Cardiac pressure - volume cycle and ions and action potentials Flashcards
Circle of Willis
Arteries on brain’s surface organised into a circle
Redundancy of blood supply
Renal circulation: special aspects
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
Skeletal muscle circulation special aspects
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
Skin circulation special aspects
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
Skin’s response to trauma
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)
The cardiac cycle
Ventricular filling
Isovolumic ventricular contraction
Ejection
Isovolumic ventricular relaxation
Isovolumic contraction
Time between closing of AV valves and subsequent opening of semilunar valves
Isovolumic relaxation
Time between closing of semilunar valves and subsequent opening of AV valves
Dicrotic notch
Small dip in the graph of aortic blood pressure that is associated with valve closure
Myocyte contraction
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
Delayed rectifier K+ channels
Open when membranes depolarise
All gating takes place with a delay
Inward rectifier K+ channels
Open when Vm goes below -60mV
Functions: to clamp membrane firmly open at rest
Action potential: initial depolarisation
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
Action potential: positive feedback of depolarisation
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
Action potential: repolarisation
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
Refractory period
Time during which neurone is incapable of reinitiating an AP
Occurs mostly after hyperpolarisation
Action potential: after hyperpolarisation
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
The plateau phase
Dynamic equilibrium
- Ca2+ current in
- K+ current out
Decreased Vm leads to Ca2+ current
Decreased Ca2+ current leads to positive feedback
Automaticity of SA node
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
Pacemaker potential
Voltage drifts positive between nodal beats
- instead of resting potential
- cells lack inward rectifiers
Slope of PP determines rate of firing
APs in SA node and AV node
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
If
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
Blocking ion channels of cardiac AP
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
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 due to capillary damage, permeability and exudation
