Congestive heart failure diuretics

Congestive Heart Failure Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology Systolic Dysfunction Diastolic Dysfunction HFpEF HFrEF
Causes
Differentiating Congestive heart failure from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Clinical Assessment
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
Cardiac MRI
Echocardiography
Exercise Stress Test
Myocardial Viability Studies
Cardiac Catheterization
Other Imaging Studies
Other Diagnostic Studies
Treatment
Invasive Hemodynamic Monitoring
Medical Therapy:
Summary
Acute Pharmacotherapy
Chronic Pharmacotherapy in HFpEF
Chronic Pharmacotherapy in HFrEF Diuretics ACE Inhibitors Angiotensin receptor blockers Aldosterone Antagonists Beta Blockers Ca Channel Blockers Nitrates Hydralazine Positive Inotropics Anticoagulants Angiotensin Receptor-Neprilysin Inhibitor Antiarrhythmic Drugs Nutritional Supplements Hormonal Therapies Drugs to Avoid Drug Interactions Treatment of underlying causes Associated conditions
Exercise Training
Surgical Therapy: Biventricular Pacing or Cardiac Resynchronization Therapy (CRT) Implantation of Intracardiac Defibrillator Ultrafiltration Cardiac Surgery Left Ventricular Assist Devices (LVADs) Cardiac Transplantation
ACC/AHA Guideline Recommendations Initial and Serial Evaluation of the HF Patient Hospitalized Patient Patients With a Prior MI Sudden Cardiac Death Prevention Surgical/Percutaneous/Transcather Interventional Treatments of HF Patients at high risk for developing heart failure (Stage A) Patients with cardiac structural abnormalities or remodeling who have not developed heart failure symptoms (Stage B) Patients with current or prior symptoms of heart failure (Stage C) Patients with refractory end-stage heart failure (Stage D) Coordinating Care for Patients With Chronic HF Quality Metrics/Performance Measures
Implementation of Practice Guidelines
Congestive heart failure end-of-life considerations
Specific Groups: Special Populations Patients who have concomitant disorders Obstructive Sleep Apnea in the Patient with CHF NSTEMI with Heart Failure and Cardiogenic Shock
Congestive heart failure diuretics On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Congestive heart failure diuretics
CDC on Congestive heart failure diuretics
Congestive heart failure diuretics in the news
Blogs on Congestive heart failure diuretics
Directions to Hospitals Treating Congestive heart failure diuretics
Risk calculators and risk factors for Congestive heart failure diuretics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Diuretics reduce circulating volume, improve symptoms and are a mainstay of therapy for congestive heart failure.

Mechanism of Benefit

• Reduce intravascular volume
• Lasix reduces preload and relaxes pulmonary venules and thereby reduce the symptoms of pulmonary edema
• Reduce wall stress
• Improve left ventricular remodeling
• Improve symptoms but not improve survival. In fact higher doses of lasix are associated with higher mortality, likely as a results of higher doses being a marker of more severe disease.

Complications

• Azotemia
• Hypokalemia
• Contraction or metabolic alkalosis
• Elevate neurohormones
• Thiazide diuretics are associated with hyponatremia

Thiazide Diuretics

• Although thiazide diuretics are effective in mild heart failure they are usually inadequate for the treatment of severe heart failure.
• Thiazide diuretics have also been associative with hyponatremia.

Lasix or Furosemide

• Fluid retention usually responds best to furosemide (Lasix)
• If there is no response to the initial dose then it can be increased by at least 50%.
• The maintenance dose of the diuretics lower than that required to initiate diuresis, and for lasix is usually 10 to 20 mg per day.
• The patient should be told to return to their physician in the next three to seven days after initiation for further assessment including assessment of their potassium concentration.
• Weight loss should not exceed 1 to 2 pounds/day.
• If the patient gains more than two pounds and they are instructed to double the dose of their loop diuretic.
• Once the baseline weight has been re-established than they can resume their previous status.
• Higher lasix doses are associated with higher mortality, likely as a surrogate of disease severity rather than part of a causal pathway.

• Intermittent use of metolazone into dose of 2.5 or 5 mg can be given if the patient is refractory to furosemide Lasix. Metolazone should be given in the inpatient setting.
• The role of potassium sparing diuretics such as spironolactone (Aldactone), amiloride, or triamterene remains the subject of controversy. Spironolactone is currently recommended as third line therapy for congestive heart failure.
• Extreme caution is necessary when adding a potassium sparing agent to the regiment that includes ACE inhibitors particularly when diabetes or renal disease is present because the patient can become hyperkalemic.

Loop Diuretics

• Agents in this class include Furosemide or lasix, bumetanide, ethacrynic acid and torsemide.
• Inhibit the Na+/K+/Cl- transporter.

Thiazide Diuretics

• Inhibit the Na+/Cl- co transporter in the distal convoluted tube.
• Recommended for management of mild chronic heart failure.

Potassium Sparing Diuretics

• Spironolactone, amiloride and triamterene.
• Inhibit principal cells in the distal convoluted tubule and cortical collecting duct.
• Inhibits Na reabsorbtion and Potassium secretion.
• Their significant side effect is hyperkalemia.

References

Template:WikiDoc Sources