Shared Flashcard Set


12 - Ischemic Heart Disease, MI, & CHF

Additional Advertising Flashcards




How far occluded do the coronary arteries need to be occluded before angina is present? What is the time at which we start to get permanent damage?
-After about 20min of reduced blood to heart we can start to get some permanent damage
-These means that in IHD, the angina last less than 20min
Define and compare stable angina, unstable angina, and prinzmetal angina in terms of causes, EKG signs, & treatment?
Stable angina; pain with exertion
-From atherosclerosis with >70% occlusion
-EKG shows ST-segment depression from subendocardial ischemia
-Relieved by rest and nitroglycerine

Unstable angina; pain at rest
-From thrombosis formation or embolization with incomplete occlusion
-Also get ST depression from subendocardial ischemia
-Relieved with nitroglycerin

Prinzmetal angina; episodic pain unrelated to exertion
-From coronary artery vasospasm (complete clamp-down)
-This time we get ST elevation because of TRANSMURAL (entire wall) ischemia
-Relieved by nitroglycerine and CALCIUM channel blockers
What is nitroglycerin and what does it do?
-Belongs to a group of drugs called nitrates which are converted to nitric oxide by mitochondrial aldehyde dehydrogenase
-NO is a potent natural vasodilator
What are causes of MI? What part is involved?
-Most typical is rupture of an atherosclerotic plaque with thrombosis and complete occlusion of the coronary a.
-Also can be from an emboli, vasospasm (from prinzmetal or cocaine use), or vasculitis
-Typically effects the left ventricle and spares the rest
What are the three common occluded arteries in MI?
-Ant. interventricular (aka left anterior descending artery, or LAD) is the most common at 40%
-Right coronary, or RCA (wraps all the way to back)
-Left circumflex artery goes over lateral wall of the LV
What are the blood markers for MI and their time frames?
-Troponin I is the gold standard; rises 2-4 hours after infarction, peaks at 24 hours, and lasts 7-10 days
-CK-MB is good for detecting reinfarction occurring days after original; rises 4-6 hours after infarction, peaks at 24, but lasts only for 3 days
What are six common treatments for MI?
1. Aspirin and/or heparin; limits thrombosis
2. Supplemental O2; minimize ischemia
3. Nitrates; vasodilatation
4. β-blocker; slows heart rate lowering O2 demand
5. ACE inhibitor; lowers blood pressure
6. Fibrinolysis or angioplasty; opens vessel
What are results that can arise from angioplasty?
-Contraction band necrosis occurs from calcium influx into irreversibly-damaged cells (can see fibers and no nucleus)
-Reperfusion injury can result from return of oxygen and inflammatory cells leading to free radical generation and further myocyte damage
What are time stages after infarct in terms of what we see grossly and microscopically along with complications?
-No visible changes
-May have cardiogenic shock, congestive heart failure, arrhythmia*

4-24 hours;
-We see dark discoloration from coagulative necrosis
-We see pyknosis>karyorrhexis>karyolysis
-Again major complication is arrhythmia

1-7 days;
-Grossly we see a yellow pallor
-Microscopically we will first see neutrophil (1-3 days) and then macrophage (4-7 days) infiltrate
-Complications of neutrophils is fibrinous pericarditis, which causes a friction rub
-Complications of macrophages is rupture of structures due to weakness (macs are eating up debris)

1-3 weeks;
-We see a red boarder of granulation tissue entering infarct with fibroblasts, collagen, and blood vessels

-White scar from fibrosis
-Complications can be an aneurisms from weakness of wall, leading to mural thrombus
-Another possible long-term complication is Dressier syndrome

CN ||DAY|| inflammation ||WEEK|| GT ||MONTH|| scar
What is Dressier syndrome?
-It is autoimmune pericarditus that is rare, but can occur 6-8 weeks after an infarct from sensitization of immune system to pericardial antigens
What are the systemic effects of left vs. right-sided heart failure? What about signs and treatment?
Left-sided will give pulmonary congestion
-Presents with dyspnea and or orthopnea (dyspnea when laying down) along with hemosiderin-laiden macrophages in lungs from intraalveolar hemorrhage
-Also get decrease flow to kidneys leading to activation of renin-angiotensis system, exacerbating CHF

Right sided failure will cause systemic congestion
-Is usually due to left-sided failure first, but can also be from things that increase right side load (like L>R shunt)
-Will present with jugular venous distention, painful hepatosplenomegaly with "nutmeg" liver, and pitting edema from increased hydrostatic pressure

-Could treat either with ACE inhibitor
What is ACE?
-Angiotensin converting enzyme
-Makes angiotensin I -----> angiotensin II (active)
-Angiotensin I is, in turn, made by RENIN
-System acts to increase BP
Supporting users have an ad free experience!