When a patient is seen in an acute setting, for example, having presented at an accident and emergency department, or is being seen by the cardiologist for the first time, often his or her heart rhythm is rapid and quite distressing for the person. By slowing down the heart rate, it makes the patient feel better and improves the working of the heart, so it is a good starting point and one to be addressed as soon as possible.

beta-blockers

There are a number of drugs used to control the heart rate. The most commonly used drugs are from a group called beta-blockers. They act through receptors that are associated with the sympathetic nervous system. These receptors are normally used to accelerate the nervous system within the body, giving us the ‘fight and flight’ response which increases the heart rate, dilates the pupils (for seeing better), increases blood flow to the muscles (to run away or fight) and increases blood pressure.

Beta-blockers act to impede these receptors. In effect, the beta-blockers dampen the sympathetic nervous system which has nerve endings supplying the atrioventricular (AV) node, thus reducing the speed of AF conduction from the atria to the ventricles and so slowing the heart rate.

However, beta-blockers can also lower blood pressure. This needs to be monitored closely. If the patient already has low blood pressure, it may mean that beta-blockers cannot be used. Beta-blockers can occasionally stir up asthma and some patients will describe fatigue and, infrequently, depression. Occasionally, though, I’ve had patients tell me they feel great, being more centred and grounded.

For most people, these agents are flexible and work well and are often used as the first-line agent in treating atrial fibrillation. They can be administered either orally, in tablet form, or intravenously, through the vein. One commonly used agent is metoprolol.
 
digoxin

Depending on the heart rate response to the first line of therapy, beta- blockers can be used in conjunction with other medications or other medications are used instead of the beta-blockers. One of the agents I like to use, often in conjunction with beta-blockers, is digoxin.
Digoxin, which is derived from digitalis which comes from the foxglove plant, acts to slow the atrioventricular node, thus slowing the ventricular rate. This leads to improved control.

On the positive side, digoxin is often very well-tolerated and does not tend to lower blood pressure. On the negative side, there can be problems if the patient’s kidneys are not working well as the drug can accumulate in the body if used longer-term. Its use must be monitored closely.

Digoxin can be administered orally or intravenously. Used alone or in combination with beta-blockers, it can work very effectively to bring down the heart rate.

calcium channel blockers

If choosing not to use beta-blockers, say for a patient with asthma, another option is a centrally acting calcium channel blocker. A calcium channel blocker is an agent that affects the way calcium flows through the cell membrane; a centrally-acting calcium channel blocker is one that acts predominantly on the heart compared with a peripherally-acting agent that has more effect on the blood vessels.

Verapamil and diltiazem are centrally-acting agents.

Although verapamil is probably used more often, both regulate ventricular reaction, slowing the response in atrial fibrillation, again through slowing the gateway between the atria and the ventricles, the AV node.

Care needs to be taken in their use by people who already have problems with their left ventricular function.

Each can be given as a tablet or through the vein.
 
amiodarone

While beta-blockers, digoxin and calcium channel blockers are the main agents for rate control, in certain emergency circumstances, amiodarone might be used.

Amiodarone is a separate sort of agent with a different class of antiarrhythmic effect. It can be given orally; however, because it takes a long time to build up its levels within the body, it is far more effective in the acute setting if given intravenously. This agent, on its own, can slow down the atrial fibrillation rate. It is also a powerful reversion (returning the patient to normal rhythm) agent. So, its use can start to slow the heart with the possibility of returning the patient to normal rhythm.

On the downside, it carries a lot of iodine that can affect the thyroid gland in the long-term. In up to 25 percent of patients thyroid problems will develop. Amiodarone can also lead to toxicity within the lungs and the liver, and cause skin pigmentation.

While it is not at the top of the list for controlling heart rate, it should not be overlooked. If needed, it should be used with care.

AN INTERESTING CONNECTION
TACHYCARDIA-INDUCED CARDIOMYOPATHY

Tachy means fast; cardia and cardio relate to the heart and myopathy refers to a problem with the muscle. So, tachycardia induced cardiomyopathy is a fast heart induced muscle problem.

This can tie in with atrial fibrillation. We see it most commonly in people who have silent, persistent atrial fibrillation; the patient is not necessarily aware of the rhythm and it lasts for an extended time, of weeks to months.

The normal heart rate is between 50 and 100 bpm. If the heart is being driven rapidly over its normal rate, say in the 130s, 140s, 150s or even above that, the heart suffers. Over time, it shows features of fatigue: dilating and not contracting as effectively as it should do. This is cardiomyopathy; the muscle of the heart becomes fatigued and ‘wears out’. If this is not treated, it can lead to heart failure and death.

By the time we see these people, the development has been gradual. They are often short of breath and their heart rate is very fast. They have a dilated heart which we can pick up on clinical examination and on ECG and even more clearly on echocardiography. They have features of heart failure and respond well to the standard therapies that have an emphasis on rate control.

Different factors may have caused the heart to dilate. Infection may have damaged the heart muscle, giving rise to an infective cardiomyopathy. The person may have consumed too much alcohol, an alcoholic cardiomyopathy. It may be related purely to the heart rate being too fast. Sometimes, we can’t be sure of the cause. Nonetheless, one of our therapy mainstays is to slow down the heart rate.

If we reduce that heart rate effectively, starting to bring it back towards the 70-odd beats per minute which is normal, then often we can see a fantastic response. Some patients respond even better if we are able to restore sinus rhythm.

The really satisfying thing about this condition is that if we can slow down the heart rate of these people for several months, say three months, they will come back feeling much better and a re-evaluation of their hearts shows marked improvement in function. It is a very satisfying outcome.

IMPORTANT POINTS    
SLOWING THE HEART RATE

•    We slow the heart rate by slowing the electrical activity passing through the AV node, the node that allows electrical impulses to pass from the atria to the ventricles.
•    Drug therapies to do this are
-    beta-blockers
-    digoxin
-    calcium channel blockers
-    amiodarone.