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69 Cards in this Set
- Front
- Back
name the waves of the 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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S3, S4 what assoc with
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S3 with dilated ventricle of CHF (volume overload)
S4 with hypertrophied ventricle (P overload) |
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phase 0 of ventricle
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rapid upstroke as VG Na open (INa)
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phase 1 ventricle
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initial repolarization, INa, Ik
1) inactivation of VG Na (INa) 2) VG K open (Ik) |
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phase 2 ventricle
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plateau, Ica, Ik
Ca influx thru VG Ca balances K efflux. Ca induces more Ca release from SR and myocyte cxn |
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phase 3 ventricle
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rapid repol, Ik
massive K efflux as VG slow K channels open VG Ca channels close |
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phase 4 ventricle
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(resting potl), Ik
hi K perm through K channels |
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phase 0 pacemaker
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upstroke Ica
opening VG Ca (these cells don't have fast VG Na--net result slow conuction used in AV node) |
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phase 2 pacemaker
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absent
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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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how change contractility
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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) |
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how catecholamines increase contractility
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incr activity of Ca pump in SR
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what decreases contractility
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b1 blockade
HF acidosis hypoxia/hypercapnia |
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how is myocardial demand increased (MVO2)
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-increased afterload
-increased contractility -increased HR -increase heart size (increase wall tension) |
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easy way to estimate SV
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pulse pressure
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changes in CO during exercise
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initially increase SV which increases CO, later increase HR makes CO high
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how does ohm's law relate to cardiac fxn
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Voltage=currentxresistance
MAP=COxTPR |
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describe process of conduction of AP to 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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which bands of muscle contract
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HIZ
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describe interaction troponin/actin in power stroke cycle
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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)
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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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normal PR segment
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<200ms (delay thru AV node)
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normal QRS
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<120ms
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name accessory path in WPW
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Bundle of Kent
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what QT interval represent
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mechanical cxn of ventricles
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Wenkebach is AKA
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Mobitz type I (progressive lengthening than drop)
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what's Mobitz II
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2nd degree AV block-drop beats without progressive lengthening of PR, often seen as 2:1 block, which can lead to 3rd degree block
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what's Mobitz I
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2nd degree AV block-Wenkebach, progressive lengthening of PR then drop
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define 1st degree AV block
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PR>200, asx, no dropped beats (that's 2nd degree)
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describe baroreceptor reponse and regulation of BP
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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 |
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what does carotid massage do
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increase P in carotid, increases carotid stretch, decrease HR
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describe peripheral chemo R
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carotid and aortic bodies respond to pCO2 increase, decr pH, pO2<60
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normal P RA
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<5
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normal P RV
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<25/5
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normal P Pul A
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<25/10
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normal PCWP
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<12
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normal LA P
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<12
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normal LV P
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<130/10
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normal aortic P
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<130/90
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autoregulation BF heart
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local metabolites, O2, adenosine, NO
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autoreg BF brain
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local metab CO2 (pH)
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autoreg BF skel mscl
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local metabolites: lactate, adenosine, K
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regul BF skin
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sympathetic control
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NO acts via
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guanylate cyclase to cGMP
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consequence of increase contractility on EDV
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greater tension developed during systole, increase SV, decrease EDV
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describe cardiac and vascular fxn curves
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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 |
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define mean systemic P
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RAP when no flow in CVS, heart stopped experimentally and P becomes equal throughout CVS
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slope of venous return curve indicates
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resistance of arterioles (increased resistance=decr VR)
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how does increase BV change VR/CO graph
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moves VR curve up with no change in slope, new equil has incr CO and incr RAP
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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 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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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 % PMN
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40-70%
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normal % lymph
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20-40%
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normal % mono
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2-10%
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normal % eos
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1-6%
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normal % baso
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<1%
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what's serum?
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plasma - clotting factors (ie fibrinogen)
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% blood that's plasma
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55% (bc formed elements=Hct=45%)
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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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starling's law
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force of sxn is proportional to inital length of cardiomyocyte (preload)
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when can viscosity of blood increase (3)
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incr RBC, incr protein (MM), here spherocytosis
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EF indicates
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ventricular contractility
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what's good indicator of ventricular contractility
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EF
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when does slow filling occur
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just before MV closure
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period of cardiac cycle with highest O2 consumption
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isovol cxn
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when isovol relavation
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bw aortic valve closing and MV open
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dicrotic notch
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notch on aortic P curve when Ao valve closes
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paradoxical splitting seen
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in As
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