Should my patient with compensated heart failure be placed on a sodium-restricted diet?

Although sodium restriction is routinely recommended for patients with heart failure (HF), the data is often conflicting with a number of studies suggesting that it may be harmful in some HF patient. 

Two randomized trials (by the same group) involving patients with compensated HF recently discharged from the hospital reported that “less restricted” sodium diet (2.8 gm/d) along with fluid restriction (1 liter/d) and high-dose furosemide (at least 125-250 mg furosemide bid) was associated with less rates of readmissions and improved levels of brain natriuretic peptide, aldosterone and plasma renin activity when compared to patients on more restricted sodium diet (1.8 gm/d).1,2

Analysis of data from the multihospital HF Adherence and Retention Trial enrolling New York Heart Association functional class II/III HF patients found that sodium restriction (<2.5 gm/d) was associated with significantly higher risk of death or HF hospitalization but only in patients not on an angiotension converting enzyme inhibitor or angiotensin receptor blocker.3

In normal subjects who are not sodium deprived, excess sodium intake has been shown to cause expansion of intravascular volume without increasing total body water.4 Thus, sodium restriction combined with diuretics may reduce intravascular volume and renal perfusion, further stimulating the renin-angiotensin-aldosterone system and fluid retention.5

Now that’s interesting! Did you know that the 2013 American College of Cardiology Foundation/American Heart Association guidelines downgraded the recommendation for sodium restriction to Class IIa (reasonable) with Level of Evidence:C? 6

 

References

  1. Paterna S, Gaspare P, Fasullo S, et al. Normal-sodium diet compared with low-sodium diet in compensated congestive heart failure: is sodium an old enemy or a new friend? Clin Sci 2008;114:221-230. https://www.ncbi.nlm.nih.gov/pubmed/17688420
  2. Paterna S, Parrinello G, Cannizzaro S, et al. Medium term effects of different dosage of diuretic, sodium, and fluid administration on neurohormonal and clinical outcome in patients with recently compensated heart failure. Am J Cardiol 2009;103:93-102. https://www.ncbi.nlm.nih.gov/pubmed/19101237
  3. Doukky R, Avery E, Mangla A, et al.Impact of dietary sodium restriction on heart failure outcomes. J Am Coll Cariol HF 2016;4:24-35. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4705447/
  4. Heer M, Baisch F, Kropp J et al. High dietary sodium chloride consumption may not induce body fluid retention in humans. Am J Physiol Renal Physiol 2000;278:F585-F595. https://www.ncbi.nlm.nih.gov/pubmed/10751219
  5. Rothberg MB, Sivalingam SK. The new heart failure diet: less salt restriction, more micronutrients. J Gen Intern Med 25;1136-7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2955483/
  6. Yancy CW, Jessup M, Bozkurt B, et al. 2013 CCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013;62:e147-239. https://www.ncbi.nlm.nih.gov/pubmed/23741058
Should my patient with compensated heart failure be placed on a sodium-restricted diet?

Is central sleep apnea-Cheyne-Stokes respirations (CSA-CSR) in the setting of heart failure (HF) detrimental?

CSA-CSR is characterized by a crescendo-decrescendo pattern of 20-30 second hyperventilation followed by 10- 40 second hypopneas or apneas during exercise, wakefulness or stages 1 and 2 non-rapid eye movement sleep (1,2). CSA-CSR is associated with elevated pulmonary capillary wedge pressure, ventricular dilatation, atrial fibrillation, and increased central and peripheral chemosensitivity to arterial C02 levels (1).

In contrast to obstructive sleep apnea whose detrimental impact is widely accepted, CSA-CSA has not consistently been shown to be associated with higher mortality rates, with some even arguing for its beneficial effects in HF by providing intrinsic positive end-expiratory pressure (PEEP), augmented stroke volume, avoidance of hypercapnic acidosis, attenuated sympathetic activity, bronchodilation and cyclic respiratory muscle rest, akin to those seen with episodic CPAP (2). This is an interesting way of looking at CSA-CSR, underscoring the importance of addressing the underlying problem (e.g. HF) rather than the symptoms alone.

1. Rosen D, Roux FJ, Shah N. Sleep and breathing in congestive heart failure. Clin Chest Med 2014, 35: 521–534. https://www.ncbi.nlm.nih.gov/pubmed/25156768

2. Naughton MT. Cheyne-Stokes respiration: friend or foe. Thorax 2012;67:357-360. http://thorax.bmj.com/content/thoraxjnl/67/4/357.full.pdf

Is central sleep apnea-Cheyne-Stokes respirations (CSA-CSR) in the setting of heart failure (HF) detrimental?