16 - Acid-base disorders Flashcards
Henderson-hasselbalch equation
H + HCO3 -> H2CO3 -> CO2 + H2O
Tissue gas exchange
Cl- in put into an RBC when CO2 is reacted with hydrogen in order to maintain charge
What happens when you shift to the right on the O2-Hb dissociation curve
Increased 2,3 diPG
Acidosis (H+)
Increased Temperature
To maintain charge in kidneys what in inputed
Na+ with HCO3-
Mineralocorticoid action in the kidney
K+/H+ go in at distal renal tubule and Na+ goes out
Acid-base in the GI tract
H+ goes to stomach
Hydrogen carbonate goes to pancreas
Acid-base balance and the liver
Dominant site of lactate metabolism
Only site of urea synthesis
Acid-base balance - liver rxns
1: proteins catabolised to NH4+ and HCO3-
2: Average proteins produce a slight XS NH4+ (balance of dicarboxylic, dibasic, neutral a/a)
3: role of urea cycle is to combine NH4+ and CO2 to neutralise HCO3 - from protein catabolism
Acid-base balance - severe liver failure
NH4 + oxo-glutarate cannot form glutamine
NH4 and CO2 cannot form urea
Metabolic alkalosis with ammonium toxicity
Why is it metabolic alkalosis in severe liver failure?
2NH4 + HCO3 -> (NH2)2CO + H+
LHS is acid
RHS is base
Compensatory mechanisms for acid-base balance
Resp.
Renal bicarb regen
Hepatic shift between urea synthesis and ammonia excretion
Metabolic acidosis - what happens
Increased H+ formation
Acid ingestion
Reduced renal H+ excretion
Loss of bicarb
Metabolic acidosis - blood gas affects
[H+] up
pCO2 down
pO2 up
Metabolic alkalosis - what happens
generation of bicarb by gastric mucosa
Renal generation of HCO3- in hypokalaemia
Administration of bicarb
Metabolic alkalosis - blood gas affects
[H+] down
pCO2 up
pO2 down
Metabolic alkalosis - consequences
K+ goes into cells and urine
PO4 goes into cells
Resp. suppression
Resp. acidosis - what happens
CO2 retention due to:
inadequate ventilation
parenchymal lung disease
inadequate perfusion
Resp. acidosis - blood gas effects
[H+] up
pCO2 up
pO2 down
Resp. alkalosis - what happens
Increased CO2 excretion due to excessive ventilation producing alkalosis
Resp. alkalosis - blood gases
[H+ down]
pCO2 down
pO2 up
Metabolic acidosis causes
increased H+ formation
Acid ingestion
Reduced renal H+ excretion
Loss of bicarbonate
Causes of increased [H+]
ketoacidosis, diabetic or alcoholic
lactic acidosis
poisoning
inherited organic acidoses
Diabetic ketoacidosis
Hyperglycaemia
Osmotic diuresis -> pre-renal uraemia
Hyperketonaemia
Increased FFA -> all lead to acidosis
Lactic acidosis types
Type a = shock
Type b = metabolic and toxic causes
Acidosis in an alcoholic
NAD+ depletion (thiamine) Thiamine deficiency (PDH co-factor) Enhanced glycolysis for ATP formation Keto-acids secondary to counter-regulatory hormones CAUSES PROFUSE VOMITING
Does high lactate = lactic acidosis? In alkalosis
Increased glycolysis
Reduced O2 delivery due to shift in O2 dissociation curve
Lactate induced vasoconstriction
Impaired mitochondrial resp.
Does high lactate = lactic acidosis? O2 debt to #2
Further anaerobic lactac
te production
Hyperventilation
Renal failure effects
Reduced volume of nephrons Increased bicarb loss Reduced NH4+ excretion NH4 to liver for urea + H+ synthesis Only fraction of NH4+ derived from glutamine
