A slow heart rate, known as bradycardia, is fewer than 60 beats per minute (bpm) in adults. While a low heart rate is common and normal in trained athletes or during sleep, it becomes a medical concern when it causes symptoms. Symptomatic bradycardia occurs when the heart beats too slowly to supply sufficient oxygenated blood to the body’s organs. This deficit in blood flow can manifest as fatigue, dizziness, lightheadedness, or fainting. When these symptoms are present, treatment is necessary to increase the heart rate, restore adequate circulation, and prevent more severe complications like syncope or heart failure.
Acute Management and Stabilization
Immediate intervention is often required when symptomatic bradycardia presents with signs of poor perfusion, such as hypotension, altered mental status, or acute heart failure. The primary goal of acute management is to temporarily raise the heart rate and stabilize the patient while the underlying cause is determined and addressed.
The first-line pharmacological agent for acute symptomatic bradycardia is Atropine. This medication works by blocking the effects of the vagus nerve, which normally slows the heart rate. Atropine is administered intravenously (IV) and is generally effective for sinus bradycardia and atrioventricular (AV) blocks that occur at the AV node level.
If Atropine is ineffective or if the patient’s condition is deteriorating rapidly, temporary pacing or alternative drug infusions are initiated. Transcutaneous pacing (TCP) involves delivering electrical impulses through pads placed on the patient’s chest and back, causing the heart muscle to contract. TCP should be started without delay in severely symptomatic patients, especially those with high-degree heart block, as Atropine is often less effective for these rhythms.
If pacing is not immediately available or while preparations are underway, alternative medications like Dopamine or Epinephrine infusions can be used. These drugs are administered as an IV infusion and increase heart rate by stimulating beta-adrenergic receptors. They act as a temporary bridge until a more definitive solution, such as transvenous pacing, can be established.
Identifying and Reversing Underlying Causes
A thorough investigation to identify reversible causes of the slow heart rate is a fundamental step after initial stabilization. If the cause can be corrected, the need for a permanent device can potentially be avoided. The workup typically includes a detailed review of all current medications, blood tests, and an electrocardiogram (ECG).
Medication toxicity is a common reversible cause, particularly with drugs used to treat hypertension or heart disease. Beta-blockers, non-dihydropyridine calcium channel blockers, and the cardiac glycoside Digoxin can all suppress the heart’s electrical activity. Simply discontinuing or reducing the dosage of the offending drug, under medical supervision, can often restore a normal heart rate.
Electrolyte abnormalities, such as excessively high or low levels of potassium, can disrupt the heart’s electrical conduction system. Correcting these imbalances with intravenous fluids or specific medications is a straightforward treatment that can resolve the bradycardia. Other potential reversible factors include hypothyroidism, which slows the body’s metabolism, and severe infections like sepsis. Treating the underlying thyroid condition with hormone replacement or managing the infection may eliminate the bradycardia.
Definitive Treatment: Permanent Pacing
When symptomatic bradycardia is persistent and not caused by a reversible factor, the implantation of a permanent pacemaker is the definitive solution. This is particularly true for intrinsic heart conditions like Sick Sinus Syndrome or advanced forms of heart block. A permanent pacemaker is a small device surgically placed under the skin near the collarbone that monitors the heart’s electrical activity.
The pacemaker consists of a pulse generator containing a battery and circuitry, connected to one or more insulated wires called leads. These leads are threaded through a vein and positioned in the heart chambers, where they sense the heart’s native electrical signals. If the device detects that the heart rate has dropped below a programmed minimum threshold, it delivers a small electrical impulse to stimulate a contraction, ensuring the heart beats at a sufficient rate.
Pacemakers are categorized based on the number of heart chambers they pace: single-chamber pacemakers typically connect to the right ventricle, while dual-chamber devices connect to both the right atrium and the right ventricle. Dual-chamber pacing is often preferred because it mimics the heart’s natural sequence of contraction, coordinating the upper and lower chambers to optimize blood flow. The implantation procedure is generally performed under local anesthesia and light sedation, usually taking only a few hours.
After the procedure, patients receive specific instructions regarding wound care and physical activity limitations for the first few weeks to allow the leads to secure themselves. Lifestyle considerations involve regular follow-up appointments to check the device’s battery life and programming, often remotely, and cautious use around strong magnetic fields. While the device provides a reliable solution, it requires ongoing monitoring to ensure its optimal function.