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Toxicology – Toxins Causing Erythema
Carbon Monoxide
Carbon monoxide poisoning may produce the classic “cherry red” skin appearance, although this is a late and often postmortem finding rather than a reliable early clinical sign.
Cyanide
Cyanide toxicity can cause skin erythema due to elevated levels of oxygenated hemoglobin in the venous system. Additionally, hydroxocobalamin, a common antidote, can itself produce noticeable skin redness.
Chinese Restaurant Syndrome (MSG Reaction)
This condition is associated with ingestion of monosodium glutamate (MSG) and may present with flushing, chest discomfort, palpitations, headache, perioral tingling, facial swelling, and sweating.
Scombroid Poisoning
Scombroid poisoning results from ingestion of histamine-rich spoiled fish, leading to vasodilation and prominent skin flushing.
Anticholinergics
Erythema is a hallmark feature of anticholinergic toxicity, often described as “red as a beet” in the classic toxidrome.
Niacin
Niacin, commonly used to manage lipid levels, frequently causes flushing even at therapeutic doses. This effect can be reduced by taking aspirin beforehand or dosing at night.
Disulfiram Reaction
This reaction occurs when aldehyde dehydrogenase is inhibited by agents such as disulfiram, metronidazole, tolbutamide, or cefotetan. When alcohol is consumed, acetaldehyde accumulates, leading to flushing along with nausea, vomiting, tachycardia, shortness of breath, headache, and confusion.
Carbon Monoxide
Carbon monoxide poisoning may produce the classic “cherry red” skin appearance, although this is a late and often postmortem finding rather than a reliable early clinical sign.
Cyanide
Cyanide toxicity can cause skin erythema due to elevated levels of oxygenated hemoglobin in the venous system. Additionally, hydroxocobalamin, a common antidote, can itself produce noticeable skin redness.
Chinese Restaurant Syndrome (MSG Reaction)
This condition is associated with ingestion of monosodium glutamate (MSG) and may present with flushing, chest discomfort, palpitations, headache, perioral tingling, facial swelling, and sweating.
Scombroid Poisoning
Scombroid poisoning results from ingestion of histamine-rich spoiled fish, leading to vasodilation and prominent skin flushing.
Anticholinergics
Erythema is a hallmark feature of anticholinergic toxicity, often described as “red as a beet” in the classic toxidrome.
Niacin
Niacin, commonly used to manage lipid levels, frequently causes flushing even at therapeutic doses. This effect can be reduced by taking aspirin beforehand or dosing at night.
Disulfiram Reaction
This reaction occurs when aldehyde dehydrogenase is inhibited by agents such as disulfiram, metronidazole, tolbutamide, or cefotetan. When alcohol is consumed, acetaldehyde accumulates, leading to flushing along with nausea, vomiting, tachycardia, shortness of breath, headache, and confusion.
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Toxicology – Nystagmus-Inducing Toxins
Sedative–Hypnotics
Medications in this class commonly produce nystagmus as part of central nervous system depression.
Alcohols (Ethanol, Methanol, Ethylene Glycol, Isopropanol)
All alcohols can induce nystagmus. Ethanol is particularly associated with horizontal and downbeat nystagmus and is often assessed clinically using the horizontal gaze nystagmus test.
Phencyclidine and Dissociatives
Dissociative agents such as PCP, ketamine, and dextromethorphan can produce a characteristic rotatory nystagmus.
Phenytoin
Phenytoin toxicity is associated with horizontal and sometimes upbeat nystagmus.
Carbamazepine (Tegretol)
Carbamazepine can cause both horizontal and downbeat nystagmus.
Lithium
Lithium toxicity may lead to downbeat nystagmus.
Solvents (Inhalants)
Exposure to inhaled solvents has been associated with positional nystagmus, with severity correlating to the degree of exposure.
Thiamine Deficiency (Wernicke Encephalopathy)
Thiamine deficiency can result in Wernicke encephalopathy, characterized by ataxia, confusion, ophthalmoplegia, and nystagmus.
Overview
Nystagmus is an involuntary, rhythmic oscillation of the eyes that may occur in toxicologic conditions. It can present as horizontal (side-to-side), vertical (upbeat or downbeat), or rotatory movement. Horizontal nystagmus is the most common and is best observed during lateral gaze. Alcohol intoxication frequently produces nystagmus, which is often assessed in clinical and roadside settings. Certain agents such as anticonvulsants and lithium may produce vertical nystagmus, while phenytoin has been associated with upbeat nystagmus and PCP with rotatory nystagmus.
Sedative–Hypnotics
Medications in this class commonly produce nystagmus as part of central nervous system depression.
Alcohols (Ethanol, Methanol, Ethylene Glycol, Isopropanol)
All alcohols can induce nystagmus. Ethanol is particularly associated with horizontal and downbeat nystagmus and is often assessed clinically using the horizontal gaze nystagmus test.
Phencyclidine and Dissociatives
Dissociative agents such as PCP, ketamine, and dextromethorphan can produce a characteristic rotatory nystagmus.
Phenytoin
Phenytoin toxicity is associated with horizontal and sometimes upbeat nystagmus.
Carbamazepine (Tegretol)
Carbamazepine can cause both horizontal and downbeat nystagmus.
Lithium
Lithium toxicity may lead to downbeat nystagmus.
Solvents (Inhalants)
Exposure to inhaled solvents has been associated with positional nystagmus, with severity correlating to the degree of exposure.
Thiamine Deficiency (Wernicke Encephalopathy)
Thiamine deficiency can result in Wernicke encephalopathy, characterized by ataxia, confusion, ophthalmoplegia, and nystagmus.
Overview
Nystagmus is an involuntary, rhythmic oscillation of the eyes that may occur in toxicologic conditions. It can present as horizontal (side-to-side), vertical (upbeat or downbeat), or rotatory movement. Horizontal nystagmus is the most common and is best observed during lateral gaze. Alcohol intoxication frequently produces nystagmus, which is often assessed in clinical and roadside settings. Certain agents such as anticonvulsants and lithium may produce vertical nystagmus, while phenytoin has been associated with upbeat nystagmus and PCP with rotatory nystagmus.
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Toxicology – Drugs Causing Tachycardia
Cocaine (Freebase)
Cocaine produces strong sympathomimetic effects by blocking the reuptake of serotonin, dopamine, and norepinephrine, leading to increased heart rate and blood pressure.
Amphetamines
Amphetamines stimulate the release of catecholamines from presynaptic nerve terminals, resulting in marked tachycardia and hypertension.
Sympathomimetics
This group of drugs elevates heart rate and blood pressure by increasing catecholamine release, decreasing reuptake, or inhibiting metabolism.
Anticholinergics
Anticholinergic agents inhibit parasympathetic activity, causing an increase in heart rate and often accompanying hypertension.
Antihistamines
Many antihistamines possess anticholinergic properties, which can lead to tachycardia as part of their toxic effects.
Theophylline (Methylxanthines)
Theophylline acts as an adenosine receptor antagonist, β-agonist, and phosphodiesterase inhibitor, all of which contribute to increased heart rate and potential arrhythmias.
Thyroid Hormone
Excess thyroid hormone elevates metabolic rate and enhances sensitivity to catecholamines, leading to tachycardia.
Solvents (Inhalants)
Inhaled solvents may displace oxygen in the lungs, causing hypoxemia and reflex tachycardia. They can also sensitize the myocardium to catecholamines, increasing the risk of fatal arrhythmias.
Fever
An increase in body temperature raises basal metabolic rate, which in turn increases heart rate.
Treatment
Benzodiazepines are the first-line treatment for undifferentiated tachycardia in toxicologic settings. Intravenous fluids should be administered in cases of hypovolemia, and active cooling measures should be initiated for patients with hyperthermia.
Cocaine (Freebase)
Cocaine produces strong sympathomimetic effects by blocking the reuptake of serotonin, dopamine, and norepinephrine, leading to increased heart rate and blood pressure.
Amphetamines
Amphetamines stimulate the release of catecholamines from presynaptic nerve terminals, resulting in marked tachycardia and hypertension.
Sympathomimetics
This group of drugs elevates heart rate and blood pressure by increasing catecholamine release, decreasing reuptake, or inhibiting metabolism.
Anticholinergics
Anticholinergic agents inhibit parasympathetic activity, causing an increase in heart rate and often accompanying hypertension.
Antihistamines
Many antihistamines possess anticholinergic properties, which can lead to tachycardia as part of their toxic effects.
Theophylline (Methylxanthines)
Theophylline acts as an adenosine receptor antagonist, β-agonist, and phosphodiesterase inhibitor, all of which contribute to increased heart rate and potential arrhythmias.
Thyroid Hormone
Excess thyroid hormone elevates metabolic rate and enhances sensitivity to catecholamines, leading to tachycardia.
Solvents (Inhalants)
Inhaled solvents may displace oxygen in the lungs, causing hypoxemia and reflex tachycardia. They can also sensitize the myocardium to catecholamines, increasing the risk of fatal arrhythmias.
Fever
An increase in body temperature raises basal metabolic rate, which in turn increases heart rate.
Treatment
Benzodiazepines are the first-line treatment for undifferentiated tachycardia in toxicologic settings. Intravenous fluids should be administered in cases of hypovolemia, and active cooling measures should be initiated for patients with hyperthermia.
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Toxicology – Drugs Causing Bradycardia
Beta-Blockers (e.g., Propranolol)
Beta-blockers reduce sinoatrial (SA) and atrioventricular (AV) nodal conduction, leading to decreased heart rate and, in severe cases, heart block.
Opiates (Poppies)
Opiates increase vagal tone and exert a depressant effect on SA and AV nodal conduction, contributing to bradycardia.
Anticholinesterase Inhibitors
By inhibiting acetylcholinesterase, these agents increase acetylcholine levels, producing a cholinergic toxidrome in which bradycardia is a prominent feature.
Clonidine
Clonidine is a central α₂ receptor agonist that can cause bradycardia along with hypotension and respiratory depression.
Calcium Channel Blockers
These medications impair SA and AV nodal conduction, resulting in decreased heart rate and potential heart block.
Digoxin
Digoxin increases vagal tone while slowing conduction through the SA and AV nodes, leading to bradycardia despite its positive inotropic effects.
Ethanol
At high doses, ethanol can depress cardiac function and contribute to bradycardia.
Treatment
Atropine may be administered to counteract increased vagal tone and raise heart rate. If ineffective, external pacing should be considered. Definitive management involves identifying the causative toxin and administering the appropriate antidote or targeted therapy.
Beta-Blockers (e.g., Propranolol)
Beta-blockers reduce sinoatrial (SA) and atrioventricular (AV) nodal conduction, leading to decreased heart rate and, in severe cases, heart block.
Opiates (Poppies)
Opiates increase vagal tone and exert a depressant effect on SA and AV nodal conduction, contributing to bradycardia.
Anticholinesterase Inhibitors
By inhibiting acetylcholinesterase, these agents increase acetylcholine levels, producing a cholinergic toxidrome in which bradycardia is a prominent feature.
Clonidine
Clonidine is a central α₂ receptor agonist that can cause bradycardia along with hypotension and respiratory depression.
Calcium Channel Blockers
These medications impair SA and AV nodal conduction, resulting in decreased heart rate and potential heart block.
Digoxin
Digoxin increases vagal tone while slowing conduction through the SA and AV nodes, leading to bradycardia despite its positive inotropic effects.
Ethanol
At high doses, ethanol can depress cardiac function and contribute to bradycardia.
Treatment
Atropine may be administered to counteract increased vagal tone and raise heart rate. If ineffective, external pacing should be considered. Definitive management involves identifying the causative toxin and administering the appropriate antidote or targeted therapy.
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Toxicology – Drugs Causing Hypoventilation
Opiates
Opiates are the most significant contributors to respiratory depression among toxicologic agents. They suppress the brainstem respiratory center, leading to decreased respiratory rate and depth. Reversal with naloxone is effective but should be carefully titrated to avoid precipitating acute withdrawal.
Sedative–Hypnotics
This class of central nervous system depressants reduces respiratory drive in overdose situations, potentially leading to hypoventilation and respiratory failure.
Liquor (Ethanol)
At very high concentrations, ethanol can cause marked central nervous system depression, resulting in clinically significant respiratory suppression.
Weed (Cannabinoids)
Cannabinoid receptor agonists such as marijuana generally have mild respiratory effects. However, slight reductions in respiratory rate may occur as part of overall central nervous system depression.
Treatment
In patients with decreased consciousness, central nervous system depression, or inadequate ventilation, airway protection with endotracheal intubation is essential. Opiate toxicity can be reversed with naloxone, and continuous infusion may be required due to its shorter duration of action compared to many opioids. Flumazenil may reverse certain sedative–hypnotics like benzodiazepines, but it must be used cautiously as it can trigger withdrawal seizures or status epilepticus in dependent individuals.
Opiates
Opiates are the most significant contributors to respiratory depression among toxicologic agents. They suppress the brainstem respiratory center, leading to decreased respiratory rate and depth. Reversal with naloxone is effective but should be carefully titrated to avoid precipitating acute withdrawal.
Sedative–Hypnotics
This class of central nervous system depressants reduces respiratory drive in overdose situations, potentially leading to hypoventilation and respiratory failure.
Liquor (Ethanol)
At very high concentrations, ethanol can cause marked central nervous system depression, resulting in clinically significant respiratory suppression.
Weed (Cannabinoids)
Cannabinoid receptor agonists such as marijuana generally have mild respiratory effects. However, slight reductions in respiratory rate may occur as part of overall central nervous system depression.
Treatment
In patients with decreased consciousness, central nervous system depression, or inadequate ventilation, airway protection with endotracheal intubation is essential. Opiate toxicity can be reversed with naloxone, and continuous infusion may be required due to its shorter duration of action compared to many opioids. Flumazenil may reverse certain sedative–hypnotics like benzodiazepines, but it must be used cautiously as it can trigger withdrawal seizures or status epilepticus in dependent individuals.
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Toxicology – Drugs Causing Hypertension
Amphetamines
Amphetamines enhance the release of catecholamines, producing significant increases in blood pressure and heart rate.
Caffeine
Caffeine stimulates adrenergic activity, causing hypertension and tachycardia. In large overdoses, it may paradoxically result in hypotension and cardiovascular collapse.
Cocaine
Cocaine increases synaptic concentrations of serotonin, dopamine, and norepinephrine by blocking their reuptake, resulting in elevated blood pressure and heart rate.
Anticholinergics
Anticholinergic drugs suppress parasympathetic activity, leading to increased heart rate and elevated blood pressure.
Nicotine
Nicotine toxicity initially presents with hypertension and tachycardia, which may later progress to bradycardia and hypotension.
Sympathomimetics
These agents increase blood pressure and heart rate by promoting catecholamine release, decreasing their reuptake, or inhibiting their breakdown.
Thyroid Hormone
Excess thyroid hormone elevates basal metabolic rate and enhances responsiveness to catecholamines. In severe overdose, this may lead to cardiac dysrhythmias followed by hypotension and cardiovascular collapse.
Treatment
Benzodiazepines are the first-line treatment for hypertension due to sympathomimetic toxicity. Pure β-blockers should be avoided because they can cause unopposed α-adrenergic stimulation and worsen hypertension. Agents such as labetalol are preferred due to their combined α- and β-blocking effects.
Amphetamines
Amphetamines enhance the release of catecholamines, producing significant increases in blood pressure and heart rate.
Caffeine
Caffeine stimulates adrenergic activity, causing hypertension and tachycardia. In large overdoses, it may paradoxically result in hypotension and cardiovascular collapse.
Cocaine
Cocaine increases synaptic concentrations of serotonin, dopamine, and norepinephrine by blocking their reuptake, resulting in elevated blood pressure and heart rate.
Anticholinergics
Anticholinergic drugs suppress parasympathetic activity, leading to increased heart rate and elevated blood pressure.
Nicotine
Nicotine toxicity initially presents with hypertension and tachycardia, which may later progress to bradycardia and hypotension.
Sympathomimetics
These agents increase blood pressure and heart rate by promoting catecholamine release, decreasing their reuptake, or inhibiting their breakdown.
Thyroid Hormone
Excess thyroid hormone elevates basal metabolic rate and enhances responsiveness to catecholamines. In severe overdose, this may lead to cardiac dysrhythmias followed by hypotension and cardiovascular collapse.
Treatment
Benzodiazepines are the first-line treatment for hypertension due to sympathomimetic toxicity. Pure β-blockers should be avoided because they can cause unopposed α-adrenergic stimulation and worsen hypertension. Agents such as labetalol are preferred due to their combined α- and β-blocking effects.
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Toxicology – Drugs causing Hypotenssion
C – Clonidine:
A central-acting α₂ receptor agonist that can initially cause hypertension followed by hypotension.
C – Calcium Channel Blockers:
A class of antihypertensive and antianginal medications that decrease heart rate and dilate peripheral vasculature.
R – Reserpine:
A sympatholytic antihypertensive medication that blocks the reuptake of norepinephrine, dopamine, and serotonin, leading to enhanced degradation by MAO in the synaptic space.
A – Antidepressants:
Tricyclic antidepressants (TCAs) can induce hypotension through α₁ receptor blockade and by causing cardiac dysrhythmias and subsequent cardiac collapse.
A – Aminophylline:
A methylxanthine that acts as an adenosine receptor antagonist, β-blocker, and phosphodiesterase inhibitor that can cause hypotension and cardiac collapse in overdose settings.
S – Sedative–Hypnotics:
Hypotension can occur secondary to myocardial depression.
H – Heroin:
Opiates can induce hypotension secondary to histamine release, direct vasodilation, or through a centrally mediated decrease of vagal tone.
Treatment:
Hypotension is best treated with large fluid boluses followed by the administration of antidotes and/or treatment of the respective toxin. Pressors may be indicated if the patient remains hypotensive after fluid resuscitation.
C – Clonidine:
A central-acting α₂ receptor agonist that can initially cause hypertension followed by hypotension.
C – Calcium Channel Blockers:
A class of antihypertensive and antianginal medications that decrease heart rate and dilate peripheral vasculature.
R – Reserpine:
A sympatholytic antihypertensive medication that blocks the reuptake of norepinephrine, dopamine, and serotonin, leading to enhanced degradation by MAO in the synaptic space.
A – Antidepressants:
Tricyclic antidepressants (TCAs) can induce hypotension through α₁ receptor blockade and by causing cardiac dysrhythmias and subsequent cardiac collapse.
A – Aminophylline:
A methylxanthine that acts as an adenosine receptor antagonist, β-blocker, and phosphodiesterase inhibitor that can cause hypotension and cardiac collapse in overdose settings.
S – Sedative–Hypnotics:
Hypotension can occur secondary to myocardial depression.
H – Heroin:
Opiates can induce hypotension secondary to histamine release, direct vasodilation, or through a centrally mediated decrease of vagal tone.
Treatment:
Hypotension is best treated with large fluid boluses followed by the administration of antidotes and/or treatment of the respective toxin. Pressors may be indicated if the patient remains hypotensive after fluid resuscitation.
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Toxicology – APPROACH TO THE POISONED PATIENT
ABC’s:
As with all emergency department patients, first ensure the patient has a patent airway, is breathing, and has a pulse. Immediate intervention is required if any or all of these are absent.
Vital Signs:
Temperature, heart rate, blood pressure, respiratory rate, and O₂ saturation will help guide the diagnosis and help categorize the intoxication or overdose into one of the more common toxidromes.
History:
Attempt to get a good history using collateral sources if possible, as the poisoned patient is often unreliable or containers altered. EMS, family members, occupation, past medical records, and empty pill bottles can provide insight into the potential toxin or overdose.
Physical:
In addition to vital signs, physical examination will help tease out the clinical toxidrome.
PEARLS
ABC’s:
As with all emergency department patients, first ensure the patient has a patent airway, is breathing, and has a pulse. Immediate intervention is required if any or all of these are absent.
Vital Signs:
Temperature, heart rate, blood pressure, respiratory rate, and O₂ saturation will help guide the diagnosis and help categorize the intoxication or overdose into one of the more common toxidromes.
History:
Attempt to get a good history using collateral sources if possible, as the poisoned patient is often unreliable or containers altered. EMS, family members, occupation, past medical records, and empty pill bottles can provide insight into the potential toxin or overdose.
- What: Consider what medications the patient has access to including his or her own, as well as those of parents, friends, significant others, children and visiting relatives. Ask if the drug is an immediate-release or sustained-release product.
- When: A time frame of suspected ingestion can influence treatment options and patient disposition. For example, some toxins have a delayed onset and some antidotes must be given within a specific time frame.
- Dose: Assume that any unreliable patient took the highest possible dose. Count the number of pills remaining in their prescription bottles and subtract that amount from the initial number prescribed. Assume all missing pills were taken as a single overdose.
- Why: Was this an accidental ingestion, a therapeutic misadventure in pursuit of a “high” or in pursuit of better treatment outcomes, or was it a suicide attempt? The answer will help determine the patient’s disposition.
- Coingestions: Multiple drug ingestions are common; alcohol is the most common coingestion.
Physical:
In addition to vital signs, physical examination will help tease out the clinical toxidrome.
- Mental Status: Agitation / somnolence / paranoid / obtunded / comatose
- Skin: Wet / dry / cyanotic / erythematous / pale / hot / cold
- Eyes: Miosis / mydriasis / nystagmus / conjunctival injection / jaundice
- Mucous Membranes: Wet and salivating / dry and chapped
- Heart/EKG: Tachycardia / bradycardia / QRS widened / QT prolongation
- Lungs: Tachypnea / bradypnea / rales / wheezing / crackles
- Bowel Sounds: Hyperactive / normal / absent
- Neurological: Hyperreflexia / hyporeflexia
PEARLS
- US Poison Control Center: 1-800-222-1222
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Toxicology – Drugs Causing Hyperventilation
Aspirin (Salicylates)
Salicylates directly stimulate the respiratory center in the central nervous system, leading to increased respiratory rate and the development of respiratory alkalosis.
Amphetamines (Speed)
Amphetamines and other sympathomimetic agents elevate catecholamine levels, resulting in increased heart rate, blood pressure, and respiratory rate, often causing hyperventilation.
Paraquat
Paraquat, a toxic herbicide, causes direct lung injury leading to impaired oxygen exchange. This results in hypoxia and compensatory hyperventilation.
Phencyclidine (PCP)
PCP is a dissociative anesthetic that produces minimal cardiopulmonary depression. Patients may fluctuate between sedation and agitation, with hyperventilation commonly occurring during agitated states.
Noncardiogenic Pulmonary Edema (NCPE)
Various toxins can lead to noncardiogenic pulmonary edema, impairing gas exchange and triggering hyperventilation. Inhaled causes include ammonia, chlorine gas, solvents, hydrocarbons, hydrogen sulfide, and phosgene. Oral or parenteral agents include heroin, methadone, naloxone, salicylates, NSAIDs, and certain chemotherapeutic drugs.
Toxin-Induced Metabolic Acidosis
Certain toxins produce metabolic acidosis, which stimulates compensatory hyperventilation (hyperpnea) as the body attempts to reduce carbon dioxide levels and correct acidemia.
Aspirin (Salicylates)
Salicylates directly stimulate the respiratory center in the central nervous system, leading to increased respiratory rate and the development of respiratory alkalosis.
Amphetamines (Speed)
Amphetamines and other sympathomimetic agents elevate catecholamine levels, resulting in increased heart rate, blood pressure, and respiratory rate, often causing hyperventilation.
Paraquat
Paraquat, a toxic herbicide, causes direct lung injury leading to impaired oxygen exchange. This results in hypoxia and compensatory hyperventilation.
Phencyclidine (PCP)
PCP is a dissociative anesthetic that produces minimal cardiopulmonary depression. Patients may fluctuate between sedation and agitation, with hyperventilation commonly occurring during agitated states.
Noncardiogenic Pulmonary Edema (NCPE)
Various toxins can lead to noncardiogenic pulmonary edema, impairing gas exchange and triggering hyperventilation. Inhaled causes include ammonia, chlorine gas, solvents, hydrocarbons, hydrogen sulfide, and phosgene. Oral or parenteral agents include heroin, methadone, naloxone, salicylates, NSAIDs, and certain chemotherapeutic drugs.
Toxin-Induced Metabolic Acidosis
Certain toxins produce metabolic acidosis, which stimulates compensatory hyperventilation (hyperpnea) as the body attempts to reduce carbon dioxide levels and correct acidemia.
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