How does electrolyte imbalance lead to heart failure

Access your subscriptions. Free access to newly published articles. Purchase access. Rent article Rent this article from DeepDyve. Access to free article PDF downloads. Save your search. Customize your interests. Hypercalcaemia can be managed initially with aggressive fluid administration, such as sodium chloride 0.

If unsuccessful, intravenous bisphosphonates can be used to slow the rate of bone turnover and reduce serum calcium levels, which is commonly undertaken in those with concomitant malignancy [8]. Hypocalcaemia will lengthen the QT interval, which can lead to AV block and cardiac arrest.

Symptoms of hypocalcaemia include cramps and tetany. Reversible causes of hypocalcaemia, including drug-induced hypocalcaemia, should be corrected if possible.

Patients treated for hypocalcaemia should also be given intravenous magnesium to aid correction of serum calcium levels [8]. Relation of electrolyte disturbances to cardiac arrhythmias.

Circulation 47; — Br J Hosp Med. Assessment of fluids and electrolytes. AACN Clin. Issues ;15 4 — Serum magnesium and stable asthma: Is there a link? Lung India 4 : — London:Blackwell Publishing European Resuscitation Council guidelines for resuscitation section 8. Cardiac arrest in special circumstances: electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution.

Bone and mineral metabolism in health and disease. Calcium and the heart: a question of life and death. J Clin Inv ; — Access provided by. Electrolytes in cardiology How potassium, magnesium, sodium and calcium imbalances can lead to serious heart complications.

The concentration of electrolytes in the body have wide-ranging implications, and imbalances can affect heart function Shutterstock. In this article you will learn: The standard serum concentrations of key electrolytes Common medicines that can affect electrolyte concentrations How to manage increases and decreases in electrolytes affecting the heart.

References [1] Fisch C. Glomerular filtration rates are a measure of renal reserve capacity, but it also includes short-term dynamic elements which help explain why it is a good predictor of long-term outcomes in HF, but also a poor short-term predictor of hour-to-hour changes in kidney health and how to respond clinically. Glomerular filtration rates can be measured directly by exogenous indicator dilutor methods using agents such as iothalamate or inulin, but it more commonly estimated from endogenously produced factors such as creatinine or cystatin C.

Cystatin C has some advantages, for unlike creatinine it is not affected by renal tubular function because it is not secreted by the tubules. Ideally, we would also have a reliable measure of renal tubular function that can be assessed acutely during an admission for decompensated HF, and although many have been proposed none has established a cemented role in routine practice. The most studied is neutrophil gelatinase-associated lipocalin.

Lastly, albuminuria can be used to assess glomerular filtration efficacy and can be abnormal in diabetes and CKD due to damage to the glomerular membrane. Albuminuria is common in HF and is linked to prognosis but the clinical implications of this remain unclear. Specialized imaging of the kidney, such as ultrasound, can be helpful but is not routinely recommended and certainly not for monitoring purposes.

Future techniques may offer better insights into dynamic changes occurring in intra-renal blood flow and the filtering tubular functions of the kidney. Electrolyte abnormalities are common in HF. They can be the result of diuretics, renal impairment neurohormonal activation, and the combination of these factors.

Sodium Na and potassium K are the most commonly perturbed electrolytes 49 but chloride is also affected. Potassium abnormalities are particularly due to the treatments given for HF with hypokalaemia complicating diuretic use and hyperkalaemia particularly associated with increasing RAAS-blockade, along with potassium-sparing diuretics and the sometime use of potassium supplements.

Magnesium, deficiency frequently co-exists with hypokalaemia. Guidelines do not specially indicate when or how frequently electrolytes should be monitored as it depends on clinical circumstances, but we believe they should be estimated daily during acute decongestive therapy, during routine post-discharge follow-up and following any dose changes in HF medication. It is difficult to be prescriptive with regards to the recommended frequency of ongoing monitoring of renal function and electrolytes usually measured together as so much depends on individual patient characteristics and inter-current clinical events but in stable HFrEF patients it appears reasonable to measure serum creatinine, urea, eGFR, and electrolytes three times per year, supplemented by re-measurement if medication or patient condition changes.

Congestion is one of the most important determinants of HF symptoms 56 , 57 and a major prognostic factor in HF. It is, therefore, of paramount importance to adequately determine the congestive status, 61 at both admission and discharge, since residual congestion at discharge is associated to higher one-year mortality and HF readmissions. On the one hand, inadequately low diuretic doses may lead to persistent congestion, one major driver of the high rate of readmission after episodes of worsening HF.

Conversely, inappropriately high loop diuretic doses may trigger hypokalaemia and hypovolaemia, with its associated risks of worsening renal function, the latter potentially leading to the down-titration or discontinuation of life-saving drugs i.

Ensuring decongestion is an essential goal during AHF hospitalization, but there is no standardized method for evaluating congestion before discharge and what defines adequate decongestion is currently unclear. Several routinely assessed biological parameters, such as serum protein, albumin, haemoglobin, 66 and haematocrit considered in isolation or in combination, enabling the indirect estimation of plasma volume 67 , 68 have been proposed as surrogate markers of de congestion and have been found to be associated with cardiovascular end-points.

Newer techniques such as lung ultrasound offer advantages over older techniques including chest X-ray. Most guidelines suggest the measurement of natriuretic peptides NPs in selected clinical settings, but this is more measure of ventricular stress or dilatation than of congestion per se, even though the two may be mechanistically linked in many cases.

NPs have a high negative predictive value for ruling out acute HF with congestion but routine monitoring of NP levels in long-term follow-up has not proven to be beneficial on outcomes or cost-effective. This pattern may be useful to identify early subclinical decompensation.

In spite of clinical improvement as result of in-hospital therapies, for a subset of patients, filling pressures and NPs levels are still persistent during hospitalization and in early post discharge period, suggesting residual congestion. Also, decrease in serum osmolality as result of the high plasma volume may signify haemodynamic congestion.

Identification and monitoring of haemodynamic congestion is crucial for preventing early post-discharge adverse events. Other potential biomarkers of congestion that can be monitored include sCD 71 and the monitoring of haemoconcentration through estimation of Hb after decongestive therapy thereby giving an estimate of the degree of relative decongestion rather than the absolute level of congestion at any point in time.

Dynamic therapy optimization using a telemedicine solution based on frequent non-invasive assessments of congestion as assessed by haemoglobin , renal function, and blood potassium may enable safe optimization of GDMT. The primary end-point of the study is the cumulative number of HF hospitalizations and cardiovascular deaths. These results will shed new light on the effectiveness of this telemonitoring system in HFrEF patients.

Renal function, congestion, and electrolyte disturbances are both inter-dependent and strong predictors of outcome in HF and can rapidly change depending on the clinical context. Accurate monitoring is essential both in the dynamic situation of acute HF as well as in up-titrating and maintaining optimized RAASi dosages.

Accurate individualized monitoring of potassium, renal function, and congestion can facilitate both HF therapy optimization and hospitalization reduction. Telemedicine, in particular, may allow a dynamic optimization of therapy over time.

Clinical trials specifically aimed at evaluating the optimal frequency of renal function monitoring in patients with HF are strongly needed. Conflict of interest : P.

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Eur Heart J Cardiovasc Pharmacother ; 3 : — Cardiovascular pharmacotherapy. Eur Heart J Cardiovasc Pharmacother ; 4 : 1. Heart failure drug treatment. Recently, ACE inhibitors have been documented to have important magnesium-conserving actions, possibly via their effect on glomerular filtration. Hyperkalemia, secondary to the use of ACE inhibitors in patients with heart failure, is well documented. Digoxin directly limits the renal tubular reabsorption of magnesium, therefore increasing magnesium excretion.

Low magnesium and potassium concentrations increase cardiac glycoside toxicity.