Diseases of the Cardiovascular System Ischemic Heart Disease – Myocardial Infartcion – Sudden Cardiac Death – Heart Failure – Stroke + A Tiny Bit on the Benefits of Exercise Nancy Long Sieber, Ph.D. October 3, 2011

Ischemic Heart Disease A mismatch between oxygen demand and oxygen delivery

What influences O 2 Delivery? O 2 carrying capacity of blood. Coronary blood flow –Influenced by neural, endothelial and metabolic factors –Can be compromised by atherosclerosis

What influences the myocardial O 2 demand? Heart Rate – Inc. HR inc. O 2 demand Cardiac contractility – Inc. contractility inc. O 2 demand Ventricular wall stress – proportional to afterload and the radius of ventricle => Law of Laplace

Law of LaPlace The ventricular wall stress (T) is the energy required to pull the cardiac muscle fibers together, so that they can contract. Tension is proportional to the product of Intraventricular pressure (P), (which = afterload) and Radius of ventricle (R) So, the greater the volume of the ventricle, the more energy required for contraction.

What enlarges the volume of the ventricle? A large blood volume (preload) => increase EDV, distends the ventricle Ventricular dilation – a pathologic condition

Manifestations of ischemia Angina chest pain associated with intermittent myocardial ischemia. Myocardial infarction (MI) is irreversible necrosis of cardiac muscle cells resulting from a prolonged period with of insufficient myocardial blood flow.

Ischemia in men vs women Men: More likely to have angina before having an MI, more likely to report chest pains during an MI Women: Less likely to experience angina. Both warning signs and symptoms of MI are vague. –Common symptoms before MI: fatigue, sleep disturbances, indigestion –During an MI: shortness or breath, weakness, fatigue, cold sweat, nausea. Less likely to have chest pain.

Vulnerable plaques are most likely to rupture, causing a myocardial infarction or a stroke

Pathophysiology of Heart Disease 3/e. Leonard S. Lilly, Ed. Lippincott Williams and Wilkins. 2003

Serum Markers of Myocardial Infarction Pathophysiology of Heart Disease 3/e. Leonard S. Lilly, Ed. Lippincott Williams and Wilkins. 2003

Sudden Cardiac Death aka: Cardiac arrest Often triggered by cardiac arrhythmia, which prevents the heart from contracting effectively. Cause is often coronary artery disease. Death of muscle tissue can make the heart more vulnerable to the type of arrhythmia that leads to SCD.

Two normal beats, followed by ventricular fibrillation

Heart Failure is a common consequence of MI Forward Failure: Inability of the heart to pump blood at a sufficient rate to meet the metabolic demands of the body Backward Failure: Ability to do so only under abnormally high cardiac filling pressures Most commonly occurs in the left ventricle. As more people are surviving MIs, the incidence of heart failure is increasing.

Types of Heart Failure Systolic dysfunction – an inability to pump blood out of the heart. Typically due to impaired myocardial contractility or increased afterload Diastolic dysfunction – problems with filling, often due to an inability of the ventricle to relax during diastole (an active process), or to ventricular stiffness.

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Compensatory mechanisms in heart failure Increased end-diastolic volume increases the stroke volume This is accomplished by –Increasing blood volume (increased thirst and retention of fluid at the kidney) –Increased sympathetic nerve activity increases venous return (moves blood from veins to the heart), and increases contractility Cardiac hypertrophy increases the muscle mass of the ventricle, and increases the heart’s ability to pump.

These compensations can become detrimental over time. The increase in blood volume leads to pulmonary congestion, in the case of left-heart failure. –Leads to dyspnea, decreased O 2 availability. –Patients are particularly uncomfortable when lying down Right heart failure can lead to peripheral edema –Fluid tends to accumulate in feet, due to gravity –Fluid may also accumulate in the abdomen

Treatment of Heart Failure ACE inhibitors are the most important drugs. –ACE (angiotensin converting enzyme) promotes activation of the renin-angiotensin system. –ACE inhibitors cause vasodilation, and decrease blood volume. Diuretics to get rid of excess. Inotropic drugs – increase availability of intracellular calcium, and thereby increase the force of contraction. Eg: digitalis. ß blockers – these drugs have a negative inotropic effect, but help some patients Other vasodilators

There are two types of strokes Ischemic or occlusive strokes, which occur when a portion of the blood flow to the brain is blocked. Intracranial hemorrhages occur when a blood vessel in the brain ruptures.

A Complete Circle of Willis Protects Against Stroke

The ischemic core is the area adjacent to the infarction. The ischemic penumbra is mildly ischemic. This is the target of therapeutic interventions schemic_penumbra.htm