lecture 4 : cardio vascular control 1 Flashcards
how is the resting membrane potential maintained?
- the membrane is only permeable to K+ at rest
- the potential across it will equal the K+ equilibrium potential
- the concentration of K+ can be further maintained using sodium potassium ATPases
- sodium gets taken out and K is put in
what would happen without the ATPases
the concentration gradients would collapse
how does the membrane potential change?
the membrane potential will change with changes to the permeability of the membrane to various ions
what can we use to calculate the membrane potential?
either with the nernst equation (less accurate)
with goldman bodkin katz equation
this takes into account the actual permeabilities
what controls the strength of the heart beat
- the duration of action potential controls the duration of the contraction of the heart
- long slow contraction is needed to provide an effective pump
what is absolute refractory period?
this is the time during which no action potential can be initiated regardless of the intensity of the stimulus
what is a relative refractory period?
this is the period after the absolute period where an action potential can happen but only with a stimulus larger than normal
what are the refractory periods caused by?
they are caused by Na+ channel inactivation
why is the relative refractory period important?
- you cannot get a thing called tetanus which is present in skeletal muscles
- this means the the heart can refill up with blood during diastole
what are the phases of the cardiac action potential?
phase 0: upstroke phase 1: early depolarisation phase 2: plateau phase 3: repolarisation phase 4: resting membrane potential
what is upstroke caused by?
the upstroke is caused by an increase in the permeability of the membrane to sodium
small repolarisation
increase in channels that give rise to a current called a transient outward current
- this is carried by potassium ions
- very brief
what brings about contraction
- the increase in the permeability of the cell to calcium ions
- the influx of calcium promotes the release of more Ca2+ channels from the stores in the sarcoplasmic reticulum
how does the depolarisation take place
- slow increased in potassium happening
- that opens up which stops the contraction and brings it back to the resting membrane potential
why is the plateau phase prolonged?
- balance of inward movement of calcium and outward movement of potassium
how does depolarisation happen?
specialised potassium current
why are there different shapes of action potential profiles?
- different parts of the heart have different action potential shapes due to different ionic currents flowing
how are the electrical properties of the heart intrinsic?
- capable of independent spontaneous generation and coordinated propagation of the electrical activity
- there is a specialised conduction system
- the heart can beat independently even after being separated from its nervous supply
what modulates the pacemaker activity?
the autonomic nervous system
show the action potential of the ventricular cell:
insert pic
show the action potential of the SA node cell?
insert pic
why does the the action potential in the SA node look different?
- this is because not all ion channels exist in the SA node
- there is no K1 ion channel
- this means there is never a stable resting potential
- the upstroke is not caused by sodium
- the upstroke is caused by calcium entry
what two types of channels are there
T type - activate at more negative potentials than L type (also present in smooth muscle)
L type-
what modulates the heart rate?
the sympathetic and parasympathetic nervous system
these are attached to the SA nodal cell
what modulates the heart rate?
the sympathetic and parasympathetic nervous system
these are synapsed to the SA nodal cell
neurotransmitter released?
parasympathetic side?
sympathetic side ?
acetylcholine
noradrenaline
what happens if you increase the sympathetic side?
there would be a lot more noradrenaline at the nerve endings
- the pacemaker cells depolarise much more quickly so they fire action potentials more quickly than normal so the
- heart rate increases
- contractility increases
affects SA node
what happens if you increase the parasympathetic side?
it slows down the depolarisation
therefore slowing down the heart rate
affects SA node
vie the vagus nerve
where does the SA node sit?
- it lies just below the epicardial surface at the boundary between the right atrium and the superior vena cava
INSERT PIC
what is the cardiac conduction pathway?
- starts at sinoatrial node
- moves across internal fibres
- conduction is slowed down at the atrioventricular node
- moves to he bundle of His
which moves the conduction to the apex of the heart - then the conduction moves to the ventricular fibres which then spread the wave of excitation across the ventricle
what is the propagation of the cardiac action potential caused by?
- a combination of passive spread of a current
- the existence of threshold which once reached can generate its own action potential
what is the function of gap junctions?
greatly reduces the membrane resistance which allows the current to leak between one cell and the next cell
what is the structure of a gap junction?
INSERT PIC
what kind of membrane does the SA node have?
an unstable membrane potential
what is the order of excitation through the heart?
- SA node - atrial bundles - AV node - bundle of His - L and R bundle branches - ventricular purkinje system
