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Anatomy Terms > Physiology > Flashcards

Physiology Flashcards

1
Q

Systole

A

Ventricular contraction

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2
Q

Systolic pressure

A

Pressure on systemic arteries when the heart contracts

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3
Q

Diastole

A

Ventricular relaxation, filling stage

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4
Q

Diastolic pressure

A

Pressure in systemic arteries when the heart is in relaxation

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5
Q

S1

A

Sound associated with the mitral valve closing and beginning of systole

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6
Q

S2

A

Sound of the aortic valve closing
Associated with the end of systole and beginning of diastole

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7
Q

EDV

A

Volume in the LV after filling during diastole, right at the end of diastole

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8
Q

ESV

A

Volume of blood in the LV right after systole

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9
Q

Stroke volume

A

Volume of blood that was ejected from the heart during systole
SV=EDV-ESV

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10
Q

Ejection fraction

A

% of blood that was pumped out from the LV during systole
EF= SV/EDVx100

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11
Q

Cardiac output

A

Volume of blood the heart pumps out per minute
CO= SV x HR

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12
Q

Preload

A

The tension put on the heart when LV is full of blood and ready to contract, end of diastole
This is the EDV or pressure
The greater the stretch of fibers the stronger the muscle contracts

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13
Q

If you increase preload

A

Increase volume of blood
Slower HR (Increase filling time), constrict veins (symp innerv)

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14
Q

Decrease preload

A

Lower volume
Increase HR
Dilate veins

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15
Q

Afterload

A

Load the heart must eject blood against, thought of as aortic pressure
Pressure the heart must overcome to eject blood during systole (use SBP or MAP to determine)
Ventricular wall tension during contraction shows how much force is needed to eject

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16
Q

Increase afterload

A

Decrease in SV

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17
Q

Cause of increase afterload

A

Raised MAP, obstruct outflow, increase TPR

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18
Q

Decrease afterload

A

Increase SV

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19
Q

Cause of decrease afterload

A

Lower MAP, relieve obstruction, decrease TPR

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20
Q

Phases of the cardiac cycle

A

Ventricular filling, atrial systole, isovolumetric contraction, ejection, isovolumetric relaxation

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21
Q

Isovolumetric contraction

A

When all of the heart valves are closed, the mitral valve closes because pressure in LV is greater than LA and the LV is pressurized and preparing to eject, building pressure to overcome aortic pressure
There is no volume change, only pressure change

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22
Q

Ventricular ejection

A

When the pressure in the LV exceeds that of the aorta so aortic valve opens and blood is pumped out of the heart

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23
Q

Isovolumetric relaxation

A

The blood has just been pumped from the heart, aorta is at higher pressure again so aortic valve closes. LV still at greater pressure than LA so all valves are closed and there is no volume change

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24
Q

Ventricular filling

A

Pressure in the LA is greater than LV so mitral valve opens and blood fills the LA

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25
Q

Atrial systole (contraction)

A

At the end of diastole the atria push a contraction to get all of the blood into the LV

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26
Q

Phases of the cardiac cycle that are systole

A

Isovolumetric contraction, ejection

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27
Q

Phases of the cardiac cycle that are diastole

A

Isovolumetric relaxation, ventricular filling, atrial systole

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28
Q

P-wave

A

Depolarization signal right before atrial contraction

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29
Q

QRS wave

A

Depolarization signal right before ventricle contraction

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30
Q

T wave

A

The repolarization of the ventricles

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31
Q

Label the diagram

A
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32
Q
A
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33
Q

Stroke work

A

Work of LV to eject a volume of blood (eject SV)
Represented by area inside the PV loop

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34
Q

Pacemaker cardiac muscle cell

A

Specialized cell that sends the electrical signal throughout the heart that allows for contractile muscle cells to contract the heart

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35
Q

Characteristics of pacemaker cells

A

Make up little muscle mass
No RMP, automaticity
AP phases are 0,3,4
Doesn’t show up on EKG

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36
Q

Contractile muscle cells

A

Cells that are responsible for making actin and myosin contract and the heart beat

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37
Q

Characteristics of contractile cells

A

Make up 99% of mass
RMP at -80mV and need an AP to activate
Phases are 0,1,2,3,4
Show up on EKG

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38
Q

Intercalated disks

A

The mechanical linkage between heart cells

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39
Q

Gap junction

A

The electrical linkage between heart cells, allows the AP to travel from one cell to the next

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40
Q

Sinoatrial node

A

The origination of the Ap traveling through the heart
Pacemaker cell that has automaticity
60-100 bpm

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41
Q
A
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42
Q

Atrioventricular node

A

Receives the signal from the SA node and slows it down, allows for atria to fully contract before ventricles contract
Rests in-between the RA and RV and is electrical link between atria and ventricles
Can take over if SA fails, 40-60bpm

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43
Q

Bundle of his

A

Receives the signal from the AV node, rapidly sends down the IV septum and then through right and left bundle branches
20-40bpm

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44
Q

Purkinje fibers

A

At the apex of the heart and receives signals from left and right bundle branches
Sends the signal back up through the rest of the heart so ventricles can contract (hits papillary muscles first so valves can contract before the ventricle does)

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46
Q

Stage 4 of SA node AP

A

Funny sodium channels are open and the amount of Na in the cell is slowly increasing until it reaches a specific threshold (-60mV to -40mV)

47
Q

Stage 0 of SA node AP

A

Once enough Na has entered the cell and the threshold has been met (-40mV), Na channels close and L-type Ca channels open causing depolarization of the cell

48
Q

Stage 3 of SA node AP

A

Once the cell has depolarized, Ca channels close and K+ channels open. As K+ exits the cell it becomes more negative allowing for repolarization
At -60mV K+ channels close and funny Na channels open again

50
Q

Phase 0 myocardial AP

A

When the Ap travels through gap junction to cell causes a depolarization, Na+ channels open rapidly causing large influx and depolarization signal
-80mV to +20mV
Once at the peak upstroke Na+ channels become inactivated

51
Q

Phase 1myocardial AP

A

Transient K+ channels (fast voltage gated) open allowing for beginning of repolarization, initial sharp downstroke

52
Q

Phase 2 myocardial Ap

A

Transient K+ channels close and K+ channels open as well as L-type Ca channels triggering contraction of the cell
Cell continues to repolarize
Influx of Ca and efflux of K is balanced so around 0mV causing plateau

53
Q

Phase 3 myocardial Ap

A

L-type Ca channels close leaving just K+ channels open causing the final repolarization of the cell

54
Q

Phase 4 myocardial AP

A

K+ channels close and cell is back at -80mV (RMP)
Na+ channels are no longer inactive
RMP stabilized by K1 ion channels that are leak channels

57
Q

EC-coupling anatomy of components

A

Sarcolemma is the cell membrane, T-tubule is the dip within the membrane that contains the L-type Ca channels (DHP)
Inside of the membrane is the RyR receptor on the sarcoplamsic reticular that is a ligand gated Ca channel and causes release of Ca from the SR
Ca then attaches to myosin and actin to contract

58
Q

EC coupling physiology

A

AP propagates down sarcolemma and T-tubule, opens voltage gated L-type channels and Ca influx that then binds to Ryr channel
SR releases Ca+ into cytoplasm and activates contractile proteins
Need to now decrease Ca in cytoplasm, use SERCA into SR, NaCaX to exchange Na and Ca, and Ca pump for ATP initiated pumping

60
Q

Tunica externa

A

Outer part of the blood vessel that is composed of connective tissue

61
Q

Tunica media

A

Middle part of the blood vessel that contains smooth muscle, receives innervation from symp and parasymp to constrict or dilate

62
Q

Tunica intima

A

Inner most layer that is composed of endothelium
Single layer of simple squamous cells, allows for diffusion and absorption

63
Q

Components of circulatory system

A

Arteries
Arterioles
Capillaries
Veins

64
Q

Arteries

A

Carries blood away from the heart, because of the large BP have thicker cell walls with more smooth muscle

65
Q

Arterioles

A

Comprise the arterioles further along in the body
Create the most resistance for the systemic vascular system because of length and radius (smallest of the arteries)

66
Q

Capillaries

A

Single stream of RBC, site of fluid exchange, diffusion, etc… Single layer of epithelium with no smooth muscle

67
Q

Veins

A

Return blood back to the heart, not pressurized and use muscle movement to return
Can create pooling before return to lessen cardiac load

68
Q

Pressure

A

Driving flow created by ventricular contraction that is transferred to the blood

69
Q

Factors that impact pressure

A

Vasoconstriction (increase)
Vasodilation (decrease)
Resistance up (increase)
Volume up (decrease)

70
Q

How the aorta is intermediate pump

A

Can lessen the outward pressure on the rest of the body because of its elasticity
Elasticity allows for increase stretch, therefore increase volume means decrease in pressure

71
Q

Aorta impact on DBP

A

Recoil in the aorta after ejection and closing of the aortic valve, elasticity allows the aorta to snap back and push in to the heart momentarily increase pressure during diastole

72
Q

Compliance in veins

A

Are able to change in volume related to change in distending pressure
Can expand and collapse for different pressures

73
Q

Pulse pressure

A

The difference between systolic and diastolic pressure
The force that the heart generates each time it contracts

74
Q

MAP (Mean arterial pressure)

A

Average blood pressure in the arteries
How much pressure is needed to push blood into the capillaries (drives blood flow)

75
Q

Main determinants of MAP

A

CO and SVR

76
Q

Calculating MAP

A

2/3DP +1/3SP = MAP

77
Q

Ohm’s law of blood flow

A

Flow= change in pressure gradient/resistance

78
Q

Determinants of blood flow

A

Pressure gradient (P1 pressure of a vessel to P2 pressure): Increase gradient increase flow
Resistance of vessel: Increase resistance decrease flow

79
Q

Relationship between volume and pressure

A

Indirect, more volume then less pressure

80
Q

Resistance

A

Opposition to flow, mostly due to friction between blood and vessel wall

81
Q

Laminar flow

A

Streamline flow of blood, each layer is same distance from wall
Velocity inside is highest and velocity close to the vessel is more turbulent due to friction

82
Q

Turbulent flow

A

Causes murmurs or bruits
High velocity flow with sharp turns, hitting rough surfaces, rapid narrowing, etc…

83
Q

Poiseuille’s law equation

A

Resistance = Ln /r^4

84
Q

Poiseuille’s law

A

Showing that the biggest influence of resistance is radius of the blood vessel

85
Q

Factors determining resistance

A

Directly proportional to length (Increase L increase R)
Inversely proportional to radius (Increase radius decrease R)

86
Q

Systemic vascular resistance

A

Resistance to blood flow offered by all systemic vasculature (total peripheral resistance)

87
Q

Systemic vascular resistance equation

88
Q

Determinants of SVR

A

If SVR increases than CO decreases
If MAP increases, SVR increases

89
Q

If SVR increases then

A

LV needs to pump harder to get blood out into the body
This results in decrease SV and drop in cardiac output
It’s harder to pump blood out of the heart

90
Q

Baroreceptor reflex

A

Primary pathway of homeostatic control of MAP
Sends signals of BP to the brain to influence pressure

91
Q

Location of baroreceptors

A

Carotid sinus in the internal carotid artery

92
Q

Baroreceptors: Increase in BP

A

Baroreceptors detect increase in pressure and start firing faster sending signals to the brain to decrease pressure and HR
Decreases symp response, decreases NE, decrease BP and HR, vasodilation, decrease TPR
Increase parasymp, increase ACh, decrease BP

93
Q

Baroreceptors: Decrease in BP

A

Detect low pressure and aren’t firing as rapidly
Increase symp, NE and vasocontriction, increase BP and HR as well as TPR
Decrease parasymp, decrease ACh, increase HR and BP

94
Q

Stroke Volume

A

Amount of blood that is pumped out the LV during systole

95
Q

Stroke volume equation

A

SV= EDV - ESV

96
Q

Cardiac output

A

How much blood the heart pumps out in one minute

97
Q

Cardiac output equation

A

CO = SV x HR

98
Q

Ejection fraction

A

% of blood that the heart pumps out of the LV during systole

99
Q

Ejection fraction equation

A

EF= SV/EDV x 100

100
Q

Frank-Starling Law

A

Heart has built in mechanism that allows it to pump automatically whatever amount of blood that flows into the right atrium from the veins
If increase stretch during filling, greater the force to pump it all out (greater stretch of actin and myosin leads to greater force generation)

101
Q

Contractility

A

Strength of contraction independent of preload and afterload

102
Q

Increase in contractility

A

Reduce ESV, squeezing harder so more blood out, increase in SV

103
Q

Decrease in contractility

A

Decrease SV

104
Q

Innervation to increase contractility

A

Symp beta 1 receptors

105
Q

Innervation to decrease contractility

A

Beta 1 receptor antagonists

106
Q

Venous return

A

Quantify of blood flowing from veins to RA/min

107
Q

To increase venous return

A

Decrease RA pressure (want to flow down a pressure gradient)
Decrease TPR (decreases the pressure against veins when returning, decrease pressure increases flow)

108
Q

Right atrial pressure

A

Equal to central venous pressure, no valves impede flow into atrium

109
Q

Decrease right atrial pressure

A

Intravascular volume depletion

110
Q

Increase right atrial pressure

A

Increases with intravascular volume overload, RV failure

111
Q

Resistance to venous return determined by

A

Venous resistance and small amount due to arteriolar and small artery resistance

Anatomy Terms (5 decks)

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