Electrical activity of the heart Flashcards
driving forces
difference between the membrane potential (Em) and the ions equilibrium potential (Ex)
ion current Ix
occurs when there is movement of an ion across the cell membrane
conditions for ions to move across membrane through ion channels
driving force on the ion
membrane has a conductance to that ion
resting membrane potential
potential difference that exists across the membrane of excitable cells at rest
what is the value of resting membrane potential
-70mV to -80mV
what is membrane potential expressed as
intracellular potential relative to extracellular potential
what do you need to know for Nerst. equation
-95 for potassium
+65 for sodium
+120 for calcium
most predominant intracellular ion
potassium
potassium movement in chemical gradient
diffuses down the chemical gradient
diffuses out
potassium movement in electrical gradient
diffuses into the cell
calcium chemical gradient
into the cell
calcium electrical gradient
out of the cell
sodium chemical gradient
into the cell
sodium electrical gradient
out of the cell
calculating ion current
Ix= Gx (Em-Ex)
Gx= ion conductance (1/ohm)
Em-Ex= driving force on ion
ohms law
V=IR
relationship between ionic current and ohms law
is a rearrangement
V=E
G is reciprocal of R
I is current
I=GV
action potential positive terms
depolarisation
inward current
threshold potential
overshoot
depolarisation
less negative
negative action potential terminology
hyperpolarisation
outward current
undershoot/repolarisation
refractory period
hyperpolarisation
more negative
threshold potential
point where action potential occurs
refractory period
no action potential
absolute refractory period
overlaps with almost entire duration of the action potential
why can no more action potentials occur in refractory period
closure of inactivation gates of sodium channel in response to depolarisation
gates closed position until cell is depolarised back to resting membrane potential and Na+ have recovered to closed but available state
relative refractory period
begins at the end of the absolute refractory period and overlaps primarily with period of the hyperpolarisation
what occurs during relative refractory period
action potential can be elicited but only if a greater than usual depolarisation current is applied
basis of relative refractory
higher K+ conductance than is present at rest
membrane potential is closer to K+ equilibrium potential, more inwards current needed to bring membrane to threshold for next action potential to be initiated
propagation
wave of depolarisation spreads via gap junctions
types of muscle cells in heart
contractile cells
conducting cells
SA node
primary pacemaker
AV node
slow conduction
bundle of his, pukinje system, ventricles
fast
sinoatrial node
AP duration 150 ms
upstroke: inward Ca current with inward Ca channels
no plateau
phase 4 depolarisation: inward Na current, normal pacemaker
atrium
action potential duration: 150 ms
inward Na current
plateau: inward Ca current, slow inward current, L-type ca channels
no phase 4 depolarisation
ventricle
250ms
inward na current
plateau: slow inward ca current, L-type ca channels
no phase 4 depolarisation
purkinje fibres
300ms
inward na current
plateau: inward ca current, slow, l-type channels
latent pacemaker
phase 0
upstroke, rapid
depolarization, Na+ influx
phase 1
nitial repolarization, Na+
influx stops & K+ efflux
phase 2
plateau, stable
depolarization, Ca2+ influx & K+
efflux
phase 3
repolarization, Ca2+ influx
stops & K+ efflux
phase 4
esting membrane
potential, or electrical diastole,
features of the Sa node action potential
automaticity: SA node can spontaneously generate AP without neural input
SA node has unstable resting membrane potential in contrast to other cardiac cells
SA node AP has no sustained plateau
cardiac action potential Sa node
Phase 0: upstroke, rapid
depolarization, Ca2+ influx
* Phase 3: repolarization, Ca2+
influx stops & K+ efflux
* Phase 4: Na+ influx (funny),
Ca2+ channels recover,
gradient restored
* The rate of phase 4 decides
the HR
sinoatrial node, pacemaker action potential
Phase 4: Prepotential (distinguishing feature of
a pacemaker action potential)
* The key to automaticity
* Pacemaker cell membranes contain HCN-gated
channels (non-specific cation channels)
* Activated by hyperpolarisation (from Phase 3)
* HCN mediates a ‘funny current’ (If);
pacemaker current
* If is a simultaneous K+ efflux and Na+ influx
* Na influx dominates and membrane slowly
depolarises to threshold
* Upstroke inactivates HCN until end of Phase 3
(hyperpolarisation)
latent pacemaker
cells in Sa aren’t only myocardial cells with intrinsic automaticity
latent pacemakers also have capacity for spontaneous phase 4 depolarisation
latent pacemakers
opportunity to drive heart rate only if SA is suppressed or intrinsic firing rate of latent pacemaker becomes faster than the SA node
effects of autonomic nervous system on heart rate
chronotropic effects
what is in the image q
positive chronotropic
what is in the image
negative chronotropic effects
positive dromotropic effect
increase in conduction velocity through AV node
negative dromotropic effect
decrease in condition velocity through AV node
what are dromotropic effects
effects of the autonomic nervous system on conduction velocity
myocardial cell structure
contractility
inotropism
It is the intrinsic ability of myocardial cells to develop force
at a given muscle cell length.
* Contractility correlates directly with the intracellular Ca2+
concentration.
amount of Ca released from SR depends on what
the size of the inward Ca2+ current
the amount of Ca2+ previously stored in the SR for release
what are inotropic effects
effects of the autonomic nervous system on contractility
positive inotropic effect
increase in contractility
negative inotropic effect
decrease in contractility
sympathetic action receptor and mechanism on the heart rate
increases
beta 1 receptor
increases If and ICa
sympathetic action receptor and mechanism on conduction velocity
increases
beta 1
increases ICa
sympathetic action receptor and mechanism on contractility
increases
beta 1
increased Ica and phosphorylation of phospholamban
sympathetic action receptor and mechanism on vascular Smooth muscle (skin renal and splanchnic)
constriction
alpha 1
sympathetic action receptor and mechanism on vascular smooth muscle (skeletal)
dilation with B2
and constriction with alpha 1
parasympathetic action receptor and mechanism on heart rate
decreased
m2
decreased If and increased K.ACh and decreased ICa
parasympathetic action receptor and mechanism on conduciton velocity
decreased
m2
decreased Ica and increased Ik.Ach
parasympathetic action receptor and mechanism on contractility
decreased in atria only
m2
decreased ICa
increased IKAch
all vascular smooth muscle parasympathetic action receptor
dilation releasing EDRF
M3
EDRF, ICa, If, IK-Ach
endothelial derived relaxing factor
inward calcium ion current
inward sodium ion current
outward potassium ion current
mechanism of action of cardiac glycosides
1.The Na+-K+ATPase is located in the cell membrane of the myocardial cell. Cardiac glycosidesinhibit Na+-K+ATPaseat the extracellular K+-binding site.
2.When the Na+-K+ATPase is inhibited, less Na+is pumped out of the cell, increasing theintracellular Na+concentration.
3.The increase in intracellular Na+concentration alters the Na+gradient across the myocardial cell membrane, thereby altering the function of aCa2+-Na+exchanger.This exchanger pumps Ca2+out of the cell against an electrochemical gradient in exchange for Na+moving into the cell down an electrochemical gradient. (Recall that Ca2+-Na+exchange is one of the mechanisms that extrudes the Ca2+that entered the cell during the plateau of the myocardial cell action potential.) The energy for pumping Ca2+uphillcomes from thedownhillNa+gradient, which is normally maintained by the Na+-K+ATPase. When the intracellular Na+concentration increases, the inwardly directed Na+gradient decreases. As a result, Ca2+-Na+exchange decreases because it depends on the Na+gradient for its energy source.
4.As less Ca2+is pumped out of the cell by the Ca2+-Na+exchanger, theintracellular Ca2+concentration increases.
5.Since tension is directly proportional to the intracellular Ca2+concentration, cardiac glycosides produce an increase in tension by increasing intracellular Ca2+concentration—apositive inotropic effect.
excitation-contraction coupling
cardiac action potential
Ca2+ enters cell during plateau
Ca2+ induced Ca2+ release from SR
Ca2+ binds to troponin C
cross bridge cycling so could lead to Ca2+ reaccumulated in SR then relaxation
or leads to tension
