L8: SA Cardiovascular Pathology (Craft) Flashcards
Sinus of valsalva =
Openings to coronary arteries
First part of heart to be damaged in hypoxic event
LV
Layers of wall of heart
Trebeculae Endocardium Myocardium Fat CT Serous pericardium (visceral layer) Pericardial space Serous pericardium (parietal layer) Fibrous pericardium
Layer of dense collagen that forms the fibrous cardiac “skeleton” and electrically insulates atria from ventricles
Central Fibrous Body (CFB)
-has occassional plates of chondroid and osseous metaplasia
Normal wall thickness ratio of LV:RV
2-3:1
3 routine sections for heart histopath:
IVS
LV free wall
RV free wall
1st place for heart degeneration
Papillary muscle
Heart failure –>
- dec. myocardial contractility and compliance (fibrosis
- dysrythmias, arrythmias
Cardiac compensation: HYPERTROPHY
- repeated stretching due to dilation of chamber (overload) can cause
- requires time, healthy myocardium, adequate nutrition of mycardium
- only works for so long as cells will outgrow blood supply
- further stretching causes dilation
Cardiac compensation: DILATION
- stretching of myofibers
- maintains connections and architecture
- degenerative
- result of chronic volume overload
Other cardiac compensatory methods
- Inc. HR, peripheral resistance, blood volume
- redistr. Of blood flow to areas of lowest pressure via shunting, peripheral vasoconstriction
Clinical syndromes of cardiac decompensation
Cardiac syncope (acute cardiac failure) CHF (chronic)
Chars. Of cardiac syncope
- arrhythmia
- massive necrosis
- extreme changes in BP and HR
- collapse, loss of consciousness, death
- may not have lesions on histo
Chars. Of CHF
- forward and/or backward failure
- eventual progression to full failure
Cycle of cardiac decompensation –> hypoxia
1) renin release from kidneys
2) aldosterone release from adrenal cortex
3) Na and H2O retention
4) increased plasma volume
5) edema, inc. BP
6) EPO stimulation
7) polycythemia
8) increased blood viscosity
*failing heart must pump a greater volume of thicker fluid