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24 Cards in this Set

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normal % lymph
20-40%
fick's principle
CO=O2 consumption/(O2 pul vein-O2 pul artery)
pul vein=peripheral artery
pul artery=systemic mixed venous blood
normal % mono
2-10%
autoregulation BF heart
local metabolites, O2, adenosine, NO
phase 2 pacemaker
absent
how change contractility
-catecholamine (incr activity of Ca pump in SR)
-increase intracell Ca
-decrease extracell Na
-digitalis (increase intracell Na, resulting in increase intracell Ca)
autoreg BF brain
local metab CO2 (pH)
how does TPR effect VR/CO graph
increasing TPR moves the equil point to lower CO, causing the slopes of each line to change
how catecholamines increase contractility
incr activity of Ca pump in SR
slope of venous curve
resistance of arterioles (increased resistance=decr VR)
changes in CO during exercise
initially incr CO is due to incr SV, later due to incr HR
phase 2 ventricle
plateau, Ica=Ik
Ca induces more Ca rel from SR and myocyte cxn
phase 3 ventricle
slow K channels open and Ca close. rapid repol, Ik
waves of jugular venous pulse
a-atrial cxn
c-RV cxn (TV bulges into atrium)
v-increse atrial pressure due to filling ag closed TV
how positive inotrope effect VR/CO graph
increases in parallel the CO curve, cauing equil pt to be at higher CO and higher RAP
how increase MVO2
-increased afterload
-increased contractility
-increased HR
-increase heart size (increase wall tension)
normal % eos
1-6%
describe plasma composition with %
92% H20, 7% proteins
of the proteins:
55% albumin
38% globulin
7% fibrinogen
describe sm m cxn
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.
phase 4, pacemaker
slow diastolic depolariz Ik
increase in Na conductance (If) causes spontaneous depolarization. gives automaticity.
slope determines HR, so symp increase rate depol, Ach decreases.
phase 1 ventricle
initial repolarization, inactivation of INa and opening of IK
describe AP->myocyte cxn
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
auto reg BF skel mscl
local metabolites: lactate, adenosine, K
key diff bw ventricle AP and pacemaker AP
-upstroke (phase 0) is Ca
(this slows conduction)
-plateau (phase 2) is ABSENT
-phase 4 uses If (Na) with spontaneous depolarization