Respiration Physiology Pt 2 Flashcards
During mammalian inhalation, ____ ____ stimulates inspiratory muscles
MOTOR NEURONS
during inhalation, ____ intercostals and diaphrahm _____
EXTERNAL intercostals and diaphragm CONTRACTS.
During mammalian inhalation, the diaphragm moves
downward
During mammalian inhalation, the volume of thorax ____, and intrathoraic pressure ___
volume increases, and intrahthoracic pressure DECREASES, this creates a transpulmonary pressure gradient INCREASE.
During mammalian exhalation, the volume of the thorax _____ and the intrathoracic pressure ____
thoracic volume DECREASES and intrathoracic Pressure INCREASES.
forced exhalation is by the contraction of ____ intercostal muscles
INTERNAL
surface tension inside the alveoli ___ expansion. how does this help? what can it cause?
OPPOSES. helps ensure elastic recoil along with elastic fibers in pulmonary connective tissue. BUT SURFACE TENSION reduces distensibility or compliance of the tissue and can potentially cause ALVEOLAR COLLAPSE Pulmonary surfactant’s role in reducing the alveoli’s tendency to recoil, thereby discouraging alveolar collapse, is important in helping maintain lung stability.
LaPlace’s law and explain its significance. How can surfactant help with this?
magnitude of the inward-directed collapsing pressure is directly proportional to the surface tension and inversely proportional to the radius of the alveoli : Pressure = 2T/R P= inward pressure T= tension (surface tension) R= radius of alveolus water molecules in alveoli have surface tension which pull inward. the holes between alveoli connect them to create a risk that larger alveolus may absorb smaller ones (causing collapse). Accordingly, if two alveoli of unequal size but the same T are connected by the same terminal airway, the smaller alveolus—because it generates a larger collapsing pressure has a tendency to collapse and empty its air into the larger alveolus. The surfactant-induced lower T of small alveoli offsets the effect of their smaller radii in deter- mining the inward-directed pressure. Therefore, the presence of surfactant causes the collapsing pressure of small alveoli to become comparable to that of larger alveoli
the holes that connect avleoli together to create a large alveoli sac are known as
pores of KAHN
two ways that we mitigate distensibility (recoil) in alveoli
1) elasticity due to elastin fibers
2) surfactant. more surfactant is secreted in smaller alveoli and less in larger to EQUALIZE PRESSURE BETWEEN ALVEOLI in the sac
What is spirometry
the tehcnique use to quantify volumes and capcities.
what is the tidal volume
the difference between end-expiratory and end-inspiratory volume= tidal volume. The volume of air moved in one ventilatory cycle
ex/ volume of lungs at end of inspiration (2700ml) and volume of lungs at end of expiration (2200 ml) therefore tidal volume is 500ml.
What is dead space? Two components of dead space
air that does not paricipate in gas exchange.
2 components: 1) anatomical dead space= volume of air of trachea and bronchi
2) alveolar dead space= volume of alveoli that are not perfused.
During expiration, 500 ml of “old” avleolar air is expired: ___ml expired to atmosphere, while ___mL remain in the dead space.
350 ml expired to atmosphere, 150 ml remain in dead space
what is alveolar ventilation volume (Va)? What is alvolar minute ventilation?
volume of fresh air that enters alveoi with each respiratory cycle.
Va= Vt- Vd= 500ml- 150 ml = 350ml
Va= alvolar ventilation volume
Vt= tidal vol
Vd= dead space
Alveolar munite ventilation is the volume of fresh air that enters the alveoli each minute :
VaDOT= f(Vt-vd)
f= brathing rate in breaths per minute.
how do you maintain alveolar minute ventilation (VdotA) with a large dead space?
you can increase tidal volume and increase respiratory rate. Recall: VDOTa= f(Vt-Vd)
T/F: during high demand exercise, increasing respiratory rate is sufficient to maintaining alveolar minute ventilation
false. you need to increase breathing rate, yes, but you also need to bood tidal volume to overcome dead space.
How do ice fish survive with no Hb or RBCs?
they have an enlarge heart and large stroke volume. extremely cold water allows higher O2 solubility and leads to low MR of the fish. therefore, diffusion and dissolved O2 in the blood is enough. Most gas exchange still occurs across the gills, some is cutaneous.
T/F: we can change the amount of dissolved O2 in the blood
false. BUT we can use respiratory pigments
Blood can’t dissolve O2 much, instead we use ___ ___ typically made of metalloproteins
respiratory pigments.
What are metalloproteins. Three major types?
metalloproteins are proteins containing metal ions which reversibly bind to O2. They increase o2 carrying capacity by 50 fold.
3 major types:
1) hemocyanin
2) hemoglobin
3) hemoerythrins
hemoglobin contains a ____ molecule in the center of a ___ ____ (heme)
Fe2+ in the center of a porphyrin ring (heme)
How many O2’s does one heme bind
- but there are 4 hemes in a hemoglobin, thus one hemoglobin can bind 4
hemoglobin is a ____ with 2 alpha and 2 beta chains. They are held together by ___ bonds and ____ ____. What structure changes during loading and offloading of O2?
hemoglobin is a tetramer. the dimers are held together by H bonds and salt bridges. It’s quarternary structure of protein changes on loading and offloading
IN addition to hemoglobin, what are the 2 primary enzymes that RBC’s contain?
1) carbonic anhydrase: for Co2 tansport, pH regulation
2) methmemoglobin reductase. reduces Fe3+ to Fe2+ in RBC
the binding of O2 to Hb is driven by ____.
PO2. Po2 decreases as Hb binds more O2 and becomes saturated
law of mass action
an increase of mas on one set of reactants then the reaction is driven to the opposite side. Hb + O2 <–> HbO2.
T/F: only dissolved O2 contributes to PO2.
true. Hb removes O2 from solution
Why is a signmoidal relationship between O2 binding and PO2 so important?
it ensures consistant supply of O2 to tissue and indicates cooperativity. as partial pressure of O2 increases, the saturation of Hb also increases, and pO2 decreases(deoxy blood), Hb saturation decreases (offloading to tissues)
R state vs T state in terms of affinity
R state: relaxed, high affinity.
T state: tense, low affinity.
what is p50
the Po2 level when Hb is 50% saturated
How can you change P50 value?
by different hemoglobin O2 affinities.
T/F: the AMOUNT of Hb can determine P50 values.
false. Low and high Hb content in blood does not define the P50. affinity does. therefore, if the blood with low and high Hb still have the same Hb isoform, they will still have the same P50 value, but the body with high Hb content will just have more O2ml on average in the blood (because of the sheer volume of respiratory pigment)
why is does myoglobin display a hyperbolic binding curve?
because it doesn’t exhibit cooperativity.
Bohr effect. What direction does it shift the Hb binding curve?
a decrease in pH (increase pCO2) REDUCES O2 affinity. Shifts it RIGHT, p50 is increased. Facilitates O2 transport to active tissues and O2 binding at respiratory surfaces
Bohr effect vs root effect
bohr effect can be mitigated by incresing O2 concentration to achieve 100% saturation again. in the root effect, the saturation will always be alower because of the pH change.
3 methods to reduce affinity for O2 by Hb
1) reduce pH
2) increase temperature
3) organic phosphates
how does an increase in temperature result in a change in Hb O2 affinity? Why is this important for ectotherms
causes a reduced affinity (stabilization of T state). it causes the curve to shift left. body temp increase allows warmer tissues to receive more O2 because Hb will readily unload them due to lack of affinity.
this is good for ectotherms because as temp increases, their Mr increases and thus they need more O2. more O2 can be delivered to them because of the increased unloading of Hb.
How do organic phosphates change Hb binding affinity? How are they produed?
they reduce affinty (right shift). They stabilize T state by reforming salt bridges. allows for O2 offloading at tissues. 2-3 DPG is produced INSIDE red blood cells.
explain cold weather adaptation in the wooley mammoth
- nucleotide difference coding for adequate O2 release in cold temp. therefore, they had a right shifted Hb curve.
Compare fetal and afult Hb
fetal Hb is not as sensitive to 2,3 BPG. They have a higher affinity for O2 then adult. this is because the Hb of the fetus has to bind O2 after blood is already partially deoxygenated from mom.
therefore, fetal Hb curve is shifted RIGHT. has a lower p50.
3 ways carbon dioxide is transported
1) dissolved CO2 in plasma and in cytoplasm of RBC
2) in the bicarbonate buffer system
3) attached to Hb and as carbamino CO2
Draw the shape of the CO2 curve (CO2 concentration in blood vs PCO2). What other chemical does this curve dependent on? Is there any cooperativity going on?
Shape of CO2 curve depends on the kinetics of HCO3- formation
- there is no sub unit cooperativity
What is the chloride shift? Where does it occur and what exchangers are present? What reaction is also occuring at the same time as chloride shift?
the chloride shift occurs on the RBC membrane, where HCO3- is pushed out of the RBC into the plasma and CL- in the plasma enters the RBC.
It involves BAND 3 PROTEIN as a shuttle system.
At the same time, HbO2 in the RBC dissociates into Hb + O2. this is so Hb is free to bind to H+ that is left when HCO3- leaves. –> this mitigates acidity levels. Hb “mops up” H+ ions, but is now stabilized in T state ( bohr effect)
peripheral chemoreceptors in the heart that control respiration are:
1) carotid bodies
2) aortic bodies
carotid body functions as a sensor: it responds to a stimulus, primarily O2 partial pressure, which is detected by the type I (glomus) cells, and triggers an action potential through the afferent fibers of the glossopharyngeal nerve, which relays the information to the central nervous system
there are also central chemoreceptors in the medulla
Why is the brain so sensitive to CO2 levels?
because brain CSF does not have much of a buffer system. CO2 from blood can easily cross into brain but it can’t be buffered. Therefore, the brain is very sensitive in increasing PCO2. this allows the medulla to detect it at very low amounts.
at PCo2 increases, the rate of ventilation____
increases
T/F: H+ ions can permeate throguh the blood brain barrier
false. therefore, pH changes due to lactic acid production can cause increased breathing rate if detected by PERIPHERAL chemoreceptors only.
___ and __ can be detected by medullary chemoreceptors and ___ and ___ can be deteced by peripheral chemoreceptors
CO2 and pH can be detected by medullary chemoreceptors and pH and O2 can be deteced by peripheral chemoreceptors
pH can be detected by both:
lactic acid/metabolic waste causes pH changes in peripheral
CO2 acidosis can be detected by medullary
