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DR Medhat MRCP

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o Treatment of chronic respiratory acidosis :<br />

1. long term oxygen therapy (LTOT)<br />

Indications (e.g in COPD) :<br />

a) FEV1 30% of the time).<br />

2. Nocturnal NIV (BIPAP):<br />

Used in COPD with chronic hypoventillation causing chronic CO2<br />

retention& respiratory acidosis<br />

Initially over-night monitoring of pco2 &PO2 has to be done to assess<br />

over-night gas exchange & decide nocturnal BiPAP.<br />

As the disease progress , the need for BiPAP will increase for longer time<br />

3. Treatment of the underlying etiology .<br />

Metabolic alkalosis :<br />

o May be caused by a loss of hydrogen ions or a gain of bicarbonate.<br />

o It is due mainly to problems of the kidney or gastrointestinal tract<br />

o Features :<br />

1. High plasma HCO3 -<br />

2. High plasma pH > 7.45<br />

3. Compensatory in PCO2 by 0.6-0.7 per every 1 mmol/L increase in<br />

Plasma HCO3 -<br />

o Causes<br />

1. Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis, nasogastric<br />

suction).<br />

2. Diuretics (= contraction alkalosis i.e loss of water to ECF & HCO3 - retention in<br />

blood.<br />

3. Liquorice, carbenoxolone .<br />

4. Hypokalemia.<br />

5. Primary hyperaldosteronism.<br />

6. Congenital adrenal hyperplasia.<br />

7. Cushing's syndrome.<br />

8. Bartter's syndrome<br />

Mechanism of metabolic alkalosis<br />

1. Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor<br />

2. Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal<br />

convoluted tubule<br />

3. ECF depletion (vomiting, diuretics) Na+ and Cl - loss activation of RAA<br />

system raised aldosterone levels<br />

4. In Hypokalemia, K+ shift from cells ECF. Alkalosis is caused by shift of H+<br />

into cells to maintain neutrality.<br />

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