In: Anatomy and Physiology
A 63year old man suddenly felt a crushing pain beneath his sternum. He became weak and began to sweat profusely. He called 911 and was taken to the hospital where it was confirmed that he had suffered a heart attack due to occlusion in a major coronary artery.
The patient had cardiac rhythm disturbances within minutes after he felt the chest pain. He was given an anti-arrhythmic drug that inactivated many of the fast Na+channels in the heart.
4.What effect would this drug have on the action potential in the SA node?
Soon after the patient arrived at the hospital, the activity in the vagus nerve fibers to the heart increased reflexively.
1. In hyperkalemia, the resting membrane potential is decreased, and the membrane becomes partially depolarized. Initially, this increases membrane excitability. However, with prolonged depolarization, the cell membrane will become more refractory and less likely to fully depolarize
2. Propagation of action potential decrease
3. Cardiac arrhythmias arise from disturbances in the functioning of the specific ion channels that normally control excitation or from the functional expression of previously latent channels. Antiarrhythmic agents act by blocking the membrane sodium, potassium, and calcium channels, but no agent has exclusive action on a given type of channel. Arrhythmias resulting from reentry form the largest group of clinically significant arrhythmias. Most arrhythmias result from depressed sodium channel function. Hence resting membrane potential dec
4. Sodium-channel blockers comprise the Class I antiarrhythmic compounds according to the Vaughan-Williams classification scheme. These drugs bind to and block the fast sodium channels that are responsible for the rapid depolarization (phase 0) of fast-response cardiac action potentials.inc duration