medic001918 Posted November 15, 2006 Share Posted November 15, 2006 Alrighty, the general concensus seems to be to try a fluid bolus prior to addressing the rate. So we administer 250cc over 5-10 min or so. Pt's BP is 78 systolic. Now what? From no BP to a BP of 78 and there was another post that stated the patients mentation had improved as well. Well the thinking of a beta blocker overdose isn't bad, and the treatment for such is correct by using glucagon I'm not sure that it would be the best choice for this sceanrio. Think of simple interventions working your way towards more advanced. You have something that's working in this case. I would stick with it as the patient is climbing his way out of the immediate danger zone. Shane NREMT-P Link to comment Share on other sites More sharing options...
Lithium Posted November 15, 2006 Share Posted November 15, 2006 Just so everyone is on the same page ... So you've been with this pt for about twenty minutes and 400cc's of NS have infused. The pts BP is 136/54, HR is still just below 50 BPM, and the Pt is responding normally and looks quite a bit better. What do you think is going on with this pt? And why or why not did you decide to treat aggressively? Now let's see you justify the glucagon :wink: Link to comment Share on other sites More sharing options...
Thunderchild145 Posted November 15, 2006 Share Posted November 15, 2006 Nope. That's it for me. Link to comment Share on other sites More sharing options...
ksemt Posted November 17, 2006 Share Posted November 17, 2006 Is this thread over? As a paramedic student I was finding it helpful. I have been learning a lot of the "what" to dos but I feel real weak on the "whys". Can someone explain the hemodynamic physiology and what is/was going on with pt. "Why" did the fluid bolus help? A "pipe" problem from the meds? I've been told to be very leary of giving fluids to the elderly. It seemed to be a small amount of fluid to make that much difference? Just trying to learn as I go... Link to comment Share on other sites More sharing options...
mountainman Posted November 17, 2006 Share Posted November 17, 2006 Well call me a beginner but I believe from the info given my P partners would not push anything besides NS. At this point we would possibly consider atropine if the HR dropped further, but then again Im confused on the Pts status....... Vitals seem fairly stable.... Link to comment Share on other sites More sharing options...
Thunderchild145 Posted November 17, 2006 Share Posted November 17, 2006 The fluid bolus increases preload. When the ventricles fill, the increase volume forces them to expland more and therefore like a rubber band, contract more forcefully. This increases the blood pressure only because of the basic equations of perfusion. Stroke Volume x Heart Rate = Cardiac Output, Cardiac Output x Periphreal Vascular Resistance = Blood Pressure. Basically in order to increase blood pressure we have to increse heart rate, stroke volume, or periphreal vascular resistance. Anyway yeah, so the fluid bolus would increase preload which would increase stroke volume, which increases cardiac output, which increase blood pressure. As far as the "pipe" problem they're referring to another part of those equations: Periphreal vascular resistance. The meds this guy took are blood pressure meds (Altace [Ramipril] and Toprol-XL [Metoprolol]), and most of them decrease one of the three componants of blood pressure. Some decrease 2 or more. Ramipril is an ACE inhibitor which would explain the vascular problem and Metoprolol is a beta blocker which is keeping his heart rate low. Also Levodopa is a dopamine precurser prescribed for Parkinson's. This guy is probably vasodilated (when combined with the slow heart rate and the physiological inability to increase said heart rate due to beta blockers, resulted in a really, really low blood pressure.) You've probably been told to be wary about giving fluid to elderly people because it can cause pulmonary edema. Just keep listening to lung sounds and make sure you don't overload them. Link to comment Share on other sites More sharing options...
ksemt Posted November 18, 2006 Share Posted November 18, 2006 Thanks Thunder, I know this sounds really basic to most of you but keep in mind I'm new to this and that's why I'm asking... I get the whole preload thing, in general anyway. But wouldn't some type of sympathetic compensatory device kick in to increase the heart rate (like the renin-angiotensin system) whether it affects the B/P or not? Doesn't hypovolemic shock usually present with an increased heart rate, at least early on? Wouldn't the respiratory rate be increased somewhat, instead of reduced (rate of 10)? Are we saying the meds are causing the entire problem by offsetting every compensatory device? I guess we've proven that by finding that the fluids worked? The pt isn't bleeding out, it's not 110 degrees out and the pt hasn't been playing golf all day, and I'm at least assuming the pt is not showing visable signs of dehydration (to cause the fluid loss). The pt is in hypovolemic shock due to the meds causing systemic vasodilation and the meds are inhibiting CNS's sympathetic responses (i.e. incereased heart rate and respiratory rate)? Hmmm, Ok, so assuming this isn't a frequent flier, not a drunk that mixes alcohol with the meds daily (he's been having a glass of wine every night with no problems), what do you guys think caused the problem TODAY? He's "probably" been on the cardiac meds for 5 years since the MIx2. The Parkinsons meds could be new I guess and causing a CNS problem that reduces HR, B/P and respiratory rate? Unless there's been a large shake up in meds lately any idea why the meds caused this today? Link to comment Share on other sites More sharing options...
Thunderchild145 Posted November 18, 2006 Share Posted November 18, 2006 The Renin-Angiotensin system is being disabled by the ACE inhibitors. Otherwise, yeah. Link to comment Share on other sites More sharing options...
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