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56 Cards in this Set
- Front
- Back
If
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Na+ inward
Phase 4 |
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Ica
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Ca2+ inward
Phase 0 |
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Ik1
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K+ outward phase 4
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Ina
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Na inward phase 0
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Icat, IcaL
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Ca inward
Phase 2 |
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Pacemaker cells
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Intiate spont. action potential (APs)
Found in SA and AV nodes |
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All pacemaker cells possess
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Automaticity- ablility to depolarize above threshold in a rhythmic fashion
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Pacemaker cells are also .... cells
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Ca2+ dependent slow-response cells (w/respect to phase 0)
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Conducting cells
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Atrial and ventricular conducting systems: His bundles, bundle branches, Purkinje fibers
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Conducting cells aka
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Na+ dependent fast-response cells
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Non-pacemaker and non-conducting cells
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Atrial and ventricular myocytes
*can acquire automaticity in pathologic conditions |
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Are ions distributed equally across the cell membrane?
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No :)
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where do you find If channels
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pacemaker cells
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what do B blockers do to If channels?
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Decrease rate of Na current by (-) cAMP production and PKA activation leading to reduced automaticity and heart rate (HR)
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Where do you find Ica channels
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Pacemaker cells
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How do beta blockers affect Ica
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Decrease Ca current by (-) PKA mediated phosphorylation
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Consequence of beta blockade of Ica channels?
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Decreased automaticity and conduction velocity (esp. in AV node)
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How do Ca channel blockers work?
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slow rise of AP in slow response cells of SA and AV nodes AND prolong repolarization of the AV node
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Consequence of Ca blockade
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Slowed conduction velocity thru AV node with prolonged repolarization increases the effective refractory period of the AV node
English: It slows the heart down |
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Two Class IV Ca channel blockers
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Verapamil
Diltiazem |
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Is Ik1 opened or closed at resting state? What is the consequence?
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Open
Membrane resting potential (-90) of fast response cells is close to the equilibrium potential for K+ (-94) |
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What is the Nernst equation?
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Ek = -61 * log [ (x)i/(x)o ]
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Explain hyperkalemia via nernst equation?
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If [Ko} is elevated to 10mM (may happen in hyperkalemia) the Ek rises to -70mV, making depolarization easier--arrythymias.
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Where do you find Ina channels?
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Fast-response cells
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What does opening of Ina channels cause?
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Membrane potential moves towards Ena (+70mV)
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What are the 3 conformational states of the Na+ channel?
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Active
Inactive Closed/resting |
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When can the Na channel be reactivated?
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In the closed state
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What is the recovery time dependent on?
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Time and voltage
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Which channel is the major determinant of the velocity of impulse conduction throughout the ventricle?
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Na channel (b.c. of refractory state)
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How do Na channel blockers work?
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Increase threshold voltage for channel activation and thereby increase the refractory period (can't reactivate as quickly)
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What is the fxn of IcaT and IcaL channels?
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Mediate plateau phase (phase 2) by transient (IcaT) and long (IcaL) currents
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How do IcaT and IcaL differ?
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IcaT inactivates with time and is insenstive to blockage by dihydropyridines, whereas IcaL channels are.
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Example of dyhydropyridine
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Nifedipine
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Which Ca channel dominates in cardiac cells?
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L-type Ca channels
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How do Ca channel blockers work
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Prolong refractory period of the fast response cells by decreasing Ca influx (increase phase 2)
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What is the consequence of Ca channel blockade?
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Decreased contractility--- decreased ventricular rate
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Uses for Ca channel blockers?
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Control ventricular rate
A fib or A flutter |
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Nifedipine vs. Verapamil and diltiazem
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All Ca blockers
Nifedipine more effective on vascular smooth muscle Verapamil and diltiazem more effective on cardiac muscle |
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Name 3 major pumps and what they do.
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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 |
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Which pump does digitalis inhibit?
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ATP-dependent Na-K pump
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Which pump do Beta blockers inhibit? How?
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ATP-dep. Ca pump
(-) PKA mediated phosphorylation of phospholamban |
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Where do normal cardiac impulses orginate?
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SA node
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Where do abnormal cardiac impulses orginate
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anywhere, including SA node
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What is refractoriness dependent on in slow-response cells?
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Recovery of Ca channels
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What is refractoriness dependent on in fast-response cells?
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Na channel recovery
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What determines basic HR? What else is important?
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Automaticity
Conduction Velocity |
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How is automaticity controlled?
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The ANS controls spontaneous depolarization (phase 4) threshold potential, and resting membrane potential
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3 categories of arrhythmias
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Defects in impulse formation
Defects in impulse conduction Defects in both |
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Mechanism of defective impulse formation
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SA node automaticity interrupted or altered--missed or ectopic beats
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Can ectopic beats occur w/o SA node alteration or interruption?
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Yes
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MA of defective impulse conduction
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AV node conduction accelerated or decreased--- irregular beats
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Two types of defective impulse formation
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Altered automaticity
Triggered automaticity: EAD and DAD |
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Give and example of early after depolarization
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Torsades de pointe
Drugs that prolong QT interval: Amiodarone, procainamide, ibutilide |
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Give causes of delayed after depolarization
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Mycardial ischemia
Adrenergic stress Digitalis intoxication |
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Two types of defective impulse conduction
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1. Re-entry e.g. Paroxysmal supraventricular tachycardia (PSVT)
2. Conduction block e.g. MI, drugs (Amiodarone, procainamide) |
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Give an example of a condition that causes both defective impulse formation and conduction.
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Atrial fib w/ AV block
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