Exam 1 Flashcards

(78 cards)

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
What is the major controlling factor of Q?
changes in resistance
26
What is the calculation for flow (Q)
Q= P / R
27
What is the equation for resistance (R)
R= 8vL / pi(r^4)
28
What has the largest effect on resistance
radius of the vessel (r^4)
29
The sum of all resistances in a series
Total peripheral resistance
30
Calculatoin for cardiac output
CO= (MAP-CVP) / TPR
31
The sum of resistances across parallel capillary beds is less than the individual resistance. What does this show about changes in flow across organs?
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.
32
What happens to velocity and pressure when cross sectional area increased across capillaries?
pressure and velocity decrease
33
What is the physiological pacemaker and where is it located?
Sinoatrial node in right atrium
34
How does the electrical signal flow through the heart?
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
how does the signal travel quickly in the perkinje fibers
large fibers with many gap junctions
36
ectopic beat
uncoordinated firing of heart
37
escape beat
ectopic beat of the ventricles
38
what is resting membrane potential
-70mV to -90mV
39
Na+K+ Pump
primary active transport using ATP | transports 3Na+ out and 2K+ into cell to repolarize the cell
40
Ca2+ ATPase
Primary active transport using ATP to move Ca2+ out of cell.
41
Na+ Ca2+ exchanger
Uses extracellular Na+ flowing along its gradient (into cell) to pump Ca2+ Secondary active transport
42
Ligand gated channels
Binding of ligand opens channels allowing flow of ions along gradient causing depolarization/ voltage change
43
Voltage gated
A change in polarity causes channels to open (flow through gap junctions).
44
What maintains resting membrane potential
Flow of K+ out (leaky channels)
45
How are funny currents activated?
Increasing negative voltage
46
What creates the decaying membrane potential in the SA node
If (funny) currents. Slow efflux of Na+ activated by increasing negative membrane potential Ca2+ slow influx (voltage gated)
47
What channels cause the depolarization in the SA node
Ca2+ fast influx channels
48
What channels repolarize SA node?
K+ fast efflux (ik)
49
What channels are lacking in the AV node
Fast Na+ channels
50
How does the excitability of the Av node compare to the SA node?
AV node have slower excitability than SA node. | -slows conduction velocity allowing full contraction of atria
51
What creates the prominent phase 1 in the action potentials of the atria, bundle of His, purkinje fibers, and ventricular myocardium?
Fast Na+ channels for rapid depolarization
52
What causes the plateau phase in the ventricular myocyte action potential? What is the heart doing in this stage?
Opening of voltage gated Ca2+ channels. | Ventricular contraction
53
What is the Pwave?
Activation/ depolarization of atria. Downward direction toward left leg lead -> positive wave
54
PR interval
Contains P wave and PS segment Depolarization of R and L atria
55
PR segment
End of Pwave to beginning of QRS complex | AV node conduction
56
Q wave
Interventricular depolarization from left to right (away from left leg lead) -> negative defection due to direction
57
R wave
Ventricular free walls activated | Largest mass depolarizing toward base -> positive wave
58
S wave
Ventricular activation | Perkins fibers base to apex -> negative direction
59
T wave
Ventricular muscle repolarization from base to apex (away from left leg lead) -> positive wave
60
QT interval
Ventricular depolarization, repolarization, and ventricular contraction
61
ST segment
Isoelectric | Ca2+ influx and contraction of ventricle
62
U wave
Usually not seen under normal conditions | Possibly due to repolarization of papillary muscles
63
What condition causes a prominent U wave?
Hyopkalaemia
64
Why does Hypokalaemia cause changes in the ECG?
Prolonged repolarization due to low K+ Flattened or negative T wave- slow repolarization of ventricles Prominent U wave - prolonged repolarization of papillary muscles
65
What are the three ways of determining heart rate from ECG Paper
Count number of boxes between two R waves (calculation) Count off method (sequence) Counting number of complexes between the 3sec markers
66
How does hypertrophy cause changes in the ECG?
Greater electrical current through the expanded chamber (increase voltage) Chamber may take longer to depolarize (increase duration)
67
What is Starlings Law?
Cardiac output/ stroke volume will increase in response to an increase in blood filling the heart Increase preload > increase CO
68
What is the length-tension relationship of the heart muscle?
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
What happens is the heart is overstretched? What Law applies to overstretched heart?
Heart failure | Law of Laplace
70
What factors affect preload?
Venous blood pressure -> blood volume and TPR | Rate of venous return (velocity) ->HR and SV
71
What is afterload?
How hard heart has to work to eject blood
72
What is the sequence of events due to increased afterload?
Decreased SV > blood left in heart > increase EDV > increased preload > increase muscle stretch (optimal length= increased contractile force) increased volume => increased stroke volume
73
What does inotropy refer to?
Force of muscle contraction
74
Name positive inotropes
Noradrenaline Adrenaline Angiotensin II Dobutamine
75
Name negative Inotropes
``` B blocker Acidosis Hypoxia Hyperkalaemia Ca2+ channel blockers ```
76
What are the autonomic controls stroke volume and where to they act?
Parasympathetic - SA and AV nodes; no ventricular innervation Sympathetic - SA node and Ventricular myocardium
77
Explain the process of sympathetic innervation
CNS efferent nerves > ganglion> postganglionic nerves> release noradrenaline > NA agonises B1-adenoreceptors > increase slope of pacemaker potential
78
Explain the process of parasympathetic innervation
CNS efferent nerves > ganglion > postganglionic PSNS > agonises cardiac m2 muscarinic receptors > decrease Ca2+ influx