Cardio

Front 1

name the waves of the jugular venous pulse

Back 1

a-atrial cxn
c-RV cxn (TV bulges into atrium)
v-increse atrial pressure due to filling ag closed TV

Front 2

S3, S4 what assoc with

Back 2

S3 with dilated ventricle of CHF (volume overload)
S4 with hypertrophied ventricle (P overload)

Front 3

phase 0 of ventricle

Back 3

rapid upstroke as VG Na open (INa)

Front 4

phase 1 ventricle

Back 4

initial repolarization, INa, Ik
1) inactivation of VG Na (INa)
2) VG K open (Ik)

Front 5

phase 2 ventricle

Back 5

plateau, Ica, Ik
Ca influx thru VG Ca balances K efflux. Ca induces more Ca release from SR and myocyte cxn

Front 6

phase 3 ventricle

Back 6

rapid repol, Ik
massive K efflux as VG slow K channels open
VG Ca channels close

Front 7

phase 4 ventricle

Back 7

(resting potl), Ik
hi K perm through K channels

Front 8

phase 0 pacemaker

Back 8

upstroke Ica
opening VG Ca (these cells don't have fast VG Na--net result slow conuction used in AV node)

Front 9

phase 2 pacemaker

Back 9

absent

Front 10

phase 4 pacemaker

Back 10

slow diastolic depolariz Ik
increase in Na conductance (If) causes spontaneous depolarization. gives automaticity.
slope determines HR, so symp increase rate depol, Ach decreases.

Front 11

how change contractility

Back 11

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)

Front 12

how catecholamines increase contractility

Back 12

incr activity of Ca pump in SR

Front 13

what decreases contractility

Back 13

b1 blockade
HF
acidosis
hypoxia/hypercapnia

Front 14

how is myocardial demand increased (MVO2)

Back 14

-increased afterload
-increased contractility
-increased HR
-increase heart size (increase wall tension)

Front 15

easy way to estimate SV

Back 15

pulse pressure

Front 16

changes in CO during exercise

Back 16

initially increase SV which increases CO, later increase HR makes CO high

Front 17

how does ohm's law relate to cardiac fxn

Back 17

Voltage=currentxresistance
MAP=COxTPR

Front 18

describe process of conduction of AP to myocyte cxn

Back 18

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

Front 19

which bands of muscle contract

Back 19

HIZ

Front 20

describe interaction troponin/actin in power stroke cycle

Back 20

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)

Front 21

describe sm m cxn

Back 21

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.

Front 22

normal PR segment

Back 22

<200ms (delay thru AV node)

Front 23

normal QRS

Back 23

<120ms

Front 24

name accessory path in WPW

Back 24

Bundle of Kent

Front 25

what QT interval represent

Back 25

mechanical cxn of ventricles

Front 26

Wenkebach is AKA

Back 26

Mobitz type I (progressive lengthening than drop)

Front 27

what's Mobitz II

Back 27

2nd degree AV block-drop beats without progressive lengthening of PR, often seen as 2:1 block, which can lead to 3rd degree block

Front 28

what's Mobitz I

Back 28

2nd degree AV block-Wenkebach, progressive lengthening of PR then drop

Front 29

define 1st degree AV block

Back 29

PR>200, asx, no dropped beats (that's 2nd degree)

Front 30

describe baroreceptor reponse and regulation of BP

Back 30

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

Front 31

what does carotid massage do

Back 31

increase P in carotid, increases carotid stretch, decrease HR

Front 32

describe peripheral chemo R

Back 32

carotid and aortic bodies respond to pCO2 increase, decr pH, pO2<60

Front 33

normal P RA

Back 33

<5

Front 34

normal P RV

Back 34

<25/5

Front 35

normal P Pul A

Back 35

<25/10

Front 36

normal PCWP

Back 36

<12

Front 37

normal LA P

Back 37

<12

Front 38

normal LV P

Back 38

<130/10

Front 39

normal aortic P

Back 39

<130/90

Front 40

autoregulation BF heart

Back 40

local metabolites, O2, adenosine, NO

Front 41

autoreg BF brain

Back 41

local metab CO2 (pH)

Front 42

autoreg BF skel mscl

Back 42

local metabolites: lactate, adenosine, K

Front 43

regul BF skin

Back 43

sympathetic control

Front 44

NO acts via

Back 44

guanylate cyclase to cGMP

Front 45

consequence of increase contractility on EDV

Back 45

greater tension developed during systole, increase SV, decrease EDV

Front 46

describe cardiac and vascular fxn curves

Back 46

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

Front 47

define mean systemic P

Back 47

RAP when no flow in CVS, heart stopped experimentally and P becomes equal throughout CVS

Front 48

slope of venous return curve indicates

Back 48

resistance of arterioles (increased resistance=decr VR)

Front 49

how does increase BV change VR/CO graph

Back 49

moves VR curve up with no change in slope, new equil has incr CO and incr RAP

Front 50

how does TPR effect VR/CO graph

Back 50

increasing TPR moves the equil point to lower CO, causing the slopes of each line to change

Front 51

how positive inotrope effect VR/CO graph

Back 51

increases in parallel the CO curve, cauing equil pt to be at higher CO and higher RAP

Front 52

fick's principle

Back 52

CO=O2 consumption/(O2 pul vein-O2 pul artery)
pul vein=peripheral artery
pul artery=systemic mixed venous blood

Front 53

normal % PMN

Back 53

40-70%

Front 54

normal % lymph

Back 54

20-40%

Front 55

normal % mono

Back 55

2-10%

Front 56

normal % eos

Back 56

1-6%

Front 57

normal % baso

Back 57

<1%

Front 58

what's serum?

Back 58

plasma - clotting factors (ie fibrinogen)

Front 59

% blood that's plasma

Back 59

55% (bc formed elements=Hct=45%)

Front 60

describe plasma composition with %

Back 60

92% H20, 7% proteins
of the proteins:
55% albumin
38% globulin
7% fibrinogen

Front 61

starling's law

Back 61

force of sxn is proportional to inital length of cardiomyocyte (preload)

Front 62

when can viscosity of blood increase (3)

Back 62

incr RBC, incr protein (MM), here spherocytosis

Front 63

EF indicates

Back 63

ventricular contractility

Front 64

what's good indicator of ventricular contractility

Back 64

EF

Front 65

when does slow filling occur

Back 65

just before MV closure

Front 66

period of cardiac cycle with highest O2 consumption

Back 66

isovol cxn

Front 67

when isovol relavation

Back 67

bw aortic valve closing and MV open

Front 68

dicrotic notch

Back 68

notch on aortic P curve when Ao valve closes

Front 69

paradoxical splitting seen

Back 69

in As