Medical Physiology - Pulmonary, Cell Membrane, Nervous System

Front 1

Normal values of Hb

Back 1

1.34mL O2/gm Hb
15gm Hb/100mL blood
20mL O2/100mL blood

Front 2

Factors that affect Hb-O2 binding (Hb-O2 dissociation curve)

Back 2

Increased CO2
Decreased pH
Increased temperature
2,3-biphosphoglycerate (BPG)

Front 3

How is CO2 transported in the blood?

Back 3

10% dissolved
30% is bound to Hb. This is called carbamino CO2.
60% is in bicarbonate (HCO3-).

Front 4

Chloride shift in non-lung tissue

Back 4

Bicarbonate is transported out of the RBC by a HCO3-/Cl- counter transporter.
Chloride is transported into the RBC.

Front 5

Chloride shift in lung tissue

Back 5

Bicarbonate is transported into the RBC, and chloride is transported out of the RBC.

Front 6

Haldane effect

Back 6

The deoxygenation of blood increases its ability to carry CO2.
In other words, it is how O2 affects Hb affinity for CO2.
Hb has greater affinity for CO2 and H+ than does HbO2. When O2 is bound to Hb, it has less affinity for CO2 and H+. When O2 is released, the opposite occurs.

Front 7

Cyanosis

Back 7

bluish color of tissue caused by the presence of more than 5 gm deoxyHb/dL in capillary bed.

Front 8

hypoxic hypoxia

Back 8

decreased O2 in blood

Front 9

Anemic hypoxia

Back 9

Decreased RBC
Decreased O2
Oxygen partial pressure is normal.
Can be caused by CO poisoning.

Front 10

Circulating hypoxia

Back 10

Too little oxygenated blood is delivered to the tissue.
Can be caused by vascular spasms, bloot clots, or CHF.

Front 11

Histotoxic hypoxia

Back 11

Cells are unable to utilize O2.
Can happen with cyanide poisoning.

Front 12

hypercapnia

Back 12

Increased CO2.
Can be caused by hypoventilation.
Results in respiratory acidosis.

Front 13

hypocapnia

Back 13

Below normal CO2.
Can be caused by hyperventilation.
Results in respiratory alkalosis.

Front 14

hyperbaric oxygen toxicity

Back 14

CNS O2 toxicity.
Requires exposure to a minimum of 1.5-2.0 atm of oxygen tension.

Front 15

Hyperbaric oxygen toxicity can cause what complications? Why?

Back 15

Can cause free radical formation, which can lead to inactivation of key enzymes essential to normal neurological function.
This can result in grand mal seizures.

Front 16

Normobaric oxygen toxicity

Back 16

Pulmonary oxygen toxicity.
Requires exposure to a minimum of 0.5 atm of oxygen tension for 18-24 hrs.

Front 17

Normobaric oxygen toxicity can cause what complications? Why?

Back 17

Can result in free radical formation, which destroy type II alveolar cells that secrete surfactant.
This can lead to pulmonary edema, atelectasis (collapse of alveoli), and hemorrhaging.

Front 18

High altitude acclimatization occurs in what five areas?

Back 18

Increased ventilation.
Increased RBC numbers and Hb concentration.
Increased diffusion capacity.
Increase in CO.
Cellular acclimatization.

Front 19

How does increased ventilation influence high altitude acclimatization?

Back 19

Arterial chemoreceptors increase alveolar ventilation to about 160% of normal initially, then up to 500% of normal after a few days.

Front 20

Increased ventilation occurs in high altitude acclimatization. What problem can this potentially create?

Back 20

Increased ventilation causes a drop in CO2 partial pressure, which will remain low as long as the person is at high altitude.
This can lead to respiratory alkalosis from blowing off too much CO2.

Front 21

How does increased diffusion capacity influence high altitude acclimatization?

Back 21

Increased diffusion capacity is a function of increased surface area and perfusion rate.
Increased tidal volume, pulmonary arterial pressure, and increased capillary numbers in the lungs also contribute to increased surface area and therefore increased diffusion capacity.

Front 22

How does high altitude acclimatization affect cardiac output?

Back 22

Initially there is an increase in CO by about 30%.
As hematocrit increases over time, however, CO decreases.

Front 23

Major respiratory control centers

Back 23

Medullary respiratory center
Pons respiratory center

These are part of the reticular nuclei.

Front 24

Medullary respiratory center

Back 24

Neurons send efferent fibers to motor neurons in C3, C4, and C5.
These neurons in turn send axons out to form the phrenic nerves, which innervate the diaphragm.

Front 25

Phrenic nerves

Back 25

Innervate the diaphragm.

Front 26

2 parts of the medullary respiration center

Back 26

Dorsal respiratory group
Ventral respiratory group

Front 27

Dorsal respiratory group

Back 27

Part of the medullary respiration center.
Mostly inspiratory neurons responsible for quiet respiration rhythm.

Front 28

Ventral respiratory group

Back 28

Part of the medullary respiratory center.
Inactive during quiet respiration.
More involved when doing something other than quiet respiration.

Front 29

Ventral respiratory group during exercise

Back 29

Expiratory neurons activate motor neurons in the spinal cord controlling the abdominal and internal intercostal muscles.
Inspiratory neurons increase input signal into the motor neurons controlling the accessory inspiration muscles as well as the diaphragm.

Front 30

2 parts of the ventral respiratory group

Back 30

rostral VRG

caudal VRG

Front 31

Rostral ventral respiratory group

Back 31

Inspiratory neurons

Front 32

Caudal ventral respiratory group

Back 32

Expiratory neurons

Front 33

The dorsal respiratory group is located mostly where?

Back 33

nucleus solitarius

Front 34

The ventral respiratory group is located mostly where?

Back 34

nucleus ambiguus and nucleus retroambiguus.

Front 35

2 parts of the pons respiratory center

Back 35

Pneumotaxic center
Apneustic center

Front 36

Pneumotaxic center

Back 36

Part of the pons respiratory center.
Sends fibers to the dorsal respiratory group that help switch off the inspiratory neurons.

Front 37

What happens when the pneumotaxic center is destroyed?

Back 37

Results in a breathing pattern consisting of prolonged inspiratory gasps abruptly interrupted by very brief expiration.
This is called apneusis.

Front 38

Apneustic center

Back 38

Part of the pons respiratory center.
Inhibits inspiratory neurons from being switched off, thus is antagonistic to the pneumotaxic center.

Front 39

Hering-Breuer reflex

Back 39

Stretch receptors in smooth muscle of bronchi and bronchioles send fibers via the vagus nerve to the dorsal respiratory group, turning these neurons off.
Prevents over-filling of the lungs.
Not active until tidal volume is about 1.5L.

Front 40

What role does the partial pressure of oxygen play regarding respiration rate?

Back 40

Under normal conditions, the partial pressure of oxygen plays little role in respiration rate.
This is b/c chemoreceptors in the carotid and aortic bodies are activated only when arterial Po2 falls below 60mmHg, which usually does not happen under normal conditions.

Front 41

What are the peripheral chemoreceptors that detect changes in the partial pressure of oxygen?

Back 41

Primarily carotid bodies and some aortic bodies.

Front 42

Aortic bodies send fibers where via what nerve in regards to respiratory control?

Back 42

Send fibers to the dorsal respiratory group via the vagus nerve.
Activated only when arterial Po2 falls below 60mmHg, which usually does not happen under normal conditions.

Front 43

Carotid bodies send fibers via what nerve in regards to respiratory control?

Back 43

Glossopharyngeal nerve.

Front 44

With CO poisoning, what happens to the partial pressure of oxygen? How does respiration change?

Back 44

The partial pressure of oxygen remains unchanged, thus there is no increase in respiration.
Neurons die of O2 starvation.

Front 45

Where are the central chemoreceptors located?

Back 45

Near the respiratory center in the medulla on the ventral lateral surface, between CN VII and CN X.

Front 46

Central chemoreceptor function

Back 46

Very sensitive to CO2 indirectly via a change in pH of ECF, not necessarily the partial pressure of CO2.
Also sensitive to H+ in the ECF, which is induced by CO2. Increase in CO2 in plasma will cause CO2 to diffuse down its concentration gradient into the ECF.

Front 47

What effect does H+ in the plasma have on central chemoreceptors?

Back 47

H+ in plasma has little effect on central chemoreceptors.
Because H+ can't cross the blood-brain barrier, whereas CO2 can.
Central chemoreceptors are sensitive to H+ in the ECF.