Signs & Symptoms Suspected Acid-Base. Laboratory Variable. Disorder Serum Bicarbonate HCO 3. Central Nervous System. Respiratory Acidosis

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1 H+ Acid base Anion gap Acid base balance Proteins lose or gain H+ according to plasma (ICF) H+ Normally the plasma H+ is very low (40nanoEq/L ie 40 x 10 9 mol/l); this is roughly one millionth the meq/l concentration of Na, K, CL- Buffering systems exist in the body to limit change of H+ after addition or removal of H+ Acid Base Acid à a substance that can donate H+ Base à a substance that can accept H+ Acidemia = of ph or elevation of [H + ] of the ECF, can be resulted from increase HCO 3- or decrease PCO Acidosis = the pathophysiological process or condition that tends to lead to acidemia even if not yet associated with of ph or of [H + ] of the ECF Metabolic acidosis à if serum PaCO2 > expected PaCO2 à additional respiratory acidosis Manifestation à depressed sensorium, depressed myocardial squeeze Anion gap = Na ( Cl + HCO3) = 3 11 Normal anion gap = Hyperchloremic AG > 30 = high AG metabolic acidisis even with normal ph a) DKA b) Lactic acidosis Alkalemia = of ph or reduction of [H + ] of the ECF, can be resulted from decrease HCO 3- or increase PCO 2 Alkalosis = the pathophysiological process or condition that tends to lead to aklakemia even if not yet associated with of ph or of [H + ] of the ECF Metabolic alkalosis à for every 10 increase in HCO3 à PaCO2 increases by 6 Manifestation à tetany; seizures, muscle weakness, ventricular arrhythmia High anion gap 1. Hi AG met. Acidosis (SLUMPED) 2. Hypocalcemia 3. Hypomagnesemia 4. Hypokalemia 5. Hyperalbuminemia 1. Hypercalcemia 2. Hypermagnesemia 3. Hyperkalemia 4. Hypoalbuminemia Low anion gap Serum albumin and anion gap For every 1.0-g/dl decrease in P. albumin, the AG is lowered by close to meq/l. The converse is true for a rise in the serum albumin. When the effective arterial blood volume is low, it appears that the valence on serum albumin becomes more negative. Negative serum AG à bromide intoxication, multiple myelopa, iodide intoxication Bromide is present in sedative drugs, pyridostigmine bromide that is used in the treatment of myasthenia gravis, and some herbal medications. Signs & Symptoms Suspected Acid-Base Disorders Central Nervous System Coma Seizures Congestive Heart Failure Shock Tachypnea, Hyperpnea Bradypnea, Hypopnea Vomiting Diarrhea Abdominal Pain Oliguria, Anuria Diuretics Polyuria DKA Polyuria Myxedema Htn (Conn s or Cushing s) Cardiovascular System Respiratory System Gastrointestinal System Renal Excretory System Respiratory Acidosis or Alkalosis Respiratory Alkalosis Respiratory Alkalosis Respiratory Acidosis Repiratory Alkalosis Endocrine System Respiratory Acidosis Laboratory Variable Increased Decreased Increased Decreased Increased Markedly AG 9 = tco 2 > 27 Disorder Serum Bicarbonate HCO 3 Metabolic alkalosis or respiratory acidosis Metabolic acidosis or respiratory alkalosis Serum Potassium Hyperkalemic distal renal tubular acidosis Metabolic alkalosis, or renal tubular acidosis Serum Anion Gap Organic acidosis Metabolic alkalosis [H + ] arterial (nmol/l) 40 (37 43) PH arterial 7.40 ( ) PCO 2 arterial (mmhg) 40 (37 43) HCO - 3 arterial (mmol/l) 24 (22 26) Total CO 2 venous (mmol/l) 28 (26 30) Anion Gap venous 12 (8 16)

2 Features high PCo2 low ph high HCo3- urine ph is low <5.4 Respiratory acidosis Respiratory alkalosis Excessive pulmonary wash of Co2 will result in alkalosis owing to directing the reaction (H2O + Co2 H2CO3 H+ HCo3-) to the left with consequent reduction in H+. Features: PCo2 ph HCo3 1. Iatrogenic in patients under ventilatory support. 2. Liver cirrhosis, salicylate intoxication, exercise and hypotension. 3. Hyperventilation syndrome in neurotic patients 4. Cerebral hypoxia and intracranial disease Causes Manifestation 1. Manifestations of the cause. 2. Confusion, hyperreactivity, headache, tremor, stupor and coma in severe cases. 3. Papillaedema and increased CSF pressure due to V.D. 4. Pulmonary and splanchnic V.C. Management

3 High AG metabolic acidosis Normal anion gap Metabolic acidosis 1. Salicylate 2. Lactate 3. Uremia 4. Methanol 5. Paraldehyde 6. Ethylene glycol 7. Diabetes Mellitus Normal A-G (Hyperchloremic) à HCO3 - effectively replaced by Cl -. It may arise from one of the following conditions: 1. HCO3 - loss from body fluids through the GIT or kidneys, with subsequent Cl - retention 2. Defective renal acidification with failure to excrete normal quantities of metabolically produced acid 3. Addition of HCl to body fluids 4. Addition or generation of another acid with rapid titration of HCO3 - and rapid renal excretion of the accompanying anion and replacement by Cl - 5. Rapid dilution of the plasma HCO3 - by saline Clinical picture GIT causes of normal anion gap metabolic acidosis 1. Diarrheal states and increased stool volume 2. Enteric fistulas and drainage of biliary, pancreatic, and enteric secretions 3. Ileus secondary to intestinal obstruction 4. Villous adenomas that secrete fluid with a high bicarbonate content Symptoms 1. Dyspnea (hyperventilation) 2. Nausea, Vomiting, Decreased apetite 3. Symptoms of underlying cause: a. History of diarrhea, DM, starvation, alcoholism b. Polyuria, polydipsia, epigastric pain, vomiting c. Nocturia, polyuria, anorexia, pruritus d. Ingestion of drugs or toxins e. Renal stones: RTA or renal failure Renal causes of normal anion gap metabolic acidosis Renal Tubular Acidosis (RTA) refers to a diverse group of tubular disorders, uncoupled from glomerular damage, characterized by impairment of urinary acidification without urea and anion retention. These disorders can be divided into 2 general categories: proximal (type II; bicarbonate wasting acidosis) distal (types I and IV) Signs 1. Kussmaul Respiration 2. Hypotension & Coma 3. Nonspiecific (according to underlying cause): a. Renal failure: xerosis, pallor, scratching in skin, fetor, astrexis, pericardial rub b. DKA: reduced skin turgor, dry mucous membranes, acetone smell Alkali therapy to keep ph>7.2 only in the following conditions: a. Continued fall in HCO - 3 with paco 2 of 15 or less in healthy young adults or even higher in elderly or patients with ventilatory disorders b. Well compensated metabolic acidosis with impending respiratory failure due to fatigue of respiratory muscles Treatment IV HCO3 HCO 3 - deficit = deficit/l (desired serum HCO measured HCO 3- ) X 0.5 X body weight (volume of distribution for HCO 3- ) To avoid hypernatremia and hyperosmolality, two 50-mL ampules of 8.4% NaHCO 3 (50 meq each) are added to 1 L of 0.25 N saline or 3 ampules are added to 1 L of 5% dextrose in water. Or add loop diuretic if not dehydrated Oral Therapy Oral HCO3 is preferred in patients with chronic metabolic acidosis NaHCO3- tablets: 325- and 650-mg (1 g of NaHCO3 is equal to 11.5 meq of HCO 3- ) Citrate salts mixtures of citric acid with sodium citrate and/or potassium citrate. Generally contain 1-2 meq of HCO3- per ml. K citrate is useful in acidosis + hypokalemia. Cautiously in renal impairment & avoided hyperkalemia.

4 Metabolic alkalosis Definition A 1ry in serum [HCO3 - ] Consequence of loss of H + from the body or gain in HCO3 - o serum [HCO3 - ] may also be observed as a compensatory response to primary respiratory acidosis. However, a [HCO3 - ] > 35 meq/l is almost always caused by metabolic alkalosis o Mild Anion Gap in metabolic alkalosis due to -ve charge of albumin and production of lactate ph In its pure form, it manifests as alkalemia (ph >7.40) Compensatory Compensatory mechanism alveolar hypoventilation with (PaCO2) Δ ph that would otherwise occur Severe alkalosis causes diffuse arteriolar VC with reduction in tissue perfusion. a) cerebral BF, may tetany, seizures, and mental status b) coronary BF refractory arrhythmias Consequences Met. Alk. hypoventilation hypoxemia, and it may impair weaning from mechanical ventilation Met. Alk. Ca 2+ by Ca 2+ binding to albumin Met. Alk. associated with hypokalemia, a) neuromuscular weakness and arrhythmias and, b) by ing NH3 production, it can hepatic encephalopathy Clinical manifestation History 1. Hypokalemia weakness, myalgia, and polyuria. 2. Hypoventilation due to the respiratory center 3. Symptoms of hypocalcemia: jitteriness, perioral tingling, muscle spasms 4. Important points in the history a. Vomiting or diarrhea - GI losses of HCl b. Age of onset and family history: eg, Bartter syndrome, which starts during childhood c. Drug use: Loop or thiazide diuretics, Licorice, Tobacco chewing, Carbenoxolone, Fludrocortisone, Glucocorticoids, Antacids (eg, magnesium hydroxide), Calcium carbonate Physical examination 1. Signs of hypocalcemia (eg, tetany, Chvostek sign, Trousseau sign), 2. Change in mental status, or seizures 3. Establish the cause o Evaluation of hypertension and volume status assessment o Volume depletion usually accompanies chloride-responsive alkalosis, while volume expansion accompanies chloride-resistant alkalosis 4. Bulimia à Because patients with bulimia frequently self-induce vomiting, they may have erosions of teeth enamel and dental caries because of repeatedly exposing their teeth to gastric acid 5. Cushing syndrome à Obesity, Moon face, Buffalo hump, Hirsutism, Violaceous skin striae, Acne 6. Congenital adrenal hyperplasia (CAH): o In CAH 2ry to 11-hydroxylase deficiency, the infants have hypertension and growth retardation. Male infants have premature sexual development, while female infants develop virilization. o In 17-hydroxylase deficiency, males develop sexual ambiguity, while females have sexual infantilism

5 Chloride responsive alkalosis Chlorideresistant Alkalosis with HTN Chlorideresistant Alkalosis w/o HTN Causes of metabolic alkalosis Etiology Urine chloride Treatment 1. Loss of gastric secretions - Vomiting, NG suction 2. Loss of colonic secretions - Congenital chloridorrhea, villous adenoma 3. Thiazides and loop diuretics (after discontinuation) 4. Posthypercapnia 5. Cystic fibrosis 1. 1ry hyperaldosteronism 2. 11B-HSD2 - Genetic, licorice, chewing tobacco, carbenoxolone 3. CAH à 11-Hydroxylase or 17-hydroxylase deficiency 4. Current use of diuretics in hypertension 5. Cushing syndrome 6. Exogenous mineralocorticoids or glucocorticoids 7. Liddle syndrome 8. Renovascular hypertension 1. Bartter syndrome 2. Gitelman syndrome 3. Severe potassium depletion 4. Current use of thiazides and loop diuretics 5. Hypomagnesemia <20mEg/L >20mEg/L >20mEg/L With volume depletion 1. intravenous infusion of isotonic sodium chloride solution 2. use potassium chloride to correct the hypokalemia Edematous states 1. use potassium chloride to correct the alkalosis 2. carbonic anhydrase inhibitor or a potassium-sparing diuretic Primary hyperaldosteronism à aldosterone antagonist spironolactone or with other potassium-sparing diuretics Cushing syndrome à Potassium-sparing diuretics until surgical therapy Licorice ingestion à Discontinuation of licorice Bartter syndrome and Gitelman syndrome à potassium supplementation, potassium-sparing diuretics, NSAIDS, or ACE inhibitors Liddle syndrome à amiloride or triamterene but not with spironolactone. Amiloride and triamterene inhibit the apical sodium ion channel in the collecting duct Other causes 1. Exogenous alkali administration NaHCO3, metabolism of lactic acid or ketoacids 2. Milk alkali syndrome 3. Hypercalcemia 4. Intravenous penicillin 5. Refeeding alkalosis 6. Massive blood transfusion All metabolic alkalosis (non-specific treatment) Intravenous HCl is indicated in severe metabolic alkalosis (ph >7.55) or when sodium or potassium chloride cannot be administered Dialysis à Both peritoneal dialysis and hemodialysis can be used with certain modifications of the dialysate to correct metabolic alkalosis