1. The necrosis which occurs is called _____________________. The area of necrosis will determine the function of the heart and the clinical manifestations. If the MI occurs in the RCA the SA node may be affected.

2. Renin Angiotensin Aldosterone System is activated by __________ renal blood flow. The end result is a release of angiotensin II and aldosterone.

3. Factors which decrease cardiac contraction?

4. The ___________ in cigarette smoke causes the release of the catecholamines which in turn causes vasoconstriction and high blood pressure.

5. A newborn has ________________ and ____________________ which increase oxygen demands may cause acute decompensation of the newborn.

6. Clinical manifestations of NSTEMI?

7. Fetal circulation: The _____________ receives oxygenated blood from the placenta.

8. ______________ decreases insulin secretion and hyperglycemia occurs. This can be seen by 72 hours post MI and is associated with increased mortality.

9. Risk factors include smoking and diabetes. Its presence is a good predictor of systemic atherosclerotic changes. Persons with ____ have more of a risk for CAD.

10. _______________ may be measured and the apolipoprotein B is the most atherogenic one and is strongly associated with coronary events.

11. The loss of ______________ is directly related to changes in the intima media.

12. The ________________ is made of connective tissue and provides the heart with stability by connecting to the sternum anteriorly and the diaphragm inferiorly.

13. Baroreceptors in the left ventricle, aortic arch and carotid sinus detect the low cardiac output (low blood pressure) and notify the medulla which in turns stimulates the sympathetic nervous system. The SNS stimulates the release of the catecholamines epinephrine and norepinephrine, which causes vasoconstriction and leads to increased afterload, increased blood pressure and increased heart rate. This increases the work load of the heart and causes hypertrophy and dilation of the left ventricle and further impairs contractility. Also, the catecholamines cause direct toxic effects to the myocytes and induce myocyte apoptosis, thus causing more damage to the heart.

14. Block the effects of the catecholamines

15. The pathogenesis of _____________ must begin with an event which sets the stage for the infection by causing damage to the endocardium. This may be trauma, congenital heart disease, valvular heart disease, the presence of a prosthetic valve, or any other risk factor.

16. ___________________ are released, one of which is endothelin which is a vasoconstrictor, and its release is associated with a poor prognosis. TNF and IL-6 both contribute to ventricular hypertrophy and remodeling. TNF prevents the synthesis of nitric oxide (thus causing vasoconstriction), induces myocyte apoptosis, and causes weakness and weight loss. IL-6 further activates the immune system.

17. Once the epithelial injury occurs and causes the endothelial cells to become inflamed, they then lack the ability to produce sufficient amounts of antithrombotic and vasodilating cytokines. Macrophages and platelets adhere to the area of injury in the endothelium and toxic oxygen radicals are released by the macrophages. Platelets further stimulate the inflammatory response. Toxic oxygen radicals create oxidative stress and oxidize LDL. This causes additional endothelial damage. Growth factors (angiotensin II, fibroblast growth factor, TGF-β, and platelet derived growth factor) are released which cause smooth muscle hyperplasia. LDL penetrates the subintima of the vessel and becomes trapped and is oxidized by the above process. Oxidized LDL is toxic and causes smooth muscle proliferation (hyperplasia). It also increases endothelial adhesion molecule expression which results in the adhesion of more macrophages which penetrate the vessel wall. The macrophages then engulf the LDL, and they are then known as foam cells. The accumulation of the foam cells increases over time and causes a fatty streak. The fatty streak produces more toxic oxygen radicals, triggers more of an immune and inflammatory response, all of which causes ongoing, progressive damage to the vessel. Smooth muscle hyperplasia is ongoing, produces collagen and migrates over the fatty streak to form a fibrous plaque. This plaque may calcify, protrude in the vessel lumen and occlude flow. Plaques can be unstable and may rupture secondary to inflammatory activations and acutely occlude blood flow and result in ischemia or infarction.

18. This is marked by ST elevation on an EKG.

19. Ideal LDL level?

20. ______________ may be caused by many things, but it is an indicator of myocardial ischemia. This simply means that blood supply is decreased.

21. ______ levels rise secondary to high fat diets (the wrong types of fat) or from genetic influences.

22. The amount of blood pushed from the left ventricle in 1 minute.

23. Supplies blood to the posterior 1/3 of the inter ventricular septum, the posterior wall of both ventricles, the posteromedial papillary muscles.

24. _____________ levels of LDL are associated with an increased risk of the development of CAD.

25. Right to left sided shunt: If the SaO2 remains at ________________ cyanosis is not likely to develop because the shunting is minimal.