Cardiac Path Robbins Part 1 Flashcards Preview

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Flashcards in Cardiac Path Robbins Part 1 Deck (64)
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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

-SA node
-AV node
-bundle of HIS (connects right atrium to ventricular septum)
-purkinje network


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
-myocardial changes:
-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
-fibrous thickening
-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

-coronary atherosclerosis
-stiffening of aorta


cardiovascular dysfxn- 6 principal mech's

-pump failure
-flow obstruction
-regurgitant flow
-shunted flow
-disorders of cardiac conduction
-rupture of the heart or a major vessel


Congestive HF

-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?

-myocytes elongate
-ventricular dilation


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
-myocyte apoptosis
-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?

-left-sided failure!!


isolated right-sided HF- results from?

any cause of pulm HTN!!!!
-parenchymal lung diseases
-primary pulm HTN
-pulm vasoconstriction