Electrophysiology of the Heart Flashcards
<p>Describe Sarcolemma</p>
<p>- Phospholipid Bilayer
- -> Controls flow of solutes based on Membrane receptors, ion channels, Semipermeable membrane)
- -> regulates electrical activity through connections between adjacent cells (Gap junctions)</p>
Describe the driving force of ions
Driving force is potential available to DRIVE ions across membrane
- differences between membrane voltage and equilibrium potential
- Resistance impedes flow of ions
OHM’s LAW USED
Describe the Resting membrane potential for Na, K+
Na+: Large conc and electrical gradient favoring SODIUM ENTRY INTO CELL
K+: Conc Gradient favors POTASSIUM EFFLUX FROM CELL; Electrical gradient favors Potassium ENTRY INTO CELL.
Cl-: Concentration gradient favors ENTRY into cell; Electrical gradient favors EFFLUX from CELL
Ca+: Large conc. and electrical gradient for CALCIUM ENTRY INTO CELL
Describe Fast Sodium Channels in a cardiac action potential
- Lots of sodium enters the cell FAST causing rapid depolarization.
- “Slaps” shut with High membrane potential
- Similar to skeletal muscle
- ONly open for 1/1000th of a second
- -> Funny current generated due to “slow” sodium current in nodal cells (NOT IN MYOCYTES) that contribute to RMP of nodal cells
Describe Slow calcium channels in a cardiac action potential
Open longer (2-3/10th of a second)
- Responsible for the PLATEAU PHASE of AP
- Calcium INFLUX required for muscle contraction
- -> difference from skeletal muscle, in that most of skeletal muscle Ca++ release by ER
- -> without EC calcium influx, heart will stop beating
- -> calcium channel blockers will affect heart and not skeletal muscle (as much) do to this property
Describe Potassium channels in a cardiac action potential
- Initiate repolarization
- Decreased potassium perm. during AP in cardiac muscles
- -> allows plateau to persist, once calcium and sodium flux stops, potassium permeability increase to return to RMP
Describe the phase 0 of the cardiac action potential.
PHASE 0: FAST depolarization due to opening of sodium channels
Decribe Phase 1 of the cardiac action potential
PHASE 1: Early repolarization due to sodium channels closing, but some potassium channels open (repolarization is incomplete)
Describe PHase 2 of the cardiac action potential
PHASE 2: PLATEAU, membrane potential approx. zero due to SLOW Ca+ Channels
- -> requires concurrent movement opposite to calcium to keep it even.
- -> allows blood to be ejected from heart
Describe PHase 3 of the cardiac action potentials
Phase 3: RAPID REPOLARIZATION
- More calcium channels are closing and opening of potassium channels
Describe PHase 4 of the cardiac action potentials
Phase 4: RESTING MEMBRANE POTENTIAL
- only Potassium channels are open
- resting potential maintained until next stimulus
Describe the time and voltage-gating of sodium channels
1) At RMP, inactivation gate is open, pore channel is closed (ready position)
2) signal is received (depolarization), pore channel opens and ions can flow (VOLTAGE DEPENDENT)
3) Inactivation gate closes (TIME DEPENDENT)
4) Dramatic change in voltage causes the pore channel to close (VOLTAGE DEPENDENT)
5) Once enough time has passed, inactivation gate opens and channel is RESET/Ready for another AP.
Describe ABSOLUTE Refractory Period of Cardiac muscle cells
- Begins at upstroke of Phase 0 (fast sodium channels open)
- Ends when sodium channels are reset to ready position (inactivation gate open, pore channel closed) (Midway through Phase 3)
- ELIMINATES POTENTIAL to TETANIZE heart muscle (tetany = summation of AP)
Describe RELATIVE refractory period of cardiac muscle cells
- AP can be elicited (requires greater than normal stimulus which results in abnormal AP)
- RRP AP
- -> fewer number of FAST SODIUM channels can participate (results in a decreased slope of Phase 0)
- -> No plateau (PHASE 2) due to potassium efflux still occurring
- -> only a portion of the ventricle will be depolarized instead of entire syncytium (some myocytes will still be in ERP)
- -> Disorganized depolarization is ventricular fibrillation
Describe Phase 2 of the Nodal AP
Phase 2: Calcium channels open (voltage Sensitive)
- -> Slow/low slope of action potential depolarization
- -> NO FAST SODIUM CHANNELS
Describe Phase 3 of the Nodal AP
Phase 3: After depolarization, potassium channels open
Describe Phase 4 of the Nodal AP
Phase 4: Slow positive slope “prepotential” (slow depolarization) until threshold is reached
- Responsible for automaticity
describe the ionic channels and their participation in Phase 4 of Nodal AP
- Na/K ATPase: pump sodium out and potassium in
- FUNNY SODIUM CHANNELS: slow leak of sodium into cell (faster than efflux)
- Potassium leaking, as in myocytes, but declining due to change in membrane potential
- Calcium influx increases during Phase 4
- *causes a slow depolarization**
Describe Phase 0 and 1 of Nodal AP
DON’T EXIST NO FAST SODIUM CHANNELS
Describe the effects of the ANS on the Cardiac action potential
= Positive chronotrophs (norepinephrine): Increase permability of nodal cells to sodium and calcium which increases slope of Phase 4, so threshold is reached faster
= Negative Chronotrophs (acetylcholine): Increase permeability of nodal cells to POTASSIUM (efflux) which lowers resting potential and thus takes longer time to reach threshold (lowers slope of Phase 4)
Describe SA Node
- Function: Primary pacemaker
- time/voltage dependent currents: Ca, K, funny current (Na+)
- Beta-Adrenergic Effect = Increased conduction velocity and increased pacemaker rate
- Cholinergic effect = Decreased conduction velocity and decreased pacemaker rate
Describe Atrial/ventricular muscle
- Expel blood from chambers
- Time/voltage dependent currents: Na, Ca, K
- Beta-Adrenergic Effect = Increased strength of contraction
- Cholinergic effect = little effect
Describe AV node
- Function: Secondary pacemaker
- Time/voltage dependent currents: Ca, K, Funny current
- Beta-adrenergic effect = increased conduction velocity and pacemaker strength
- Cholinergic effect = decreased pacemaker rate and decreased conduction velocity
Describe purkinje fibers
Function: Rapid conduction of action potentials/ Tertiary pacemaker
- Time/voltage dependent currents: Na, Ca, K, funny current
- Beta-adrenergic effect = Increased pacemaker rate
- Cholinergic effect = decreased pacemaker rate
Describe the sequence of depolarization
SA node Atria AV node Septum Apex Ventricular free walls
Describe the sequence of contraction of cardiac muscle
1) AP enters from adjacent cells
2) voltage-gated Ca+ channels open and Ca+ enters the cells
3) Ca+ induces Ca+ release through ryanodine receptor channels
4) local release causes Ca+ spark
5) summed Ca+ sparks create a Ca+ signal
6) Ca+ ions bind to troponin to initiate contraction
7) relaxation occurs when Ca+ unbinds from toponin
8) Ca+ is pumped back into SR for storage
9) Ca+ is exchanged with Na
10) Na+ gradient is maintained by Na/K ATPase
Describe the result of hyperkalemia
Extracellular potassium excess:
- Slows HR
- Dilates Heart
- Can block conduction through AV bundle
- due to decerased RMP (excess potassium depolarizes cell membrane to be less negative, which reduces the intensity of the action potential produced and makes heart progressively weaker.
Describe the result of Hypocalcemia
Excess calcium = increases contraction the direct initiation of cardiac contractile apparatus
- Deficient calcium = causes decrease in the contractile potential of the heart
Describe the affects of acetylcholine on the heart
- Decreases rate of sinus node discharge
- decreases excitability of AV nodal cells (slows or at high concentration can block ocnduction)
- Increases potassium permeability (slow leakage hyperpolarizes cell and makes it HARDER to reach threshold.
Describe the affects of Norepinephrine on the Heart
- Increases rate of SA node discharge
- increases rate of conduction and excitability
- increases force of contractions’
- Through changes in sodium and calcium permeability
Describe effects of Potassium channel blockers
- increase AP duration and Effective refractory period
- extends QT interval on ECG
Describe effects on calcium channel blockers
- slows rate of conduction at SA and AV nodes by delaying Ca+ entry
ex: Verapamil
Describe effects of sodium channel blockers
- reduces phase 0 and slope of depolarization
- increases effective refractory period
- ex: lidocaine
