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Cardio Exam 1 > Cardio Physiology > Flashcards

Cardio Physiology Flashcards

1
Q

What is nernst potential equation?

A

Ex = RT/zF * ln [Xo]/[Xi]

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2
Q

What is resting membrane voltage?

A
  • 85 mV

- membranes are permeable to K+ but not Na or Ca

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3
Q

What is K equilibrium potential [Ek]?

A

-89 mV

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4
Q

What is Na equilibrium potential [Ena]?

A

+70 mV

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5
Q

What is Ca equilibrium potential [Eca]?

A

+ 133 mV

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6
Q

Which ion sets the resting voltage?

A

K+

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7
Q

What is phase 0 of ventricular AP? What channels open/closed?

A

rapid upstroke and depolarization

due to voltage gated Na channels opening [ Na in]

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8
Q

What is phase 1 of ventricular AP? What channels open/closed?

A

initial repolarization

  • inactivation of voltage gated Na channels
  • voltage gated K channels begin to open [K out]
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9
Q

What is phase 2 of ventricular AP? What channels open/closed?

A

plateau phase = voltage decreasing at very slow rate

  • Ca in through voltage gated Ca channels [depolarizing]
  • balanced by K out [repolarizing]

Ca in triggers Ca release from SR and myocyte contraction

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10
Q

What is phase 3 of ventricular AP? What channels open/closed?

A

rapid repolarization

lots of K out due to opening voltage-gated slow K channels

  • slow voltage gated K open [K out]
  • voltage gated Ca close
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11
Q

What is phase 4 of ventricular AP? What channels open/closed?

A

resting potential

high K permeability through K channels

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12
Q

What is path of action potential propagation in a heartbeat?

A
  • SA node generates AP
  • propagated to atrial muscle
  • activates AV node between atria and ventricles
  • goes down bundles of his to left and right bundle branches
  • reaches purkinje fibers of L and R ventricles which excite subendocardium then epicardial surface
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13
Q

How many contractions per AP in cardiac cell? why?

A

one contraction per AP

because of refractory period after AP –> need time to recover until 2nd AP

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14
Q

What is the absolute refractory period?

A

time that must elapse before 2nd stimulus can cause an AP

–> impossible to trigger second AP during this time

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15
Q

What is the relative refractory period?

A

period of time when very large stimulus can produce weak action potential [AP]

stronger signal than normal is required to produce a normal AP

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16
Q

What is phase 0 for SA node?

A

upstroke

  • opening Ca voltage-gated channels
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17
Q

What is phase 2 for SA node?

A

no phase 2 in SA node

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18
Q

What is phase 3 for SA node?

A

inactivation of Ca channels and activation of K channels

–> lots of K efflux to repolarize

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19
Q

What is phase 4 for SA node?

A

slow diastolic depolarization

membrane potentially spontaneously depolarizes as Na conductance increases [If= funny current] , slope of phase 4 determines HR

  • If in
  • Ca out and Na in [NCX]
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20
Q

What is difference phase 0 ventricular vs SA node cells?

A

ventricle: Na open/in

SA: Ca channels open/in, no fast voltage-gate Na b/c less negative resting voltage of these cells

phase 0 for ventricular myocyte = much faster [300 V/s]

SA = 20 V/s

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21
Q

What is funny current [If]?

A

current that depolarizes in phase 4 of SA node contraction

mixed Na/K inward current

not present in ventricle

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22
Q

What is inward rectifier current?

A

Ik = in ventricle but not SA node

responsible for flat phase 4

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23
Q

How does phase 3 differ ventricle vs SA?

A

comparable

both have delayed rectifier K channels responsible for repolarization

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24
Q

What is baseline voltage for SA node cells?

A

-60 mV

[compared to ventricle -85 mV]

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25
Q

What is NCX current?

A

Na Ca exchanger current

  • 3 Na in for 1 Ca out
  • net Ca out and Na in
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26
Q

What is single electrode whole cell voltage clamping?

A
  • voltage clamp controls cellular voltage and measure of corresponding ionic current
  • record changes in ionic current in response to series of depolarizations
  • plot peak current vs voltage to understand underlying characteristics
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27
Q

What is convention inward vs outward currents?

A 
inward = negative
outward = positive
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28
Q

What direction does current travel when voltage across membrane is greater than the nernst potential for an ion?

A

pos current

  • ion will move out of cell [assuming + charge ion]
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29
Q

What direction does current travel when voltage across membrane is less than the nernst potential for an ion?

A

neg current

  • ion will move into cell [assuming + charge ion]
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30
Q

What direction will Na/Ca/K go if voltage = 80?

A
  • K out
  • Na out
  • Ca in
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31
Q

What is mech of activation and speed of activation of Ik/Ach vs If [funny]?

A

Ik,Ach = activated by gprotein By subunits

If = activated by increased CAMP
- requires intermediate enzyme AC thus much slower

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32
Q

Is parasympathetic or sympathetic effect on HR faster?

A

parasympathetic = by activation Ik by G protein By subunit

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33
Q

When do voltage gated Na channels [Ina] open? Close?

A
  • open at greater than -60 mV
  • close milliseconds later

thus not open at -85 mV resting potential

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34
Q

When do L-type Ca channels [Ica] open? close?

A
  • open at more positive membrane potential than Na

- activates and inactivates 10x slower than Na

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35
Q

What mediates parasympathetic stimulation of heart cells?

A

via muscarinic ACh receptors

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36
Q

What is effect of parasympathetic stimulation in SA? AV? ventricular?

A

SA: slower firing by activation of Ik, Ach by G protein By subunits

AV: slower electrical conduction through AV by reduced Ica due to decreased PKA activity

ventricle: no effects

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37
Q

What is the inward rectifying K channel [Ik1]? when is it open/closed?

A
  • open at resting potential
  • closes at positive potentials and closed completely at 0 mV

keeps ventricle membrane potential constant at -85 mV

not present in SA node

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38
Q

What are the delayed rectifying K channels [Ikr and Iks]? when are they open/closed?

A
  • closed at resting potential
  • open in plateau [phase 2] positive potential
Ikr = rapid delayed rectifier = can be blocked by meds
Iks = slow delayed rectifier
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39
Q

What is effect of sympathetic stimulation of heart cells on SA? AV? ventricles?

A

SA: faster firing by activation If by increase CAMP

AV: faster electrical conduction through AV by increased Ica due to increase PKA activity

ventricle: stronger contraction, faster relaxation
- increased Ica due to increased PKA
- phosphorylation phospholamban, increased SERCA

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40
Q

What receptors mediate sympathetic stimulation of heart cells?

A

B-adrenergic receptors

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41
Q

What is difference AP vs ECG voltage?

A

AP = Vin - Voutside of cell

ECG = V2 - V1 = voltages outside of cells at 2 different locations = AP1 - AP2 = subtract APs

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42
Q

What is funny current? another name for the channel?

A

If = HCN = hyperopolarization-activated cyclic nucleotide gated channel

present in SA and AV node but not ventricle
- closed at more positive potentials, opens when membrane potential less than -50

mixture of Na and K [mostly Na]
depolarizing

43
Q

Is heart under parasympathetic or sympathetic control? blood vessels?

A

heart = both; except ventricles just sympathetic

blood vessels = just sympathetic

44
Q

What is chronotropy?

A

HR

45
Q

What does a positive chronotrope do?

A

increase HR

46
Q

What is inotropy?

A

contractile strength

47
Q

What does a positive inotrope do?

A

increases force of contraction

48
Q

What is action of digoxin?

A

positive inotrope

49
Q

What is dromotropy?

A

speed at which electrical impulses propogate through heart

50
Q

What is lusitropy?

A

speed of relaxation of ventricle

51
Q

Upward or downward deflection [wave] in ECG?

  • depolarization toward + electrode
  • depoarlization away from + electrode
  • repolarization toward + electrode
  • repolarization away from + electrode
A
  • depolarization toward + electrode
    == pos deflection [wave]
  • depoarlization away from + electrode
    == neg deflection [wave]
  • repolarization toward + electrode
    == neg deflection [wave]
  • repolarization away from + electrode
    == pos deflection [wave]
52
Q

What part of heart is main determinant of dromotropy?

A

SV node!

53
Q

What is parasympathetic innervation of SA node?

A

vagus nerve

54
Q

Is resting HR in a heart transplant patient higher or lower than normal?

A

resting HR in heart transplant 90-100 bpm compared to healthy = 60-80

55
Q

What happens to heart if you give atropine?

A

atropine = parasympathetic antagonist

–> increase HR

56
Q

What happens to heart if you give B-blocker?

A

blocks sympathetics –> HR decrease

57
Q

Do you get bigger change in HR if you block parasympathetic or sympathetic?

A

block PNS = much greater rise in HR compared to blocking SNS = not as much decrease HR

58
Q

What is the cellular basis for T wave?

A

endocardium activates before and repolarizes after epicardium

if you do Vendo-Vepi you get an upward deflecting t wave

== ventricular repolarization

59
Q

What is the cellular basis for p wave?

A

atrial depolarization

60
Q

What is the cellular basis of QRS complex?

A

ventricular depolarization

61
Q

What is equation for aVL from other leads?

A

aVL = 0.6 * (V1-V3) [L is for left]

62
Q

What is equation for aVR from other leads?

A

aVR = 0.6 * (-V1-V2) [R is for Right]

63
Q

What is equation for aVF from other leads?

A

aVF = 0.6*(V2 + V3) [F is for food

64
Q

What angle for aVL?

A

-30

65
Q

What angle for aVR?

A

-150

66
Q

What angle for II?

A

+60

67
Q

What angle for aVF?

A

+90

68
Q

What angel for III?

A

+120

69
Q

What is Ohm’s equation for BP control?

A

MAP = CO * TPR

MAP = mean arterial pressure
CO = cardiac output
TPR = total peripheral resistance
70
Q

What does increase in MAP do to CO?

A

nothing!

71
Q

What are the 3 phases of baroreceptor reflex?

A
  1. something happen to change MAP
  2. reflex response tries to return MAP to level that existed before
  3. after changes, new steady state reached
72
Q

What is cellular meaning of PR interval?

A

propagation through AV node

73
Q

Why don’t you see a signal from atrial repolarization?

A

atria are much smaller = the muscle mass is too small

74
Q

What does baroreceptor reflex do when there is hemorrhage to return MAP to steady state? Effect on myocardium + vessels?

A

on myocardium:

  • increase HR –> increase CO
  • increase contractility –> increase CO

on vessels:

  • arteriolar smooth muscle contraction –> increase TPR
  • venous smooth muscle contraction –> increase preload –> increase CO
75
Q

What is renin-angiotensin-aldosterone system [RAAS] action to regulate BP?

A
  • detect decreased pressure in kidneys –> release renin from juxtaglomerular cells
  • increase renin –> increase angiotensin I –> ACE [angiotensin converting enzyme] –> angiotensin II
  • angiotensin II
  • -> increase aldosterone –> increase Na reabsorption in kidney –> increase blood volume
  • -> vasoconstriction –> increase TPR
76
Q

What are the 4 phases of cardiac PV Loop?

A
  1. isovolumic contraction
  2. ejection
  3. isovolumic relaxation
  4. diastolic filling
77
Q

What is preload?

A

amount of pressure/stretch in heart muscle before contraction

78
Q

What is afterload?

A

pressure that exists in the aorta/vasculature against which

79
Q

When does MV close on PV loop?

A

bottom right = after diastolic filling at start of isovolumic contraction

80
Q

When does AoV open in PV loop?

A

top right = after isovolumic contraction at start of ejection

81
Q

When does AoV close in PV loop?

A

top left = after ejection at start of isovolumic relaxation

82
Q

When does MV open in PV loop?

A

bottom left = after isovolumic relaxation at start of filling

83
Q

What is EDPVR?

A
  • end diastolic pressure-volume relationship

- bottom right of PV loop [MV closure] occurs along it

84
Q

What is ESPVR?

A
  • end systolic pressure-volume relationship

- top left of PV loop [AoV closure] occurs along it

85
Q

What happens to PV loop if increase preload with constant afterload and contractility?

A

shift up along both ESPVR and EDPVR curves

–> increase stroke volume and arterial BP

86
Q

What are 2 ways to increase preload?

A
  • increase blood volume

- venoconstriction –> decrease venous compliance

87
Q

What is starling curve?

A

relationship preload and stroke volume

increase preload [LVEDP] –> increase stroke volume

88
Q

What are some things that cause increased preload?

A
  • fluid retention [as in advanced heart failure]

- constriction of veins

89
Q

What are some things that cause decreased preload?

A
  • blood loss

- dilation of veins

90
Q

What happens to PV volume if increased TPR with constant preload and contractility?

A
  • stays in same place along EDPVR
  • moves up on ESPVR [end systolic volume increases]
  • SV decreases [width of loop]
91
Q

How do you get increased TPR?

A

arteriolar constriction

92
Q

What does TPR represent?

A

afterload

93
Q

How do you calculate SV from PV loop?

A

SV = width of loop

= EDV - ESV

94
Q

What are some things that cause increase afterload?

A
  • temporary constriction of arterioles
  • chronic hypertension
  • aortic stenosis [valve narrowing or block]
95
Q

What are some things that cause decrease afterload?

A

dilation of arterioles

96
Q

What happens to PV loop if increase contractility with constant preload and afterload?

A
  • increase stroke volume
  • increase ejection fraction
  • decrease end systolic volume
  • shits ESPVR line to the left
97
Q

What are some ways you can increase contractility?

A
  • B adrenergic stimulation ventricles
  • increase plasma Ca
  • increase muscle mass [ physiological hypertrophy]
98
Q

What are some ways you can decrease contractility?

A
  • B adrenergic blockade
  • Ca channel blocker
  • decrease energy supply [ischemia or hypoxia]
  • decrease muscle mass [MI]
99
Q

How does venous return change with venous/atrial pressure?

A

as venous return/flow increases, atrial/venous pressure decreases

100
Q

In steady state was is relationship CO and venous return?

A

in steady state CO = venous return

101
Q

What does increased blood volume do to venous return curve?

A

line shifts up

102
Q

What does decrease TPR do to venous return curve?

A

y intercept increases = steeper slope

103
Q

What does venoconstriction do to venous return curve?

A

x intercept [mean systemic pressure] increases = shallower slope

Cardio Exam 1 (16 decks)

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