Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
72 Cards in this Set
- Front
- Back
What allows for a long refractory period in cardiac mm?
|
Plateau
|
|
What is the source of Ca in cardiac mm? How is this different from sk mm?
|
Cardiac mm: extracellular Ca
Sk mm: intracellular Ca from SR |
|
How is the depolarization wave spread in cardiac mm? How is it spread in sk mm?
|
Cardiac mm uses gap junctions so depolarization comes from neighboring cell.
Sk mm has T tubules that propagate the depolarization into the mm. |
|
What is calcium induced calcium release?
|
Ca from extracellular sources induces Ca from the Sr to be released in cardiac mm. (Ca induces RyR receptors)
|
|
What is the mech that allows actin/myosin binding in cardiac mm
|
Ca binds troponin, just like Sk mm!
|
|
What are two ways Ca is cleared from cardiac mm. What is the result from decreased Ca
|
1. SERCA: ATPase on SR
2. 2nd Active Transport: Ca leaves and Na enters the cell When Ca decreases it no longer binds troponin so Actin/Myosin cant bind. |
|
How many AP in autorythemic cells are needed to elicit 1 AP in contractile cells?
How does an AP reach contractile cells? |
1
**the AP in autorhythmic cells are carried by PK fibers to the contractile cells. The AP spreads through contractile cells via gap junctions in intercalated disk |
|
Trace the conduction path of the heart
|
SA
AV Bundle of HIS R/L Bundle Branch PK Fibers |
|
What mechanical event follows atrial depolarization?
|
Atrial Contraction?
|
|
What allows depolarization to spread rapidly among the contractile cells of the heart?
|
Intercallated disks
|
|
Do autorhythmic cells do mechanical work?
|
NO
|
|
What increases the force of contractility of cardiac mm?
|
Ca
|
|
What is a distinguishing characteristic of cardiac mm?
|
it has intrinsic control
|
|
Does Cardiac mm rely on motor neurons?
What mechanism allows this? |
NO
the AP generated by AR cells frees the heart from needing motor neurons |
|
Intercalated disks are made of what two features. What is the function of each
|
1. Desmosomes: resist mechanical force
2. Gap junctions: eletrical coupling, cytoplasm is continuous Together, these allow the cardiac mm to act as a single unit |
|
What are the major cell types in cardiac mm?
|
1. Contractile Cells: more abundant, respond to depolarization by contracting, do the mechanical contraction, AP has a characteristically long refractory period, Fast AP
2. Autorhythmic (conductile) Cells: rapid spread of eletrical signal, conducting system, dont contract, initiate and propagate the AP that triggeres contraction, 'pacemaker', myogenic, self excitable, gives rise to a coordinated rhythmic pumping, Slow AP |
|
When is a contractile cell stimulated, what happens at stimulation?
|
contractile cell is stimulated by an AR cell. At this time ALL channels are stimulated to open, but do so at differing speeds
|
|
In AR cells what ion channel allows AP generation (depolarization) once threshold has been reached
|
L type Ca channels
|
|
What leads to depolarization in AR cells
|
F type Na channels open
T type Ca channels open (L type open at threshold to cause upstroke) K channels close |
|
name the 4 ion channels involved in AP of AR cells
|
T type: transient Ca. When these open, Depolarization
F type: funny Na. When these open, Depolarization L type: long lasting Ca. Generates depolarization of AP (upstroke), close during repolarization K+. Open to repolarize the cell |
|
Describe the general characteristics of the AP for a contractile cell.
time resting potential refractory period |
long period of time!
stable resting potential LONG refractory period to ensure NO tetnus |
|
What occurs during phase 0 of an AP created by contractile cells?
|
this is the upstroke of the AP
Na enters the cell cell is DEPOLARIZED **recall in AR cells phase 0 occurs due to Ca entering the cell |
|
What occurs during phase 1 of an AP created by contractile cells?
|
breif repolarization due to a little K (fast K channels)leaving the cell and Na channels closing
|
|
What occurs during phase 2 of an AP created by contractile cells?
|
plateau period: inward/outward currents are about equal
Responsible for the LONG AP seen in cardac contractile cells Ca will enter the cell K leaves the cell |
|
what is the major difference btwn cardiac contractile cell AP and sk mm AP?
|
Phase 2 PLATEAU. the cardiac cells have a period when Ca into the cell is about equal to the K out of the cell so there is a broad flat peak in the AP. This ensures cardiac cells will NOT have tetnus
|
|
Ca inhibitors will block which phase of AP in contractile cells?
|
phase 2
plateau |
|
What occurs during phase 3 of an AP created by contractile cells?
|
Repolarization!
Ca no longer enters the cell K leaves the cell to hyperpolarize the cell to resting |
|
What occurs during phase 4 of an AP created by contractile cells?
|
Resting membrane potential
|
|
How long does a mm contraction take in relation to the AP that generated it (contractile cells). What does this mean and why is it important to have this response?
|
the contraction lasts longer than the AP
ie by the time the AP is over the mm is just finishing up contraction, this restricts summation and tetnus in cardiac mm. Good so that mm can contract AND relax: its a pump! |
|
What does an AP in a contractile cell elitic?
|
a mm contraction
|
|
Where are the AR cells that conduct AP located?
|
SA node
|
|
What is the pacemaker of the heart? What is a unique feature?
|
SA node
Unstable resting membrane potential |
|
Why is the pacemaker of the heart the SA node?
|
the SA node has the highest rate of intrinisic depolarization (HR)
|
|
Name 3 differences in the AP of contractile cells vs AR cells
|
1. automaticity in AR only
2. Plateau in contractile only 3. unstable resting membrane potential in AR only |
|
What phases are missing in AR AP?
|
1
2 |
|
What occurs during phase 0 of an AP created by AR cells?
|
upstroke of an AP
caused by Ca entering the cell **recall an inflow of Na is responsible for phase 0 in contractile cells |
|
What occurs in phase 3 of an AP created by AR cells?
|
Repolarization
K leaves the cell Ca channels close |
|
What occurs in phase 4 of an AP created by AR cells?
|
Pacemaker potential: Automaticity
Spontaneous depolarization |
|
What causes depolarization of cells in the SA node?
|
Spontaneous depolarization to threshold fires an AP
Pacemaker Potential F type Na channles (turned on by previous repolarization) T Ca open at threshold |
|
What causes the upstroke of AP in AR cells? Contractile cells? What phase
|
AR: Ca
Contractile: Na Phase 0 |
|
The rate of what phase of what AP sets HR
|
Phase 4
AP by AR **when the slope of the depolarization is more steep more AP will fire and so HR increases |
|
From what node does NSR (normal sinus rhythem) occur? What is the BPM for normal conduction
|
SA node
60-100 |
|
When will a latent pacemaker take over for the heart?
|
When the SA node is blocked
the fastest pacemaker will take over. The pacemaker potential is highest at the begining of the condiction path and slowest at the end of the conduction path ie SA>AV>Bundle of HIS> R/L bundle branch> PK fibers |
|
Is conduction through the AV node slow or fast?
|
Slow
|
|
Is conduction through the PK fibers slow or fast?
|
fast
|
|
What does conduction velocity refer to?
|
the spread of an AP through the heart
**conduction velocity has physiological implications |
|
name 2 factors that dictate conduction velocity
|
1. upstroke of AP (how membrane pot changes over time)
2. resistance |
|
What cardiac cell type fires fast AP?
|
contractile cells
|
|
What cardiac cell type fires slow AP?
|
Pacemaker (AR cells)
|
|
Where are T Tubules more developed in the heart?
|
ventricles
|
|
State the steps of Excitation Contraction Coupling in cardiac mm
|
1. AP brings depolarization down the T tubule
2. L type Ca channels open as part of AP (phase 2, plateau) 3. The L type (DHP) receptors that allow Ca into the cell induce more Ca to enter the cell via RyR on SR 4. Ca binds troponin and moves tropomyosin out of the way 5. Actin/Myosin bind and cross bridging occurs 6. Relaxation occurs when Ca is cleared by SERCA |
|
What is the tension/force/contractility of a cardiac mm contraction proportional to?
|
Ca levels!
|
|
What determines how much Ca is released from the SR
|
Ca induced Ca release
1. amt of Ca in Sr 2. Amt of Ca that enters via L type |
|
What contributes to the majority of Ca flux?
|
SERCA pump
|
|
Name 2 drugs that enhance the force of contraction of cardiac mm?
|
Digitalis
Digitoxin |
|
How do digitalis/digitoxin work?
|
They block the Na/K ATPase so that the Na/Ca exchanger works in reverse and pumps Na out of the cell and Ca into the cell.
Increased Ca leads to increased force of contraction |
|
In what direction does the Na/Ca exchanger normally work?
|
Allows Na INto the cell along conc grad
Pumps Ca OUT of the cell |
|
When the Na/K ATP ase no longer functions what happens to the Na/Ca exchanger?
|
Ca is moved INTO the cell!
This increases the force of contraction of the heart ex digitalis/digitoxin |
|
Does the heart undergo tentus or summation?
How does the heart regulate the force of contraction? |
NO
strength of contraction increases when cardiac mm fibers are stretched |
|
Does cardiac mm work at the optimal length tension relationship?
|
NO
|
|
What does the force of contraction of cardiac mm rely on?
|
initial fiber length
|
|
What does increasing the length of a cardiac mm fiber do?
|
1. increases affinity of Ca and troponin
2. Increases release of Ca from SR |
|
what is the realtionship btwn ca, length, force?
|
increased ca leads to increased force. ca can be increased by stretching cardiac mm fibers
|
|
how does contractility alter tension?
|
independent of fiber length
|
|
positive ionotropic effect
3 examples |
increasaed contractility and rate of tension at a fixed length
sympathetic NS catecholamines HR |
|
negative ionotropic effect
2 examples |
decreased contractility and rate of tension at a fixed length
parasympathetic activity heart failure |
|
what causes faster relaxation in cardiac mm?
|
phospholamban is Pi and increases activity of SERCA
|
|
What two things will increase the rate of tension development in cardiac mm?
|
1. phosphorylation of Ca channels on the SR increase the Ca that comes into the cell during the Plateau
2. Increased ca induced ca release (increased tension) |
|
What is increased peak tension due to in cardiac mm?
|
increased intracellular Ca
|
|
Where do T tubules and SR meet?
|
Z line
|
|
is cardiac mm single nuclei or multinucleate
|
SINGLE
|
|
waht things increase contractility
|
SNS
Catecholamines HR Contractility is decreased by: Heart Failure and PNS **Recall contractility (inotropism) is a way to increase the force of contraction without changing fiber length, this method increaes Ca to increase contractility |