physio 3
Terms
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- 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 - -
25/2
3
120/4
5
120/80
25/9 - 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 - CPL =
- 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
-
bradykinin
prostaglandins
leukotrines
IL-1 - Autocoid constrictors
- thromboxane, serotonin