Acid Base Disorders J. Vymětal
ph alkalinity/acidity of internal enviroment 7,4 ± 0,04 mmol/l pco 2 respiratory component of ABB 4,5-6,5 kpa po 2 partial pressure O 2 10-13,3 kpa shco 3 metabolic component of ABB 24 ±2,0 mmol/l (amount of HCO3- in blood saturated O 2 by 37 C. and pco 2 5,3 kpa) ahco 3 metabolic component of ABB 24±2 mmol/l (amount of HCO3- in blood saturated O 2 by 37 C and actual pco 2 ) BE base excess /base lack HCO3 in 1 litre ECF 0 ± 2,5 mmol/l SpO 2 saturation O 2 95-98% -------------------------------------------------------------------------------------------------------------------------------- Anion gap AG = Na + K [ Cl + HCO 3 ] (propotion of acids accumulation) 16 mmol/l AG = Na + K + Ca + Mg [ Cl + HCO3 + 0.28 x alb + 1,8 P ] 8,2 mmol/l
SID strong ion difference SID = [Na + ]+[K + ]+[Ca ++ ]+[Mg ++ ]-[Cl - ]-[UA - ] SID eff = [HCO 3- ]+[Alb x- ]+[Pi y- ] SID eff = SID 37 41 mmol/l Cation superiotity = fluids alkalisation Anion superiority = fluids acidification
SID strong ion difference SID eff = [Na + ]+[K + ]+[Ca ++ ]+[Mg ++ ]-[Cl - ]-[UA - ] SID eff = [HCO 3- ]+[Alb x- ]+[Pi y- ] SID eff = SID 37 41 mmol/l Acidosis SID decreases (chlorides acummulation, and/or organic acids acummulation, plasma dilution by free water, esp. hyponatremia Alkalosis - SID increases (renal or extrarenal hypochloremie, positive intake Na + without adequate chlorides balance, free water lost and hypernatremia
Useful rules Hypoalbuminemia causes alkalosis decrease of albumin 10g/l ~ BE + 3 mmol/l Hyperchloremia causes acidosis
Blood buffer systems Bicarbonate system (35%) concentration is affected by kidneys and breathing the only system in ISF and cerebrospinal fluid, participates in the regulation of respiratory centre activity Hemoglobin (35%) vital to maintain the ph (H + binding) in tissues anemia in crtitically ill Protein (7%) Phosphate (5%) the most important intracellular buffer, its partner K+
Compensantion of ABB disorders lungs (respiration) change of activity of the respiratory center - ph of the cerebrospinal fluid hyperventilation in acidosis Hypoventilation in alkalosis (disadvantageous hypoxia) response within minutes, the full development 24 h kidneys (renal) synthesis or exrection of bicarbonate changes of NH3 and phosphates excretion response within hours, maximum in 5-7 days inertia of compensating process!
ABB examination (Astrup previosly) ABB diseases related to ABB disorders in all critically ill patients In all acute patients within differential diagnosis Blood sample arterial lung function evaluation capillary metabolic situation assesment in tissues venous (v. cubiti) in critically ill patiants no sense (CVC mixed venous blood) - AV difference po2 a pco2
Primary ABB disorders acidosis alkalosis ph < 7,35 ph > 7,45 [H + ] > 45 mmol/l [H + ] < 35 mmol/l metabolic respiratory metabolic respiratory HCO 3- <22 mmol/l pco 2 > 5,8 kpa HCO 3- >26 mmol/l pco 2 <4,8 kpa 9
Metabolic acidosis (MAC) ph < 7,35 [H + ]> 45 nmol/l HCO 3- < 22 nmol/l pco2 < 4,5 Without bicarbonate lost (increased AG) Lactic acidosis typ A - hypoxia anaerobic metabolism in tissue (šokové stavy, sepse, embolie a. mesenterica, ARDS) typ B - Reduced lactate utilization in the liver (biguanids, metanol, etanol, salicylates, hepatorenal syndrom, quick sorbitol infusion) Ketoacidosis diabetes mellitus starvation (increased lipolysis, ketons formation) Renal failure inability of the kidneys to excrete acids, phosphates supply of strong acids intoxication salicylates, methanol (formic acid), ethylene glycol (oxalic acid), ingestion of HCl, H2SO4
Metabolic acidosis (MAC) ph < 7,35 [H + ]> 45 nmol/l HCO 3- < 22 nmol/l pco2 < 4,5 from bicarbonate loss (normal AG ) prolonged diarrhea, intestinal and pancreatic fistulas, suction of doudenal secretion, drains hyperchloremic acidosis increased influx of chloride ions (0,9% NaCl, Ringer ) renal tubular acidosis
Metabolic acidosis diagnosis and therapy Diagnosis ph < 7,35 [H + ]> 45 nmol/l HCO 3- < 22 nmol/l pco2 < 4,5 presence of lactate, ketones hyperkalemia Therapy NaHCO3 4,2% (1ml = 0,5 mmol/l), resp. 8,4% (1ml = 1mmoll/l) BE x body weight (kg) x 0,3 absolute indication: severe MAC from acids influx a lactic acidosis B type renal failure (aimed ph 7,3) in hypoxaemic (A type) LAC, ketoacidosis, treatment of the underlying disease, correct ph < 7,1 treat the underlying disease cause, not acidosis itself Repeated control not to overshoot to alkalosis
Metabolic alkalosis ph > 7,44 [H + ] < 45 nmol/l HCO 3- > 22 nmol/l BE > 2,0 pco2 > 6,0 less frequent serious consequences, more difficult treatment loss of strong acids (HCl) repeated vomiting, aspiration of gastric juice Increased losses Cl - diuretics aplication primary and secondary hyperaldosteronismus increased reabsorption Na+ and exchange for K+ a H+ hypokalemia of any cause impaired exchange Na+ for za K +, exretion H+ prolonged hypokalemia always leads to the development of metabolic alkalosis Supply salts of organic acids K-citrát (blood tranfusion, Na-lactate (Ringer lactate) are metabolized, HCO3- replaced
Metabolic alkalosis (diagnosis and therapy) ph > 7,44 [H + ] < 45 nmol/l HCO 3- > 22 nmol/l BE > 2,0 pco2 > 6,0 hypokalemia hypochloremia Treatment: should always be treated (attenuation ventilation, decreased fraction of ionized calcium and myocardial contractility, impaired release of oxygen from hemoglobin) NaCl, KCl, NH4Cl, arginin-hcl BE x body weight (kg) x 0,3 The aim - ph 7,4, light acidosis is less harmful
Respiratory acidosis (RAC) at the lack of ability to eliminate pco2 by lungs, or overproduction of pco2 by glucose feeding (400g-600g) restrictive and obstruktive lung disease in stage of global respiratory infufficiency, large pneumotorax, pulmonary emphysema Demage of the respiratory center hypoxia and brain trauma (hypercapnia impairs brain edema due to vasodilating effect) opioids, sedatives and hypnotics intoxication decreased cardiac output severe or multiple pulmonary embolism
Respiratory acidosis (diagnosis and therapy) ph < 7,35 pco2 > 6,5 po2 < 8 increased lactate, HCO 3- < 22 mmol/l, but longer lasting and kidney compensated increase HCO 3 - Cyanosis Treatment: improving ventilation (bronchodilators, NIV, MV) Increasing CO in heart failure (inotropic therapy) Oxygen therapy (careful, repeated blood gases check, there is possibility of the pco2 rise - eliminating hypoxia - failure) reducing carbohydrate intake, increase intake of fats Bicarbonate contraindicated
Respiratory alkalosis (RAL) ph > 7,44 [H + ] < 45 nmol/l HCO 3- > 22 nmol/l BE > 2,0 pco2 < 4,7 Hyperventilation physiological stress response, regularly present in the acute stage (critically ill) pulmonary embolism, the initial stages of sepsis, shock, ARDS inappropriately set ventilation Hyperventilation in tetany irritation of the respiratory center lesion of the CNS, head trauma, encephalitis compensatory response to metabolic acidosis
Respiratory alkalosis (diagnosis and therapy) ph > 7,45 ph < 4,7 kpa hypocapnia leads to cerebral vasoconstriction and brain ischemia pco2 < 3 kpa can significantly reduce cerebral perfusion and brain function Treatment: treatment of the underlying cause pharmacological sedation (risk of hypoxia) increased dead space controlled ventilation with analgosedation
Clinical status and history diagnosis Hypoxaemia = lactate (acidosis) Vomiting = HCl lost (alkalosis) diarrhoea and fistulas = HCO3- lost (acidosis) starvation and diabetes = ketons (ketoacidosis)
Mixed acid base disorders MAC + RAC cardiac arrest, respiratory insufficiency (ARDS) + septic shock MAC + RAL septick shock, hepatorenal syndrome MAC + MAL vomiting with alcohol intoxication, uraemia, diabetic ketoacidosis, lactic acidosis MAC + MAL + RAC. + respiratory insufficiency MAL + RAL vomiting + liver insuficiency, alkalisation therapy of diabetic ketoacidosis
woman, 1951 Typ krve: Arterial; Arterial; Arterial; Arterial, ph B: 6,88; 6,97; 7,16; 7,18 PCO2 B: 2,94; 4,07; 6,55; 4,95, PO2 B: 16,20; 15,00; 8,41; 7,62, Stdn bikarbonát: 5,3; 7,5; 15,0; 13,6 Akt bikarbonát: 3,9; 6,7; 16,6; 13,3, Base excess: -27,1; -23,6; -12,2; -13,8, Saturace Hb B: 96,0; 95,0; 90,0; 87,7
woman, 1951 ph B: 6,88; 6,97; 7,16; 7,18 PCO2 B: 2,94; 4,07; 6,55; 4,95, PO2 B: 16,20; 15,00; 8,41; 7,62, Stdn bikarbonát: 5,3; 7,5; 15,0; 13,6 Akt bikarbonát: 3,9; 6,7; 16,6; 13,3, Base excess: -27,1; -23,6; -12,2; -13,8, Saturace Hb B: 96,0; 95,0; 90,0; 87,7 Lactate: >23,30
Man, 1961 vzorek venous arterial capillar datum 01/09/15 01/09/15 02/09/15 ph B: 7,50 7,73 7,42 pco2: 7,92 7,66 8,80 po2 B 7,26 11,20 5,65 SBC: 42,8 77,4 37,3 HCO3: 46,2 77,9 41,5 BE: 18,7 45,2 14,0 SAT B: 85,3 97,8 73,9
Man, 1961 Výsledky z 01/09/15: Natrium: 129; 133, Kalium: 2,72; 2,52 Chloridy: <61; 68, Urea: 43,4; 38,3, Kreatinin: 751; 407????
Man, 1961 Výsledky z 01/09/15: Natrium: 129; 133, Kalium: 2,72; 2,52 Chloridy: <61; 68, Urea: 43,4; 38,3, Kreatinin: 751; 407 Alfa-amyláza: 9,13; 13,95, Lipáza: 18,49; 25,34 lactate: 1,0