mmHg 75 %
26mmHg 50%
40 mmHg 75 %
60mmHg 90%
PARTIAL PRESSURE AT
WHICH Hb IS 50 %
SATURATED IS P50
In venous blood 75 %
saturation
TONY SCARIA 2010
KMC
OXYGEN DISSOCIATION CURVE
• sigmoid shape
• due to the T–R configuration interconversion
• D/T COOPERATIVE BINDING
• In deoxyhemoglobin, the globin units are tightly bound in a tense (T) configuration,
which reduces the affinity of the molecule for O2. When O2 is first bound, the bonds
holding the globin units are released, producing a relaxed (R) configuration, which
exposes more O2 binding sites
• Combination of the first heme in the Hb molecule with O2 increases the
affinity of the second heme for O2, and oxygenation of the second
increases the affinity of the third, and so on, so that the affinity of Hb for
the fourth O2 molecule is many times that for the first
• The net result is a 500-fold increase in O2 afnity.
TONY SCARIA 2010
KMC

29-04-2018
Te higher the P50, the lower the afnity
of hemoglobin for O2
TONY SCARIA 2010
KMC
SHIFT OF OXYGEN DISSOCIATION CURVES
SHIFT TO RIGHT  LOWER AFFINITY
(HIGHER P50) INCREASED O2
DELIVERY TO TISSUES
• INCREASED TEMPERATURE
• LOW pH
• HIGH Pco2
• Raised 2,3 BPG
SHIFT TO LEFT HIGHER AFFINITY
(LOWER P50) INCREASED O2
DELIVERY TO TISSUES
• Low temp
• High pH
• Low Pco2
• Low 2,3 BPG
• Fetal Hb low affinity to 2 3 BPG
• Stored blood  low 2,3 BPG
• CO poisoningTONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
• Right shift of oxygen dissociation curve  muscle & other tissues
• BOHR EFFECT AT TISSUE LEVEL
• Left shift in lungs  to help in oxygen uptake
• HALDANE EFFECT AT LUNG LEVEL
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
2,3 BPG
• formed from 3-phosphoglyceraldehyde, which is a product of
glycolysis via the Embden-Meyerhof pathway.
• highly charged anion that binds to the β chains of deoxyhemoglobin.
One mole of deoxyhemoglobin binds 1 mol of 2,3-DPG
• Increase in 2,3 BPG  shift of ODC to right
TONY SCARIA 2010
KMC

29-04-2018
It is a highly charged anion
that binds to the β chains of
deoxyhemoglobin
TONY SCARIA 2010
KMC
2,3 BPG binds to beta chain of deoxyHb
TONY SCARIA 2010
KMC

29-04-2018
an increase in the concentration of
2,3-DPG shifs the reaction to the
right, causing more O2 to
be liberated
TONY SCARIA 2010
KMC
• Thyroid hormones,
• growth hormones,
• Androgens
• Exercise
• High altitude anemia
• Chemical agents  inosine
Increased
concentration
of 2 3 BPG
• acidosis inhibits red cell glycolysis, the 2,3-DPG
concentration falls when the pH is low
• Stored blood
Decreased
concentration
of 2 3 BPG TONY SCARIA 2010
KMC

29-04-2018
Effect of CO on ODC
• Decreases O2 concentration
& shifts curve to left
• CO has 240 times greater
affinity to Hb than O2
• Decreases p50 and makes
curve less sigmoidal
TONY SCARIA 2010
KMC
CO at varous concentration
TONY SCARIA 2010
KMC

29-04-2018
Anemia
• No change in shape
• Curve shifts to right
• d/t increased 23 BPG
TONY SCARIA 2010
KMC
bohR effect  shift to R
• The decrease in O2 afnity of hemoglobin when the pH of blood falls is
called the Bohr eﬀect
• deoxygenated hemoglobin (deoxyhemoglobin) binds H+ more actively than
does oxygenated haemoglobin
• Decrease pH can occur d/t increased pCO2
• Occurs at tissue level
TONY SCARIA 2010
KMC

29-04-2018
Mechanism of bohr effect
Deoxygenated Hb binds H+ ion more
actively than oxygenated Hb 
decreases affinity of deoxygenated
Hb for O2
TONY SCARIA 2010
KMC
the leftward shift of the myoglobin
O2 binding curve when compared
with hemoglobin demonstrates a
higher affinity for O2, and thus
promotes a favourable
transfer of O
2 from hemoglobin in the blood The steepness
of the myoglobin curve also
shows that O2 is released
only at
low Po2 values (eg, during
exercise)
TONY SCARIA 2010
KMC

29-04-2018
Fetal Hb
• Is having gamma chain with less affinity to 2 3 BPG
• Therefore HbF is having greater affinity for HbA
TONY SCARIA 2010
KMC
Double bohr effect occurs at placenta level
TONY SCARIA 2010
KMC

29-04-2018
Myoglobin
• rectangular hyperbola
• D/t lack of cooperative binding is reﬂected in the myoglobin dissociation
curve
• Myoglobin binds 1
• Low P50 (5 mmHg ) higher affinity left shift of curve
TONY SCARIA 2010
KMC
• DISSOLVED O2 IS
DIRECTLY PROPORTIONAL
TO PaO2
• STRAIGHT CURVE RATHER
THAN SIGMOID
TONY SCARIA 2010
KMC

29-04-2018
Transport of CO2
TONY SCARIA 2010
KMC
• 70 %
Plasma HCO3-
• 23 %
Carbamino Hb
• 7 %Dissolved in
plasma TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
• 1. Dissolved
• 2. Formation of carbamino-Hb
• 3. Hydration, H+ buﬀered, 70% of HCO3– enters the plasma
• 4. Cl– shifts into cells; mOsm in cells increases
In RBC
(89%)
• 1. Dissolved
• 2. Formation of carbamino compounds with plasma protein
• 3. Hydration, H+ buﬀered, HCO3– in plasma
In plasma
(11%) TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
• Blood carries 4ml /dL of CO2 to lungs
• Transports 200ml/min to lung
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
Haldane effect
TONY SCARIA 2010
KMC

29-04-2018
Haldane effect
• Occurs in lungs
• Effect of pO2 in CO2 dissociation curve
TONY SCARIA 2010
KMC
• The Haldane eﬀect refers to the increased
capacity of deoxygenated hemoglobin to
bind and carry CO2. Consequently, venous
blood carries more CO2 than arterial blood,
CO2 uptake is facilitated in the tissues, and
CO2 release is facilitated in the lung
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
• At point V
• P CO2 = 45 mmHg
• 52 volumes combine wih blood
• At point A
• P CO2 = 40 mmHg
• Higher PaO2  loses 4ml of CO2
• Loses 4 ml & becomes 48 mL
• At point C
• In the absence of Haldane effect
• PCO2 = 40 mmHg
• CO2 concentration will fall only to 50 ml from 52 mL
c
TONY SCARIA 2010
KMC

29-04-2018
Chloride shift or hamburger shift
anion exchanger 1 (AE1; also called
Band 3)
TONY SCARIA 2010
KMC
Hematocrit of venous blood is larger than
arterial blood
• the hematocrit of venous blood is normally 3% greater than that of
the arterial blood
• Note that for each CO2 molecule added to a red cell, there is an
increase of one osmotically active particle in the cell— either an
HCO3 − or a Cl− Consequently, the red cells take up water and
increase in size.
• a small amount of ﬂuid in the arterial blood returns via the lymphatics
rather than the veins
TONY SCARIA 2010
KMC

29-04-2018
In the lungs, the Cl− & h2O
moves back out of the cells
and they shrink.
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
respiratory quotient (RQ)
• The is the ratio in the
steady state of the volume
of CO2 produced to the
volume of O2 consumed
per unit of time at
equilibrium
respiratory exchange ratio
(R)
• the ratio of CO2 to O2 at
any given time whether
or not equilibrium has
been reached.
• R is aﬀected by factors
other than metabolismTONY SCARIA 2010
KMC
RQ
Carbohydrate 1
Fat 0.7
Protein 0.8
Mixed diet 0.825
TONY SCARIA 2010
KMC

29-04-2018
Hypoxia
Hypoxemia
•Decrease in partial
pressure of oxygen in
arterial blood <80
mmHg
•Does not consider Hb
Hypoxia
•O2 deficiency at
tissue level
TONY SCARIA 2010
KMC
4 types of hypoxia
• Hypoxic hypoxia
• Anemic hypoxia
• Stagnant hypoxia
• Histotoxic hypoxia
TONY SCARIA 2010
KMC

29-04-2018
Hypoxia Hypoxic hypoxia Anemic hypoxia Stagnant hypoxia Histotoxic hypoxia
d/t decrease in oxygen
supply
Most common hypoxia
Decrease in oxygen
carrying capacity of blood
d/t sluggish blood
flow
Tissues are unable to
use O2 brought to
them by blood
Cause • High altitude
• Pneumonia
• VP imbalance
• AV malformation
• Anemia
• CO poisoning
• Methaemoglobinemia
• Heart failure
• Shock
• Haemorrhage
• Cyanide poisoning
PaO2 Low Normal Normal Normal
PvO2 low Low low high
A-V o2
difference
Decreased Increased Maximum
difference  d/t
maximum
extraction
Decreased
difference or even
may be zero
Dissolved O2 Decreased Normal Normal normal
Peripheral
chemoreceptor
Stimulated Not stimulated bcz
peripheral
chemoreceptors are
sensitive only to PO2
Stimulated Stimulated
Central
chemoreceptor
Stimulated if there is
associated high PCO2
Not stimulated Not stimulated Not stimulated
TONY SCARIA 2010
KMC
Hypoxemic hypoxia
• Decreased PO2 in inspired air
• Decreased FiO2
• Low barmetric pressure at high altitude
• Ventilation perfusion mismatch
• Right to left shunt
• Impairement of diffusion acroos respiratory membrane
TONY SCARIA 2010
KMC

29-04-2018
Oxygen treatment
Not useful for
• Anemic hypoxia
• Hypoxic hypoxia d/t ventilation
perfusion mismatch ie
oxygenated blood bypasses
well ventilated alveoli
Useful for
• Hypoxic hypoxia
Useful in condition where PaO2 decreases
TONY SCARIA 2010
KMC
Hyperbaric oxygen therapy
• 100 % O2 @ 2-3 atm P
• CO poisoning
• Gas gangrene
• Very severe blood loss anemia
• Decompression sickness & air embolism
• Radiation induced injury
TONY SCARIA 2010
KMC

29-04-2018
Hypoxia induced factor
• Hypoxia induces formation of
hypoxia (HIF α)
• in normal cells they are
ubiquitinated
• In hypoxic cells dimerises with HIF
β activate genes  angiogenic
factors & erythropoietin formed
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
Effect of hypoxia
• Effect on brain
• Less severe hypoxia impaired judgement & head ache
• Severe  loss of consciousness in 10-20 sec & death in 4-5 min
• Respiratory stimulation syndrome
• Dyspnea & hyperpnea
TONY SCARIA 2010
KMC
Pulmonary toxicity
TONY SCARIA 2010
KMC

29-04-2018
CO poisoning
• Gaseous transmitter vasodilator like NO & H2S
• CO has 210 more affinity for Hb
• PaO2 is normal  doesnot stimulate respiratory centre
• ANEMIC HYPOXIA
• Cannot take up O2  liberate CO slowly
• Shift of ODC to left
• Brain is the first organ to be affected
TONY SCARIA 2010
KMC
CO poisoning
• Rx
• Hyperbaric oxygen
• Mixture of 95 % O2 & 5% CO2
• As CO2 stimulates respiratory centre
TONY SCARIA 2010
KMC

29-04-2018
Methaemoglobinemia
• Heme iron is ferric rather than ferrous
• MetHb can neither bind or transport oxygen
• Chocolate cyanosis & chocolate colured blood (d/t dark colored
blood)
TONY SCARIA 2010
KMC
Sulfhaemoglobinemia
• Excess sulfHb  greenish colour pigment
• Even low level  cyanosis
TONY SCARIA 2010
KMC

29-04-2018
Cyanosis
• Bluish discolouration of skin & mucus membrane
• Cyanosis is present when
• deoxyHb >4-5 g/dL
• metHb >1.5g/dL
• sulfHb>0.5 g/dL
TONY SCARIA 2010
KMC
• SaO2<85 %
• Any cause of hypoxic hypoxia
• All sites including mucus membrane
Central
cyanosis
• Stagnation of blood
• Any cause of stagnant hypoxia
• Manifested in ear lobe finger tips
Peripheral
cyanosis TONY SCARIA 2010
KMC

29-04-2018
Cyanosis does not occur in
• Anemic hypoxia
As total Hb content is low
• CO poisoning
Masked by cherry red
colour of COHb
Blood gas content is
normal
Cyanosis will occur in
• Hypoxic hypoxia
TONY SCARIA 2010
KMC
Regulation of respiration
TONY SCARIA 2010
KMC

29-04-2018
Regulation of
respiration
Chemical
regulation
Peripheral
chemoreceptor
Central
chemoreceptor
Neural
regulation
Cerebral cortex
pons medulla
TONY SCARIA 2010
KMC
chemoreceptors
Peripheral
chemoreceptors
• Carotid body
• Glossopharyngeal
nerve
• Aortic body
• Vagus
Central chemoreceptor
• Just beneath ventral
surface of medulla
TONY SCARIA 2010
KMC

29-04-2018
MECHANISM OF PERIPHERAL
CHEMORECEPTOR ACTIVATION
TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
CAROTID BODIES & AORTIC BODIES
• MAXIMUM BLOOD SUPPLY/100gm OF TISSUE
• 2000ml/mim/100gm tissue
TONY SCARIA 2010
KMC
The type II
cells are glia-like, and each
surrounds four to six type I cells.
The function of type II cells is not
fully defined
The type I or glomus cells are
closely associated with cuplike
endings of the aﬀerent nerves
TONY SCARIA 2010
KMC

29-04-2018
Peripheral chemoreceptor Sensitive to
• Increase in H+
• Increase in PaCO2
• Decrease in PaO2 most potent stimuli
TONY SCARIA 2010
KMC
Powerful stimulants of chemoreceptor
• Cyanideprevents O2 utilisation
• Nicotine & lobeline
• Infusion of K+  increase discharge rate
• Exercise  increase plasma K+ • Not stimulate respiratory
centre
• Anemic hypoxia & CO
poisoning (dissolved O2 is
normal)
TONY SCARIA 2010
KMC

29-04-2018
Central chemoreceptor
On ventral surface of medulla
TONY SCARIA 2010
KMC
Stimulation of central chemoreceptor
• H+ ion
• Respond to H+ ion of CSF of
medulla
• But not to increase in H+ in blood as
BBB is impermeable to charged ions
• CO2
• BBB Readily permeable to CO2
• Indirectly form H+ stimulate
chemoreceptor
• O2
• Doesnot stimulate
• Depress chemoreceptor
TONY SCARIA 2010
KMC

29-04-2018
Ventilatory response to
increased CO2
• Linear relationship b/w RMV & alveolar pCO2
• PaCO2 <37mmHg  temporary cessation of
respiration
When the CO2 content of
the inspired gas is more than 7%, the alveolar and
arterial
Pco 2 begin to rise abruptly in spite of
hyperventilation. Te
resultant accumulation of CO
2 in the body (hypercapnia)
depresses the central nervous system, including the
respiratory center, and produces headache, confusion,
and eventually
coma (CO2 narcosis)
TONY SCARIA 2010
KMC
Ventilatory response to CO2
• No increase in ventilation till PAO2 <60 mmHg
• Hb is a weaker acid than HbO2, there is a slight decrease in the H+
concentration of arterial blood when the arterial Po2 falls and
hemoglobin becomes less saturated with O 2.
• CO2 is washed out
• Apnoea point
TONY SCARIA 2010
KMC

29-04-2018
Voluntary hyperventilation
•  Raises alveolar & arterial PO2 &lower PCO2
• Low PCO2  depress respiratory centre
TONY SCARIA 2010
KMC
Breath holding
• The point at which breathing can no
longer be voluntarily inhibited is
called the breaking point.
• due to the rise in arterial Pco2 and the
fall in Po2
• Breaking point increased by
• removal of the carotid bodies.
• Breathing 100% oxygen
• hyperventilating room air
• Encouragement TONY SCARIA 2010
KMC

29-04-2018
Neural regulation of respiration
TONY SCARIA 2010
KMC
Automatic
control
Upper medulla
Pons
Voluntary
control
Cerebral cortex
via corticospinal
tract
Cervical motor
neuron thoracic
spinal neuron
TONY SCARIA 2010
KMC

29-04-2018
• Prebotzinger
complex
• DRG & VRG
Medulla
• Pneumotaxic
centre
• Apneustic centre
pons TONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
DRG & VRG project in to prebotzinger
complex
TONY SCARIA 2010
KMC
Dorsal respiratory group
• Contain inspiratory neurons
• Innervate primary muscle of inspiration diaphragm & external
intercostal
TONY SCARIA 2010
KMC

29-04-2018
TONY SCARIA 2010
KMC
• Botzinger
• Contains expiratory neurons supply accessory muscles of
expiration
Rostral VRG
• Prebotzinger complex
• Contains Inspiratory neurons
• Also supply accessory muscles inspiration
Intermediate
VRG
• Conatins expiratory neurons
• Supply accessory muscles of expiration
• Silent most of time as expiration is passive
Caudal VRG TONY SCARIA 2010
KMC

29-04-2018
Prebotzinger complex
• Pacemaker cells
• Regulate rate of
respirationdischarge
rhythmically phrenic N
• Inhibited by opiods
• Stimulated by substance P
TONY SCARIA 2010
KMC
prebot
TONY SCARIA 2010
KMC

29-04-2018
Pontine centres
• Not normally required for eupnea
Pneumotaxic centre
• Medial parabrachial &
kolliker fuse nuclei
• Control rate & fine
tuning of breathing
• Limits inspiration by
inhibiting apneustic
centre
Apneustic centre
• Lower pons
• Produces prolonged
inspiratory drive by
stimulating inspiratory
neurons of
prebotzinger complex
• Tonically active &
control depth of
breathing
TONY SCARIA 2010
KMC
Strong stimulation of pneumotaxic centre 
inhibit apneustic centre  early termination of
inspiratory drive decrease Tidal volume
TONY SCARIA 2010
KMC

29-04-2018
Section at D
• Cut below medulla
• Complete transection of brain
stem
• Stops all respiration
TONY SCARIA 2010
KMC
Section at C
• Cut at inferior portion of pons
• Vagi intact
• Irregular gasping
• rhythmic as pacemaker is intact
• Vagi cut
• Same as above as vagi are
connected to apneustic centre
TONY SCARIA 2010
KMC

29-04-2018
Section at B
• Cut at mid pons
• Apneustic centre is intact
• But pneumotaxic is lost (inhibitory
control on depth is lost)
• Vagi intact
• Regular respiration
• Deep & slow breathing
• vagi cut
• Lost stretch reception
• Arrest of respiration in maxmm
inspiratory phase interrupted by brief
expirationTONY SCARIA 2010
KMC
Section at A
• Decerebration
• Normal rhythmic breathing
continues
• Loss of voluntary breath
holding
• If vagi are cut increased rate &
depth
TONY SCARIA 2010
KMC

29-04-2018
Administration of O2 in hypoxia
inhibit peripheral chemoreceptor
 apnea
TONY SCARIA 2010
KMC
Ondines curse
• Voluntary control intact
• Automatic control is lost
• In case of bulbar poliomyelitis
TONY SCARIA 2010
KMC

29-04-2018
Airway reflexes
TONY SCARIA 2010
KMC
Vagal innervation Type Location Stimulus Response
Myelinated Slow adapting Among airway
smooth muscle
Lung inflation • Shorten
inspiratory time
• HB reflex
• Bronchodilation
& tachycardia
Rapidly adapting
(irritant recpetors)
Among airway
epithelium
Lung hyperinflation
Exo & endogenous
substances
• Cough
• Bronchoconstrict
ion
• Hyperpnea
Unmyelinated Pulmonary C
receptors
Close to the blood
vessels
• Lung
hyperinflation
• Exo &
endogenous
substance
• Apnea followed
by rapid
breathing
• Bronchoconstrict
ion
• Hypotension
• Mucus
Bronchial C fibres • Pulmonary
chemoreflex
TONY SCARIA 2010
KMC

29-04-2018
Coughing
• Deep inspiration
fb forced
expiration
• Against closed
glottis (glottis
opened
suddenly)
sneezing
• Similar
expiratory effort
• Continuously
open glottis
Hiccup
• Spasmodic
contraction of
diaphragm that
produce
inspiration
• Glottis closes
suddenlyTONY SCARIA 2010
KMC
TONY SCARIA 2010
KMC

29-04-2018
High altitude physiology
TONY SCARIA 2010
KMC
• Total barometric P decreases at high altitudes
• Fractional concentration of O2 in the atmosphere remains normal
• Partial pressure of oxygen decreases d/t decrease in total barometric
P  hypoxic hypoxia
TONY SCARIA 2010
KMC

29-04-2018
High altitude
illness
a/c mountain
sickness
Develops 8-24
hours after
arrival
Last 4-8 dys
c/c mountain
sickness
(monges ds)
Develops in
some high
altitude settlers
• a/c syndrome May also be a/w
• High altitude pulmonary
edema (HAPE)
• High altitude cerebral
edema(HACE)
TONY SCARIA 2010
KMC
a/c mountain sickness
• Head ache in setting of recent altitude again
• With typical symptoms of
• Hypoxia
• Tachycardia
• Anorexia N V
• Insomnia
• Dizzziness & fatigue
TONY SCARIA 2010
KMC

29-04-2018
• Hypoventilation interstitial edema &
increased sympathetic drive
Mild to
moderate
• White matter edema in edema d/t
cerebral vasodilation (leak of fluid)
Moderate
to severe TONY SCARIA 2010
KMC
Rx of AMS
• Halting descent
• O2 therapy
• Hyperbaric chamber
• Drugs
• Acetazolamide
• Dexamethasone
• Analgesic
• Promethazine
TONY SCARIA 2010
KMC

29-04-2018
High altitude syndromes
High altitude cerebral edema
(HACE)
• Ataxia + or – mental status
changes
• In the absence of AMS
• Failure of cerebral
autoregulation Cerbral
vasodialtaion  white
matter edema
High altitude pulmonary
edema (HAPE)
• Vasoconstriction of
pulmonary capillaries 
raised capillary hydrostatic P
 pulmonary edema
TONY SCARIA 2010
KMC
Rx of high altitude syndrome
• Immediate descent
• O2 therapy
• CCB
• Glucocorticoids
TONY SCARIA 2010
KMC

29-04-2018
c/c mountain sickness
• Peripheral chemoreceptors insensitive to hypoxia severe hypoxic
symptoms
• Widespread pulmonary vasoconstriction  right ventricular failure 
cor pulmonale
• Exaggerated other adaptive changes
TONY SCARIA 2010
KMC
Deep sea diving physiology
TONY SCARIA 2010
KMC

29-04-2018
• Pressure exerted by every 10m (33 feet) descent in water increases P
by 1 atm
TONY SCARIA 2010
KMC
• Therefore at depth partial pressure of each gas increases (daltons
law)
• As partial pressure of gas increases amount gas dissolved in tissue
also increases(henerys law)
• Divers are exposed to O2 N2 CO2 toxicity
TONY SCARIA 2010
KMC

29-04-2018
N2 toxicity or N2 narcosis
• CF similar to alcohol intoxication  rapture of depth
• N2 dissolved in body fluids & even more easily in to fat
• Dissolves in fatty substance in neuronal membrane
• Euphoria is earliest symptom
TONY SCARIA 2010
KMC
Caisson disease
• Decompression sickness
• Sudden lowering of atmospheric P
• Rapid ascend of SCUBA & deep sea divers
• N2 bubbles develop in body fluids
• Formation of bubble in skeletal muscle  bends most common symptom
• Microbubbles blocking pulmonary capillaries  shortness of breath
pulmonary edema  chokes
TONY SCARIA 2010
KMC

29-04-2018
Isocapnic buffering
TONY SCARIA 2010
KMC

Respiratory physiology REVISION NOTES PHYSIOLOGY

Empfohlen

Empfohlen

Weitere ähnliche Inhalte

Was ist angesagt?

Was ist angesagt? (20)

Ähnlich wie Respiratory physiology REVISION NOTES PHYSIOLOGY

Ähnlich wie Respiratory physiology REVISION NOTES PHYSIOLOGY (12)

Mehr von TONY SCARIA

Mehr von TONY SCARIA (20)

Kürzlich hochgeladen

Kürzlich hochgeladen (20)

Respiratory physiology REVISION NOTES PHYSIOLOGY