Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio > Zachow Physio Lecture > Flashcards

Zachow Physio Lecture Flashcards

1
Q

T tubules funciton

A

allow for AP to move from cardiomyocyte to other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

DHPR function

A

Activated by AP from T-tubule

Activates Ryr=results in calcium influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

RYR function

A

activatesd by DHPR=results in calcium influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

SERCA function

A

activated by phosphohalidin

moves Ca2+ into sarcoplasmic reticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Troponin I or T function

A

reveals tropomyosin under Ca2+ heavy conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

NCX function

A

trade extraceullar Na+ for intracellular Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ckMB

-when see?

A

makes ATP from ADP

  • released during heart damage
  • start seeing at 8 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

CtnI/CTnT

-when see

A

cardiac troponins

see at heart damage at 4 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

SV=

A

EDV-ESV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

CO=

A

SVxHR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gs protein

A

activated by epi/noreepi
has cADP downstream
activates PKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Troponin I

A

makes Ca2+ leave troponin C

activates by PKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Na/K ATPase function

A

Na out for K+ in

=drives NCX-Na in for Ca out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

HCN channel

A

funny current

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

(also T type Ca open at same time)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

L=fast

T=flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

outward rectifying K+

A

activated by CM2 which are activated by PNS ACh

-dump K+ out-harder to hit threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

pressure volume curve corners

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Primary HB mech/sx

A

M-delayed conduction through AV doe

Sx-PR interval elongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

2nd HB mech/sx

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Complete HB mech/sx

A

M-no transfer from atrium to ventricle

Sx-random pattern of P to QRS-atrial p waves are okay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

A fib

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

A flutter

A

M-tons of irregular SA/ectopic atrium pacemaker activity

Sx-SAW TOOTH ECG
-variable ventricular response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

V fib

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

V tach

A

M-ectopic pacemaker in ventricle-tach means beating fast-LMAO-beating just really fast

Sx-the huge version of fib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

bundle branch block

A

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
Q

rogue QRS waves

A

due to ectopic pacemakers-usually ventricular myocytes slowly creating a circus rhythm

35
Q

Hypokalemia

A

M-weak repol

Sx-small T waves

36
Q

Hyperkalemia

A

M-lots o salt, repol is strong

Sx-tented t waves-possibly bigger QRS

37
Q

Hypocalcemia

A

M-longer plateu (Ca2+ opens and stays open for a long time), more time before depol occurs

Sx-longer QT interval

38
Q

Hypercalcmia

A

M-type L opens fast, tons of Ca2+ rush in, short plateu

Sx-short QT interval

39
Q

Antiarrythmic meds

on myo

on pacemaker

A

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
Q

MI on ECG

  • minutes
  • hours/days
  • weeks
A

m-peaked T
H/D-inverted T, ST elevation/dep, strong Q
weeks-T inverse, strong Q

41
Q

massive Q waves indicate

A

irreversible cell death

42
Q

localizing MI posteriorly

A

reciprocal changes (than normal MI) in V1, normal changes in lead aVr

43
Q

chronic systolic wall stress vs diastoloic

A

sys-concentric LVH-parallel-bigger/thicker

dais-eccentric LVH-seriers-more flimsy/thin

44
Q

AVP vs AII vs ANP vs renin vs ACE

A

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
Q

pressure volume reg system steps

-6

A

sensory, afferent vehicles (9/10/blood), central integration (medulla/hypo), effector sent out, response, feedback

46
Q

sys BP=?

dias BP=?

A

sys BP=CO

dias BP=vascualr resistance=pressure used to do LV diastole

47
Q

RAAS and pathologic HTN

A

RAAS causes change in gene expression that creates hypertrophy with fibrosis-not reverisble

48
Q

TPR=

what vessel creates most of this

A

(Pa-Pv)/TPR

arterioles

49
Q 
arteriolar BP and ECG
-when highest
when starts going up
down?
lowest
A

highest at ST interval

goes up after R

starts dropping at T

lowest a few ms after T to next R

50
Q

change in pressure=

A

Flow times resistance

51
Q

Arachnoid acid function and pathway

A

decrease SERCA=more contraction

from alpha 1/PKC
-changes arach acid into PGF that decreases SERCA

52
Q

effects of alpha 1

A

PKC up (also stimulated by Ca+ in sarco)

  • opens type L calcium channels
  • changes brach acid into PGF-decrease SERCA
53
Q

how do things leave cap

  • h2o soluble
  • lipid solube
A

h20-through pores
-fast

lipid soluble-like gases-diffusion through PM
-very fast

54
Q

vasodilatory pathway

A

vaso dil factors, recepotr, NO, PKG

PKG inhibit membrane Ca2+ channels
-increase SERCA stim

55
Q

NO and PKG

A

downstream b2/vasodilation factor

NO results in PKG

PKG-inhib membrane Ca2+ channels
-increase SERCA stim-open

56
Q

beta 2 pathway

A

use small amount of epi

downstream b2/vasodilation factor

NO results in PKG

PKG-inhib membrane Ca2+ channels
-increase SERCA stim-open

57
Q

graded vasoconstrict

A

starts as norepi, then tap, then npy, then epi

58
Q

what does EF down essentially do

A

make all pressures go up

-LVV up, LVP up, LAP up-etc.

59
Q

angina causes what?

A

cell death=expelling of K, Na, troponins, creatines, etc.

60
Q

what happens under low flow

high flow?

A

less ox-less ox phos-vasodilation
ADP/AMP up, adenosine up, vasodilation

more oxygen, ox phos-ATP-vasoconstrict

61
Q

primary receptor in coronary VSN

A

alpha 1

-need lots of metabolites to overcome SNS

62
Q

2 functions of adenosine

A

vasodilation

pain ligand

63
Q

chronic stabilized angina ecg

A

inverted/flat t waves

horizontal/sloping ST depression

only when physically actvie

64
Q

2 main effects of hypoxia

A

Adenosine used for adenosine vs ATP

lactate increases-pH acidosis-sarcolemma integrity gets fucked-dumps ions/adenosine out

65
Q

ranolazine function

A

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
Q

main receptor in sphalnic circulation

-significance?

A

alpha 1

very easy to shunt blood out and get to where you need it

67
Q

compensation for loss of plasma volume?

A

low pressure baroreceptors fire
SNS up
contractility (and HR up)
CO, MAP, RAP up

68
Q

working out

  • initial
  • vigrous
A

initally-ionotropy up, CO up, RAP down, MAP up

vigorous-vasodilation b/c not enough oxygen-RAP up, MAP down

69
Q

what is S3 gallop signifiy

A

early diastole/volume overload due to CHF

70
Q

systolic heart failre

A

ionotropy down, CO down, ESV up, EDV up, EF down

71
Q

diastolic heart failure

A

stiff ventricle

EF preserved

EDV down, ESV same but increase in ionotropy

72
Q

LOW MAP

A

FLUID CONSERVATION BY KIDNEYS

ARTERIOLES CONSTRICT

73
Q

once LV muscle fibers are stretched to optimal length

A

intracellular Ca2+ is increase and systole begins

74
Q

starling law

A

EDV up=CO up
EDV up=SV up

all because preload up

75
Q

ACH in PNS vs SNS

A

lower membrane potential

vs increase inward Calcium and charge

76
Q

high pressure baroreceptors activate fibers where and go where

A

9 and 10

go to medulla

77
Q

conductance and diameter

A

conductance is diameter to the fourth

78
Q

MAP=

A

2xdiastolic+systolic all over 3

-ESSENTAILLY CO AND TPR

79
Q

flow vs pressure and resistance

A

flow is directly proportional to pressure

and inversely prop to resistance

80
Q

common sx for angina

A

tachy, diaphoresis

81
Q

SNS vasoconstriction in arterioleses vs venules

A

arterolies -increase TPR

venules-no increase TPR-but more venous return

Cardio (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions