Test 2 (Lectures 1-4) Flashcards
P (indicates)
- Partial pressure of a gar: must specify which gas you are referring to. The units are mm Hg
PO2= Partial pressure of Oxygen
PCO2= Partial pressure of Carbon Dioxide
Q or a Q with a dot over it (indicates)
- Blood Flow
V (indicates)
- Volume of Gas
V with a dot over it named “V Dot” (indicates)
- Airflow or Volume per unit time
F (indicates)
- Fractional concentration of gas (again you specify what gas you are referring to). There are no units
FO2: Partial Pressure of Oxygen (100% Oxygen = 1.0; 21% = 0.21)
FCO2: Partial pressure of Carbon Dioxide
A (indicates)
- ALVEOLAR Gas
- Conventional use: PAO2
a (indicates)
- ARTERIAL Gas
- Conventional use: PaO2
E (indicates)
- EXPIRED Gas
- Can indicate that the volume in question was measured during Expiration
I (indicates)
- INSPIRED Gas
- FIO2: Fraction of Inspired Oxygen
Muscles of Inspiration
1) The DIAPHRAGM
- Innervated by the PHRENIC NERVE
- When contracting, flattens or moves down in Abdomen
- INCREASES VOLUME of the Thorax as a result
2) EXTERNAL Intercostal Muscles
- Between ribs
- Slope DOWN and FORWARD
- When CONTRACTION, they RAISE the ribs
- INCREASING the ANTEROPOSTERIOR Diameter of the Thorax (BUCKET HANDLE MOTION)
3) There are additional muscles that participate in Inspiration under certain CIRCUMSTANCES (Ex: Exercise)
- SCALENE: Raise 1st and 2nd Ribs
- STERNOMASTOIDS: Raise Sternum
- Some muscles in Head and Neck
What are the Pros and Cons of the Respiratory muscle being Skeletal (and therefore dependent on the Brain for Activation)?
PROS:
- For talking because we can control this since its under Central Control
- RAPID Uniform ACTIVATION
- Respond rapidly to different conditions
CONS:
- Brain or Spinal cord damage can STOP BREATHING
- Length/ Tension Curve: If the lungs get too big, can stretch the Muscle
**The LENGTH TENSION DIAGRAM can start working against me in the Diaphragm during something that causes HYPERINFLATION, which causes the Diaphragm to MVOE TO SHORTER LENGTHS!
Events in Inspiration
STEP 1:
- CONTRACTION of the Inspiratory Muscles
- INCREASE in the THORACIC Volume
- ***Under NORMAL Conditions, the LUNGS and the MUSCLES/ RIBS are NOT PHYSICALLY CONNECTED to one another!!!!!
- Parietal Pleura and Ribs are NOT CONNECTED
- ***In between the VISCERAL and PARIETAL Pleura there is FLUID
- This fluid effectively CONNECTS the two Pleura together!!!
Side Note: The Intrapleural Pressure
- Because of their Anatomy and Physical characteristics, the LUNGS and the CHEST Wall are CONSTANTLY trying to PULL AWAY from Each Other (Even at Rest)
- This results in an INTRAPLEURAL PRESSURE that is BELOW ATMOSPHERIC PRESSURE
**Because these two are pulling away from each other, this means that the Intrapleural Space is NEGATIVE!!!!
Conventions in Respiratory Physiology
- Because the pressure we are dealing with are Relatively Small (and due to some history), the pressures we will all about are measure in CM H2O, not mm Hg!!!
- A 1 cm H2O change in Pressure is almost exactly the same as a 1 mm Hg due to the DENSITY of Hg
- We also NORMALIZE Atmospheric Pressure to 0 cm H2O (so a Pb of 760 mm Hg becomes 0 cm H20 in Respiratory Physiology)
- If you are in a place with a different Barometric Pressure, it is still 0 cm H2O
Side Note: The Intrapleural Pressure
- At REST, the Intrapleural Pressure is generally near -5 cm H2O!!!!!!
Events in Inspiration
- As the Thorax INCREASES Volume, the Intrapleural Pressure will DECREASE (as Volume Increases, Pressure DECREASES) to about -8 cm H2O!!!
Events in Inspiration
- Because of the Coupling of the Lungs and the Chest Wall, the lungs will EXPAND as the Thorax Expands
Events in Inspiration
- As the Lungs INCREASE in SIZE, the ALVEOLAR PRESSURE (Pressure within the Alveoli) DECREASES!!!!
A) At rest, Alveolar Pressure is the same as Atmospheric (0 cm H2O)B) During a NORMAL INSPIRATION, it will go to -1 cm H2OC) Due to the INCREASE in ALVEOLAR SIZE
***Make the ALVEOLAR PRESSURE LOWER than the Atmospheric Pressure and then the Air will flow in
Events in Inspiration
- When the ALVEOLAR PRESSURE drops BELOW the Atmospheric pressure, AIR FLOWS INTO THE LUNGS
The Respiratory Cycle
As Inspiration Proceds:
- Intrapleural Pressure will reach its lowest point at the end of Inspiration (in a normal breath, about -8cm H2O)
- Airflow into the lungs will Decrease as Alveolar Pressure returns back to 0 cm H2O
- The amount of air inhaled in a given breath is known as the TIDAL VOLUME and abbreviated VT. In a typical breath, VT is about 500 mL!!!
1) VOLUME CHANGE (Liters)
- Volume increases from 0 to +0.5 at the END of INSPIRATION
2) ALVEOLAR PRESSURE (cm H2O)
- Starts off at 0 then goes down to -1 half way through Inspiration and then finishes off at 0 at the END of INSPIRATION
3) INTRAPLEURAL PRESSURE (cm H2O)
- Starts off at -5 at the beginning of Inspiration and then proceeds to -8 at the END of INSPIRATION
4) AIR FLOW (L/sec)
- Starts off at 0 and then drops to -1 half way through Inspiration and then off at o at the END of INSPIRATION
The Expiratory Muscles
1) Abdominal Muscles
- Action: to PUSH into the abdomen displace the Diaphragm UPWARDS
2) INTERNAL INTERCOSTALS
- Orientated at (more or less) a RIGHT ANGLE to the External Intercostals
- DECREASES the AP Diameter of the Thorax
3) There are also ACCESSORY Muscles of Expiration
IMPORTANT: In a NORMAL BREATH, we don’t have to use these Muscles. EXPIRATION IS PASSIVE because the Lungs “WANT” to be Smaller (Like a balloon)
**The ELASTIC RECOIL od the lungs will be sufficient so the the expiration muscles will not be needed unless we are exercising
Events in Expiration
- As the Inspiratory Muscles Relax, the VOLUME of the THORAX DECREASES as the Diaphragm and rib cage RETURN to their STARTING POSITIONS
Events in Expiration
- The DECREASING VOLUME causes the Intrapleural Pressure to return to its STARTING POINT (-5)
Events in Expiration
- The Alveolar Pressure also INCREASES due to the Action of the Rib Cage
- It will reach a PEAK of about +1 cm H2O at MID-EXPIRATION
The Respiratory Cycle
- As EXPIRATION proceeds and the Volume of air in the Lungs DECREASES, the Alveolar pressure will begin to go back to 0
- Eventually, all the air that entered during INSPIRATION is EXHALED
1) VOLUME CHANGE (Liters)
- Went from +0.5 at the start of Expiration to 0 at the END of EXPIRATION
2) ALVEOLAR PRESSURE (cm H2O)
- Went from 0 at the start of Expiration to +1 mid way through and then back down to 0 at the END of EXPIRATION
3) INTRAPLEURAL PRESSURE (cm H2O)
- Started at -8 at the start of Expiration and ended at -5 at the END of EXPIRATION
4) AIR FLOW (L/sec)
- Started at 0 at the start of Expiration, went to +1 mid way through and then ended at 0 at the END of EXPIRATION
Compare and Contrast Intrapleural and Alveolar Pressures
INTRAPLEURAL:
1) -5 cm H2O at Rest
2) Becomes more Negative with Inspiration
3) Peak negative value at End- Inspiration
4) In Normal Expiration, remains Negative
5) Reaches Peak Value at END- Expiration
ALVEOLAR:
1) 0 cm H2O at rest
2) Becomes negative with Inspiration
3) Peak Negative value at MID-Inspiration
4) In any Expiration, becomes POSITIVE
5) Peak Positive value at MID-Expiration
Why does the Intrapleural Pressure not Return to resting value until the end of the Respiratory Cycle?
- In the Intraplearal space no air should be present so this doesn’t happen and ti won’t return to zero
Why did the Alveolar Pressure return to 0 at the end of Each Phase?
- Alveolar pressure returned to zero because Air Molecules came in and took up the extra space
Ventilation
MINUTE VENTILATION
- How much air is INHALED EVERY MINUTE
- Calculate as: V(dot) = VT x Frequency
- A a patient’s respiratory rate is 14 breaths/ min and their Tidal Volume is 500 mL/ Breath. What is their minute Ventilation?
- 14 breaths/ min x 500 mL/ breath = 7,000 mL/ min or 7 L/min
Alveolar Ventilation
- Although it is nice to know how much air enters the lungs each minute, what REALLY matters is how much gets to the Alveoli
- the FIRST 16 GENERATIONS of Airway don’t have any ALVEOLI- they re considered ANATOMIC DEAD SPACE!!!!!!!!!
- Dead space because the blood cant get Oxygen there
- ANATOMIC because they weren’t designed to EXCHANGE OXYGEN
***Some of the effort when I go to breath in is USELESS!!!
Alveolar Ventilation
- The ANATOMIC DEAD space can be estimated by knowing the patient’s WEIGHT in POUNDS!!!
- A 150 lb individual is estimated to have an ANATOMIC DEAD SPACE of 150 mL. (So just take the weight in lbs and put mL when lbs used to be)
Minute Alveolar Ventilation
- The MINUTE ALVEOLAR VENTILATION is calculated by:
a) Subtracting the Anatomic Dead Space Volume form the Tidal Volume :
- Valv = Vt- Vds
- So a 150 lb person who breaths in 500 mL with each breath:
- 500 - 150 = 350 mL of every breath gets to the Alveoli
- Minute Alveolar Ventilation is equal to the Alveolar Ventilation x Frequency
V (dot) ALV = V alv x Frequency
- If our 150 lb patient is breathing 12 breaths/ min the V (dot)ALV is 350 x 12 or 4,200 mL/ min (4.2 L/ min)
Intrapleural Pressure
- Pressure in the Intrapleural Space
Alveolar Pressure
- Pressure in the Alveoli
Tidal Volume
- How much air you take in during Inspiration
Anatomic Dead Space
- the Volume of air that remains in the CONDUCTING AIRWAYS
Alveolar Ventilation
VT- VDS
Minute Ventilation
VT x Frequency
Minute Alveolar Ventilation
VALV x Frequency
Tidal Volume
- Amount of AIR INSPIRED (or EXPIRED) in a Single Breath
- VARIES with CIRCUMSTANCES (Resting versus Exercises)
Inspiratory Reserve Volume (IRV)
- The volume of air you can breathe in after (on top of/ in addition to) the VT
Expiratory Reserve Volume (ERV)
- The volume of air you can FORCE OUT in addition to the VT
- Requires activation of EXPIRATORY MUSCLES (Active Respiration)
Residual Volume
- No matter how hard you try, you cannot voluntarily force this air
- “Having the wind knocked out of you” - something forced you to EXHALE into RV
Respiratory Capacities
- A capacity is the SUM of TWO of more of the RESPIRATORY VOLUMES
- There are FOUR CAPACITIES
- Like the Respiratory Volumes, they are influenced by size, gender, and age
a) Absolute VOLUME less important than present of predicted
b) Percent predicted is based on POPULATION NORMS and REGRESSION ANALYSIS
Respiratory Capacities
VITAL CAPACITY
- Inhale as deeply as you can
- Exhale all the air that you can (force it out at the end)
VC = IRV + VT + ERV
- Because it does not include the RV, it can be MEASURED using SPIROMETRY
Inspiratory Capacity
- Inhale as deeply as you can
- The TOTAL VOLUME of air you can INHALE from a NORMAL RESTING POINT
IC = IRV + VT
- Because it does not the RV, it can be measured using SPIROMETRY
Functional Residual Capacity
- All the AIR that REMAINS in your LUNGS at end of a NORMAL (passive) RESPIRATION
FRC = ERV + RV
- Because it DOES include the RV, it CANNOT be measured using SPIROMETRY
Total Lung Capacity
- The Total Volume of air in your lungs after a Maximal Inhalation
TLC = ERV + RV + IRV + Vt
- Because it DOES INCLUDE the RV, it CANNOT be measured using SPIROMETRY
TLC
= ERV + IRV + VT + RV
FRC
= ERV + RV
IC
= IRV + VT
VC
= ERV + IRV + VT
Dead Space
- Dead Space is REGIONS of the LUNG that receive AIR BUT NOT BLOOD
- Work done to bring air into these regions ay be WASTED!!!
Dead Space is divided into THREE KINDS:
1) ANATOMIC: this is the conducting airways that were never meant to exchange O2 and CO2
2) ALVEOLAR DEAD SPACE: Alveoli that get air, but do not get blood. No exchange occurs here (because there is no blood to exchange with) so the work it took to get the air into these alveoli is wasted!
3) PHYSIOLOGIC DEAD SPACE: The sum of Anatomic and Alveolar Dead Space
***GAS EXCHANGE refers to the exchange between the Alveolar Air and the Blood!!!!
Alveolar Capillaries
- Arise from the RIGHT VENTRICLE
- Are involved in the EXCHANGE of O2 and CO2 between the BLOOD and AIR
- Millions of ALVEOLAR CAPILLARIES make it so the Alveoli are effectively a SHEET OF CAPILLARIES
***In the Pulmonary Capillaries, the tissue Hydrostatic Pressure is a NEGATIVE NUMBER!!!
**Alveolar Pressure can actually EXCEED Capillary Pressure and BLOCK OFF BLOOD FLOW!!!
Extra-Alveolar Capillaries
- Arise from the LEFT VENTRICLE
- Deliver OXYGEN and CO2 to the Tissue of the LUNGS
- Return to the HEART in the PULMONARY VEINS (VENOUS ADMIXTURE)
a) Reduces the PaO2 of the Arterial Blood by a few mm Hg
b) INCREASES the PaCO2 to a Small Degree
***Receives blood form the Bronchial Arteries
Venous Admixture
- The addition of Venous Blood into the Pulmonary Veins
Compare and Contrast the Alveolar and Extra-Alveolar Vessels
ALVEOLAR CAPILLARY:
1) Source:
- Right Ventricle
2) PaO2:
- Low
3) PaCO2:
- High
4) Function:
- Gas Exchange
5) Return to the Heart:
- Pulmonary Vein
6) Blood Gases:
- High PaO2/ Low PaCO2
7) Notes:
- None
EXTRA-ALVEOLAR CAPILLARY
1) Source:
- Left Ventricle
2) PaO2:
- High
3) PaCO2:
- Low
4) Function:
- Provide Nutrients/ remove waste from the tissue of the Lungs
5) Return to the Heart:
- Pulmonary Vein
6) Blood Gases:
- Low PaO2/ High PaCO2
7) Notes:
- VENOUS ADMIXTURE
Pulmonary Vascular Resistance
- Important reminder: BP = CO x TPR
CO = SV x HR
- Holds true in the Lung as well, but substitute in PULMONARY VASCULAR RESISTANCE (PVR) for TPR:
PBP = CO x PVR
What do we know of these numbers right now?
- Pulmonary Blood Pressure: 25/ 15 (MAP about 18?)
MAP= Mean Arterial Pressure
Compare to Systemic Side:
- Systemic MAP: 90 mm Hg
- Cardiac Output: 4 L/min
The PULMONARY Vascular Resistance must be about 1/4 of the SYSTEMIC!!!!!!!!
Pulmonary Vascular Resistance
Determined by:
- HIGH number of Capillaries
- HOW MANY are OPEN at any given moment in Time (It is perfectly normal NOT to be using all your lungs at rest)
- Much LESS SYMPATHETIC Tone/ Vasoconstriction Forces
What is the Major Stimulus that causes an INCREASE in Pulmonary Vascular Resistance?
- The presence of HYPOXIA in a region of the LUNG!!!!
***Hypoxia is the LOCAL CONTROL of Blood Flow so the Blood Vessels CONSTRICT because there is NO OXYGEN
What is the Major role of the Vasoconstriction produced by Hypoxia?
- INCREASE Blood Flow to areas of the Lung with GOOD Oxygenation
**BEcause if we send the blood to areas with Poor Oxygenation, then the Blood will be POORLY OXYGENATED!!!
-
**HIGH ALTITUDE and COPD are when the ENTIRE LUNG is HYPOXIC, so that there is VASOCONSTRICTION in the ENTIRE VASCULATURE of the Lung!!!!!!!!
- THIS IS VERY BAD!!!!!!
Pulmonary Vascular Resistance
- During EXERCISE, PVR drops as more PULMONARY CAPILLARIES open up to accommodate the INCREASED CARDIAC OUTPUT!!!
Pulmonary Vascular Resistance
- Also depends on LUNG VOLUME
- At LOW or VERY HIGH Lung Volumes, the resistance INCREASES a little because the STRETCH of the tissue COMPRESSES the CAPILLARIES!!!!
- Just like a rubber band gets a little thinner when stretched, the diameter of the Capillaries DECREASES a little
Compare and Contrast the Pulmonary Vascular Resistance and the Systemic Total Peripheral Resistance
PVR:
1) Normal Value:
- LOW
2) Major Constrictor:
- Hypoxia
3) Change with Exercise:
- Decrease
4) Major Control:
- Local
SYSTEMIC RESISTANCE:
1) Normal Value:
- Moderate
2) Major Constrictor:
- Sympathetics
3) Change with Exercise:
- Decrease
4) Major Control:
- ANS
Regional Blood Flow in the Lungs
- As you already know, GRAVITY works on the Blood in our bodies, when we STAND, the Hydrostatic Pressure in our Legs in INCREASED Compared to the Level of the HEART or in the BRAIN
- The same is TRUE in the LUNGS
Apex of the Lung
- At the APEX of the Lung, the BLOOD PRESSURE is REDUCED because it is slightly above the level of the heart
- However, the ALVEOLI are somewhat EXPANDED
- The BLOOD FLOW is LESS
Middle of the Lung
- In the MIDDLE regions of the LUNG, the BLOOD PRESSURE is a LITTLE HIGHER because we are at the level of the Heart
- The ALVEOLI are AVERAGE SIZE
- The BLOOD FLOW is “NORMAL”
Base of the Lung
- At the BASE of the Lung, the BLOOD PRESSURE is HIGH because we are Below the level of the Heart
- The ALVEOLI are SMALLER
- The BLOOD FLOW is GREATER than in Other Regions
Starling Forces in the Systemic Circulation
- In a Systemic Capillary there is a balance. Arterial end is the net filtration while the venous end sucks that fluid back in
1) We have a NEGATIVE INTRAPLEURAL Pressure ———————–>
2) The HYDROSTATIC PRESSURE in the Tissue appears to be a NEGATIVE NUMBER. This now becomes a FORCE FAVORING FILTRATION!!! ———————————————————->
3) It appears now that we have a NET FORCE FAVORING FILTRATION over the Capillary and Alveoli
Starling Forces in the Lung
- It appears that the same forces that give rise to NEGATIVE Intrapleural pressure (the Lung always trying to COLLAPSE, the Chest wall trying to SPING AWAY) creates a NEGATIVE HYDROSTATIC PRESSURE in the TISSUE!!!!!!!
- This means it si now a Force Favoring Filtration of fluid from the CAPILLARY into the ALVEOLUS!!!!
The net result of this:
- The Starling Forces favor NET FILTRATION of the FLUID into the ALVEOLI
- But, that fluid is BAD FOR GAS EXCHANGE
What do we do???
- The Intact LYMPHATICS SYSTEM REMOVES the FLUID IN THE LUNGS!!!!!!!!
Describe the mechanism by which the alveoli are kept “dry”
- The Interstitial Hydrostatic Pressure is believed to be NEGATIVE and favors FILTRATION of Fluid from the CAPILLARY to the Alveolus
- The Net Startling Forces are believed to favor Filtration along the length of the Pulmonary Capillary
- The Lymphatics are CRUCIAL in removing the filtered fluid form the ALVEOLUS!!!
What is the Direct Stimulus for the release of Renin?
- DECREASED Sodium delivery to the Kidney
What is the source of the peptide acted on by Renin?
- Angiotensinogen comes from the LIVER!!!!
Review of Renin
- Renin is an Enzyme that CONVERTS Angiotensinogen (a protein added to the Plasma by the LIVER) to Angiotensin 1!!!!!!
- Angiotensin 1 is converted to the more active Angiotensin 2 by ACE (Angiotensin Converting Enzyme) in the Lungs
- ACE also Inactivates BRADYKININ. About 10 - 15% of people who are placed on ACE Inhibitors for blood pressure control develop a Cough due to accumulation of Bradykinin
Metabolic Functions of the Lung
- The Lungs also participate in the Metabolism of the ARACHIDONIC ACID Metabolism
- Both Leukotrienes and Prostaglandins/ Thromboxane A2 are produced by IMMUNE SYSTEM Activation in the Lungs
- Prostaglandin E2 and F2alpha are also almost COMPLETELY REMOVED from the circulation in the Lungs, as are the Leukotrienes!!!!
Regional Blood Flow in the Lungs
- As you already know, gravity works on the blood in our bodies, when we stand the Hydrostatic Pressure in our legs is INCREASED compared to the level of the Heart or in the Brain
- The same is true in the Lungs
- We’ve already seen what it does to Blood Flow, because that is relatively “big”
Regional Blood Flow in the Lungs Cont
Zone 1) At the APEX of the lung, the blood pressure if REDUCED because it is slightly above the Level of the heart
Zone 2) In the MIDDLE regions (at the level of the Heart) Blood Flow is “Normal”
Zone 3) At the BASE of the Lungs, the Blood Flow is High (were below the Heart)
***There is PROGRESSIVELY MORE BLOOD Flow going to each of these three zones! Increasing from Zone 1 to Zone 3!!!
Regional Ventilation in the Lungs
The Intrapleural Pressure is also acted on by GRAVITY:
1) At the APEX, there is LESS Intrapleural Fluid, so the Intrapleural PRESSURE is MORE NEGATIVE
- (-7 to -10)
2) At the BASE, there is more Intrapleural Fluid, so the PRESSURE is LESS NEGATIVE than you expect!!!
- (-2 to -3)
- Slightly less negative because we have more fluid molecules here
Regional Ventilation in the Lungs Cont
The Intrapleural Pressure is also acted on by GRAVITY:
1) At the APEX, the Intrapleural PRESSURE is MORE NEGATIVE, so the ALVEOLI ARE BIG!!!
2) At the BASE, the PRESSURE is LESS NEGATIVE than you would expect, so those ALVEOLI are SMALL (not as expanded by Pressure)
*****VENTILATION is HIGHER at the APEX than the BASE!!!!!!!!!!!!!!!!
The Ventilation (V)/ Perfusion (Q) Ratio
- The mathematical ratio between Ventilation and perfusion
- OVER THE ENTIRE LUNG
- A [4 L/ min (V)] / [5 L/ min (Q)]
- May vary in different regions
Often spore as a “High” V/Q or “Low” V/Q
1) HIGH V/Q: Ventilation is HIGH relative to Perfusion
2) LOW V/Q: Ventilation LOW compared to Perfusion
Altering the V/Q Ratio
Normal:
- V/Q = 0.8
PaO2: 40 —> 100
PaCO2: 45 —> 40
Altering the V/Q Ratio: LOW V/Q Ratio
1) - Extreme condition: V = 0; the ARWAY is BLOCKED by something
PaO2: 40 —> 100
PaCO2: 45 —> 40
2) In a SHORT TIME, the O2 in that Alveolus DECREASES while the CO2 INCREASES> The same change occur in the Arterial Blood
PaO2: 40 —> 80
PcCO2: 45 —> 42
3) With TIME, the alveolus will equilibrate with the Non-arterialized (Venous) blood entering the Pulmonary Capillary and the blood leaving that Alveolus will leave WITHOUT EXCHANGING Oxygen or Carbon Dioxide
PaO2: 40 —> 40
PaCO2: 45 —> 45
Altering the V/Q Ration: HIGH V/Q Ratio
1) The Extreme example: NO BLOOD is coming to the Alveolus (Alveolar Dead Space)
PaO2: 40 —> 100
PaCO2: 45 —> 40
2) With LESS BLOOD removing Oxygen/ Adding CO2, the alveolar O2 will INCREASE/ CO2 DECREASES, brining the Alveolus closer to ATMOSPHERIC CONDITIONS!!!!
PaO2: 40 —> 120
PaCO2: 45 —> 20
3) Eventually, the Alveolar Air in these areas will be MOST SIMILAR to the AIR outside the BODY
PaO2: 40 —> 150
PaCO2: 45 —> 1
**This sounds great but remember we don’t have any substantial blood flow, so not much blood (if any) “benefits” from this situation!!!!!!
***Even worse, the blood that couldn’t get to this ALVEOLUS has to go SOMEWHERE, turning this Normal Alveolus …………………..
……Into an Alveolus with a LOW V/Q Ratio (Even though the airflow is Normal, the INCREASE in Blood Flow causes the LOW V/Q Ratio)!!!!!!!
CONCLUSION: Because we have more Blood coming from the LOW V/Q Ratio areas, the OVERALL PaO2 and PaCO2 DECREASES!!!!!!!!!!!
Compare and Contrast the Arterial Blood cases that are attained by region and a HIGH V/Q ratio versus a LOW V/Q ratio
(APEX) HIGH V/Q Region:
1) PaO2:
- HIGH
2) PaCO2:
- LOW
3) pHa:
- HIGH
4) Volume of Blood
- LOW
(BASE) LOW V/Q Region:
1) PaO2:
- LOW
2) PaCO2:
- HIGH
3) pHa:
- LOW
4) Volume of Blood
- HIGH
**THE MIDDLE OF THE LUNG REPRESENTS THE NORMAL CONDITIONS (PaO2: 100, PaCO2: 40)!!!!!!!!*****
Minor V/Q Inequalities exist in all of us
- The influence of Gravity on the Blood Flow and Ventilation in our lungs when we stand is a V/Q INEQUALITY!!!!!
- Because the Alveolar gases have changes, the arterial blood gases also change.
- In an ideal world. they are Identical to the Alveolar gases…
- They are always SLIGHTLY LESS due to the Venous Admixture from the Bronchial and Coronary Sinuses!!!!!
Arterial Oxygen (PaO2)
Range: 80 to 100 mm Hg (Age dependent)
Arterial Carbon Dioxide (PaCO2)
Range: 35 to 45 mm Hg
- For calculations, use 40 mm Hg
Arterial pH (pHa)
Range: 7.35 to 7.45
- For calculations, use 7.40
Arterial Bicarbonate (HCO3)
Range: 22 to 26 mEq/ L
- For calculations, use 24 mEq/L
pH
pHa 7.45 ALKALOSIS
Bicarbonate
INCREASE in HCO3 —> INCREASE in pHa
DECREASE in HCO3 —> DECREASE in pHa
What can Change HCO3?
1) The KIDNEYS can change HCO3 a LOT because they can MOVE HCO3 into the URINE or KICK out H+ into the URINE
- If kidneys not working properly, the pH will GO DOWN!
2) The GI Tract SECRETES a lot of HCO3 or H+. If have Vomiting or Diarrhea, i can lose the HCO3
3) I can ingest too many TUMS
4) I can use it up by making an Acid i hadn’t planned on- LACTIC ACID, KETOACIDOSIS
Changes in Bicarbonate are?
METABOLIC DISTURBANCES!!!!
Increasing CO2 causes
- An INCREASE in H2CO3
- An INCREASE in H+
***An INCREASE in CO2 ALWAYS leads to ACIDOSIS because of the H2CO3 and H+
***Less CO2 means Less H2CO3 and Less H+. Therefor a DECREASE in CO2 leads to ALKALOSIS because of DECREASED H2CO3 and H+
CO2
INCREASE CO2 —-> DECREASE pHa
DECREASE CO2 —> INCREASE pHa
Changes in CO2?
RESPIRATORY DISTURBANCES!!!!!!
