Management of bradycardia depends on the severity of symptoms, as bradycardia is usually not a dangerous condition and does not require treatment. Bradycardia that does not cause symptoms such as dizziness, weakness, or fainting is usually not treated.
Factors that influence whether any treatment plan is used in cases of bradycardia include:
- severity of symptoms
- Correlation between bradycardia and its symptoms
- Have a serious underlying medical condition, such as heart block
- There is a potentially reversible cause that can be treated
Listed below are some examples of the types of treatments that can be used to treat bradycardia.
- In cases of bradycardia caused by drugs that slow the heartbeat, the drug is usually discontinued.
- For example, in cases of bradycardia caused by low or high potassium levels, electrolyte imbalances may need to be corrected.
- A pacemaker may be implanted to regulate the heart's rhythm. Pacemakers are tiny devices that generate electrical pulses if they detect an abnormality in the pulses produced by the heart's sinoatrial node. A pacemaker is implanted under the skin and permanently attached to the heart. When they detect a slow or abnormal heart rhythm, they send impulses to correct the heart rate.
According to the guidelines of the American College of Cardiology and the American Heart Association, pacemaker implantation is only performed under certain conditions. These include:
- Third-degree heart block (or atrioventricular block) occurs when the patient's heartbeat is missing for 3 seconds or more or when the patient's heart rate is less than 40 bpm while awake.
- Third degree heart block or second degree Mobitz type heart block combined with chronic bifascicular and trifascicular block.
- Congenital third-degree heart block with a wide QRS escape rhythm (as shown on the electrocardiogram), ventricular dysfunction (disordered ventricular pumping), or age-inappropriate bradycardia.
Less commonly accepted indications for pacemaker use in bradycardia are known as Class II recommendations. These include:
- In third-degree heart block, the escape rate is faster in awake patients and there are no obvious symptoms.
- Second-degree Mobitz type heart block in patients without bifascicular or trifascicular block.
- There is a block under or within the His bundle
When the bradycardia occurs only during sleep, even if the bradycardia is severe, the use of a pacemaker is usually not recommended. These patients may benefit from pindolol, a beta-blocker with intrinsic sympathomimetic activity.
Patients with impending heart failure or unstable bradycardia require immediate treatment. The drug of choice is usually atropine 0.5-1.0 mg administered intravenously at intervals of 3 to 5 minutes, with a maximum dose of 0.04 mg/kg. Other emergency medications that may be given include adrenaline and dopamine.
Pindolol, sold under the brand name Visken and others, is a non-selective beta blocker used to treat high blood pressure. It is also an antagonist of serotonin 5-HT 1A receptors, preferentially blocking inhibitory 5-HT 1A autoreceptors, and has been studied as an add-on therapy to selective serotonin reuptake inhibitors (SSRIs) for the treatment of depression disease.
It is used to treat high blood pressure in the United States, Canada, and Europe, and also to treat angina pectoris outside the United States. When used alone in high blood pressure, it can significantly reduce blood pressure and heart rate, but the evidence base for its use is weak due to the small number of participants in published studies. In some countries, Pindolol is also used for the prevention of cardiac arrhythmias and acute stress reactions.
Contraindicated in hyperthyroidism. The possible harmful effects of long-term use of Pindolol have not been fully evaluated in patients with thyrotoxicosis. Beta-blockers may mask clinical signs of persistent hyperthyroidism or complications and give a false impression of improvement. Therefore, sudden discontinuation of Pindolol may worsen the symptoms of hyperthyroidism, including thyroid storm. Pindolol has intrinsic sympathomimetic activity and should be used with caution in angina.
Pindolol is a first-generation non-selective beta-blocker in the beta-adrenergic receptor antagonist class. At the receptor level, it is a competitive partial agonist. It has intrinsic sympathomimetic activity, meaning that it has some degree of agonist action in the absence of competing ligands. Pindolol shows membrane stabilizing effects like quinidine, which may be responsible for its antiarrhythmic effects. It also acts as a partial agonist (intrinsic activity = 20–25%) or functional antagonist of the serotonin 5-HT 1A receptor
Pindolol is rapidly and well absorbed in the gastrointestinal tract. It undergoes some first-pass metabolism, resulting in an oral bioavailability of 50-95%. Bioavailability may be reduced in uremic patients. Food does not alter bioavailability but may increase absorption. Peak plasma concentrations are reached within 1-2 hours after a single oral dose of 20 mg. The effect of Pindolol on pulse rate (reduction) is evident after 3 hours. Although the half-life of 3-4 hours is rather short, the hemodynamic effects persist for 24 hours after administration. The plasma half-life increases to 3-11.5 hours in patients with renal insufficiency, to 7-15 hours in elderly patients, and from 2.5 hours to 30 hours in patients with cirrhosis. Approximately two-thirds of pindolol is metabolized in the liver to produce hydroxylates, which are present in the urine as glucouridine and ether sulfate. The remaining 1/3 of pindolol is excreted unchanged in the urine.
Pindolol was patented by Sandoz in 1969 and launched in the United States in 1977. In February 2020, the FDA added the product to its "drug shortage" list, noting that it was due to a "shortage of active ingredients" that was potentially related to the coronavirus outbreak and related supply chain impacts.