These changes come on the heels of a new tactic by death penalty opponents: getting European countries to ban their pharmaceutical manufacturers from exporting drugs that may be used to execute people. These bans were partially responsible for nationwide shortages of several anesthetic drugs a few years ago.
Long story short, propofol, the “Michael Jackson drug,” went into shortage due to the contamination of a major supplier, and a perfect storm of low prices (due it being a generic drug) and extreme difficulties in manufacturing it correctly and with sterility. Sodium thiopental, the older back-up to propofol, came into demand. Promptly thereafter, the manufacturer stopped selling it in the US due to it’s use in lethal injections, leading to a nationwide shortage of anesthetic drugs and the temporary importation of drugs from Canada.
In any case, because of chronic shortages and problems with vein access (more on this later), the traditional method that had been used: a three drug combo of sodium thiopental, pancuronium bromide, and potassium chloride has been abandoned in many states.
Let’s go back in time: What did this three drug combo do? It was originally developed by a Dr. Jay Chapman. He observed that animals were killed more humanely than people (the firing squad and electric chair were the options in use at the time for executions in Oklahoma). So, he developed a three drug protocol that has been widely adapted since.
The first drug is sodium thiopental, a barbiturate. Barbiturates produce different effects at different doses, but in the dose used in lethal injections produces an anesthetic coma. The patient has no awareness, and no consciousness of anything around them. As the patient is in a state of deep anesthesia, the patient loses their brain stem reflexes, and stops breathing. As the patient stops breathing however and O2 saturation drops, involuntary movements start taking place. These are known as “agonal” movements. Not because the patient is in agony — the term just refers to the movements of a patient when they are close to death (a heart that has suffered blocked artery and is dying is in an “agonal” rhythm, a patient who is dying experiences “agonal” breathing). The patient is not conscious of these: think of people moving in their sleep. On it’s own, sodium thopental is lethal due to the suppression of breathing — but it would take a long while. The human body has reserves of oxygen, and the agonal movements may supply just enough air to prolong the execution.
To stop these agonal movements (which might be distressing to onlookers), the second drug is administered: pancuronium bromide, a non-depolarizing muscle relaxant (aka, a paralytic) — it completely stops all muscle movement. This drug too can be lethal all on it’s own, but the sensation it would produce (think of feeling the need to breathe but not being able to move a muscle — until death) was deemed too cruel on its own. Thus, it’s only given after the sodium thiopental takes away consciousness. It’s really a bit redundant: the only function is to prevent onlookers from being alarmed at the dying, “agonal” movements. And if given to an improperly anesthetized condemned inmate (due to dosing issues, vein issues, or a variety of reasons), it can result in a rather terrible way to die. But it would stop agonal breathing more completely and reliably than the sodium thiopental. But even this isn’t what ultimately killed inmates executed under the protocol.
The two drugs would kill given enough time, but Dr. Chapman decided on a rapid final method: potassium chloride. This drug produces rapid cardiac arrest by disrupting the electric balance of the heart. If given on it’s own, it would produce brief, agonizing pain (the most painful heart attack you can imagine). Hence why it’s given after the sodium thiopental puts the patient into an anesthetic coma.
As you can imagine, this is a hideously complicated protocol, with a few critical failure points. The sodium thiopental may not produce an anesthesia effect if too small a dose is given. This is extremely unlikely however, as a massive overdose of the drug is given to prevent just that occurrence.
More likely is this: venous access problems. To give any of these drugs, intravenous access must be established — that is to say, a route to give fluids directly into the patient’s bloodstream. IVs actually can be pretty difficult to establish — you have to get a line directly into a vein which might move or roll around, or be very small, or might break, etc. The people establishing these lines are prison workers — who have probably never started an IV in their lives. It is possible that they start two IVs — one in each arm. One of these lines is good. The other one isn’t — and instead goes through the vein or otherwise isn’t capable of delivering drugs. A medical provider would recognize this instantly. A prison worker probably not so much. The bad IV is used for the sodium thiopental, the good IV is used for the pancuronium bromide, and the bad IV for the potassium chloride. What would be the result? The inmate would be paralyzed, and unable to tell anyone that the sodium thiopental didn’t work while they suffocated to death over the course of 5-10 minutes.
This outcome is considered inhumane, and thus many states have developed variations on this “traditional” approach.
Back to the present day. Ohio’s new protocol used just two drugs: midazolam and hydromorphone. These are two entirely different classes of drugs: a benzodiazepene and an opioid. Why? Because these drugs don’t need an IV. Instead of prison workers poking around, looking for a vein, they can just inject the drugs into the muscle — like an epinephrine auto-injector for allergic reactions. Plus, there was no paralytic — meaning that it would be impossible for the inmate to be aware but paralyzed and unable to say anything. What’s the downside? IM drugs’ absorption into the bloodstream takes longer and is more inconsistent — meaning it might take awhile to get to the dose needed to suppress breathing.
So what happened in the execution chamber? Exactly what was expected. The drugs kicked in, the patient lost consciousness, and proceeded to die due to oxygen deprivation. Here’s the thing: he couldn’t have experienced any sensation at all. Why? Because consciousness is a higher order brain function than breathing. For an inmate to “experience” pain, the inmate’s brain stem has to be functioning. The only reason the inmate wouldn’t be breathing is if consciousness has already been suppressed. If anything, the inmate ironically died having the high of his life. Don’t believe me? Ask an overdose victim. Because really, that’s all this new protocol is: a massive overdose.
However, due to the slow absorption into the bloodstream and the agonal movements of the chest wall, some air exchange still went on for a while, some movement was witnessed, and the inmate died more slowly than if they had been paralyzed. The inmate appeared to move around and struggle for 25 minutes — which led to a lot of people claiming it was botched when in reality what happened was exactly what was expected.
All the media excitement about a “botched” execution is just that: media excitement. The method used in Ohio is probably as humane as it can get.
That said, there is another consideration: why use medical drugs in executions at all? I commend Dr. Chapman for his intent: to execute inmates more humanely. But his recent suggestion is right: the most rapid, painless, and reliable method to execute anyone is probably the guillotine. We shouldn’t mix medicine and executions.
But, the real reason to oppose the death penalty isn’t the method. After all, if we’re going to kill someone, do we really care about how much pain they might experience in the last few minutes or seconds of their life? No, the real reason is because it is incredibly arbitrary and racist. I believe in the death penalty in the abstract — I think killing a person is actually more merciful than locking them in a 6′ by 6′ box for 50 years. But as currently applied, it is utterly ridiculous and demonstrably ineffective.
Vamsi Aribindi is a medical student who blogs at Follies of an Amateur Intellectual.