You are moonlighting in the ED at 0300 when a very big ruckus occurs in the vestibule. A disheveled 21 y/o male enters shortly thereafter with each of his extremities covalently bonded to no less than two police officers. This wave of sweating, screaming, undulating humanity proceeds to the trauma room. Secreatries scatter. Nurses run like rats. The North end of a Southbound Psych resident is the only hint he was there. A pair of hands on your scapulae gently push you into the room where you press as close to the wall as you can get.
The patient tosses burly police officers about like a petulant child might a rag doll. He sits upright in bed bellowing like a bull elk in mid-rutting season. James Brown would be proud. After much difficulty, he is finally restrained in leather and a cuff is applied to his arm yielding a blood pressure (you think) of 130/60. His heart rate on the monitor is 145 before the leads slime off. Every single muscle in his body stands out in bass relief. He is beet red and bathed in sweat. The room is alive with a cacophony of screaming and bellowing. A pretty young girl claiming to be his girlfriend appears at the door with an apprehensive look and states that he had some LSD and seems to not be enjoying his trip. She suggests possibly an exorcist. You note for all to hear that if his head turns 360 degrees you are outta there.....
You gingerly raise an eyelid just enough to see one pupil react normally from mid-position. He slimes out of one wrist restraint and waves three cops around in the breeze.
Well, here you are just hanging around helping support some of your habits by picking up a few bucks in the pit. What do you do now?
Don Chalfin:
Before I would do, administer, or order anything, I would at least consider the possibility of other wonderful substances that may be circulating in this patient's vasculature. Specifically, PCP comes to mind, judging by the patients "presentation" and "demeanor". Treatment?: Consider haloperidol or lorazepam,(both are helpful in the treatment of LSD and PCP) however, initial nonpharm measures may help prevent the patient from injuring himself or others. Prior to this however, consider administering flumazenil, D50, naloxone (again the possibility of a mixed drug cocktail should be strongly considered; drug users aren't always particular and the wonderful "labs" that process these street drugs don't seem to pay too much attention to CQI and TQM. Also, if PCP is shown to be present, consider urine acidification.
Daniel Joyce:
however, initial nonpharm measures may help prevent the patient from injuring himself or others. Prior to this however, consider administering flumazenil, D50, naloxone....This patient is not toxic from benzos nor opiates, antidotes can only cause problems. I would avoid them. A fingerstick is on the to-do list, but not an imperative during this dangerous period.
Malcolm Fisher:
I dont have much experience of either the substances or animals that US citizens choose to put in their veins and orifices as I live in a genteel hospital in Sydney"s Volvo belt. However prior to getting one of the American fellows down to grill him I would want to control the situation rapidly before someone got hurt. I would do this with whatever it took while the plods held any bit with a vein. Probably pentothal or a benzodiazepine and if it took enough to stop him breathing so be it. The pancuroniun would be handy. Then I would get a load of haloperidol on board, get him up to the unit and anchor his four limbs to something solid for when he came around. And because of personal prejudice and once nearly scheduling a similar patient with meningococcal meningitis I would think about an LP. Then I would go and read the book about acid,cocaine,crack and the like.
I note though that he doesn't fill Leigh Thompson's diagnostic criteria as the girl with him should have said "He never took nothing Doctor."
Dick Burrows:
This is the sort of thing you laugh about later but which at the time is deadly serious. It happened to me twenty years ago working in the delightful climes of Barbados. A big bugger built like a brick s***house and obviously given to pumping large amounts of iron presented in casualty and landed up at my desk. A few seconds of history taking showed him to be totally out of his tree and shortly he began talking about Jesus and how wonderful it was that everybody got on so well together! I took that as info that meant that in a very short space of time his deranged connections were going to look on me as something from under the floorboards and therefore something to be dispatched without due process. I called for a verrrry large aliquot of largactil (anything would have done as far as I was concerned and nothing is as fast as an ounce of lead). When said drug was placed in my hand I found myself and the patient looking at it with not another soul within a metric mile. Gently but quite deliberately I placed the syringe on the table, excused myself, backed out of the door and ran like ****. The next day he was apprehended by the cops stark naked directing the traffic in the middle of Bridgetown. He knocked hell out of most of em but was eventually committed for observation.
I make no excuse for my blatent cowardice - I'm not fighting for king and country with the distinct possibility of being executed for lack of moral fibre. When this situation occurs it is the responsibility of the authorities to ensure the safety of their staff. If the individual has to be restrained then so be it. I didn't ask him to sniff crack/Angel dust whatever. To be quite honest there are times when I think a dart gun would suffice.
Stephen Streat:
Ugh. This does have a deja-vu feel about it. I agree with Malcolm that the girlfriend should have said `he didn't take anything doctor' to make it more realistic - even more realistically he has smashed his arm through the window of the police car and is spraying God knows what all round the room in a fine red spray from his radial artery. I hate this problem - round here the ED staff arrive at an expedient solution via a two neuron reflex (eyes see the patient - fingers dial Critical Care pager) - I guess that puts us in the same bag as all those other guys who take the `low rent' approach.
I would try and manage him without endotracheal anaesthesia if it was possible - I reckon ataraxis is what he needs - hence butyrophenone or phenothiazine first off. Failing that there is nothing like thiopentone and sux - it wins every time. follow that up with some morphine and a good shot of a long acting bender (diazepam 20-40 mg). Such approach does have the advantage that instrumentation, CT scan, toxicology testing, gastric lavage etc are all much much easier but it does mean you have just bought a critical care admission - and one that want make you any friends among the cynical critical care nursing staff either most likely. Such is life. Oh yeah I almost forgot, stay away from flumazenil, naloxone and anything like them. That way danger lies (seizures, pulmonary odema, even`he gets even more lively than he is' - you dont need that).
Louis Brusco:
Succinylcholine 4 mg/kg IM, intubate him, and let the poor intensivist deal with the problem. No, seriously, my management would be decided by what further I plan to do with the patient. If I felt that any radiologic work-up would be needed, I would intubate and paralyze him. If I felt sure that it was pure drug related and I would just observe him, then I would ATTEMPT to sedate him. My choice here would be for IM Haloperidol. He may need 100-200 mg to be able to get him to the point that an IV could be started. My other choice for LSD but not PCP would be IM Ketamine, but I would save that for sedation for intubation early on. I would not hesitate to consider IM Vecuronium or pancuronium also, if the succinylcholine didn't work. The succ may weaken him enough to get an IV in and continue.
Steve Stowe:
Thankfully I am an anesthesiologist. Put 'im to sleep. Maybe with PAVLOX (That is a combination of Pancuronium (Pavulon) and Oxygen. May be crude but is a very effective restraint. Patients will rarely attack staff after a good dose of Pancuronium. Seriously, it is a difficult problem and sometimes these patient do arrive in the OR in this state after a street battle. These do occur here in New York on rare ocassions, not more than several times a night.
I learned a long time ago that the only way I can help the next patient is not to allow the current patient to render me incapable of functioning. The Other staff and I come first. If the men in Blue with badges and guns can't control the patient then the patient may be denied care until such a time as his care will not endanger others.
David Crippen:
Tim Buchman sez: There is some question as to why the patient is here. I sez: When the police are called to a "disturbance", they have a strong incentive to assume the disturbee has a medical problem...in this fashion they do not have to deal with these people in their facility. They are always brought straight to us..because we are a big Psychiatric Center with one of the few Psychiatric Emergency Departments Headed by a full time Emergency Interventional Psychiatrist. As soon as the psych folks get a gander at someone like this, they point their bony fingers toward the medical ED and the progression is complete. If there is no concern regarding trauma, medical emergencies and so on other The psychiatrists will not deal with unruly patients suspected of having drug ingestions. They are all sent forthwith to the medical side for "medical clearance", then shipped to the psych side when they calm down.
The patient was held down by enough people so that a tenuous IV could be placed in his left upper arm. Next question-what to give? Here was my thinking process.
I gave him 5 mg of midazolam and he settled down in about five minutes, at least enough for the nurses to manage. I thin got a central line in his femoral artery and started esmolol at 50 mcg/kg/min titrated up to get his heart rate down from 150 to around 110. Following calming, he remained confused and somewhat combative as if being pursued by demons real or imagined. Blood samples are drawn for routine stuff and tox screen. The Shrinks slowly accumulate and suggest they might take him now that he is calmed down.
Further questions at this point:
David Crippen:
He needed to be monitored closely and his sedation highly titrated, which is why I kept him on a midazolam infusion in the ICU and also an esmolol infusion to keep his heart rate and catechols down. He did well on about 2 mg per hour of midazolam and 50 mcg/kg/min of esmolol. After a few hours he started making sense and by morning he was pretty sheepish. Psych types evaluated him in the AM and he was transferred later that morning off all drips.
His tox screen came back PCP. Later his girlfriend said they had no idea what they were using...thought it was LSD. Curry tells me there is a big difference and I am sure he will elucidate on this.
So, in the end, I left him to the tender mercies of the shrinks...God knows he is probably in just as much trouble as when he started.
Thoughts to take home from this case:
David Carpenter:
A short story. While working as an EMT in a county hospital in a medium sized southern city we had the following happen to our quiet room. The police brought in a rather large gentleman who had taken an undetermined amount of PCP. Our ER physician decided to put him in the "quiet room" to cool off. We listened to him rhythmically slamming himself into the walls and sat back to wait for the noises to stop. Unknownst to us, one of the bean counters (the kind the immortal Dr. Crippen rails about) had designed the "quiet room" as an afterthought. They had taken a alcove with cinderblock walls and put a framed wall (2x4's and plasterbaord) across it. Needless to say, until this night the room had never been properly tested. In a seen that would have more properly been in Terminator, our guest came crashing through the wall. Worse, his hands were still handcuffed, but the chain connecting them was seperated in the middle. The local gendarmes broke two night sticks over his head, which just seemed to make him angry. He was finnaly coralled after our 5'2" triage nurse applied an aluminum baseball bat to the back of his head as he lapped the desk chasing the police. Finally total, the incredible hulk= 1 broken wrist, and a skull fracture. The police suffered a total of two broken arms and eleven broken ribs. At the trial the judge before sending said hulk to jail for more than 40 years said to the police, "why didn't you just shoot the SOB". The police replied they thought that might make him madder.
Pauline L. Wong:
There's a terrific blow dart system (Telinject) for animals that is simply powered by blowing on the end of a tube -- propells a plastic syringe dart that empties on impact, plunger simply driven by compressed air. Only needs 20g needle, so requires much less impulsion & is much less traumatic than dart gun (eg Capchur pistol).
Alan Meakes:
We, too have the main psych facility and "process" psych patients through medicine by default. The scenario described is not rare, but in my experience I have found extreme variability in many of the routine calming agents. One patient comes to mind who after 400mg of Diazepam iv, followed by 50mg iv Haldol was still bending the stainless steel railings to which he had been secured (the security were bloodied by this point). The "fire extinguisher" was Propofol 1.5mg/kg. For most of these patients we now control with an initial dose of propofol and immediately begin regular Nozinan 25mg im q4h till calmed without top-up agents. (We call Nozinan "the equalizer"). If an iv simply cannot be started, I give 2mg/kg Sux to gain control, followed by propofol for amnestic calming. Most of the time. however, I try to refer... ;-)
Steven Curry:
The question was how do you handle such an agitated patient. There are no scientific studies in humans that tell us the best answer. My opnions are entirely based on personal experience in handling lots of these guys, the known pharmacology of commonly used drugs of abuse, and reviews of case reports and case series. Thus, my opinions are just that. Feel free to ignore anything you wish.
First, if your goal is to have NO concern for whether the patient lives or dies or suffers severe morbitity, but is only how to keep him from interfearing with your time and resources, then comments (many obviously humorous) from reviewers on strapping him down until he agrees to cooperate, or giving an IM benzo and waiting 30 to 60 minutes until it works or he calms down on his own are fine. But you will be burned with this rather apathetic treatment plan sooner or later with sudden and unexpected demise and death.
Hallucinating, agitated, combative patients who are thought to be suffering from drug intoxication have usually ingested sympathomimetics (e.g., cocaine, methamphetamine, ephedrine, etc.), LSD and derivatives (much less common as they are usually happy, not fighting), PCP and derivatives, or anticholinergic drugs (e.g., Jimson weed, cogentin). If they are going to die in the emergency department, it will usually be from being unable to breath from restraints, hyperthermia, rhabdomyolysis,and hyperkalemia. All of these are aggravated by leather restraints, bed sheets, and other methods of restraining that, admitedly, are necessary until you get control of the situation. Patients do not die from sinus tachycardia and usually not from hypertension, although such is commonly seen.
So, your goals are to QUICKLY get control of the situation so you can
I agree with everyone that the patient must be initially restrained until you can get a line. I am afraid to use succinylcholine in these patients because many or most have rhabdomyolysis and I am afraid of hyperkalemia. However, the suggestion of using 2 mg/kg of succinylcholine IM just to weaken the patient might be fine - I have no idea and have seen no reports of hyperkalemia with this dose. For sympathomimetics and PCP, I frequently find that many patients do not respond to benzos. If I can wait a few minutes and am not too worried about hyperthermia or rhabdo, I find that 5-20 mg haldol usually works nicely - but not always. I treat seizures with lorazepam and phenobarbital. I'm sure that midazolam or other benzos may work just as well.
If I am concerned that significant hyperthermia, hypoxia, or rhabdomyolysis are present or will be developing shortly given extreme agitation and combativeness, I do not hesitate one second to paralyze the patient with a nondepolarizing blocking agent so that I can assess temperature, begin cooling, and start pouring in the fluids. If someone would rather just push an ultrashort-acting barbiturate or propofol rather than paralyze the patient, I have no great problem with that as long as it does not delay STOPPING motor activity and as long as the patient or kept deep with propofol after intubation to prevent excessive muscle activity. Axillary temperatures are a joke, and anyone who uses them to assess a patient for hyperthermia is asking for trouble. I have seen an axiallary temperature of 97 when the rectal temperature was 108. As noted earlier, patients do not die from sinus tachycardia. Therefore, giving a beta blocker to decrease the heart rate mainly treats the physician, not the patient. Furthermore, I like to see the heart rate because is gives me an objective sign as to whether the sympathomimetic oranticholinergic drug is still producing toxicity.
Giving beta blockers to patients with increased adrenergic activity (e.g., amphetamines, cocaine, PCP, pheochromocytoma, clonidine withdrawal) can produce unopposed alpha stimulation and can raise blood pressure to dangerous and fatal levels. IV labetaolol is NOT a reasonable substitute. While oral lebatolol has a beta/alpha blocking ratio of about 3:1, IV lebetalol's ratio os about 6:1, making it about identical to IV propranolol. In fact, labetolol has produced hypertensive crises in patients with pheochromocytomas, and has been found to be inferior to the combination of propranolol and regitine in treating hypertension in pigs poisoned with cocaine. I agree that I would not use ketamine. Both ketamine and PCP bind to the identical site in the calcium channel of the NMDA glutamate receptor. Ketamine, also a drug of abuse, would be expected to worsen PCP toxicity. The ability of ketamine to cause catecholamine release (explaining its occasional use in asthma) would not help the situation.
Patients poisoned with sympathomimetics or PCP can suffer from a wide range of acid/base disorders, most commonly respiratory alkalosis and metabolic acidosis (respiratory acidosis is seen when they are restrained). Acidosis may worsen cocaine cardiotoxicity, as a fall in pH enhances sodium channel binding by cocaine and worsens myocardial toxicity - evidenced by further widening of the QRS (can be mistaken for hyperkalemia), hypotension, ventricular arrhythmias, and bradyrrhythmias.
Marjorie Lazoff:
Since I'd not leave any such patient alone in even an observation room until after a directed medical assessment is completed, the question is how can I most safely and expeditiously complete my initial accessment -- environmental control/divine inspiration, chemical restraints, or sedation-paralysis-intubation. Such patients can have a sudden decompensation in the ED so I prioritize obtaining IV access higher than I've heard others here -- in fact, the more agitated and combative the patient, the higher a priority for me.
The trick in starting an IV line in a combative patient is to go for the femoral line -- safer and faster than trying to immobilize an arm and hunt for peripheral access. (Once in restraints it only takes 1-2 people to control the patient from the waist up, and 1-2 people to immobilize the legs). Like several here we also usually 'dart throw' IM benzos but in the severly agitated/combative patient I think we're just treating ourselves. If they are going to die in the emergency department, it will usually be from being unable to breath from restraints, hyperthermia, rhabdomyolysis, and hyperkalemia.
Excellent point(s). I've heard the stats show the most common cause of death in these patients is medical/nursing neglect -- carted off to the corner of the ED, the now quiescent patient dies without having had periodic medical and restrains reassessment. Those you mentioned would be the missed causes. How does one die of rhabdo in the ED? Patients do not die from sinus tachycardia and usually not from hypertension, although such is commonly seen. But I try to normalize extreme vital signs, since the cardiovascular andneurologic stress can precipitate MIs and strokes.
Begin hydration and keep those kidneys open in an attempt to lessen or prevent hyperkalemia and myoglobinuric renal failure. Rhabdo-induced hyperkalemia is almost only seen in those who are oliguric or anuric. Again, excellent point. My concern is with overhydrating the unknown acutely head-injured or cardiomyopathic patient. But between sweating and osmotic diuresis, these patients are usually mildly hypovolemic anyway.
I agree with everyone that the patient must be initially restrained until you can get a line. I am afraid to use succinylcholine in these patients because many or most have rhabdomyolysis and I am afraid of hyperkalemia. However, the suggestion of using 2 mg/kg of succinylcholine IM just to weaken the patient might be fine - I have no idea and have seen no reports of hyperkalemia with this dose. I understand the logic, but I'd be concerned low dose paralytics would impair the muscles of respiration.
For sympathomimetics and PCP, I frequently find that many patients do not respond to benzos. If I can wait a few minutes and am not too worried about hyperthermia or rhabdo, I find that 5-20 mg haldol usually works nicely - but not always. I treat seizures with lorazepam and phenobarbital. I'm sure that midazolam or other benzos may work just as well.
Are you familiar with Robert Hoffman's/Lewis Goldfrank's work on cocaine toxicity? I've heard them both lecture about the increased mortality with haldol (and b-blockers) and the DECREASED mortality with benzodiazepams in this patient population, but in a quick medline search I couldn't find the documentation. I know many use IV haldol liberally in ICU patients but in the ED I'm concerned crossreactivity with unknown substances can induce cardiac arrhythmia. As noted earlier, patients do not die from sinus tachycardia. Therefore, giving a beta blocker to decrease the heart rate mainly treats the physician, not the patient. Furthermore, I like to see the heart rate because is gives me an objective sign as to whether the sympathomimetic or anticholinergic drug is still producing toxicity.
So many things affect heart rate, I never thought of using it as an indicator for drug toxicity except in the most benign clinical scenarios. Toxicology is neat because drugs/toxins cause patterned changes in many different organ systems, but all that's superimposed on a patient's underlying medical condition and other drug interactions -- a real diagnostic challange.
Giving beta blockers to patients with increased adrenergic activity (e.g., amphetamines, cocaine, PCP, pheochromocytoma, clonidine withdrawal) can produce unopposed alpha stimulation and can raise blood pressure to dangerous and fatal levels. IV labetaolol is NOT a reasonable substitute.
Daniel Joyce:
Unfortunately, the esmolol does not 'keep the catechols down' but, instead, just blocks the beta effects. I don't believe I would have used this agent. This patient was tachycardic from agitation +/- dehydration, (there was no description suggestive of an anticholinergic toxidrome) and would have given drugs/fluids to address this issue, as you did. There is potential 'theoretical' concern that if there was coingestion of cocaine, there would have been unapposed alpha stimulation and worsening of his condition. I don't believe you needed more than the benzos (you spent a few bucks on this guy), fluids and a little time. If something atypical develops, then one can get a little more extravagant. I agree that this type of patient is not a quick dump to psych and deserves intensive monitering, unfortunately, in our perpetual no ICU bed city hospital, these 12-24 hours are usually spent in the ED.
Pauline L. Wong:
For sympathomimetics and PCP, I frequently find that many patients do not respond to benzos. If I can wait a few minutes and am not too worried about hyperthermia or rhabdo, I find that 5-20 mg haldol usually works nicely - but not always. [rest deleted] Dogs anesthetized w/ IV ketamine/diazepam commonly appear to be dysphoric in the recovery room. They often overreact to hands reaching out to touch them & sometimes appear to see things which are not visible to us. Involuntary muscle activity in these unrestrained animals is not unusual & is associated w/ hyperthermia. Occasionally a dog will vocalize during recovery from ketamine.
IV administration of diazepam doesn't do much to ameliorate these signs - just seems to slow the dogs down a bit & make them ataxic. Actually, small doses of acepromazine (phenothiazine derivative) titrated IV seems more efficacious in reducing muscle activity & abnormal behavior. We treat hyperthermia symptomatically w/ ice packs & a fan; as soon as abn muscle activity ceases, body temp comes down. I've seen dogs w/ rectal temp up to 105F during ketamine recovery. We always treat them, so I don't know how hot untreated dogs would get b/f the transient period of hyperactivity ended. Hyperthermia doesn't seem to be a problem in cats recovering from ketamine anesthesia, but seizures sometimes occur & can be terminated by IV acepromazine.
Marjorie Lazoff:
How does one die of rhabdo in the ED? Mainly from hyperkalemia?
Are you familiar with Robert Hoffman's/Lewis Goldfrank's work on cocaine toxicity? I've heard them both lecture about the increased mortality with haldol (and b-blockers) and the DECREASED mortality with benzodiazepams in this patient population, but in a quick medline search I couldn't find the documentation. I know many use IV haldol liberally in ICU patients but in the ED I'm concerned crossreactivity with unknown substances can induce cardiac arrhythmia.
There is no documentation to be found demonstrating that humans have increased mortality mortality with haloperidol when the are poisoned with cocaine. I agree with Hoffman and Goldfrank that benzos work in many cocaine patients, and find them less effective for amphetamines. Bob and Lewis are in New York and see much more cocaine, while here in Phoenix, we see more methampetamine. Although I find that benzos fail, I nevertheless always try high dose benzos as my first choice (unless I decide to paralyze them right off the bat). It ends up, then, that I use haldol only when benzos fail. The contraindication of beta blockers in cocaine extends beyond inducing hypertension. Human, yes human, studies demonstrate that a beta blocker will induce coronary artery vasospasm in the face of cocaine. Furthermore, with regard to propranolol, it is also a sodium channel blocker like cocaine.
I'm not aware of any studies suggesting that haldol would produce cardiac arrhythmias in such patients based on primary effects or drug effects unless much larger doses that 5 to 20 mg were used, and find that these lower doses are usually effective.
David Crippen:
This person was in deep metabolic trouble and he needed to get fixed very fast. There is no role for restraints except to protect him and you while VERY timely action tales place. Metabolic and hemodynamic disaster is looming, you do not have time for IM drugs or lorazepam. I needed to get control of this situation VERY quickly.
I had no real problem harpooning him with a non-depolarizing neuromuscular blocker such as vecuronium (not Sux for reasons previously discussed) but I was willing to give him a very brief shot at midazolam, which is very potent and rapid acting, first. If he had not began a rapid improving trend (within a few minutes) I would have cheerfully, and with no malice aforethought, paralyzed him to stop the hemodynamic and metabolic effect of hyperactive musculoskeletal activity.
IMHO I have found haloperidol very iffy for acute, life threatening agitation. It sometimes works, sometimes does absolutely nothing in very high doses. I didn't want to wait around and see what I was going to get. Midazolam is normally potent and predictable.
Interestingly, there is some evidence that diazepam is a better drug than both of Steve's recommendations for the INITIAL treatment of convulsions. It gets into the brain fast, then it can be quickly replaced by midazolam or lorazepam. I have never been impressed with phenobarb except as a long term drug for ambulatory patients.
I get to quibble with Steve's otherwise impeccable advice when it comes ot beta blockade. The human body reacts to acute physiological stresses by a well recognized catecholamine surge and tachycardia to increase cardiac output in preparation for "fight or flight". Though compensatory tachycardia may increase cardiac output, the amount of excessive myocardial oxygen consumption and decreased coronary artery perfusion may result in a net hemodynamic detriment. It has been consistently shown than cardiac metabolic efficiency (measured as a ratio of cardiac work to myocardial oxygen consumption) is decreased with tachycardia. Since tachycardia disproportionally restricts diastolic filling time, stroke volume and coronary artery perfusion may be severely compromised, resulting in paradoxical hemodynamic disaster.
There is a difference between "compensatory" tachycardia in which the heart must make up in speed what it has lost in contractility or preload, and "decompensated" tachycardia, in which the heart gets horsewhipped into beating itself to death for nonsensical reasons. This guy has a heart rate running around 150-160, but a relatively normal blood pressure never higher than 160 systolic. His tachycardic response was clearly "decompensatory" and deleterious. By physical exam he had a visible heave and a harsh murmur that disappeared the next day. I did not think this was cocaine...for which I think Steve's comments on beta blockade are more appropriate. I didn't know what it was, but I knew it was causing a big problem. Has it been LSD, as originally billed, I don't think a short acting, titratable beta blocker would have been contraindicated.
Now, I have heard all about this "unopposed alpha" argument but I have never seen it happen in real life that I can remember. Also, being somewhat of a Philistine, I tend to believe none of what I hear and only half of what I see. This punk had a big time decompenastory cardiac situation and I resolved to fix it. After the esmolol his heart rate calmed down to 100-110 and the blood pressure did not change significantly. My job it to titrate hemodynamics and metabolism to the patient's best advantage and that's what I did. The whole point is bedside monitoring and titrated care. If there had ben an untoward reaction, I would have picked it up quickly and fixed it.
Decreasing stress related tachycardia by the use of super-selective, ultra-short acting beta adrenergic blocking agents MAY result in an aggregate benefit to hemodynamics in heart failure by improving cardiac function proportionally more than the small amount of negative inotropyinherent to the drug. I personally like this idea and I use it frequently. I have never seen "unopposed alpha effect", and even if it appears, the whole point of esmolol is it's short action and high titratablility. It goes away quickly if an untoward effect is seen.
REFS: