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Acid Base Disturbances Ian Chan MS4 Eliza Long R2 10/30/06
ABG analysisWhy do we care ?– Critical care requires a good understanding– Helps in the differential and final diagnosis– Helps in determining treatment plan– Treating acid/base disorders helps medications work better (i.e. antibiotics, vasopressors, etc.)– Helps in ventilator management– Severe acid/base disorders may need dialysis– Changes in electrolyte levels in acidosis (increased K+ and Na+, and decreases in HCO3)
Gap AcidosisMethanolUremiaDiabetic ketoacidosisParaldehydeINHLactic acidosisEthylene GlycolSalicylate
Non Gap AcidosisH: hyperalimentationA: acetazolamideR: RTAD: diarrheaU: rectosigmoidostomyP: pancreatic fistula
Metabolic AcidosisRespiratory compensation process takes 12-24 hours to become fully active. Protons areslow to diffuse across the blood brain barrier.In the case of LA this will be faster becauseLA is produced in the brain.The degree of compensation can beassessed by using Winter’s Formula. It isINAPPROPRIATE to use this formula beforethe acidosis has existed for 12-24 hours.– PCO2 = 1.5 (HCO3) + 8 +/-2.
Decreased anion gapDecrease in unmeasured anions– HypoalbuminemiaIncrease in unmeasured cations– Hypercalcemia– Hypermagnesemia– Hyperkalemia– Multiple myeloma– Lithium toxicity
Metabolic AlkalosisGeneration by gain of HCO3 and maintainedby abnormal renal HCO3 absorption.This is almost always secondary to volumecontraction (low Cl in urine, responsive toNaCl, maintained at proximal tubule)– Vomiting: net loss of H+ and gain of HCO3.– Diuretics: ECFV depletion– Chronic diarrhea: ECFV depletion– Profound hypokalemia– Renal failure: if we cannot filter HCO3 we cannot excrete it.Mineralocorticoid excess: increased Hsecretion, hypokalemia (Na/K exchanger),saline resistant).
Respiratory AcidosisAcute or Chronic: has the kidney hadenough time to partially compensate?The source of the BUFFER (we need toproduce bicarb) is different in these statesand thus we need to make this distinction.
Respiratory AcidosisAcute : H is titrated by non HCO3 organic tissuebuffers. Hb is an example. The kidney has littleinvolvement in this phase.– 10 mm Hg increase in CO2 / pH should decrease by . 08Chronic: The mechanism here is the renalsynthesis and retention of bicarbonate. AsHCO3 is added to the blood we see that [Cl] willdecrease to balance charges.– This is the hypochloremia of chronic metabolic acidosis.– 10 mm H increase in CO2 / pH should decrease by . 03
Respiratory AcidosisElevation of CO2 above normal with a drop inextracellular pH.This is a disorder of ventilation.Rate of CO2 elimination is lower than theproduction5 main categories:– CNS depression– Pleural disease– Lung diseases such as COPD and ARDS– Musculoskeletal disorders– Compensatory mechanism for metabolic alkalosis
Respiratory AlkalosisInitiated by a fall in the CO2 activateprocesses which lower HCO3.Associated with mild hypokalemia. Cl isretained to offset the loss of HCO3 negativecharge.Acute response is independent of renalHCO3 wasting. The chronic compensation isgoverned by renal HCO3 wasting.Causes– Intracerebral hemorrhage– Drug use : salicylates and progesterone– Decreased lung compliance Anxiety– Liver cirrhosis– Sepsis
Arterial Blood Gas (ABG) AnalysisABG interpretationFollow rules and you will always be right !! 1) determine PH acidemia or alkalemia 2) calculate the anion gap 3) determine Co2 compensation (winters formula) 4) calculate the delta gap (delta HCO3)
ABG analysisArterial Blood Gas (ABG) –interpretation– Always evaluate PH first Alkalosis – PH > 7.45 Acidosis – PH < 7.35– Determine anion gap (AG) – AG = NA – (HCO3+ CL) AG metabolic acidosis Non AG acidosis – determined by delta gap– Winters formula Calculates expected PaCO2 for metabolic acidosis PaCO2 = 1.5 x HCO3 + 8
ABG analysisDelta gap– Delta HCO3 = HCO3 (electrolytes) + change in AG Delta gap < 24 = non AG acidosis Delta gap > 24 = metabolic alkalosis– Note: The key to ABG interpretation is following the above steps in order.
ABG analysis33 y/o with DKA presents with thefollowing:– Na = 128, Cl = 90, HCO3 = 4, Glucose = 800– 7.0/14/90/4/95%– PH = acidemia– AG = 128 – (90 + 4) = 34– Winters formula – 1.5(4) + 8 = 14– Delta gap = 4 + (34 – 12) = 26
ABG analysisAnswer– AG acidosis with appropriate respiratory compensation– History c/w ketoacidosis secondary to DKA with appropriate respiratory compensation
ABG analysis56 y/o with COPD exacerbation and hypotensionand associated diarrhea x 7 days presents withthe following ABG: – 7.22/30/65/10/90% 139 110 20 120 PH(7.22) = acidemia 4.0 10 1.5 AG = 139 – (10 + 110) = 19 (nl AG = 8-12) Winters formula – PaCO2 = 1.5 (HCO3) + 8 = 1.5 (10) + 8 = 23 Delta gap – Delta gap = HC03 + change in the AG = 24 – Delta gap = 10 + (19 – 12) = 10 + 7 = 17 – Delta gap = 17
ABG - exampleTriple disorder – AG acidosis - – Incomplete respiratory compensation – Non AG acidosisHistory would suggest AG acidosis is secondary tohypotension with lactic acid build up and the patient is notable to compensate with his COPD therefore there is norespiratory compensation and the non AG acidosis issecondary to diarrhea with associated HCO3 loss.
Look at the pH. – pH < 7.35, acidosis – pH > 7.45, alkalosisLook at PCO2, HCO3- • Main pathology will be the change correlates with the pH. • If alkalosis pCO2 will be low or Bicarb high • If acidosis pCO2 will be high or Bicard low • The other abnormal parameter is the compensator responseRespiratory or Metabolic • pCO2 - respiratory • Bicarb - metabolic
Metabolic Acidosis? Anion Gap? • >12 - ketoacidosis, uremia, lactic acidosis, or toxins • Delta ratio to check for gap and non gap disorders , or metabolic alkalosis happening simultaneously • Normal anion gap - diarrhea OR unknown. If unknown calculate urine anion gap, if positive likely RTA, if neg liekly diarrheaMetabolic Alkalosis If urin Cl is > 20 it is chloride-resistant alkalosis (increased mineralcorticoid activity If <20 chloride responsive alkalosis (vomitting or gastric loss)
Example # 144 yo M 2 weeks post-op from totalproctocolectomy for ulcerative colitis.Na+ 134, K+ 2.9, Cl- 108, HCO3- 16, BUN31, Cr 1.5BG: 7.31/ 33 /93 / 16
Example #29 yo M presents with N/V.Na 132 , K 6.0, Cl 93, HCO3- 11 glucose650BG: 7.27/23/96/11/-8
Example #370 yo M s/p lap chole, on the morning ofPOD #1. Pt received 2L bolus ofcrystalloid throughout pm for tachycardia.Now with SOB.7.24 / 60 / 52 / 27 /+3
Example #454 yo F s/p mult debridements fornecrotizing fasciitis, now on vassopressinto maintain blood pressureBG - 7.29/40/83/17/-6
Example #535 yo M involved in crush injury, bouldervs body.Na 135 , K 5.0, Cl 98, HCO3- 15 BUN 38,Cr 1.7, CK 42,346BG: 7.30/32/96/15/-4
Example #64 wks M with projectile emesisNa: 140, K:2.9, Cl: 927.49/40/98/30/+6