60 ish yo with weakness and diaphoresis

[kemple]

60 yo male called EMS 2/2 weakness and dizziness. EMS found him to have a HR in the 30s and gave 2 x 0.5mg atropine getting the HR to the 50s.
Pt EKGs are




below about 60 minutes between EKG 1 and 2


another 30 from 2 to 3,






Dopamine started after EKG 1 with BP in the 60s-70s, took 15 mcg/kg to get his HR and bp up. Hx of CAD, DM, CKD Stage 1, HTN, and other non important stuff. In ED no CP, no SOB, only c/o feeling weak. 


What do you think? 

[Bjs04f]

Comes in with a junctional escape rhythm and bradycardia. Gets dopamins it sounds like which sped up you junctional rhythm, i dont see a p anywhere so SA node is not working. Two questions 1-whats his K+, 2 what eds does he take, three whats renal function

[kemple]

GFR was 35, K+ hemolyzed needs redraw, meds weren't significant

[Bjs04f]

K is gonna be high, give him some calcium gluconate, insulina dn D50, and send me the EKG after that

[pbruss]

would like to know mag level. with the 3 ekgs would be worried about early infarct as the peaked t waves eventually got to a more focal appearance. other things are hypothermia as well as accidental betablocker, calcium channel blocker or oral hypoglycemic agents.

[kemple]

So final K was 7.9, Mg was normal. The last EKG was after 2 grams Ca, D50, Insulin, and Albuterol. Went to ICU with CVVHD. Still had a GFR of 35...interesting case.

[tyson]

nice ekg's.

why do you think patient's t-waves were not peaked on first ecg? typically peaked t waves are first sign, then lengthening of pr interval with no p waves. seems this guy is backwards in his progression! this case is a good example of why we need i-stat in our department. shouldn't have to wait 1.5 hrs to find out k+ is 7.9.

dopamine i think is a good selection in this guy.

any thought on transcutaneous pacing initially vs. pressors?

is there an advantage or major disadvantage to one or the other?

[slevittMD]

Did you give dopamine because you thought it was the best pressor or because that's what was easiest to give in the ED? Weingart seems to think that dopamine is a junk dirty pressor that has no place in the ED, although I'm not exactly sure where he gets such a harsh view from. I probably would have gone with levophed.

Couldn't agree more that every hospital should have an istat!! I wrote up an incident report recently where it took about 2 hours to find out that a dialysis patient had a K of over 7. Ideally should have istat troponin as well, but having it available for K+ at a minimum should be standard of care for a modern ED.

Transcutaneous pacing sucks for the patient, particularly one who has no complaints except feeling weak. His HR wasn't so atrocious that I'd want to do that to him right away. I like the idea of medical therapy first for this guy.

[tyson]

the only reason why i think dopamine is a good pressor in this guy because he's bradycardic and hypotensive. dopamine has a lot of B1 agonism (and alpha) at the rate he was giving. really what the heart needs. increases HR and CO and BP.


i would not argue ever w/ levaphed, however, it seems everywhere this has to be ordered from pharmacy and i don't see a major issue with running dopamine on most patients, providing that the pressor i really want, is coming up shortly.

if this was a heart block of some sort rather than a K+ issue, would you transcutaneously pace? if not, what situations have you paced in?

[kemple]

I had the pads on him once 10mcg/kg/min wasn't doing the trick, expecting to have to give some Edison's medicine. Luckily for him that never happened as my max of 15 did the trick. I know it has gotten a bad rap but I have had nothing but success with dopamine for these 3rd degree or similar block type situations.

[slevittMD]

It's not that dopamine doesn't work, it's that it has a high morbidity compared to other pressors. There is a paper out there about a head-to-head study of levophed versus dopamine which really turned the tide against dopamine. I'm driving right now or I'd look it up, but you can definitely find it on emcrit

[kemple]

NO change in mortality, but increased arrythmias.

N Engl J Med. 2010 Mar 4;362(9):779-89. doi: 10.1056/NEJMoa0907118.
Comparison of dopamine and norepinephrine in the treatment of shock.
De Backer D1, Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C, Brasseur A, Defrance P, Gottignies P, Vincent JL; SOAP II Investigators.
Collaborators (12)
Author information
Abstract
BACKGROUND:
Both dopamine and norepinephrine are recommended as first-line vasopressor agents in the treatment of shock. There is a continuing controversy about whether one agent is superior to the other.
METHODS:
In this multicenter, randomized trial, we assigned patients with shock to receive either dopamine or norepinephrine as first-line vasopressor therapy to restore and maintain blood pressure. When blood pressure could not be maintained with a dose of 20 microg per kilogram of body weight per minute for dopamine or a dose of 0.19 microg per kilogram per minute for norepinephrine, open-label norepinephrine, epinephrine, or vasopressin could be added. The primary outcome was the rate of death at 28 days after randomization; secondary end points included the number of days without need for organ support and the occurrence of adverse events.
RESULTS:
The trial included 1679 patients, of whom 858 were assigned to dopamine and 821 to norepinephrine. The baseline characteristics of the groups were similar. There was no significant between-group difference in the rate of death at 28 days (52.5% in the dopamine group and 48.5% in the norepinephrine group; odds ratio with dopamine, 1.17; 95% confidence interval, 0.97 to 1.42; P=0.10). However, there were more arrhythmic events among the patients treated with dopamine than among those treated with norepinephrine (207 events [24.1%] vs. 102 events [12.4%], P<0.001). A subgroup analysis showed that dopamine, as compared with norepinephrine, was associated with an increased rate of death at 28 days among the 280 patients with cardiogenic shock but not among the 1044 patients with septic shock or the 263 with hypovolemic shock (P=0.03 for cardiogenic shock, P=0.19 for septic shock, and P=0.84 for hypovolemic shock, in Kaplan-Meier analyses).
CONCLUSIONS:
Although there was no significant difference in the rate of death between patients with shock who were treated with dopamine as the first-line vasopressor agent and those who were treated with norepinephrine, the use of dopamine was associated with a greater number of adverse events. (ClinicalTrials.gov number, NCT00314704.)