Acid Base physiology Flashcards
Normal blood pH, and ways body produces acid
7.37-7.42
Oxidative metabolism producing CO2: water and carbon dioxide making carbonic acid, weak acid. Known as volatile, as in equilibrium with dissolved CO2
Protein catabolism: far less, oxidation of sulphur aa residues, sulphuric acid. Non volatile/fixed acid. Rises markedly under: Ischaemia/extreme exercise, due to lactic acid; Insulin deficiency, diabetes, due to formation of aceto-acetic acid and B hydroxybutyric acid
The bicarbonate buffer system: what acids is it particularly good at buffering? Henderson Hasselbach equation
What is the bicarbonate buffer system thus determinant on?
Fixed acids
H+ + HCO3- = H2CO3 = CO2 + H2O
So when acid is added, equilibrium shifts to right, more dissolved Co2, at cost of lowering the bicarbonate.
HH: pH= pKa + log10( [HCO3-}/[H2CO3])
(Where Ka = [H+][HCO3-]/[H2CO3]
Can be simplified by using dissolved CO2 instead
pH= 6.1 + log10([HCO3-]/0.03 x PCO2)
Thus determinant on bicarb and PCO2
Other buffer systems of non volatile/fixed acids
Short term: bicarb in the ECF
Blood acts as a buffer (organic phosphates), also quick
H+ will be buffered by intracellular proteins and organic phosphates in tissue (proteins) and bone(phosphate). H+ is transported across cell membrane in exchange for Na+ and K+. Is a slow process (hours to days)
What is the isohydric principle
Buffers in the same solution are in equilibirum, thus pH can be calculated from the status of one buffer system.
reasonable for ECF but not intracellularly as not homogenous.
How are volatile acids buffered (i.e if increased carbonic acid from tissues due to oxidative metabolism not being matched by alveolar ventilation which is removing the Co2 to remain in equilibrium) 6% of total buffer capacity.
diagram in Smaill
Bicarbonate buffer is not very good for this, as you are just essentially adding buffer.
Blood acts as a buffer!
-Tissue produces CO2, readily diffuses into plasma and dissolves, forming volatile acid.
-Also readily diffuses into RBC’s along a concentration gradient where there is a high concentration of carbonic anhydrase
-This makes H2CO3, which dissociates into H+and HCO3-
-Bicarb moves out of the red cell, in exchange for chloride.
Some of CO2 in red cell will combine with Hb, carbaminohaemoglobin, making more H+ ions in red celll
-H+ ions combine with OXY haemoglobin to cause oxygen dissociation, which diffuses into tissues
-The small amount of H+ formed by CO2 hydration in plasma is buffered by bicarbonate formed in red cells, and organic phosphates/proteins
The blood buffer line, consequence of reduced haematocrit. Addition of an acid or base
Capacity of the blood buffer system
High CO2will have higher H+ and bicarbonate, with a lower pH.
lies next to bicarbonate buffer system, in equilibrium.
reduced haematocrit, less red cellsso less efective red cell buffer. Blood buffer line will flatten out, as less bicarb will be produced for any unit of PCO2. So ph will be lower, due to relationship with bicarb buffer line
fixed Acid added: Blood buffer line moves down, as bicarb concentration drops, but blood buffer ine same gradient, still works.
Alkali added, more bicarb conc, moves line up
Base excess
Amount of acid needed to correct an alkalosis
Will increase in metabolic alkalosis! As This is an increase in bicarb, lowers acid. is negative in metabolic acidosis
(Bicarb buffer line)
Acid base disurbances on the buffer graphs
Resp acidosis: raised PCO2, little increase in bicarbonate. Moves along blood buffer line
Resp alkalosis: Lowered pCO2, slightly lower bicarb, moves along blood buffer line
Metabolic acidosis: Blood buffer line shifts down, bicarb drop, low pH same PCO2
Metabolic alkalosis: blood buffer line raises, high pH, high bicarb, same PCO2
Respiratory regulation of acid base
PCO2 is proportional to _______/_________.
Arterial PCO2 and pH are sensed by chemoreceptors in brain and aortic/carotid bodies
Increased PCO2 will ____ alveolar ventilation to bring it down
Hypoxia also stimulates respiratory drive
PCO2 is proportional to Ventilation of CO2/Alveolar ventilation.
Arterial PCO2 and pH are sensed by chemoreceptors in brain and aortic/carotid bodies (note peripheral particularly sensitive to hypoxia)
Increased PCO2 will increase alveolar ventilation to bring it down
Hypoxia also stimulates respiratory drive
Renal regulation of bicarbonate: Maintenance and control requires. Controlled by the kidneys!
- Reabsorption of all bicarb filtered by the kidneys
- Regeneration of all bicarb lost to non-volatile acids (metabolic acidosis)
- Removal of fixed acids incorporated into non-bicarbonate buffer system
The process of renal hydrogen excretion and bicarbonate reabsorption. Where does it occur? All passive
___
- Driven by Sodium, __ exchange, sodium ___ cell, H+ into ___
- These H+ combine with HCO3- from _____ blood, making _____
- Carbonic anhydrase in brush ___ breaks down to CO2 and water, where ___ diffuses into cell
- Intracellular CA converts this CO2, with water to ____ acid
- This carbonic acid dissociates, the H+used in the ____, and HCO3- absorbed into blood, by ______ symport (3 bicarb)
PCT
- Driven by Sodium, H+ exchange, sodium into cell, H+ into lumen
- These H+ combine with HCO3- from filtered blood, making H2CO3
- Carbonic anhydrase in brush border breaks down to CO2 and water, where CO2 diffuses into cell
- Intracellular CA converts this CO2, with water to carbonic acid
- This carbonic acid dissociates, the H+used in the exchanger, and HCO3- absorbed into blood, by Na+/Bicarb symport (3 bicarb)
Renal bicarbonate regeneration and acid excretion
Two ways, ____ cells? ____ tubule
Ammonia:
-Ammonia diffuses from blood into cell, and into tubule. H+ resulting from action of ____ ____dissociation (originally made by ___) is _____ transported into lumen. Combines with ammonia, to make ammonium ion
-Bicarb made from this ____ ____, made from CA is exchanged with __ into the blood ____. New ___
Phosphate: Same idea, however phosphate ions originally in filtrate, H+ still actively transported out
Can take ___, as ammonia may . need synthesising for example
Two ways, Intercalated cells? Distal tubule
Ammonia:
-Ammonia diffuses from blood into cell, and into tubule. H+ resulting from action of carbonic acid dissociation (originally made by CA) is ACTIVELY transported into lumen. Combines with ammonia, to make ammonium ion
-Bicarb made from this carbonic acid, made from CA is exchanged with Cl- into the blood passively. New bicarb
Phosphate: Same idea, however phosphate ions originally in filtrate, H+ still actively transported out
Can take time, as ammonia may . need synthesising for example
Fill in the gaps
In acidosis, H+ secretion is ___, and bicarb reabsorption is nearly ___
In alkalosis, H+ secretion ____, ___ bicarb reabsorption
Bicarb reabsorption in kidney:
-Directly related to ____, so increase in PCO2 ____ bicarb absorption
-Inversely related to ____ and ____ concentrations
-Increased in response to adrenal corticosteroids, such as cortisol/aldosterone
In acidosis, H+ secretion is increased, and bicarb reabsorption is nearly full
In alkalosis, H+ secretion lowered, less bicarb reabsorption
Bicarb reabsorption in kidney:
-Directly related to PCO2, so increase in PCO2 increases bicarb absorption
-Inversely related to potassium and chloride concentrations
-Increased in response to adrenal corticosteroids, such as cortisol/aldosterone
Common causes of all the acute acid base disturbances
MAC: DKA, lactic acid accumulation, failure to excrete sufficient acid, loss of bicarbonate (diarrhoea)
MALK: addition of alkali, e.g. antacids, loss of fixed acids due to vomiting/NG suction
RAC: Inadequate ventilation (drug induced, COPD, asthma), pulmonary oedema
RALK: Hyperventilation, due to drug induction, self induction or anxiety/fear
Time course of events to regulate an acid or alkali load
Use case of acidosis
- ECF buffer system works first, within 2 hours peaked, cellular buffer next peaking at 6-8 hours. starting to rise a lot after 2
- Respiratory compensation next, so hyperventilation in this instance. Starts early, but takes some hours to reach effect, peak at about 12 hours
- renal base excretion, in this case reduced, slightly slower than respiratory compensation. Turned on with alkalosis
- Last is renal acid excretion, slow for 0-14 hours, picks up now and peaks at 72 hours. Will be increased. Slow due to ammonia synthesis etc
