Կարող է արդյոք LAD-Ին առաջացնել աջ փորոքի ինֆարկտ՞
66տ կին, գանգատվում է արտահայտված հետկրծոսկրային ցավից, սրտխառնոցից
ԷՍԳ-1 (ԷՍԳ-ն իրականացվել է Շ/Օ բրիգադի կողմից ժ14:00)
ԷՍԳ-2 (Իրականացվել է հիվանդանոցում, նշված ժամանակ հիվանդի ցավի ինտենսիվությունը նվազել էր)
ԷՍԳ-3 Ստենտավորումից հետո, ռեպերֆուզիա
Բացատրություն
ԷՍԳ-1 ում առկա են կորոնար
T-ատամիկներ, ինչպես նաև R-ատամիքի աճի դեֆիցիտ V2-V4 արտածումներում
Նրանք լայն են, բարձր և ուշադրություն
դարձրեք որ V4-արտածման մեջ այն ուռուցիկ է (Upwardly Convex) որը նույնպես ապացուցում
է նրա իշեմիկ բնույթը, իսկ aVF-արտածման մեջ այն ավելի մեծ է քան ամբողջ QRS-կոմպլեքսը։
ԷՍԳ-2 ում P-ատամիկ չկա, առկա է ՀԽՁՈՊ
մորֆոլոգիա ՍԿՀ մոտ 95զ/ր QRS>120մվ, առկա է արագացած փորոքային ռիթմ (AIVR) այն ռեպերֆուզիայի
նշան է, ինչի պատճառով իսկ հիվանդի ցավի ինտենսիվությունը մեղմացել էր։
ST-սեգմենտը
նշված ԷՍԳ-ում ակնհայտ բարձր է, հատկապես V1-V3 արտածումներում, ուստի Scarbossa-ի մոդիֆկացված օրենքը
կիրառելի չէ արագացած փորոքային ռիթմի ժամանակ`քիչ ապացուցողական հիմք ունենալու պատճառով,
այն կիրառելի է ՀԽՁՈՊ և Արհեստական ռիթմավարի ռիթմի ժամանակ սրտամկանի սուր ինֆարկտին
բնորոշ ST-T փոփոխությունները գնահատելու ժամանակ, Ինչը կքննարկվի այլ հիվանդի շրջանում,
Աջ կրծքային արտածումներում առկա են ST-սեգմենտի էլևացիաներ RV3-RV5, ինչը
Հիպոպլաստիկ աջ կորոնար զարկերակը
Wraparaound Type III երկար LAD-ին, նրա պրօքսիմալ և միջին հատվածի նեղացումներով
Ստորև պատկերված է ԷՍԳ-ն կորոնարոպլաստիկայից հետո որտեղ առկա են ռեպերֆուզիայի ԷՍԳ-նշաններ II,III,aVF և V1-V5 արտածումնեորւմ ինչը ապացուցում է որ LAD-Ին սնուցել է նաև ստորին պատը,
- Ինչու են առկա ST-սեգմենտի էլևացիաներ աջ կրծքային արտածումներում՞,
- Արդյոք աջ կրծքային արտածումներում ST էլևաիաների առկայությունը պարտադիր է Աջ փորոքի ինֆարկտը ախտորոշելու նպատակով (Նշված Case-ում նրանք առկա են, սակայն արդյոք առկա է ԱՓ-ի ինֆարկտ՞)
- Եթե աջ կրծքային արտածումներում առկա են ST-սեգմենտի էլևացիաներ, սակայն մեղավոր անոթը ձախ առաջային վայրէջ զարկերակն է (LAD) արդյոք դա կարելի է համարել աջ փորոքի ինֆարկտ՞
- Ինչ կարևորություն ունի LAD-ին աջ փորոքի պերֆուզիայի համար, կորոնար շրջանառության ձախ դոմինանտ տիպի դեպքում
Ken Grauer-ի կարծիքը նշված Case-ի վերաբերյալ
Yes — VERY interesting. I made a PDF of the illustrations. I'd love to publish this as a Blog IF I can get some more answers! My thoughts are the following:
ECG #1 (in the ambulance) — Sinus tach — narrow QRS — obvious hyperacute T waves in V2-thru-V6, with some abnormal ST elevation beginning in lead V1. Limb lead changes are more subtle — with really no ST elevation in the inferior leads, but a hyperacute T wave in led aVF. Lead aVF has a flat ST segment. My impression on seeing this would be acute proximal LAD occlusion — with the somewhat surprising finding of a lack of reciprocal ST dep in inferior leads and a lack of at least some ST elevation in aVL (as both are typically seen with acute proximal LAD occlusion).
In retrospect, knowing the cath film results — I suspect this acute prox. LAD occlusion with "wraparound" DID have acute inferior ST elevation (as suggested by the hyperacute T in aVF) — but that this was attenuated by what otherwise would have been inferior lead reciprocal depression from the proximal LAD occlusion. It's a pretty SEVERE lesion when you have a hypoplastic RCA + acute prox. LAD occlusion + "wraparound" affecting the inferior wall — so a miracle that the patient survived!
ECG #2 — You call this LBBB — but WHERE is the P wave !!!!!!!! Answer — The P wave is retrograde, seen best in the inferior leads — because this is AIVR and not a sinus rhythm (ie, so NO "LBBB" — but rather a ventricular rhythm!). Note lack of monophasic R in V6 and the triphasic bizarre complex in lead I which is another hint that this is NOT "LBBB". Spontaneous reperfusion must have occurred to cause this AIVR. (Was there ANY decrease in chest pain at ANY point near the time this ECG #2 was done ????)
ECG #3 (Right-Sided Leads) — I agree that there DOES seem to be ST elevation in V3,4,5 — and that suggests acute RV involvement! Perhaps the HYPOPLASTIC RCA resulted in an anatomical variation in blood supply to the RV, in which the LAD does give off a branch to supply the RV, therefore acute RV MI (and in retrospect, the DIFFERENT SHAPE of the elevated ST segment in V1 of ECG #1 could be because this ST elev. in V1 is a result of the RV MI and NOT of the anterior MI (for which ST elevation began in V2).
CATH RESULTS — As I've told you before, I am NOT expert in this (as I am not a cardiologist). I see the obvious high-grade stenosis in the LAD (RED arrow). Is the 2nd LAD lesin by the YELLOW arrow (this is not as obvious ...). Please draw arrows on a picture so that I can add the cath film with arrows to Blog post. I'll make the arrows pretty — but I need your assistance in figuring out where the 2 LAD lesions are.
ECG #4 (post-Cath) — Here we see obvious reperfusion T waves, which are most prominent in the anterior leads.
The above my thoughts. I'll await more follow-up from you. How is the patient now doing?
Nelson — You didn’t say how much time passed between the ECG with AIVR and the right-sided leads? Were they done right after each other? Realize that AIVR is often transient — it could last seconds, minutes, or much longer — but seems like no one noticed AIVR — so no one probably noticed when it began and when it ended. This is why CLOSE correlation of the amount of chest pain is an essential part of interpreting serial tracings. I’d expect (not 100% — but usually) — that either just before or shortly after AIVR, that there should be a reduction in the amount of chest pain (might not go away — but the severity SHOULD CHANGE) — but that might be missed if not actively looked for …
The QRS looks narrow on the right-sided leads — and you can again see P waves IN FRONT of the QRS.
During AIVR — it looks like a P wave MIGHT be in front of the QRS in V4 — but too much artifact for me to be sure — but this was not thought of, so “the moment” for recording the change from AIVR back to sinus rhythm was missed.
So — spontaneous reperfusion usually means the “culprit” artery has reopened — but what reopens may reclose — sometimes multiple times (Steve Smith has MANY cases of this on his Blog) — so one needs to remain alert.
I am only guess re RV MI. I DOES look like with a narrow QRS, there IS ST elevation in V3,4,5 — so that goes along with acute RV involvement — so I am just wondering (???) if perhaps with a hypoplastic RCA (was this a “congenital hypoplastic RCA”?) — if perhaps since the RV blood supply has to come from somewhere — perhaps it is congenitally coming from the LAD?
Hope that helps — 
P.S. As to Sgarbossa criteria with AIVR — in my opinion (which probably differs from Steve Smith's opinion) — there just is NOT ENOUGH DATA to draw ANY conclusions about fixed millimeter criteria with AIVR (for which QRS morphology will vary tremendously, therefore NO consistent picture to "measure") — therefore — Give me the case and show me the tracings — and I'll individualize my judgement as to whether an AIVR rhythm is likely to reflect acute ST elevation — but NO generalizations are possible (in my opinion). SHAPE counts more. That said — IF you have a good history for new chest pain AND you have AIVR — then the IMPLICATION is that there has just been an acute MI, and now there is reperfusion (especially if the new chest pain is now gone
P.S. As to Sgarbossa criteria with AIVR — in my opinion (which probably differs from Steve Smith's opinion) — there just is NOT ENOUGH DATA to draw ANY conclusions about fixed millimeter criteria with AIVR (for which QRS morphology will vary tremendously, therefore NO consistent picture to "measure") — therefore — Give me the case and show me the tracings — and I'll individualize my judgement as to whether an AIVR rhythm is likely to reflect acute ST elevation — but NO generalizations are possible (in my opinion). SHAPE counts more. That said — IF you have a good history for new chest pain AND you have AIVR — then the IMPLICATION is that there has just been an acute MI, and now there is reperfusion (especially if the new chest pain is now goneTHANKS for the follow-up! Am I correct that these are the 2 LAD lesions (proximal & mid-LAD) = RED arrows ??? As to your Professor. We ALL agree this is a big STEMI in need of revascularization — as this is OBVIOUS on the initial ECG. But it sounds like your professor missed the AIVR. NO, this does NOT change management in the least — but I’m glad that at least YOU are attentive to what the ECG findings are. In this case — whether or not AIVR was recognized does not change management — but in some cases, it MIGHT change management, which is why I think ( = my opinion) that it is good to recognize it.
Otherwise — I like to verify cath findings before I publish anything, because this is not my expertise. Do you agree that the RCA may be congenitally hypoplastic? And does it seem reasonable to you to postulate that because of the hypoplastic RCA — blood supply to the RV may have come from the LAD, which is why we seem to be seeing an acute RV MI on your right-sided leads? What do YOU think?
THANKS Nelson for your follow-up on this. It really helps me to know that the RCA Marginal Branch is the KEY — and that as per your diagram. this Marginal Branch IS intact in this patient — so I agree that makes it less likely that that the LAD was supplying the RV in this case. That said — ST elevation persists in right-sided leads as FAR OVER as lead V5R! — so WHAT is the most likely reason for this?
I have not yet begun to write this case up — but based on your info — I'd be tempted to say something like this: The question arises as to WHY we see ST elevation in right-sided leads? Given the presence of a "hypoplastic" RCA in this case — I contemplated the possibility that this might be a rare case in which the the RV was supplied by the LAD. That said — against this possibility, is the presence of the Marginal Branch to the RCA. This leaves us with uncertainty as to the cause of ST elevation as far rightward as lead V5R. Input from readers on this question is WELCOME! — Thanks again for all your input!
The fact remains that there is substantial ST elevation in V3, V4 (less in V5) — and we still do not (in my opinion) have a good explanation for this. I am well aware that many RCA occlusions do not cause RV MI (I have always looked for signs of RV MI for years with each inf. MI I see). I also commented on a couple of Steve Smith's blog posts about isolated ST elevation in lead V3 in the setting of isolated acute inferior MI — in which we'd postulate that a branch from the RCA was probably vascularizing a portion of the anterior wall. But without a better appreciation for how/when the RCA in your patient became "hypoplastic" — nor more specifics from the cath as to precise vascularization of the medial RCA branch (I agree that it cetainly LOOKS like this branch IS adequate to supply the RV wall) — I think we still find ourselves without good explanation for why there is so much ST elevation in V3,V4. In the original ECG — there is some ST elev. in V1, but much more in V2. Now, on a regular ECG — lead V1 = V2R — and lead V2 = V1R — so IF this is accurate, then the AMOUNT of ST elevation is decreasing as you go from V1R to V2R — but then INCREASES in V3R and V4R — and we still do not have explanation for why.
All that said — we lack serial ECGs soon after that first ECG — and we do NOT have a normal 12-lead at the time of those right-sided leads (because there was the unrecognized AIVR) — so all I'm saying is that AMONG the "active theories" needs to be the possibility that the LAD may have been supplying the RV ...
Without more info on cath, clinical and more serial ECGs close to the time of those right-sided ECGs — we just can never know for certain in my view.
Հետագայի համար
Comments
Post a Comment