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MS2 Renal > 9/9- Physiology of Metabolic Acidosis and Alkalosis I & II > Flashcards

9/9- Physiology of Metabolic Acidosis and Alkalosis I & II Flashcards

1
Q

What is the difference between acidemia and acidosis? (or alkalosis and alkalemia)

A

Acidosis is the process while acidemia is the net result of all “processes” (the same pt can have acidosis and alkalosis at the same time)

  • Acidemia is only clear when you known the pH in ABG
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2
Q

pH values for acidemia? alkalemia?

A

Acidemia: pH under 7.35

Alkalemia: pH > 7.45

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3
Q

What are some consequences of acidemia (in terms of O2 affinity and also systemic effects?)

A
  • Hgb has increased O2 affinity
  • Impairs bone structure and formation
  • Decreased contractility of myocardium
  • Decreased excitability of the brain: Metabolic Encephalopathy
  • Decreased peripheral vascular resistance
  • Increased K+ levels – cellular shifts
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4
Q

What are some consequences of alkalemia (in terms of O2 affinity and also systemic effects?)

A
  • Hgb binds O2 avidly
  • Decreased respiratory center causing hypoventilation
  • Decreased ionized Ca++ results in weakness
  • Decreased K+ by cellular shifts

Increased irritability:

  • Myocardium: arrhythmias
  • CNS: seizures
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5
Q

When do you apply the concept of anion gap?

A

Metabolic acidosis

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6
Q

What is the anion gap?

A

Na + unmeasured cations = Cl + HCO3 + unmeasured anions

Na - (Cl + HCO3) = UMA - UMC = AG

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7
Q

Ex)

  • pH = 7.13
  • Na = 140
  • Cl = 105
  • HCO3 = 5

What is AG?

A

AG = Na - (Cl + HCO3)

AG = 140 - (105 + 5) AG = 30 (high)

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8
Q

What is pathogenesis of metabolic acidosis?

A

(From acid accumulation or low bicarbonate)

Normal acid production:

  • Under excretion of acid (kidney failure)
  • HCO3 wasting (renal, GI)

Excess acid production:

  • Endogenous acid (lactate, ketones)
  • Exogenous acid (salicylates, methanol, ethylene glycol, proylene glycol, acetaminophen)
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9
Q

What are chemical hallmarks of high AG metabolic acidosis?

Pathogenesis?

A

Hallmarks:

  • Acid accumulation
  • Low bicarbonate

Pathogenesis:

Normal acid production:

  • Kidney failure -> underexcretion of acid

Excess acid production:

  • Endogenous acid (lactate, ketones)
  • Exogenous acid (salicylates, methanol, ethylene glycol, proylene glycol, acetaminophen)
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10
Q

What are chemical hallmarks of normal AG metabolic acidosis?

Pathogenesis?

A

Hallmarks:

  • Loss of bicarbonate as sodium bicarb
  • Sodium reabsorbed as sodium “chloride”
  • High Cl
  • Low bicarb compensated by high chloride

Pathogenesis:

Normal acid production:

  • HCO3 wasting (renal, GI)
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11
Q

Case)

Frustrated by this acid-base talk, a medical student flies to Cancun for a break

  • drinks tap water
  • diarrhea
  • On exam: PR 120/mt, BP 80/40.
  • pH 7.26, pCO2 24, HCO3- 10
  • Na 133, K 2.1, Cl 112 and HCO3 11

Analyze

A
  • pH is low; acidemia
  • Low K (lost in diarrhea)
  • AG = 133 - (11 + 112) = 10 (normal)

This is normal AG metabolic acidosis from diarrhea

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12
Q

Summary of causes of metabolic acidosis

A
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13
Q

How can you calculate osmolarity?

A

Osm = 2Na + BUN/2.8 + glucose/18

(Osm in mmol/L and glucose in mg/dL)

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14
Q

Stepwise approach for acid-base problems?

A
  • Look at pH (acidemia or alkalemia?)
  • Determine if metabolic (HCO3 problem) or respiratory (PCO2 problem)
  • AG and calculate delta AG
  • Delta bicarbonate
  • Adequate compensation?
  • Simple vs. mixed
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15
Q

What is the equation for delta anion gap?

What does delta AG reflect?

A

Pt AG - Normal AG

Normal AG ~ 10

Delta AG indicates how much bicarbonate fell

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16
Q

Delta AG is equal to what?

A

Delta bicarbonate

17
Q

What is the equation for delta bicarbonate?

What does it reflect?

A

Delta bicarbonate = 24 - pt’s bicarbonate

In simple high anion gap metabolic acidosis: Delta AG = Delta bicarbonate

In other terms: Initial HCO3 = Delta AG + pts HCO3

18
Q

What is the expected pCO2 in terms of compensation? (For metabolic acidosis)

A

Expected pCO2 = (HCO3 x 1.5) + 8 +/- 2

(Winter’s formula)

19
Q

In metabolic acidosis, if HCO3 is 10, what is expected PCO2?

A

EpCO2 = (10 x 1.5) + 8 +/- 2

= 21 -25 mmHg

20
Q

What do the possible PCO2 values tell you about compensation (for metabolic acidosis)?

A

- PCO2 under 20: lungs hyperventilating; also has primary* respiratory alkalosis

- PCO2 21-25: just right

- PCO2 > 25: lungs hypoventilating; also has primary* respiratory acidosis

21
Q

Example)

  • 25 yo man consumes ethylene glycol and takes overdose of “sleeping pills” ABG:
  • pH under 7
  • pCO2 = 25
  • HCO3 = 5
  • Na = 140
  • Cl = 105
  • HCO3 = 5

Analayze

A
  • Acidosis
  • AG = 140 - (105+5) = 30 (high)
  • Delta AG = 30 - 10 = 20
  • Delta bicarbonate = 24 - 5 = 19
  • Delta mismatch? No
  • expected PCO2 = (5 x 1.5) + 8 +/- 2 = 13.5 - 17.5; not compensated!

This is high AG metabolic acidosis + respiratory acidosis

22
Q

Example)

  • Na 136
  • HCO3 8
  • Cl 108
  • pH 7.44
  • PaCO2 12

Analyze

A
  • Normal pH - AG = 136
  • (8 + 108) = 20 (high)
  • Delta AG = 20 - 10
  • Delta bicarbonate = 24 - 8 = 16
  • Delta mismatch? Yes
  • Expected PCO2 = (8 x 1.5) + 8 +/- 2 = 18 -22

This is:

- High AG metabolic acidosis

- Non AG metabolic acidosis

- Respiratory alkalosis

Could be due to: ARF + diarrhea + sepsis

23
Q

T/F: A secondary response can bring the pH back to normal.

A

False!

Under NO circumstances, can a secondary response bring the pH back to normal. If the patient is normal, either:

  • Pt is normal - Mixed disorder
24
Q

What can cause lactic acidosis?

A

Type A: poor tissue perfusion

  • Shock/circulatory failure
  • Mitochondrial enzyme defect

Type B: adequate perfusion

  • Malignancies
  • Liver/renal failure
  • Seizures
  • Drugs
25
Q

What is therapy for lactic acidosis?

A
  • Treat underlying condition: restore perfusion
  • Bicarb therapy: if pH is under 7.1
  • Enough bicarbonate to increase pH to 7.2: lactate is “potential” bicarbonate once underlying condition is treated (risk of overshoot alkalosis)
26
Q

Fun fact: in mild to moderate metabolic acidosis (7.1ish- 7.35), you expect the last 2 digits of your pH to be roughly equal to your pCO2 if it is compensated (not confirmative, but rough idea)

A

Ex)

  • pH = 7.26
  • pCO2 = 24

Compensated metabolic acidosis

27
Q

What can cause ketoacidosis (broadly)?

A
  • Diabetes mellitus
  • Alcoholism
28
Q

Pathogenesis of DM ketoacidosis?

  • What is seen on dipstick?
  • Treatment?
A
  • Insulin deficiency AND any stress like infection, MI etc
  • Dipstick picks up ONLY acetoacetate (not beta- OH-B)
  • Bicarbonate used only with severe acidemia
  • Ketones are “potential” bicarbonate
29
Q

Pathogenesis of alcoholic ketoacidosis?

  • What is seen on dipstick?
  • Treatment?
A
  • Predominantly beta-OH-B: not strongly (+) on dipstick
  • Hypoglycemia, insulin low
  • Treatment: volume replacement with saline and glucose.
30
Q

Pathogenesis of ethylene glycol causing metabolic acidosis?

  • Diagnosis?
  • Treatment?
A
  • Metabolized to oxalic acid, glycolic acid, lactic acid, and other acids

Gaps to remember:

  • EG (before metabolism) causes “osmolar” gap
  • Metabolites cause “anion” gap with acidosis

Diagnosis:

  • Wood’s lamp of urine detects fluorescence that was added to anti-freeze (in which ethylene glycol is used)

Treatment:

  • Fluids, thiamine, etc.
  • Fomepizole or ethanol (alcohol dehydrogenase)
  • Dialysis
31
Q

What is seen in the pH, serum bicarb, and PCO2 with metabolic alkalosis?

A
  • Increased arterial pH (pH > 7.45)
  • High serum bicarbonate
  • High PCO2 due to compensation
32
Q

Recall: What are the consequences of alkalemia (systemically)?

A
  • Hgb binds O2 avidly -> less O2 released to tissues
  • Decreased respiratory center -> hypoventilation

Increased irritability:

  • Myocardium: arrhythmias
  • CNS: seizures

Also:

  • Decreased ionized Ca++ -> weakness
  • Decreased K+ by cellular shifts
33
Q

What ion transport is occurring in Type A Intercalated Cells?

A

Volume contraction -> Aldosterone -> more H-ATPase action (excreting H from cell into tubular lumen)

K depletion -> increased NH3, which combines with H in tubular lumen -> NH4 excreted in urine

K depletion -> increased H-K-ATPase, getting K into the cell and H into tubular lumen

34
Q

What are causes of metabolic alkalosis?

A
  • Exogenous bicarbonate load: alkali therapy

- Loss of acid: vomiting (HCl loss), NG suction, etc.

- Decreased ECF volume/normal BP (sec hyperaldosterone)

—- Renal: diuretics/Bartter’s and Gitelman syndrome

- ECF expansion/hypertension

—- Mineralocorticoid excess (renal artery stenosis/primary aldosterone excess/adrenal enzyme defects/Cushing’s, etc.)

—- Low mineralocorticoid: Liddle’s syndrome

(Diuretics: alkali-free fluid lost in urine: concentration of bicarbonate increases)

35
Q

Maintenance phase of alkalosis involves what?

A

- Persistent hyperaldosterone state/continued acid loss or alkali therapy

- Chloride depletion:

—- H loss in Type A intercalated cells

—- Alkali retention in Type B cells

36
Q

How does chloride deficiency and H secretion (bicarb retention) affect Type A intercalated cells?

A
  • Less H-ATPase function (excreting Cl into tubular lumen instead??)
37
Q

How does chloride deficiency and H secretion (bicarb retention) affect Type B intercalated cells?

A
  • HCO3-Cl exchange (main drive is Cl concentration gradient) sending Cl into cell and bicarb into tubular lumen
38
Q

Treatment of metabolic alkalosis?

A

If volume contracted: “Chloride-sensitive”
- Replenish volume with normal saline

If volume overloaded and ECF expanded

  • Treat primary disorder that resulted in high renin and aldosterone state
  • “Chloride insensitive”
  • Replace K+

MS2 Renal (25 decks)

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