acid/base it’s all about… - ceconsultants,...

9/13/12

Clin J Am Soc Nephrol 3: 554-561, 2008 1

Dilemmas in the Diagnosis & Management of Acid Base

Disorders

Paula Dennen, MD Assistant Professor of Medicine

Nephrology and Critical Care Medicine September 27, 2012

Background

Acid/Base

It’s all about…

pH

Acid Base

Balance

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Acid Base Balance:

  DEFINITION: Simply the maintenance of a normal hydrogen ion concentration

pH Acid Base

Balance

Acid Base Balance

  What is a normal hydrogen ion concentration?

  40 nMol   (1/1,000,000,000 of a mole vs. mMol which is

1/1,000 of a mole)

  0.00004 mEq/L (pretty small amount!)

Definitions: “emia” vs “osis”

  “osis” is the process   Metabolic alkalosis

  Metabolic acidosis

  Respiratory alkalosis

  Respiratory acidosis

  “emia” is the actual pH of the blood   Acidemia   Alkalemia

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Acid Base Basics

  Interpretation: need ABG (or VBG*) & Chem 7   ABG

  Measured: pH, pCO2, pO2

  Calculated: HCO3-, O2 sat

  Chem 7 total CO2 includes dissolved CO2, H2CO3 and HCO3

- (mostly HCO3-)

  About 2mmol/L difference between ABG & Chem 7

  *VBG – pH ~ 0.03 lower, pCO2 ~ 6 higher   “Pretty good”   Underutilized for pH and pCO2

Acid Base Basics: “4” Step Approach   Step 1 Calculate anion gap

  IF anion gap, calculate ΔΔ (potential bicarb)

  Step 2 Look at the pH (ABG or VBG)   > 7.4 alkalemia   < 7.4 acidemia

  Step 3 Look at HCO3-

  If pH & HCO3- same direction, 1° metabolic

  If pH & HCO3- opposite direction, 1° respiratory

  Acute or chronic

  Step 4 Evaluate compensation

Compensation

HCO3- Controlled

by the kidneys CO2 Controlled by

the lungs

Normal HCO3- 24 mEq/L Normal pCO2

40 mmHg

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Remember: Compensation is ALWAYS in the same direction as the primary

change!!

Compensation

  Metabolic acidosis   Expected pCO2 = 1.5 x HCO3

- + 8 ± 2

  Metabolic alkalosis   Expected pCO2 = (0.7 x HCO3

-) + 20 ± 2

  Respiratory acidosis   ↑ HCO3

-: ↑ pCO2, acute* 1:10, chronic** 3:10

  Respiratory alkalosis   ↓ HCO3

-: ↓ pCO2, acute* 2:10, chronic** 4:10

* Acute: before full renal compensation; **Chronic:after full renal compensation

Compensation:

Renal compensation 2-3 day delay…

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Metabolic Acidosis

Anion Gap vs Non Anion Gap

Metabolic Acidosis

? Is it bicarbonate loss (NAGMA) or

? Is it gain of acid (AGMA) (bicarbonate

consumption)

H+ + HCO3- H2CO3 H2O + CO2

H+ + HCO3- H2CO3 H2O + CO2

Non Anion Gap Metabolic Acidosis (NAGMA)

Loss of Bicarbonate

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Metabolic Acidosis: NAGMA

? Blame the kidney Or blame the gut…

The normal anion gap

=

Na – (HCO3- + Cl-) = 12*

Normally,

*Adjust downward by 2.5 for every 1 mg/dL decrease in albumin

Remember…we are electroneutral!

Daily Acid Load

  Product of dietary protein & cellular metabolism

  Acids produced: sulfuric & phosphoric acid, etc.

  Estimated 1 mmol/kg/day (50-100mmol/day)

  50-100 meq of H+ buffered daily

  HCO3- lost during buffering, replaced in distal

nephron

  If bicarbonate production impaired, NAGMA occurs

  Anions of daily load are excreted ( IF normal kidney function) therefore AG is normal

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“Blame the Kidney”: RTAs Key Points

  Diagnosis: kidney function must be normal

  Mechanism: disorders of impaired tubular function

  Consequence: systemic metabolic acidosis due to an inability of the kidney to handle the daily acid load

  UAG:   unreliable when urine pH > 6.5 or when other measured

anions such as ketones or unmeasured anions (lithium) are present

  Tracks unmeasured cations (like NH4+) vs. unmeasured

anions (serum anion gap)

Proximal RTA: Type II

  Reduced Tm for HCO3-

  Distal tubule function normal

  Hypokalemia is common   Lose K+ with HCO3

-

  Treatment: lots and lots of bicarbonate

  Acetazolamide (Diamox) essentially produces a proximal RTA

  Wastes HCO3- and K+

Distal RTA: Type I

  problem with urine acidification

  Positive urine anion gap (UAG)

  Urine pH ≥ 5.5

  Defect in H+ secretion

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Hyperkalemic RTA – Type 4

  Problem of NH3 production   Hyperkalemia   Hypoaldosteronism contributes

  Not a problem of acidifying the urine

  Urine pH can be <5.5

  Urine anion gap (UAG) is positive

Hyperkalemic RTA, secondary

  Mineralocorticoid deficiency   Addison disease, DM

  Mineralocorticoid resistance   Interstitial nephritis

  Drug induced   ACE-I, COX inhibitors, heparin   K sparing diuretics, trimethoprim   Beta-blockers

NAGMA in CKD   Problem is NOT decreased tubular function

  Problem is decreased functioning nephrons (tubules)

  “over function” to compensate

  As CKD progresses functioning nephrons increase amount of NH3 they make

  Eventually (GFR ~ 30 to 40)

  reduction in functioning nephrons exceeds ability of remaining nephrons to compensate

  daily acid load (~ 1meq/kg/day) cannot be excreted

  systemic acidosis occurs

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Cases

Case #1 50 yo with stage 4 CKD (75kg) admitted with 5 day history of diarrhea 2 weeks after being hospitalized for PNA. c/o SOB. Serum Alb 3.2

131 112

3.0 10

40

3.2 94

7.1/40/75/10 on 2L NC

What acid/base disturbance(s) are present? (choose all that apply)

1.  AGMA 2.  Metabolic alkalosis 3.  NAGMA 4.  Respiratory acidosis 5.  Respiratory alkalosis

Acid Base Basics: “4” Step Approach

  Step 1 Calculate anion gap   IF anion gap, calculate ΔΔ (potential bicarb)

  Na – (HCO3- + Cl-) =

  131 – (10 + 112) = 9   Corrected AG (~ 3 x 3.2 = 9.6)

  NAGMA   “blame the kidney” (history of diarrhea)

  Note…UAG not helpful in CKD

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  Step 2 Look at the pH (ABG or VBG)   < 7.4 acidemia



  Step 4 Evaluate compensation   Expected pCO2 = 1.5 x HCO3

- + 8 ± 2   Expected pCO2 = 1.5 x 10 + 8 ± 2 = 21-25   Respiratory Acidosis (pCO2 = 40 = inappropriate

respiratory compensation)

Case #1 continued… 50 yo with stage 4 CKD (75kg) admitted with 5 day history of diarrhea 2 weeks after being hospitalized for PNA. c/o SOB. Serum Alb 3.2

131 112

3.0 10

40

3.2 94

7.1/40/75/10 on 2L NC

What acid/base disturbance(s) are present? (choose all that apply)

1.  AGMA 2.  Metabolic alkalosis 3.  NAGMA 4.  Respiratory acidosis 5.  Respiratory alkalosis

Case #1   Would you give bicarbonate?   Why?

  Symptomatic (SOB, can’t compensate)   Ongoing loss   Unable to “generate” bicarb with CKD

  How would you give it?   Calculate & replace deficit IV   Continue 1meq/kg PO after repleted for CKD

  What should you do before giving bicarbonate?   Replace potassium   Check ionized Ca++ & replace if low

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Case #1: HCO3- deficit

  How much HCO3- should be given to raise the

HCO3- to 15? To 20?

  mEq HCO3- = weight x ∆ HCO3 x bicarb space

= 75 kg x 5 mmol/L x 0.5 = 187.5 mmol (goal 15) = 375 mmol (goal 20)

7.1 / 40 / 75 / 10 pH / pCO2 / pO2 / HCO3

Bicarb Replacement (for NAGMA)

  1 amp of HCO3- is 50 mmol of Na+ & 50 mmol of HCO3

-

  3 amps in a liter of D5W:   Na+ of 150 mEq/1150 mL or 130 mEq/L   Can leave out the D if hyperglycemic

  2 amps in 1L 1/4NS:   Na+ of 38 + 100 / 1100 mL or 125 mEq/L

  NaHCO3- tablets – 7meq per 650mg tablet

  Example – deficit ~ 200 meq (+ “losses”) = 28 tabs/day   Useful for maintenance of 1meq/kg/day

  Tough for replacement!

Case #2

Mr. V is a 75 yo male with a 2 day h/o N/V admitted with septic shock 2/2 aspiration pneumonia (on vasopressors), respiratory failure and oligoanuric AKI (albumin 3.3).

134

6

90

2.5

70

24

7.2/60/75/22 on 100% NRB

Lactate 6

140

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Case #2

What acid/base abnormalities does he have? (choose all that apply)

1)  AGMA

2)  Metabolic Alkalosis

3)  Respiratory Acidosis

4)  NAGMA


  Step 1 Calculate anion gap   IF anion gap, calculate ΔΔ (potential bicarb)

  Na – (HCO3- + Cl-) =

  134 – (24 + 90) = 20

  AGMA

ΔΔ “AKA” Potential Bicarbonate

  Potential or Corrected HCO3- -> what would the

HCO3- have been without the AGMA?

  Measured HCO3- +(delta gap)= 24 + 10 (20-10) = 34

  If > 24 then metabolic alkalosis present

  If < 24 then NAGMA present

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  Step 2 Look at the pH (ABG or VBG)   < 7.4 acidemia



  Step 4 Evaluate compensation   Expected pCO2 = 1.5 x HCO3

- + 8 ± 2   Expected pCO2 = 1.5 x 24 + 8 ± 2 = 42-46   Respiratory Acidosis (pCO2 = 60 = inappropriate

respiratory compensation)

Case #2

What acid/base abnormalities does he have? (choose all that apply)

1)  AGMA

2)  Metabolic Alkalosis

3)  Respiratory Acidosis

4)  NAGMA

Triple Acid/Base Disorder

Case #2 Key Points -> Always… ● Calculate the anion gap ● Look for concomitant NAGMA or met alkalosis ● Look for appropriate respiratory compensation

134

6

90

2.5

70

24

7.2/50/75/22 on 100% NRB

Lactate 6

140

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Anion Gap Metabolic Acidosis (AGMA)

Gain of Acid

What is the Acid?

AGMA: Gain of H+Anions-   Metabolism

  Starvation (ketones)   DKA (ketones)

  Ingestions   Ethylene glycol (-> -> glycolic acid -> -> oxalic acid)   Methanol (formaldehyde -> formic acid)   Ethanol (ketones) (also lactic acid if “too much substrate”)   Aspirin (Acetylsalicylic acid -> salicylic acid)

  Hypoperfusion and Hypoxia (Lactic acid)

  Renal failure (sulfate, urate, phosphate, hippurate…)   MUDPILES or whatever works for you…

What about an AGMA is bad for you? AKA: Why do we care?

  The anion?

  The H+?

  The disease?

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“Bad” Anions: Methanol

  Methanol (Sterno, shellac, varnish, de-icing)

HC3 – OH H – C – H

= O

Alcohol dehydrogenase

Methanol Formaldehyde Formic acid

H – C – OH

= O

Fomepizole or ethanol Hemodialysis Hemodialysis Rx:

“Bad” Anions: EG

  Ethylene glycol (EG) (antifreeze, solvents)

H2C

Alcoho

l

dehy

drog

enas

e

Ethylene glycol

Glyco- aldehyde

Oxalic acid

Fomepizole or ethanol Hemodialysis Rx:

HO

HO

H2C

–

–

–

Glycolic acid

Glycoxalic acid

– H

= O

C

H2C

–

HO

–

– OH

= O

C

H2C

–

HO

–

H – = O

C

– OH

= O

C

–

HO – = O C

– OH

= O

C

–

Ethylene Glycol

  Not itself toxic   Converted to toxic metabolites   Dependent on alcohol dehydrogenase   Suspect in a patient with AGMA & osmolar gap

  MW is 62, small amount can increase osmolar gap

  Symptoms: AMS, tachypnea, pulm edema…   Renal failure is a LATE finding

  Toxic effects of glycolic acid on tubules   Oxalic acid crystalizes in tubules

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Serum Osmolality   Osmolality = Osmoles/kg of water

  What makes of serum osmolality?

2 (Na+) + Glucose/18 + BUN/2.8

  Normal serum osmolality is 285-295   Kidney runs a pretty tight ship!

  Osmolar Gap = Osmmeasured – Osmcalculated

  Normal ~ 10

+ Ethanol/4.6

To convert mg/dL to mmol/L:

Divide by the molecular weight and multiply by 10

Osmolar Gap…

MW Example concentration

Contribution to osmolality

Methanol 32 80 mg/dL 25 mMol

Ethylene glycol

62 80 mg/dL 13 mMol

Salicylic acid

180 50 mg/dL 3 mMol

Ethanol 46 100 mg/dL 22 mMol

Osmolar Gap…   Classic workup

  Ethanol   Ethylene glycol   Methanol   Isopropyl alcohol

  What else increases it   DKA or alcoholic ketoacidosis   Lactic acidosis   Chronic renal failure   Mannitol infusion   Hypertriglyceridemia

  If no other explanation, or greater than 25 it is suggestive of methanol or ethylene glycol poisoning

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Bad Anions: Salicylates   Aspirin: acetylsalicylic acid

  Active form: salicylic acid   90% protein bound   10% therapeutically active

  At toxic doses:   Limited protein binding   Liver detoxification overwhelmed

  Respiratory alkalosis (brain stimulation)   Often the 1st sign

  AG metabolic acidosis 50 mg/dL of salicylic acid (MW 180) is 3 mEq/L

Bad Anions: Salicylcates

Salicylate anion: S- (impermeable to cell membranes)

Salicylic acid: HS (freely crosses cell membranes)

H+ + S- HS

Ion trapping: Alkalinizing the serum and the urine increases the formation of S- which allows elimination of the drug

CAUTION: risk of bicarbonate is severe alkalemia (mixed respiratory and metabolic) (Resp alkalosis: 1st acid/base disturbance seen in salicylate toxicity)

Non-toxic Anions: Ketones

  Ketones:

  Alternate fuel when glucose is scarce   Starvation, DKA, alcohol

  Produced in the liver from triglycerides

  Beta-hydroxybuterate, acetoacetate, acetone

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Lactate

  1400 mmol produced daily

  Production of lactic acid from pyruvate via lactate dehydrogenase yields NAD+ for glycolysis

  Buffered by bicarbonate to form lactate

  Liver oxidizes lactate to form bicarbonate

  Kidney responsible for 10 to 20% of lactate removal

  Generation increases when glucose or glycogen are required to generate ATP in the absence of oxygen

Lactate Clearance   Conversion to Bicarbonate

  Clearance Elevated Lactate due to

  Decreased metabolism

  Decreased Clearance

  Increased production

  Combination of above

Lactic Acidosis

  Absence of mitochondrial function from

  Tissue hypoxia (Type A)

  Impaired mitochondrial oxygen utilization (Type B)   (cyanide, metformin, thiamine deficiency)

  Mortality is 60 to 90%

  Sepsis is most common cause

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Lactic Acidosis: Causes   Type B

  Propylene glycol

  Nitroprusside

  Metformin

  Malignancies

  Lymphoma, leukemia

  Liver failure

  Ingestions…

  Type A

  Sepsis

  Ischemia

  Hypoperfusion

  Seizures

  Exercise

Reminder…Case #2 cont’d

Mr. V is a 75 yo male with a 2 day h/o N/V admitted with septic shock 2/2 aspiration pneumonia (on vasopressors), respiratory failure and oligoanuric AKI (albumin 3.3).

134

6

90

2.5

70

24

7.2/60/75/22 on 100% NRB

Lactate 6

140

Case #2

After 6L volume resuscitation with IVNS his ABG is 7.1/50/100/12 with AGMA 20. Mr. V becomes more obtunded, requires intubation and is initiated on CRRT. The next morning he has an increase in his vasopressor requirement.

What do you expect his pH to be on his AM ABG?

Why does he have an increased pressor requirement?

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Case #2 What is his most likely pH on his AM ABG?

1.  7.15 2.  7.32 3.  7.40 4.  7.58 5.  7.7

CAUTION: Don’t forget to adjust the vent (minute ventilation) as the metabolic acidosis is being corrected!

(cuz CRRT is just that good)

Mixed respiratory and metabolic alkalosis

Case #2 Why an increased pressor requirement?

1.  Worsening sepsis 2.  Volume Depletion 3.  Hypocalcemia 4.  Tension pneumothorax 5.  Bleeding

CAUTION: free or ionized calcium drops with alkalemia which can lead to clinically significant hypotension

Bicarbonate and Calcium

  Data from ICU patients with lactic acidosis

  Given 2 mEq/kg of NaHCO3 or saline

  pH from 7.22 to 7.36   Ionized calcium fell

8.5% (from .95 to 0.87)   pH correction vs.

hypocalcemia effect on cardiac contractility

Cooper, DJ et al, Annals 1990;112:492-8.

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Calcium

  HCO3- binds Ca++ decreasing ionized or

“available” calcium

  IF Ca++ is low and patient is acidemic, IMPORTANT to correct Ca++ as reversal of acidemia will decrease free Ca++

  Similar to K+, IF patient is hypokalemic and acidemic, IMPORTANT to correct hypokalemia before acidemia

Case #3 50 yo with decompensated heart failure on NIPPV for acute hypoxemic respiratory failure 2/2 volume overload and increased work of breathing. Aggressively diuresed on lasix gtt for management of pulmonary edema. After 24 hours on a lasix gtt his urine output drops to 10cc/hr.

What additional information would be helpful?

1) Hemodynamics 2) Serum sodium 3) Serum creatinine 4) Pulmonary pressures 5) All of the above

Case #3

What is the risk of metabolic alkalosis in this patient:

1)  Respiratory depression

2)  Hypoxia due to hypoventilation

3)  Increased affinity of hemoglobin for O2

4)  Hypocalcemia

5)  All of the above

134

30 2.5

89 39 134

1.3 7.5/48/75/29 on 70% 12/5

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Case #3 Based on the previous labs what should be your

next order (s) ? Choose all that apply:

1)  Diamox 500mg IV x 1

2)  Intubation

3)  KCl at 20meq/hr x 6

4)  Check an ionized calcium

5)  Give IVF

Acetazolamide (Diamox)

  Confirm alkalemic pH   Contraindicated for primary respiratory acidosis

  Increases bicarbonate loss in proximal tubule

  CAUTION with hypokalemia   Must replace BEFORE diamox

  CAUTION with hypocalcemia   Must replace BEFORE diamox

  Important to assess volume status   IVF treatment for hypovolemic (chloride

responsive metabolic alkalosis)

Case #4 54 yo female with h/o DM on metformin, schizoaffective D/O, COPD admitted with AMS, lethargy and decreased PO intake per family report. 1st chem 7:

Albumin 2

What acid/base disturbances are present? (choose all that apply)

1)  AGMA 2)  Metabolic alkalosis 3)  NAGMA 4)  Respiratory acidosis 5)  Respiratory alkalosis

129 86

4.5 27

65

10.5 85

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  Na – (HCO3- + Cl-) =

  129 – (27 + 86) = 16

 AGMA   Potential Bicarb

  HCO3- + (delta gap) = 27 + 10 = 37

  If > 24 then metabolic alkalosis present

Case #4 54 yo female with h/o DM on metformin, schizoaffective D/O, COPD admitted with AMS, lethargy and decreased PO intake per family report. 1st chem 7:


1)  AGMA 2)  Metabolic alkalosis 3)  NAGMA 4)  Respiratory acidosis 5)  Respiratory alkalosis

129 86

4.5 27

65

10.5 85

Need an ABG or VBG!

Case #4

  What is the most likely cause of her acid/base disturbances?

  What additional information do you want?   Lactate 1   Albumin 2   Toxic Alcohol Screen Negative   Salicylate negative   Other?

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Case # 4: Labs 24 hours later


1)  AGMA 2)  Metabolic alkalosis 3)  NAGMA 4)  Respiratory acidosis

5)  Respiratory alkalosis

136 108

4.7 12

59

8.2 94



  Na – (HCO3- + Cl-) =

  136 – (12 + 108) = 16

 AGMA   Potential Bicarb

  HCO3- + (delta gap) = 12 + 10 = 22

  If < 24 then NAGMA present

Case # 4: 24 hours later


1)  AGMA 2)  Metabolic alkalosis 3)  NAGMA 4)  Respiratory acidosis

5)  Respiratory alkalosis

136 108

4.7 12

59

8.2 94

Need an ABG or VBG!

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Case #4

  What is the most likely cause of her acid/base disturbances?

  What additional information do you want?

 Serum KETONES  Large!!!

“Normoglycemic” DKA

  Don’t need hyperglycemia to be in DKA

  Be complete in your workup of AGMA

  Don’t let a high bicarbonate mask your AGMA   ALWAYS calculate the anion gap

 Don’t be fooled by “normoglycemic” DKA!

Metformin: MALA Metformin Associated Lactic Acidosis

  Risk Factors   AKI/CKD/elderly

  Symptoms   Lethargy, N/V/abd pain

  Signs   VERY high lactate (Note…lactate was only 1)

  Can be confused with mesenteric ischemia   No hypoglycemia in therapeutic doses but

hypoglycemia seen in toxic doses

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Metformin: MALA

  Decreased lactate uptake by liver and decreased conversion of lactate to glucose

  Can check levels but not very predictive

  Toxicity   Acute AP   Acute on chronic (new med or illness that decreases

clearance)   Chronic – develop other cause of lactic acidosis

(e.g. sepsis), see delayed clearance w/metformin

  Treatment: Dialysis

Case #5 48 yo alcoholic male admitted with N/V/abd pain. Diagnosed with acute pancreatitis. Serum ketones +, toxic alcohol screen negative. Alb 1.6.

139 103

3.3 20

18

0.8 82 7.38/28/75/20 on 4L NC

What acid/base disturbances are present?

1)  Mixed AGMA/NAGMA

2)  Mixed metabolic alkalosis/AGMA/resp acidosis

3)  Mixed AGMA/metabolic alkalosis/respiratory alkalosis

4)  Mixed AGMA/NAGMA/respiratory alkalosis

5)  AGMA with appropriate respiratory compensation

Case # 5 What is the treatment for “non-diabetic” ketosis

(AKA or “starvation”)?

 Glucose! Glucose! Glucose!   Need substrate (i.e. glucose) to clear ketones

  Insulin appropriately suppressed   IV fluids

  Need volume to correct metabolic alkalosis   KCl

  Need K replacement to avoid maintenance of metabolic alkalosis

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Case # 6   32 yo found down at home by roomate. Obtunded

and tachypneic but protecting airway. Foley placed with good UOP. BAL 300, tox screen negative, lactate 20. AG 16. Difficult physical exam due to obtundation. Hemodynamically stable. No other history available?

  What other lab value (s) or imaging studies do you want right away?

Case #6

Which of the following causes of AGMA does NOT cause a severely elevated lactate

1.  Metformin

2.  Ethylene glycol

3.  Methanol

4.  Mesenteric Ischemia

Ethylene Glycol (EG)

  Typically does NOT cause severe lactic acidosis

  Acidosis due to breakdown product   Major toxin is glycoaldehyde   Dependent on alcohol dehydrogenase

  Blocked by ethanol or fomepizole

  Can be masked if elevated BAL

  Don’t forget to use your serum osm

  IMPORTANT: False + lactate 2/2 interference of metabolite of EG in analyzer

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Bicarbonate in AGMA?

Consequences of Acidemia…

  Cardiovascular   Decreased cardiac contractility   Arterial dilatation/venoconstriction   Increased pulmonary vascular resistance   Predisposition to arrhythmias   Decreased response to catecholamines

  Exogenous or endogenous

  Respiratory   Hyperventilation

Consequences of Acidemia…

  Metabolic   Insulin resistance   Inhibition of glycolysis   Reduced ATP synthesis   Hyperkalemia (shfit)

  Cerebral   Altered mental status   Coma

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Acidemia   Does arterial pH reflect tissue pH?

  If blood flow to a tissue decreases 50%   Tissue PCO2 will double   Local intracellular pH will decrease (acidosis)   Arterial pH and PCO2 do not change

  What about mitochondrial pH?   In isolated hepatocytes   Mitochondrial pH gradient did not change when

extracellular pH was lowered from 7.4 to 6.9

Chest 2000; 117:260-267

Respiratory Acidosis

  Elevated pCO2 dilates cerebral vessels

  “Permissive” hypercapnia (e.g. in ARDS) is potentially dangerous and contra-indicated in patients with TBI or CVA   Don’t need hyperventilation but should

avoid hypoventilation

Should I give Bicarbonate?

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Bicarbonate in DKA?

  Can be detrimental in DKA

  Ketones reduce pH, and decreased pH blocks ketogenesis, negative feedback

  Increasing pH turns off the negative feedback, stimulating ketogenesis

  Consensus statement from ADA 2006 recommends bicarb for pH < 6.9 (no prospective study)

Bicarbonate in Lactic Acidosis Why Not?

  Causes CSF acidosis

  Intracellular acidosis

  Impairs oxygen delivery to tissues

  Increases carbon dioxide and worsens acidosis

  Increases lactic acid production

  Worsens hypocalemia

Bicarbonate in Lactic Acidosis Controversial…

  pH < 7.2 ?

  pH < 7.15

  pH < 7.1

  pH < 7

  Who knows?

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Summary of Bicarbonate in Metabolic Acidosis

  Reasonable/recommended to give in disorders where HCO3

- is lost   RTA, diarrhea with severe acidosis

  Acidemia well tolerated in permissive hypercapnea, DKA

  Lactic acidosis   No improvement in hemodynamics   Potentially detrimental – although clinical

significance unknown

What to worry about with bicarbonate administration…

  Alkalemia – know the pH 1st

  Hypokalemia – replete K+ 1st

  Hypocalcemia – replete Ca++ 1st

Take Home Pearls   Acidemia likely better tolerated than we think

  Caution with bicarbonate (watch electrolytes)

  Sometimes treatment worse than condition

  Appreciate integration between metabolic and respiratory physiology (e.g. vent & CRRT)

  Don’t forget the osmolar gap

  Think twice (or 3x) about bicarbonate in AGMA

  Analyze acid/base status in all patients (can uncover other diagnoses)

  Integrate clinical and laboratory data

9/13/12


Email: [email protected]

acid/base it’s all about… - ceconsultants,...

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