Respiratory acid-base balance and control of ventilation Flashcards

(77 cards)

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
What is the difference in chemical concentration between chronic and acute respiratory alkalosis
Chronic respiratory alkalosis has a lower HCO3- level, a lower pH, and a higher H+ concentration.
26
Why do chronic respiratory acidosis and alkalosis have more stabilized values than the acute versions?
Because the kidneys have time to secrete or hold onto H+ and HCO3 ions, so they can balance the levels
27
What is the difference in CO2 levels in respiratory vs metabolic acidosis
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.
28
What is the difference in CO2 levels in respiratory vs metabolic alkalosis
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.
29
What is the primary concern in hypoxemia (Hypoxic hypoxemia)
Not enough O2 in the blood, the arterial blood has low O2 levels
30
What is the primary concern in anemic hypoxia
low hemoglobin levels-->not enough hemoglobin to hold the oxygen needed in the blood
31
What is the primary concern in ischemic hypoxia
low blood flow to tissues
32
What is the primary concern in histotoxic hypoxia
Toxins impair O2 USAGE in a cell-- the tissue can't use O2
33
Why is there a large increase in ventilation at high altitude
decrease in O2 in blood, decreased O2 saturation
34
What effect does high altitude have on CO2 and pH?
Decrease CO2 levels, Decrease levels of H+ which increases pH
35
What effect does high altitude have on the O2 hemoglobin dissociation curve
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
What type of anemia occurs at high altitude
hypoxemia due to high altitude--> decreased O2 blood saturation so not enough O2 in blood
37
What type of anemia is caused by Right to Left shunting in the heart
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
What happens to O2 levels and ventelation when there is a hypoxic V/Q Mismatch (i.e. ventilation problems)
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
Walk through the steps of the shifting of the oxygen-hemoglobin dissociation curve at high altitude
Decreased O2 in blood-->increased Ventilation-->Decreased CO2-->Left shift-->Increased O2 saturation
40
Hypernea vs hyperventilation
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
What is voluntary control of respiration due to
respiratory motor neurons (intercostal muscles under voluntary control)
42
What is automatic control of respiration due to
Pacemaker cells in the medulla (Pre-botzinger complex is a grouping of automatically depolarizing cells) - Have cervical portion and thoracic portion
43
Where is automatic control of respiration in the body
In the medulla in pre- Botzinger complex, automatically depolarizing cells)
44
What are the 2 portions of the autonomic control of respiration
Cervical portion- connects to phrenic nerve and controls diaphragm Thoracic portion- Controls intercostal muscles (intercostal nerves innervate these)
45
The dorsal respiratory group nuclei connects to which nerve and muscle
Connects to phrenic nerve that innervates diaphragm (cervical portion)
46
The Ventral respiratory group nuclei connects to which nerve and muscle
Connects to intercostal nerve and internal/external intercostals for the thoracic portion of autonomic control
47
Where is the location of central chemoreceptors
Medulla oblongata- sense the CSF
48
What is the location of peripheral chemoreceptors
Carotid and aortic bodies (sense in blood and sinusoidal capillaries)
49
What stimulates central chemoreceptors
the level of CO2 (strongest) and O2/H+ in the CSF
50
What do chemoreceptors do when they sense high levels of CO2, H+, and low levels of O2
Increase ventilation to get rid of CO2 and decrease pH
51
What do chemoreceptors do when they sense Low levels of CO2, low levels of H+, and high levels of O2
Decrease ventilation to hold onto CO2 and increase H+/decrase pH
52
What is the hering-breuer reflex driven by? Describe the inflation and deflation reflexes
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
What is the slowly adapting reflex for non-chemical reflexive action on ventilation
Hering-breuer reflex
54
What is the rapidly adapting reflex for non-chemical reflexive action on ventilation
Irratent receptors- activate quickly and cause coughing.
55
What is the rapidly adapting receptor stimulated by
chemicals like histamine
56
What does activation of the rapidly adapting receptor cause
activation in the trachea leads to coughing, bronchoconstriction, and mucous secretion Activation in lungs leads to hyperpena(increased ventilation)
57
Where are C-fibers found and what are they stimulated by
Found next to pulmonary capillaries (Juxtacapillary receptors, J receptors). Stimulated by hyperinflation or capsacin
58
What does C-fiber stimulation cause
Pulmonary chemoreflex: stimulated by apnea --> rapid breathing, bradycardia, hypotension
59
What is the non-chemical reflexive action that relates to joints and muscles in our body?
Proprioceptors and the active and passive movements of joints stimulate respiration. Important for exercise ventilation, drives ventilation
60
What are the nerves related to coughing vs sneezing
Coughing: Vagus and glosopharyngeal Sneezing: Trigeminal nerve
61
Where does irritation occur in coughing vs sneezing
Coughing: Irritation of trachea, bronchi Sneezing: Irritation of nasal mucosa
62
Is the glottis open or closed in coughing vs sneezing
Coughing: Closed glottis Sneezing: Open glottis
63
What is a hiccup
spasmodic contraction of diaphragm. Inspiration leads to the diaphragm suddenly closing
64
What does a yawn increase
Increases venous return May open collapsed alveoli
65
What are the factors in exercise that increase ventilation
1. Chemoreceptors in muscle sensing CO2 levels 2. Psychological stimuli (anticipation and beyond) 3. Proprioceptors
66
What is the primary driver of ventilation
CO2
67
Where does an increasing level of CO2 come from
Byproduct of oxidative metabolism (primarily) and buffering acid (buffering of H+ that comes from lactate in anaerobic buildup)
68
From the beginning of exercise until minute 2-3, what systems do we rely on
Use Creatine phosphate and anaerobic systems. Get into an O2 deficit since we can't get it caught up immediately
69
What system begins to work after minute 3 of exercise
Aerobic system--> catches up and steady state oxygen uptake is achieved.
70
What is the phenomenon of EPOC
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
What causes ventilation to increase immediately after beginning exercise
no buildup of CO2 yet, but the anticipation of exercise and the proprioceptors cause the ventilation to increase immediately
72
What causes ventilation to increase in moderate exercise
Driven by an increase in CO2 levels from oxidative metabolism Increase in body temperature and extracellular K stimulates chemoreceptors around muscles
73
What causes Ventilation to increase in vigorous exercise
Increase in CO2 from oxidative metabolism and buffering
74
What type of neuron increases in sensitivity with exercise
Afferent neuron sensitivity to CO2 increases with exercise (the same amount of CO2 leads to an increase in ventilation)
75
What is the relationship between lactate and ventelation
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
What changes in ventilatory response with exercise training
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