The Nation’s #1 Killer

CARDIOVASCULAR DISEASE

The Cardiovascular SystemThe Cardiovascular System

The heart weighs between 7 and 15 ounces 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 more than 3.5 billion times. In fact, each day, the average heart beats 100,000 times, pumping about 2,000 gallons of blood. It is almost all muscle; made up of unique muscle tissue called the myocardium. Within the heart there are four hallow chambers. Two collecting chambers, the atria, and two pumping chambers, the ventricles. Between the chambers of the heart there are valves that prevent the blood from flowing in the wrong direction. The valve between the left atrium and the left ventricle is the mitral valve. The valve between the right atrium and right ventricle is the tricuspid. There are two other valves within the heart where blood exits. When oxygen rich blood exits from the left ventricle it passes through the aortic valve and into the aorta. When oxygen depleted blood exits from the right ventricle it passes through the pulmonary valve into the pulmonary artery.

CardioCardio – the heartVascularVascular – blood vessel system, circulation of nutrients.

STRUCTURE OF THE HEARTSTRUCTURE OF THE HEART

The heart is separated down the middle by a strong, muscular wall called the septum. The heart is enclosed in a fibrous sac called the pericardian (or pericardial sac).

The left side of the heart (left atria and left ventricle) are responsible for pumping oxygen rich blood to all cells, tissues and organs. Conversely, the right side of the heart is responsible for collecting and pumping oxygen depleted blood back to the lungs to receive fresh O2. Oxygenated blood enters the left atria and is passed to the left ventricle where it is pumped through the aortic valve into the aorta. Oxygen depleted blood enters the right atria of the heart through two large veins, the superior vena cava (carrying all DeO2 above the heart) and the inferior vena cava (carrying all DeO2) from below the heart. The heart muscle itself receives oxygen and nutrients from the all important coronary arteries, which branch off from the base of the aorta. There are four major branches off the coronaries. These are the arteries where most heart issues occur.

STRUCTURE OF HEARTSTRUCTURE OF HEART

STRUCTURE OF THE HEART

This is the external appearance of a normal heart. The epicardial surface is smooth and glistening. The amount of epicardial fat is usual. The left anterior descending coronary artery extends down from the aortic root to the apex.

VASCULAR SYSTEM – BLOOD VESSELS AND CELLSVASCULAR SYSTEM – BLOOD VESSELS AND CELLS

The circulatory (vascular) system is made up of arteries, veins and capillaries. Blood (plasma) travels through these vessels carrying nutrients, oxygen and waste products to and from cells. Within blood plasma are three blood cells. Red blood cells carry the oxygen within a pigment called hemoglobin.

Arteries carry oxygen rich blood away from the heart branching into smaller and smaller arteries then into the arterioles which feed the capillary beds in tissues.

Diffusion occurs at the capillary bed level where oxygen is diffused into tissue and carbon dioxide is picked up. Capillary beds then drain waste blood into venules which empty into veins and finally into the superior vena cava (blood from above the heart) and inferior vena cava (blood from below the hear).

Major arteries and veins of the circulatorysystem

BLOOD CELLSBLOOD CELLS

Plasma, the liquid portion of blood, is approximately 90%. Over 100 different substances are dissolved in this fluid including nutrients, salts (electrolytes, respiratory gases, hormones, proteins and various wastes.

Red blood cells (erythrocytes) carry oxygen, inside a pigment called hemoglobin, to all the cells of the body.

White blood cells (leukocytes), produce a variety of antibodies to combat everything from the common cold to tumors and viruses.

Platelets, responsible for clotting of blood, are not really cells but fragments of bizarre multinucleate cells called megakaryocytes.

CARDIOVASCULAR DISEASES (CVD’s)CARDIOVASCULAR DISEASES (CVD’s)Refers to diseases of all parts of the cardiovascular system, including

both the heart and blood vessels.

Atherosclerosis, or hardening of the arteries, is the most common form of CVD. It begins early on with deposits of fat along the inner walls of arteries. These deposits harden and form plaques. The passageway narrows and blood supply lessens.

Atherosclerosis not only weakens the heart but it leads to HIGH BLOOD PRESSURE. High blood pressure, hypertension, is a major contributor to CVD. Hypertension damages artery walls.

Aneurysm occur when the pressure becomes so great a part of the artery balloons out and can burst. When this happens to small vessel it results in death to surrounding tissue. If it happens to a major vessel like the aorta or coronary artery massive hemorrhage occurs resulting in death.

CARDIOVASCULAR DISEASE (CVD’s) CARDIOVASCULAR DISEASE (CVD’s) cont.cont.

Atherosclerosis can cause blockage of an artery in any of three ways:

1. The plaques themselves can enlarge to block flow of blood.

2. A blood clot may form, stick to a plaque, and grow until it cuts off the blood supply like a plug. This is called a thrombus. In the arteries of the heart it is called a coronary thrombosis (a type of heart attack). In a vessel that feeds the brain , the blockage is called a cerebral thrombosis (a type of stroke).

3. A clot may also break loose, become a traveling clot, an embolus and can circulate until it reaches an artery too small to allow its passage. The sudden blockage of the vessel is an embolism.

Strokes occur in the same way heart attacks do – by the blockage of arteries – the cerebral arteries. Strokes do not occur as often as heart attacks and many arise from the bursting of an aneurysm in a small vessel.

CARDIOVASCULAR DISEASE (CVD’s) CARDIOVASCULAR DISEASE (CVD’s) cont.cont.

Congestive Heart Disease – occurs because the heart muscle is damaged or overworked. This can result from high blood pressure, artherosclerosis or heart attack. The heart lacks strength to keep blood circulating throughout the body. The result is congestion in the tissues resulting in swelling (edema) in legs and ankles. Sometimes fluid collects in lungs and can interfer with breathing.

Rheumatic Heart Disease – condition in which heart valves are damaged by a disease process that begins with strep throat. If not treated it can develop into rheumatic fever.

Bacterial Endocarditis – a bacterial infection of the heart lining or valves. People with abnormal heart valves or congential heart defects are at increased risk of developing this disease.

Congenital Heart Defects – malformation of the heart or of its major blood vessels present at birth.

ATHEROSCLEROTIC CARDIOVASCULAR DISEASEATHEROSCLEROTIC CARDIOVASCULAR DISEASESome Pictures Some Pictures

This is the tricuspid valve. The leaflets thin and delicate. Just like the mitral valve, the leaflets have thin chordae tendineae that attach the leaflet margins to the papillary muscles of the ventricular wall below.

This is a normal coronary artery. The lumen is large, without any narrowing by atherosclerotic plaque. The muscular arterial wall is of normal proportion.

The coronary artery shown here has narrowing of the lumen due to build up of atherosclerotic plaque. Severe narrowing can lead to angina, ischemia, and infarction.

This is about as normal as an adult aorta in America gets. The faint reddish staining is from hemoglobin that leaked from RBC's following death. The surface is quite smooth, with only occasional faint small yellow lipid streaks visible.

Put down that jelly doughnut and look carefully at this aorta. The white arrow denotes the most prominent fatty streak in the photo, but there are other fatty streaks scattered over the aortic surface. Fatty streaks are the earliest lesions seen with atherosclerosis in arteries.

These three aortas demonstrate mild, moderate, and severe atherosclerosis from bottom to top. At the bottom, the mild atherosclerosis shows only scattered lipid plaques. The aorta in the middle shows many more larger plaques. The severe atherosclerosis in the aorta at the top shows extensive ulceration in the plaques.

Here is an example of an atherosclerotic aneurysm of the aorta in which a large "bulge" appears just above the aortic bifurcation. Such aneurysms are prone to rupture when they reach about 6 to 7 cm in size. They may be felt on physical examination as a pulsatile mass in the abdomen. Most such aneurysms are conveniently located below the renal arteries so that surgical resection can be performed with placement of a dacron graft.

This is severe atherosclerosis of the aorta in which the plaques have undergone ulceration along with formation of overlying mural thrombus.

A coronary artery has been opened longitudinally. The coronary extends from left to right across the middle of the picture and is surrounded by epicardial fat. Increased epicardial fat correlates with increasing total body fat. There is a lot of fat here, suggesting one risk factor for atherosclerosis. This coronary shows only mild atherosclerosis, with only an occasional yellow-tan lipid plaque and no narrowing.

This is the left coronary artery from the aortic root on the left. Extending across the middle of the picture to the right is the anterior descending branch. This coronary shows severe atherosclerosis with extensive calcification. At the far right, there is an area of significant narrowing.

This is coronary atherosclerosis with the complication of hemorrhage into atheromatous plaque, seen here in the center of the photograph. Such hemorrhage acutely may narrow the arterial lumen.

At high magnification, the dark red thrombus is apparent in the lumen of the coronary. The yellow tan plaques narrow this coronary significantly, and the thrombus occludes it completely.

The anterior surface of the heart demonstrates an opened left anterior descending coronary artery. Within the lumen of the coronary can be seen a dark red recent coronary thrombosis. The dull red color to the myocardium as seen below the glistening epicardium to the lower right of the thrombus is consistent with underlying myocardial infarction.

A thrombosis of a coronary artery is shown here in cross section. This acute thrombosis diminishes blood flow and leads to ischemia and/or infarction, marked clinically by the sudden onset of chest pain.

MYOCARDIAL INFARCTION MYOCARDIAL INFARCTION HEART ATTACKHEART ATTACK

When the myocardium (heart muscle) is deprived of oxygen the result could be crushing chest pain called anginas pectoris (anginas). This pain is a warning that should never be ignored because, if angina is prolonged, the ischemic heart cells may die, forming an infarct. The resulting myocardial infarction is commonly called a “heart attack” or “coronary”.

Most heart attacks are brought on by atherosclerosis.

WARNING SIGN OF HEART ATTACKWARNING SIGN OF HEART ATTACK

Even though not every heart attack is announced by clear cut symptoms, you should get help immediately if you:

1. Feel uncomfortable pressure, fullness, squeezing or pain in the center of the chest lasting for more than two minutes.

2. Experience pain that spreads to the shoulders, neck, or arms.

3. Become dizzy faint, sweats for no apparent reason or have nausea or shortness of breath – especially when other symptoms are present.

WARNING SIGN OF STROKEWARNING SIGN OF STROKE

Report to a physician immediately any of the following:

1. Sudden, temporary weakness or numbness in any part of one side of the body.

2. Temporary loss of speech or of understanding of speech.

3. Dizziness, unsteadiness, or unexplained falls.

4. Temporary dimness or loss of vision, particularly one eye.

DIAGNOSIS AND TREATMENT FOR HEART DISEASEDIAGNOSIS AND TREATMENT FOR HEART DISEASE

Most patients, when symptoms of anginas appear, will have diagnostic tests to determine what course of treatment is best.

There are also many who must first survive a heart attack before determining best course of action.

HEART ATTACK HEART ATTACK – The most common of life-threatening events brought on by lack of blood supply to the myocardium. It requires immediate intervention with CPR (Cardio-Pulmonary Resuscitation) and Emergency Medical Treatment (see handout on CPR performance.

DIAGNOSTIC TESTSDIAGNOSTIC TESTS

ELECTROCARDIOGRAM (ECG or EKG) – a graphic record of electrical impulses by the heart.ECHOCARDIOGRAPHY – sound waves are transmitted into the body and the echoes returning record a picture of the heart’s silze, shape and movements.ANGIOCARDIOGRAPHY – an X-ray picture of blood vessels or chambers of the heart that show the course of dye injected into the bloodstream. The X-ray pictures made are called angiograms.ARTERIOGRAPHY - X-ray opaque dye shows pictures to show artery damage.CATHETERIZATION – examining an artery by introducing a thin tube (catheter) into a vein or artery and passing it into the heart.

TREATMENTTREATMENT

CORONARY BYPASS SURGERY – surgery to improve blood supply to the myocardium (heart muscle). This surgery is the most often performed procedure when narrowed coronary arteries reduce the flow of oxygen-containing blood to the heart itself.

ANGOOPLASTY (Balloon Angioplasty) – a procedure sometimes used to dilate (widen) narrowed arteries. A catheter with a deflated balloon on its tip is passed into the narrowed artery segment, the balloon inflated, and the narrowed segment widened. Often times a mesh stint is also put in to hold the inflated artery open.

REPERFUSION THERAPY – if a victim gets to an emergency room fast enough, a form of reperfusion therapy (called thrombolytic) sometimes can be performed. It involves injecting a thrombolytic (clot-dissolving) agent, to dissolve a clot in a coronary artery and restore some blood flow.

NITROGLYCERIN – a drug that causes dilation of blood vessels and is often used in treating angina pectoris.

RISK FACTORS FOR HEART AND ARTERY DISEASERISK FACTORS FOR HEART AND ARTERY DISEASE

Heredity (history of CVD prior to age 55 in family members.

Gender – males suffer more CVD’s than female although current research shows that heart disease in females is approaching males.

Smoking and use of other tobacco products.

High blood pressure – Hypertension

High blood cholesterol, high LDL, and/or low HDL.

Glucose intolerance – Diabetes

Lack of cardiovascular exercise.

Obesity – 30% or more overweight.

STRESS

BLOOD BLOOD CHOLESTEROL CHOLESTEROL

CHARTCHART

HIGH BLOOD PRESSURE – THE “SILENT KILLER”HIGH BLOOD PRESSURE – THE “SILENT KILLER”

HYPERTENSION, the medical term for high blood pressure is called the “silent killer” because it often has no recognizable symptoms.

Blood pressure is the measure of pressure within the walls of arteries. It is read as a two number notation:

SYSTOLIC PRESSURE SYSTOLIC PRESSURE - a measure of pressure when the ventricles contract and force more blood into the system.

DIASTOLIC PRESSURE DIASTOLIC PRESSURE – a measure of pressure when the ventricles are refilling and the heart is in relaxation phase.

Normal blood pressure reading would be systolic in the 120-130 range and diastolic in the 70-80 range. Systolic pressure over 140 and diastolic over 90 would indicate pressure in the high range.

CONTRIBUTING FACTORS:CONTRIBUTING FACTORS: 1. Smoking2. High Saturated Diet3. Stress4. Family History5. Pregnancy – increase

in blood pressure

6. BMI in the overweight range and above

7. Age – pressure goes up with age8. The Pill – two times greater in women

who use oral contraceptives

MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION – – HEART ATTACKHEART ATTACKSome PicturesSome Pictures

This is the left ventricular wall which has been sectioned lengthwise to reveal a large recent myocardial infarction. The center of the infarct contains necrotic muscle that appears yellow-tan. Surrounding this is a zone of red hyperemia. Remaining viable myocardium is reddish- brown.

This cross section through the heart demonstrates the left ventricle on the left. Extending from the anterior portion and into the septum is a large recent myocardial infarction. The center is tan with surrounding hyperemia. The infarction is "transmural" in that it extends through the full thickness of the wall.

One complication of a myocardial infarction is rupture of the myocardium. This is most likely to occur in the first week between 3 to 5 days following the initial event, when the myocardium is the softest. The white arrow marks the point of rupture in this anterior-inferior myocardial infarction of the left ventricular free wall and septum. Note the dark red blood clot forming the hemopericardium. The hemopericardium can lead to tamponade.

The heart is opened to reveal the left ventricular free wall on the right and the septum in the center. There has been a remote myocardial infarction that extensively involved the anterior left ventricular free wall and septum. The white appearance of the endocardial surface indicates the extensive scarring.

There has been a previous extensive myocardial infarction involving the free wall of the left ventricle. Note that the thickness of the myocardial wall is normal superiorly, but inferiorly is only a thin fibrous wall. The infarction was so extensive that, after healing, the ventricular wall was replaced by a thin band of collagen, forming an aneurysm. Such an aneurysm represents non-contractile tissue that reduces stroke volume and strains the remaining myocardium. The stasis of blood in the aneurysm predisposes to mural thrombosis.

A cross section through the heart reveals a ventricular aneurysm with a very thin wall at the arrow. Note how the aneurysm bulges out. The stasis in this aneurysm allows mural thrombus, which is present here, to form within the aneurysm.

This left ventricle is very thickened (slightly over 2 cm in thickness), but the rest of the heart is not greatly enlarged. This is typical for hypertensive heart disease. The hypertension creates a greater pressure load on the heart to induce the hypertrophy.

This patient underwent coronary artery bypass grafting with saphenous vein grafts. The largest of these runs down the center of the heart to anastomose with the left anterior descending artery distally. Another graft extends in a "Y" fashion just to the right of this to branches of the circumflex artery. A white temporary pacing wire extends from the mid left surface.

The left ventricle is markedly thickened in this patient with severe hypertension that was untreated for many years. The myocardial fibers have undergone hypertrophy.

This is a mechanical valve prosthesis of the more modern tilting disk variety. Such mechanical prostheses will last indefinitely from a structural standpoint, but the patient requires continuing anticoagulation because of the exposed non-biologic surfaces. The superior aspect (here the left atrium) is seen at the left, while the outflow, with the two leaflets tilted outward toward the left ventricle, is at the right in this mitral valve prosthesis.

REDUCING THE RISK OF CVDREDUCING THE RISK OF CVD

1. Learn about your heredity, and use the information. Control the lifestyle factors that may affect you.

2. Don’t smoke. If you do smoke, STOP!STOP!

3. Keep your blood pressure below 125/80 if you are a teenage girl; 130/80 if you are a teenage boy.

4. Keep; your blood cholesterol within the normal range (below 170 milligrams per deciliter for teenagers).

5. Keep your blood sugar under control.

6. Exercise vigorously for at least 20 minutes 4-6 times a week.

7. Maintain appropriate body weight.

8. Control stress. LEARN TO RELAX!!!LEARN TO RELAX!!!.

TAKE CARE OF YOUR HEARTTAKE CARE OF YOUR HEART

ITIT’’S THE ONLY ONE YOU HAVES THE ONLY ONE YOU HAVE