L5 Heart- Cardiac Resting Membrane and AP Flashcards
Define the sequence of electrical activation (conduction) within the heart.
Automatic electrical activity starts in SA node, spreads through RA tissue to AV node, then signal sent through bundle of His then throughout heart by Purkinje fibers
Define the relationship between extracellular K and the cardiac resting Vm.
Vm and extracellular K concentrations are directly proportional until K conc. drops below normal, then Vm levels off while K continues to drop
-B/c of small Na influx and decrease in K permeability
Define inward (anomalous) rectification of K conductance.
Decrease in K permeability that occurs when the electrical or chemical driving force on K is increased
- K in the heart affects its own permeability- as K is reduced outside or as Vm depolarizes, K permeability is decreased
- Way of conserving K, limits how much leaks out, especially at rest
- It would be a waste of energy to fight against Ca influx during AP plateau, so better to turn K current off
Explain the effects of hyperkalemia on the cardiac resting Vm.
Hyperkalemia= abnmlly high extracellular K (>5meq/L)
Increases membrane K permeability
Decreases K gradient across membrane
More positive membrane potential
Explain the effects of hypokalemia on cardiac resting Vm.
Hypokalemia= abnmlly low extracellular K (
Define the ionic current (channel) mechanisms responsible for cardiac action potentials
Phase 0- Na channels activate, open and rapid depolarization brings Vm to E(Na)
Phase 1- Na channels inactivate, close and K channels transiently open
Phase 2- Ca channels activate (slow) and K conductance decreases (inward rectification), long plateau phase
Phase 3- Delayed activation of K channels, repolarization, Vm back to baseline
Phase 4- K conductance high, delayed K channels closed, Ca and Na channels closed, at resting Vm
Explain how a fast response AP can become a slow response AP.
Fast response AP activate both fast Na and slow Ca channels during the upstroke depolarization
- If abnormal conditions occur, fast responses can become slow
- Conduction slows dramatically
How does the change from fast to slow response AP affects conduction characteristics of the AP?
- If all fast response cells affected, the heart could not conduct or contract normally= cardiac arrest
- If small portion affected, conduction there slows= arrhythmias from reentry of excitation
What are the components of an EKG?
P- atrial activation/depolarization
Q- ventricular activation
T- ventricular recovery
PR interval- time between A depol and V depol
QRS complex- beginning of V depol to end of V depol
ST interval- time of rest before V recovery
Describe the actions of the Na-K pump and the Na-Ca exchange.
- Na-K pump pumps Na out and K in to maintain Na gradient
- Na-Ca exchanger exchanges 3 Na in for 1 Ca out to maintain low intracellular Ca
- Na-Ca exchanger uses the Na gradient from the pump, so it is affected by pump alterations
How does digitalis affect the Na-K pump?
Digitalis inhibits the Na-K pump, so the Na gradient isn’t maintained, less Na outside the cell means the Na-Ca exchange isn’t as active, build-up of Ca in the cell which causes stronger heart beats
-Digitalis used for CHF, classic glycoside
What role does Ca play in cardiac AP?
Ca is the cause and the reason for the long plateau- Ca depolarizes the membrane and is the signal for contraction, then CICR keeps the membrane depolarized for a while
-Need long depol. for contraction to take place
How does the SA node function?
- Slope on SA node cell is much less than ventricle- no Na channels in node cells and Ca channels are slower
- SA node cells never really rest, just drift until they reach threshold, then AP occurs
- Control HR by controlling slope of drift
- This is how they are automatic
