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The Minimalist approach to acid/base disturbances ABG’s so easy….a GEICO rep can do it
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OBJECTIVES Acid/Base terminology and definitions Normal physiologic acid/base regulation Acid/base disturbances ABG interpretation Case studies
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Acid/Base terminology and definitions Acid/Base regulation / Control of( H+)concentration –Acid—proton (H+) donor increases (H+) –Base—proton (H+) acceptor decreases (H+) Ph is the logarithmic/exponential representation of (H+) concentration in eq/liter
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What is log???? 10 =10(1) log 10= 1 100=10(2) log 100=2 1000=10 (3) log1000=3 0.1= 10 (-1) log 0.1 = -1 0.01 = 10 (-2) log 0.01= -2
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ph = - Log (H+) ph = 6 (H+) = 10 (-6) eq/liter 0.000001 eq/liter ph = 7 (H+) = 10 (-7) eq/liter 0.0000001eq/liter ph = (H+) = 10(-8) eq/liter 0.00000001 eq/liter
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H20 <<<<< (H+) + ( OH-) (H+) = 10(-7) eq/liter Pure Water has a ph 7(chemical neutral)
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Physiologic regulation of extracellular ph Normal physiologic ph = 7.4 Essential for normal enzymatic reactions
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Control Mechanisms/ Normal physiology Buffer systems (immediate) Respiratory (seconds) Renal (hours-days)
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Buffer solutions Solution of two or more compounds Prevent marked changes in ph when acid or base is added
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Bicarbonate Buffer H20 + CO2 <<< H2CO3 <<( H+)+ HCO3-
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Henderson/Haselbalch Equation ph = 6.1 + log HCO3-/ CO2 HCO3-/CO2= 20 Ph= 7.4
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Ph is dependent on HCO3- (direct) and CO2(inverse) HCO3 increases--- ph increases HCO3 decreases ---- ph decreases CO2 increases---- ph decreases CO2 decreases--- ph increase
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Physiologic Response to chronic acid load Bicarbonate Buffer system (immediate) –HCL + NaHCO3 >>>H2CO3 (CO2) +NaCL Pulmonary Control (seconds to minutes) –Ventilation of newly created CO2 in buffer system Renal control (hours to days) –Secretes H+ to reabsorb and regenerate HCO3 consumed by buffer
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Pathophysiology/ Acid/Base disturbances Acidosis---any process that lowers ph –Lowers HCO3- or raises PCO2 Alkalosis--- any process that raises ph –Raises HCO3- or lowers PCO2
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Definitions Neutral –Ph 7.35-7.45 Acidemia –Ph < 7.35 Alkalemia –Ph > 7.45
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More Definitons More Definitons Isoelectric principle –+ ions (cations) = -ions (anions) Anion Gap—(Na + K) – (CL + HCO3) nl =15 –Measures minor/unmeasured anions –Endogenous/exogenous anions
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Acid/Base disturbances Primary Secondary- a response to a primary disturbance –Opposite direction from primary –Compensation is partial and incomplete
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Acid/Base disturbaces Respiratory--- alteration in pCO2 Metabolic --- alteration in HCO3
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Acute Respiratory Acidosis- Elevation in PCO2 CNS vs. pulmonary –CNS – coma, stroke –Pulmonary-asthma, COPD, pneumonia (very late).08 ph drop for every 10mm increase in PCO2 –Typical abg’s 7.32/50/62 7.24/60/47 No metabolic compensation/ HCO3 unchanged Treatment- Fix the problem –Bronchodilators/cpap/bipap/intubation
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Chronic Respiratory Acidosis Chronic/slow PCO2 elevation –COPD/sleep apnea/obesity Compensatory metabolic alkalosis a major component –Kidneys increase H+ secretion –increase HCO3.02 ph drop / 10 mm increase in PCO2 –Typical abg’s 7.38/50 /50 7.36/60/55 Treat underlying condition –Beware excess O2
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Acute Respiratory Alkalosis/ decreased PCO2 CNS vs pulmonary –CNS stress, drugs, anxiety, sepsis, toxins –Pulmonary pneumonia/asthma/pulmonary embolism.08 ph increase 10 mm decrease in PCO2 –Typical abg’s 7.48/30/62 No metabolic compensation Treat underlying condition –Supplement O2 –Beware of paper bag
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Chronic Respiratory Alkalosis Extremely rare…some other time….
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Acute Metabolic Acidosis Decreased HCO3 –Direct HCO3 loss via GI/kidneys –Decreased HCO3 from H+ buffering
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Metabolic Acidosis - defined by the associated anion Anion gap acidosis- increased minor anions –Endogenous/Exogenous Non anion gap acidosis-hyperchloremic –HCO3 loss from GI/kidneys –Increased reabsorption of CL-
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Acute metabolic acidosis Compensatory respiratory alkalosis Compensation is rapid but incomplete PCO2 drop= HCO3 drop –Typical abg 7.34/35/98 serum HCO3 =20
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Treatment of Metabolic Acidosis Define and treat the underlying condition Watch for elevations in K+ Beware HCO3-
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Pitfalls of HCO3- treatment Paradoxical CNS and intracellular acidosis Over correction alkalosis Aggressive Na load
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Indications for HCO3- therapy HCO3 < 5 Ph <7.10 Cardiovascular instablity or irritability More likely to use on ventilated patients as CO2 is “blown off”
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Anion Gap Acidosis MUDPILES MethanolUremia Diabetic (ketones) ParaldehydeIronLactate Ethylene glycol Salicylate
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Alternative Classification of anion gap acidosis Ketoacidosis Lactic acidosis Exogenous poisonings Uremia
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Ketoacidosis Diabeticalcoholic
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Diabetic ketoacidosis Insulin lack –Hyperglycemia –Fatty acid breakdown Ketone accumulation Treatment –Correct underlying disorder –fluids –insulin –maintenance of electrolytes especially K+
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Alcoholic Ketoacidosis EtOH use followed by vomiting/starvation –Excessive ketone accumulation –Dehydration –Hypo or normoglycemia Treatment –Fluids –Maintenance of electrolytres –Glucose
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Lactic Acidosis Lactic Acidosis Type A tissue hypoxia/underperfusion Type B abnormal lactate utilization
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Treatment Treatment Correct underlying cause –Antibiotics –Blood transfusion –Goal directed sepsis therapy –Fluids/pressors
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Exogenous toxins Alcohols –Methanol/ethylene glycol Salicylate
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Alcohol poisoning Ethanol not usually a major cause of acidosis MethanolEthylene Glycol –Formate/Oxylate accumulation –Increased osmolar gap –Renal failure/oxylate crystals Treatment for methanol/ethylene glycol –Ethanol drip –Dialysis
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Clues to diagnosis for ethylene glycol/methanol intox History –“sterno” or anti freeze ingestion Altered mental status Unexplained visual disturbances/coma Unexplained anion gap acidosis Renal failure
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Diagnostic Aides ABG/ HCO3 Serum osm ETOH level Osmolar gap Oxylate crystals
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Salicylate Toxicity Altered mental status Anion gap acidosis Primary respiratory alkalosis as well –Typical abg 7.35/20/110 serum HCO3 15 Treatment –Alkalinazation of the urine –K+ replacement –Dialysis
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Lab Evaluation of anion gap Metabolic Acidosis KetonesSalicylateLactate Etoh/serum osm Osmolar gap = measured-calc serum osm
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Non Anion Gap-Hyperchloremic acidosis GI or renal HCO3- loss Compensatory CL- resorption Usually associated with hypo/hyperkalemia
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Metabolic Alkalosis Primary elevation in extracellular HCO3- –H + losses from GI (vomiting) –Excessive renal H+ excretion/ elevated HCO3 resorpbtion –Exogenous ingestion Respiratory compensation –If HCO3 goes up by 10 pco2 goes up by 7 –Typical abg 7.47/47/100 HCO3 =34
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Metabolic Alkalosis Physical effects –Tetany –Neuromuscular hyperactivity –Seizures –Decreased K+/ionized Ca 2+ Treatment –Correct underlying cause –Acetazolamide---causes renal HCO3 loss –Correct electrolytes
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ABG interpretation Step 1 obtain ABG/ HCO3- (electrolytes SMA7/Istat) Step 2 ph determination to determine – ph 7.35-7.45 = nuetral – ph < 7.35 = academia – ph > 7.45 + alkalemia
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Acidemia Flow chart to determine underlying process HCO3 low- primary process is metabolic acidosis pCO2 elevated- primary process is respiratory acidosis
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Metabolic Acidosis What is the anion gap???? Is the respiratory compensation appropriate –Appropriate PCO2/HCO3 =1 HCO3 =15/ PCO2 =30 –PCO2/HCO3 > 1 resp alkalosis HCO3=15 PCO2= 20 PCO2/HCO3 < 1 resp acidosis HCO3= 15 PCO2 =43
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Respiratory Acidosis Is the acidosis acute/chronic? –Acute –ph down.08/10 mmPCO2 elevation –Chronic ph down.03/10mm PCO2 elevation –Acute on chronic 7.35/50/50 –Outside limits—second primary process
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Alkalemia flow chart HCO3 elevated- primary metabolic alkalosis pCO2 decreased- primary respiratory alkalosis
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Metabolic Alkalosis Is the respiratory response appropriate? –PCO2/HCO3 =.7 7.48/47/75 HCO3 =35
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Respiratory Alkalosis Acute—is the ph response appropriate –Ph.08 up for every 10 mm decrease in PCO2
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Nuetral ph Look for mixed primary disturbances –PCO2 –Anion gap –HCO3
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Case studies Having FUN yet???/ Follow the flow charts!!!!!
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Case #1 57 y.o acutely SOB 7.32/60/55 HCO3=32 HCO3=32 SMA 7 and anion gap otherwise normal
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Case #2 31 y.o homeless male unresponsive in park 7.24/29/107 Na 140 K 5.4 Cl 97 HCO3 14 glucose 110 Renal function normal
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Case #3 61 y.o with severe arthritis confused and agitated 7.34/18/110 Na 142 K 2.9 CL 99 HCO3 12 Glucose/renal function wnl
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Case #4 19 y.o. diabetic with vomiting 7.38/38/110 Na 140 K 2.8 CL 95 HCO3 24 Glucose 440 renal function wnl
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