Metabolic alkalosis. ICU Fellowship Training Radboudumc

Transcription

1 Metabolic alkalosis ICU Fellowship Training Radboudumc

2 Case History 28-year-old male Discovered by roommate at home in bewildering state During transport by EMS possible tonicclonic seizure Arrival in ER at with GCS E1-M5-V2

3 Case History Medication Venlafaxin (Effexor ) - SNRI Methylphenidate (Ritalin ) Disulfiram (Refusal )

4 Case History Temperature C Airway - accepts oral airway Breathing - SpO2 100% on 12 L O2 Circulation - BP 170/100 mm Hg Disability - E1-M5-V2

5 Laboratory results Na K ph Lactate 95 mmol/l 1.4 mmol/l 7.54 mmol/l 8.9 mmol/l 7.54 / 19.1 / 6.1 / 37.8 / 13.3

6 Things always get worse Lactate 2.9 mmol/l 7.61 / 17.2 / 5.7 / 40.0 / 16.5 Is the respiratory response appropriate? What are the immediate life-threatening dangers?

7 Respiratory response Expected PaCO2 (mm Hg) = 0.7 [HCO3-] + 20 ± [40] + 20 ± 5 = mm Hg = ( kpa) Actual PaCO2 5.7 kpa = appropriate

8 Metabolic alkalosis Decrease in cardiac output Depression of central ventilation Leftward shift of the oxyhemoglobin saturation curve Worsening of hypokalemia and hypophosphatemia

9 Why K + shift with metabolic alkalosis? Na + H + Na + -K + - ATPase 3 Na + 2 K + K + Insulin β-mimetics Potassium enters the cell because of a negative transmembrane gradient

10 Stewart-Figge theory Body water is inexhaustible source of H + ions Three independent components influence the dissociation of water PCO2 Total concentration of weak acids (ATOT) Strong Ion Difference

11 Strong Ion Difference Electrical neutrality Apparent SID Effective SID Na + Cl - Na + Cl - Lact - - Lact - Total negative charges of K + HCO3 - K + HCO3 - Ca 2+ Mg 2+ Alb - P - Ca 2+ Mg 2+ Normal SIDa meq/l Alb - P - Strong Ion Gap = SIDa - SIDe

12 Pathophysiology Acidosis Alkalosis Respiratory PaCO2 PaCO2 Metabolic 1 Changes in SID a) H20 or b) Change in strong anions - chloride or - unmeasured anions 2 Changes in weak acids a) Albumin b)anorganic phosphate SID [H2O ] SID [Cl - ] SID [Xa - ] [Alb] [P] SID [H2O ] SID [Cl - ] [Alb] [P] Unmeasured cations?

13 What about our patient? Na + 96 K Ca Mg Cl - 44 Lact Apparent SID (normal meq/l) Albumen 44 Phosphate 0.78 Total negative charges of HCO3-40 Alb P No strong ion gap Effective SID 54.76

14 Metabolic alkalosis solely explained by Cl - Why does hypokalemia due to an intracellular shift not result in an acid-base disturbance?

15 If you believe in Stewart

16 If you believe in HH Bicarbonate 15L 25 mmol from 375 to 345 mmol (23 mmol/l) 30 mmol H + 30 mmol Na + -K + - ATPase K + 15 L 2 mmol

17 Where do we loose chloride? HCl loss - vomiting NH4Cl loss - diuretics / specific disorders KCl loss (GI tract) NaCl loss Urinary chloride is low in all cases except 2

18 Case record History compatible with extensive vomiting Urinary chloride excretion 44 mmol/l, ph 7 Patient does not use diuretics Differential diagnosis of high urinary chloride loss?

19 Differential diagnosis with high Cl - excretion Bartter syndrome Gitelman syndrome Other causes of excess aldosterone Severe potassium deficiency

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21 Upregulated by Inhibited or blocked by Thiazides Gitelman syndrome K + depletion Cotransporter Cl - depletion alkalosis Cl - HCO3 - Early distal nephron Na + Cl - Connecting tubule PENDRIN Distal tubule Flow and alkali stimulation Thiazides Loop diuretics Gitelman Bartter GI Cl - loss Inhibited or blocked by Loop diuretics Bartter syndrome K + depletion Loop of Henle Na + K + 2Cl - Cotransporter Secondary to ENaC activity K + H + Secondary to K + depletion ROMK Maxi K H + - ATP-ase Collecting duct ENaC Na + Direct stimulation Conn GRA Cushing Liddle Congenital adrenal disease 11 β HS dehydrogenase Proximal tubule 80% HCO3 - reabsorption K + H + /K + - H + ATP-ase

22 Treatment Correct volume depletion Correct chloride depletion Correct potassium depletion

23 Additional therapy Hydrochloric acid Acetazolamide How does acetazolamide decrease ph?

24 Metabolic alkalosis Moviat M. Crit Care 2006;10:R14

25 Metabolic alkalosis Moviat M. Crit Care 2006;10:R14

26 Conclusion Severe metabolic alkalosis due to gastric chloride loss (vomiting) and inappropriate urinary chloride loss due to hypokalemia Correction with chloride and potassium suppletion

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30 Gennari FJ. AJKD 2011;58: