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Metabolic Acidosis Mendoza, Donn Paulo; Mendoza, Gracielle; Mendoza, Trisha; Mindanao, Malvin Ace, Miranda, Maria Carmela; Molina, Ramon Miguel; Monzon,

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Presentation on theme: "Metabolic Acidosis Mendoza, Donn Paulo; Mendoza, Gracielle; Mendoza, Trisha; Mindanao, Malvin Ace, Miranda, Maria Carmela; Molina, Ramon Miguel; Monzon,"— Presentation transcript:

1 Metabolic Acidosis Mendoza, Donn Paulo; Mendoza, Gracielle; Mendoza, Trisha; Mindanao, Malvin Ace, Miranda, Maria Carmela; Molina, Ramon Miguel; Monzon, Jerry West; Morales, Arriane; Musni, Merwen Mitchel; Nallas, Anna Pauline; Naval Ayne Rangel C7

2 Salient Features:

3 Acid Base Disturbance:

4 Algorithm for the Diagnosis of the acid base disorder

5 Steps in acid base diagnosis
Obtain arterial blood gas (ABG) and electrolytes simultaneously Compare [HCO3-] on ABG and electrolytes to verify accuracy Calculate anion gap (AG) Know four causes of high-AG acidosis ketoacidosis lactic acid acidosis renal failure toxins)

6 Steps in acid base diagnosis
Know two causes of hyperchloremic or nongap acidosis bicarbonate loss from GI tract renal tubular acidosis Estimate compensatory response Compare AG and HCO3- Compare change in [Cl-] with change in [Na+]

7 Prediction of compensatory responses

8 Rule of Thumb: Metabolic acidosis or PaCO2= (1.5x HCO3-) + 8
PaCO2 will mmHg per mmol/L in HCO3- PaCO2= HCO

9 Rule of Thumb Metabolic alkalosis
PaCO2 will mmHg per mmol/L in HCO3- or PaCO2 will 6 mmHg per 10 mmol/L in HCO3- PaCO2= HCO

10 Rule of Thumb Respiratory alkalosis Acute: Chronic:
HCO3- will 2 mmol/L per 10 mmHg in PaCO2 Chronic: HCO3- will 4 mmol/L per 10 mmHg in PaCO2

11 Rule of Thumb Respiratory Acidosis Acute: Chronic:
HCO3- will 1 mmol/L per 10 mmHg in PaCO2 Chronic: HCO3- will 4 mmol/L per 10 mmHg in PaCO2

12 Pattern of Compensatory Changes
Disorder pH HCO3 PaCO2 Metabolic Acidosis Low Metabolic Alkalosis High Respiratory Alkalosis Respiratory acidosis

13 Anion Gap

14 Anion Gap represents the concentration of all the unmeasured anions in the plasma concentrations are expressed in units of milliequivalents/liter (mEq/L) NV: 8-16 mEq/L

15 Major Clinical Uses of the Anion Gap
To signal the presence of a metabolic acidosis and confirm other findings Help differentiate between causes of a metabolic acidosis: high anion gap versus normal anion gap metabolic acidosis. To assist in assessing the biochemical severity of the acidosis and follow the response to treatment In an inorganic metabolic acidosis (eg due HCl infusion), the infused Cl- replaces HCO3 and the anion gap remains normal. In an organic acidosis, the lost bicarbonate is replaced by the acid anion which is not normally measured. This means that the AG is increased.

16 Anion Gap With potassium = ( [Na+]+[K+] ) − ( [Cl−]+[HCO3−] ) = ( ) – (108+10) = 24.2 mEq/L - HIGH Without potassium = ( [Na+] ) − ( [Cl−]+[HCO3−] ) = (138) – (108+10) = 20.0 mEq/L - HIGH It is calculated by subtracting the serum concentrations of chloride and bicarbonate(anions) from the concentrations of sodium plus potassium (cations): potassium is frequently ignored because potassium concentrations, being very low, usually have little effect on the calculated gap. This leaves the following equation:

17 Causes of high anion gap acidosis and normal anion gap acidosis

18 Anion Gap Sodium - (chloride + bicarbonate)
High Anion Gap Acid retention Examples: Lactic Acidosis: most common Ketoacidosis Advanced Renal Failure Drug and Toxin Induced Normal Anion Gap Hyperchloremic acidosis GI or renal Loss of bicarbonate Impaired renal acid secretion Reabsorption of Chloride Examples: Diarrhea Renal Tubular Acidosis Carbonic Anhydrase Inhibition High anion gap acidosis: The most common causes of a high anion gap metabolic acidosis are Ketoacidosis, Lactic acidosis Renal failure Toxic ingestions Ketoacidosis is a common complication of type 1 diabetes mellitus, but it also occurs with chronic alcoholism, undernutrition, and, to a lesser degree, fasting. In these conditions, the body converts from glucose to free fatty acid (FFA) metabolism; FFAs are converted by the liver into ketoacids, acetoacetic acid, and β-hydroxybutyrate (all unmeasured anions). Ketoacidosis is also a rare manifestation of congenital isovaleric and methylmalonic acidemia. Lactic acidosis (see Acid-Base Regulation and Disorders: Lactic Acidosis) is the most common cause of metabolic acidosis in hospitalized patients. Lactate accumulation results from a combination of excess formation and decreased utilization of lactate. Excess lactate production occurs during states of anaerobic metabolism. The most serious form occurs during the various types of shock. Decreased utilization generally occurs with hepatocellular dysfunction from decreased liver perfusion or as a part of generalized shock. Renal failure causes anion gap acidosis by decreased acid excretion and decreased HCO3 − reabsorption. Accumulation of sulfates, phosphates, urate, and hippurate accounts for the high anion gap. Toxins may have acidic metabolites or trigger lactic acidosis. Rhabdomyolysis is a rare cause of metabolic acidosis thought to be due to release of protons and anions directly from muscle. Normal anion gap acidosis: The most common causes of normal anion gap acidosis are GI or renal HCO3 − loss Impaired renal acid excretion. Normal anion gap metabolic acidosis is also called hyperchloremic acidosis, because instead of reabsorbing HCO3 − with Na, the kidney reabsorbs Cl−. Many GI secretions are rich in HCO3 − (eg, biliary, pancreatic, and intestinal fluids); loss from diarrhea, tube drainage, or fistulas can cause acidosis. In ureterosigmoidostomy (insertion of ureters into the sigmoid colon after obstruction or cystectomy), the colon secretes and loses HCO3 − in exchange for urinary Cl− and absorbs urinary ammonium, which dissociates into ammonia (NH3 +) and hydrogen ion (H+). Ion-exchange resin uncommonly causes HCO3 − loss by binding HCO3 −. The renal tubular acidoses (see Renal Transport Abnormalities: Renal Tubular Acidosis [RTA]) either impair H+ secretion (types 1 and 4) or HCO3 − absorption (type 2). Impaired acid excretion and a normal anion gap also occur in early renal failure, tubulointerstitial renal disease, and when carbonic anhydrase inhibitors (eg, acetazolamide)

19 Management

20 Treatment Depends primarily on the cause
Need to control diabetes with insulin 

21 High Anion Gap Acidosis Treatment
Diabetic Ketoacidosis Fluid resuscitation with isotonic saline IV regular insulin

22 High Anion Gap Acidosis Treatment
Lactic Acidosis Alkali therapy  acute acidemia to improve cardiac funtion and lactate utilization Infuse sufficient NaHCO3 to raise arterial pH to no more than 7.2 over minutes

23 Treatment Metabolic acidosis may also be treated directly
If the acidosis is mild - administration of intravenous fluids may be all that is needed If the acidosis is very severe - bicarbonate may be given intravenously However, bicarbonate provides only temporary relief and may cause harm

24 Treatment Potential Complications of Bicarbonate Therapy
Volume overload Hypokalemia CNS acidosis Hypercapnia Tissue hypoxia Continuous monitoring of pH and electrolytes

25


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