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lecture 11 kemp

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
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
causes of left sided heart failure ischemic heart dz, systemic HTN, mitral or aortic valve dz, primary dz of myocardium
causes of right sided heart failure L sided heart failure (most commonly), pulmonary parenchymal or vascular dz like COPD, fibrosis, etc.
clinical findings of L heart failure pulmonary edema, cough, dyspnea/cough, orthopnea, PND. chronic passive congestion with hemosiderin-filled macrophages, resultant fibrosis over time
clinical findings of R heart failure congestion in body: peripheral edema, HSM, pleural or pericardial effusions, ascites. nutmeg liver due to chronic passive congestion
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
4 manifestation of ischemic heart dz ACS: angina pectoris, AMI, sudden cardiac death & then chronic ischemic heart dz
70-75% stenosis less than this usually won't cause ischemia or sx. greater than this may cause ischemia with exertion
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
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
vulnerable plaque plaques with a thin fibrous cap and thick core that are less stable and prone to rupture
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
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)
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
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
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
general morphology/location of MI most involve LV and/or interventricular septum, most commonly transmural (>50% of wall thickness) in the distribution of LAD.
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.
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
reperfusion injury appearance microscopically is hemorrhage and contraction band necrosis (Ca++ rushed in and caused intense contraction of myocytes)
most common complications of MI heart failure, arrhythmias, myocardial ruptures, pericarditis, infarct expansion, mural thrombus, ventricular aneurysm, papillary muscle dysfunction
types of myocardial rupture free wall (hemopericardium or cardiac tamponade), interventricular septum (L-R shunt), mitral valve papillary muscle (mitral insufficiency)
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
most common cuases of cor pulmonale COPD, CF or interstitial fibroses, PE, kyphoscoliosis, metabolic acidosis or hypoxia that cause arterial constriction
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
Created by: sirprakes