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Physiology unit 4 > Respiratory acid-base balance and control of ventilation > Flashcards

Respiratory acid-base balance and control of ventilation Flashcards

1
Q

What is the purpose of the chloride shift

A

Allows the bicarbonate reaction to happen in RBCs

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2
Q

What does the chloride shift exchange and where

A

Exchange Cl- for HCO3- across RBC membrane

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3
Q

What are the 2 functions for Cl shift

A
  1. remove product of the bicarb reaction to keep the raction going
  2. maintain membrane potential
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4
Q

Which membrane protein is needed for the cl shift

A

Anion exchanger (AE1)

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5
Q

What are the 3 methods of transporting CO2

A
  1. in the form of bicarbonate
  2. CO2 dissolves in bicarbonate
  3. CO2 binds to hemoglobin
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6
Q

Where does Bicarbonate move in tissues for chloride shift

A

HCO3 out, Cl- in to deal with High CO2

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7
Q

Where does Bicarbonate move in lungs for chloride shift

A

HCO3 in, Cl out so that CO2 is released into lungs

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8
Q

Why does venous blood have a higher hematocrit

A

RBCs swell with water because they have - ions inside of them (either bicarbonate or chloride inside of them) which increases osmotic pressure (once passes into arterial side, doesn’t have these bicarb or cl)
Also water loss in capillaries

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9
Q

Where does carbonic anhydrase work

A

Inside of RBCs

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10
Q

Rank the 3 buffer systems in the body

A
  1. Carbonic acid bicarb system
  2. Hemoglobin
  3. Plasma proteins
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11
Q

What is the definition of acidosis

A

pH of 7.35 or lower

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12
Q

Most common cause of respiratory acidosis

A

hypoventilation
AcidOOOOsis= hypOOOventilation

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13
Q

What are causes of respiratory acidosis

A

HypOOOventilation, short term rise in CO2 above 40mmHG
emphysema
overdose on morphine/narcotics affects medulla

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14
Q

Compensation of respiratory acidosis

A

increased urine secretion of H+ in the PCT, DCT, or Collecting duct!
Increased retention of HCO3- in the the PCT

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15
Q

Respiratory alkalosis definition

A

pH of 7.45 or Higher

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16
Q

Most common cause of respiratory Alkalosis

A

Hyper ventilation

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17
Q

Metabolic acidosis causes

A

Ketone bodies in DM
Starvation (liver form ketone bodies)
Severe diarrhea–>loss of bicarb rich juices

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18
Q

Metabolic alkalosis causes

A

Diuretics
Vomitting (flu or self-induced bulimia)
Loss of stomach acid

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19
Q

Compensation for respiratory alkalosis

A

Increased reabsorbtion of H+ in kidneys (In PCT)
Decreased retention of HCO3-

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20
Q

Compensation for metabolic acidosis

A

Increased ventilation to get rid of CO2
Increased H+ secretion in kidneys
Increased retention of HCO3-

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21
Q

Does increased ventilation increase or decrease CO2

A

Decreases CO2
(Hypoventilation= acidOsis, so breathing less leads to buildup of acid and CO2)

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22
Q

Metabolic alkalosis causes

A

diuretics, vomiting (bulimia or loss of stomach acid)

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23
Q

Compenstion for metabolic alkalosis

A

Increased reabsorbtion of H+
Decreased retention of HCO3-
Decreased Ventilation (Hold onto more CO2, Hypoventilation leads to Acidooosis, so retain more CO2 when in alkalosis is good)

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24
Q

What is the difference in chemical concentration between chronic and acute respiratory acidosis

A

Chronic respiratory acidosis has a higher pH, lower H+ concentration, and higher HCO3

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25
Q

What is the difference in chemical concentration between chronic and acute respiratory alkalosis

A

Chronic respiratory alkalosis has a lower HCO3- level, a lower pH, and a higher H+ concentration.

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26
Q

Why do chronic respiratory acidosis and alkalosis have more stabilized values than the acute versions?

A

Because the kidneys have time to secrete or hold onto H+ and HCO3 ions, so they can balance the levels

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27
Q

What is the difference in CO2 levels in respiratory vs metabolic acidosis

A

CO2 levels are lower in metabolic acidosis because lungs can help get rid of CO2- they can hyperventilate, but in respiratory acidosis, they are the problem and can’t be used to fix it.

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28
Q

What is the difference in CO2 levels in respiratory vs metabolic alkalosis

A

Alkalosis means that there is a lack of CO2 and H+. Metabolic alkalosis can use the lungs, so CO2 levels are higher in metabolic alkalosis because the lungs can hypoventilate and hold onto CO2.

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29
Q

What is the primary concern in hypoxemia (Hypoxic hypoxemia)

A

Not enough O2 in the blood, the arterial blood has low O2 levels

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30
Q

What is the primary concern in anemic hypoxia

A

low hemoglobin levels–>not enough hemoglobin to hold the oxygen needed in the blood

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31
Q

What is the primary concern in ischemic hypoxia

A

low blood flow to tissues

32
Q

What is the primary concern in histotoxic hypoxia

A

Toxins impair O2 USAGE in a cell– the tissue can’t use O2

33
Q

Why is there a large increase in ventilation at high altitude

A

decrease in O2 in blood, decreased O2 saturation

34
Q

What effect does high altitude have on CO2 and pH?

A

Decrease CO2 levels, Decrease levels of H+ which increases pH

35
Q

What effect does high altitude have on the O2 hemoglobin dissociation curve

A

Leftward shift
Easier loading of O2 at lungs, harder to unload at tissues because blood is desaturated (67% at top of everest)
Low O2 stimulates EPO to increase hematocrit

36
Q

What type of anemia occurs at high altitude

A

hypoxemia due to high altitude–> decreased O2 blood saturation so not enough O2 in blood

37
Q

What type of anemia is caused by Right to Left shunting in the heart

A

Congenital heart diseases result in a right to left shunt that causes hypoxemia (hypoxic hypoxemia) because there is not enough O2 in arterial blood

38
Q

What happens to O2 levels and ventelation when there is a hypoxic V/Q Mismatch (i.e. ventilation problems)

A

Leads to a decrease in O2 saturation and decrase in Ventilation, it is compensated for by lungs, but there is still an overall decrease in saturation.

39
Q

Walk through the steps of the shifting of the oxygen-hemoglobin dissociation curve at high altitude

A

Decreased O2 in blood–>increased Ventilation–>Decreased CO2–>Left shift–>Increased O2 saturation

40
Q

Hypernea vs hyperventilation

A

Hypernea: Increased ventilation in response to a true increase in O2 demand such a metabolism
Hyperventilation: Pathological increase in ventilation not triggered by O2 demand (Decrease in CO2 levels because the O2 is not low to start with)

41
Q

What is voluntary control of respiration due to

A

respiratory motor neurons (intercostal muscles under voluntary control)

42
Q

What is automatic control of respiration due to

A

Pacemaker cells in the medulla (Pre-botzinger complex is a grouping of automatically depolarizing cells)
- Have cervical portion and thoracic portion

43
Q

Where is automatic control of respiration in the body

A

In the medulla in pre- Botzinger complex, automatically depolarizing cells)

44
Q

What are the 2 portions of the autonomic control of respiration

A

Cervical portion- connects to phrenic nerve and controls diaphragm
Thoracic portion- Controls intercostal muscles (intercostal nerves innervate these)

45
Q

The dorsal respiratory group nuclei connects to which nerve and muscle

A

Connects to phrenic nerve that innervates diaphragm (cervical portion)

46
Q

The Ventral respiratory group nuclei connects to which nerve and muscle

A

Connects to intercostal nerve and internal/external intercostals for the thoracic portion of autonomic control

47
Q

Where is the location of central chemoreceptors

A

Medulla oblongata- sense the CSF

48
Q

What is the location of peripheral chemoreceptors

A

Carotid and aortic bodies (sense in blood and sinusoidal capillaries)

49
Q

What stimulates central chemoreceptors

A

the level of CO2 (strongest) and O2/H+ in the CSF

50
Q

What do chemoreceptors do when they sense high levels of CO2, H+, and low levels of O2

A

Increase ventilation to get rid of CO2 and decrease pH

51
Q

What do chemoreceptors do when they sense Low levels of CO2, low levels of H+, and high levels of O2

A

Decrease ventilation to hold onto CO2 and increase H+/decrase pH

52
Q

What is the hering-breuer reflex driven by? Describe the inflation and deflation reflexes

A

stretch receptors in the lungs
Inflation reflex: Increased duration of expiration produced by lung inflation
Deflation reflex: Decrease in duration of expiration produced by lung deflation

53
Q

What is the slowly adapting reflex for non-chemical reflexive action on ventilation

A

Hering-breuer reflex

54
Q

What is the rapidly adapting reflex for non-chemical reflexive action on ventilation

A

Irratent receptors- activate quickly and cause coughing.

55
Q

What is the rapidly adapting receptor stimulated by

A

chemicals like histamine

56
Q

What does activation of the rapidly adapting receptor cause

A

activation in the trachea leads to coughing, bronchoconstriction, and mucous secretion
Activation in lungs leads to hyperpena(increased ventilation)

57
Q

Where are C-fibers found and what are they stimulated by

A

Found next to pulmonary capillaries (Juxtacapillary receptors, J receptors). Stimulated by hyperinflation or capsacin

58
Q

What does C-fiber stimulation cause

A

Pulmonary chemoreflex: stimulated by apnea –> rapid breathing, bradycardia, hypotension

59
Q

What is the non-chemical reflexive action that relates to joints and muscles in our body?

A

Proprioceptors and the active and passive movements of joints stimulate respiration. Important for exercise ventilation, drives ventilation

60
Q

What are the nerves related to coughing vs sneezing

A

Coughing: Vagus and glosopharyngeal
Sneezing: Trigeminal nerve

61
Q

Where does irritation occur in coughing vs sneezing

A

Coughing: Irritation of trachea, bronchi
Sneezing: Irritation of nasal mucosa

62
Q

Is the glottis open or closed in coughing vs sneezing

A

Coughing: Closed glottis
Sneezing: Open glottis

63
Q

What is a hiccup

A

spasmodic contraction of diaphragm. Inspiration leads to the diaphragm suddenly closing

64
Q

What does a yawn increase

A

Increases venous return
May open collapsed alveoli

65
Q

What are the factors in exercise that increase ventilation

A
  1. Chemoreceptors in muscle sensing CO2 levels
  2. Psychological stimuli (anticipation and beyond)
  3. Proprioceptors
66
Q

What is the primary driver of ventilation

A

CO2

67
Q

Where does an increasing level of CO2 come from

A

Byproduct of oxidative metabolism (primarily) and buffering acid (buffering of H+ that comes from lactate in anaerobic buildup)

68
Q

From the beginning of exercise until minute 2-3, what systems do we rely on

A

Use Creatine phosphate and anaerobic systems. Get into an O2 deficit since we can’t get it caught up immediately

69
Q

What system begins to work after minute 3 of exercise

A

Aerobic system–> catches up and steady state oxygen uptake is achieved.

70
Q

What is the phenomenon of EPOC

A

Excess post-exercise oxygen consumption
- Increase in body temp, increase in epi levels in blood, O2 storage, need to take the build up lactic acid and turn to pyruvate in cycle. All of these things take oxygen

71
Q

What causes ventilation to increase immediately after beginning exercise

A

no buildup of CO2 yet, but the anticipation of exercise and the proprioceptors cause the ventilation to increase immediately

72
Q

What causes ventilation to increase in moderate exercise

A

Driven by an increase in CO2 levels from oxidative metabolism
Increase in body temperature and extracellular K stimulates chemoreceptors around muscles

73
Q

What causes Ventilation to increase in vigorous exercise

A

Increase in CO2 from oxidative metabolism and buffering

74
Q

What type of neuron increases in sensitivity with exercise

A

Afferent neuron sensitivity to CO2 increases with exercise (the same amount of CO2 leads to an increase in ventilation)

75
Q

What is the relationship between lactate and ventelation

A

The point of lactate threshold is when the point of ventallatory threshold increases ( Don’t always increase at the same time, but when there is more lactate in the blood we need a buffer, so more cO2 from the buffer which increases ventelation rate)

76
Q

What changes in ventilatory response with exercise training

A

The ventaltory threshold occurs at a higher percent of max effort (from 50% to 75%) after training.

This is due to an increased power of the oxidative system, so there is less reliance on anaerobic system, so there is no production of extra CO2 until later in exercise (and therefore higher ventilation occurs later in exercise)

77
Q
A

Physiology unit 4 (5 decks)

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