[fatoma]

hey everybody,
I am wondering how alkalosis and acidosis interfere with capturing and result in faliure to capture...is this some thing related to potassium level???
and why don't we use atropine immediatly in case of bradycarrdia?

thank you

[dianah]

Are you referring to a patient who has a permanent pacemaker?

(welcome to the forum, by the way [BTW] )

If so, alkalosis and acidosis will increase the pacing threshold.

Decreased extracellular potassium level changes the RMP (resting membrane potential), making capture more difficult.
Acute increase in extracellular potassium level (as with myocardial ischemia or rapid K+ replacement) also changes the RMP, resulting in easier capture.
(I had to google to review. )

Also: what is the background of your last question re: giving atropine for bradycardia?

[fatoma]

Thank you very much Dianah,


I am referring to a patient with temporary pacemaker at the bed side...that's why I asked about the atropine b/c it increases the heart rate ...why is it not the first intervention?
if the pacing failed what is the next step...is it the atropine?
I am still a student and I want to construct the whole picture to be clear for me

thank you again dear

[dianah]

You're right, always have atropine at the bedside, say, for a patient having an MI (heart attack), especially if it's involving the inferior leads' (RCA = right coronary artery) territory.
These patients are certainly at high risk for developing dysrhythmias.
Having the temp. pacer at the bedside is ALSO smart, as some pts (see above) need it ASAP.
Placing a temp pacer is safer for the pt than standing at the bedside waiting to give repeated doses of atropine (silly scenario, yes, but I'm just making a point).

[preciosa]

And also there is a limit in giving atropine so the best is still to have a temporary pacer at bedside.