Heart rhythm disorders, called arrhythmias, pose one of the paradoxes of medicine. Almost anyone’s heart will occasionally produce an extra beat or two, and the distressing symptoms that may accompany the extra beats, such as palpitations or dizziness, do not necessarily signal a serious health problem. Yet an undetected arrhythmia also may set off a chain of events leading to sudden death from cardiac arrest.

heart-celec conduction

Your heart is an organ which pumps about 4,300 gallons of blood each day through the vascular network of our body.  Although movement of blood is its primary function, each and every beat of this unique muscular pump is initiated and finely regulated by electrical impulses that originate in the heart itself.  Electrical currents, not in the form of electrons like those that course through the wires of our house, but in the form of ions, flow across the membrane of each cell causing voltage surges that set the heart in motion.  Sodium ions rush into the cells, to be followed by potassium and chloride ions making a quick exit. The resulting voltage spike or action potential regulates the influx of calcium ions that mediate the sliding motion of filaments within each cell causing their shortening or contraction.

This process, repeated in each adjoining cell of the heart, causes the orderly spread of electrical activity and the synchronous contraction of the myocardium (heart muscle).  Like other “excitable” tissues, the cells of the heart are electrically connected through low resistance pathways.  These pathways facilitate the spread of the electrical impulse, ensuring efficient activation and pumping motion.  Without electrical activity, the heart lies motionless and serves no useful purpose.  Disorderly electrical activity also known as arrhythmias may also render the heart inefficient or totally useless as a pump.

Arrhythmias are not always life-threatening.  Some, including extrasystoles or “extra beats” may be quite innocuous.  Others like AV nodal tachycardia, although not lethal, may be incapacitating.  Still others like atrial fibrillation may be less crippling, but could lead to a stroke. In the United States, more than 300,000 deaths result each year from sudden cardiac arrest. Abnormal heart rhythms fall into two general classes: excessively slow heart rates, known as bradyarrhythmias or bradycardias, and overly rapid heart rates, known as tachyarrhythmias or tachycardias. Nearly every minute of every day someone in this country dies of sudden cardiac death, very often the result of an arrhythmia known as ventricular fibrillation.

Scientists at the  Masonic Medical Research Laboratory have been on the cutting edge of  the identification of  a number of mechanisms by which cardiac arrhythmias arise.  Prevention, diagnosis and treatment have advanced at a steady pace offering a better quality of life for some and a new lease on life for many sufferers of heart disease.  Many of these advances are directly attributable to research done at the Masonic Medical Research Laboratory (MMRL), a leading center for the study of cardiac arrhythmias for over 50 years.

Mechanism of Cardiac Arrhythmias

The electrical signal that sets the heart in motion originates in the right upper chamber (right atrium) in a structure known as the sinus node.  Traveling through specialized pathways, the impulse spreads throughout the right and left atria and then squeezes through an isthmus that connects the upper and lower chambers (ventricles) of the heart.  This junction known as the atrioventricular (AV) node delays the impulse, providing enough time for the blood in the atria to empty into the ventricles.  Because it serves as the gatekeeper for the ventricles, the AV node is also referred to as a “safety valve”, regulating the rate at which impulses can propagate from the atria to the ventricles.  From there the electrical impulse journeys down a divided cellular highway (bundle branches), simultaneously activating both ventricles.  The conduction system terminates in a webbed network of specialized (Purkinje) fibers that permit nearly synchronous activation of the cells of the ventricles from the bottom up so as to effectively squeeze out the blood.  This well organized sequence of activation, the result of millions of years of evolution, allows for quiet and efficient pumping of blood by the heart for the purpose of providing oxygen and nutrients to the rest of the body.

heart conduction and ecg

The healthy heart follows this same pattern of electrical activation about 70 times each minute; this is the basis for the normal heart rate.  The efficiency of the heart as a pump can become seriously compromised when the electrical distribution system breaks down.  Just as a faulty distributor can cause a car to stutter and sputter, a faulty distribution system in the heart can cause rhythm disturbances, or arrhythmias, that can alter its normal function.  An arrhythmia occurs when the heart beats too slowly (bradycardia), too rapidly (tachycardia) or erratically.

A very slow heart rate results when either the sinus node, the primary pacemaker of the heart, is defective, or the AV node, the structure through which the sinus impulse must pass to activate the ventricles, is defective.  When impulse conduction between the atria and ventricles is blocked (heart block), the heart does not stop completely because subsidiary (backup) pacemakers located in the ventricles take over control of the heart.  However, their rate, usually less than 40 beats per minute, is too slow to maintain normal function and in some cases is too slow to maintain consciousness.  Fortunately, the problem is easily remedied by the implantation of an artificial pacemaker, a device that provides electrical pulses to stimulate the heart and thus restore normal rate and rhythm.  Although very slow heart rates can be life-threatening, most arrhythmic deaths result from abnormally rapid heart rates.

tachy atrial and ventrical

A tachycardia results when either the atria or the ventricles beat too rapidly.  There are several mechanisms by which this can occur.  Abnormal impulse formation due to altered movement of ions across the membrane of pacemaking cells is one mechanism.  Another, more common mechanism, involves the recirculation (reentry) of the electrical impulse around a real or functional obstacle in a never ending loop characteristic of a dog chasing its tail.  The normal pattern of electrical distribution is therefore disrupted, resulting a short-circuiting of a part of the heart.  Tachycardia can degenerate into fibrillation, also known as sudden cardiac death when it occurs in the ventricles, if the electrical activity becomes further disorganized.

 

Because the ventricles do most of the pumping, a rapid rate in the ventricles is generally more serious than in the atria.  Inasmuch as the AV node limits the number of atrial beats that reach the ventricles, an abnormally fast heart rhythm can exist in the atria while the ventricles beat at a near normal rate.  Medical treatment of fast heart rhythms ideally should be tailored to the underlying mechanism responsible for the arrhythmia.  Artificial pacemakers, automatic defibrillators, antiarrhythmic drugs and ablation techniques are today available to treat and prevent the development of life-threatening cardiac arrhythmias.

These therapeutic modalities are available today due in part to research conducted by the Experimental Cardiology team at the Masonic Medical Research Laboratory.  The research findings of the MMRL’s scientists together with researchers at other institutes worldwide have translated into therapies and preventative measures that have saved countless lives.  In the next segment of this series, I hope to expand on the causes of tachycardia and fibrillation and to further discuss how research can provide a new lease on life for many patients.

Detecting Cardiac Arrhythmias

Like a metronome, our heart maintains a steady beat helping us to keep time with the musical interludes of life. But that faithful pace can be interrupted, slowed or accelerated disrupting the harmony of our lives. Cardiac arrhythmias can take many forms ranging from single extra beats, sensed as occasional palpitations,  to totally uncoordinated contractions known as fibrillation. Fibrillation of the upper chambers of the heart (atria) usually leads to a fast somewhat irregular heart rate, accompanied by fatigue, chest discomfort and, in people with coronary disease, anginal pain. Fibrillation of the main pumping chambers (ventricles) is a bit more serious in that it leads to death unless reversed in a timely manner. Between these two extremes exist a wide variety of irregular rhythms that impact on the quality of our lives and in some cases are life-threatening.

To diagnose a heart arrhythmia, your doctor will review your symptoms and your medical history and conduct a physical examination. Your doctor may ask about — or test for — conditions that may trigger your arrhythmia, such as heart disease or a problem with your thyroid gland. Your doctor may also perform heart-monitoring tests specific to arrhythmias. These may include:

ecg strip

  • Electrocardiogram (ECG). During an ECG, sensors (electrodes) that can detect the electrical activity of your heart are attached to your chest and sometimes to your limbs. An ECG measures the timing and duration of each electrical phase in your heartbeat.
  • Holter monitor. This portable ECG device can be worn for a day or more to record your heart’s activity as you go about your routine.
  • Event monitor. For sporadic arrhythmias, you keep this portable ECG device available, attaching it to your body and pressing a button when you have symptoms. This lets your doctor check your heart rhythm at the time of your symptoms.

echo-2

  • Echocardiogram. In this noninvasive test, a hand-held device (transducer) placed on your chest uses sound waves to produce images of your heart’s size, structure and motion.
  • Implantable loop recorder. This device detects abnormal heart rhythms and is implanted under the skin in the chest area.

If your doctor doesn’t find an arrhythmia during those tests, he or she may try to trigger your arrhythmia with other tests, which may include:

  • Stress test. Some arrhythmias are triggered or worsened by exercise. During a stress test, you’ll be asked to exercise on a treadmill or stationary bicycle while your heart activity is monitored. If doctors are evaluating you to determine if coronary artery disease may be causing the arrhythmia, and you have difficulty exercising, then your doctor may use a drug to stimulate your heart in a way that’s similar to exercise.
  • Tilt table test. Your doctor may recommend this test if you’ve had fainting spells. Your heart rate and blood pressure are monitored as you lie flat on a table. The table is then tilted as if you were standing up. Your doctor observes how your heart and the nervous system that controls it respond to the change in angle.
  • Electrophysiological testing and mapping. In this test, doctors thread thin, flexible tubes (catheters) tipped with electrodes through your blood vessels to a variety of spots within your heart. Once in place, the electrodes can map the spread of electrical impulses through your heart.