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PHSI 208 > Gas Exchange and Transport > Flashcards

Gas Exchange and Transport Flashcards

1
Q

what is hypoxia?

A

decreased O2, from impaired diffusion or improper transport

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2
Q

what is hypercapnia?

A

excess CO2

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3
Q

1

A

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4
Q

2

A

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5
Q

2

A

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6
Q

sensors which prevent hypoxia and hypercapnia?

A

O2 sensor (needed for ATP production); CO2 (CNS depressant, acid precursor); pH (protein denaturation)

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7
Q

what are the two causes of low alv Po2 assuming perfusion is constant?

A
  1. Inspired air has low O2 content (high elevation = low Po2); 2. Alveolar ventilation–hypoventilation decrease rate and depth of breathing= increased airway resistance; or decreased lung compliance, CNS respiratory control issue
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8
Q

how can rate of diffusion be impaired?

A

low conc gradient, reduced SA, and reduced barrier permability

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9
Q

what affects the movement of gas from air to liquid?

A
  1. The pressure gradient of the gas
  2. Solubility of gas in liquid
  3. Temperature-relatively constant
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10
Q

what is mass flow?

A

movement of a substance per minute = O2 transport = CO x O2 conc

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11
Q

what is mass balance?

A

any substance in the body must remain constant

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12
Q

mass flow and balance together?

A

= Fick eq’n; CO x (Arterial [O2] - Venous [O2]) = QO2

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13
Q

Arterial conc of O2 under resting conditions?

A

200 mL O2/ L blood

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14
Q

Venous conc of O2 under conditions?

A

150 mL O2/ L blood

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15
Q

how does pH affect % sat of Hb?

A

the lower the pH, the more H to change the conformation of Hb–>less O2 binds–>more O2 for active tissues

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16
Q

what is the bohr effect?

A

shift in Hb saturation curve as a result of pH or CO2 change

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17
Q

how does CO2 affect Hb saturation?

A

increase aerobic metabolism results in increase CO2 production–>increases Pco2 in the blood->CO2 binds Hb & competes wtih oxygen, and is also converted to HCO3- + H

18
Q

how does temperature affect Hb saturation?

A

active muscles produce heat–>heat causes conf change of Hb, leading to decrease affinity for O2–>more O2 dropped off at very active muscles

19
Q

how does 2,3-BPG affect Hb saturation?

A

by-product of glycolysis–chronic hypoxia increases 2,3 BPG (RBCs release ATP during hypoxia), or ascending to igher altitudes increases 23BPG–> competes with Oxygen, decreases Hb’s affinity for O2

20
Q

what are the factors that affect % sat of Hb?

A

temp, pH, PCO2, and 2,3 BPG conc

21
Q

waht affects the total number of binding sites?

A

Hb content per RBC x # of RBCs

22
Q

what affects O2 bound to Hb?

A

% sat x total number of binding sites

23
Q

what is total artieral O2 content determined by?

A

PO2 of plasma (oxygen dissolved in plasma) and O2 bound to Hb

24
Q

what is PO2 of plasma determined by?

A

composition of inspired air, alveolar ventilation, oxygen diffusion between blood and alveoli, and adequate perfusion to alveoli

25
Q

what is alveolar ventilation controlled by?

A

rate and depth of breathing; airway resistance; lung compliance;

26
Q

what is oxygen diffusion between alveoli and blood determined by

A

surface area and diffusion distance

27
Q

what is diffusion distance influenced by?

A

membrane thickness and amount of interstitial fluid

28
Q

why is it important to remove CO2 from the body?

A
  1. excess CO2 can cause acidosis–>low pH disrupts H-bonds and causes denaturing of proteins;
  2. high amounts can cause CNS depression–>leads to confusion, coma, and maybe death
29
Q

how much CO2 can be dissolved in plasma, usually?

A

7% of the CO2

30
Q

how else is CO2 carried in the blood?

A

23% binds to Hb–> carbaminoHb; 70% is converted to HCO3 (bicarbonate) + H

31
Q

what is the purpose to convert CO2 to HCO3?

A
  1. Provides an additional means of CO2 transport from cells to the lungs
  2. HCO3- is available to act as a buffer for metabolic acids, stabilizing
    body’s pH
32
Q

what ensures equil is not reach from the conversion f CO2 to HCO3 + H?

A

removal of HCO3 from RBC via chloride exchanger, and binding excess H by Hb

33
Q

what is the current model for control of respiration?

A
  1. Respiratory neurons in the medulla control inspiratory and expiratory muscles
  2. Neurons in the pons integrate sensory information and interact with medullary neurons to influence ventilation
  3. Rhythmic pattern of breathing arises from a neural network with spontaneously discharging neurons
  4. Ventilation is continuously modulated by various chemo and mechano receptor-linked reflexes and by higher brain centers.
34
Q

what groups are involved in medulla-mediated respiration?

A

the nucleus tractus solitaris which contains the dorsal respiratory group of neurons;
the pontine resp group;
the ventral resp group

35
Q

how does the NTS/DRG function?

A

the nucleus tractus solitaris in the medulla contains the dorsal respiratory group of neurons–>mainly control inspiratory muscles via phrenic nerve and intercostal nerve during quiet respiration; the NTS receives input from the peripheral mechano and chemoreceptors;

36
Q

how does the PRG function in respiration

A

the pontine resp group provides tonic (always active) input to the DRG to help the medullary networks create a smooth resp rhythm (not essential for resp itself, but essential for smoothness)

37
Q

how does the VRG function in respiration?

A 
has a few areas with different functions:
•  Pre-botzinger complex: contain
pacemaker neurons that may
ini8ate respira8on
•  control muscles of active
inspira8on and expiration, remain
quiet otherwise
•  outputs that keep upper airways
open (tongue, larynx, pharynx), Some8mes outputs slow down too much while asleep: sleep apnea, snoring.
38
Q

what are the peripheral chemoreceptors, and what do they monitor?

A

aortic and carotid bodies (main sensors), sense changes in artieral PO2, PCO2, and H–>adjust ventilation rates accordingly; NOT always active

39
Q

where are central chemoreceptors located?

A

medulla

40
Q

how do central chemoreceptors function?

A

always active–>continuously providing input to resp control centre; mainly respond to changes in CO2–>CO2 in cerebrospinal fluid converts to HCO3 + H, and the central chemo receptors also sense the increase in H; H activates ASIC (acid-sensing ion channels) in neurons and transmit APs to resp control centre

41
Q

what ae the protective reflexes that guard the lungs from damage?

A
  1. irritant receptors–respond to inhaled particles or noxious gases; – Send input into the CNS, parasympathetic outputs then respond by causing bronchoconstriction
    – Leads to rapid shallow breathing and turbulent airflow to deposit irritant in mucosa
  2. stretch receptors–in lungs, prevent lung over-inflation–> Hering-Breuer inflation reflex
42
Q

how can receptors in muscles and joints affect respiration?

A

will anticipate physical exertion–>start increasing vent rates before any chemical changes have occurred in the blood

PHSI 208 (32 decks)

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