Disorders of acid base balance

1. Disorders of acid base balance Gamal El Naggar Internal Medicine Department Tanta Faculty of Medicine Nephrology Unit. by

2. Acid-base disorders • The diagnosis and mangement of acid-base disorder s in acutely ill patients requires an accurate and timely interpretatation of the laboratory parameters associated with any specific acid-base disorder. Appropriate interpretation requires simultaneous measurement of serum electrolytes and arterial blood gases • Primary changes in serum concentrations of fixed acid or bace lead to either metabolic acidosisor alkalosis and are reflicted in the serum HCO3 concentration ,where as primary change s in parial pressure of arterial carbon dioxide (PCO2) lead to either respiratory acidosis or alkalosis.

3. Simple acid-base disorders *= change due to compensation.

4. Disorders of acid-base balance Normally pH (7.35-7.45) will vary as the bicarbonate and PCO2 Change so pH depends on (HCO3)- = (22-28mEq/L) PCO2 (35-48mmHg) There are two types of disorders: 1- metabolic disorders: due to alternation arterial blood of bicarbonate concentration. Types: • metabolic acidosis : due to decrease plasma bicarbonate --decrease pH • Metabolic alkalosis : due to increase plasma bicarbonate -increase pH 2-respiratory disorders: due to changes in arterial blood Co2 tension. Types: • Respiratory acidosis: due to increase of PCO2-decrease pH • Respiratory alkalosis: due to decrease of PCO2increase pH

5. Metabolic acidosis Metabolic acidosis is characterized by a fall in both the bloob pH and the serum HCO3- concentration and is normally accompanied by a compensatory respiratory alkalosis. It develops as the result of amarked increase in endogenous production of acid (such as lactic acid and ketoacids),loss of HCO3 stores (diarrhea or renal tuular acidosis (RTA), or progressive accumulation of endogenous acids (renal failure).

6. Metabolic acidosis ANION GAP: • It is the difference between plasma concentration of Na+ and sum of CL- and HCO3- (Na - (CL- + HCO3-) =6-16mmol). • This gap represent substances which combine with Na+ (other than CL- and HCO3-) which are not measured in routine chemistry such as amino acid. Causes: Two mechanisms: • Increased acid production • Decreased alkali reserve. • Normal anion gap • Renal causes • Bicarbonate loss (proximal tubular defects). • Proximal RTA ,type II • Dilutional acidosis • Carbonic anhydrase inhibitors • Primary hyperparathyroidism

7. Failure of bicarbonate regeneration (distal tubular defect) • Distal RTA ,type I • Distal RTA ,type IV • Diuretics :amilorid ,spironolactones , triamterene • Gastrointestinal causes (increased alkali loss) • Diarrheal states • Small bowel drainage • Ureterosigmoidostomy iliostomy • Acidifying salts (increase acid) • Ammonium chloride • Lysine hydrochloride • Arginine hydrochloride • Parentral hyperalimentation • Inceased anion gap (>16 mmol) • Endogenous causes II.Exogenous causes • Uremic acidosis > salicylates • Lactic acidosis > paraldehyde • Ketoacidosis > methanol • Hydroxybutyric acidosis > ethylene glycol

8. Clinical features • Manifestation of the cause • Varies widely • Hyperventilation ( Kussmal’s respiration) deep and rapid respiration (air hunger ) due to stimulation of the respriatory center. • Hyperkalaemia • Cardiac depressant effects. • Cerebral depression: confusion and even coma. • Bone decalcification in chronic case. INVESTIGATION • Low pH • Low HCO3 • Low PCO2

9. Treatment • Treatment of the cause: • Insuline for DKA or restoration of tissue perfusion in lactic acidosis • Treatment with alkali shoud be reserved for severe acidemia only (pH<7.2) • In distal RTA: correction should be gradual by NaHCO3 should be provided 1-3mmoL/Kg/day.K+ and Ca++ supplementation may de needed 1/6 Na+ lactate could be used if NaHCO3 is not available. • In proximal RTA: large amount of alkali (10 -25 mmol/Kg/day)with Ca++ or K+ supplement. • HCO3 deficit ×body weight (Kg) × 0.5 if the deficit less than 10mEq/L or HCO3 deficit ×body weight (Kg) × 0.8 if the deficit more than 10mEq/L • Dialysis and ultrafiltration may be used in severe and refractory cases.

10. Respiratory acidosis • Respiratory acidosis occurs as the result of severe pulmonary disease, respiratory muscle fatigue ,or depressed ventoratory control. The increase in PCO2 caused by reduced alveolar ventilation is the primary abnormality leading to acidamia • In acute respiratory acidosis there is immediate compensatory elevation HCO3 concentration(1mEq/L for every 10 mmHg increase in PCO2 ) • In chronic respiratory acidosis(> 24hours)renal adaptation is achieved and HCO3 increases by 4 mEq/L for 10mmHg increase in PCO2 • The serum HCO3 dose not usually increase more than 38mEq/L Causes: Hypercapnic respiratory failure that caused by hypoventilation • Acute respiratory failure. • Chronic respiratory failure

11. Clinical manifestations CLINICAL FEATURES OF RESPIRATORY ACIDOSIS: • Vary according to the severity , duration , underlying diseases , and absence or presence of hypoxemia • Vary widely depending on the rate and severity of CO2 retention. • Cerebral depression: somnolence , irritability asterixis , CO2 narcosis , confusion and even coma in severe cases. • Cerebral vasodilatation: cerebral oedema , headache , papilloedema. • Features of respiratory failure. EINVSTIGATION: • Low pH of the blood • High HCO3 and PCO2

12. TREATMENT: • Treating the underlying cause • ventilatory support • Treament of respiratory acidosis depends on the severity and the onset • In acute respiratory acidosis measures to reverse the underlying cause must be taken • Adequate alveolar ventilation relieve hypoxemia and acidemia • O2 should be carefully titerated • Aggressive and rapid correction of hypercapia should be avoid(cardic arrhysmia ,reduced cerebral perfusion and siezures) • In chronic respiratory acidosis measures to improve lung function (cessation of smoking, use of O2 ,bronchdilators , corticosteroids , duiretics , respiratoty stimutant , and physiotherapy)

13. Metabolic alkalosis • Metabolic alkalosis is a primary acid-base disturbance that is manifestated as alkalemia (elevated arterial pH) together with an increase in PCO2 as a result of compensatory alveolar hypoventilation . • A rise in the serum HCO3 concentration requires either exogenous administration of HCO3 or a net acid loss from the kidney or GIT. • The maintenance of a metabolic alkalosis thereafter represents a failure of the kidneys to eliminate HCO3 at the normal capacity .

14. Causes • Volume depleted type • Gastric acid loss • Vomiting • Renal chlorid loss • Diuretics • Volume –repleted type • Mineral corticoid excess • Hyperoldosteronism • Batter’s syndrome (hypokalemia ,alkalosis ,hypercalsoria ,normal blood pressure ,elevated plasma renin & aldesterone • Licorice excess • Profound K+ depletion. • Iaterogenic:(excess HCO3 load) • Excess ingestion of bicarbonate • Milk alkali syndrome

15. Other causes : • Ampicilline ,pinicilline therapy • Recavery from starvation • hypoalduminemia

16. Clinical features • Manifestation of the cause • In severe alkalosis there may be : • Cardiac irritability and dysrhythmia • Neuromuscular irritability and tetany • Hypocalaemia (low ionised Ca++) • Hypoventilation:shallow slow breathing • Shift to the left of the oxyheamoglobin dissociations curve INVESTIGATION: • High pH of the blood • High HCO3 • High PCO2

17. Treatment • Treatment of the cause • Support the respiratory and renal compensatory mechanisms • Correction of hypercalaemia. • NB: because of high capacity of the kideny to secret HCO3 , metabolic alkalosis commonly persist if there is a renal dysfunction with a reduction in HCO3- secretion. • In Chlorid dependant metabolic acidosis isotonic saline soulution is used provied there is extrcellural volume depletion • If there is volume over load isotonic saline is contraindicated and the used of ammoniun chlorid can be considared

18. If GFR is adequate use acetasolamide (induced bicarbonate diaylasis) • If the kidney is severe affected and unable to responed dialysis is indicated • In case of metabolic alkalosis due to potasium depletion treat the cause and replace the potasium by oral potasium chlorid in mild cases & by IV KCLadministration in severe cases

19. Respiratory alkalosis Causes (hyperventilationCO2 wash) • Hypoximia and tissue hypoxia: as high altitude ,drowning , bacterial or viral pneumonia , pulmonary oedema , cyanotic heart disease , and hypotension: • Stimulation of chest receptor: asthma , pneumonia , pneumothorax , cardiac failure. • CNS stimulation: • Psychosis ,anxiety , voulantary • Subarachinoid haemorrhage , CV accidents. • Tumour ,truma. • Drugs and hormones:salicylates , angiotension II , catachelamines , nicotine. • Iaterogenic: under ventilatory support • Recavery from metabolic acidosis

20. Clinical features (usually minimal) • Manifestation of the cause • Neurological manifestation :irritation (low ionized Ca++): parathesia , tinnitus , neuromuscular irritability , tetany ,and • Cerebral vasoconstriction • Hyperventilation. • Cardiac arrhythmia , INVESTIGATION: • High pH of the blood • Low HCO3 & PCO2 TREATMENT: • Correction of the underlying causes • Reassurance • Rebreathing into a closed system (eg paper bag )to inspire the expired air with its high level of CO2.