National Registry Paramedic Exam: Toxicological Emergencies

The paramedic will need to, at some point in his or her career, treat a patient who has overdosed on some form of drug. The drug could be alcohol, prescription or over-the-counter medication, illicit street drugs such as marijuana or heroin, or any other substance that alters the mind, produces euphoria, or could result in death as the desired outcome.

A drug is any substance that in appropriate quantities can bring about a therapeutic effect, whereas a poison is a substance that is toxic in some capacity, regardless of dose and route of entry into the patient.
Toxicologic emergencies can involve either a drug or a poison and can be intentional, as in cases of attempted suicide or applying the concept of “if some is good more is better,” or unintentional, such as in cases of a person taking acetaminophen along with a cold medicine that also contains acetaminophen or an elderly person accidentally taking the same medication multiple times because he or she forgot that a dose had already been taken. Unintentional or accidental overdoses also can occur in the workplace through exposures to chemicals. Children can be particularly susceptible to accidental poisoning, either because everything naturally goes into their mouths when they are young or in a case of mistaken identity when they take a pill thinking it is candy.
As a provider, it is nearly impossible to keep up with the amount of poisons and drugs available to the public, their toxidromes—the signs and symptoms associated with a particular drug or poison or class of drugs or poisons—and steps to take when a patient has taken them. Some bottles will say drink water, some drink milk; still others advise to induce vomiting, whereas others advise against it.

Here, only some of the more common drugs and poisons a paramedic may encounter will be highlighted. Some major toxidromes and classes of drugs and poisons will be referred to during the discussion of specific poisons later. Don’t worry, however. The Poison Control Centers are available to help with the paramedics’ diagnosis of what poison was taken or to what the patient was exposed. Always call the Poison Control Center, 1-800-222-1222, and solicit their help. Identify who you are and provide all the information possible to the toxicologist on the other end of the line.


Toxidromes
 

Routes of Absorption
When a poison is ingested, it is consumed in the same way as food. Depending on the poison, the damage to the body can begin immediately, such as in the consumption of strong acids or bases or petroleum products. Conversely, the effects of the poison can be delayed if the toxin must first be digested and absorbed into the bloodstream. In this case, the medical team may have a bit more time to prevent a negative outcome for the patient. The paramedic may be able to prevent it from being digested and absorbed by inducing vomiting or administering activated charcoal. Because the effects will come on slowly, paramedics and physicians may be able to administer an antagonist (antidote) for what was ingested until it can be safely eliminated from the body.
There are 2 ways in which a person can be poisoned through inhalation. First, the toxin can cross the alveolar wall and get into the bloodstream, where it can be carried to the brain, heart, or other organs to exert its effects. This is similar to what happens in carbon monoxide poisoning. Second, the toxin can simply take the place of O2 in the atmosphere, effectively suffocating the patient in air. The best examples for such a poisoning are enclosed environments where other gases are present. This might be inside a silo, in a walk-in refrigerator with a refrigerant leak, or in a room where bottled gases are stored.
Injection involves the toxin being placed directly into the body where absorption and time to onset of the effects are the fastest. This involves the injection of street drugs, such as cocaine or heroin, but it also includes snake, spider, scorpion, and jellyfish bites and stings. The effects of injection are directly related to what was injected. For street drugs, they can have wide-ranging systemic effects, including death. For insect and animal bites, the effects tend to start as localized to the area of the bite and then, often slowly over several hours, cause systemic problems.
Toxins that can cross the skin can be absorbed. Absorption often is the slowest of all routes. Pesticides, petroleum products, and some prescription medications can be absorbed through the skin.

Terms Related to Toxicology
The following terms are related to toxicology:

- Antagonist. One medication acts in opposition to another drug or system.
- Drug Abuse. The recurrent use of illegal street drugs or the intentional misuse of prescription or over-the-counter medications for purposes other than what is described on the label.
- Drug Addiction. The compulsive use of a medication or street drug despite the harm that may happen (or is happening) to the user, the user’s family, job status, or social status.
- Habituation. A conditioned decrease in response to a stimulus resulting from repeated exposures. Also the act of becoming part of the routine.
- Physical Dependence. A physiological addiction to a drug such that suddenly stopping the medication or drug will cause physical signs and symptoms.
- Potentiation. One drug or medication increases the effect of another drug.
- Psychological Dependence. The emotional attachment to the way a drug makes the user feel. Alternatively, thinking that the drug is what is responsible for the feelings experienced.
- Synergism. Two drugs when taken together have a greater effect than the sum of each individual drug. In other words, the 2 drugs work together to create a greater effect.
- Tolerance. Needing an ever-increasing quantity or dose of a drug to achieve the same effect.
- Withdrawal Syndrome. Predictable signs and symptoms that occur when a drug is suddenly stopped.

Factors Specific to Assessment of Toxicological Emergencies
In addition to typical assessment points, including OPQRST, SAMPLE, and vital signs, the paramedic needs to assess specific factors related to drug overdose and poisonings. The questions below can help determine the severity of the overdose and the course of treatment the paramedic will employ or be prepared to employ for the care of the patient.

- What was the agent? This may not always be obviously known and may require sleuthing. Recently filled but empty prescription bottles could provide a clue if it was a prescription overdose. A spoon and a lighter nearby could indicate heroin or some other cooked drug, including methamphetamines; crack cocaine can be inhaled when heated. The police are great resources for this because they can look around while the paramedic begins treatment.
- How was it taken? Refer to the routes of absorption earlier in this section. Some routes are faster to circulation than others, and, therefore have a faster onset of effects.
- How long ago was it taken? Here again is a question that may not have a definitive answer, especially if the patient was alone at the time. If it was taken orally and it is within an hour, the Poison Control Center may advise you to induce vomiting or have the patient drink an activated charcoal slurry if the person is capable of maintaining his or her own airway. In some cases, the paramedic may be able to insert a nasogastric tube to provide a route of administration for the activated charcoal if the patient is obtunded.
- How much was taken? This may be an estimate only if it was a prescription medication or if the patient is unable to relate this information. Street drugs may be even more difficult to quantify.
- Were any other drugs taken? This can include washing down the poison or the medication with lethal amounts of alcohol, but it also can be an overdose where multiple medications are taken in a desperate attempt to either get high or die trying.
- Has the patient vomited? If the agent was ingested, vomiting may limit the effects.
- Why did the patient take the medication? This is another question that may garner an unreliable answer. Whatever the answer, simply document what was said.

Toxicological Emergencies

Alcohol (Ethanol)

Pathophysiology
Three pathophysiologies are to be considered when talking about alcohol, the most abused drug in the United States. The 1st is acute intoxication, the 2nd is the chronic effects on the body as a result of alcoholism, and the last is withdrawal and delirium tremens (DTs) associated with a sudden stop of alcohol consumption in a long-term alcoholic.
Acute alcohol intoxication can be just as lethal as an overdose of just about any other drug. Alcohol has the effect of being a CNS depressant, which can cause slowed breathing and heart rate. The patient also may become unconscious as a result of the intoxication and is no longer able to protect his or her airway. Vomiting is common as the body reflexively tries to get rid of the poison in the stomach. If the patient vomits while unconscious, there is a high likelihood of aspirating the vomit. Death is a very real possibility when the blood alcohol content exceeds 400 mg/dL.
For patients believed to have acute alcohol intoxication, it is best to treat them as patients with an altered mental status. Evaluate their vital signs and perform a thorough physical assessment. Although it is easy to chalk a patient’s behavior up to alcohol, it may not be the only issue at hand. Furthermore, it may not be the most life-threatening issue. With this in mind, take steps to rule out other causes of altered mental status, particularly hyperglycemia or hypoglycemia, head injury, hypoxia, or other drug use. Establish an intravenous line and run it by keeping the vein open (KVO). Check the blood sugar level and treat the value appropriately. Be prepared to manage the patient’s airway if he or she vomits, passes out, or both. If available, administer 100 mg thiamine intravenously to help the body process the alcohol.

Chronic Alcohol Use (Alcoholism)
Alcohol dependence is still one of the top 5 causes of death in the United States. Typically, dependence begins as a psychological dependence, where the consumer likes how he or she feels when drinking. The person feels that he or she needs to have alcohol to function properly, particularly in social situations. Eventually, needing alcohol this frequently evolves into a physical dependence heralded by the fact that when the person stops consuming alcohol, withdrawal symptoms begin, including restlessness, anxiety, agitation, and muscle tremors. To relieve these symptoms, the person returns to alcohol, further deepening the dependence and volume of consumption. Chronic abuse leads to damage to multiple different organs of the body, including the liver, the esophagus, the stomach, the pancreas, and the brain.
Alcohol has a direct effect on the entire digestive system, particularly the stomach. Alcohol causes alcoholic gastritis, which is an irritation and inflammation of the lining of the stomach and sometimes the small intestine. This leads to pain; reflux; and, in more extreme cases, hematemesis, or bloody vomit. The accessory organs to the digestive system also are taxed in heavy drinkers. The pancreas is prone to inflammation called pancreatitis, which can be either acute, lasting a few days, or chronic, repeating over and over again with no extended wellness period between episodes. Chronic pancreatitis can lead to diabetes or the highly lethal pancreatic cancer.
The liver is the site of detoxification in the body, so it is where alcohol will go to be metabolized and removed from the body, eventually through the kidneys. The chronic abuse of alcohol will lead to inflammation of the liver followed by fatty deposits throughout the liver cells. Eventually, this will lead to hepatitis, cirrhosis, and liver failure. Cirrhosis causes venous vascular pressures to build up within the liver, and in the veins leading to it, causing them to distend and possibly turn into varicose veins. These varicose veins are most concerning when they occur in the lining of the esophagus. Here, esophageal varices are subject to the abrasion of food passing by, increasing their likelihood of rupturing. The rupture of esophageal varices can be lethal because of the amount of blood stored in those veins and the pressure to which they are subjected.
The brain and the peripheral nerves are not immune from the destructive effects of chronic alcohol consumption. The brain will sustain damage to the cerebrum and the cerebellum. Damage to the cerebrum will lead to problems with the memory, motor coordination, and speech areas of the brain. This combination of ataxia, memory, and speech problems is called Wernicke encephalopathy and is a result of chronic thiamine deficiency. In addition, the brain may actually shrink in size from neuronal destruction. This shrinking from alcoholism combined with the natural shrinking caused by aging predisposes a patient to serious head injuries and intracranial bleeding from falls. In this situation, the brain has more room to shake around the cranial vault, allowing for the increased possibility that blood vessels will tear as the brain sloshes back and forth. As if the motor coordination problem from cerebral damage was not enough, cerebellum damage diminishes the patient’s ability to balance, resulting in more falls.

Delirium Tremens and Alcohol Withdrawal
Suddenly stopping alcohol consumption in the long-term alcoholic can be fatal. Over time, however damaging, the body essentially comes to need the alcohol to function; stopping it suddenly can be similar to eliminating a nutrient from the diet. Initial alcohol withdrawal symptoms begin within 6–12 hours of the last drink and can include sweating, nausea and vomiting, and headache. Heavier drinkers who stop drinking may experience visual, auditory, or tactile hallucinations beginning within 24 hours after the last drink. Unlike the hallucinations associated with DTs discussed later, the patient is usually aware that the sensations felt are not real. Throughout the first 2 days after the last drink, the patient is at risk of having withdrawal seizures. Symptoms of DTs peak within 5 days and can be characterized with any of the following: profuse sweating, seizures, intense visual hallucinations that the patient cannot distinguish from reality, continuous full body tremors, high blood pressure, and a light fever. In DTs, the hallucinations and disorientation can become so intense and disturbing to the patient that he or she may opt for suicide to escape the situation.
Treatment for alcohol withdrawal and seizures can be difficult because of the realism of the hallucinations possibly increasing the patient’s agitation. Make every attempt to reassure the patient that you are there to help him or her feel better and work to keep the patient calm. Although restraints may be necessary, they should be a last resort because this can be more agitating to the patient who is hallucinating. Once it is safe, initiate cardiac monitoring, establish vascular access, and consider volume replacement with normal saline. If available, administer 100 mg thiamine via a slow intravenous piggyback. Be prepared to administer benzodiazepines for seizures as they occur.

Stimulants
Stimulants have the highest potential for abuse and the lowest chances for recovery because of the feelings of excitement they tend to cause. Stimulants can be smoked, snorted, injected, or taken orally. Patients who have taken any stimulant are excited or hyper, often with tachycardia, hypertension, and dilated pupils. Patients also may be in a state of agitated delirium. As the dose increases, patients can have seizures, high fevers, or suddenly collapse in cardiac arrest from either the increased workload on the heart or the coronary artery spasms these drugs often cause. The stimulant abuser also can appear jittery or on edge and hypersensitive to touch. In this state, the patient could easily be set off and become combative or even violent.
Common drugs in this class include cocaine and amphetamines. Cocaine can be taken in any of the ways previously mentioned, but it is most often snorted or smoked. If the patient snorted the cocaine, the effects are felt within 2 minutes, and the peak high will last for about 20–30 minutes, at which point the high begins to fade. When smoked, the effects are felt within seconds, and the high is much more intense but shorter lasting. This results in a person wanting to redose much more quickly. As the high fades and the effects of cocaine are no longer felt, the patient “crashes,” which is characterized by depression with sleeplessness, irritability, and exhaustion.
Amphetamines, methamphetamines, and amphetamine-like drugs have legitimate clinical applications as nasal decongestants and in medications for attention deficit disorder (ADD) and attention deficit with hyperactivity disorder (ADHD). Methamphetamines can be made relatively easily in the home from the nasal decongestant pseudoephedrine and other household chemicals, making it easier and cheaper to use than cocaine but with the added benefit that the high from methamphetamine can last up to 12 hours, compared with 30 minutes for cocaine. Although treatment for the amphetamine abuser is largely supportive, patients can become violent with little notice.

Treatment for Stimulants
EMS systems do not typically carry an antidote to any of the stimulant classes of drugs, so treatment is limited to symptoms. As with any patient, ensure an adequate airway and oxygenation; these patients may be necessarily tachypneic to keep up with myocardial and skeletal O2 demands. Titrate supplemental O2 to a pulse oximetry of 95% or higher and initiate cardiac monitoring. Appropriately treat any dysrhythmias found. For seizures, violent behavior, combativity, or anxiety, administer a benzodiazepine and be prepared to manage the airway. The patient may have a very high fever, sometimes in excess of 106°F, which will require aggressive cooling measures, including ice packs to the groin, axillae, and neck.

Opiates
Opiates are drugs derived directly from the poppy seed, whereas opioids are typically synthetic medications. The term opiate will be used to refer to any narcotic drug. Opiates act on opiate receptors found primarily in the brain to produce euphoria and analgesia. They can be absorbed through the nasal mucosa (snorted); smoked, entering the bloodstream through the alveoli; taken orally; or injected. Oral opiates are subjected to first-pass metabolism and, therefore, have their effects lessened compared with absorption via other routes. Heroin, for example, when injected, does not appreciably change when first metabolized in the liver. This means that heroin can outlast the antidote naloxone.
Patients who have taken opiate derivatives present as being sedated, sometimes with respiratory depression, hypotension, and pinpoint pupils. Sometimes, the patient’s respiratory status can be depressed to the point that he or she becomes bradycardic. Narcotics also are well known for affecting the GI tract by slowing overall transit. This can present as nausea, vomiting, and constipation.
Treatment for opiates is primarily the administration of the reversal agent, naloxone. Naloxone can be given intravenously, intraosseously, intranasally, or endotracheally, but the onset of reversal is fastest via the intravenous or intraosseous route. Naloxone should be given slowly and titrated to the improvement of the respirations rather than waking the patient all the way up. It is recommended to draw up 2 mg in a 10 mL syringe, creating a 0.2 mg/mL concentration and giving 2 mL at a time until the respiratory rate improves. If the patient is given all of it at once, he or she will likely vomit, possibly creating an airway problem, but, at the very least, a dirty ambulance problem. The patient also may get very agitated that his or her expensive high is now gone, creating a safety issue for the paramedics and the hospital staff.

Sedatives and Hypnotics: Barbiturates and Benzodiazepines
Barbiturates were once commonly prescribed as antiseizure medications; however, they were frequently combined with alcohol in successful suicides because of the combined CNS depressant effects of both drugs. There are long- and short-acting versions of barbiturates. Benzodiazepines have largely replaced barbiturates for seizure control and other medical applications for a variety of reasons. Benzodiazepines have a lower possibility for abuse and a significantly lower chance for toxicity. They also have a wider range of uses, including general sedation and anxiolysis, none of which are possible with barbiturates.
Both barbiturates and benzodiazepines have a similar mechanism of action in the CNS. Both bind to the gamma-aminobutyric acid (GABA) receptor and exert their effects by hyperpolarizing the postsynaptic cell. Because the cell is now hyperpolarized, it takes a larger stimulus for it to depolarize, resulting in sedation and the cessation of seizure activity.
Patients who overdose on benzodiazepines, or low doses of barbiturates, will appear intoxicated with alcohol: slurred speech, drowsy, ataxic gait, and decreased mentation. Even in high doses of benzodiazepines, the assessment will be similar; however, in high doses of barbiturates, the patient becomes increasingly lethargic until he or she is unconscious and possibly apneic. If a patient who is suspected of a benzodiazepine overdose is suffering from severe respiratory depression or is unresponsive, it is very likely that the patient took other depressants, alcohol, or opiates with the benzodiazepine.
Overdoses of either benzodiazepines or barbiturates is symptom-based for the most part. Manage the airway as for any other unresponsive or minimally responsive patient and consider intubation and ventilation. Respiratory depression is far more likely in barbiturate overdoses but could be significant with barbiturates when other drugs are involved. Establish vascular access and administer a fluid bolus if hypotension is present. Fluid resuscitation is the first-line treatment for hypotension; only after about 1–2 L have been administered should dopamine be considered for continued hypotension.

Marijuana
Classified as a hallucinogen despite not actually producing true hallucinations, marijuana does sometimes cause the user to have a distorted sense of time, space, and reality. Marijuana is most commonly smoked; however, it can be eaten as well. If consumed, the onset of effects can take several hours, whereas the onset of the relaxing effects start within a few minutes if smoked. Either way, the effects tend to last about 2–4 hours before waning.
Rarely will smoking marijuana result in an emergency visit to the hospital, unless it is laced with some other drug. Patients who have smoked marijuana will have bloodshot eyes, drowsiness, and euphoria. Patients will occasionally have a bad reaction and feel paranoid or anxious. Low-dose benzodiazepines are recommended here; alternatively, simply talk to the patient to calm the person.

Hallucinogens
Any substance that causes changes in senses of perception, including vision, hearing, and touch, is called a hallucinogen. Hallucinations of taste and smell are extraordinarily uncommon. Effects and sensations can be impacted by the user’s social setting, history of drug use, and mere expectations of what the drug will do. For this guide, the effects of each will be discussed, which will be followed by general treatment guidelines for patients who have taken hallucinogens.

Ketamine
Until recently, ketamine was not commonly used in human medicine; it was primarily used in veterinary medicine as a tranquilizer or anesthetic. However, now it is being used in pediatrics and adults to control seizures. Street ketamine often is snorted or taken orally and is physically and psychologically addicting. Low doses result in patients who seem intoxicated but have a reduction of inhibitions and slurred, dreamy speech. At higher doses, patients may appear anesthetized and have difficulty moving.

LSD
LSD saw its use peak in the 1960s, with a brief resurgence in the 1990s. It is a highly potent hallucinogen, with users achieving the desired effects with <100 mcg. It often is taken orally or sublingually, and the effect typically lasts between 3 and 4 hours, with effects occasionally lasting in excess of 12 hours with larger doses. Patients often report synesthesias with LSD, which are total changes in perception, such as hearing colors or touching sounds. The hallucinations are very real and can cause anxiety for the patients during so called “bad trips.”

Peyote and Mescaline
Found in the dried flower “buttons” of the peyote cactus in the American Southwest, native tribes have used peyote and mescaline for religious purposes for centuries. People typically ingest the “buttons” and vomit them back up after a short while because it is a powerful gastric irritant to begin the hallucination. Hallucinations have been described as a psychedelic experience complete with bright flashes of color often in geometric shapes being reported, thus people also experience out-of-body sensations and floating feelings.

Phencyclidine
Phencyclidine (PCP) often is referred to as angel dust on the streets and is occasionally used to lace other drugs, such as marijuana. In smaller doses, it can cause symptoms similar to alcohol intoxication: slurred speech, a staggering gait, and horizontal gaze nystagmus (bouncing of the eyes when the person looks as far right or left as possible). With larger doses, patients can experience what is known as mind-body separation or violent outbreaks that PCP is reputed to cause. Patients at this level of overdose are extremely combative and violent. They often have no response to attempts at physical containment, including being hit with tasers. These patients combine an almost complete lack of sensation of pain with superhuman strength and now pose a significant threat to law enforcement and EMS on scene until they can be subdued.

Psilocybin Mushrooms
Certain species of “shrooms” contain a psychoactive drug called psilocybin. The patient eats these mushrooms and after about 30 minutes to an hour, begins to have hallucinations similar to those experienced with LSD. Though less intense, the hallucinations last slightly longer, up to 6 hours. It is rare to need emergent medical care directly related to a shroom overdose.

Treatment for Hallucinogens
Most hallucinogens rarely cause life-threatening problems, so treatment is symptom related. Providing a calm environment for the patient is important. If there is extensive anxiety from the hallucinations, anxiolysis with benzodiazepines is recommended in low doses sufficient to bring about a state of relaxation. Do not play into patient’s hallucinations because that adds confirmation to what he or she is experiencing and can increase anxiety or agitation. If the patient is or becomes combative, higher doses of benzodiazepines may be required, likely via the intramuscular route first until an intravenous line can be safely established.

Organophosphate and Cholinergic Poisoning
Insecticides, pesticides, and fertilizers fall into a chemical category called organophosphates. The most common causes for overdose of these materials are intentional for purposes of suicide or accidentally during regular agricultural use and pesticide applications. ACh is the neurotransmitter of the PNS. Organophosphates inhibit AChE, an enzyme responsible for the breakdown of ACh in the synapse. With AChE no longer able to break down and remove the ACh from the synapse, the parasympathetic nerve will continuously produce its parasympathetic response. This is systemic.

Consequently, in organophosphate poisoning, the patient will show symptoms consistent with parasympathetic stimulation, including marked bradycardia and bradypnea and other symptoms contained in the mnemonic SLUDGE:

- Salivation: continuous drooling
- Lacrimation: excessive tear production
- Urination: urine incontinence
- Defecation/diarrhea: continuously moving the bowels
- GI upset: excessive continuous vomiting and GI cramping if conscious
- Eyes: pinpoint pupils (Some have emesis for the “E.”)

For the treatment of the patient poisoned by organophosphates, first ensure that the patient has been completely decontaminated and that he or she is not going to share the organophosphate with the ambulance crew and the entire emergency department. Once the patient is no longer a direct threat to the paramedics, assess and treat the ABCs as appropriate, including endotracheal intubation. Monitor the ECG, SpO2, and capnography. Administer 2 mg atropine as soon as an intravenous line is available and flush the line. Repeat this every 3–5 minutes until the secretions dry up. In the case of poisoning, the 0.3 mg/kg limit that is imposed during cardiac arrest or other bradycardic situations is not in play because atropine is the primary antidote for organophosphate poisoning. Fluid resuscitation sometimes in excess of 1 L is recommended for hypotension. If available, administer 2 mg pralidoxime chloride over 5 minutes.

Anticholinergic Overdose
Overdoses of drugs that inhibit the parasympathetic side of the CNS also are possible. Anticholinergic medications are available both over the counter and by prescription. Examples of anticholinergics include diphenhydramine and other antihistamines, certain cough suppressants, medications for overactive bladder such as oxybutynin, among others. Anticholinergic drugs competitively inhibit the ACh receptors in the synapse and prevent ACh from stimulating the postsynaptic nerve, essentially allowing the sympathetic side of the CNS to run amok.

The symptoms of anticholinergic overdose are listed below, along with a common memory aid for such overdoses.

- Blind as a bat (dilated pupils)
- Red as a beet (vasodilation/flushing)
- Hot as a hare (hyperthermia)
- Dry as a bone (dry skin and mucous membranes/no secretions)
- Mad as a hatter (hallucinations/agitation)

Management of this overdose is rooted in relieving and treating symptoms. Give benzodiazepines for any seizures that may happen. Be prepared to manage the patient’s airway. Because of decreased systemic secretions, it is recommended to judiciously lubricate the ETT before insertion. Monitor the ECG, establish an intravenous line, and observe the patient for changes during rapid transport to the nearest appropriate facility.

Carbon Monoxide
Carbon monoxide (CO) is a colorless, odorless, and tasteless gas that is produced during the incomplete combustion of hydrocarbon fuels, including oil, natural gas, and wood. CO can be found in gases from a malfunctioning furnace, a blocked chimney, or car exhaust. CO is a poison because it attaches to red blood cells at the same spot of attachment as O2; however, the CO attaches 200 times more strongly than O2. This means 2 things: (1) Once attached, it takes a long time for it to detach and make space for the O2 again; and (2) in the presence of both O2 and CO, the red blood cell will attach to the CO.
Patients with CO poisoning may be difficult to identify if it is early in the poisoning process. Early on a patient’s complaints are general and flu-like: nausea, vomiting, headache, confusion, and weakness. Having multiple people in the same location with similar complaints is characteristic of CO poisoning. Late in CO poisoning, usually near death, the patient will have a cherry red appearance to his or her face, though at that point the poisoning is seldom survivable. The patient who has CO poisoning will have an SpO2 of 100% because it will read that the hemoglobin is saturated, but the sensor cannot tell if it is CO or O2.
Treatment of CO poisoning is primarily high-flow O2, regardless of the SpO2 reading. Evaluate the ECG and consider intubation if the patient is unresponsive or has severe altered mental status. Check the blood sugar level to rule out hypoglycemia. Transport the patient to a hospital where the patient can receive emergent hyperbaric O2 therapy.

Cyanide
Cyanide is used in chemical and industrial processes and also is produced when certain plastics burn, which can happen in house fires. It is found in the pits and seeds of certain fruits, though not in any quantity that could inflict harm on a person. It is an extremely fast-acting poison that works by shutting down cytochrome oxidase, a cellular enzyme responsible for more than 80% of cellular energy production, and blocks the use of O2 at the cellular level.
The patient will present as being weak and lethargic. Breathing will initially be rapid but will slow and eventually stop as the muscles are no longer able to function. As lactic acid builds up in the cell’s last ditch effort to make energy, the patient becomes increasingly acidotic and will have a decreasing level of consciousness. Eventually, the patient will become unresponsive. It has been reported that patients have a smell of bitter almonds; however, nearly 60% of the population cannot smell that.

Treatment for known or suspected cyanide poisoning includes the following:
- If available, begin the administration of the antidote. 

- Hydroxocobalamin: 5 g infusion over 15 minutes
- Amyl nitrite: inhaled for 20 seconds out of every minute for 5 minutes, alternating with 40 seconds of high-flow O2
- Sodium nitrite: 10 mL of a 3% solution infused over 5 minutes. This is the 2nd medication to be given after hydroxocobalamin
- Sodium thiosulfate: 12.5 g over 5 minutes- Rapidly transport to the nearest medical facility, especially if EMS does not have access to the above antidotes.

Hydrogen Sulfide
Hydrogen sulfide has a distinctive rotten egg smell. It is a highly toxic, colorless gas. Poisoning can be created by reacting household chemicals, and it has been gaining popularity as a method of suicide because it will be successful. People are locking themselves in cars, mixing the chemicals that react to form the lethal hydrogen sulfide, and dying in their cars.

EMS should not open the car door, and the people have been known to put up signs in the car’s window that will say something like, “Chemical suicide in progress. Do not open the door.” Obey the sign, unless a full hazardous material suit is available. Even ventilating the patient after he or she has been poisoned and inhaling the patient’s exhalation can be enough to make the providers sick and possibly kill them. There is no proven antidote for hydrogen sulfide poisoning.