ATCEMSEA Forums: My Fair Brady

You are not logged in. [Log In] ATCEMSEA.org » Forums » Clinical Discussion » Interesting Calls » My Fair Brady

Page 1 of 1

Topic Options

Rate This Topic

#7962 - 11/23/05 02:48 PM

My Fair Brady

Tony Pope
Member
ATCEMSEA

Registered: 06/22/03
Posts: 56

Offline

To take your mind off the growing madness.

You are dispatched to the residence of a 50yo black male for a priority 2 diabetic. As you arrive on scene with your FD in tow you see the rather obese patient lying supine on the couch. Introducing yourself and reaching for his wrist you notice that he looks rather pale

, is extremely diaphoretic and although he answers all questions he is a bit altered. No recent illness or injury, no CP, no SOB no signs of CVA. Your pulse check reveals a weak slow pulse of 38. Placing the patient on O2 NRB, attaching the EKG with pacer pads and noting a sinus bradycardia, elevating his legs and noting profound hypotension, your partner reports his meds to include Verapamil and Glucophage with a Hx of HTN, DM2, Liver Failure and GERD. Pt has been compliant with all meds, Dstick is WNL. You start pacing your patient while attempting IV access. Shortly after your pacing begins and you have set your mA at 80 with great capture, strong pulses at a rate of 80, the patient becomes more alert, diaphoresis subsides, normotensive and besides the discomfort caused by the pacer is compensating well. 12lead non-diagnostic due to pacer induced T wave changes, you assess recent Hx further without significant findings and note no abnormal physical findings. Enroute to the ER the patient continues to improve and all care is supportive. You arrive at the ED and all care/report is transferred to ED staff without incident.

"Hint" Not an MI or cardiac in origion.

Your thoughts on why this patient is bradycardic?

Differential Diagnosis?

Treatment plan?

Top

#7963 - 11/23/05 02:57 PM

Re: My Fair Brady [Re: Tony Pope]

Sean Norton
Member
ATCEMSEA

Registered: 03/05/03
Posts: 74
Loc: SanMarcos

Offline

verapamil O.D.

treat with calcium, Calcium channel blocker O.D. will produce the bradycardia, hypotention, confusion, and overall shock symptoms.

Top

#7964 - 11/23/05 02:59 PM

Re: My Fair Brady [Re: Sean Norton]

Tony Pope
Member
ATCEMSEA

Registered: 06/22/03
Posts: 56

Offline

good thoughts but elaborate......he has been compliant with all meds and dosing schedules, has been on Verapamil of 4 yrs....

Top

#7965 - 11/23/05 03:08 PM

Re: My Fair Brady [Re: Tony Pope]

Cory Crouch
Member
ATCEMSEA

Registered: 11/19/03
Posts: 144
Loc: Right Here Right Now

Offline

Could liver failure have something to do with it??

Top

#7966 - 11/23/05 03:12 PM

Re: My Fair Brady [Re: Tony Pope]

Sean Norton
Member
ATCEMSEA

Registered: 03/05/03
Posts: 74
Loc: SanMarcos

Offline

You mentioned the patient has a history of liver disease since verapamil is processed by the liver the serum levels will increase with additional failure of liver function a quick search found this.

http://www.rxlist.com/cgi/generic/verapsr_wcp.htm

Use in Patients with Impaired Hepatic Function: Since verapamil is highly metabolized by the liver, it should be administered cautiously to patients with impaired hepatic function. Severe liver dysfunction prolongs the elimination half-life of verapamil to about 14 to 16 hours; hence, approximately 30% of the dose given to patients with normal liver function should be administered to these patients. Careful monitoring for abnormal prolongation of the PR interval or other signs of excessive pharmacologic effects (see OVERDOSAGE) should be carried out.

Top