Benefit of natriuresis and cardiac resynchronisation therapy in acute decompensated heart failure with cardiorenal syndrome and hypernatraemia

  1. Abdulrahman Tawfiq Khojah 1,
  2. Emma Katz 2,
  3. Romina Pace 3 and
  4. Rajkumar Rajendram 4 , 5
  1. 1 Heart Center, King Faisal Specialist Hospital and Research Center, Riyadh, Central Region, Saudi Arabia
  2. 2 Department of Medicine, McGill University, Montreal, Quebec, Canada
  3. 3 Centre for Outcomes Research and Evaluation, Department of Medicine, McGill University, Montreal, Quebec, Canada
  4. 4 College of Medicine, King Saud bin Abdulaziz University for Health Sciences College of Medicine, Riyadh, Al Riyadh Province, Saudi Arabia
  5. 5 Department of Medicine, King Abdulaziz Medical City, Riyadh, Al Riyadh Province, Saudi Arabia
  1. Correspondence to Dr Rajkumar Rajendram; rajkumarrajendram@doctors.org.uk

Publication history

Accepted:22 Jun 2022
First published:04 Jul 2022
Online issue publication:04 Jul 2022

Case reports

Case reports are not necessarily evidence-based in the same way that the other content on BMJ Best Practice is. They should not be relied on to guide clinical practice. Please check the date of publication.

Abstract

A man in his eighties with acute heart failure and cardiorenal syndrome developed severe hypernatraemia with diuresis. In this situation, palliation is often considered when renal replacement therapy is inappropriate. The literature to guide treatment of dysnatraemia in this setting is limited. Diuretics often worsen hypernatraemia and fluid replacement exacerbates heart failure. We describe a successful approach to this clinical Catch-22: sequential nephron blockade with intravenous 5% dextrose. Seemingly counterintuitive, the natriuretic effect of this combination had not previously been compared with diuretic monotherapy for heart failure. Yet this immediately effective strategy generated a high natriuresis-to-diuresis ratio and functioned as a bridge to cardiac resynchronisation therapy (CRT). In conjunction with a low salt diet, CRT facilitated the maintenance of sodium homeostasis and fluid balance. Thus, by improving the underlying pathophysiology (ie, inadequate cardiac output), CRT may enhance the outcomes of patients with cardiorenal syndrome and hypernatraemia.

Background

Severe heart failure with volume overload is usually associated with normal or low serum sodium.1 This typically improves with diuresis and restriction of salt intake.1 While less common in the setting of hypervolaemia due to decompensated heart failure, hypernatraemia poses a therapeutic challenge and carries a dismal prognosis.1–3 There are few data regarding hypernatraemia in heart failure with cardiorenal syndrome. The literature to guide management is lacking. Diuretics can worsen hypernatraemia and fluid replacement may exacerbate volume overload. The present case report describes a novel solution to this clinical challenge.

Case presentation

A man in his 80s with heart failure with reduced ejection fraction (HFrEF) presented to the emergency department with breathlessness at rest, orthopnoea and bilateral lower limb swelling. He had atrial fibrillation with complete heart block for which he had received a ventricular pacemaker. He also had coronary artery disease and valvular heart disease. These had been treated with bypass surgery and mechanical mitral and aortic valve replacement. However, he had developed moderate paravalvular aortic regurgitation (AR) and severe tricuspid regurgitation. Other relevant comorbidities included hypertension, chronic kidney disease (CKD) stage 3b (baseline serum creatinine 140 µmol/L) and early dementia.

The patient was frequently admitted to hospital with decompensated HFrEF despite maximal tolerated medical therapy (bisoprolol 2.5 mg one time a day, sacubitril/valsartan 24/26 mg two times a day, spironolactone 12.5 mg one time a day and furosemide 40 mg two times a day) and regular outpatient follow-up.

On this presentation to the emergency department, he was afebrile and haemodynamically stable (heart rate 62 beats/min, paced atrial fibrillation; blood pressure 115/64 mm Hg) but oxygen dependent (oxygen saturation 94% on 40% oxygen delivered via a Venturi mask).

Physical examination found New York Heart Association (NYHA) class IIIb dyspnoea and severe pitting oedema of the lower limbs. The jugular venous pressure was markedly raised with a large cv wave (due to tricuspid regurgitation) and absent a wave. The abdominal jugular reflex was also positive. The regular (paced) pulse was collapsing in nature. On auscultation, the first and second heart sounds were mechanical and a grade 3 early diastolic murmur (consistent with the known paravalvular AR) was audible.

Sacubitril/valsartan and spironolactone were held, salt and fluid restrictions were recommended and intravenous furosemide was administered (80 mg). Regular intravenous furosemide (20 mg three times a day) was started the following morning. While this therapy improved the symptoms and signs of volume overload, the patient developed hypernatraemia (serum sodium 152 mEq/L), and contraction alkalosis (pH 7.5) while the renal function deteriorated.

Investigations

Transthoracic echocardiography performed 7 months before this presentation demonstrated a severely dilated left ventricle with several regional wall motion abnormalities (hypokinesis–akinesis) and moderate paravalvular AR. The left ventricular (LV) ejection fraction reported (LVEF; 30%–35%) overestimated the effective cardiac output as AR was present. Moderate right ventricular hypokinesis was also seen with severe tricuspid insufficiency (estimated right atrial pressure>20 mm Hg) and severe pulmonary hypertension (estimated pulmonary artery systolic pressure>80 mm Hg).

On this presentation with acute biventricular decompensation, the patient also had acute renal impairment (serum creatinine 225 µmol/L). The serum sodium concentration was initially 138 mEq/L. Hypernatraemia developed on diuresis. The ECG showed atrial fibrillation and a paced ventricular rhythm with left bundle branch block (LBBB) morphology (figure 1). The chest X-ray (CXR; figure 2) showed severe cardiomegaly with bilateral interstitial oedema. The COVID-19 PCR test was negative.

Figure 1

The ECG performed prior to initiation of cardiac resynchronisation therapy. The ECG performed on day 21 (prior to implantation of the cardiac resynchronisation therapy pacemaker) shows atrial fibrillation and a paced ventricular rhythm with left bundle branch block morphology (QRS duration 226 ms). The ECG performed on admission was similar.

Figure 2

The chest X-ray (CXR) performed on admission. The CXR performed on admission shows cardiomegaly, mechanical mitral and aortic valves and a ventricular pacemaker with bilateral pulmonary oedema.

Figure 3 illustrates the effect of treatment on the patient’s functional status, weight and laboratory test results over the first 4 weeks of his admission. Table 1 provides further details and also correlates the patient’s symptoms, physical signs and volume status with his laboratory test results and treatment. Figure 4 shows a CXR performed 3 weeks after admission.

Figure 3

The effect of select therapeutic interventions on the patient’s functional status, weight and laboratory data. This figure illustrates the effect of select therapeutic interventions on the patient’s weight and functional status (measured using the New York Heart Association classification). These variables are also correlated with changes in serum creatinine, sodium, chloride and bicarbonate over the first 4 weeks of the patient’s admission. Further details are provided in table 1. The grey bands superimposed on the graphs indicate the reference ranges of serum sodium (133–143 mmol/L), chloride (100–109 mmol/L) and bicarbonate (23–29 mmol/L). D5W: dextrose 5% water.

Figure 4

The chest X-ray performed on day 21. The chest X-ray performed on day 21 (after implantation of the cardiac resynchronisation therapy pacemaker) demonstrates clear lung fields without pulmonary oedema. At this point, the furosemide had been stopped and the salt restriction had been relaxed slightly.

Differential diagnosis

The patient presented with pulmonary oedema, peripheral oedema and acute renal impairment then developed hypernatraemia after diuresis. Proteinuria was absent. The liver enzymes and coagulation profile were unremarkable. These findings excluded nephrotic syndrome and liver cirrhosis. The nature of the peripheral oedema (ie, pitting) and improvement with diuresis excluded lymphoedema. In the context of the patient’s multiple cardiac comorbidities including HFrEF, previous similar presentations and raised brain natriuretic peptide (BNP; 469 pg/mL) the most likely cause of the initial presentation was acute decompensation of heart failure.

The patient also had an acute kidney injury (AKI). Obstruction of the renal tract was excluded on insertion of a urinary catheter and renal tract ultrasound. Intrinsic renal injury and urinary tract infection were excluded by urine analysis.

The low fractional excretion of urea and high serum urea:creatinine ratio indicated prerenal AKI. However, the patient initially presented with volume overload. So, intravascular hypovolaemia was unlikely to have caused the AKI. The absence of liver disease excluded hepatorenal syndrome. Reduction of renal perfusion and renal congestion due to HFrEF with severe tricuspid regurgitation were thought to have caused the AKI (ie, cardiorenal syndrome). Improvement in renal function with natriuresis and cardiac resynchronisation therapy (CRT) supported this diagnosis.

Hypernatraemia is classified by changes in sodium mass balance (EMB) relative to the water mass balance (VMB).4 On presentation, the serum sodium was normal. After administration of furosemide the oedema improved, but hypernatraemia developed despite the persistent fluid overloaded (ie, hypervolemic hypernatraemia). Furosemide had induced diuresis such caused a greater fall in VMB than in EMB.

When hypernatraemia developed, the only cause of significant water loss was diuresis. Excessive salt intake was unlikely as the patient was salt restricted and his oral intake was poor. The improvement in the signs and symptoms of hypervolaemia, and initial worsening of renal function with high serum urea:creatinine ratio and metabolic alkalaemia supported the diagnosis of diuretic-induced hypernatraemia.

Treatment

As the patient’s oral intake was poor, the hypernatraemia and contraction alkalaemia did not resolve with oral free water alone. Intravenous 5% dextrose (80 mL/hour) was started on day 4. However, despite ongoing therapy with intravenous furosemide (20 mg three times a day), this worsened the fluid overload. Pulmonary oedema and peripheral oedema manifested on day 5. The dextrose was stopped and an additional dose of intravenous furosemide (40 mg) was given. A vicious cycle arose; increased diuresis-induced severe hypernatraemia (venous blood gas sodium 160 mEq/L) with altered mental status.

Renal replacement therapy was considered. However, in view of the patient’s advanced age, significant comorbidities, dementia and frailty, palliation was also discussed with the patient’s relatives. The patient’s family stated that he would not want renal replacement therapy or cardiopulmonary resuscitation to be attempted. Nevertheless, it was decided that active management should continue while the AKI was improving.

The navigation of Scylla and Charybdis remained. Diuresis for hypervolaemia risked worsening hypernatraemia while administration of free water for severe hypernatraemia could induce pulmonary oedema. This clinical Catch-22 was resolved by infusion of 5% dextrose alongside furosemide, metolazone and spironolactone to achieve a higher natriuresis-to-diuresis ratio. This was started on day 6 with meticulous monitoring of fluid balance. Spironolactone and bisoprolol were resumed the next day.

The assessments included hourly measurements of fluid intake and urine output, 6 hourly monitoring of vital signs, and daily assessment of symptoms, neurological status, 24-hour fluid balance, and weight. The 5% dextrose infusion was titrated using 6 hourly measurements of the serum sodium concentration to prevent overzealous correction of the hypernatraemia.

By day 11, the patient’s mental status, renal function and electrolytes had returned to their preadmission baselines. The patient’s oral intake also increased. Despite stopping the 5% dextrose on day 12, the serum sodium concentration remained stable. The patient’s exercise tolerance had improved significantly, but he continued to desaturate on exertion. Therefore, a CRT pacemaker was implanted to enhance cardiac contractility on day 21.

The postprocedure ECG (figure 5) confirmed resolution of pacemaker-induced ventricular dyssynchrony (figure 1). To simulate the outpatient setting, the salt and fluid restrictions were relaxed slightly, volume status was monitored less rigorously, metolazone was stopped and furosemide was administered only as required.

Figure 5

ECG performed after initiation of cardiac resynchronisation therapy. The ECG performed on day 21 (after implantation of the cardiac resynchronisation therapy pacemaker) shows atrial fibrillation and a paced ventricular rhythm. In comparison to the ECG performed prior to cardiac resynchronisation therapy (figure 1), the QRS complexes have narrowed demonstrating successful biventricular synchronisation (QRS duration<120 ms).

Outcome and follow-up

Success was evidenced by improvement in clinical and laboratory markers of fluid and sodium homeostasis (figure 3, table 1). Serum BNP improved from 469 pg/mL on admission to 76 pg/mL after CRT. Some reduction in BNP is to be expected with improvement in renal function and on withholding sacubitril/valsartan. However, serial 2 min walk tests also confirmed improvement in functional status. The patient had become less frail, engaging in physiotherapy with minimal limitation. Thus, the precipitous fall in BNP is likely to reflect the recovery of some cardiac function.

The patient was discharged home in a stable condition. He and his family were given clear recommendations for fluid restriction and salt intake. They were also advised to administer furosemide if the patient’s weight increased by 1 kg or more.

The patient attended outpatient follow-up with internal medicine and heart failure specialists, one and 2 months post discharge, respectively. At each visit clinical, laboratory and imaging variables confirmed that functional status, sodium homeostasis and fluid balance were maintained. Sacubitril/valsartan was restarted. Echocardiography performed 1 year post discharge revealed normalisation of the dimensions of the LV cavity and improvement of LVEF to 35%–40%.

Telephone interviews were conducted with the patient’s family 5 and 12 months post discharge. These confirmed that salt and fluid restrictions were being respected. The patient’s weight was being monitored daily and had plateaued around 70 kg. As a result, the patient remained stable with NYHA class II dyspnoea allowing for an autonomous lifestyle in his own home.

Discussion

Hypernatraemia is associated with increased mortality and morbidity in heart failure.1–3 The present case report describes successful treatment of acute decompensated HFrEF and cardiorenal syndrome when severe hypernatraemia developed with loop diuretic monotherapy. The patient required greater natriuresis than diuresis but therapeutic options were limited by refusal of dialysis.

A quantitative approach to hypervolaemic hypernatraemia5 was applied. The calculated doses of furosemide and 5% dextrose improved the signs of heart failure at the cost of severe symptomatic hypernatraemia. A thiazide diuretic and a mineralocorticoid receptor antagonist were added to increase the natriuresis-to-diuresis ratio. Sodium-glucose co-transporter-2 inhibitors also intensify natriuresis and reduce mortality in heart failure.6 However, these were contraindicated by poor oral intake and AKI.

Doses of spironolactone below 50 mg daily are not thought to induce natriuresis.7 However, natriuresis increased slightly when spironolactone 25 mg daily was added to furosemide and metolazone (table 1).

Table 1

Correlation of the relevant clinical findings, laboratory data and therapeutic interventions

Clinical sign/
investigation/intervention		 Admission time line (days after admission)
Days after admission 0 2 3 4 5 9 11 14 27 88
Metolazone 2.5 mg one time a day 2.5 mg one time a day 2.5 mg one time a day 2.5 mg one time a day, last dose.
Furosemide 20 mg intravenously three times a day 20 mg intravenously three times a day 20 mg intravenously three times a day, extra 40 mg intravenously was given for acute overload. 20 mg intravenously three times a day 40 mg intravenously two times a day 40 mg intravenously two times a day until day 13 80 mg PO two times a day until day 15 40 mg PO two times a day 20–40 mg PO PRN 20–40 mg PO PRN
Spironolactone Held Resumed 25 mg one time a day 25 mg one time a day 25 mg one time a day 25 mg one time a day 25 mg one time a day 25 mg one time a day
D5W 80 mL/h for 8 hours, stopped due to overload. Held 80–120 mL/hour 80–120 mL/hour 80–120 mL/hour stopped day 12
Sacubitril/
valsartan		 Held Resumed 24/26 mg two times a day 24/26 mg two times a day
Bisoprolol Held Resumed 2.5 mg one time a day 2.5 mg one time a day 2.5 mg one time a day 2.5 mg one time a day 2.5 mg one time a day 2.5 mg one time a day
NYHA IIIb IIIa IV IIIa IIIa IIIa II II II II
Extremity oedema +++ +++ ++++ ++ ++ ++ + – – –
AJR* ++ + +++ + + + + + -/ND -/ND
Walking test Frail, unable. Frail, unable. Frail, unable. Frail, unable. Frail, unable. Exertional desaturation ++ ++ +++ +++
Weight (kg)** ND ND ND 73.2 75 76 69.9 69.5 69.5 70
O2 saturation 94% 98% 95% 92% 92% 90% 90% 92% 95% ND
Oxygen (L/min) 4 2 1 RA RA RA RA RA RA RA
Days after admission 0 2 3 4 5 9 11 14 27 88
Serum BNP (pg/mL) 469 148 76 106
Serum Cr (μmol/L) 225 259 258 221 210 199 207 183 160 153
Serum Na (mEq/L) 138 → 147 on day 3 152 → 150 post D5W 154 after stopping D5W 156 152 → 145 on day 8 146 145 147 → 142 on day 18 139 141
Serum osmolality (mmol/kg) 361 342 → 336 on day 9 347 340
Serum K (mEq/L) 6.2 5.1 4.9 4.6 4.5 5.3 4.3 4.4 4.2 4.1
Serum Cl (mEq/L) 115 122 119 125 118 104 100 102 101 104
Serum bicarbonate (mmol/L) 22 24 25 28 28 30 34 32 27 24
Venous pH 7.27 7.50 7.36
Serum urea (mmol/L) 41 34.4 33.9 21
Urine Na (mmol/L) 19 101, 9 hours post MTZ 105 108 15
Urine Cr (mmol/L) 6.2 3.9 3.7 4.1 8.8
Urine K (mmol/L) 4.9 18.9 20.9 19.2 54.8
Urine Cl (mmol/L) 118 100 105
Urine urea (mmol/L) 159 150 289
Urine osmolality (mOsm/kg) 434 411 391

  • Some of these data are also presented in figure 3.

  • *AJR was used instead of jugular venous distention as the patient has severe pulmonary hypertension and severe tricuspid regurgitation with a large cv wave.

  • †Baseline weight 1 year before presentation was 68.3 kg.

  • AJR, abdominal jugular reflex; Cl, chloride; Cr, creatinine; D5W, dextrose 5% water; iv, intravenously; K, potassium; MTZ, metolazone; Na, sodium; ND, not documented; NYHA, New York Heart Association classification of dyspnoea; PO, peroral; PRN, as required; RA, room air.

Thiazides and mineralocorticoid receptor antagonists amplify the effect of loop diuretics. This sequential nephron blockade overcomes the diuretic resistance and antinatriuretic rebound seen with prolonged loop diuretic monotherapy.8

In advanced CKD (estimated glomerular filtration rate (eGFR) <30 mL/min) torsemide and butizide induced greater natriuresis than torsemide alone.9 Urine output (diuresis) and weight loss were similar.9 Hitherto, the natriuretic effect of sequential nephron blockade with furosemide, metolazone and spironolactone had not been compared with that of monotherapy in the setting of decompensated HFrEF with cardiorenal syndrome and acute hypernatraemia. The monitoring required to balance the patient’s sodium and volume status would have been challenging in the outpatient setting. The aetiology of the disequilibrium had to be addressed.

CRT improves LV function and reduces both hospitalisation and mortality in patients with symptomatic HFrEF and ventricular desynchrony (LBBB or QRS duration >120 ms).10 Increasing LV function improves organ perfusion, reducing sympathetic and renin–angiotensin–aldosterone system activity.10 This may improve cardiorenal syndrome and reduce renal events.10

‘Cardiorenal resynchronization therapy’ has been explored.10 11 However, advanced CKD and hypernatraemia have been associated with increased mortality post CRT.11 Indeed, the present case is the first to demonstrate the favourable impact of CRT on hypernatraemia and cardiorenal syndrome in the context of decompensated heart failure. This beneficial effect was sustained at follow-up 1 year after discharge home.

Patient’s perspective

  • In view of the patient’s dementia, he was unable to provide the patient’s perspective himself. This was provided on his behalf by his daughter.

  • We, his family, were very concerned with the various health complications that he experienced while admitted to the hospital. He has now been home for the past couple of months. He is doing much better now than when he was admitted to the hospital.

  • Presently, he is functioning reasonably well with assistance from the local community service and family. He is able to manage a limited daily routine. He is also able to remain living in his own home which was very important to him.

  • We, his family, greatly appreciate the extraordinary efforts made by the multidisciplinary medical team at the Montreal General Hospital.

Learning points

  • Sequential nephron blockade, combining loop and thiazide diuretics, generates significant natriuresis so close monitoring of fluid balance, renal function and serum electrolytes is required.

  • In cardiorenal syndrome with severe hypernatraemia administration of intravenous 5% dextrose alongside sequential nephron blockade can achieve a high natriuresis-to-diuresis ratio.

  • Medication-induced natriuresis may avoid the need for more invasive therapy for cardiorenal syndrome (eg, renal replacement therapy).

  • By improving cardiac contractility and the neurohormonal pathophysiology of heart failure, cardiac resynchronisation therapy (CRT) can improve cardiorenal syndrome and dysnatraemia.

  • Hypernatraemia and cardiorenal syndrome should not preclude CRT.

Ethics statements

Patient consent for publication

Footnotes

  • Contributors All authors were involved with the conceptualisation, design, preparation and editing of the manuscript. ATK, EK and RP acquired, analysed and interpreted the data. All authors approved the final manuscript for publication.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests Dr RR has received fees for lectures sponsored by Novartis.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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