What is the effectiveness of a sodium restricted diet on reducing weight gain and edema formation in adult patients with chronic heart failure?
Heart failure is a pathophysiologic state in which the heart is unable to generate sufficient cardiac output to the extent that there is inadequate perfusion of tissues or increased diastolic filling pressure of the left ventricle, or both, so that pulmonary capillary pressures are increased.1,2 Consequently, this results in typical manifestations of heart failure which are dyspnea, fatigue, exercise intolerance, fluid retention, pulmonary congestion and peripheral edema. It is estimated that nearly 10% of Americans older than age 65 have symptomatic heart failure and about 20% of adults older than 40 have some signs of myocardial dysfunction. According to statistics, in the past thirty years, heart failure related hospitalizations have increased an incredible 171%. The most common risk factors for heart failure are increasing age, hypertension, ischemic heart disease, obesity, diabetes, and renal failure. The most common cause for heart failure related hospitalizations is volume overload due to failure to manage a low-sodium diet.3 As heart failure incidence, prevalence, morbidity and mortality increase, personal and societal costs of this disease increase as well. Annual United States health care costs are 29.6 billion to care for persons with heart failure. At least 70% of this cost relates to hospitalization. Once patients with heart failure are discharged following an exacerbation, approximately 44% are readmitted within six months4. Frequent hospitalizations is one characteristic of heart failure, other consequences are seen in the reduced quality of life, increased caregiver burden, as well as a high rate of death.5
The climbing costs of heart failure make patient adherence to pharmacologic and non-pharmacologic treatment regimens absolutely essential. The foundation for non-pharmacologic recommendations is the maintenance of a low-sodium diet. However, the rate of adherence to a low-sodium diet is minimal. The non-adherence rates range from 35% to 71%. Consequently, this non-adherence results in symptom exacerbations and re-hospitalizations.6 It has been estimated that adherence to the medical regimen most importantly in the area of medications and diet, could prevent at least half of hospital admissions.7
To understand the basis of sodium restriction, it is important to understand the pathophysiology of heart failure. Sodium homeostasis and fluid balance are critical to the function of the human body. The regulation of blood pressure through the maintenance of blood volume is an adaptive mechanism that is controlled by the kidney's interpretation of sodium concentration in renal circulation that is a gauge for volume status in the body.8 In the presence of low cardiac output, resulting from decreased blood volume (regardless of the cause of the decreased volume), the macula densa of the renal glomerulus identifies a state of lower sodium concentration. Consequently, this stimulates the neurohormonal activation which in essence activates renin generation. Renin in turn sets in motion the cycle of biological responses that preserve blood pressure by means of sodium concentration, and in turn volume expansion.8 The therapies that target heart failure must target this cycle of events. If there are not adequate interventions that address this cycle, then vasoconstriction results, cardiac contraction increases, and the kidney enters a sodium-retentive state.8
Excessive sodium retention by the kidneys has been repeatedly shown to be a characteristic of heart failure, which essentially is the rationale for sodium restriction9. Abnormal distribution of sodium is a trait of even mild heart failure. Diuretics are known to improve symptoms of shortness of breath caused by pulmonary congestion, as well as edema and increased body weight caused by fluid retention. However, diuretics are known to adversely affect renal function, which is an independent risk factor for mortality in patients with heart failure. 10 One study showed that furosemide treatment (a loop diuretic), resulted in increased renin activity and aldosterone concentration in a low sodium diet as opposed to use with a high sodium diet. These results suggest direct activation of the renin-angiotensin-aldosterone system by furosemide, an indication that in the presence of a low sodium diet, the effect of diuretics may be more noticeable.11
Many identified physiologic mechanisms allow human beings to respond to increased salt intake. An increase in salt ingestion results in a reduction in the activity of the renin-angiotensin-aldosterone system (salt-retaining hormones) and an increase in the release of atrial natriuretic peptides (salt-losing hormones).12 These systems interact in turn with other paracrine systems within the kidney, such as the kalikrenin-kinin system and prostaglandins, which respond by enhancing or buffering the signals. Furthermore, an increase of salt intake results in less sympathetic nerve activity to the kidneys. The net effect of these responses is an increased daily elimination of sodium.12
Other factors that have a role in salt elimination are the plasma colloid oncotic pressures and renal arterial blood pressures. Dilution of plasma proteins reduces colloid oncotic pressure within the renal capillaries, which increases glomerular filtration and reduces tubular reabsorption of sodium and water. One factor, however, supersedes the others in maintaining the homeostasis of sodium and water and that is the arterial blood pressure to the kidney. 12 A rise in arterial blood pressure to the kidneys results in an increased excretion of sodium and water, a process known as pressure natriuresis (diuresis). The kidney's response to changes of arterial pressure defines the salt sensitivity of individuals and for the most part there seems to a genetic predisposition in individuals to be salt sensitive or salt resistant.12
In the Dahl S (salt-sensitive) rat, the primary animal model for heart failure with preserved systolic function, high sodium intake caused hypertension, ventricular and vascular stiffening, adverse renal modeling and subsequent heart failure. Target organ damage was precipitated by oxidative stress, local neurohormonal upregulation, and vascular inflammation in the heart and kidney caused by high sodium intake.13 In salt-sensitive humans, there is a propensity in some individuals to be more reactive to the effects of sodium, as evidenced by short term responses including but not limited to endothelial dysfunction, altered neurohormonal responses, oxidative stress and increased plasma volume. The research that was done with Hummel's group indicates that patients with a preserved systolic function who received documented sodium-restricted diet recommendations had decreased odds of 30-day combined death and readmission. No other discharge recommendation predicted 30-day outcomes.13
In a meta-analysis of 13 studies, it was noted that less salt was associated with lower blood pressure and lower risk of heart attacks, strokes and other cardiovascular events.14 In one research study published in 2011,15 a correlation was seen between a high sodium diet and acute decompensatory heart failure in ambulatory heart failure patients.15 It is documented that many early rehospitalizations, especially in elderly heart failure patients, are a result of sodium indiscretion. In hypertensive animal models and susceptible human beings, high dietary sodium intake leads to structural and physiologic changes that are implicated in the pathophysiology of the heart failure with preserved systolic function.15
In a pilot study16 done to evaluate dietary restriction instructions and effectiveness of recommendations by Philipson and others, it was noted that patients with congestive heart failure were able to reduce sodium and fluid intake when given specific guidelines with these recommendations as opposed to general information on heart failure.16Hence, the importance of a low salt diet, as part of comprehensive heart failure management, should be further explored for its utility in preventing hospitalizations by reducing edema and weight gain and consequently improving the quality of life for patients with this chronic illness. A preliminary search of the Joanna Briggs Library of Systematic Reviews, the Cochrane Library, CINAHL, PubMed and Current Contents has revealed that there is not currently a systematic review (either published or underway) on this topic.