Hypocalcemia causes tetany because calcium ions normally keep your nerve cells from firing too easily. When blood calcium drops below about 8.8 mg/dL, nerves become hyperexcitable and start sending signals on their own or with very little provocation, triggering involuntary, sustained muscle contractions. Understanding exactly how this works requires a closer look at what calcium does on the surface of your nerve cell membranes.
How Calcium Keeps Nerves in Check
Your nerve and muscle cells fire when tiny channels in their membranes open and let sodium rush in. This is called an action potential, and it only happens when the electrical charge across the membrane reaches a specific trigger point known as the threshold potential. Calcium ions play a critical gatekeeper role here: they sit on the outer surface of voltage-gated sodium channels and neutralize negative charges that would otherwise make those channels easier to open.
This is sometimes called charge screening. The outer surface of sodium channels carries negative charges, and calcium ions, which carry two positive charges each, are attracted to those negative spots. By parking there, they effectively raise the bar for how much stimulation is needed before the channel swings open. The nerve stays quiet until it receives a strong enough signal.
What Changes When Calcium Drops
When extracellular calcium falls, fewer calcium ions are available to screen those negative charges on sodium channels. The channels become easier to open, meaning the threshold potential shifts closer to the resting potential of the cell. The gap between “resting” and “firing” shrinks. A nerve that previously needed a solid push to fire now goes off with minimal provocation, or even spontaneously.
This is a key distinction: low calcium doesn’t change the resting potential of the membrane itself. It changes how easily the cell reaches the point of firing. The smaller the gap between resting and threshold, the greater the excitability. In practical terms, your peripheral nerves start generating action potentials they were never asked to generate.
From Nerve Firing to Muscle Spasm
Once a motor nerve fires, it releases chemical signals at the neuromuscular junction that tell the muscle to contract. Under normal conditions, this is a tightly controlled process. But when nerves are hyperexcitable, they fire repeatedly and in rapid bursts. The muscle doesn’t get a chance to relax between signals. This sustained, involuntary contraction is tetany.
The classic presentation is carpopedal spasm, where the hands and feet lock into characteristic positions. The wrist flexes, the fingers draw together at the knuckle joints, and the finger joints themselves extend stiffly. Feet can cramp into similar forced postures. These spasms happen because the long peripheral nerves supplying the hands and feet are particularly sensitive to changes in calcium levels.
Milder forms of tetany include muscle cramps and tingling or numbness in the hands, feet, and around the mouth. On the severe end, the same hyperexcitability can cause laryngospasm, where the muscles controlling the vocal cords contract involuntarily and partially or fully close the airway. Seizures can also occur when the hyperexcitability spreads to the brain. Laryngospasm from low calcium is more common in infants but can happen in adults, particularly those with very low magnesium levels.
Clinical Signs That Reveal Tetany
Two bedside tests can unmask latent tetany even before full-blown spasms develop. Trousseau’s sign is tested by inflating a blood pressure cuff on the upper arm to about 20 mmHg above systolic pressure and holding it for two to three minutes. This briefly reduces blood flow to the arm and lowers local calcium availability, which is enough to trigger the characteristic hand spasm in someone with borderline-low calcium. Chvostek’s sign involves tapping over the facial nerve just in front of the ear. In a positive test, the facial muscles twitch involuntarily on that side. Neither test is perfectly reliable on its own, but together with symptoms and a blood draw, they help confirm the diagnosis.
What Causes Calcium to Drop This Low
The most common cause of hypocalcemia leading to tetany is hypoparathyroidism, where the parathyroid glands don’t produce enough hormone to maintain calcium levels. This frequently happens after thyroid or neck surgery, when the parathyroid glands are accidentally damaged or removed. Vitamin D deficiency is another major contributor, since vitamin D is essential for absorbing calcium from food in the gut.
Low magnesium is a particularly important and often overlooked trigger. Magnesium is required for the parathyroid glands to secrete their hormone properly and for tissues to respond to it. Chronic alcohol use, gastrointestinal disorders, and certain medications can deplete magnesium, indirectly dragging calcium down with it. Correcting the calcium in these cases won’t work unless the magnesium is fixed first.
Alkalosis, a shift toward more alkaline blood pH, can also provoke tetany even when total calcium levels look normal. This happens because more calcium binds to proteins in alkaline conditions, leaving less ionized (free) calcium available. Hyperventilation from anxiety is a well-known trigger: rapid breathing blows off carbon dioxide, raises blood pH, and drops ionized calcium enough to cause tingling and hand spasms within minutes. The total calcium on a blood test might read as normal, but the fraction that actually matters, ionized calcium, has fallen below the functional threshold of about 4.7 mg/dL.
How Acute Tetany Is Treated
When tetany is severe, with laryngospasm, seizures, or significant carpopedal spasm, intravenous calcium is given to rapidly restore levels. This is typically administered over about 10 minutes with heart rhythm monitoring, and the dose can be repeated every 10 to 60 minutes until symptoms resolve. Relief is usually fast once calcium reaches the bloodstream, because restoring the extracellular calcium concentration immediately re-stabilizes those sodium channels and raises the firing threshold back to normal.
For milder or chronic cases, oral calcium and vitamin D supplements are the mainstay. If low magnesium is part of the picture, that gets replaced as well. The goal is to keep ionized calcium in the normal range of 4.7 to 5.2 mg/dL, which maintains the safety margin between resting potential and threshold potential that prevents nerves from misfiring.