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75 Cards in this Set

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Gas Exchange Definition (2 systems)

- the ability to transfer gases from gases from the respiratory system with the atmosphere (alveolar), and CV system with the tissues (thus two different areas of gas exchange)


- occurs due to differences in partial pressures of gases

What creates gas pressure?

- the weight of all the molecules in the atmosphere being pulled down by gravity that are exerting a force

Atmospheric Pressure (sea level vs moon)

- Barometric Pressure - PB


- at sea level, barometric pressure is 760 mmHg


- PB on the moon = 0


Measurement of PB

- pan filled with mercury with a vacuum


- all molecules exert a force (as they have a weight)


- atmosphere weight of molecules will push down on the mercury and send it up the test tube, and measure the pressure based on how high it goes

Dalton's Law of Partial Pressures

- in a mixture of gases, each gas will contribute to the total pressure of the system in direct proportion to its percentage in the mixed gas

Why is partial pressure important?

- determines direction of diffusion


- ex) the only reason O2 moves rom atmosphere (160mmHg) to alveoli (105 mmHg) to arterial blood (100) to tissue (40) is that it is constantly going down partial pressure gradient

Calculation of Partial Pressure

[pressure] x [gas%]= Pgas

Atmosphere at Sea Level (N, O, H20 and CO2)

Diffusion of gases (how does it occur)

- highest to lowest partial pressure


- regardless of total pressure difference


- each individual gas moves according to it's own partial pressure

Nomenclature of Partial Pressures in the Respiratory System (Room air, Alveoli, Arterial, Venous)

Room Air (inspired air) = I


PP of oxygen in room air = PI02


Alveoli= A


PP of nitrogen in alveoli = PAN2


Arterial = a


PP of carbon dioxide in artery = PaCO2


Venous = v


PP of oxygen in veins = PvO2

ex) Gas exchange taking place between alveoli and blood (vein) (oxygen and CO2)

PAO2 > PvO2


- from alveoli to blood: PP of O in alveoli is greater than venous blood



PACO2 < PvCO2


- from blood to alveoli: PP of CO2 in alveoli is less than venous blood

Partial Pressure Gradients in the Body: Inspired to alveoli (PO2 and PCO2)

PO2 (160--> 105) decreases


- Due to increase in PH20 (air humidified, changes contribution of each PP)


- due to increase in PCO2 (displaces O2)



PCO2 increases (0.3 --> 40)


- due to CO2 addition into alveoli from blood


As air moves from Alveoli to atmosphere (expiration)

PO2 increases


- due to mixing with deadspace air



PCO2 decreases


- due to mixing with deadspace air

Different PP in the body (need to know numbers)


- Arterial Blood, Systemic Tissue Cells, Alveoli

Arterial Blood


PO2 = 100


PCO2 = 40



Systemic Tissue Cells


PO= 40


PCO2= 45


- tissue cells use up O2 and produce CO2 so PvCO2 has higher CO2 content than arteries



Alveoli


PAPO2 = 104


PAPCO2 = 40


- PCO2 goes back down to 40 from 45 as you offload the extra CO2 into the expired air (thus 40 at arterial end)

Why is PaO2 (arterial) < PAO2 (alveolar)?

- as blood passes alveoli in capillary, equilibrates with alveolar air (PO2 105 mmHG), and so right at the capillary, there is PO2 105mmHg, but as soon as blood leaves the lung, you lose 5 mmHg to get 100mmHg WHY



- The bronchiole circulation, which keeps the conducting passages alive, travels with/beside the pulmonary circuit, so these vessels all come in to the hilus of the lung (at the primary bronchi), then all go down together until they reach the respiratory regions of the lungs (this is where the bronchiole circulation stops, and the pulmonary circulation continues)


- when the pulmonary circuit picks up oxygen from the alveoli, it has to go back up beside the veins for the bronchiole circuit (which have used deox blood), and this leeches some of the oxygen off of the pulmonary circuit

Normal Gas Exchange

Alveoli


PAPO2 = 105


PAPCO2 =40



Venous


PvPO2= 40


PvPCO2= 45



Arterial


PaPO2 = 105 (100)


PaPCO2= 40

Process of Gas Exchange (Normal)

Blood from pulmonary artery is called venous blood (not oxygenated). Physiologically speaking it has come from tissue and has had O2 leeched off and CO2 put in. It quickly equilibrates as it passes the alveoli with PP of gases there, so it picks up O2 and dumps CO2

Note: Speed of Gas exchange process

Occurs very quickly.


Oxygen: oxygen equilibrium is achieved as soon as blood passes 1/3 of the alveoli.


CO2: Even quicker. Since CO2 is more soluble.


PO2 is approx 5% in water vs 20% in atm, this is why we need hemoglobin to move it through the liquid blood.

Pathological Gas Exchange (Respiratory Disease)

Mechanism: Diffusion barrier is created between alveoli and blood. There is something sitting in your airway that is preventing oxygen from diffusing. (pulmonary edema- adds more water to airways)


Effect of Pathological Gas Exchange (Respiratory Disease)

CO2 diffusion in unaffected- it dissovles well in water so you can get rid of it easy. If you had a CO2 barrier you would die as the O2 for sure would not move.


O2 diffusion is affected- it takes more time to dispel in the water, so blood O2 content gets lower over time.


May become hypoxic

Ventilation/Perfusion Ratios

Ventilation differs throughout the lungs. This imbalanced is referred to as an abnormal Vdot/Qdot ratio


Solution: The lung is always trying to match ventilation to blood perfusion of the lungs.. they try to send the blood coming in areas of the lung that actually get air.

Nomenclature

Dot on top is rate of change


Vdot=volume of air (ventilation)


Qdot= volume of liquid or blood (perfusion)


Cases (Normal Vdot/Qdot ratio)

High V, high Q


Good ventaltion, and good blood flow going across the alveolus

Cases (High Vdot/Qdot ratio)

Abnormal- high, V low Q


Not enough perfusion to a well ventilated area.


Apex of the lung (naturally)- top of the lung will naturally have low perfusion due to gravity, most perfusion is at the bottom.


Pulmonary Embolism: Blood clot occludes pulmonary arteries, lung may be functional (not dead), but there is not enough blood to support gas exchange.

Result of High Vdot/Qdot ratio

PaO2 increases- oxygen pressure will be high (not take O2 out but bringing lots in)


PaCO2 decreases

Cases (Low Vdot/Qdot)

Abnormal- Low V, high to normal Q


Low ventilation of lung area (something that obstructs air flow)


Asthma ,Lung Cancer


This causes hypoxia (no gas exchange)


Causes low alveolar pressure of oxygen (big problem)

Result of Low Vdot/Qdot

PaO2 decreases


PaCO2 increases

Compensations: Correcting for V/Q mismatch

Pulmonary arteries- either constrict or relax to allow blood to move to different regions of the lung.


High V/Q: Relax is PaCO2 is low or PaO2 is high, this allows more blood to come and lowers V/Q ratio to normal


Low V/Q: Constrict if PaCO2 is high or PaO2 is low, this allows less blood to leave poorly ventilated area (increase V/Q ratio to normal)

Problems (altitude)

How do the pulmonary arteries respond when moving to high elevations? PP of O2 is low in the entire lung. Therefore constrict all vessels. Results in pulmonary hypertensions.

Problems ( COPD)

What happens to pulmonary arteries in COPD?


Chronic obstruction of airways=poor ability to ventilate. So pulmonary arterioles contract to try to move blood around to a better place. But there is no better place. Causes pulmonary hypertension. Can lead to damage of the right ventricle, and heart failure.

CO2 Diffusion in Blood

Diffusion: From tissue to blood based on gradient of pressures. Higher in tissue than blood. From blood to alveoli due to pressure gradient of PvCO2 and PaCO2. Higher in blood than alveoli so goes to alveoli.


CO2 Transport in Blood (3)

Dissolved (7%)


HCO3- (70%): Bicarbonate anion in blood plasma


Bound to hemoglobin (22%)


Remember H+ + HCO3- <--> H20 +CO2


As Co3 enters the blood it can combine with water to form HCO3 and proton

Normal Co3 Tensions (PPs)

Alveolus: 40 mmHg


Arteriole Blood: 40 mmHg


Tissues: >45 mmHg


Venous Blood: 45 mmHg

Co2 from tissues to Blood, 3 things can happen

1. some in dissolved (7%)


2. Some combines with water to be converted to a bicarb anion


3. Binds to haemoglobin

Ways that Co2 combines with water to from a bicarb anion (2)

In the plasma: Slow, there are no enzymes to catalyze the reaction


In the RBC: Some goes into red blood cells and then combine with water. Same equation as before but faster since there is carbonic anhydrase. HCO3- tranposted by Cl- out of RBC and into plasma

Way that CO2 binds to hemoglobin (22%)

Binds to the outer stutter of haemoglobin. Not the same spot as O2. This association creates carbomino hemoglobin. This is different from carboxy hemoglobin where CO attaches and competes with O2

CO2 from Blood to Alveoli

CO2 thats dissolved foes out of blood and into the alveoli. All of the previous reaction occur in reverse.


1. Bicarbonate in plasma come out slow Co2 +H2O <-- H2Co3 <-- HCO3- + H+


2. Bicarbonate from RBC (fast reaction) comes out


3. Hemoglobin bound CO2 come out as well (as PCO2 is higher in RBC than alveolus.


Haldane Effect

As blood passes the lungs is releases CO2 and picks up O2. Oxygen saturated hemoglobin does not bind well to CO2, so O2 kicks CO2 off.

O2 Transpot in Blood

Dissolved (1.5%)


Bound to hemoglobin (98.5%)

Normal Oxygen Tensions

Alveolus: 105 mmHg


Venous: 40 mmHg (use about 60 mmHg)


Arterial: 100 mmHg


Tissue: 40 mmHg

Hemoglobin Structure

4 protein chains (2 aplha, 2 beta) with central global surrounded by 4 heme portions.



Heme: Includes ferrous iron. Loos binding with O2 (reversible). Bind to O2 in relation to PP. Higher affinity for CO (230x). Treatment for CO poisoning? - give 100% O2

Globin

Globular protein chains (2 alpha, 2 beta)

Forms of Hemoglobin

A=Adult: Normally 140-165g/L (male), 120-150 (female). Characteristic dissociation for O2


F=fetal: Higher affinity for O2 than adult. Allows fetus to lech O2 from mother hemoglobin.


S=sickle: next slide

Sickle Cells

Crystallizes within cell-results in fragile RBC. Genetic mutation of protein so whens its not bound to O2 it makes a weird shape. This is a problem reduces lifespan of RBC. RBC production controlled by homeostasis

Oxygen Saturation

O2 binds to Hb proportionally to PO2. 2 Hb sites can be filled:


0 filled= blue blood (unsaturated)


4 filed = red blood (saturated)


After 1 O2 binds the other 3 binds easily since the shape of the protein changes, know as cooperativity. This results in the slope of the O2-Hb dissociation crime is not a straight line.

Oxygen Saturation Cont.

O2Sat= % of Hb that has bound to O2


Detected by infrared "Sat" moniters. Normal - >97%. Measuring saturation alone will not account for anemia (low RBCs). An anemic person will have little Hb but is well saturated with O2. This means that O2 stat can be normal but you don't have enough O2 going to tissues and become cyanotic.

Solution to Measure O2stat and anemia

Must measure Hct and Hb levels


Hct= hematocrit (volume of RBCs) tells you if you have too much or too little

What does 97% O2stat imply?

The average Hb-O2 saturation in a sample of blood is 97%. There are a lot with 4 and some with 3 O2 bound. Is an average (actually Hb can only have 0,25,50,75,100%)

O2-Hb Dissociation Curves

At lung-100% saturated (Normally): In the lungs the PO2 is 100 mmHg and the hemoglobin is almost 100% saturated


At tissues- Release 25% of O2- As of the blood passes tissues the PO2 decease to 40 mmHg which represents offloading of O2 from 25% of Hb molecules. So you have 75% go Hb that has oxygen (huge reverse for exercise)

O2-Hb Dissociation Curves (exercising tisse)

Please 70% of oxygen: Increases cellularl respiration can can drive PO2 to 20 mmHg.

Benefits o the Shape of the O2-Hb dissociation Curve (first reason)

1. Flat top portion: allows lots of O2 pick up even with respiratory failure. Large Decrease in PO2 results in only small decrease in O2 stat. You drop PO2 from 100 to 60, stat goes from 100 to 90%. Good when you in mountains. Also you have to have a big disease (COPD, edema) to affect you.

Benefits o the Shape of the O2-Hb dissociation Curve (2nd reason)

Steep portion: Allows tissues to pull off O2 as needed. Moving down a little bit in PO2 means that you release lots of O2 off of Hb

The shifted Curve

You can shift the curve to your advantage in situations to allow tissues to pull off more oxygen. Tissues with high metabolism (cell resp) change the shape of the curve due to:


Increases PCO2


Increased Temp


Decrease pH (increase in H+)


Shifting Curve due to lactic acid

When you generate lactic acid, you have a lot of H+ and therefore a decrease in pH. This causes a right sifted, which means that the tissue can pull off oxygen at any given PO2.

Carbon Monoxide Saturation

100%stat when PP is 0.5 (as compared to 100 for O2). Thus less Co is need to fully statute Hb than O2

Control of Breathing (purpose)

To ensure that alveolar ventilation is at appropriate level.

Brain

Medulla-Respiratoy Center : Dorsal and ventral reparatory group (RG) sends signals to muscles of breathing. Simplest is a contractile signal.


Dorsal RG

Inspiration area of the medulla: Is active when breathing quietly.


Active (inspiration): Signals to muscles of inspiration (external intercostals, diaphragm) to contract then turns off.


Inactive (Expiration): Relaxation of muscles followed by elastic recall of lungs.

Ventral RG

Expiatory area of medulla: recruits the muscle of forced expiration. Anterior abdominal muscles, and internal intercostals. Expiratory centre turns on when inspiratory centre is working hard. (suggests you needs forceful breathing)

Regulation of Respiratory Groups (Dorsal)

Control by higher centre in the Pons:


Apneustic Center: agonizes the dorsal RG, allowing you to breather quicker in and more forcefully (accessory muscles of inspiration)


Pneumptaxic Center: Turns off the dorsal RG



To increase breathing rate you use both centres, to quickly inspire then shut it off (gas brake)

What influences rate/depth of ventilation?

Centers in the pons, receive input from many site to ensure that level of ventilation matches body demand.

Inputs to the apneustic and pneumotaxic sites

Higher brain centre (cortical influences): Allows conscious control, also sends corollary input when sending signals to skeletal muscles. This is why you can hold your breath an hyperventilate. Swimmers hyperventilate to release CO2. But can result in fainting.

Hering-Breuer Reflexes (stretch receptors in the lungs)

Prevents overinflation of lungs. Can tear elastic components. Stretch receptors prevent this by feedback to medulla.

Irritant Cough Receptors

Sit in the carina, triggers cough reflex. Any particle that sits here trigger it

Proprioreceptors in muscles and joints

Increases breathing when activity is increased. Info sent up through proprioceptors occurs when you increase muscle activity, some of this info peels off and gets sent to the respiratory group. This reopens is all anticipatory for what will occur as a result of skeletal muscle activity

Central Chemoreceptors

In the brain: measure blood CO2 levels

Peripheral Chemoreceptors (PCs)

Arch of the aorta and carotid artery. PCs enable fine control of PaO2 and PaCO2. When CO2 goes down/up causes problem with blood chemistry (pH)

Baroreceptors

Can sense change in blood pressure.


BP drops: increase ventilation


BP rises: shut off breathing


Natural reflex from baroreceptors

Other input from hypothalamus

Pain, stress, emotional state.


Temp: during fever increase ventilation


Emotion: Crying, leads to hyperventilation. Limbic system sends info to hypothalamus affecting breathing


Stretching and Anal Sphincter: increases rest rate, is useful if you have a comatose patient who stopped breathing ....?

Chemoreceptors

Ensure that blood gas pressures remain constant. PaCO2 = 40 mmHg

Central Chemorecptors

Located on ventral surface of medulla. Sense CSF H+ levels which are influenced by PaCO2. Can only sense things that cross the blood brain barrier (BBB). High levels of CO2 results in CO2 coming out of circulation crossing BB and making H+. Causes you to ventilate more to get rid of CO2. Is an insuppressible signal, why you can't hold your breath forever.

Note on Central Chemoreceptors

Receptors itself is responsive to H+, not pH

Peripheral Chemoreceptors

Location: Carotid bodies, aortic arch


Responsive to: increase PaCO2, decrease arterial pH, decrease PaO2.


Note: can directly monitor above. but biggest stimulus os PaCO2. Best way to correct for abnormalities is to breath more.

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for good