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28 Cards in this Set

  • Front
  • Back
S1 split
Rigbht his block - M closes first anway, so T would be even farther behind - would slow RV ejection, so S2 split too (A then P)
S2 slipt
- ventricular septal defect - LV first and stronger - if some LV blood goes to RV, less is ejected from LV, so A earlier and P later
- Right his block (S1 slipt too)
Heart contraction and closure order
RA contracts
LA contracts
LV contracts
M closes
RV contracts
T closes
P opens
A opens
A closes
P closes
T opens
M opens
Normal Values
RV -
RA -
LV -
LA -
aorta -
pulmonary -
a wave
pressure wave from atria to vein during atrial systole - T stenosis will increase it
c wave
pressure wave from atria to vein - at onset of isovolumetric contraction - T insufficiency or conginital V septal defect will increase
v wave
pressure wave from atria to vein - in V ejection, flow from vein to atria - T insufficiency will increase b/c blood is leaking backward
valvular stenosis
causes harsh systolic murmur - causes increase in blood velocity
incompetent valve
causes aortic or mitral regurgitation murmurs
coarcitation (artery narrowing)
hear a murmur over vessel - called a bruit
Excessive CO (murmur)
ejection murmurs in anemics
mitral or tricuspid prolapse
bulging of vavle into atria
Determinants of preload
#1 is atrial pressure, which is governed by CVP

CVP determinants
- venous smooth muscle (VSM) tone
- blood volume
- body position
Determinants of afterload
- aortic aterial diastolic P - hihger P, higher afterload
- Aortic compliance - lower comliance, higher afterload
- aortic valve resistance - stenosis increases afterload
CTY definition
contractile force at a GIVEN preload and afterload
CTY determinants
- Ca kinetics - increase IC Ca, increase CTY (Catecholamines)
- myosin ATPase activity
- ATP levels
- # of sarcomeres
Q= (Long def)
[(pi*r^4)/(8/n)] where n=viscocity
Mitral valve stenosis causes
diastolic murmur
Aortic valve stenosis causes
systolic murmur
T(tension) =
Pr/h h is wall thickness
arterial pressure wave form determinants
- Systolic P - determined by stroke volume, diastolic P, CPL
- Diastolic P - determined by SVR, systolic pressure, age, HR
change in V/change in P
How to increase CVP
1) contrict venules
2) decrease large vein CPL
3) indrease BV
4) take away gravity
5) decrease CO
7 Bed components
1) resistance vessels have thicker walls
2) 1/3 caps have flow
3) single epi and BM
4) capacitance vessles - veunles major resiviour
5) P cells surrounding SM
6) Autonomic innervation
7) autociod dilators from epi
Q controllers (intrinsic)
1) Autoregulation
2) Myogenic reg
3) metabolic reg of VSM
4) Autacoids
metabolic reg of VSM
1) [vasodilator metabolites] depends on metabolic rate - if decreased (from Q increase), arterioles constrict
2) When MR changes, so does [VD] in proportion
Autocoid dilators
Autocoid constrictors
thromboxane, serotonin