2 - Pulmonology Flashcards
Lectures Respirator Mechanics O2 Transport CO2 Transport Regulation of Respiration Shunt and Ventilation Respiratory Failure (36 cards)
Define TLC, FRC, and RV.
Total Lung Capacity - volume from max inhalation to max exhalation (Inspiratory Reserve Volume + Tidal Volume + Expiratory Reserve Volume)Functional Reserve Capacity - volume in lungs after normal exhalation (ERV + RV)Reserve Volume - volume in lungs after max exhalation
Define compliance of lung tissue.
Compliance is a measure of the relationship between the change in pressure required to change the volume of the lungs. C=dV/dP
Why don’t alveoli collapse on themselves?
Interconnected alveoli are exposed to the same airflow, but according to Law of LaPlace (P=2T/r) the alveoli with smaller radii see more pressure (to collapse). To compensate, the Type II pneumocytes secrete surfactant. The high lipid concentration decreases surface tension. So as the radius decreases, the surfactant becomes more concentrated and decreases the surface tension. This creates a balance in tension between the larger and smaller alveoli, thus maximizing surface area available for gas exchange.
Discuss changes in the rate of inhalation and exhalation with progressive increases in effort.
Inhalation - increasing effort results in proportional increase in volume and rate of air flow until max effort is reached Exhalation - increading effort results in a proportional increase in volume, changes in rate are limited. The increased contractions during forced exhalation place pressure on the smaller (without cartilage) bronchioles. This causes them to narrow and increases the resistance to flow. Therefore, the rate of exhalation is mostly set regardless of effort.
Describe the layers of the Respiratory Membrane. How is O2/CO2 transported across this membrane during inhalation and exhalation?
The Respiratory Membrane is everything that O2/CO2 must pass through when traveling between the alveoli lumen to the RBC.
Air -> water/surfactant layer -> Type I pneumocyte -> interstitial space -> capillary endothelium -> blood plasma -> RBC
All transport is by SIMPLE DIFFUSION.
What is the partial pressure of a gas? Are the partial pressures of the alveolar air the same as atmospheric air? Why?
Partial pressure = total pressure x fractional gas concentration
NO - since the concentrations of the different components of air are different in the alveolar space, the partial pressures are different. This is driven by 4 factors:
1) alveolar air is moistened during inhalation (water vapor UP)
2) alveolar air is not replaced completely replaced with each breath
3) CO2 is constantly entering from blood
4) O2 is constantly exiting to blood
What factors drive the rate of diffusion of fluids through the Respiratory Membrane?
Factors that affect rate of diffusion PROPORTIONALLY:
1) solubility of gas
2) difference in partial pressures across membrane(MAJOR)
3) cross-sectional area for diffusion (MAJOR)
4) temperature
Factors that affect the rate of diffusion INVERSELY:
1) molecular weight (technically the square root of MW)
2) distance of diffusion (MAJOR)
What are the typical partial pressures for O2 and CO2 in the RBCs and in the lungs?
O2 - Lung->104mmHG; RBC -> 40mmHG
CO2 - Lung -> 40mmHG; RBC -> 45mmHG
Describe the effect of allosteric binding in hemoglobin. Why is this important for O2 transport?
When one O2 molecule binds to a heme in hemoglobin (Hb), there is a conformational change in Hb that makes it easier to bind O2 to the three other hemes.
This makes it possible for Hb to preferentially release O2 in tissue (where O2 concentration is low) and bind it in the lung (where O2 concentration is high). Without this effect there would be a linear pattern of binding and release of O2, leaving the distant tissue badly deoxygenated.
What are the factors that affect the shape of the oxygen-hemoglobin dissociation curve?
1) hydrogen ions (pH)
2) CO2
3) Temperature
4) 2,3-biphosphoglycerate (2,3-BPG is a glycolysis biproduct)
Increases in each of these items (drop in pH) shifts the curve to the right. This means hemoglobin has a DECREASED affinity for O2.
What is the affect of exercise on O2-hemoglobin binding?
Exercise uses O2 in tissue. This causes the tissue PO2 to drop and “pull” more O2 from hemoglobin. At rest Hb saturation only drops to 72% (a 25% drop from the lungs). However, during exercise Hb saturation drops as low as 7%. This results in a 93% O2 delivery to the tissue!
The low saturation during exercise is helped by a shift in the O2-Hb dissociation curve to the RIGHT by increases in:
1) hydrogen ion concentration (pH drop)
2) CO2 concentration
3) temperature (minor)
4) 2,3-BPG
What is the affect of anemia on O2 tansport?
Anemia decreases the blood’s capacity to transport O2 to the tissue. This means that even though there is no change in PO2 or percent Hb saturation, MUCH less O2 is reaching the tissue. This can be partially compensated for by increased cardiac output, but will likely be evident during strenuous exercise.
How is CO2 transported in the blood?
1) Dissolved CO2 (7%) -> due to increased solubility of CO2 (20x»>O2) the small pressure difference allows CO2 to just diffuse into the blood plasma
2) As bicarbonate ions (HCO3 -) (70%) -> CO2 + H2O -> H2CO3 -> H+ + HCO3- –> HCO3- is transported across RBC membrane and is dissolved in plasma
3) as carbamino compounds (Hb-CO2) (23%) -> CO2 reacts slowly with proteins (especially Hb) in RBC which makes it more soluble in RBCs and plasma
What is a the chloride shift with regard to CO2 transport in blood?
This is referring to an increase in chloride inside RBCs when there is a high concentration of CO2 in the blood (venous blood).
This is due to how the bicarbonate ion is transported out of the RBC. Once CO2 and H2O have formed bicarbonate, it is transported out of the RBC by facilitated diffusion via the BICARBONATE-CHLORIDE EXCHANGER. This allows HCO3- to travel down its concentration gradient and pulls Cl- into the RBC => Chloride Shift. This is reversed when CO2 concentration falls.
Why does CO2 form H2CO3 more rapidly in RBC vice plasma?
1) RBCs have a high concentration of CARBONIC ANHYDRASE (the enzyme catalyst for this reaction)
2) Cl/HCO3- Exchanger removes HCO3- from the cell, preventing a build up of HCO3- from slowing the reaction
3) the intracellular buffers (mostly Hb) prevent a build up of H+ from slowing the reaction
What is the Haldane Effect with regard to CO2 transport in blood?
O2 binding to Hb promotes the release of CO2 from blood, thus doubling the amount of CO2 exchanged at physiological pressure differences.
1) O2 binding to Hb makes it a stronger acid, therefore releasing H+ it had been “buffering” –> this pushes the HCO3- equilibrium back to H2CO3 and CO2/H2O
2) O2 binding to Hb also displaces CO2 that had been bound as carbamino compounds
3) The resulting increase in CO2 concentration in the RBCs increases the pressure difference across the Respiratory Membrane and helps with diffusion
What is the affect of CO2 concentration on blood pH?
CO2 + H2O -> H2CO3 -> HCO3- + H+
This means that as CO2 increases, pH drops. Normally arterial pH is ~7.41 where venous pH is ~7.38.
This change is related to CO2 concentration by the Henderson-Hasselbach Eqn, which is how CO2 is measured in a standard Arterial Blood Gas sample.
Define Respiratory Acidosis. What are some (general) physiologic causes?
Acidosis: Arterial Pco2 > 44mmHG (norm=40) OR Blood pH drop pH
1) poor ventilation (mechanical breathing failure)
2) poor diffusion (pulmonary edema/alveoli injury)
3) low pressure difference (high atm CO2 ie. rebreathing)
Define Respiratory Alkalosis. What are some (general) physiologic causes?
Alkalosis: Arterial Pco2 7.45 (norm=7.41)
Causes: decreased CO2 concentration -> pH rise
1) hyperventilation (blow off too much CO2)
2) fever (temperature affects CO2 diffusion)
What sensory receptors are involved in respiratory control?
1) Central chemoreceptors -> H+ (this is driven by CO2 concentration, but H+ interacts directly with receptor)
2) Peripheral chemoreceptors -> O2, CO2, H+
3) Pulmonary receptors -> stretch
4) Joint/Muscle receptors -> stretch and tension
What neurologic areas are responsible for automatic respiratory control? What is their GENERAL function?
1) Upper pons -> Pneumotaxic Center -> “off switch” to transition from inspiration to expiration
2) Lower pons -> Apneustic Center -> unknown; may be involved with taking deep breaths
3) Medulla -> Dorsal Regulatory Group -> innervate “breathing muscles” to help with forced breathing
4) Medulla -> Ventral Regulatory Group -> pacemaker function to control rate of breathing
How do central chemoreceptors respond to changes in blood chemistry?
CO2 diffuses freely across the blood brain barrier. This shifts the equilibrium with HCO3-, freeing more H+. These ions directly stimulate the chemoreceptors and cause increased ventilation.
Describe the peripheral mechanical pulmonary receptors.
Slow adapting stretch - located in smooth muscle of airways; respond to changes in air volume
Rapidly adapting stretch - located in epithelium of airways; respond to the rate of change of air volume
J (Juxtaposed) Receptors - located near pulmonary capillaries to respond to changes in capillary interstitial pressure (as in edema) -> these are responsible for sense of dyspnea during edema
Describe the Hering-Breuer Reflex.
Summary: mechanically inflating the lungs promotes exhalation, and a decrease in lung volume promotes inhalation
Inspiration -> lung inflation -> stretch receptors (slow/fast activate @~1.5L) -> vagal fibers increase stimulation -> Apneustic center inhibition -> “stop” inhalation -> exhalation