Illegal Drugs - What affect on the EKG, the 12 lead?

[spenac]

On a recent call I had a patient with obvious st elevation and depression in continous and reciprical leads. At the hospital the doctor said he thought patient was on illegal drugs and that he was not having an MI. Patient was under 40 with severe chest pain. Ran the full MONA by time at hospital. My question is what should I look for different on my EKG or 12 lead that might indicate drug use rather than MI. Doctor could not explain to me why and the drug screen had not returned prior to leaving hospital. Dr mention crack and a couple of other drugs that he suspected. Pupils were equal and reactive normal pupil size to.

Thanks for helping in advance. Please don't just say stupid Doctor if that is your only thought. I want facts or real possibilitys. Thanks.

[Mateo_1387]

Spenac, I do not know of any specific ECG findings that say 'drug abuse.' There are however street drugs that do affect the heart. Drugs that are stimulants can affect the heart rate, contractility force, and increase oxygen demand. Depending on the health level of the patient, these drugs may affect how the heart reacts to the drugs. Cocaine, for example, can cause an increase in HR, increased oxygen demand, and an increased contractility force, and cause arterial spasm. A patient, who OD's on say cocaine, may show symptoms of heart problems. The effect of cocaine on the heart can cause the same effect as say a thrombus in the heart, which is ischemia. A history may clue you in to suspect something such as a drug induced AMI.

There has been a problem lately in NC with some cocaine being cut with a veterinary grade drug called Clenbuterol. Its effects are similar to albuterol and ephedrine. These patients would present with a 'high' unlike their others, with tachycardia, and anxiety. The albuterol effects would push potassium into the cells, causing the patient to become hypokalemic. Standardized treatment with Sodium Bicarbonate is not advised with these patients. More information can be found at http://www.jems.com/news_and_articles/tips...l_outbreak.html

Any more specifics on the XII leads you ran? Did you have any changes on the XII lead and patient condition with your treatments?

[spenac]

Patients pulse was in the 160-180 range. Normal QRS. Had ST elevation with Reciprical ST depression.

So even if drug use, which patient denied, I should still assume MI based also on S/S's? I just know I have not found anything that says with cocaine expect to see these EKG changes.

[scott33]

I was always led to believe that Cocaine use was one of the causes of Prinzmetal's Angina.

http://en.wikipedia.org/wiki/Prinzmetal's_angina

Still right to treat as MI

Edit: More here...

http://content.nejm.org/cgi/content/full/349/1/e1

[fiznat]

Maybe the doc meant that the ischemia/injury was demand related and not the typical arteriosclerosis/clotting that we usually see? Not that it wasn't an MI, but just that it wasn't the normal cath-able kind...?

[Arizonaffcep]

Either way, can be solved easily with a good magazine and a laxative...

[Camulos]

Various backyard pharmaceuticals can have numerous effects on the ECG. Really depends on the actual substance taken. Sometimes it is not the active that causes the problem but rather the other substances it has been “cut” with. Perhaps the most prevalent example I have seen of this is with GHB overdoses that presented with peaked T waves on the ECG. It was not the GHB that caused this change however it was due to the potassium that the GHB had been mixed with to derive the finished product.

In this particular case you presented it sounds classical for a possible case of cocaine induced MI - if of course an illegal drug was being considered as the cause. History is a big determinant here and I note your pt denied illegal drugs. Guess the drug screen is the only way to tell if they’re lying or not. Happy to elaborate further on cocaine induced MI if necessary however I am unfortunately short on time. I’m sure Mr Google can provide some answers here for any interested parties though. Hope this helps.

Stay safe,

Curse

[jwraider]

Patients pulse was in the 160-180 range.

-That's pretty quick and might lend to the cocaine differential

Normal QRS. Had ST elevation with Reciprical ST depression.

- Just wondering which leads?

[MSDeltaFlt]

Patients pulse was in the 160-180 range. Normal QRS. Had ST elevation with Reciprical ST depression.

So even if drug use, which patient denied, I should still assume MI based also on S/S's? I just know I have not found anything that says with cocaine expect to see these EKG changes.

Following MONA is indicated, as you well know, but street drug use can cause SVT. Granted they always deny, but the HR is high enough technically. What was the BP? What were the other S/S's?

Now we weren't there. Did your pt, according to your assessment, warrant Adenosine? Could it have been an option?

[ccmedoc]

Cocaine induced chest pain presents a potential problem and can definitely lead to complications. Studies have shown that most individuals will present within three hours of use of cocaine (although S/S have been attributed to cocaine up to 4 days after use), and should be monitored for 12 hrs following cardiac presentations; i.e. chest pain, dyspnea, etc. I have read one study that cited mid 40% of patients presenting with ST elevation of greater than 1mm in two contiguous leads, but ruled out of MI by serial enzyme studies; whereas it is thought that only 6% of cocaine induced chest pain result from AMI . Who's going to make the call of 'just another cocaine ST elevation chest pain' and not treat accordingly? Not me...

Generally speaking, the cocaine chest pain can certainly lead to mortality and morbidity, and should be taken seriously and treated accordingly. In theory this is limited to nitro, aspirin, and benzodiazepines. There is a theoretical problem with aggressive beta blockade and increasing hypertension due to unopposed alpha blockade.

In concluding the 12 lead answer, some ST elevation may be seen, S/S of LVH, RVH, maybe early repolarization changes, and of course the tachycardia you see. It is possible to see Tachycardia dependant BBB also.

At any rate, do not dismiss them as just another cocaine chest pain. Especially if they have had a cocaine induced MI before, the chances are greatly increased of resultant heart failure and rapid decompensation.

The tachycardia should be managed with benzos and CCB. The adenosine is not going to be warranted in this situation.