Phys lecture 1: Cardiac excitation contraction Flashcards
Describe the parasympathetic and sympathetic innervation of the heart.
parasympathetic fibers originate in the cardioinhibitory center of the medulla oblongata, travel along the vagus N to innervate the SA node (left vagus N) and the AV node (right vagus)
sympathetic fibers arise in the cardioacceleratory center of the medulla oblongata, travel along the sympathetic trunk–> cardiac Ns to terminate on the SA and AV nodes and ventricles
Describe the conduction system of the heart.
- SA node spontaneously depolarizes
2a. AP travels rapidly thru internodal pathways to the AV node
2b. depolarization travels (more slowly) thru atrial myocytes and they contract - AV node slows conduction signal
- AP moves to bundle of His and purkinje fibers to the apex of the heart
- depolarization wave spreads upward from the apex (thru myocytes –> contraction)
Why does the AV node need to slow doen the depolarization?
to allow time for the ventricles to fill before contracting
T or F: In health, the ventricles do not spontaneously depolarize
T (want the contraction to be in synchrony)
Describe the phases of the ventricular action potential (AP)
describe polarization and channels for each phase
phase 4 = resting potential (-85mV)
- I-K1 potassium channel active
phase 0 = rapid depolarization (to +50mV)
- from opening/activating of Na channels when cells reach threshold of -60 mV
phase 1 = small and transient repolarization
- I-TO K+ channels open and allow some K+ to exit)
phase 2 = stable depolarized state
-balance of Ca-in and K-out channel activity
phase 3 = repolarization
-activation of K+ channels (IK1, IKATP, IKAch) and inactivation of Ca channels
4 = resting potential
T or F: all the cells in the heart have the same electrical profile
F: they all are different
Describe the electrical profile (AP) of the SA node
- the SA node is hyper/re-polarized at -60 mV
- this hyperpolarized state activates I-f channels
- Na enters cell and depolarizes it
- at -40 mV, I-f (Na) channels inactivate and Ca channels activate and moves into cells
- at peak of depolarization Ca channels close and K+ channels open
- repolarization of cell
What is the minimum potential of ventricular cells? SA node?
- 85 mV
- 60 mV
Rank the parts of the conduction system from fastest to slowest.
Bundle of HIis and Purkinje cells > ventricular muscle > atrial muscle > SA and AV nodes
What part of the cardiac conduction system has the highest rate of spontaneous discharge? Why is this important?
SA node = it sets the pace of AP firing (pacemaker cells)
Does atrial and/or ventricular muscle have spontaneous discharge activity?
No, but they will if damaged
Does the AV node, bundle of His, and Purjunke cells have spontaneous discharge activity?
Yes, BUT it is at a slower rate than the SA node, therefore the SA node sets the pace of AP firing
These cells can take over if the SA node is not operating or cannot transmit signals!!!!!!
What is the intrinsic rate of the SA node (parasympathetic and sympathetic activity absent)?
100-120 bpm
**SA node is the pacemaker
If the SA node is damaged, who will take over?
V node, bundle of His, and Purjunke cells BUT it will be a slower pace than the SA node
What are 3 effects that parasympathetic activity has on the heart?
- dec HR
- decreases conduction velocity (esp at AV node)
- dec excitability of LATENT pacemakers (BOH, PJF)
What are 3 effects that sympathetic activity has on the heart?
- inc HR
- inc conduction velocity (esp at AV node)
- increases excitability of LATENT pacemakers
- decreases (makes more negative) the threshold for Ca channel activation (=inc depolarization at SA node)
What effect does Ach have on the time to conduct an AP thru the AV node?
Norepi?
ACh: inc time = slower (parasympathetic)
Norepi: dec time = faster (sympathetic)
What effect does Ach have on the time to conduct an AP thru the bundle of his?
Norepi?
no effect = symp and para symp act on the AV node to control conduction velocity… once the signal is fired in the AV node and reaches the BOH it will travel v quickly
How is our resting HR different than the spontaneous rate of the SA node? Why is the important?
At rest, parasympathetic activity prevails (over sympathetic) to keep our HR ar ~60 bmp which is less than the spontaneous SA rate of 100 bmp
T or F: At rest, parasymp NS is at work and not the symp NS
How has this been proven?
F: both are firing at rest, but parasympathetic prevails
**giving alpha and beta blockers experimentally (blocks both para and symp activity) shows that resting HR is lower than spontaneous SA rate (= parasymp prevails at rest!)
How do we go from an AP to a contraction?
depolarization of cells (from an AP) causes Ca channels to open and Ca to enter the cell –> this inc in intracell Ca triggers Ca release from SR (Ca induced Ca release)
What 2 things regulates the strength of muscle contraction?
- intracell Ca levels
2. initial length of cardiac fibers (determines sensitivity of myofilaments to Ca)
How is muscle contraction reversed? (normal process, i.e. we dont want the muscle to always be contracted)
Ca uptake by SR
Why must the Ca that enters the cell eventually be efflux-ed?
if not, the cell will become calcified
How is Ca efflux-ed? What are the transporters?
Ca-ATPase
NaCa antiporter that is driven by NaK-ATPase created Na gradient
How is Ca taken into the cells? (Transporters)
Ca channels NaCa antiporter (ATP driven)
Describe the mechanism of chatecholamine-induced cardiac cell sympathetic activation
Epi/Nor epi binds B-AR ->
activation of GPCR ->
Adenylate cyclase active ->
cAMP increases ->
PKA active and phosphorylate/activate ramadine receptor and Ca channels
Ca released from SR
= increase intracell Ca = inc contractility
Describe the mechanism of chatecholamine-induced cardiac cell parasympathetic activation
Ach binds M2R inhibits AC dec cAMP PKA inactive Ca stays in SR and power stoke is blocked (troponin not released)
Why would sympathetic activity accelerate both cardiac contractility and relaxation
relaxation accelerated do that you can have contraction occur sooner
What is lusitrophy?
cardiac relaxation
What is inotrophy?
cardiac contraction
What do chatecholamines accelerate the rate of?
cardiac contraction and relaxation
intracell Ca decline
EDV - ESV =
SV
What determines preload?
EDV
What determines SV?
EDV
How muscle muscle cell stretch cause an inc on contractility
stretch …
- stretch activated Ca channels open (slow response)
- increases Ca sensitivity/less Ca needed to generate tension (fast response)
T or F: increasing the length of the sarcromere increases the cardiac force generated
T
