Zachow Physio Lecture Flashcards
T tubules funciton
allow for AP to move from cardiomyocyte to other
DHPR function
Activated by AP from T-tubule
Activates Ryr=results in calcium influx
RYR function
activatesd by DHPR=results in calcium influx
SERCA function
activated by phosphohalidin
moves Ca2+ into sarcoplasmic reticulum
Troponin I or T function
reveals tropomyosin under Ca2+ heavy conditions
NCX function
trade extraceullar Na+ for intracellular Ca2+
ckMB
-when see?
makes ATP from ADP
- released during heart damage
- start seeing at 8 hours
CtnI/CTnT
-when see
cardiac troponins
see at heart damage at 4 hours
EF=
and what is avg EF
SV/EDV
STROKE VOLUME AND EDV HAVE NO EFFECT ON EF WHEN IONOTROPY SINCE BOTH GO UP
SV=
EDV-ESV
CO=
SVxHR
what does PKA regulate and what regulates it
- activated by Gs protein cascade (epi/norepi)
- actvites phospholambin, troponin I, open type L Ca2+
Gs protein
activated by epi/noreepi
has cADP downstream
activates PKA
Troponin I
makes Ca2+ leave troponin C
activates by PKA
Na/K ATPase function
Na out for K+ in
=drives NCX-Na in for Ca out
myocyte/purkinje ions going in at out in the 4 stages (and stage 0)+what is open
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)
pacemaker ions and channels and stages (4)
- slow depol-T type Ca2+ for slow Ca2+ n
- HCN-slow inward Na+ for outward K+ - fast depot-lots of Ca2+ by T and L type channels
- outward K+
- refractory
HCN channel
funny current
- outward K and slow inward Na+
- very slow depol
(also T type Ca open at same time)
when is sarcoplasmic Ca2+ at peak during cardiomycyte AP+why
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
what is difference between type L and type T ca2+ channels
L=fast
T=flow
what is open during plateau phase/what is closed
what is the point
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
how does SNS /PNS affect pacemaker
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
outward rectifying K+
activated by CM2 which are activated by PNS ACh
-dump K+ out-harder to hit threshold
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
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
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
Primary HB mech/sx
M-delayed conduction through AV doe
Sx-PR interval elongation
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
Complete HB mech/sx
M-no transfer from atrium to ventricle
Sx-random pattern of P to QRS-atrial p waves are okay
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
A flutter
M-tons of irregular SA/ectopic atrium pacemaker activity
Sx-SAW TOOTH ECG
-variable ventricular response
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
V tach
M-ectopic pacemaker in ventricle-tach means beating fast-LMAO-beating just really fast
Sx-the huge version of fib
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
rogue QRS waves
due to ectopic pacemakers-usually ventricular myocytes slowly creating a circus rhythm
Hypokalemia
M-weak repol
Sx-small T waves
Hyperkalemia
M-lots o salt, repol is strong
Sx-tented t waves-possibly bigger QRS
Hypocalcemia
M-longer plateu (Ca2+ opens and stays open for a long time), more time before depol occurs
Sx-longer QT interval
Hypercalcmia
M-type L opens fast, tons of Ca2+ rush in, short plateu
Sx-short QT interval
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)
MI on ECG
- minutes
- hours/days
- weeks
m-peaked T
H/D-inverted T, ST elevation/dep, strong Q
weeks-T inverse, strong Q
massive Q waves indicate
irreversible cell death
localizing MI posteriorly
reciprocal changes (than normal MI) in V1, normal changes in lead aVr
chronic systolic wall stress vs diastoloic
sys-concentric LVH-parallel-bigger/thicker
dais-eccentric LVH-seriers-more flimsy/thin
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
pressure volume reg system steps
-6
sensory, afferent vehicles (9/10/blood), central integration (medulla/hypo), effector sent out, response, feedback
sys BP=?
dias BP=?
sys BP=CO
dias BP=vascualr resistance=pressure used to do LV diastole
RAAS and pathologic HTN
RAAS causes change in gene expression that creates hypertrophy with fibrosis-not reverisble
TPR=
what vessel creates most of this
(Pa-Pv)/TPR
arterioles
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
change in pressure=
Flow times resistance
Arachnoid acid function and pathway
decrease SERCA=more contraction
from alpha 1/PKC
-changes arach acid into PGF that decreases SERCA
effects of alpha 1
PKC up (also stimulated by Ca+ in sarco)
- opens type L calcium channels
- changes brach acid into PGF-decrease SERCA
how do things leave cap
- h2o soluble
- lipid solube
h20-through pores
-fast
lipid soluble-like gases-diffusion through PM
-very fast
vasodilatory pathway
vaso dil factors, recepotr, NO, PKG
PKG inhibit membrane Ca2+ channels
-increase SERCA stim
NO and PKG
downstream b2/vasodilation factor
NO results in PKG
PKG-inhib membrane Ca2+ channels
-increase SERCA stim-open
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
graded vasoconstrict
starts as norepi, then tap, then npy, then epi
what does EF down essentially do
make all pressures go up
-LVV up, LVP up, LAP up-etc.
angina causes what?
cell death=expelling of K, Na, troponins, creatines, etc.
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
primary receptor in coronary VSN
alpha 1
-need lots of metabolites to overcome SNS
2 functions of adenosine
vasodilation
pain ligand
chronic stabilized angina ecg
inverted/flat t waves
horizontal/sloping ST depression
only when physically actvie
2 main effects of hypoxia
Adenosine used for adenosine vs ATP
lactate increases-pH acidosis-sarcolemma integrity gets fucked-dumps ions/adenosine out
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
main receptor in sphalnic circulation
-significance?
alpha 1
very easy to shunt blood out and get to where you need it
compensation for loss of plasma volume?
low pressure baroreceptors fire
SNS up
contractility (and HR up)
CO, MAP, RAP up
working out
- initial
- vigrous
initally-ionotropy up, CO up, RAP down, MAP up
vigorous-vasodilation b/c not enough oxygen-RAP up, MAP down
what is S3 gallop signifiy
early diastole/volume overload due to CHF
systolic heart failre
ionotropy down, CO down, ESV up, EDV up, EF down
diastolic heart failure
stiff ventricle
EF preserved
EDV down, ESV same but increase in ionotropy
LOW MAP
FLUID CONSERVATION BY KIDNEYS
ARTERIOLES CONSTRICT
once LV muscle fibers are stretched to optimal length
intracellular Ca2+ is increase and systole begins
starling law
EDV up=CO up
EDV up=SV up
all because preload up
ACH in PNS vs SNS
lower membrane potential
vs increase inward Calcium and charge
high pressure baroreceptors activate fibers where and go where
9 and 10
go to medulla
conductance and diameter
conductance is diameter to the fourth
MAP=
2xdiastolic+systolic all over 3
-ESSENTAILLY CO AND TPR
flow vs pressure and resistance
flow is directly proportional to pressure
and inversely prop to resistance
common sx for angina
tachy, diaphoresis
SNS vasoconstriction in arterioleses vs venules
arterolies -increase TPR
venules-no increase TPR-but more venous return
