Heart 1 Flashcards
Working myocardium
Atrial and ventricular muscle
Specialized conduction system
SA node, internodal pathways, AV node, bundle of His, bundle branches, Purkinje fibers
P wave
Atrial activation
QRS complex
Ventricular activation
T wave
Ventricular recovery
Difference between Nernst and Goldman-Katz equations
Nernst gives the theoretical equilibrium potential with only taking into account the ions in question; Goldman-Katz gives the actual resting membrane potential considering ALL ions in the solution
What pharmaceutical inhibits the Na-K pump?
Digitalis - has been in use in medicine for the last 200 years, but the mechanism of action has only been known for the last 30
Na-Ca exchange
Exchanges 3 sodium ions in for one calcium ion out to produce an electrogenic net inward current
How is the sodium-calcium exchange indirectly affected?
Since sodium is also being used to exchange potassium, the concentrations of sodium will flux within the cell and indirectly affect calcium exchange
Anomalous rectification
A decrease in potassium permeability that occurs when either the electrical or chemical driving force on potassium is increased
What are the two reasons for the deviation between the predicted Ek by Nernst and the actual Vm?
Small amount of sodium influx and a decrease in potassium permeability when the concentration is within normal limits and lower
Which is better for the heart: hyperkalemia or hypokalemia?
Hypokalemia, due to anomalous rectification
What happens with K current during the action potential plateau?
K permeability decreases, which then delays repolarization
Normal physiological concentration of potassium
3-5 meq/L
Describe the consequences of hyperkalemia
It increases membrane potassium permeability, which decreases K+ concentration gradient across the membrane. This creates a more positive membrane potential
Describe the consequences of hypokalemia
Decreases membrane potassium permeability due to inward rectification. It then increases the potassium gradient across the membrane, but there is no measurable effect due to the anomalous rectification.
Waveform in the SA node
Continuous rise and fall; no true “resting” phase
Phase 0
Upstroke of AP due to influx of sodium
Phase 1
Peak and fall due to closing of sodium channels and opening of the potassium channels
Phase 2
Plateau phase: continuation of efflux of potassium (inward rectification), net influx of calcium
Phase 3
Fall of plateau due to closing of calcium channels. Potassium channels remain open
Phase 4
Resting phase; only potassium channels remain open. Sodium channels are available, but non-active
Effect of TTX on phase 0
Fast sodium channels are blocked so fast upstroke is now the responsibility of slow Ca2+ channels
Effect of TTX on phases 2-4
None
Fast response action potentials activate what?
Both fast sodium AND slow calcium channels during initial upstroke
What happens with local damage to heart tissue?
Fast responses can become slow responses from infarct, so the damaged region can slow dramatically and cause arrhythmias due to reentry of excitation
Where do slow responses happen in the heart?
The SA node and AV node
What phases do slow response waves lack?
1 and 2
Membrane potential for slow response tissue and its threshold
-40 to -60 with threshold of -40 mV
In what tissues do fast responses happen?
Atrial, His-Purkinje, ventricular
Membrane potential and threshold for fast response cells
-90 to -80 with a threshold of -65 mV
