Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

Safety and Effectiveness of Field Nitroglycerin in Patients with Suspected ST Elevation Myocardial Infarction

 

Is prehospital use of NTG (NiTroGlycerin; GTN GlycerylTriNitrate in Commonwealth countries) safe for treating prehospital suspected STEMI (ST segment Elevation Myocardial Infarction) patients?

The evidence is limited, but does not suggest that prehospital NTG produces enough harm to discourage use in suspected STEMI. These researchers looked at the emergency department assessments of patients following prehospital NTG for suspected STEMI.  

Despite the theoretical risk, the limited retrospective studies of NTG in the prehospital setting for multiple indications suggest that the medication is safe.(10-13) However, with regard to NTG use for STEMI, the AHA International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care concluded that there was not enough evidence to determine the benefit or harm of out-of-hospital use of NTG.(14) Given the high false positive rates for STEMI identified in the field, an additional concern is that many patients treated with NTG for presumed STEMI will ultimately have an alternate etiology for their pain.(15, 16) Therefore, it is not clear that the benefits outweigh the risks of administering NTG to all patients with suspected STEMI in the field.[1]
 

This paper helps to show the safety of prehospital NTG for suspected STEMI, providing evidence that blood pressure changes were similar in suspected STEMI patients with an SBP (Systolic Blood Pressure) of 100, or higher, regardless of whether they were treated with NTG. The study is a retrospective chart review, so we do not know why some of the patients were not treated with NTG.

One reason mentioned, but not discussed, is that only 22% (96 of 440) suspected STEMI patients not treated with NTG are documented to have had pain, but there is no information on the type of pain or other cardiac symptoms of the patients. Were the paramedics avoiding treating atypical chest pain, such as pressure, heaviness, gastric discomfort, difficulty breathing, et cetera? We do not know. Was only chest pain being documented, rather than shoulder, or arm, or jaw, pain? We do not know. Did the pain resolve prior to EMS arrival? We do not know. Were the paramedics correctly recognizing when the machine interpretation of the ECGs (ElectroCardioGrams) were wrong? We do not know.

The median Initial Pain Score is documented as 8, with an IQR (Inter-Quartile Range) of 5-9 for those treated with NTG. For those not treated with NTG the Initial Pain Score is documented as 0, with an IQR of 0-0. We do not know the Initial Pain Score of those who did have pain, but were not treated with NTG. All of these patients were in an IQR that was not documented in the paper. The good news is that the suspected STEMI patients not treated with NTG act as a control group, although possibly with important differences that are not discussed in the paper.

Click on the image of the LA County protocol to make it larger.[2]

What about the 17% of suspected STEMI patients with SPB <100 mmHg who were treated with NTG?

Was medical command (California has certified MICNs [Mobile Intensive Care Nurses] providing medical command on the radio, with physicians available, as well) contacted for authorization to deviate from the protocol? If so, that is something that should be documented in the charts, which were reviewed for this paper. That information is not included in this paper. Those patients are much more interesting to me.

I do not object to using NTG to treat suspected STEMI with an SBP below 100 mmHg, but the authors seem to think that EMS should not even consider it. Do the outcomes of those patients support the approach of the authors? We do not know.

I suspect that the fears of bottoming out the blood pressure are very exaggerated, but it would be nice to have some evidence either way.

An important secondary end point was the differences between those with inferior/right ventricular STEMI, but treated with NTG.  

By vasodilating all blood vessels, and the venous system in particular, it causes a drop in blood pressure and preload. Thus, there is concern for precipitating hypotension in ACS involving the right ventricle.(1-3) Contraindications to the use of NTG, as outlined by the American Heart Association (AHA) Guidelines on the treatment of ACS, include right ventricular infarction.(4) This raises concern for use in inferior ST-segment elevation myocardial infarction (STEMI) in the prehospital setting, since many inferior STEMI result from proximal right coronary artery (RCA) occlusion and 50% involve the right ventricle.(3) Traditional 12-lead ECG is focused mainly on the left side of the heart and typically EMS protocols do not include acquisition of right-sided ECG leads. Further, in many systems, Basic Life Support (BLS) protocols allow for administration of NTG without differentiating the location of STEMI. There is also risk of other adverse events including bradycardia and cardiac arrest.(5-9)[1]
 

I have aggressively promoted the use of NTG for even hypotensive CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure). Many physicians are not comfortable with that, even though the available evidence shows that aggressive IV NTG doubled the survival rate for these hypotensive patients. More research is needed on the use of NTG, especially in hypotensive patients.  

Further, we did not find an increased risk of hypotension among patients with proximal or mid RCA occlusions confirmed on coronary angiography. There are several possible reasons for our findings. First, while right ventricular involvement in inferior STEMI is common, hemodynamic instability is actually rare due to the right ventricle’s more favorable oxygen supply-demand ratio compared to the left heart and more extensive collateral flow.(3, 22) In addition, left heart occlusions may also involve the right ventricle and result in a preload dependent condition.(23-25) While limited by sample size, our results suggests that specifically avoiding NTG use in inferior STEMI, which is common in EMS systems, may be misguided. One quarter of the local EMS agencies in the state of California, for example, currently prohibit the use of NTG in inferior STEMI.(26) This analysis would benefit from additional study with a larger sample size and specific information about the infarct territory. Further studies are needed to determine which patients, in particular, are at increased risk for hypotension when treated with NTG.[1]
 

Perhaps NTG is also safe for treating patients with inferior ischemia and even right ventricular ischemia.

Footnotes:

[1] Safety and Effectiveness of Field Nitroglycerin in Patients with Suspected ST Elevation Myocardial Infarction.

Bosson N, Isakson B, Morgan JA, Kaji AH, Uner A, Hurley K, Henry TD, Niemann JT.

Prehosp Emerg Care. 2018 Dec 17:1-9. doi: 10.1080/10903127.2018.1558318. [Epub ahead of print]

PMID: 30556765

[2] Treatment Protocol: Chest Pain */ Acute MI

Reference No. 1244

LA County Paramedic Protocols

Los Angeles County Department of Health Services – Emergency Medical Services

Protocol

.

ILCOR wants the appearance of public comments with less than half the substance

 

The International Liaison Committee on Resuscitation (ILCOR) shows its priorities in the way it handles its problem with public comments.
 

Last week ILCOR posted the two new draft CoSTRs listed below for public comment. It became apparent that the commenting link was broken and those who visited the site could not comment. We apologize for the inconvenience. The commenting link is now fixed and we invite you to comment at ilcor.org/costr.

  • Advanced Airway Management During Adult Cardiac Arrest
  • Vasopressors in Adult Cardiac Arrest
  • As a reminder, the public comment period will close on 4 April 2019.[1]

     

    ILCOR made a mistake that prevented public comments from being submitted for most of the public comment period.

    ILCOR is so interested in your public comments that they have decided to send out an email to let people know that they have the same drop dead date for the comments as before, but this time they might actually be able to get the comments to work. Maybe.

    The lack of evidence of benefit of epinephrine (adrenaline in Commonwealth countries) has lasted over half a century, so what is the rush to get these new guidelines out?

    There is only one outcome that matters – survival without severe brain damage.
     


     

    ILCOR evaluates 23 outcomes.

    ILCOR considers 15 of these outcomes critical, but they are really just 5 outcomes, with some of them repeated over different rhythms. These are (in increasing order of importance to the only one that matters):

    1. For the critical outcome of survival to hospital discharge, 2. For the critical outcome of survival at 3 months, 3. For the critical outcome of favorable neurologic outcome at hospital discharge, 4. For the critical outcome of survival with unfavorable neurologic outcome at 3 months, 5. For the critical outcome of favorable neurologic outcome at 3 months,

    Many of them are repeated for each cardiac arrest rhythm or for each vasopressor, or vasopressor cocktail:

    1. Epinephrine plus vasopressin compared to epinephrine only – Any rhythm 2. Initial vasopressin compared to initial epinephrine – Any rhythm 3. Epinephrine compared to placebo – Non-shockable rhythms 4. Epinephrine compared to placebo – Shockable rhythms 5. Epinephrine compared to placebo – Any initial rhythm

    There is only one outcome that matters – survival without severe brain damage.

    There is only one study that was large enough to answer this:
     

    CONCLUSIONS
    In adults with out-of-hospital cardiac arrest, the use of epinephrine resulted in a significantly higher rate of 30-day survival than the use of placebo, but there was no significant between-group difference in the rate of a favorable neurologic outcome because more survivors had severe neurologic impairment in the epinephrine group.[2]

     

    If the people at ILCOR really think that epinephrine is beneficial in cardiac arrest, they should encourage a much larger study.

    There were 4,000 patients in each group – 4,000 placebo and 4,000 epinephrine.

    Maybe with 8,000 patients in each group, the ever decreasing “trend toward better outcome” will reach significance. Maybe it will be shown to be just another insignificant appearance of a “trend” that is the result of having so few survivors to compare.

    There were only 161 survivors without severe brain damage out of 8,000 cardiac arrest patients – 74 placebo and 87 epinephrine.

    Those resuscitated before receiving epinephrine/placebo were excluded from the study, so this is not a case of EMS that only has a 2% resuscitation rate. The focus on epinephrine is a focus on the patients least likely to be resuscitated and a focus on counterproductive outcomes.

    Almost all of our good outcomes (without severe brain damage) will be without epinephrine, because these resuscitations happen before epinephrine can be give by even the most aggressive epi enthusiast.

    What we are doing is making excuses for memorizing ineffective interventions and requiring their application is a specific way, in order to determine the quality of care. We are promoting fantasy.

    We learned that distracting from the quality of chest compressions is the most deadly thing we can do in resuscitation.

    CPR = only chest compressions – the exception is when the arrest is believed to be due to a respiratory event, such as when the Smurf sign or a respiratory/choking history is present. Chest compressions provide all of the pulmonary resuscitation that a human needs for a non-respiratory event and the respiratory events are not easily missed.

    Why require a whole bunch of skills be applied for such a tiny portion of good outcomes among cardiac arrest patients?

    Why not give up on requiring these skills when the evidence makes it clear that there is no benefit?

    All we are doing is adding cognitive load to make us feel like we are doing something special.

    We could learn something that actually benefits patients, such as how to assess patients when giving high-dose NTG (NiTroGlycerin or GTN GlycerylTriNitrate in Commonwealth countries) for even hypotensive CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure), where we can make much more of a difference and prevent cardiac arrest, but we don’t.[3],[4],[5]
     


     

    Cognitive load is not just a problem for paramedics and nurses, or med/surg doctors, but also for emergency physicians:

    Cognitive Load and the Emergency Physician
    April 12, 2016
    James O’Shea
    emDocs
    Article

    Why are we distracting everyone from things that do improve the only outcome that matters, in order to promote things that do not improve any outcome that matters?

    Here is what I wrote –
     

    The primary source for the recommendation to keep things the same is a brand new study – PARAMEDIC2.

    This showed no statistically significant improvement in the only outcome that matter – survival without severe brain damage.

    A larger study might show that there is a real improvement – or it may put the epi hypothesis out of its misery.

    I will eventually have a cardiac arrest. If I am resuscitated, whom will ILCOR send to change my diaper, and attend to the other things I can no longer attend to?

    We need evidence of a significant benefit in order to justify distracting everyone from interventions that actually do improve survival without severe brain damage.

    .

     

    The commenting link is now fixed and we invite you to comment at ilcor.org/costr

    Maybe they will pay attention. Dr. Rory Spiegel of EM Nerd has a detailed comment that is also critical of ILCOR’s proposed “strong recommendation” of epinephrine.

    Footnotes:

    [1] Vasopressors in Adult Cardiac Arrest
    Time left for commenting: 11 days 15:49:49
    ILCOR staff
    Created: March 21, 2019 · Updated: March 21, 2019
    Draft for public comment
    Consensus on Science with Treatment Recommendations (CoSTR)
    Vasopressors in Adult Cardiac Arrest page for comments until April 04, 2019 at 06:00 Eastern Time

    [2] A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest.
    Perkins GD, Ji C, Deakin CD, Quinn T, Nolan JP, Scomparin C, Regan S, Long J, Slowther A, Pocock H, Black JJM, Moore F, Fothergill RT, Rees N, O’Shea L, Docherty M, Gunson I, Han K, Charlton K, Finn J, Petrou S, Stallard N, Gates S, Lall R; PARAMEDIC2 Collaborators.
    N Engl J Med. 2018 Aug 23;379(8):711-721. doi: 10.1056/NEJMoa1806842. Epub 2018 Jul 18.
    PMID: 30021076

    Free Full Text from N Engl J Med.
     

    In a Bayesian analysis that used an assumption of no benefit from adrenaline, the posterior probability that the absolute rate of survival was at least 1 percentage point higher in the epinephrine group than in the placebo group was 37% (Fig. S3 in the Supplementary Appendix). The probability that the absolute survival rate was at least 2 percentage points higher was 0.2%. With respect to the rate of survival with a favorable neurologic outcome at hospital discharge, the probabilities that the rate was at least 1 or 2 percentage points higher with epinephrine were 1.9% and 0%, respectively (Fig. S4 in the Supplementary Appendix).

     

    The probability of a good outcome (no severe brain damage) is not improved with epinephrine.

    If we want to improve outcomes, we need to look elsewhere, because there is nothing to be gained with epi.

    [3] Intravenous nitrates in the prehospital management of acute pulmonary edema.
    Bertini G, Giglioli C, Biggeri A, Margheri M, Simonetti I, Sica ML, Russo L, Gensini G.
    Ann Emerg Med. 1997 Oct;30(4):493-9.
    PMID: 9326864 [PubMed – indexed for MEDLINE]

    [4] Unreasonable Fear of Hypotension and High-Dose NTG – Part I
    Thu, 29 Aug 2013
    Rogue Medic
    Article

    [5] Unreasonable Fear of Hypotension and High-Dose NTG – Part II
    Wed, 04 Sep 2013
    Rogue Medic
    Article

    .

    This Rhythm is Hilarious

     


    Click on the image to make it larger.
     

    Apparently, the second 12 lead was after 150 mg of amiodarone. The hilarity is the amiodarone.

    I received this in an email. It is reported to have been posted on Facebook, but I choose not to have access to Facebook, so I do not have any more details. I am occasionally tempted to set up an account again, but I generally prefer intentional comedy.

    Everything you need to know is in the first 12 lead.

    Things that do not matter:

    Distance to the hospital.

    Time of onset.

    Last meal.

    National Registry certification.

    Et cetera.

    .

    Why do people deny they are having heart attacks? NSFW language in video

     

    Why is this NSFW (Not Safe For Work)? Because some of the language in the video is not appropriate for some workplaces.

    Why have Keven Smith talk about a heart attack?

    Because we generally do not get an opportunity to have the patient explain what they were thinking while they were having the heart attack. We have to negotiate with the patient to be able to assess the medical condition properly, but we don’t usually have the time to have an extended discussion about why the patient is not feeling cooperative.
     


     

    When did he realize that his significant family history of heart disease was causing his problems? Apparently, not until after the words heart attack were used by EMS.

    How can people try to deny that the chest pressure, difficulty breathing, diaphoresis, nausea, et cetera are not a heart attack? Because it is natural for our species to assume either of two extremes – that bad things happen to other people or that bad things always happen to me. We are not good at being reasonable.

    I had a cardiologist as a patient. He had the same presentation.

    I was able to show him 9 of the 12 leads (not the augmented leads, because we did not have a 12 lead capable monitor). He admitted that the ST segment elevation was consistent with an acute myocardial infarction. He refused to leave.

    As a cardiologist, he could easily explain that he understood cardiology better than I do, and therefore did understand the gravity of the situation.

    He was answering all questions appropriately.

    He felt that he would ruin the event he was attending if he left in an ambulance. His shirt was covered with what had been the contents of his stomach an little earlier. Nobody suggested that he should stay at the event.

    Some men you just can’t reach.

    How do you get someone to accept reality, when he adamantly insist that his opinion is real and that the evidence is wrong?

    We did not end up back at that location the rest of the night and nobody else was dispatched to that location, so it appears that he did not drop dead right away. Beyond that, I don’t know. Maybe he was smart enough to see a fellow cardiologist soon after. Maybe it was something other than a heart attack. If it was a heart attack, maybe it was minor.

    .

    Cardiac arrest victim Trudy Jones ‘given placebo’ – rather than experimental epinephrine

     

    As part of a study to find out if epinephrine (adrenaline in Commonwealth countries) is safe to use in cardiac arrest, a patient was treated with a placebo, rather than the inadequately tested drug. Some people are upset that the patient did not receive the drug they know nothing about.[1]

    The critics are trying to make sure that we never learn.

    We need to find out how much harm epinephrine causes, rather than make assumptions based on prejudices.

    When used in cardiac arrest, does epinephrine produce a pulse more often?

    Yes.

    When used in cardiac arrest, does epinephrine produce a good outcome more often?

    We don’t know.

    In over half a century of use in cardiac arrest, we have not bothered to find out.
     


     

    We did try to find out one time, but the media and politicians stopped it.[2]

    We would rather harm patients with unreasonable hope, than find out how much harm we are causing to patients.

    We would rather continue to be part of a huge, uncontrolled, unapproved, undeclared, undocumented, unethical experiment, than find out what works.

    Have we given informed consent to that kind of experimentation?

    Ignorance is bliss.

    The good news is that the enrollment of patients has finished, so the media and politicians will not be able to prevent us from learning the little that we will be able to learn from this research.[3]

    Will the results tell us which patients are harmed by epinephrine?

    Probably not – that will require a willingness to admit the limits of what we learn and more research.

    What EMS treatments have been demonstrated to improve outcomes from cardiac arrest?

    1. High quality chest compressions.
    2. Defibrillation, when indicated.

    Nothing else.

    All other treatments, when tested, have failed to be better than nothing (placebo).

    Footnotes:

    [1] Cardiac arrest victim Trudy Jones ‘given placebo’
    BBC News
    23 March 2018
    Article

    [2] Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
    Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL.
    Resuscitation. 2011 Sep;82(9):1138-43. Epub 2011 Jul 2.
    PMID: 21745533 [PubMed – in process]

    Free Full Text PDF Download from semanticscholar.org
     

    This study was designed as a multicentre trial involving five ambulance services in Australia and New Zealand and was accordingly powered to detect clinically important treatment effects. Despite having obtained approvals for the study from Institutional Ethics Committees, Crown Law and Guardianship Boards, the concerns of being involved in a trial in which the unproven “standard of care” was being withheld prevented four of the five ambulance services from participating.

     

    In addition adverse press reports questioning the ethics of conducting this trial, which subsequently led to the involvement of politicians, further heightened these concerns. Despite the clearly demonstrated existence of clinical equipoise for adrenaline in cardiac arrest it remained impossible to change the decision not to participate.

     

    [3] Paramedic2 – The Adrenaline Trial
    Warwick Medical School
    Trial Updates
     

    Trial Update – 19 February 2018:
    PARAMEDIC2 has finished recruitment and we are therefore no longer issuing ‘No Study’ bracelets. The data collected from the trial is in the process of being analysed and we expect to publish the results in 2018. Once the results have been published, a summary will be provided on the trial website.

     

    Edited 12-27-2018 to correct link to pdf of Jacobs study in footnote 2.

    .

    Is placebo better than aggressive medical treatment for patients NOT having a heart attack?

    Also to be posted on ResearchBlogging.org when they relaunch the site.
     

    Is cardiac catheterization placebo better than aggressive medical treatment for patients not having a heart attack?

    No.
     

    The answer is not really different from before. This should not be surprising for anyone who pays attention to EBM (Evidence-Based Medicine). We should all pay attention to EBM, because it is the best way to find out what works.

    Many routine treatments are not beneficial to patients, but are considered to be standards of care. We continue to give these treatments out of unreasonable optimism, a fear of litigation, or fear of criticism for not following orders. The difference between the banality of evil and the banality of incompetence does not appear to be significant in any way that matters.

    PCI (Percutaneous Coronary Intervention) treatment does not add any benefit – unless you are having a heart attack.

    The placebo group received sham PCI in addition to optimized medical treatment. this did not provide any benefit over actual PCI in addition to optimized medical treatment. The patients in the placebo group received all of the same medications that the patients in the PCI group received.

    Why is this news today?

    A recent article in The Lancet is encouraging snake oil salesmen and snake oil saleswomen to claim that it shows the miracle healing power of placebos, but this is not true.

    Apparently, Big Placebo (the multi-billion dollar alternative medicine industry) is trying to use this to promote their scams (homeopathy, acupuncture, Reiki, naturopathy, prayer, . . . ).

    Big Placebo seems to think that this study shows that placebo is better than medical treatment. A placebo is an inactive intervention that is undetectable when compared with the active treatment. The placebo group received the same aggressive medications that the treatment group received.
     

    All patients were pretreated with dual antiplatelet therapy. In both groups, the duration of dual antiplatelet therapy was the same and continued until the fial (unblinding) visit. Coronary angiography was done via a radial or femoral arterial approach with auditory isolation achieved by placing over-the-ear headphones playing music on the patient throughout the procedure.[1]

     

    What is new about this?

    A much larger study a decade ago showed that aggressive medical therapy was as good as PCI and aggressive medical therapy. The difference is the use of sham PCI to create a placebo group for comparison, rather than using a No PCI group for comparison.
     

    CONCLUSIONS:
    As an initial management strategy in patients with stable coronary artery disease, PCI did not reduce the risk of death, myocardial infarction, or other major cardiovascular events when added to optimal medical therapy.
    [2]

     

    Compare that with the conclusion (interpretation) of the new paper.
     

    INTERPRETATION:
    In patients with medically treated angina and severe coronary stenosis, PCI did not increase exercise time by more than the effect of a placebo procedure. The efficacy of invasive procedures can be assessed with a placebo control, as is standard for pharmacotherapy.
    [1]

     

    The unfortunate outcome is that we will have fewer hospitals providing PCI, so patients with heart attacks (STEMI – ST segment Elevation Myocardial Infarctions) may have to wait longer for emergency PCI, which really does improve outcomes.
     

    What other Standards Of Care are NOT supported by valid evidence?

    Amiodarone is effective for cardiac arrest, whether unwitnessed, witnessed, or witnessed by EMS.

    Kayexalate (Sodium Polystyrene) is a good treatment for hyperkalemia. Anything that causes diarrhea will lower your potassium level, but that does not make it a good treatment, unless you are in an austere environment (in other words – not in a real hospital).

    Amiodarone is effective for VT (Ventricular Tachycardia).

    Backboards are effective to protect against spinal injury while transporting patients.

    Blood-letting is effective for anything except hemochromatosis (and some rare disorders).

    More paramedics are better for the patient.

    Prehospital intravenous lines save lives.

    IV fluid saves lives in hemorrhagic shock.

    Oxygen should be given to everyone having a heart attack.

    The Golden Hour is important.

    Driving fast saves lives. For only some rare conditions, it probably does – and that depends on traffic.

    Flying people to the hospital saves lives. Again, for only some rare conditions, it probably does – and that depends on traffic and distance.

    Tourniquets are dangerous. As with anything else, if used inappropriately, they are dangerous, but tourniquets save lives.

    Prehospital intubation saves lives.

    Ventilation in cardiac arrest improves outcomes (other than for respiratory causes of cardiac arrest, which are easy to identify).

    Epinephrine improves outcomes in cardiac arrest. It does produce a pulse more often, but at what cost to the long-term survival of the patient and the patient’s brain? PARAMEDIC2 should help us to identify which patients benefit from epinephrine, since it is clear that many patients are harmed by epinephrine in cardiac arrest. If we limit treatment to patients reasonably expected to benefit from the treatment, we can improve long-term survival.

    And there are many more.

    Footnotes:

    [1] Percutaneous coronary intervention in stable angina (ORBITA): a double-blind, randomised controlled trial.
    Al-Lamee R, Thompson D, Dehbi HM, Sen S, Tang K, Davies J, Keeble T, Mielewczik M, Kaprielian R, Malik IS, Nijjer SS, Petraco R, Cook C, Ahmad Y, Howard J, Baker C, Sharp A, Gerber R, Talwar S, Assomull R, Mayet J, Wensel R, Collier D, Shun-Shin M, Thom SA, Davies JE, Francis DP; ORBITA investigators.
    Lancet. 2017 Nov 1. pii: S0140-6736(17)32714-9. doi: 10.1016/S0140-6736(17)32714-9. [Epub ahead of print]
    PMID: 29103656

    [2] Optimal medical therapy with or without PCI for stable coronary disease.
    Boden WE, O’Rourke RA, Teo KK, Hartigan PM, Maron DJ, Kostuk WJ, Knudtson M, Dada M, Casperson P, Harris CL, Chaitman BR, Shaw L, Gosselin G, Nawaz S, Title LM, Gau G, Blaustein AS, Booth DC, Bates ER, Spertus JA, Berman DS, Mancini GB, Weintraub WS; COURAGE Trial Research Group.
    N Engl J Med. 2007 Apr 12;356(15):1503-16. Epub 2007 Mar 26.
    PMID: 17387127

    Free Full Text from N Engl J Med.

    .

    Normal Sinus Rhythm is Not a Good Description

    What is the rhythm 1a
     

    Is Normal Sinus Rhythm a good description of this rhythm?

    Is it sinus?

    Is it normal?

    Dr. Steven Novella writes about normal and some of the meanings of normal.
     

    This findings, if confirmed, has several implications. First, it is just good to know how our brains typically work. “Normal” is a combined judgment about what is actually happening and what “should” be happening. This confirms what was observed in health care, especially psychiatry, that there is a moral judgment in deciding what is normal.[1]

     

    Too often, we seem to try to apply what we think something should be to our mistaken description of what something is.

    As an example, an ECG (ElectroCardioGram) showing a regular, or slightly irregular, sinus rhythm is often described using the misleading term normal sinus rhythm.

    Normal suggests that there is nothing wrong with the rhythm, or with the heart, when it is not unusual for a patient to have a heart attack with a normal sinus rhythm being accurately displayed on the ECG.

    We are subconsciously telling ourselves, Nothing to see here. Move along.

    We are fooling ourselves and discouraging investigation of what may be causing problems by unnecessarily adding the term normal.

    In this setting, normal does not add any information, but suggests that we know more than we actually know.

    Why lie to ourselves?

    Because we trust ourselves and don’t bother to check our assumptions to see if they are valid.
     

    What is the rhythm 1
     

    It is clearly sinus, but what information do we add by calling it normal?

    Footnotes:

    [1] What Is Normal?
    Steven Novella
    Feb 02, 2017
    Neurologica
    Article

    .

    Valsalva the SVT or Shock the Monkey?


     

    The Skeptics’ Guide to Emergency Medicine should be on your podcast list. The podcasts are short, so there is not much reason to avoid them. This one is 13 minutes.

    Valsalva for SVT (SupraVentricular Tachycardia) is supposed to come before medication. At least that is the order of treatments of every EMS SVT protocol I have seen. Since medicine is expected to have more, and more serious, side effects, this is reasonable.

    What medicines?

    Adenosine has the side effects of –
     

    Cardiovascular

    Prolonged asystole, ventricular tachycardia, ventricular fibrillation, transient increase in blood pressure, bradycardia, atrial fibrillation, and Torsade de Pointes

    Respiratory

    Bronchospasm

    Central Nervous System

    Seizure activity, including tonic clonic (grand mal) seizures, and loss of consciousness.[1]

     

    It appears to be reasonable to try to avoid those side effects.

    Too much of this could become more of a problem than an SVT.
     


    Click on images to make them larger. Image credit.[2] This is not the actual strip, but a strip of an adenosine pause edited to produce more asystole, which I have seen.
     

    The side effect becomes much more of a problem when someone decides to treat the side effect, rather than wait for it to wear off.

    We SLAM adenosine in because it wears off quickly. A minute, or two, of asystole is not a problem.

    Giving a dose of epinephrine to a patient who had an SVT a minute ago and now has adenosine quickly wearing off – that may be a fatal problem.

    But how effective is the Valsalva maneuver (VM)?
     

    The VM is a non-invasive way to convert patients from SVT to sinus.It increases myocardial refractory period by increasing intrathoracic pressure thus stimulating baroreceptors in the aortic arch and carotid bodies Increases vagal tone (parasympathetic).[3]

     

    Here is a big problem with the use of the Valsalva maneuver. It is just one method of attempting to stimulate the vagus nerve.

    There are many other methods and they may be more successful. Carotid sinus massage (after auscultation for bruits), facial immersion in ice water (assuring that the airway does not become a problem), bearing down, blowing through a straw (even better may be a swizzle stick), digital circumferential sweep of the anus, coughing, . . . .

    There are many ways of activating the vagal nerve, but my favorite is to act as if I have not started an IV before, go very s l o w l y with the insertion of the largest IV catheter I think I can get in the vein, and this has almost always broken the rhythm.

    Yes, that is anecdotal, but I have only rarely needed to follow that with medication.

    Yes, pain is not a nice thing, but it is much nicer than the side effects listed above.
     

    Bottom Line: There is no standardized methods to perform a VM to terminate uncomplicated SVT that are evidence based.

    Clinical Application: VM is a viable technique that is poorly researched for the conversion of SVT and should not be considered essential to attempt prior to chemical cardioversion.[2]

     

    We need better vagal maneuvers.

    We need good evidence on what works.
     

    Go read the article and listen to the podcast.
     

    Footnotes:

    [1] ADENOCARD (adenosine) solution
    [Astellas Pharma US, Inc.]

    DailyMed
    FDA Label

    [2] Atrioventricular Re-entrant Tachycardia
    Thumbnail Guide to Congenital Heart Disease
    edited version of their adenosine ECG strip
    Article

    [3] SGEM#67: Shock the Monkey Tonight (Valsalva Maneuver for SVT)
    Podcast Link: SGEM67
    Date: March 23, 2014
    Skeptics’ Guide to Emergency Medicine
    Article and link to podcast

    .