Transesophageal echocardiography, which physicians call TEE, is a Special form of echocardiography. Echocardiography is the second most commonly ordered test in Cardiology. It utilizes high frequency sound waves which are not audible to the human ear. These sound waves are emitted from a special device called a transducer which is held onto the chest wall next to the heart (transthoracic echocardiography ). Heart tissue reflects these sound waves, and the reflection is recorded onto the screen of an echocardiography machine. With this information, cardiac anatomy, and how this anatomy functions, can bedetected, such as the atrial and ventricular chambers and the cardiacvalves. Blood flow direction and velocity can also be determined from any ofthe valves, and this helps in determining whether or not a valve is abnormal,Sound waves from a transducer held onto the the chest wall are absorbedby skin, fat, bone and lung tissue. Because of this, and In spite of the remarkable advances in the transthoracic method of echocardiography since it was initially developed in the 1950’s, 15% of all echoes do not provide sufficient information for the physician. Consequently, TEE was developed in the 1970’s in order to overcome the limitations of transthoracic echocardiography.

TEE utilizes an especially designed ultrasound transducer that can beswallowed. TEE emits sound waves that reflect off the heart that aregenerated from inside the esophagus, which is next to the heart. None of theimages that are obtained by TEE suffer from the sound interruptions that atransducer on the chest wall shows.

Besides providing echo images where transthoracic echo is notsatisfactory, TEE has been found very useful in locating and determining thefunction of various cardiac structures that cannot be imaged at all with a transthoracic echo.

Some examples of the other information available from TEE include:

1. evaluation of artificial heart valves and valve infection

2. evaluation cardiac anatomy in stroke patients

3. evaluation of tears of the aorta

4. evaluation of congenital heart disease

TEE has been found to be very useful in the emergency department andquickly resolves issues such as the cause of cardiovascular shock whenpatients are too unstable to be sent for tests such as a CT scan or MRI.

Its use in the critical care area is well recognized because it providescardiac images when there are chest bandages present and when patients are on ventilators. Routine echocardiography in the critical care area is frequentlyinadequate for the above reasons. It is used routinely in cardiac surgery to provide monitoring of cardiac function.

TEE for an outpatient is performed with the patient supine and rolled onto his side. Individuals which are usually present include the cardiologist, a nurse and an echo technician who controls the echo machine. The head of thepatient is elevated slightly with a pillow. An intravenous line is started for administration of mild sedation, and the throat is sprayed with an anesthetic. Patients are not put to sleep during this procedure.

During the procedure the EKG is monitored, and blood oxygen is monitored with a finger optical device. A suction tube is available to remove secretions from the throat which usually accumulate. The TEE transducer is a cable about the diameter of an adult’s small finger and is inserted into the esophagus by having the patient swallow when it is placed in the back of the throat. There is usually some initial gagging, but once the transducer is in the correct place to obtain images, the patients become more comfortable.

Breathing is not disturbed; patients can talk; and occasionally watch their own echoes during the procedure. The procedure requires about 10 minutes to perform. If sedation is used patients are observed for one hour after the procedure. Patients are also told not to drink or eat for 2 hours until the throatanesthetic wears off.

Since its inception, TEE has provided a major leap in diagnostice chocardiography, and has become the gold standard of practical ultrasonic cardiac imaging.

** Dr. Frazin holds the proud distinction and honor of inventor of the Transesophegeal Echocargiogram. This incredible accomplishment has literally changed the face of Cardiology and made Dr. Frazin internationally reknown.

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CARDIOMYOPATHY is as the name implies, i.e., pathology of the myocardium, (heart muscle), of the cardia (heart). Initially, it was applied to unknown causes of deteriorating heart muscle function, principally in young, otherwise healthy persons, although, it may also include the old as well. As our knowledge of causes and pathology has improved, there has been a blurring of the distinction between heart muscle malfunction of unknown causes and those of known causes. This classification, exclusively, still focuses on heart muscle abnormalities, in contradistinction to those maladies involving the heart valves, or the covering over the heart (pericardium).

The best classification has revolved around distinct functional or hemodynamic properties. Since most Cardiomyopathies result in Congestive Heart Failure and/or arrhythmias, this classification is of great utility in the treatment of these conditions. Five major forms are recognized: (i) dilated cardiomyopathy, (ii) hypertrophy cardiomyopathy,(iii) restrictive cardiomyopathy, (iv) right ventricular cardiomyopathy and (v) non-classifiable cardiomyopathies with distinct hemodynamic properties. Some of the specific dysfunctions of the heart muscle may overlap in this classification, but the clinical usefulness is still helpful. These functions are expressed as 1.)Dilatation (ventricular enlargement), 2.) Thickness of the heart muscle (Hypertrophy), or 3.) Stiffness of the heart muscle.

Known causes of heart muscle dysfunction, often referred to as Secondary Cardiomyopathies, are also included in categories of Cardiomyopathies. The new World Health Organization’s, World Health Foundation’s (WHO/WHF) definition comprises Inflammatory cardiomyopathy, defined as MYOCARDITIS in association with cardiac muscle dysfunction. Also, Autoimmune, and Infectious forms of cardiomyopathy are recognized. Viral Cardiomyopathy, which may be accompanied by inflammation, has been recognized in some instances. Some cardiomyopathies have a relationship with other organ systems, while still others are hereditary.

The end result of all these different forms of Cardiomyopathies is the worsening of cardiac work. This results, either, from failure of the pump function or from failure of the heart muscle to relax, called ventricular compliance. Hence, the clinical presentation of these Cardiopathies as Congestive Heart Failure. This muscle damage may also interfere with the electrical properties of the heart and result in severe Arrhythmias.

FUNCTIONAL IMPAIRMENT

DILATED CARDIOMYPOATHY

This is a syndrome characterized by a large dilated heart, often accompanied by Congestive Heart Failure. It is frequently referred to as “Congestive Cardiomyopathy”. This is because a dilated heart with stretched cardiac muscle acts like a rubber band, which has been stretched too far and therefore lacks the power to contract. This results in a flabby heart unable to propel the blood forward, i.e., pump failure. The muscle thickness may be normal, increased, or decreased. Most often, the cause of Congested Dilated Cardiomyopathy is elusive and unknown, but it is probably the end result of many forms of heart muscle damage caused by a variety of toxic, metabolic, or infectious agents. Alcohol, pregnancy, hypertension, are a few of the known causes of his syndrome. Once these are ruled out, as well as infection, the syndrome is often referred to as Idiopathic Congestive Cardiomyopathy.

The pathology demonstrates enlargement and dilatation of all four chambers of the heart. The ventricles are more dilated than the atria. Histological examination reveals interstitial and peri- vascular fibrosis in the walls of the ventricles.

The symptoms are those of left ventricular failure, i.e., congestive heart failure. Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, and rest dyspnea occur. Fatigue and weakness due to diminished cardiac output are prominent. Physical examination reveals a weak pulse, gallop heart rhythm and in the late stages, swollen feet and a swollen liver, associated with abdominal swelling (Ascites).

Treatment, as the syndrome suggests, is directed in strengthening the heart muscles, diminishing the fluid backup, and relieving the heart muscle of resistance to pump against. So Digitalis, which strengthens the heart muscle; diuretics to promote fluid mobilization, and peripheral vasodilators to decrease peripheral resistance are of great help. Other more recent medications, which facilitate the same goals are being incorporated in the treatment with fair results.

Alcoholic cardiomyopathy is probably the most common cause of congestive dilative cardiomyopathy in the western world.

HYPERTROPHIC CARDIOMYOPATHY

This is a condition where the left ventricular wall is thickened (hypertrophied), and the cavity is perforce small. Hypertension is the most common cause of this form of Cardiomyopathy, but an inheritable form, (IHSS-Idiopathic hypertrophy sub-aortic stenosis) is the originator of this classification. Actually, the wall of the left ventricle may be symmetrically hypertrophied, or the hypertrophy may involve the sub aortic, valvular, or supravalvular areas of the ventricle, or only the septum may be asymmetrically involved (ASH).

The pathological examination reveals a marked increase in myocardial mass, with the ventricular cavities being small. The atria are also often hypertrophied and dilated. Myocardial fiber disarray is seen in the interventricular septum in the IHSS cases.

The clinical symptoms include dyspnea from impaired ventricular filling do to the small cavities and the rapid buildup of pressure do the thickened wall stiffness. Fatigue and syncope, as well as angina pectoris are common. Understandably, exertion tends to exacerbate the symptoms. The physical examination may reveal a prominent chest wall thrust of the thickened heart against the inner chest wall in systole. There is often a systolic heart murmur which may vary in intensity with respiration and can be accentuated by having the patient bear down and strain. This, understandably, increases the peripheral resistance and the heart has to push the blood out harder against this increased pressure, causing the murmur from turbulence of this fast moving blood through the narrow passageway to emit a higher pitched and louder sound.

The EKG and especially, the Echocardiogram have made the diagnosis of all forms of this disorder more easily identifiable. Treatment consists of medication to rest the heart muscle in order to increase the ventricular volume, or the use of medication to decrease peripheral resistance.

RESTRICTIVE CARDIOMYOPATHY

This condition occurs either as an inheritable condition or when a disease state occurs which enables the heart muscle to be infiltrated by the disease pathology. In this condition, the heart muscle becomes stiff and unpliable, such that it cannot relax and therefore the quantity of blood which enters the heart chambers and the force of muscular contractility exerted by the heart muscle are both severely limited, causing poor blood flow. Sarcoidosis and Amyloidosis are examples of disease states which can be associated with this condition.

SUMMARY: Cardiomyopathies refer to diseases or conditions which weaken the heart muscle, either exclusively or in conjunction with other organ involvement. Many of the Cardiomyopathies are from unknown causes. This damage to the heart muscle impairs its function and the blood either backs up into the lungs causing Congestive Heart Failure or is unable to be propelled forward and hypotension ensues. The internal damage to the muscle may interfere with electrical conduction and life threatening arrhythmias may occur. Their prognosis is very grave.

Classifying the Cardiomyopathies into the functional categories of dilatation of the heart muscle, thickening of the muscle, or stiffening of the muscle, is helpful in therapeutic decision making. Medications which rest the heart muscle, allowing it to expand more leisurely and thus, allow the chambers to fill with more blood, and those which strengthen the muscle’s contractile properties, as well as those medications which diminish peripheral resistance are of substantial utility in the treatment of these conditions.

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Congestive Heart Failure (CHF) is a condition, not a disease. It is a constellation of signs and symptoms, caused by a multitude of diseases, not all of which, primarily involve the heart muscle. This explains why most states, Louisiana in particular, preclude the use of heart failure, as well as respiratory and cardiac arrest as a cause of death, on the Death Certificate. These are all modes of dying, not causes of death.

Congestive Heart Failure (CHF) is exactly what it’s name implies-failure of the heart muscle to keep the lung from becoming congested. This congestion occurs when fluid leaks out of the blood vessels into the air sacs and displaces the air. When the pressure in the blood vessels is elevated by the heart muscle’s inability to propel the blood forward, out of the lungs into the rest of the body, fluid leaks out of the blood stream, through micropermeable vessel walls into the air sacs (alveoli). This manifests itself, clinically, as Congestive Heart Failure.

So any inability of the heart muscle to pump the blood out of the lungs, whether from a weakening of the muscle or by an overburdening of the heart muscle can result in CHF.

Weakening of the heart muscle, most commonly, in Western Societies comes from Coronary Artery disease, whereby cholesterol plaques build up in the lining of the blood vessels. This build up of cholesterol plaques results in obstruction of blood flow and death of a portion of the heart muscle. Other causes of heart muscle injury vary from viral infections of the muscle (called myocarditis), to toxins such as alcohol, to disease states, such as hypertension, kidney or liver failure.

Over-burdening of the heart muscle, on the other hand, occurs in hypermetabolic states such as hyperthyroidism, vitamin deficiency (Beri Beri), severe anemias, and cardiac valvular defects, such as Aortic Stenosis or Mitral Regurgitation.

SIGNS AND SYMPTOMS

The signs and symptoms of CHF include, getting tired easily, weakness, confusion, shortness of breath (initially with exercise, but, as the CHF worsens, at rest and associated with the inability to lie or sleep lying flat in bed. This necessitates sleeping with 2 or more pillows called 2 pillow Orthopnea), a persistent cough from congested lungs, swelling of the feet and abdomen, from fluid accumulation as the heart muscle weakens, along with darkening of the finger and toenails (cyanosis), from oxygen poor blood perfusing the extremities at a slower rate of flow.

Physically, fluid in the air sacs can be heard with a stethoscope, as well as the addition of one or two additional heart sounds. Instead of just the lub-dub, lub-dub of the 1st. and 2nd. heart sounds, a 3rd. and 4th. heart sound are added, either da-lub-dub or lub-dub-da (Ken-tuc-ky or Ten-ne-see). The pulse may even vary in intensity on alternate beats (pulsus alternans). There is, of course, a faster pulse at rest and with exercise, as the heart tries to mitigate its weakness, by increasing its rate. The patient will often complain of the heart feeling as if he had run around the block, when all he did is cross the room. Prominent engorged veins, from blood backup, is noticeable as prominent neck and abdominal wall veins and a large palpable swollen liver is detected. Swollen feet and ankles, initially occurring after prolonged sitting or standing and disappearing overnight, but later persisting all the time, becomes evident.

Congestive Heart Failure is divided into many categories:

Acute and Chronic CHF
Compensated and Decompensated CHF
Systolic and Diastolic CHF
Right and Left sided CHF
High and Low output CHF

I.) Acute and Chronic CHF

A.) Acute CHF- As the name implies; when the heart muscle suddenly becomes too weak to propel the blood forward, sudden CHF ensues. This is usually heralded by the abrupt onset of Shortness Of Breath.

The classic example of this occurrence is from the onset of a fairly extensive heart attack (myocardial infarction). This occurs from Coronary Atherosclerotic Artery disease. With so much muscle damage at one time, the remaining muscle cannot compensate and CHF develops. Occasionally, the patient will present to the Emergency Room in acute CHF from a myocardial infarction, but without a history of chest discomfort (Silent myocardial infarction). Therefore it is incumbent upon the physician to suspect and to check for a myocardial infarction in all and any cases of acute CHF, even if there is no antecedent pain. This is the standard of care, since, if detected early enough, possibly something can be done to save the heart muscle and reverse some or all of the damage.

Other causes of Acute CHF are: 1.) Arrhythmias, such as a very fast or very slow heart rate; 2.) Rhythm irregularities between the upper and lower chambers of the heart as in Heart blocks; 3.) Sepsis; 4.) Pulmonary Emboli; 5.) Acute stroke; 6.) Viral infections.

B.) Chronic CHF- This is, most often, an insidious condition, occurring slowly over a period of months or years. In this condition, shortness of breath on exertion is often the only first symptom. Sometimes the feet will swell during the afternoon and go down at night, assisted by frequent nocturnal trips to urinate this excessive fluid. As the weakened heart muscle , which is too weak during the active daytime, is able to mobilize the fluid from the subcutaneous tissues during a horizontal and restful night, the kidneys are presented with more blood and, therefore, more urine is produced. Later, sleeping with 2 pillow Orthopnea becomes necessary.

Causes of Chronic CHF are of a more chronic duration, but can occur from some of the same causes as with Acute CHF. 1.) Repetitive small myocardial infarctions; 2.) hypertension; 3.) valvular defects; 4.) slow renal deterioration 5.) multiple recurrent small pulmonary emboli; 6.) and diseases that infiltrate the heart muscle.

II. Compensated and Decompensated CHF

Compensated CHF simply refers to the chronic form of CHF that is under control with medication. Whereas, if symptoms are frequent, such as nocturnal shortness of breath, which goes away in the morning or when sitting up and moving around, with or without treatment, the condition is referred to as Decompensated.

III. Systolic and Diastolic CHF

If the heart muscle is too weak to push the blood in the ventricular chambers forward, but still fill up with the usual quantity of blood, as they do in the healthy state, and do so without creating a greatly increased pressure in those chambers, then Systolic CHF is present. In other words, even though the muscle is too weak to propel enough blood forward, the muscle can still dilate to comfortably handle the incoming blood without stress on the chamber walls and, therefore, without an increase in the pressure inside those chambers.

If, as in Hypertensive Heart Disease, the chambers hold less blood, in part because the wall is thickened from having to push against increased resistance, i.e., high Blood Pressure, then the chamber wall muscles are not as elastic, do not have the give to dilate as much and the pressure builds up, such that, even less blood can be pushed into that chamber from the upper chambers (Atria). Then Diastolic CHF is present, because less blood can enter the lower chambers (Ventricles) and must, perforce, back up into the lungs, causing CHF.

IV. Right and Left CHF

The heart is divided into 2 lower chambers (Ventricles). The Right Ventricle sends blood to the lung. The Left Ventricle sends blood out of the heart to the rest of the body. Failure of the Right Ventricle, before the blood reaches the lungs, results in the backup of blood in the venous return system of the body, resulting in distended veins, a swollen liver, occasionally with fluid in the abdominal cavity (ascites) and with swollen legs. Failure of the Left Ventricle, after the blood has gone through the lungs results in the classical symptoms of shortness of breath, cyanosis, etc., because of inability to propel the oxygenated blood forward to the distal tissues. If Left sided CHF lasts long enough, it will result in Rt. sided CHF also developing. Because the Kidney puts out hormones which regulate salt and fluid retention, when it does not receive enough blood, as in Lt . sided heart failure, it will hold salt and fluid in the body hoping to increase the fluid volume, since it interprets this lack of blood and oxygen as one of an anemic state. If the liver becomes engorged with backed up blood, as in Rt. sided CHF, it will not destroy these kidney hormones in it’s usual efficient manner and they will accumulate, holding more salt and water in the body.

V.) High and Low Output CHF

Low Output CHF results from a weakened heart muscle and is commensurate with the classical sign and symptoms of CHF. High Output CHF occurs in the overburdening types of CHF, such as Beri Beri, or Hyperthyroidism or severe Anemia, where the heart is in a feverish state of activity, having to move the blood around vigorously, and wearing itself out.

TREATMENT OF CHF

Since CHF occurs from the presence of excessive fluid in the air sacs due to an absolute or relative weakened heart muscle, the solution is directed at these two problems. Of course, once the patient is comfortable, then the underlying disease should be sought for and addressed, such as treating the Hyperthyroidism, or balloon dilating and stenting the Coronary Arteries, or giving blood, etc.

So, first we try and remove the fluid from the lungs so the patient can breath.

Then, we try and increase the strength of the heart muscle if possible, or, at least, relieve the burden on the heart muscle.

1.) Relieve the lungs of fluid – By simply dehydrating the blood stream with the use of Diuretics, leaving less free fluid to be available to infiltrate the tissues, leak into the air sacs or for the heart muscle to have to move around, in it’s weakened state.

2.) Strengthen the heart muscle – Unfortunately, this is our biggest problem. We have very few medications which can be absorbed orally and not be destroyed by the stomach juices, which will strengthen the heart muscle.

A.) Digitalis – This drug has been in use for a century and is still very useful in treating CHF. It has been shown to improve the stamina and life style of CHF patients, but, for some unknown reason, not prolong life. At present, this is the only oral heart muscle strengthening muscle (IONOTROPIC AGENT) available.

B.) Other Ionotropic Agents – Intravenously, we do have some very good agents, but, of course, the route of administration is cumbersome and expensive. Dobutamine and Dopamine are examines of this genre. On the horizon, however, there are plenty of candidates, which should be available shortly, some of which can be taken orally. What about a patch?

3.) Decrease the burden against which the heart muscle must push against. (Peripheral Vascular Dilators).

A.) ACE Inhibitors – Stands for Angiotensin Converting Enzyme Inhibitors. These ACE Inhibitors are the 1st. drugs of choice in early CHF. They have been proven to increase the quality of life and to prolong life. They work by decreasing the work of the heart by decreasing the peripheral resistance against which the heart muscle must work. They also work on the kidney vessels to prevent them from deteriorating and compounding the congestive state. They do so by inhibiting the enzymes which tell the kidney to retain salt and water, a mechanism the body uses when the tissues do not receive enough oxygen and blood nutrients. In this case it is self-destructive. A new improved and more selective class of ACE Inhibitors has come on the market with great promise. (I will update that shortly).

B.) Other types of peripheral vascular vasodilators exist and have been found to be beneficial in difficult CHF cases, which work on either the arteries or veins, such as Alpha Blockers or Nitroglycerine.

4.) Decrease the frenatic activity of the heart muscle so that it can relax, allowing more blood to enter its chambers without elevating the pressure.

A.) Beta Blockers – Unique in that these drugs allow the heart muscle to rest and slow down and thereby become more efficient, even in their weakened state. Of course, we do not want weakened muscles to fall asleep and not work at all, making the CHF worse, so these drugs must be carefully monitored.

SUMMARY

Congestive Heart Failure occurs when the heart muscle is, eitherweakened or overburdened. It occurs because of the inability of the heart to effectively pump blood out into the lungs or to the rest of the body. This blood in the vessels, principally in the lungs, builds up increasing the pressure and causesfluid to leak out into the surrounding tissues, such as the air sacs, in the lungs, or the subcutaneous tissue in the extremities. Symptoms vary from Shortness of Breath to swelling of the lower extremities. Signs include liquid heard in the air sacs (rales), compressionable swelling of the extremities (edema), and purplish fingers and/or toes (cyanosis), among others. Treatment is directed towards mobilization of fluid plus strengthening and reducing the stress on the heart muscle. So, diuretics, Ace Inhibitors, vasodilators, Ionotropic agents and Beta blockers may be employed, separately or together to effect this relief.

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Heart attack is a leading cause of death and disability in the United States. There are major efforts underway to find improved methods for prevention, detection and treatment. These efforts are sponsored by many organizations including the American Heart Association, the American College of Cardiology, and the federal government.

In order to best understand the science of heart attack, a basic knowledge of heart ( cardiac ) anatomy and function is necessary. The heart is basically a pump that receives blood lacking oxygen from the veins ( venous system ), pumps it to the lungs for oxygenation, and then returns it to the body thru the arteries ( arterial system ).

Anatomically the heart consists of 4 chambers whose walls are made of muscle. The right atrium initially receives unoxygenated blood from the venous system. Blood then enters the right ventricle, but contraction of the atrium helps pump more blood into the right ventricle. As the right ventricular chamber begins to contract, the tricuspid valve closes so that blood does not reenter the right atrium. Contraction of the right ventricle rejects blood into the pulmonary artery which is the major conduit carrying blood to the lungs.

As the right ventricle finishes its contraction, the pulmonic valve closes so that blood does not reenter the right ventricle from the pulmonary artery. Once blood is oxygenated in the lungs, it is returned via the pulmonary veins to the left atrium and left ventricle. When the left ventricle begins to contract, the mitral valve closes so that blood does not reenter the left atrium. The oxygenated blood from the left ventricle is pumped into the aorta which delivers blood via the many branches of the arterial system throughout the body. Once the left ventricle finishes its contraction, the aortic valve closes which prevents blood from reentering the heart.

There are microscopic and biochemical differences between heart muscle and regular muscle which is attached to skeletal bones. However, both types of muscle require their own nutrient blood supply through arteries. This nutrient blood supply provides oxygen and sugars without which contraction would not occur. The nutrient blood supply of the heart is supplied by the coronary arteries of which there are 2 and, in fact, they are the first branches off the aorta. They are located just beyond or distal to the aortic valve. The right coronary artery supplies the right ventricular chamber, and the left coronary artery supplies the left ventricular chamber.

The main portions of both arteries are 4 to 8mm. in diameter. Both arteries have many branches all of which decrease in size the farther they are from the main or proximal part. The atria receive blood from small branches of both of these arteries. It is the interruption of the coronary artery blood supply which causes a heart attack.

The bottom line determinant of whether or not a heart attack occurs is the oxygen and sugar (nutrient) demands of the heart muscle. One of these determinants is the thickness of the muscle making up the cardiac chamber walls. The atria are 2 to 3 mm. thick. The right ventricle is about 5 mm. thick, and the left ventricle is 10 to 12 mm. thick. The thicker the chamber wall, the more nutrient it requires, and, consequently, the left ventricular chamber is more vulnerable to heart attack. Another determinant is how often the heart contracts. A heart contracting at 150 time per minute uses substantially more oxygen and sugar than one contracting at 70 per minute.

Coronary artery occlusion is caused in the far majority of people by accumulation of cholesterol within the lumen and walls of the coronary arteries. The rate at which this cholesterol accumulates, the degree of blood supply interruption, and what happens to the cholesterol plaque itself in combination with nutrient demands determines what happens to the cardiac muscle.

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The manner in which an individual presents with coronary artery disease depends upon the location of the interruption in the coronary artery, how quickly the interruption occurs, and the nutrient demands of the myocardium at the time. Acutely damaged heart muscle appears as a red purple bruise which has a reduced amount or no contraction.

The individual may have chest pain that is better described as chest discomfort, chest tightness or a constricting sensation. The discomfort may travel to the shoulders and arms including elbows and wrists. It also may travel to the lower jaw including the teeth, to the back between the shoulder blades and to the upper abdomen. The discomfort is not affected by breathing in or out. It may be accompanied by shortness of breath, sweating, and nausea and vomiting.
If complete occlusion (blockage) is within the proximal or main portion of the coronary artery, a significant amount of heart muscle may be destroyed. Enough blood may not be ejected and blood pressure will not be supported. Fainting with unconsciousness may occur if the blood pressure drops. If recovery from an acute event such as this occurs, a remaining large area of non contracting scar which does not eject blood may leave an individual easily fatigued and possibly short of breath, even at rest. This known as congestive heart failure.

Before the actual heart attack (myocardial infarction or MI) occurs, the individual may have warning signs. These are the above described symptoms known as angina pectoris and occur with the increased myocardial nutrient demands of exertion or anxiety. These symptoms indicate that the coronary artery is only partially closed by the cholesterol plaque. Plaques can completely occlude a coronary artery suddenly by causing tiny particles in the blood called platelets to clog up the remaining part of the narrowed channel, or the plaques can hemorrhage into themselves increasing their size causing complete coronary occlusion.

If complete coronary occlusion never occurs, or if it occurs slowly, the individual may never have the unremitting chest discomfort of a classic heart attack, but rather just periodic chest discomfort described as angina pectoris above. In this situation the appearance of the myocardium may appear normal but also may reveal patchy areas of scar or fibrous tissue which does not contract very well. If the scarred area is extensive, the amount of ejected blood from each beat may be significantly reduced causing symptoms of congestive heart failure.
A significant percent of individuals never have chest discomfort at all. The classic warning signs of angina pectoris or impending heart attack are absent. This is especially noted in the elderly or diabetics. One of the challenges in cardiology is to identify these people.

Besides the mechanical contraction problems of the myocardium with a heart attack, the ability of the mitral valve to close may be impaired resulting in a leak between the left ventricle and left atrium when the left ventricle contracts. Also a rupture of heart muscle between the 2 ventricular chambers can occur, and the heart muscle can rupture into the fibrous sac (pericardium) which contains the heart.

All living cells are electrically active, and this activity is determined by a balance of chemicals within each cell and across the cell membrane which separates it from other cells. In mammals these chemicals are sodium, potassium, chlorine, and calcium. They create a measurable mini- potential across the cell membrane just like a battery. The myocardium therefore consists of millions of cells that have electrical potential. When a myocardial cell contracts it is the temporary interchange of these chemicals across the membrane that cause the myocardial protein elements within each cell to inter connect and change the shape of the cell; ie, making it shorter. In cardiac muscle this whole system is coordinated by a nerve conduction system that may be compared to conductive wires that extend from the atria to the ventricles. This nerve conduction system is located just beneath the inner surface of the cardiac chambers and ensures that the atria and ventricles contract on time and in a coordinated manner. It is this
conduction system that can be recorded by the electrocardiogram (EKG). The wire network works automatically, and in an adult at rest, it emits chemical electric current thru its distribution at 72 times per minute.

A heart attack not only damages heart muscle, it damages the electrical activity of the heart. If one of the myocardial cell membranes is injured, the chemical balance maintaining potential across its membrane is disturbed. This cell may then contract independently of the networked coordinating system, and in addition, the damaged cell will transmit its irritability to many contiguous cells. The entire myocardium may then be affected causing potentially fatal heart rhythms as ventricular tachycardia and ventricular fibrillation. These rhythm disturbances cause rapid, uncoordinated and weak myocardial contractions and can lead to full cardiac arrest.

Cardiac rhythm disturbances are a frequent cause of complications from a heart attack, including death. It is one of the major reasons for dealing with chest pain as a possible life or death situation.

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