Mechanisms of acid/base balance Flashcards
(30 cards)
Summary of Acid base homeostasis diagram
slide 3, lecture 7
Change in lung function could be effectiveness as well as volume (e.g. fluid accumulation in lungs)
Lungs react quicker than kidneys so compensation for a metabolic disorder happens quicker than compensation for a respiratory disorder
The lungs excrete how much acid compared to kidneys?
The lungs excrete 99% of the volatile acid in the blood (13,000mmols/d) while the kidneys excrete only 1%
Normal arterial blood ranges in pH from
7.35 → 7.45
The minimum and maximum ranges of pH that are compatible with human life are
6.7 → 7.9.
Plasma [H+] usually sits around:
40nmolL-1
H+ concentration is much smaller than other electrolytes
Normal arterial bicarbonate:
22-26 mEq/L
Urine pH range
5-9
pH will vary quite a lot because it’s the regulator not the regulatee (broad range is expected)
Importance of HCO3-?
Responds rapidly to changes in?
Can be produced by?
High Capacity Chemical Barrier
Responds rapidly to changes in metabolic acid
Can be produced by volatile respiratory acid
Proportion of HCO3- reabsorption across nephron
80% reabsorbed in PCT
10% reabsorbed in ascending loop of Henle
6% reabsorbed in DCT
4% reabsorbed in CD
Henderson-Hasselbach equation in relation to pH
Normal values to be inputted?
𝑝𝐻=𝑝𝐾+𝑙𝑜𝑔_(10 ) ([H𝐶𝑂3−])/([𝐶𝑂2])
pK= 6.1 doesn't change [HCO3-]= 24 mmol/L [CO2]= 1.2 mmol/L
Know how to explain changes in this equation depending on changes in CO2
Davenport diagram discription
Axes?
Draw on normal ranges
Draw segments for: Chronic respiratory acidosis? Metabolic alkalosis? Metabolic acidosis? Acute respiratory acidosis? Acute respiratory alkalosis? Chronic respiratory alkalosis? Explanation for shape?
Why are respiratory disorders split into acute+ chronic
How is BE calculated?
A graphical representation of the association between pH, bicarbonate and carbon dioxide in blood.
X axis= pH
Y axis= Plasma bicarbonate [HCO3-] (mmol/L)
Top axis= [H+] (nmol/L), gaps aren’t equivalent to bottom axis (pH= logarithmic)
Extra axis that curves round on the right= PCO2 (kPa)
Intersection of all normal ranges= ideal
Meatbolic alkalosis= pH increases, HCO3 increases too which actually drives metabolic acidosis, curves up because moves along CO2 lines
Respiratory disorders split into acute+ chronic because rapid changes in breathing rapidly affect homestasis, or slower ones steadily make things worse
BE is measured as amount of deviation from normal range so you would state it by counting difference from 24mmol/L plasma HCO3-
Chronic respiratory acidosis actually overlaps a lot with normal pH because physiology changes over time to try and bring back to green zone
HCO3- reabsorption
diagram on slide 8, lecture 7
Isoenzyme of CA reverses equation above in a 1:1 ratio
Trying to retain HCO3 so no point in bring H+ in
ATPase used to pump H+ : Gradient for secdonary active transport used to antiport H+ out
Peritubular capillaries are part of vasa recta
HCO3 taken out by anion exchanger+ Na coupled transport
Cl- moves cyclically to aid this
Acid secreting cell
Bicarbonate secreting cell
(slide 9, lecture 7)
α cell
HCO3 diffuses in cells but also uses carbonic anhydrase: combines with H+ to form CO2 and H20, CO2 moves into cell
Lots of mechanisms to move H+ back out of apical membrane out of filtrate+ save HCO3
High energy process
β cell
Same mechanisms as alpha but flipped upside down
Bring H+ back into body
Push HCO3- out
HCO3- generation by cells
slide 10, lecture 7
Glutamine split into HCO3- and NH4
NH4 is got rid of, HCO3- is reabsorbed
SGLT1= irrelevant
HCO3- titratable mechanism
slide 11, lecture 7
Secretion H+ with all the mechanisms before contribute to HPO42- equation which can be titrated
Compensatory mechanisms for:
Respiratory acidosis
Cause
Compensatory response
Compensatory mechanism (Acute/ Chronic?)
Respiratory acidosis
Cause= ↑ PaCO2
Response= ↓ H+, ↑ HCO3-
Mechanism= Acute: Intracellular buffering
Chronic: HCO3- generation & ↑ ammonium excretion
Compensatory mechanisms for:
Respiratory alkalosis
Cause
Compensatory response
Compensatory mechanism (Acute/ Chronic?)
Cause= ↓ PaCO2
Response= ↑ H+, ↓ HCO3-
Mechanism= Acute: Intracellular buffering
Chronic: ↓HCO3- reabsorption & ↓ ammonium excretion
Compensatory mechanisms for:
Metabolic acidosis
Cause
Compensatory response
Compensatory mechanism
Cause= ↑ H+, ↓ HCO3- Response= ↓ PaCO2 Mechanism= Hyperventilation to ↑ CO2 excretion
Compensatory mechanisms for:
Metabolic alkalosis
Cause
Compensatory response
Compensatory mechanism
Cause= ↓ H+, ↑ HCO3- Response= ↑ PaCO2 Mechanism= Hypoventilation to ↓ CO2 excretion
Graph depicting compensation pH begins to normalise
for Respiratory acidosis
(slide 13, lecture 7)
Initial accumulation of CO2 in arterial blood
Subsequent fall in arterial blood pH
PCO2 stimulus and acidaemia effect plateau
Nephrons increase HCO3- retention/production and H+ secretion
pH begins to normalise
Full compensation
Graph depicting compensation pH begins to normalise
for Respiratory alkalosis
(slide 14, lecture 7)
Initial loss of CO2 in arterial blood
Proportional rise in arterial blood pH
PCO2 stimulus and alkalaemia effect plateau
Kidneys increase HCO3- excretion and reduce H+ excretion
pH begins to normalise
Full compensation
Graph depicting compensation pH begins to normalise
for metabolic acidosis
(slide 15, lecture 7)
Initial loss of HCO3- in arterial blood
Subsequent fall in arterial blood pH
HCO3- stimulus and acidaemia effect plateau
Lungs increase ventilation to eliminate volatile PCO2
pH begins to normalise
Full compensation
Graph depicting compensation pH begins to normalise
for metabolic acidosis
(slide 16, lecture 7)
Initial loss of free H+ in arterial blood
Proportional rise in arterial blood pH
H+ stimulus and alkalaemia effect plateau
Lungs decrease ventilation to retain volatile PCO2
pH begins to normalise
Full compensation
If PCO2 and BE compensation go in opposite directions
mixed disorder
