Anatomy and Physiology Exam 4 - Respiratory Physiology

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respiratory physiology

Respiration

Process of exchanging O2and CO2between the body & the external environment
•Involuntary
•Responsive the changes in blood chemistry, mood, activity, NT & hormone release, alertness
Occurs in 2 stages:
•Gas exchange
•Cellular respiration

Conducting Zone

Conducts air to respiratory zone
-No gas exchange between lung and blood
Must function to:
-Warm and humidify inspired air
-Distribute air evenly to deeper parts of lungs
-"Cleanse" air

Mucociliary transport system

Whether a foreign substance gets into the mucous is a matter of size.
Generally, particles < 1 um make it to the alveolus.
This is an important issue in drug delivery and toxicology.

Respiratory Zone

defined by the presence of alveoli
-Gas exchange
Must be:
-thin-walled
-moist, so gases can dissolve in fluids
-richly supplied with blood vessels

Blood-gas interface

site of exchange
-extremely thin
-type 1 alveolar cell: make up the alveolar surface
-type 2 alveolar cell: secrete surfactant (polar and non polar- breaks up surface tension and prevents small aveoli from collapsing) (RDS in premature infant is lack of surfactant)

Thoracic Cavity

•Thoracic cage:
-12 ribs
-sternum
-Internal and external intercostalmuscles (lie between the ribs)
•Diaphragm
-separates from abdominal cavity

Pleurae

•Thin, double-layered serous membrane
•Parietal pleura
-Covers the thoracic wall and superior face of the diaphragm
-Continues around heart and between lungs
•Visceral, or pulmonary, pleura
-Covers the external lung surface

Stages of Respiration

1) Venilation: exchange of air between atmosphere and alveoli by bulk flow
2) Exchange of O2 and CO2 between alveolar air and blood in lung capillaries by diffusion
3)Transport of O2 and CO2 through pulmonary and systemic circulation by bulk flow
4) Exchange of O2 and CO2 between blood in tissue capillaries and cells in tissues by diffusion
5) Cellular utilization of O2 and production of CO2

Muscles of inspiration

-Sternocleidomastoid muscles
-External intercostal muscle
-Diaphragm

Muscles of expiration

-Internal intercostal Muscle
-External oblique muscle
-Rectus abdominis muscle
-diaphragm relaxes

Pressure relationships in the thoracic cavity

•Alveolar pressure (Palv)
-Pressure inside of the alveoli
•Pleural pressure (Ppl)
-Pressure within the pleural cavity (between lung & chest wall)
•Atmospheric pressure(Patm)
-Pressure exerted by the air surrounding the body
•If pressure inside the lungs and alveoli decreases, outside air will be pushed into the airways

Inspiration and Expiration pressure relationships..

Inspiration- Palv lower than Patm
Expiration- Patm lower than Palv

Boyle's Law

•The relationship between the pressure and volume of gases P1V1= P2V2
-P=pressure of a gas in mm Hg
-V=volume of a gas in cubic millimeters
-Subscripts 1 and 2 represent the initial and resulting conditions, respectively

Transpulmonary pressure

the difference between the intrapleural pressure and the intra-alveolar pressure

Transplural pressure

the difference in pressures between the inside and outside of a structure: Ptm=Pi-Po. Positive, pressure greater on outside; negative, pressure is greater on inside, zero=resting volume

Pressure at rest..

Intrapleural(Pip) = -4
Alveolar (Palv) = 0
Transpulmonary(PTP) = 4
Chest wall (Pcw) = -4

inspiration sequence of events

1)inspiration muscles contract- diaphragm descends- rib cage rises
2)thoracic cavity volume increases
3)lungs stretched; intrapulmonary volume increases
4)intrapulmonary pressure drops (so air can travel down gradient)
5)air flows into lungs down its pressure gradient until intrapulmonary pressure is 0 (equal to atmospheric pressure)

Expiration sequence of events

1) inspiratory mucles relax- diaphragm rises- rib cage descends due to recoil of costal cartilages
2)thoracic cavity volume decreases
3)elastic lungs recoil passively; intrapulmonary volume decreases
4)intrapulmonary pressure rises (t0 +1 mm Hg)
5) Air flows out of lungs down its pressure gradient until intrapulmonary pressure is 0

Elasticity in the lung

•Important feature of elastic material is that it recoils back into original position after being stretched
•Compliance: how easily a lung can be stretched or inflated (inversely related to elastic recoil)

Concept of Compliance

*Lung compliance= 1/lung recoil
*Compliance changes with disease states
*Emphysema shows high compliance, low recoil (expiration difficult)
*Fibrosis slow low compliance (inspiration difficult)

Factors the determine lung compliance

*Stretchability of lung tissues (elasticity)
*Surface tension within the alveoli - surface tension tends to cause smaller alveoli to collapse
*The lung produces a natural surfactant to reduce surface tension
*Increased pressure with smaller radius

airway resistance

•Airway resistance is a ratio of the change in pressure (mouth ->aveoli) to the volume of air taken in (airflow)
•Same dynamics as with blood flow-R is determined by r4, and smooth muscle determines r.
•β2 receptors: Dilate bronchioles and relax smooth muscle in walls of airway

Tidal volume

Amount of air that moves in and out of the lungs during a normal breath

Inspiratory reserve volume

Amount of air that can be forcefully inhaled after a normal tidal volume inhalation

Expiratory reserve volume

Amount of air that can be forcefully exhaled after a normal tidal volume exhalation

residual volume

The amount of air that remains in the lungs after a person exhales as forcefully as he or she can

inspiratory capacity

TV + IRC, Max amount of air that can be inspired after a normal expiration

functional residual capacity

ERV + RV, volume of gas remaining in the lungs at normal resting expiration

vital capacity

The maximum volume of air that a respiratory system can inhale and exhale.

total lung capacity

The maximal volume of air that the lungs can contain. Total lung capacity is the sum of the vital capacity and the residual volume

Alveolar ventilation

amount of air reaching the alveoli each minute. The point is: to increase alveolar ventilation, increasing depth of respiration is more effective than increasing the frequency of respiration. respiratory rate x tidal volume = minute ventilation

Pulmonary blood supply to lungs

•Pulmonary arteries -supply systemic venous blood to be oxygenated
-Branch profusely, along with bronchi
-Ultimately feed into the pulmonary capillary network surrounding the alveoli
-High flow, low pressure, low resistance
•Pulmonary veins
-carry oxygenated blood from respiratory zones to the heart
*Pulmonary blood pressure is relatively low
*As cardiac output increases, pulmonary blood pressure increases

Bronchial blood supply to lungs

•Bronchial arteries
-provide systemic (oxygenated) blood to the lung tissue itself
-Arise from aorta
-Supply all lung tissue except the alveoli

Ventilation perfusion inequality

Hypoxic Pulmonary vasoncnstriction
*Local blood flow decreased to match a local decrease in ventilation
*Local ventilation decreased to match a local decrease in perfusion
**Diversion of blood flow and air flow away from local area of disease to healthy areas of the lung

Oxygen carrying capacity

The volume of O2 in arterial blood:
1000 ml O2/5000 ml blood
or
10 ml O2/100 ml blood
*This is also called "The volume percent" Normal oxygenated blood is "20 volumes percent"

Hyperventilation

increased alveolar ventilation through increased respiratory rate or tidal volume, more O2 to alveoli and more CO2 removed (exercise)

Hypoventilation

reduced alveolar ventilation, less O2 to alveoli and less CO2 removed (respiratory depression)

Oxygen transport

*99% of O2 is bound
*Hemoglobin with O2 bound is called "oxyhemoglobin"
*Each hemoglobin binds 4 molecules of O2
*1 O2 binds to a ferrous iron atom (Fe2+) in the center of the heme group

Oxygen-hemoglobin dissociation curve

*Increase in heat- right shift- unloading of O at tissue
*Lower pH (higher acidity)- also shift right- drop O off at tissues

Transport of CO2 in the blood

* 10% dissolved
* 30% bound to hemoglobin (carbaminohemoglobin)
* 60% HCO3 in plasma
-action of carbonic anydrase
*As CO2 diffuses into the blood stream, it is absorbed by red blood cells before the majority is converted into H2CO3 by carbonic anhydrase (makes bicarbonate), an enzyme that is not present in the plasma. The H2CO3 dissociates into H+ and HCO−3. The HCO−3 moves out of the red blood cells in exchange for Cl− (chloride shift). The hydrogen ions are removed by buffers in the blood (Hb).
**At lungs:
1) CO2 leaves plasma > aveoli
2)CO2 unbinds Hb > aveoli
3)HC03 enters RBC, rxn occurs in reverse (CA) (reverse cl shift- CO2 released into aveoli)

Transport and exchange of O2 and CO2 at tissue

CO2 -> blood
O2 -> tissue

Central (Brain) Respiratory Centers

Two systems regulate
these respiratory centers
according to the metabolic needs of the body:
1. Central chemoreceptors
-located in the brain
stem
2. Peripheral chemoreceptors
-located in carotid aortic bodies

Central chemoreceptors that regulate ventilation

Ventilation is stimulated by H+ from H2CO3 that comes from CO2.
1. Respond to H+
2. Depend on the actions of the enzyme Carbonic Anhydrase
H2CO3 <-->CO2 + H2O

Peripheral chemoreceptors

Same location as baroreceptors
*Respond to:
O2 and H(CO2)
**Respond to PO2 not O2 content!
(because O2 contents also takes into account hemoglobin)

Effect of decreasing Po2

substantial drops to Po2 (to 60mm Hg) are needed before oxygen levels become a major stimulus for increased ventilation
1) decrease in inspired Po2
2) decrease in alveolar and arterial Po2
3)increase in peripheral chemoreceptor firing and respiratory muscle contractions
4) increase in ventilation

Effect of increasing PCO2

1) increase in alveolar and arterial Pco2 lead to..
2) increase in brain fluid PCO2 and H (thus increase in central chemoreceptors)** - increase in arterial H (thus increase in peripheral chemoreceptors)
3) Both increase respiratory muscles- thus increase ventilation!

Metabolic acidosis stimulates peripheral chemoreceptors

1) increase in production of non-CO2 acid
2) increase in arterial H concentration
3) thus increase in peripheral chemoreceptors firing and respiratory muscle contractions
4) increase in ventilation, decrease in alveolar PCo2 and decrease in arterial PCo2

Predicting metabolic vs. respiratory acidosis and alkalosis...

does the Co2 level predict the pH level?
-yes- respiratory problem
-no- metabolic problem

ex: pH= 7.3 low pCO2 levels
-metabolic acidosis
ex: pH= 7.5 low pCo2 levels
-respiratory alkalosis
ex: pH=7.25 high pCo2 levels
-respiratory acidosis
ex: pH=7.55 high pCo2 levels
-metabolic alkalosis

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