Metabolic alkalosis Flashcards

1
Q

Metabolic alkalosis

A

pH > 7.45, increased HCO3-, and a compensatory hypoventilation resulting in increased PaCO2

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2
Q

Pathophysiology

A

Primary rise in HCO3- can occur through:

  1. Loss of acid from GI tract or urine
  2. Administration of HCO3- or a bicarbonate precursor
  3. Contraction alkalosis

Sometimes, there is an impairment in renal function that results in the maintenance of metabolic acidosis

Volume and chloride depletion

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3
Q

Saline Responsive

A

Urinary chloride < 10-20 mEq/L

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4
Q

Diuretic therapy

A

most common cause of saline responsive alkalosis

Enhances excretion of NaCl and water, resulting in extracellular volume contraction

Volume contraction stimulates aldosterone release

Aldosterone increases distal tubular Na+ reabsorption and induces H+ and K+ secretion

H+ secretion is associated with HCO3- reabsorption in the proximal tubule and HCO3- generation in distal tubule

Na and H exchange in distal tubule

In response to hypokalemia, there is stimulation of movement of hydrogen ions intracellularly

K+ moves extracellularly to fight off hypokalemia, in exchange for K+, Na+ gets reabsorbed

Hypochloremic state: normally Cl- is anion absorbed with Na+, without Cl-, Na is reabsorbed with HCO3-

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5
Q

Vomiting and NG suction

A

2nd most common cause of alkalosis

1L/day may be lost with vomiting

1L of fluid contains: 200 mEq Cl-, 25-100 mEq H+

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6
Q

Exogenous HCO3- administration or blood transfusions

A

Blood transfusions: HCO3- in fluids, LR, TPN’s

Citrate (preservative in blood products) breaks down to HCO3-

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7
Q

Saline resistant alkalosis

A

urinary chloride > 20 mEq/L

Enhanced renal H+ excretion and HCO3- reabsorption

Key difference: no chloride depletion or this is an inability to reabsorb chloride

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8
Q

Increased mineralcorticoid activity

A

Causes of saline resistance

Directly stimulates collecting duct H+ secretion and indirectly increase ammoniagenesis by causing hypokalemia

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9
Q

Hypokalemia

A

Cause of saline resistance

Increased H+ secretion with HCO3- reabsorption and ammoniagenesis

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10
Q

Renal tubular chloride wasting (Bartter’s syndrome)

A

Impaired NaCl reabsorption

Volume depletion activates RAA system–>increase aldosterone

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11
Q

Symptoms of alkalosis

A

Muscle cramps, weakness, paresthesias

Postural dizziness

Cellular hypoxia, mental confusion, coma, seizures

Direct myocardial suppression; CV collapse; arrhythmias

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12
Q

Treatment of alkalosis

A

Treat underlying cause

Rapid correction not necessary but treatment still needed

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13
Q

Treatment for saline responsive

A

SALINE

Fluid/electrolyte replacement with NaCl or KCl

Allows more Na+ to be reabsorbed with Cl- vs. getting exchanged with H+ or reabsorbed with HCO3-

Increases the plasma K+ concentration which reduces renal H+ secretion

Use caution in patients with HF or hepatic/renal failure

Potassium supplementation

May also use lactated ringers for certain patients

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14
Q

Monitoring

A

I/O, BP, HR, lung sounds, electrolytes, edema

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15
Q

Carbonic anhydrase inhibitors for treatment of saline responsive

A

Used in patients who cannot tolerate excess fluids or sodium

Decreases HCO3- reabsorption in proximal tubule

Adverse consequence is K+ wasting: caution in already hypokalemic patients

Not helpful in volume depletion, renal dysfunction, or severe alkalosis (pH > 7.55)

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16
Q

Other alternatives for persistant alkalosis

A

HCl: for failure of previous therapies, or confirmed severe metabolic alkalosis pH >7.55 or HCO3- > 50

Ammonium chloride

17
Q

Adjunct therapies

A

For patients with vomiting or NG suction as their cause: H2 antagonist or PPIs

18
Q

Treatment of saline resistant

A

Correct hypokalemia with potassium-sparing diuretic or KCl supplementation

Decrease dose of mineralcorticoid or change steroids to one with less activity

Spironolactone

Correct hyperaldosteronism-fluids