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RUSVM Physiology 1 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What anchors the AV valves and the semilunar valves?

A

Annulous fibrosis

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2
Q

What valves lie between the atria and ventricles?

A

Atrioventricular valve
Right - tricupid valve
Lepf- bicuspid or mitral valve

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3
Q

What valve lie between the aorta, pulmonary system and ventricles

A

semilunar valves

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4
Q

What are the layers of the blood vessel wall?

A

Tunica intima
Tunica media
Tunic adventitia

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5
Q

Tunica intima

A

endothelium and elastic lamina

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6
Q

Tunica media

A

smooth muscle and elastic lamina

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7
Q

Tunica adventitia

A

connective tissue

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8
Q

What vasculature is distributive?

A

Elastic and muscular arteries

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9
Q

What vasculature is creates resistance?

A

Arterioles

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10
Q

What vasculature is for exchange

A

capillaries

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11
Q

What are the capacitance vessels?

A

venules and veins

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12
Q

What layer is significant in elastic arteries and what is its effect?

A

Tunica media with a large amount of collagen and elastin

Windkessel effect- elastic reservoir expanding and recoiling over a cardiac cycle

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13
Q

What is the main layer on muscular arteries? What does it prevent?

A

Tunica media

Prevents kinking at joints

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14
Q

What is the main layer in arterioles? What controls this?

A 
Tunica media (smooth muscle)
sympathetic nervous system and adrenoreceptors (b receptors)
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15
Q

Capillary walls are made of?

A

single layer of epithelium

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16
Q

What do venules lack?

A

smooth muscle

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17
Q

What innervates veins? What is the effect of this innervation?

A

sympatheic nervous system

venoconstricion -> increased CVP -> increased cardiac output

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18
Q

systole

A

contraction phase

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19
Q

diastole

A

relaxation phase

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20
Q

heart rate

A

beat per min

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21
Q

stroke volume

A

volume ejected per beat

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22
Q

cardiac output

A

volume ejected per min

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23
Q

pulse pressure

A

systolic - diastolic

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24
Q

What is resistance

A

how hard it is for flow (Q) to occur through vessels

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25
Q

What is the major controlling factor of Q?

A

changes in resistance

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26
Q

What is the calculation for flow (Q)

A

Q= P / R

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27
Q

What is the equation for resistance (R)

A

R= 8vL / pi(r^4)

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28
Q

What has the largest effect on resistance

A

radius of the vessel (r^4)

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29
Q

The sum of all resistances in a series

A

Total peripheral resistance

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30
Q

Calculatoin for cardiac output

A

CO= (MAP-CVP) / TPR

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31
Q

The sum of resistances across parallel capillary beds is less than the individual resistance. What does this show about changes in flow across organs?

A

flow in one organ can be altered without effecting flow of another organ.
flow through an individual bed is dependent on the individual resistance of that bed.

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32
Q

What happens to velocity and pressure when cross sectional area increased across capillaries?

A

pressure and velocity decrease

33
Q

What is the physiological pacemaker and where is it located?

A

Sinoatrial node in right atrium

34
Q

How does the electrical signal flow through the heart?

A

SA node -> AV node (slight pause to allow atria to contract) -> Bundle of His in interventricular septum -> Perkinje fibers up sides of heart to myocardium

35
Q

how does the signal travel quickly in the perkinje fibers

A

large fibers with many gap junctions

36
Q

ectopic beat

A

uncoordinated firing of heart

37
Q

escape beat

A

ectopic beat of the ventricles

38
Q

what is resting membrane potential

A

-70mV to -90mV

39
Q

Na+K+ Pump

A

primary active transport using ATP

transports 3Na+ out and 2K+ into cell to repolarize the cell

40
Q

Ca2+ ATPase

A

Primary active transport using ATP to move Ca2+ out of cell.

41
Q

Na+ Ca2+ exchanger

A

Uses extracellular Na+ flowing along its gradient (into cell) to pump Ca2+

Secondary active transport

42
Q

Ligand gated channels

A

Binding of ligand opens channels allowing flow of ions along gradient causing depolarization/ voltage change

43
Q

Voltage gated

A

A change in polarity causes channels to open (flow through gap junctions).

44
Q

What maintains resting membrane potential

A

Flow of K+ out (leaky channels)

45
Q

How are funny currents activated?

A

Increasing negative voltage

46
Q

What creates the decaying membrane potential in the SA node

A

If (funny) currents. Slow efflux of Na+ activated by increasing negative membrane potential
Ca2+ slow influx (voltage gated)

47
Q

What channels cause the depolarization in the SA node

A

Ca2+ fast influx channels

48
Q

What channels repolarize SA node?

A

K+ fast efflux (ik)

49
Q

What channels are lacking in the AV node

A

Fast Na+ channels

50
Q

How does the excitability of the Av node compare to the SA node?

A

AV node have slower excitability than SA node.

-slows conduction velocity allowing full contraction of atria

51
Q

What creates the prominent phase 1 in the action potentials of the atria, bundle of His, purkinje fibers, and ventricular myocardium?

A

Fast Na+ channels for rapid depolarization

52
Q

What causes the plateau phase in the ventricular myocyte action potential? What is the heart doing in this stage?

A

Opening of voltage gated Ca2+ channels.

Ventricular contraction

53
Q

What is the Pwave?

A

Activation/ depolarization of atria. Downward direction toward left leg lead -> positive wave

54
Q

PR interval

A

Contains P wave and PS segment

Depolarization of R and L atria

55
Q

PR segment

A

End of Pwave to beginning of QRS complex

AV node conduction

56
Q

Q wave

A

Interventricular depolarization from left to right (away from left leg lead) -> negative defection due to direction

57
Q

R wave

A

Ventricular free walls activated

Largest mass depolarizing toward base -> positive wave

58
Q

S wave

A

Ventricular activation

Perkins fibers base to apex -> negative direction

59
Q

T wave

A

Ventricular muscle repolarization from base to apex (away from left leg lead) -> positive wave

60
Q

QT interval

A

Ventricular depolarization, repolarization, and ventricular contraction

61
Q

ST segment

A

Isoelectric

Ca2+ influx and contraction of ventricle

62
Q

U wave

A

Usually not seen under normal conditions

Possibly due to repolarization of papillary muscles

63
Q

What condition causes a prominent U wave?

A

Hyopkalaemia

64
Q

Why does Hypokalaemia cause changes in the ECG?

A

Prolonged repolarization due to low K+
Flattened or negative T wave- slow repolarization of ventricles
Prominent U wave - prolonged repolarization of papillary muscles

65
Q

What are the three ways of determining heart rate from ECG Paper

A

Count number of boxes between two R waves (calculation)
Count off method (sequence)
Counting number of complexes between the 3sec markers

66
Q

How does hypertrophy cause changes in the ECG?

A

Greater electrical current through the expanded chamber (increase voltage)

Chamber may take longer to depolarize (increase duration)

67
Q

What is Starlings Law?

A

Cardiac output/ stroke volume will increase in response to an increase in blood filling the heart
Increase preload > increase CO

68
Q

What is the length-tension relationship of the heart muscle?

A

Resting cardiac muscle is less than optimal length for tension.
Increase length by increased filling (EDV or preload) => fibers at optimal length creating a greater force of contraction

Increases stroke volume

69
Q

What happens is the heart is overstretched? What Law applies to overstretched heart?

A

Heart failure

Law of Laplace

70
Q

What factors affect preload?

A

Venous blood pressure -> blood volume and TPR

Rate of venous return (velocity) ->HR and SV

71
Q

What is afterload?

A

How hard heart has to work to eject blood

72
Q

What is the sequence of events due to increased afterload?

A

Decreased SV > blood left in heart > increase EDV > increased preload > increase muscle stretch (optimal length= increased contractile force) increased volume => increased stroke volume

73
Q

What does inotropy refer to?

A

Force of muscle contraction

74
Q

Name positive inotropes

A

Noradrenaline
Adrenaline
Angiotensin II
Dobutamine

75
Q

Name negative Inotropes

A 
B blocker
Acidosis 
Hypoxia 
Hyperkalaemia 
Ca2+ channel blockers
76
Q

What are the autonomic controls stroke volume and where to they act?

A

Parasympathetic - SA and AV nodes; no ventricular innervation
Sympathetic - SA node and Ventricular myocardium

77
Q

Explain the process of sympathetic innervation

A

CNS efferent nerves > ganglion> postganglionic nerves> release noradrenaline > NA agonises B1-adenoreceptors > increase slope of pacemaker potential

78
Q

Explain the process of parasympathetic innervation

A

CNS efferent nerves > ganglion > postganglionic PSNS > agonises cardiac m2 muscarinic receptors > decrease Ca2+ influx

RUSVM Physiology 1 (2 decks)

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