Cardiac pressure - volume cycle and ions and action potentials

Question 1

Circle of Willis

Answer 1

Arteries on brain’s surface organised into a circle

Redundancy of blood supply

Question 2

Renal circulation: special aspects

Answer 2

20-25% cardiac output

• kidenys form only 0.5% of body weight
• 50-fold over perfused volume/weight

Portal system
- glomerular capillaries to peritubular capillaries

Makes both ACE and renin

• endocrine functions
• controlling blood volume
• responding to renal blood pressure

Question 3

Skeletal muscle circulation special aspects

Answer 3

Adrenergic input -> vasodilation

Can use 80% cardiac output during strenuous exercise

• 40% adult body mass
• major site of peripheral resistance

Muscle pump
- augments venous return

Question 4

Skin circulation special aspects

Answer 4

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

Question 5

Skin’s response to trauma

Answer 5

Red reaction (dilation or precapillary sphyncters by histamine and bradykinin, leading to bright red spot/ line)

Flare (warm red area surrounding the damage due to dilation of arterioles based on C fibres of nervous system)

Wheal (swelling die to capillary damage, permeability and exudation of plasma)

Question 6

The cardiac cycle

Answer 6

Ventricular filling

Isovolumic ventricular contraction

Ejection

Isovolumic ventricular relaxation

Question 7

Isovolumic contraction

Answer 7

Time between closing of AV valves and subsequent opening of semilunar valves

Question 8

Isovolumic relaxation

Answer 8

Time between closing of semilunar valves and subsequent opening of AV valves

Question 9

Dicrotic notch

Answer 9

Small dip in the graph of aortic blood pressure that is associated with valve closure

Question 10

Myocyte contraction

Answer 10

Sliding filament model
Myosin pulls on actin
Actin-myosin activity breaks down ATP and is triggered by increased free Ca2_ near contractile machinery
Increase in Ca2+ triggered initially by transient increase in voltage

Question 11

Delayed rectifier K+ channels

Answer 11

Open when membranes depolarise

All gating takes place with a delay

Question 12

Inward rectifier K+ channels

Answer 12

Open when Vm goes below -60mV

Functions: to clamp membrane firmly open at rest

Question 13

Action potential: initial depolarisation

Answer 13

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

• depolarisation: inside the cell the voltage becomes less negative
• could be a nearby cell depolarisation
• could be synaptic transmission where a neurotransmitter opens a ligand gated channel

Question 14

Action potential: positive feedback of depolarisation

Answer 14

Initial depolarisation causes few Na+ channels to open

Additional Na+ causes more depolarisation

Acts as positive feedback loop

Voltage above threshold, cell is committed to an AP

Question 15

Action potential: repolarisation

Answer 15

The voltage becomes less positive inside the cell

2 delayed action events occur:

• Na+ channel inactivation leads to decrease Na+ going in
• delayed rectifier K+ channels open so increased K+ going out

Question 16

Refractory period

Answer 16

Time during which neurone is incapable of reinitiating an AP

Occurs mostly after hyperpolarisation

Question 17

Action potential: after hyperpolarisation

Answer 17

At the end of AP the voltage inside goes slightly more negative than at rest then returns to resting potential

Below -60mV, inward rectifier K+ channels open again and stay open until next depolarisation

Question 18

The plateau phase

Answer 18

Dynamic equilibrium

• Ca2+ current in
• K+ current out

Decreased Vm leads to Ca2+ current

Decreased Ca2+ current leads to positive feedback

Question 19

Automaticity of SA node

Answer 19

SA node cells autorhythmic

• resting potential is unstable
• resting potential is close to threshold

Cells independently beat at 100bpm

• increased by sympathetic activity
• decreased by parasympathetic activity

SA node is normally pacemaker

Question 20

Pacemaker potential

Answer 20

Voltage drifts positive between nodal beats

• instead of resting potential
• cells lack inward rectifiers

Slope of PP determines rate of firing

Question 21

APs in SA node and AV node

Answer 21

At rest spontaneously depolarise

• not stable at rest
• there’s no inward rectifier

Upstroke of AP due to transient increase in inward Ca
- nodal uptake slower than in ventricular myocytes

K conductance increases shortly after depolarisation

• which initiates repolarisation
• as in nerve and skeletal muscle

Question 22

If

Answer 22

Makes the SA node cells spontaneously active

• HCN channel
• autorhythmicity
• during the pacemaker potential

Increases upon hyperpolarisation
- rather than depolarisation

Leads to net inward current

• lots of Na+ current inward and tiny K+ current outward
• depolarises cell toward 0mV

Question 23

Blocking ion channels of cardiac AP

Answer 23

Only block percentage of ion channels (if you block all it would kill patient)
- e.g. tetrodotoxin

Na+ channel block leads to decreased conduction velocity

• changes organisation of firing in different regions of heart
• can prevent arrhythmias
• does not prevent depolarisation or affect HR

Calcium channel block can lead to decreased heart rate
- and decreased contractile force

Question 24

Red reaction

Answer 24

Dilation or precapillary sphyncters by histamine and bradykinin, leading to bright red spot/ line

Question 25

Flare

Answer 25

Warm red area surrounding the damage due to dilation of arterioles based on C fibres of nervous system

Question 26

Wheal

Answer 26

Swelling due to capillary damage, permeability and exudation