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Module 103: The Heart, Lungs and Blood > Theme 3: Lecture 9 - The cardiac pressure volume cycle > Flashcards

Theme 3: Lecture 9 - The cardiac pressure volume cycle Flashcards

1
Q

Features of cerebral circulation

A
  • Constant blood flow and pressure (auto regualtion)
  • Circle of Willis - This is an anatomical feature of arteries on the brain’s inferior surface arranged in a surface
  • If one branch gets blocked, blood can still reach that part of the brain through another artery
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2
Q

Features of renal circulation

A
  • 20-25% of Cardiac Output. Kidneys form only a 0.5 % of body weight so 50-fold over-perfused vol/weight
  • Portal system, glomerular capillaries to peritubular capillaries
  • Makes both ACE & Renin (Endocrine functions, Controlling blood volume, Responding to renal blood pressure)
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3
Q

Features of skeletal muscle circulation

A
  • Adrenergic Input leads to vasodilatation
  • Can use 80% of Cardiac Output during Strenuous Exercise (40% Adult Body Mass)
  • Major Site of Peripheral resistance
  • Muscle Pump Augments Venous Return
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4
Q

Features of skin circulation

A
  • Perfusion can increase 100X: role in thermo–regulation
  • Arterio–Venous anastomoses: primary role in thermoreg. The anastomoses allow rapid cooling
  • Sweat Glands: role in thermoreg, produce a plasma ultrafiltrate
  • Response to Trauma: red reaction (skin becomes activated and allows for unusual amounts of blood to go to area), flare (capillaries are more permeable), wheal (leakage of fluid which causes a bump)
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5
Q

What are the four events in a cardiac cycle (pressure volume loop)

A
  • Ventricular filling
  • Isovolumic* ventricular contraction
  • Ejection
  • Isovolumic ventricular relaxation
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6
Q

What is isovolumic ventricular contraction

A
  • The heart muscle is generating force but no contraction occurs
  • Begins when mitral valve closes and ends when aortic valve opens
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7
Q

What is isovolumic ventricular relaxation

A
  • Ventricle relaxes but cells don’t get any larger

- Begins when aortic valve closes and ends when mitral valve opens

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8
Q

What is the dicrotic notch

A
  • Seen in a cardiac pressure volume loop

- It’s a brief moment just before the aortic valve completely closes

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9
Q

When does the P wave occur in the cardiac cycle

A

Near the end of ventricular filling

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10
Q

When the QRS complex occur in the cardiac cycle

A

At the start of isovolumic contraction

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11
Q

What causes a change in shape of the cardiac pressure volume loop in the ejection portion

A

Change in afterload

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12
Q

What causes a change in shape of the cardiac pressure volume loop in the isovolumic ventricular relaxation portion

A

Change in afterload

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13
Q

What causes a change in shape of the cardiac pressure volume loop in the isovolumic ventricular contraction

A

Change in preload

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14
Q

How does mitral stenosis affect preload and afterload

A
  • Decreased preload

- Decreased afterload

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15
Q

How does aortic stenosis affect preload and afterload

A
  • No change in preload

- Increased afterload

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16
Q

How does mitral regurgitation affect preload and afterload

A
  • Increased preload

- Decreased afterload

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17
Q

How does aortic regurgitation affect preload and afterload

A
  • Increased preload

- No change in afterload

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18
Q

Describe the shape of a pressure volume loop in mitral stenosis

A
  • Graph shifted to the left
  • Maximum pressure slightly decreased
  • Still has neat corners
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19
Q

Describe the shape of the pressure volume loop in aortic stenosis

A
  • Graph squashed to the (maximum volume in the ventricle remains the same but minimum volume is raised)
  • Graph elongated (max pressure is raised but minimum volume stays the same )
  • Still has neat corners
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20
Q

Describe the shape of the pressure volume loop in mitral regurgitation

A
  • Oval shaped, no neat corners
  • Maximum pressure is decreased
  • Minimum volume is decreased and maximum volume is raised and minimum volume stays the same
  • Maximum pressure raised
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21
Q

Describe the shape of the pressure volume loop in aortic regurgitation

A
  • Oval shaped, no neat corners
  • Maximum volume raised and minimum volume stays the same
  • Maximum pressure raised
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22
Q

What causes myocytes to contract

A

myosin pulling actin:

  • Sliding filament model
  • Thin filaments (actin) & thick filaments (myosin)
  • Myosin is a “motor protein”
  • consumes ATP
  • Trigger is increase in free Ca2+
  • Initiated by increase in Voltage
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23
Q

Name two different types of K+ channels

A
  • Delayed rectifier K+ channels

- Inward rectifier K+ channels

24
Q

Describe the delayed rectifier K+ channels

A
  • Open when membrane depolarises

- But all gating takes place with a delay

25
Q

Describe the inward rectifier K + channels

A
  • Open when Vm goes below -60 mV (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
26
Q

Which channels are open when the cell is at rest

A

-Inward rectifier K+ channels are open, K+ flowing out of the cell is the dominant current

27
Q

What is the cell’s resting potential

A

-70mV

28
Q

Describe how an AP causes a cell to depolarise

A
  • The initial depolarisation causes a few of the Na+ channels to open
  • Na+ permeability increases, Na+ current flows through channels into cell
  • The additional current of Na+ going into the cell leads to more depolarisation
  • This acts as a positive feedback loop
  • When the voltage goes above the threshold voltage (-50 mV), the cell is committed to an AP
  • APs are “all-or-none”.
29
Q

Describe how a neural cell becomes repolarised

A

Due to the passage of time, 2 delayed-action events occur:

  • Na+ channel inactivation leads to ↓ Na+ current going in
  • Delayed rectifier K+ channels open leads to ↑ K+ going out
30
Q

What is the refractory period

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
31
Q

What is after hyperpolarisation

A

at the end of an AP the voltage inside temporarily goes slightly more negative than at rest, followed by a return to the resting membrane potential

32
Q

What are the 5 phases of a ventricular myocyte action potential

A

Phase 0 - Depolarisation: Na+ gates open in response to wave of excitation from pacemaker
Phase 1 - Transient Outward Current: tiny amount of K+ leaves cell
Phase 2 - Plateau phase: Inflow of Ca2+ just about balances outflow of K+
Phase 3 - Rapid repolarisation phase: Vm falls as K+ leaves cell
Phase 4 - Back to resting potential, inward rectifier K+ channels stabilise membrane current

33
Q

Compare cardiac and neural action potentials

A

Neural:

  • Roughly 1ms
  • Always the same size
  • AP completed before contraction begins in skeletal muscle
  • Short refractory period means that repeated APs lead to tetany

Cardiac:

  • Much longer, roughly 500ms
  • Vary in duration and size
  • Overlap between AP and contraction
  • Long refractory period, no tetany
34
Q

What is happening in the plateau phase (phase 2) of the cardiac AP in ventricular myocytes

A

Dynamic equilibrium:

  • Ca2+ going into cell
  • K+ going out of cell
35
Q

How does the cardiac AP in ventricular myocytes move from the plateau phase to the repolarisation phase

A
  • A lower membrane potential leads to a smaller Ca2+ current going into the cell
  • This also affects K+ so that there is less going out of the cell but to a much lesser extent
  • A decrease in the amount of Ca2+ going into the cell leads to even less Ca2+ going into the cell (positive feedback)
  • There’s a lot more K+ going out of the cell than Ca2+ going into the cell leading to rapid repolarisation
36
Q

How does the cardiac AP change in different areas of the heart

A

It varies in timing and shape

37
Q

What determines the ECG

A

The timing of the different cardiac APs

38
Q

What does the QT interval align with

A

The ventricular AP

39
Q

What does the QRS complex represent

A

Ventricular depolarisation

40
Q

What does the T wave represent

A

Ventricular repolarisation

41
Q

What causes the delay to repolarisation in ventricular myocyte APs

A
  • The depolarisation of the cell that causes it to go very positive
  • Opening of voltage dependant Ca2+ channels in the Plateau phase
42
Q

Why do nodal cells spontaneously depolarise

A
  • They aren’t stable at rest because they don’t have inward rectifier channels
  • The voltage slowly creeps up until it reaches the threshold at which point the cell rapidly depolarises
43
Q

What are the phases of a nodal AP

A 
Phase 0 = depolarisation phase
Phase 1 = does not exist
Phase 2 = does not exist
Phase 3 = repolarisation phase
Phase 4 = pacemaker potential
44
Q

Which ion causes the depolarisation of nodal cells

A
  • Due to a transient increase in inward Ca2+

- NOT Na+

45
Q

What causes repolarisation of nodal cells

A
  • the K conductance increases shortly after depolarization

- Which initiates repolarisation (as in nerve and skeletal muscle)

46
Q

How long do nodal APs last

A

roughly 300ms

47
Q

What allows SA node cells to be autorhythmic

A
  • Their resting potential in unstable

- The resting potential is close to the threshold potential

48
Q

Why does the SAN normally beat slower than 100bpm when that is the rate that it will beat at when left to its own devices

A

Due to parasympathetic input

49
Q

Why are SA nodal cells responsible for initiation of a heart beat in a healthy heart

A

They have the fastest natural rate

50
Q

What does the steepness of the slope in the pacemaker potential determine

A
  • The rate of APs firing

- AKA the diastolic potential

51
Q

What causes the upward slope of nodal APs between the depolarisations

A

The funny current

52
Q

Describe the funny current

A
  • Due to the HCN channel
  • Increases upon hyperpolarisation (rather than depolarisation)
  • Allows Na+ into cell and K+ out of cell
  • Leads to a net inward current (lot of Na+ in and tiny amount of K+ out)
  • Depolarises cell towards 0mV
53
Q

During drug therapy, why do you only block a percentage of the ion channels that you target

A

If you blocked them all you would kill the patient

54
Q

What does Na+ channel block lead to regarding cardiac APs

A
  • Lowered conduction velocity
  • Changes the organisation of firing in different regions of the heart
  • This can prevent (or sometimes cause) arrhythmias
  • It does NOT prevent depolarisation or affect HR
55
Q

What does Ca2+ channel block lead to regarding the cardiac APs

A
  • Slower heart rate

- Reduced contractile force

Module 103: The Heart, Lungs and Blood (51 decks)

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