Electrical activity of the heart

The pumping activity of the heart is dependent on the electrical impulses generated by specialized fibers in the heart itself called the pacemaker or the SA node (sinoatrial node). The SA node is located in the wall of the right upper chamber of the heart called the right atrium. The muscle fibers of the heart are structurally different from muscle fibers in other parts of the body and are connected to each other in a special arrangement such that the impulses generated in that special spot in the right atrial wall are propagated and programmed to arrive at each of the other 3 heart chambers (left atrium, right ventricle and left ventricle) in perfect timing.




Electrical conduction pathway of the heart.
Original heart diagram illustrated by Patrick J. Lynch; illustrator; C. Carl Jaffe; MD; cardiologist Yale University Center for Advanced Instructional Media

The result is that the 2 atria receive electrical impulses at the same time and contract in unison, pushing blood out into the ventricles while the ventricles receive electrical impulses a bit later and are thus relaxed when the atria are contracting. By the time the ventricles finally begin to contract, the atria have emptied out, the building pressure in the ventricles cause the atrioventricular valves to close and blood is pushed out of both ventricles; from the right to the lungs and from the left to the aorta, the biggest artery in the body.

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HEART ATTACK (2)

How do I know if I'm having a heart attack?

A person having a heart attack(myocardial infarction) may experience severe central chest pain often described as squeezing or pressure which may radiate to the shoulders, neck or jaw, with or without headache, dizziness, breathlessness, sweating, vomiting or fainting. The pain lasts longer than a few minutes and is not relieved by nitroglycerin (a drug that widens the coronary arteries, prescribed for patients with angina).Unfortunately however, some people,  will not experience any symptoms at all. This is called silent infarction and is more common in diabetics. If not immediately treated, the heart muscle fibers affected will undergo irreversible damage/infarction/death within 4-5 minutes, lose their functionality and be replaced by scar tissue in a few weeks. Depending on the size of the area affected, this damage may lead to heart failure, arrhythmias, heart rupture, cardiac arrest or death.    A heart attack can occur suddenly but many patients have warning signs days or weeks before the actual event. These warning signs may be in form of recurrent chest pain which is precipitated by exertion and relieved by rest, or increasing frequency and severity of chest pain in people who have already been diagnosed with ischemic heart disease. If medical intervention is sought early, the process can be halted or reversed with appropriate therapy.

In what ways may you be increasing your risk for ischemic disease?

Although there are some predisposing factors which are not modifiable or controllable such as male gender, age(˃40) and heredity (family history of IHD), most of the risk factors for IHD are modifiable. Interestingly, modifying these risk factors simply implies adopting a healthy lifestyle i.e. engaging in regular physical exercises, eating a healthy balanced diet low in saturated fat, avoiding smoking and maintaining optimal body weight. Also, screening for hypertension, diabetes and hypercholesterolemia and controlling them if present will significantly reduce the risk of IHD. Thus, you may be increasing your own risk for heart disease by living a physically inactive life, living on junk foods high in saturated fats and carbohydrate, smoking and not having regular medical checkups.

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Back to Heart attack 1

HEART ATTACK (1)

Myocardial infarction also known as heart attack is an irreversible damage (death) to the heart muscles due to loss of blood supply following narrowing and occlusion of a coronary artery. The coronary arteries are the arteries which supply the heart muscles (myocardium). The right and left main coronary arteries are the first branches of the aorta, carrying oxygenated blood from the left ventricle. These 2 arteries divide into many branches which supply every part of the heart. Unlike many other parts of the body, the heart does not have an alternate source of oxygenated blood. This is why the coronary arteries are called end arteries. Narrowing of these arteries therefore puts the heart tissue at risk of ischemic injury (Ischemic heart disease -IHD). Also, unlike other parts of the body which get continuous blood supply, the muscle layer of the heart only gets blood supply in pulses. This is because each time the heart muscles contract (systole), they squeeze the arteries running through them and temporarily stop blood flow, when they relax (diastole), the arteries become patent again and blood flows to supply the muscles and inner lining of the heart. [An average heart contracts and relaxes about 70 times each minute]. This intermittent oxygen supply contributes to the susceptibility of the hard working heart muscles to hypoxic damage. Fortunately, the heart muscles are capable of extracting more oxygen from blood than any other tissue in the body. Also, the blood flow to the heart increases almost proportionately to increase in workload and corresponding increase in oxygen consumption, by dilatation of the coronary arteries. These measures normally prevent hypoxia and tissue damage.

Patrick J. Lynch, medical illustrator

Coronary arteries may become narrowed or blocked by plaques (in coronary artery disease), blood clot building over a ruptured plaque or rarely, loose clot (embolus) formed within a heart with damaged valve or wall and carried in blood into the aorta.  Narrowing can also occur due to spasm of the artery. A plaque is mainly composed of fat (in form of cholesterol), calcium and fibrous tissue. Plaques take years to develop. They are commonly seen with ageing but may occur in younger people with high cholesterol levels, diabetes mellitus or hypertension.   The presence of plaques in any artery is called atherosclerosis- meaning hardened artery. Apart from narrowing the lumen, the plaque also hardens the walls of the artery preventing it from dilating to supply more blood in response to increased oxygen demand.

However, even in the presence of a plaque, symptoms of ischemia do not occur until about 70% of the lumen of the artery is occluded. The individual experiences squeezing chest pain (angina) brought on by any increase in workload on the heart such as with exertion (e.g. climbing stairs, physical exercise), in cold weather, emotional situations etc., and relieved by rest. If the plaque ruptures, a raw surface is exposed on the arterial wall and this stimulates the formation of a blood clot much like a bleeding injury anywhere in the body. This further narrows the lumen; worsening the angina which may now occur even at rest. Sometimes, the clot or thrombus can grow large enough to completely occlude the artery, totally depriving the part of the heart muscle (supplied by this artery) of oxygenated blood. This is what is referred to as a heart attack.

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See Heart attack (2)

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