L5-6 Acid-Base Balance Flashcards
Describe the pH scale
Logarithmic and reciprocal
Fall in pH leads to ________ in H+
Increase
Rise in pH leads to ________ in H+
Decrease
What would the result of a 1 unit pH change be in H+
x10 change
Why must pH be carefully controlled
A small pH change will have profound phyisological effects
Normal pH range
7.35 - 7.45
Describe the effects fluctuations in H+ may have
Change the excitability of muscles/nerves
Enzyme activities changed
Change in K+ levels
What organ does hyperkalaemia have a hug effect on in praticular
Heart
pH of gastric secretions
0.7
pH of CSF
7.3
pH of pancreatic secretions
8.1
pH of the final urine
5.4
How many moles of CO2 metabolised per day
15
Diet is a huge source of
Acid
How many mmol net H+ due to metabolism
40
One source of alkali
Fruit
Western diet contributes to
Excess ingestion of acid
How many mmole of H+ in per day through diet
20
Net H+ gain per day
70 mmol
3 Systems involved in the control of acid-base balance
Blood and tissue buffers
Respiration
Renal
Which is the only method which directly allows the extrusion of H+/OH-
Renal
Examples of buffers
Hb HCO3- Pi Weak acids/bases on proteins
Equation for the primary ECF buffer
CO2 + H2O H2CO3 HCO3- + H+
What is the name of the primary ECF buffer
Carbonic acid/bicarbonate buffer
Describe what would happen to the Carbonic acid/bicarbonate buffer if there was an increase in CO2
Eqbm shift right to minimise change
More H+ produced
What is the equation for pH in the Carbonic acid/bicarbonate buffer system
Ph = pK + [HCO3/H2CO3]
What can be said about the concentrations of H2CO3 + CO2 at eqbm
Equal
Rewrite the equation of the Carbonic acid/bicarbonate buffer system to include CO2
pH = pK + [HCO3/CO2]
What is pK at 37 deg
6.1
Describe what would happen to the Davenport diagram if acid was added
Conc of HCO3- decreases
pH decreases
Metabolic acidosis
What is the normal [HCO3]//[CO2]
20:1
Using the normal [HCO3]/[CO2] calculate pH
pH = 6.1 + log 20 pH = 7.4
Describe what would happen to the Davenport diagram if CO2 conc was increased
Increase in [hco3]
Decrease in pH
Respiratory acidosis
Describe what would happen to the Davenport diagram if base was added
Increase in [hco3]
Increase in pH
Metabolic alkalosis
Describe what would happen to the Davenport diagram if concentration of CO2 decreases
Decrease in [hco3]
Increase in pH
Respiratory alkalosis
Two chemoreceptors involved in the control of blood gas composition
Central and peripheral
Hypoxia is
Decrease in O2
Hypercapnia is
Increase in CO2
Peripheral chemoreceptors are found
Carotid and aortic bodies
Main stimulus for the peripheral chemoreceptors
Hypoxia
What 3 nerves are involved with the peripheral chemoreceptors
Sinus
Vagus
Glossopharyngeal
Weight of the carotid bodies
2mg
Supporting cells of the carotid body are called
Type II supporting cells
What two stuructures of the carotid body help increase blood flow
Arteriole
Siusoid
What is the receptive cell of the carotid body
Glomus cell
Compare blood flow through the carotid body to the brain
Carotid body has over 40x per unit mass than the brain
Describe the mechanism of activation of the glomus cell in response to
Dec PO2 Inc PCO2 Dec pH
Inhibition of the BK K channels Depolarisation Action potential firing VGCC open Ca influx NT release Afferent nerve fibre stimulation
What NTs are released from the glomus cell
Ach, dopamin, NA, 5-HT, Substance P, ANP
What is different in SIDs babies and normal babies in terms of the peripheral chemoreceptors
Increase [] of dopamine and NA in SIDs babies glomus cell
Describe how the sensitivity to PO2 of the peripheral chemoreceptor changes with acid-base status
At lower pH they are more sens. to pO2
Describe how sensitivity to pCO2 of the peripheral chemoreceptor changes with pH
At the higher pH they are less sensitive to changes in pCO2
Central chemoreceptors are the primary source for the
Tonic drive for breathing
What is the main activator for the central chemoreceptors
Hypercapnia
A change in CO2 P from 40-45 mmHg will have what affect on the central chemoreceptors, how does this compare to what would be seen in response to pO2
double the ventilation rate
this would only be seen with a 50% decrease in PO2
What is the experiemental evidence for the central chemoreceptors
Perfusion of the cerebral ventricles with an acidic solution and hyperventilation was observed
Descrive the location of the central chemoreceptors
Within the brain parenchyma
Bathed in BECF
Separated from the arterial blood by the BBB
Describe the effect an increase in arterial pCO2 would have on the BECF, what long term compensation may be involved
Inc Arterial pCO2
Inc BECF pCO2
Dec BECF pH
Less bicarbonate buffering power (fewer proteins) so a larger pH fall
LONG TERM - Bicarbonate may be transported out of the blood
Describe what effect the poor ionic perm of the BBB has on metabolic disorders compared with respiratory disorders
Metabolic - no change in Co2 - only change in H+ - these can’t cross the BBB
Respiratory - CO2 can cross the BBB and affect pH
METABOLIC DISORDERS CHANGE THE BECF BY 10-35% OF THAT OBSERVED WITH RESPIRATORY DISORDERS FOR THE SAME PH CHANGE IN THE BLOOD
Can H+ cross BBB
No
Can HCO3- cross BBB
No
Can CO2 cross BBB
Yes
Where do the central chemoreceptors project to
The ventrolateral medulla and other brainstem nuclei
How many neuronal populations of the central chemoR, what are they called
2
Acid activating + inhibiting
Acid inhibiting release
GABA
Acid activating release
Serotonin
What is seen in SIDS babies in terms of the central chemoreceptors
Lack the serotonergic neurones
Response of both ChemoR to respiratory acidosis
Both central and peripheral
Normoxic central 65-80%
Peripheral faster
As PO2 falls the response to PCO2 is enhanced
Response of both ChemoR to metabolic acidosis
Severe - hyperventilation - --- Kussmaul breathing Descrease in PCO2 Peripheral acute response Central longer term role
Effect of breathing faster or CO2 and pH
Dec CO2, Dec H+, Inc pH
Effect of breathing slower on CO2 and pH
Inc CO2, Inc H+, Dec pH
Effect of dec pH on resp rate
Inc rate to increase loss of CO2
Effect of inc pH on resp rate
Dec rate to decrease loss of CO2
Three renal mechanisms
HCO3- handling
Urine acidification
Ammonia synthesis
90% of HCO3- handling takes place in the
Proximal tubule
10% of HCO3- handling takes place in the
Distal tubule
Describe how HCO3- handling takes place in the proximal cell
Na/K ATPase sets up low IC Na
NHE (1 Na in, 1 H+ out)
H+ out combines with filtered HCO3-
Forms H2CO3
Carbonic anhydrase catalyses the breakdown of H2C03 –> CO2 + H20
Both move into the cell when in the cell an intracellualr form of carbonic anhydrase reforms the H2CO3
H+ out through the NHE
HCO3- out through a basolateral HCO3/Na co transporter
What is different in HCO3- handling in the proximal and distal tubule
Proton pump instead of NHE in the distal tubule
Acidification of the urine accounts for what percentage of base conservation
25%
Is NAH2PO4 an acid phosphate or alkaline
Acid
Is NAHPO4 an acid phosphate or alkaline
Alkaline
Describe how NaH2PO4/NaHPO4 is used in the acidifcaiton of the urine
Na/K ATP establishes a low IC Na
CO2 and H2O enter cell, combine under influence of carbonic anhydrase to H2CO3 this disociates to HCO3- and H+, H+ out through apical NHE, HcO3- out through basolateral channel
Na in H+ out through NHE
Filtered NaHPO4- combines with the H+ forms the acid salt
What other two substances can be used in acidification of the urine
Uric acid and creatinine
Is ammonia permeable to the membrane
Yes
Is ammonium permemable, why?
No, charged
What chemical can ammonia form from
Glutamine
Describe how ammonia can be formed from glutamine
Glutamine to a-ketoglutarate
With loss of two ammonia and 2 H+ released
Describe how ammonia production can be used for base conservation
Glutamine to a-keto in the cell (produces 2NH3 and 2H+)
NH3 diffuses out
H+ out through NHE
Combine out of the cell to form ammonium
Cant diffuse back into the cell
Ammonia production base conservation is an example of
Diffusion trapping
What is the renal response for acidosis for : H+ excretion HCO3- excretion pH of urine Change in plasma pH
Increase
Zero no change
Decrease
Increase
What is the renal response for alkalosis for : H+ excretion HCO3- excretion pH of urine Change in plasma pH
Decrease
Increase
Increase
Decrease
Describe respiratory acidosis and the renal compensations
CO2 elimination decreases
Due to lung disease (emphysema, chronic bronchitus)
Inc secretion of H+, inc reab of HCO3- rise in blood pH but the further rise in HCO3-
Describe respiratory alkalosis and the renal compensations
CO2 eliminaition increases
Hyperventilation as cause due to fear/stress/pain
Dec secretion of H+, Dec reab of HCO3- fall in pH but the further drop in HCO3-
Describe metabolic acidosis, the respiratory compensation and then subsequent renal correction
Due to ingestion of acid/ loss of alkaline fluid
e.g. diahorrea, diabetic ketoacidosis
Inc resp rate to dec arterial pCO2, increase pH and drop in PCO2
Increased secretion of H+ and increased reabsorption of HCO3-
Describe metabolic alkalosis, the respiratory compensation and subsequent renal correction
Due to ingestion of alkaline fluid, loss of acid (may be from vomitting)
Dec resp rate, to increase arterial PCO2, decrease in pH
NO RENAL CORRECTION IN THIS INSTANCE IT IS UNABLE TO HELP
What is a mixed dissorder
More than one primary alkalosis/acidosis
If they are both the same type of dissorder the pH will be
Additive
If the disorders are opposite then the pH will be
Subtractive
How do alcoholic patients have a mixed disorder
Metbolic acidosis from the breakdown of the alcohol
Metabolic alkalosis from vomitting
How is asthma a mixed dissorder
Respiratory acidosis Lactic acidosis (form of metabolic acidosis)
How are COPD an example of a mixed dissorder
Respiratory acidosis
Metabolic alkalosis
What is the treatment for COPD
Diuretics
How is salicylate poisoning an example of a mixed dissorder
Respiratory alkalosis (aspirin stimulates the respiratory centre) Metabolic acidosis (Increases the ammount of acid)
