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Post by kemple on Jul 30, 2014 16:51:58 GMT -5
80 yo male not feeling right all day, weak and dizzy. Wife states he wasn't eating well the last 2 days and thought that might be the cause, made him eat dinner which he did. After he went to bed and curled up with his clothes on which was unsual. Shortly after he goes to the bathroom, comes out and collapses. Pt is combative and altered mental in the ED, RSI successful. What do you see here? Anything concerning? Would you want any other EKGs or testing, is this enough? EKGWhat treatments do you want to start first? a. Heparin, ASA, Nitro b. Cath Lab Stat c. Plavix, ASA, Integrilin d. CT Brain no contrast
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Post by DD on Jul 30, 2014 21:11:57 GMT -5
good ecg
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Post by jeanpaul1 on Jul 31, 2014 4:38:57 GMT -5
Very good ECG indeed. Come on first years!
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Post by pbruss on Jul 31, 2014 6:30:01 GMT -5
Nice case and EKG. Now some first year impress me with an answer
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Post by mwiepking on Jul 31, 2014 17:21:13 GMT -5
ECG shows a regular rhythm with a tachycardia of ~120bpm. R waves are dominant in leads I and aVL; S waves dominant in leads II and aVF so I feel this is left axis deviation. V2 and V3 look striking due to the height of the QRS complex, suggestive of left ventricular hypertrophy. Given his age and the fact he had a collapse--possibly after straining and then standing at the toilet--followed by altered mental status, I would want to consider aortic stenosis leading to an ischemic event. V1, which looks very much like an M with associated T-wave inversion, and V6, which looks like a W, I feel that this is a right bundle branch block though I thought the QRS complex would be wider. This could also be related to significant aortic stenosis. ST depression is present in V2-4 so there may be an element of coronary ischemia as well.
Given his presentation, I would also want a finger-stick glucose. Given his reluctance to eat and drink, a basic metabolic panel. Since he was cold, weak, dizzy, and now collapsed, thyroid function tests (I'm dying to say those were J-waves on the ECG but that I like aortic stenosis-related issues more). Because the ECG looks disconcerting, I would get troponins. Because I think he could have had an cerebrovascular ischemic event, I would like to get INR, PT, aPTT.
I'm going to go with D and say CT brain non-contrast and I would also like to get a chest x-ray (calcified valve, maybe cardiomegaly) and ECHO. Then I would want to consider anti-platelet therapy.
I am very much open to constructive criticism.
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Post by pbruss on Jul 31, 2014 21:17:46 GMT -5
Mildly impressed. Let's see what kemple thinks of your interp.
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Post by kemple on Aug 1, 2014 13:16:37 GMT -5
1) Kudos for being the only one in your class to take a stab at it. 2) Completely agree when you don't have a true cause for AMS you need a CT before anticoagulation or antiplatelets as this could have been a CVA, especially if there was prolonged down time, unwitnessed, or any neuro deficits. 3) Let's suppose an astute ED resident decides to get a second EKG b/c they are rolling the patient....anything specific you would want? You were close with the V2-4 comment.
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Post by mwiepking on Aug 1, 2014 14:49:08 GMT -5
A posterior ECG if you're rolling him because of the V2-4 ST depression to evaluate for posterior infarct?
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Post by kemple on Aug 1, 2014 17:50:44 GMT -5
What do you see here? How do we do a posterior EKG?
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Post by mwiepking on Aug 3, 2014 11:41:02 GMT -5
A posterior ECG involves places left-sided infrascapular leads, V7-9. V7 is placed below the tip of the scapula along the posterior axillary line, V8 just below the tip of the scapula, and V9 at the left paraspinal position, again below the tip of the scapula in the same plane.
This ECG shows ST elevation in leads V5-6and Q-waves in V4-6. I see ST elevation in leads labeled II and III as well. Is it a posterior ECG--are V4-6 actually V7-9 in this case? If so, I can diagnose a posterior MI from this tracing.
If that's what's going on, I would like to contact cardiology and discuss getting this gentleman to the cathlab provided he did not have documented wishes for comfort measures only. I will give him oxygen via a vent (he's intubated?) to titrate to 94-98% saturation, morphine 2.5mg IV, not entirely sure how I'd give him aspirin or clopidogrel (NG tube?) but I think getting him to the cathlab is more important anyway. I'd hold off on nitrates as I think those are not recommended in aortic stenosis (which I'm still contending is a factor!) and he's already had RSI and given morphine. I'd start my ACS adjuncts as well including a beta-blocker and, provided there was no bleed on the CT Brain, heparin (4000U bolus followed by 1000U/hr, but I would confirm those doses) as directed by hospital guidelines. Inform the family of the situation and discuss the treatment plan.
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Post by kemple on Aug 4, 2014 7:49:32 GMT -5
Well done, yes in the case you don't have extra leads you take 4-6 and make them 7-9 which is what I did. He did get a head CT prior to heparin due to questionable hx of facial droop but ultimately ended up in the cath lab. Bonus points...what do you want to have before giving heparin to a STEMI and why? It's something simple we get on all chest pains.
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Post by mwiepking on Aug 4, 2014 11:14:13 GMT -5
Aside from prothrombin time? Make sure an accurate weight is recorded. Get a platelet level in case HIT develops.
Something else?
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Post by pbruss on Aug 4, 2014 15:16:56 GMT -5
there are few points i wanted to make. 1. i think it is GREAT that you guys are starting to post your own cases in board format. i guarantee you will retain more information and you will do better on the boards. writing the question helps you figure out how the boards are formatted. for example in this question if you had no idea you could still get it right if you notice that all of the questions are about ACS except for D. 2. some of the therapy listed were aspirin, O2, morphine, beta blockers, heparin, and nitro. A. you can give ASA rectally and ASA has been one of the only things that has been proven to reduce morbidity and mortality. B. O2 has NEVER been show to reduce morbidity and mortality and may even cause harm. I attached a Chocrane review on the subject for your review but put the relevant parts below: -"Three trials were found. None demonstrated that oxygen therapy in patients with acute myocardial infarction (AMI) does more good than harm on clinical outcomes. " C. there is some publications and some opinions of doc i have seen that morphine use in MI increases morbidity and mortality. i attached the CRUSADE study which this view point is based on. take a look at the study and tell me if you agree with that conclusion. D. Lovenox has been shown multiple time to be superior to heparin for all ACS patients (MI, unstable angina, NSTEMI). the dose of lovenox for any ACS is supposed to be 40mg IVP and 1mg/kg SQ. see attached E. I never use IV beta blockers with STEMIs. There is clear evidence thatt IV beta blockers for STEMIs causes more harm then good (see below). if the cardiologist wants it i will give it po, and the guidelines and core measures say "beta blocker with in the first 24hours" so we dont really need to give them in the ED. "The use of IV beta blockers has also changed based on the results of the COMMIT Trial, which showed a significant increase in complications in STEMI patients who received IV beta blockers within hours of STEMI onset.[3] Intravenous beta blocker administration within the first 24 hours of a myocardial infarction (MI) should occur only after the adequacy of myocardial function has been determined. Thus, EMS administration of IV beta blockers, with drugs such as metoprolol, should no longer be considered in any ACS patient." i tried to attach the COMMIT trial but its too large. you can get it free online. F. Nitro has been shown to be beneficial in only certain high risk groups. see below from The Merck Manual Acute Coronary Syndromes (ACS) and the official 2013 ACCF/AHA guidelines. The risk was based on the TIMI score. "In high-risk patients, nitroglycerin given in the first few hours reduces infarct size and short-term and possibly long-term mortality risk. Nitroglycerin is not routinely given to low-risk patients with uncomplicated MI." "Nitrates - Although nitroglycerin can ameliorate symptoms and signs of myocardial ischemia by reducing LV preload and increasing coronary blood flow, it generally does not attenuate the myocardial injury associated with epicardial coronary artery occlusion unless vasospasm plays a significant role. Intrave- nous nitroglycerin may be useful to treat patients with STEMI and hypertension or HF. Nitrates should not be given to patients with hypotension, marked bradycardia or tachycardia, RV infarction, or 5????phosphodiesterase inhibitor use within the previous 24 to 48 hours. There is no role for the routine use of oral nitrates in the convalescent phase of STEMI." G. A chest x-ray is not too good for ruling out a dissection. see below from Emerg Med J 2004;21:199-200 - Best evidence topic reports - The sensitivity of a normal chest radiograph in ruling out aortic dissection. "A short cut review was carried out to establish the sensitivity of a normal chest radiograph as a rule out test for aortic aneurysm. Altogether 557 papers were found using the reported search, of which four presented the best evidence to answer the clinical question. The author, date and country of publication, patient group studied, study type, relevant outcomes, results, and study weaknesses of these best papers are tabulated....The classic chest radiological findings of a wide mediastinum or abnormal aortic contour do not seem sufficiently sensitive to rule out aortic dissection in a patient with chest pain." i am interested to see what you guys think. Attachments:O2MI.pdf (722.65 KB)
CRUSADE.pdf (563.32 KB)
HepvLov.pdf (816.19 KB)
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Post by kemple on Aug 5, 2014 23:33:25 GMT -5
I was going with the CXR before heparin (or lovenox) bolus to go to cath lab. I agree it's not sensitive but I would imagine it's better than nothing and could possibly be useful no? Completely agree with morphine increasing M and M and ASA only true benefit to mortality. I HATE that at UTMC Nitro is a nursing protocol if the CP is associated with diaphoresis or arm pain. This could be deadly as we discussed with R sided MI's. Ultimately this patient was cathed with 95% occlusion to a branch of the RCA.
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