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24 Cards in this Set
- Front
- Back
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normal % lymph
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20-40%
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fick's principle
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CO=O2 consumption/(O2 pul vein-O2 pul artery)
pul vein=peripheral artery pul artery=systemic mixed venous blood |
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normal % mono
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2-10%
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autoregulation BF heart
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local metabolites, O2, adenosine, NO
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phase 2 pacemaker
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absent
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how change contractility
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-catecholamine (incr activity of Ca pump in SR)
-increase intracell Ca -decrease extracell Na -digitalis (increase intracell Na, resulting in increase intracell Ca) |
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autoreg BF brain
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local metab CO2 (pH)
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how does TPR effect VR/CO graph
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increasing TPR moves the equil point to lower CO, causing the slopes of each line to change
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how catecholamines increase contractility
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incr activity of Ca pump in SR
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slope of venous curve
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resistance of arterioles (increased resistance=decr VR)
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changes in CO during exercise
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initially incr CO is due to incr SV, later due to incr HR
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phase 2 ventricle
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plateau, Ica=Ik
Ca induces more Ca rel from SR and myocyte cxn |
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phase 3 ventricle
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slow K channels open and Ca close. rapid repol, Ik
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waves of jugular venous pulse
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a-atrial cxn
c-RV cxn (TV bulges into atrium) v-increse atrial pressure due to filling ag closed TV |
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how positive inotrope effect VR/CO graph
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increases in parallel the CO curve, cauing equil pt to be at higher CO and higher RAP
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how increase MVO2
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-increased afterload
-increased contractility -increased HR -increase heart size (increase wall tension) |
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normal % eos
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1-6%
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describe plasma composition with %
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92% H20, 7% proteins
of the proteins: 55% albumin 38% globulin 7% fibrinogen |
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describe sm m cxn
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sm m membrane is depolarized causing VG Ca channels to open, Ca in cytoplasm increases and binds to calmodulin which then activates myosin light chain kinase resulting in cross bridge formation and cxn. so cxn controled by balance of MLC kinase and MLC phosphorylase.
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phase 4, pacemaker
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slow diastolic depolariz Ik
increase in Na conductance (If) causes spontaneous depolarization. gives automaticity. slope determines HR, so symp increase rate depol, Ach decreases. |
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phase 1 ventricle
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initial repolarization, inactivation of INa and opening of IK
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describe AP->myocyte cxn
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NT binds cardiomyocyte, causes depolariz which travels down T tubule to activate dihydropyridine R (voltage sensing Ca channel) which allows Ca in which then activates ryanidine R which opens Ca channel of SR and causes Ca release
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auto reg BF skel mscl
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local metabolites: lactate, adenosine, K
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key diff bw ventricle AP and pacemaker AP
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-upstroke (phase 0) is Ca
(this slows conduction) -plateau (phase 2) is ABSENT -phase 4 uses If (Na) with spontaneous depolarization |
