1.7 - Metabolic Acidosis & Alkalosis Flashcards

1
Q

What is metabolic acidosis?

A
  • It is a nonventilatory process that increases H+; pH is less than 7.35. The HCO3 is usually less than 22 mEq/L.
  • Respiratory alkalosis (decreased pCO2) is seen as compensating process
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2
Q

What are the 2 types of metabolic acidosis?

A

There are two types of metabolic acidosis: those that cause an anion gap and those with a normal anion gap

  1. Normal AG metabolic acidosis – the AG is less than 12 mEq/L. Indicates primary HCO3- loss or H+ plus Cl- gain. AG = [Na+] – ([Cl-] + [HCO3-]). Normal AG is 10 + 2mEq/L.
  2. High AG metabolic acidosis – AG greater than 15 mEq/L. Indicates addition to serum of non-chlorine acid anion (e.g. lactate from lactic acid)
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3
Q

What causes a normal AG metabolic acidosis?

A
  • GI bicarbonate loss with diarrhea or pancreatic drainage
  • Insufficient renal acid excretion seen in renal tubular acidosis, types I, II and IV.
  • Also seen in mild to moderate kidney failure where the GFR is greater than 20-30 ml/min. Renal causes that are due to renal excretion of HCO3- or disorders of renal acid handling are referred to collectively as renal tubular acidosis.
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4
Q

What causes a high AG metabolic acidosis?

A

1. Endogenous acids

  • Lactic acidosis: hypoxia, sepsis, circulatory shock. Lactic acidosis will resolve once the underlying cause is identified and appropriately treated. At that point tissue perfusion is restored. The administration of alkali does not appear to be affective and may lead to a rebound metabolic alkalosis.
  • Diabetic ketoacidosis: lack of insulin
  • Alcoholic ketoacidosis: binge drinking ending in nausea and vomiting with poor nutrition. Usually resolves when drinking stops and calories are consumed.
  • Advanced renal insufficiency: GFR less than 15-20 ml/min

2. Exogenous acids

  • Salicylate poisoning: aspirin or salicylic acid
  • Methanol: formic acid metabolite
  • Ethylene glycol: glycolic and oxalic acid metabolites
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5
Q

What are the subjective and PE findings associated with metabolic acidosis?

A

Subjective findings

  • Anorexia and nausea
  • Weakness, lethargy to coma
  • Symptoms of underlying condition/disease/disorder

Physical exam findings

  • Kussmaul breathing: rapid, regular, deep breathing
  • Hypotension
  • Signs of underlying disorder. Example: sweet breath in DKA
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8
Q

How do you treat metabolic acidosis due to methanol or ethylene glycol ingestion?

A
  • Infuse ethanol to maintain blood level at 100-150 mg/day limits acid metabolites
  • Fomepizole 15 mg initial infusion then 10 mg q 12 hr; limits acid metabolites
  • Dialysis indicated for severe intoxications, toxic levels greater than 50 mg/dl
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9
Q

How do you treat metabolic acidosis due to salicylate poisoning?

A
  • Alkalinize urine with isotonic NaHCO3 infusion to maintain urine pH at 8 or above
  • Dialysis indicated for severe intoxications, levels greater than 100 mg/dl acute or greater than 40 mg/dl chronic
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10
Q

How do you treat metabolic acidosis due to DKA?

A
  • Intravenous NS (0.9% NS) and insulin infusions
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11
Q

How do you treat metabolic acidosis due alcoholic ketoacidosis?

A
  • IV glucose (D5W or 5% dextrose in 0.9% NS at 100-150 ml/hr) plus thiamine (100 mg)
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12
Q

How do you treat metabolic acidosis due to the accumulation of lactic acid?

A
  • Maintain tissue perfusion
  • Intravenous 0.9% NS more effective than intravenous NaHCO3
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15
Q

What lab/diagnostic tests are used to diagnose metabolic acidosis?

A

To diagnose metabolic acidosis obtain these labs:

1.Arterial blood gases

  • pH
  • pCO2
  • Calculated HCO3

2. Serum sodium, bicarbonate, and chlorine Cl - calculate AG

3. BUN and serum creatinine - to identify renal failure

4. Urine pH

  • If greater than 5.5, suspect renal acidifying defect
  • If less than 5.5, suspect GI bicarbonate loss or anion gap acidosis

5. Serum and urine ketones: positive in ketotic states

6. Serum salicylate, methanol or ethylene glycol levels

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16
Q

In general, how do you treat a patient with metabolic acidosis?

A

In general:

  • NaHCO3 therapy; intravenous NaHCO3 infusion is controversial
  • NaHCO3 isotonic infusion
  • Stop or limit GI HCO3- losses​
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17
Q

What is metabolic alkalosis?

A
  • It is a nonventilatoryprocess that decreases H+;; pH greater than 7.45
  • Identified by an increase in HCO3 , usually exceeding 28 mEq/L
  • Respiratory acidosis (increased pCO2 ) is seen as a compensating process
  • Development of a persistent metabolic alkalosis requires both generation and maintenance causes. (See acid base disorders flashcards)
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18
Q

What are the 3 main causes of metabolic alkalosis?

A

1. GI hydrogen loss

  • Vomiting
  • NG aspiration

2. Renal hydrogen loss

  • Secondary hyperaldosteronism from volume contraction
    • Diuretic therapy
    • Vomiting, NG aspiration/losses
    • Potassium depletion with or without magnesium deficiency
  • Hyperaldosteronism with normal or expanded volume
    • Primary aldosteronism
    • Cushing’s syndrome
    • Renal artery stenosis

3. Bicarbonate gains; only occurs in renal insufficiency

  • NaHCO3 administration
  • Massive organic anion infusion
    • Citrate from blood or FFP
    • Acetate from parenteral nutrition or dialysis solutions
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19
Q

What are the subjective and PE findings of metabolic alkalosis?

A

Since the key causes of metabolic alkalosis are related to volume contraction, patients may present initially with signs of volume depletion. Others are listed below:

Subjective findings:

  • CNS symptoms
    • Headache
    • Lethargy to coma
  • Tetany or seizure: may be associated with decreased Ca2+
  • Cardiac arrhythmias, especially with sympathetic nerve stimulation

Physical findings;

  • Postural hypotension or tachycardia
  • Respiratory depression
  • Signs of primary disorder
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20
Q

What laboratory/diagnostic tests are used to diagnose metabolic alkalosis?

A

1. Arterial blood gases

  • pH
  • pCO2
  • Calculated HCO3

2. Check Serum electrolytes, for decreased potassium, magnesium and ionized calcium

3. Check Urine Cl because it is a marker of volume status

  • Urine Cl than 20 mEq/Line Cl
    • Vomiting
    • Low NaCl intake
    • Diuretic use after drug stopped
  • Urine Cl greater than 40 mEq/L
    • Aldosterone excess (primary or secondary)
    • Active diuretic use
21
Q

How do you treat a patient with metabolic alkalosis?

A

1. If they are Volume depleted:

  • IV 0.9% NS at 100-150 ml/hr. Metabolic alkalosis is most effectively treated with saline resuscitation until euvolemia is achieved.
  • The increase in filtered chloride leads to improved renal handling of the bicarbonate load.
  • These are chloride responsive.

2. Give KCL replacement for all potassium depleted or potassium losing states

3. Patients with metabolic alkalosis who are chloride unresponsive do not respond to NS administration and are often associated with a normal or expanded ECF volume.

  • Mineralcorticoid excess can be managed with a potassium sparing diuretic (amiloride or spironolactone) and replacing the potassium deficit
  • The alkalosis caused by excessive alkali administration will respond when the medication is discontinued
  • Acetazolamide (Diamox), 250-500 mg IV or PO BID; especially useful in volume expanded states. This therapy promotes bicarbonaturia although you will see an effect on lowering potassium levels also.
  1. Metabolic alkalosis caused/induced by excess aldosterone states may require spironolactone or eplerenone
  2. Severe alkalemia (pH > 7.70) with ECF volume excess and/or renal failure can be treated with isotonic (150 mEq/L) HCl through a central vein only.
  3. Hemodialysis against a low [HCO3 -] bath