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Zachow Physio Lecture Flashcards

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1
Q

T tubules funciton

A

allow for AP to move from cardiomyocyte to other

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2
Q

DHPR function

A

Activated by AP from T-tubule

Activates Ryr=results in calcium influx

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3
Q

RYR function

A

activatesd by DHPR=results in calcium influx

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4
Q

SERCA function

A

activated by phosphohalidin

moves Ca2+ into sarcoplasmic reticulum

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5
Q

Troponin I or T function

A

reveals tropomyosin under Ca2+ heavy conditions

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6
Q

NCX function

A

trade extraceullar Na+ for intracellular Ca2+

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7
Q

ckMB

-when see?

A

makes ATP from ADP

  • released during heart damage
  • start seeing at 8 hours
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8
Q

CtnI/CTnT

-when see

A

cardiac troponins

see at heart damage at 4 hours

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9
Q

EF=

and what is avg EF

A

SV/EDV

STROKE VOLUME AND EDV HAVE NO EFFECT ON EF WHEN IONOTROPY SINCE BOTH GO UP

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10
Q

SV=

A

EDV-ESV

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11
Q

CO=

A

SVxHR

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12
Q

what does PKA regulate and what regulates it

A
  • activated by Gs protein cascade (epi/norepi)

- actvites phospholambin, troponin I, open type L Ca2+

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13
Q

Gs protein

A

activated by epi/noreepi
has cADP downstream
activates PKA

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14
Q

Troponin I

A

makes Ca2+ leave troponin C

activates by PKA

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15
Q

Na/K ATPase function

A

Na out for K+ in

=drives NCX-Na in for Ca out

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16
Q

myocyte/purkinje ions going in at out in the 4 stages (and stage 0)+what is open

A

0-Na+in-huge depot
1-k+ out-FAST repol
2-Type L brings Ca2+ in, and also K+ out-delayed rectifier current
3-K+ out (also Na+ somewhat recovered-rel refractory starts)
4-refractory (relative)

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17
Q

pacemaker ions and channels and stages (4)

A
  1. slow depol-T type Ca2+ for slow Ca2+ n
    - HCN-slow inward Na+ for outward K+
  2. fast depot-lots of Ca2+ by T and L type channels
  3. outward K+
  4. refractory
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18
Q

HCN channel

A

funny current

  • outward K and slow inward Na+
  • very slow depol

(also T type Ca open at same time)

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19
Q

when is sarcoplasmic Ca2+ at peak during cardiomycyte AP+why

A

right after the huge depol of Na+ in

  • NCX not working
  • DHPR and RYR at full effect
  • Type L calciums are open!

during quick repol-also plateu phase of type L open and delayed rectiferir allows for Ca2+ to stay at high level for longer

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20
Q

what is difference between type L and type T ca2+ channels

A

L=fast

T=flow

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21
Q

what is open during plateau phase/what is closed

what is the point

A

Na+ and K+ closed

Type L Ca+ open/K+ delayed rectifier open (slow K+ out)

Point-Ca2+ rushes in, when hits threshold stops, then allows fast K+ to open-GIVE CELL SOME TIME BETWEEN DEPOL AND REPOL

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22
Q

how does SNS /PNS affect pacemaker

A

makes pacemaker hit threshold faster (Na+ in faster)-T type Ca2+ open earlier
-CM2 (CN2?)-increase RMP keeping K+ in
(apparently CM2 is PNS)

makes pacemaker slower-Na+ n slower-Ca2+ open (t type) open later
-CM2-R-decrease RMP by dumping K+ out

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23
Q

outward rectifying K+

A

activated by CM2 which are activated by PNS ACh

-dump K+ out-harder to hit threshold

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24
Q

coupling mech and electric events

what happens right after S depression(3)

during t wave

right after T wave

roughly .12 after T wave (2)

@ p wave

A

after S dep-isovol contraction, aorta open, rapid ejection (in that order)

during T -slow ejection

right after T-aorta closes

after t-mitral valve open, and diastolic filling

later after t-atrial systole

at r- mitral valve closes

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25
pressure volume curve corners
bot left-mitral open-2nd part atrial systole/2nd part vent diastole bot right-mitrel closes-1st part vent systole top right-aortic opens-2nd part vent systole top left-aortic valve closes-being atrial sys/ventricular diastoly
26
Primary HB mech/sx
M-delayed conduction through AV doe | Sx-PR interval elongation
27
2nd HB mech/sx
M-not every p wave is conducted through AV node (can also be his-purkinje block-worse) Sx-more than 1 p before q, P-R elongated
28
Complete HB mech/sx
M-no transfer from atrium to ventricle Sx-random pattern of P to QRS-atrial p waves are okay
29
A fib
M-lots of AP's from ectopic/SA pacemakers in atrium, AV node stops some but not all Sx-NO P WAVES SEEABLE!!!!! can have rapid/normal ventricular response -irregularlaly irregular beat
30
A flutter
M-tons of irregular SA/ectopic atrium pacemaker activity Sx-SAW TOOTH ECG -variable ventricular response
31
V fib
M-ectopic pacemaker in ventricle-CO extremely low b/c very low diastole time-not really beating Sx-p waves masked by large QRS-not as large as Vtach-just looks like small squiggles
32
V tach
M-ectopic pacemaker in ventricle-tach means beating fast-LMAO-beating just really fast Sx-the huge version of fib
33
bundle branch block
M-delayed conduction in R or L bundle branch Sx-wide QRS (conduction of affected side relayed by unaffected side=slow) -R splitting!!!! (again from slow conduction through cardiomyocytes
34
rogue QRS waves
due to ectopic pacemakers-usually ventricular myocytes slowly creating a circus rhythm
35
Hypokalemia
M-weak repol Sx-small T waves
36
Hyperkalemia
M-lots o salt, repol is strong Sx-tented t waves-possibly bigger QRS
37
Hypocalcemia
M-longer plateu (Ca2+ opens and stays open for a long time), more time before depol occurs Sx-longer QT interval
38
Hypercalcmia
M-type L opens fast, tons of Ca2+ rush in, short plateu Sx-short QT interval
39
Antiarrythmic meds on myo on pacemaker
inhibit SNS, delay depol, prolong repeal -increase ABS refraction length/impair phase 0 mho-longer phase 0 repol, longer plateu, higher threshold-block Na+ channels (maybe block K+ out/add more Ca+ in during plateu/repol) pacemaker-raise threshold for Ca2+ to open/increase time to get there (block Na+ channels)
40
MI on ECG - minutes - hours/days - weeks
m-peaked T H/D-inverted T, ST elevation/dep, strong Q weeks-T inverse, strong Q
41
massive Q waves indicate
irreversible cell death
42
localizing MI posteriorly
reciprocal changes (than normal MI) in V1, normal changes in lead aVr
43
chronic systolic wall stress vs diastoloic
sys-concentric LVH-parallel-bigger/thicker dais-eccentric LVH-seriers-more flimsy/thin
44
AVP vs AII vs ANP vs renin vs ACE
AVP=vassopressin=ADH AII=stimulates AVP secretion ANP=turns off AVP secretion (by turning off renin-thus turning off AII) AVP and AII made in adrenal renin-precursor to AI ACE-makes AII from AII
45
pressure volume reg system steps | -6
sensory, afferent vehicles (9/10/blood), central integration (medulla/hypo), effector sent out, response, feedback
46
sys BP=? | dias BP=?
sys BP=CO dias BP=vascualr resistance=pressure used to do LV diastole
47
RAAS and pathologic HTN
RAAS causes change in gene expression that creates hypertrophy with fibrosis-not reverisble
48
TPR= what vessel creates most of this
(Pa-Pv)/TPR arterioles
49
``` arteriolar BP and ECG -when highest when starts going up down? lowest ```
highest at ST interval goes up after R starts dropping at T lowest a few ms after T to next R
50
change in pressure=
Flow times resistance
51
Arachnoid acid function and pathway
decrease SERCA=more contraction from alpha 1/PKC -changes arach acid into PGF that decreases SERCA
52
effects of alpha 1
PKC up (also stimulated by Ca+ in sarco) - opens type L calcium channels - changes brach acid into PGF-decrease SERCA
53
how do things leave cap - h2o soluble - lipid solube
h20-through pores -fast lipid soluble-like gases-diffusion through PM -very fast
54
vasodilatory pathway
vaso dil factors, recepotr, NO, PKG PKG inhibit membrane Ca2+ channels -increase SERCA stim
55
NO and PKG
downstream b2/vasodilation factor NO results in PKG PKG-inhib membrane Ca2+ channels -increase SERCA stim-open
56
beta 2 pathway
use small amount of epi downstream b2/vasodilation factor NO results in PKG PKG-inhib membrane Ca2+ channels -increase SERCA stim-open
57
graded vasoconstrict
starts as norepi, then tap, then npy, then epi
58
what does EF down essentially do
make all pressures go up | -LVV up, LVP up, LAP up-etc.
59
angina causes what?
cell death=expelling of K, Na, troponins, creatines, etc.
60
what happens under low flow high flow?
less ox-less ox phos-vasodilation ADP/AMP up, adenosine up, vasodilation more oxygen, ox phos-ATP-vasoconstrict
61
primary receptor in coronary VSN
alpha 1 | -need lots of metabolites to overcome SNS
62
2 functions of adenosine
vasodilation | pain ligand
63
chronic stabilized angina ecg
inverted/flat t waves horizontal/sloping ST depression only when physically actvie
64
2 main effects of hypoxia
Adenosine used for adenosine vs ATP lactate increases-pH acidosis-sarcolemma integrity gets fucked-dumps ions/adenosine out
65
ranolazine function
inhibits second inward Na wave - less sodium in cell - more NCX - more calcium out of cell-LV relax - reduced tension on wall - decrease O2 demand
66
main receptor in sphalnic circulation | -significance?
alpha 1 | very easy to shunt blood out and get to where you need it
67
compensation for loss of plasma volume?
low pressure baroreceptors fire SNS up contractility (and HR up) CO, MAP, RAP up
68
working out - initial - vigrous
initally-ionotropy up, CO up, RAP down, MAP up vigorous-vasodilation b/c not enough oxygen-RAP up, MAP down
69
what is S3 gallop signifiy
early diastole/volume overload due to CHF
70
systolic heart failre
ionotropy down, CO down, ESV up, EDV up, EF down
71
diastolic heart failure
stiff ventricle EF preserved EDV down, ESV same but increase in ionotropy
72
LOW MAP
FLUID CONSERVATION BY KIDNEYS | ARTERIOLES CONSTRICT
73
once LV muscle fibers are stretched to optimal length
intracellular Ca2+ is increase and systole begins
74
starling law
EDV up=CO up EDV up=SV up all because preload up
75
ACH in PNS vs SNS
lower membrane potential vs increase inward Calcium and charge
76
high pressure baroreceptors activate fibers where and go where
9 and 10 | go to medulla
77
conductance and diameter
conductance is diameter to the fourth
78
MAP=
2xdiastolic+systolic all over 3 -ESSENTAILLY CO AND TPR
79
flow vs pressure and resistance
flow is directly proportional to pressure | and inversely prop to resistance
80
common sx for angina
tachy, diaphoresis
81
SNS vasoconstriction in arterioleses vs venules
arterolies -increase TPR | venules-no increase TPR-but more venous return

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