What is the relationship between intravenous (IV) Furosemide (Lasix) and metabolic alkalosis?

From the Guidelines

IV Lasix (furosemide) can cause metabolic alkalosis, and clinicians should monitor for this condition, especially in patients receiving high doses or prolonged therapy, as it can lead to increased morbidity and mortality. When administering IV Lasix, it is essential to be aware of the potential for metabolic alkalosis, which can occur through several mechanisms. Lasix causes metabolic alkalosis by promoting excessive urinary excretion of chloride and hydrogen ions while enhancing sodium reabsorption in the distal tubule, leading to increased bicarbonate retention 1. Additionally, volume contraction from diuresis activates the renin-angiotensin-aldosterone system, further exacerbating alkalosis.

To manage Lasix-induced metabolic alkalosis, consider the following strategies:

• Reducing the Lasix dose
• Administering chloride replacement (normal saline or potassium chloride if hypokalemic)
• Using acetazolamide 250-500mg IV/PO to promote bicarbonate excretion in severe cases Potassium levels should be monitored and repleted as needed, as hypokalemia can worsen alkalosis 1. In patients requiring ongoing Lasix therapy but developing alkalosis, switching to a thiazide diuretic or adding spironolactone may help mitigate the metabolic derangement while maintaining diuretic effect. Addressing the underlying condition necessitating diuresis is also crucial for long-term management.

Some key points to consider when using IV Lasix include:

• High doses of frusemide are associated with severe electrolyte disturbance and metabolic alkalosis, and should be used cautiously 1
• Simultaneous administration of frusemide and spironolactone increases the natriuretic effect 1
• The thiazide and loop diuretics can cause hypokalemia and metabolic alkalosis, which in turn can exacerbate CO2 retention in patients with chronic lung disease 1
• Periodic monitoring of serum electrolytes is essential in infants and children treated with chronic diuretic therapy 1

From the FDA Drug Label

All patients receiving furosemide therapy should be observed for these signs or symptoms of fluid or electrolyte imbalance (hyponatremia, hypochloremic alkalosis, hypokalemia, hypomagnesemia or hypocalcemia): dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia or gastrointestinal disturbances such as nausea and vomiting.

The use of IV Lasix (furosemide) may cause metabolic alkalosis, specifically hypochloremic alkalosis, as a result of excessive diuresis and electrolyte depletion.

• Key points to consider:
  • Electrolyte imbalance: Patients should be monitored for signs of fluid or electrolyte imbalance.
  • Hypochloremic alkalosis: A type of metabolic alkalosis that can occur with furosemide therapy.
  • Monitoring: Serum electrolytes, particularly potassium, CO2, creatinine, and BUN, should be determined frequently during the first few months of furosemide therapy and periodically thereafter 2, 2.

From the Research

IV Lasix and Metabolic Alkalosis

• IV Lasix, also known as furosemide, is a loop diuretic that can cause metabolic alkalosis as a side effect 3, 4, 5.
• Metabolic alkalosis is a condition characterized by an increase in blood pH due to a primary increase in serum bicarbonate (HCO3-) 3, 6.
• The pathogenesis of metabolic alkalosis involves either a loss of fixed acid or a net accumulation of bicarbonate within the extracellular fluid 3.
• Furosemide can cause metabolic alkalosis by increasing the excretion of hydrogen ions and decreasing the excretion of bicarbonate ions in the kidney 3, 5.
• The treatment of metabolic alkalosis depends on the underlying cause and severity of the condition, but may include the administration of acidifying agents such as ammonium chloride or hydrochloric acid 7.
• In patients with heart failure, IV acetazolamide may be preferred to treat diuretic-induced metabolic alkalosis 4.
• It is essential to monitor patients taking furosemide for signs of metabolic alkalosis, such as hypokalemia, hypochloremia, and elevated blood pH 3, 5.

Mechanisms and Risk Factors

• The kidney plays a crucial role in maintaining acid-base balance, and factors that interfere with renal function, such as volume contraction, low glomerular filtration rate, and potassium deficiency, can contribute to the development of metabolic alkalosis 3.
• Other risk factors for metabolic alkalosis include aldosterone excess, hypochloremia, and elevated arterial carbon dioxide 3.
• Certain clinical states, such as vomiting, licorice ingestion, and genetic diseases like Bartter syndrome and Gitelman syndrome, can also increase the risk of developing metabolic alkalosis 3.

Clinical Implications

• Metabolic alkalosis can have significant clinical implications, including increased mortality in critically ill patients 3, 6.
• Severe metabolic alkalosis can lead to respiratory depression, cardiac arrhythmias, and other complications 3, 6.
• Early recognition and treatment of metabolic alkalosis are essential to prevent these complications and improve patient outcomes 7, 4.