Pharmacological Emergencies

These questions and answers are designed to give you an opportunity to use some of the pharmacological knowledge you have acquired during the semester, by exploiting observation and data collected during five emergency room admissions in order to develop a differential diagnosis of each patient’s problem. ( Non-drug-related diagnoses will not be considered here, but they will be among your first choices when actually working in a hospital emergency room. ) You should first review each case history, and then prepare yourself to answer the following questions about each case before attempting to answer the specific questions following it, keeping in mind that the object is to treat a sick patient, not a drug:

  • What drug class is most likely to have caused the signs and symptoms in the patient at hand? [N.B.: There may be several possibilities, but in no instance is more than one drug implicated in the following cases, even if multiple exposures are the rule.]
  • What are the sites and modes of action of the drug or drug class that appears to have been responsible for the patient’s signs and symptoms?
  • What other effects would be expected if the patients is not treated?
  • What do you anticipate to be the time course of the patient’s illness? What is the likely prognosis for complete recovery?
  • What supportive or specific treatments are appropriate for the patient?
  • What is the epidemiology of the agent that was probably responsible for his sympton? Are recurrences likely, or possible?

Before you begin to study these cases, you may wish to review normal values for the various vital signs, including pulse, blood pressure, respiratory rate, and pupil diameter.

Vital Sign Normal Values
Pulse 60-80 at rest, awake; 50-70 asleep
Blood pressure 100-140/60-90 mm Hg
Respiratory rate 14-18 / min
Temperature 96.5 – 99.0 F oral, for rectal add 0.5 to 1.0F to oral
Pupil diameter 3-4 mm in average lighted room
Urine output 0.4 – 1.0 ml/min


The patient is a slightly overweight 50 year-old man who is brought to the emergency room by ambulance after his wife found him unconscious in their garage. He does not respond to verbal or painful stimuli, and his deep tendon reflexes are diminished. Neither alcohol nor fruity odors are detectable in his breath. His vital signs are: Pulse = 90 bpm; BP = 140/90 mmHg; Respirations = 32/min; Temp. (rectal) = 97.4F. His pupil diameter is 4mm, and his pupils respond sluggishly to light. Routine blood cell counts are within normal limits. The patient is moderately cyanotic, and ausculation reveals fluid in his lungs. His bladder is catheterized at admission; two hour later his total urine output is measured at 20 ml. At that time, his BP is 120/60 mmHg, his pulse is 52bpm, and his respirations are 8-10/min.

I. This patient’s signs and symptoms might plausibly have been produced by:

No. Although a large first-ever dose of heroin can’t be ruled out from the data given, you’d certainly have expected to find miosis; since the respiratory rate falls during your examination, you might well be justified in pursuing an opioid diagnosis. (Since no needle tracks are reported, addiction seems unlikely.) What drug might you administer in order to rule an opioid in or out of further consideration? On the other hand, another agent could better fit the clinical picture described here. Make another choice.

No. Well, a benzodiazepine is a possibility, but it’s highly unlikely to produce such a serious clinical picture of progressive deterioration. Since you don’t have time to wait for a definitive drug screen to come from the lab, you might wish to make another choice. If an empty bottle of diazepam tablets had been brought in with this patient, what agent might you administer in order to both reverse the drug’s toxic effects and confirm your diagnosis?

Good thinking. This case was adapted from a case report of a patient who had ingested an overdose of a barbiturate that had been prescribed to help him sleep; was it a very short- or a long-acting agent? (However, barbiturates are seldom prescribed for ambulatory patients these days, since benzodiazepines are equally effective and much safer as sleep medications.) Characteristically, such patients first lose consciousness, then their pain reflexes followed by their deep tendon reflexes, and go into shock, hypothermia, and renal failure as respiration and circulation fail. The pupils are usually somewhat dilated; are this patient’s pupils dilated? They’ll grow larger as hypoxia paralyzes the ciliary muscles. However, you might want to consider other possibilities for your differential diagnosis. For instance, if the patient’s symptoms had been produced by a barbiturate but you diagnosed an opioid, would the administration of naloxone be expected to further depress his respiration? (No.) Now go on to Item II.

Come on, now; cocaine will not reduce either pulse or blood pressure. Try again.

No. Well, alcohol is a possibility, despite the absence of its odor on the patient’s breath. Indeed, alcohol can produce symptoms virtually indistinguishable from those of other non-selective central depressants. Since there’s no evidence of a night with a bottle at the scene, you might want to expand your differential diagnosis to include at least one other agent.

II. Appropriate therapy for this patient should include:

1) Gastric lavage and/or other techniques for removing the drug from the gastrointestinal tract.
2) Oxygen.
3) A diuretic.
4) Dopamine or dobutamine.
5) Naloxone.

Yes, gastric lavage will be most helpful if the poison was ingested within 24 hours, as seems likely here. The “intestinal dialysis” technique of administering activated charcoal by mouth, to speed removal of barbiturates from the blood, should provide additional protection against further reduction of the patient’s vital signs. But, might any other treatment be necessary? Better think about this patient’s clinical status a bit more.

Yes, he’ll certainly need oxygen, perhaps administered via a tracheostomy tube. CO2 should not be added to the oxygen, however, because the CO2-sensitive respiratory drive is more seriously impaired by barbiturates than is the hypoxic drive. Is any other treatment indicated for this patient?

Yes, you’re right; minimizing the amount of drug in the body and shortening its half-life are important (see comment to Item IIa), as are oxygen (see comment to Item IIb) and a diuretic, probably furosemide (why this one?), to help remove fluid from the chest. However, the diuretic may need a little help, so you may need to add something else from the list given in Item II.

Yes, you’re right; minimizing the amount of drug in the body and shortening its half-life are important (see comment to Item IIa), as are oxygen (see comment to Item IIb), a diuretic, probably furosemide (why this one?), to help remove fluid from the chest, and perhaps dopamine or dobutamine, to restore the failing circulation, so that blood can actually get to the kidneys. (On the other hand, if the blood pressure falls no further, vasopressors may not be needed.) Now go on to Case 2.

Well, yes, minimizing the amount of poison in the body and shortening it’s half-life (see comment to Item IIa), oxygen (see comment to Item IIb), and a diuretic and a vasopressor (see comment to Item IId), are all likely to be needed here. It’s true that some emergency room physicians treat all apparent drug-induced coma patients with naloxone, playing the odds as it were, but we have no evidence of heroin use, such as needle tracks, in this case. (See, e.g., comment to Item Ia)


The patient, a well-developed, well-nourished, 33 year-old man, is brought to the Emergency Room by the police officers who found him staggering along a street near the hospital. He tells you this is the worst headache he’s had since he began having them every week or two about a year ago. Although he seems oriented in respect of time and place, emergency room personnel agree that his affect is inappropriate, partly because he refuses to answer further questions about his medical history, including illicit drug use. Neurological exam reveals left ataxic hemiparesis, although deep tendon and pain reflexes are normal. No recognizable odors are detectable in his breath. His vital signs are: Pulse = 104 bpm; BP = 170/116; Respirations = 22/min; Temp. = 99.0F. Both pupils measure 6mm in diameter and respond promptly to light. He is able to provide a urine sample with ease. The hospital computer tells you that the patient was admitted for a myocardial infarction eight months ago, and that his record will be delivered to you shortly.

III. This patient’s signs and symptoms might plausibly have been produced by:

Come on now, there’s absolutely nothing in this man’s history or vital signs that suggests opioid toxicity. Try again.

No. Some of the physical signs in this case might suggest the presence of antimuscarinic compounds, but the entire picture is atypical of poisoning by, e.g., the little red berries of the climbing nightshade (Solanum dulcamara) that look like “Tic-Tacs” to the unwary. For instance, the patient’s vision is not blurred, his pupils can respond to light, and urination is not difficult. Make another choice.

No. The history might be consistent with an amphetamine habit, but in overdoses the deep tendon reflexes are usually enhanced, and sweating is a prominent sign of increased body temperature and involuntary skeletal muscle activity. Try again.

You’re right; this is an actual case of acute cocaine overdose in a regular cocaine user. Because it blocks reuptake of norepinephrine and dopamine, its peripheral effects are identifiable in the tachycardia and hypertension that result from the underlying vasoconstriction. Cocaine’s local anesthetic effect is synergistic with its sympathomimetic effect, resulting in ventricular arrhythmias and, in this case, a previous myocardial infarct. Similarly, the premonitory headaches and now the right-handed stroke (it could be either occlusive or hemorrhagic) are secondary to cerebral vasoconstriction (although the headaches might also be associated with cocaine’s greater potency for inhibiting the uptake of serotonin than that of norepinephrine or dopamine). Cocaine usually kills by respiratory depression; however, fatal cardiac and CNS events have been increasing in frequency as cocaine abuse becomes more widespread. Now go on to Item IV.

No. You’re right that heroin, antimuscarinic compounds, and amphetamines are highly unlikely. However, there is one more choice, if only by default.

IV. Appropriate therapy for this patient should include:

No. You might want to acidify the urine to speed the removal of amphetamine, which has a half-life of 6-8 hours, but it won’t affect the half-life of cocaine. Besides, its half-life is somewhat less than an hour, so nothing much is to be gained by enhancing its removal. Try again.

No. Is there any good evidence that this patient actually needs more oxygen? Try again.

No. Diazepam would certainly be indicated if the patient were convulsing or showing other signs of excessive CNS activity. However, this seems not to be the case here; that is, this man’s CNS symptoms are clearly referable to anatomic damage in the CNS. Any other good therapeutic choices?

Yes, since this patient’s tachycardia and hypertension are signs of potential hazard, especially in light of his previous MI. You might, therefore, want to administer labetalol; why might it be preferable to propranolol? Evidence from the EKG might also lead you to prescribe verapamil if ventricular fibrillation seems imminent, or phentolamine might be indicated. It all depends. Now you can move on to Case 3.

What would be the point of giving bicarbonate to this patient? That is, is anything special to be gained by alkalinizing his blood or urine? Try again.


The patient is a rather overweight 19 year-old male aspring college athelete who has been sent by ambulance by the college health service because he had complained of severe headache, and because his BP is 230/142. Upon admission to the Emergency Room, he is highly agitated. His BP is unchanged and his pulse is 48. Respirations = 20/min; Tmep. = 98.2F; Pupil diameter = 3mm. The patient denies any history of illicit drug use, and you find no reason not to believe him. His past medical history is not remarkable, and he appears in all respects save for his headache and vital signs. Urinalysis and blood counts are normal. While you are completing the essentially unremarkable neurological examination of this patient, he slumps forward and falls off the examining table.

V. This patient’s signs and symptoms might plausibly have been produced by:

No. The signs of chlorpromazine toxicity generally range from orthostatic hypotension to extrapyramidal symptoms to an extreme form of Parkinsonism, marked by antidopaminergic effects. Nothing within this range seems to be present here. Try again.

No. Pseudoephedrine would be expected to increase the heart rate, because it is a beta-agonist. Try again.

No. Phencyclidine often confuses the differential diagnosis of drug-related emergencies. However, the typical victim of PCP has a fast pulse, is hallucinating, is hyper-reflexive, and becomes extraordinarily anxious; he may go into coma and then shock, but that is not what is described in this case. Try again.

Yes, the best bet here is phenylpropanolamine (PPA), although we don’t know whether the patient acquired it as a so-called “mail-order stimulant,” or as an appetite suppressant so that he could make one of his college’s teams; it also appears in dozens of over-the-counter “cold remedies.” Since PPA is highly selective for alpha-receptors (more than for B-receptors), it increases total peripheral resistance and BP, and induces reflex bradycardia. It also releases neuronal norepinephrine. Although PPA stimulates the CNS, producing anxiety, agitation, and sometimes even psychotic behavior, the mechanism has not yet been ascertained; it may be via adrenergic stimulation, but that’s still hypothetical. The greatest hazard is the hypertension which, if left unchecked, can result in a fatal encephalopathy, as seems imminent here. Many PPA preparations also contain B-agonists such as ephedrine. In patients poisoned by such combination drugs, the heart rate will usually increase, instead of fall, which further increases the risk of hypertensive encephalopathy. Now go on to Item VI.

VI. Appropriate therapy for this patient should include:

Right. Since the greatest hazard to patients with PPA toxicity is unchecked hypertension, its appropriate treatment begins with sodium nitroprusside or IV nitroglycerin. But this may not be quite enough. Would you like to consider some additional therapy before moving on to Case 4?

No. You don’t really mean to prescribe a vasopressor for a man with serious hypertension and a reflex bradycardia, do you? Try, try again.

Yes, phentolamine or some other alpha-antagonist may well be required to help maintain vasodilation in such a patient. Anything else?

No. Considering the patient’s neurological status at the end of the case report, he’s not going to need a sedative. Make another choice.

Yes. Since PPA is a weak base, usually it’s fairly easily excreted as long as the urine pH is not too alkaline; thus, acidification is not usually needed unless the urinary pH climbs above 7.0. The drug’s half-life is as long as 5 to 6 hours, however, so it might be necessary to speed its removal if the patient has taken a truly gargantuan overdose, or if his CNS symptoms seem to be out of control (even so, a potent vasodilator should facilitate recovery). If you’ve already considered choice VIa, you can feel free to go on to Case 4.

Of course; a direct vasdolator (which?) and a longer-lasting one (which?). Once you’ve sorted them out, move along to Case 4.


A 55 year-old professor of biochemistry is brought to the Emergency Room by ambulance. His wife had found him unconscious in their large apple and peach orchard two hours previously, and summoned help when she was unable to rouse him. She tells you that her husband has been complaining of stomach cramps, severe nausea that “made him feel like he was always going to throw up”, and diarrhea, all for about ten days, and that a couple of days ago he mentioned that things looked “fuzzy”, that maybe he should see an ophthalmologist. Otherwise, he has been in fairly good health for many years, although a cardiologist has been following his mild hypertension. On physical examination the patient is sweating profusely (although the examining room is well air conditioned), copious saliva is drooling from his mouth, and his skin is cyanotic. BP = 148/92; Pulse = 72 bpm; Respirations = 36/min; Temp. (rectal) = 97.8 F. Pupil diameter = 1.5 min; both pupils are unresponsive to light, but his fundi are normal. Ausculation reveals fluid in the lungs. He is in deep coma, perhaps worsening; he does not respond to painful stimuli. At the time you first see him his muscles are twitching, but by the end of your examination, his limbs are completely flaccid, and deep tendon reflexes are absent. His bladder empties spontaneously (of 100 ml urine) before it can be catheterized. Conventional blood chemistries and blood cell counts are normal.

VII. This patient’s signs and symptoms might plausibly have been produced by:

No. If you chose this diagnosis, you should go to Goodman & Gilman (especially page 158) to refresh your memory and discover why another choice is necessary.

You got it. This case was abstracted from a published case of organophosphate poisoning. Whether the culprit was malathion or parathion was never established, but the latter has caused many more cases of human poisoning. The physical exam is typical of generalized cholinergic stimulation: miosis, sweating, salivation, bronchospasm (although that’s only a secondary inference from the increased respirations and cyanosis), fasciculations progressing toward complete flaccidity, and apparent urinary incontinence. Moreover, the patient’s history is entirely consistent: GI hyperactivity, blurring, and now urinary incontinence. In short, SLUD, for the most distinguishing features of AntiChE poisoning: Salivation, Lacrimation (for which we have no certain evidence in this case), Urination, & Defecation. Patients usually die of respiratory failure due to bronchoconstriction, increased secretions, and respiratory muscle paralysis, with, perhaps, secondary cardiovascular complications. The time course varies with the agent which caused the poisoning, but this is more likely a case of organophosphate than carbamate poisoning because of the prominence of the patient’s CNS symptoms. He probably inhaled the AChE inhibitor, whatever it was, during repetitive seasonal spraying of his orchard for the past couple of weeks. Now go on to Item VIII.

No. Nicotine poisoning by this route would be highly unusual; serious toxicity is usually from ingesting it, or following accidental topical application to the skin, and its course is very short, usually only a few minutes until death. Moreover, nicotine poisoning usually produces hypotension, a weak, rapid pulse, and respiratory failure, none of which are occuring in this patient. Better try again.

No. Acetaminophen toxicity has not been reported to have the kind of chronic prodromal GI distress that has affected this patient, although the analgesic may, of course, produce such symptoms as part of its acute toxicity syndrome seen within 24 hours of an overdose. Keep in mind that the principal toxic effects of acetaminophen are on the liver, and, to a lesser extent, on the kidneys. Better choose another diagnosis.

No. This would be a cop-out answer! Choose one of the poisons on the list, and go on from there.

VIII. Appropriate therapy for this patient would include:

Atropine is, of course, the obvious antimuscarinic agent, to block the toxin’s muscarinic and CNS manifestations. But it’s probably not enough all by itself. Make another choice before going on to the next case.

No. What would a vasopressor get you — or, more precisely, your patient — therapeutically? His cardiovascular signs reveal no discernible damage. But at least one other choice is far more likely to benefit him. Better pick it before he dies on you.

Why? Try again.

No. Neither acidification nor alkanization of the urine is likely to speed up the elimination of organophosphates, but restoring the normal mechanism for their detoxification is virtually guaranteed to do so; better make another choice.

Sure; the usual treatment is with pralidoxime (2-PAM), which restores AChE activity at both nicotinic and muscarinic receptors by dephosphorylating the enzymes, even if it has little effect on the patient’s CNS symptoms. However, if this is the only agent you chose for treating this man, you should probably consider at least one additional and highly selective agent. Then go on to Case 5.

Yes, you’d probably want to antagonize the insecticide’s muscarinic effects (with what?) as well as to counteract the insecticide directly, at its site of action (with what?)


A 36 year-old man who has been widowed recently is found unconscious in his apartment by a neighbor who calls for an EMT team. Because he is in a deep coma, the EMTs elect simply to start IV fluids (without any medication) and bring him to the Emergency Room. BP = 120/65; Pulse = 285/min (as recorded on the EKG); Respirations = 18/min; Temp. = 99.5 F; Pupil diameter is 5mm, with only slight response to light. Otherwise, the physical examination is generally unremarkable, although the bladder is palpable a handsbreadth above the symphysis pubis. Babinski signs are present, and deep tendon reflexes are absent. Conventional blood chemistries and cell counts are normal. The friend who found the patient tells you he had appeared highly agitated earlier in the day, and assures you that the patient has no history of drug abuse.

IX. This patient’s signs and symptoms might plausibly have been produced by:

No. Well, diazepam might have produced the CNS symptoms you’ve observed here (although probably not the Babinski reflex), but it would not have produced tachycardia and moderate hypotension, nor would it have affected the lower urinary tract. Better think this one through again.

Very good. This is a classic case of accidental poisoning (although a suicide attempt is not out of the question, considering the patient’s recent bereavement) with a tricyclic antidepressant, probably amitryptiline (other tricyclics, such as desimipramine, fluoxetine, and trazodone, have fewer anticholinergic effects, and this is an unusually serious case). Here the problem is to differentiate the patient’s anticholinergic (and quinidine-like) symptoms from his CNS symptoms. The first include tachycardia and hypotension (since tricyclics block cardiac cholinergic receptors, sympathetic tone to the heart increases; the hypotension may be due to reflex vasodilation or to peripheral alpha-blockade), urinary retention, and mydriasis (peripheral alpha-blockade may produce orthostatic hypotension, but not in this patient. Why not?). The tachycardia suggests the presence of A-V dissociation; if so, the EKG will very likely show prolongation of the QRS wave, which is the single best index of the severity of tricyclic toxicity. Fatal ventricular fibrillation seems imminent. Secondly, CNS signs, which may be followed by seizures, may be frightening, but they are unlikely to have fatal consequences all by themselves. The mechanism underlying the abnormal reflexes is unknown, although a Babinski reflex (but not absent deep tendon reflexes) often accompanies coma. Now that you’ve identified this patient’s problem, go on to the last Item.

No. Would you really have expected hypotension and tachycardia in a patient who had taken a large dose of an indirectly acting sympathomimetic agent? Also, see comment to Item IIIc. Better think this one through again.

No. Well, a very large dose of an anticholinergic agent like atropine might have produced many of this man’s signs and symptoms, but then one might wonder where he had obtained it — it’s not usually prescribed for self-administration at home. However, other prescription drugs have marked anticholinergic properties, as well as direct effects on the CNS. Try again.

No. Quinidine can cause hypotension, because of its alpha-adrenergic blocking effect. High grade A-V block is probably present, as well as a widened QRS complex, even if we don’t have details of the EKG here. However, quinidine is unlikely to affect the CNS or the lower urinary tract, so you might want to think more about this problem.

X. Appropriate therapy for this patient might include many different agents, such as:

Right. Either of these agents can help control the arrhythmia; phenytoin can also help control seizures, but the coma will probably disappear over 24 to 72 hours anyway if the cardiac problems can be resolved. Because tricyclics block alpha-receptors, an alpha-adrenergic agonist (e.g., norepinephrine) or perhaps an inotropic agent (e.g., dobutamine), may also be indicated. On the other hand, although it might be difficult to predict, alkalinization with sodium bicarbonate alone will usually reduce the QRS interval, correct the mild hypotension, and control the arrhythmia. At any rate, some intervention will be necessary, since the half-life of amitryptiline is about 16 hours. Congratulations on completing this program. We hope you’ve enjoyed these previews of life in the E.R.

Come on, now, this patient is in a coma. (However, seizures can occur during tricyclic poisoning; in such cases, diazepam would be appropriate therapy.) You’d probably better continue to study the choices in Item X.

No. Well, physostigmine might seem to be appropriate for treating an overdose of a drug with prominent anticholinergic symptoms, but it is not recommended here, since the major toxic symptoms are not related to the anticholinergic effects of tricyclics but to cardiac conduction defects. Please go back to the drawing board at Item X.

Not entirely correct; see the comment to Item Xa, which will reassure you that you’re on the right track, while the comment to Item Xb will remind you of the clue you overlooked.

Not a good choice; better see the comment to Item Xb and the comment to Item Xc.