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Acid-Base Disorders Acidemia vs Acidosis • Acidemia • Describes concentration of hydrogen ions [H+] in plasma; this it includes all conditions where H+ in plasma is higher than the values observed in normal subjects (40 +/- 2nmol/L), or a pH less than 7.38 • Acidosis • Any process by which there is increased H+ and a decrease in the concentration and/or content of bicarbonate (HCO3-) in the extracellular fluid compartment • 2 causes • High CO2 tension in arterial blood (PaCO2) – Respiratory Acidosis • High H+ in plasma from a low bicarb – Metabolic Acidosis Alkalemia vs Alkalosis • Alkalemia • It includes all conditions where H+ in plasma is lower than the values observed in normal subjects (40 +/- 2nmol/L), or a pH greater than 7.42 • Alkalosis • Any process by which there is decrease H+ and an increase in the concentration and/or content of bicarbonate (HCO3-) in the extracellular fluid compartment Acid-Base Disorder • Step 1: Measure pH • Step 2: Check the Compensatory or secondary response of PCO2 or HCO3- to see if the disorder is simple or mixed • Step 3: Calculate serum Anion Gap • Step 4: Determine cause of acid-base disorder • Step 5: Treat Identifying the Disorder • Check pH, pCO2, and HCO3- (CO2 in Basic Metabolic Panel) • Normal pH 7.40 • Normal pCO2 40 • Normal HCO3- 24 • First determine if acidemia or alkalemia is present • Then determine primary generating change (check pCO2) • Finally determine degree of compensation, or secondary/tertiary disturbances Consequences of Severe Acid-Base Disturbances Organ System Cardiovascular Respiratory Acidemia (pH < 7.38) contractility , arteriolar vasodilation MAP and CO; response to catecholamines risk of arrhythmias Hyperventilation, resp muscle strength Alkalemia (pH > 7.42) Arteriolar vasoconstriction coronary blood flow risk of arrhythmias Hypoventilation Metabolic K, insulin resistance K, ICa, Mg, PO4 Neurologic MS MS, seizures, tetany ABG vs VBG • Concordant for pH (~0.04 difference) • HCO3 changes by ~2 mEq but not PaCO2 (8+/-17 mmHg) • VBG can be used to screen for hypercarbia w PaCO2 cutoff >/= 45 mmHg (100% sensitive) • Does not accurately assess degree of hypercarbia Metabolic Acidosis • pH <7.40 • pCO2 > 40 (compensatory mechanism) • Remember: Hyper/Hypoventilation alters pCO2 to counteract 1ry metabolic process • HCO3 < 24 • Check for AG always!! • AG = Na – (Cl + HCO3-) • Increased AG = there are increased unmeasured anions • Organic acids, phosphates, sulfates • Decreased AG = decreased Albumin or increased unmeasured cations • Ca, Mg, K, Li, bromine, immunoglobulins • If increased AG, • Check delta-delta (delta AG / delta bicarb) • Delta = change in Increased Anion Gap Met Acidosis • 3 major causes • Ketoacidosis • When glucose is not available to cells because of lack of insulin, cell dysfunction, or glucose depletion • Fatty acids are oxidized to yield energy • Acetone and 2 ketoacids (acetoacetic and B-hydroxybutyric) • H+ produced are consumed by HCO3- (buffered), producing carbonic acid CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3 – • Ketoanions accumulate in serum, increasing AG • Lactic acidosis • Glucose anaerobic glycolysis to pyruvate ! lactate • Type A lactic acidosis: primary inadequate delivery of oxygen to tissues • Shock most common cause • Type B lactic acidosis: tissue oxygenation is normal but they cannot use oxygen normally or need excessive amounts • Hepatic failure, malignancy, drugs, seizures • Toxicities Increased Anion Gap Met Acidosis • 3 major causes • Ketoacidosis • Lactic acidosis • Toxicities • Ethylene glycol, methanol, salicylate intox, pyroglutamic acidosis from acetaminophen • Check Osmolal gap • Calc Sosm = 2xNa + glu/18 + BUN/2.8 • If difference is greater than 10 suggests ingestion; >25 mOsm/kg of serum, the presence of a toxic alcohol is probable Ingestions AG OG nl nl Ingestion Other manifestations Acetaminophen Hepatitis Salicylates Fever, tachycardia, tinnitus; met acid + resp alk Ethanol Alcoholic fetor, changes mental status, hepatitis, keto + lactic acid +/- met alkalosis (vomiting) Methanol Changes mental status, blurred vision, pupillary dilation, papilledema Ethylene Glycol Changes mental status, cardiopulmonary failure, hypocalcemia, Ca oxalate crystals ! renal failure; urine flouresces under UV light Prolylene gluycol AKI Isopropyl alcohol Changes mental status, fruity breath (acetone) Normal Anion Gap Met Acidosis • 3 causes • GI HCO3- loss • Diarrhea and external drainage of pancreatic, biliary, or small bowel juices • Chloride-rich fluid remains behind generating a hyperchloremic met acidosis (normal AG) • Renal • HCO3- loss or H+ retention • Renal Tubular Acidosis • Inorganic acid intake Normal Anion Gap Met Acidosis • Work-up • History • Urine Anion Gap • UAG = (Urine Na + Urine K) – Urine Cl • UAG = unmeasured anions – unmeasured cations • As NH4+ is primary unmeasured cation, UAG is indirect assay for renal NH4+ excretion • Negative UAG ! increased renal NH4+ excretion (appropriate response to acidemia • DDx: GI causes, proximal RTA, ingestions or dilutional • Positive UAG! failure of kidneys to secrete NH4+ • DDx: distal or hypoaldo RTA, early renal failure Renal Tubular Acidosis • Proximal (old type II RTA) • Defect in proximal tubular HCO3- reabsorption • Most common cause in children is cystinosis (causing Fanconi Syndrome) • Most common cause in adults are paraproteinemias and autoimmune disorders • Distal (old type I RTA) • Defect in collecting duct with defect in net distal H+ secretion • 2 varieties • Hypokalemic distal RTA • Hyperkalemic distal RTA Renal Tubular Acidosis • Distal • Hypokalemic • Collecting duct potassium secretion is intact • Enhanced by small amount of bicarbonaturia • Seen with Sjögren’s syndrome, ampho B tox, cirrhosis of liver, medullary sponge kidney, etc • Hyperkalemic • Hypoaldosteronism (old type IV RTA) • Can be caused by DM, mild chronic renal failure • Tubular defect • Can be caused by chronic obstruction of kidney, SLE, and sickle cell disease Recall Aldosterone… https://cjasn.asnjournals.org/content/10/2/305 Hypoaldosteronism • Increase K ! Decrease in NH3 synthesis/delivery ! carrying capacity • 3 variants: • Decrease Renin • • • • diabetic nephropathy NSAIDs CIN HIV • Normal Renin • Decrease aldo synthesis (1ry adrenal disorders, ACEi, ARBs, Heparin) • Decrease response to aldosterone • • • • • K-sparing diuretics TMP-SMX Pentamidine CIN (calcineurin inhibitors) Tubulointerstitial disease (sickle cell, SLE, amyloid, diabetes) decrease urine acid Treatment (severe met acidosis pH <7.2) • DKA: insulin and IVFs • Replete K, Mg, PO4 as needed • Lactic acidosis • Treat underlying condition • Renal failure • Hemodialysis • Methanol and ethylene glycol • Early fomepizole, Vit B6, folate, HD (especially if late presentation) • Alkali therapy: NaHCO3 Metabolic Alkalosis • 3 causes • Loss of volume • Cl depletion from extrarenal losses of hydrogen ion or chloride • Gastric acid loss, vomiting, renal chloride loss, diuretics, posthypercapnia, cystic fibrosis • Gain of volume due to mineralocorticoids • Chloride replete Urine Cl spot > 20 mmol/L • Kidney is not avid for salt because of volume expansion and therefore excretes the daily Na+ and Clload without difficulty • • • • • Hyperaldosteronism Gitelman’s syndrome Bartter’s syndrome Cushing’s syndrome Licorice excess • Miscellaneous factors • Profound K depletion Approach to Metabolic Alkalosis • Urine Cl • < 20 Saline-Responsive • GI losses, Prior diuretics, posthypercapnia • > 20 Saline-Resistant • Hypertensive • 1ry Hyperaldo • 2ry Hyperaldo • Non-aldosterone • Hypo- or normotensive • Current diuretics • Severe Hypokalemia • Exogenous alkali • Barter’s • Gitelman’s Respiratory Acidosis • Increase in pCO2 • Etiologies: • CNS depression • Sedatives, CNS trauma, O2 in chronic hypercapnia (decreases hypoxemic drive), central sleep apnea • Neuromuscular disorders • MG, Guillain-Barré, poliomyelitis, ALS, muscular dystrophy, severe hypophosphatemia, high spinal cord injury, drugs (paralytics) • Upper airway abnormalities • Obstruction, laryngospasm, OSA, esophageal intubation • Lower airway abnormalities • Asthma, COPD Respiratory Alkalosis • Decrease in PCO2 • Hypoxia ! hyperventilation • Pneumoniae, pulm edema, PE, restrictive lung disease • Primary hyperventilation • CNS stimulation, pain, anxiety, fever, trauma, stroke, voluntary • Drugs: salicylates, progesterone, methylxanthines, nicotine, pregnancy, hepatic failure, sepsis • Pseudorespiratory alkalosis • Decreased perfusion with preserved ventilation • CPR, severe HoTN ! increase tissue CO2 decreased delivery of CO2 to lungs for excretion; low PaCO2 but Compensations • Metabolic Acidosis • Winter’s Formula • PaCO2 = (1.5 x HCO3) + 8 ±2 • PaCO2 last two digits of pH • Metabolic alkalosis • PaCO2 = 0.7 x ΔHCO3 Compensations • Respiratory Acidosis • Acute • HCO3 = 0.1 x ΔPaCO2 • Chronic • HCO3 = 0.35 x ΔPaCO2 • Respiratory Alkalosis • Acute • HCO3 = 0.2 x ΔPaCO2 • Chronic • HCO3 = 0.4 x ΔPaCO2 Examples You are evaluating a 55 y/o man who just arrived to ED with shortness of breath. He has a history of emphysema • pH 7.32 • PCO2 80 mmHg • HCO3- 40 mmol/L Examples You are evaluating a 55 y/o man who just arrived to ED with shortness of breath. Patient also complains of episodes of diarrhea He has a history of emphysema. Calculated AG 11 • pH 7.10 • PCO2 80 mmHg • HCO3- 26 mmol/L Examples You are evaluating a 55 y/o man who just arrived to ED with shortness of breath. AG 35. • pH 7.44 • PCO2 12 mmHg • HCO3- 8 mmol/L Examples You are evaluating a 55 y/o man who just arrived to ED with shortness of breath. BP on arrival 70/30. AG 33. • pH 7.14 • PCO2 22 mmHg • HCO3- 8 mmol/L Examples You are evaluating a 55 y/o man who just arrived to ED with shortness of breath. • pH 7.55 • PCO2 35 mmHg • HCO3- 30 mmol/L Examples You are evaluating a 55 y/o man who just arrived to ED with shortness of breath. • pH 7.55 • PCO2 21 mmHg • HCO3- 20 mmol/L