Electrolytes Effect on Heart

Written by Ben Bunting: BA, PGCert. (Sport & Exercise Nutrition) // British Army Physical Training Instructor // S&C Coach.


Electrolyte abnormalities can be a dangerous complication for patients with heart failure.

This may be due to the pathophysiological alterations seen in the heart failure state leading to neurohumoral activation (stimulation of the renin-angiotensin-aldosterone system, sympathoadrenergic stimulation), and due to the complications of therapy with diuretics, cardiac glycosides or ACE inhibitors. 

Electrolytes Explained

Electrolytes are essential minerals found in fluids like water, stomach juices, poop, sweat and urine that make up our blood and are essential in making heart, muscles and nerves function as well as hydrating the body while simultaneously balancing acidity levels in blood and transporting nutrients and waste out.

Your kidneys play an essential role in managing electrolytes in your blood, and having too many or too few can cause health issues.

Key electrolytes include sodium, potassium, calcium, magnesium, chloride bicarbonate phosphate (CBCP) and phosphate; they're commonly found in food and sports drinks as well as in whole fruits like bananas.

Electrolytes, or electrically conductive solutions, contain positively and negatively charged particles known as ions that easily move through the water medium.

When an electric potential is applied to this solution, positively charged cations such as cations (positively charged particles) migrate towards electrodes with abundant electrons while negatively charged anions move towards the other electrode and this movement of anions and cations creates currents of electricity flow that form currents of current.

Your body relies on electrolytes to balance voltage across cell membranes, carry nerve impulses and muscle contractions, hydrate your body, regulate blood acidity levels and pressure, help repair damaged tissue and rebuild lost muscle mass.

If these levels become out of whack, they could lead to fatigue or even heart attacks; to maintain balanced levels, getting enough of the right electrolytes in your diet while drinking plenty of water can be effective at mitigating potential issues.

Cardiovascular System Explained

The cardiovascular system (your heart and blood vessels) supplies your cells with oxygen and other essentials as well as eliminating waste products, while helping maintain a steady temperature throughout your body.

Your blood vessels, commonly referred to as the cardiovascular or circulatory system, form an intricate network that supplies your cells with food, oxygen, hormones and other substances they need.

Your capillaries connect these blood vessels directly to individual cells for nutrients and oxygen delivery while simultaneously transporting waste products away.

Furthermore, capillaries transport heat away from tissues back into the circulatory system to maintain a constant temperature throughout your body.

Your cardiovascular system consists of two circulation circuits, the pulmonary and systemic circulations.

The former transports deoxygenated blood from your heart to your lungs for oxygenation before being returned through its pulmonary veins to your heart for distribution to all organs in your body.

Your heart relaxes between its upper chambers (atria), and then pumps blood down through its lower chambers (ventricles).

As it beats, the left ventricle sends blood rushing into arteries throughout your body while the right side receives non-oxygenated blood that's sent directly to the lungs via arteries, where oxygenated blood is exchanged for carbon dioxide to return back into the left side of the heart via right ventricle.

Your blood vessels contain red, white and platelet cells - all essential elements for the proper functioning of the cardiovascular system.

Red blood cells carry oxygen around your body while white cells identify and attack infections or threats to its wellbeing.

Platelets adhere to tears in blood vessels to help clot them quickly to stop bleeding at the site of injury.

Electrolytes and the Heart

The electrolytes sodium, potassium, magnesium and calcium are essential for the proper function of myocardium (the muscular tissue in the heart).

The movement of these ions along the semi-permeable membrane of the myocardial cells causes the voltage to exceed a certain threshold, which results in muscle contraction.

The heart functions properly when electrolytes are kept in a tight concentration.

An imbalance of these electrolytes may have adverse effects on the heart. It can cause or contribute to arrhythmias and cardiac arrest.

Arrhythmias that are life-threatening are often associated with potassium disorders. Hyperkalaemia, or an elevated potassium level, is one of the most common.

Less commonly, arrhythmias can be caused by disorders of serum magnesium and calcium. 

The kidneys play a key role in maintaining the electrolyte equilibrium in the body. Therefore, changes in renal function may affect the electrolyte levels in the heart.

All of these conditions, including kidney disease, hypoaldosteronism, and adrenal insufficiency, can affect the balance of electrolytes.

Some drugs, in addition to their role in maintaining the electrolyte equilibrium, can cause significant changes in serum electrolyte levels through various mechanisms.


Potassium is by far the most abundant intracellular (positively-charged) cation in the human body.

This gradient is due to the fact that the intracellular concentration of potassium is approximately 20 times higher than extracellular fluid. This keeps nerve and muscle cells excitable.

Potassium is primarily regulated by aldosterone, catecholamines and insulin.

pH also affects potassium concentrations.

When serum pH falls (acidaemia), potassium is moved from cells to the vascular area; however, when pH rises (alkaemia), potassium is transferred back into the cells. 


Magnesium, along with potassium and calcium influences cardiovascular function.

Magnesium and potassium deficiencies are important in the development of arrhythmias.

Magnesium is necessary for the maintenance of intracellular potassium concentration.

Multiple studies have shown that patients with heart failure have lower magnesium levels than normal controls.

Magnesium and potassium are mainly intracellular, so measurements in serum or plasma have limited value for assessing magnesium status.

Hyperkalemia secondary to ACE inhibitors is well documented in patients with heart failure.

Digoxin reduces the renal tubular absorption of magnesium and increases magnesium excretion.

Low magnesium and potassium concentrations can increase cardiac glycoside toxicity.

Magnesium levels that are elevated reduce the sensitivity of the human myocardium towards antiarrhythmogenic effects of cardiac glycosides without affecting maximally-developed tension.

Magnesium increases the affinity of cardiac glycosides for receptors.

Magnesium's antiarrhythmic effect is thought to be mediated through a reduced sensitivity of electrophysiological changes caused by Ca2+.

This indicates Ca2+ antagonistic qualities of magnesium. Magnesium deficiencies have also been linked to sudden death, particularly in patients with congestive cardiac failure.


Magnesium is the second most abundant intracellular anion.

This interaction between magnesium and sodium-potassium enzyme ATPase, which pumps potassium into the cells in exchange for sodium, is crucial in regulating cell concentration gradients.


Sodium is the most important extracellular cation and it has a significant effect on serum osmolality.

Together with potassium, it plays a major role in controlling the membrane potentials of myocardium and therefore has an important role in governing action potentials.

Unlike potassium, however, changes in serum sodium levels are rarely associated with significant cardiac problems unless they exceed normal physiological values.

Untreated sodium deficiency can cause seizures and comas. ECG variations are rare.

In patients with severe heart failure, excess total body water is seen relative to sodium. This occurs because the compensatory mechanisms of sodium regulation have been compromised.

Fluid restriction should be implemented and a diuretic used to reduce the water content and correct serum sodium levels.


Calcium is a powerful substance that affects the cells of the myocardium. It can influence conduction, intracellular signals, and muscle contraction.

Calcium levels, in particular, can affect the heart conduction and the duration of phase 2 of the myocardial potential plateau.

Calcium deficiency or excess can cause a short QT, while calcium deficiency causes a longer QT. Conduction abnormalities may lead to cardiac arrest at extremes. 


According to various studies, elevated phosphorous levels are associated with coronary arteries and increased left ventricular masses, carotid atherosclerosis, increased arterial rigidity, and calcification in the aorta.

The risk of cardiovascular mortality and morbidity is also higher in patients with chronic kidney disease and those without.

The study by Lopez et al. concluded that higher levels of serum phosphorus and calcium-phosphorus products in the large population study were associated with a higher incidence of AF.


The most abundant electrolyte in serum, after sodium, is chlorine. It plays a vital role in the regulation and balance of body fluids as well as the acid-base status.

It is also essential for the assessment of different pathological conditions.

Chloride abnormalities can be a sign of more serious metabolic disorders, such as alkalosis and acidosis.

The function of chloride channels in the plasma membrane includes cell volume regulation, excitability regulation, ionic balance, trans-epithelial transport etc.

It has been reported that the chloride channels were related to a variety of cardiovascular diseases, including hypertension, myocardial failure, ischemic heart disease, and myocardial hypertrophy.


Electrical remodelling is responsible for the persistence of atrial fibrillation. This could be due to a change in the expression of calcium, sodium, and potassium channels, fibrosis development, gene transcription, and channel redistribution.

Atrial fibrillation is a leading cause of heart failure, stroke and cardiac death. Calcium and magnesium can influence this risk.


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