Flashcards in Cardiac Path Robbins Part 1 Deck (64)
cardiac valves- tri-layered architecture
-dense collagenous core (fibrosa) at the outflow surface and connected to the valvular supporting structures
-central core of loose CT (spongiosa)
-layer rich in elastin (ventricularis or atrialis) on inflow surface
valves- critical to fxn
valvular interstitial cells (most abundant cell type in heart valves)
-syn ECM and express matrix degrading enzymes
pathologic changes to valves- 3 types
-damage to collagen that weakens the leaflets (example- mitral valve prolapse)
-nodular calcification beginning in interstitial cells (calcific aortic stenosis)
-fibrotic thickening (rheumatic heart disease)
components of conduction system
-bundle of HIS (connects right atrium to ventricular septum)
3 major epicardial coronary a's
-LAD (left ant descending) and LCX (left circumflex) a's arise from left coronary a
-right coronary a
LAD and LCX divisions
-LAD- diagonal branches
-LCX- marginal branches
aging and the heart- myocardium and chambers
-dec LV chamber size (sigmoid septum- bulging of vasal ventricular septum into left ventricular outflow tract)
-inc epicardial fat
-lipofuscin and basophilic degeneration (gray-blue byproduct of glycogen metabolism)
-fewer myocytes, inc collagen fibers
aging and the heart- valves
-aortic and mitral valve annular calcification
-mitral valve leaflets buckling towards left atrium- inc left atrium size
-lambl excrescences (small filiform processes on the closure lines of aortic and mitral valves- due to small thrombi)
aging and the heart- vascular changes
-stiffening of aorta
cardiovascular dysfxn- 6 principal mech's
-disorders of cardiac conduction
-rupture of the heart or a major vessel
-when heart is unable to pump blood at a rate to meet peripheral demand, or can only do so with inc filling pressure
CHF- result from?
-loss of myocardial contractile fxn (systolic dysfxn)
-loss of ability to fill the ventricles during diastole (diastolic dysfxn)
CHF- mech's that maintain arterial P and organ perfusion
-Frank-Starling mech- inc filling volumes dilate the heart- inc actin-myosin cross-bridge formation- enhance contractility/SV
-myocardial adaptations- hypertrophy w/ or w/o cardiac chamber dilation
-act of neurohumoral systems- NE inc HR, act of renin-ang-aldosterone system, release of ANP
cardiac hypertrophy- caused by
-sustained inc in mechanical work due to P or volume overload
-trophic signals (B-R's)
cardiac myocytes become hypertrophic when?
-sustained pressure or volume overload
-sustained trophic signals (B-adrenergic stim)
pressure overload- causes what?
-myocytes become thicker
-left ventricular wall thickness inc concentrically
volume overload- causes what?
cardiac hypertrophy- accompanied by?
-not accompanied by a inc in blood supply
-vulnerable to ischemia-related decompensation
best measure of hypertrophy
heart weight (rather than wall thickness)
the molecular/cellular changes in hypertrophied hearts that initially mediate enhanced fxn may contribute to the development of HF- thru?
-abnormal myocardial metabolism
-alterations of intracellular handling of ca ions
-reprogramming of gene expression
increases cardiac work, causing hypertrophy
-HTN (p overload)
-valvular disease (p and or volume overload)
-MI (volume overload)
CHF- characterized by?
-dec CO and tissue perfusion (forward failure)
-pooling of blood in venous capacitance system (backward failure)- causes pulm edema and/or peripheral edema
left-sided heart failure- most commonly a result of?
(can be systolic or diastolic failure)
-left-sided valve disease
-primary myocardial disease
left-sided heart failure- clinical effects are due to?
-congestion in pulm circulation
-stasis of blood in left-sided chambers
-dec tissue perfusion
left-sided heart failure- morphologic changes
-left ventricular hypertrophy
-left ventricular dysfxn- left atrial dilation (leads to atrial fibrillation, stasis, thrombus)
-pulm congestion and edema (cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea)
-heart failure cells (hemosiderin-laden macrophages)- signs of pulm edema!!
left-sided heart failure- dec ejection fraction may result in?
-dec glomerular perfusion- stim release of renin- inc volume- prerenal azotemia
-dec cerebral perfusion-hypoxic encephalopathy
left-sided HF- divided into
-systolic failure- insuff ejection fraction
-diastolic failure- abnormally stiff and cannot relax during diastole- heart unable to inc its output in response to inc metabolic demands of peripheral tissues- cant expand normally so any inc in filling P goes back to pulm circulation (flash pulm edema)
diastolic failure- most common in?
->65 age, women
-HTN- most common cause!!
-diabetes, obesity, b/l renal a stenosis
right-sided heart failure (cor pulmonale)- most common cause is?