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CARDIAC ELECTROPHYSIOLOGY
Microscopic Structure of Myocardial Cells
Myocardial cells are long, narrow and often branched.
1.
Sarcolemma
The sarcolemma is a thin bilayer of phospholipids separating the intracellular
and extracellular spaces.
2.
Intercalated disc
The intercalated disc forms a mechanical and electrical junction between
adjacent cells.
3.
Nexus
A specialized type of cell-to-cell connection, the nexus (sometimes called the gap
junction), is present within the intercalated disc and is the site of direct exchange
of small molecules.
4.
T-tubule
Another specialized membrane structure, the T-tubule system, carries electrical
excitation to the central portions of the myocardial cells, thereby allowing
simultaneous activation of the deep and superficial portions of the cells.
5.
Myofibrils
The myofibrils are long, rod-like structures that extend the length of the cell.
Contraction of the muscle involves the generation of force, shortening by the
myofibrils.
6.
Mitochondria
Mitochondria are small, rod-shaped membranous structures located within the
cell. They are the major sites of breakdown of substrates and synthesis of
high-energy compounds.
7.
Sarcoplasmic reticulum
The sarcoplasmic reticulum is an extensive, self-contained internal membrane
system. Calcium ions are stored in the sarcoplasmic reticulum and released for
use after depolarization.
Myocardial Cells Properties
1.
Automaticity
The ability of the cell to spontaneously generate and discharge an electrical
impulse (pacemaker potential)
2.
Excitability
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The ability of the cell to respond to an electrical impulse.
3.
Conductivity
The ability of the cell to transmit an electrical impulse from one cell to another.
4.
Contractility
The ability of the cell to shorten and lengthen its muscle fibers in response to an
electrical stimulus.
5.
Extensibility
The ability of the cell to stretch.
Electrical Characteristics of the Myocardial Cells
Each cardiac cell is surrounded by and filled with a solution that contains
positively charged ions (+) and negatively charged ions(-). Electrical potential, or
transmembrane potential refers to the relative electrical difference between the
interior of the cell and that of the fluid surrounding the cell. Ionic channels are pores
in cell membranes that allow for passage of specific ions at specific times or signal.
Transmembrane potentials and ionic channels are extremely important in
myocardial cells because they form the basis for electrical impulse conduction and
muscular contraction.
1.
Resting state
The inside of the cell membrane is considered negatively charged while the
outside of the cell membrane is considered positively charged. It is also called
membrane resting potential which is a stable period where there is no net ionic
motion or electrical events.
2.
Depolarization
It is the process of changing the ionic state of a cell from a resting state to an
activated state. The result is a reversal of net charges. The outer surface is
now more negative than positive and the cell is said to be depolarized.
3.
Repolarization
It is the process of rearranging the ionic state of the depolarized cell from an
activated state back to the original resting state.
The depolarization-repolarization cycle is known as the action potential. Some
myocardial cells have an intrinsic ability to spontaneously depolarize and initiate an
action potential that can be propagated throughout the cardiac tissue. Depolarization
of one cardiac cell initiates depolarization of adjacent cells and ultimately leads to
cardiac muscle contraction.
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Cardiac Action Potential
Excitation of the cell begins with a small depolarization to threshold potential
which evokes a large depolarization, the cardiac potential. It propagates the full
length of the cell membrane and communicates to adjacent cells by means of current
flow. It is divided into 5 phases:
Phase 4: Resting membrane potential
The resting membrane potential (RMP) of the cardiac cells are approximately
-80 to -90 millivolts (mV). When the cell is at rest, the intracellular K+ is very high
and sodium is low, compared with a high concentration of Na+, Ca++ also has a much
higher concentration outside the cell.
Chemical gradients
Electrical gradient
Membrane permeability
Phase 0: Depolarization
On electrical stimulation, innervation starts to conduct to conduct to cardiac cell
membrane causing the membrane resting potential to move toward to 0 mV. As the
membrane is depolarized, Na+ begins to enter the cell, thus causing the interior of the
cell to become more positive. At approximately -65 mV, the membrane reaches
threshold, the sodium-channel activation gates open. The influx of Na+ extremely
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rapid and causes the inside of the cell to become slightly more positive than the
outside cell. The peak voltages attained are +20 to +40mV.
Phase 1: Early and rapid repolarization
When the rapid influx of Na+ is terminated and rapid influx of chloride ions is
started, the transmembrane potential returns rapidly from +20 mV to 0 mV.
Phase 2: Slow repolarization (Plateau)
During this phase, slow Na+ and Ca++ channels open and allow the influx of Ca++
and Na+. K+ tens to diffuse out of the cell, balancing the slow inward flux of Na+ and
Ca++. The Ca++ entering the cell at this phase causes cardiac contraction.
Phase 3: Final repolarization
The inactivation of the slow channels preventing further influx of Ca++ and Na+
and the efflux K+ out of the cell causing the intracellular environment to become more
negative, thereby reestablishing the RMP.
Phase 4: Resting membrane potential
On returning to the RMP, the excess Na+ that entered the cell during
depolarization is now removed from the cell in exchange for K+ by means of the Na+
and K+ pump. This mechanism returns the intracellular concentrations of Na+ and
K+ to the levels before depolarization and is essential for normal ionic balance.
Conduction of Cardiac Action Potentials
Action potentials are conducted over the surface of individual cells because
active depolarization in any one area of the membrane produces local currents in the
intracellular and extracellular fluids which passively depolarize immediately adjacent
areas of the membrane to their voltage threshold for active depolarization.
Action potentials are propagated from cell to cell in the heart because adjacent
heart muscle cells have regions of close membrane association called gap junctions
(nexuses) through which the local internal electrical currents can easily pass.
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Refractory period
The period following depolarization, during which the cardiac cells may or may
not be depolarized by an electrical stimulus, depending on the strength of the
electrical impulse. It is divided into the absolute refractory period and the relative
refractory period.
Absolute refractory period
During this period, the cell cannot be depolarized regardless of the amount or
intensity of the stimulus. This period lasts from the beginning of depolarization to
approximately -50 mV during phase 3.
Relative refractory period
During this period, the cell is not fully repolarized, but can be depolarized with
strong electrical stimulus. This period lasts from approximately -50 mV during
phase 3 to when the cell returns to RMP.
Electrical Conduction System of the Heart
Action potentials of cells from different regions of the heart are not identical but
have varying characterisitics that are important to the overall process of cardiac
excitation. Some cells within the specialized conduction system have the ability to
act as pacemakers and to spontaneously initiate action potentials whereas ordinary
cardiac muscle cells do not.
Specific electrical adaptations of various cells in the heart are reflected in the
characteristic shape of their action potentials.
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Mechanical Activity
Muscle action potentials trigger mechanical contraction through a process called
excitation-contraction coupling.
As the myocardial cell is depolarized, specifically during phase 2 of the AP, the
majority of Ca++ enters the cytoplasm from stores in the sarcoplasmic reticulum, then
binds with troponin and tropomyosin, molecules that are present on the actin
filaments, resulting in contraction.
Once contraction has occurred, Ca++ is taken back up into the sarcoplasmic
reticulum and the cytplasmic concentration of Ca++ falls, leading to muscular
relaxation.
Cardiac Vectors
The wave of depolarization that spread through the heart during each cardiac
cycle has vector properties defined by its direction and magnitude. At any instant
depolarization occurs in multiple directions as the activation wave is propagated.
Thus the instantaneous direction of the wave recorded at the skin surface is the
resultant of multiple ‘minivectors’ through the heart.
Cardiac vectors of each cardiac cycle include:
1. Atrial depolarization vector
2. Septal depolarization vector
3. Apical and early ventricular depolarization vector
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4.
5.
Late ventricular depolarization vector
Ventricular repolarization vector
References
Mohrman, D.E. & Heller, L.J. (1981). Cardiovascular physiology (4th Ed.).
U.S.A.:McGraw-Hill.
Thelan, L.A., Davie, J.K., Urden, L.D. & Lough, M.E. (1994). Critical Care Nursing:
diagnosis and management (2nd Ed.). St. Louis: Mobsy.
Huff, J. (1997). ECG workout Exercises in Arrhythmia Interpretation (3rd Ed.).
Philadelphia: Lippincott.
Wood, S.L., Froelicher, E.S.S., Halpenny, D.J. & Motzer, U.S. (1995). Cardiac
Nursing (3rd Ed.). Philadelphia: J.B. Lippincott.
MAK WAI LING
Nurse Specialist
YCH ICU
2002
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