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103 theme 3 > The cardiac pressure volume cycle > Flashcards

The cardiac pressure volume cycle Flashcards

1
Q

what are the special aspects of cerebral circulation

A

Brain maintains all vital functions
Constancy of flow & pressure (auto-regulation)
Circle of Willis (arteries on brains inferior surface organised into a circle, redundancy of the blood supply)

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2
Q

what are the special aspects of renal circulation

A

20-25% CO
Kidneys form only 0.5% of body weight, 50 fold over-perfused vol/weight)
Portal System
Glomerular capillaries to peritubular capillaries
Makes both ACE and Renin
Endocrine functions. Control blood vol and respond to renal pressure

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3
Q

what are the special aspects of skeletal muscle circulation

A 
Adrenergic input > vasodilation
Can use 80% of CO during strenuous exercise
40% adult body mass
Major site of peripheral resistant 
Muscle pump to augment venous return
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4
Q

what are the special aspects of skin circulation

A

Role in thermo-regulation
Perfusion can increase 100X
Arterio-venous anastomoses (primary role in thermoregulation)
Sweat glands – role in thermoregulation, plasma ultrafiltrate
Response to trauma (red reaction, flare, wheal)

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5
Q

what is the cardiac cycle

A 
Can be considered 4 sequential events
Ventricular filling
Isovolumic ventricular filling
Ejection
Isovolumic ventricular relaxation
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6
Q

how is filling and ejection shown on a pressure time graph

A

Sharons increase, round peak and sharp decrease for ejection and flat line for ventricular filling/ relaxation (diastolic pressure)

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7
Q

when does the aortic valve close

A

when left ventricular pressure < aortic pressure

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8
Q

what is isovolumic contraction

A

ventricles contract with no vol change as all heart valves close

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9
Q

what is isovolumic relaxation

A

ventricles relax within no volume change (ventricles empty, blood in aorta and aortic valve is closed)

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10
Q

how is aortic pressure shoes on a pressure time graph

A

slight dip at IVR, slight decrease across filling but far above diastolic pressure

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11
Q

how does IVR and IVC compare to S1 and S2

A

(mitral) S1 = IVC aortic valve opens at end, no sound

(aortic) S2 = IVR mitral valve opens at end, no sound

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12
Q

how do ECG waves link to ventricular pressure changes

A

P wave before ejection (filling)

QRS complex immediately before ejection

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13
Q

what is the pressure volume loop

A 
pressure on y axis and volume on x axis
IVR parallel to pressure, furthest left 
MO
Filling along y axis, bottom
MC
IVC increase
AO
Ejection curves back to start
AC
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14
Q

how does preload and afterload link to PV loops

A

IVC affected by preload

Ejection and IVR effected by after load

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15
Q

how do valve pathologies link to valve pathologies

A

Mitral stenosis _ dec in pre and afterload
Aortic stenosis - incr afterload
Mitral regurgitation - inc preload and dec after load
aortic regurgitation - inc preload

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16
Q

what are the valve sounds on auscultation

A

S1 AV valves close normally loudest
S2 SL valves close
Systole occurs between S1 and S2 (diastole has a longer duration than systole)
Murmurs are due to turbulence caused by obstacles

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17
Q

what causes a systolic murmur

A

Fluid leaves ventricle, AV regurgitation or SL stenosis

18
Q

what causes a diastolic murmur

A

Fluid enters ventricle, AV stenosis or SL regurgitation

19
Q

what causes myocytes to contract

A 
Myosin pulling actin 
Sliding filament model 
Thin Filaments (actin) and thick filaments (myosin)
Myosin – motor protein 
Consumes ATP 
Trigger is increase in free Ca2+
20
Q

what is cardiac action potential

A

Initiated by increase in voltage (the cardiac action potential)
Cardiac action potential is longer, Ca2+ and K+ flow during plateau phase
Nodal action potential – calcium-based depolarisation

21
Q

what are delayed rectifier K+ channels

A

Open when membrane depolarises, all gating has a delay

22
Q

what are inward rectifier K+ channels

A

Open when Vm goes below -60mV
Very unusual, more open when cells are at rest
Functions: to clamp membrane firmly at rest
K+ channel lets K+ out of cell, repolarising it

23
Q

what happens at the initial depolarisation of an AP

A

The cell starts at rest (-70mV)
Inward rectifier K= channels are open, k+ flowing out is dominant current
Resting membrane potential is near Ek
Something causes cell to become less negative

24
Q

What is depolarisation

A

inside the cell the voltage becomes less negative (or more positive)
Could be nearby cell depolarising or could be a synaptic transmission where a neurotransmitter opens a ligand-gated channel

25
Q

what is the positive feedback of depolarisation of an AP

A

The additional current of Na+ going into the cell > more depolarisation (membrane potential moves closer to 0mV)
Acts as a positive feedback loop
When the voltage goes above the threshold voltage (-50mV), the cell is committed to an AP (all or nothing)
quite positive (>+30mV)
Vm >0, period is the overshoot

26
Q

What is depolarisation of an AP

A

voltage becomes less positive (or more negative) inside the cell
Due to the passage of time, 2 delayed-action events occur
Na+ channel inactivation > decrease Na+ current going in
Delayed rectifier K+ channels open > increase K+ going out
These cause the membrane to be less positive and more negative inside

27
Q

What is the refractory period of an AP

A

Period of time during which neuron is incapable of reinitiating an AP
The amount of time it takes for neuron’s membrane to be ready for a second stimulus once it returns to its resting state following an excitation
The amount of time it takes for a neuron’s membrane to be ready for a second stimulus once it returns to its resting state following an excitation
Refractory period occurs mostly during after-hyperpolarisation

28
Q

what is the after-hyperpolarisation of an AP

A

voltage inside temporarily goes slightly more negative than at rest, followed by a return to the resting membrane potential
When the voltage goes below -60mV, the inward rectifier K+ channels open again, they stay open until next depolarisation
These normally clamp the voltage toward Ek and are responsible for maintaining the resting potential
During APH: increase the K+ permeability and decrease Na+ permeability

29
Q

how do cardiac and skeletal action potentials compare

A 
Neural action potentials: ~1 ms
Always the same size 
In skeletal muscle 
Action potential completed before contraction begins 
short refractory period means that repeated action potentials > tetany 
cardiac action potentials 
much longer up to 500 ms
varies in duration and size
long refractory period, no tetany
30
Q

what are the phases of cardiac action potential

A

0 depolarisation: Na+ gates open in response to wave of excitation from pacemaker
1 transient outward current: tiny amount of K+ leaves cell
2 plateau phase:inflow of Ca2+ about balances outflow of K+
3 rapid repolarisation phase: Vm falls as K+ leaves cell
4 back to resting potential

31
Q

what is the plateau phase

A 
Dynamic equilibrium 
Ca2+ current in and K+ current out 
Decrease Vm, decrease Ca2+ current 
Also for K+, but much less
In decreasing Ca2+ current > positive feedback 
Repolarisation by K+
32
Q

how does the cardiac AP vary in different regions of the heart

A

Vary in timing and shape, atrial AP occurs earlier also a steeper and narrower shape

33
Q

what are the shape and timing of the cardiac action potentials

A 
SA node= pacemaker
Av node and Bundle of His = potential pacemakers in case of atrio-ventricular conduction failure
QT interval aligns with ventricular AP
QRS= ventricular depolarisation
T = ventricular repolarisation
34
Q

what do the ventricular myocytes do in cardiac action potential

A

At rest, inward rectifier K= channel > outward current stabilising membrane (phase 4)
The rapid rising phase (or upstroke) of the action potentials is, exactly as in nerve and skeletal muscle, due to transient increase in inward Na current (with positive feedback, phase 0)
Depolarisation also leads to transient opening of time and voltage dependant Ca Channels (phase 2)
The total K conductance decreases rather than increases upon depolarisation
Repolarisation delayed due to b and c

35
Q

how do action potentials occur in the SA and AV node

A

At rest spontaneously depolarises (not stable at rest because no inward rectifier)
The upstroke of the AP is due to a transient increase in inward Ca2+ (nodal upstroke slower than in ventricular myocytes)
The K conductance increases shortly after depolarisation
Initiates repolarisation as in nerve and skeletal muscles
Duration nodal AP (phases 0-3) = ~300ms

36
Q

what are the phases of the nodal AP

A

0 depolarisation
1 & 2 don’t exist
3 depolarisation phase
4 pacemaker potential

37
Q

is the SA node automatic

A

SA node cells are autoarhythmic
(resting potential is unstable and close to threshold)

Cells independently beat at 100bpm
SA node is normally the pacemaker (initiation of heart beat in healthy heart as have fastest rate)
Other cardiomyocytes can be too

38
Q

what is the pacemaker potential

A

In myocytes of SA node, AV node conduction system only
Voltage drifts positive between nodal beats
Instead of resting potential because cells lack inward rectifiers
Slope of PP determines rate of firing (aka diastolic potential)
Drifts up slowly

39
Q

what is the funny current

A 
If the funny current 
Makes SA node cells spontaneously active 
HCN channel, Not a sodium channel 
Autorhythmicity
During pacemaker potential
40
Q

what does the If current lead to

A

Increases upon hyperpolarisation (rather than depolarisation)
Leads to net inward current
If > Na+ inward and only tiny K+ out
Depolarises towards 0mV

41
Q

Blocking Ion channels of cardiac AP

A

During drug therapy you only block a percentage of ion channels
(block all kill patient, eg tetrodotoxin from fugu fish)
Na+ blocked to decrease conduction velocity
Changes organisation of firing in different regions of the heart, can prevent (or sometimes cause) arrythmias
Doesn’t prevent depolarisation or affect HR
Calcium channel block can decrease heart rate and decrease contractile force

103 theme 3 (20 decks)

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