Furosemide (Lasix) Nursing Considerations: Administration, Patient Teachings, and More

Furosemide, brand name Lasix, is a potent loop diuretic and first-line treatment in the management of volume overload. In this article we'll walk through proper administration, indications, contraindications, and more.

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Furosemide (Lasix) Nursing Considerations: Administration, Patient Teachings, and More

Furosemide (Lasix) Indications

Furosemide (Lasix) is used to treat acute pulmonary edema, pleural effusions, and volume overload of different etiologies, including the following (1)

  • Congestive heart failure 
  • Ascites from cirrhosis or end-stage liver disease (ESLD) 
  • Edema in renal failure 
  • Nephrotic syndrome

Furosemide has antihypertensive effects (1).

Table of Contents

Pharmacology

Furosemide is metabolized 100% by the kidneys (2).

Most loop diuretics reach peak serum concentrations within 0.5 to 2 hours of administration. Depending on the condition of the kidney, the heart, or the liver, the effects of the drug may last up to 8 hours. Furosemide's short half-life means it is dosed at least twice daily(2).  

Mechanism of Action

Furosemide is an inhibitor of electrolyte reabsorption from the proximal and distal tubules and the ascending loop of Henle.  It increases renal excretion of water, sodium, chloride, magnesium, potassium, and calcium (3).

Contraindication/Precautions

Furosemide is contraindicated in patients with (1) 

  • Anuria 
  • Hypersensitivity to furosemide 
  • Hepatic coma 

Patients with sulfonamide allergy may also be allergic to furosemide.

Adverse Reactions/Side Effects

Furosemide causes several adverse side effects, especially in patients with chronic kidney disease (1, 4). 

  • Hypotension caused by diuresis and vasodilation 
  • Hypokalemia 
  • Hypocalcemia
  • Metabolic alkalosis 
  • Hyperuricemia 
  • Hypomagnesemia
  • Hyponatremia
  • Hyperglycemia
  • Increased BUN and serum creatinine 
  • Increased serum glucose
  • Increased uric acid levels 

Ototoxicity is an uncommon complication and occurs in patients who receive (2, 5)

  • High doses of the medication
  • Have kidney disease 
  • Are older adults
  • Have concomitant use of aminoglycoside antibiotics 

Interactions

  • Digoxin toxicity can occur in patients taking digoxin (5).
  • Signs of digoxin toxicity are anorexia, nausea, vomiting, muscle cramps, paresthesia, and confusion.
  • Concomitant use of cyclosporine is associated with an increased risk of gouty arthritis (5).
  •  There is a risk of hearing loss if high doses of salicylates and furosemide are given concomitantly (1).
  • May cause lithium toxicity (1).
  • NSAIDs may cause increased BUN and serum creatinine (1).
  •  Nephrotoxicity of cisplatin may be enhanced (1).

There is a risk of ototoxic effects with the concomitant use of:

  • Ethacrynic acid(1).
  • Aminoglycosides (especially in the presence of impaired renal function)(1, 4).

Furosemide Administration

Furosemide is available in oral, oral solution, and intravenous formulations. 

Oral Dosage

Ultimately, the effective dose is determined by urine output response(2). Dosage should be individualized according to the desired diuretic effect.

For edema

  • 20–80 mg/day as a single dose initially
  • May repeat in 6–8 hr for insufficient diuresis 
  • May increase the dose by 20–40 mg every 6–8 hr until the desired response

Maintenance doses may be given once or twice daily.

For antihypertensive effects

  • 40 mg twice daily initially

The onset of oral furosemide is 

  • 30-60 minutes
  • Peak effect is at 1-2 hrs 

Parenteral Dosage

Rapid diuresis is achieved with intravenous furosemide. Dosage should be individualized according to the desired diuretic effect.

Edema IM/IVP (1)

  • 20–40 mg slowly ( over 1-2 minutes) 
  • May repeat in 1–2 hr 
  • May increase  by 20 mg every 1–2 hr until the desired response is obtained

The maintenance dose may be given every 6–12 hrs. 

Acute pulmonary edema IV(1)

  • 40 mg injected slowly intravenously (over 1 to 2 minutes).
  • After 1 hour dosage may be increased to 80 mg injected slowly intravenously (over 1 to 2 minutes)

Peak and onset (1)

  • Diuresis begins within five minutes of intravenous administration
  • Peak occurs approximately half an hour after the start of the effects
  • Diuretic effects last roughly two hours

Furosemide Slow IV Push

Furosemide drug inserts and drug books caution to administer furosemide slow IVP to avoid ototoxicity. However, there is a paucity of evidence suggesting that the administration rate of furosemide, when given IVP, causes ototoxicity. 

Additionally, the definition of slow IVP varies widely.

What is slow IVP?

The manufacturer alternately defines slow IVP (1) as:

  • 10 mg/minute or
  • 20 mg/minute or
  • 40 mg/minute or 
  • 80 mg/minute 

Conversely, continuous infusions are directed to run at no faster than 4 mg/minute (1). However conventional practice is to administer furosemide IVP slowly and there is no harm in doing so.

Nursing Considerations

  • Oral tablets may be taken with food or milk to minimize gastric irritation. Tablets may be crushed if needed. Lasix comes in an oral solution.
  • Place patients on fall risk due to potential postural hypotension.
  • Ensure ambulatory patients do not flush the toilet after urinating, preventing accurate I&O. Provide a hat or urinal.
  • If patient has a foley, use a urometer for hourly measurements
  • Make sure to place the call light within easy reach for bedridden patients and give males a urinal. They will have urinary urgency.
  • Notify the monitor tech to be alert for PVCs or set alarm limits to notify

Nursing Assessment and Interventions

Assess for response to furosemide administration to see if fluid overload was reduced, or blood pressure decreased pulmonary congestion.

Assess for signs of volume overload:

  • Dyspnea and activity intolerance
  • Peripheral and dependent edema (sacral area if bedridden)
  • S3 gallop, bilateral crackles
  • Pulse oximetry readings

Monitor fluid changes 

  • Measure I &O and daily weights 
  • Maintain fluid restriction if ordered
  • Monitor urine output 30 minutes to 1 hour after IV push administration
  • Monitor BP for orthostatic hypotension

Monitor labs

  • Monitor for S&S of hypokalemia 
  • Monitore BUN, creatinine and electrolytes
  • Obtain potassium and magnesium before and after rapid diuresis

Potential Diagnoses

Fluid or electrolyte imbalance.

Desired Outcomes

  • Decreased edema
  • Increased urinary output
  • Decreased blood pressure
  • Weight loss 
  • Dyspnea relief

Patient Teaching

Nursing TIP: Patients often refer to furosemide as their "water pill" and may not know the name of the drug.

  • This medication causes frequent urination in large amounts for 1-2 hours after taking the medication. Plan out-of-the-house activities accordingly.
  • Take medication early at night or in the evening so sleep is not disturbed. 
  • Change position slowly. You may feel dizzy when standing up suddenly. 
  • Take potassium supplements as ordered.
  • Anticipate temporary hyperglycemia (patients with diabetes mellitus).
  • Avoid prolonged exposure to direct sun. It may cause photosensitivity.
  • Follow any salt and fluid restrictions.
  • Keep potassium-rich foods on hand (e.g., bananas, oranges, peaches, dried dates).
  • Check with your provider if you are breastfeeding. 
  • Take with food or meals to prevent stomach upset.
  • Weigh daily at the same time, in the same clothing, and after urination.
  • Consider purchasing a smart scale to automatically communicate readings to your provider.

Notify your provider of the following:

  • Dizziness, muscle weakness, or cramps
  • Increasing shortness of breath or needing to sleep upright
  • Weight gain of more than 2 pounds in 1 day or 5 lbs in one week (6)
  • Swelling in lower legs, ankles, and feet
  • Gout
  • Sensation of irregular heart beats 

Go to the emergency department or urgent care for sudden, sustained shortness of breath.

Nursing TIP: When teaching patients, ask them to repeat back what you told them (called teach-back method) to ensure they understood.

NCLEX Questions

On the NCLEX, you are likely to be tested on the following key points.

  • Hypokalemia, hypomagnesia, and ototoxicity are potential adverse effects of furosemide 
  • Foods that are rich in potassium include bananas, broccoli, and Swiss chard, avocados, spinach
  • Furosemide affects the ascending limb of the loop of Henle

Nursing pharmacology 

  • Differentiate between loop diuretics (such as furosemide) and thiazide diuretics (such as hydrochlorothiazide)
  • Differentiate between potassium-sparing diuretics (such as spironolactone, an aldosterone inhibitor) and potassium-wasting diuretics (such as furosemide)

Anecdotal Experience

Furosemide is a wonder drug that decongests patients with fluid overload rapidly.

Hypomagnesemia and hypokalemia are the most severe side effects. Premature ventricular contractions (PVCs) can cause ventricular tachycardia and ventricular fibrillation, both of which are lethal arrhythmias. 

If your patient develops PVCs, order magnesium and potassium levels stat and replace as ordered in the facility's replacement protocols or orders.

PVCs are a lethal arrhythmia but when caused by hypomagnesemia and hypokalemia respond well to IV magnesium or potassium replacement.

 

STAFF NOTE: Original Community Post 

This article was created in response to a community post. The comments and responses have been left intact as they may be helpful. Here's the original post:

Quote

Can anybody tell me why Lasix needs to be pushed slowly? I keep getting different answers. I want to understand why it is that I have to push it over 1-2 minutes. Thank you.

References

1.Furosemide Injection insert. 2016. Hospira. Reference ID: 3989427 https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/018667s036lbl.pdf

2. Novak, J. E., & Ellison, D. H. (2022). Diuretics in states of volume overload: core curriculum 2022. American Journal of Kidney Diseases. https://pubmed.ncbi.nlm.nih.gov/35190215/

3. Khan, T. M., Patel, R., & Siddiqui, A. H. (2022). Furosemide. In StatPearls. StatPearls Publishing.

4. Oh SW, Han SY.   Loop Diuretics in Clinical Practice.   Electrolyte Blood Press. 2015 Jun;13(1):17-21. https://doi.org/10.5049/EBP.2015.13.1.17

5. Ding, Dalian, Hong Liu, Weidong Qi, Haiyan Jiang, Yongqi Li, Xuewen Wu, Hong Sun, Kenneth Gross, and Richard Salvi. "Ototoxic effects and mechanisms of loop diuretics." Journal of otology 11, no. 4 (2016): 145-156. https://www.sciencedirect.com/science/article/pii/S1672293016300629

6. Daily Weights. Internet. Obtained Feb 23, 2023. American Association of Heart Failure Nurses AAHFN. https://www.aahfn.org/mpage/dailyweights

 

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Nurse Beth

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Hi! Nice to meet you! I especially love helping new nurses. I am currently a nurse writer with a background in Staff Development, Telemetry and ICU.

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Ototoxicity is associated with rapid injection, severe renal impairment, use of higher than recommended doses, concomitant therapy with aminoglycoside antibiotics, ethacrynic acid, or other ototoxic drugs.

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Yes I understand but exactly what causes that ototoxicity? I keep reading that in the drug books but I don't understand the cause based on slow vs. rapid push.

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Loop diuretics (e.g., furosemide, ethacrynic acid, bumetanide) affect the potassium gradient of the stria vascularis, as well as the electrical potential of the endocochlear structure.[2,3]These medications produce tinnitus and hearing loss. The hearing loss may be perceptible to patients or may be apparent only with audiometric testing. Their toxicity is dose-related.[12] Thus, ototoxicity is more likely when the patient receives a rapid infusion of injectable loop diuretics in renal failure, which allows the medications to accumulate. Furosemide-related ototoxicity is usually reversible but may be permanent in rare instances (e.g., in patients with renal failure).[7] Ethacrynic acid is virtually obsolete, partly due to the potential for ototoxicity, especially when it was given intravenously to patients whose regimen also included aminoglycosides.[7]

Found on first page of a Google search. Source is Medscape.

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pepino23 said:
Yes I understand but exactly what causes that ototoxicity? I keep reading that in the drug books but I don't understand the cause based on slow vs. rapid push.

There are Na/K/Cl transporters in the stria vascularis. Large rapid doses disrupt or damage the transporters which will damage the stria vascularis which will kill the hair cells.

No hair, no hearing.

How the actual molecules bind and disrupt is beyond my knowledge of chemistry.

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