Snapshot: 58 year old male CC: Epigastric pain

From time to time, we may have an interesting ECG, but without enough information (including final diagnosis) or additional ECGs to make a full case study.  In these instances, we will share the ECG and whatever information we have in our "Snapshot" series.  As always, some information may be changed to protect patient confidentiality.  Hope you enjoy!

Our first "Snapshot" involves a 58 year old male, with a chief complaint of epigastric pain. This pain has gone on for three days, and EMS is called by his girlfriend after "a couple" of syncopal episodes. Upon your arrival, he is alert and oriented, with an auscultated BP of 92/50, and a palpable radial pulse of 36. RR was 18, with an SpO2 of 95% on room air and clear lung sounds. He does, however, look anxious and is cool and diaphoretic. He complains of some shortness of breath, which he attributes to his epigastric pain. He has no significant medical history.

Here is the 12 lead ECG:

 

 

So, 

What do you think is going on here?

What would you do about it?

73 Comments

  • Brian says:

    Looks like Inferoposterior MI w/ 3rd degree AV block. I'd give a dose of Atropine while I readytranscutatneous pacing. 

  • gary goodman says:

    Inferior wall mi. Pacemaker time.

  • gary goodman says:

    Geez….no atropine

  • Bob says:

    My initial thought was dopamine…and I don’t see a third degree.

  • E. Sowers says:

    Inferior MI with III degree block (would like to see a longer printoff in just one lead as well).  Pt needs to be paced and on a bird.

  • Newer EMT-I says:

    3rd degree block with an MI present.  O2, IV.  Atropine (I don't expect this to help).  Pace.  Diazepam prior to pacing.  Emergent transport to closed facility.  

  • Craig Richey says:

    Inferior MI with 2* type 1 AV block… Looks like it's been ischemic for quite a while.  Tx: Pace it and run hot to the cath lab.  It's a gamble to speed up his rate; as it may increase oxygen demand and worsen the infarction… but he's symptomatic and beginning to decompinsate so the benefit outweighs the risk… Regardless be prepared for a crash.

  • Drew says:

    Syncope, chest pain, and hypotension=unstable bradycardia. Go straight to pacing. Obviously having an MI … the pump is now the problem, not vagal overstimulation so the Atropine isn’t going to do anything.

  • Craig Richey says:

    Whoops, ment to say 2* type 2.

  • E. Sowers says:

    Look at the PRI in lead I compared to lead VI.   Also in V4 you can see a couple of P waves there.  Thats why i would like to see a longer strip of one lead rather than short ones in the 12.  Just by looking at this, im assuming a 3rd degree.

  • Liz says:

    His BP being as low as it is along with his obvious signs of hemodynamic instability would lead me to also bypass the atropine and move straight to pacing.

  • Janell Stultz says:

    Agree with the inferior wall MI. Try to obtain v4r, O2, ASA, pacing and code 3 to stemi center. Consider fluids just to maintain BP. No atropine due to causing increased workload on an already damaged muscle.

  • Bill says:

    I agree with a inferior MI probably explains the hypotension and brady rate..

  • Janell Stultz says:

    Agree with the inferior MI.  I'd try to obtain a v4r, O2, ASA (if no contraindications), pacing, IV – consider fluids to maintain BP, code 3 to STEMI center.  WIthhold atropine since it will cause increased work for an already compromised muscle.

  • Mdelgado says:

    Let's get ready to pace and get Dope with it!!!

  • CCC says:

    I’m with Gary. Inferior MI an a complete heart block. He needs a pacer and certainly not atropine.

  • Don says:

    Can’t call it a third degree because you don’t have enough complexes in each lead. Shoot a right sided 12 lead to check for posterior wall involvement. Inferior wall MI but he’s AAOx4 with a decent systolic pressure. Try a fluid bolus to increase preload and use TCP as an absolute last resort. I wouldn’t want to make a dying heart die faster.

  • StormyMedic says:

    3rd Degree Complete A-V Block with an active MI.
    Apply TCP and rapid transport to a reperfusion center (Cath Lab capable ED).

    Change your uniform when it’s all done.

  • Brian N says:

    atropine=fail for complete heart block. it wont hurt, but it wont help. he needs PCI and a transvenous pacer. 

  • Ridgegirl says:

    Agree, no atropine. I'd obtain a right v4 to rule out RVI with those posterior changes. His pressure is holding I would start my STEMI protocol, get those stat pads on, rapid transport or fly to interventional facility, monitor BP and consider pacing should his pressure drop below 90. 

  • Nick Adams says:

    12 Lead:  CHB with a ventricular rate of 33 bpm secondary to an inferior/posterior wall MI.  St elevation in II, III, aVF with reciprocal ST depression in the left lateral leads.  The ST depression in the Anteroseptal leads are reciprocal changes from the posterior ST elevation (right dominant). QRS axis approx 80* (still normal, but rightward).
    TX:  ECG (3), ECG (12), ECG (15), ASA, IV x2, O2 @ 2 lpm via NC.  100 mcg of Fentanyl for pain management with a soft B/P prior to paceing this pt with an A/P pad placement.  HR and B/P increases?, NTG IV starting @ 10 mcg/min and titrating up until pain resolved or B/P < 100 mmHg.  IV fluid challange of 500 mL's and recheck lung sounds.  transport to a hospital with interventional cath lab capabilities and back-up CABG.
    DX:  Inferoposterior STEMI in a right dominant pt.  More then likely a proximal RCA.  Also, you should be thinking of a class I or II DeBakey aneurysm.  Do a good pt hx and physical exam.
     

  • Rob Ingram says:

    O2, IV, repeat 12 lead, consider fluid challenge if only for raising bp to medicate during pacing.  Looks like brady with 2nd or 3rd deg block, lead 2 and 3 show possible ST elevation.  No atropine, it's time for that external battery.

  • firemedic24 says:

    Atropine won't help, but it will definitely hurt.  If the atropine works, the atrial rate will speed up increasing the chances of a p wave landing in the absolute refractory period.
    TCP immediately without hesitation (while TCP does increase the oxygen demand, it is necessary to override the SA node) also evn though the systolic is greater than 90 the MAP is <65.
    Not saying that atropine and waiting on TCP is wrong or harmful, just giving my 2 cents and the reasoning behind it.
    Otherwise I agree with most people on here.  Inferior MI 3rd degree block.  I would be interested if anyone could tell me what the deal is with the biphasic T-Waves though.  Not that it changes my differential diagnosis or the actions I would take, just curious.

  • Joann says:

    Obviously bradycardia with what looks like III block, inferior MI, maybe some posterior involvement. Do right sided 12 lead for RVI, ASA, fluids, and get ready to pace while transporting to closest PCI center.

  • HarleyGirl says:

    I really don't see an MI, help me out there…need to see the lead two strip. There is some type of block…

  • George B says:

    It looks like an inferior MI with a third degree block. Bizarre EKG due to the patient sitting on the MI for three days. STEMI alert to cardiac cath lab. IV x 2, ASA, O2, Fluid challenge and listen to lung sounds. Prepare pads for pacing and run subsequent EKG. In NH we have heparin protocols with med control. This should be considered as well as getting you dopamine calculations done for possible administration.

  • firemedic24,

    I'm not sure I follow as to the problem with a P-wave (atrial impulse) falling during the absolute refractory period. The usual concern with increasing the atrial rate during AV dissociation is the atria kicking against contracted ventricles, exacerbating filling problems.

    The usefulness of atropine in AV dissociation will be determined by how big of a role hypervagotonia is playing.

  • Stephen says:

    Usual STEMI treatment w/o NTG.  I would apply pads but would not pace, as he is mentating well and has a blood pressure of 92/50.  Lots of fluids.

  • OdieO says:

    I want to see a longer strip as well.  Looks like 3rd degree with MI.  STEMI  activation and treat the pain.  With a stable BP no need to get agressive just yet.  The heart is already being insulted- why put that extra load on it to obtain a "more stable" BP?

  • Aut says:

    I'd go with posterior MI because of the depression in V1-V4, fluid bolus for the hypotension, Atropine while preparing to pace if his bp drops or LOC changes. I don't agree with the 3rd degree block only because the complexes are still so narrow, looks more like a second degree block to me (leaning towards type 1, but it really isn't going to change treatment either way). Definitely need a longer strip to confirm.

  • Aut says:

    On second thought, probably no Atropine or at least contacting med control before giving it.

  • Mike says:

    Guys, I dont know your local protocol.
    He is very brady but He is maintaining a pressure over 90. Thats beautiful! Why would you want to increase cardiac O2 consumption? Because of a pulse number? I know He reports syncope. So what? Is He loopy now? Are you going to kill heart muscle because of a history of syncope?

  • BigWoodsMedic says:

    I split the visible P waves and found there were little blips in the middle of QRS or T waves about halfway between. So I'd call this a 3rd degree block with Inferior changes. I would grab a quick V4R and one or two posterior leads, ASA, a line or two if time allows, and apply the patches. I hesitate to pace an alert patient without sedation. I'm able to send ekgs to the receiving hospital capable of PCI, so I'd consult with med command quick as well. He is borderline stable. I'd be keeping copies of his EKGs in my "neat things" folder. 

  • David Baumrind says:

    Great comments so far! 

    For those of you considering V4R or a 15 lead… are there clues on a standard 12 lead that lead you toward an RVI or posterior involvement? What are they?

  • Holly says:

    Inferior MI. The beadycardia is a natural defense mechanism to help lower the oxygen demand on the heart. Do a right side ECG to confirm right side involvement and HOLD NTG. 2 large bore IVs with fluid bolus 500-1000cc, ASA, high flow 02, have pacer/dfib pads ready in case of arrest or AMS (pace at a rate of about 60 instead of 80bpm to help keep o2 demand lower). Transmit ECG to ER or talk to medical control about what is coming in so the hospital is prepared for the worst.

  • David says:

    He is alert at this time, so I would be interested in changes during syncope. The qtc is prolonged. would be concerned with MI. Would like more history. It is plausible that the patient could be having periods of torsades. I would treat with ASA, fluid challenge, transmit EKG, continuous 12-lead monitoring. Rapid transport to STEMI center. I would apply combo pads and be prepared to pace or Dfib if nessisary.

  • steve says:

    Atropine is still in ACLS protocols! .5mg and follow with pacing and/or dopamine/EPI drip. I’m not sure how anyone could get 2nd type 2 or 3rd degree out of this strip. It’s not a 2/type 1 cause the p-r is not constant. The strip has to be longer. But doesn’t matter. Both treated the same. My opinion is everyone is missing the most important thing. Syncopal episodes. He isn’t perfusing the brain. Atropine increases p waves and may increase ventricular response do to that(depends on who you ask). His brain needs oxygen. If a P-wave falls in an absolute refractory period, NOTHING WILL HAPPEN. Since it’s been said in here. Pain management, easy fluids,and asa I agree with. The more agressive the treatment, the more that can go wrong. Pt needs rapid transport and cath lab.

  • FB says:

    I question whether he needs the cath lab. Symptoms ongoing for 3 days, q waves starting to develop in the inferior leads with inverting of the T-waves. I believe the damage is done. I question what the evidence based benefit would be of taking him to the lab after 3 days of infarcting and I think his ST-T changes agree.
    As to atropine, if he becomes unstable or more bradycardic I think you should use it (but to be honese the bradycardias in IWMI are sometimes short lived and usually not permanent). I think we agree there is an AV-block. He also has a narrow QRS. This is common for IWMI. These tend to be more responsive to atropine (because RCA supplies blood to the AV node in 80% of patients and the AV node is innervated by the vagus). It generally won't work with the AV block and a wide complex because these escape beats are originating distal to the AV node and these foci are not innervated by the vagus.
    ACLS says to use atropine with caution in the setting of MI but it is not contraindicated. Talk to your interventional cardiologists. They use it in this setting quite a bit. Plus if you use it, it works, increases rate, cardiac output, diastolic BP then you increase perfusion to the coronary arteries. If they go into V-fib (happens whether or not you give atropine) then you have a defib ready.
    I think he gets maximum medical therapy but doesn't need the cath lab emergently. I think ASA and some saline. Fentanyl.

  • IDB says:

    Inferior MI w/ 2* type I AVB. O2, ASA, 15-lead, IV, pacing, maybe dopamine. Definitely be ready for this PT to crash.

    Not seeing where the 3* is coming from, the PRI clearly lengthens during the strip and then drops a QRS in the V4 column.

  • BigWoodsMedic says:

    David Baumrind: The ST elevation in II, III, aVF, with reciprocal changes (esp. ST depression in V1!) lean towards an inferior MI, which can involve the right side or RCA. I'm sure there is more but that was a big one to me. I also tend to do a V4R following a regular 12 lead regardless simply because it takes a few more seconds while I'm setting up other stuff, I see no reason not to. 

  • BigWoodsMedic says:

    IDB: take that measurement between the P waves of the V4 column and go backwards across the lines, you'll find they line up with the visible P waves and some blips in the QRS complexes. I thought 2nd Deg type I initially too, but I'm leaning more to 3rd Deg. I know it was said above, I'd love to see a longer strip too, that would really be able to confirm which it is. 

  • Keith says:

    Obviously he needs 20 mg of Morphine followed up with 3 Nitros. Also I would consider placing a 22 gauge IV cathader, just in case. I would have him flown to the closest hospital with orthopedic services. This guys funny bone in oviously infarcting. Sorry couldn't resist…… ::
     

  • FB says:

    To Holly,
    The bradycardia in this case is probably not a protective mechanism but instea secondary to an RCA occlusion decreasing blood flow to the SA/AV node. Bradycardia here is secondary to an AV block (common in IWMI and may come and go with treatment but usually isn’t permanent).

  • Medic-Minx says:

    3* AVB w/ IWMI; definite STEMI Alert. I’d be putting the pt in tredendelenberg, pacer/defib pads on at once, & getting fluids going with an 18ga cath MINIMUM (if possible, & also bilateral if I gave an extra set of hands available). Hang some Dopamine after fluid bolus, multiple 12-Leads & trend vitals en route. If he becomes +AMS then I’d be starting the TCP at 60 PPM (pre-med w/ 2mg Versed) & introducing some electricity. *NO* Atropine..I’d never want to increase myocardial workload & increase oxygen demand/consumption, plus it’s rare it will work in a 3rd* since the block is so low & atropine works on the SA node.
    And HOLY CRIPES to anyone that wants to give one, let alone THREE NTG…you’ll kill him, especially if he has right-sided involvement. If you get his SBP >110 mmHg then I’d go for the Tridil (IV NTG) before even considering SL NTG…you can’t take sublingual back, but you can control the IV form much better. And consider what Morphine does…it has good preload decreasing effects & drops pressure (that w/ 3 NTG, might as well call him DRT); while Morphine is an excellent cardiac drug, Fentanyl is better in some sense because it doesn’t cause as much of a histamine release, therefore maintaining the pressure.

    He needs rapid & emergent transport to a cardiac facility, cath lab activated, & leave it up to the team whether they are going to send him up or treat another way. Everyone’s protocol varies but think about what drugs do in the setting of different MI’s.

  • Don says:

    Steve- I think your missing the point a well. You have two problems here. Two ACLS protocols STEMI and symptomatic brady. Question is which do you treat? Treating one hurts the other so which is more important? Bradycardia or an MI? Treat the cause not just the rate. The cause if the bradycardia is the MI. He can’t perfuse the brain sure to cardiac output. In an inferior wall MI give fluids to increase preload or think of it as the starlings law effect.
    Posterior involvement suspicions without a right sides 12, look for more ST elevation in less two than lead three.

  • Jarrod F. says:

    Does anyone that knows see a posibility for PE? I know thats a long shot but the S1 Q3 T3 seems to fit for this pt. Just inquiring. I would love some feedback. Thank you.

  • Rob M. says:

    Jarrod, I don't see anything that would indicate a PE.  Although you can't rule it out, the epigastric pain is an "atypical" presentation of STEMI.  This guy is going to be a high priority patient in my mind.  I'm going to get a quick HPI, inquire about allergies, place him on high flow O2, obtain my 1st 12-lead (prior to moving him), & then get him loaded & start rolling wheels to the ED.  I think that a decent length 3-lead strip is in order as I'm not too comfortable determining which HB (3rd degree or 2nd Type I) is present, given the extremely slow rate, I'd lean towards 3rd degree.  Either way, its unstable bradycardia (no need to overthink it at this time), just go to the cable & be done with it.  En route I'm going to put him on the pacer, start a large-bore IV & run LR (plus place in in trandellenberg) to bolster his pressure.  Once I've gotten that accomlished I'm gonna get V4R.  If that shows no RVI, then I'll start him on SL NTG & possibly MS).  Once thats done I'm going to get the ED on the horn, transmit the 12-lead(s), request orders for MS or versed to achieve mild sedation for the pacing (given an appropriate BP).  Obviously serial 12-leads & transport emergency.  Also, if I'm relatively close to the ED, I'll also draw labs to help speed things up in the ED.  This guy is acutely sick & needs the cath lab.

  • Chris R says:

    This is a STEMI. Little q waves, so maybe sub acute. STE more in lead 2 than lead 3, so probably a RCX occlussion. But, looking at lead 1 I see depression; that would fit a RCA occlussion. V4R is needed for better research. Treat with medication following protocol. Monitor bp and give fluid, if V4R agree RCA is the culprit. 3 degree av-block with a narrow, regular escape rhythm originate from bundle of His or higher. Send to PCI centre

  • Mike M. says:

    3rd degree AVB. Inferior wall injury with septal and lateral wall reciprocal ischemic changes. I do not think there is posterior wall involvement as the R wave progression seems normal, not showing any prominent anterior forces. Bezold jarisch causing hypervagatonia as said by Chris W.
    O2, 2 large bore IV's, 250 cc bolus on repeat with clear breath sounds, ASA, Pads on for pacing. No atropine. Monitor BP, pace if you have to. 
    AND… Are those t-u fusion waves?

  • Doc whit says:

    Well we have thrown down, 4r would be good what about a postierior 12 lead 7, 8, 9, I would snap the cap ETCO2 can tell you alot about this pt, inferior septal MI the decreased rate and electrical conduction is a compemsatory mechanism "Atropine" no, pacing yes and a Benzo. Thrombolitic check list, Nitro drip, think LMWH.
    MAI may be considered if pt becomes more stmptomatic to protect Homeostasis  

  • Mike says:

    I have to disagree, Atropin is contraindicated in high level blocks, like this one. You may wipe out all conduction. The nodes are already taxed to the point of failure.
    Pacing engages all the muscles in the electrical field VASTLY increasing work load. Turn the monitor around and look at your PT. if he is not in distress DONT PUT HIM IN DISTRESS! remember “do no harm”.

  • Nick Adams says:

    MEDIC-MINX:  If I'm having the "Big One", I would like for you to come get me please. 
    For other commentors, It is a 3rd degree HB…..not a 2nd type I or type II.  In a 2* type I, the ventricular rate would be irregular.  A 2* type II, you would see a "set" PRI in front of EVERY QRS.  With both, this is not the case so it is a 3rd degree HB (CHB).
    I even stated to pace this patient, but let me add it would depend on my physical exam and how the patient presents.  Sure he had a syncopal episode, but I bet it was secondary to a change in position (sitting to standing or laying to sitting).  Maybe the infaction is growing and even thought he's had CP (epigastric) pain for 3 days, he just went into a CHB 30 minutes prior to calling).  Oh wait……He's anxious, cool and diaphoretic.  I would definately try a fluid bolus to increase B/P.  Maybe, just maybe, paceing might help him.  An increase in oxygen demand by increasing ventricular rate?  An increase in ventricular rate will definately increase demand.  But an increase rate will also increase the patients cardiac output and increase coronary perfusion pressure which will increase flow and oxygenation to the tissues.  The rate is NOT a compensatory mechanism for the MI…..that's silly.  It is secondary to ischemia of the AV node and junction.  Now that you have his pressure up, you can give NTG (gtt) to vasodilate, which will further increase oxygenation to the tissues.  Granted, this pt has had CP for 3 days and the damage is ongoing, but who has the right to say that the damage is DONE and nothing can help him now.  Most MI's have normal (or increased) ventricular rates so increasing his rate to a normal level of 60 shouldn't hurt him……it should help.
    If you do decide to pace this patient, I noticed some of you would give the pt Versed…..nice.  Versed will relax him a little bit at 2mg.  To sedate a patient for a painful procedure, you'd need more like 4mg……and benzo's do NOTHING for analagesia.  If you are going to do a painful procedure on me….please give me some Fentanyl too (100mcg atleast)…..TY.
    Please stop it with the Atropine.  Yes, Atropine is contraindicated in a CHB.  Not because it's bad for him, but because it increases SA nodal discharge, which will just give him more PW's and does nothing for the ventricular rate.
    Someone mentioned that the pt's MAP is 65mmHg.  Ok, so the pt's has a normal MAP.
    Some other things that would help you diagnose a proximal RCA occlusion without doing a V4Ror 15 lead EKG is the fact that the ST elevationis greater in lead III then in lead II.  Not so much that the pt is in a 3rd degree HB, but the atrial rate is very bradycardic too.  This is secondary to ischemia to the SA node from a proximal RCA occlusion.
     

  • Stephen says:

    Bezold-Jarisch Reflex.
    I believe it has been discussed here before. 

  • Firemedic24 says:

    This thread has definitely given me something to think about.
    Previously I always considered atropine to be contraindicated in CHB.
    I always thought pacing to be a better treatment for CHB. I know that pacing increases myocardial oxygen demand in the setting of MI, but with CHB the rhythm in and of itself is very dangerous.

    It seems that there is a big difference of opinion here. I am interested to take a look at some of the original studies and hear some more expert opinions.

  • David Baumrind says:

    Firemedic24,

    it is important to remember that to a large degree, there is parasympathetic innervation to the SA node as well as the AV node, but not the ventricles… It will not help in CHB, and is not indicated for high degree heart block (2nd degree type II and 3rd degree).

  • B. DaY says:

    Some of these responses scare me.  But of course IV, O2 on a NC and monitor and capnography.  You can't really determine the degree of the block because you don't have a long enough strip to look at but given the rate you can say it's one of the higher degree blocks.  If I had a longer 4-lead strip I could better identify it.  Yeah he's hypotensive but not bad considering he is having an inferior wall MI so no Dopamine.  Do a V4R and V9P to see if there's any posterior involvement and to confirm the right sided MI.  No Atropine, No Nitro and No Dopamine.  If the bradycardia wasn't complicated by a block and an MI then I would say go for the Atropine but otherwise forget it.  As for the Nitro with the right sided involvement we don't want to knock out our preload that's helping that heart contract as well as it is.  ASA, if lung sounds are clear a fluid bolus, and TCP should take care of it and a benzo like Versed in small doses to keep from interfering with the hemodynamics if you have time.  Along with hauling tail to the hospital and hopefully bypassing the ER to the cath lab that's it.  Some people are going way overboard and making it too complicated.  Keep it simple! 🙂

  • DAn says:

    I agree with B. Day, most people seem to be going way overboard! The BP is a fairly benign number that doesn’t concern me too much. The pulse may be low, but it is palpable radially. This EXACT scenario is one that I was thinking about the other day, and there are certainly many things to think about. Anyone who says nitro is just plain scary. Look at that BP with an inferior (possibly rvi as well) MI! As far as trying to speed up the rate, I’m not so sure that’s a great idea either. This is a very irritable heart, and I do not believe that increasing the O2 demand would do much good. The pulse is palpable radially, and the systolic pressure is over 90. Just my thinking… I would love to be pointed in the right direction for more expert opinions!

  • h dawg says:

    WHY ATROPINE?!? Yall guys are jumping the gun bigtime on this one. Skipping lots of steps.
    Try a fluid bolus. Check out 'dem big ol' Q's and inferior elevations.
    This is the big one
     
    Fentanyl for the preload and pain in place of morphine due to non-hypotensive effects, nitro bolus AND drip if tolerable, o2 prn, anticoagulant of your desire and ship them off priority mail to the cath lab.

  • Firemedic24 says:

    WHY NITRO?!?
    you are jumping the gun big time with that one.

  • The Hungry Medic says:

    Hi everyone. We can see from the 12 lead Ecg that the patient is experiencing to major disruptions within the heart. The first being an inferior wall STEMI. We know that this is caused by an occlusion of the right coronary artery. We also know that this could include an infarction of the right ventricle as the RCA also supplies its blood flow. If i had the help and time I would do a Right-sided 12 lead, but if not I wouldn't worry about it as the patient is already unstable. The second problem is the resulting third degree heart block. My treatment would include placing the patient on 10 lpm of O2 by non rebreather mask. I would administer 324 mg of chewable baby ASA. I would position the patient supine on the cot. I would place pacemaker electrodes in preparation for Transcutaneous Pacing. I would establish IV access. Granting that the patient has clear lung sounds I would administer a 250 ml bolus of NS. I would not administer larger amount of fluid to this patient as I expect that it would precipitate congestive heart failure and pulmonary edema. I would certainly not administer Atropine as it would increase myocardial oxygen demand as the heart rate increased. Atropine is contraindicated in the setting of an acute MI in the Massachusetts State Protocols which i work under. I would consider transcutanous pacing. I would probably refer to medical control in regards to pace or to not pace. My reasoning for this is that transcutaneous pacing will also increase the heart rate therefore also increasing myocardial oxygen demand. The bradycardia may be acting as a compensatory mechanism. The slower the rate, the less oxygen the myocardium requires to operate, staving off further myocrdial tissue death until the infarction can be remediated. I am thinking that as long as the patient remains conscious and alert, as well as without congestive heart failure I would hold off from pacing. If he does develop pulmonary edema I would be inclined to contact medical control for on-line orders for Dopamin infusion. Maybe someone can shine some more light on the topic of TCP in the setting of an acute MI. My transport decision is to take this patient to a PCI center with a STEMI alert. Luckily the city I work for has a PCI capable hospital so we are never further than ten minutes away.

  • firemedic24 says:

    Not to beat a dead horse, but I did a little bit of research and learned alot.  Here is what I found.  It seems there are different types of Complete AV Blocks.  High CAVBs are in or near the AV node.  Low CAVBs are lower, in the pukinje fibers.  High CAVBs are more stable than low CAVBs.  A low CAVB or a CAVB with bifasicular block is at risk of sudden asystole regardless of the rate or the pressure.  A heart rate of 35 in the presence of a high CAVB is actually safer than a heart rate of 60 in a low CAVB.
    Atropine is inneffective in second degree type II and in low CAVBs.  CAVBs that are high can actually be responsive to atropine.  That being said, atropine will not fix the rhythm, it will only increase the rate.  Atropine will also increase the oxygen demand of the heart.  I personally would not administer atropine unless the pt condition deteriorated despite a fluid bolus and pacing.
    Pacing is still a little fuzzy for me, but I will share what I learned.  In low CAVB the pt is at high risk for asystole and the decision to start pacing needs to be made on whether the pt is symptomatic (as opposed to stable).  At this point the decision to withhold pacing in a stable patient with a high CAVB is one I am not comforatable with, but I am still trying to find the answer to that one.  It should go without saying that sedation should be consider in conjunction with pacing in this case.
    I think we can all agree that asa, and heparin are safe choices in this pt as long as they are not contraindicated.
    Nitro is currently contraindicated due to hypotension.  If by some miracle the pt dramatically improved with a fluid bolus there is still concern about right sided involvement.

  • Ian Boucher says:

    Inferior MI with signifigant bradycardia. Would like a longer lead II strip to tease out what kind of block is present. 
    Management plan: O2 via NC, IV, monitor, ASA. I would probably call up the doc and ask her opinion on whether to sedate and pace or not. 

  • apneic says:

    I won't discuss treatment, because that has been covered already in discussion.  However, I would like to weigh in on the decision making between AV-blocks.  
    To me this is clearly a 3rd degree block.  P-waves can be seen marching out throughout the total 10 second strip that includes I, aVR, V1, and V4.  In some areas, it can be difficult to find the P's, but measuring a set that is clearly seen can make the task easier.  Remember that the amplitude of P-waves, whether positive or negative, add to or subtract from the amplitude of other electricity at the same time.  
    In this example, 2 P-waves are clearly seen in V4.  Measuring them (I eyeball, use a pen, or hashes drawn on a paper), and marching backwards finds the previous P-wave buried in the very beginning of the v4 QRS complex.  Next one back is the inverted wave 5 boxes to the left of the V1/V4 break.  Before that is the inverted wave 1 box after the V1 QRS complex.  So on and so forth.  The most difficult to identify are found in AVR, as their locations superimposed over both T-wave areas can lead to confusion.
    The P-waves are regular, as are the QRS's.  3rd degree.
     

  • medic says:

    Treat the pt not the monitor….O2 via NC at 6LPM, Vitals, ECG monitoring, 12L, if time permits perform R12L, IV access, start with 250-500cc fluid bolus or KVO. I would hold off on pain analgesics due to the fact the A) this could be a right sided MI following a CHB and B) In most state protocols it's contraindicated to administer anagelsics to abdominal pain pt's. The pt's pressure is 92/50 and he's been complaining of all this for x3days so theres no immediate life threats or immediate unstability here. As along as you keep the pt's pressure to >90 or titrated til pt's perfusion increases and keep pt's airway patent you should be good. I would still apply pacer pads and explain to pt why just for precautionary. I would not pace until pt should s/s of severe unstability (chest pain, pulmonary edema, altered mental status). reasess q5min, txp class 2.

  • Hereandthere says:

    Inferior MI in the presence of a 3rd degree heart block. o2 w/ capnography, supine position, IV w/ a 250-500 cc fluid bolus, 2nd line/saline lock, pacer pads, serial 12 leads, R sided 12 lead, and call for a consult and orders for fentanyl (I agree with fentanyl vs morphine due to morphine's hypotensive effects but we only have standing orders for up to 10 mg of morphine for ACS pt's)

  • Jess says:

    Inferior MI with 3rd degree block causing significant cardiac compromise. Treat the cause, ACA, fluid bolus if lungs remain clear. Only pace if he gets significantly more cardiovascularly compromised.

  • jeff says:

    the strip is too short to confirm any kind of heart block, even though the 2:1 ratio of p waves to QRS can be seen in V3-6.  Nitro is contraindiated due to hypotension. Although it would be an atypical presentation, with diffuse ST changes in all leads hypotension and bradycardia we should not rule out an AAA or STEMI.  Id begin with O2, trendelenburg position and a fluid bolus (BLS before ALS) and go from there.  As long as the patient remains alert and oriented I would stray away from pacing.

  • Bradlee G says:

    If I was the medic onscene and I saw this 12 lead I would first: take a deep breath, do a repeat 12 lead to amke sure it is accurate.  I would immediately give him ASA, do a 15 lead to see about possible RV involvement and treat accordingly.  The hypotension is from RV involvement and pre-load issues, so no nitro due to possible killing the pt.  double large bore IVs and fluid wide-open as long as no respiratory issues.  Call the ER and get him to the cath lab, and if possible, get medical command orders for possible pain management orders for pain if his blood pressure will hold.  Just keep it simple and breath.

  • Bradlee G says:

    And  also to everybody who is saying that this is a 2nd or 3rd degree block, there is only one way to determine the rhythm and that is with at a least a six second strip.  We can speculate all day that this might be a 2nd or 3rd degree block but you can't be positive without a rhythm strip.

  • I'm not so sure I agree; by that logic we shouldn't diagnose VT from a 12-Lead…you can see AV blocks on 12-Leads and often times they are the only way to accurately differentiate 2:1 AVB from blocked/non-conducted PACs.

    A 12-lead is simply a 10 second strip. I will agree though, that sometimes you need more than just 6 or 10 seconds to make a positive diagnosis. In this case I'd be very confident in a 3rd Degree AVB even without a rhythm strip.

  • David Baumrind says:

    Also, just to add, sometimes atrial activity will be best seen in lead V1, which for most people, will not be on a rhythm strip. Often, we will have to use all the tools at our disposal to diagnose rhythm, including the 12 lead.

  • JB Wallace says:

    The thing that confuses me is that the complexes are narrow.  In a CHB, I would expect them to be wide.

  • JB,

    Heart blocks of any type do not relate to the width of the ventricular complexes. The width of the complex is based on the origination and travel of the electrical impulse. In a complete heart block, the origination of the impulse can come from the junctional tissue or the ventricles. If it originates in the AV Node then the resulting ventricular complexes will be narrow.

    Does this help?

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