Clinical Reasoning Acid Bases Flashcards
First four steps of analyzing an acidotic/alkalotic patient?
- 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.
If the anion gap is elevated, what do we do and what does it mean?
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.
Henderson hasselbach shortcut
Differential diagnoses for metabolic acidoses
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
Differential diagnoses for metabolic alkaloses
Loss of acid (chloride responsive)
Gain of alkali (chloride unresponsive)
Differential diagnoses for respiratory alkaloses
Hyperventilation (hypoxemia vs. central)
Pulmonary disease
Differential diagnoses for respiratory acidoses
Airway obstruction
Respiratory depression
Hypoventilation (central vs. musculoskeletal)
What is Winter’s Formula and when do we use it?
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
Formula we use for projected change in pCO2 with metabolic alkalosis
Metabolic alkalosis:
Expected ΔpCO2 = 0.6* ΔHCO3
When do the two types of compensation occur?
Acute metabolic compensation occurs over minutes-to-hours
Chronic metabolic compensation occurs over 3-5 days
What bicarbonate compensation do we expect in respiratory acidosis? (provide formulae)
Respiratory acidosis:
Acute: eΔHCO3 = 0.1 * ΔpCO2
Chronic: eΔHCO3 = 0.35 * ΔpCO2
What bicarbonate compensation do we expect in respiratory alkalosis? (provide formulae)
Respiratory alkalosis:
Acute: eΔHCO3 = 0.2 * ΔpCO2
Chronic: eΔHCO3 = 0.5 * ΔpCO2
In general, metabolic acidoses can be one of three processes
Increased acid production
Decreased acid excretion
Loss of base (bicarbonate)
Serum anion gap is defined as:
Serum anion gap is defined as: [Na] −[Cl] −[HCO3] = 12 ± 3 (normally)
What si Anion Gap essentially?
AG = ANIONS WE DON’T MEASURE
Due to electroneutrality, increases in the AG are reflected as:
Due to electroneutrality, increases in the AG are reflected as decreases in [HCO3]
AG > 16 indicates a high-likelihood (index of suspicion) of:
AG > 16 indicates a high-likelihood (index of suspicion) of excess organic acids
MUDPILES and what we use it for
Causes of an elevated AG: “MUDPILES”
Methanol
Uremia
Diabetic ketoacidosis (alcoholic, starvation)
Paraldehyde (pyroglutamic acid)
Iron/isoniazid
Lactic acidosis
Ethanol/ethlyene glycol
Salicylates
Discuss diabetic ketoacidosis
Insulin deficit causes metabolism of fatty acids resulting in excess acetoacetate and β-hydroxybutyrate
Treatment for ketoacidoses
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)
What are the two types of lactic acidosis and when do we see them?
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
HARDASS and what it indicates
Causes of a normal AG: “HARDASS”
Hyperalimentation
Addison disease
Renal Tubular Acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
Addison’s disease on acid/baase and why
results in net bicarb loss (secondary to hypoaldosteronism)
What does RTA result in and how do we divide the effects?
Discuss proximal RTA and what we see with it.
Proximal (type II) RTA due to impaired reabsorption of bicarbonate
Associated with other signs of proximal tubular dysfunction (Fanconi’s syndrome):
Glycosuria
Aminoaciduria
Phosphaturia
Distal RTA, discuss it and when we see it/what we see with it
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)
Diarrhea results in what acid/base changes?
Diarrhea
results in net bicarb loss
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?
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
UAG decreases as ____ increases. Why?
Principle unmeasured cation is NH4+, thus UAG decreases as NH4+ increases
With normal kidneys in metabolic acidosis, ___ ___ should increase and UAG should be ____.
With normal kidneys in metabolic acidosis, NH4+ excretion should increase and UAG should be negative
Common causes of metabolic alkaloses
Loss of chloride (hypochloremic, Urine Cl < 10):
Excess of bicarbonate (Urine Cl > 20):
Causes of loss of chloride
Loss of chloride (hypochloremic, Urine Cl < 10):
vomiting, gastric drainage, villous adenoma/chloride diarrhea, diuretics, posthypercapnia, cystic fibrosis
Causes of bicarbonate excess
exogenous bicarbonate administration, hyperaldosteronism, Cushing’s syndrome, licorice intoxication
Bartter syndrome (defective chloride absorption in thick ascending loop of Henle)
