Physiology of respiratory system

1. RESPIRATORY PHYSIOLOGY
LUNG VOLUMES AND CAPACITIES
VENTILATION PERFUSION

2. LUNG VOLUMES AND CAPACITIES

3. INTRODUCTION
• Volumes are most commonly measured by
spirometry and capacities are then calculated as the
sum of specific volumes
• The lung volumes tend to vary depending on the
depth of respiration, gender, age as well as in certain
respiratory diseases.

4. LUNG VOLUMES
1. TIDAL VOLUME (TV)– Volume of air inspired and expired
during a relaxed breathing cycle. Normal value is 500ml or 5-
10 ml/kg
2. RESIDUAL VOLUME (RV) – Volume remaining in the lung
after a maximal expiratory effort. Normal value is 1200ml
3. INSPIRATORY RESERVE VOLUME (IRV)– Volume of air that
can be inspired with maximal effort above the normal
resting end expiratory position of a TV. Average value is
3000ml
4. EXPIRATORY RESERVE VOLUME (ERV)- Volume of air that can
be forcibly exhaled between the resting end expiratory
volume and residual volume. Average value is 1100ml
5. FORCED EXPIRATORY VOLUME IN 1 SECOND (FEV1)- The
volume of air that can be exhaled in 1 second with maximal
effort from the point of maximal inspiration. Normally it is
80% of forced vital capacity.

5. LUNG CAPACITIES
1. VITAL CAPACITY (VC) – The maximum volume of air exhaled
from the point of maximum inspiration.
VC = TV + IRV + ERV Normal value – 4600ml
2. FUNCTIONAL RESIDUAL CAPACITY(FRC) – Amount of air in
the lung at the end of a quiet exhalation.
FRC = ERV + RV Normal value – 2300ml
3. TOTAL LUNG CAPACITY(TLC) – Total volume of air in the
lungs after a maximal inspiration.
TLC = TV + IRV + ERV + RV Normal value 5800ml

6. 4. INSPIRATORY CAPACITY(IC) – The maximum volume of air
inhaled after normal expiration.
IC = TV + IRV Normal value 3500ml
5. EXPIRATORY CAPACITY( EC) – The maximum volume of air
that can be expired after normal inspiration
EC = TV + ERV Normal value 1600ml
6. FORCED VITAL CAPACITY (FVC) – The volume of air that can
be exhaled with maximal effort from TLC

7. LUNG VOLUMES AND CAPACITIES

9. VARIATIONS IN VITAL CAPACITY
• Physiological variations:
1. Gender – Females < Males
2. Body built – It is more in heavily built persons.
3. Posture – More in standing and less in lying.
4. Athletes – More than average people.
5. Occupation – Less in sedentary jobs, more in people who play musical
wind instruments like flute
• Pathological variations: Vital capacity is decreased in :
1. Asthma
2. Emphysema
3. Weakness or paralysis of respiratory muscles.
4. Pulmonary congestion
5. Pneumonia
6. Haemothorax
7. Pyothorax
8. Hydrothorax
9. Pulmonary oedema
10. Pulmonary tuberculosis

10. FACTORS KNOWN TO ALTER FRC
• Body habitus: FRC is directly proportional to height. Obesity, however, can
markedly decrease FRC (from reduced chest wall compliance and
increased abdominal pressure on the diaphragm). Kyphosis can adversely
impact both lung volumes and rib mobility.
• Sex: FRC is reduced by about 10% in females compared with males.
• Increased intraabdominal pressure: Decreased FRC is associated with
laparoscopic procedures, pregnancy, and significant ascites due to
increased pressure on the diaphragm from the laparoscopy
pneumoperitoneum, the gravid uterus, or from ascitic fluid, respectively.
• Posture: FRC decreases as a patient is moved from an upright to a supine or
prone position. This is the result of reduced chest compliance as the
abdominal contents push up againstthe diaphragm. The greatestchange
occurs between 0° and 60° of inclination.
• Lung disease: Decreased compliance of the lung, chest, or both is
characteristic of restrictive pulmonary disorders, all of which are
associated with a low FRC.
• Diaphragmatic tone: This normally contributes to FRC, and its contribution
is evident with unilateral or bilateral phrenic nerve paralysis.

11. CLOSING CAPACITY AND CLOSING VOLUME
• Closing capacity is the sum of closing volume and
residual volume
• Closing volume is the lung volume below which small
airways begin to close (or atleast cease to contribute to
expiratory gas) during expiration.
• Closure of small airways in the basal portions of the
lung during deep expiration is a normal phenomenon
due to gravity dependent increase in pleural pressure
at the bases and due to the lack of parenchymal
support in the distal airways.
• Normal values for closing capacity in seated healthy
young adults is 15-20% of vital capacity

12. Closing capacity is
normally well below FRC ,
but rises steadily with age .
This increase is probably
responsible for the normal
age related decline in
arterial O2 tension. For
individuals at an average
age of 44 years, closing
capacity equals FRC in the
supine position; by age 66,
closing capacity equals or
exceeds FRC in the upright
position in most
individuals. Unlike FRC,
closing capacity is
unaffected by posture.
Closing capacity also
approaches or exceeds FRC
in morbid obesity.

13. FORCED EXPIRATORY
VOLUME
SIGNIFICANCE OF FEV1/FVC
• IN OBSTRUCTIVE DISEASES
➢ FEV1 reduced < 80% predicted
normal
➢ FVC is reduced but to a lesser
extent than FEV1
➢ FEV1/FVC ratio reduced < 0.7
• IN RESTRICTIVE DISEASES
➢ FEV1 reduced < 80% predicted
normal
➢ FVC reduced< 80% predicted
normal
➢ FEV1/FVC ratio normal >0.7
It is the volume of air that
can be expired forcefully in
a given unit of time.
FEV1 = Volume of air
expired forcefully in 1
second.
FEV can be used to
diagnose restrictive and
obstructive lung diseases
The ratio of the forced
expiratory volume in the
first second of exhalation
(FEV1 ) to the total forced
vital capacity (FVC) is
proportional to the degree
of airway obstruction.

14. AIRWAY RESISTANCE
At low lung volumes, loss
of radial traction increases
the contribution of small
airways to total resistance;
airway resistance becomes
inversely proportional to
lung volume . Increasing
lung volume up to normal
with positive end-
expiratory pressure (PEEP)
can reduce airway
resistance.

15. ❖INTRUMENTS used to measure lung function
• Spirometer • Respirometer • Plethysmograph •
Wright Peak Flow Meter
❖ BEDSIDE PULMONARY FUNCTION TEST
• Breath holding test
• Single breath test
• Match blowing test
• Cough test
• Forced expiratory time
• Whistle blowing test

17. VENTILATION PERFUSION

18. VENTILATION
• Ventilation is usually measured as the sum of all exhaled gas
volumes in 1 min (minute ventilation).
• MINUTE VENTILATION = RESPIRATORY RATE X TIDAL VOLUME
• For the average adult at rest, minute ventilation is about 5
L/min.
• Not all of the inspired gas mixture reaches alveoli; some of it
remains in the airways and is exhaled without being
exchanged with alveolar gases. The part of the VT not
participating in alveolar gas exchange is known as dead space
• Alveolar ventilation is the volume of inspired gases actually
taking part in gas exchange in 1 min.
• ALVEOLAR VENTILATION = RESPIRATORY RATE X (TIDAL
VOLUME – DEAD SPACE)

19. DEAD SPACE
Dead space is actually
composed of gases in non
respiratory airways(anatomic
dead space) and alveolithat
are not perfused (alveolar
dead space). The sum of the
two componentsis referred to
as physiological deadspace.
In the upright position,dead
space is normally about 150
mL for most adults
(approximately2 mL/kg) and
is nearly all anatomic.Dead
space can be affected by a
variety of factors.

20. DISTRIBUTION OF VENTILATION
• Alveolar ventilation is unevenly distributed in the lungs.
• The right lung receives more ventilation than the left lung (53% vs 47%),
and the lower (dependent) areas of both lungs tend to be better
ventilated than the upper areas because of a gravitationally induced
gradient in intrapleural pressure (transpulmonary pressure).
• Pleural pressure decreases about 1 cm H2O (becomes less negative) per 3-
cm decrease in lung height. This difference places alveoli from different
areas at different points on the pulmonary compliance curve .
• Because of higher transpulmonary pressure, alveoli in upper lung areas
are near-maximally inflated and relatively noncompliant, and they
undergo little expansion during inspiration. In contrast, the smaller alveoli
in dependent areas have lower transpulmonary pressure, are more
compliant, and undergo greater expansion during inspiration
• Airway resistance can also contribute to regional differences in pulmonary
ventilation.

21. DISTRIBUTION OF VENTILATION

22. PULMONARY PERFUSION
• Of the approximately 5 L/min of blood flowing through the lungs, only
about 70 to 100 mL at any one time are within the pulmonary capillaries
undergoing gas exchange.
• Although capillary volume remains relatively constant, total pulmonary
blood volume can vary between 500 mL and 1000 mL.
• Large increases in either cardiac output or blood volume are tolerated
with little change in pressure as a result of passive dilation of open vessels
and recruitment of collapsed pulmonary vessels.
• Small increases in pulmonary blood volume normally occur during cardiac
systoleand with each normal (spontaneous) inspiration.
• A shift in posture from supine to erect decreases pulmonary blood volume
(up to 27%). Trendelenburg positioning has the opposite effect.
• Changes in systemiccapacitance also influence pulmonary blood volume:
Systemic venoconstriction shifts blood from the systemicto the
pulmonary circulation, whereas vasodilation causes a pulmonary-to-
systemicredistribution. In this way, the lung acts as a reservoir for the
systemiccirculation.

23. • Hypoxia is a powerful stimulus for pulmonary vasoconstriction
(HPV).
• Both pulmonary arterial (mixed venous) and alveolar hypoxia
induce vasoconstriction, but the latter is a more powerful stimulus.
• This response seems to be due to either the direct effect of hypoxia
on the pulmonary vasculature or increased production of
leukotrienes relative to vasodilatory prostaglandins.
• Inhibition of nitric oxide production may also play a role.
• Hypoxic Pulmonary Vasoconstriction - is an important physiological
mechanism in reducing intrapulmonary shunting and preventing
hypoxemia.
• Hyperoxia has little effect on the pulmonary circulation in normal
individuals.
• Hypercapnia and acidosis have a constrictor effect, whereas
hypocapnia causes pulmonary vasodilation.

24. DISTRIBUTION OF PULMONARY PERFUSION
• Pulmonary blood flow is not uniform.
• Regardless of body position, dependent areas of the lung
receive greater blood flow than nondependent areas. This
pattern is the result of a gravitational gradient of 1 cm
H2O/cm lung height.
• The normally low pressures in the pulmonary circulation allow
gravity to exert a significant influence on blood flow.
• Also, in vivo perfusion scanning in normal individuals has
shown an “onion-like” layering distribution of perfusion, with
reduced flow at the periphery of the lung and increased
perfusion toward the hilum.
• Although the pulmonary perfusion pressure is not uniform
across the lung, the alveolar distending pressure is relatively
constant.
• The interplay of these pressuresresults in the division of the
lung into four distinct zones (ie, the West zones).

25. ZONES OF LUNG
• In zone 1 (PA > Pa > PV), alveolar pressure (PA) is greater
than both the arterial pulmonary pressure (Pa) and venous
pulmonary pressure (PV), resulting in obstructionof blood
flow and creation of alveolar dead space. West zone 1 is
fairly small in a spontaneouslybreathing individual, but it
can enlarge during positive pressure ventilation.
• In zone 2 (Pa > PA > PV), Pa is greater than PA, but PV
remains less than both, resulting in blood flow that is
dependent on the differential between Pa and PA.
• In zone 3 (Pa > PV > PA), both Pa and PV are greater than PA,
resulting in blood flow independent of the alveolar pressure.
• Zone 4, the most dependent part of the lung, is where
atelectasis and interstitial pulmonary edema occur, resulting
in blood flow that is dependent on the differential between
Pa and pulmonary interstitial pressure.

26. ZONES OF LUNG PERFUSION

27. VENTILATION PERFUSION RATIO
• Alveolar ventilation is normally about 4 L/min, and
pulmonary capillary perfusion is 5 L/min. The overall V/Q
ratio is about 0.8.
• The V/Q ratio can range from 0 (no ventilation) to infinity (no
perfusion). The former is referred to as intrapulmonary shunt,
whereas the latter constitutesalveolar dead space.
• V/Q ratio normally ranges between 0.3 and 3. The majority of
lung areas, however, are close to 1.
• Because perfusion increases at a greater rate than ventilation,
nondependent (apical) areas tend to have higher V/Q ratios
than do dependent (basal) areas.

28. SIGNIFICANCE OF V/Q RATIO
• The importance of V/Q ratios relates to the efficiency with which
lung units resaturate venous blood with O2 and eliminate CO2 .
• Pulmonary venous blood from areas with low V/Q ratios has a
low O2 tension and high CO2 tension. Blood from these units
tends to depress arterial O2 tension and elevate arterial CO2
tension.
• The arterial CO2 tension often decreases from a hypoxemia-
induced reflex increase in alveolar ventilation. An appreciable
compensatory increase in O2 uptake cannot take place in
remaining areas where V/Q ratio is normal because pulmonary
end-capillary blood is usually already maximally saturated with
O2.
• COVID-19 is associated with increased ventilation–perfusion
mismatch, resulting in reduced oxygenation. Alveolar and
interstitial damage contribute to impaired ventilation of alveoli.
Additionally, prothrombotic effects of COVID-19 contribute to the
development of pulmonary emboli, reducing lung perfusion and
increasing dead space ventilation.

29. SHUNTS
• Shunting denotes the process whereby desaturated, mixed
venous blood from the right heart returns to the left heart
without being oxygenated in the lungs.
• The overall effect of shunting is : decrease (dilute) arterial
O2 content. this type of shunt is referred to as right-to-left.
• Intrapulmonary shunts are often classified as absolute or
relative.
• An absolute shunt refers to anatomic shunts and lung units
where is V/Q ratio is zero.
• A relative shunt is an area of the lung with a low V/Q ratio.
• Clinically, hypoxemia from a relative shunt can usually be
partially corrected by increasing the inspired O2
concentration. Hypoxemia caused by an absolute shunt
cannot achieve such correction.

30. RESPIRATORY FUNCTION DURING ANAESTHESIA
❖ Lung volume and respiratory mechanics during anesthesia
• FRC is reduced by 0.8 to 1.0L by changing body position from
upright to supine, and there is another 0.4-0.5L decrease after
induction of anaesthesia.
• Anaesthesia causes a fall in FRC whether breathing is
controlled or spontaneousand whether anaesthetic is
inhalational or intravenous.
• Compliance of the total respiratory system is reduced during
anaesthesia due to increased resistance from volume loss
• Cranial shift of the diaphragm and a decrease in transverse
diameter of the thorax contribute to lowered functional
residual capacity (FRC) during anesthesia

31. ❖ Atelectasis and airway closure during anesthesia
• Atelectasis appears in approximately 90% of all patients, who
are anesthetized. It is seen during spontaneous breathing and
after muscle paralysis and with either intravenous or inhaled
anesthetics. 15-20% of lung is atelectatic during uneventful
anesthesia, before surgery has commenced.
• After thoracic surgery and cardiopulmonary bypass, more
than 50% of the lung can be collapsed even several hours
after surgery.
• The amount of atelectasis decreases toward the apex, which
is mostly spared.
• Obese patients showing larger atelectatic areas .
• The atelectasis is independent of age, with children and young
people showing as much atelectasis as elderly patients.
• Patients with COPD showed less atelectasis. The mechanism
being airway closure precedes alveolar collapse.

32. ❖ Distribution of ventilation and blood flow during anesthesia
• Ventilation was shown to be distributed mainly to the
upper lung regions, and there was a successive decrease
down the lower half of the lung.
• PEEP increases dependent lung ventilation in anesthetized
subjects.
• Thus, restoration of overall FRC towards awake level
returns gas distribution toward the awake pattern.
• During anaesthesia , a successive increase in perfusion
occurs from upper towards lower regions, with a slight drop
in the lowermost portion of the lung.
• PEEP redistributes blood flow towards dependent lung
regions, which may increase shunt through atelectatic lung.
• Anaesthetic agents may also reduce hypoxic pulmonary
vasoconstriction

33. ❖Dead space, shunt, and ventilation perfusion
relationships
• Both CO2 elimination and oxygenation of blood are
impaired in patients during anesthesia.
• The impended CO2 elimination can be attributed to
reduced minute ventilation because of respiratory
depression or increased dead space ventilation.
• Anatomic dead space is unchanged, indicating that the
“alveolar” dead space must have increased during
anesthesia.
• The impaired CO2 elimination is most easily corrected
by increasing the ventilation.
• The impairment is arterial oxygenation during
anesthesia is more marked with increased age, obesity
and smoking.

34. ❖Effects of anesthetics on respiratory drive
• Spontaneousventilation is frequently reduced
during anesthesia because inhaled
anesthetics, as well as barbituratesreduce
sensitivity to CO2
• Anesthesia also reduces the response to
hypoxia because of effects on the carotid body
chemoreceptors

35. FACTORS INFLUENCING RESPIRATORY FUNCTION
DURING ANAESTHESIA
❖ Breathing
• During spontaneous breathing, the lower, dependent portion of the
diaphragm moved the most, whereas with muscle paralysis, the upper,
nondependent part showed the largest displacement.
❖ Body position
• FRC is dramatically reduced by the combined effect of the supine position
and anesthesia. Steep head down position can reduce FRC considerably.
❖ Age
• Arterial oxygenation is less efficient with increasing age of the patient.
• There appears to be increasing V /Q mismatchwith age, with enhanced
perfusion of low V/Q regions both in awake subjects and when they are
subsequently anesthetized.
• Major cause of impaired gas exchange during anesthesia at ages younger
than 50 years is shunt, whereas at higher ages V/Q mismatchbecomes
increasingly important.

36. ❖ Obesity
• Obesity worsens the oxygenation of blood. A major explanation appears
to be a markedly reduced FRC, resulting in greater propensity to airway
closure
❖ Pre-existing lung disease
• Smokers and patients with lung disease have more severe impairment of
gas exchange in the awake state than healthy subjects do and this further
deteriorates during anaesthesia.
❖ Regional anesthesia
• Ventilatory effects of regional anesthesia depend on the type and
extension of motor blockade.
• With extensive blocks that include all the thoracic and lumbar segments,
inspiratory capacity is reduced by 20% and expiratory reserve volume
approaches zero. Diaphragmaticfunction however, is often spared

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