Hyponatremia in Congestive Failure: Evidence Based Management

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Austin Internal Medicine
Review Article
Hyponatremia in Congestive Failure: Evidence Based
Management
Wessly P, Soherwardi S and Gandotra C*
Department of Internal Medicine, Howard University,
USA
Abstract
*Corresponding author: Charu Gandotra, Department
of Internal Medicine, Howard University, Clinical
Educator Track, Division of Cardiovascular Medicine,
College of Medicine, Howard University Hospital, 2041
Georgia Ave NW Washington DC 20060, USA
Received: June 14, 2016; Accepted: July 08, 2016;
Published: July 11, 2016
Hyponatremia frequently complicates management of Congestive Heart
Failure (CHF), either due to disease severity and/or due to diuretic use. It is an
independent predictor of increased morbidity and mortality in CHF. Evidence
suggests that there is significant variability among health care professionals
in the understanding of pathophysiology and management of hyponatremia
in hospitalized CHF patients. Adequate management of hyponatremia in CHF
may reduce in hospital mortality and CHF related hospital readmission rate.
This article will review the mechanism of hyponatremia in CHF; its prognostic
implications; and the available evidence based management strategies.
Keywords: Hyponatremia; Congestive heart failure; Ultrafiltration; Arginine
vasopressin antagonist; Tolvaptan
Introduction
Heart failure is a growing problem with more than 23 million
individuals affected worldwide and over 5.8 million affected in the
United States (US) [1]. In 2015, the medical cost related to Congestive
Heart Failure (CHF) in US was estimated at 31 billion dollars and is
projected to increase 3 fold by 2030 [2]. Hospital readmissions for
CHF are a major driver of this expense [3-5]. Hyponatremia is one of
the major predictors of hospital readmission in CHF [3,4]. Inadequate
treatment of hyponatremia in CHF is seen in 41.9% of patients and is
independently associated with about 50% increase in the odds of 30 day
unplanned readmission or death [5]. Management of hyponatremia,
especially in the setting of acutely decompensated CHF can be
challenging. Lack of a consistent approach causes hyponatremia to
be inappropriately managed in about 43.6% of patients [6]. Evidence
suggests that adequate management of hyponatremia in hospital
setting may help decrease CHF related morbidity, mortality, and
health care cost [6-10]. This article will review the mechanism of
hyponatremia in CHF; its prognostic implications; and the available
evidence based management strategies.
Pathophysiology of Hyponatremia
Congestive Heart Failure
in
Hyponatremia is defined as a serum sodium concentration of <
135 mEq/l. In CHF there is decrease in cardiac output and systemic
blood pressure which decreases the perfusion pressure of the carotid
sinus baroreceptor and renal afferent arteriole. This leads to release
of “hypovolemic hormones” such as renin, angiotensin II, Arginine
Vasopressin (AVP) and norepinephrine. These neuro-hormonal
changes limit salt and water excretion disproportionately leading to
volume overload and dilutional hyponatremia (Figure 1).
AVP binds to the Vasopressin-2 (V2) receptor subtype and
increases the number of Aquaporin-2 water channels, leading to
increased permeability of water in the collecting duct and enhanced
free water retention. Angiotensin II and norepinephrine release
limit distal sodium and water delivery by lowering Glomerular
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Filtration Rate (GFR) and by increasing proximal sodium and water
reabsorption. Angiotensin II also stimulates the thirst center of the
brain promoting increased water intake and further release of AVP
[7].
Besides these neuro-hormonal changes, concomitant diuretic use
in CHF worsens hyponatremia. As these neuro-hormonal changes are
related to the severity of CHF, hyponatremia is often seen in advanced
stages of CHF. This confounds the poor prognostic implications of
hyponatremia. It is uncertain if hyponatremia is directly associated
with increased mortality or if the serum sodium level is a surrogate
marker of a more severe underlying disease [8].
Prognostic Value of Hyponatremia
Congestive Heart Failure
in
Hyponatremia is an independent predictor of increased morbidity
and mortality in CHF. The prevalence of hyponatremia in acute heart
failure ranges from 8-28% [9,10]. Studies have shown that in patients
hospitalized with acute CHF, hyponatremia was independently
associated with lower short term and long term survival; longer
hospital stay, and increased readmission rates [11,12]. Table 1
summarizes the landmark studies elucidating the prognostic value of
hyponatremia in CHF.
Pharmacological
Management
of
Hyponatremia in Congestive Heart Failure
Fluid restriction
As described in the introduction, AVP dysregulation and the
Renin Angiotensin Aldosterone System (RAAS) are involved in
the pathogenesis of hyponatremia in CHF. Fluid restriction is the
most inexpensive modality to achieve a negative water balance in
these patients. Fluid restriction to less than 1000ml/day in patients
with sodium less than 137mg/dl leads to significant improvement in
heart failure symptoms [13]. Many patients with heart failure have
increased thirst which reduces compliance with strict fluid restriction
[14].
Citation: Wessly P, Soherwardi S and Gandotra C. Hyponatremia in Congestive Failure: Evidence Based
Management. Austin Intern Med. 2016; 1(1): 1004.
Austin Publishing Group
Gandotra C
serum sodium levels, but there is only modest improvement in CHF
outcomes, such as reduction of length of stay and readmission rates.
Thus, this strategy is not as effective as tolvaptan [21,23] and may
worsen fluid overload in advanced CHF patients with cardio renal
syndrome and diuretic resistance.
HEART FAILURE
DECREASED CARDIAC OUTPUT
Non Pharmacological
Hyponatremia in CHF
INCREASE IN
SYMPATHETIC
RAAS ACTIVATION
INCREASED
ALDOSTERONE
INCREASED NON OSMOTIC AVP RELEASE
INCREASED
ANGIOTENSIN II
DECREASED SODIUM AND WATER
DELIVERY TO THE COLLECTING DUCT
INCREASED THIRST
INCREASED WATER
RETENTION
INCREASED FREE
WATER INTAKE
DECREASED FREE WATER
EXCRETION
HYPONATREMIA
Figure 1: Schematic representation of hyponatremia in CHF.
AVP antagonist, Tolvaptan is another available treatment
modality for hyponatremia in CHF. AVP plays a pivotal role in the
decline of sodium concentration in CHF. AVP antagonist, Tolvaptan
potentiates excretion of electrolyte free water and increases serum
sodium concentration. Tolvaptan has been shown to reduce
body weight, increase urine volume, and increase serum sodium
concentration in patients with CHF. Meta-analytical studies suggest
that tolvaptan is safe, as it does not cause worsening of renal function
or hypotension [15-16]. CHF patients on tolvapatan should not be
placed on fluid restriction. It is also essential to monitor serum sodium
levels every 6-8 hours to avoid rapid correction of hyponatremia [17].
Tolvaptan may confer some mortality benefit in a subgroup of CHF
patients with hyponatremia. However, evidence supporting mortality
benefit is inconsistent 15 [18].
EVEREST trial, a double blind randomized control trial, studied
the use of tolvaptan in patients with worsening CHF. In acute CHF
patients with mild to moderate hyponatremia, tolvaptan use showed
reversal of hyponatremia. Tolvaptan group had an improvement in
serum sodium level of 6.6 mEq/L over 5 days, however, there was no
effect on long term mortality or morbidity [19].
Hypertonic saline with Furosemide has been the mainstay
of treatment of hyponatremia in patients with CHF with fluid
overload. Loop diuretics are preferred because they increase
electrolyte-free water clearance [20]. Addition of loop diuretic
to Angiotensin Converting Enzyme Inhibitors (ACEI) also helps
reverse hyponatremia in CHF patients [21]. This combination of loop
diuretic with ACEI has been effective in moderate hyponatremia due
to improvement in diluting capacity of the kidneys [22]. Though,
hypertonic saline with furosemide is associated with increase in
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Management
of
Ultra-Filtration (UF) is a method of removing fluid from the
vasculature without removal of solutes or electrolytes. This method
was described as early as 1974 to treat volume overload in CHF
patients [24]. Since then several studies have compared UF with
pharmacological therapies in CHF. UF improves congestion, lowers
right atrial and pulmonary capillary wedge pressure, decreases neurohormone levels, corrects hyponatremia, restores diuresis, and reduces
diuretic requirement [23,25]. However, UF has not been shown to
improve CHF related outcomes such as hospital re-admission rate or
mortality.
In the EUPHORIA trial, Coztanzo et al [26] showed that early UF
safely and effectively reduced congestion in Acute Decompensated
Heart Failure (ADHF). In this trial UF was initiated within 4.7 ± 3.5
hours of hospitalization in 20 CHF patients with volume overload
and diuretic resistance (age 74.5 ± 8.2 years; 75% ischemic disease;
ejection fraction 31 ± 15%). UF was initiated at a maximum rate
of 500 cc/h and was continued until euvolemia was achieved and
symptoms resolved. If systolic BP fell to ≤ 80 mm Hg, UF rate was
reduced to 200 cc/h. Re-evaluation was done each hospital day
during hospitalization, at 30 days, and at 90 days. Results showed
that early UF permitted discharge of 60% of the high risk acutely
decompensated CHF patients in ≤ 3 days compared to the ADHERE
study where median CHF hospital length of stay was 4.3 days [27].
In spite of the large amount of fluid removed by UF, there was no
associated worsening of renal failure, electrolyte abnormalities or
symptomatic hypotension. Thus, UF is an effective management
strategy for patients with hyponatremia and ADHF.
UNLOAD trial [28] compared UF with standard intravenous
(IV) diuretic treatment in ADHF patients. This was a multicenter
prospective randomized control trial of 200 ADHF patients (mean
age 63 ± 15 years, with 69% men, 71% had LVEF ≤ 40%). The
duration and rate (maximum 500 ml/h) of fluid removal by UF were
decided by treating physicians. In the UF group, fluid was removed
at an average rate of 241 ml/h for 12.3 ± 12 hours. In the standardcare group, average IV daily diuretic dose during the 48 hours after
randomization was 181 ± 121 mg. At 48 hours, the UF group lost
significantly more weight (5.0 ± 3.1 kg vs. 3.1 ± 3.5 kg; p = 0.001)
and fluid (4.6L vs. 3.3 L; p = 0.001) than the diuretic cohort. Dyspnea
scores did not differ significantly between the two groups. The CHF
readmission rate was significantly lower in the UF group (32% versus
18%; p = 0.037). Neither serum creatinine (baseline 1.5 mg/dl) at
hospital discharge nor length of hospital stay differed between the
treatment groups. No clinically significant changes in serum blood
urea nitrogen, sodium, chloride, and bicarbonate, occurred in either
group.
The findings of significant weight loss and fluid removal without
change in serum creatinine with UF in EUPHORIA and UNLOAD
Austin Intern Med 1(1): id1004 (2016) - Page - 02
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Gandotra C
Table 1: Prognostic implications of hyponatremia in CHF.
Source
Aim
Sample
size
Prevalence of
hyponatremia
Inclusion criteria
Outcome
ESCAPE
2005 [31]
Association of serum sodium
level with 6-month post-discharge
all- cause mortality and CHF rehospitalization
433
23.8%
Heart failure with reduced
ejection fraction(HFrEF)
NYHA class IV
OPTIMIZE-HF
2007 [32]
Relationship between admission
serum sodium and clinical
outcomes in hospitalized CHF
patients.
48,612
19.7%
New-onset or worsening
CHF
Baldasseroni
et al
2011 [33]
Investigate the relation between
hyponatremia and mortality
4670
≈10%
Hospitalized due to
worsening CHF
Analysis from the
Clinical impact of hyponatremia
Korean Heart Failure improvement during hospitalization
(KorHF) registry
on post discharge outcome in
2012 [34]
patients admitted for acute CHF
2888
19.9%
Patients with acute CHF
Banish etal.
2014 [35]
Prevalence, risk factors, and longterm outcomes of hyponatremia
in ambulatory heart failure with
preserved ejection fraction
(HFpEF) and HFrEF
8862
12.9% in HFpEF
and
13.8% in HFrEF
Cohort of veterans with CHF
treated in ambulatory clinics
JCARE-CARD
database
2014 [36]
Association of hyponatremia with
in-hospital and long-term outcomes
1659
10.6%
Hospitalized due to
worsening CHF; mean left
ventricular ejection fraction
(LVEF) was 42.4%
COAST
2015 [37]
Predictive value of hyponatremia in
hospitalized Asian CHF patients
1470
16.8%
≥ 18 years of age who were
hospitalized for CHF with
LVEF< 45%
HARVEST
registry
Lu etal
2016 [38]
Association of the severity of
hyponatremia and changes of
serum sodium levels with longterm outcome
2556
14.08%
New or exacerbated
symptoms and signs of CHF
trials are contrary to the results seen in CARRESS-HF trial. CARESSHF trial [29] was a randomized control trial, that randomly assigned
188 patients with ADHF to receive either IV diuretic therapy (n=94)
or UF (n=94). Patients were followed for 60 days. In the patient subset
with ADHF and abnormal renal function, UF did not cause fluid or
weight loss at 96 hours, but led to an increase in serum creatinine.
There was no significant difference between the two groups with
respect to mortality and re-hospitalization. At 96 hours, serum
sodium level in IV diuretic group increased more than the UF group
(0.0 ± 3.6 vs. -2.3 ± 3.5, p < 0.001). These findings illustrate that,
despite significant relief of congestion with or without preservation of
renal function, UF did not lead to reduction in CHF re-hospitalization
rates or mortality.
While UF removes isotonic fluid without exchange in solute or
electrolytes, Hemodialysis (HD) involves significant exchange of
electrolytes and solutes between dialysate solution and blood across
a semi-permeable membrane. Combination of HD and UF is often
used in patients with renal failure to correct volume overload and
electrolyte abnormalities, with clearance of toxins [30]. Thus UF is an
available treatment modality for ADHF patients with hyponatremia;
however, its use should be individualized based on the severity of
renal dysfunction associated with ADHF.
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Hyponatremia was an independent
predictor of all-cause mortality (p value
= 0.04), CHF re-hospitalization (p
value 0.03) and combined death or rehospitalization (p value = 0.01).
Hyponatremia was associated with
longer length of stay; and greater inhospital and post-discharge mortality
(p value <0.0001)
Serum Sodium decrease of 1 mEq/L
was associated with 10% increase in
all cause mortality(p<0.001) and 3%
increase in risk for hospitalization( p=
0.005)
Persistent hyponatremia is associated
with increased incidence of death or rehospitalization
(HR 1.345, 95% CI 1.075 to 1.683,
p=0.010)
Hyponatremia was a predictor of allcause mortality in both HFrEF(p <0.001)
and HFpEF(p = 0.004); and predictor
of all-cause hospitalization in HFrEF (p
<0.001)
but not in HFpEF (p = 0.21)
Hyponatremia was independently
associated with in-hospital(p <0.001);
and long-term adverse outcomes –all
cause death, cardiac death and rehospitalization due to CHF (p < 0.001)
Hyponatremia was an independent
predictor of 12-month mortality (p<
0.008) and increased 12-month rehospitalization rate (p = 0.002)
Independent predictor for all-cause and
cardiovascular mortality
( P value = <0.001);
Severe hyponatremia (<125 mEq/L) was
associated with worse clinical outcomes
Given the above study the question that arises is whether UF
seems justified due to its high cost and no advantage in comparison
to pharmacologic therapy. CARESS-HF study cannot lead us to a
definitive conclusion because in CARESS-HF, the duration of UF was
longer than other studies which could have resulted in elevated serum
creatinine secondary to intravascular volume depletion.
Conclusion
Hyponatremia in CHF is associated with increased morbidity
and mortality. Inadequate treatment of hyponatremia in patients
admitted for acutely decompensated heart failure is frequent and
is associated with poor outcomes. Fluid restriction; Tolvaptan use;
hypertonic saline with loop diuretic use; and dialysis are the available
treatment modalities which improve morbidity but not mortality.
Patients with CHF complicated by hyponatremia should be carefully
evaluated in terms of their fluid status, cardiorespiratory status,
and renal function prior to initiating any of the above mentioned
therapeutic approaches. Treatment of hyponatremia in HF needs to
be tailored to the individual patient.
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Gandotra et al. © All rights are reserved
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Citation: Wessly P, Soherwardi S and Gandotra C. Hyponatremia in Congestive Failure: Evidence Based
Management. Austin Intern Med. 2016; 1(1): 1004.
Austin Intern Med 1(1): id1004 (2016) - Page - 05

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