Beachey: Respiratory Care Anatomy and Physiology, 2nd Edition

Answers to Concept Questions

Chapter 17: Cardiac Electrophysiology

17-1	High extracellular [K+] decreases the gradient for potassium diffusion out of the cell. Because less potassium diffuses out of the cell, less electronegativity develops inside the cell. This makes the resting membrane potential less negative (closer to 0), and the membrane is easier to depolarize.

17-2	Because they inhibit the opening of fast sodium channels, antiarrhythmic drugs raise the threshold potential (bring it closer to 0). Because the resting membrane potential stays constant at 90 mV, a longer time is required for the membrane potential to decay from the resting to the threshold potential. These drugs make the heart muscle more difficult to depolarize (i.e., they make the heart less excitable).

17-3	If the sinoatrial (SA) node fails to generate an impulse, the next most excitable myocardial tissue spontaneously depolarizes and becomes the pacemaker. This tissue continues to function as the pacemaker as long as SA nodal impulses are absent. The heart rate would then be slower than normal because the new pacemaker’s spontaneous depolarization rate is less than that of the SA node.

17-4	If atrial tissue other than the sinus node (an ectopic focus) is pacing the heart, it must have a higher firing rate than the sinus node. Otherwise, this atrial focus would not be pacing the heart.

17-5	Decreased filling time leads to low end-diastolic volumes and thus low stroke volumes. Low stroke volumes diminish the pulse amplitude, making the pulse weaker and more difficult to palpate.