CVS 1 previous semester Flashcards Preview

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

Flashcards in CVS 1 previous semester Deck (120)
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1
Q

what is the contractile unit of the myocardial cell

A

sarcomere

2
Q

what is similar to contractile unit in skeletal muscle

A

sarcomere

3
Q

it runs from z line to zline

A

sarcomere

4
Q

contains thick filament called

A

myosin

5
Q

the sarcomere contains thin filaments called (3)

A

actin, troponin, tropomyosin

6
Q

myocardial cells are disarrayed in what condition

A

hypertrophic cardiomyopathy

7
Q

in skeletal muscles shortening occurs when what?

A

thin filament slide along adjacent thick filaments

8
Q

where do intercalated disk occur

A

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

9
Q

what do intercalated disks do

A

maintain cell to cell cohesion

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

11
Q

how are the heart cells electrically connected with one another

A

by gap junctions

12
Q

the heart behaves as an_____ unit

A

electrical syncytium

13
Q

what do T tubules do

A

carry action potential into the cell interior

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

15
Q

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

A

SR

16
Q

Where do you find the SR in the muscle?

A

small diameter tubules in close proximity to the contractile elements

17
Q

what is important in excitation-contraction coupling

A

calcium

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

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
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).

21
Q

the trigger for SR release in the cardiac muscle

A

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

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)

23
Q

cardiac muscle - t-tubule membrane has

A

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

24
Q

what is the ryanodine receptor for skeletal muscle and cardiac muscle

A

Ca release channel

25
Q

skeletal muscle ca release is proportional to

A

membrane voltage

26
Q

cardiac muscle- the ryanodine receptor ..

A

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

27
Q

where does the action potential spread from the cell membrane

A

into the t tubules

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

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

30
Q

what is the result of calcium coming from the ryanodine receptors

A

intracellular Ca++ increases

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

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

33
Q

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

A

relaxation

34
Q

what also moves Ca++ from the cell

A

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

35
Q

calcium channel blockers block which receptors

A

L-Type Ca++ channels (dihydrophyridine receptors)

36
Q

what does dantrolene do

A

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

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)

38
Q

what is Contractility

A

the intrinsic ability of the cardiac muscle to develop force

39
Q

Contractility is related to what intracellular concentration

A

Is related to intracellular Ca++ concentration

40
Q

what do we use to estimate contractility

A

EF (stroke volume/end diastolic volume ) 55%

41
Q

what do Ve+ inotrops do to contractility

A

increase contractility

42
Q

what does -Ve inotrops do to contractility

A

decrease contractility

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

44
Q

Factors that decrease contractility

A

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

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.

46
Q

Preload is equivalent to… related to…..

A

equivalent to end-diastolic volume related to right atrial pressure

47
Q

Afterload for RV=

A

For RV = pulmonary artery pressure

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

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