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Post by pbruss on Mar 31, 2015 13:59:05 GMT -5
its been a while, i have not had any interesting cases. Here is one for you to ponder: 71 yo MALE presentS to ED WITH SOB. Has been going on for 2 weeks. its worse in the AM and improves during the day. No CP, orthopnea, doe, or cough. He states it feels like he just can't catch his breath. He had a heart cath after a positive stress test 2 weeks ago. He says this current SOB did not start in till AFTER the heart cath. He says, "That Indian guy gave me a sh*t load of meds to take doc! I feel like a f*cking hippie who needs his dope!" (Metoprolol, Crestor. Brilinta, HCTZ, ASA, Pepcid). His physical exam is all normal. His labs, including trop, d dimer and CXR and all normal. Attached is his ECG. His cardiologist says to send him home. What do you say? by the way i really liked this guy. He was old school and hardcore. I had to deal with a combative patient in the room next to his and he heard the whole thing. First thing he told me was, "I'm glad you aint no p*ssy!". ecg.webarchive (818.38 KB) |
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Post by Bjs04f on Mar 31, 2015 15:34:23 GMT -5
ekg doesnt work.
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Post by pbruss on Apr 1, 2015 14:25:02 GMT -5
you are so high maintaince. you should just know what the EKG is supposed to look like. fail. ECG.bmp (562.55 KB) |
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Post by pbruss on Apr 1, 2015 15:16:20 GMT -5
ok how bout now Attachments:ECG.bmp (562.55 KB)
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Post by kemple on Apr 1, 2015 20:13:42 GMT -5
Brillinta www.ncbi.nlm.nih.gov/pubmed/23070079 In studies that compared the reversible P2Y12 inhibitor ticagrelor with the irreversible inhibitor clopidogrel, dyspnea was observed more frequently among ticagrelor-treated patients than among clopidogrel-treated patients. Because dyspnea was not associated with acidosis, pulmonary or cardiac dysfunction, alterations in the mechanisms and pathways of the sensation of dyspnea may be involved in its pathogenesis. It has been hypothesised that the sensation of dyspnea in ticagrelor-treated patients is triggered by adenosine, because ticagrelor inhibits its clearance, thereby increasing its concentration in the circulation. However, dipyridamole, a much stronger inhibitor of adenosine clearance than ticagrelor, usually does not cause dyspnea. We hypothesise that inhibition of P2Y12 on sensory neurons increases the sensation of dyspnea, particularly when reversible inhibitors are used. We base our hypothesis on the following considerations: 1) cangrelor and elinogrel, which, like ticagrelor, are reversible P2Y12 inhibitors, also increase the incidence of dyspnea; 2) it is biologically plausible that inhibition of P2Y12 on sensory neurons increases the sensation of dyspnea; 3) inhibition of P2Y12 on platelets (which do not have a nucleus) by clopidogrel is permanent, despite the once daily administration and the short plasma half-life of the inhibitor; 4) in contrast, inhibition of P2Y12 on neurons by clopidogrel may be temporary and transient, because neurons have a nucleus and can therefore rapidly replace the inhibited receptors with newly synthetised ones; 5) inhibition of P2Y12 on neurons by reversible inhibitors is permanent, because the plasma drug concentration is maintained high by repeated dosing, in order to ensure permanent inhibition of platelet P2Y12. |
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Post by Bjs04f on Apr 2, 2015 7:17:48 GMT -5
dan your study doesnt exist when clicked on, so your point is invalid. EKG is fine, some signs of biatrial enlargement looking at V1 biphasic p. AM dyspnea improving during the day sounds like sleep apnea. Not sure what cath would do to make that happen unless there was an issue during cath or need for intubation. Maybe more rare phrenic nerve damage, air embolism in pulmonary system, maybe a slowly accumulating pericardial fluid
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Post by mwiepking on Apr 2, 2015 10:38:44 GMT -5
Not fussed about the ECG and didn't see an issue with the medications, but I hadn't heard of Dan's ticagrelor/Brillenta study (though now I can't unsee it). I would've gone for a mild iatrogenic pericarditis/peridcardial effusion myself, especially since Stranksy invalidated Dan's point on technical grounds. Would've expected more on ECG and exam though.
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Post by pbruss on Apr 3, 2015 14:15:52 GMT -5
ekg is not impressive, the teaching point on this one was SOB 2nd to brilinta. brilinta is similar to adenosine and causes SOB mostly for the first 2 weeks someone is on it, like this guy. it goes away eventually but if you take the brilinta with caffiene the symptoms are drastically improved. this SOB from brilinta is the most common reason patients stop it (up to 30% in some cases).
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Post by mwiepking on Apr 3, 2015 14:32:39 GMT -5
Righteous
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Post by kemple on Apr 12, 2015 0:36:45 GMT -5
dan your study doesnt exist when clicked on, so your point is invalid. EKG is fine, some signs of biatrial enlargement looking at V1 biphasic p. AM dyspnea improving during the day sounds like sleep apnea. Not sure what cath would do to make that happen unless there was an issue during cath or need for intubation. Maybe more rare phrenic nerve damage, air embolism in pulmonary system, maybe a slowly accumulating pericardial fluid I could gloat but....nah I'll gloat. Sucker! Even though I pasted the important part of the study in the previous message, this is for Brandon Click here Brandon! |
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