Clinical Reasoning Acid Bases

Question 1

First four steps of analyzing an acidotic/alkalotic patient?

Answer 1

1. Acidemia vs. alkalemia - look at their pH, 7.4 is the cutoff 2. Metabolic vs. respiratory - Normal HCO3 is 24, normal pCO2 is 40 3. Is the compensation correct? If respiratory, compare bicarb to expected. If metabolic, compare pCO2 to expected. 4. Is there an elevated anion gap? AG = Na - Cl - Bicarb, we want less than or equal to 12.

Question 2

If the anion gap is elevated, what do we do and what does it mean?

Answer 2

Secondary process as well. 1. If AG = [HCO3-], then the elevated anion gap completely explains the change in bicarbonate, and there is no additional process. 2. If AG > [HCO3-], then the change in bicarbonate is less than the change in anion gap, and there must be an additional metabolic alkalosis present. 3. If AG < [HCO3-], then the change in bicarbonate is greater than the change in anion gap, and there must be an additional non-AG metabolic acidosis present.

Question 3

Henderson hasselbach shortcut

Question 4

Differential diagnoses for metabolic acidoses

Answer 4

If there is an elevated AG:

Renal vs. extrarenal (ingestion, metabolism derangements, etc) Remember MUDPILES here

If NOT an elevated AG:

Renal vs. a GI source specifically

Question 5

Differential diagnoses for metabolic alkaloses

Answer 5

Loss of acid (chloride responsive)

Gain of alkali (chloride unresponsive)

Question 6

Differential diagnoses for respiratory alkaloses

Answer 6

Hyperventilation (hypoxemia vs. central)

Pulmonary disease

Question 7

Differential diagnoses for respiratory acidoses

Answer 7

Airway obstruction

Respiratory depression

Hypoventilation (central vs. musculoskeletal)

Question 8

What is Winter’s Formula and when do we use it?

Answer 8

Metabolic acidosis: use Winter’s formula

Expected pCO2 = 1.5 x [HCO3] + 8 (±2)

if there was ever a formula you should remember, the COL said it should be this one b/c most Pts will clinically present with metabolic acidosis

Question 9

Formula we use for projected change in pCO2 with metabolic alkalosis

Answer 9

Metabolic alkalosis:

Expected ΔpCO2 = 0.6* ΔHCO3

Question 10

When do the two types of compensation occur?

Answer 10

Acute metabolic compensation occurs over minutes-to-hours

Chronic metabolic compensation occurs over 3-5 days

Question 11

What bicarbonate compensation do we expect in respiratory acidosis? (provide formulae)

Answer 11

Respiratory acidosis:

Acute: eΔHCO3 = 0.1 * ΔpCO2

Chronic: eΔHCO3 = 0.35 * ΔpCO2

Question 12

What bicarbonate compensation do we expect in respiratory alkalosis? (provide formulae)

Answer 12

Respiratory alkalosis:

Acute: eΔHCO3 = 0.2 * ΔpCO2

Chronic: eΔHCO3 = 0.5 * ΔpCO2

Question 13

In general, metabolic acidoses can be one of three processes

Answer 13

Increased acid production

Decreased acid excretion

Loss of base (bicarbonate)

Question 14

Serum anion gap is defined as:

Answer 14

Serum anion gap is defined as: [Na] −[Cl] −[HCO3] = 12 ± 3 (normally)

Question 15

What si Anion Gap essentially?

Answer 15

AG = ANIONS WE DON’T MEASURE

Question 16

Due to electroneutrality, increases in the AG are reflected as:

Answer 16

Due to electroneutrality, increases in the AG are reflected as decreases in [HCO3]

Question 17

AG > 16 indicates a high-likelihood (index of suspicion) of:

Answer 17

AG > 16 indicates a high-likelihood (index of suspicion) of excess organic acids

Question 18

MUDPILES and what we use it for

Answer 18

Causes of an elevated AG: “MUDPILES”

Methanol

Uremia

Diabetic ketoacidosis (alcoholic, starvation)

Paraldehyde (pyroglutamic acid)

Iron/isoniazid

Lactic acidosis

Ethanol/ethlyene glycol

Salicylates

Question 19

Discuss diabetic ketoacidosis

Answer 19

Insulin deficit causes metabolism of fatty acids resulting in excess acetoacetate and β-hydroxybutyrate

Question 20

Treatment for ketoacidoses

Answer 20

Insulin (necessary in DKA, contraindicated in starvation, EtOH) inhibits lipolysis, thus limiting ketone production

Volume repletion: usually ~ 3 liters in adults, but may required as much as 10-15 liters

Electrolyte repletion: initial hyperkalemia but net total body K depletion, hypophosphatemia, hypomagnesemia.

Bicarbonate therapy not recommended unless pH < 7.2 (with appropriate respiratory compensation)

Question 21

What are the two types of lactic acidosis and when do we see them?

Answer 21

Lactic acidosis - comes in two types

Type A: tissue hypoxia - Sepsis, hypovolemia, cardiogenic shock

Type B: non-hypoxic, Drug induced: Metformin, anti-retrovirals

Alcoholic, Malignancy

Question 22

HARDASS and what it indicates

Answer 22

Causes of a normal AG: “HARDASS”

Hyperalimentation

Addison disease

Renal Tubular Acidosis

Diarrhea

Acetazolamide

Spironolactone

Saline infusion

Question 23

Addison’s disease on acid/baase and why

Answer 23

results in net bicarb loss (secondary to hypoaldosteronism)

Question 24

What does RTA result in and how do we divide the effects?

Question 25

Discuss proximal RTA and what we see with it.

Answer 25

Proximal (type II) RTA due to impaired reabsorption of bicarbonate

Associated with other signs of proximal tubular dysfunction (Fanconi’s syndrome):

Glycosuria

Aminoaciduria

Phosphaturia

Question 26

Distal RTA, discuss it and when we see it/what we see with it

Answer 26

Distal (type I and IV) RTA due to impaired secretion of acid (NH4+)

Urine pH usually inappropriately high (>5.5)

Associated with tubulointerstitial diseases:

• Autoimmune disorders
• Kidney stones
• Chronic kidney disease
• Inborn errors of metabolism

Type IV associated with hyperkalemia and hypoaldosteronism (seen in diabetes)

Question 27

Diarrhea results in what acid/base changes?

Answer 27

Diarrhea

results in net bicarb loss

Question 28

If serum bicarb is low, what do we know about the urine anion gap, or rather, what can we use our UAG to find out?

Answer 28

If serum bicarb is low…

UAG = -20 to -30 ⇒ appropriate ammonium excretion/normal renal function ⇒ extrarenal causes of non-AG metabolic acidosis

UAG = 0 to +40 ⇒ inappropriate renal response ⇒ renal causes of non-AG metabolic acidosis

Question 29

UAG decreases as ____ increases. Why?

Answer 29

Principle unmeasured cation is NH4+, thus UAG decreases as NH4+ increases

Question 30

With normal kidneys in metabolic acidosis, ___ ___ should increase and UAG should be ____.

Answer 30

With normal kidneys in metabolic acidosis, NH4+ excretion should increase and UAG should be negative

Question 31

Common causes of metabolic alkaloses

Answer 31

Loss of chloride (hypochloremic, Urine Cl < 10):

Excess of bicarbonate (Urine Cl > 20):

Question 32

Causes of loss of chloride

Answer 32

Loss of chloride (hypochloremic, Urine Cl < 10):

vomiting, gastric drainage, villous adenoma/chloride diarrhea, diuretics, posthypercapnia, cystic fibrosis

Question 33

Causes of bicarbonate excess

Answer 33

exogenous bicarbonate administration, hyperaldosteronism, Cushing’s syndrome, licorice intoxication

Bartter syndrome (defective chloride absorption in thick ascending loop of Henle)