Cardiac Ischemia (is-kē-mē-uh)

Transcription

1 Chapter 21 Cardiac Ischemia (is-kē-mē-uh) By: Alejandra & Lindsay

2 I. Cardiac Ischemia =the most common cause of death in Western Culture ~35% of deaths. -Suddenly from acute coronary occlusion or fibrillation of the heart. -Or slowly over a period of weeks to years as a result of progressive weakening of heart pumping.

3 Main Focus: Acute coronary ischemia caused by acute coronary occlusion and myocardial infarction.

4 A.Atherosclerosis as a cause of ischemic heart disease = A disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls. Who s at risk to have atherosclerosis? -People with a genetic predisposition -People who have high blood pressure and damage to epithelial cells of the coronary blood vessels

5 How? 1. Large quantities of cholesterol gradually become deposited beneath the endothelium at many points in arteries throughout the body (cholesterol plaques). 2. Deposit areas are invaded by fibrous tissue. These can then become calcified (calcification). Results in atherosclerotic plaques that actually protrude into the vessel lumens and either block or partially block blood flow. Common sites of atherosclerosis are the first few centimeters of major coronary arteries.

6 Acute Coronary Occlusion -Most frequently occurs in a person who already has underlying atherosclerotic coronary heart disease, but almost never in a person with a normal coronary circulation. Acute occlusion could result from 1. Thrombus, a local blood clot from an atherosclerotic plaque, which can occlude the artery. A thrombus that flows along the artery and occludes an artery more distally is a coronary embolus. 2. Secondary thrombosis of the vessel, from a local muscular spasm that results from direct irritation of the smooth muscle of the arterial wall by the edges of an atherosclerotic plaque.

7 * Corrected from lecture: Thrombosis (primary or secondary) remain attached to vessels. Thrombosis will plug arteries locally, where they are. Embolus detach and occlude arteries away from where they detached.

8 B.Collateral Circulation offers protection In a normal heart, there are almost no large communications among large coronary arteries. But, there are anastomoses. Anastomoses= a connection between adjacent blood vessels, parts of the intestine, or other channels of the body. -Developing collateral channels ~1 month to reach normal (almost normal) coronary flow Fig. 21-6: Minute anastomoses in the normal coronary arterial system.

9 C.Myocardial Infarction 1. Immediately after acute coronary occlusion, blood flow ceases in coronary vessels. 2. Area of muscle with little or no blood flow cannot sustain cardiac muscle function (infarcted) Onset of Infarction - Small amounts of collateral blood seep into infarcted area - Dilation of blood vessels causes area to become overfilled with stagnant blood. - Cardiac muscle begins to swell Within a few hours of almost no blood supply, the cardiac muscle cells die

10 D.Causes of Death following Infarction Decreased Cardiac Output Overall pumping strength of the infarcted heart is often decreased more than expected because of systolic stretch=instead of contracting, the ischemic portions of the ventricular muscle bulges out. Heart can no longer contract with sufficient force peripheral ischemia. AKA: coronary shock, cardiogenic shock, or low cardiac output failure. -Cardiac almost always occurs when more >40% of left ventricle is infarcted; death in >70% of patients. Fig. 21-7: Systolic stretch in an area of ischemic cardiac muscle.

11 Blood Damming in Venous System - Heart not pumping enough blood forward, so it dams blood in the atria and blood vessels of the lungs capillary pressures, especially in the lungs. Symptoms develop few days later due to: - Diminished blood flow to the kidneys - Kidneys fail to excrete enough urine This progressively adds to the total blood volume and leads to congestive symptoms. -Develop acute pulmonary edema and die within hours of symptom appearance

12 Fibrillation Two periods which fibrillation can occur: 1. First 10 min after infarction occurs 2. Days after the infarction occurs Four factors for the heart to fibrillate 1. Acute loss of blood to cardiac muscle - Rapid depletion of K+ from ischemic musculature 2. Ischemia of the muscle causes an injury current - Ischemic musculature cannot repolarize its membranes after a heartbeat 3. Sympathetic reflexes develop after infarction - Reduced blood pressure 4. Myocardial infarction causes ventricle to dilate excessively

13 Rupture of Infracted Areas After acute infarction, little danger of rupture of ischemic part of the heart - Dead muscle fibers begin to degenerate - Heart wall is stretched very thin - Dead muscle bulges outward with each heart contraction - Systolic stretch becomes greater until heart ruptures

14 Recovery from Acute Myocardial Infarction When area of ischemia is small, little to no muscle death may occur (Left) but part of the muscle does become nonfunctional. When area is large (right) some muscle fibers dies in the center. Area around dead tissue contracts weakly. Fig. 21-8: Top, small and large areas of coronary ischemia. Bottom, stages of recovery from myocardial infarction.