From a journal entry.

Male in his mid 50’s arrived to ED via EMS around noon complaining of shortness of breath related to covid-19. The patients initial vitals were within normal limits aside from elevated heart and respiratory rates. On arrival, the patient was initially conscious and alert with an oxygen saturation of 96%

The CT scan showed a very progressive viral pneumonia related to covid-19 with extensive infiltrates.

Here is a still image of the CT scan.

As the night progressed, the patient was placed on a bipap as his oxygen saturation began to fall and respiratory rate steadily increased. At approximately 2200, the patient experienced an extremely increased work of breathing, began hyper ventilating, and his oxygen saturation plummeted to 70%. The patient was RSI’d and intubated. As the night progressed, the patient’s oxygen saturation would not come above 72% while on the ventilator. The patient became hypotensive requiring the pressors to maintain blood pressure.

Here is a chest X-ray after intubation. The patient also has a central line and a nasogastric tube.

Given the patient’s present illness and deteriorating condition, evidenced by the lack of improvement on a ventilator and worsening lab values, a call was made to his wife.

The patient remained in the emergency room for three days until he died. There were no ICU beds available in any hospital within a 500 mile radius.

https://doi.org/10.1016/j.yebeh.2021.108334

https://pubmed.ncbi.nlm.nih.gov/34600281

Abstract

Patients with uncontrolled epilepsy have a high risk of sudden unexpected death in epilepsy (SUDEP). Seizure-induced respiratory arrest (S-IRA) is thought to be the determining cause of death in many cases of SUDEP. The goal of the present study was to use Scn1a^(R1407X)^(/ ) (Dravet Syndrome, DS) and DBA/1 mice to determine: (1) the effect of a ketogenic diet (KD) on S-IRA and (2) the relationship between serum ketones and the protective effect of a KD. Ketogenic diet treatment significantly decreased spontaneous seizure-induced mortality in DS mice compared to control (8% vs 39%, p = 0.0021). This protective effect was not abolished when ketosis was prevented by supplementing the KD with glucose (10% mortality, p = 0.0007). In DBA/1 mice, the latency to onset of S-IRA due to audiogenic seizures was delayed from 7.6 to 20.8 seconds by a KD on treatment day (TD) 7 compared to control (p < 0.0001), an effect that was reversed on TD14 when mice were crossed over to a control diet on TD7. β-Hydroxybutyrate (BHB) levels were significantly decreased in DBA/1 mice on a KD supplemented with glucose (p = 0.0038), but the protective effect was maintained. Our findings show that a KD decreases SUDEP in DS mice and increases the latency to audiogenic S-IRA in DBA/1 mice. In both mouse models, a KD was protective against S-IRA. This effect may be due in part to specific dietary components rather than generation of ketone bodies.

------------------------------------------ Info ------------------------------------------

Open Access: False

Authors: Megan S. Crotts - YuJaung Kim - Eduardo Bravo - George B. Richerson - Frida A. Teran -

Additional links: None found

I recently had a dmt induced seizure I thought others should know about I have no history of Epilepsy never had a seizure prior and have used DMT and other hallucinogens MANY times im an avid tripper but just threw everything out. I took 2 very small puffs off my yocan and my chest got instantly tight I couldn't breathe I was super confused tripping way harder than what I had smoked and felt like I was having a heart attack. Please be careful when using these substances.

I thanked my lucky stars that the coroner seemed to be one of the 40% of the population who could not smell cyanide.

https://twitter.com/AshAgony/status/1270409845238312960

I've noticed in my research that 5-MeO-DMT and Bufotenine cause respiratory arrest in sheep, rats and (anecdotally) in humans, reports below. Chemical Structures of the two molecules. 5MeODMT is converted to bufotenine in vivo but based on looking at their receptor binding profiles I can't see any reason why they would cause respiratory arrest. I have heard reports of other psychedelics causing elongated orgasm-like states which are accompanied by difficulty breathing but I don't think this would be A: So translational or B: Fatal.

TIHKAL #38 (with an unknown but large amount, smoked) I observed the subject pass very quickly into an almost coma-like state. Within seconds his face became purple and his breathing stopped. I pounded his chest, and breathed for him, and he seemed to emerge in consciousness, with the comment, “This is absolute ecstasy.” He stopped breathing a second time, and both heart massage and mouth-to-mouth resuscitation was provided. Again, he recovered and managed to maintain a continuing consciousness and achieve a partial recovery. In the awake condition he was increasingly lucid, but on closing his eyes he became possessed with, what he called, “The energy of terror.” He could not sleep, as upon closing his eyes he felt threatened in a way he could not tolerate. Three days later, medical intervention with antipsychotic medication was provided, which allowed the recovery of an acceptable behaviour pattern in a few more days

Shulgin & Shulgin. Tryptamines I have known and loved. (Transform Press, 1997).

A women on a shamanic retreat is given 5-MeO-DMT inhaled from a pipe and suffers a transient respiratory arrest. This resolves without pharmacological intervention

Bowers, J. Personal Story: My 5-MeO-DMT Experience. Reset.me http://reset.me/personal-story/personal-story-my-5-meo-dmt-experience/ (2015)

Bufotenine causes acute toxicity in rats between 200 and 300mg/kg wherein death occurs via respiratory arrest

Mice, rats, sheep and monkeys have been shown to demonstrate ataxia, mydriasis, head nodding, tremor, convulsion and shivering following 5-MeO-DMT ingestion. Sheep are particularly susceptible to 5-MeO-DMT toxicity and experience stringy salivation, tachycardia and respiratory failure when exposed to 1mg/kg 5-MeO-DMT

Here are some old school human studies showing respiratory arr

tl;dr: 50F, 35 year history asthma/COPD, smoker, 4LPM home O2 wakes up, can't breathe. No relief from DuoNeb, doesn't want to do CPAP, don't have BiPAP. Gets real sleepy in transport, stops breathing, gets bagged for ~2 minutes, wakes back up, no other changes. What caused her to arrest / how could I have managed this patient better to get out ahead of that?

Suburban service called out for difficulty breathing, find patient tripodded on bed puffing on DuoNeb. Discharged from hospital a week ago for COPD exacerbation. Says its been getting worse for the last two days. 3-word dyspnea. Let her finish the neb while we move furniture / get doors propped to fit stairchair down trailer hallway and into room just big enough to fit it and a queen bed. HR 130 RR 30 BP 130/80 SpO2 97%

Chair down icy deck steps to stretcher, stretcher into the truck, and patient onto the main O2. Hand IV gets good flash, advances easily, won't flush. No good. Get going to the hospital expecting success on the second stick and improvement with second neb. No changes in vitals so far.

Takes a few minutes to set up for second IV (switched cuff / pulse ox, moved supplies to patient's right for better access). Notice she's started to get drowsy and go a bit pale, now speaking single-words. SpO2 down to 92%. RR falls. Try NRB at 15LPM (Looking back, probably the wrong choice here).

Head flops forward. Apneic. Still has a pulse ~120. SpO2 now 89%. Drop head of cot and get BVM. Connected to O2. Mask seal sucks. Get a better jaw-thrust, mask seal improves, 4 or 5 breaths later she wakes back up. Assist ventilations until full return of consciousness. Drop her off in the ED with no further changes. Seems like there was a lot of room for improvement in how I managed this patient.

Encourage / persuade better for CPAP?

Bag sooner?

Treat the patient not the monitor, perhaps?

This incident happened in Las Vegas, NV.

About a week ago, I underwent an ACL reconstruction surgery using a part of my patella ligament as a graft for the ACL. The surgery took place in an outpatient center. Everything was looking good during pre-op and the day of the surgery prior to the surgery. I had only undergone surgery once before with general anesthesia, to remove my wisdom teeth. Everything was ok then, so I wasn’t too concerned about the surgery. The last time remember before going into surgery was approximately 0830.

At some point, I remember waking up, but not opening my eyes, with what felt like intubation, as there was something in my throat. I was trying to resist it, but then I blacked out. I assume they had sedated me to put me to sleep again.

When I woke up at around 1115, I woke up in a hospital a few blocks from the center in the ER. My chest and throat felt sore and I felt completely exhausted. I had an ER doctor come to me, along with the orthopedic surgeon that was performing the surgery, and explained that there were complications during the surgery.

When they gave me toradol (I’m pretty sure that’s what it was from what I kept hearing, to increase the anesthesia when they started cutting into the bone), my body started to negatively react and my blood pressure spiked and my heart rate increased. They then gave me metoprolol to stabilize me, but it apparently reacted with the toradol and dropped my blood pressure, down to around 50/30, before I went into respiratory failure and cardiac arrest. They had already taken out a piece of the ligament when it happened, so they had to discard it and pack and close the site to transport me to the hospital. They were forced to perform chest compressions until the paramedics arrived.

At the hospital, they were concerned for my liver as the AST and ALT levels were alarmingly high as a result of the stress on my body. They wanted me to stay overnight to observe me to make sure I was stabilizing for a good period of time. They wanted to perform an U/S of my abdomen to ensure everything was ok with my liver, but bloodwork from later in the day showed that the AST and ALT levels were lowering down to normal levels, so they dismissed it. The surgeon and anesthesiologist that were performing my surgery visited during my recovery in the hospital to check and redress the wound. They were confused as to what had happened with the surgery and were still trying to find the root cause of the incident

Hello all, I kind of had a broad question for the community, and I also wanted to see if anyone else has had this experience. So recently, my seizures have come back after almost 5 months. As usual, they start off as focal, soon progressing to convulsive. What’s different now is that I stop breathing and turn blue during the convulsive phase. It’s scary as shit, but I have midazolam rescue med that my parents give me. This stops the seizure, therefore making me start to breathe again. My Neuro and I have a long and complicated theory about a mind-gut connection (I know that sounds weird) but we think that certain foods have been exacerbating the seizure severity. I won’t go into too much detail though, as this is an extremely long story. My 2 broad questions: has anyone else ever had to deal with resp. arrest? Also, if you do, how do your family members take care of you when you are not breathing? Do you have oxygen at home for those occasions? I know my rescue med gets me breathing again, but my O2 stays kinda low for a while, and the paramedics/ambulance have to give me some.

TL;DR: I have had convulsive seizures where I stop breathing. Rescue midazolam starts my lungs back up almost immediately, but O2 stays pretty low until I get O2 from ambulance (sometimes dips into the 80s). Does this happen to anyone else? What do you do to keep your oxygen up during these? Moreover, why do these happen in the first place? Thank you all so much for your help. Have a great day!

I have a character who is going to die from a respitatory failure caused by laudanum overdose, but I couldn't find any resources on how long it might take, or what it might feel like, and I want my writing to feel convincing.

Sorry if this isn't the place for this kind of question, I don't know where else to look.

Any insight would be very appreciated!

So, I’ve been learning about excited delirium and have been told that patients go through hyperthermia which leads to respiratory and ultimately cardiac arrest. I’m confused about how this happens though and what actually kills these people. In one paper, I read that patients can experience respiratory arrest secondary to cerebral edema which would make sense. But wouldn’t that process happen slower than one minute they’re losing their cookies and the next minute they’ve stopped breathing? I’m just very confused and need some help understanding this.

I've been reading the news stories, and they seem to be mostly agreed that

1. There was no sign of botulism, and that wouldn't cause a coma anyway

2. There weren't any signs of beatings, such as bruises or broken bones

3. The brain damage was most likely caused by respiratory arrest leading to a lack of oxygen

And they've avoided speculating after that, which is reasonable obviously, but I was wondering what some causes of respiratory arrest could be?

Is it just something that comes from being suffocated? Can panic cause it? Or malnutrition? Could waterboarding?

If there anything you can say is likely to have lead to it? Or unlikely?

Thanks,

Oh, for anyone who doesn't know the background, Otto Warmbier was the American student held in North Korea, and sentenced (about a year ago) to 15 years hard labour. He's been recently returned to the US, but is in a state of 'wakeful unresponsiveness' (apparently another term for a vegetative state), and has brain damage. North Korea's claim is that he had botulism shortly after sentencing, was given a sleeping pill, and fell into a coma.