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Physiology > Lecture 13 Respiratory System Part 2 > Flashcards

Lecture 13 Respiratory System Part 2 Flashcards

1
Q

daltons law

A

total pressure of gas mixture is the sum of each gas partial pressure

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2
Q

percent of O2 in air

A

21%

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3
Q

pressure at sea level

A

760 mmHg

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4
Q

pressure H2O in wet air

A

47 mmHg

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5
Q

PO2 in wet air vs dry air - include calculations

A
  • wet = .21(760-47) = 150mmHg
  • dry = .21(760) = 159 mmHg
  • not a large difference
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6
Q

at sea level

  • atmospheric pressure
  • PO2 in air
  • PO2 in alveoli
  • PO2 arterial
A
  • 760mmHg
  • 159 PO2 in air
  • 105 PO2 in alveoli (large decrease because O2 is removed so quickly in lungs)
  • 100 PO2 arterial
  • think of PO2 alveoli as pressure pushing O2 into blood vessels of lungs
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7
Q

affect of altitude on air pressure

A

increased altitude decreases air pressure

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8
Q

arterial PO2 at 10k and 20k

A
  • 10k = 65mmHg

- 20k = 35mmHg

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9
Q

henry’s law aka 3 factors effecting gas movement

A
  • solubility of gas in liquid (CO2 is more soluble)
  • partial pressure of gas (this is the determining factor)
  • temperature - more can be dissolved in cold liquid
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10
Q

dissolve/free O2

  • what is it a good measure of
  • amount in blood
  • what does it depend on
A
  1. 3ml/100ml
    - very little and depends on PO2
    - good measure of lung function
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11
Q

total O2 content

  • what does it depend on
  • amount in blood
A

20ml/100ml

- depends on hematocrit

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12
Q

why do we intubate/ventilate people

A
  • ventilation only increases hemoglobin saturation from 97-100%
  • increases dissolved O2 which can be used by cells
  • cells cannot use bound O2
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13
Q

increase in hemoglobin saturation from intubation/ventilation

A

97 to 100%

not much!

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14
Q

PCO2 pressure in veins and arteries - specific numbers

A
  • veins = 46mmHg

- arteries = 40 mmHg

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15
Q

what happens if pressure in pulmonary circulation is too high

A
  • high pressure –> fluid leaves capillaries causing pulmonary edema –> short of breath and cant lay down
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16
Q

ventilation perfusion matching - how is this opposite of systemic circulation

A
  • pulmonary capillaries and arteries dilate in more ventilated area of lungs (more O2 means more O2 to be absorbed by more blood)
  • in systemic circulation, more O2 means the area has enough blood –> vasconstriction –> blood shunting to other areas where blood is needed
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17
Q

apex vs base of lungs - ventilation vs perfusion

A
  • apex = overventilated and under perfused

- based = underventilated and overperfused

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18
Q

hemoglobin structure

A
  • 4 polypeptides 2 alpha and 2 beta

- 1 heme group on each polypeptide

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19
Q

heme group structure and 6 bonds

A
  • porphoryin ring with a metallic ion in the center
  • in this case Fe
  • 4 bonds to N to attach to prophoryin ring, 1 attaches to polypeptide, 1 attaches to oxygen
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20
Q

oxyhemoglobin and deoxyheomglobin, what type of iron

A
  • oxyhemoglobin when O2 attached, deoxyhemoglobin when no O2 attached
  • Fe2+ ferrous ion
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21
Q

oxyhemoglobin saturation - definition and normal value

A

oxyhemoglobin / total hemoglobin - normally 97%

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22
Q

methemoglobin - what type of iron, mechanism to make i able to carry oxygen

A
  • Fe3+, cannot bind to O2

- methemoglobin reductase to convert Fe3+ to Fe2+

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23
Q

carboxyhemoglobin

A
  • CO bound, bond is 200x stronger than oxygen
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24
Q

anemia

A
  • low hemoglobin
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25
Q

polycythemia - definition and absolute vs relative

A
  • relative = transient, could be due to dehydration

- absolute = more RBC made due to hypoxia, high altitude, infection, smoking

26
Q

erythropoietin

A
  • hormone made by kidneys to increase RBC production in red bone marrow
27
Q

oxygen dissociation curve and importance of plateau

A
  • x axis = PO2, y axis = oxyhemoglobin saturation

- plateau means that life at high elevation is supported

28
Q

Bohr effect and relation to increased metabolism

A
  • as pH decreases and more acidic graph shifts right and hemoglobin affinity is lowered
  • increased metabolism = more acid produced adn more O2 reelased
29
Q

temperature, oxygen dissociation curve, and increased metabolic activity

A
  • high temp = curve shifted to the right, affinity for oxygen decreases
30
Q

CO2, oxygen dissociation curve, and increased metabolic activity

A

-high CO2 shifts curve to the right, lowers oxygen affinity, CO2 produced during metabolism so more O2 released

31
Q

2,3 DPG - where does it come from, what conditions cause it, mechanism and affect on hemoglobin

A
  • intermediate in glycolysis/anaerobic respiration

- binds to beta polypeptide and causes change that decreases O2 affinity so more O2 released

32
Q

fetal hemoglobin

A
  • 2 alpha and 2 gamma
  • 2,3 DPG cannot bind to gamma so it has higher affinity for O2
  • this way O2 is transferred from maternal to fetal blood
33
Q

sickle cell anemia

  • hemoglobin type and affect
  • sickle cell crisis
  • heterozygous vs homozygous for trait
A
  • hemoglobin S due to 1 amino acid change
  • during hypoxia the hemoglobin polymerize causing sickle shaped RBC that have a shorter life span and cannot fit through blood vessels
  • sickle cell crisis = wide spread ischemia and whole body pain
  • heterozygous = sickle cell trait, occasional crisis
  • homozygous = sickle cell disease, many crisis and constant need for blood transfusions
34
Q

thalassemia and 2 types

A
  • common in mediterranean people

- alpha/beta thalassemia based on if alpha/beta polypeptide cannot be made properly

35
Q

myoglobin and comparison to hemoglobin

A
  • only found in muscle
  • higher affinity for O2 and only releases O2 when O2 is very low
  • only carries 1 O2 vs the 4 that hemoglobin carries
36
Q

different forms of CO2 in body and percentage distribution

A
  • dissolved 20%
  • carbaminohemoglobin 10%
  • bicarbonate 70%
37
Q

CO2 and bicarbonate chemical equation

A

CO2 + H2O –> carbonic anhydrase enzyme catalyzes reaction –> carbonic acid –> freely dissociates to H+ and bicarbonate ion

38
Q

why CO2 is a volatile acid

A
  • can be released /exhaled
39
Q

chloride shift

A
  • in tissues
  • CO2 produced in tissues –> enters RBC and becomes bicarbonate –> bicarbonate leaves RBC and goes into blood and Cl- goes in so RBC is electrically neutral
40
Q

reverse chloride shift

A
  • in lungs

- bicarbonate enters RBC to be converted to CO2 –> Cl exits RBC so that RBC is electrically neutral

41
Q

le chatliers principle

A
  • for a reaction that can occur in both directions, reaction moves from higher concentration to lower concentration
42
Q

acid production and 2 systems that maintain pH

A
  • produced by metabolic reactions
  • kidneys/renal system release H+ in urine
  • respiratory system and bicarbonate buffering gets ride of H+ as CO2
43
Q

respiratory acidosis and causes

A
  • hypoventilation (high CO2 concentration) –> H+ builds up
  • caused by opioids and heroin which decrease breathing rate
44
Q

respiratory alkalosis and causesa

A
  • hyperventilation, low CO2 and H+
45
Q

metabolic acidosis and 2 causes

A
  • high H+ due to metabolic causes –> high CO2 in blood –> brain increases rate of breathing
  • diabetes - lots of acidic ketone bodies made, cause s kussmal breathing that is tachypnea and hyperpnea
  • bicarbonate loss through diarrhea so H+ cannot be buffered
46
Q

metabolic alkalosis

A
  • too much bicarbonate so not enough H+ in blood
47
Q

3 respiratory control centers

A
  • rhythmicity center in MO

- pneumotaxic and apneustic center in pons

48
Q

rhythmicity center - 2 type of neurons and function

A
  • inspiratory neurons innervate LMN that control inspiratory muscles like diaphragm
  • expiratory neurons inhibit inspiratory neurons
  • exhalation is passive
49
Q

apneustic center

A
  • excites inspiratory neurons causing inhalation
50
Q

pneumotaxic center

A
  • inhibits apneustic center ultimately leading to exhaation
51
Q

peripheral chemoreceptor location, what is monitored, and through what nerve is information sent

A
  • located in aortic and carotid bodies
  • monitors blod CO2, H+, and O2
  • sends information to rhythmicity cente via vagus nerve
52
Q

central chemoreceptors - location

A
  • located in MO
53
Q

describe connection between other parts of the brain and rhythmicity center

A
  • other parts of brain send info to rhythmicity center explaining why thoughts, emotions, and visual information can cause changes in breathing rate
54
Q

voluntary breathing - what parts of the brain are involved

A
  • frontal cortex sends commands directly to LMN

- autonomic responses can override voluntary breathing control

55
Q

blood brain barrier - can H+ and CO2 pass through?

A
  • CO2 can pass through but H+ cannot
56
Q

central chemoreceptor vs peripheral chemoreceptor - how do they detect hypoventilation and how long does it take

A
  • peripheral: stimulated by H+
  • central - stimulated by CO2 which crosses blood brain barrier and is then converted to H+
  • central has a larger affect but takes a longer amount of time
57
Q

total minute volume - definition and normal amount

A
  • amount of volume exhaled in a minute
  • tidal volume * breath per minute
  • 4L/minute
58
Q

PCO2 range and link to rhythmicity cente r

A

PCO2 = tight range of 40mmHg +- 2

- rhythmicity center tries to regulate this amount in the blood

59
Q

effect of PCO2 vs PO2 on ventilation - describe the graph

A
  • overall PCO2 has a much larger effect
  • as PCO2 rises total minute volume gradually then steeply rises
  • total minute volume only increases when PO2 is very low and even then it doesnt increase that much
60
Q

hypoxic drive - when does it occur and what is the mechanism

A
  • PO2 = 70mmHg = 10k altitiude

- carotid bodies respond directly to low O2

61
Q

why is there greater sensitivity to CO2 then O2

A
  • high CO2 = high H+ = acidic and protein denaturation

Physiology (25 decks)

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