CVPR Week 2: Cardiac Muscle Physiology I Flashcards
(81 cards)
1
Q
Objectives
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2
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Question
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3
Q
Speed of conduction in the heart
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Highest Purkinje > Atria & Ventricles > AV node Lowest
4
Q
AV Node conduction velocity
A
the slowest and is important because it delays electrical conduction between the atria and the ventricles
5
Q
Identify
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6
Q
SA Node innervation
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- innervated by Autonomic nervous system but does not require it to generate potentials (spontaneous generation of action potentials)
- this is why you can perform a heart transplant
7
Q
Question
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8
Q
Cardiac Electrophysiology concentration gradients
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- Na+ and Ca2+ are of higher concentration outside the cell
- K+ concentration inside the cell is higher than outside the cell
9
Q
Cardiac Electrophysiology ion movement
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- 3Na+ out of the cell for 2K+ into the cell
- Action potential Na+ and Ca2+ into the cell and K+ out of the cell
10
Q
Cardiac Electrophysiology: resting membrane potential
A
other leak currents help keep the resting potential a little more depolarized than Ek such as Ca and Na leak currents keeping the membrane slightly more depolarized than the K+ equilibrium
11
Q
K+ equilibrium potential
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when the net movement of K+ is 0
12
Q
Fast response action potentials
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Do more on this!!!
Phase 0 iNa+ channel Na influx
Phase 1 iK+ rectifying channels open repolarizing the membrane outward K+
Phase 2 L-type calcium channels lead to Ca2+ influx into the cell causing membrane depolarization (inward Ca2+ and outward K+ causes the semi-plateau)
Phase 3 coincides with T wave (ventricular myocyte repolarization
Phase 4
13
Q
Question
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14
Q
Question
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15
Q
Question
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16
Q
Fast response action potentials
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17
Q
Effective refractory period
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18
Q
Effective Refractory period AKA
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ERP
19
Q
The ERP is resultant from?
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20
Q
Fast-response action potentials phase specific ion permeability
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21
Q
Question
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22
Q
Slow-response action potentials: phase specific ion permeabilities
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Phase 0: iCaL Ca2+ influx
Phase 3: K+ efflux
Phase 4: Na+ , Ca2+ L , Ca2+ T
23
Q
Conduction Summary
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24
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Fast and slow-response action potential summary
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25
Question
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Skeletal vs cardiac muscle intracellular Ca2+ release mechanisms
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Question
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Excitation-contraction coupling
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Excitation-contraction coupling and cross-bridge cycling summary
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Objectives
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Structural characteristics of cardiac muscle
3 listed
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Describe Gap Junctions
where ions and small molecules can diffuse and allow for electric communication between cardiac myocytes
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Ultrastructural characteristics of cardiac muscle
* Mitochondrion
* Sarcolemma
* T-tubule
* Sarcoplasmic reticulum
* myofribrils
* sarcomere
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Identify
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Sarcomere structural features
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cross-section of a sarcomere
every thick filament is surrounded by 6 thin filaments
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Longitudinal section of a sarcomere
this sarcomere is stuck in contraction and so cross-bridges formed between the thick and thin filaments
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Identify
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Conduction system
SA node generates action potentials without nervous input
↓
Atria contract and AV node
↓ delay
propagates action potential to the ventricles through the bundle of His and left and right bundle branches to the Purkinje fibers (delivered to the apex first allows the ventricles to contract from the bottom up)
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What are latent pacemakers
cells other than the SA node exhibiting automaticity
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Pacemaker rates
SA \> AV \> bundle of HIS \> Purkinje
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Ectopic pacemakers
Latent pacemakers that become the pacemaker of the heart
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Pacemakers of the conduction system
3 listed
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Speed of conduction in the heart
Purkinje \> Atria & Ventricles \> AV node
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Describe Na+ concentration inside and outside the cell
High outside
Low inside
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Describe K+ concentration inside and outside the cell
* High inside
* low outside
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Describe Ca2+ concentration inside and outside the cell
Low inside
High outside
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driving force for potassium
the concentration gradient exceeds the electrical gradient driving it outside the cell
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Na/K ATPase
* helps establish the electrochemical gradients and requires ATP
* Pumps potassium into the cell against its concentration gradient
* Pumps Na out of the cell against its electrochemical gradients
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Nernst Equation
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What determines Em ?
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Electrogenic ion pumps and exchangers in cardiac electrophysiology
3 listed
defines Em
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hyperpolarization cause
K+ channels open to let more out causing hyperpolarization
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Depolarization ion channels
* Na+ channels
* Ca2+ channels
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Resting membrane potential is closer to what equilibrium potential?
K+ because the membrane is more permeable to K+ because more K+ channels are open during this time
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Net Na/K ATPase
net hyperpolarizing influence because 1 more positive charge out of the cell than in
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Plasmalemmal Ca2+ ATPase
net hyperpolarizing influence because Ca2+ out of the cell
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Na+/Ca2+ exchanger
3 Na into the cell for every Ca2+ out of the cell
so net depolarizing effect
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Net influence of electrogenic pumps and exchangers
Net hyperpolarizing = -2 overall
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Types of cardiac action potentials
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Fast-response action potentials: Phase 4
* Resting Em (Er)
* Near EK due to high K+ permeability
* Dominated by iK1 (outward current due to activation of inwardly rectifying K channels)
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Fast-response action potentials: Phase 0
* Rapid depolarization
* Mediated by iNa (inward current due to activation of voltage-dependent Na channels)
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Fast-response action potentials: Phase 1
* Transient repolarization
* Mediated by
1. Na channel inactivation
2. Activation of transient outward K current (iKto)
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Fast-response action potentials: Phase 2
* Plateau
* Mediated by:
1. i CaL (inward current due to L-type voltage-gated Ca channels (VGCC)
2. Outward iK1
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Fast-response action potentials: Phase 3
* Rapid repolarization
* mediated by
1. iK (outward current due to activation of voltage-dependent K channels)
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Fast-response action potentials: Phase 4
resting Em
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Slow-response action potentials: Phase 4
Pacemaker potentials
* inward funny current (if) carried mainly by Na+
* Inward Ca2+ currents
1. iCaT (mediated by T-type VGCC)
2. iCaL (carried by L-type VGCC)
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Slow-response action potentials: Phase 0
* slow depolarization
* mediated by iCaL
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Slow-response action potentials: Phase 3
* Mediated by iK (outward current due to activation of voltage-dependent K channels)
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Summary
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Summary
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What is Excitation-Contraction Coupling?
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Identify
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Skeletal muscle calcium channel
Dihydropyridine receptor exhibits a mechanical linkage to the Ryanodine receptor
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Cardiac muscle calcium channel
* Voltage-gated Ca2+ channel stimulated by Ca2+ influx by L-Type Ca channels during phase 2 of the fast-response action potential
* CICR (Calcium-Induced Calcium Release)
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Excitation-Contraction Coupling How?
* a couple of mechanisms
* T tubules of sarcoplasmic reticulum
* phase 2 of fast response action potential L type Ca channels open
* high concentration of Ryanodine receptors at the apex of the sarcoplasmic reticulum Calcium-induced calcium release causes the release of Ca from SR
* when SR releases Ca, Ca binds to Troponin C and allows myosin head to bind to actin like in skeletal muscle (however this is different than in smooth muscle)
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Ca2+ in skeletal, cardiac and smooth muscle
* In cardiac and skeletal muscle Ca2+ binds to a thin regulatory filament (troponin C)
* In smooth muscle, Ca2+ binds to a regulatory thick filament to facilitate contraction
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How to get the cell to relax for the next action potential?
3 main mechanisms
* Ca2+ binds to calmodulin leading to decreased Ca2+ influx and decreases CICR through the Ca2+/CAM complex
* SERCA (Sarcoendoplasmic reticulum calcium ATPase)pumps Ca2+ up its concentration gradient into the sarcoplasmic reticulum from the cytoplasm) responsible for ~ 70% of cytosolic Ca2+
* The other ~ 30% by Ca2+ extrusion by 2 mechanisms
1. 3Na+/Ca2+ exchanger
2. plasma level Ca2+ATPase
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Summary
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Summary objectives
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What phase of the action potential represents the T-wave on the ECG?
Phase 3 of the fast response action potential
