Bradycardia

Bradycardia is a physiologically incompatible slow heart rate. Generally speaking, this is a rate of 60 beats per minute or less. However, some healthy individuals, most notably athletes, sustain slower rates without problems thanks to highly efficient heart muscles. The differentiating factor between a healthy and a diseased heart rate is whether sufficient quantities of oxygen-enriched blood are being pumped to the other organs. It is not unusual for the heart rate of a healthy individual to drop during deep sleep or meditation. However, symptomatic bradycardia (such as fainting, fatigue, dizziness, and/or lightheadedness) requires evaluation.

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The condition is more prominent in the aged, those with diseased hearts, and frequently by a few common medications such as beta blockers and non-dihydropyridine (DHP) calcium-channel antagonists (verapamil and diltiazem are examples). There is, additionally, a relationship between apnea (delayed breathing) and bradycardia. This is of particular concern in neonates with immature lungs.

Overview

The heart is a complex organ that is best viewed, for this discussion, as an electrical engine, albeit quite unique. Each beat is normally triggered by the sinoatrial node; which is composed of myocyte cells situated on the right atrium wall, at the heart’s center, near the superior vena cava entrance. The impulse from the SA node, in normal action, causes the contraction of both atria, which pumps the oxygenated blood through the arterial system.

It is somewhat easier to comprehend the nature of bradycardia if the functioning of the cardiac cells is better appreciated. Myocytes are specialized cells. In this instance, we are referring to cardiac myocytes. These units are made of myofibril bundles, which in turn are composed of myofilaments. Each of these contains the essential contractile units of the myocyte: sarcomeres. The sarcomeres have thick (myosin) and thin (actin) filaments. It is the chemical reactions between these two bands which permit the ions to pass across and initiate contractions of the fibers.

Basically, the SA node fires and triggers a sequence of depolarization and repolarization of cardiac muscle. The impulse goes from the SA node to the gatekeeper AV (atrioaventricular) node where it is delayed slightly to allow the atria to contract before the ventricles. From there the impulse normally goes to the HIS-Pukinje pathway which distributes the charge to the ventricular walls so they contract and force the blood into its next stage.

One of the unique features of cardiac cells is the ability of each cell to initiate the electrical impulse to the cell next to it in a synchronous manner. Here too lies another source of interrupted stimulus and bradycardia if individual cells become out of sync. Coronary artery disease often impedes circulation within the heart, which can impact myocardial tissue by decreasing perfusion. In a healthy heart, the firing of the SA node and subsequent points of the cycle repeat in a uniform and consistent pattern. An impaired heart may well find itself with blocked impulses and bradycardia. Another source of impeded firing is hypoxia, often a side effect of lung disease.

Impact

The Centers for Disease Control and Prevention’s 2012 statistical report indicates 36.6 million American adults, representing 11.3 percent of the population, have been diagnosed with heart disease. In 2011 the cost to treat heart disease exceeded $215 billion. It is the leading healthcare expenditure, as well as the number one cause of death.

Bradycardia can be a direct result of sick sinus syndrome. There are no hard statistics breaking down how many cases are due to sinus irregularities versus a host of other problems that result in impeded impulses. When the arrhythmia is the result of a damaged sinus node, the five year survival rate for 47–59 percent of the patients is estimated at five years.

Treatment is dependent on causative factors. With sinus dysfunction, implanted pacemakers can resolve the issue in most cases. However, it is not uncommon for sick sinus syndrome induced bradycardia to convert to atrial fibrillation, which can be resolved with medication or ablation.

As mentioned elsewhere, the SA node is not the sole source of bradycardia. In some instances it is caused by medications. One would imagine discontinuing the pharmaceutical would be a reasonable and logical remedy. In some cases, that is the resolution. However, many of those drugs are life-sustaining and cannot, therefore, be discontinued. A partial list of the most common are:

  • alfentanil
  • clonidine
  • dimethyl sulfoxide (DMSO)
  • fentanyl
  • lithium
  • paclitaxel
  • reserpine
  • sufentanil
  • toluene
  • topical ophthalmic acetylcholine

The first source to examine is the heart itself. Heart disease is a component in any bradycardia differential diagnosis. A simple EKG can demonstrate one of four common blocks.

  • First degree: the atria signals are slightly slowed to the ventricles. It is usually asymptomatic, requiring no treatment if no other problem exists.
  • Second degree: signals and beats are lost, which translates to slower, and sometimes irregular, rhythms
  • Third degree: the atrial impulses do not reach the ventricles. The bundle of His or the Purkinjee network become a pacemaker.
  • Bundle branch block: one or both bundle branches fail to respond to electrical impulses somewhere along the pathway.

Other factors may include allergic reactions, environmental and chemical toxins, plus physical illness. Hypertension has a tendency to impair the resiliency of chamber walls, as do congenital heart defects. Some systemic infections and that of the heart itself (myocarditis) has deleterious effects on heart rate. Hypoxia is a large factor in some bradycardia patients as a result of sleep apnea. The frequent disruption of breathing causes the heart to slow due to hypoxia. Smoking, as well, reduces the amount of available oxygen saturation needed to perfuse the heart. Surgery on the heart can disrupt the electrical conduits of the myocardium. Rheumatic fever, lupus, or inflammatory disease can slow the heart rate.

There is no shortage of bradycardia etiologies. Hypothyroid conditions are common causes, as are electrolytic imbalances that come from too much or too little essential minerals. Bradycardia is often a result rather than a primary and easily diagnosed entity.

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