First Pass Miss Flashcards
What is the purpose of Ik1 channel? How does it’s activity change?
It is the inward rectifier potassium channel. It’s activity decreases during the plateau phase to prevent rapid repolarization
Where do IKur channels exist and why?
Atrial myocytes. (ultra rapid) They shorten the atrial action potential so the plateau phase isn’t is long since it is a thinner wall and is not as necessary for them to contract as long
Where is the IKach channels vs IKatp?
IKach - atrial myocytes + SA/AV nodes, opens to shorten action potentials in atrial myocytes only
IKatp - atrial and ventricular myocyes - opens to shorten both atrial and ventricular in response to low ATP levels. (unbinds when the ATP/ADP ratio is low)
Why is there always a slow diastolic depolarization in slow fibers?
There is no Ik1 inward rectifier channel to keep the membrane hyperpolarized
What is the sequence of events leading to a cardiac slow fiber contraction?
If = Ifunny, nonspecific channels respond to membrane hyperpolarization when membrane potential goes below -50 mV. This is a nonspecific channel.
Inward flux from If causes a depolarization via the voltage gated calcium channels (slower AP rise than sodium channels)
K+ outward current via Ik starts immediately and ensures no plateau phase to re-hyperpolarize the membrane to start next cycle
What channels mediate the activity of positive and negative chronotropic effects on pacemakers?
Positive - Sympathetic - increased activity of If + Ica channels to produce a higher sloping and thus quicker diastolic depolarization (phase 4). Ik activity is decreased
Negative - Parasympathetic - IKach channels keep the membrane more hyperpolarized so it takes longer to reach threshold potential. Also reduces Ica and If activity.
What causes an early afterdepolarization (triggered activity)?
Typically at low HRs or altered electrolyte levels.
Due to another depolarization in relative refractory period since Ca+2 is no sufficiently cleared from the cytoplasm and repolarization via Iks is not as good at slow heart rates (we are sitting much closer to Ca+2’s threshold, giving enhanced automaticity)
What causes a delayed afterdepolarization?
Typically with high heart rates / sympathetic activity, may occur due to genetic mutations causing increased intracellular concentrations and RyR dysfunction.
What is depolarization-induced automaticity?
Something that occurs in ventricular or atrial myocytes that can be induced by never reaching resting potential (i.e. ischemia). Membrane potential sits close enough to Na+ or Ca+2 threshold to trigger a depolarization.
What is first degree heart block characterized by?
PR intervals longer than 200 msec (slowed AV conduction)
What are the two types of second degree AV block characterized by?
Mobitz I - gradually lengthening PR intervals so that a ventricular beat will be dropped
Mobitz II - normal PR intervals and random dropping of a beat
What characterizes third degree AV block?
Complete dissociation between PR intervals and ventricular contraction, an ectopic pacemaker distal to the block of the AV node will cause the ventricular contraction
What is atrial fibrillation vs atrial flutter?
Atrial flutter - a single ectopic firing that is propagated through a re-entry circuit. May not lead to a ventricular tachycardia if physiological AV block is good
Atrial fibrillation - One or more ectopic foci are firing causing to chaotic, discoordinated atrial depolarization and random conductions to the ventricles. May lead to clotting since blood is net not moved.
What is the most common cause of Ventricular Tachycardia?
Re-entry, especially due to areas of slowed conduction (ischemic tissue during myocardial infarction)
How can ventricular tachycardia be caused by the AV node?
AV nodal re-entrant tachycardia:
alpha-pathway is refractory due to premature atrial contraction
beta-pathway is slow-travelling but lower refractory period, stimulated on next normal AV rhythm.
beta to alpha pathway stimulates re-entry loop and Vtach ensues