RESPIRATORY PHYSIOLOGY Anatomy review Pressures Atmospheric pressure Alveolar pressure (intrapulmonary pressure) Intrapleural pressure Boyle’s Law More volume=less pressure Less volume=more pressure.
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Transcript RESPIRATORY PHYSIOLOGY Anatomy review Pressures Atmospheric pressure Alveolar pressure (intrapulmonary pressure) Intrapleural pressure Boyle’s Law More volume=less pressure Less volume=more pressure.
RESPIRATORY PHYSIOLOGY
Anatomy review
Pressures
Atmospheric pressure
Alveolar pressure
(intrapulmonary
pressure)
Intrapleural pressure
Boyle’s Law
More volume=less
pressure
Less volume=more
pressure
Diaphragm is chief respiratory muscle
(80%)
Intercostal muscles are secondary (20%)
- Diaphragm is controlled by phrenic nerve
(C3,4,5)
- Range of movement: from 1 cm (normal
breathing) to 10cm in heavy breathing.
Parietal pleura attaches to diaphragm
Visceral pleura attaches to parietal pleura
(thin space in b/w filled with serous fluid)
Lungs attach to visceral pleura.
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Inspiration:
Before inspiration pressure in lung equals
atmospheric pressure: 760 mm Hg or 1 atm
Increasing the size of the lungs will cause
pressure to drop and air to rush in. How does
lung increase in size?
Boyle’s law: the pressure of a gas in a closed
container is inversely proportional to the volume
of the container.
- incr. in size of container pressure will decrease
pressure..
Intrapleural pressure is 756 mm Hg and during
inspiration (as diaphragm is pulling down) pressure
drops to 754 mm Hg.
External intercostals contract and pull rib cage up and
When volume increases, pressure inside lung
(alveolar, intrapulmonic pressure) drops from
760 to 758. A pressure gradient is established
between the atmosphere and the alveoli.
Air rushes in (pressure gradient) to alveoli from
atm.
Expiration: pressure in lungs is greater than
atm.
- diaphragm relaxes and dome shape muscle
pushes up (elasticity). Internal intercostals cause
a-p diameter to decrease
- lung pressure increases to 762. Air will flow
from higher to lower pressures.
Thoracic Volume and Inspiration
Thoracic Volume and Expiration
Changes in Thoracic Volumes
Factors Influencing Pulmonary
Ventilation
Airway Resistance:
Amount of drag air encounters in respiratory
passageways; not significant since airway diameters
are large and at terminal bronchioles gasses travel by
diffusion
Surface Tension:
At gas-liquid boundaries, liquids are more attracted to
each other (cohesiveness), surfacant at the alveoli
keeps water from being cohesive and allows alveoli to
be more functional (less energy needed for breathing)
Lung Compliance:
The distensibility of the lungs, ability to stretch;
higher compliance leads to better ventilation (fibrosis,
airway blockages, decreased surfacant, and
decreased thoracic cage flexibility lead to less
compliance)
Respiratory Volumes and
Capacities
Respiratory Volumes
Tidal Volume:
Inspiratory Reserve Volume:
The amount of air that can be inspired forcibly
beyond the tidal volume (2100-3200 mL)
Expiratory Reserve Volume:
The amount of air that moves in and out of the lungs
with a normal breath at rest (~500 mL)
The amount of air that can be expired forcibly beyond
a tidal expiration (1000-1200 mL)
Residual Volume:
The amount of air remaining in the lungs even after
the most forceful expiration (1200 mL)
Respiratory Capacities
Inspiratory Capacity:
Functional Residual Capacity:
Total amount of air remaining in lungs after a tidal
expiration; ERV + RV
Vital Capacity:
Total amount of air that can be inspired after a tidal
expiration; TV + IRV
Total amount of exchangeable air; TV + IRV + ERV
Total Lung Capacity:
Sum of all lung volumes
Volumes and Capacities
Dead Space
Anatomical dead space:
Alveolar dead space:
The volume of air found in the conduits of the
respiratory system NOT involved in gas exchange
Regions where alveoli cease to function due to
collapse or obstruction
Total dead space:
Alveolar dead space + Anatomical dead space
Non-Respiratory Air Movements
Cough
Laughing
Sneeze
Hiccups
Crying
Yawn
Regulation of Respiration
Medullary respiratory
center
Dorsal respiratory center
(DRC)
Ventral respiratory center
(VRC)
Pontine center
formerly called the
Pneumotaxic center
Hypothalamus
Gas Transport
Oxyhemoglobin: HbO2
Deoxyhemoglobin: HHb
Carbaminohemoglobin: HbCO2
External Respiration:
Oxygen and Carbon Dioxide concentration is
measured as a unit of pressure called partial
pressure (p)
Blood coming into the lungs (pulmonary arterycapillary) is deoxygenated blood= PO2 is 40 mm
Hg. PCO2 is 45 mm Hg
Air in the alveoli:
PO2= 105 mm Hg
PCO2= 40 mm Hg
Oxygen and Carbon dioxide are highly fat soluble
and can diffuse through membranes with ease.
As gases pass from the blood pass an alveolus
gases will diffuse from areas of higher
concentration to lower. (diffusion gradients)
PO2 in blood after passing alveolus is 105 mm Hg
PCO2 in blood after passing alveolus is 40 mm Hg
Internal respiration: Exchange of gases in
the tissues.
CO2 is a byproduct of cellular metabolism.
PCO2 in tissue space: 45 mm Hg
PO2 in tissue spaces: 40 mm Hg
O2 will diffuse into tissue spaces (105) and
CO2 will diffuse into blood (45)
Gas Transport at the Tissues
Carbon dioxide transported to and from the lungs
and tissues in three ways:
Dissolved in plasma 7%
Chemically bound to hemoglobin (carbaminohemoglobin)
23%
As Bicarbonate in plasma (Reaction between carbon
dioxide and water, catalyzed by carbonic anhydrase)
pH buffer system. 70% of CO2 is transported this way.
Chloride shift (Chloride anions diffuse into RBCs to
counteract bicarbonate anions leaving RBCs)
Process results in diffusion of Oxygen from RBC to
tissues and from Carbon dioxide from tissues to
RBCs
This process is reversed in the Lungs
At the Lungs
At the Tissues
Oxygen Transport
Molecular oxygen carried in blood or
bound to hemoglobin
HbO2- hemoglobin bound to oxygen
HHb + O2 -- HbO2 + H+
Hb can bind 4 oxygens; after first binding,
there is a higher affinity for other 3
Hemoglobin is fully saturated when all 4
heme sites bound to oxygen
Clinical corner
Eupnea - quiet breathing
Tachypnea - rapid breathing
Costal breathing - shallow
Diaphragmatic breathing - deep
Atelectasis - collapse or incomplete
expansion of lungs
Cheyne-Stokes respiration - irregular
breathing (increase/decrease in depth and
rapidity)
Laryngitis - inflammation of the vocal cords
Pleurisy - inflammation of the pleura Infant
respiratory distress syndrome (IRDS) - insufficient
surfactant produced, surface tension forces collapse of
the alveoli
Hypoxia - inadequate amount of oxygen is delivered to
body tissues anemic - to few RBCs, or RBCs with
inadequate hemoglobin stagnant - blood circulation is
impaired or blocked interference with gas exchange
Hypercapnia - apnea (breathing cessation) increase in
carbon dioxide levels in cerebrospinal fluid, causing pH
to decrease, exciting chemoreceptors to increase rate of
breathing (compensating)
Hypocapnia- low levels of CO2 in plasma and CSF due
to depth and rate of breath increase (hyperventilation)
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Chronic Obstructive Pulmonary Disease (COPD), common
features:
Patients with history of smoking
Dyspnea - difficult or labored breathing
Coughing and frequent pulmonary infection
Will develop respiratory failure
COPDs: Obstructive emphysema - permanent enlargement of the
alveoli, deterioration of alveolar walls
Chronic inflammation leads to lung fibrosis (lungs lose their
elasticity)
Victims sometimes called "pink puffers" - breathing is labored, but
doesn't become cyanotic because gas exchange remains adequate
until late in the disease
Chronic bronchitis - inhaled irritants lead to chronic excessive
mucus production by the mucosa of lower respiratory passageways
and inflammation and fibrosis of that mucosa
Victims sometimes called "blue bloaters" - hypoxia and carbon
dioxide retention occur