Sodium is an essential mineral and electrolyte that is crucial for maintaining fluid balance, nerve transmission, and muscle contraction, including the contraction of the heart muscle. It is the primary positively charged ion in the fluid surrounding cells (extracellular fluid), and its concentration is tightly regulated by the kidneys and hormonal systems.
Excess sodium in the body draws water with it, increasing circulating volume and blood pressure. High sodium intake is a significant risk factor for hypertension and worsens oedema in heart failure. NHS guidelines recommend adults consume no more than 6g of salt (approximately 2.4g of sodium) per day. Low sodium levels (hyponatraemia, below 135 mmol/L) can cause confusion, nausea, and seizures; in critical care patients this can result from excessive fluid administration, diuretic use, or SIADH. Elevated sodium (hypernatraemia), reflecting dehydration, is managed by careful fluid replacement.
Sodium plays a direct role in generating electrical impulses in the heart. Sodium channels open rapidly during the initial phase of the cardiac action potential, allowing sodium to rush into cells and triggering depolarisation. Long QT syndrome type 3 (LQT3) involves a mutation in the cardiac sodium channel gene (SCN5A), causing abnormal persistent channel opening that prolongs the action potential and predisposes to ventricular arrhythmias.
Monitoring sodium levels via regular blood tests is standard practice in cardiac patients, particularly those taking diuretics, ACE inhibitors, or other medications affecting kidney function. Abnormal sodium levels should be corrected carefully, as overly rapid correction of hyponatraemia can cause serious neurological injury.
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