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GAS ANALYSIS
l Normal body pH is 7.35–7.45 /40Nmol/l H l Other buffers
l Fall in pH is Acidemia, rise is Alkalaemia l Haemoglobin
l Major buffer is l Phosphates
l bicarbonate- carbonic acid pair Proteins
l Normal plasma HCO is 25mmol/L
Respiratory Acidosis
l Due to retention of CO
l PaCO & H+ rise. --- pH decrease
l HCO3 is used-up for buffering
l Compensation is by HCO retention by kidneys
l In chronic conditions H+ has returned closer to normal due to HCO retention
Causes : Clinical features of RAc
1) Ventilatory failure Increases cerebral blood flow and raises intracranial pressure
2) COPD (type 11 RF) 1) Impairs cardiac contractility
3) Emphysema 2) Cardiac arrythmias
4) Polyneuropathy 3) Confusion
5) Drug-overdose 4) Coma
5) Hyperkalaemia
6) ODC shifts to the right
Respiratory Alkalosis
l H+ & PaCO fall. pH increase 3) Spontaneous hyperventilation
l Due to increased ventilation 4) High altitudes
l Compensation is by slight decrease in HCO 5) Septic shock
Causes : 6) Pneumonia
1) Mechanical ventilation 7) Hyperkalaemia
2) Hypoxaemia (type 1 RF)
Metabolic Acidosis
l H+ increase. pH decrease Causes : Acid administration
l HCO is largely decreased acid generation (Diabetic ketoacidosis, anaerobic metabolism/
l Is due to accumulation of acid otherthan HCO lactic acidosis (shock, cardiac arrest)) impaired acid excretion
l Compensation is by decrease in PaCO by hyperventilation (chronic renal failure),
hyperkalaemia,
loss of HCO from gut or kidney (renal tubular acidosis)
To see whether MAc is due to H Cl retention or other cause, need anion gap (plasma & urinary)
Normal anion gap acidosis
l Normal AG with acidosis
l When HCO3 is lost via the gut or kidney Cl is retained. (H CL is retained or Na HCO is lost)
E.g renal tubular acidosis – plasma HCO < 21mmol/l, urinay pH > 5.3
l Urinary anion gap (Urinary Na + K - Cl) is useful in distinguishing RTA1 (UAG +ve) & diarrhoea (UAG -ve)
Increased anion gap acidosis
l Due to retention of unmeasured anions (organic acids)
l HCO3 is utilized to maintain normal [H+] and therefore decreases. Cl is normal or low
E.g. Commonest is lactic acidosis:
type A- lack of O :cardiac arrest, sepsis, type B- metabolic ablormality :diabetes, metformin
Uraemic acidosis/ renal disease
Ketoacidosis : diabetes, alcohol excess, stravation
Exogenous acids : salicylates
Clinical features of MAc 6) Coma
1) Impairs cardiac contractility - -ve ionotrophic 7) Hyperkalaemia if renal function is impaired or
2) Cardiac arrythmias hypokalaemia if normal
3) Arteriolar vasodilation 8) ODC shifts to the right
4) venoconstriction 9) Air hunger / Kussmaul erspiration
5) Confusion
Metabolic Alkalosis
l H+ is decreased. pH increased
l HCO is very much increased
l PaCO is slightly increased as respiratory compensation
Causes : Hypochloraemia/Loss of acid ; gastric (nasogastric suction, Clinical features of MAl
vomiting, intestinal obst) Tetany
Chloruretic diuretics (furosemide), Headache
Hypokalaemia/ mineralocorticoid excess (remove H+) ; Confusion
aldosteronism Seizures
Impaired cerebral perfusion
Hypercaicaemic states Coma
Increased Rx with IV Na HCO , antacid abuse, Hypokalaemia
Cardiac arrhythmias
Nueromuscular irritability
ODC shift to left
Why S electrolytes?
l To determine the Anioin gap
l Anioin gap = (Na + K) – (Cl + HCO3)
l Usually 10 – 18 mmol/l
because of unmeasured albumin mainly & organic acids, phosphate
l Reduced albumin cause reduction in anion gap