How the Heart Works
The heart consists of four chambers: two upper chambers, called atria, which receive the blood, and two lower ones, called ventricles, which push the blood out from the organ. The atria and ventricles alternately contract and relax to pump blood through the heart and to the rest of the body.
A heartbeat originates as electrical impulses are generated and pass through a pre-determined pathway in the heart. These electrical impulses originate in the sinoatrial (SA) node, which is a small mass of specialized tissue located in the right atrium; it is also known as the heart’s pacemaker. This electrical impulse first causes the atria to contract and squeeze blood into the ventricles. It then passes through the atrioventricular (AV) node and triggers the ventricles to contract, which having just been filled with blood by the contracting atria, pump blood out to the rest of the body (Patterson 2002).
A “normal” range for resting heart rate is approximately 60-100 beats per minute, with evidence suggesting that a heart rate at rest over 80 beats per minute may be cause for possible concern for underlying heart disease. For example, a study published in The Journal of Epidemiology & Community Health followed 50 000 healthy men and women over 20 years and found that for each increase of 10 heart beats per minute, the risk of dying of a heart attack increased 18% among women and about 10% in men (Nauman 2010). Any irregularities in the heart rhythm can affect the efficiency at which the heart pumps blood to the body, and may thereby lead to damage in various tissues and organs (NHLBI 2011a,b).
The normal conduction of electric impulses and normal heart muscle contractions depend on the levels of various electrolytes in the body. Impulses are generated due to the movement of electrolytes through passages called ‘ion channels’ that are present in the heart cells. Sodium, potassium, calcium, and magnesium are the chief ions required for generating electric impulses under normal circumstances. Inadequate levels of these ions prevent the proper formation of impulses, and/or their normal conduction, resulting in the development of arrhythmias. Most anti-arrhythmic drugs act by modulating these ion channels (Sanguinetti 2003).