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physiology and pharmacology > Cardiac stuff > Flashcards

Cardiac stuff Flashcards

1
Q

how can you work out the duration of a cardiac cycle?

A

60 (s/m)/ Heart rate (beats/m)

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2
Q

what kind of variety is the cardiac pump? what phases does this alternate between?

A

it is of the two stroke variety

it alternates between filling and emptying phases.

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3
Q

under normal circumstances what determines duration?

what determines the relative duration of contraction and relaxation?

A

duration determined by pacemaker
duration of contraction and relaxation is determined by the electrical properties of the cardiac conductive system and cardiac myocytes.

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4
Q

what enters the right and left atrium?

A

Right - deoxygenated blood from superior and inferior vena cava.
left - oxygenated blood from pulmonary circulation.

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5
Q

what do atria act as?

A

passive reservoirs

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6
Q

do atria contract?

A

they do contracts, this enhances ventricular filling and cardiac output to a small extent.

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7
Q

where are the AV valves found?

A

between the atria and ventricles,these are inlet valves of the ventricles.

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8
Q

what valve is between the right atrium and right ventricle?

A

tricuspid valve

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9
Q

what valve is between the left atrium and left ventricle?

A

mitral valve

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10
Q

what are semi lunar valves?

A

outlet valves of the ventricles

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11
Q

where is the pulmanory valve located?

A

between the right ventricle and the pulmanory artery

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12
Q

where is the aortic valve located?

A

between the left ventricle and aorta.

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13
Q

what are the four phases of the cardiac?

A

inflow phase
isovolumetric contraction
outflow phase
isovolumetric relaxation

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14
Q

what occurs with valves during the inflow phase?

A

inlet valve is open and outlet valve closed

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15
Q

what occurs with valves during isovolumetric contraction?

A

both inlet and outlet valve are closed, there is no blood flow.

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16
Q

what occurs with valves during the outflow phase?

A

outlet valve is open and inlet valve is closed

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17
Q

what happens to valves during isovolumetric relaxation?

A

both valves vlosed resulting in no blood flow,

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18
Q

which phases are systole?

A

isovolumetric contraction and outflow phase as systole is during contraction of the ventricles

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19
Q

which phases are diastole?

A

inflow phase and isovolumetric relaxation as these are when the ventricles are relaxing.

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20
Q

what is excitation - contraction coupling? how is this caused?

A

the way in which electrical stimulation (depolarisation) is turned into a physical contraction
t-tubules and intercalated discs rapidly transmit action potentials to the myocardium

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21
Q

what happnes to intracellular calcium during the plateau phase?

A

it rises from about 100nm - 1-10 micromoles.

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22
Q

where does the calcium come from that enters?

A

from extracellularly and from also in calcium stores. however the moving around of calcium in stores is difficult.

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23
Q

what does calcium entry cause?

A

it binds and displaces troponin/tropomyosin from actin

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24
Q

what happens when troponin/tropomyosin displaces from actin?

A

myosin contracts actin, this commencing sliding of filaments. the sliding of thin filaments in comparison with thick brings in the ends of the sarcomere.

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25
Q

what should muscle tension be proportional to?

A

should be proportional to the crossbridges

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26
Q

what should crossbridges be proportional to?

A

sarcomere length

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27
Q

what are the thin filaments like in short sarcomeres? what happens when these are drawn out?
what does this make tension proportional to?

A

they are overlapping. when these are drawn out they have more contact with thick filament myosin
this making tension proportional to muscle length.

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28
Q

what happens when the sarcomere is overstretched?

A

there is less contact between thin and thick filaments resulting in less tension

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29
Q

what’s the difference between isometric conditions and isotonic conditions?

A

isometric there is no change in length of the muscle, contraction doesn’t change the length.
isotonic - there’s a change in length however no change in tension

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30
Q

what is tension actually proportional? what are the limits to this?

A

proportional to starting length, the limits are that the muscle can be overstretched this making it hypoeffective

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31
Q

what is Lmax?

A

maximum tension

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32
Q

when is the Lmax of actin?

A

at 2.2 micrometeres

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33
Q

when is Lmax of crossbridges?

A

2.2 micrometers

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34
Q

what is a crossbridge?

A

myosin head with actin

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35
Q

what filling pressure produces a 2.2um sarcomere in the intact heart?

A

10-12mmHg, i.e. pre-systole.

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36
Q

what thinking about length tension relationships what’s it important to remember about different muscles?

A

they have different profiles meaning they have different length tension relationships

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37
Q

when measuring the force-velocity relationship why is an isotonic concentration used with the papillary muscle?

A

as measuring how fast the muscle shortens

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38
Q

what is the pre-load when measuring force-velocity

what is the afterload

A

preload is the stretch applied to the muscle

the after load is what we want the muscle to do, so it is stimulated to lift the afterload.

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39
Q

what is the relationship between preload and maximal force(Po)

A

an increase in preload gives an increase in maximal force. this is because of the length tension relationship.

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40
Q

what is the relationship between preload and velocity for any given afterload?

A

as preload increases, velocity increases.

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41
Q

what happens to Vmax during force-velocity experiments? what does this indicate?

A

remains constant, indicates the contractility of cardiac muscle

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42
Q

when is a change in contractility shown?

A

when the intact heart changes it’s output per beat when the end diastolic volume is constant

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43
Q

what can contractility reflect?

A

can reflect the number of crossbridges that are formed (amount of ca2+ per stimulus) or the qualitative state of the actin/myosin crossbridges (how well they are working)

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44
Q

what are changes in contractility called?

A

positive or negative ionotropc effects

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45
Q

what are changes in rate called?

A

chronotropic effects

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46
Q

what does NorA do to Po and Vmax? what effects is this?

A

increases Po and Vmax, these are positive ionotropic and chronotropic effects.

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47
Q

what does interbeat duration influence?

A

the force of contraction.

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48
Q

what does an increase in frequency result in? when doesn’t this occur

A

an increase in force apart from the first contraction

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49
Q

if there’s an extra stimulus what happens?

A

over the next 4 beats there’s an increase in tension

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50
Q

if a stimulus is missed what happens?

A

over the next three beats there’s an increase in tension

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51
Q

what is the treppe/bowditch staircase

A

as frequency increases, contractility increases.

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52
Q

what happens if there’s a beat missed or extra beat?

A

tension increases

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53
Q

what happens if there is more cytosolic calcium?

A

more crossbridges are formed

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54
Q

what does the amount of ca2+ around the sarcomere depend on?

A

ca2+ entry, Ca2+ stores, Ca2+ pump rate, Ca2+ stores refilling, Ca2+ and tropomysoin interactions, stretch activated Ca2+ channels etc.

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55
Q

Before the P-Wave what does the S.A node do?

A

The S.A node fires action potentials to trigger the atrial muscle to contract

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56
Q

are there heart sounds during atrial contraction?

A

no it is quiet

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57
Q

are there heart sounds during the P-wave?

A

no there’s no sound

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58
Q

what is the blood in the ventricals like during the p-wave? why?

A

a lot of blood present in ventricals during p-wave. This is because during the p-wave the atria are contracting meaning the ventricles are filling with blood.

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59
Q

why is there low pressures in both the left atria and ventrical during the p-wave?

A

because at this point the mitral valve is open meaning there is free flow of blood so pressure in both is the same.

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60
Q

what does the S.A node trigger?

A

atrial muscle contraction

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61
Q

what happens to the pressure when the muscles begin to relax?

A

the pressure decreases.

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62
Q

Why is there a time delay between the P wave and the QRS complex?

A

because there’s a AV node delay

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63
Q

what is occuring from the beginning of the QRS until the end of the T- wave?

A

Ventricular contraction

64
Q

Why is there a dramatic increase in pressure during the QRS complex?

A

because the inlet and outlet valves have shut

65
Q

when can the ‘Lub’ sound be heard?

A

during the closure of the mitral valve

66
Q

what valve closes after the mitral valve?

A

the triscupid valve

67
Q

why is there a rise in pressure in the left atrium during the QRS complex?

A

because there is such a large pressure in the ventricles this causes the mitral valve to bulge back into the atrium.

68
Q

why is it that isovolumetric contraction is occuring during a point during the QRS complex?

A

because the volume of blood in the ventricles stays the same at one point when both inlet and outlet valves are closed.

69
Q

what has to happen for blood to leave the ventricles and enter the Aorta?

A

ventricular pressure has to become greater than aortic in order for the aortic valves to open and allow blood to exit the ventricles.

70
Q

what is isovolumetric ventricular contraction?

A

occurs early systole as the ventricles are contracting however there’s no corresponding volume change at that point.

71
Q

what does it mean by end systolic volume? why does this occur?

A

it’s the volume left in the ventricles after contraction, there’s always some blood left, the volume in the ventricles never drops to 0.

72
Q

why can pressure changes be tracked back to veins?

A

there’s no valves between veins and atria

73
Q

what is jugular venous pressure?

A

indirectly observed pressure over the venous system via visualization of the internal jugular vein.

74
Q

what is postitive blood flow?

A

blood flows towards the aorta

75
Q

what is negative blood flow?

A

blood flowing backwards into coronary circulation

76
Q

when does the aortic valve shut?

A

when pressure in the aorta is greater than the pressure in the ventricles

77
Q

what causes the second heart sound ‘dub’?

A

when the aortic and pulmanory valves shut

78
Q

what happens when the pressure in the left atria is greater than the ventricle?

A

the AV valve opens and the ventricle fills with blood.

79
Q 
during the jugular phase:
what does the a wave represent?
the c wave?
the x descent?
the V wave?
the Y descent?
A

the a wave is created by atrial contraction
c wave = AV valve bulging into the atrium
X descent = ejection phase of blood
V wave= blood flowing back into heart before opening of the AV valve
Y descent = rapid filling of the ventricle.

80
Q

what happens during heart blocks?

A

the conducting pathways are impaired.

81
Q

what happens during first degree heart blocks?

A

there’s a slowing of SA-AV conduction
the PR interval increases
this can be seen as a training effect in athletic training.
these are incomplete heart blocks.

82
Q

what happens during second degree heart blocks?

A

some SA impulses fail to evoke a QRS
wenckeback - PR increases over ~3.5 beats, the 4th PR interval is so long it doesn’t trigger the QRS
repeated pattern - there’s 2:1 PR : QRS or 3:1 etc etc.
again this is an incomplete heart block as still some electrical activity from the SA node = still contracting.

83
Q

what happens during a third degree heart block?

A 
there is a complete heart block
no SA impulses reach AV
can lead to death
can be: no p waves but still has QRS
or can be lots of p waves with a random low rate of QRS
84
Q

does third degree heart block always mean death?

A

no it can also mean there’s a dissociation of chamber contraction.
the atria and ventricles can be acting independantly
this is caused by them being driven by alternative pacemakers.
this can cause atrial contraction to be greater than ventricular.

85
Q

how can alternative pacemakers arise?

A

other cells in the heart can start showing pacemaker activity. (Av node, bundles of hiss, sometimes even the myocardial tissue)

86
Q

what is overdrive supression?

A

where numerous cells in the heart show pacemaker activity however the SA node is going too fast so overdrives the other cells.

87
Q

what is an infranodal block? what is the heart rate and why is it like this?

A

when the blockage is below the AV node

heart rate is 15-35 bpm, it’s this slow as it’s the bundle of hiss taking over the pacemaker role.

88
Q

what are the consequences of 1st degree heart blocks?

A

they are usually benign

89
Q

what are the consequences of 2nd degree heart blocks?

A

can be benign (some can be seen due to intense training) or they may require a pacemaker to be fit.

90
Q

what are the consequences of 3rd degree heart blocks?

A

chamber contractions out of synchrony.
the jugular a waves (atria) may mismatch arterial pulse.
there may be atrial contraction against a close triscupid due to the ventricles contracting, the energy produced by atria may cause pressure to build up and there be a cannon wave in jugular (blood back into veins)
can be reduced perfusion to tissues causing dizziness and fainting if cerebral perfusion is comprimised.

91
Q

what are the consequences of branch block?

A

there may be delayed contraction as the electrical activity down a branch slowed. this can lead to a longer QRS.

92
Q

what happens during sick sinus syndrome?

A

there’s impaired SA node firing

93
Q

who discovered the SA node?

A

Keith arthur.

94
Q

what happens in the familial types of sick sinus? what does this effect?

A

there is an Na v1.5 mutation, this effects Na channel.

95
Q

what is wolff-parkinson-white syndrome? what causes this?

A

it is an arrythmia.

caused by an abnormal connection between the atria and ventricles, this causes a short circuit.

96
Q

what are the cardiac effects caused by wolff-parkinson-white syndrome? what may it also form?

A

The AV delay is short circuited.
this causing ventricular pre-excitation.
the p wave is normal, there’s a short PR interval, a delta wave and a prolonged QRS.
may also form a transcient refractory block

97
Q

what happens during a transcient refractory block?

A

fibrillation is elicited via circus movement.

98
Q

what can circus movement also be called? why can this cause confusion?

A

re entry

can cause confusion as this is also the name for when blood is flowing the wrong way.

99
Q

why is there usually no re-excitation of myocardial cells in the atria?

A

because there’s normally a long refractory period

100
Q

what can happen to myocardial cells during circus movement? what can this cause?

A

they can be re-excited due to there being no refractory period. this can cause atrial flutter and atrial fibrillation.

101
Q

during chronic cardiac failure what is unable to happen? what does this do?

A

there’s an inability to perfuse the tissue at normal filling pressures.
this reduces contractility.

102
Q

what happens to the ventricular function curve for some one with chronic cardiac failure?

A

there’s a decrease in the ejection fraction.

103
Q

what is chronic cardiac failure often called? why is it called that?

A

congested heart failure.

this is because it is congested with blood.

104
Q

what is chronic cardiac failure evoked by?

A

infarct (dead tissue), poor energy production/ poor energy utilization, ca2+ transport.

105
Q

what happens to the at rest stroke volume during chronic cardiac failure?

A

stroke volume is maintained until severe heart failure.

106
Q

what happens to those with chronic cardiac failure during exercise?

A

there is no raise in stroke volume.
this is because they are already at the top of the frank starling curve due to the myocardial already being stretched at rest.
there’s a decreased catecholamine response, this would normally increase HR.
there’s a decrease in NorAdrenaline.(normally increases heart rate)
plasma catecholamines increase.

107
Q

what are the early mechanisms for compensation during chronic cardiac failure?

A

peripheral vasoconstriction (especially in veins as so much blood in veins.
there’s an increase in sympathetic activity.
an increase in angiotensin II activity - this can help supply and protect vital organs.
there’s a decrease in renal flow, this increasing Na/ water retention. - this increases plasma volume and an increase in volume results in increased filling and output.

108
Q

during the progression of chronic cardiac failure, what does cardiac dilation cause? what does this lead to?

A

it impairs muscle and valve function as the cusps don’t come back together properly. this leads to regurgitation and re-entry of blood.

109
Q

what promotes oedema during chronic cardiac failure?

A

and increase in ventricular pressure and a decrease in plasma COP

110
Q

what happens if Right ventrical pressure > Left ventrical pressure?

A

there’s a pressure build up in the lungs.

= oedema in the lungs.

111
Q

what happnes if the left ventrical pressure > right ventrical pressure?

A

there are peripheral oedemas, these tend to be at the end of limbs.

112
Q

if there is an oedema in either the lung or the periphery does this mean one of the ventricles is failing?

A

no, both can be failing, there could just be one failing more than the other.

113
Q

what is the aim of the treatment for chronic cardiac failure?

A

to reduce cardiac work.

114
Q

what are the ways in which to treat CCF? what drugs are used?

A

decrease plasma volume and cardiac dilations
- diuretics
vaso and venodilation - this meaning more blood is away from the heart - reduced cardiac output, improves contractility.
digitoxin, increases Ca2+ retention and contractility.

115
Q

what kind of syndromes are long and short QT syndromes?

A

inherited syndromes.

116
Q

what is the QT interval?

A

the start of the QRS to the end of the T wave

this is the start of ventricular depolarisation to the end of ventricular repolarisation.

117
Q

what is happening during short QT?

what is happening during a long QT?

A 
short = repolarisation is accelerated
long = repolarisation is delayed.
118
Q

where are the changes seen in short and long QT syndrome (electrocardiogram)

A

Changes seen in T-wave

not much change seen to P wave and QRS complex.

119
Q

how long is the ventricular AP normally?
how long is it if it’s long?
how long is it if it’s short?

A

normally 0.36s
long 0.45 s
short 0.34 s

120
Q

what are the phases of ventricular action potential?

A

phase 1 - partial repolarisation
phase 2 -plateau
phase 3 -repolarisation
phase 4 - resting.

121
Q

what channels are involved during depolarisation?

A

sodium channels

122
Q

what channel is involved in phase 1 of ventric repol -partial repolarisation

A

a K channel (Ito)

123
Q

which channels are involved in phase 2 of ventric repol - the plateau phase

A

sodium and calcium channels - mainly calcium

124
Q

what kind of channels are involved in phase 3 of ventric repol -which is repolarisation
which channels?
why is having more than one channel a positive

A

K channels
- IKS, IKR, IKur, IKATP, IKACh (don’t need to learn these)
there’s multiple channels meaning if one channel doesn’t work properly there’s still repolarisation. however repolarisation is altered

125
Q

what happens during triggered activity of the ventricles?

A

there’s an additional beat after the depolarisations reach threshold.
there’s normal repolarisation but they sometimes can reach threshold again before they should due to changes in times.

126
Q

what is ventricular tachycardia?

A

there’s an increase in contraction of ventricles but not in the atria

127
Q

what is ventricular fibrilation?

A

no co-ordinated contractions of the ventricles.

128
Q

what happens during re-entrant excitation?

what can this cause?

A

this effects different layers of cells (multicellular)
this means some cells are effected and delayed.
these then impact on the cells that have already depolarised.
this means there’s temporal and spacial dispersion of refractory period, means there’s re-entry and AP proppagation.
this can cause ventricular tachycardia or ventricular fibrillation.

129
Q

what happens to the QT interval during long QT?

what can this cause?

A

prolonged QT interval

can cause synscope or even sudden death

130
Q

how many forms of long QT are there?

A

there are 12 forms of long qt

131
Q

what kind of mutation is involved in long QT?

A

can be either gain of function or loss of function depending on what protein is effected.

132
Q

what happens in a self limiting ECG of long QT?

A

there’s a short and specific duration, the heart then corrects itself to the right ECG.

133
Q

what happens to the ECG of someone with Long QT that is leading to ventricular fibrilation?
what is required when this happens?

A

it is extended with lack of co-ordination of electrical activity in ventricular myocytes.
there’s no ventricular contraction
defibrillation is needed when this occurs.

134
Q

describe the rarity of LQT1 to LQT12

A

goes from LQT1 being the most common to LQT12 being the rarest.

135
Q

give 3 examples of voltage gated potassium channels in LQT…. what kind of mutations occur in these?

A

LQT1 (Kv7.1alpha)
LQT2 (Kv11.1alpha)
LQT5 (minK)
all of these occur loss of function mutations.

136
Q

what are the other two names of LQT1?

A

Kv7.1alpha and KCNQ1

137
Q

what is the structure of LQT1 like?

A

it has 6 transmembrane domains, a pore region and a voltage sensing region.

138
Q

how many LQT1 subunits are needed to make a channel?

A

4

139
Q

what kind of mutation is it in LQT1?
is the disease present if dominant negative?
is the disease present if heterozygote?
explain….

A

it is a loss of function mutation.
if dom negative then have disease
if heterozygote then still have the disease.
this is because 50% of the subunits are mutants, if there are any mutants in the channel then the whole channel won’t function.

140
Q

which long QT mutations effect the ear? how do these effect the ear? explain.

A

KCNQ1(LQT1)and KCNE1 (minK/LQT5)
because there is a channel that is Q1/E1 channel
this channel is made up of 4 X Q1 subunits and 1 X E1 subunits.
if have a mutation in either LQT1 or LQT5 will have similar effects as both loss of function mutation in the same channel.

141
Q

what happens if there’s mutations in the Q1/E1 in the ear?

A

if Q1/E1 is removed / mutated there is no longer a potassium secretion in the ear.
this leads to the reissners membrane in the ear to collapse as there’s no endolymph in the ear due to lack of potassium secretion.

142
Q

what does a loss of function mutation in a potassium channel ultimately do?

A

it effects repolarisation, there’s a delay in repolarisation and an extension of the QT interval.

143
Q

what happens when there’s a gain of function in the Na+ and Ca2+ channels (long QT)

A

Na+ channels open but don’t close as quickly as they should.
this means there’s a high Na+ potential pushing the Vm closer to the Nernst for Na+.
this means that the K+ channels have to work for longer to repolarise.
the Ca2+ channel also doesn’t close as quickly.

144
Q

what drugs can be used to treat long QT syndrome?

A

B-blockers and atenolol

145
Q

what kind of drugs are beta-blockers?

A

it’s a class 2 antidysrhymic drug

146
Q

how does atenolol work?

are ther conta-indications?

A

it’s a B1 selective antagonist, whihc means there’s a cAMP linked receptor, this has negative chronotrophic and ionotrophic action.
cannot be given to some one with an obstructive lung disease as there’s a risk of broncoconstriction.

147
Q

what happens to the QT interval with short QT syndrome?

A

it’s reduced

148
Q

what can short QT lead to?

A

arrythmias, palpitations, synscope, ventricular fibrilation and sudden death.

149
Q

how many forms are there of short QT?

A

5

150
Q

what kind of mutations are there in short QT?

A

gain of function and loss of function.

151
Q

how does short QT effect the patients ECG?

A

there’s a short/ absent ST segment
there’s tall/peaked T wave
the QT interval is fixed, doesn’t shorten during exercise.

152
Q

which voltage gated potassium channels are effected in short QT? what mutations do these undergo?

A

Kv11.1alpha (SQT1) Kv7.1alpha (SQT2) Kir2.1alpha (SQT3)

these incur a gain of function mutation.

153
Q

which voltage gated calcium channels are effected in short QT? what mutations do these undergo?

A

Cav1.2alpa (SQT4) and Cav1.2beta2 (SQT5)

thes incur a loss of function mutation

154
Q

how do the channel mutations in short QT compare to long QT?

A

in short the potassium channels gain function where as in long they lose function,
in short the calcium channel lose function where as in long QT they gain function.

155
Q

what is the effect of gaining function in potassium channels?

A

there’s enhanced repolarisation

156
Q

what is the effect of losing function of calcium channels?

A

the calcium channels usually maintain plateu phase, but this makes the plateau phase shorter as the calcium channels aren’t opening, this makes repolarisation earlier and faster.

157
Q

what’s the treatment for short QT?

A

an implant defibrillator.

research also suggests that quindin may be effective as it is a K channel blocker as this may lengthen the QT.

physiology and pharmacology (7 decks)

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