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Acid-Base Abnormalities During Cardiopulmonary Resuscitation (CPR) Anakapong Phunmanee M.D. Associated Professor Faculty of Medicine, Khon Kaen University.

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Presentation on theme: "Acid-Base Abnormalities During Cardiopulmonary Resuscitation (CPR) Anakapong Phunmanee M.D. Associated Professor Faculty of Medicine, Khon Kaen University."— Presentation transcript:

1 Acid-Base Abnormalities During Cardiopulmonary Resuscitation (CPR) Anakapong Phunmanee M.D. Associated Professor Faculty of Medicine, Khon Kaen University

2 Cardiac Output During CPR Del Guercio LRM, et al. Circulation 1965; 32:I Normal CO = L/m2(BSA)/min

3 Metabolism During CPR Aerobic Metabolism Anaerobic Metabolism Progressive increase CO2 in cells PCO mmHg PCO2 >475  EMD Confusion Following CPR MacGregor DC,et al. J Thorac Cardiovasc Surg Niemann JT,et al. Ann Emerg Med 1984.

4 Intamyocardial pH and cardiac venous blood Planta M, et al. Circulation 1989;80:

5 CO2 transport during CPR Planta M, et al. Circulation 1989;80:

6 Arterial pH and PCO2 different

7 Arterial vs Veneous blood during CPR CO2 Vein Arterial blood venous blood pH less acidotic pH acidotic pH 7.1 PvCO2 74 Venous paradox Weil MH,et al. N Eng J Med 1986; 314:

8 Myocardial K uptake during experimental CPR Von Planta M, et al. Crit Care Med 1989;17:

9 Arterial blood during CPR Severe Acidotic arterial blood Inadequate V/Q Improved mechanical technique Hyperventilation Correct intubation Alternate method for circulation Open-chest compression Venoarterial bypass Ornato JP, et al. Am J Emerg Med 1985;3:

10 Composition and physiochemical of buffer agents Anorganic NaHCO3 Na2CO3 Organic THAM (Tris-hydroxymethyl amino-methane) Mixtures CABICARB (NaHCO3, Na2CO3) TRIBONATE (NaHCO3, THAM, Phosphate, Acetate) NaHCO3 pH 8.0 Na2CO3 pH 11.7 THAM pH 8.4 CARBICARB pH 9.6 TRIBONATE pH 8.1

11 NaHCO3 H + HCO3 H2CO3 H2O2 +CO2 Na 1000, Osm 2000 mOsm/l Na2CO3 Na2CO3+ CO2 +H2O 2HCO3 + 2Na HCO3 + H Na 1000, Osm 1500 mOsm/l CARBIBARB NaHCO3 + Na2CO3 Na 1000, Osm 1667 mOsm/l

12 Buffering agents and CPR Kette F, et al. Clin Res 1988;36:10. Myocardial pH

13 Comparison of coronary perfusion pressure Shijie Sun Pharmacology and Experimental Therapneutics;1999:

14 NaHCO3 administration during CPR: A Mistake NaHCO3(PCO ) CO2 HCO3 Na Falling Intracellular pH HyperosmolarityNa overload

15 DETRIMENTBENEFIT 95%CI CPR OUTCOME AFTER NaHCO3 Von Planta M. Circulatoire Aigue

16 NaHCO3 administration during CPR Should not be used until other proven interventions (ET tube, defibrillation, cardiac compression, adrenaline) Should not be used until other proven interventions (ET tube, defibrillation, cardiac compression, adrenaline) Estimated that this interventions required at least 10 min. Estimated that this interventions required at least 10 min.

17 Guideline for NaHCO3 administration during CPR Known preexisting metabolic acidosis with or without hyperkalemia Known preexisting metabolic acidosis with or without hyperkalemia Known hypercalcemia Known hypercalcemia Doasage Doasage 1 mEQ/kg then no more than half for subsequent dose 1 mEQ/kg then no more than half for subsequent dose No more frequently than every 10 min No more frequently than every 10 min Postresuscitation phase, guideed by arterial blood gas Postresuscitation phase, guideed by arterial blood gas

18 Alternate buffer agents during CPR THAM (tromethamine), potent amine buffer THAM (tromethamine), potent amine buffer DCA (Dichloroacetate), stimulating pyruvate dehydrogenase (oxidative enzyme in step of lactate to pyruvate) DCA (Dichloroacetate), stimulating pyruvate dehydrogenase (oxidative enzyme in step of lactate to pyruvate) However, no alternate buffer agents improve survival during CPR However, no alternate buffer agents improve survival during CPR Lee WH, et al. Am Surg Stacpoole PW, et al. N Engl J Med 1983.

19 Buffering agents and survival Shijie Sun Pharmacology and Experimental Therapneutics;1999:

20 Capnography Normal respiration, circulation, the PETCO2 about 4-5 % (1% approximately 7 mmHg)

21 Capnography

22 Minute Ventilation PETCO2 PETCO2 & Hyperventilation Normal CO; PETCO2 ~ PCO2

23 PETCO2 PETCO2 & Cardiac Output Cardiac Output PETCO2 ¼ of normal ROSC  Increase PETCO2

24 Common causes of low PETCO2 (< 2%) Inadequate ventilation Inadequate ventilation Esophageal intubation Esophageal intubation Airway obstruction Airway obstruction V/Q mismatch V/Q mismatch Pulmonary emboli Pulmonary emboli Inadequate blood flow Inadequate blood flow Inadquate chest compression Inadquate chest compression Hypovolumia Hypovolumia Tension pneumothorax Tension pneumothorax Pericardial tamponade Pericardial tamponade Decrease metabolic production eq. hypothermia Decrease metabolic production eq. hypothermia

25 End-tidal CO2 concentration (PETCO2) Clinical indication Clinical indication Confirm ET tube placement (sen, spec, 100, 90%) Confirm ET tube placement (sen, spec, 100, 90%) Esophageal intubation results in PETCO2 < 0.5% Esophageal intubation results in PETCO2 < 0.5% Guide hemodynamic status: inadequate chest compression PETCO2 < 1% Guide hemodynamic status: inadequate chest compression PETCO2 < 1% Prognostic value: PETCO2 20 min after CPR < 10 mmHg accurately predicts death Prognostic value: PETCO2 20 min after CPR < 10 mmHg accurately predicts death

26 Acid-Base Abnormalities During CPR: Conclusion Intracellular acidosis plays an important role Intracellular acidosis plays an important role The treatment is properly performed CPR and airway management The treatment is properly performed CPR and airway management Pharmacologic buffers have no benefit and potentially risk Pharmacologic buffers have no benefit and potentially risk

27 จบการบรรยายขอขอบคุณทุกท่านที่ฟังการบรรยาย ขอขอบคุณกรรมการหน่วยช่วยฟื้นคืนชีพ โรงพยาบาลศรีนครินทร์


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