cardiac pressure-volume cycle Flashcards
what is the circle of Willis?
- arteries on brains inferior surface organised into a circle
- redundancy of blood supply
what capillaries are in the portal system?
glomerular capillaries to peritubular capillaries
what proportion of body weight is made from the kidneys?
0.5%
what does ACE and renin do?
- endocrine functions
- controlling blood volume
- responding to renal blood pressure
what does the skeletal muscle pump do?
augments venous return
what does adrenergic input lead to?
vasodilation
how does skin circulation have a role in thermo-regulation?
perfusion can increase 100x
how does skin circulation affect arterio-venous anastomoses?
primary role in thermoregulation
how does skin circulation affect sweat glands?
role in thermoregulation and plasma ultrafiltrate
how does skin circulation affect the response to trauma?
red reaction, flare, wheal
what are the 4 sequential events of the cardiac cycle?
- ventricular filling
- isovolumic ventricular contraction
- ejection
- isovolumic ventricular relaxation
what are the 2 valve sounds for S1 and S2?
- S1: AV valves close, normally loudest
- S2: semi lunar valves close, systole occurs between S1 and S2, duration: systole < diastole
what is a systolic murmur?
fluid leaves ventricle, AV regulation of SL stenosis
what is a diastolic murmur?
fluid enters ventricles, AV stenosis or SL regurgitation
what causes myocytes to contract?
- sliding filament model
- thin filaments (actin) and thick filaments (myosin)
- consumes ATP
- trigger is increase in free calcium
- initiated by increase in voltage: the cardiac action potential
what happens when an ion channel in the membrane opens?
causes a current flow
what are delayed rectifier K+ channels?
open when membrane depolarised but all gating takes place with a delay
what are inward rectifier K+ channels?
open when Vm goes below -60mV and its function is to clamp the membrane firmly at rest
what happens in initial depolarisation?
- the cell starts at rest (-70mV)
- inward rectifier K+ channels are open, K+ flowing out is the dominant current
- resting membrane potential is near
- something causes the cell to become less negative
- depolarisation: inside the cell the voltage becomes less negative
- could be a nearly cell depolarising
- could be synaptic transmission where a neurotransmitter open ligand-gated channel
what happens with positive feedback of depolarisation?
- 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: positive feedback loop
- when the voltage goes above the threshold voltage (-50mV) the cell is committed to an AP
- the positive feedback of increased Na+ channel conductance and increased voltage continues until the membrane becomes quite positive
what is repolarisation?
voltage becomes less positive (or negative) inside the cell
what happens in repolarisation?
- due to the passage of time, 2 delayed-action events occur: Na+ channel inactivation leads to decreased Na+ current going in
- delayed rectifier K+ channels open leads to increased K+ going out
- these cause the membrane to be less positive and more negative inside
what happens in the refractory period?
- period of time during which neuron is incapable of reinstating an AP
- the amount of time it takes for neurons membrane to be ready for a second stimulus once it returns to its resting state following an excitation
- refractory period occurs mostly after hyperpolarisation
what is after-hyperpolarisation (AHP)?
at the end of an AP the voltage inside temporarily goes slightly more negative than at rest, followed by a return to the testing membrane potential
what happens during after-hyperpolarisation?
the increase in K+ permeability and decrease in Na+ permeability leads to the membrane potential moving closer to Ek
how big is a neural action potential?
approx 1ms, always the same size
how big is a cardiac action potential?
up to 500ms, varies in size and duration, long refractory period, no tetany
what are action potentials like in skeletal muscle?
action potentials completed before contraction begins, short refractory period means that repeated action potentials leads to tetany
what is the plateau phase?
- dynamic equilibrium: Ca2+ current in, K+ current out
- decreased Vm leads to decreased Ca2+ current
- so decreased Ca2+ current leads to positive feedback
what is the SA node?
heart pacemaker
what are the AV node and bundle of His?
potential pacemakers in case of atrio-ventricular conduction failure
what do QRS an T peaks show?
QRS = ventricular depolarisation T = ventricular repolarisaiton
how do ventricular myocytes work?
1) at rest, the inward rectifier K+ channel leads to the outward current stabilising membrane
2) the rapid upstoke of the action potential is exactly as in nerve and skeletal muscle due to a transient increased in inward Na current
3) depolarisation also leads to transient opening of time and voltage dependent Ca channels
4) the total K conductance decreases rather than increases upon depolarisation
5) repolarisation is greatly delayed due to 2 and 3
what happens with action potentials in the SA node and AV node?
- at rest spontaneously depolarises: not stable at rest because there is no inward rectifier
- the upstroke of the action potential is due to transient increase in inward Ca: not Na, Ca current, nodal upstroke is slower than in ventricular myocytes
- the K conductance increases shortly after depolarisation: initiates repolarisation
- duration nodal AP (phases 0 + 3) = approx 300ms
what does it mean that sinoatrial node cells are autorhythmic?
resting potential is unstable, resting potential is close to threshold
what cells and where is the pacemaker potential found?
in the myocytes of SA node, AV node and conduction system only
what determines the rate of firing (diastolic potential)?
slope of pacemaker potential
when does If increase?
upon hyperpolarisation rather than depolarisation
what happens when the If leads to a net inward current?
- leads to a lot of Na+ current inward and a tiny K+ current outward
- depolarises cell towards 0mV
why does drug therapy only block a percentage of the ion channels you target?
if you blocked them all the patient would die
what happens when the Na+ block leading to decreased conduction in velocity?
- the changes of 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
- calcium channel block can lead to decreased heart rate and decreased contractile force
