Metabolic acidosis: 1] Calculate the anion gap: Anion gap = Na+ - [CL- + HCO3-] Difference between calculated serum

anions and cations. Based on the principle of electrical neutrality, the serum concentration of cations (positive ions) should equal the serum concentration of anions (negative ions). However, serum Na+ ion concentration is higher than the sum of serum Cl- and HCO3- concentration. Na+ = CL- + HCO3- + unmeasured anions (gap). Normal anion gap: 12 mmol/L (10 - 14 mmol/L) 2] Based on the anion gap and patient history - review potential causes: Normal anion gap (hyperchloremic) metabolic acidosis: Normal anion gap acidosis: The most common causes of normal anion gap acidosis are GI or renal bicarbonate loss and 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 bicarbonate (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 bicarbonate in exchange for urinary Cl- and absorbs urinary ammonium, which dissociates into NH3+ and H+. Loss of HCO3 ions is accompanied by an increase in the serum Cl- concentration. The anion gap remains normal. Disease processes that can lead to normal anion gap (hyperchloremic) acidosis. Useful mnemonic (DURHAM): a) Diarrhea (HCO3- and water is lost). b) Ureteral diversion: Urine from the ureter may be diverted to the sigmoid colon due to disease (uretero-colonic fistula) or after bladder surgery. In such an event urinary Cl- is absorbed by the colonic mucosa in exchange for HCO3-, thus increases the gastrointestinal loss of HCO3-. c) Renal tubular acidosis: dysfunctional renal tubular cells causes an inappropriate wastage of HCO3- and retention of Cl-. d) Hyperalimentation e) Acetazolamide f) Miscellaneous conditions: They include pancreatic fistula, cholestyramine, and calcium chloride (CaCl) ingestion, all of which can increase the gastrointestinal wastage of HCO3-.

Increased anion gap metabolic acidosis High anion gap acidosis: The most common causes of a high anion gap metabolic acidosis are ketoacidosis, lactic acidosis, renal failure, and toxic ingestions. Renal failure causes anion gap acidosis by decreased acid excretion and decreased bicarbonate reabsorption. Accumulation of sulfates, phosphates, urate, and hippurate accounts for the high anion gap. Toxins may have acidic metabolites or trigger lactic acidosis. In increased anion gap metabolic acidosis, the nonvolatile acids are organic or other inorganic acids (e.g., lactic acid, acetoacetic acid, formic acid, sulphuric acid). The anions of these acids are not Cl- ions. The presence of these acid anions, which are not measured, will cause an increase in the anion gap. Useful mnemonic (MUD PILES): Methanol poisoning: Methanol is metabolized by alcohol dehydrogenase in the liver to formic acid. Uremia: In end-stage renal failure in which glomerular filtration rate falls below 10 20 ml/min, acids from protein metabolism are not excreted and accumulate in blood. Diabetic ketoacidosis: incomplete oxidation of fatty acids causes a build up of betahydroxybutyric and acetoactic acids (ketoacids). Paraldehyde poisoning. Ischemia: causes lactic acidosis. Lactic acidosis: Lactic acid is the end product of glucose breakdown if pyruvic acid, the end product of anaerobic glycolysis, is not oxidized to CO2 and H2O via the Tricarboxylic Acid Cycle. (Causes: hypoxia, ischemia, hypotension, sepsis). Ethylene glycol poisoning: Ethylene is metabolized by alcohol dehydrogenase to oxalic acid in the liver. Usually there is also a coexisting lactic acidosis. Salicylate poisoning

Causes of common acid-base disturbances: Metabolic acidosis (non-respiratory)

High anion gap. Ketoacidosis (diabetes, chronic alcoholism, malnutrition, fasting). Lactic acidosis. Renal HCO3- loss: Tubulointerstitial renal disease. Renal tubular acidosis, types 1, 2, 4. Hyperparathyroidism.

Renal failure. Toxins metabolized to acids: Methanol (formic acid) Ethylene glycol (oxalate) Paraldehyde (acetate, chloracetate) Salicylates Toxins causing lactic acidosis CO2 Cyanide Iron Isoniazid Toluene (initially high gap, subsequent excretion of metabolites normalizes gap) Ingestions (acetazolamide, CaCl2, MgSO4) Others Hypoaldosteronism, Hyperkalemia Parenteral infusion of arginine, lysine, NH4Cl. Rapid NaCl infusion. Toluene (late). Formulas (Compensation): pCO2 decreases 1.2 for each mEq/L change in HCO3 or pCO2 = last two digits of pH

Compensation Ventilation of the lungs increases through stimulation of central chemoreceptors (H+ Rhabdomyolysis (rare) ion receptors) in the medulla and peripheral chemoreceptors in the carotid and aortic Loss of base Normal anion gap (hyperchloremic bodies. Consequently PCO2 falls below normal, and H+ ion concentration falls. acidosis) GI HCO3- loss (diarrhea, ileostomy, Respiratory compensation increases the colostomy, enteric fistulas, use of ion- acidic pH towards normal. The respiratory system responds to metabolic acidosis exchange resins) quickly and predictably by hyperventilation, Ureterosigmoidostomy, ureteroileal so much so that pure metabolic acidosis is seldom seen. conduit

Respiratory Alkalosis:
CNS disorders or lesions, hypoxia [Hypoxia-causing conditions], pulmonary receptor stimulation (asthma, pneumonia, pulmonary edema, PE), Pulmonary vascular disease, anxiety, fear, pain, drugs (ASA, theophylline), liver failure, sepsis. Formulas (Compensation): - Acute: HCO3 decreases 0.22 for every mmHg change in pCO2 - Chronic: HCO3 decreases 0.5 for every mmHg change in pCO2

Compensation: In the presence of respiratory alkalosis the kidneys compensate for the increase in pH by retaining H+ ions and excreting HCO3 ions. As a result, pH falls towards normal and HCO3 - concentration falls below normal. Renal compensation to respiratory alkalosis is a slow process and the pH does not completely return to normal.

Metabolic (non-resp) alkalosis:

Respiratory Acidosis:

Increase in base Administration/ingestion of HCO3Hypochloremia (HCO3 retained). Diuretic therapy Contraction of blood volume. Loss of fixed acid. Severe vomiting (loss of H+). Nasogastric suction. Hypokalemia - Potassium deficiency. Corticosteroid administration.

Central nervous depression: sedatives etc. Neuromuscular disease (Guillain-Barr, myasthenia gravis). Trauma. Severe restrictive disorders: scoliosis. COPD. Acute airway obstruction: choking etc. CVA, pneumothorax, chest wall disorder, tumor. Acute and chronic lung disease. Formulas (Compensation): - Acute: HCO3 increases 0.1 for every mmHg change in pCO2

Formulas (Compensation): pCO2 increases 0.6 for each mmol/L change in HCO3 - Chronic: HCO3 increases 0.35 for every mmHg change in pCO2 Compensation: The respiratory response to metabolic Compensation: In the presence of alkalosis is hypoventilation. PCO2 respiratory acidosis the kidneys compensate rises above normal. Respiratory for the fall in pH by excreting H+ ions and compensation to metabolic alkalosis retaining HCO3 - ions. As a result, pH rises is variable and unpredictable. It is towards normal and HCO3 - concentration unlikely that a conscious patient rises above normal. Renal compensation breathing spontaneously will (also called metabolic compensation) to hypoventilate to a PCO2 > 7.3 kPa respiratory acidosis is a slow process. (55 mmHg) to compensate for Compensation is not obvious for several metabolic alkalosis. hours and takes 4 days to complete.

Sample Problems - Arterial Blood Gases

Respiratory alkalosis (chronic alveolar hyperventilation) Respiratory acidosis. Chronic ventilation failure pH: PaCO2: HCO3: BE: pH: PaCO2: HCO3: BE: pH: PaCO2: HCO3: BE: pH: 7.44 24 16 -6 7.38 76 42 +14 7.56 44 38 +14 7.26

Uncompensated metabolic alkalosis (Respiratory acidosis.

acute ventilation failure

PaCO2: HCO3: BE: pH: PaCO2: HCO3: BE: pH: PaCO2: HCO3: BE: pH: PaCO2: HCO3: BE:

56 24 -4 7.56 40 34 +11 7.44 26 18 -4 7.40 56 34 +7 7.44 20 16 -7 7.24 36 14 -13 7.52 28 22 +1

uncompensated metabolic alkalosis

Respiratory alkalosis (chronic alveolar hyperventilation) Respiratory acidosis. Chronic ventilation failure

pH: Respiratory alkalosis. PaCO2: Chronic alveolar hyperventilation HCO3: BE: Uncompensated metabolic acidosis pH: PaCO2: HCO3: BE: pH: PaCO2: HCO3: BE:

Respiratory alkalosis (acute alveolar hyperventilation)

Acute Respiratory Acidosis

Dx - heroin overdose. Breathing - shallow, slow. ABGs: pH: 7.30 PaCO2: 55 mm/Hg HCO3-: 27 mEq/L Hx/Dx: 73yo, emphysema, labored breathing at rest. ABGs: pH: 7.36 PaCO2: 64 mmHg HCO3-: 35 mEq/L Hx/Dx: 77yo, anxiety, psychosomatic origin. Rapid breathing and slurred speech.

Chronic Respiratory Acidosis

Acute Respiratory Alkalosis

ABGs: pH: 7.57 PaCO2: 23 mmHg HCO3-: 21 mEq/L Persistent bacterial pneumonia. Mild cyanosis and labored breathing. ABGs: pH: 7.44 PaCO2: 26 mmHg HCO3-: 17 mEq/L PaO2: 53 mmHg 80 yo with heart disease. RX: diuretic ABGs: pH: 7.58 PaCO2: 48 mmHg HCO3-: 44 mEq/L BE: + 19 mEq/L Serum CL- 95 mEq/L

Compensated Respiratory Alkalosis

Metabolic Alkalosis