Z Approach to Acid-Base Disorders Flashcards
What is arterial pH regulated between?
What is intracellular pH regulated between?
- 35-7.45
7. 0-7.3
Acidic metabolites are constantly produced by the cell. How is pH regulated in the extracellular compartment?
The bicarbonate buffer system (HCO3- and CO2)
What is the equation for the bicarbonate buffer system?
CO2 + H2O <> H2CO3- <> H+ + HCO3-
What is the Henderson Hasselbalch equation?
pH = 6.1 + log ([HCO3-]/(0.03x[PCO2]))
Increase in HCO3- leads to:
Increase in PCO2 leads to:
Increased pH (more basic)
Decreased pH (more acidic)
How do the lungs affect the bicarbonate system?
They control the [PCO2] by adjusting RR.
Increased RR = more CO2 blown off (dec. CO2, inc. pH)
Decreased RR = less CO2 blown off (inc. CO2, dec. pH)
How do the kidneys affect the bicarbonate buffer system?
How?
They regulate pH by excreting either acidic or alkaline urine.
Large amounts of HCO3- are filtered into the urine and lots of H+ are secreted into the tubular lumen by the tubular epithelial cells, so the kidneys are able to adjust the pH quickly by adjusting these concentrations.
Metabolic acidosis =
Metabolic alkalosis =
Respiratory acidosis =
Respiratory alkalosis =
Metabolic acidosis = low serum HCO3-
Metabolic alkalosis = high serum HCO3-
Respiratory acidosis = high PCO2
Respiratory alkalosis = low PCO2
What is HAGMA vs. NAGMA?
HAGMA is “high anion gap metabolic acidosis”
NAGMA is “normal anion gap metabolic acidosis”
What is associated with saline-responsive metabolic alkalosis?
What is associated with saline-non-responsive metabolic acidosis?
Saline-responsive metabolic alkalosis - hypovolemia (contraction alkalosis)
Saline-non-responsive metabolic acidosis - euvolemia
Respiratory acidosis and alkalosis can be either…
Acute or chronic
How is metabolic acidosis compensated?
The lungs increase RR and cause a respiratory alkalosis.
Decrease HCO3- and PCO2.
How is metabolic alkalosis compensated?
The lungs decrease RR and cause a respiratory acidosis.
Increase HCO3- and PCO2.
How is respiratory acidosis compensated?
The kidneys reclaim and generate new HCO3- and lead to metabolic alkalosis.
Increase PCO2 and HCO3-.
How is respiratory alkalosis compensated?
The kidneys decrease the rate of HCO3- reclaimation and leads to a metabolic acidosis.
Decrease PCO2 and HCO3-.
Compensation formula for metabolic acidosis =
Winter’s formula
PCO2 = 1.5[HCO3-] + 8 +/- 2
How is compensation for metabolic alkalosis determined?
PCO2 will increase by 0.7 mmHg for each 1.0 mEq/L increase in HCO3- from normal (24).
How is compensation determined for acute vs. chronic respiratory acidosis?
Acute: HCO3- will increase by 1 mEq/L for every 10 mmHg increase in PCO2 from normal (40)
Chronic: HCO3- will increase by 3.5 mEq/L for every 10 mmHg increase in PCO2 from normal (40)
How is compensation determined in acute vs. chronic respiratory alkalosis?
Acute: HCO3- will decrease by 2 mEq/L for every 10 mmHg decrease in PCO2 from normal (40)
Chronic: HCO3- will decrease by 5 mEq/L for every 10 mmHg decrease in PCO2 from normal (40)
Anion gap is….
Not real. All cations must equal the amount of anions in the body.
What are the major cations and anions in the body?
Cations: Na+, K+, Mg+, etc.
Anions: Cl-, HCO3-, proteins- (albumin-), etc.
What is the equation for anion gap?
What is a normal value?
Anion gap = Na+ - (HCO3- + Cl-)
Normal = 12+/- 2
When is determining anion gap useful?
Differentiating between etiologies of metabolic acidosis (HAGMA vs. NAGMA)
NAGMA is AKA as:
Why does the anion gap remain normal?
Hyperchloremic metabolic acidosis
If an acid like HCl is added to blood, H+ is buffered by HCO3-, so HCO3- levels drop. However, Cl- levels rise as a result, so the AG remains normal.
What does hypoalbuminemia do to AG?
What calculation adjustment is made as a result?
It falsely lowers AG, thus it must be corrected.
For every 1 g/dL drop in albumin, the AG increases by 2.5 mEq/L (ex: if someone had a normal anion gap of 12, but now has an [albumin] that is 2 g lower than normal, the AG is now 17).
What is the calculated serum osmolality equation?
What is the equation for osmolar gap?
Serum Osm = 2(Na+) + (Glc/18) + (BUN/2.8)
Osmolar gap = measured serum Osm - calculated serum Osm
- normal is < 10 mOsm/L
- if > 10 mOsm/L, it’s suggestive of additional solutes
When is the osmolar gap clinically useful? (3)
In screening for alcohol ingestions, particularly in HAGMA cases (AG > 20 should be suspicious for EtOH ingestion)
Screening for ketoacidosis
Sceening for lactic acidosis
When is the delta-delta gap useful?
How is it calculated?
In patients with HAGMA to determine if there is a coexistent NAGMA or metabolic alkalosis present.
For every increase in AG, there should be an equal decrease in serum HCO3-.
What is the normal delta HCO3-?
What is present if it is greater than that value?
What is present if it is less than that value?
Approx. 16
> 16 means a metabolic alkalosis is present in addition to the HAGMA
< 16 means a NAGMA is present in addition to the HAGMA
What is the 4 step approach to acid-base disturbances?
- Determine if it is acidosis or alkalosis
- Determine if it is primarily metabolic or respiratory
- If metabolic acidosis is present, calculate the anion gap
- if hypoalbuminemia is present, calculate the corrected anion gap
- if HAGMA is present, calculate the osmolar gap (screen for possible EtOH ingestion) and the delta-delta gap (screen for NAGMA or metabolic alkalosis w/ HAGMA) - Determine if there is appropriate compensation for primary acid-base disorder (is it a simple acid-base disorder, or a mixed disorder, etc.)
Normal ABG values for:
pH (normal, acidosis, alkalosis) HCO3- PCO2 Anion gap Osm gap
Normal pH: 7.35-7.44
Acidosis: pH < 7.35
Alkalosis: pH > 7.44
HCO3-: 24
PCO2: 40
AG: 12
Osm gap: 10
What is on the DDx for HAGMA?
GOLD MARK
Glycols
Oxoproline (acetaminophen toxicity)
L-lactic acid
D-lactic acid
Methanol
Aspirin
Renal failure
Ketoacidosis (alcoholic, diabetic, starvation, etc)
Pyroglutamic (5-oxoproline) acidosis is seen mostly in…
How is it diagnosed?
What is the pathophysiology?
Malnourished or critically ill females who use lots of acetaminophen.
Urinary organic acid screening.
Glutathione is depleted due to increased acetaminophen. Pyroglutamic acid build up and causes and acidosis.
What is on the DDx for increased osmolar gap?
ME DIE
Methanol Ethanol Diethylene glycol (mannitol) Isopropyl alcohol (rubbing alcohol) -not associated w/ metabolic acidosis Ethylene glycol
What is the relationship between acidosis and alkalosis and K+ levels?
Acidosis is associated with hyperkalemia, due to transcellular shift of cations (H+ and K+) into and out of cells, so the electroneutrality is maintained. In acidosis, H+ enters the cell and K+ exits.
Alkalosis is associated with hypokalemia, due to H+ exiting the cells and K+ entering.
What is on the DDx for NAGMA?
DURHAAM
- Diarrhea
- Ureteral diversion, ileal conduit or fistula
- RTA
Hyperalimentation
Acetazolamide (a CA inhibitor)
Addison’s Dz (adrenal insufficiency)
Miscellaneous (meds, glue sniffing, toluene toxicity, etc.)
What drives HCO3- reabsorption?
H+ secretion leads to HCO3- reabsorption.
Urine anion gap (UAG) is used to differentiate what?
What is it a marker of?
What is the equation to find UAG?
-what does it mean if it is negative vs. positive?
Renal from non-renal causes of NAGMA and the function of the DCT.
Marker of NH4Cl excretion, which indicates appropriate urinary acidification.
UAG = (urine Na+ + urine K+) - urine Cl-
- if negative, acidification is appropriate
- if positive, acidification by the distal nephron is not appropriate
What is a major consideration for cause of metabolic alkalosis?
Hypokalemia Vomiting or NG tube placement *Diuretics (thiazide and loop) Volume depletion Mineralcorticoid excess
Overall, what can cause metabolic alkalosis?
Factors that stimulate Na+ reabsorption, secondarily increase H+ secretion and thus stimulate HCO3- reabsorption leading to potentially to a metabolic alkalosis.
Beta-intercalated cells and alpha-intercalated cells are…
HCO3- generated from these cells exits via…
In contraction alkalosis, what must the intercalated cells do?
Mirror images
Cl-/HCO3- exchanger into the tubular lumen
Replete Cl- to help with HCO3- secretion
What is on the DDx for respiratory alkalosis?
Anything that leads to an increase in RR - pneumonia, PE, pulmonary edema, PTX, sepsis, HF, meds, etc.
What is on the DDx for respiratory acidosis? (3)
Anything that lowers RR/tidal volume, increases dead space or worsens airway obstruction.
Inadequate ventilator settings
Increases in CO2 production
What is the main problem in Type 1 RTA?
Where does it occur?
What is the urine pH?
What are [K+] levels?
What is associated with it? (3)
Is the UAG + or -?
a-intercalated cells do not secrete H+ into the lumen, due to defects in transporters or gradient.
DCT
Urine pH > 6
Hypokalemia
Renal stones, Sjogren’s, elevated urine Ca++
UAG is +
What is the main problem in Type 2 RTA?
Where does it occur?
What happens to the urine pH?
What are [K+] levels?
What is it associated with? (3)
Is the UAG + or -?
PT cells do not filter HCO3-.
PCT
Increased urine pH initially, but after time it stabilizes and reaches a steady state.
Mild hypokalemia
Fanconi syndrome, multiple myeloma, cystinosis in kids
Can be either + or -*
What is the main problem in Type 4 RTA?
What happens to [K+] levels?
What is the UAG?
Decreased aldosterone at DCT leads to decreased ENaC activity, which decreases excretion of H+ and K+, leading to NAGMA and hyperkalemia.
Hyperkalemia
Always +
The only RTA associated with hyperkalemia is…
What are the symptoms of these patients?
Type 4 RTA
They are usually asymptomatic, but are 50-70 w/ a history of DM
