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Fall'20 A&P III > CVS 1 previous semester > Flashcards

CVS 1 previous semester Flashcards

1
Q

what is the contractile unit of the myocardial cell

A

sarcomere

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2
Q

what is similar to contractile unit in skeletal muscle

A

sarcomere

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3
Q

it runs from z line to zline

A

sarcomere

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4
Q

contains thick filament called

A

myosin

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5
Q

the sarcomere contains thin filaments called (3)

A

actin, troponin, tropomyosin

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6
Q

myocardial cells are disarrayed in what condition

A

hypertrophic cardiomyopathy

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7
Q

in skeletal muscles shortening occurs when what?

A

thin filament slide along adjacent thick filaments

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8
Q

where do intercalated disk occur

A

at the end of cells- its the interconnecting nature of cardiac muscle fibers

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9
Q

what do intercalated disks do

A

maintain cell to cell cohesion

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10
Q

gap junctions or communication junctions are present where?

A

Are present at the intercalated disks. They are low resistance path between cells that allow for rapid electrical spread of AP

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11
Q

how are the heart cells electrically connected with one another

A

by gap junctions

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12
Q

the heart behaves as an_____ unit

A

electrical syncytium

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13
Q

what do T tubules do

A

carry action potential into the cell interior

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14
Q

what are t tubules and what do they invaginate

A

are continuous with the cell membrane and invaginate the cells at the z lines

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15
Q

what is the site of storage and release of Ca++ for excitation-contraction coupling

A

SR

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16
Q

Where do you find the SR in the muscle?

A

small diameter tubules in close proximity to the contractile elements

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17
Q

what is important in excitation-contraction coupling

A

calcium

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18
Q

name the 6 sequence of events of excitation. contraction coupling skeletal muscle

A

AP moves along T-tubule The voltage change is sensed by the DHP* receptor. Is communicated to the ryanodine receptor which opens. Contraction occurs. Calcium is pumped back into SR. Calcium binds to calsequestrin to facilitate storage. Contraction is terminated

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19
Q

Excitation/Contraction Coupling – Cardiac muscle sequence of events 1-5

A
  1. AP moves along T-tubule. 2. During the plateau of the AP , Ca++ conductance is increased and Ca++ enters the cell from the extracellular fluid ( inward Ca++ current ) 3. Ca++ then binds to the ryanodine receptor which opens, releasing a large amount of Ca++. (Calcium induced calcium release) 4. Calcium is pumped back into sarcoplasmic reticulum, and back into T-tubule. 5. Contraction is terminated
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20
Q

what is the trigger for SR release in the skeletal muscle

A

The trigger for SR release is voltage (Voltage Activated Calcium Release - VACR).

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21
Q

the trigger for SR release in the cardiac muscle

A

The trigger for SR release is calcium (Calcium Activated Calcium Release – CACR).

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22
Q

in the skeletal muscle, what causes the t tubule membrane to open?

A

The T-tubule membrane has a voltage sensor (DHP receptor)

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23
Q

cardiac muscle - t-tubule membrane has

A

The T-tubule membrane has a Ca channel (DHP receptor)

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24
Q

what is the ryanodine receptor for skeletal muscle and cardiac muscle

A

Ca release channel

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25
Q

skeletal muscle ca release is proportional to

A

membrane voltage

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26
Q

cardiac muscle- the ryanodine receptor ..

A

The ryanodine receptor is Ca gated and Ca release is proportional to Ca entry.

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27
Q

where does the action potential spread from the cell membrane

A

into the t tubules

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28
Q

Dihydropyridine receptors

A

Ca++ conductance is increased and Ca++ enters the cell from the extracellular fluid (inward Ca++ current ) through L-type Ca++ channels

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29
Q

Ryanodine receptors

A

This Ca++ entry (Ca++ spark ) triggers the release of even more Ca++ from the sarcoplasmic retinaculum (Ca++ induced Ca++ release) through Ca++ release channels

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30
Q

what is the result of calcium coming from the ryanodine receptors

A

intracellular Ca++ increases

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31
Q

Ca++ binds to ___ , and ____ is moved out of the way removing the inhibition of the actin and myosin binding

A

Troponin C and Tropomyosin

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32
Q

Actin and myosin bind, the thick and thin filaments slide past each other and the muscle contract. (____)The magnitude of the tension that develops is proportional to the intracellular [Ca++]

A

power stroke

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33
Q

_____ occurs when Ca++ is reaccumulated by the SR by an active Ca++ ATPase Pump

A

relaxation

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34
Q

what also moves Ca++ from the cell

A

by Na+/Ca++ exchanger, Ca++ clears off

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35
Q

calcium channel blockers block which receptors

A

L-Type Ca++ channels (dihydrophyridine receptors)

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36
Q

what does dantrolene do

A

Dantrolene (Dantrium®) blocks Ca++ release channels (Ryanodine receptors) on sarcoplasmic retinaculum.

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37
Q

how does norepinephrine act on beta 1 receptors in the heart

A

increase cAMP which increase Ca++ influx through L-type Ca++ channels leading to increase force of contraction. (Acetylcholine does the opposite)

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38
Q

what is Contractility

A

the intrinsic ability of the cardiac muscle to develop force

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39
Q

Contractility is related to what intracellular concentration

A

Is related to intracellular Ca++ concentration

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40
Q

what do we use to estimate contractility

A

EF (stroke volume/end diastolic volume ) 55%

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41
Q

what do Ve+ inotrops do to contractility

A

increase contractility

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42
Q

what does -Ve inotrops do to contractility

A

decrease contractility

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43
Q

Factors that increase contractility (3)

A

increase heart rate

(Positive staircase: due to increase intracellular Ca++ in a stepwise way, Post-extrasystolic potentiation: due to extra Ca++ entered during extrasystole)

Sympathetic stimulation via b1 receptor increases the inward Ca++ current during the plateau of AP

Digitalis by increasing Ca++ by inhibiting Na+/K+ ATPase

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44
Q

Factors that decrease contractility

A

Parasympathetic stimulation (Ach) via muscarinic receptor in atria - decreases inward Ca++ flow during the plateau

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45
Q

how does digitalis work on the heart?

A

Cardiac glycosides (digitalis) increase the force of contraction by inhibiting Na+/K+ ATPase in the myocardial cell membrane. As a result of this inhibition, the intracellular [Na+] increases, diminishing the Na gradient across the cell membrane Na+/Ca++ exchange (a mechanism that extrudes Ca++ from the cell) depends on the size of the Na+ gradient and thus is diminished, producing an increase in intracellular Ca++. Higher the Ca++, more forceful will be the contraction of myocardial cell.

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46
Q

Preload is equivalent to… related to…..

A

equivalent to end-diastolic volume related to right atrial pressure

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47
Q

Afterload for RV=

A

For RV = pulmonary artery pressure

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48
Q

Frank-Starling relationship- explain what happens to the heart with greater venous return.

A

increase venous return (EDV), increase muscle fiber length, increase force of contraction, increase cardiac output The heart will pump what it receives Greater the venous return, the greater the CO

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49
Q

Depolarization

A

Makes the cell membrane potential less negative due to movement of positively charged sodium ions (Na+) into the cell. increase excitability

50
Q

Repolarization

A

Change after depolarization, that returns the membrane potential back to resting potential. Repolarization results from the movement of positively charged potassium ions (K+) out of the cells.

51
Q

Hyperpolarization

A

Makes the membrane potential more negative due to movement of negatively charged chloride ions (Cl-) into the cell. decrease excitability

52
Q

Inward current

A

Is the flow of positive charge into the cell. Inward current depolarizes the membrane potential.

53
Q

Outward current

A

Is the flow of positive charge out of the cell. Outward current hyperpolarizes the membrane potential.

54
Q

Action potential

A

Is a property of excitable cells (nerve & muscle) that consists of a rapid depolarization, or upstroke, followed by repolarization of the membrane potential. Action potential have stereotypical size and shape, are propagating and are all-or-none

55
Q

Threshold

A

Is the membrane potential at which the action potential is inevitable. At threshold potential, net inward current becomes larger that net outward current. The resulting depolarization becomes self-sustaining and gives rise to upstroke of action potential. If net inward current is less than net outward current, no action potential will occur (i.e. all- or- none response)

56
Q

Ventricular Muscle Action Potential what is the resting membrane potential value

A

The resting membrane potential is determined by the conductance to K+ Is equal to -90 mV Is STABLE and of longer duration ~ 300 msec (c.f. neuron AP ~ 1 to 2 msec)

57
Q

Phase 0- ventricle

A

Is the rapid upstroke Is caused by transient increase in Na+ conductance leads to inward Na+ movement that depolarizes the membrane.

58
Q

Phase 1- ventricle

A

Is brief period of initial repolarization caused by and outward movement of K+

59
Q

Phase 2- ventricle

A

Is the plateau of action potential Is caused by transient increase in Ca++ conductance leads to inward movement of Ca++ (L-type Ca++ channels open in this phase) During plateau, Ca++ influx balances K+ efflux. Ca++ influx triggers myocyte contraction

60
Q

Phase 3- ventricle

A

Rapid repolarization – massive K+ efflux leads to Hyperpolarization of the membrane Ca++ conductance decreases

61
Q

Phase 4- ventricular muscle action potential

A

Is the resting membrane potential – high K+ permeability through K+ channels

62
Q

what happens to skeletal muscle placed in calcium free solution

A

nothing

63
Q

what happens to cardiac muscle placed in calcium free solution

A

it stops beating

64
Q

Action Potential in SA node (Pacemaker)

A

Occurs in SA and AV nodes (SA node is normal pacemaker of heart) Has an UNSTABLE resting potential Exhibits phase 4 depolarization or automaticity

65
Q

Rate : greater pacemaker to least

A

Rate : SA node > AV node > His-Purkinje ;

66
Q

Phase 0- SA node

A

Is the upstroke of action potential Is caused by an increase Ca++ conductance inward Ca++ influx. These cells lack fast Na+ channels. Results in slow conduction velocity that is utilized by the AV node to prolong transmission from the atria to ventricles

67
Q

Phase 1 & 2 (plateau) SA node

A

are absent in the SA node action potential

68
Q

Phase 3 -SA node

A

Is repolarization Is caused by an increase K+ conductance  outward K+ movement

69
Q

Phase 4 SA node

A

Is slow depolarization- membrane spontaneously depolarizes as Na+ conductance increase Accounts for the pacemaker activity of the SA and AV nodes ( automaticity) Is caused by an increase Na+ conductance , which result in an inward Na+ current

70
Q

Ca++ Channel Blockers examples

A

Nifedipine, Verapamil , Diltiazem,

71
Q

Ca++ Channel Blockers MOA

A

Block voltage dependent L-type Ca++ channels of cardiac and smooth muscles and thereby reduce muscle contractility

72
Q

Ca channel blockers : Clinical use (5)

A

Hypertension Angina Arrhythmia (not nifedipine) Prinzmetal’s angina Raynaud’s

73
Q

Ca channel blockers toxicity

A

Flushing Dizziness, fatigue Hypotension, headache Constipation

74
Q

Pharmacolgical therapy of SVT is 1 drug of choice 3 drug alternatives

A
  1. IV adenosine - agent of choice; decreases SA and AV nodal activity 2. IV verapamil and IV esmolol or digoxin are alternatives in patients with preserved left ventricular function.
75
Q

SVT treatment if medication unsuccessful or patient becomes unstable

A

DC cardioversion if drugs are not effective or if unstable; almost always successful.

76
Q

For prevention of SVT 1 drug of choice 2 drugs for alternatives

A

Digoxin is drug of choice Verapamil or beta blockers are alternatives

77
Q

what is Conduction Velocity

A

Reflects the time required for excitation to spread throughout cardiac tissue

78
Q

conduction is slowest in ?

A

Is slowest in the AV node ( seen as the PR interval on the ECG),

79
Q

Absolute refractory period (ARP)

A

NO action potential can be initiated, regardless of how much inward current is supplied

80
Q

Effective refractory period (ERP)

A

Is slightly longer than ARP No action potential can be generated

81
Q

Relative refractory period (RRP)

A

Is the period immediately after ARP - AP can be elicited , but more than the usual inward current is required

82
Q

+ve Chronotropic effect =

A

increase heart rate by increasing the firing rate of SA node

83
Q

-ve Chronotropic effect =

A

decrease heart rate by decreasing the firing rate of SA node

84
Q

+ve Dromotropic effect =

A

increase conduction velocity through AV node, speeding the conduction of AP from the atria to the ventricles and decreasing the PR interval.

85
Q

-ve Dromotropic effect =

A

= decrease conduction velocity through the AV node, slowing the conduction of AP from the atria to the ventricles and increasing PR interval.

86
Q

Parasympathetic where in the heart in vagal innervation, where is there not vagal innervation

A

SA node, atria, and AV node have parasympathetic vagal innervation, but the ventricle do not

87
Q

Sympathetic NE works on which receptor

A

Neurotransmitter is Norepinephrine which acts on b1 receptor

88
Q

Heart Rate sympathetic parasympathetic

A

increase B1 decrease muscarinic

89
Q

conduction velocity sympathetic parasympathetic

A

increase B1 decrease muscarinic

90
Q

contractility sympathetic parasympathetic

A

increase B1 decrease muscarinic (atria only)

91
Q

vascular smooth muscle skin, splanchnic- sympathetic effects

A

constriction a1

92
Q

vascular smooth muscle skeletal muscle- sympathetic

A

relaxation B2

93
Q

sa node phase 0

A

depolarization inward ca current

94
Q

sa node phase 3

A

outward K current

95
Q

sa node phase 4

A

slow depolarization inward na current

96
Q

action potential in sa node add epinephrine

A

phase 4 depolarization is accelerated,

97
Q

Preload

A

increase venous return, increase end diastolic volume, increase length of ventricular muscle fibers

98
Q

after load lv=?

A

aortic pressure

99
Q

increasing arterial pressure will…

A

increase after load

100
Q

what is the effect of parasympathetic stimulation on phase 4 of the sa node action potential

A

decreasing heart rate-decreases rate of phase 4 depolarization

101
Q

what is the effect of sympathetic stimulation on phase 4 of the sa node action potential

A

increases HR increasing rate of phase 4 depolarization

102
Q

vascular smooth muscle calcium channel blockers greatest to least

A

Vascular smooth muscles : nifedipine > diltiazem > verapamil

103
Q

Heart- calcium channel blockers greatest to least

A

Heart : verapamil > diltiazem > nifedipine (Verapamil = Ventricle)

104
Q

ARP of the ventricle muscle

A

ARP of ventricular muscle is 250msec

105
Q

why does the conduction need to be slow in the AV node.

A

allowing time for ventricular filling before ventricular contraction.

106
Q

what happens in the conduction through the av node is fast

A

If conduction velocity through the AV node is increased, ventricular filling may be compromised.

107
Q

av node and HPS are considered?

A

AVN&HPS are latent pacemakers

108
Q

which ventricle phase is reduced by calcium channel blockers

A

phase 2

109
Q

what receptor does acetylcholine stimulate on the heart

A

Neurotransmitter is Acetylcholine which acts on muscarinic receptors

110
Q

parasympathetic stimulation effects on the heart and decreases which phase

A

decrease HR by slowing rate of phase 4 depolarization decrease conduction velocity through AV node, increase PR interval

111
Q

sympathetic stimulation effects on the heart increasing which phase

A

increase HR by accelerating rate of phase 4 depolarization increase conduction velocity through AV node, decrease PR interval

112
Q

define excitability

A

Is the ability of cardiac cells to initiate AP in response to inward depolarizing current

113
Q

Absolute refractory period (ARP) when does it begin and end

A

Begins with the upstroke of the AP and ends after the plateau

114
Q

where is conduction velocity fastest

A

Purkinje system

115
Q

what is this from

A

parasympathetic stimulation- due to increase permability to K

116
Q
A

−Due to the permeability to Na+ and Ca++

117
Q

what is this picture of

A

normal firing

118
Q

Name 4, 0, 3

A

• Phase 4 (slow depolarization)

−inward Na+ current

• Phase 0 (depolarization)

−Inward Ca++ current

• Phase 3

−outward K+current

119
Q

Name 0, 1, 2, 3, 4

A

Phase 0- rapid upstroke-Fast Na+ channels open, inward Na+ flow

Phase 1- initial repolarization- K+ channels open, outward K+ flow

Phase 2- plateau-Ca++ channels open, inward Ca++ flow

Phase 3- rapid repolarization- K+ channels open more, massive outward K+ flow

Phase 4- Resting membrane potential- high K+ permeability through leaky K+ channels

120
Q

Name the three boxes

A

Fall'20 A&P III (13 decks)

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