Metabolic acidosis Flashcards
Metabolic acidosis
pH < 7.35
low serum HCO3- (<24 mEq/L)
decrease in PaCO2 from hyperventilation
Anion gap
Na+ - (Cl + HCO3-)
Normal 3-11 mEq/L
Pathophysiology of non-anion gap acidosis
Loss of plasma HCO3- replaced by Cl-
Gastrointestinal bicarbonate losses
Diarrhea: can lose 5-10 L of fluid; one L has 3050 mEq/L of HCO3-
Pancreatic fistulas/biliary drainage: fluids are rich in HCO3-
Renal bicarbonate loss
Type 2 renal tubular acidosis
Causes: can result from various diseases or toxins (heavy metal toxicity, carbonic anhydrase inhibitors, topiramate, fanconi’s syndrome)
Reabsorptive threshold for HCO3- is reduced in the proximal tubule
With enhanced bicarb loss there will be an increase in Na+ and fluid loss, which will then activate angiotensin system leading to hyperaldosteronism
Increased aldosterone augments K+ excretion–>hypokalemia
Urine pH ofter < 5.3
Reduced renal H+ excretion
distal tubule RTA’S
Type I RTA
hypokalemia RTA
Causes: primary tubule defect, SLE, myeloma, sickle cell, Li+, ampho B, toluene
H+ cannot be pumped into tubule lumen by cells of collecting duct
Urine pH > 5.3
Increase in K+ excretion: H+ cannot be secreted in response to Na+ reabsorption
Type IV RTA
hyperaldosteronism or hyperkalemia RTA
Aldosterone stimulates H+ excretion, so with less aldosterone=H+ retention
Hyperkalemia conditions also lead to H+ retention=acidosis
Chronic renal failure
decrease H+ excretion
less ammonia production which can’t pick up H+ to make new bicarb
Acid and chloride administration
TPN administration
HCl or Ammonium Cl administration
Pathophysiology of anion gap acidosis
M: methanol intoxication
U: uremia
L: lactic acidosis
E: ethylene glycol
P: paraldehyde ingestion
A: aspirin
K: ketoacidosis
Characteristics of anion gap acidosis
Elevated anion gap
HCO3- losses are replaced with another anion besides Cl-
How to calculate delta gap
difference between the patient’s anion gap and the normal anion gap
if the delta gap is added to the measured HCO3- and the answer is an elevated HCO3-, it tells you there is also the presence of a metabolic alkalosis as well as acidosis
Causes of anion gap metabolic acidosis
Lactic acidosis
Ketoacidosis
Drug intoxications
Lactic acidosis
Lactate formation essential for tissues that need NAD+ to generate energy anaerobically
RBC’s, exercising muscle
1 mEq/L=normal
> 5 mEq/L=diagnostic
Normally enters circulation in small amounts and is promptly removed by the liver
Possible causes of lactic acidosis
Shock
Drugs/toxins: ethanol, metformin, NRTIs, linezolid, isoniazid, propofol, topiratmate, propylene glycol
Seizures: self-limiting
Leukemia
Hepatic/renal failure
Diabetes
Malnutrition
Rhabdomyolysis
Ketoacidosis
increase acetoacetic acid and B-OH butyric acid
Drug intoxications
Salicylate toxicity: respiratory alkalosis from stimulation of respiratory drive, metabolic acidosis from accumulation of acid
Methanol/ethanol glycol ingestion
Symptoms of lactic acidosis
Kussmaul respirations
Peripheral vasodilation causing flushing and tachycardia; as acidosis worsens, ventricular arrhythmias may occur
Hyperkalemia
Lethargy/coma
N/V
Bone demineralization in chronic acidotic states
Treatment of lactic acidosis
Treat the underlying cause!
Acute bicarbonate therapy
-Consider use if pH < 7.10-7.15
Good indications of bicarb
Hyperkalemia, pH < 7.10 with cardiac arrest after defibrillation, ventilation, and medications have been utilized, and overdoses
Bicarbonate dose
(mEq)= [0.5 L/kg (IBW)] x (desired HCO3- - actual HCO3-)
desired HCO3- is 12 mEq/L
give 1/3 to 1/2 the calculated dose; monitor ABG
during cardiac arrests, 1 mEq/kg may be given
supplement K+, if needed
Hazards of bicarbonate therapy
Overalkanization can reduce cerebral blood flow and can impair oxygen release from Hgb to tissues
-A “shift to the left” on the oxygen-hemoglobin saturation curve
-For any given pO2, Hgb has increase saturation
Hypernatremia, hyperosmolality
CSF acidosis occurs from the CO2 that is generated
Electrolyte shifts
Potassium
With acidosis, K+ moves extracellularly and is excreted
When bicarbonate therapy is used to treat the acidosis, K+ moves back into the cells creating even more hypokalemia
Calcium
Decreased ionized calcium–>decrease myocardial contractility
Chronic bicarbonate therapy
for chronic metabolic acidosis
average dose: 1-3 mEq/kg/day (may go up to 10+ mEq/kg/day