ACUTE CORONARY SYNDROME

Background: The initial diagnosis of acute coronary syndrome (ACS) is based entirely on history, risk factors, and, to a lesser extent, ECG findings. The symptoms are due to myocardial ischemia, the underlying cause of which is an imbalance between supply and demand of myocardial oxygen.

Patients with ACS include those whose clinical presentations cover the following range of diagnoses: unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). This ACS spectrum concept is a useful framework for developing therapeutic strategies.

Pathophysiology: Myocardial ischemia is most often due to atherosclerotic plaques, which reduce the blood supply to a portion of myocardium. Initially, the plaques allow sufficient blood flow to match myocardial demand. When myocardial demand increases, the areas of narrowing may become clinically significant and precipitate angina. Angina that is reproduced by exercise, eating, and/or stress and is subsequently relieved with rest, and without recent change in frequency or severity of activity that produce symptoms, is called chronic stable angina. Over time, the plaques may thicken and rupture, exposing a thrombogenic surface upon which platelets aggregate and thrombus forms. The patient may note a change in symptoms of cardiac ischemia with a change in severity or of duration of symptoms. This condition is referred to as unstable angina.

Patients with STEMI have a high likelihood of a coronary thrombus occluding the infarct artery. Angiographic evidence of coronary thrombus formation may be seen in more than 90% of patients with STEMI but in only 1% of patients with stable angina and about 35-75% of patients with unstable angina or NSTEMI. However, not every STEMI evolves into a Q-wave MI; likewise, a patient with NSTEMI may develop Q waves.

The excessive mortality rate of coronary heart disease is primarily due to rupture and thrombosis of the atherosclerotic plaque. Inflammation plays a critical role in plaque destabilization and is widespread in the coronary and remote vascular beds. Systemic inflammatory, thrombotic, and hemodynamic factors are relevant to the outcome. Evidence indicates that platelets contribute to promoting plaque inflammation as well as thrombosis. A new theory of unbalanced cytokine-mediated inflammation is emerging, providing an opportunity for intervention.

Coronary vasospasm is a frequent complication in patients with connective tissue disease. Other causes include arterial inflammation and secondary unstable angina. Arterial inflammation may be caused by or related to infection. Secondary unstable angina occurs when the precipitating cause is extrinsic to the coronary arterial bed, such as fever, tachycardia, thyrotoxicosis, hypotension, anemia, or hypoxemia. Most patients who experience secondary unstable angina have chronic stable angina as a baseline medical condition.

An early clinical suspicion of this disease is necessary for a good outcome. Cardiology consultation should be obtained for consideration for urgent percutaneous coronary intervention.

• ACS may occur with Marfan syndrome; Kawasaki disease; Takayasu arteritis; or cystic medial necrosis with aortic root dilatation, aneurysm formation, and dissection into the coronary artery.
• Anomalous origin of the left coronary artery from the pulmonary artery may occur as unexplained sudden death in a neonate.
• Coronary artery ostial stenosis may occur after repair of a transposition of the great arteries in the neonatal period.
• An aberrant left main coronary artery with its origin at the right sinus of Valsalva may cause ACS, especially with exertion.
• Traumatic myocardial infarction can occur in patients at any age.
• Accelerated atherosclerosis is known to occur in cardiac transplant recipients on immunosuppressive therapy.
• Progeria

Irrespective of the cause of unstable angina, the result of persistent ischemia is myocardial infarction (MI)

Mortality/Morbidity: When the only treatment for angina was nitroglycerin and limitation of activity, patients with newly diagnosed angina had a 40% incidence of MI and a 17% mortality rate within 3 months. A recent study shows that the 30-day mortality from ACS has decreased as treatment has improved, a statistically significant 47% relative decrease in 30-day mortality among newly diagnosed ACS from 1987-2000. This decrease in mortality is attributed to aspirin, glycoprotein (GP) IIb/IIIa blockers, and coronary revascularization via medical intervention or procedures.

Clinical characteristics associated with a poor prognosis include advanced age, male sex, prior MI, diabetes, hypertension, and multiple-vessel or left-mainstem disease.

Sex: Incidence is higher in males among all patients younger than 70 years. This is due to the cardioprotective effect of estrogen in females. At 15 years postmenopause, the incidence of angina occurs with equal frequency in both sexes. Evidence exists that women more often have coronary events without typical symptoms, which might explain the frequent failure to initially diagnose ACS in women.

Age: ACS becomes progressively more common with increasing age. In persons aged 40-70 years, ACS is diagnosed more often in men than in women. In persons older than 70 years, men and women are affected equally.

History:

• Typically, angina is a symptom of myocardial ischemia that appears in circumstances of increased oxygen demand. It usually is described as a sensation of chest pressure or heaviness that is reproduced by activities or conditions that increase myocardial oxygen demand.
• Not all patients experience chest pain. Some present with only neck, jaw, ear, arm, or epigastric discomfort.
• Other symptoms, such as shortness of breath or severe weakness, may represent anginal equivalents.

• A patient may present to the ED because of a change in pattern or severity of symptoms. A new case of angina is more difficult to diagnose because symptoms are often vague and similar to those caused by other conditions (eg, indigestion, anxiety).
• Patients may have no pain and may only complain of episodic shortness of breath, weakness, lightheadedness, diaphoresis, or nausea and vomiting.

• Patients may complain of the following:

• Palpitations
• Pain, which is usually described as pressure, squeezing, or a burning sensation across the precordium and may radiate to neck, shoulder, jaw, back, upper abdomen, or either arm
• Exertional dyspnea that resolves with pain or rest
• Diaphoresis from sympathetic discharge

• Nausea from vagal stimulation

• Decreased exercise tolerance

• Patients with diabetes and elderly patients are more likely to have atypical presentations and offer only vague complaints, such as weakness, dyspnea, lightheadedness, and nausea.

• Stable angina

• Involves episodic pain lasting 5-15 minutes

• Provoked by exertion

• Relieved by rest or nitroglycerin

• Unstable angina: Patients have increased risk for adverse cardiac events, such as MI or death. Three clinically distinct forms exist, as follows:

• New-onset exertional angina

• Angina of increasing frequency or duration or refractory to nitroglycerin

• Angina at rest

• Variant angina (Prinzmetal angina)

• Occurs primarily at rest

• Triggered by smoking

• Thought to be due to coronary vasospasm

• Elderly persons and those with diabetes may have particularly subtle presentations and may complain of fatigue, syncope, or weakness. Elderly persons may also present with only altered mental status. Those with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever.
• As many as half of cases of ACS are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient. Maintain a high index of suspicion for ACS especially when evaluating women, diabetics, older patients, patients with dementia, and those with a history of heart failure.

Physical:

• Physical examination results are frequently normal. If chest pain is ongoing, the patient usually will lie quietly in bed and may appear anxious, diaphoretic, and pale.

• Hypertension may precipitate angina or reflect elevated catecholamines due to either anxiety or exogenous sympathomimetic stimulation.

• Hypotension indicates ventricular dysfunction due to myocardial ischemia, infarction, or acute valvular dysfunction.

• Congestive heart failure (CHF)

• Jugular venous distention

• Third heart sound (S₃)

• A new murmur may reflect papillary muscle dysfunction

• Rales on pulmonary examination, suggesting left ventricular (LV) dysfunction or mitral regurgitation

• Presence of a fourth heart sound (S₄), a common finding in patients with poor ventricular compliance due to preexisting ischemic heart disease or hypertension

Causes:

• Atherosclerotic plaque is the predominant cause. Coronary artery vasospasm is less common.

• Alternative causes of angina include the following:

• Ventricular hypertrophy due to hypertension, valvular disease, or cardiomyopathy

• Embolic occlusion of the coronary arteries

• Hypoxia, as in carbon monoxide poisoning or acute pulmonary disorders

• Cocaine and amphetamines, which increase myocardial oxygen demand and may cause coronary vasospasm

• Underlying coronary artery disease, which may be unmasked by severe anemia

• Inflammation of epicardial arteries

• Coronary artery dissection

• Risk factors for ACS should be documented and include the following:
  • Male gender
    
    
  • Diabetes mellitus (DM)
    
    
  • Smoking history
    
    
  • Hypertension
    
    
  • Increased age
    
    
  • Hypercholesterolemia
    
    
  • Hyperlipidemia
    
    
  • Prior cerebrovascular accident (CVA) - These patients constitute 7.5% of patients with ACS and have high-risk features.
    
    
  • Inherited metabolic disorders
    
    
    
  • Occupational stress
    
    
  • Connective tissue disease

TREATMENT

How is a heart attack treated? Special treatments to open up your arteries Heart attack treatment begins immediately. Once symptoms are identified, call 9-1-1 to set in motion rapid diagnosis and treatment. Medications thrombolytic medications are used to break up clots blocking the artery The knowledge gained in the past years regarding acute coronary syndromes and what happens in the artery during a heart attack has helped guide medical treatment. The goals of medication therapy are to break up or prevent blood clots, prevent platelets from gathering and sticking to the plaque, stabilize the plaque, and prevent further ischemia. These medications must be given as soon as possible (within 30 minutes from the start of heart attack symptoms) to decrease the amount of damage to the heart muscle. The longer the delay in starting these drugs, the more damage that occurs and the less benefit they can provide. Medications given right after the start of a heart attack may include: aspirin thrombolytic therapy ("clot busters") heparin other antiplatelet drugs any combination of the above Other drugs, given during or after a heart attack lessen your heart's work, improve the functioning of the heart, widen or dilate your blood vessels, decrease your pain, and guard against any life-threatening heart rhythms. Your doctor will prescribe the appropriate medications for you. Door to Balloon Time The ACC/AHA practice guidelines suggest a 90-minute goal from the patient’s arrival in the Emergency Department to balloon inflation for percutaneous coronary intervention (PCI) procedures unless there is uncertainty about diagnosis or delays associated with informed choice. Interventional procedures During or shortly after a heart attack, you may go to the cardiac catheterization laboratory to directly evaluate the status of your heart, arteries and the amount of heart damage. In some cases, procedures (such as angioplasty or stents) are used to open up your narrowed or blocked arteries. These procedures may be combined with thrombolytic therapy to open up the narrowed arteries, as well as to break up any clots that are blocking them. Coronary artery bypass surgery If necessary, bypass surgery may be performed to restore the heart muscle's supply of blood.

HEART ATTACK : an ACUTE CORONARY SYNDROME

Types of Acute Coronary Syndromes - or heart attacks Acute Coronary Syndrome is a name given to three types of coronary artery disease that are associated with sudden rupture of plaque inside the coronary artery: unstable angina, Non-ST segment elevation myocardial infarction or heart attack (NSTEMI), or ST segment elevation myocardial infarction or heart attack (STEMI). The location of the blockage, the length of time that blood flow is blocked and the amount of damage that occurs determines the type of acute coronary syndrome. These life-threatening conditions require emergency medical care. Unstable angina is a new symptom or a change from stable angina. The angina may occur more frequently, occur more easily at rest, feel more severe, or last longer. Although this angina can often be relieved with oral medications, it is unstable and may progress to a heart attack. Usually more intense medical treatment or a procedure is required. Unstable angina is an acute coronary syndrome and should be treated as a medical emergency. Heart attack: Non-ST segment elevation myocardial infarction (NSTEMI): This heart attack, or MI, does not cause changes on an electrocardiogram (ECG). However, chemical markers in the blood indicate that damage has occurred to the heart muscle. In NSTEMI, the blockage may be partial or temporary, and so the extent of the damage relatively minimal. Heart attack: ST segment elevation myocardial infarction (STEMI): This heart attack, or MI, is caused by a prolonged period of blocked blood supply. It affects a large area of the heart muscle, and so causes changes on the ECG as well as in blood levels of key chemical markers. Other terms associated with a heart attack: Stunned myocardium: If blood flow is returned to an area of heart muscle after a period of ischemia (lack of blood supply), the heart muscle may not pump normally for a period of days following the event. This is called "stunned" heart muscle or myocardium. Hibernating myocardium: After a heart attack, some areas of heart muscle do not pump as they should. Some areas will have permanent damage. Other areas are able to return to their normal function if blood flow is returned to that area (by medications or a procedure). Hibernating myocardium is heart muscle that is "resting" and may possibly return to normal function.

HEART ATTACK SYMPTOMS

If you are having any one of the symptoms described below that lasts for more than 5 minutes, SEEK EMERGENCY TREATMENT WITHOUT DELAY. These symptoms could be the signs of a heart attack and immediate treatment is essential. Symptoms of a heart attack include: Symptoms of a heart attack include: Angina: Chest pain or discomfort in the center of the chest; also described as a heaviness, tightness, pressure, aching, burning, numbness, fullness or squeezing feeling that lasts for more than a few minutes or goes away and comes back. It is sometimes mistakenly thought to be indigestion or heartburn. Pain or discomfort in other areas of the upper body including the arms, left shoulder, back, neck, jaw, or stomach Difficulty breathing, shortness of breath Sweating or “cold sweat” Fullness, indigestion, or choking feeling (may feel like “heartburn”) Nausea or vomiting Light-headedness, dizziness Extreme weakness or anxiety Rapid or irregular heart beats Women often have different symptoms of a heart attack than men and may report symptoms before having a heart attack, although the symptoms are not typical “heart” symptoms. In a multi-center study of 515 women who had an acute heart attack (MI), the most frequently reported symptoms were unusual fatigue, sleep disturbances, shortness of breath, indigestion and anxiety. The majority of women (78 percent) reported at least one symptom for more than one month before their heart attack. Only 30 percent reported chest discomfort, which was described as an aching, tightness, pressure, sharpness, burning, fullness or tingling. Silent MI: Some people have a heart attack without having any symptoms (a “silent” myocardial infarction). A silent MI can occur among all patients, though it is more common among people with diabetes. A silent MI may be diagnosed during a routine doctor’s exam. If you have been prescribed nitroglycerin and you experience angina, stop what you are doing and rest. Take one nitroglycerin tablet and let it dissolve under your tongue, or if using the spray form, spray it under your tongue. Wait 5 minutes. If you still have angina after 5 minutes, call 9-1-1 to get emergency help. DO NOT DELAY. Emergency personnel may tell you to chew an aspirin to break up a possible blood clot, if there is no medical reason for you to avoid aspirin. After you have called 9-1-1, continue to take your nitroglycerin as prescribed. The first symptoms start the clock At the first signs of a heart attack, call for emergency treatmen.Do not wait for your symptoms to “go away.” Early recognition and treatment of heart attack symptoms can reduce the risk of heart damage and allow treatment to be started immediately. Even if you’re not sure your symptoms are those of a heart attack, you should still be evaluated. Do not delay The best time to treat a heart attack is within one hour of the onset of the first symptoms. When a heart attack occurs, there’s a limited amount of time before significant and long-lasting damage occurs to the heart muscle. If a large area of the heart is injured during the heart attack, full recovery becomes much more difficult. Studies show that the people who have symptoms of a heart attack often delay, or wait to seek treatment, for longer than seven hours. People who delay tend to be older, female, African-American and to have a history of angina, high blood pressure or diabetes. People who delay also consult their family members or try to treat themselves first before seeking treatment. Reasons people delay: They are young and cannot believe it is happening to them Symptoms are not what they expected They may deny the symptoms are serious and wait until they go away They may ask the advice of others, especially family members They may first try to treat the symptoms themselves, using aspirin or antacids They may think the symptoms are related to other health problems (upset stomach, arthritis) They may put the care of others first (take care of children or other family members) and not want to worry them Waiting just a couple hours for medical help may limit your treatment options, increase the amount of damage to your heart muscle, and reduce your chance of survival. Call 9-1-1 – Not a friend Calling 9-1-1 or nearest hospital is almost always the fastest way to get life-saving treatment. When you call, emergency personnel may tell you to chew an aspirin to break up a possible blood clot, if there is not a medical reason for you to avoid aspirin. When they arrive, emergency personnel can promptly begin treatment, and they are trained to revive someone whose heart has stopped. Also, you’re likelier to get treated faster at the hospital if you arrive by ambulance. If you are having symptoms, do not drive yourself unless there is absolutely no other option. If you’ve had prior heart treatments Even if you’ve been treated for a prior heart attack or if you’ve had other treatments for coronary artery disease, a heart attack CAN happen again. Treatments such as medications, open heart surgery and interventional procedures DO NOT cure coronary artery disease. Know in advance: The symptoms of a heart attack. If you are at risk for a heart attack. Ask your doctor about your risk and what you should do to reduce your risk. Be sure to ask about aspirin and nitroglycerin. Who to call for emergency help. Do not call a friend or family member. Call for an ambulance to take you to the nearest emergency room. Share this information with your family members and caregivers so they learn to recognize the symptoms of a heart attack and when to help you seek emergency treatment.

WHAT HAPPENS DURING A HEART ATTACK?

A closer look inside your coronary arteries Your heart muscle needs to receive a good supply of blood at all times to function properly. Your heart muscle gets the blood it needs to do its job from the coronary arteries. What is coronary artery disease? Coronary artery disease is the narrowing or blockage of the coronary arteries caused by atherosclerosis. Atherosclerosis (sometimes called “hardening” or “clogging” of the arteries) is the buildup of cholesterol and fatty deposits (called plaque) on the inner walls of the arteries that restricts blood flow to the heart. Without adequate blood, the heart becomes starved of oxygen and the vital nutrients it needs to work properly. This can cause chest pain called angina. When one or more of the coronary arteries are completely blocked, a heart attack (injury to the heart muscle) may occur. A closer look at coronary artery disease
When fat builds up inside your arteries it causes slight injury to your blood vessel walls. In an attempt to heal the blood vessel walls, the cells release chemicals that make the blood vessel walls stickier. Other substances traveling through your blood stream, such as inflammatory cells, cellular waste products, proteins and calcium, begin to stick to the vessel walls. The fat and other substances combine to form a material called plaque.
Over time, the inside of the arteries develop plaques of different sizes. Many of the plaque deposits are soft on the inside with a hard fibrous “cap” covering the outside. If the hard surface cracks or tears, the soft, fatty inside is exposed. Platelets (disc-shaped particles in the blood that aid clotting) come to the area, and blood clots form around the plaque.
If a blood clot totally blocks the blood supply to the heart muscle, called a coronary thrombus or coronary occlusion, the heart muscle becomes "starved" for oxygen and nutrients (called ischemia) in the region below the blockage. Within a short time, an acute coronary syndrome can occur. Acute Coronary Syndrome is a name given to three types of coronary artery disease that are associated with sudden rupture of plaque inside the coronary artery: unstable angina, Non-ST segment elevation myocardial infarction or heart attack(NSTEMI),or ST segment elevation myocardial infarction or heart attack(STEMI).
spasm A heart attack can also occur less frequently by a spasm of a coronary artery. During coronary spasm, the coronary arteries constrict or spasm on and off, causing lack of blood supply to the heart muscle (ischemia). It may occur at rest and can even occur in people without significant coronary artery disease. If coronary artery spasm occurs for a long period of time, a heart attack can occur.
Each coronary artery supplies blood to a region of the heart muscle. If an artery is occluded (blocked) there is no blood supply to that region.
dark red = artery	blue = outlines region of heart affected by blockage
Circumflex occlusion back of heart	Left anterior descending (LAD) occlusion front of heart	Right coronary artery (RCA) occlusion front of heart
The amount of damage to the heart muscle depends on the size of the area supplied by the blocked artery and the time between injury and treatment. Quick treatment to open the blocked artery is essential to lessen the amount of damage. Learn the symptoms of a heart attack and what to do if they occur. Healing of the heart muscle begins soon after a heart attack and takes about 8 weeks. Just like a skin wound, the heart’s wound heals and a scar will form in the damaged area. The new scar tissue does not contract or pump as well as healthy heart muscle tissue. So, the heart’s pumping ability is lessened. The amount of lost pumping ability depends on the size and location of the scar.

HEART ATTACK

What is heart attack

A heart attack, or myocardial infarction (MI), is permanent damage to the heart muscle. "Myo" means muscle, "cardial" refers to the heart, and "infarction" means death of tissue due to lack of blood supply.

Heart Beat

A heartbeat is a two-part pumping action that takes about a second. As blood collects in the upper chambers (the right and left atria), the heart's natural pacemaker (the SA node) sends out an electrical signal that causes the atria to contract. This contraction pushes blood through the tricuspid and mitral valves into the resting lower chambers (the right and left ventricles). This part of the two-part pumping phase (the longer of the two) is called diastole.

The second part of the pumping phase begins when the ventricles are full of blood. The electrical signals from the SA node travel along a pathway of cells to the ventricles, causing them to contract. This is called systole. As the tricuspid and mitral valves shut tight to prevent a back flow of blood, the pulmonary and aortic valves are pushed open. While blood is pushed from the right ventricle into the lungs to pick up oxygen, oxygen-rich blood flows from the left ventricle to the heart and other parts of the body.

After blood moves into the pulmonary artery and the aorta, the ventricles relax, and the pulmonary and aortic valves close. The lower pressure in the ventricles causes the tricuspid and mitral valves to open, and the cycle begins again. This series of contractions is repeated over and over again, increasing during times of exertion and decreasing while you are at rest. The heart normally beats about 60 to 80 times a minute when you are at rest, but this can vary. As you get older, your resting heart rate rises. Also, it is usually lower in people who are physically fit.

Your heart does not work alone, though. Your brain tracks the conditions around you—climate, stress, and your level of physical activity—and adjusts your cardiovascular system to meet those needs.

The human heart is a muscle designed to remain strong and reliable for a hundred years or longer. By reducing your risk factors for cardiovascular disease, you may help your heart stay healthy longer

Heart Valves

Four valves regulate blood flow through your heart:

* The tricuspid valve regulates blood flow between the right atrium and right ventricle.

* The pulmonary valve controls blood flow from the right ventricle into the pulmonary arteries, which carry blood to your lungs to pick up oxygen.

* The mitral valve lets oxygen-rich blood from your lungs pass from the left atrium into the left ventricle.

* The aortic valve opens the way for oxygen-rich blood to pass from the left ventricle into the aorta, your body's largest artery, where it is delivered to the rest of your body

Coronary Arteries

Diagram of the Coronary Arteries

Coronary Circulation

The heart muscle, like every other organ or tissue in your body, needs oxygen-rich blood to survive. Blood is supplied to the heart by its own vascular system, called coronary circulation.

The aorta (the main blood supplier to the body) branches off into two main coronary blood vessels (also called arteries). These coronary arteries branch off into smaller arteries, which supply oxygen-rich blood to the entire heart muscle.

The right coronary artery supplies blood mainly to the right side of the heart. The right side of the heart is smaller because it pumps blood only to the lungs.

The left coronary artery, which branches into the left anterior descending artery and the circumflex artery, supplies blood to the left side of the heart. The left side of the heart is larger and more muscular because it pumps blood to the rest of the body.

Bundle Branch Block

Your heart has a natural "pacemaker" called the sinoatrial (SA) node. The SA node is a specialized group of cells at the top of your heart's upper-right chamber (the right atrium). Anywhere between 60 and 100 times a minute, the SA node sends an electrical impulse throughout your heart to cause it to beat (contract).

When the SA node sends an electrical impulse, that impulse first travels through the heart's upper chambers (the atria). It then passes through a small group of cells called the atrioventricular (AV) node. The AV node checks the impulse and sends it along a track called the bundle of His. The bundle of His divides into a right bundle branch and a left bundle branch, which lead to your heart's lower chambers (the ventricles)

Sometimes the electrical impulse cannot travel throughout the heart because part of the heart's conduction system is "blocked." If an impulse is blocked as it travels through the bundle branches, you are said to have bundle branch block.

What causes bundle branch block?

For the left and right ventricles to contract at the same time, an electrical impulse must travel down the right and left bundle branches at the same speed. If there is a block in one of these branches, the electrical impulse must travel to the ventricle by a different route. When this happens, the rate and rhythm of your heartbeat are not affected, but the impulse is slowed. Your ventricle will still contract, but it will take longer because of the slowed impulse. This slowed impulse causes one ventricle to contract a fraction of a second slower than the other.

The medical terms for bundle branch block are derived from which branch is affected. If the block is located in the right bundle branch, it is called right bundle branch block. If the block is located in the left bundle branch, it is called left bundle branch block.

The block can be caused by coronary artery disease, cardiomyopathy, or valve disease. Right bundle branch block may also occur in a healthy heart.

What are the symptoms of bundle branch block?

If there is nothing else wrong with your heart, you probably will not feel any symptoms of bundle branch block. In fact, some people may have bundle branch block for years and never know they have the condition. In people who do have symptoms, they may faint (syncope) or feel as if they are going to faint (presyncope).

So why should we worry about bundle branch block? Because it can be a warning sign of other, more serious heart conditions. For example, it might mean that a small part of your heart is not getting enough oxygen-rich blood. Also, researchers have found that people who have left bundle branch block may be at greater risk for heart disease than are people who do not have the condition.

How is bundle branch block diagnosed?

Doctors can use an electrocardiogram (EKG or ECG) machine to record the electrical impulses of your heart. Bundle branch block shows up on the EKG tracing. The electrical patterns recorded by the EKG machine can even show your doctor whether the block is located in the right or left bundle branch.

How is bundle branch block treated?

In most cases, bundle branch block does not need treatment. But patients who have bundle branch block along with another heart condition may need treatment. For example, if bundle branch block develops during a heart attack, you may need a pacemaker. After a heart attack, your heart is fragile, and bundle branch block may cause a very slow heart rhythm (bradycardia). A pacemaker will help regulate the heart's rhythm after a heart attack.

For patients with both bundle branch block and dilated cardiomyopathy, a new type of pacing called cardiac resynchronization treatment (CRT) may be used. Normally, pacemakers pace only one of the lower heart chambers (the ventricles) at a time. But CRT re-coordinates the beating of the two ventricles by pacing them at the same time. Recent studies have shown that CRT works for certain patients with both bundle branch block and dilated cardiomyopathy.

Even if you do not have other conditions, you should still see your doctor regularly so that he or she can be sure there are no other changes in your heart

Conduction System

Electrical impulses from your heart muscle (the myocardium) cause your heart to beat (contract). This electrical signal begins in the sinoatrial (SA) node, located at the top of the right atrium. The SA node is sometimes called the heart's "natural pacemaker." When an electrical impulse is released from this natural pacemaker, it causes the atria to contract. The signal then passes through the atrioventricular (AV) node. The AV node checks the signal and sends it through the muscle fibers of the ventricles, causing them to contract. The SA node sends electrical impulses at a certain rate, but your heart rate may still change depending on physical demands, stress, or hormonal factors

Anatomy and physiology of the Heart

The heart weighs between 7 and 15 ounces (200 to 425 grams) and is a little larger than the size of your fist. By the end of a long life, a person's heart may have beat (expanded and contracted) more than 3.5 billion times. In fact, each day, the average heart beats 100,000 times, pumping about 2,000 gallons (7,571 liters) of blood.
Your heart is located between your lungs in the middle of your chest, behind and slightly to the left of your breastbone (sternum). A double-layered membrane called the pericardium surrounds your heart like a sac. The outer layer of the pericardium surrounds the roots of your heart's major blood vessels and is attached by ligaments to your spinal column, diaphragm, and other parts of your body. The inner layer of the pericardium is attached to the heart muscle. A coating of fluid separates the two layers of membrane, letting the heart move as it beats, yet still be attached to your body.
Your heart has 4 chambers. The upper chambers are called the left and right atria, and the lower chambers are called the left and right ventricles. A wall of muscle called the septum separates the left and right atria and the left and right ventricles. The left ventricle is the largest and strongest chamber in your heart. The left ventricle's chamber walls are only about a half-inch thick, but they have enough force to push blood through the aortic valve and into your bodthpulmonary arteries, which carry blood to your lungs to pick up oxygen.