Electrophysiology & Wigger’s Diagram Flashcards
what 2 components maintain the resting membrane potential?
- 3Na+/2K+/ATPase pump
- K+ outwards leakage
the ratio of intra/extracellular K+ establishes RMP!
how would hyperkalemia and hypokalemia alter the resting membrane potential, respectively?
ratio of intra/extracellular K+ establishes RMP - usually more K+ extracellular relative to intracelular
thus…
hyperkalemia —> makes RMP less negative - depolarizing effect
hypokalmeia —> makes RMP more negative - hyperpolarizing effect
activation of which membrane channels are responsible for depolarization and repolarization, respectively?
activation of voltage-gated Na+ channels —> depolarization
activation of voltage-gated K+ channels (and inactivation of voltage-gated Na+ channels) —> repolarization
[reestablishment of resting Na+/K+ gradients via Na+/K+/ATPase]
absolute vs relative refractory period
absolute (effective) refractory period: Na+ channels inactive and non-stimulatable
relative refractory period: some Na+ channels are resting, can elicit sub-threshold potentials with sufficient stimulus
how do voltage-gated sodium channels respond to prolonged voltage that is sufficient to cause depolarization?
voltage-gated Na+ channels are time-sensitive, so give transient excitability
if voltage is prolonged (clamped), voltage-gated Na+ channels depolarize at different timings, resulting in populations of voltage-gated Na+ channels in various activation-inactivation-resting states
explain how hyperkalemia can cause cardiac arrhythmia
hyperkalemia reduces threshold needed to cause depolarization, and membrane voltage is clamped at a less negative voltage
however, voltage-gated Na+ channels are time-sensitive (give transient excitably, sort of fail-safe), so what results in populations of Na+ channels in various stages of activation/inactivation/resting
this causes non-uniform contraction, and thus, cardiac arrhythmia
what channels allow the SA node of the heart to spontaneously depolarize?
HCN channels (hyperpolarize-activated, cyclic nucleotide dependent Na+ channels): allows slow depolarization via slow inward Na+ current (“funny current”)
T-type Ca2+ channels also allow slow inward current of Ca2+
once threshold achieved, rapid depolarization via influx of calcium
what effect does ACh have on heart rate? Describe the mechanism
ACh from parasympathetic neurons slows down HR by increasing the interval between action potentials
binds type 2 cholinergic muscarinic receptors (CM2) and cause outflow of K+ —> membrane potential is more hyperpolarized, and longer time is required to reach threshold of depolarization
what are the phases of non-SA node cardiac action potentials?
phase 0: voltage-gated Na+ channels open (depolarizing)
phase 1: 1 isoform of voltage-gated K+ channels opens (repolarizing)
phase 2: different isotypes of K+, Ca2+, and Na+ channels are open - Ca2+ influx offsets K+ efflux (plateau phase)
phase 3: only K+ channels are open, but a different isotype
phase 4: refraction (all channels close)
*in each stage, different isotypes of ion channels are used
describe how Lidocaine disrupts pain signals, in terms of membrane potentials?
Lidocaine has high-affinity for voltage-gated Na+ channels, blocking generation of action potentials for afferent pain signaling
what is the last event in the cardiac cycle that occurs during diastole
remember systole/diastole conventionally refer to the ventricles
and
systole = ventricular contraction/ejection, diastole = everything else (including ventricular relaxation and filling)
atrial systole is the last event in [ventricular] diastole - this makes sense because most of ventricular filling is passive, followed by a little dump from the atrium, and then ventricular contraction/systole occurs
for the most part, ventricles can passively fill adequately without atrial assistance (like when someone has atrial fibrillation)… however, there are times when atrial contraction is really important
can you name 2 situations?
- at times of high heart rate - there is less time for diastolic passive filling
- when the ventricle is stiff - the ventricle is less able to fill
in both of these scenarios, atrial contraction contributes a larger portion of ventricular volume
when would you heart a fourth heart sound (S4)?
S4 is pathological finding - sound of atrial trying to contract to fill a stiff ventricle
so it is the sound of atrial contraction
the beginning of [ventricle] systole coincides with the peak of the ___ wave and represents phase __
the beginning of [ventricle] systole coincides with the peak of the R wave
QRS complex represents phase 0 of ventricular action potential
what’s happening during this time? ventricles depolarize (Ca2+ induced Ca2+ release) and myocyte contraction leads to abrupt increase in IV pressure (IVP)
what causes the first heart sound, and what is this event caused by?
S1 = closure of AV valves = “lubb”
when ventricular pressure (IVP) exceeds atrial pressure, the AV valves close
the cusps are pushed back by blood trying to go backwards, and the valve closes
first heart sound marks the beginning of ventricular systole
what is occurring during isovolumentric contraction of the heart?
AV valves and semilunar valves are ALL closed
intraventricular pressures (RVP/LVP) rise rapidly with no change in volume
what causes the semilunar valves to open (mechanically)?
during isovolumetric contraction, all valves are closed - IVP (both sides) is rising rapidly with no change in volume
when IVP exceeds pressure in the outflow tract, semilunar valves open
*no heart sounds should be heard during ejection
which heart sound represents the beginning of diastole?
S2 (“dubb”) = semilunar valves closing (once IVP falls below that of outflow tracts) = beginning of diastole
what would a third heart sound correspond to?
S3 correlates to rapid filling in ventricles that are larger than they should be
usually pathological (but normal in children)
