Acid base balance. Grzegorz Szewczyk M.D. Chair & Department of General & Experimental Pathology

Átírás

1 Acid base balance Grzegorz Szewczyk M.D. Chair & Department of General & Experimental Pathology Physiology ph (log [ ]) [ ] 5 45 nmol/l essential for normal cellular function because of the high reactivity between and other compounds, especially proteins Every day metabolism produces to a total of about 70 mmol (1 mmol/kg) as nonvolatile sulphuric acid (5 mmol) from aminoacid catabolism, nonmetabolised organic acids (40 mmol) and phosphoric and other acids. 1

2 Physiology Buffer solution of constant ph (mixture of weak acid/base and its salt) HA+HCO H CO +A CO +H O+A HCO 1) H CO ) HPO4 ) H PO 4) protein buffer 4 Hb HHb Physiology 1. Blood buffers. Intra/extracellular transport Na + K +

3 Physiology. Lungs ventilation is regulated by brainstem chemoreceptors for PCO, PO, and ph, by neural impulses from arterial chemoreceptors and lungstretch receptors, and by impulses from the cerebral cortex PCO, PO, ph make hyperventilation PCO, PO, ph make hypoventilation Physiology Proximal tubule 4. Kidneys lumen Na + + HCO H CO Carbonic anhydrase H O + CO Na + HCO H CO Carbonic anhydrase CO + H O Tubule cell Cl HCO blood Bicarbonates reabsorption

4 Physiology Kidneys Distal tubule HPO 4 H PO 4 Titration acidity lumen K + ATP ATP HCO H CO Carbonic anhydrase CO + H O Tubule cell Cl blood HCO HCO Bicarbonates regeneration K + HCO HCO HCO NH 4 + NH ATP ammoniogenesis H CO CO + H O Carbonic anhydrase Cl Physiology Excretion into lumen is increased by: PCO increase [K + ] decrease Hypovolemia Aldosterone 4

5 ph = pk a HCO + log H CO HCO ph = 6.1+ log 0. PCO Respiratory acidosis Reasons 1. Depression of central respiratory centre due to: Drugs, anaesthetics, neurologic diseases (stroke). Abnormalities of motor neurons: poliomyelitis, myasthenia gravis, Guillain Barre syndrome, currare. Abnormalities of chest Pickwick syndrome, scoliosis, crush injuries 4. Reduction of gas exchange area: COPD, pneumonia, asthma, pulmonary edema, pneumothorax, laryngeal or tracheal obstruction 5. Inefficient mechanical ventilation incorrect gas mixture 5

6 Respiratory acidosis Respiratory acidosis arises from a primary increase in blood PCO HCO ph = 6,1 + log 0, PCO Increased [ ] is buffered by: a) Blood buffers b) Intracellular transport hyperkalemia c) Kidneys in chronic diseases only K + Na + The effect of buffering is increase in HCO and return in ph to normal value HCO ph = 6,1 + log 0, PCO Respiratory acidosis Symptoms 1. Symptoms of primary disease. Dilation of cerebral, coronary and peripheral vessels, constriction of pulmonary and renal vessels. Encephalopathy due to increased intracranial pressure with headache and drowsiness progressing to stupor and coma. 4. Asterixis and multifocal myoclonus can also occur 5. Peripheral edema 6. Cardiac arrythmia (bradycardia) due to hyperkaliemia most common reason of death 6

7 Respiratory alkalosis Reasons anxiety(hyperventilationsyndrome) overventilation of patients on assisted ventilation, primary CNS disorders (multiple sclerosis, vascular dementia) salicylism, hepatic cirrhosis, hepatic coma, hypoxemia, fever, pain, gramnegative septicemia. Respiratory alkalosis Respiratory alkalosis arises from a primary decrease in blood PCO HCO ph = 6,1 + log 0, PCO Decrease in plasma [ ] leads to releasing protons from: a) Blood buffers b) Intracellular transport hypokaliemia c) Kidneys decreasing in bicarbonates regeneration d) Metabolism processes increase in lactates and ketoacids production The effect of buffering is decrease in HCO and return in ph to normal value ph Na + K + HCO = 6,1 + log 0, PCO 7

8 Respiratory alkalosis Symptoms Cerebral vasoconstriction may produce cerebral hypoxia Tetany, circumoral paresthesias, acroparesthesias, lightheadedness and syncope may occur ANION GAP (AG) [Na + ]+[NK]=[Cl ]+[HCO ]+[NA] [Na + ]([Cl ]+[HCO ])=[NA][NK] Ref value: 5 1 meq/l groups of met. acidosis: with normal and with elevated AG 8

9 Reasons 1. Due to increased acid production a) Ketonic acidosis diabetes, hyperthyreosis, alcoholism, poor dietary intake b) Lactic acidosis hypoperfusion of tissue in shock, hepatic disorders, diabetes mellitus treated with metphormine c) Congenital metabolic block Reasons. Due to exogenous acid administration a) After nonconsumption alcohol ingestion (methanol, ethylene glycol) b) Salicylate overdosing. Renal failure accumulation in plasma: phosphates, sulphates, urate, creatinine 9

10 Hyperchloremic acidosis (with normal anion gap) RTA (renal tubular acidosis) type 1 distal RTA lumen Tubule cell HCO blood HCO HCO NH 4 + NH ATP ammoniogenesis H CO CO + H O Carbonic anhydrase Cl RTA type 1 Distal RTA can occur secondary to sickle cell anemia, hypercalcemia, amphotericin B toxicity, toluene toxicity (glue or paint sniffing), or lithium toxicity. Patients cannot reduce their urine ph below 5.5, even in the presence of a severe metabolic acidosis. Symptoms: excessive diuresis, dehydratation, increased calcium release from bones, urolithiasis, growth impairment at children 10

11 RTA type proximal Na + + HCO H CO Carbonic anhydrase Na + HCO H CO Carbonic anhydrase CO + H O Cl HCO H O + CO lumen Tubule cell blood After the initial bicarbonaturia, plasma [HCO ] and the amount of bicarbonate filtered both decrease, and a new steady state is reached within hours, with hyperchloraemic acidosis and urine free of bicarbonate. RTA type RTA is due to: myeloma light chain nephropathy, nephrotoxins and genetic diseases. Symptoms and laboratory findings: Random urinary ph above 5.5 Dehydratation, hypokalemia Significant increase in urine ph after administration of bicarbonates, with a low plasma level of bicarbonates 11

12 4. Loss of alkali Excessive GI fluid losses due to: protracted diarrhea, villous adenoma of the colon, drainage of biliary, pancreatic, or intestinal fluid Early beginning: HCO ph = 6,1 + log 0, PCO [ ] excess is buffered by: Blood buffers Intracellular buffers Increased ventilation Regeneration of bicarbonates in kidneys HCO ph = 6,1 + log 0, PCO 1

13 The major symptoms and signs of acidosis are difficult to separate from those of the underlying disease. Mild acidosis may be asymptomatic or may be accompanied by nausea and vomiting. The most characteristic finding in severe metabolic acidosis is increased ventilation.(kussmaul respiration). Signs of ECF volume depletion, especially in patients with diabetic ketoacidosis or GI volume losses. Severe acidosis may cause circulatory shock due to impaired myocardial contractility (hyperkalemia) and impaired peripheral vascular response to catecholamines Metabolic alkalosis Reasons 1. Loss of [ ] protracted vomiting, nasogastric suction, excessive losses of chloride via stool or urine. Excessive alkali administration milkalkali syndrome (Calcium carbonate). transcellular movement of into cells hypokalemia, hypovolemia 1

14 Metabolic alkalosis Compensation 1. Blood buffers. Intracellular buffers are most important buffer increased production of [H+] lactic acid, ketonic acids. Decrease of ventilation may give partial compensation only due to hypoxemia, that limits hypoventilation 4. Renal mechanism insufficient paradoxical aciduria Metabolic alkalosis Signs and symptoms: There are no specific signs nor symptoms Severe alkalosis may cause apathy, confusion and stupor. If serum calcium is borderline rapid development of alkalosis may lead to tetany 14