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Cardiovascular > Physiology > Flashcards

Physiology Flashcards

1
Q

5 general features of cardiac muscle

A 
Myogenic
Striated
Cells electrically coupled
Mainly oxidative metabolism
AP triggers calcium-induced calcium release
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2
Q

Main cell types of myocardium

A 
Cardiac fibroblasts
Myocytes
Endothelial cells
Vascular smooth muscle cells
Neurons
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3
Q

Function of cardiac fibroblasts

A

Secrete and maintain connective tissue fibres

Majority of cells in the heart

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4
Q

Function of myocytes

A

Provide majority of myocardial mass
Carry out contraction
Can be specialised e.g. purkinje and nodal cells
About 30% of heart cells - 20 microns thick and 100 microns long

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5
Q

Things you will see in a longitudinal section of myocardium

A

Striations
Endocardial spaces containing collagen
Intercalated discs at intercellular junctions

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6
Q

3 types of junction in the heart

A

Gap junctions
Intermediate junctions
Desmosomes

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7
Q

Extracellular matrix composition

A 
60% vascular
23% glycocalyx-like substance
7% connective tissue cells
6% empty space
4% collagen
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8
Q

Sarcolemma

A

Forms a permeability barrier between the inside and outside of the cell
Continuous with t-tubules

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9
Q

Glycocalyx

A

Outer surface of sarcolemma abundant in acidic mucopolysaccharides and sialic acid residues
Divided into surface coat and external lamina

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10
Q

T-tubules

A

Invaginations of sarcolemma
Rich in L-type calcium channels (DHPRs)
Bigger than in skeletal muscle

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11
Q

Caveolae

A 
Small invaginations of sarcolemma
Scaffolding proteins (cavoelin-3) and signalling molecules (NOS and PKC) found here
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12
Q

Sarcoplasmic reticulum

A

Intracellular membrane-bound compartment
Internal calcium store
Junctions with t-tubules and external sarcolemma
Junctional sarcoplasmic reticulum contains ryanodine receptors or calcium release channels
Contains SERCA and calseqeuestrin

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13
Q

SERCA

A

Sarcoplasmic reticulum calcium ATPase
Responsible for re-uptake of calcium into sarcoplasmic reticulum
Phospholamban modulates activity

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14
Q

Calsequestrin

A

Calcium buffer (calcium sequester)

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15
Q

Excitation-contraction coupling

A

The process by which electrical changes at the surface membrane lead to changes in intracellular calcium levels which activate contraction

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16
Q

5 steps of EC coupling

A

1) AP from adjacent cell spread across sarcolemma
2) Depolarisation opens L-type calcium channels
3) Calcium influx opens ryanodine receptors causing sarcoplasmic reticulum calcium release
4) Calcium ions bind to TnC and initiate crossbridge cycling
5) Contraction

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17
Q

Calcium-induced calcium release

A

DHPRs form functional voltage-gated calcium channels in cardiac muscle
Depolarisation opens channels and influx of calcium triggers further calcium release from sarcoplasmic reticulum via ryanodine receptors

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18
Q

2 sources of calcium to activate contraction

A

1) extracellular
- voltage dependent calcium channels in the sarcolemma membrane
- passive leakage channels in the sarcolemma
2) intracellular
- sarcoplasmic reticulum
- mitochondria

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19
Q

L-type calcium channels (DHPRs) stimulation

A

Catecholamines

Depolarisation

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20
Q

L-type calcium channels (DHPRs) function

A

Carries inward calcium current
Contributes to AP plateau
Triggers EC coupling

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21
Q

L-type calcium channels (DHPRs) inhibition

A

Sarcoplasmic reticulum calcium release
Calcium channel blockers
Magnesium
Low plasma calcium concentration

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22
Q

High sarcoplasmic reticulum calcium load leads to:

A

Increased calcium available for release

Enhanced gain of EC coupling

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23
Q

Microscopic sarcoplasmic reticulum release events

A

Calcium sparks - summate to make the whole cell calcium transient
Amplitude and number of calcium sparks determines the calcium transient amplitude

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24
Q

Myocyte relaxation

A

Occurs when intracellular calcium concentration is reduced and calcium unbinds from TnC
Bulk of calcium pumped back into sarcoplasmic reticulum for storage
Small amount leaves cell in exchange for sodium

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25
Q

4 important calcium transport proteins

A

SERCA (calcium into sarcoplasmic reticulum)
SELCA (calcium out of cell)
NCX (calcium out of cell, sodium in)
Mitochondrial uniporter (calcium into mitochondria)

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26
Q

If calcium efflux is decreased:

A

Calcium accumulates in cell leading to

  • higher sarcoplasmic reticulum calcium content
  • increased calcium extrusion to balance influx
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27
Q

SELCA pump

A

Sarcolemma calcium ATPase pump
Minor contributor to calcium extrusion at rest
Electroneutral - brings protons into cell

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28
Q

Electrogenic sodium calcium exchanger

A 
Reverse mode (calcium entry) follows depolarisation
Forward mode (calcium exit) promoted by repolarisation
Contributes to myocyte membrane potential, both depend on electrochemical gradient
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29
Q

Two ways that calcium can be removed from the cytoplasm

A

1) Extrusion across the sarcolemmal membrane

2) Sequestration into the sarcoplasmic reticulum

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30
Q

3 properties of cardiac myocytes

A

Excitability
Conductivity
Automaticity

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31
Q

Cells with a fast excitability response

A

Atrial cells
Ventricular cells
Fast parts of specialised conduction system

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32
Q

General fast response action potential

A 
Phase 0: Rapid depolarisation
Phase 1: Early repolarisation
Phase 2: Plateau
Phase 3: Repolarisation
Phase 4: Resting
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33
Q

Phase 0 key points

A

-90 mV resting potential to -70 mV threshold potential
Rapid increase in sodium permeability causes fast inward sodium current
Causes upstroke

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34
Q

Phase 1 key points

A

Early repolarisation to near 0 mV

Transient outward potassium current

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35
Q

Phase 2 key points

A

Sodium channels inactivate
Cell becomes refractory
Inward and outward currents nearly balanced
Slow inward calcium current and outward potassium current

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36
Q

Phase 3 key points

A

Outward potassium currents

  • iK switched on after delay
  • iK1 reactivated as membrane potential drops
  • iK,ATP activated when ATP drops
  • iK,ACh activated when ACh drops
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37
Q

Phase 4 key points

A

iK1 high potassium conductance defines resting potential

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38
Q

Timespan of fast response AP

A 
Phases 0 - 1 = about 10 msec
Phases 1 - 2 = about 100 msec
Phases 2 - 3 = about 150 msec
Phases 3 - 4 = about 50 msec
Overall, about 290 - 310 msec
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39
Q

Ions of calcium pump

A

Outward current

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40
Q

Ions of Na/Ca exchanger

A

Ongoing
3Na in, 1 Ca out
Electrogenic
At resting potential, current is inward and depolarising

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41
Q

Ions of Na/K ATPase

A

3Na out, 2K in
Electrogenic
Current is outward and repolarising

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42
Q

Slow response cells are driven by:

A

Calcium, not sodium

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43
Q

2 reasons by slow response cells might not be driven by sodium

A

1) sodium channels already inactive

2) no sodium channels present

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44
Q

Slow response cell locations

A

SA node

AV node

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45
Q

Slow response cell key points

A

Can be pacemaker or non-pacemaker
Resting potential around 55 mV
Similar to fast response but phase 0 is slow upstroke due to slow inward calcium current

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46
Q

4 refractory periods

A

1) Absolute refractory period
2) Relative refractory period
3) Supranormal period
4) Full recovery time

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47
Q

Absolute refractory period

A

Time when membrane cannot be re-excited

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48
Q

Relative refractory period

A

Need larger than normal stimulus to get propagated AP (slow propagation)

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49
Q

Supranormal period

A

Get propagated AP from weaker than normal stimulus (slow propagation)

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50
Q

Full recovery time

A

May extend beyond return to resting potential

Time dependent

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51
Q

Refractoriness over long periods advantage

A

Prevents tetanising of heart

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52
Q

Interval-duration relationship

A

Duration of action potential is determined partly by preceding diastolic interval
Rapid heart rate = shorter AP
Related to properties of various ion channels

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53
Q

Conductivity of cardiac muscle cells

A

Myogenic, not neurogenic
Do not contract in response to neural signal
All cells interconnected
Electrical activation spreads through myocardium from cell to cell
Due to electrical coupling between neighbouring cells

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54
Q

Pacemaker cells

A

SA node
Some cells around AV node
His-Purkinje network

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55
Q

Automaticity

A

Ability to initiate electrical impulse through own pacemaker activity or diastolic depolarisation

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56
Q

Pacemaking is based on:

A

The membrane slowly depolarising in phase 4

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57
Q

3 mechanisms for altering intrinsic rate of pacemaker discharge

A

Alter rate of depolarisation
Alter threshold potential
Alter maximum diastolic potential

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58
Q

Funny current

A

Mainly inward sodium current
Activated at negative potentials when the cell has repolarised
Some K+ current

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59
Q

Conduction velocity of SA node

A

Less than 0.01 m/s

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60
Q

Conduction velocity of AV node

A

0.02 - 0.05 m/s

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61
Q

Conduction velocity of bundle branches and purkinje network

A

2.0 - 4.0 m/s

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62
Q

AV delay is due to:

A

Slow conduction in the AV node

Activation subject to block because of this

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63
Q

ECG

A

Sum of electrical activity of heart
Voltage over time recording
Electrodes measure potential difference between different sites on the body caused by the electrical activity of the heart

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64
Q

ECG electrodes don’t need to be on the heart because:

A

Body tissues act as conductors

65
Q

3 main deflections on ECG

A

P wave - atrial depolarisation
QRS complex - ventricular depolarisation
T wave - ventricular repolarisation

66
Q

P wave

A

Atrial depolarisation
Relatively small mass therefore small height deflection
Slow, therefore wide

67
Q

PR segment

A

Isoelectric

Reflects time taken for wave to pass through AV node, AV bundle and bundle branches

68
Q

QRS complex

A

Ventricular depolarisation
Greater magnitude than P wave due to greater mass of tissue
Relatively shorter than P wave because of rapid spread to Purkinje fibres
Atrial repolarisation present, but not visible

69
Q

PR interval

A

Reflects total time for wave to pass from atria to ventricles

70
Q

ST segment

A

Isoelectric
All depolarised therefore no moving wavefront
Plateau of ventricular AP

71
Q

T wave

A

Asynchronous ventricular repolarisation

Slower than depolarisation

72
Q

QT interval

A

Reflection of ventricular action potential duration

73
Q

3 things that affect electrode recording

A

Magnitude of charges
Orientation of dipole and electrodes
Distance between dipole and electrodes

74
Q

Q wave

A

Ventricular septum depolarising

75
Q

R wave

A

Ventricular apex depolarising

76
Q

S wave

A

Ventricular base depolarising

77
Q

T wave orientation

A

Ventricular depolarisation is endocardium to epicardium, therefore +ve QRS
Ventricular repolarisation is epicardium to endocardium, therefore +ve T wave

78
Q

Limitations of ECG

A

Body has varying conductivity

Single dipole not good representation of wavefront

79
Q

Bipolar system

A

Measures difference between two electrodes

80
Q

Three bipolar limb leads

A

Lead I = LA - RA
Lead II = LL - RA
Lead III = LL - LA

81
Q

Einthovens law

A

Equivalent to connecting the electrodes to 3 corners of an equilateral triangle with the heart at the centre
At any instant during the cardiac cycle, I + III = II

82
Q

Three augmented unipolar limb leads

A

aVR, aVL, aVF

83
Q

Unipolar chest leads

A

V1 - V6

Look at heart from front and side in the horizontal plane

84
Q

Calibration signal is always:

A

1 mV

85
Q

Normal QR axis values

A

-30 to +110 degrees

0 degrees = horizontal

86
Q

Calculation of mean QRS vector

A

Biggest +ve minus biggest negative (both from 0)

87
Q

EC coupling summary

A

Depolarisation via DHPR or L-type calcium channels opening
Ryanodine receptors release sarcoplasmic reticulum calcium
Crossbridge cycling begins
Relaxation occurs when cytosolic calcium returns to resting levels

88
Q

Result of SERCA inhibition

A

Slower contraction

89
Q

Result of activity on calcium release

A

Phospholamban is phosphorylated by PKA, can no longer inhibit SERCA, calcium release is quicker

90
Q

3 key points about the electrogenic NCX

A

1) Reverse mode (calcium entry) follows depolarisation
2) Forward mode (calcium exit) is promoted by repolarisation
3) Carries one net charge per cycle and contributes to myocyte membrane potential

91
Q

How do we know that force of contraction varies?

A

The heart has to pump out all the blood that comes in, but all muscle fibres already contribute to contraction so we can’t recruit more. Therefore the heart must be modulating the rate of activation of the fibres or the contractility of the actin or myosin.

92
Q

4 ways to modulate force

A

Increase ventricular stretch
Increase automaticity
Use neurotransmitters to alter rate and calcium handling
Inotropic drugs

93
Q

Two main ways to change the strength of contraction

A

Alter calcium transient (amplitude and duration)

Alter myofilament calcium sensitivity

94
Q

Frank-Starlings Law

A

Increase in end diastolic ventricular volume increases stroke volume via stretch induced increase in cardiac contractility

95
Q

Inotropy

A

Strength of muscular contraction

96
Q

Chronotropy

A

Heart rate and rhythm

97
Q

Lusitropy

A

Muscular relaxation

98
Q

6 factors that can increase myofilament calcium sensitivity

A 
Alkalosis
Longer sarcomeres
Lower catecholamines
Decreased ATP
Caffeine
Lower phosphate
99
Q

4 important effects of beta-adrenergic stimulation

A

Decreased myofilament calcium sensitivity
Increased inner calcium
Enhanced sarcoplasmic reticulum calcium-ATPase rate
Altered ryanodine receptor gating

100
Q

Beta adrenergic agonist mechanism

A

Stimulate adenylyl cyclase to increase cAMP levels

Activates PKA which phosphorylates phospholamban, decreases troponin I and increases sarcolemma calcium channels

101
Q

Biphasic response to stretch

A

Rapid response
Slow force response
Increase in amplitude of calcium transient

102
Q

Effect of increased rate of AP activation

A

Less time for calcium extrusion
Decrease in average membrane potential
Decreased overall calcium efflux via NCX
Increased intracellular sodium and calcium

103
Q

Parasympathetic effects on heart

A

Decreased SA node discharge rate

Decreased force

104
Q

Sympathetic effects on heart

A

Increase SA node discharge rate
Increase calcium influx
Increased sarcoplasmic reticulum pump rate
Decreased sensitivity of troponin for calcium

105
Q

Regulation of stroke volume and heart rate

A

Adrenaline and sympathetic activity:
Increases contractility which increases stroke volume which increases CO
Increases heart rate which increases CO
Increased preload also increases stroke volume and therefore CO

106
Q

3 main force modulation drugs

A

Cardiotonic steroids
Sympathomimetics
Bypyridines

107
Q

Cardiotonic steroids

A

Digoxin

Inhibit sodium pump therefore increase intracellular sodium which reduces calcium extrusion via sodium/calcium pump

108
Q

Sympathomimetics

A

Act via beta-1 receptors

Can get desensitised to these

109
Q

Bypyridines

A

Act via phosphodiesterase which increases cAMP

Limited use

110
Q

3 current therapies to reverse the increase in cardiac dimensions

A

NO - relaxation
Diuretics - decrease blood volume
ACE inhibitors - depress angiotensin axis

111
Q

Events of the cardiac cycle

A 
Atrial systole
Isovolumic contraction
Rapid ejection
Reduced ejection
Isovolumic relaxation
Rapid filling
Reduced filling
112
Q

Atrial systole

A

Atrial depolarisation starts soon after start of P wave
Top up of ventricle by atrial contraction
Can contribute to ventricular filling depending on heart rate
‘a’ wave

113
Q

Isovolumic contraction

A

Onset coincides with peak of R wave
Ventricular volume unchanged
Closure of AV valves causes 1st heart sound
‘c’ wave

114
Q

Rapid ejection

A

Semilunar valve opens
Rapid increase in aortic flow
Rapid decrease in left ventricle volume
Atrial pressure drops

115
Q

Reduced ejection

A

Runoff from aorta to periphery exceeds left ventricular output so aortic pressure drops, but just about left ventricular pressure so ejection is still occurring
Aortic flow drops
Atrial pressure rises
End systolic volume

116
Q

End systolic volume

A

Volume of blood left after contraction finishes
About 60 mLs
55 - 75% LV blood has been ejected at this point

117
Q

Isovolumic relaxation

A

Beginning of diastole
Aortic valve closes
Produces notch in aortic pressure curve (incisura)
Closing of semilunar valves produces 2nd heart sound
Rapid fall in left ventricular pressure
Aortic pressure remains high

118
Q

Rapid filling

A

LA pressure greater than LV pressure causing AV valve to open
Rapid increase in LV volume
3rd heart sound sometimes heard

119
Q

Slow filling

A

Diastasis
Equalised pressures
Slow rise in atrial and ventricular pressures

120
Q

3 positives of ECG

A

Non-invasive
Fast
Measures cardiac function

121
Q

Venous pulse wave

A 
Upwards deflections:
'a' = atrial contraction
'c' = ventricular contraction
'v' = venous filling
Downwards deflections:
'x' = atrial relaxation
'y' = ventricular filling
122
Q

Valve openings and closings

A

Mitral valve closes just before tricuspid
Pulmonary valve opens before aortic
Aortic valve closes before pulmonary
Tricuspid opens before mitral
Right ventricle valves open sooner and close later due to differences in electrical activation and pressures

123
Q

1st heart sound

A

AV valve closure at onset of ventricular systole

Low frequency

124
Q

2nd heart sound

A

Closure of semilunar valves
Higher frequency but shorter duration
Splitting of second heart sound occurs when pulmonary valve closes after aortic

125
Q

3rd heart sound

A

Early diastole
Rapid filling of ventricle causes wall vibrations
Can be heard in healthy children or in ventricular failure

126
Q

3 reasons a murmur might be heard

A

Regurgitation
Mitral valve prolapse
Stenosis

127
Q

LA pressure measurement

A

Fluid filled catheter with balloon on the end inserted into pulmonary artery
Balloon wedges and blocks channel, stopping flow
Pressure seen is representative of LA

128
Q

2 measurements of cardiac output

A

Fick method
- based on conservation of mass
- requires arterial puncture
- indicator dilution using dye
Thermodilution
- indicator dilution technique using cold saline
- measures downstream temperature change instead of dye concentration

129
Q

Emphysema and vascular resistance

A

Increases pulmonary vascular resistance
Much of lung tissue destroyed causing high vascular resistance
To maintain flow, RV increases pumping pressure leading to RV hypertrophy and eventually failure

130
Q

Wolff-Parkinson White Syndrome

A

Pre-excitation syndrome where ventricles are electrically activated earlier than normal
Accessory pathway is abnormal connection between atria and ventricles which does not have delaying properties of AV node

131
Q

ECG properties of WPW

A

Normal sinus rhythm
Shortened PR interval
Wide QRS complex
Delta wave

132
Q

Symptoms of WPW

A

Ventricular tachyarrhythmia
Syncope
Palpitations
Small risk of sudden death

133
Q

Treatment of WPW

A

Drugs to control fast rhythms

Ablation of accessory pathway

134
Q

Long QT syndrome

A

Abnormally long delay between depolarisation and repolarisation of ventricles
Drug-induced or genetic

135
Q

Drug induced LQTS

A

Anti-arrhythmics
Antihistamines
Potassium channel blockers

136
Q

Genetic LQTS

A

Mutation in gene for ion channels prolongs duration of ventricular action potential which lengthens the QT interval

137
Q

Hyperkalaemia ECG

A

Tall, peaked T waves due to faster repolarisation

138
Q

Hypokalaemia ECG

A

Flat T waves due to slower depolarisation

139
Q

Ventricular and atrial hypertrophy ECG

A

Bigger waves on all leads

140
Q

Hypercalcaemia ECG

A

Shortened QT interval due to reduced action potential duration

141
Q

Hypocalcaemia ECG

A

Lengthened QT interval due to increased action potential duration

142
Q

Digitalis ECG

A

ST segment depression
T wave inversion
PR interval prolongation

143
Q

Sequence of changes of Q-wave infarction

A 
Tall peaked T waves
ST segment elevation
Reduced R wave amplitude
T wave inversion
Pathological Q waves
ST segment returns to normal
T waves often return to normal (within weeks)
144
Q

T wave changes in MI

A 
Tall and peaked
Earliest sign
Localised to leads facing areas of injury
5-30 minutes after onset
Later, symmetrically inverted
145
Q

ST segment changes in MI

A

Elevation often earliest observed sign
Seen in leads facing infarcted area
Often followed by definitive QRS changes
May return to normal

146
Q

QRS changes in MI

A

Low R wave voltages and pathological Q waves in local area
Wavefronts coming toward electrode reduced or absent
Wavefronts moving away from electrode emphasised

147
Q

Reciprocal changes in MI

A

In leads opposite those facing the infarct, ST segment depression and tall T waves

148
Q

Preload

A

Degree of filling

Stretch of muscle just before contraction

149
Q

Afterload

A

Pressure against which the ventricle contracts

150
Q

Four determinants of ventricular performance

A

Preload
Afterload
Inotropic state
Heart rate

151
Q

Inotropic state

A

Intrinsic ability of myocardium to contract with given preload and afterload

152
Q

Chronotropic state

A

Heart rate

Increased HR = increased CO but decreased SV

153
Q

Factors that affect preload

A 
Blood volume
Venous tone
Posture
Heart rate
Atrial contraction
Intrathoracic pressure
Ventricular compliance
154
Q

Factors that affect afterload

A

Systemic pressure
Vasoconstriction
Aortic stenosis
Ventricular stress

155
Q

Factors that affect inotropic state

A 
ANS
Catecholamines
Force-frequency relation
Action potential changes
Cardiomyopathy
Inotropic drugs
156
Q

Factors that affect heart rate

A

ANS

Catecholamines

157
Q

Ejection fraction

A

(EDV - ESV) / EDV

x 100

158
Q

Normal ejection fraction

A

55-60% at rest
85% during exercise
<50% = depressed contractility

159
Q

Stroke work

A

about MAP x SV

Cardiovascular (6 decks)

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