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Physiology > Exam 2 Cadrio > Flashcards

Exam 2 Cadrio Flashcards

1
Q

define automaticity

A

the heart is self excitable, which means it can depolarize without an impulse from outside of the heart

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2
Q

excitability

A

the response it has to an electrical stimulation

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3
Q

conductivity

A

the ability to propagate an impulse from cell to cell

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4
Q

contractility

A

the ability to contract.

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5
Q

is the action potential longer in the atrium or the ventricles

A

its longer in the ventricles

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6
Q

describe what happens in each of the phases the ventricular action potential

A

0: fast Na channels open ,and then the slow Ca channels
1: K channels open
2: Ca channels open more
3: K channels open more
4: resting membrane potential

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7
Q

phase 0 of the action potential

A

Na rushes in, when it reaches a certain point, the activation gate closes (inactivation gate still open), which stops the influx of Na ions.

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8
Q

in a slow response, what ion causes the phase 0 of the action potential

A

Ca

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9
Q

what role does tetrodotoxin play

A

it inhibits the fast Na channels.. phase 0 diminishes until you no longer have an upstroke. when the Na current is blocked, you can still get the slow AP (from the Ca channels)

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10
Q

Phase 1:

A

early repolarization this is a brief repolarization that is caused by the transient outward current channels with K (fast to open and close)

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11
Q

phase 2:

A

the plateau caused by the slow L-type calcium channels that have opened at the end of depolarization. they take a much longer time to inactivate (compared to Na). the plateau is caused by the counterbalance of the influx of Ca and the efflux of K (delayed rectifier channels)

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12
Q

what phase are the rectifier channels and the transient outward current channels present

A

the transient outward current channels are present in the phase 1, because those are the ones that open the K channels for a brief repolarization
the rectifier channels open in Phase 2 during the plateau

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13
Q

effects of beta adrenergic stimulation (catecholamines)

A

this causes the increase of Ca conductance through the L-type calcium channels which will increase contractility

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14
Q

effects of verapamil and amlodipine which are ca channel blockers

A

this will reduce contractility. if the calcium channels are blocked, the plateau is much shorter and the duration of the AP decrease which will decrease force produced but the heart.

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15
Q

relationship of calcium and heart contraction

A

the more calcium the stronger the contraction.

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16
Q

phase 3:

A

the efflux of K will be greater then the influx of Ca. the inward rectifying K channels open, which leads to rapid repolarization.

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17
Q

does the atrium or ventricle have a smaller plateau

A

the atrium

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18
Q

phase 4:

A

restoration happens here. membrane goes back to the K equilibrium (Thanks to the Na/K pump)

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19
Q

positive inotropic effect on the heart

A

this will increase contractility (by inhibiting the Na/K Pump). no Na is pumped back out which cannot work the NCx pump, so Ca is not Brought back to the SR. The NCx only works when there is a gradient for Na. So there is less of a drive to push Ca out. the intracellular Ca concentration increase with will allow the binding of troponin to keep happening and this will keep the heart contracting.

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20
Q

what happens with rigor mortis

A

there is no ATP, so the cross-bridges are still intact, since ATP is needed to break the cross bridges.

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21
Q

Ischemia on Cardiac tissue

A

blood t the heart is reduced, so less ATP. less ATP, the Na/K pump doesn’t pump the Na out so there is more Na inside the cell then usual, and more K outside. this bring RMP closer to that of the Na, which means that it is more positive inside. This will mess up the repenting of the activation gate of the Na channel (because it usually needs to get depolarized and reach that negative value to open again). therefore, you lose phase o and this makes a slower action potential. This can lead to changes in conduction velocity and rhythm which can lead to arrhythmia and even death

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22
Q

what is missing in a slow AP

A

phases 1 and 2

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23
Q

what is phase 0 in a slow AP

A

this is the net inward flow of Ca vie L-type channels (since Na is not present due to the funky RMP that doe not allow the activation gate of the Na channel to open)

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24
Q

why is it important for things like the AV node to have a slow action potential

A

this causes a delay between the atrium and ventricle contraction giving het ventricle to fit with enough blood for an efficient contraction. If they went at the same time, there would be no time for adequate filling.

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25
Q

what is the funny current

A

this happens in phase 4 of the slow AP. the repolarization and even hyperpolarization of the phase 3 of the slow AP causes the opening of Na channels that allows Na ions to move in, nice and slowly. this accounts for the slow depolarization to the threshold, which will ultimately open the Ca channels for the faster depolarization and the AP

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26
Q

what determines HR

A

the Funny current in phase 4 of the SA node.

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27
Q

what is the relative refractory period

A

this is when a greater than normal stimulation can make an action potential, but it could have an abnormal configuration.

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28
Q

RRP in fast vs slow AP

A

in a fast AP, the RRP… if the membrane is more negative when a stimulus comes, it will look like a normal AP

slow RRP… same thing

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29
Q

what is essential for normal contraction and preventing backward spread of an action potential

A

RRP and ARP

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30
Q

what is ARP

A

absolute refractory period when no stimulus at all will make an action potential

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31
Q

chemical versus electrical synapse. what does this mean for an action potential

A

chemical happens at the Neuro Junction with NT
an electrical synapse happens in the heart, and ions trace and diffuse rapidly via gap junctions. this also allows for rapid transition of AP’s

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32
Q

what are the conduction pathways in the heart

A

it starts at the SA node, the impulse then travels to the atrium and the AV node (electrical delay), at the AV node, the impulse will travel down the bundle of His and into the right and left bundle branches to the intraventricular septum to the apex of the heart
then it goes to the ventricles

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33
Q

sequence of depolarization

A

the SA node causes depolarization of the atria
then the AV node down the septa towards the apex
then the ventricles
endocardium before epicardium to make a torsional force and allow it to contract from the inside out for optimal contraction.
then the posterior portion of the left base of the left ventricle (ventricles contract together)

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34
Q

the ___ always proceeds the ____

A

the electrical (AP) always precedes the mechanical (contractile forces)

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35
Q

the peak contractile force happens about ____ way through the repolarization of the AP

A

half (1.2)

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36
Q

SA node fires at 0seconds, then it takes ___ seconds to reach the AV node. So the total delay for the impulse to travel from the SA node to the ventricles is ____

A
  1. 03
  2. 13
  3. 16
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37
Q

why is conduction delayed at the AV node

A

the conduction in the AV node is delayed because of the nature of the slow response AP and the decreased amount of gap junctions in the AV node and bundle compared to the rest of the heart.

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38
Q

what is the consequence of the delay

A

there is plenty of time for the atrium to dump their contents into the ventricles, and allows for optimal ventricular pumping.

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39
Q

why is it important for the AV node to act as a gatekeeper? what happens when there is an abnormal rhythm?

A

the AV node ensures there is optimal filling of the ventricles. If there is an abnormal rhythm, then the ventricles don’t optimally fill with blood and may not pump enough out and we may get cardiac arrest

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40
Q

the depolarization starts at the ___ cardiac and spreads to the ___

A

endo spreads to epi.

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41
Q

what is the purpose of ventricular fibrillation

A

to try and get the heart into a refractory period so the SA node can take over and the ventricles don’t just pump wily nilly without the optimal filling.

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42
Q

what are the intrinsic firing rates of the SA and AV node

A

the SA is about 60-100 impulses per minute and the AV is 40-60

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43
Q

in what three instances can a latent pacemaker take over control of HR

A
  1. when there is vagal stimulation and the SA node is suppressed
  2. when the intrinsic firing rate of a latent pacemaker exceeds the rate of the SA node
  3. conduction block (if the AV node can’t conduct)
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44
Q

what are the ventricles, atria and nodes under? SNS or PNS

A

the ventricles are under SNS, and the Sa and AV nodes and part of the atria are under the PNS (vagus nerve)

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45
Q

what do the following effect
chronotropic
dromotropic
inotropic

A

chronotropic: HR
dromotropic: conduction velocity
inotropic: contractility and force production

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46
Q

what does the SNS and PNS do to HR, conduction velocity and contractility. Via what receptors

A

SNS will increase them via beta 1 and norepinephrine

PNS suppresses

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47
Q

how do the SNS and PNS modulate the HR

A

the SNS will cause an increase is I-calcium and I-funny which will cause a faster depolarization and therefore a faster AP, so the HR will increase
the PNS will decrease I-calcium and increase I-potassium, which will decrease the rate of the depolarization. There will be a delay in the firing of the SA node, which will translate to a decrease in the firing of the AV node, and therefore decrease the HR and firing rate.

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48
Q

what are two other ways the HR is modulated.

A
  1. decreasing, making the diastolic potential more negative. ACh does this by increasing I-potassium. This means that the membrane is more negative and further away from the threshold, so there is a slow down because it takes more time to increase to the threshold. This slows the HR
  2. increasing the threshold: ACh will decrease the I-calcium, meaning you need a higher depolarization to reach that threshold.
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49
Q

Describe a dromotropic effect. where do these affects happen? what does this do to the heart?

A

this affects conduction velocity (I-calcium and upstroke) and the rate of the upstroke (I-funny) in the AV nodes.

a positive dromotropic effect is the SNS, this is where you increase I-calcium for a faster conduction velocity at the AV node. This shortens the ERP

a negative dromotropic effect is the PNS, where the I-calcium is decreased and the I-potassium is increased, which will slow down the conduction.

50
Q

an inotropic response affects what about the heart?

A

contractility and force production.

51
Q

What two aspects of Ca affect the heart in an inotropic effect.

A

the more Ca stored, the more released and the bigger the next AP.
The more Ca that comes in the bigger the AP

52
Q

what does SNS stimulation do and by what NT and receptors

A

Beta 1 adergenic and norepinephrine and epi

this increases tension and rate of tension development and faster relaxation.

53
Q

describe the cardiac cycle

A

at first, all the chambers are relaxed, and the ventricles can fill with 80% of the blood. Then, there is atrial systole, which fills the remaining 20% blood to the ventricles. (4th sound). then there is atrial diastole at the same time as ventricular systole. the first phase of V-systole is Isovolumetric contraction. the AV valves are shut (1st sound), but there is not enough P to open the semilunar valves. then in phase 2 V-systole, the pressure int he ventricles is more then the atrium so the semilunar valves open and you have ventricular ejection. Early ventricular diastole happens when the ventricles relax, and the blood flows back on the semilunar valve which smashes them shut (2nd sound). Blood will flow into the relaxed atria: Isovolumetric relaxation, and then there will be late ventricular diastole where everything is relaxed and the ventricle fills with 80% again (3rd sound).

54
Q

what is the P wave

A

atrial depolarization (contraction)

55
Q

QRS wave

A

ventricular contraction

56
Q

T-wave

A

ventricular repolarization (relaxation)

57
Q

at the beginning of diastole the AV valve ___

A

opens

58
Q

why is there an increase in atrial pressure when the ventricle is contracting

A

when the AV valve shuts because the ventricle is contracting, there is a pushback of blood onto that mitral valve, and some of the leaflets of the mitral valve try to encroach and push back into the atrium

59
Q

when does the aortic valve open

A

when the pressure in the ventricle is high enough so it can contract

60
Q

what causes the dichotic notch

A

the closure of the aortic valve

61
Q

what causes the insisura

A

the pushback of blood on the aortic valve

62
Q

the greater the after load on the muscles the ___ the velocity of contraction

A

slower

63
Q

Increasing the preload (EDV) is going to ___ the velocity of contraction

A

increase

64
Q

a positive inotropic effect will do what to CO or SV

A

it will increase it

65
Q

an increase in preload does what to EDV, SV and VR

A

the increase in preload increases the EDV because there is an increase in VR. This means there will also be an increase in stroke volume

66
Q

there is an increase in after load when there is an increase in pressure in what?

A

aorta

67
Q

what happens to SV with an increase in afterload and why

A

there is a decrease in SV because the heart needs to pump out against a higher pressure (in the aorta). So the ESV will increase (because not as much is being pumped out)

68
Q

what happens to SV if there is an increase in contractility (and ESV)

A

stroke volume will increase and ESV will decrease because the increased contractility pumps way more blood out, so there is less volume of blood remaining after the systole.

69
Q

PNS causes a/an ____ in CO because it does what to HR. in SNS

A

a decrease in CO because there is a decrease in HR. opposite for SNS

70
Q

an increase in afterload does what to CO

A

decreases Co because the heart needs to work harder to pump blood out against the higher P in the vessel just outside of the ventricle

71
Q

under normal conditions, 95% ATP for myocardium comes from

A

oxidative phosphorylation which is aerobic.

72
Q

what does it mean that the heart is metabolically flexible

A

it will burn any substance it can get (glucose, fat, lactate)

73
Q

the heart normally burns more ___ then ____

A

fat than CHO

74
Q

how does hypertension and diabetes lead to heart failure with regard to metabolic activity

A

in diabetes, burn less glucose and more fat

in hypertension, burn pretty much just CHO and no fat

75
Q

in what vessel does the greatest pressure drop occur and why

A

arterioles because of their resistance.

76
Q

is the pressure high or low in the capillaries why?

A

it is low because the capillaries have a he cross sectional area. Velocity is inversely proportional to the area.

77
Q

what makes a vessel susceptible to turbulent flow

A

high diameter, high velocity, a local decrease in diameter (stenosis), low viscosity (anemia)

78
Q

three reasons you want laminar flow

A
  1. it makes a shear stress on the endothelium which will produce NO, and will cause the smooth muscle around vessels to relax. This will then cause the diameter to increase and the flow will be smooth
  2. KLF-2 is an immune response brought on by the shear stress, and the vessel will be less susceptible to athlerscleriosis
  3. additionally, the SOD (supra oxide dimutase) will prevent certain reactive oxygen species like lipids and macrophages which could also promote things like athlerscleriosis
79
Q

what happens to resistance when you increase viscosity (and to flow)

A

if you increase viscosity, you increase resistance which will decrease flow

80
Q

why is it important to take in fluids when you exercise

A

when you exercise, blood volume will decrease. if the blood volume decreases, there will be a decrease in VR, and SV and therefore CO. Additionally, this will make the blood more viscous and increase resistance and decrease flow and CO.

81
Q

why is it important to have blood flow in series and in parallel

A

in series, the blood flow is continuous (within a system). in parallel, the blood flow is going to be cut off in one system and increased in another (like during exercise increase blood to the skeletal muscle and decrease it to the renal system)

82
Q

when the BP increases, what do you do to resistance and how does this affect flow

A

when it increases, you decrease the resistance so the flow is maintained. when BP decreased, increase resistance by vasoconstriction and therefore maintaining flow.

83
Q

what does it mean when you say vessels are distensible

A

they are elastic and can expand and recoil with each systole. they can adapt to pulsatile outputs so that blood flow doesn’t pulsate (which could cause ischemia and hypo perfusion).

84
Q

which is more distensible veins or arteries

A

veins and they make better reservoirs.

85
Q

what is delayed compliance and how does it come into play with hemorrhage

A

delayed compliance is when the blood volume increases, the vessel expands and the smooth muscle around it relaxes. when someone is losing a lot of blood, the smooth muscle will constrict the vessel in hopes of normalizing the pressure.

86
Q

how is blood flow affected by stiff arteries

A

when the vessel is compliant (not stiff) the blood will be pumped into the vessel during systole, and the vessel wall will expand. PE will be stored in the wall. then when systole is over, the walls will recoil and continue to push the blood along. In stiff arteries, the PE is not there, so during diastole, there is no further pushing of the blood because the vessels are non compliant, and therefore the flow becomes pulsatile.

87
Q

do people with hypertension have increased or decreased compliance (and what about stiffness)

A

hypertension, increased stiffness and decreased compliance.

88
Q

how are PP transmitted

A

the blood goes into the aorta and it distends and stores PE. then the energy will continue to push the blood along

89
Q

what happens to velocity as you go downstream. why

A

velocity decrease as you go down stream because the compliance of the vessels decreases. If you cannot expand and store PE there is nothing to propel the blood forward.

90
Q

where is the PP dampened the most. why

A

at the arterioles because that is where there is the most resistance and the least compliance

91
Q

what dampens the PP

A

an increase in resistance and a decrease in compliance

92
Q

right arterial pressure is identical to what

A

central venous pressure

93
Q

what happens to RAP with a transfusion

A

the RAP will increase because of the increase in blood volume

94
Q

what happens with right sided heart failure

A

there is a blockage when the right ventricle tries to pump to the pulmonary artery. the blood backs up in the ventricle, atrium and then the systemic circulation, can cause edema.

95
Q

what two things affect RAP

A

the ability of the blood to go from the heart to the lungs and the ability of blood to go from the periphery to the right atrium

96
Q

what increases RAP

A

an increase in blood volume
HF
factors that decrease CO (pneumothorax, pleural effusion)
increase vessel tone (decreases venous compliance)
dilation of arterioles

97
Q

what decreases RAP

A 
hypovolemia 
deep inhalation (when the diaphragm descends, and the inter thorax pressure becomes more negative, the blood is sucked in)
98
Q

when veins are distended, what is the pressure like

A

almost 0

99
Q

what does a higher venous pressure do in regard to RAP

A

it increases venous return to the right atrium (because the venous pressure is higher than RAP)

100
Q

what happens with a high RAP

A

blood pools in the systemic venous circulation return, so there could be excess blood in the jugular vein. it becomes distended. if it increases too much, then there will be a build u pin the peripheral venous pressure.

101
Q

what affect does high intra-abdominal pressure have. with what conditions does this occur

A

pregnancy, tumors, obesity and an increase in fluid. prevents blood from moving from the legs to the heart, so you get swelling in the lower limbs.

102
Q

gravity and venous pressure

A

the blood will pool in the legs.

103
Q

what do varicose veins do to venous pressure

A

they increase the venous pressure because the blood valves in the legs do not pump blood forward and it stagnates.

104
Q

why do venous ulcers happen

A

the increase in blood pooling in the legs causes fluid to leak from capillaries and you can get such bad edema that it leads to ulcers.

105
Q

what are the purpose of pre capillary sphincters

A

these can constrict blood flow to an area. so if the area doesn’t need blood, it will bypass the capillaries that lay beyond the sphincter

106
Q

what is the purpose of the smooth muscle around the arterioles

A

to provide resistance. If you constrict the vessel, resistance increases. This means the arterioles are highly innervated by nerves.

107
Q

as the radius increases, what happens to the flow

A

it increases

108
Q

as the amount of tissue decreases, what happens to diffusion

A

it increases because the oxygen doesn’t have to travel was far.

109
Q

high flow means ___ diffusion

A

high

110
Q

which has a lower permeably

urea, albumin, hemoglobin, NaCl, H2O glucose

A 
water
NaCl
Urea
Glucose
Hemoglobin
Albumin
111
Q

flux greatly favors ____ over ____

A

ultrafiltration over absorption

112
Q

stroke volume is calculated how

A

systolic-diastolic

113
Q

a decrease in capacitance leads to a/an ____ PP

A

increase

114
Q

what has to happen to these factors to increase the chance of turbulent flow

A

increase the velocity and decrease the viscosity

115
Q

MAP can be calculated by

A

diastolic plus 1/3 PP

116
Q

an increase in capillary hydrostatic pressure favors…

A

filtration

117
Q

increasing venous pressure does what to capillary hydrostatic pressure (Pc)

A

it increases it, favors filtration

118
Q

an increase in ISF hydrostatic pressure and a dears in capillary osmotic pressure favors

A

absorption

119
Q

what happens to lymph flow during exercise

A

it increases (because of the contraction of muscles around it and arterial pulsations)

120
Q

relationship between blood flow and metabolic rate

A

proportional

Physiology (7 decks)

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