ACID – BASE BALANCEMetabolic causes of acid – base disturbances are indicated
by changes in the standard
bicarbonate level and base excess or deficit
Respiratory causes of ABD are indicated by changes in Po2 and
there is deficit of base or excess of any acid other than H2CO3
1- over production of organic acids
- lactic acidosis of sepsis and shock.
2- renal failure.
3- excessive loss of bicar.
- pancreatic or small bowel fistula.
Pathology :Standard bicar level is lowered and there is a base deficit .
Compensation:Respiratory stimulation of respiration wash out of CO2 decrease PCO2 bringing HCO3\PCO2 ratio and PH back to normal .
Renal later occur- renal excretion of acid increase .
Clinical:Increase rate and depth of breathing ( Kussmauls respiration).
Treatment:mild to moderate acidosis – treat primary cause.
severe acidosis ( PH 7.3 or HCO3 less than 15) IV bicar .
required amount ( body wt kg *0.3*bsae deficit)
Metabolic alkalosis:the main rise in PH due to accumulation of HCO3.
1- GIT losses of H + due to vomiting , suction (pyloric stenosis).
2- bicar retention NaHCO3 administration and milk alkali syndrome.
respiratory inhibition raises PCO2.
Normal hypoxic respiratory drive when PO2 reach 50 mmHg .
1- severe alkalosis – cheyne – stocks respiration with period of apnea.
2- tetany occasionally occur.Treatment:
1- If metabolic alkalosis due to gastric juice loss replacement of chloride is essential . Administration of normal saline is sufficient in mild cases without hypokalaemia , since kidney will complete the job by retaining chloride and excreting sodium along with excess bicar , hypokalaemia treated by IV K+ infusion.
2- severe not responding to saline and KCL give IV aluminum chloride or hydrogen chloride very slowly.
3- tetany is treated by slow IV 10 ml calcium gluconate.
Respiratory acidosis:Decrease in the PH and increase in PCO2 is called RA usually associated with hypoxia.
Increase in PCO2 result in respiratory depression (CO2 narcosis) with hypoxia and endanger life.
Renal compensatory mechanisms are too slow to affect the outcome significantly.
1- inhibition of respiratory derive .
* drugs as opiates or anesthetics.
* CNS lesions.
2- disorders of respiratory muscle or chest wall.
* muscle weakness as in myasthenia gravis or poliomyelitis.
* morbid obesity .
* flail chest.
3- other disorder of ventilation.
* obstructive pulmonary disease.
* pulmonary oedema.
Compensation:In acute RA the HCO3 may be not elevated,thus renal mechanism has no time to work , in chronic RA the HCO3 elevated.
Restless , cyanosis , hypertension and tachycardia in immediate post operative period (pain also increase BP and pulse).
Respiratory alkalosis :Carbon dioxide tension in the arterial blood Pco2 is below normal and the PH increase .
It results from hyperventilation
3- in patient who are hyperventilated by mechanical ventilator.
Compensation:Increase renal excretion of bicar but usually is in adequate .
Clinical features :
In most cases is short lived and well tolerated , when hyperventilation stops PH return to normal.
Decrease in ionized Ca+ may manifest by parasthesia in the extremities and carpopedal spasm.
In severe cases respiratory arrest follows.
When it is due to HYS the patient instructed to breath into paper bag.
Add small amount of CO2 to the inspired air.
Normal Po2 80-110 mmHgNormal Pco2 36-44 mmHg
Hco3 22-26 mmol/liter
Post operative fluid and electrolytes therapyWe will give and observe
1- basal and requirements
2- pre existing dehydration , electrolytes loss and acid base disturbances
3- continuing losses over the basal requirement
The basal daily requirement of water and electrolytes
- water 35ml/kg
- sodium 1mmol/kg
- potassium 1mmol/kg
The usual daily post operative fluid for adult uncomplicated surgery
3 liters of fluid , add 200 ml for each 1 degree C of increase temperature
-500ml of saline (0.9% NaCl) give requirement of Na+ and Cl-