Initiation of atherosclerosis
-begins w endothelial damage
-accumulation of oxidized LDL cholesterol in intima
-inflammatory response and recruitment of immune cells
-monocytes differentiate into foam cells
-foam cells form a plaque that ruptures and causes a clot
-leads to MI or stroke
primary hypertension
essential, no identifiable cause
secondary hypertension
due to identifiable underlying condition (renal disease, endocrine disorders)
peripheral arterial disease
-extremity does not receive enough blood supply most likely from atherosclerotic obstruction (blue, pallor, shiny)
-ischemic ulcer
peripheral venous insufficiency
↑hydrostatic pressure in capillary bed, pushes fluid out into interstitial space, edema, swelling, redness compresses blood supply
superior vena cava syndrome
-compression -> venous congestion in face, head, upper extremities
-compresses trachea, larynx, and esophagus
true aneurysm
all 3 layers involved
2 types: fusiform, saccular
fusiform aneurysm
symmetrical bulge, both sides of vessel
saccular aneurysm
asymmetrical, only one side of vessel bulges
pseudoaneurysm
hole in a side of the vessel, causes pooling in connective tissue (not 3 layers involved)
raynaud phenomenon
-vasospasm in fingers/toes triggered by cold or stress
-white -> blue -> red
varicose veins & venous insufficiency
valve incompetence -> venous pooling -> itching, burning, worse w standing
How does the RAAS worsen the heart’s workload after injury?
antiotensin II causes vasoconstriction, ↑afterload, ↑cardiac stress
HFrEF
systolic heart failure impaired contraction, things aren’t squeezing the way they’re supposed to, reduced ejection fraction
-dyspnea, orthopnea, frothy sputum, fatigue, SOB, edema
HFpEF
diastolic heart failure, hypertrophy, weakening of muscle which results in preserved ejection fraction, impaired relaxation, stroke volume reduced
STEMI
ST-elevation MI - full thickness myocardial necrosis; emergency
NSTEMI
non-ST-elevation MI - subendocardial infarction (not entire wall); ST depression or T wave inversion, myocardium at risk for further ischemia, serious and requires monitoring but not emergent
pericarditis
-inflammation of the pericardium sac surrounding the heart
-sharp chest pain that gets worse when taking deep breath and is relieved when sitting up
what chest pain features distinguish pericarditis from MI?
pericarditis chest pain is worse supine, relieved leaning forward
dilated cardiomyopathy
-systolic pump failure; chamber dilation
-large, thin walled LV, ↑ volumes
-↓EF
hypertrophic cardiomyopathy
-diastolic dysfunction; asymmetric septal hypertrophy
-small LV cavity, thick septum/walls
-normal/↑EF
restrictive cardiomyopathy
-diastolic dysfunction from stiff/noncompliant ventricles
-normal size ventricles; thick/rigid appearance
-usually normal or mildly ↓EF
mitral regurgitation
-mitral valve fails to close properly during systole
-blood leaks back from LV into LA
-fatigue, dyspnea
mitral stenosis
impaired flow from LA to LV
dyspnea, orthopnea
