Cardio 03 - "the course with a heart!"

Applied Cardiac Cellular Electrophysiology (revision 2- 9/23/03)

(in B&L extend your reading 31-34, 39-40 + fig. 2-34)

 

1) In the case of a single missed sinus beat, overdrive suppression provides a safety margin of protection against takeover of the heart by a potentially dangerous ectopic pacemaker.

 

2) The differing conduction velocities of the AV node and the Purkinje system are each adaptive in facilitating a coordinated cardiac contraction.

 

3) Digitalis overdose can lead to serious AV nodal block.

 

4) Hyponatremia (low blood Na) can lead to intraventricular conduction disturbances.

 

5) Explain the following drug actions on the basis of ion and channel theory:

         a) Ca++ antagonists- slow HR and stabilize ectopic pacemakers

         b) Verapamil and nefedipine (Ca L channel blockers) decrease cardiac contractility.

         c) Norepinephrine (E) increases pacemaker firing rate (and therefore HR).

         d) Catecholamines (e.g. NE, E) increase myocardial contractility.

         e) local anesthetics (e.g. lidocaine) stabilize ventricular arrhythmias.

 

6) Absolute and relative "refractoriness" in fast fibers are explainable as due to the inactivation (h) process.

 

7) Myocardial ischemia (compromised cardiac blood flow) tends to induce ventricular cells to become ectopic pacemakers.

 

8) Increased heart rate (i.e. shorter cycle lengths) tends to cause a shorter action potential.

        

9) Tetrodotoxin (TTX, puffer fish toxin) tends to affect ventricular force less than rate.

 

10) Reentry, thought to be the main cause of ectopic pacemaking, requires the presence of a unidirectional block to occur. (see B&L fig. 2-34 8^th ed.)

 

Notes on order of discussion leaders - 1) rotation as usual Amanda, Kristin, Max, Roy 2) treat question #5 as 5 individual questions.