Contractility

Contractility is the ability of muscle cells to contract after depo-

larization. This ability depends on how much the muscle fibers are

stretched at the end of diastole. Overstretching or understretching

Contractility is the heart's ability to stretch -- like a balloon!

Nerve supply to the heart

two branches of the autonomic

The heart is supplied by the

nervous system--the sympathetic, or adrenergic, and

the parasympathetic, or cholinergic.

The sympathetic nervous system -the heart's

accelerator. Two sets of chemicals--norepinephrine
and epinephrine influenced by this system. These
chemicals increase heart rate, automaticity, AV
conduction, and contractility.

Braking the heart

The parasympathetic nervous system, --the

heart's brakes. One of this system's nerves, the
vagus nerve, carries impulses that slow heart rate
and the conduction of impulses through the AV node
and ventricles. Stimulating this system releases the
chemical acetylcholine, slowing the heart rate.
The vagus nerve is stimulated by baroreceptors,
specialized nerve cells in the aorta and the internal
carotid arteries. Conditions that stimulate the
baroreceptors also stimulate the vagus nerve.

For example, a stretching of the baroreceptors, which can oc-

cur during periods of hypertension or when applying pressure to

the carotid artery, stimulates the receptors. In a maneuver called

carotid sinus massage, baroreceptors in the carotid
arteries are purposely activated in an effort to slow a
rapid heart rate.

Transmission of electrical impulses

The heart can't pump unless an electrical stimulus occurs first.

Generation and transmission of electrical impulses depend on

four characteristics of cardiac cells:

· Automaticity -- cell's ability to spontaneously initiate

an impulse. Pacemaker cells possess this ability.

· Excitability - shifts of ions across the cell membrane (occurs due to shifts of ions )
and indicates how well a cell responds to an electrical stimulus.

· Conductivity - ability of a cell to transmit an electrical im-

 pulse to another cardiac cell.

· Contractility - how well the cell contracts after receiv-

ing a stimulus.

"De"-cycle and "re"-cycle

As impulses are transmitted, cardiac cells undergo cycles of

depolarization and repolarization. (See Depolarization-repolar-

ization cycle, page 14.) Cardiac cells at rest are considered polar-

ized, meaning that no electrical activity takes place. Cell mem-

branes separate different concentrations of ions, such as sodium

and potassium, and create a more negative charge inside the cell.

This is called the resting potential. After a stimulus occurs, ions

cross the cell membrane and cause an action potential, or cell

depolarization.

When a cell is fully depolarized, it attempts to return to its rest-

ing state in a process called repolarization. Electrical charges in

the cell reverse and return to normal.

A cycle of depolarization-repolarization consists of five phas-

es--0 through 4. The action potential is represented by a curve

that shows voltage changes during the five phases. (See Action

potential curve, page 15.)

Many phases of the curve

During phase 0, the cell receives an impulse from a neighboring cell

 and is depolarized. Phase 1 is marked by early, rapid repolarization.

Phase 2, the plateau phase, is a period of slow repolarization.

During phases 1 and 2 and at the beginning of phase 3, the

cardiac cell is said to be in its absolute refractory period. During

that period, no stimulus, no matter how strong, can excite the

cell.

Phase 3, the rapid repolarization phase, occurs as the cell re-

turns to its original state. During the last half of this phase, when

the cell is in its relative refractory period, a very strong stimulus

can depolarize it.

Phase 4 is the resting phase of the action potential. By the end

of phase 4, the cell is ready for another stimulus.

All that electrical activity is represented on an electrocardio-

gram (ECG). Keep in mind that the ECG represents electrical ac-

tivity only, not actual pumping of the heart.

Pathway through the heart

After depolarization and repolarization occur,

the resulting electrical impulse travels through the
heart along a pathway called the
conduction system. (See The cardiac conduction system, page
16.)

Impulses travel out from the SA node and through the inter-
 nodal tracts and Bachmann's bundle to the AV node. From there,

they travel through the bundle of His, the bundle branches, and

lastly to the Purkinje fibers.

Setting the pace

The SA node is located in the upper right corner of the right

atrium, where the superior vena cava joins the atrial tissue mass.

It's the heart's main pacemaker, generating impulses 60 to 100

times per minute. When initiated, the impulses follow a specific

path through the heart. They usually can't flow backward

because the cells can't respond to a stimulus immediately after

depolarization.

Bachmann's bundle of nerves

Impulses from the SA node next travel through Bachmann's bun-

dle, tracts of tissue extending from the SA node to the left atrium.

Impulses are thought to be transmitted throughout the right atri-

um through the anterior, middle, and posterior internodal tracts.

Whether those tracts actually exist, however, is unclear. Impulse

transmission through the right and left atria occurs so rapidly that

the atria contract almost simultaneously.

AV: The slow node

The AV node, located in the inferior right atrium near the ostium

of the coronary sinus, is responsible for delaying the impulses that

reach it. Although the nodal tissue itself has no pacemaker cells,

the tissue surrounding it (called junctional tissue) contains pace-

 maker cells that can fire at a rate of 40 to 60 times per minute.

The AV node's main function is to delay impulses by 0.04 sec-

ond to keep the ventricles from contracting too quickly. This delay

allows the ventricles to complete their filling phase as the atria

contract. It also allows the cardiac muscle to stretch to its fullest

for peak cardiac output.

Branch splitting

The bundle of His, a tract of tissue extending into the ventricles

next to the interventricular septum, resumes the rapid conduction

of the impulse through the ventricles. The bundle eventually di-

vides into the right and left bundle branches.

The right bundle branch extends down the right side of the

interventricular septum and through the right ventricle. The left

bundle branch extends down the left side of the interventricular

septum and through the left ventricle.

The left bundle branch then splits into two branches, or fas-

ciculi: the left anterior fasciculus, which extends through the ante-

rior portion of the left ventricle, and the left posterior fasciculus,

which runs through the lateral and posterior portions of the left

ventricle. Impulses travel much faster down the left bundle branch

(which feeds the larger, thicker-walled left ventricle) than the

right bundle branch (which feeds the smaller, thinner-walled right

ventricle).

The difference in the conduction speed allows both ventricles

 to contract simultaneously. The entire network of specialized

nervous tissue that extends through the ventricles is known as the

His-Purkinje system.

Those perky Purkinje fibers

Purkinje fibers extend from the bundle branches into the endo-

cardium, deep into the myocardial tissue. These fibers conduct

impulses rapidly through the muscle to assist in its depolarization

and contraction.

Purkinje fibers can also serve as a pacemaker and are able

to discharge impulses at a rate of 20 to 40 times per minute,

sometimes even more slowly. (See Pacemakers of the heart,

page 18.) Purkinje fibers usually aren't activated as a pacemaker

unless conduction through the bundle of His becomes blocked or

a higher pacemaker (SA or AV node) doesn't generate an impulse.

(See Pediatric pacemaker rates, page 18.)

Abnormal impulses

Now that you understand how the heart generates a normal im-

pulse, let's look at some causes of abnormal impulse conduction,

including automaticity, backward conduction of impulses, reentry

abnormalities, and ectopy.

When the heart goes on "manual"

 Automaticity is a special characteristic of pacemaker cells that

generates impulses automatically, without being stimulated to do

If a cell's automaticity is increased or decreased,

so.

an arrhythmia can occur. Tachycardia, for example, is commonly caused by

an increase in the automaticity of pacemaker cells below the SA

node. Likewise, a decrease in automaticity of cells in the SA node

can cause the development of bradycardia or an escape rhythm

(a compensatory beat generated by a lower pacemaker site).

Out of synch

Impulses that begin below the AV node can be transmitted back-

ward toward the atria. This backward, or retrograde, conduction

usually takes longer than normal conduction and can cause the

atria and ventricles to beat out of synch.

Coming back for more

Sometimes impulses cause depolarization twice in a row at a

faster-than-normal rate. Such events are referred to as reentry

events. In reentry, impulses are delayed long enough that cells

have time to repolarize. In these cases, the active impulse reenters

the same area and produces another impulse.

Repeating itself

An injured pacemaker (or nonpacemaker) cell may partially de-

polarize, rather than fully depolarizing. Partial depolarization can

lead to spontaneous or secondary depolarization, which involves

repetitive ectopic firings called triggered activity.

The resultant depolarization is called afterdepolarization.

Early afterdepolarization occurs before the cell is fully repolarized

and can be caused by hypokalemia, slow pacing rates, or drug tox-

icity. If it occurs after the cell has been fully repolarized, it's called

delayed afterdepolarization. These problems can be caused by

digoxin toxicity, hypercalcemia, or increased catecholamine re-

lease. Atrial or ventricular tachycardias may result. You'll learn

more about these and other arrhythmias in later chapters.