electrical activation of the heart Flashcards
define membrane potential
the difference in electric potential between the interior and the exterior of a cell.
if there is a charge outside the cell is that positive or negative membrane potential
negative
if there is a charge inside the cell is that positive or negative membrane potential
positive
how to calculate membrane potential
interior potential - exterior potential
what is the membrane potential of a cardiac myocyte at rest
-90mV
what are the units for membrane potential
mV
millivolts
compare action potentials of the heart to action potentials of skeletal muscle
the action potential of the heart is 100x longer than skeletal muscle.
because cardiac muscle has slow calcium channels
skeletal muscle cells: 2-5ms duration
cardiac muscle cells: 200-400ms duration
what are the phases of myocyte action potential
- resting state
- depolarisation
- partial depolarisation
- plateau
- repolarisation
- resting state
what is phase 4 of myocyte action potential
it is resting state
pd is -90 mv
SAN generates action potential
causes depolarisation
if threshold is reached
phase 0 starts
what is phase 0 of myocyte action potential
depolarisation
action potential arrives
threshold potential (-60mV) reached
Na+ channels open.
inflow of Na+
causes slightly positive pd
what is phase 1 of myocyte action potential
partial repolarization
At +30mV, Na+ channels close and transient K+ channels open.
slightly negative pd due to K+
what is phase 2 of myocyte action potential
plateau
L-type Ca2+ channels allow a slow influx of Ca2+ to balance K+ efflux.
so pd remains constant
what is phase 3 of myocyte action potential
repolarisation
the Ca2+ channels close allowing repolarisation.
K+ channels open allowing influx of K+
causes pd to become more negative
2 types of refractory period
abolsute
relative
what is the absolute refractory period
- period after an action potential where the cell is completely unexcitable so second impulse CANNOT cause a second contraction of cardiac muscle
- longer for cardiomyocytes
what is the relative refractory period
when a greater than normal stimulus can depolarise the cell
purpose of refractory period
- to prevent excessive FREQUENT
contraction - To allow adequate filling time
how is resting potential of cardiac myocyte membrane maintained
by Na+ & K+ ATPase pumps
pumping 3Na+ ions OUT
for every
2K+ ions pumped IN
why is resting membrane potential much closer to the K+ equilibrium potential (-90mV) than to the Na+
equilibrium potential (+60mV)
The resting cardiac myocyte membrane (sarcolemma) is much more permeable to K+ than to Na+ - meaning the resting membrane potential is much closer to the K+ equilibrium potential (-90mV) than to the Na+ equilibrium potential (+60mV)
what is K+ equilibrium potential
-90mv
what is Na+ equilibrium potential
+60mv
why is resting cardiac myocyte membrane (sarcolemma) is much more permeable to K+
since K+ channels are open meaning K+ is leaving the cell -
what happens when an action potential arrives in myocardial cell
- Na+ voltage gated ion channels are OPENED
- Na+ entry depolarises the cell
- triggering more Na+ channels to open
-positive feedback effect - At the same time that the Na+ voltage gated ion channels are triggered to open Ca2+ voltage gated ion channels are ALSO triggered
- however these channels open much more slowly than the Na+ channels.
what happens when the potential in cell is positive (+52)
voltage gated Na+ channels CLOSE,
at the same time voltage gated K+ channels OPEN - partially REPOLARISING the cell
what happens during the partial repolarisation causes by the outflow of K+
- Ca2+ voltage gated channels finally OPEN at T-TUBULES which are part of the sarcolemma
- resulting in the INFLOW of Ca2+ into the cell
- since these channels remain open for a long duration of time they are often referred to as Ltype Ca2+ channels (L=long lasting), these channels are modified versions of the
dihydropyridine (DHP) receptors that function as voltage sensors in excitationcontraction coupling of skeletal muscles
why are Ca2+ voltage-gatted channels located in t-tubules called L-type Ca2+
because these channels remain open for a long duration of time
they are modified versions of the
dihydropyridine (DHP) receptors that function as voltage sensors in excitation-contraction coupling of skeletal muscle
what keeps the membrane DEPOLARISED at the PLATEAU VALUE of roughly 0mV.
2 reasons:
- because the flow of Ca2+ ions into the cell just balances the flow of K+ ions out of the cell
- the K+ channels open at the start close as well - maintaining depolarisation
what causes repolarisation to eventually occur
the eventual closure of the L-type Ca2+
channels
and
the reopening of the K+ channels (the ones open at the start) - these
are similar to the ones in neurons & skeletal muscle;
they open in response to depolarisation (after a delay) and close once the K+ current has depolarised the
membrane back to negative values
which ions are responsible for rapid depolarisation in phase 0
Na+ inflow
which ions are responsible for partial repolarisation in phase 1
K+ outflow
Inflow of Na+ stops
which ions are responsible for plateau in phase 2
Ca2+ slow inflow
which ions are responsible for repolarisation in phase 3
K+ outflow
Inflow of Ca2+ stops
which ions are responsible for pacemaker potential in phase 4
Na+ inflow
Slowing of K+ outflow
what is excitation-contraction coupling
refers to the series of events that link the action potential (excitation) of the muscle cell membrane (the sarcolemma) to muscular contraction
describe excitation - contraction coupling process
- wave of depolarisation/AP spreads into myocardial cells via T tubules
- L-type Ca2+ channels open –> Ca2+ enters the muscle cell
- causing small increase in cytosolic Ca2+ concentration
- the small amount of Ca2+ ions bind to ryanodine receptors on the sarcoplasmic reticulum
- this causes sarcoplasmic reticulum to release many Ca2+ ions into the cytoplasm of the cell
- this initiates cardiac muscle contraction - the start of the cross bridge cycle
- Ca2+ binds to Ca2+ binding site on troponin on actin
- troponin changes shape and displaces tropmyosin, exposing myosin binding sites
- mysoin head binds to actin via myosin binding site
- inorganic phosphate is dropped in order for mysoin head to bind to actin but the ADP is still attached to the head - this is cross bridge formation
- myosin head then drops ADP to contract and pull actin over mysoin
- this decreases the Z lines resulting in muscle contraction - the power stroke
- ATP binds to myosin head, detaching the head from actin and moving it to its start position
- ATPase in myosin head hydrolyses ATP into ADP and Pi ready for next contraction if the mysoin binding sites remain open
- contraction stops when cytosolic Ca2+ conc is restored to is original extremely low resting value by primary active Ca2+ - ATPase pumps in the sarcoplasmic reticulum and sarcolemma AND Na+/Ca2+ counter transporters in the sarcolemma
- the amount of Ca2+ returned to extracellular fluid and sarcoplasmic reticulum exactly matches the amounts that entered the cytosol during excitation
how are myocardial cells supplied with blood
by the coronary ateries
the coronary arteries exit from behind the aortic valve cusps in the very first part of the aorta
most of the coronary arteries drain into a single vein called the coronary sinus, which empties into the right atrium
what is the force of contraction directly proportional to
levels of cytosolicic Ca2+
what is the effect of drugs and chemicals that c
increased cytosolic calcium levels
examples of drugs that increase myocardial contractility
Adrenaline
Digoxin
cardiac glycosides
what happens in rigour mortis
person is dead
no ATP
myosin head cannot detach from actin
resulting in stiffness of skeletal muscles
what is the conducting system of the heart
approx 1% of cardiac cells dont function in contraction
instead they have specialised features essential for normal heart excitation
they form the conducting system of the heart and are in electrical contact with cardiac myocytes via gap junction
what does the conducting system do
initiates the heartbeat & helps spread the action potential rapidly throughout the heart
what do gap junctions do
interconnect myocardial cells and allow action potentials to spread from one cell to another
how does the initial excitation of one cardiac celleventually result in the excitation of all cardiac cells
the action potential spreads over cell membranes,
the positive charge from the Na+ affects adjacent cells, resulting in depolarisation,
the newly depolarised cells can cause further depolarisation,
and the gap junctions enable ions to travel directly to other cells.
where is the sinoatrial node (SAN)
right atrium
near entrance of superior vena cava
how does action potential spread to ventricles
it arises in SAN
spreads from SAN throughout atria and into and throughout ventricles
what is the SAN
the natural pacemaker of the heart
determines heart rate in mammals - tho no. of times the heart contracts per minute
characterized by the ability to generate spontaneous action potentials that serve to excite the surrounding atrial myocardium
what is resting membrane potential of SAN
-55 to -60 mV
this is closer to the threshold of depolarisation so it depolarises first
its closer to depolarisation threshold because of it’s slow Na+ inflow not found anywhere else in the body
what are the phases for pacemaker action potential
phase 4
phase 0
phase 3
what is pacemaker potential
SA node has no steady resting potential
instead it undergoes slow depolarisation
this is pacemaker potential
it brings membrane potential to a threshold at which ap occurs
which 3 ion channel mechanisms contribute to pacemaker potential
- K+ channels
- F - type channels
- Ca2+ channels
how do k+ channels affect pacemaker potential
- the K+ channels that opened during the repolarisation phase of the previous action potential gradually
close due to the membrane returning to negative potentials - leads to progressive reduction in K+ permeability.
how do F type channels affect pacemaker potential
- these open when the membrane potential is at NEGATIVE values - these nonspecific cation (positive ions) conduct mainly an inward Na+ current
- since this is not normal these channels are referred to as “funny” and are thus
called F-type channels
how do Ca2+ channels affect pacemaker potential
- these open VERY BRIEFLY but contribute to an inward current of Ca2+ which acts as an important final depolarising boost to the pacemaker potential.
- Since the channel is only opened briefly it can be called transient so these channels are known as T-type Ca2+ channels
compare action potentials in SA node and AV node
both similar in shape
but
pacemaker currents in SA node bring them to threshold more rapidly than the AV node
this is why the SA node normally initiates action potentials and determines the pace of the heart
why is cardiac excitation slow in AV node
because the depolarising phase is caused by Ca2+ influx through L type Ca2+ channels instead of Na+
the Ca2+ currents depolarise the membrane more slowly than voltage gated Na+ channels
so the ap propagate ire slowly along nodal cells than in other cardiac cells
what does the pacemaker potential provide the SA node with
automaticity
- the ability for spontaneous, rhythmic self excitation
how is ap spread to ventricles
using the atrioventricular node
the ap is conducted relatively fast from the SA node to the V node via internodal pathways
where is the atrioventricular node (AVN)
Located at the base of the right atrium
what does AVN do
transmits cardiac impulse from atria to
ventricles
structure of AVN
Consists of modified cardiac cells that have lost contractile capability but conduct action potentials with LOW RESISTANCE
Elongated structure with an important
feature; the propagation of action potentials through the AV node is RELATIVELY SLOW (requiring approximately 0.1 secs) - this is
IMPORTANT since it enables the atria to
EMPTY BLOOD into the ventricles, enables atrial contraction to be completed before ventricular excitation occurs
what happens after the AV node has been excited
the action potential progresses down the interventricular septum
- this pathway of conducting fibres is called the bundle of His
what is the only electrical connection between the atria and ventricles
The AV node and the bundle of His constitute the ONLY electrical connection between the atria and ventricles -
except from THIS PATHWAY the atria are completely isolated from the ventricles by a layer of nonconducting connective tissue
describe structure of bundle of His
Within the interventricular septum, the bundle of His divides into right & left bundle branches, conducting fibers that separate at the bottom (apex) of the heart and enter the walls of both ventricles
These fibers in turn make contact with Purkinje fibers, large-diameter conducting
cells that rapidly distribute the impulse throughout much of the ventricles
* Finally the Purkinje fibres make contact with ventricular myocardial cells - which spread the action potential through the rest of the ventricles
why is conduction from the AV node to the ventricles is RAPID
to enable coordinate ventricular contraction
rate of discharge in SAN
60-100/min
highest rate of discharge
thats why its the primary pacemaker
how is the heart innervated
via a rich supply of parasympathetic (rest & digest) & sympathetic
(fight or flight) nerve fibres
what is sympathetic stimulation
Sympathetic postganglionic fibers innervate the entire heart
what is sympathetic stimulation controlled by
controlled by adrenaline & noradrenaline
effect of sympathetic stimulation
*Increases heart rate (positively chronotropic)
* Increases force of contraction (positively inotropic)
* Increases cardiac output (by up to 200%
what happens if there’s decreased sympathetic stimulation
decreased heart rate & force of
contraction and a decrease in cardiac output by up to 30%
what does noradrenaline do
increases Ca2+ channel opening
= faster depolarisation
what is parasympathetic stimulation
Fibers are transmitted via the vagus nerve (CN10)
what is parasympathetic stimulation controlled by
by acetylcholine which bind to muscarinic receptors
effect of parasympathetic stimulation
- Decreases heart rate (negatively chronotropic)
- Decreases force of contraction (negatively inotropic)
- Decreases cardiac output (by up to 50%)
what happens if there’s decreased parasympathetic stimulation
an increased heart rate
what does ACH do (acetylcholine)
ACH activates potassium channels = Hyperpolarizes membrane = longer to reach TP
Also decreases calcium influx= decreases slope of pacemaker potential
