introduction to cardiac pathology Flashcards
coronary arteries originate from
ostia behind aortic valve
coronary arteries
- run in connective tissue on surface of heart
- supply blood from outer to inner layers of myocardium
most of coronary blood flow occurs
during diastole
LAD
apex of heart
anterior LV
anterior 2/3 of ventricular septum
RCA
RV free wall
posterior 1/3 of ventricular septum
posterior LV
Left circumflex
lateral left ventricular wall
can also supply posterior aspect of LV
left main
both LAD and left circumflex
occulsio to what CA(s) results in damage to LV wall and ventricular septum
RCA or LCA
endocardium
- thickness varies inversely with myocardium
- subendocardial region at greatest risk of ischemia
anatomy of conduction system
- specialized myofibers
- myocytes have a certain automaticity without impulse conduction will either fire an impulse aberrantly (premature complexes) or contract in an unorganized fashion (fibrillation)
SA anatomy
location at junction of SVC and right atrium
serves as pacemaker
AV anatomy
AV node near atrium-ventricular junction
organizes and fires impulses into Bundle of His
bundle of his anatomy
- runs thru ventricular septum to insure coordination contraction of both ventricles
- movement of contraction in a wave of depolarization to maximize pumping action
P wave
atrial contraction
Q wave
atrial systole
R wave
atrial diastole
S wave
ventricular contraction
T wave
ventricular systole
chamber function
- left/right synchronous
- dependent on directional wave of depolarization
- sequential upper chamber to lower chamber contraction to help in directional flow
valvular function
- one directional flow valve to prevent back flow
- essential for maintaining stroke volume and attaining pressure differential across valve
- most passive, mitral valve is assisted papillary muscle and chordae tendonae, tricuspid has similar structures
valvular dysfunction
stenosis
insufficiency
anatomic distortion
loss of papillary muscle
inflow
- systemic-> inflow through IVC, dependent on systemic blood pressure and ventricular volume
- pulmonary-> interruption of flow secondary to pulmonary emboli
outflow
- pulmonary: specialized vessels to pump large volume of blood through lungs under low pressure
- two main problems:
1. pulmonary HTN resulting in cor pulmonale
2. pulmonary emboli
-systemic: collective peripheral resistance, blood volume, vessel diameter, elasticity, HTN
cardiac cycle
diastole systole
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S2 S1 S2
starlings law
stretch versus contractility
cardiac dysfunction: primary causes of cardiovascular dysfunction
- Hypovolemia
- Arrhythmia
- Cardiac muscle failure
- ischemia (hypertrophy+ cardiac artery disease)
- metabolic - Decreased end diastole volumes
- decreased diastolic relaxation
- decreased ventricular volume
cardiac failure
hypertrophied muscle may lead to end stage dilation and heart failure
left heart failure
->80% ischemia, 1-3% HTN, 1% rheumatic
signs and symptoms of left heart failure
- cardiac enlargement with:
LVH-> heart increases in both volume and mass
actual cardiac dilatation is end point decompensation
2.Obstruction to venous return-> pulmonary congestion - obstruction of systemic outflow
-insufficient renal perfusion leads to fluid retention and further exacerbation of problem
-hypoxic encephalopathy
-coronary insufficiency and cardiac ischemia - LA enlargement may be secondary to left ventricular enlargement or may be primary (MS) often associated with atrial fibrillation
- atrial fibrillation is associated with formation of mural thrombi (stasis of atrial blood flow) increased risk of embolic stroke
right heart failure
- occurs in only a few diseases
- usually consequence of left sided (global) failure
- most common pure form-> cor pulmonale (pul. HTN)
- associated with valvular disease
right heart failure
- engorgement of systemic and portal congestion (nutmeg liver, dependent pitting edema)
- liver congestion: chronic passive congestion (nutmeg liver)
- stasis of blood in central vein with hypoxia of adjacent cells
- vascular congestion with local hemorrhage, phagocytosis of red cells
- fibrosis of long-standing ischemic tissue cardiac sclerosis
global heart failure
- long standing right or left sided failure
- constrictive disease (tamponade)
- massive infarct
- shock
signs of symptoms of global heart failure
degree of symptomology depends on the rapidity of development of cardiac failure
pressure of volume overload
response: Hypertrophy
Microscopic features:
- increased myocyte size with prominent and sometimes reduplicated nuclei
- decreased capillary density
- increased deposition of ECM
chronic ischemia
response: myocardial atrophy, apoptosis
microscopic changes:
- decreased cell numbers
- increased fibrosis
acute ischemia
response: necrosis, accompanying inflammation around margins
microscopic features: coagulative necrosis, with evolving inflammatory infiltrates, eventual replacement by fibrosis and scar
reperfusion
response: reperfusion injury
microscopic features: contraction bands
infection
response: acute inflammation
microscopic features: depends on nature of infectious agent, variable infiltration of inflammatory cells and myocyte damage
aging
microscopic features: fewer myocytes increased collagen senile amyloidosis basophillic degeneration (by product of glycogen metabolism) brown atrophy-> lipofuschin pericardial fat
