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56 Cards in this Set

  • Front
  • Back
Na+ inward
Phase 4
Ca2+ inward
Phase 0
K+ outward phase 4
Na inward phase 0
Icat, IcaL
Ca inward
Phase 2
Pacemaker cells
Intiate spont. action potential (APs)

Found in SA and AV nodes
All pacemaker cells possess
Automaticity- ablility to depolarize above threshold in a rhythmic fashion
Pacemaker cells are also .... cells
Ca2+ dependent slow-response cells (w/respect to phase 0)
Conducting cells
Atrial and ventricular conducting systems: His bundles, bundle branches, Purkinje fibers
Conducting cells aka
Na+ dependent fast-response cells
Non-pacemaker and non-conducting cells
Atrial and ventricular myocytes
*can acquire automaticity in pathologic conditions
Are ions distributed equally across the cell membrane?
No :)
where do you find If channels
pacemaker cells
what do B blockers do to If channels?
Decrease rate of Na current by (-) cAMP production and PKA activation leading to reduced automaticity and heart rate (HR)
Where do you find Ica channels
Pacemaker cells
How do beta blockers affect Ica
Decrease Ca current by (-) PKA mediated phosphorylation
Consequence of beta blockade of Ica channels?
Decreased automaticity and conduction velocity (esp. in AV node)
How do Ca channel blockers work?
slow rise of AP in slow response cells of SA and AV nodes AND prolong repolarization of the AV node
Consequence of Ca blockade
Slowed conduction velocity thru AV node with prolonged repolarization increases the effective refractory period of the AV node
English: It slows the heart down
Two Class IV Ca channel blockers
Is Ik1 opened or closed at resting state? What is the consequence?
Membrane resting potential
(-90) of fast response cells is close to the equilibrium potential for K+ (-94)
What is the Nernst equation?
Ek = -61 * log [ (x)i/(x)o ]
Explain hyperkalemia via nernst equation?
If [Ko} is elevated to 10mM (may happen in hyperkalemia) the Ek rises to -70mV, making depolarization easier--arrythymias.
Where do you find Ina channels?
Fast-response cells
What does opening of Ina channels cause?
Membrane potential moves towards Ena (+70mV)
What are the 3 conformational states of the Na+ channel?
When can the Na channel be reactivated?
In the closed state
What is the recovery time dependent on?
Time and voltage
Which channel is the major determinant of the velocity of impulse conduction throughout the ventricle?
Na channel (b.c. of refractory state)
How do Na channel blockers work?
Increase threshold voltage for channel activation and thereby increase the refractory period (can't reactivate as quickly)
What is the fxn of IcaT and IcaL channels?
Mediate plateau phase (phase 2) by transient (IcaT) and long (IcaL) currents
How do IcaT and IcaL differ?
IcaT inactivates with time and is insenstive to blockage by dihydropyridines, whereas IcaL channels are.
Example of dyhydropyridine
Which Ca channel dominates in cardiac cells?
L-type Ca channels
How do Ca channel blockers work
Prolong refractory period of the fast response cells by decreasing Ca influx (increase phase 2)
What is the consequence of Ca channel blockade?
Decreased contractility--- decreased ventricular rate
Uses for Ca channel blockers?
Control ventricular rate
A fib or A flutter
Nifedipine vs. Verapamil and diltiazem
All Ca blockers

Nifedipine more effective on vascular smooth muscle

Verapamil and diltiazem more effective on cardiac muscle
Name 3 major pumps and what they do.
ATP-dependent Na-K pump: 3Na out 2K in, generates repol

ATP-dependent Ca pump (SERCA): moves Ca back into Sarc reticulum

Na-Ca exchanger (NCX): 3 Na in for 1 Ca out
Which pump does digitalis inhibit?
ATP-dependent Na-K pump
Which pump do Beta blockers inhibit? How?
ATP-dep. Ca pump

(-) PKA mediated phosphorylation of phospholamban
Where do normal cardiac impulses orginate?
SA node
Where do abnormal cardiac impulses orginate
anywhere, including SA node
What is refractoriness dependent on in slow-response cells?
Recovery of Ca channels
What is refractoriness dependent on in fast-response cells?
Na channel recovery
What determines basic HR? What else is important?
Conduction Velocity
How is automaticity controlled?
The ANS controls spontaneous depolarization (phase 4) threshold potential, and resting membrane potential
3 categories of arrhythmias
Defects in impulse formation
Defects in impulse conduction
Defects in both
Mechanism of defective impulse formation
SA node automaticity interrupted or altered--missed or ectopic beats
Can ectopic beats occur w/o SA node alteration or interruption?
MA of defective impulse conduction
AV node conduction accelerated or decreased--- irregular beats
Two types of defective impulse formation
Altered automaticity
Triggered automaticity: EAD and DAD
Give and example of early after depolarization
Torsades de pointe
Drugs that prolong QT interval: Amiodarone, procainamide, ibutilide
Give causes of delayed after depolarization
Mycardial ischemia
Adrenergic stress
Digitalis intoxication
Two types of defective impulse conduction
1. Re-entry e.g. Paroxysmal supraventricular tachycardia (PSVT)

2. Conduction block e.g. MI, drugs (Amiodarone, procainamide)
Give an example of a condition that causes both defective impulse formation and conduction.
Atrial fib w/ AV block