Bergdahl- Chapter 13 and 14 Flashcards Preview

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Flashcards in Bergdahl- Chapter 13 and 14 Deck (92):

What is the % of different gases in ambient air ?

20.93 % O2
79.04% N2
0.03% CO2


what is partial pressure ? how does it compute ?

partial pressure is the pressure exerted by the molecules of a specific gas.
PP = % concentration x TP


what are the partial pressures of gases in dry ambient air at sea level ?

PO2 = 159 mmHg
PCO2 = 0.2 mmHg
PN2 = 600 mmHg


what happens to the partial pressures in tracheal air ? what are the partial pressures in tracheal air ?

the air "saturates" with the water vapor, and the latter dilutes the air mixture.
PO2 decreases by 10 mmHg from 159 mmHg to 149 mmHg.
little effect on inspired PCO2 since the gas only has a negligible contribution.


what happens to the partial pressures in alveolar air ? what are the partial pressures in alveolar air ?

CO2 is continually entering alveoli from the blood. Therefore its concentration increases. Air becomes 14.5% O2, 80% N2, and 5.5% CO2.

PO2 = 103 mmHg
PCO2 = 39 mmHg


what is Henry's law ? what are the two factors that govern the rate of diffusion of gas into liquid ?

at a given temperature, the mass of a gas that dissolves in a fluid (solubility) varies in direct proportion to the pressure of the gas over the liquid.

another way to phrase it is: solubility of a gas into a solution increases when the partial pressure of a gas above the liquid increases. makes sense because then the pressure difference enhances diffusion

2 factors:
- pressure difference between the gas above the fluid and the gas dissolved in the fluid
- the solubility of the gas in the fluid


what creates the driving force for gas diffusion across the pulmonary membrane ?

the pressure difference between alveolar and pulmonary gases, especially where CO2 is concerned


what is the net result of gas exchange in the lungs ?

O2 : travels from higher to lower pressure, diffuses through alveolar membranes into the blood
CO2: net diffusion from blood into lungs because higher pressure in venous blood than in alveoli
N2: stays unchanged


how fast does the alveolar gas- blood gas equilibrium happen ?

0.25 s


what are 3 factors that impair gas transfer capacity at the alveolar-capillary membrane ?

1) buildup of pollutant layer that thickens the alveolar membrane. as we learned, the longer the distance, the harder diffusion is
2) reduction in alveolar surface area (although it is pretty big, usually. so probably if remove a lung or in a pathology)
3) low perfusion


at rest. circuit with alveoli and muscle. what are the pressure differences of O2 ? what are the implications ?

going to alveoli: PO2 40 mmHg, which means that since the 100 mmHg pressure in the alveoli is much higher, oxygen will diffuse from the alveolis to the blood.
it will then go to the muscles.

PO2 in blood (outside) is around 100 mmHg (same as alveoli). Inside, it;'s about 40 mmHg. This means that this induces oxygen entry into the muscle cell.


what is PO2 and CO2 within muscle tissue during exercise ? what are the implications ?

some values don't change with physical activity, like blood leaving the lungs (PO2 of 100 mmHg, PCO2 40 mmHg).

PO2 in muscle falls to 0 mmHg approximately. This drives a pressure difference for more O2 to leave the blood and diffuse towards cells.
PCO2 approaches 90 mmHg


what are the two ways blood carries oxygen ?

1) dissolved in blood. This establishes the PO2 plasma, regulates breathing (especially at high altitudes) and determines oxygen loading of hemoglobin in lungs.
2) loose combo with hemoglobin


what is hemoglobin ?

iron-containing globular protein pigment


how powerful is Hb? meaning, how much more can it carry O2 than plasma ?

65-70 times more


how many iron atoms does Hb have ? how many O2 molecules can Hb therefore bind to ?

4 iron atoms. each can loosely bind one oxygen molecule.
1 Hb- 4 O2

oxygenation of hemoglobin to oxyhemoglobin.


what catalyst does Hb need to bind to O2 ?

the reaction does not need an enzyme. it proceeds only with the dictation of the partial pressure of oxygen dissolved in physical solution (in plasma).


what is the joining of O2 and hemoglobin called ?

cooperative binding. (the binding of an O2 molecule to one of the irons facilitates the binding of subsequent O2 molecules)


what shape does the Hb - O2 dissociation curve have ?



what is the oxygen transport cascade ?

basically, as you go from air to myoglobin, step by step O2 partial pressure decreases.


at low pressures (in what conditions?) what is oxygen bound to ?

myoglobin (more of a logarithmic graph) facilitates oxygen transfer to the mitochondria when cellular PO2 declines rapidly (eg in intense exercise or as exercise begins)


how is myoglobin different from hemoglobin?

- hemoglobin is for oxygen TRANSPORT whereas myoglobin is stationary and works as a localized oxygen reserve

- one myoglobin can only hold one oxygen, unlike hemoglobin which can hold 4 . however, myoglobin has a higher affinity for oxygen (curve elevated throughout range of PO2)

- during rest & moderate exercise, myoglobin maintains high saturation levels
greatest myoglobin binding when PO2


what is the use of myoglobin ?

muscles use it to accelerate oxygen diffusion


what affects myoglobin's oxygen-binding affinity?

NOT acidity, CO2, temperature


what is the only way for CO2 to "escape the body"?

diffusion and subsequent transport in venous blood


what are the three ways CO2 is transported in the blood ?

- in physical solution in plasma
- combined with hemoglobin in RBC
- as plasma bicarbonate


what is the Bohr effect ?

looking at the O2- hemoglobin dissociation curve, it's the phenomenon that states that H+ and CO2 alter hemoglobin's structure to decrease its oxygen-binding ability. This particularly holds between 20-50 mmHg

This means more oxygen releases to tissues in a low PO2 due to three factors:
- metabolic heat (temperature)
- CO2 (produced by tissues)
- acidity from blood lactate accumulation


after exercise, what whill happen with the % composition of hematocrit ?

it will decrease (decrease of RBC concentration)


what is the a-vO2 difference ? how much is it usually ?

represents difference between the O2 content of arterial blood and mixed-venous blood

usually about 4-5 mL / dL blood


what limits aerobic exercise capacity, O2 supply or muscle O2 use ?

O2 supply, since the muscle has an "uncompromising capacity to use available O2"

THEREFORE, Hb does not need input from local tissue blood flow to supply more O2.


what is 2,3-DPG ?

2,3- diphosphoglycerate is a compound produced by RBC
in its anaerobic consumption of energy


what does 2,3- DPG do ?

it binds loosely with subunits of hemoglobin, which reduces the affinity for oxygen, which causes greater O2 release to tissues for a given decrease in PO2


in what conditions is 2,3-DPG increased ? what are the implications of this ?

in cardiopulmonary patients, or those who live at high altitudes, or those who exercise a lot

this facilitates O2 release to the cells
(compensatory adjustment for low Hb for example)


what happens to the a-vO2 difference during intense activity ?

tissue PO2 decreases since the cell's use of O2 will increase. therefore, Hb will release a higher amount of O2 (see curve).
Extracellular PO2 may decrease to nearly 15 mmHg with only 5 mL O2 bound to hemoglobin
Therefore, the a-v O2 difference may increase to 15 mL of O2 / 1 dL of blood.

so a-v O2 difference will increase with increased metabolic activity and ATP production


a person with lower Hb levels will have higher or lower 2,3-DPG ?

higher (as a compensatory adjustment)


what determines the P(GAS) in the blood ?

just the gas in the plasma


arterial blood releases how much of its total oxygen content at rest ?

75% returns unused to heart through venous blood


what does the a-vO2 difference indicate ?

that there is an automatic reserve of oxygen for rapid use should metabolism increase suddenly.


in what conditions does a-v O2 difference increase or decrease ?

it proportionally increases with higher metabolic activity and ATP production (straight line starting from 5 mL)

same O2 on arterial side, but less on venous side because more O2 has been extracted.


in what conditions does the a-v O2 difference slope increase ?

for an endurance athlete who is more capable of using O2


carbon dioxide in 1) physical solution - what percentage ? what does this do ?

5% of CO2
establishes the PCO2 in blood


carbon dioxide as 2) sodium bicarbonate
how ? how much ?

CO2+H2O H2CO3 (carbonic acid) HCO3- (bicarbonate) + H+

usually carbonic acid ionizes into bicarbonate and hydrogen ions (shifts right)
60-80% of CO2 exists as bicarbonate


explain how the equilibrium shifts in metabolism.

CO2 will leave the blood via the lungs, which will lower plasma PCO2

therefore, the equilibrium will shift left and HCO3- + H+ will combine to form H2CO3, carbonic acid. another shift to the left will form more CO2


carbon dioxide as 3) carbamino compounds - when do they form ?

form when CO2 reacts directly with the aa of blood proteins


carbon dioxide as 3) carbamino compounds - what's an example ?

globin portion of hemoglobin forms a carbamino compound by binding to CO2
carries 20% of body's CO2


what will affect carbamino compound concentration ?

a decrease in PCO2 will reverse carbamino formation (carbaminohemoglobin will become CO2+ Hb)


what is the Haldane effect ?

a decrease in PCO2 will decrease carbamino formation (binding of Hb to Co2), causing Co2 to move into solution so that O2 binds to hemoglobin which reduces the ability of Hb to bind to CO2


ventilatory control- what is the purpose?

to maintain a relatively constant alveolar and arterial gas pressure throughout a broad range of exercise intensities.


where is the normal ventilatory cycle controlled ?

by the INHERENT activity of inspiratory neurons in the medial portion of the medulla.


how is the normal ventilatory cycle controlled ? when do these neurons stop firing?

inherent inspiratory neurons in medulla activate the diaphragm and intercostal muscles to cause the lungs to inflate.

they CEASE firing due to self-limitation and inhibitory influence of expiratory neurons in medulla.

therefore, they are automatically on, just get inhibited during expiration and then they're passively on again. as expiration proceeds, the inspiratory center becomes progressively less inhibited and once again becomes active.


ok, so the normal ventilatory cycle is because of medullar neurons. but what is the duration and intensity of the inspiratory cycle due to ?

neural center in hypothalamus
it integrates input from descending neurons in higher areas. it can also adjust during exercise due to input from mechanical or chemical changes (info from ascending signals, due to feedback control)


what humoral factors exert ventilatory control?

variations in arterial PO2, PCO2, pH, and temperature


what exerts the greatest control of pulmonary ventilation at rest ?

the chemical state of the blood (humoral factors)


how do humoral factors exert ventilatory control?

variations in arterial PO2, PCO2, pH, and temperature activate sensitive neural units in the medulla and arterial system to adjust ventilation and maintain arterial blood chemistry within narrow limits.


how does the body detect change in O2, a humoral factor ?

peripheral chemoreceptors are sensitive to reduced oxygen pressure in the blood
the carotid bodies monitor the state right before it perfuses the brain
aortic chemoreceptors


what is the only thing that protects the organism against reduces oxygen pressure in inspired air?

(aortic and carotid)


how is plasma CO2 and H+ monitored by the ventilatory control system (humoral factors)?

PCO2 and plasma acidity exert command over minute ventilation


at rest, what is the most important respiratory stimulus ?

PCO2 in arterial plasma
small increases trigger large increases in minute ventilation


do the peripheral chemoreceptors only work when there's a lack of O2 ?

nope, in exercise they react to changes in other humoral factors.


how do variations in plasma acidity command minute ventilation ?

pH decrease: acidosis, meaning the curve is shifted to the left (there is a lot of CO2 and carbonic acid)

H+ ions accumulate, so inspiratory activity increases to eliminate CO2 and carbonic acid


in breath holding, where does the stimulus to breathe come from ?

NOT a lack of O2.
rather, and increase of PCO2 and H+
the breaking point for PCO2 is at 50 mmHg


what happens to the gases in the body with hyperventilation?

alveolar PCO2 to decrease from 40 mmHg to 15 mmHg, meaning a larger than normal quantity of CO2 leaves the blood to go to alveoli

arterial PCO2 decreases due to this considerable diffusion gradient


during exercise, how is ventilatory control different ?

there is chemical and non-chemical control.
however, chemical control is not enough to explain an increase in ventilation during exercise. alveolar PO2 does not decrease to an extent that would increase ventilation through chemoreceptor stimulation. therefore, there are also non-chemical control factors involved (neurogenic, temperature)


what suggests that there is non-chemical control of ventilation?

the fact that the ventilatory response at the start & end of movement is so rapid suggests that there is other input than arterial PCO2 and H+ that mediate ventilation.


what is non-chemical control of ventilation during exercise

neurogenic factors


what are the 2 neurogenic influences for non-chemical control of ventilation in exercise ?

- cortical influence = neural outflow from regions of the motor cortex in anticipation of exercise stimulates respiratory neurons in medulla to initiate abrupt increase in exercise ventilation.
- peripheral influence = sensory input from joints, tendons, and muscles influences the ventilatory adjustments throughout exercise


does temperature influence ventilatory regulation ?

nope not really except in extreme hyperthermia. the rise in ventilation at activity onset and decline at end of mvmt are too fast for it to be due to temperature input.


what initiates and modulates exercise alveolar ventilation ?

combined and perhaps simultaneous effects of several chemical and neural stimuli


phases of minute ventilation in exercise and recovery

phase I: central neurogenic stimuli from cerebral cortex and feedback from active limbs stimulate the medulla. abrupt increase of ventilation

phase II: short plateau, then, with central command (due to continued activity of respiratory neurons) + input from peripheral chemoreceptors, increase to achieve a steady level related to metabolic gas exchange demands

phrase III: peripheral fine-tuning of steady-state ventilation through peripheral sensory feedback mechanisms.

then, when exercise stops:
abrupt decline
and then slow recovery phase


after cessation of exercise, what can the abrupt decline in ventilation be attributed to ? (2 reasons)

- the removal of central command drive
- the sensory input from previously active muscles `


what can the slow recovery phase after the abrupt phase be attributed to ? ( 2 reasons)

- gradual diminution of the short-term potentiation of the respiratory center
- reestablishment of the body's homeostasis


in steady-rate exercise, how does ventilation look ?

increases linearly with O2 consumption and CO2 production
ventilation increases through increases in tidal volume, but then in higher intensities breathing frequency also plays a role

Ve= Vt x f

PO2 and PCO2 remain near resting levels due to the change in ventilation


in non-steady rate exercise, how does ventilation look ? how does the ventilatory equivalent look ?

moves sharply upward and increases disproportionately in relation to oxygen consumption

the ventilatory equivalent can increase to 35-40 L of air breathed / L of O2 consumed


what is ventilatory equivalent ?

Ve / Vo2


what is ventilatory threshold ?

the point at which pulmonary ventilation increases disproportionately with oxygen consumption


what causes the ventilatory threshold ?

excess ventilation comes from CO2 release from the lactic acid buffering that begins to accumulate
the sodium bicarbonate is being used to buffer it, which leaves CO2
this disproportionately increases VT and ventilatory equivalent


what are the three functions of measuring lactate threshold ?

1) provides a sensitive indicator of aerobic training status
2) predicts endurance performance, often with greater accuracy than VO2 max
3) establishes an effective training intensity geared to the active muscles' aerobic metabolic dynamics


what are the three indicators of lactate threshold ?

- ventilatory threshold
- blood lactate- exercise VO2 response


what is OBLA ?

onset of blood lactate accumulation
when blood lactate concentration systematically increases to 4 mM
excess production of lactate basically


what does lactate threshold represent ?

the highest oxygen consumption achieved with less than 1 mM increase in blood lactate concentration above the pre-exercise level


what are the 4 causes for excessive lactate appearance in OBLA ?

1) imbalance between rate of glycolysis and mitochondrial respiration
2) decreased redox potential
3) lower blood oxygen content
4) lower blood flow to skeletal muscle


endurance training at OBLA will change OBLA, VO2max, or both ?

only OBLA (some independence between VO2max and OBLA)
improves exercise intensity at OBLA without changing VO2 max


what are the two factors that influence endurance performance ?

2) VO2 max


what is buffering ?

chemical and physiologic mechanisms that minimize changes in H+ concentration


what are the three buffering mechanisms we have ?

first line of defense:

second line of defense:
physiologic (ventilatory and renal)


what is chemical buffering ? give an example.

a weak acid and a salt are necessary
eg carbonic acid and sodium bicarbonate

bicarbonate binds to excess H+ to produce a weak acid, carbonic acid.
H+ + Buffer => H-Buffer

when H+ decreases, the inverse reaction will happen.
H-Buffer => H+ + Buffer


what are the three kinds of chemical buffers we have ?



what is the second line of defense for buffering ?

physiologic buffers, occur only when a change in pH has already occured.


what is ventilatory buffering ?

a physiologic buffer (second line of defense)
H+ increases, which stimulates the respiratory center to increase alveolar ventilation. reduces alveolar PCO2, which accelerates the recombination of H+ and HCO3- into carbonic acid (shift left) which reduces the H+ concentration in plasma


what is renal buffering

physiologic buffer (second line of defense)
renal tubules regulate acidity through complex chemical reactions that secrete ammonia and H+ into urine and reabsorb alkali, chloride, and bicarbonate


when renal problems occur, what happens to breathing ?

hyperventilation to compensate for excessively low plasma pH


how does pH regulation work in intense exercise ?

increased H+ concentration from CO2 production and lactate formation makes regulation more difficult

esp when blood lactate 30 mM or higher (extreme, brief bouts)

humans can temporarily tolerate these disturbances. however, pH below 7 means nausea, dizziness, headache + pain in active muscles.

anaerobic exercise makes buffering progressively more difficult.