View Full Version : "Too Fat To Safely Execute,Tell Them To Use An Enema Bag Filled with the drugs !"

08-04-2008, 05:49 PM
Killer Says He's Too Fat To Safely Execute

COLUMBUS -- A death row inmate scheduled for execution in October says he's so fat that Ohio executioners would have trouble finding his veins and that his weight could diminish the effectiveness of one of the lethal injection drugs. Lawyers for Richard Cooey argue in a federal lawsuit that Cooey had poor veins when he faced execution five years ago and that the problem has been worsened by weight gain. They cite a document filed by a prison nurse in 2003 that said Cooey had sparse veins and that executioners would need extra time. "When you start the IV's come... snip

The lawsuit, filed Friday in federal court in Columbus, also says prison officials have had difficulty drawing blood from Cooey for medical procedures. Cooey is 5 feet 7 inches tall and weighs 267 pounds, according to the lawsuit.

Cooey, 41, was sentenced to die for raping and murdering two female University of Akron students in 1986. After a federal judge granted Cooey a last-minute reprieve in 2003, Cooey was returned to death row. In May, he lost a challenge to Ohio's lethal injection process when the U.S. Supreme Court said he had missed a deadline to file a lawsuit.


08-04-2008, 06:50 PM
The following drugs are a representation of a typical lethal injection as practiced in the United States for capital punishment.

Euthanasia protocol

Euthanasia can be accomplished either through oral, intravenous, or intramuscular administration of drugs. In individuals who are incapable of swallowing lethal doses of medication, an intravenous route is preferred. The following is a Dutch protocol for parenteral (intravenous) administration to obtain euthanasia, with the old protocol listed first and the new protocol listed second:

First a coma is induced by intravenous administration of 1 g thiopental sodium (Nesdonal), if necessary, 1.5-2 g of the product in case of strong tolerance to barbiturates. Then 45 mg alcuronium chloride (Alloferin) or 18 mg pancuronium bromide (Pavulon) is injected. In order to ensure optimal availability, these agents are preferably given intravenously. However, there are substantial indications that they can also be injected intramuscularly.

In severe hepatitis or cirrhosis of the liver, alcuronium is the agent of first choice.[2]
Intravenous administration is the most reliable and rapid way to accomplish euthanasia and therefore can be safely recommended.

A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium in a small volume (10 ml physiological saline).

Then a triple intravenous dose of a non-depolarizing neuromuscular muscle relaxant is given, such as 20 mg pancuronium bromide or 20 mg vecuronium bromide (Norcuron).

The muscle relaxant should preferably be given intravenously, in order to ensure optimal availability. Only for pancuronium dibromide are there substantial indications that the agent may also be given intramuscularly in a dosage of 40 mg.[3]

Sodium thiopental: ultra-short action barbiturate, an anaesthesic agent capable of rendering the person unconscious in a few seconds.

Pancuronium: non-depolarizing muscle relaxant, causes complete, fast and sustained paralysis of the skeletal striated muscles, including the diaphragm and the rest of the respiratory muscles; this would eventually cause death by asphyxiation.

Potassium chloride: stops the heart, and thus causes death by cardiac arrest.

Sodium thiopental
Lethal Injection dosage: 2-5 grams
Sodium thiopental (US trade name: Sodium Pentothal) is an ultra-short acting barbiturate, often used for anesthesia induction and for medically induced coma. The typical anesthesia induction dose is 3-5 mg/kg (a person who weighs 200 pounds, or 91 kilograms, would get a dose of about 300 mg). Loss of consciousness is induced within 30-45 seconds at the typical dose, while a 5 gram dose—14 times the normal dose—is likely to induce unconsciousness in 10 seconds.

Thiopental reaches the brain within seconds and attains a peak brain concentration of about 60% of the total dose in about 30 seconds. At this level, the subject is unconscious. Within 5 to 20 minutes the percentage in the brain falls to about 15% of the total dose, since the drug redistributes to the rest of the body. At this concentration in the brain, the anesthetic effects wear off and consciousness returns. These are the typical pharmacokinetics for the induction dose.

The half-life of this drug is about 11.5 hours[11], and the concentration in the brain remains at around 5-10% of the total dose during that time. When a 'mega-dose' is administered, as in lethal injection, the concentration in the brain during the tail phase of the distribution remains higher than the peak concentration found in the induction dose for anesthesia. This is the reason why an ultra-short acting barbiturate, such as thiopental, can be used for long-term induction of medical coma.

After a 5 gram dose consciousness will be regained in about 5 to 6 half-lives, which occurs in about 57-69 hours. The effects of such a high dose, however, include profound respiratory depression (depression of the brainstem respiratory center) and vascular collapse (vasodilatation and myocardial depression), which is in itself lethal.

Historically, thiopental has been one of the most commonly used and studied drugs for the induction of coma. Protocols vary for how the medication is given, but the typical doses are anywhere from 500 mg up to 1.5 grams. It is likely that these data were used to develop the initial protocols for lethal injection, according to which one gram of thiopental was used induce the coma. Now, most states use 5 grams to be absolutely certain it is effective.

Barbiturates are the same class of drugs used in medically assisted suicide, but it is the only drug used, in contrast to the three drug cocktail typically employed for capital punishment. In euthanasia protocols, the typical dose of thiopental is 20 mg/kg[12] and a 91 kilogram man would receive 1.82 grams. The lethal injection dose used in capital punishment is therefore about 3 times more than the dose used in euthanasia.

Pancuronium bromide
Lethal Injection dosage: 100 milligrams
Pancuronium bromide (Trade name: Pavulon) is a non-depolarizing muscle relaxant (a paralytic agent) that blocks the action of acetylcholine at the motor end-plate of the neuromuscular junction. Binding of acetylcholine to receptors on the end-plate causes depolarization and contraction of the muscle fibre; non-depolarizing neuromuscular blocking agents like pancuronium stop this binding from taking place.

The typical dose for pancuronium bromide is 0.2 mg/kg (a person who weighs 200 pounds, or 91 kilograms, would get a dose of around 9 mg). With a 100 milligram dose, the onset of paralysis occurs in around 15 to 30 seconds, and the duration of paralysis is around 4 to 8 hours. Paralysis of respiratory muscles will lead to death in a considerably shorter time.

Other drugs in use are tubocurarine chloride and succinylcholine chloride, both considerably stronger, but most states stick to using Pavulon.

Pancuronium bromide is a derivative of the alkaloid malouetine from the plant Malouetia bequaertiana. [1]

Potassium chloride
Main article: Potassium chloride
Lethal Injection dosage: 100 mEq (milliequivalents)
Potassium is an electrolyte, 98% of which is intracellular. The 2% remaining outside of the cell has great implications for cells that generate action potentials. Doctors prescribe potassium for patients when there is insufficient potassium, called hypokalemia, in the blood. The potassium can be given orally, which is the safest route; or it can be given intravenously, in which case there are strict rules and hospital protocols on the rate at which it is given.

The usual intravenous dose is 10-20 mEq per hour and it is given slowly since it takes time for the electrolyte to equilibrate into the cells. When used in lethal injection, bolus potassium injection affects the electrical conduction of heart muscle. Elevated potassium, or hyperkalemia, causes the resting electrical potential of the heart muscle cells to be higher than normal. Without a negative resting potential, cardiac cells cannot generate impulses that lead to contraction.

Depolarizing the muscle cell inhibits its ability to fire by reducing the available number of Na channels (they are placed in an inactivated state). EKG changes include faster repolarization (peaked T-waves), PR interval prolongation, widening of the QRS, and eventual sine-wave formation and asystole. The heart eventually stops in systole. Cases of patients dying from hyperkalemia (usually secondary to renal failure) are well known in the medical community, where patients have been known to die very rapidly, having previously seemed to be normal.