PHYSIOLOGY OF RESPIRATION
OBJECTIVES
The student should be able to:
Explain how partial gas pressures are calculated, and their
significance in measurement of arterial blood gases.
Describe gas exchange in alveoli and tissues.
Define standard lung volumes and capacities and show how they
are measured by spirometry.
Explain how pulmonary function test relate to pulmonary
disorders
Differentiate between alveolar ventilation and pulmonary
ventilation.
Define anatomic dead space and physiological dead space in
healthy and diseased person.
Differentiate between obstructive and restrictive lung diseases.
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GAS EXCHANGE IN THE
LUNGS
• Dalton’s Law:
– Total pressure of a gas mixture is equal to the sum of the
pressures that each gas in the mixture would exert
independently.
• Partial Pressure of A Gas:
– The pressure that a particular gas exerts independently.
• PATM = PN2 + P02 + PC02 + PH20= 760 mm Hg.
– 02 is humidified = 105 mm Hg.
• H20 contributes to partial pressure (47 mm Hg).
– P0 = 150 mm Hg.
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– PC0 = 40 mm Hg.
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PARTIAL PRESSURES OF GASES
IN INSPIRED AIR AND
ALVEOLAR AIR
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GAS EXCHANGE
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GAS EXCHANGE
• Gas exchange occurs by diffusion.
• Partial pressure of oxygen in the alveoli is higher than the
pulmonary vein. The pulmonary vein carry the blood to the
heart and then, blood carried to the systemic arteries. The
oxygen in the systemic capillaries has a high partial pressure
(100 mmHg) compared to tissue cells, (40 mmHg).
• The partial pressure for carbon dioxide in the systemic
capillaries is low (40 mmHg) compared to the tissue cells (46
mmHg). Then, blood is carried by veins back to the heart and
then the lungs. The partial pressure of carbon dioxide is higher
in the pulmonary artery than the alveoli.
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PULMONARY CIRCULATION
• Rate of blood flow through the pulmonary circulation equal rate of
flow through the systemic circulation.
– Driving pressure is about 10 mm Hg.
• Pulmonary vascular resistance is low.
• Autoregulation:
– Pulmonary arterioles constrict when alveolar P0 2 decreases.
• In a fetus:
– Pulmonary circulation has a higher vascular resistance, because
the lungs are partially collapsed.
• After birth, vascular resistance decreases:
– Opening the vessels as a result of sub-atmospheric intrapulmonary
pressure.
– Dilation of pulmonary arterioles in response to increased alveolar
P02.
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PULMONARY FUNCTION
TESTS
• Spirometry is a method of assessing lung function by
measuring the volume(amount) & flow(speed) of air the
patient can expel from the lungs after a maximal inspiration.
• Subject breathes into a closed system in which air is trapped
within a bell floating in H20.
• The bell moves up when the subject exhales and down when
the subject inhales.
• Measurement of lung volumes provides a tool for
understanding normal function of the lungs as well as disease
state.
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Spirometry
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LUNG VOLUMES AND
CAPACITIES
Description Average
Value
Tidal volume (TV) Volume of air entering or leaving lungs 500 ml
during a single breath
Inspiratory Extra volume of air that can be maximally 3000 ml
reserve volume inspired over and above the typical resting
(IRV) tidal volume
Inspiratory Maximum volume of air that can be 3500 ml
capacity (IC) inspired at the end of a normal quiet
expiration (IC =IRV + TV)
Expiratory Extra volume of air that can be actively 1000 ml
reserve volume expired by maximal contraction beyond the
(ERV) normal volume of air after a resting tidal
volume
Residual volume Minimum volume of air remaining in the 1200 ml
(RV) lungs even after a maximal expiration
LUNG VOLUMES AND
CAPACITIES
Description Average
Value
Functional residual Volume of air in lungs at end of 2200 ml
capacity (FRC) normal passive expiration
(FRC = ERV + RV)
Vital capacity (VC) Maximum volume of air that can 4500 ml
be moved out during a single
breath following a maximal
inspiration (VC = IRV + TV +
ERV)
Total lung capacity Maximum volume of air that the 5700 ml
(TLC) lungs can hold (TLC = VC +
RV)
Forced expiratory Volume of air that can be expired
volume in one second during the first second of
(FEV1) expiration in a VC determination
ANATOMICAL DEAD SPACE
• As we breath in, all air does not go to alveoli for gas
exchange but some of the air remains in trachea and
bronchi [conducting zone] and does not take part in gas
exchange.
• It is called ‘Anatomic Dead Space’.
• Normally, there is no alveolar dead space in healthy person.
• In case of disease, where alveoli are abnormal e.g.
pneumonia, gas exchange does not take place in affected
alveoli, therefore, alveolar dead space is there.
• Physiological Dead Space
= Anatomical Dead Space + Alveolar Dead Space
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PULMONARY VENTILATION
• Pulmonary Ventilation or Minute Ventilation
• It is volume of air breathe in and out in one (1)
min.
• Pulmonary Ventilation=
= Tidal Volume X Respiratory Rate
= 500 ml/breath X 12breath/min =
6000 ml/min or 6 L/min
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ALVEOLAR VENTILATION
Alveolar Ventilation is Less Than Pulmonary Ventilation
Because of the Presence of Dead Space
• Alveolar ventilation: is volume of air reaching the alveoli/min.
• Alveolar air that takes part in gas exchange.
Alveolar Ventilation= F x (TV- DS).
= 12x (500-150)
= 4200 ml/min
F = frequency ( 12 breaths/min.)
TV = tidal volume.(500 ml)
DS = dead space. (150 ml)
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AIRWAY RESISTANCE
• Primary determinant of resistance to airflow is the radius of the
conducting airway.
• Autonomic Nervous System: controls contraction of smooth
muscle in walls of bronchioles (changes the radii).
• Pulmonary Disorders:
Chronic Obstructive Pulmonary Disease (COPD): abnormally
increases airway resistance. Expiration is more difficult than
inspiration due to obstruction of bronchi.
Examples: Chronic bronchitis, Asthma and Emphysema.
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PULMONARY DISORDERS
Lung disease is often divided into two broad categories:
1. Chronic Obstructive Pulmonary Diseases:
Asthma:
• Caused by inflammation and mucus secretion. Inflammation
contributes to increased airway responsiveness to agents that
promote bronchial constriction.
Emphysema:
• Chronic progressive condition that reduces surface area for gas
exchange (Alveolar tissue is destroyed)
• Cigarette smoking stimulates macrophages and leukocytes to
secrete protein digesting enzymes that destroy tissue.
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PULMONARY DISORDERS
2. Chronic Restrictive Pulmonary Diseases:
• Lungs are smaller than normal, therefore, vital capacity and
total lung capacity are decreased as lungs can not expand.
• Examples: abnormalities of the spine and chest and diseases
within the lungs that make them less elastic (“stiffer”), such
as pulmonary fibrosis.
Pulmonary fibrosis:
• Normal structure of lungs disrupted by accumulation of
fibrous connective tissue proteins (Anthracosis).
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FVC - Forced vital capacity:
The total volume of air that can be forcibly exhaled in one breath
FEV1 - Forced expiratory volume in one second:
The volume of air expired in the first second of the blow
FEV1/FVC ratio:
The fraction of air exhaled in the first second relative to the total volume exhaled
Normal Restrictive diseases
FEV1/FVC: > 0.7 FEV1/FVC: > 0.7
Obstructive diseases: FEV1/FVC: < 0.7
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PULMONARY DISORDERS
Sudden Infant Death Syndrome (SIDS)
• In SIDS, Apnea occurs (stoppage of breathing) Infant is unable
to recover from Apnea and death occurs.
• SIDS or crib death – It is the leading cause of death in the first
year of life, usually 2-4 months old infant is found dead in his
or her crib for no apparent reason.
• Cause is not clear but different possibilities may be a reason:
- Baby forgets to breath – as respiratory control mechanism are
immature.
- Abnormal lung development.
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DISORDERS CAUSED BY CHANGES IN
PARTIAL PRESSURES OF GASES
• Nitrogen Narcosis:
– At sea level nitrogen is physiologically inert.
– Under hyperbaric conditions:
• Nitrogen dissolves slowly.
– Can have deleterious effects.
» Resembles alcohol intoxication.
• Decompression Sickness:
– Amount of nitrogen dissolved in blood as a diver ascends
decreases due to a decrease in PN . 2
• If occurs rapidly, bubbles of nitrogen gas can form in tissues and
enter the blood.
– Block small blood vessels producing the “bends.”
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DISORDERS CAUSED BY CHANGES IN PARTIAL
PRESSURES OF GASES
Hypoxia
• Condition of having insufficient O2 at the cellular level
• Categories
• Hypoxic Hypoxia: occurs in lung disease, at high altitude.
• Anemic Hypoxia: occurs in Anemia and CO Poisoning.
• Circulatory Hypoxia: occurs in slow circulation e.g. Cardiac
failure.
• Histotoxic Hypoxia: occurs when tissues are not able to use O2.
It occurs in Cyanide Poisoning.
Hyperoxia
• Condition of having an above-normal arterial P O2
• Can only occur when breathing supplemental O2
• Can be dangerous
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DISORDERS CAUSED BY CHANGES IN PARTIAL
PRESSURES OF GASES
Hyperventilation:
Increased pulmonary ventilation in excess of metabolic requirements,
resulting in decrease PCO2.
Hypoventilation:
Decreased pulmonary ventilation in relation to metabolic
requirements, resulting in increased PCO2 and respiratory acidosis.
Hypercapnia:
Condition of having excess CO2 in arterial blood. Caused by
hypoventilation.
Hypocapnia:
Below-normal arterial PCO2 levels. Brought about by hyperventilation
which can be triggered by: Anxiety states, Fever and Aspirin
poisoning.
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PNEUMOTHORAX
• Puncture in the chest wall as a result of trauma will allow air to
enter the pleural cavity and the transmural pressure gradient will
be disturbed causing collapse of the lung.
• Collapse of the lung creates a condition known as pneumothorax.
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CLINICALLY IMPORTANT RESPIRATORY
STATES
Eupnea: Normal breathing rate and tidal volume for a typical person at rest.
Apneusis: termination of breathing at end-inspiration requiring continual active
contraction of respiratory inspiratory muscles.
Apnea: Transient cessation of breathing. During apnea, the muscles of respiration are
not actively contracting.
Dyspnea: Difficult breathing.
Tachypnea: High frequency ventilation (f> 20 bpm at rest) characterized by low tidal
volume (rapid shallow breathing). Tachypnea is a frequent sign of respiratory distress.
Respiratory arrest: Permanent cessation of breathing.
Suffocation: O2 deprivation as a result of inability to breath oxygenated air.
Asphyxia: Lack O2 in the tissue caused by lack of O2 in the air.
Cyanosis: Blueness of skin resulting from insufficiency oxygenated blood in the arteries
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REFERNCES
• Human physiology by Lauralee Sherwood, Seventh edition.
• Text book physiology by Guyton &Hall,11th edition.
• Text book of physiology by Linda S. Contanzo, Third edition.
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