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Correction to Cohn, N Engl J Med 335(7):490-498 August 15, 1996.

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Volume 336:295-296 January 23, 1997 Number 4
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The Management of Chronic Heart Failure

 

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To the Editor: In his discussion of diuretic therapy in his excellent review of congestive heart failure (Aug. 15 issue),1 Dr. Cohn did not mention that resistance to diuretics frequently develops in patients with severe refractory heart failure. The underlying mechanisms include decreased drug delivery to the nephron due to reduced renal blood flow, competition with organic acids for active secretion, compensatory sodium retention, hypochloremia, and decreased absorption of sodium due to edema of the gastrointestinal tract. Resistance can often be overcome by administering large intravenous doses or continuous infusions of diuretics. For example, furosemide, in doses of up to 4000 mg daily, is well tolerated and can cause a diuresis of 3 to 10 kg of body weight per day.2 In a group of patients with congestive heart failure who were resistant to 250-mg intravenous bolus doses of furosemide, continuous infusions at rates as high as 168 mg per hour were effective.3 Most patients required oral doses of up to 1000 mg daily to prevent recurrent edema.

Congestive heart failure is the most common diagnosis-related group among patients over 65 years of age, with annual hospitalization costs estimated at $8 billion.4 Aggressive diuresis is essential in order to avoid prolonged hospitalization and excessive costs.


Patricia A. Howard, Pharm.D.
Marvin I. Dunn, M.D.
University of Kansas Medical Center
Kansas City, KS 66160-7231

References

  1. Cohn JN. The management of chronic heart failure. N Engl J Med 1996;335:490-498. [Free Full Text]
  2. Gerlag PGG, van Meijel JJ. High-dose furosemide in the treatment of refractory congestive heart failure. Arch Intern Med 1988;148:286-291. [Free Full Text]
  3. van Meyel JJ, Smits P, Dormans T, Gerlag PG, Russel FG, Gribnau FW. Continuous infusion of furosemide in the treatment of patients with congestive heart failure and diuretic resistance. J Intern Med 1994;235:329-334. [Medline]
  4. Garg R, Packer M, Pitt B, Yusuf S. Heart failure in the 1990s: evolution of a major public health problem in cardiovascular medicine. J Am Coll Cardiol 1993;22:Suppl A:3A-5A.
 
To the Editor: In his review of the management of heart failure, Dr. Cohn failed to mention that the fundamental pathophysiologic mechanism responsible for the clinical features and the eventual outcome of heart failure is the imbalance between the delivery of oxygen and the oxygen requirements in various tissues and organs. Heart failure can be defined, in essence, as the inability of the cardiac output to sustain the level of oxygen delivery necessary for the preservation of aerobic metabolism. The different mechanisms and indicators of cardiac function, such as preload, afterload, contractility, cardiac output, and ejection fraction, subserve this physiologic goal. The therapies for heart failure outlined in the article will fail if adequate oxygen delivery is not maintained. It is therefore puzzling that terms such as oxygenation, oxygen delivery, aerobic metabolism, and oxygen therapy were not mentioned.


Hamid Sahebjami, M.D.
Veterans Affairs Medical Center
Cincinnati, OH 45220

 
Dr. Cohn replies:

To the Editor: I agree with Drs. Howard and Dunn, who stress the importance of adequate diuresis in treating patients with intense sodium retention. Maintenance of normovolemia is a key to avoiding recurrent hospitalization. I prefer to use a second diuretic (metolazone, as outlined in my review) instead of massive doses of furosemide to achieve the desired effect. In most patients this therapy delivers enough solute to the ascending limb to render the loop diuretic more effective. Clearly, when this approach is not successful, the intravenous or oral high-dose regimens of furosemide that Howard and Dunn describe may be necessary.

Dr. Sahebjami's concept that heart failure is fundamentally a deficiency in tissue oxygen delivery is a simple, traditional view that probably can no longer be defended. In states of cardiogenic shock inadequate tissue oxygenation leads to organ system failure. In chronic heart failure the neurohormonal stimulation, cardiac and vascular structural remodeling, sodium retention, and exercise intolerance are not easily attributable to oxygen debt. Therapies that probably do not directly affect oxygen delivery appear to have long-term favorable effects, whereas some therapies that augment oxygen delivery may have a deleterious effect. Although hemodynamic abnormalities resulting in impaired oxygen delivery may be fundamental to the genesis of heart failure, they do not appear to account for the clinical manifestations that characterize the chronic disease.

There was an error in the second footnote of Table 3. The correct formula for creatinine clearance is as follows: (140 - age) ÷ serum creatinine concentration.


Jay N. Cohn, M.D.
University of Minnesota Medical School
Minneapolis, MN 55455

 


 

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