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Physiology Flashcards

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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
4 important calcium transport proteins
SERCA (calcium into sarcoplasmic reticulum) SELCA (calcium out of cell) NCX (calcium out of cell, sodium in) Mitochondrial uniporter (calcium into mitochondria)
26
If calcium efflux is decreased:
Calcium accumulates in cell leading to - higher sarcoplasmic reticulum calcium content - increased calcium extrusion to balance influx
27
SELCA pump
Sarcolemma calcium ATPase pump Minor contributor to calcium extrusion at rest Electroneutral - brings protons into cell
28
Electrogenic sodium calcium exchanger
``` Reverse mode (calcium entry) follows depolarisation Forward mode (calcium exit) promoted by repolarisation Contributes to myocyte membrane potential, both depend on electrochemical gradient ```
29
Two ways that calcium can be removed from the cytoplasm
1) Extrusion across the sarcolemmal membrane | 2) Sequestration into the sarcoplasmic reticulum
30
3 properties of cardiac myocytes
Excitability Conductivity Automaticity
31
Cells with a fast excitability response
Atrial cells Ventricular cells Fast parts of specialised conduction system
32
General fast response action potential
``` Phase 0: Rapid depolarisation Phase 1: Early repolarisation Phase 2: Plateau Phase 3: Repolarisation Phase 4: Resting ```
33
Phase 0 key points
-90 mV resting potential to -70 mV threshold potential Rapid increase in sodium permeability causes fast inward sodium current Causes upstroke
34
Phase 1 key points
Early repolarisation to near 0 mV | Transient outward potassium current
35
Phase 2 key points
Sodium channels inactivate Cell becomes refractory Inward and outward currents nearly balanced Slow inward calcium current and outward potassium current
36
Phase 3 key points
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
37
Phase 4 key points
iK1 high potassium conductance defines resting potential
38
Timespan of fast response AP
``` 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 ```
39
Ions of calcium pump
Outward current
40
Ions of Na/Ca exchanger
Ongoing 3Na in, 1 Ca out Electrogenic At resting potential, current is inward and depolarising
41
Ions of Na/K ATPase
3Na out, 2K in Electrogenic Current is outward and repolarising
42
Slow response cells are driven by:
Calcium, not sodium
43
2 reasons by slow response cells might not be driven by sodium
1) sodium channels already inactive | 2) no sodium channels present
44
Slow response cell locations
SA node | AV node
45
Slow response cell key points
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
46
4 refractory periods
1) Absolute refractory period 2) Relative refractory period 3) Supranormal period 4) Full recovery time
47
Absolute refractory period
Time when membrane cannot be re-excited
48
Relative refractory period
Need larger than normal stimulus to get propagated AP (slow propagation)
49
Supranormal period
Get propagated AP from weaker than normal stimulus (slow propagation)
50
Full recovery time
May extend beyond return to resting potential | Time dependent
51
Refractoriness over long periods advantage
Prevents tetanising of heart
52
Interval-duration relationship
Duration of action potential is determined partly by preceding diastolic interval Rapid heart rate = shorter AP Related to properties of various ion channels
53
Conductivity of cardiac muscle cells
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
54
Pacemaker cells
SA node Some cells around AV node His-Purkinje network
55
Automaticity
Ability to initiate electrical impulse through own pacemaker activity or diastolic depolarisation
56
Pacemaking is based on:
The membrane slowly depolarising in phase 4
57
3 mechanisms for altering intrinsic rate of pacemaker discharge
Alter rate of depolarisation Alter threshold potential Alter maximum diastolic potential
58
Funny current
Mainly inward sodium current Activated at negative potentials when the cell has repolarised Some K+ current
59
Conduction velocity of SA node
Less than 0.01 m/s
60
Conduction velocity of AV node
0.02 - 0.05 m/s
61
Conduction velocity of bundle branches and purkinje network
2.0 - 4.0 m/s
62
AV delay is due to:
Slow conduction in the AV node | Activation subject to block because of this
63
ECG
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
64
ECG electrodes don't need to be on the heart because:
Body tissues act as conductors
65
3 main deflections on ECG
P wave - atrial depolarisation QRS complex - ventricular depolarisation T wave - ventricular repolarisation
66
P wave
Atrial depolarisation Relatively small mass therefore small height deflection Slow, therefore wide
67
PR segment
Isoelectric | Reflects time taken for wave to pass through AV node, AV bundle and bundle branches
68
QRS complex
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
PR interval
Reflects total time for wave to pass from atria to ventricles
70
ST segment
Isoelectric All depolarised therefore no moving wavefront Plateau of ventricular AP
71
T wave
Asynchronous ventricular repolarisation | Slower than depolarisation
72
QT interval
Reflection of ventricular action potential duration
73
3 things that affect electrode recording
Magnitude of charges Orientation of dipole and electrodes Distance between dipole and electrodes
74
Q wave
Ventricular septum depolarising
75
R wave
Ventricular apex depolarising
76
S wave
Ventricular base depolarising
77
T wave orientation
Ventricular depolarisation is endocardium to epicardium, therefore +ve QRS Ventricular repolarisation is epicardium to endocardium, therefore +ve T wave
78
Limitations of ECG
Body has varying conductivity | Single dipole not good representation of wavefront
79
Bipolar system
Measures difference between two electrodes
80
Three bipolar limb leads
Lead I = LA - RA Lead II = LL - RA Lead III = LL - LA
81
Einthovens law
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
Three augmented unipolar limb leads
aVR, aVL, aVF
83
Unipolar chest leads
V1 - V6 | Look at heart from front and side in the horizontal plane
84
Calibration signal is always:
1 mV
85
Normal QR axis values
-30 to +110 degrees | 0 degrees = horizontal
86
Calculation of mean QRS vector
Biggest +ve minus biggest negative (both from 0)
87
EC coupling summary
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
Result of SERCA inhibition
Slower contraction
89
Result of activity on calcium release
Phospholamban is phosphorylated by PKA, can no longer inhibit SERCA, calcium release is quicker
90
3 key points about the electrogenic NCX
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
How do we know that force of contraction varies?
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
4 ways to modulate force
Increase ventricular stretch Increase automaticity Use neurotransmitters to alter rate and calcium handling Inotropic drugs
93
Two main ways to change the strength of contraction
Alter calcium transient (amplitude and duration) | Alter myofilament calcium sensitivity
94
Frank-Starlings Law
Increase in end diastolic ventricular volume increases stroke volume via stretch induced increase in cardiac contractility
95
Inotropy
Strength of muscular contraction
96
Chronotropy
Heart rate and rhythm
97
Lusitropy
Muscular relaxation
98
6 factors that can increase myofilament calcium sensitivity
``` Alkalosis Longer sarcomeres Lower catecholamines Decreased ATP Caffeine Lower phosphate ```
99
4 important effects of beta-adrenergic stimulation
Decreased myofilament calcium sensitivity Increased inner calcium Enhanced sarcoplasmic reticulum calcium-ATPase rate Altered ryanodine receptor gating
100
Beta adrenergic agonist mechanism
Stimulate adenylyl cyclase to increase cAMP levels | Activates PKA which phosphorylates phospholamban, decreases troponin I and increases sarcolemma calcium channels
101
Biphasic response to stretch
Rapid response Slow force response Increase in amplitude of calcium transient
102
Effect of increased rate of AP activation
Less time for calcium extrusion Decrease in average membrane potential Decreased overall calcium efflux via NCX Increased intracellular sodium and calcium
103
Parasympathetic effects on heart
Decreased SA node discharge rate | Decreased force
104
Sympathetic effects on heart
Increase SA node discharge rate Increase calcium influx Increased sarcoplasmic reticulum pump rate Decreased sensitivity of troponin for calcium
105
Regulation of stroke volume and heart rate
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
3 main force modulation drugs
Cardiotonic steroids Sympathomimetics Bypyridines
107
Cardiotonic steroids
Digoxin | Inhibit sodium pump therefore increase intracellular sodium which reduces calcium extrusion via sodium/calcium pump
108
Sympathomimetics
Act via beta-1 receptors | Can get desensitised to these
109
Bypyridines
Act via phosphodiesterase which increases cAMP | Limited use
110
3 current therapies to reverse the increase in cardiac dimensions
NO - relaxation Diuretics - decrease blood volume ACE inhibitors - depress angiotensin axis
111
Events of the cardiac cycle
``` Atrial systole Isovolumic contraction Rapid ejection Reduced ejection Isovolumic relaxation Rapid filling Reduced filling ```
112
Atrial systole
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
Isovolumic contraction
Onset coincides with peak of R wave Ventricular volume unchanged Closure of AV valves causes 1st heart sound 'c' wave
114
Rapid ejection
Semilunar valve opens Rapid increase in aortic flow Rapid decrease in left ventricle volume Atrial pressure drops
115
Reduced ejection
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
End systolic volume
Volume of blood left after contraction finishes About 60 mLs 55 - 75% LV blood has been ejected at this point
117
Isovolumic relaxation
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
Rapid filling
LA pressure greater than LV pressure causing AV valve to open Rapid increase in LV volume 3rd heart sound sometimes heard
119
Slow filling
Diastasis Equalised pressures Slow rise in atrial and ventricular pressures
120
3 positives of ECG
Non-invasive Fast Measures cardiac function
121
Venous pulse wave
``` Upwards deflections: 'a' = atrial contraction 'c' = ventricular contraction 'v' = venous filling Downwards deflections: 'x' = atrial relaxation 'y' = ventricular filling ```
122
Valve openings and closings
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
1st heart sound
AV valve closure at onset of ventricular systole | Low frequency
124
2nd heart sound
Closure of semilunar valves Higher frequency but shorter duration Splitting of second heart sound occurs when pulmonary valve closes after aortic
125
3rd heart sound
Early diastole Rapid filling of ventricle causes wall vibrations Can be heard in healthy children or in ventricular failure
126
3 reasons a murmur might be heard
Regurgitation Mitral valve prolapse Stenosis
127
LA pressure measurement
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
2 measurements of cardiac output
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
Emphysema and vascular resistance
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
Wolff-Parkinson White Syndrome
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
ECG properties of WPW
Normal sinus rhythm Shortened PR interval Wide QRS complex Delta wave
132
Symptoms of WPW
Ventricular tachyarrhythmia Syncope Palpitations Small risk of sudden death
133
Treatment of WPW
Drugs to control fast rhythms | Ablation of accessory pathway
134
Long QT syndrome
Abnormally long delay between depolarisation and repolarisation of ventricles Drug-induced or genetic
135
Drug induced LQTS
Anti-arrhythmics Antihistamines Potassium channel blockers
136
Genetic LQTS
Mutation in gene for ion channels prolongs duration of ventricular action potential which lengthens the QT interval
137
Hyperkalaemia ECG
Tall, peaked T waves due to faster repolarisation
138
Hypokalaemia ECG
Flat T waves due to slower depolarisation
139
Ventricular and atrial hypertrophy ECG
Bigger waves on all leads
140
Hypercalcaemia ECG
Shortened QT interval due to reduced action potential duration
141
Hypocalcaemia ECG
Lengthened QT interval due to increased action potential duration
142
Digitalis ECG
ST segment depression T wave inversion PR interval prolongation
143
Sequence of changes of Q-wave infarction
``` 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
T wave changes in MI
``` Tall and peaked Earliest sign Localised to leads facing areas of injury 5-30 minutes after onset Later, symmetrically inverted ```
145
ST segment changes in MI
Elevation often earliest observed sign Seen in leads facing infarcted area Often followed by definitive QRS changes May return to normal
146
QRS changes in MI
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
Reciprocal changes in MI
In leads opposite those facing the infarct, ST segment depression and tall T waves
148
Preload
Degree of filling | Stretch of muscle just before contraction
149
Afterload
Pressure against which the ventricle contracts
150
Four determinants of ventricular performance
Preload Afterload Inotropic state Heart rate
151
Inotropic state
Intrinsic ability of myocardium to contract with given preload and afterload
152
Chronotropic state
Heart rate | Increased HR = increased CO but decreased SV
153
Factors that affect preload
``` Blood volume Venous tone Posture Heart rate Atrial contraction Intrathoracic pressure Ventricular compliance ```
154
Factors that affect afterload
Systemic pressure Vasoconstriction Aortic stenosis Ventricular stress
155
Factors that affect inotropic state
``` ANS Catecholamines Force-frequency relation Action potential changes Cardiomyopathy Inotropic drugs ```
156
Factors that affect heart rate
ANS | Catecholamines
157
Ejection fraction
(EDV - ESV) / EDV | x 100
158
Normal ejection fraction
55-60% at rest 85% during exercise <50% = depressed contractility
159
Stroke work
about MAP x SV

Cardiovascular (6 decks)

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