ABR: acid-base balance Normal pH - very close ranges Normal 7 35 - . 7 í F Acidosis ^ Alkalosis ^^^J YJ 7.00 **»c ^ \ ^ V- 7.80 Analyte Unit Reference intervale pH 7.35 - 7.45 pC02 kPa 4.8-5.6 p02 kPa 10-13 actual HCO3 mmol/l 22-26 standart HC03 mmol/l 22-26 BE (base exces) mmol/l ±2 pH - activity of hydrogen ions . pH: 7.35-7.45 • Acidosis: pH < 7.35 ► „common": 7.35-7.10 ►serious: 7.10-6.80 ► extremely: < 6.80 (life threatening) . Alkalosis: > 7.45 ► serious: 7.45 - 7.70 ► extremely: > 7.70 Not serious acid-base disorders • „Common" acidosis: pH 7.35-7.10 ► „Physiological" situation • Physiologic acids ► Kenotic acids ► Lactic acid • There is no „common" alkalosis ► Alkalosis is always serious disorder ► It often results from inadequate therapy of acidosis • Normal pH ► Aide-base disorder may be present Correction of pH changes • Buffers ► To correct the influence of acids and bases • Reaction of buffers ► Immediately • Compensation ► With delay ► Lungs and/or kidney Buffers • Bicarbonate ► Extracellular fluid (blood, interstitial fluid) ► Cerebrospinal liquor - activity of the respiratory centre • Haemoglobin ► Intravasal fluid • Phosphate ► Intracellular fluid ► Connection to the concentration of K+ ! • Proteins ► Both intra and extracellular fluid ► Small capacity . Blood ► Bicarbonate 53 ► Phosphate 5 ► Haemoglobin 35 ► Proteins 7 Fers % % % % HC03" a Hb system • Bicarbonate ► Concentration: 24 + 2 mmol/l ► Regulation of their blood level: kidney ► Standard x actual HC03_ • Haemoglobin ► Similar capacity as HC03_ ► HbO is stronger acid than Hb: it releases H+ •Tissues: HbO -> Hb: binding of H+ •Lunqs: Hb -» HbO: release ofÍH+) Compensation of A-B disorders • Respiratory A-B disorder ► Renal compensation • „Metabolic" A-B disorder ► Lung and renal compensation Respiratory compensation of A-B disorders T or i of ventilation Acidosis Respiratory compensation of A-B disorders T or i of ventilation • Metabolic acidosis: hyperventilation ► Stimulation of respiratory centre by low pH ► Very effective mechanism ► i pC02, improved tissues saturation with 02 • Metabolic alkalosis: hypoventilation = hypoxia !! ► Inhibition of respiratory centre by elevated pH ► Low effective mechanism ► T pC02, i p02, hypoxia = hypoventilation is cancelled Respiratory compensation of A-B disorders T or i of ventilation • Respiratory compensation started immediately, but ► Maximal compensation: 24 hours ► Hyperventilation persists after adjustment of acidosis •Risk of respiratory alkalosis development Renal compensation of A-B disorders Return do the blood Excretion to the urine Renal compensation of A-B disorders • Acidosis ► Synthesis of HC03- ► Excretion of H+to urine •Ammonium ions (NH4+) •Phosphate ions (H2P04_) • Alkalosis: ► Excretion of HC03_ to the urine ► Inhibition of H+ elimination •Stop of NH4 synthesis •HP042_ synthesis is started Renal compensation of A-B disorders • Renal compensation starts during 24 hours ► It is complete is after 1 week ► When is acidosis or alkalosis removed (therapy), compensation continues several days •Risk of reverse A-B disorder! Acid-base disorders • Simple disorders 1. Metabolic acidosis 2. Metabolic alkalosis 3. Respiratory acidosis 4. Respiratory alkalosis • Combined acid-base disorders ► Result of compensation mechanisms ► Primary combined disorders Metabolie acidosis • Laboratory diagnosis: ► i pH ► ÍHC03- ► <-> pC02 (acute), i (lung compensation) • Causes: a) Without HCO3- loss • T acids b) Duetolossof HCO3- Acidosis without HC03" loss • T production of acids ► Kenotic acids •Starvation, decom. DM, high grade fever ► Others acids • Intoxications ■»Salicylate, ethylene glycol (oxalic acid), methanol (formate) • Acid retention ► Acute renal failure, chronic renal failure Acidosis without HC03" loss Lactic acidosis • Type A (hypoxic): hypoxia from any causes ► Respiratory insufficiency, shock ► Anaemia (Hb < 70 g/l), carbon monoxide poisoning, extreme muscular activity ► Blood stagnation • Type B (insufficient utilization of lactic acid) ► Hepatic failure ► Biguanide poisoning ► Sepsis Acidosis due to bicarbonate loss • Real bicarbonates loss ► Diarrhoea ► Pancreatic fistula • Decline of bicarbonates: Hyperchloremic acidosis ► T chloride intake • KCl, NaCI, NH4CI Therapy of . NaHC03 ► How much ? • Calculation ► mmol HCO3 the metabolic acidosis : BE x 0.3 x weight (kg) Therapy of the metabolic acidosis The rules for therapy of met. ac. • Therapy must be causal (if possible)!!! • Maximal dose of bicarbonate ► 1/3 -1/2 of the calculated dose • HCO3- is indicated only when ► Causal therapy is not possible ► pH<7,1 • Chronic met. ac: treatment with caution ► Compensation with both hyperventilation and kidney •Risk of alkalosis after therapy Therapy of MAC with HC03" :YES or NO ? • Ketoacidosis: No ► Starvation - nutrition ► Decom. DM - insulin ► Intoxication (ethylene glycol, methanol) •Dialysis • Renal failure: No ► Haemodialysis Therapy of MAC with HC03" :YES or NO ? • Lactic hypoxic acidosis type A: NO !!! ► Oxygen therapy • Type B ► Hepatic failure, sepsis: specific therapy ► Biguanide poisoning: Yes, but dialysis and/or hemoperfusion is necessary • Loss of bicarbonates ► Diarrhoea, pancreatic fistula: Yes ► Hyperchloremic acidosis: No •Thiazid diuretics Metabolic alkalosis • Dg: ► T pH ► THC03 ► <-> pC02 (acute), T (lung compensation) • Types of MAL: ► Responding for treatment with chlorides • MAL due to loss of CI ► Not responding for treatment with chlorides Metabolic alkalosis 45 -cl:i - [HCO3-] 55~ (mmolíL) M ■ 25-ZJ pH 7J- 7.6-7.5-7.4-7.3-7.2- Pco2 C mmHg) BO- SO ■ ; Primary Lesion Pcuz (mmHg) = 0.9 x [HCO3J + S Limit: ^6Q mmHg Ücjmponsjitk>n MAL due to loss of CI • Vomiting • Drainage of gastric juice • Overdosing of diuretics (thiazides) Concentration of the ions in the extracel. fluid o £ £ Na: 140; 4 1 2.5 K Mg Ca CI: 102 HC03: 24 RA, Prot: 26 Lack of chlorides = alkalosis o £ £ Na: 140 4 1 2,5 K Mg Ca CI: 94 (102) HC03: 32 ___(24)___ RA, Prot: 26 MAL due to lack of CI: therapy . CI- ► NaCI, KCl, NH4CI, arginin hydrochlorid • How much of Cľ ? ► BE x 0.3 x weignt (kg) ► Deficite of Ch x 0.3 x weight (kg) • The rules for therapy of met. alkalosis ► Therapy is always indicated ► The full calculated dose of Ch should be given • Alkalosis is more dangerous than acidosis! MAL not responding for treatment with Cľ • Hyperaldosteronism • Long-term therapy with glukocorticoides • Iatrogenic ► T supplementation of HC03_ MAL not responding for treatment with Ch • Therapy must be causal • Hypokalemia - KCl • Live- threatening MAL - Hemodialysis Respiratory acidosis (RAC) • It is characterized by retention of C02 • Dg: ►ipH ► T pC02 ► <-> HCO3, then T (kidney compensation) • Cause of RAC: retention C02 ► Central ► Ventilatory ► Cardiac Respiratory 45 40 [KCD3-] 35 {m mo ľ L) 3Ů 25 20. 7.5 7 -i 7.3 7.2 7.1 7.0 pH f mmHg) Limit*: Acute -32 mmoLL Chronic -45 mmn-lŕL Compensation Chronic: [HCO3-] = G 43 v Pcoj + 7 6 ímrndíL) |mmHg) 10 min acidosis Deviation of pH may be greatly reduced by the process of compensation Respiratory acidosis (RAC) • Central (depression of respiratory centre) ► Drug induced - sedatives, narcotics ► Lesions of resp. centre - tumour, trauma, ... Respiratory acidosis (RAC) • Ventilatory ► Neuromuscular (myastenia gravis, botulism) ► Muscles (myositis, muscular dystrophy) ► Thorax (pneumothorax) ► Respiratory tract (asthma, bronchostenosis, tumour) ► Lung parenchyma (lung oedema, ARDS, pneumonia) Respiratory acidosis (RAC) • Cardiac ► Low minute volume of cardiac output Respiratory acidosis: Therapy • Therapy must be causal!! • Hypoxia is more serious problem then acidosis !!! • Improvement of ventilation, sometime oxygen • In the life threatening RAC ► Mechanical ventilation • Bicarbonate is contraindicated !!! • Oxygen must be done with caution ! ► Hypoxia stimulated respiratory centre • High 02 doses can stop respiration Respiratory alkalosis (RAL) • Stimulation of the respiratory center • Dg: ► T pH ► i pC02 ► <-> HCO3, then i (kidney compenzation) Respiratory 35 30 [HCP3] 25 (mmol/L) 20 15 10 7.7 7.6 7.5 ?X 7.3 7-2 pH (mmHg) m - Compensation Limit»: Ac úl* ~18 mmolJL Chronic -12mmůl/L Acute pH 10 -T.4Q |f>7d*yt Chronic . Primary Legion; 1 n rTwl alkalosis Respiratory alkalosis (RAL) • Causes of RAL ► Hyperventilatory syndrom ► Anxiety, hysteria ► Lesions of the CNS ► Encephalitis, meningitis, tumours, trauma Respiratory alkalosis (RAL): Therapy • Depression of the respiratory center • Hyperventilatory syndrom ► Sedatives • Life threatening RAL ► Mechanical ventilation Combined A-B disorders • Primary combined A-B disorders • Result of the compensation mechanisms ► Metabolic acidosis is compensated by respiratory alkalosis ► Metabolic alkalosis is compensated by respiratory acidosis ► Respiratory acidosis is compensated by metabolic alkalosis ► Respiratory alkalosis is compensated by metabolic acidosis How to recognized combined A-B disorders ? • Respiratory component can be found easy ► pC02 is changed • Metabolic components may be sometimes difficult to detect, as both acidosis and alkalosis may be present and they result to the relatively normal laboratory values (pH, HCO3, pC02, p02): ► Concentration of Ch , K+, Na+ must be measured ! ► Some calculation may be useful How to recognized combined A-B disorders ? • An interpretation of the blood's A-B status must take into account the electrolyte status • CI and K deserve special attention! • Changes in Ch cone, are followed by the changes in A-B status ► t of Ch results in i of HC03" and it is followed by metabolic acidosis (hyperchloremic acidosis) ► i of Ch results in T of HC03" and it is followed by metabolic alkalosis (hypochloremic alkalosis) Formulas that can contribute to the detection of the combined disorders: . Buffer Base = Na+ + K+ - Cľ ► Normal result: 42 mmol/l ► T = metabolic alkalosis is probably present Formulas that can contribute to the detection of the combined disorders: . Anion gap = (Na+ + K+) - (Cľ + HC03) • Normal result =18 mmol/l) • T = metabolic acidosis is probably present (Tconcentration of organics anions) ► Lactate, kenotic acids, multiple acid radicals How to recognized combined A-B disorders ? • Normal pH do not exclude A-B disorders ! • What we need for interpretation of A-B status ? ► pH, HCO3-, pC02, p02 ► Na, K, CI ► Patients s history and clinical examination! Physiologie values of AB balance Parameter Unit Reference ranges Critical values pH 7.35 - 7.45 <7.1; >7.6 pC02 kPa 4.8-5.6 < 3.3; > 8.1 p02 kPa 10-13 <6.7 akt.-HC03 mmol/l 22-26 < 5; > 55 stan.-HC03 mmol/l 22-26 < 5; > 55 BE mmol/l ±2 Laboratory diagnostic of A-B disorders HCO3 pH pC02 Metabol. acidosis Acute II II N Chron. 1 1 1 Metabol. alkalosis Acute TT TT N Chron. T T T Respir. acidosis Acute N,T II TT Chron. T 1 TT Respir. alkalosis Acute N, 1 TT II Chron. 1 T II