4: Hsf A9: Respiration Ii

Front 1

What is alveolar ventilation adjusted to do?

Back 1

Keep constant PO2 and PCO2 in the alveoli as the body's oxygen demands change.

Front 2

What do the following do:

1) Pneumotaxic center
2) Ventral respiratory group
3) Dorsal respiratory group
4) Vagus and glossopharyngeal
5) Respiratory motor pathways

Back 2

1) Regulate depth of inspiration. High output increases frequency.
2) Control inspiration and expiration. Increases Va with exercise
3) Active inspiration only. Tidal "quiet" breathing, passive expiration.
4) Stretch receptors in lung (Hering-Breuer reflex), chemoreceptors (brain, carotid, aorta)
5) To inspiratory and expiratory muscles

Front 3

1) What do sensory neurons in the brain, aorta, and carotid do?
2) What gives rise to intrinsic breathing rhythm of the respiratory muscle?

Back 3

1) Detect changes in blood composition, stimulate or inhibit intrinsic pattern of ventilation
2) Spontaneously active "pattern generator" in the respiratory center of the medulla

Front 4

If all inputs to the respiratory center are cut off, what kind of pattern does breathing follow?

Back 4

"Ramp" signal

Front 5

During normal breathing, the instrinsic ramp signal is modified by inputs from what 3 areas of the body?

Back 5

1) Lungs (stretch receptors)
2) Higher brain centers (emotion, anticipation of exercise)
3) Chemoreceptors (blood gas composition)

Front 6

1) What in the lungs controls the intrinsic breathing rhythm?
2) What happens if you cut input from the area?

Back 6

1) Stretch receptors - Hering Breuer reflex.
2) Cutting stretch receptor input from lungs will produce deeper inspiration

Front 7

1) What two things does athletic training increase?
2) What do these increase do?
3) What else becomes more sensitive to increase PCO2 levels?

Back 7

1) Affects cerebral cortex, increases alveolar ventilation, sensitivity of the respiratory center to increased arterial PCO2.
2) Anticipate level of activity based on motor memory
3) Chemoreceptors

Front 8

1) What controls ventilation based on blood gas composition?
2) How does CSF react to increased PCO2?

Back 8

1) Chemosensitive neurons in the medulla that detect elevated PCO2 and lowered pH.
2) It's well buffered so a chance in PCO2 will create a greater reduction of pH.

Front 9

1) What happens to patient with reduced blood flow from lungs to brain?
2) What is Cheyne-Stokes breathing? What causes it?

Back 9

1) Increase brain PCO2, causes burst of ventilation that lowers PCO2.
2) Episodic breathing with periods of apnea. Conditions where respiratory control is diminished.

Front 10

How does a small increase in arterial PCO2 eventually stimulate Va?

Back 10

Small increase in arterial CO2 -> lowers pH of CSF bathing chemosensitive cells of medulla -> stimulates Va

Front 11

1) How do small increases in arterial PCO2 affect ventilation?
2) What causes sleep apnea?
3) What is the function of hyperventilation?
4) Why do snorkeling divers hyperventilate to stay underwater longer? What happens if ventilation is suppressed long enough that PCO2 falls too low?

Back 11

1) Cause LARGE increases in ventilation
2) Lower sensitivity to CO2 during sleep
3) Lower alveolar and arterial PCO2.
4) Lower arterial PCO2 and raise pH, blocking "inspiratory drive" by pH sensitive neurons. Shallow water blackout.

Front 12

1) What is the output of the carotid body like under normal O2 conditions? Abnormal?
2) What normally dictates rates of ventilation?

Back 12

1) Normally low, but increases rapidly under abnormally low conditions
2) PCO2

Front 13

What is oxygen carried by? Describe its makeup.

Back 13

Hemoglobin - tetramer - 4 subunits - 2 alpha and 2 beta dimers. Each subunit has a heme group that attracts/reversibly binds O2. Bound in lungs to hemoglobin, unbound at tissues.

Front 14

1) What is the first thing that happens upon oxygen binding hemoglobin?
2) How does oxygen get uncoupled from hemoglobin?

Back 14

1) One pair of alphabeta subunits rotates to increase oxygen binding affinity
2) 2,3 BPG interacts with beta subunits to decrease oxygen binding affinity

Front 15

1) At what PO2 do you find a greater amount of oxygen unloading from hemoglobin to support increase metabolic activity?
2) What is the affinity for hemoglobin measured as?

Back 15

1) 40 mmHg
2) p50 - partial pressure at which hemoglobin is half saturated. Lower p50 = greater affinity for oxygen

Front 16

Hemoglobin:

1) Where is it located?
2) How much O2 can it bind?
3) What is the normal Hb level in blood?
4) What is the normal oxygen binding capacity /100 ml of blood?
5) What is the status of Hb at alveolar PO2?
6) At tissue PO2, how much HBO2 has dissociated?

Back 16

1) RBCs
2) 1.34 ml O2/gram
3) 15 g/100 ml
4) 20 ml O2/100 ml blood (20% of blood is oxygen)
5) Near saturation
6) 20-25%, more is delivered during exercise

Front 17

What 4 factors cause a decrease in Hb affinity for O2 and increased unloading?

Back 17

1) Increased hydrogen ions
2) Increased CO2
3) Increased temp
4) Increased BPG (metabolite of glycolytic pathway)

Front 18

What is the Bohr effect?

Back 18

Regulation of oxygen binding by hydrogen ions produced by carbon dioxide from the tissues. Facilitates O2 loading at lungs, unloading at tissues (pH lower at tissues)

Front 19

Describe the formation of H+ that eventually decreases affinity of Hb for oxygen.

Back 19

1) CO2 and H2O combine due to carbonic anhydrase, make H2CO3
2) H2CO3 dissociates, makes H+ that binds to Hb, decreases affinity for O2, unloading and delivery to tissue occurs
3) HCO3- leaves RBC in exchange for Cl- entry (chloride shift)

Front 20

Describe what happens with low PCO2 in alveolar air to facilitate loading of O2

Back 20

HCO3- taken up by chloride shift, H+, HCO3- associated, raises pH and increases O2 affinity to facilitate O2 loading by Hb.

Front 21

1) How does the curve of fetal hemoglobin compare to the curve of adult hemoglobin?
2) Why does fetal hb have a higher affinity than maternal RBCs?
3) What vein carries fetal blood?

Back 21

1) Much steeper curve, greater affinity so fetus can load oxygen from maternal circulation
2) It doesn't bind 2,3, BPG as well as maternal Hb
3) Umbilical vein

Front 22

Myoglobin:

1) Where is it found?
2) What does it do?
3) What is its affinity for oxygen like? What is its p50?
4) Where is it abundant?
5) Why is carbon monoxide fatal?

Back 22

1) Red skeletal muscle
2) Permits O2 storage, allows oxygen transfer to tissues
3) High O2 affinity. p50 = 5 mmHg, ~pO2 of muscle in mitochondria
4) In skeletal muscle of diving animals
5) It has an extremely high affinity for O2, competes for the binding.

Front 23

Besides O2, what can hemoglobin transport?

Back 23

Nitric oxide, so area of vasodilation can spread with circulation

Front 24

What three forms is CO2 carried in the blood? Which one is the main form?

Back 24

Dissolved CO2, bicarbonate, carbamino CO2. Bicarbonate is most common

Front 25

What is the Haldane effect?

Back 25

Unloading of O2 at the tissues facilitates formation of carboxy hemoglobin (HBCO2, 23%)

Front 26

What does hyperventilation do and what does it cause?

Back 26

Lowers alveolar PCO2 (alveolar PCO2 is where CO2 gets unloaded), and thus lowers PCO2 returning to heart and systemic circulation (hypocapnia)

Front 27

1) Cytosol pH? H+?
2) Arterial pH? H+?
3) Venous pH? H+?
4) What does an increase in PCO2 result in?

Back 27

1) 7.0 (most CO2), 10^-7
2) 7.4 (least CO2), 4x10^-8
3) 7.35 (middle CO2), 4.5x10^-8
4) Increased carbonic acid formation and acidosis

Front 28

What is the equation for carbonic acid formation? What effect do increasing Va have on this? What maintains HCO3- concentrations?

Back 28

CO2 + H2O -> H2CO3 -> H+, HCO3-

Increasing Va decreases ECF CO2, decreases carbonic acid in plasma.

HCO3- maintained at 23-25 mM by renal tubular absorption

Front 29

What is the Ka equation for H2CO3 dissociation?

What does pH =?

Back 29

H2CO3- -> H+ + HCO3-

so Ka = ([H+] [HCO3-]) / [H2CO3]

pH = pKa + log10 of [HCO3-]/ [H2CO3]
= 6.1 + log10 [HCO3-, 24] / alpha x PCO2 (.03 x PCO2)

Front 30

What is metabolic acidosis with compensatory respiratory alkalosis?

Back 30

Addition of acid is buffered by HCO3 to form H2CO3, formation of CO2 can be reduced by increasing Va

Front 31

What causes mountain sickness? What compensates for depressed PCO2 in the long run?

Back 31

Va increasing to maintain PO2, which causes a drop in PCO2 .

Decrease in plasma bicarbonate due to decreased HCO3- reabsorption by the kidneys.

Front 32

At high altitude, what is the primary stimulator of ventilation?

Back 32

PO2 - PCO2 is reduced.