Patients with congestive heart failure (CHF) readily present with electrolyte imbalance which commonly includes deficiencies of sodium, potassium, and magnesium.
Hyponatremia is the most common electrolyte abnormality observed in hospitalized subjects; it is defined as a serum sodium concentration lower than 136 mmol/L [6].
The electrolytes potassium, magnesium, sodium and calcium play a crucial role in the function of the myocardium, the muscular tissue of the heart.
Monitoring your electrolytes.
Low potassium, magnesium, or calcium can all raise your risk of having a dangerous ventricular arrhythmia. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and spironolactone, on the other hand, can increase the level of potassium in your blood.
Electrolyte imbalance cardiomyopathy
Electrolyte imbalance is a common finding in many diseases [9,10]. The most important and prevailing electrolyte imbalances include hypo- and hyper-states of sodium, potassium, calcium and magnesium (Table 1).
In healthy patients, elevated aldosterone levels lead to potassium excretion. However, in patients with heart failure, elevated aldosterone promotes sodium reabsorption, thus less sodium is delivered to the distal nephron resulting in impaired excretion of potassium [17].
Maladaptive neurohormonal activation and acid-base changes during the chronic HF progression can affect the serum chloride concentration by activating the neural thirst center and impairing the vasopressin secretion (1).
In cardiac patients, hypokalemia and potassium depletion are often caused by an increased loss of potassium through the kidneys due to nonpotassium-sparing diuretic therapy.
A patient presented with hypernatremia (plasma sodium level equals 171 mEq/L), marked congestive heart failure, and fluid retention. A high-salt intake and an inappropriate lack of thirst in this patient with poor cardiac function resulted in hypernatremia accompanied by edema.
However, at late-stage congestive heart failure, patients exhibit an impairment in the renal excretion of water (aquaresis or water diuresis), predisposing them to the development of hyponatremia.
The common electrolyte imbalance seen in these patients include deficiencies of sodium, potassium, and magnesium. Deficiencies of magnesium and potassium pose a serious risk of cardiac arrhythmias [2]. Hyponatremia occurs in advanced stages of CHF because of impaired urinary water excretion.
Low potassium in combination with low magnesium is a risk factor for severe arrhythmias. Thus, magnesium balance is closely tied to sodium, calcium, and potassium balance.
Intravenous potassium is often used to treat hypokalaemia cardiac arrhythmias as the cardiac effects of hypokalaemia include excitability and contractility changes [77].
Metabolic acidosis is a common complication of CHF, which is closely related to ischemia and hypoxia of tissue caused by hemodynamic disorders and the use of diuretics. In turn, acidosis and accompanying hyperkalemia can further weaken myocardial contractility, creating a vicious circle.
Potassium (+)
Your cells use potassium alongside sodium. When a sodium ion enters a cell, a potassium ion leaves, and vice versa. Potassium is also especially critical to your heart function. Too much or too little can cause serious heart problems.
Hypervolemic hyponatremia in HF patients is multifactorial and occurs mainly due to the persistent release of arginine vasopressin (AVP) in the setting of ineffective renal perfusion secondary to low cardiac output.
Hyponatremia or low serum sodium level is typically defined as a serum sodium concentration of <135 mEq/L and is one of the most common biochemical disorders featured in heart failure patients, with a prevalence close to 25% [2–4].
Sodium intake is associated with fluid retention, hence the puffiness and bloating that may follow a very salty meal. And excessive sodium intake may worsen high blood pressure, or hypertension. High blood pressure increases the risk of developing heart failure and can worsen existing heart failure.
Hyperkalemia is routinely defined as a serum potassium level >5 mmol/L and is a common occurrence in patients with acute and chronic heart failure (HF).
Almost 4 in 10 patients with HF develop hyperkalemia, and many patients have recurrent hyperkalemia episodes. Hyperkalemia risk is strongly associated with degree of reduced kidney function and use of spironolactone. Hyperkalemia is associated with severe clinical outcomes and death in HF.
Disturbance in acid-base balance is commonly observed in patients with heart failure. The most common disturbance is metabolic alkalosis combined with hypokalemia, as a result of the excessive use of loop diuretics. Occasionary, hypoxia due to pulmonary edema stimulates ventilation, resulting in respiratory alkalosis.
In patients with worsening HF and an increase in the serum chloride concentration (Fig. 1, left half), the accumulation of serum chloride acts to maintain or increase intravascular volume, which places a greater burden on the failing heart.
Congestive Heart Failure
In addition, the disease state itself results in neurohormonal activation (renin-angiotensin system, sympathetic nervous system, and endothe- lin) that further amplifies the tendency toward alkalosis.
Taking too much potassium chloride may result in hyperkalemia, which may also need treatment. Hypokalemia and hyperkalemia can cause serious health conditions, such as heart and kidney failure.