High Anion Gap Metabolic Acidosis Flashcards
Define blood gas values seen in acidemia (metabolic and respiratory)
pH < 7.35
Metabolic acidosis:
HCO3 < 20
Respiratory acidosis:
pCO2 > 45
[identify primary disorder based on HCO3 and PCO2]
Define blood gas values seen in alkalemia (metabolic and respiratory)
pH > 7.45
Metabolic alkalosis:
HCO3 > 30
Respiratory alkalosis:
pCO2 < 35
[identify primary disorder based on HCO3 and PCO2]
Causes of acidosis
Increased endogenous acids: Ketoacidosis Lactic acidosis (diabetic, alcoholic, starvation)
Ingestion of acids: Ethylene glycol Methanol Propylene glycol Salicylates
Loss of bicarb:
Diarrhea
Decreased secretion of acids:
AKI or CKD
Differentiate definition of AKI and CKD
AKI is defined as rate of rise in SCr
CKD is defined as decrease in GFR over time
Signs and symptoms of acidosis
Complaint of headache Abdominal pain Malaise AMS — confusion, stupor, coma Increased respirations Variations in BP Tachycardia (catecholamine release) Pulmonary edema Increased serum glucose
Anion gap is a way of demonstrating the accumulation of unmeasured anions. How is anion gap calculated?
What is a normal anion gap?
AG = Na - (Cl + HCO3)
Normal AG is 10 +/- 2 mEq/L (range of 8-12)
An elevated anion gap suggests metabolic acidosis with circulating anions
How does the body attempt to compensate for metabolic acidosis?
Increasing respiratory rate to blow off CO2 —> creating respiratory alkalosis
Formula to determine appropriate compensation for metabolic acidosis
PCO2 = (1.5 x [HCO3]) + 8 (+/- 2)
If the calculated PCO2 doesn’t match, then there is likely a respiratory alkalosis
Common causes of anion gap
MUDPILES
Methanol, metformin Uremia DKA (usually type 1) Paraldehyde, propylene glycol, phenformin Isoniazid/iron toxicity Lactic acidosis Ethanol/ethylene glycol Salicylates
[note that starvation ketoacidosis also causes anion gap; lactic acidosis includes cyanide and CO poisoning, seizures, sepsis, and ischemia]
**Toluene first causes HAGMA, then NAGMA
Lactic acidosis typically occurs via one of which two mechanisms?
- Hypoxia —> buildup of lactate (ex: seizure, extreme exercise, CO poisoning, shock, cardiac arrest, low cardiac output, severe anemia, early toluene poisoning)
- Impaired OxPhos (ex: sepsis, hypovolemic shock, uncontrolled DM, ethanol, metformin, isoniazid, cyanide, salicylate, malignancy)
Condition characterized by muscle aches, hypotension, and renal failure d/t release of intracellular contents into extracellular space
Rhabdomyolysis
Causes of rhabdomyolysis
Drugs/supplements: statins, SSRIs, colchicine, cocaine, amphetamines, heroin, creatine, ephedra
Toxins: alcohol, toluene, CO, hydrocarbons, quail poisoning, mushroom poisoning
Other: hypokalemia, hypophosphatemia, excessive fluid shifts, vasculitis, influenza, dermatomyositis, polymyositis
Urinalysis and lab findings with rhabdomyolysis
Dipstick: heme positive, but no RBCs on microscopy (myoglobinuria)
Microscopy would show granular casts
Serum labs: elevated CK, hyperkalemia, hypocalcemia, hyperphosphatemia
How does DKA cause HAGMA?
Polyuria = osmotic diuresis d/t high serum glucose —> dehydration leads to polydipsia
With T1D, intracellular hypoglycemia activates fatty acid degradation —> large amounts of ketones (anions) that are rapidly excreted in urine
[vomiting is a compensatory mechanism]
How does alcoholic ketoacidosis cause HAGMA?
Degradation of alcohol depletes NAD which curtails hepatic gluconeogenesis —> depletion of liver stores of glycogen
Metabolism increases NADH/NAD ratio, favoring conversion of pyruvate to lactate
Lactic acid builds up d/t impaired hepatic conversion of lactate to glucose
