Metabolic alkalosis Flashcards
Metabolic alkalosis
pH > 7.45, increased HCO3-, and a compensatory hypoventilation resulting in increased PaCO2
Pathophysiology
Primary rise in HCO3- can occur through:
- Loss of acid from GI tract or urine
- Administration of HCO3- or a bicarbonate precursor
- Contraction alkalosis
Sometimes, there is an impairment in renal function that results in the maintenance of metabolic acidosis
Volume and chloride depletion
Saline Responsive
Urinary chloride < 10-20 mEq/L
Diuretic therapy
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-
Vomiting and NG suction
2nd most common cause of alkalosis
1L/day may be lost with vomiting
1L of fluid contains: 200 mEq Cl-, 25-100 mEq H+
Exogenous HCO3- administration or blood transfusions
Blood transfusions: HCO3- in fluids, LR, TPN’s
Citrate (preservative in blood products) breaks down to HCO3-
Saline resistant alkalosis
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
Increased mineralcorticoid activity
Causes of saline resistance
Directly stimulates collecting duct H+ secretion and indirectly increase ammoniagenesis by causing hypokalemia
Hypokalemia
Cause of saline resistance
Increased H+ secretion with HCO3- reabsorption and ammoniagenesis
Renal tubular chloride wasting (Bartter’s syndrome)
Impaired NaCl reabsorption
Volume depletion activates RAA system–>increase aldosterone
Symptoms of alkalosis
Muscle cramps, weakness, paresthesias
Postural dizziness
Cellular hypoxia, mental confusion, coma, seizures
Direct myocardial suppression; CV collapse; arrhythmias
Treatment of alkalosis
Treat underlying cause
Rapid correction not necessary but treatment still needed
Treatment for saline responsive
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
Monitoring
I/O, BP, HR, lung sounds, electrolytes, edema
Carbonic anhydrase inhibitors for treatment of saline responsive
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)