conducting system Flashcards
cellular electrical activity: explain membrane potential and changes in ionic permeability; draw action potentials for the ventricle and sino-atrial node; explain the role of the sino-atrial node and importance of refractory periods
what is the potassium hypothesis of membrane potential
K+ can move over semi-permeable cell membranes and Cl- cannot, so K+ diffuse out of the cell down their K+ gradient and reach equilibrium when positive charge outside the cells repels the efflux of K+, resulting in no net movement over the membrane
when is membrane potential equilibrium achieved
when electrical gradient exactly balances chemical gradient
define driving force
difference between electrical gradient and chemical gradient (at equilibrium, driving force is 0mV)
what does membrane potential depend on most
efflux of K+
what is the equation used to predict what the potential difference will be across semi-permeable membrane
Nernst
if the membrane is uniquely permeable to K+ at diastole (resting membrane potential), what is the potential difference across the membrane equal to
K+ equilibrium potential
how is [K+] in the cell restored after depolarisation
Na+/K+-ATPase pumps
what changes membrane potential in the heart, causing different action potential profiles
relative permeabilities of membrane to various ions (different cell types in heart express different ion currents flowing and different ion channel expression in membrane)
if the membrane is uniquely permable to Na+ at upstroke of action potential, what is the potential difference across the membrane equal to
Na+ equilibrium potential
why is Goldman-Hodgkin-Katz equation used
takes into account relative permeabilities of several ions simultaneously
diagram to show change in membrane potential over time
benjis
what happens in phase 0 (upstroke)
reaches threshold potential so hugely increased permeability to Na+ due to open channels so Na+ influx; more dependent on Na+ influx than Ca2+ influx; membrane potential depolarised from -70mV to +40mV
what happens in phase 1 (early repolarisation)
transient outward current due to brief K+ efflux
what do phases 1 and 2 occur simultaneously with and what channel does it enter through
Ca2+ influx through L-type channels
what does Ca2+ influx promote
release of further internal Ca2+ (binds to SR Ca2+ release channel), prolonging action potential
what does Ca2+ trigger
contraction
what happens in phase 2 (plateau)
K+ efflux is electrically balanced with Ca2+ influx due to gradual activation of K+ currents
what happens in phase 3 (repolarisation)
K+ permeability slowly increases to partially repolarise, and when potential becomes low enough (overcome influx of Ca2+, and the Ca2+ channels slowly close (Ca2+ ATPase starts to pump Ca2+ back into SR), IK1 opens significantly to efflux large amount of K+, returning cell to resting membrane potential
what happens in phase 4 (resting membrane potential)
IK1 open to allow flow during diastole, stabilising resting membrane potential
ventricle and SAN action potential differences
SAN keeps oscilating, SAN has no IK1 current so no resting membrane potential, Na+ channels open in SAN diastole to produce small dissociation, but upstroke provided by Ca2+ influx
what Ca2+ channels are activated in SAN
T-type
what is the significance of T-type Ca2+ channels being present in the SAN
activate at more negative potentials than L-type, so require smaller depolarisation
how is repolarisation brought about in the SAN
inactivation of Ca2+ channels so reduced Ca2+ influx
where is the SAN located
below epicardial surface at right atria/superior vena cava boundary
structure of SAN
group of specialised cells
role of SAN
spontaneously depolarise to allow autorhythmic contraction, starting conduction pathway, by nerves synapsing to it
which nervous system is the extrinic nerve supply of the heart
autonomic nervous system
what does the autonomic nervous system do to the heart
modulate pacemaker activity and control intrinsic beating established by heart
what nervous systems control heart rate and what neurotransmitters do each secrete
sympathetic (noradrenaline) and parasympathetic (acetylcholine) nervous system, which synapse with SAN cells
effect on heart rate and contractility of increasing sympathetic stimulation
membrane depolarises and reaches threshold potential more quickly, increasing heart rate (positive chronotropy) and contracilitiy (positive inotropy)
effect on heart rate of increasing parasympathetic stimulation
membrane depolarises and reaches threshold potential more slowly, decreasing heart rate
what nerves modulate intrinsic heart rate
vagus nerve (parasympathetic nerve), accelerans nerve (sympathetic nerve)
where are the cardioregulatory and vasomotor centres from where the vagus nerve begins
medulla
what is the duration of cardiac action potential and purpose
200-300ms (very long), allowing it to be an effective pump
define absolute refractory period
time during which no action potential can be inititated regardless of stimulus intensity
define relative refractory period
period after absolute refractory period where an action potential can be elicited, but only with stimulus strength larger than normal (leading to reduced risk of arrhythmias in specialised IK1)
what are refractory periods caused by
Na+ channel inactivation
when do Na+ channels recover from inactivation
during membrane repolarisation (more negative membrane potential = more channels reactivated to allow heart filling)
why don’t tetanic (summation) contractions occur in cardiac muscle
long refractory period so not possible to re-excite muscle until process of contraction well underway
