There are currently five methods of
execution that various States in the United States use to carry out executions:
lethal injection, electric chair, gas chamber, hanging, and firing squad.  Most of the States use lethal injection as
their main method, and keep another method as a backup in case the first method
fails.  Death is certain in these
situations, but how exactly do these methods cause death?  In this paper I have researched the various
physiologic mechanisms of action for three methods of execution—lethal
injection, the electric chair, and the gas chamber.

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Lethal Injection

was the first State in the US to adopt lethal injection for execution
(Descriptions of execution methods, n.d.). 
This method of execution uses three different drugs to cause death:
sodium thiopental (Pentothal ®), pancuronium bromide (Pavulon ®), and potassium
chloride.  These three drugs are used in
a stepwise fashion to induce death, with a saline flush in between intravenous
administration of each drug.  The first
drug that is administered is sodium thiopental.

            Sodium thiopental is an ultra-short acting barbiturate
anesthetic that depresses activity in the central nervous system (Sergo, 2007) (Intravenous
anesthetics, n.d.).  According to PubChem,
thiopental sodium:

ultrashort-acting barbituric acid derivative, with anesthetic activity.
Thiopental binds to the chloride ionophore site of the gamma-aminobutyric acid
(GABA)-A/chloride ionophore receptor complex, thereby enhancing the inhibitory
actions of GABA-A in the brain. This leads to synaptic inhibition, decreased
neuronal excitability and induction of anesthesia.”  (“Thiopental Sodium,” n.d.).

       There has been some controversy over the
effectiveness of sodium thiopental in executions.  It has been argued that sodium thiopental
does not induce respiratory arrest with certainty or that the specific dose
administered might not provide surgical anesthesia for the extent of the
execution (Zimmers et al., 2007).  Sodium
thiopental has been banned in the United States and the European Union.

       The second drug administered during a
lethal injection execution is pancuronium bromide.  Pancuronium bromide is a nondepolarizing
agent that produces skeletal muscle paralysis by blocking the myoneuronal
junction and competing with acetylcholine (ACh) for cholinergic receptors.  The relaxation of the skeletal muscles
progress in the following order: muscles associated with fine movements (such
as the eyes, face, neck, and fingers) and are followed by the muscles of the
limbs, chest, abdomen, and lastly the diaphragm (“Pancuronium Bromide,” n.d.).  Once the diaphragm has ceased movement, the
ability to breathe is quickly stopped which causes suffocation.

       The last drug administered is potassium
chloride.  Potassium plays a significant
role in cardiac function (and dysfunction). 
The potassium concentrations in the intracellular and extracellular
compartments have a role in electrophysiologic function of the myocardium.      The
administration of potassium chloride induces hyperkalemia in a rapid
fashion.  As the concentration of
potassium increases, the resting membrane potential becomes more
depolarized.  As the resting membrane
potential depolarizes to around -65mV, the voltage dependent sodium channels
are inactivated which prevents the sodium induced spike in the action potential.  During this time, energy dependent
transmembrane pumps remain active and try to correct the abnormal ionic
gradients (Chambers, 2003). 

 The concentration gradients are maintained by
sodium-potassium adenosine triphosphatase pumps (Na-K ATPase) on the wall of
the cell which pump sodium out of the myocyte and bring potassium into the
cell.  These gradients create an
electrical potential across the cell membrane which leads to a resting
potential of -90 mV.  The first phase of
the action potential (phase 0) occurs when the voltage-gated sodium channels
are open, and sodium enters the myocyte down its electrochemical gradient.  As the resting membrane potential becomes more
positive (less than -70 mV) the percentage of free sodium channels decrease,
leading to a decrement in the inward sodium flow and a coexisting decrease in
the action potential.  This causes the
resting membrane potential to become more positive causing a slowing of the
impulse through the myocardium and a prolonging of the membrane
depolarization.  This ultimately causes
the duration of the QRS wave to lengthen (Parham et al., 2006).

potassium levels keep increasing, the resting membrane potential becomes even
more positive, and decreases the action potential.  The decrease in the action potential leads to
a slowing of myocardial conduction, which is manifested by a prolonged P wave,
PR interval, and QRS wave.  As the
potassium levels continue to rise and myocyte depression occurs, and action
potential continues to decrease.  After
the influx of sodium across the membrane in phase 0, the potassium ions leave
the cell along the electrochemical gradient. 
As the membrane potential becomes more positive (-40 to -45 mV) during
phase 0 the calcium channels are stimulated to begin entering the myocyte
(Parham et al., 2006).

 During phase 2 the potassium efflux and the
calcium influx offset one another, causing the electrical change going across
the cell membrane to remain the same. 
This is the plateau phase of the action potential.  In phase 3 the calcium channels close and the
potassium channels continue to move potassium out of the cell thus restoring
the electronegative membrane.  As the
amount of potassium increases, the rate of phase 0 of the action potential
decreases which leads to a longer action potential, wider QRS complex, and a
prolonged PR interval.  This would appear
as a delayed intraventricular and atrioventricular conduction.  This delay continues through the QRS wave
(Parham et al., 2006). 

the level of potassium increases the SA node activity may begin to stimulate
the ventricles without evidence of atrial activity, thus producing a
sinoventricular rhythm.  This happens
because the SA node is much less susceptible to the effects of hyperkalemia and
can keep stimulating the ventricles without evidence of atrial electrical
activity.  As the potassium increases
even more the sinoatrial conduction stops and the passive junctional pacemakers
begin taking over the electrical stimulation of the myocardium.  The QRS wave continues to widen and
eventually blends in with the T wave. 
Once this happens, ventricular fibrillation and asystole will follow
(Parham et al., 2006).  This effectively
causes cardiac arrest.

Gas Chamber

In 1924 the use of cyanide gas was introduced in
Nevada as a humane way of executing inmates. 
For execution using cyanide gas, the condemned person is strapped to a
chair within an airtight chamber, and then the chamber is sealed with only the
condemned person inside.  A long
stethoscope is affixed to the inmate so that a doctor outside of the chamber
can determine if the person is dead.  The
warden then gives the signal to the executioner who then flicks a lever that
releases crystals of sodium cyanide into a pail of sulfuric acid underneath the
chair that the person is sitting in.  The
crystalline sodium cyanide reacts with the sulfuric acid and releases hydrogen
cyanide gas (“Descriptions of execution methods”, n.d.).  The following chemical equation details this

absorbed either through inhalation or ingestion, the cyanide enters the blood
stream and is distributed very rapidly to the rest of the body.  Inside the cells, the cyanide attaches itself
to ubiquitous metalloenzymes which renders them inactive (Leybel et al.,
2016).  Most of the toxicity results from
the inactivation of cytochrome oxidase at cytochrome a3 which causes an uncoupling
of the mitochondrial oxidative phosphorylation and inhibits cellular
respiration even when there are adequate oxygen stores.  Cellular metabolism shifts from aerobic to
anaerobic and begins producing lactic acid, and the tissues with the highest
need for oxygen (the brain and the heart) are most affected (Leybel et al., 2016).  Vapor exposure in high doses usually cause
death in 6-8 minutes.


            New York built the first electric
chair in 1888 (“Descriptions of execution methods, n.d.).  Prior to execution the person has their head
and their legs shaved.  The person is escorted
into the execution chamber, and then they are strapped into the chair using ties
made of leather or webbing straps across their chest, thighs, legs, and arms.  A metal or leather helmet is placed on the
person’s head, the helmet contains one to two copper electrodes in direct
contact with a brine soaked sponge.  The
brine works because the salt in the solution is very conductive compared with
the human body (Fish et al., 2009).  The
brine soaked sponge is used because the brine improves the electrical
conductivity and the sponge fills the gap between the electrodes and the
person’s head when the chin strap is tightened. The person who is receiving the
electric shock will have at least 2 contact points to a source of voltage, one
of which may be the earth ground (Fish et al., 2009).  The leg electrode is sometimes coated with a
gel to increase conductivity and to reduce burning.  The person’s leg is strapped securely to
this.  The helmet is connected to the wiring
and once the warden gives the signal the executioner presses a button on the
control panel to deliver the first shock of electricity that is between 1,700
and 2,400 volts at 7.5 amps for 30-60 seconds. 
After a short interval the process is repeated and then the body is left
to remain in the chair with the electricity off for five minutes.  A doctor then examines the body and
pronounces death (“The electric chair”, n.d.).

            The first high voltage shock destroys
both the brain and the central nervous system. 
Electrocution causes complete paralysis due to all the muscles in the
body contracting and staying contracted while the electricity is still flowing
this makes the heartbeat and respiration impossible (“The electric chair”,
n.d.).  This is known as the “let-go
phenomenon” (Fish et al., 2009).  The “let-go
current” (6-9 mA) is the level above which muscular tetany prevents the release
of the current source (Bernius & Lubin, n.d.). The path of the flow of
electricity determines the tissues at risk and the type of injury.  Current passing through the heart and thorax
can cause arrhythmias and myocardial damage. 
Nerves, blood vessels, mucous membranes and muscles tend to have the
least resistance due to their high concentration of electrolytes.  Tissues that have the highest to electricity
are skin, bone, and fat.  These tend to
increase in temperature and coagulate. 
The conversion of electrical energy to thermal energy usually results in
massive external and internal burns.  The
direct effect of the current on the body tissues lead to asystole, ventricular
fibrillation, or apnea (Bernius & Lubin, n.d.).




All three methods of execution that are described in
this paper have benefits and shortcomings, as well as controversies that
surround each method.  After researching
each method, I have found that all three methods involve stopping the heart,
but each method does so differently.  Reflecting
upon my previous science classes (physiology, anatomy, biochemistry, etc.) I
can appreciate how intricate our body functions are.