Respiratory Acidosis
Due to retention of CO
PaCO & H+ rise. --- pH decrease
HCO3 is used-up for buffering
Compensation is by HCO retention by kidneys
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
H+ & PaCO fall. pH increase 2) Hypoxaemia (type 1 RF)
Due to increased ventilation 3) Spontaneous hyperventilation
Compensation is by slight decrease in HCO 4) High altitudes
5) Septic shock
Causes :
6) Pneumonia
1) Mechanical ventilation 7) Hyperkalaemia
Metabolic Acidosis
H+ increase. pH decrease Causes : Acid administration
HCO is largely decreased acid generation (Diabetic ketoacidosis, anaerobic metabolism/
Is due to accumulation of acid otherthan HCO lactic acidosis (shock, cardiac arrest)) impaired acid excretion
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
Normal AG with acidosis
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
Urinary anion gap (Urinary Na + K - Cl) is useful in distinguishing RTA1 (UAG +ve) & diarrhoea (UAG -ve)
Increased anion gap acidosis
Due to retention of unmeasured anions (organic acids)
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
H+ is decreased. pH increased
HCO is very much increased
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
Base Excess – The concentration of acid or base in mEq/l to bring the pH back to normal when PCO & PO are normal.HCO is the base. ‘+’ BE
means there are more HCO than H+
Standard HCO3 – Plasma HCO3 after equilibrating with whole blood at pCO2 of 40mmHg at 37 C and fully oxygenated. This totally eliminates the
respiratory component and relates to the metabolic change.
Why S electrolytes?
To determine the Anioin gap
Anioin gap = (Na + K) – (Cl + HCO3)
Usually 10 – 18 mmol/l
because of unmeasured albumin mainly & organic acids, phosphate
Reduced albumin cause reduction in anion gap