6-19-10 Patho II CAD
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| What percent of all deaths in western society are caused by CAD | 33%
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| How do you know if your old | All elderly have at least some impairment of CAD
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| How many ml/min is resting coronary flow | 225ml/min (8ml of o2/100g of tissue/min)
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| What percent of cardiac output becomes coronary blood flow | 4-5 % of total CO
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| Exercise can increase coronary demand by ? many times (in relation to CO) | 4 times
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| How many ml of O2 is required to maintain cell life | 1.3 ml of O2/100g of tissue/min
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| Coronary blood flow is controlled by | the local metabolism
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| What is the most important factor in local blood flow regulation of the coronary perfussion | O2 demand
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| What does stimulation of the SNS have on the heart | increase HR, strength, and vasoconstriction
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| What does PNS (parasymp) stimulation do to the heart | decreases strength and HR
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| 70% of the metabolism of the cardiac muscle uses what as its energy source | Fatty acids, but in emergencies glycolysis is used
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| Death due to CAD is the result of (2 things) | Acute occlusion or Cardiac Fibrillation
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| The most frequent cause of decreased coronary flow is | Atherosclerosis
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| Atherosclerosis starts at what age | childhood
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| Atherosclerosis causes - besides lipid accumulation, what are 3 other causes | necrotic debis, proliferation of internal vessel (intimal) smooth muscle cell, the formation of large amounts of connective tissue matrix (collagen and elastic fibers) by proliferated cells
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| Proliferated cells form large amounts of | Connective tissue matrix (collagen and elastic fibers
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| Name 3 independant predictors for the development of athrosclerosis | cigarett smoking, High BP, plasma cholesterol
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| What Theory is this: some form of injury in the endothelium will trigger the events by changing the fx activity of the endothelium which combined with incr. cholest, smooth muscle prolif. and platlet activity lead to the atherosclerosis plaque | Response-To-Injury theory
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| What theory is this: each lession of athrosclerosis is originated from a single smooth muscle cell that serves as a source of all of the cells within a lesion - each lesion is a benign neoplasm - caused by viruses, chemicals, or mutants | Monoclonal
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| ??? is when coronary demand is greater than supply | Coronary insufficiency
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| Adequate perfussion with decreased O2 supply is called | Hypoxia
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| Zero O2 supply with adeqate perfusion is called | Anoxia
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| Ischemia is the result when what 3 things decrease | O2 supply, perfusion, removal of metabolic waste
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| Angina Pectoris is pain felt due to | Ischemia (not necrosis, no pain with necrosis)
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| Angina Pectoris is describes as | hot, pressing, and constricting
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| Per slide 13, which of the following 2 are not related to myocardial ischemia pain: [Throat, neck jaw][shoulder][retrosternal][epigastric][right chest pain][left chest pain][back pain] | left chest pain and right chest pain (per the slide)
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| T/F: there is necrosis in angina | Give Fernandez's cell phone a ring and get the scoop (IN BOLD LETTERS, NO!!!!)
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| What are the classes of angina (3 of them) | Chronic (or Stable), Acute (or Unstable), and Variant (Prinzmetal's angina)
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| Angina that starts gradually and gets worse over minutes than dissipates after trigger is gone is classified as ? angina | Chronic or Stable angina
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| Chronic or stable angina is caused by | Increase O2 demand over supply (physical activity, emotions, eating, Mary Beth, hurrying, fever, chills, tachycardia, motion of hands over head)
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| In chronic or stable angina there is a "fixed coronary occlusion" which means | The O2 "flow" to the heart(coronaries) is max'd out but is not meeting the O2 demand
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| T/F: "Angina Of Effort" is caused by decreased O2 flow | False, it results from increased demand with fixed supply
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| T/F: Chronic angina disappears with rest | True
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| Other diagnosis that could mimic angina (MI)- (6 of them) | Esophagus dz, biliary colic, GI syndrome, cervical radiculitis, PE (dyspnea), Acute pericarditis
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| Chronic angina findings include (3 things) | HTN, non-specific S-T and T changes, left bundle branch blocks
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| What is the name of the cardiac diagnostic test that injects a radionuclide and compares peak exercise to rest periods | Stres thalium 201 Myocardial perfusion imaging - it shows defects
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| A defect found in a stress test that last 2-3 hrs in consistant with the diagnosis of | MI
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| Name a definative coronary diagnostic test | Coronary arteriography with left ventricular arteriography
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| Management of an MI (3 things) | Lifestyle changes, drug tx, revascularization
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| Four types of revascularization | PTCA, CABG, Laser angioplasty, Coronary atherectomy
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| What is the difference between Acute (unstable) Angina and Chronic (Stable) Angina | Acute (unstable) angina happens at rest or with minimal effort, Chronic (stable) needs significant trigger event
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| T/F: Acute (unstable) angina is when O2 demand is increased with a fixed O2 supply | False (that is the definition of Chronic/Stable angina). A true statement would be: fixed O2 demand with decreased O2 supply
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| What are the clinical symptoms that differ between Acute and Chronic angina | Acute symptoms include more intense pain and longer duration and usually while the patient is resting
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| What things (2 of them ) do not relieve symptoms in Acute angina but do in Chronic angina | Bed rest and nitroglycerin cannot eliminate acute pain completely or permanently
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| What are clinical findings that differ between Acute and Chronic Angina | In acute angina there is less collateral flow, higher number of vessles dz (more than one), increased incidence of coronary thrombi, faster progression of atherosclerosis, increased platlet aggregation, and thrombosis + coronary spasms
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| What are the different diagnosive test between Acute and Chronic angina | None
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| Management of Acute angina (8 of them) | Hospitalization, Quietness, keeping cardiac O2 demand down (no fevers, anemia, infections, arrhythmias), drug tx (beta blockers, nitrates, anticoagulants), thrombolitic tx, ballon pump, PTCA, and Surgical intervention
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| What is the difference between Ischemia and Infarction (MI) | Dead tissue (from prolonged ischemia)
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| Transmural infarction includes | The whole thickness of the ventricular wall
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| Sub-endocardial infarction includes | the subendocardium, the intramural myocardium or both --does not extend into the epicardium
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| What is the most common cause of transmural infarction | Acute coronary thrombosis
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| What are the variables with Acute coronary occlution that determine whether the damage will be transmural, subendocardial or no damage | How fast the onset of the occlution occurs, and the number and quality of distal collaterals involved
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| Enzymes tested related to MI (4 of them) | Troponin, Creatine Kinase, Lactic Dehydrogenase, and Glutamic-Oxalacetic Transaminase (GOT)
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| MI management includes (4 things) | Drugs (b-blockers, nitrates, analgesics, and O2), Controll of physical activity, Thrombolitics (intracoronary and intravenously), and PTCA (easier through fresh thrombus)
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| T/F: In a CABG, the harvested vessle can be from either a venous or arterial source | True
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| In a CABG, revascularization occurs by connecting the harvested vessle distal to the coronary blockage and into the ? or the ? | Subclavian artery or the Aorta
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| What makes a CABG the treatment of choice | When the PTCA was not successful (or could not be performed), or multiple vessles need intervention
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| CABG is containdicated in what patients | Patients with uncomplicated Transmural infarcts more than 6 hours after the onset
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| How many hours after an AMI should a CABG be performed to be most successful. | 4-6 hours (before 2 hours should be the goal)
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| The pain associated with Variant Angina Pectoris is related to | Coronary artery spasm
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| T/F: Variant Angina is like Acute angina, it can occur at rest | True - occurs almost exclusively at rest
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| T/F: Varient angina is like Chronic angina, it is related to physical exertion or emotion stress | False, Varient angina does is not related to physical activity or emotional stress; Chronic angina is
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| Does anything happen with the ST segment with Variant Angina | Yes, it is associated with ST elevation
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| T/F: Variant angina is like Acute angina, the onset of pain gets progressively worse with time | False, Variant angina pain does not get worse (Acute angina pain gets worse)
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| The key component to diagnosing Variant angina is | the development of ST segment elevation with pain
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| What oxytocic drug in give to diagnose Variant angina | Ergonovine
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| What will the administration of Ergonovine cause in a patient with Variant angina | ST elevations
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| What is the best management treatment for patients with Variant angina | The best treatment is to combine nitrates and Ca++ antagonists (calciun channel blockers)
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| What circumstance makes it appropriate to perform a PTCA or CABG on a Variant angina patient | When the spasm is present with obstruction (PTCA and CABG are contraindicated in Variant angia without obstruction)
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