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Re: [ekg_club] Beta Blockers In AMI - "the Answer … " - KG [8 Attachments]

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  • David Rand
    Hi Ken, Thanks for posting those articles. I queried an interventional cardiologist and another fellow, both of whom told me IV beta blockers should not be
    Message 1 of 7 , Mar 1, 2012
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      Hi Ken,

      Thanks for posting those articles. I queried an interventional cardiologist and another fellow, both of whom told me IV beta blockers should not be given (generally) in the setting of STEMI.  I think we solved our question. 

      Thanks for the discussion,
      Dave


      On Wed, Feb 22, 2012 at 5:16 PM, Ken Grauer <ekgpress@...> wrote:
      Hi Dave and fellow EKG Club Members,

      After consulting with one of my esteemed colleagues, I believe I finally have some of the answers to this question about acute use of Beta-Blockers in ACS/Acute MI that would seem to be simple, but amazingly is more complex the more things come to light ... My colleague sent me these 3 references which I have included as PDFs in attached to this e-mail. 

      Below a screen shot from the BEST of these 3 = Editorial by Miller - with yellow highlight of his concluding paragraph that I believe says it all ...  Great review of the overall situation in his 2-page Editorial - more support for these views in the other two articles. Summary of ACC/AHA Guidelines in screen shot below (I don't know that these are further updated ... ) - though one can clearly question the path to follow (which explains why some of you work in EMS systems that routinely do use beta-blockers - and others of you work in systems that don't ... ). My impression is that there is potential harm from acute (IV use) of beta-blockers in the field (increased risk of cardiogenic shock, so far from a meaningless potential to harm .. ) - with questionable (at most) benefit in most patients vs waiting until you arrive in the ED - so my bias in 2012 would be against IV beta-blockers in the field, deferring that decision (and decision for subsequent PO beta-blockers or not) to the in-hospital team. We probably just DON'T KNOW if beta-blockers are truly helpful in the PCI era - since much (most) data obtained before that, such that a patient getting acute reperfusion may have their overall risk lowered to such an extent that potential downside of beta-blocker therapy may outweigh any positives .... but whether we'll get good data studying this prospectively is another question ...

      FINAL POINT to CONTEMPLATE: Quality indicators (that GREATLY affect hospital reimbursement) are based on old data that much more heartily used to support early use of beta-blockers - such that even if it is proven that beta-blockers in ACS are not beneficial - it is possible that this practice might not take hold (at least for a while .... ) because of concern for losing "quality points" (and therefore reimbursement ...).

      Hope this is helpful.

      Ken















      Ken Grauer, MD (
      KG/EKG Press, Professor Emeritus in Family Medicine)
       E-Mail: ekgpress@...
       Free Educational ECG Blog: www.ecg-interpretation.blogspot.com
       ECG Competency DEMO: http://demo.ecgcompetency.com/

      ====================


      ==================
      On Feb 22, 2012, at 1:07 PM, David Rand wrote:

      [Attachment(s) from David Rand included below]

      HI Ken and Gene,

      All good points and questions. As an internal medicine resident, I'm not "up" enough on cardiology research to comment on the impact of these articles vs the braunwald text and certainly publication date is an issue (per Ken). When I discussed this issue with one of the cardiology fellows, he did reiterate that IV B blockers in STEMI was not passe. I'll try to seek some more expert input. Clearly, the Kontos abstract below (I'm attaching the full text) does seem to make a compelling argument that early beta blockers are dangerous, especially in the presence of risk factors for heart failure (which they note include  age >70 years, systolic blood pressure (SBP) <120 mm Hg, heart rate >110 beat/min, and prolonged time from symptom onset to presentation). The article also points out that the COMMIT trial included many patients treated by fibrinolytics/medically and not by PCI. Hence, perhaps the implications for rural vs other EMS systems where primary PCI is the norm may be different.  To answer your question about "stability" Gene, I think that at least in this last article  stability refers to hemodynamics as opposed to clot.

      When interpreting any literature, I always remind myself that it usually takes many years and multiple studies to change medical practice and for updated guidelines to emerge...which is both good and bad. 
      Thanks for the great discussion.
      Dave




      On Tue, Feb 21, 2012 at 6:55 AM, Ken Grauer <ekgpress@...> wrote:
      David - I think the key to assessing the 2011 Braunwald text is to look at the year of the references used for this chapter. It doubtlessly took 1 (if not 2) years to publish this new 2011 edition given its size (that's the typical time it takes to publis

      h large medical texts ... ). Sometimes late changes can be made - but the date of references used should reflect that if it occurred.

      I'm no longer directly involved with these acute care protocols - so I don't have a feel for current national practice - but had the impression from the references Brandon supplied and the Kontos abstract below that current practice had changed ....  I'm sure that from other EKG Club members we could "build" a good picture as to how prevalent routine acute use of IV beta-blockers in the pre-hospital (and then in the hospital) setting still is.

      Ken



      On Feb 21, 2012, at 12:55 AM, David Rand wrote:

      While I cannot comment on why EMS folks are no longer giving beta
      blockers in the setting of STEMIs, the practice is still common in the
      hospital, especially if the patient's heart rate is over 70. According
      to the 2011 edition of Braunwald's heart disease, the practice
      decreases all cause mortality as well as cardiac arrest.A key point is
      that it is contrandicated in patients with STEMI and concomitant heart
      failure. I've pasted the entire section from Braunwald's at the
      bottom, with the most relevant section here:

      Given the evidence of the benefits of early beta blocker
      administration in STEMI, patients without a contraindication (see
      Table 55-8), irrespective of administration of concomitant
      fibrinolytic therapy or performance of primary PCI, should promptly
      receive oral beta blockers.It is also reasonable to administer
      intravenously beta blockers promptly to STEMI patients, especially if
      a tachyarrhythmia or hypertension is present, in the absence of signs
      of heart failure or low output, increased risk of developing shock,
      indicators of high risk of developing shock, or other relative
      contraindications to beta blockers.[35] We use metoprolol 5 mg
      intravenously every 2 to 5 minutes for three doses, provided the heart
      rate does not fall below 60 beats/min and the systolic blood pressure
      does not drop below 100 mm Hg. Oral maintenance dosing is initiated
      with metoprolol, 50 mg every 6 hours for 2 days, and then 100 mg twice
      daily

      David Rand DO MPH EMT-P

      The effects of beta blockers for the treatment of patients with STEMI
      can be divided into those that are immediate (when the drug is given
      early in the course of infarction) and those that are long term
      (secondary prevention). The immediate intravenous administration of
      beta blockers reduces cardiac index, heart rate, and blood
      pressure.[120] The net effect is a reduction in myocardial oxygen
      consumption per minute and per beat. Favorable effects of acute
      intravenous administration of beta blockers on the balance of
      myocardial oxygen supply and demand are reflected in reductions in
      chest pain, in the proportion of patients with threatened infarction
      who actually evolve STEMI, and in the development of ventricular
      arrhythmias.[121] Because beta-adrenergic blockade diminishes
      circulating levels of free fatty acids by antagonizing the lipolytic
      effects of catecholamines, and because elevated levels of fatty acids
      augment myocardial oxygen consumption and probably increase the
      incidence of arrhythmias, these metabolic actions of beta-blocking
      agents may also benefit the ischemic heart. Despite these favorable
      effects of early administration of intravenous beta blockers, there
      are potentially detrimental effects for some patients,[43] which have
      led to the modification of guidelines for early administration of
      intravenous beta blockers.[35]

      More than 52,000 patients have been randomized in clinical trials
      studying beta-adrenergic blockade in acute MI. These trials cover a
      range of beta blockers and timing of administration and were largely
      conducted in the era before reperfusion strategies were developed for
      STEMI. The available data in the prereperfusion era have suggested
      there were favorable trends toward a reduction in mortality,
      reinfarction, and cardiac arrest. However, in the reperfusion era, the
      addition of an intravenous beta blocker to fibrinolytic therapy was
      not associated with a reduction in mortality but was helpful in
      reducing the rate of recurrent ischemic events.[122] Concern arose
      regarding the potential risk of provoking cardiogenic shock if early
      intravenous followed by oral beta-adrenergic blockade was routinely
      administered to all patients with STEMI.[121] The largest trial
      testing beta blockade in patients with acute MI was COMMIT, which
      randomized 45,852 patients within 24 hours of MI to metoprolol given
      as sequential intravenous boluses of 5 mg, up to 15 mg, followed by
      200 mg/day orally or placebo.[43] There was no difference in the rate
      of the composite endpoint of death, reinfarction, or cardiac arrest in
      the metoprolol group (9.4%) compared with the placebo group (9.9%).
      But significant reductions occurred in reinfarction and episodes of
      ventricular fibrillation in the metoprolol group, translating into
      five fewer events for each of these endpoints per 1000 patients
      treated. However, there were 11 more episodes of cardiogenic shock in
      the metoprolol group per 1000 patients treated. The risk of developing
      cardiogenic shock, which was recorded as part of the COMMIT protocol
      in contrast to earlier studies, was greatest in those patients
      presenting with moderate to severe left ventricular dysfunction
      (Killip Class II or higher).

      Combining the results of the low-risk patients from COMMIT with the
      data from earlier trials, an overview of the effects of early
      intravenous therapy followed by oral beta blocker therapy can be seen
      (Fig. 55-24). There is a 13% reduction in all-cause mortality (7 lives
      saved/1000 patients treated), 22% reduction in reinfarction (5 fewer
      events/1000 patients treated), and 15% reduction in ventricular
      fibrillation or cardiac arrest (5 fewer events/1000 patients
      treated).[43] To achieve these benefits safely, it is important to
      avoid the early administration of beta blockers to patients with
      relative contraindications, as outlined in Table 55-8.



      FIGURE 55-24  Meta-analysis of effects of intravenous and then oral
      beta blocker therapy on death, reinfarction, and cardiac arrest during
      the scheduled treatment periods in 26 small randomized trials, MIAMI,
      ISIS-1, and the low-risk subset of COMMIT. For COMMIT, data are
      included only for patients who presented with systolic blood pressure
      105 mm Hg, heart rate > 65 beats/min, and Killip Class I (as in
      MIAMI). Five small trials included in the ISIS-1 report did not have
      any data on reinfarction. In the ISIS-1 trial, data on reinfarction in
      hospital were available for the last three quarters of the study,
      involving 11,641 patients. Odds ratios (ORs) in each (blue squares
      with area proportional to number of events) comparing outcome in
      patients allocated beta blockers to that in patients allocated
      controls, along with 99% CIs (horizontal line). Overall OR and 95% CI
      are indicated by diamonds.
      (From Chen ZM, Pan HC, Chen YP, et al: Early intravenous then oral
      metoprolol in 45,852 patients with acute myocardial infarction:
      Randomised placebo-controlled trial. Lancet 366:1622, 2005.)

      TABLE 55-8   -- Contraindications to Early Intravenous Beta Blocker
      Therapy in STEMI
         Signs of heart failure

         Evidence of a low-output state

         Increased risk for cardiogenic shock*


      * The more risk factors present, the higher the risk of developing
      cardiogenic shock: age older than 70 years, systolic blood pressure
      <120 mm Hg, sinus tachycardia >110 beats/min or heart rate <60
      beats/min, and increased time since onset of symptom of STEMI.


      Recommendations

      Given the evidence of the benefits of early beta blocker
      administration in STEMI, patients without a contraindication (see
      Table 55-8), irrespective of administration of concomitant
      fibrinolytic therapy or performance of primary PCI, should promptly
      receive oral beta blockers. It is also reasonable to administer
      intravenously beta blockers promptly to STEMI patients, especially if
      a tachyarrhythmia or hypertension is present, in the absence of signs
      of heart failure or low output, increased risk of developing shock,
      indicators of high risk of developing shock, or other relative
      contraindications to beta blockers.[35] We use metoprolol 5 mg
      intravenously every 2 to 5 minutes for three doses, provided the heart
      rate does not fall below 60 beats/min and the systolic blood pressure
      does not drop below 100 mm Hg. Oral maintenance dosing is initiated
      with metoprolol, 50 mg every 6 hours for 2 days, and then 100 mg twice
      daily.

      Beta blockers are especially helpful for patients in whom STEMI is
      complicated by persistent or recurrent ischemic pain, progressive or
      repetitive serum enzyme level elevations suggestive of infarct
      extension, or tachyarrhythmias early after the onset of
      infarction.[123] If adverse effects of beta blockers develop or if
      patients present with complications of infarction that are
      contraindications to beta blockade, such as heart failure or heart
      block, the beta blocker should be withheld. Unless there are
      contraindications (see Table 55-8), beta blockade probably should be
      continued in patients who develop STEMI.[35] Moreover, patients who
      initially have contraindications to a beta blocker, such as heart
      failure, should be reevaluated with respect to their candidacy for
      such therapy after 24 hours.

      Selection of Beta Blocker

      Favorable effects have been reported with metoprolol, atenolol,
      carvedilol, timolol, and alprenolol; these benefits probably occur
      with propranolol and with esmolol, an ultrashort-acting agent, as
      well. In the absence of any favorable evidence supporting the benefit
      of agents with intrinsic sympathomimetic activity, such as pindolol
      and oxprenolol, and with some unfavorable evidence for these agents in
      secondary prevention, beta blockers with intrinsic sympathomimetic
      activity probably should not be chosen for treatment of STEMI. The
      CAPRICORN trial randomized 1959 patients with MI and systolic
      dysfunction (ejection fraction < 40%) to carvedilol or placebo in
      addition to current pharmacotherapeutic agents, including
      angiotensin-converting enzyme (ACE) inhibitors in 98% of patients.
      All-cause mortality was reduced over a mean follow-up of 1.3 years
      from 15.3% in the placebo group to 11.9% in the carvedilol group (23%
      RR reduction; P = 0.031), with a similar pattern during the first 30
      days.[124] Thus, CAPRICORN confirms the benefit of beta blocker
      administration in addition to ACE inhibitor therapy for patients with
      transient or sustained left ventricular dysfunction after MI. An
      algorithm for the use of beta blockers in STEMI patients is shown in
      Figure 55-25.



      FIGURE 55-25  Algorithm for use of beta blockers in the treatment of
      patients with STEMI. COPD = chronic obstructive pulmonary disease; DM
      = diabetes mellitus; ER = extended release; HF = heart failure; PVD =
      peripheral vascular disease.
      (From Gheorghiade M, Goldstein S: Beta-blockers in the post-myocardial
      infarction patient. Circulation 106:394, 2002.)





      Occasionally, the clinician may wish to proceed with beta blocker
      therapy even in the presence of relative contraindications, such as a
      history of mild asthma, mild bradycardia, mild heart failure, or
      first-degree heart block. In this situation, a trial of esmolol may
      help determine whether the patient can tolerate beta-adrenergic
      blockade. Because the hemodynamic effects of this drug, with a
      half-life of 9 minutes, disappear in less than 30 minutes, it offers
      considerable advantage over longer acting agents when the risk of a
      beta blocker complication is relatively high.





      On 2/21/12, krin135@... <krin135@...> wrote:
      As Gene noted, that's enough to be clearly identifying information.

      Might want to seek advice of counsel if you are using personal equipment to
      transmit those images....

      Chuck


      In a message dated 02/20/12 21:45:50 Central Standard Time,
      christopher.watford@... writes:




      Our strips include the age, gender, and unit, which should be enough given
      pre-notification.


      -Christopher

      On Mon, Feb 20, 2012 at 10:41 PM, <_krin135@..._
      (mailto:krin135@...) > wrote:



      no, but you do need to be able to positively link the transmitted image
      with the patient on arrival...tad hard to do that if you have stripped all
      of
      the demographics off.

      ck




      In a message dated 02/20/12 21:37:28 Central Standard Time,
      _brandon@..._ (mailto:brandon@...)
      writes:


      Yes, thanks. Although I wonder if the HIPPA side couldn't be simplified  by
      just stripping transmitted strips of all patient identifiers. You don't
      need a name to recognize a STEMI.


      Brandon


      ***
      _http://degreesofclarity.com/_ (http://degreesofclarity.com/)
      _http://emsbasics.com/_ (http://emsbasics.com/)








      On Feb 20, 2012, at 10:26 PM, _krin135@..._ (mailto:krin135@...)
      wrote:






      sorry for the blank  post.

      you forgot one important point: Securability.

      Remember this is one place where HIPAA really does have teeth- the
      electronic transmission of medical records with identifiable patient
      information.

      Add in some of the questions about how well certain web/cloud  programs
      and providers handle en route and stored  security....

      and you really need to have a secure (HTTPS or VPN) linkage or the
      equivalent to send something like this over cell phone or web pad
      connections.

      ck
      Retired FM/EM/EMS Physician; Educator and Author


      In a message dated 02/20/12 20:08:05 Central Standard Time,
      _brandon@..._ (mailto:brandon@...)
      writes:


      I'm far from an expert, but I suspect the reasons are linked to  concerns
      like:


      -- Standardization. Even if it's not particularly important what  system is
      used, everyone does need to agree to use *one* system, a  goal which can be
      challenged by lack of cooperativity and  difficult-to-eradicate legacy
      hardware/software.


      -- Liability. When a system is put in place formally, the  hospitals and
      ambulance services are placing themselves behind its  functionality. This
      means they'll demand a lot from it, and THAT means  it's a big job -- one
      it's
      tempting to avoid until next year.


      -- Reliability. A casual system that works fine when it works is  great,
      but probably not adequate for a formal implementation. You need  to know
      that
      connections will be successfully established (you should  see the challenges
      we've faced with on-board computer-based ePCRs),  that it'll transmit
      quickly, that the results will have essentially  100% fidelity (imagine a
      bad
      call based on a transmission artifact),  and that nobody will get an error
      message or bluescreen. Big demands  considering that the system probably has
      five interacting components  and each is from a different manufacturer.


      Brandon


      ***
      _http://degreesofclarity.com/_ (http://degreesofclarity.com/)
      _http://emsbasics.com/_ (http://emsbasics.com/)








      On Feb 20, 2012, at 8:57 PM, David Baumrind wrote:




      For me, the issue is more that if the  technology (via iphone or anything
      else) is available to transmit  these ECG’s in seconds, why are we tethered
      by system which does not  make it easy or standardized to transmit and
      receive the ECGs.  I know in my system, the ECG takes a circuitous route
      from my
      monitor to med control.  I am using technology costing tens of  thousands of
      dollars, and in some cases with subscription fees, yet  can be outperformed
      by an iphone.  Is It a harbinger of  change?


      On 2/20/12 8:36 PM, "Ken Grauer" <ekgpress@...>  wrote:








      Brandon  - Understood - and I suspected this might be what was occurring.
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