Acid Base DisturbancesAcid Base Disturbances

Ian Chan MS4Ian Chan MS4

Eliza Long R2Eliza Long R2

10/30/0610/30/06

ABG analysisABG analysis

Why do we care ?Why do we care ?– Critical care requires a good understanding Critical care requires a good understanding – Helps in the differential and final diagnosisHelps in the differential and final diagnosis– Helps in determining treatment planHelps in determining treatment plan– Treating acid/base disorders helps medications Treating acid/base disorders helps medications

work better (i.e. antibiotics, vasopressors, etc.)work better (i.e. antibiotics, vasopressors, etc.)– Helps in ventilator managementHelps in ventilator management– Severe acid/base disorders may need dialysisSevere acid/base disorders may need dialysis– Changes in electrolyte levels in acidosis Changes in electrolyte levels in acidosis

(increased K+ and Na+, and decreases in HCO3)(increased K+ and Na+, and decreases in HCO3)

Acid bufferingAcid buffering

The Anion GapThe Anion Gap

Na – (Cl + HCO3)Na – (Cl + HCO3)

NaHCO3 + HCL NaHCO3 + HCL NaCL + H2CO3 NaCL + H2CO3

NaHCO3 + HXNaHCO3 + HX NaX+ H2CO3 NaX+ H2CO3

Unmeasured cations: calcium, Unmeasured cations: calcium, magnesium, gamma globulins, potassium.magnesium, gamma globulins, potassium.

Unmeasured anions: albumin, phosphate, Unmeasured anions: albumin, phosphate, sulfate, lactate.sulfate, lactate.

Gap AcidosisGap Acidosis

MethanolMethanolUremiaUremiaDiabetic ketoacidosisDiabetic ketoacidosisParaldehyde Paraldehyde INHINHLactic acidosisLactic acidosisEthylene GlycolEthylene GlycolSalicylateSalicylate

Non Gap AcidosisNon Gap Acidosis

H: hyperalimentationH: hyperalimentation

A: acetazolamideA: acetazolamide

R: RTAR: RTA

D: diarrheaD: diarrhea

U: rectosigmoidostomyU: rectosigmoidostomy

P: pancreatic fistulaP: pancreatic fistula

Metabolic AcidosisMetabolic AcidosisRespiratory compensation process takes 12-Respiratory compensation process takes 12-24 hours to become fully active. Protons are 24 hours to become fully active. Protons are slow to diffuse across the blood brain barrier. slow to diffuse across the blood brain barrier. In the case of LA this will be faster because In the case of LA this will be faster because LA is produced in the brain. LA is produced in the brain. The degree of compensation can be The degree of compensation can be assessed by using Winter’s Formula. It is assessed by using Winter’s Formula. It is INAPPROPRIATE to use this formula before INAPPROPRIATE to use this formula before the acidosis has existed for 12-24 hours. the acidosis has existed for 12-24 hours. – PCO2 = 1.5 (HCO3) + 8 +/-2. PCO2 = 1.5 (HCO3) + 8 +/-2.

Decreased anion gapDecreased anion gap

Decrease in unmeasured anionsDecrease in unmeasured anions– HypoalbuminemiaHypoalbuminemia

Increase in unmeasured cationsIncrease in unmeasured cations– HypercalcemiaHypercalcemia– HypermagnesemiaHypermagnesemia– HyperkalemiaHyperkalemia– Multiple myelomaMultiple myeloma– Lithium toxicityLithium toxicity

Metabolic AlkalosisMetabolic AlkalosisGeneration by gain of HCO3 and maintained by Generation by gain of HCO3 and maintained by abnormal renal HCO3 absorption. abnormal renal HCO3 absorption. This is almost always secondary to volume contraction This is almost always secondary to volume contraction (low Cl in urine, responsive to NaCl, maintained at (low Cl in urine, responsive to NaCl, maintained at proximal tubule)proximal tubule)– Vomiting: net loss of H+ and gain of HCO3.Vomiting: net loss of H+ and gain of HCO3.– Diuretics: ECFV depletionDiuretics: ECFV depletion– Chronic diarrhea: ECFV depletionChronic diarrhea: ECFV depletion– Profound hypokalemiaProfound hypokalemia– Renal failure: if we cannot filter HCO3 we cannot excrete it. Renal failure: if we cannot filter HCO3 we cannot excrete it.

Mineralocorticoid excess: increased H secretion, Mineralocorticoid excess: increased H secretion, hypokalemia (Na/K exchanger), saline resistant).hypokalemia (Na/K exchanger), saline resistant).

Respiratory AcidosisRespiratory Acidosis

Acute or Chronic: has the kidney had Acute or Chronic: has the kidney had enough time to partially compensate? enough time to partially compensate?

The source of the BUFFER (we need to The source of the BUFFER (we need to produce bicarb) is different in these states produce bicarb) is different in these states and thus we need to make this distinction. and thus we need to make this distinction.

Respiratory AcidosisRespiratory Acidosis

Acute : H is titrated by non HCO3 organic tissue Acute : H is titrated by non HCO3 organic tissue buffers. Hb is an example. The kidney has little buffers. Hb is an example. The kidney has little involvement in this phase. involvement in this phase. – 10 mm Hg increase in CO2 / pH should decrease by .0810 mm Hg increase in CO2 / pH should decrease by .08

Chronic: The mechanism here is the renal synthesis Chronic: The mechanism here is the renal synthesis and retention of bicarbonate. As HCO3 is added to and retention of bicarbonate. As HCO3 is added to the blood we see that [Cl] will decrease to balance the blood we see that [Cl] will decrease to balance charges. charges. – This is the hypochloremia of chronic metabolic acidosis. This is the hypochloremia of chronic metabolic acidosis. – 10 mm H increase in CO2 / pH should decrease by .0310 mm H increase in CO2 / pH should decrease by .03

Respiratory AcidosisRespiratory AcidosisElevation of CO2 above normal with a drop in Elevation of CO2 above normal with a drop in extracellular pH. extracellular pH. This is a disorder of ventilation. This is a disorder of ventilation. Rate of CO2 elimination is lower than the Rate of CO2 elimination is lower than the productionproduction5 main categories: 5 main categories: – CNS depressionCNS depression– Pleural diseasePleural disease– Lung diseases such as COPD and ARDSLung diseases such as COPD and ARDS– Musculoskeletal disordersMusculoskeletal disorders– Compensatory mechanism for metabolic alkalosisCompensatory mechanism for metabolic alkalosis

Respiratory AlkalosisRespiratory AlkalosisInitiated by a fall in the CO2 Initiated by a fall in the CO2 activate processes which activate processes which lower HCO3. lower HCO3. Associated with mild hypokalemia. Cl is retained to offset Associated with mild hypokalemia. Cl is retained to offset the loss of HCO3 negative charge. the loss of HCO3 negative charge. Acute response is independent of renal HCO3 wasting. The Acute response is independent of renal HCO3 wasting. The chronic compensation is governed by renal HCO3 wasting. chronic compensation is governed by renal HCO3 wasting. CausesCauses– Intracerebral hemorrhageIntracerebral hemorrhage– Drug use : salicylates and progesteroneDrug use : salicylates and progesterone– Decreased lung compliance AnxietyDecreased lung compliance Anxiety– Liver cirrhosisLiver cirrhosis– SepsisSepsis

Arterial Blood Gas (ABG) AnalysisArterial Blood Gas (ABG) Analysis

ABG interpretationABG interpretationFollow rules and you will always be right !!Follow rules and you will always be right !!

1) determine PH 1) determine PH acidemia or alkalemiaacidemia or alkalemia

2) calculate the anion gap 2) calculate the anion gap 3) determine Co2 compensation (winters 3) determine Co2 compensation (winters

formula) formula)4) calculate the delta gap (delta HCO3)4) calculate the delta gap (delta HCO3)

ABG analysisABG analysis

Arterial Blood Gas (ABG) –interpretationArterial Blood Gas (ABG) –interpretation– Always evaluate PH firstAlways evaluate PH first

Alkalosis – PH > 7.45Alkalosis – PH > 7.45

Acidosis – PH < 7.35Acidosis – PH < 7.35

– Determine anion gap (AG) – AG = NA – (HCO3+ CL)Determine anion gap (AG) – AG = NA – (HCO3+ CL)AG metabolic acidosisAG metabolic acidosis

Non AG acidosis – determined by delta gapNon AG acidosis – determined by delta gap

– Winters formulaWinters formulaCalculates expected PaCO2 for metabolic acidosisCalculates expected PaCO2 for metabolic acidosis

PaCO2 = 1.5 x HCO3 + 8 PaCO2 = 1.5 x HCO3 + 8

ABG analysisABG analysis

Delta gapDelta gap– Delta HCO3 = HCO3 (electrolytes) + change in AGDelta HCO3 = HCO3 (electrolytes) + change in AG

Delta gap < 24 = non AG acidosisDelta gap < 24 = non AG acidosis

Delta gap > 24 = metabolic alkalosisDelta gap > 24 = metabolic alkalosis

– Note: The key to ABG interpretation is Note: The key to ABG interpretation is following the above steps in order.following the above steps in order.

ABG analysisABG analysis

33 y/o with DKA presents with the 33 y/o with DKA presents with the following:following:– Na = 128, Cl = 90, HCO3 = 4, Glucose = 800Na = 128, Cl = 90, HCO3 = 4, Glucose = 800– 7.0/14/90/4/95%7.0/14/90/4/95%– PH = acidemia PH = acidemia – AG = 128 – (90 + 4) = 34AG = 128 – (90 + 4) = 34– Winters formula – 1.5(4) + 8 = 14Winters formula – 1.5(4) + 8 = 14– Delta gap = 4 + (34 – 12) = 26Delta gap = 4 + (34 – 12) = 26

ABG analysisABG analysis

AnswerAnswer– AG acidosis with appropriate respiratory AG acidosis with appropriate respiratory

compensationcompensation

– History c/w ketoacidosis secondary to DKA History c/w ketoacidosis secondary to DKA with appropriate respiratory compensationwith appropriate respiratory compensation

ABG analysisABG analysis

56 y/o with COPD exacerbation and hypotension 56 y/o with COPD exacerbation and hypotension and associated diarrhea x 7 days presents with and associated diarrhea x 7 days presents with the following ABG:the following ABG:– 7.22/30/65/10/90% 7.22/30/65/10/90%

PH(7.22) = acidemiaPH(7.22) = acidemiaAG = 139 – (10 + 110) = 19 (nl AG = 8-12)AG = 139 – (10 + 110) = 19 (nl AG = 8-12)Winters formulaWinters formula

– PaCO2 = 1.5 (HCO3) + 8 = 1.5 (10) + 8 = 23PaCO2 = 1.5 (HCO3) + 8 = 1.5 (10) + 8 = 23

Delta gap Delta gap – Delta gap = HC03 + change in the AG = 24Delta gap = HC03 + change in the AG = 24– Delta gap = 10 + (19 – 12) = 10 + 7 = 17Delta gap = 10 + (19 – 12) = 10 + 7 = 17– Delta gap = 17Delta gap = 17

1394.0

11010

201.5

120

ABG - exampleABG - example

Triple disorderTriple disorder– AG acidosis - AG acidosis - – Incomplete respiratory compensationIncomplete respiratory compensation– Non AG acidosisNon AG acidosis

History would suggest AG acidosis is secondary to History would suggest AG acidosis is secondary to hypotension with lactic acid build up and the patient is not hypotension with lactic acid build up and the patient is not able to compensate with his COPD therefore there is no able to compensate with his COPD therefore there is no respiratory compensation and the non AG acidosis is respiratory compensation and the non AG acidosis is secondary to diarrhea with associated HCO3 loss.secondary to diarrhea with associated HCO3 loss.

Look at the pHLook at the pH. . – pH < 7.35, acidosispH < 7.35, acidosis– pH > 7.45, alkalosispH > 7.45, alkalosis

Look at PCO2, HCO3- Look at PCO2, HCO3- • Main pathology will be the change correlates with the Main pathology will be the change correlates with the

pH.pH.• If alkalosis pCO2 will be low or Bicarb highIf alkalosis pCO2 will be low or Bicarb high• If acidosis pCO2 will be high or Bicard lowIf acidosis pCO2 will be high or Bicard low• The other abnormal parameter is the compensator The other abnormal parameter is the compensator

responseresponseRespiratory or MetabolicRespiratory or Metabolic

• pCO2 - respiratorypCO2 - respiratory• Bicarb - metabolicBicarb - metabolic

Metabolic Acidosis? Anion Gap?Metabolic Acidosis? Anion Gap?• >12 - ketoacidosis, uremia, lactic acidosis, or >12 - ketoacidosis, uremia, lactic acidosis, or

toxinstoxins• Delta ratio to check for gap and non gap disorders Delta ratio to check for gap and non gap disorders

, or metabolic alkalosis happening simultaneously, or metabolic alkalosis happening simultaneously• Normal anion gap - diarrhea OR unknown. If Normal anion gap - diarrhea OR unknown. If

unknown calculate urine anion gap, if positive unknown calculate urine anion gap, if positive likely RTA, if neg liekly diarrhealikely RTA, if neg liekly diarrhea

Metabolic AlkalosisMetabolic AlkalosisIf urin Cl is > 20 it is chloride-resistant alkalosis If urin Cl is > 20 it is chloride-resistant alkalosis

(increased mineralcorticoid activity(increased mineralcorticoid activityIf <20 chloride responsive alkalosis (vomitting or If <20 chloride responsive alkalosis (vomitting or

gastric loss)gastric loss)

Example # 1Example # 1

44 yo M 2 weeks post-op from total 44 yo M 2 weeks post-op from total proctocolectomy for ulcerative colitis.proctocolectomy for ulcerative colitis.

Na+ 134, K+ 2.9, Cl- 108, HCO3- 16, Na+ 134, K+ 2.9, Cl- 108, HCO3- 16, BUN 31, Cr 1.5BUN 31, Cr 1.5

BG: 7.31/ 33 /93 / 16 BG: 7.31/ 33 /93 / 16

Example #2Example #2

9 yo M presents with N/V.9 yo M presents with N/V.

Na 132 , K 6.0, Cl 93, HCO3- 11 Na 132 , K 6.0, Cl 93, HCO3- 11 glucose 650glucose 650

BG: 7.27/23/96/11/-8BG: 7.27/23/96/11/-8

Example #3Example #3

70 yo M s/p lap chole, on the 70 yo M s/p lap chole, on the morning of POD #1. Pt received 2L morning of POD #1. Pt received 2L bolus of crystalloid throughout pm bolus of crystalloid throughout pm for tachycardia. Now with SOB. for tachycardia. Now with SOB.

7.24 / 60 / 52 / 27 /+37.24 / 60 / 52 / 27 /+3

Example #4Example #4

54 yo F s/p mult debridements for 54 yo F s/p mult debridements for necrotizing fasciitis, now on vassopressin necrotizing fasciitis, now on vassopressin to maintain blood pressureto maintain blood pressure

BG - BG - 7.29/40/83/17/-67.29/40/83/17/-6

Example #5Example #5

35 yo M involved in crush injury, boulder 35 yo M involved in crush injury, boulder vs body. vs body.

Na 135 , K 5.0, Cl 98, HCO3- 15 BUN Na 135 , K 5.0, Cl 98, HCO3- 15 BUN 38, Cr 1.7, CK 42,34638, Cr 1.7, CK 42,346

BG: BG: 7.30/32/96/15/-47.30/32/96/15/-4

Example #6Example #6

4 wks M with projectile emesis4 wks M with projectile emesis

Na: 140, K:2.9, Cl: 92 Na: 140, K:2.9, Cl: 92

7.49/40/98/30/+67.49/40/98/30/+6