Acid Base Regulation Flashcards
Death due to pH
Below 6.8
Above 8.0
Formation of acid
Most H+ ions originate from cellular metabolism
Carbonic acid
Aerobic respiration of glucose
Metabolic production of CO2
CO2 + H20
about 15mol/d
Lactic acid
Anaerobic respiration of glucose
Sulfuric acid
Oxidation of sulphur-containing amino acids
Acidic ketone bodies
Incomplete oxidation of FAs
Phosphoric acid
Hydrolysis of phosphoproteins + nucleic acid
Pathological increase of H+
Formic acid
Glycolic acid
Lactic acid
Acetoacetate
Mechanisms limiting changes in pH
Chemical buffer system in blood + ICF - immediate
Resp centre in brain stem- 1-3 mins
Renal mechanisms - hours to days
Buffer
Solution that can resist pH change upon addition of an acid or base
Acts quick to bind or release H+
Consist of weak acid + salt of that acid functioning as weak acid
3 Major Chemical buffer systems
Bicarbonate
Proteins (haemoglobin + albumin)
Phosphate
Buffer systems in ICF
Phosphate
Protein
Buffer system in ECF
Protein
Carbonic acid
Acidaemia + K+
Acidaemia leads to HYPERKALAEMIA
–> tissues release K+
Alkalemia + K+
Alkalemia leads to HYPOKALAEMIA
–> cells take up K+
ECF
Plasma + IF
Cations- Na+ mainly, K+ small
Anions- Mainly Cl-, some HCO3-
ICF
Cations- K+ mainly, Na+ small
Anions- PO43- mainly, protein anions
Anion gap with Na+, K+, HCO3- and Cl-
12-16mEq/L
Anion gap Na+, Cl-, HCO3-
8-12mEq/L
Normal gap acidosis
Metabolic acidosis = hyperchloremic acidosis Seen in loss of bicarbonate Reduced kidney H + excretion Cl- increases to make up for HCO3- loss
Normal gap acidosis causes (loss of bicarbonate)
Severe diarrhoea
Chronic laxative
Fistulas
Losses via NG tube
Normal gap acidosis causes (kidney)
If kidney not excreting acid efficiently, more bicarbonate needed to buffer them
–> bicarbonate drop
Elevated gap acidosis causes
Ketoacidosis
Lactic acidosis
Renal failure
Toxic ingestion
Low gap acidosis
Haemorrhage Nephrotic syndrome Intestinal obstruction Liver cirrhosis Decreased Albumin, but increased HCO3- and Cl-