Uploaded byEmad Zarief Kamel
Metabolic acidosis - physiologic approach
This document discusses metabolic acidosis, including its underlying causes, effects on the body, and diagnostic steps. It notes that metabolic acidosis can be caused by conditions like diabetic ketoacidosis, renal failure, intoxication, or shock. The 6 key steps for arterial blood gas interpretation are outlined, including evaluating pH, pCO2, HCO3, and determining the primary cause. Mixed disorders can complicate the diagnosis and treatment. Anion gap and delta gap help identify underlying causes of high anion gap metabolic acidosis. Respiratory compensation and renal responses are also addressed.
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Metabolic acidosis - physiologic approach
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- 2. EMADZARIEF 2019 ❖ Theunderlying cause DKA, RF, Intoxication, shock , hypoxia ❖ M. Acidosis on systems
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- 6. EMADZARIEF 2019 ▪ Resuscitatethe patient/ hist. exam. ▪ ABG ▪ Try to catch a diagnosis ..and treat ▪ Evaluate the body response ▪ Anion gap ▪ Don’t miss mixed disorders Mixed problems→ could change the ttt. Ensure diagnosis / catch diagnosis / detect the mix ER actions.. Variable types of M. acidosis, and alkalosis
- 7. 6 STEPS FOR ABG INTERPRETATION 1-Evaluate the pH 2- evaluate the PaCO2 3- evaluate HCO3 4-Determine the 1ry 5-Assess the compensation 6- Any mixed disorder EMADZARIEF 2019
- 8. EMADZARIEF 2019 The 1rychange is in HCO3- and base deficit Check PaCO2compensation ABG with low pH Anion Gap metabolic Acidosis Delta Gap Unhide underlying cause(s)
- 9. EMADZARIEF 2019 Respiratory compensation forMetabolic Acidosis Resp.c. for M. Alkalosis
- 10. EMADZARIEF 2019 ▪ Theamount of strong acid or alkali that must be added to each L. of fully oxygenated blood to return the pH to 7.40 at a temperature of 37°C and a pCO2 of 40 mmHg (5.3 kPa). ▪ Normally −2 to +2 mEq/L
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- 12. EMADZARIEF 2019 ▪ Increasein the generation of H + from endogenous (eg, lactate, ketones) or exogenous acids (eg, salicylate, ethylene glycol, methanol). ▪ Inability of the kidneys to excrete the H + from dietary protein intake (type I, IV renal tubular acidosis). ▪ The loss of bicarbonate (HCO 3) due to wasting through the kidney (type II renal tubular acidosis) or the gastrointestinal tract (diarrhea). ▪ The kidneys response to a respiratory alkalosis
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- 15. EMADZARIEF 2019 = 12± 2 mmol
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- 17. ▪High Ag >20 mmol/l is helpful, but >30 is usually indicative of HAGMA ▪Falsely high AG in metabolic alkalosis with volume depletion, increased charge of albumin (anion), or compensatory increase of lactate. ▪Falsely low AG in hypoalbuminemia, bromide or lithium toxicity, multiple myelomas EMADZARIEF 2019
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- 19. Causes of wide AG Metabolic Acidosis ▪Non-volatileAcid Loads e.g. ▪DKA ▪Renal Failure ▪Lactic Acidosis ▪Mixed causes: inborn errors of metabolism, non ketotic hyperosmolar diabetic coma, rhabdomyolysis ▪Intoxication by Acids e.g. Aspirin, methanol, ethylene glycol, paraldehyde, toluene EMADZARIEF 2019
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- 23. EMADZARIEF 2019 Retention ofhydrogen+ along with CL- Hyperchloremic metabolic acidosis
- 24. EMADZARIEF 2019 +ve urinaryAG indicates that renal cause of metabolic acidosis
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- 28. EMADZARIEF 2019 1ry MAcidosis full resp. compensation Wide anion gap
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- 31. EMADZARIEF 2019 High anion-gapmetabolic acidosis
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- 33. EMADZARIEF 2019 3x2 Vol ofdistribution x ½ correction
- 34. ▪Hypernatremia ▪hyperosmolarity ▪Volume overload ▪Hypercapnia &intracellular acidosis ▪Higher HB affinity to O2 ▪Decrease pf ionized calcium ▪Rebound alkalosis EMADZARIEF 2019
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