ABR: acid-base balance Normal pH - very close ranges Analyte Unit Reference intervale pH 7.35 - 7.45 pCO2 kPa 4.8 - 5.6 pO2 kPa 10 - 13 actual HCO3 mmol/l 22 - 26 standart HCO3 mmol/l 22 - 26 BE (base exces) mmol/l ± 2 pH - activity of hydrogen ions • pH: 7.35-7.45 • Acidosis: pH < 7.35 4„common“: 7.35 - 7.10 4serious: 7.10 - 6.80 4extreme: < 6.80 (life threatening) • Alkalosis: > 7.45 4serious: 7.45 - 7.70 4extreme: > 7.70 Not serious acid-base disorders • „Common“ acidosis: pH 7.35-7.10 4„Physiologic" situation • Physiologic occur acids 4Ketonic acids 4Lactic acid • There is no „common“ alkalosis 4Alkalosis is always serious disorder 4It often results from inadequate therapy of acidosis • Normal pH 4Aide-base disorder may be present Correction of pH changes • Buffers 4To correct the influence of acids and bases • Reaction of buffers 4Immediately • Compensation 4With delay 4Lungs and/or kidney Buffers • Bicarbonate 4Extracellular fluid (blood, interstitial fluid) 4Cerebrospinal fluid - activity of the respiratory centre • Haemoglobin 4Intravascular fluid • Phosphate 4Intracellular fluid 4Connection to the concentration of K+ ! • Proteins 4Both intra and extracellular fluid 4Small capacity Relationship between K a pH 1 2 3 4 5 6 7 8 9 6,9 7 7,1 7,2 7,3 7,4 7,5 7,6 7,7 pH K(mmol/ Kmmol/L K and pH • Acidosis = excess of H+ ions 4H+ move to ICF, where is bound to phosphate buffer, K+ is released from buffer and move out to maintain electroneutrality 4Concentration of K+ increase K and pH • Alcalosis = lack of H+ ions 4H+ is released in ICF from phosphate buffer, K+ move into cells and is bound to P buffer 4Concentration of K+ decrease Buffers • Blood 4Bicarbonate 53 % 4Phosphate 5 % 4Haemoglobin 35 % 4Proteins 7 % HCO3 - a Hb system • Bicarbonate 4Concentration: 24 ± 2 mmol/l 4Regulation of HCO3 - level: kidney • Haemoglobin 4Similar capacity as HCO3 - 4Oxidized HbO is stronger acid: it releases H+ Tissues: HbO → Hb: binding of H+ Lungs: Hb → HbO: release of H+ Compensation of A-B disorders • Respiratory A-B disorders 4Renal compensation • „Metabolic“ A-B disorders 4Lung and renal compensation Respiratory compensation of A-B disorders ↑ or ↓ of ventilation • Metabolic acidosis: hyperventilation 4Stimulation of respiratory centre by low pH 4Very effective mechanism to ↓ pCO2 4Good tissues saturation with O2 • Metabolic alkalosis: hypoventilation = hypoxia !! 4Inhibition of respiratory centre by elevated pH 4Ineffective mechanism 4↑ pCO2, ↓ pO2, hypoxia = hypoventilation is cancelled Respiratory compensation of A-B disorders ↑ or ↓ of ventilation • Respiratory compensation started immediately, but 4Maximal compensation: 24 hours 4Hyperventilation persists after adjustment of acidosis Risk of respiratory alkalosis development Renal compensation of A-B disorders • Acidosis 4Synthesis of HCO3 - 4Excretion of H+ to urine Ammonium ions (NH4 +) Phosphate ions (H2PO4 -) • Alkalosis: 4Excretion of HCO3 - to the urine 4Inhibition of H+ excretion Stop of NH4 synthesis HPO4 2- synthesis is started Renal compensation of A-B disorders • Renal compensation starts during 24 hours 4It is complete is after 1 week 4When 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 4 Result of compensation mechanisms 4 Primary combined disorders Metabolic acidosis • SOURCES OF HYDROGEN IONS 44Cell MetabolismCell Metabolism 44Food ProductsFood Products 44MedicationsMedications 44Metabolic Intermediate byMetabolic Intermediate by--productsproducts 44SomeSome ddisease processesisease processes METABOLIC ACIDOSIS • Metabolic acidosis is always characterized by a reduction in plasma HCOHCO33 -- while COCO22 remains normal Metabolic acidosis • Laboratory diagnosis: 4 ↓ pH 4 ↓ HCO3 - 4 ↔ pCO2 (acute), ↓ (respiratory compensation) • Causes: a) Without HCO3 - loss ↑ acids b) Due to loss of HCO3 - Acidosis without HCO3 - loss • ↑ production of acids 4Kenotic acids Starvation Unregulated DM High grade fever 4Ketones AcetoneAcetone Acetoacetic acidAcetoacetic acid ββ--hydroxybutyrhydroxybutyrousous acidacid Acidosis without HCO3 - loss • Others acids 4Ingestion of Ethylene glycol (antifreeze) → oxalic acid Methanol → formate acid Salicylate Acidosis without HCO3 - loss • Acid retention 4Acute renal failure, chronic renal failure 4Kidneys are unable To rid the plasma of even the normal amounts of HH++ generated from metabolic acids To conserve an adequate amount of HCOHCO33 -- Acidosis without HCO3 - loss • Lactic acidosis type A (hypoxia) 4Respiratory insufficiency, shock 4Anaemia (Hb < 70 g/l), carbon monoxide poisoning, extreme muscular activity 4Blood stagnation Acidosis without HCO3 - loss • Type B (insufficient utilization of lactic acid) 4 Hepatic failure 4 Biguanide poisoning 4 Sepsis Acidosis due to bicarbonate loss • Real bicarbonates loss 4Severe diarrhoea 4Pancreatic fistula • Decline of bicarbonates: Hyperchloremic acidosis 4↑ chloride intake KCl, NaCl, NH4Cl Therapy of the metabolic acidosis • NaHCO3 4How much ? • Calculation 4mmol HCO3 = BE x 0.3 x weight (kg) The rules for therapy of met. ac. • Therapy have to be causal (if possible) ! 4If the acidosis is mild, treatment for the underlying disorder may be all that's needed Therapy of the metabolic acidosis The rules for therapy of met. ac. • HCO3 - may be given only when 4Causal therapy is not possible 4Acidosis is severe: pH < 7,1 • Maximal dose of bicarbonate 41/3 - 1/2 of the calculated dose Therapy of the metabolic acidosis Metabolic alkalosis • Dg: 4 ↑ pH 4 ↑ HCO3 4 ↔ pCO2 (acute), ↑ (pulmonary compensation) Breathing suppressed to hold CO2 • Types of MAL: 4 Responding for treatment with chlorides MAL due to loss of Cl 4 Not responding for treatment with chlorides MAL due to loss of Cl • Vomiting • Drainage of gastric juice • Diuretic use (thiazides) • Cl- (HCO3 - ions replaced by Cl- ions) 4NaCl, KCl, NH4Cl, arginin hydrochlorid • How much of Cl- ? 4BE x 0.3 x weignt (kg) 4Deficiency of Cl- x 0.3 x weight (kg) MAL due to lack of Cl: therapy • The rules for therapy of met. alkalosis 4Therapy of alkalosis should be started in all cases 4The full calculated dose of Cl- should be given • Alkalosis is more dangerous than acidosis! MAL due to lack of Cl: therapy MAL not responding for treatment with Cl• Hyperaldosteronism • Long-term therapy with glukocorticoides • Iatrogenic 4↑ supplementation of HCO3 - • Therapy have to be causal • Hypokalemia - KCl • Live- threatening MAL - Haemodialysis MAL not responding for treatment with Cl-: Respiratory acidosis (RAC) • It is characterized by retention of CO2 • Dg: 4↓ pH 4↑ pCO2 4↔ HCO3, then ↑ (renal compensation) • Cause of RAC: retention CO2 4Central 4Pulmonary 4Cardiac Respiratory acidosis (RAC) • Central (depression of respiratory centre) 4Drug induced - sedatives, narcotics 4Lesions of resp. centre - tumour, trauma, ... Respiratory acidosis (RAC) • Pulmonary 4Neuromuscular (myastenia gravis, botulism) 4Muscles (myositis, muscular dystrophy) 4Thorax (pneumothorax) 4Respiratory tract (asthma, bronchostenosis, tumour) 4Pulmonary parenchyma (pulmonary edema, ARDS, pneumonia) Respiratory acidosis (RAC) • Cardiac 4Low minute volume of cardiac output Respiratory acidosis: Therapy • Therapy must be causal !! • Hypoxia is more serious problem then acidosis !!! • Improvement of respiration, sometime oxygen • In the life threatening RAC 4Artificial ventilation • Bicarbonate is contraindicated !!! • Oxygen must be done with caution ! 4Hypoxia stimulate respiratory centre Increased pO2 may inhibite respiration Respiratory alkalosis (RAL) • Stimulation of the respiratory center • Dg: 4↑ pH 4↓ pCO2 4↔ HCO3, then ↓ (kidney compenzation) Respiratory alkalosis (RAL) • Causes of RAL 4Anxiety, emotional disturbances, hysteria 4Pulmonary embolism 4Lesions of the CNS (respiratory center) 4Encephalitis, meningitis, tumours, trauma 4Pregnancy 4Fever 4High altitude (low pO2) 4 Too much CO2 is “blown off” • Depression of the respiratory center • Sedatives • Life threatening RAL 4Arteficial ventilation Respiratory alkalosis (RAL): Therapy Combined A-B disorders • Primary combined A-B disorders • Result of the compensation 4Metabolic acidosis is compensated by respiratory alkalosis 4Metabolic alkalosis is compensated by respiratory acidosis 4Respiratory acidosis is compensated by metabolic alkalosis 4Respiratory alkalosis is compensated by metabolic acidosis How to recognized combined A-B disorders ? • Respiratory component is present, if 4pCO2 is changed • Sometimes it may be difficult to detect metabolic components, as both acidosis and alkalosis may be present, resulting in the normal laboratory values (pH, HCO3, pCO2, pO2): 4Concentration of Cl- , K+, Na+ must be measured ! 4Some calculation may be useful Calculations that help recognize combined disorders • Buffer Base = Na+ + K+ - Cl- 4Normal result: 42 mmol/l 4↑ = metabolic alkalosis is probably present • Anion gap = (Na+ + K+) - (Cl- + HCO3 -) • Normal result = 18 mmol/l • ↑ = metabolic acidosis is probably present (↑concentration of organics anions) 4Lactate, kenotic acids, multiple acid radicals Calculations that help recognize combined disorders • Normal pH do not exclude A-B disorders ! • What we need for correct interpretation of AB status ? 4pH, HCO3 -, pCO2, pO2 4Na, K, Cl 4Patients´s history and clinical examination! How to recognized combined A-B disorders ? • An interpretation of the blood´s A-B status must take into account the electrolyte status • Cl and K deserve special attention! • Changes in Cl- conc. are followed by the changes in A-B status 4↑ of Cl- results in ↓ of HCO3 - and it is followed by metabolic acidosis (hyperchloremic acidosis) 4↓ of Cl- results in ↑ of HCO3 - and it is followed by metabolic alkalosis (hypochloremic alkalosis) How to recognized combined A-B disorders ?