lecture 11 kemp
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| mechanisms of cardiac compensation | NE to inc HR/contractility, angiotensinII and aldosterone to inc PVR and blood vol, ANP for vasodilation, natri- & diuresis. Frank-Starling. myocardial hypertrophy
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| concentric vs eccentric hypertrophy | concentric: diameter of cells increases, thicker ventricle without chamber size growing // eccentric: length of cells increases, heart size and wall thickness increase
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| causes of left sided heart failure | ischemic heart dz, systemic HTN, mitral or aortic valve dz, primary dz of myocardium
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| causes of right sided heart failure | L sided heart failure (most commonly), pulmonary parenchymal or vascular dz like COPD, fibrosis, etc.
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| clinical findings of L heart failure | pulmonary edema, cough, dyspnea/cough, orthopnea, PND. chronic passive congestion with hemosiderin-filled macrophages, resultant fibrosis over time
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| clinical findings of R heart failure | congestion in body: peripheral edema, HSM, pleural or pericardial effusions, ascites. nutmeg liver due to chronic passive congestion
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| cor pulmonale | RVH with dilation caused by primary lung disorders: acute - usually due to PE obstructing @ least 50% of vasculature, chronic - develops more insidiously as from pulmonary fibrosis from sarcoidosis
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| 4 manifestation of ischemic heart dz | ACS: angina pectoris, AMI, sudden cardiac death & then chronic ischemic heart dz
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| 70-75% stenosis | less than this usually won't cause ischemia or sx. greater than this may cause ischemia with exertion
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| cutoff for stenosis amt that will cause ischemia even at rest | 90% stenosis; however even with 100% stenosis, there may not be ischemia if it's developed over time and collaterals have been created
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| ACS is usually due to sudden acute plaque change that alters the degree of stenosis * | rupture, fissuring or ulcertation of atherosclerotic plaque will expose lipid core, which is highly thrombogenic
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| vulnerable plaque | plaques with a thin fibrous cap and thick core that are less stable and prone to rupture
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| stable angina | CP occurring with fixed amt of exertion, due to ~ 70-75% stenosis of vessel lumen. does not occur at rest but IS relieved by resting
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| Prinzmetal angina | CP that occurs at rest, due to vasospasm of a vessel that can either be nl or atherosclerotic. (similar to what's seen with cocaine use)
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| unstable angina | CP can occur at rest or otherwise, isn't constant, due to acute plaque change. can be reversible; known as pre-infarction angina due to possibility of progressing to MI
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| critical time window with respect to AMI | if revascularized within 20-40 min, damage may be reversible; takes 3-6 hrs for completion of infarct
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| layer of myocardium most typically affected during MI | subendocardial region is the last to receive blood but has high O2 demand due to amt of intramural stress it sees. expands to epicardium within 3-6 hrs
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| general morphology/location of MI | most involve LV and/or interventricular septum, most commonly transmural (>50% of wall thickness) in the distribution of LAD.
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| MIs are not apparent on gross tissue before 12 hrs | no reliable microscopic changes before 4 hrs, then coag necrosis starts. neutrophilic infiltrate makes yellow gross appearance. granulation tissue 7-10 days causes sunken appearance as macrophages eat tissue.
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| all MIs are readily visualized dense scars after 2 months | collagen deposition starts around 10-14 days and continues for the next 6 weeks or so
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| reperfusion injury | appearance microscopically is hemorrhage and contraction band necrosis (Ca++ rushed in and caused intense contraction of myocytes)
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| most common complications of MI | heart failure, arrhythmias, myocardial ruptures, pericarditis, infarct expansion, mural thrombus, ventricular aneurysm, papillary muscle dysfunction
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| types of myocardial rupture | free wall (hemopericardium or cardiac tamponade), interventricular septum (L-R shunt), mitral valve papillary muscle (mitral insufficiency)
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| chronic ischemic dz | due to one or more past MIs, can cause heart failure. dilated and hypertrophied heart. may see fibrous scars in myocardium and subendocardial vacuolization
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| most common cuases of cor pulmonale | COPD, CF or interstitial fibroses, PE, kyphoscoliosis, metabolic acidosis or hypoxia that cause arterial constriction
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| causes of sudden cardiac death | aortic stenosis, mitral valve prolapse, myocarditis, dilatory or hypertorphic cardiomyopathy, pulmonary HTN, abnormalities of conduction (long QT), coronary artery dissection, congenital artery anomalies
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