MSAP Physiology Respiratory System Flashcards
Gauge scale vs Absolute Scale
Ex. °F °C
O° C= Point at which water freezes (arbitrary) (doesn’t mean anything in energy terms)
100°C= Point at which water boils Relativistic information (arbitrary scale)
0°K= no heat or movement associated with it
Kelvin is the better scale to use (absolute temperature scale) 0
Degrees Farenheight: how cold he could make water before it froze 100 Degrees F: temperature underneath his armpit (arbitrarily driven) Kelvin: 0°C= 273K
Gauge scale pulmonary physiology
mmHg, cmH2O (pressures) (P)
Atmospheric = 0
Gauge scale starts at zero
+ cmH2O (positive pressure) = higher atmospheric pressure
-cmH20 (negative pressure) = lower atmospheric pressure
What happens when you punch a balloon?
The hand is enveloped by the balloon
Something similar happens to the lungs
Lungs are surrounded by pleural membrane full of fluid
plural fluid allows lungs to inflate and have layers of pleural membrane rub against each other without damage
Viseral Pleura
covers the outside of the lung
Parietal Pleura
Covers the inside of the chest wall
Static Conditions in the Lung
Pleural space pressure = (-)ve at static conditions
Lungs are trying to collapse inwards and thorax is trying to push outwards; expansionist force is generated which decreases the pressure
Alveolar pressure= 0
Transmular pressure (pressure across the alveolar wall)= Pressure alveolar-Pressure pleural membrane= 0-(-5)=+5
How does pleural pressure, alveolar pressure, airflow and lung volume change during Inspiration?
As the thorax expands (recruited muscles to expand the thorax) the pleural pressure decreases even further; Pp= more (-)ve
Alveolar pressure= O
Transmular pressure=PA-PP=0-(-10)= +10 à this causes the alveolar walls to move outwards
Pressure inside alveolar drops and now there is a slight negative pressure inside; Barometric (atmospheric) pressure is still zero.
Pressure differential causes gases to start filling the lungs.
How does pleural pressure, alveolar pressure, airflow and lung volume change during expiration?
Relax muscles–> thorax decreases in volume–> increase pleural pressure–> decrease transmular pressure which makes the pressure inside the alveolar (+)-ve –>pressure differential allows air to go outwards into the atmosphere
Sequence of events for one breathing cycle
Expiration:
All driven by contraction of diaphragm muscle –> increase in thoracic volume–> drop in pleural pressure–> increase in transmeural pressure across the alveoli–> expansion of the alveoli –> drop in alveoli pressure–> pressure differential between alveolar pressure and atmospheric pressure allows for gas to start filling the lungs –> as gas continues to fill the lungs pressures then equilibrate–> flow will slow down and stop–> flow leaves–> lung volume declines–> back to normal lung volume
Movement related to atmospheric and alveolar pressures during the breathing cycle
Expiration
Elastic force cause alveolar to contract and causes positive pressure inside alveolar which moves air back into the atmosphere; once PA and PB have equilibrated then flow is stopped movement related to
Compliance
Change in volume per given change in pressure (think of a balloon)
As the mechanical properties of the lungs change, the compliance changes
What causes a drop in compliance
Clinically Lung Fibrosis; extra collagen gives us very stiff lungs that make them difficult to inflate; large pressure needed for small changes in volume
What causes high compliance?
High Compliance= little resistance to changes in volume
Clinically: Emphysema; the walls of the aveoli are eaten away by protease activity; lungs becomes like plastic bag (easy to inflate, but there is very tough low elasticity alveoli )
What is spirometry? What is a weakness of the system?
Main method through which we measure certain parameters of lung function
Weakness: have to be able to exhale that air to measure it
Spirometry: What is tidal volume?
Measure difference between shallow breaths
How much you breath in a average cycle (usually 500ml) ;how much we breath in and out during FRC
Spirometry: Total Lung Capactity
Breathing in as much as possible
Spirometry:Residual volume
Still 2L of gas in the lungs after we exhale fully
Important Clinical Parameters
4 main parameters to predict lung volume: Need to know height of pt, age,
sex, race
Spirometry: FRC
Function residual capactiy = rest volume of lungs
Spirometry: Vital Lung Cpacity
Vital lung capacity= total lung capacity- rest volume of lungs
- maximum dynamic volume (as much as you can breath in or out)
- Forced vital capacity (when pt is asked to force air out of lung) ; name reflects the method that the patient was asked to do
What is the VC in a normal pt?
80% VC from TLC is FEV1= In one second you should be able to get 80% of the vital capacity out of the lungs
What are the steps of spirometry?
Volume/Time spirometry; amount of air the pt can breath over time
Ask pt to go to total lung capacity (breathing in as much as possible) and then forcefully exhale for as long as possible
Measuring the volume that the pt exhales from total lung capacity over time
Spirometric abnormalities with restrictive lung diseases
Pt with Restrictive Lung Disease (low lung volumes):
Abnormalities: Dampening of entire curve so that FVC is low and FEV1 is low; both parameters lower than predicted, but FEV1 to FVC ratio is normal (80%)
Clinically: Lung Fibrosis (difficult to fill mechanically tight lungs)
Spirometric abnormalities with obstructive lung diseases
Pt with Obstructive Lung Disease (Problem with rate at which air can flow in and out of the lung):
Abnormalities: FVC is normal but FEV1 is very low and FEV1:FVC ratio is <<80%
Clinically: Asthma, COPD
Partial Pressure
Partial Pressure: In a mixture of gases, each gas has a partial pressure which is the hypothetical pressure of that gas if it alone occupied the volume of the mixture at the same temperature
Dalton’s Law
Daltons Law: The total pressure of a mixture of gasses is equal to the sum of the partial pressures of the individual gases in the mixture
Fraction of inspired oxygen
the assumed percentage of oxygen concentration participating in gas exchange
Partial pressures in alveolar during constant ventilation
P02: 100mmHg
PCO2: 40 mmHg
Steady state values
Partial Pressures in arterial blood system
P02: 100mgHg
PCO2: 40mmHg
Partial pressures in venous blood system
PO2: 40mmHg
PCO2: 45mmHg
Partial pressure gradient for O2 deliver into and out of hte body
Partial pressure gradient for O2 delivery into the body= 100mmHg (alveolar)- 40mmg(venous)= 60mmHg
Partial pressure gradient for CO2 delivery out of the body= 40(alveolar)-45(venous)= -5mmHg
Fick’s Law Correlation
- Flux of gases, driving pressure (partial pressure), SA (lung is approximately the size of a tennis court), and thickness (minimized diffusion thickness by decreasing the distance between the alveolus and the blood)
We have evolved to maximize flux
Enhance the delivery of oxygen by increasing the rate of ventilation; opposite if you slow the rate of ventilation
Pulmonary Edema
Increases the distance between the alveolus and the blood
Fibrosis
increases the thickness of the diffusing difference
Driving Partial Pressure of O2
Partial pressure of O2 in the systemic venous is about 40mmHg and in the alveolus is about 100mmHg; gives a DeltaPO2 (driving partial pressure) = 60mmHg
Capillary Reserve Time
It only takes 0.25 seconds for blood to get fully equilibrated with alveolus (fully oxygenated so……
Q: Why is full resting transit time 0.75 seconds?
Answer: When cardiac output increase the velocity flow increases and so the transit time lessens; blood is still able to get fully oxygenated even if it spends less than 0.75 seconds in contact with alveolus
Darcy’s Law
Q= ΔP/R ; driving pressure over resistance
What is the normal flow throughout the pulmonary circulation?
Q= flow= 5L/min (has to be continuous and constant throughout cardiac output)
What is the driving pressure and resistance in the pulmonary system?
ΔP in pulmonary: 20 mmHg
Resistance in pulmonary: 4 (low so we can maintain constant flow with minimal pressure driving it) (tissue is delicate and if pressure is too high we will cause pulmonary edema)
What is the driving pressure and resistance in the systemic system?
ΔP in systemic: 100 mmHg
Resistance in systemic: 20
Why is the lung a good place to modify blood?
The lung is the only organ that receives almost all of the cardiac output
Factors that affect diffusion of gas between the alveolus and the pulmonary capillary
Flux of gases, driving pressure (partial pressure), SA (lung is approximately the size of a tennis court), and thickness (minimized diffusion thickness by decreasing the distance between the alveolus and the blood)
What is the oxygen content of plasma?
0 xygen is not very soluble
O2 solubility: is 0.003ml per deciliter of blood per mmHg
PAO2: 100mmHg…….0.3 ml dl-1
What is the oxygen consumption rate?
Oxygen consumption: 200ml/min
Why do we need Hb? why can we rely on the dissolved oxygen in our plasma?
Cannot rely on dissolved oxygen content in plasma; does not supply needs; that is why we need hemoglobin!
Vast majority of blood carried in hemoglobin
What is the oxygen contect of Hb?
20.4 ml dl-1
What is the percent hemoglobin saturation of arterial blood?
Arterial blood: High saturation (96-98%),
O2 content (21 ml dl-1)
As we increase the partial pressure of O2 we increase the amount of binding sites occupied and increase the oxygen content of blood
What is the percent hemoglobin saturation in venous blood?
Venous blood: Low saturation;
O2 content: About 16 ml dl-1
How would a RT Bohr Shift change the affinity of oxygen for Hb?
Decrease in pH (acidification, increase temp, and increase in CO2;
RT shift is so we can unload more oxygen: Blood comes out of lungs and into tissues–> higher PP CO2 and lower pH–> helps to drive the unloading of blood and give it to tissues that are metabolically active
How would a LT Bohr Shift change the affinity of oxygen for Hb?
Alkalizations, drop in temperature, drop in CO2; Increase the affinity of Hb for O2 and O2 does not get unloaded; would reduce the supply of O2 to the tissues
Peripheral Chemoreceptors
in carotid and aortic; When PO2 is <60 then there is an increase in ventilation.
There is no direct sensor for CO2
CO2 can turn into H+ and HCO3-
Central Chemoreceptors
Cerebral spinal fluid pH receptor
CO2 easily crosses the blood brain barrier into the CSF; broken down to H+ and Bicarb
H+ receptors in CSF measure CO2
Rise in H+ in CSF= Increase in VA
PCO2= 40 mmHg
CO2 usually drives the ventilation regulation in most individuals
Respiratory acidosis (adding protons)
If you slow ventilation CO2 will increase; increased CO2= increased H+; causes acidosis
Respiratory alkalosis (removing protons)
Increased ventilation CO2 decreases and so there are less H+ ions= alkalosis
Respiratory Acid-Base Compensations
HEY THIS IS KIND OF COOL: The protons produced from the carbonate anhydrase reaction binds to Hb and helps O2 unload from Hb; cause the dissociation of O2 from Hb
If CO2 is high from high metabolic demand then there is a lot of H+–> what is going to help? More oxygen; See the feedback? CO2 essentially regulates itself almost (feedback)
High metabolic demand–>High CO2–> lots of H+–> H+ binds to Hb and delivers oxygen where it is needed (the site of high metabolic demand)
- Bicarb rapidly taken out of cell and into the plasma ( CO2 in plasma) so that intracellular levels are low and the the conversion of CO2 to bicarp and protons can occur quickly and efficiently
- Did not need carrier protein for CO2; partial pressure of CO2 goes up the actual content of CO2 will continue to go up (does not happen with Oxygen because sites are saturated on carrier proteins)
Henry’s Law
Amount of gas concentration in solution is equal to the partial pressure of that gas multiplied by the solubility of the gas
Carbonate Anhydrase
CO2+H2O–> H+ + HCO3-; largely controls blood pH
CO2 in the tissues
Vast majority converted to bicarbonate ion (HCO3-) and is thought of as primary carrier of CO2 in blood
CO2 in the lungs
Bicarbonate is recombined with hydrogen ion to reform CO2
Alveolar partial pressure of CO2 low; drives CO2 in opposite direction
keeps the partial pressure of CO2 in the blood cell very low
favor H ions to dissociated from Hb recombine with bicarbonate to form CO2 and be released out through the lung
Acidosis
If you slow ventilation CO2 will increase; increased CO2= increased H+;
Alkalosis
Increased ventilation CO2 decreases and so there are less H+ ions
Clinical Correlation of Emphysema
- Imbalance in the protease/antiprotease activity in the lung
- Anti-protease activity is greater than the protease activity (starts to break down alveolar walls and lose surface area for gas exchange)
- Less tissue causes mechanical effect; lose the elasticity
- Decrease SA for gas exchange; lose volume of gas flux (gas diffusion)
- Decrease in CSA of vasculature (may cause problems in the RT side of the heart since there will be an increase in pressure)
- RV has to work much harder to increase the flow into the lungs (increase in afterload)
- Increases pressures in pulmonary pressure we increase filtration (causes pulmonary edema)
- Increased compliance (shift to the left)
- No elastic elements means that there is little elastic recoil which makes it difficult to exhale; easy inspiration, difficult exhalation (resembles a plastic bag (have to squeeze the bag) instead of a balloon)
- Airways are easily collapsed with loss of alveolar wall leads in reduction in airway diameter (Obstructive)
Respiratory Acidosis
Respiratory Acidosis
Clinical situation: Pt is not ventilating sufficiently; CO2 increases; PCO2; move up buffer line to greater PCO2; acidic; slow ventilation you developed acidosis with bicarbonate excess
Respiratory Alkilosis
Clinical Situation: Pt is ventilating too much; Lower PCO2; alkilinic and have a base deficit; lose bicarbonate and H+
Metabolic Acidosis
Cardiac output is low and there is not enough O2 to tissues; anaerobic metabolism; produces many H+
Increase of H+, but CO2 stays the same; acidification, but will stay on the same PCO2 isopleth
Excess protons produced by metabolic disorder protons are buffered by bicarbonate; lose bicarbonate and produces a deficit
PT with COPD (respiratory acidosis). What kind of compensation would take them back to baseline? How do we get rid of the excess H+?
Metabolic compensation which would takes you back to baseline pH (7.4pH)
Excess protons. How do we get rid of them? Kidney increases protonic secretion and slows down bicarbonate excretion; keep bicarbonate and get rid of H+ which takes you back towards baseline
Metabolic Alkilosis
Alkalinic and an excess of bicarbonate; lose protons (excess vomiting); CO2 remains normal
