Cardiac volume-pressure cycles, ions and APs

Question 1

Cerebral circulation

Answer 1

Contains constant flow and pressure of blood as it is unable to store energy.

Circle of Willis- anastomosis or arteries on brain’s inferior surface

Question 2

Renal circulation

Answer 2

Despite the kidney making 0.5% of body weight, it contributes to 20-25% of cardiac output.

Involved in the synthesis of ACE and Renin- controls blood volume in response to renal perfusion.

Contains portal system- Glomerulus and peritubular capillaries are in series- connected by efferent arteriole.

Question 3

Skeletal muscle circulation

Answer 3

Adrenergic input causes vasodilation- sympathetic activation.

During strenuous exercise muscles can use up tp 80% of CO.

Muscle pumps facilitates venous return

Question 4

Skin circulation

Answer 4

Thermoregulation- can increase perfusion up tp 100X.

Arteriovenous anastomoses - when arterioles join with venules.

Sweat glands- plasma ultrafiltrate and used in thermoregulation.

Trauma- Red reaction, flare wheal.

Question 5

Ventricular filling and ejection

Answer 5

Ventricles fills when pressure is lower than atrial (and importantly aortic) pressure.

Ventricle eject blood when the pressure is higher than the aorta.

Question 6

Isovolumic contraction

Answer 6

When the ventricle contract with no change in volume.

This occurs between the AV valves closing and the opening of the semilunar valves.

Both the AV and Semilunar valves are shut- hence pressure increases without volume change.

Question 7

Isovolumic relaxation

Answer 7

When the ventricles relax with no change in volume.

The left ventricular pressure is lower than aortic pressure, causing the aortic valve to close.

This occurs between the closing of the semilunar valves and opening of the AV valves.

All valves are closed during this process.

Question 8

Dicrotic notch

Answer 8

The small dip in aortic blood pressure (in the Wiggers diagram).

Occurs when the aortic valve closes, there is a slight dip in aortic pressure,

Question 9

ECG waves during cardiac pressure changes

Answer 9

ECG waves always precede ventricular pressure changes.

Electrical changes occur before heart contractions.

Heart contractions cause the pressure changes.

P wave cause atrial contraction. P waves proceed atrial contraction and AV closing.

QRS complex precedes ventricular ejection.

Question 10

Pressure volume loop

Answer 10

Graph that shows volume (x) against pressure (y) in the heart.

Moving in an anti-clockwise direction:
Filling—> AV valves close at the corner—-> Isovolumic contraction—> Ejection —> SL valves close —-> Isovolumic relaxation at the corner.

Question 11

Preload and afterload in the pressure-volume loop

Answer 11

Between the mitral valve closing and the aortic valve opening- this is affected by preload. This is during isovolumic contraction.

Ejection is affected by afterload. This is between the aortic valve opening and closing.

Isovolumeric relaxation is affected by afterload. This is between the aortic valve closing and the mitral valve opening.

Question 12

Low L.ventricle volume at the end of ejection

Answer 12

End systolic volume is low because:

Afterload was low.

Ventricles fill with less blood due to mitral stenosis.

Escape of blood back into the atrium during mitral regurgitation.

Question 13

High L.ventricle volume at the end of filing

Answer 13

Occurs because:

Excess filling of ventricle due to high preload.

Aortic regurgitation- blood from aorta entering back into ventricle.

Mitral regurgitation- XS blood from atrium into ventricle.

Question 14

High LV pressure during ejection

Answer 14

High levels of afterload

Question 15

High LV volume at the end of ejection

Answer 15

Occurs when ejectio is incomplete:

• Myocardial weakness/damage, thus less contractile force
• High after load

Question 16

Aortic stenosis pressure-volume loop

Answer 16

There is an increase in afterload.

The loop will show a narrower loop on the right hand side.

Question 17

Mitral stenosis pressure-volume loop

Answer 17

There is a decrease in preload and afterload:
Less volume of blood enters the ventricle and aorta.

This shifts the loop to the left, from the normal loop.

Question 18

Mitral regurgitation pressure-volume loop

Answer 18

There is an increase in preload BUT decrease in afterload:
There is more blood escaping into the ventricles but it also leaves back into the atrium during ejection, decreasing afterload.

Therefore the loop forms an oval shape- widens at the right and left.

Question 19

Aortic regurgitation pressure-volume loop

Answer 19

There is an increase in preload: blood from aorta leaks into the ventricle.

Isovolumic relaxation doesn’t really happen because the aortic valve is never close so blood from aorta leaks into the ventricle.

Question 20

Two types of K+ channels in cardiomyocytes

Answer 20

Both channels let K+ out of the cells.

Delayed rectifier K+ channels:
Only opens when membrane depolarises but does so in a slow fashion.

Inward rectifier K+ channels:
Opens when membrane potential is below -60 mV
This clamps membrane firmly at rest towards the equilibrium potential for K+.

Question 21

After hyperpolarisation.

Answer 21

The stage at the end of the AP where the Vm gets more negative than resting potential.

The voltage goes below -60mV due to opening of inward rectifier K+ channels- which stay opened until depolarisation.

The membrane becomes less permeable to Na+ and more permeable to K+. This pushes the Vm closer to K+ equilibrium potential.

Question 22

Phases of ventricular myocyte action potential

Answer 22

0= Always depolarisation

1- Transient outward current: small amount of K+ leaves the cell.

2= Plateau phase: dynamic equilibrium b/w K+ and Ca2+.

3- Rapid repolarisation

4- Back to resting potential. The current is maintained by inward rectifier K+ opened.

Question 23

Action potentials in skeletal muscle

Answer 23

ALWAYS occurs before contraction begins.

Contains a short refractory period- repeated APs causes tetany.

Question 24

Cardiac action potentials

Answer 24

Length: up to 500ms

Always varies in duration and size

Contains a long refractory period- no tetany can occurs. This prevents fibrillation.

Question 25

The plateau phase

Answer 25

Phase 2 of ventricular myocytes action potential.

Ca2+ channels open when membrane is depolarisation.

This is when there is a dynamic equilibrium between the Ca2+ going in and K+ going out of the cell.
- This causes the voltage to become depolarised VERY slowly due to K+ current slightly outweighing the Ca2+ current.

The more negative the membrane goes, the more Ca2+ channels close- positive feedback mechanism.

Question 26

Atrial vs Ventricular AP

Answer 26

Atrial AP occurs earlier than ventricular AP- The P wave on the ECG.

Ventricular AP aligns with QT interval.

Question 27

Automaticity of SAN

Answer 27

SAN cells are autorhythmic:
Resting potential is unstable and close to threshold potential (-40mV).

The cells always independently beat at 100 bpm if not affected by autonomic system.

SAN cells initiate the heartbeat as it has the fastest rate- even though other cardiomyocytes can initiate it.

Question 28

Pacemaker potential/ Diastolic potential

Answer 28

Pacemaker cells lack inward rectifier cells so it drifts towards the positive between nodal beats- instead of the resting potential (-40mV).

The slope of this diastolic potentials determines rate of firing.

Question 29

AP in SAN and AVN

Answer 29

There is no inward rectifier so it spontaneously depolarises at rest- the resting Vm is not stable.

The nodal upstroke is slower than in ventricular myocytes - when Ca2+ flows inwards.

K+ conductance increases after depolarisation which initiates repolarisation.

Question 30

Phases of nodal AP

Answer 30

0= depolarisation phase

1+2= does not exist. There is no transient outflow of K+ and plateau phase.

3- repolarisation- after K+ conductance increases.

4- return to pacemaker potential.

Question 31

The funny current (If)

Answer 31

In SAN- this is maintained by the hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels. channel which makes the nodal cells spontaneous.

This leads to a net INWARD current- a lot of Na+ inward, with small K+ outward. This causes the cell to depolarise towards 0 mV.

This current increases during hyperpolarisation.

Question 32

Tetrodotoxin

Answer 32

A toxin found in fugu fish that blocks all the Na+ channels.

This causes DEATH.

Question 33

Blocking K+ channels

Answer 33

This decreases conduction velocity- changes organisation of firing in the heart.

This can be used to prevent arrhythmias.

Does not prevent depolarisation of affect HR.

Question 34

Blocking Ca2+ channels

Answer 34

This can decrease heart rate and contractile force.

This is because the SAN is dependant on Ca2+ channels.

Diminishing Ca2+ influx decreases the rate of voltage depolarisation (Phase 0)

Question 35

Dihydropyridine

Answer 35

Drugs that targets Ca2+ channels in the blood vessels more than the heart.

They are used as anti-hypertensives.

Example: Amlodipine

Question 36

Amlodipine

Answer 36

A dihydropyridine that is used as an anti-hypertensives.

The drug blocks Ca2+ channels in the blood vessel.

Question 37

Diltiazem

Answer 37

Anti-anginal drug that lowers heart contractility.

Does so by blocking Ca2+ channels.

Question 38

Verapamil

Answer 38

Antiarrhythmic agent in the heart that blocks Ca2+ channels.