Metabolic acidosis Flashcards

1
Q

Metabolic acidosis

A

pH < 7.35

low serum HCO3- (<24 mEq/L)

decrease in PaCO2 from hyperventilation

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2
Q

Anion gap

A

Na+ - (Cl + HCO3-)

Normal 3-11 mEq/L

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3
Q

Pathophysiology of non-anion gap acidosis

A

Loss of plasma HCO3- replaced by Cl-

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4
Q

Gastrointestinal bicarbonate losses

A

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-

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5
Q

Renal bicarbonate loss

A

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

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6
Q

Reduced renal H+ excretion

A

distal tubule RTA’S

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7
Q

Type I RTA

A

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

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8
Q

Type IV RTA

A

hyperaldosteronism or hyperkalemia RTA

Aldosterone stimulates H+ excretion, so with less aldosterone=H+ retention

Hyperkalemia conditions also lead to H+ retention=acidosis

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9
Q

Chronic renal failure

A

decrease H+ excretion

less ammonia production which can’t pick up H+ to make new bicarb

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10
Q

Acid and chloride administration

A

TPN administration

HCl or Ammonium Cl administration

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11
Q

Pathophysiology of anion gap acidosis

A

M: methanol intoxication
U: uremia
L: lactic acidosis
E: ethylene glycol
P: paraldehyde ingestion
A: aspirin
K: ketoacidosis

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12
Q

Characteristics of anion gap acidosis

A

Elevated anion gap

HCO3- losses are replaced with another anion besides Cl-

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13
Q

How to calculate delta gap

A

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

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14
Q

Causes of anion gap metabolic acidosis

A

Lactic acidosis

Ketoacidosis

Drug intoxications

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15
Q

Lactic acidosis

A

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

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16
Q

Possible causes of lactic acidosis

A

Shock

Drugs/toxins: ethanol, metformin, NRTIs, linezolid, isoniazid, propofol, topiratmate, propylene glycol

Seizures: self-limiting

Leukemia

Hepatic/renal failure

Diabetes

Malnutrition

Rhabdomyolysis

17
Q

Ketoacidosis

A

increase acetoacetic acid and B-OH butyric acid

18
Q

Drug intoxications

A

Salicylate toxicity: respiratory alkalosis from stimulation of respiratory drive, metabolic acidosis from accumulation of acid

Methanol/ethanol glycol ingestion

19
Q

Symptoms of lactic acidosis

A

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

20
Q

Treatment of lactic acidosis

A

Treat the underlying cause!

Acute bicarbonate therapy
-Consider use if pH < 7.10-7.15

21
Q

Good indications of bicarb

A

Hyperkalemia, pH < 7.10 with cardiac arrest after defibrillation, ventilation, and medications have been utilized, and overdoses

22
Q

Bicarbonate dose

A

(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

23
Q

Hazards of bicarbonate therapy

A

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

24
Q

Potassium

A

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

25
Q

Calcium

A

Decreased ionized calcium–>decrease myocardial contractility

26
Q

Chronic bicarbonate therapy

A

for chronic metabolic acidosis

average dose: 1-3 mEq/kg/day (may go up to 10+ mEq/kg/day