Lecture 02: Basic Structural and Electrical Chars. of Myocardial Cells (Hayward) Flashcards
diastole. where is pressure greatest during this time?
period of ventricle relaxation as blood from atria fill ventricles. Pressure outside ventricle is greater than inside ventricle
Pacemaker cells
specialized myocardial cells in SA node that undergo spontaneous depolarization (produces SELF-GENERATED action potentials) to instigate sequential depolarization of heart muscle, followed by synchronized rhythmic contractions of the heart chambers (systole)
systole. where is pressure greatest during this time?
period of ventricular contraction as ventricle pump blood out to pulmonary and systemic circulation. Pressure is greater inside ventricle than outside
How is rapid impulse conduction/depolarization achieved across myocardium?
Direct ELECTRICAL COUPLING between cells via intercalated disks with gap junctions
How do action potentials of myocardial cells compare to those generated by skeletal muscle cells?
much broader (almost 300x longer)
Why do pacemaker cells not have input from external control system?
they spontaneously depolarize and produce their own APs
sarcolemma =
myocardial cell membrane
2 most important physiological characteristics of the myocardial cell membrane
1) ability to maintain appropriate ion concentration gradients b/w intracellular and extracellular environments
2) ability to respond to electrical depolarization
Resting membrane potential of cardiac myocytes is fx of:
1) high permeability of membrane to K+
2) low permeability of membrane to other ions (i.e. Na, Ca)
3) high concentration of K+ in myocardial cells at rest
Why is K+ concentration in myocardial cells higher than extracellular environment at rest? (3 main reasons)
1) Myocardial cells have high permeability to K+
2) negatively charged proteins in cells draw K+ in
3) Na+/K+ contributes to negative balance inside cell, which also draws more K+ in
Nernst Equation
used to determine the equilibrium potential for different ions across a semi-permeable membrane at rest
Changes in extracellular concentrations of Na+ and Ca++ –> myocardial RMP
little effect
increased extracellular K+ —> myocardial cells
depolarize the RMP of cardiac muscle fibers
What does Na/K pump pump in/out of cell?
3 Na+ out, 2 K+ in. Driven by ATP
2 types of action potentials in myocardial cells
fast type and slow type
Why is AP of myocardial cells longer than normal cells?
due to large influx of Ca++ during depolarization IN ADDITION to normal Na+ influx
Most common type of AP in myocardial cells
fast response AP
Where do fast response APs occur?
atrial and ventricular myocytes + Purkinje fibers
Where do slow response AP occur?
pacemaker cells of SA and AV nodes
What do myocardial cells have a high concentration of?
glycogen
Phase 0: Rapid Depolarization (precursor + 2 main events)
Before Phase 0, pacemaker cells fire in wave of membrane depolarization. Causes:
1) opening of abundant fast-type voltage sensitive Na+ channels of myocardial cells
2) rapid influx of Na+ down Na+ concentration and charge gradient
RAPID Na+ INFLUX
Where are “backup” pacemakers located?
AV node
4 phases of typical fast response cardiac AP
0) Rapid depolarization
1) Initial repolarization
2) Plateau phase
3) Rapid repolarization
4) Resting membrane potential
RAPID Na+ INFLUX –> Ca++ INFLUX –> K+ EFFLUX –> return to RMP
decrease in extracellular K+ –> myocardial cells
hyperpolarizes
Phase 1: Initial repolarization (2 main events)
1) Na+ channels rapidly close
2) Transient K+ outward current activated by the depolarization
Phase 2: Plateau phase (3 main events)
1) Ca++ channels SLOWLY open
2) Ca++ influx according to its conc. gradient
3) Decreased K+ efflux
Phase 3: Rapid Repolarization (3 main events)
1) Ca++ channels slowly close/Ca++ conductance decreases
2) K+ efflux increases via delayed rectifier channel that was activated in plateau phase
3) Cell is repolarized/hyperpolarized as membrane potential returns to original resting negative potential
Why is plateau phase a plateau?
Low conductance of K+ during this time.
Also, slow Ca++ channel opening and closing(<–main regulator)
Why is slow nature of Ca++ channel opening/closing important?
Allows for prolonged AP in cardiac cells. Length of AP is directly related to the rate of intracellular sequestering of Ca++
When do delayed rectifier channels become activated?
During plateau phase
Phase 4: Resting membrane potential (3 main events)
1) High K+ conductance, low Na+ and Ca++ conductance
2) Na+/K+ pumps correct Na+/K+ concentrations from preceding AP
3) Na/Ca++ channels and sarcolemma restore internal Ca++ concentration
Long AP is associated with long:
refractory period
refractory period fx
allows for sufficient time between heart beats for adequate cardiac filling time and Ca++ reuptake into intracellular stores
When does absolute/effective refractory period occur?
Phase 1-3
When does relative refractory period occur?
phase 3
When is cell completely unexcitable to new input?
During phase 1-2 in absolute/effective refractory period
Stimulation of myocardial cell in beginning of phase 3 will result in:
local AP only with no propagation
Stimulation of myocardial cell during middle/end of phase 3 during relative refractory period will result in:
AP conducted, but with slower velocity. AP may not depolarize the rest of the heart and generate a heart beat.
What is amplitude of AP directly relate to?
Driving force to open Na+ channels
Normal RMP of myocardial cell
-90mV
