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69 Cards in this Set

  • Front
  • Back
name the waves of the jugular venous pulse
a-atrial cxn
c-RV cxn (TV bulges into atrium)
v-increse atrial pressure due to filling ag closed TV
S3, S4 what assoc with
S3 with dilated ventricle of CHF (volume overload)
S4 with hypertrophied ventricle (P overload)
phase 0 of ventricle
rapid upstroke as VG Na open (INa)
phase 1 ventricle
initial repolarization, INa, Ik
1) inactivation of VG Na (INa)
2) VG K open (Ik)
phase 2 ventricle
plateau, Ica, Ik
Ca influx thru VG Ca balances K efflux. Ca induces more Ca release from SR and myocyte cxn
phase 3 ventricle
rapid repol, Ik
massive K efflux as VG slow K channels open
VG Ca channels close
phase 4 ventricle
(resting potl), Ik
hi K perm through K channels
phase 0 pacemaker
upstroke Ica
opening VG Ca (these cells don't have fast VG Na--net result slow conuction used in AV node)
phase 2 pacemaker
absent
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.
how change contractility
1) increase intracell Ca
2) decrease extracell Na
for ex:
-catecholamine (incr activity of Ca pump in SR)
-digitalis (increase intracell Na, resulting in increase intracell Ca)
how catecholamines increase contractility
incr activity of Ca pump in SR
what decreases contractility
b1 blockade
HF
acidosis
hypoxia/hypercapnia
how is myocardial demand increased (MVO2)
-increased afterload
-increased contractility
-increased HR
-increase heart size (increase wall tension)
easy way to estimate SV
pulse pressure
changes in CO during exercise
initially increase SV which increases CO, later increase HR makes CO high
how does ohm's law relate to cardiac fxn
Voltage=currentxresistance
MAP=COxTPR
describe process of conduction of AP to 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
which bands of muscle contract
HIZ
describe interaction troponin/actin in power stroke cycle
Ca released from SR binds to troponin C causing conformational change moving tropomyosin out of the way so that myosin can bind. as myosin hydrolyzes its ATP power stroke created. When new ATP binds needed myosin is released (cause rigor mortis)
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.
normal PR segment
<200ms (delay thru AV node)
normal QRS
<120ms
name accessory path in WPW
Bundle of Kent
what QT interval represent
mechanical cxn of ventricles
Wenkebach is AKA
Mobitz type I (progressive lengthening than drop)
what's Mobitz II
2nd degree AV block-drop beats without progressive lengthening of PR, often seen as 2:1 block, which can lead to 3rd degree block
what's Mobitz I
2nd degree AV block-Wenkebach, progressive lengthening of PR then drop
define 1st degree AV block
PR>200, asx, no dropped beats (that's 2nd degree)
describe baroreceptor reponse and regulation of BP
increase BP at aortic arch causes message sent via vagus to medulla.
decrease BP at carotid sinus causes decrease in signal sent by Hering's n (CN9) to medulla
classic baroR response is via carotid
what does carotid massage do
increase P in carotid, increases carotid stretch, decrease HR
describe peripheral chemo R
carotid and aortic bodies respond to pCO2 increase, decr pH, pO2<60
normal P RA
<5
normal P RV
<25/5
normal P Pul A
<25/10
normal PCWP
<12
normal LA P
<12
normal LV P
<130/10
normal aortic P
<130/90
autoregulation BF heart
local metabolites, O2, adenosine, NO
autoreg BF brain
local metab CO2 (pH)
autoreg BF skel mscl
local metabolites: lactate, adenosine, K
regul BF skin
sympathetic control
NO acts via
guanylate cyclase to cGMP
consequence of increase contractility on EDV
greater tension developed during systole, increase SV, decrease EDV
describe cardiac and vascular fxn curves
cardiac output shows Starling curve, venous return curve shows relationship of VR to RAP.
x intercept=mean systemic P
where intersect=equilibrium, steady state point
define mean systemic P
RAP when no flow in CVS, heart stopped experimentally and P becomes equal throughout CVS
slope of venous return curve indicates
resistance of arterioles (increased resistance=decr VR)
how does increase BV change VR/CO graph
moves VR curve up with no change in slope, new equil has incr CO and incr RAP
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 positive inotrope effect VR/CO graph
increases in parallel the CO curve, cauing equil pt to be at higher CO and higher RAP
fick's principle
CO=O2 consumption/(O2 pul vein-O2 pul artery)
pul vein=peripheral artery
pul artery=systemic mixed venous blood
normal % PMN
40-70%
normal % lymph
20-40%
normal % mono
2-10%
normal % eos
1-6%
normal % baso
<1%
what's serum?
plasma - clotting factors (ie fibrinogen)
% blood that's plasma
55% (bc formed elements=Hct=45%)
describe plasma composition with %
92% H20, 7% proteins
of the proteins:
55% albumin
38% globulin
7% fibrinogen
starling's law
force of sxn is proportional to inital length of cardiomyocyte (preload)
when can viscosity of blood increase (3)
incr RBC, incr protein (MM), here spherocytosis
EF indicates
ventricular contractility
what's good indicator of ventricular contractility
EF
when does slow filling occur
just before MV closure
period of cardiac cycle with highest O2 consumption
isovol cxn
when isovol relavation
bw aortic valve closing and MV open
dicrotic notch
notch on aortic P curve when Ao valve closes
paradoxical splitting seen
in As