Kidneys and acid base

why does the concentration of H+ need to be controlled in the body

• H+ is highly reactive and reacts very easil ywith proteins, despite its comparatively low concentration compared to other electrolytes

how do the lungs aid with H+ homeostasis

• alveolar ventilation removes CO2 - involved in H+ buffering

what 3 organs are involved in H+ concentration

• liver

• lungs

  • kidneys

why do the kidneys need to be involved in H+ homeostasis

• non volatile lipids and proteins are made and cant be exhaled

how does the body deal with non-volatile proteins and lipids produced that contain H+

• secretion in the kidney

how are H+ secreted in the urine

bound to filtered buffers as it cant be excreted freely

what buffers are used to excrete urine

• ammonium

  • phosphate

which metabolite of H+ buffering must be reabsorbed into the blood during excretion and why

• HCO3-

• if it’s not reabsorbed it’s the same as adding H+ to the plasma

what metabolites does the liver produce to aid with H+ secretion

• NH4+

once the liver has produced NH4+, how is the proton accessed for excretion?

• NH4+ + CO2 → HCO3- and H+

  • HCO3 is titrated, H+ is then excreted through methods back as NH4+

describe the cycle of H+ synthesis and secretion

• NH4+ produced in the liver from metabolism

• HCO3- and H+ are produced from a reaction with CO2

• H+ and HCO3- go through process in the kidney

• H+ is excreted bound to NH3 → NH4+ or with PO43- as HPO3,2-

what are the 3 lines of defence for pH control?

• buffers

• respiratory system

• kidneys

How does acid secretion take place in the kidney?

1. glutamine is converted to alpha-ketoglutarate

2. this becomes NH4+, glucose and HCO3-

• NH4+ is secreted into tubular lumen (H+ secretion)

• glucose is metabolised

• HCO3- is reabsorbed

How does bicarbonate reclamation take place in the kidney?

• H2O and CO2 react together → H+ and HCO3-

• bicarbonate is reabsorbed

• protons are pumped out into the tubular lumen via co-transport of Na+ (uses the concentration gradient to power this)

• H+ binds with HCO3- in the tubular lumen via the action of carbonic anhydrase → H2O and CO2 (cycle repeats again

• HCO3- is reabsorbed into the blood via 3Na+ : HCO3- co-transporter

what are 4 factors that control bicarbonate reabsorption

1. luminal HCO3- concentration

2. luminal flow rate

3. arterial pCO2

4. angiotensin II

which hormone contributes to bicarbonate reabsorption, how?

• PTH - it increases cAMP and decreases bicarbonate reabsorption

which 2 places in the nephron does acidification take place

• PCT

• DCT

how does acidification in the DCT compare to that in the PCT/

• uses H+-ATPase due to lack of Na+ reabsorption rather than Na+/H+ co-transport

describe acidification in the distal tubule

• H+ is secreted in cortical medullary collecting tubule by active secretion via H+-ATPase

• H+ combine with phosphate buffers

where in the nephron does excretion of H+ take place with:

1. NH4+

2. PO43-?

1. PCT

2. DCT

how does the pKa of the bicarbonate system compare to the phosphate system, what does this mean in terms of acidification at the initial filtrate pH of 7.4?

• bicarbonate - 6.8

• phosphate - 6.1

• more bicarbonate base than phosphate base as buffer

What does this infographic tell us?

• acidification and excretion along the nephron affects each other and itsn’t an isolated process

• ammonium is essential along the tubule for the removal of H+

how does increased PCO2 affect H excretion

• tubular cells respond directly to its increase in the blood by increasing the rate of H+ secretion

how does ECF level affect hydrogen secretion?

• if ECF volume decreases, Na+ reabsorption is stimulated, increasing H+ secretion and HCO3- reabsorption

• increased Angiotensin II directly stimulates the Na+/H+ exchanger

• increased aldosterone stimulate H+ secretion by cortical collecting tubules

what tends to occur after H+ secretion is affected by decreasing extracellular fluid levels?

• alkalosis due to excess H+ secretion and HCO3- reabsorption

how does plasma potassium affect h+ excretion?

• when high

• when low

• hypokalaemia stimulates H+ secretion in PCT

• hyperkalaemia inhibits H+ secretion in PCT

what effect does a decreased plasma K conc have on H+ concentration?

• increases H+ concentration in renal tubular cells

• this stimulates H+ secretion and HCO3- reabsorption → alkalosis

how does incresaed K+ affect H+ secretion?

• hyperkalaemia descreases H+ secretion and HCO3- reabsorption → acidosis

how does hypochloraemia affect H+ excretion?

• it causes secretion and HCO3- reabsorption

• Na+ must be absorbed in exchange for H+/K+ secretion

• causes paradoxical aciduria

state 6 factors that cause increased H+ secretion and HCO3- reabsorption

1. increased pCO2

2. increased [H+'], decreased [HCO3-]

3. decreased ECF volume

4. increased angiotensin

5. increased aldosterone

6. hypokalaemia

state 6 factors that cause a decreased H+ secretion and HCO3- reabsorption

1. decreased pCO2

2. decreased [H+], increased [HCO3-]

3. increased ECF volume

4. decreased angiotensin

5. decreased aldosterone

6. hyperkalaemia

what measure can we take during surgery to help us determine how well the kidneys/lungs/liver are secreting H+

• arterial or venous blood gas

what is arterial blood gas useful to measure?

• assessing respiratory stats

what won’t arterial blood gas help detect?

• changes in the periphery

what is venous blood gas useful for?

• measuring metabolic scenarios

how will venous blood gas differ from arterial?

• lower pH and higher CO2

what may peripheral blood gas not be accurate in?

• in low flow states

what do we want blood pH to be?

• around 7.4

what is the typical range of pCO2 mmHg?

• 40 (range of 31-49 but want in the 40 area)

what do we want HCO3- to measure in blood gas?

• 18-29 mmol/l

what do we want pO2 mmHg to be

• arterial

  • venous

• 90-100

• 24-48

if a patient presents with pO2mmHg at 90, which is in range, should we just presume this is fine?

• NO - need to look at patient entirely and see if they amy need additional O2 support

what blood gas marker hsould we always look at first?

• O2

where do we take an arterial sample from for blood gas?

• dorsal metatarsal

• facial

• transverse facial

• femoral

• auricular

what needle to we use for arterial sample collection?

• heparinised

how do we set up a blood gas reader?

• insert cartridge needed for calibration

• attach syrings and inject sample smoothly

• interpret results

if arterial pH is decreased what do we call this?

• acidaemia

if arterial pH is elevated, what do we call this?

• alkalaemia

what are the 2 additional blood gas markers which correlate to acidaemia?

• elevated paCO2

• reduced HCO3-

what type of acidaemia is it for the following markers:

• elevated paCO2

• reduced HCO3-

• respiratory acidosis

• metabolic acidosis

what are the 2 additional markers of alkaelimia in a blood gas sample?

• decreased PaCO2

• increased HCO3-

what do the following tell us about the type of alkalaemia?

• decreased PaCO2

• increased HCO3-

1. respiratory alkalosis

2. metabolic alkalosis

if both PaCO2 and HCO3- are changed in a blood gas sample, how do we determine whether the patient is in respiratory or metabolic distress?

• which one of the markers is worse - use this initially and go from there

What is our dignosis?

• look at O2 first - well saturated

• pH is low, therefore acidosis

• pCO2 is within range but HCO3- is low, therefore metabolic acidosis

Interpret

• Oxygen is LOW - needs immediate oxygen support!

• pH is low = acidosis

• paCo2 is elevated

• HCO3- is also elevated

• paCO2 elevated most therefore respiratory acidosis

what does an anion gap tell us?

• the grreater the anion gap, the more we can assume other acid is being added from another body system contributing to acidosis

Interpret

• oxygen is lower end of acceptable range - as pet has been in an RTA - GIVE O2 ANYWAY

• pH is low

• PaCo2 is elevated

• HCO3- is within range

• respirtaory acidosis duet o RDA