Week 1 Flashcards
Two components of the heart
electrical and mechanical
Cells in electrical portion and difference in response to action potential
- nodal cell: slow - myocyte: fast
Why would fibrosis slow down conduction
interrupts gap junctions which are needed/responsible for conduction of ions from one cell to the next.
Where does automaticity start?
SA node
Electrical pathway in the heart
SA node–> atria–> AV node–> Bundle of His–> Purkinje Fibers–> Ventricles
What happens when a cell depolarizes?
inside of the cell becomes more positive
How does the electrical response travel from cell to cell?
positive charge comes into the cell then flows through the gap junction to depolarize the neighboring cell
Why is size important for conduction
larger the diameter of the cell, the greater the conduction
Importance of difference in size between the SA and AV node
- SA node has large and fast fibers compared to the AV node which has small and slow fibers which allows time for blood from atrial contraction to fill the ventricles. - Also, allows for separation of atrial contraction from ventricular contraction
Action potential in Purkinje fibers
fast action potentials that depolarize ventricular cells almost spontaneously to achieve one fluid beat of the ventricles.
what differentiates slow and fast action potentials? - values?
- resting membrane potentials - Fast action potentials go down to a lower, more negative resting membrane potential (-85) and includes Purkinje fibers and cardiac myocytes. - Slower acting potentials include nodal cells and are at (-65)
What establishes the resting membrane potential? What amount of it is inside the cell?
- K+ - high concentrations
How does depolarization occur?
- Na+ and Ca++ are in greater concentration outside the cell. When they enter the cell, they make it more positive causing depolarization
How to repolarize the cell?
- Na+/K+ ATPase helps get the Na+ out of the cell - K+ channels also allow for K+ to move out of cell and make it more negative - During hyper-polarization (more negative than usual resting potential) Na+/K+ ATPase will pump K+ in to get back to resting membrane potential
Slow-Response Action Potential
- Phase 4 (funny current=slow depolarization): HCN channel is open during this phase allowing for influx of Na+, Ca++, and K+ and as resting membrane changes the closer it gets the threshold, the less permeable it is to K+ - Phase 0 (depolarization): Ca++ channels open up, allowing for influx of Ca++ through L-type channels - Phase 3 (repolarization): Ca++ channels close and K+ channels open, K+ leaves the cell allowing it to repolarize
How do the ions get in and out of the cell?
- Through ion gates
How do we have fast and slow depolarization?
- We have activation and inactivation gates in the channel and fast cells have faster reacting gates making them depolarize and repolarize faster
Fast-Response Action Potential Phases
- Phase 0 (rapid depolarization): Influx of Na+ into the cell - Phase 1 (initial repolarization): K+ channel opens and K+ leaves the cell and Na+ innactivation gates close so Na+ influx stops - Phase 2: Ca++ comes in through L-type channels but results in plateau due to K+ going out of cell through K channels - Phase 3: More K+ channels open and efflux out of the cell which then causes impermeability to Ca++ so now CA isn’t coming into the cell - Phase 4: Voltage-gated K+ channels close but K+ leak channels are still open, allowing for a return to resting membrane potential
Sympathetic regulation of electrical current of heart - what is being released and what is it binding to?
- post ganglionic adrenergic nerve terminals release norepinephrine, epinephrine, and dopamine which bind adrenergic receptors such as α, β1, and β2 that are coupled to the heteromeric G proteins
receptors coupled to the heteromeric G proteins
- α is located in arteries - β1 is located in the heart - β2 is located in the lungs
Pathway of Sympathetic regulation of electrical current of heart myocytes
- Myocyte: NE binds the β1 on the myocyte–> GDP is exchanged for GTP–> heteromeric G protein dissociates–> Gαs stimulated AC–> increases cAMP–> Activated PKA–> Phosphorylates L-type Ca++ channel, SR, and ryanodine 2 receptor (RyR2)–> increases Ca++ influx into the cytosol as well as increases Ca++ storage in the SR–> Increases heart rate
What does sympathetic innervation do to heart rate for myocytes? Why?
- Increases heart rate - Refractory period is shortened and repolarization can happen quicker because there is a large increase in intracellular Ca++ as well as Ca++ stores which will increase the permeability of K+ so it will efflux out of the cell to help balance the positive intracellular charge caused by the high [Ca++].
Pathway of Sympathetic regulation of electrical current of heart noda cells
- Dopamine (DA) binds β1–> Gαs is activated –> acts on “effectors”–> modulate signaling at HCN funny current and L-type channels–> Increases heart rate
What does sympathetic do to nodal cells and what does it do heart rate? - what happens to phase 4?
Increases heart rate because it is opening channels faster and allowing for faster influx of ions which allows for an increase in action potential frequency and allows for threshold to be lowered -Phase 4 of depolarization becomes steeper








