Physiology 7: Electrophysiology of the Heart Flashcards
What is different about AV/bundle branches (from SA node) that causes slowed conduction and therefore allows increased ventricular filling ?
Decreased number of gap junctions ! Slows conduction through these two areas.
Is conduction through the Purkinje system slow or fast ?
Fast !
On an EKG which interval correlates to the time it takes the impulse to go from the SA node through the bundles ?
PR interval (P is atrial depol, QRS is ventricular depol)
Beginning of P to Beginning of QRS
Ions that have voltage gated channels include…
Na+
Ca++
K+
Funny Na+ Channels (I-f) lead to…
Pacemaker activity in the SA, AV and Purkinje fibers
Fast Na+ Channels (I-Na+) lead to …..
rapid depolarization in atrial and ventricular myocytes and Purkinjie fibers
Calcium Channels (I-Ca++) lead to
Rapid depolarization in Sa and AV nodal cells, triggers contraction in all myocytes
Potassium channels (I-k+) lead to
repolarization in all cardiomyocytes
Describe Phases 0 of the Myocyte AP
Phase 0 –> Rapid depolarization due to Voltage gated Na+ Channels opening leading to Na+ influx
Describe Phases 1 of the Myocyte AP
Na+ channels close while K+ and Cl- channels open leading to a short but strong repolarization (will not repolarize completely due to Phase 2 Ca++ influx)
Describe Phases 2 of the Myocyte AP
Ca++ open leading to a slower repolarization from k+ channels. This is the plateau portion of the AP.
Describe Phases 3 of the Myocyte AP
Ks and Kr channels open and Ca++ channels close leading to de/hyperpolarization.
Describe Phases 4 of the Myocyte AP
Kr and Ks channels close while Na+ channels activate but are still closed…. this is resting membrane potential
What does hyperkalemia do to resting membrane potential ? How does this effect AP propagation ?
Hyperkalemia will raise the resting membrane potential
This,however, does not make the cell hyperexcitable due to the inactivation of Vgated Na+ channels at this higher membrane potential (fail to reset). This will cause decreased ability to propogate and AP in myocytes.
Describe Phases 4 of the Nodal AP
Phase 4 represents depolarization
The first portion in slow due to I-f Na+ channels opening.
This is then precipitated by T-type calcium channel opening and finally the opening of L-Type Ca++ leading to full depolarization.
Describe Phases 0 of the Nodal AP
Primarily the influx of calcium from L-Type Channels
Describe Phases 3 of the Nodal AP
Closing of L-Type Ca++ channels coupled with opeing of K+ channels –> Re-polarization.
Fastest Phase _______ will lead to overdrive suppresion by that tissue.
4 (Phase 4 =depolarization in SA/AV nodes.)
Explain how hypokalemia leads to automaticity
Steps for hypokalemia induced automaticity:
EKbecomes more negative (Nernst equation prediction)
A more negative EKcauses the maximum diastolic Vm to become more negative
A more negative diastolic Vm activates more If, which produces enhanced phase 4 depolarization
A low [K+]oreduces IK1; fewer K channels are open in hypokalemia
In Short: Hyperpolarization turns on the I(f) channel Na+ influx. (Phase 4 current will be stimulated, especially in the Perkinje system Ectopic pacemaker)
Ultra Rapid K+ Channels —>
Lead to shorter AP in Atria than in other myocytes due to faster depolarization ( Phase 1 and 2…these channels shorten both)
Absolute Refractory Period (ARP)
– absolute, no action potential can be fired, Na+ channels inactivated
Relative Refractory Period
relative, stimulation triggers an action potential, but not all the Na+ channels are ready to go, lower rate of rise of AP
Supranormal period
less than normal signal can trigger an action potential (hyper-excitable)
What may occur from stimulation of the relative refractory period ?
Premature contraction–> decreased CO due to decreased pre-load.
Class IA AA drugs: Increase or decrease ARP ?
Increase ARP
Class IB AA drugs: Increase or decrease ARP ?
Decrease ARP
Class IC AA drugs: Increase or decrease ARP ?
NO EFFECT !
Class III AA drugs : Increase or Decrease ARP ?
Increase
Class IV AA drugs : Increase or Decrease ARP ?
Decrease
Delayed After Depolarization are caused by excess Ca++. What can cause excess Ca++ ?
Digitalis intoxication
Excessive catecholamine stimulation–> increase Ca++ entry
Sympathetic molecule activation of HCN channels lead to which kind of Na+ current ?
I-f
Parasympathetic effect of nodal action potentials lead to activation K+ channels as well as Gi Receptors. What will these two do respectively ?
K-Ach channels lead to increased K+ current out of cells
Gi will decrease cAMP and stop I-f (less marked depolarization)
Brugada syndrome
Mutation in the fast acting Na+ Channel leading to loss of function
Increased risk of ventricular tachyarrhythmia
Prolonged conduction interval
Slowed conduction due to prolonged phase 0
Na+ channel blockers may evoke/aggravate symptoms
Treatment: implantable cardioverter-defibrillator (ICD)
LQT1 and LQT2 – ventricular arrhythmias that occur during….
exercise or stress
LQT3
occur during rest
What channels mutations are involved in Long QT intervals ?
KCNQ1 (Ks) - impair
KCNH2 (Kr) - impair
SCNA (Na+) - enhance
Long QT intervals can lead to …
Torsades de Pointes
What drugs can be given to help alleviate symptoms of Long QT syndromes ?
Beta Blockers
There was a lot on channelopathies that we did not get to because of Raymond’s whole spiel about his awful podcasts.
Yupp had to put something on the back of this one
