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28 Cards in this Set
- Front
- Back
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S1 split
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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)
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S2 slipt
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- 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) |
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Heart contraction and closure order
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RA contracts
LA contracts LV contracts M closes RV contracts T closes P opens A opens A closes P closes T opens M opens |
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Normal Values
RV - RA - LV - LA - aorta - pulmonary - |
25/2
3 120/4 5 120/80 25/9 |
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a wave
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pressure wave from atria to vein during atrial systole - T stenosis will increase it
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c wave
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pressure wave from atria to vein - at onset of isovolumetric contraction - T insufficiency or conginital V septal defect will increase
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v wave
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pressure wave from atria to vein - in V ejection, flow from vein to atria - T insufficiency will increase b/c blood is leaking backward
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valvular stenosis
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causes harsh systolic murmur - causes increase in blood velocity
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incompetent valve
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causes aortic or mitral regurgitation murmurs
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coarcitation (artery narrowing)
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hear a murmur over vessel - called a bruit
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Excessive CO (murmur)
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ejection murmurs in anemics
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mitral or tricuspid prolapse
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bulging of vavle into atria
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Determinants of preload
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#1 is atrial pressure, which is governed by CVP
CVP determinants - venous smooth muscle (VSM) tone - blood volume - body position |
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Determinants of afterload
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- aortic aterial diastolic P - hihger P, higher afterload
- Aortic compliance - lower comliance, higher afterload - aortic valve resistance - stenosis increases afterload |
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CTY definition
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contractile force at a GIVEN preload and afterload
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CTY determinants
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- Ca kinetics - increase IC Ca, increase CTY (Catecholamines)
- myosin ATPase activity - ATP levels - # of sarcomeres |
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Q= (Long def)
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[(pi*r^4)/(8/n)] where n=viscocity
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Mitral valve stenosis causes
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diastolic murmur
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Aortic valve stenosis causes
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systolic murmur
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T(tension) =
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Pr/h h is wall thickness
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arterial pressure wave form determinants
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- Systolic P - determined by stroke volume, diastolic P, CPL
- Diastolic P - determined by SVR, systolic pressure, age, HR |
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CPL =
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change in V/change in P
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How to increase CVP
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1) contrict venules
2) decrease large vein CPL 3) indrease BV 4) take away gravity 5) decrease CO |
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7 Bed components
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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 |
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Q controllers (intrinsic)
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1) Autoregulation
2) Myogenic reg 3) metabolic reg of VSM 4) Autacoids |
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metabolic reg of VSM
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1) [vasodilator metabolites] depends on metabolic rate - if decreased (from Q increase), arterioles constrict
2) When MR changes, so does [VD] in proportion |
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Autocoid dilators
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bradykinin
prostaglandins leukotrines IL-1 |
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Autocoid constrictors
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thromboxane, serotonin
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