STEMI Limitations

STEMI Limitations

In 2000, the ST-Elevation Myocardial Infarction (STEMI) paradigm revolutionized the management of Acute Coronary Syndrome (ACS), substituting the previous dichotomy between Q-wave versus non-Q wave myocardial infarcts (MI). Subcategorizing aimed to predict completely occluded arteries and the need for immediate intervention, namely, emergent cardiac catheterization to open an occluded coronary artery in STEMI. However, literature has shown that STEMI and occlusion myocardial infarction (OMI) are not interchangeable, with clear evidence of benefit from early reperfusion in both entities. Moreover, definitions STEMI and Non-ST-elevation myocardial (NSTEMI) can miss a large proportion of acute coronary occlusions; STEMI as a category can miss 30% of occlusion MI up to 50% in left circumflex, and NSTEMI was only associated with total MI in a quarter of cases.

As any Emergentologist at any level can relate, it was only recently when my ED held a morbidity and mortality meeting for a presumably delayed cath lab activation. The patient had all the risk factors, a typical chest pain which resolved in the ED, normal vitals and an ECG that didn’t meet the STEMI criteria; however, when he went for urgent angiography, the LAD was totally occluded.

A new paradigm: OMI vs. NOMI

The OMI manifesto, introduced by Dr Stephen Smith, Dr Pendell Myers, and Dr Scott Weingart might provide a better solution in the management of ACS. The fundamental question is: Does the patient have an acute coronary occlusion that would benefit from immediate intervention? Based on this question, the following diagram was suggested to substitute STEMI versus NSTEMI paradigm. The manifesto also contains rules to diagnose acute MI in certain categories of patients, such as patients with left bundle branch block (LBBB), left ventricular paced rhythm, terminal QRS distortion, normal ST-elevation vs. left anterior descending artery (LAD) occlusion, anterior ventricular aneurysm vs. acute MI, ST depression in aVL.

Basic concepts

ACS is a spectrum of clinical presentations divided into STEMI, NSTEMI and unstable angina, based on ECG findings and cardiac markers. The American Heart Association/American College of Cardiology (AHA/ACC) and European Society of Cardiology (ESC) define STEMI as new ST elevation at the J point in the absence of LV hypertrophy or LBBB in at least 2 contiguous leads. The elevation must be at least 2 mm (0.2 mV) in men or 1.5 mm (0.15 mV) in women in leads V2–V3 and/or 1 mm (0.1 mV) in other contiguous chest leads or the limb leads.

AHA/ACC recommends primary percutaneous coronary intervention (PCI) for patients with STEMI and ischemic symptoms of less than 12 hours’ duration. In NSTEMI, the recommendation is to perform urgent/immediate angiography with revascularization if appropriate in patients who have refractory angina or hemodynamic or electrical instability.

A meta-analysis of 46 trials with a total of 37 757 patients, including data from the International Study of Comparative Health Effectiveness with Medical and Invasive Approaches (ISCHEMIA) and Complete versus Culprit-Only Revascularization Strategies to Treat Multi-vessel Disease after Early PCI for STEMI (COMPLETE) trials demonstrated that PCI prevents death, cardiac death, and MI in patients with unstable coronary artery disease (CAD). The study defined unstable CAD as post-MI patients who haven’t received reperfusion therapy, multi-vessel disease following STEMI, non–ST-segment–elevation acute coronary syndrome.

STEMI Equivalents

For patients with persistent chest pain, hemodynamic instability and certain patterns of EKGs, it’s advisable to consider immediate/urgent PCI. The following patterns were found consistent with total occlusion or critical ischemia of the coronaries so every Emergentologist should familiarize her/himself with those: (All displayed ECGs are from Life in the Fast Lane ECG library)

De Winter T-wave: LAD occlusion.

Prominent T wave with upsloping ST depression in precordial leads
Prominent T wave with upsloping ST depression in precordial leads. https://litfl.com/de-winter-t-wave-ecg-library/

Wellen's Syndrome: Severe proximal LAD stenosis.

Biphasic or deep inverted T waves in V2 V3
Biphasic or deep inverted T waves in V2 V3 https://litfl.com/wellens-syndrome-ecg-library/

LBBB with positive Sgarbossa criteria

New LBBB without meeting Sgarbossa criteria is not considered an indication for cath lab activation any longer. Smith modified Sgarbossa criteria are:

  • Concordant ST elevation ≥ 1 mm in ≥ 1 lead
  • Concordant ST depression ≥ 1 mm in ≥ 1 lead of V1-V3
  • Proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the preceding S-wave

Positive Sgarbossa criteria in ventricular paced rhythm

Posterior MI: Left Circumflex (LCx) Artery or right coronary artery (RCA) occlusion

Infero-lateral STEMI with ST depression in V1 to V4 suggesting posterior MI
Infero-lateral STEMI with ST depression in V1 to V4 suggesting posterior MI https://litfl.com/posterior-myocardial-infarction-ecg-library/
Same patient with posterior EKG showing ST elevation in posterior leads
Same patient with posterior EKG showing ST elevation in posterior leads https://litfl.com/posterior-myocardial-infarction-ecg-library/

Right Ventricular MI: Complicates inferior STEMI, RCA occlusion

ST elevation in V1, ST elevation in III more than II
ST elevation in V1, ST elevation in III more than II https://litfl.com/right-ventricular-infarction-ecg-library/

ST elevation in aVR with diffuse ST depression: Left Main Coronary Artery (LMCA), proximal LAD, or triple vessel occlusion

ST elevation in aVR with diffusion ST depression
ST elevation in aVR with diffusion ST depression https://litfl.com/st-elevation-in-avr/

ST depression and T-wave inversion in aVL: RCA, LCx, or LAD occlusion

Reciprocal ST depression in avL
Reciprocal ST depression in avL https://litfl.com/inferior-stemi-ecg-library/

Hyperacute T-waves: LCx occlusion

Broad asymmetrical T wave
Broad asymmetrical T wave https://litfl.com/t-wave-ecg-library/

References and Further Reading

  • Amsterdam, E. A., Wenger, N. K., Brindis, R. G., Casey, D. E., Ganiats, T. G., Holmes, D. R., … & Zieman, S. J. (2014). 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes. Journal of the American College of Cardiology, 64(24), e139-e228.
  • Chacko, L., P. Howard, J., Rajkumar, C., Nowbar, A. N., Kane, C., Mahdi, D., … & Ahmad, Y. (2020). Effects of percutaneous coronary intervention on death and myocardial infarction stratified by stable and unstable coronary artery disease: a meta-analysis of randomized controlled trials. Circulation: Cardiovascular Quality and Outcomes, 13(2), e006363.
  • Coven, D. L. (2020). Acute Coronary Syndrome. Retrieved April 9, 2021, from https://emedicine.medscape.com/article/1910735-overview
  • Khan, A. R., Golwala, H., Tripathi, A., Bin Abdulhak, A. A., Bavishi, C., Riaz, H., … & Bhatt, D. L. (2017). Impact of total occlusion of culprit artery in acute non-ST elevation myocardial infarction: a systematic review and meta-analysis. European heart journal, 38(41), 3082-3089.
  • Kreider, D., Berberian, J. (2019). STEMI Equivalents: Can’t-Miss Patterns. EMResident. Retrieved April 9, 2021, from https://www.emra.org/emresident/article/stemi-equivalents/
  • Life in the Fast Lane. (n.d.). ECG Library. Retrieved April 9, 2021, from https://litfl.com/ecg-library/
  • Meyers, P. (2018). Guest Post – Down with STEMI – The OMI Manifesto by Pendell Meyers. EM Crit RACC. Retrieved April 9, 2021, from https://emcrit.org/emcrit/omi-manifesto/
  • O’gara, P. T., Kushner, F. G., Ascheim, D. D., Casey Jr, D. E., Chung, M. K., De Lemos, J. A., … & Zhao, D. X. (2013). 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. Circulation, 127(4), 529-555.
  • Wang, T. Y., Zhang, M., Fu, Y., Armstrong, P. W., Newby, L. K., Gibson, C. M., … & Roe, M. T. (2009). Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non–ST-elevation acute coronary syndromes undergoing diagnostic angiography. American heart journal, 157(4), 716-723.
Cite this article as: Israa M Salih, UAE, "STEMI Limitations," in International Emergency Medicine Education Project, May 31, 2021, https://iem-student.org/2021/05/31/stemi-limitations/, date accessed: July 28, 2021

Recent Blog Posts By Israa Salih

The Future of Resuscitation in the ED: ECMO-CPR (Part 2)

ecmo-cpr 2
Part 2 of this post continues with the use of ECMO during CPR. To learn more about ECMO, here is the link to Part 1

What is E-CPR?

E-CPR is defined as the utilization of veno-arterial extracorporeal membrane oxygenation (V-A ECMO) in patients who experience a sudden and unexpected pulseless condition secondary to the cessation of cardiac mechanical activity.

Rationale for E-CPR

The idea of E-CPR originated due to deficiencies in conventional CPR (C-CPR), which, even under optimal conditions, only delivers 15-25% of normal cardiac output. This leads to rapid hypoperfusion and ischemic damage to vital organs (what is known as the low-flow state). However, E-CPR is able to supply near-normal levels of organ perfusion; therefore, preserve the brain and other vital organs for days or weeks until cardiac recovery takes place.

In addition, E-CPR facilitates coronary interventions, even in patients with sustained ventricular fibrillation, because V-A ECMO provides stable systemic perfusion. Therefore, E-CPR has been considered a way to buy tome for the subsequent diagnosis and treatment of the underlying cause of cardiac arrest. Moreover, it provides better survival rates and neurologic outcomes.

Indications and patient selection for E-CPR

Up to date, there are no universal inclusion criteria for E-CPR. Inclusion criteria commonly used in E-CPR studies are the following:

  • Patients aged 18 to 65 or 18 to 70 years
  • Witnessed refractory cardiac arrest
  • Immediate bystander CPR
  • Initial shockable rhythm
  • Access to immediate coronary angiography
  • An anticipated low-flow period <60 minutes

Other common inclusion criteria for E-CPR include signs of life and end-tidal CO2 level >10 mm Hg on arrival to the emergency department. Their value in E-CPR is yet to be systematically assessed.

When should the transition to E-CPR occur?

No consensus is available regarding the ideal time to switch from C-CPR to E-CPR. Starting E-CPR too early may predispose patients who could potentially recover without it to a complicated and expensive procedure. On the other hand, delaying E-CPR may take away the core benefit of the intervention, which is, reducing low-flow state time and organ ischemia.

Studies showed that after 35 minutes of C-CPR, only less than 1% of patients achieve ROSC with good neurological outcomes. One study revealed that 16 minutes after the initiation of C-CPR by emergency medical services might be the optimal time to proceed to E‐CPR. Another study showed superior neurological outcome with the transition after 21 minutes in selected patients. However, delivering patients to a hospital within ab appropriate time frame presents a challenge to EMS staff. Prehospital E-CPR provides an alternative solution to this challenge.

Outcomes of C-CPR versus E-CPR:

Up to date, no published randomized controlled trial compared C-CPR versus E-CPR. Most of the evidence comes from retrospective and prospective observational studies, and meta-analysis. These studies included patients with out-of-hospital cardiac arrest (OHCA) and in-hospital cardiac arrest (IHCA). For example, the SAVE-J study, a prospective observational study, revealed that patients with OHCA who underwent E-CPR had a better neurological outcome, measured by a cerebral performance category of 1 or 2, compared to those with C-CPR, at 1 month (12.3% vs 1.5%, P<0.0001) and at 6 months (11.2% vs 2.6%, P=0.001). Kim et al. also reported favourable neurological outcomes at 3 months in the E-CPR group. Moreover, some recent systematic reviews have demonstrated trends that link E-CPR with improved survival and neurologic outcomes. Overall, factors that were associated with better outcomes included young age, witnessed arrest, bystander CPR, rhythm of sustained VF/VT, time from OHCA to E-CPR initiation, and acute coronary syndrome.

The latest study regarding E-CPR for OHCA was published in June 2020. It took place in Paris and included 13.191 OHCA cases. Of the 12,396 patients managed with C-CPR, 1061 (8.6%) survived to hospital discharge, compared with 44 (8.4%) of 523 E-CPR patients. E-CPR was attempted but failed in 58 (11%) patients. Factors associated with survival in the E-CPR group included an initial shockable rhythm and transient return of spontaneous circulation (ROSC) prior to E-CPR. This study posed major questions regarding the effectiveness of E-CPR in patients with OHCA. The fact that there was no statistical difference between C-CPR and E-CPR made the science community to realize the need to reevaluate the literature and for more and larger randomized clinical trials.

Prehospital E-CPR:

Pre-hospital ECMO aims to reduce the time to E-CPR initiation and increase potential positive outcomes (Figure 2). A cohort performed in Paris attempted to initiate E-CPR after 20 minutes of failed C-CPR and within 60 minutes of arrest. Outcomes revealed reduced low-flow state by 20 minutes and improved survival with neurologically intact patients up to 29% (21% absolute increase, P<0.001). This concluded that prehospital E‐CPR reduced low‐flow duration significantly and increased the rate of ROSC, but it was not an independent predictor of survival to discharge.

APACAR2 (A Comparative Study Between a Pre‐hospital and an In‐hospital Circulatory Support Strategy (ECMO) in Refractory Cardiac Arrest), an ongoing promising RCT, is randomizing patients with OHCA to either prehospital or hospital E‐CPR groups, depending on their location and predicted transport time to the hospital. It will reveal more about E-CPR use in the prehospital setting.

Limitations and closing remarks:

Current evidence concerning the effectiveness of E-CPR seems low quality, making drawing strong conclusions on OHCA E-CPR impossible. Additionally, positive outcomes may be associated with the whole “E-CPR bundle of care”, which include rapid hospital transfer, C-CPR and coronary angiography. Consequently, the effectiveness of E-CPR on its own is uncertain and more RCTs are needed.

Lastly, the survival rate of approximately 25-30% with E-CPR for IHCA already represents a huge financial and resource burden to the family and healthcare systems. If survival with OHCA E-CPR is potentially less than 10%, is it worth the burden or should we better invest in reducing cardiovascular morbidity and improve conventional bystander CPR?

prehospital ecmo-cpr
Figure 2: Prehospital ECMO (Ref: 11 - Nickson, C. (2020). Extracorporeal Membrane Oxygenation. Accessed Feb 26, 2021, from https://litfl.com/ecmo-extra-corporeal-membrane-oxygenation/)
Cite this article as: Amani Khalouf, UAE, "The Future of Resuscitation in the ED: ECMO-CPR (Part 2)," in International Emergency Medicine Education Project, March 24, 2021, https://iem-student.org/2021/03/24/ecmo-cpr-part-2/, date accessed: July 28, 2021

References and Further Reading

  1. Berdowski, J., Berg, R. A., Tijssen, J. G., & Koster, R. W. (2010). Global incidences of out-of-hospital cardiac arrest and survival rates: systematic review of 67 prospective studies. Resuscitation, 81(11), 1479-1487.
  2. Bougouin, W., Dumas, F., Lamhaut, L., Marijon, E., Carli, P., Combes, A., … & Jouven, X. (2020). Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest: a registry study. European Heart Journal, 41(21), 1961-1971.
  3. Dennis, M., Lal, S., Forrest, P., Nichol, A., Lamhaut, L., Totaro, R. J., Burns, B., & Sandroni, C. (2020). In-Depth Extracorporeal Cardiopulmonary Resuscitation in Adult Out-of-Hospital Cardiac Arrest. Journal of the American Heart Association, 9(10), e016521.
  4. Gräsner, J. T., Lefering, R., Koster, R. W., Masterson, S., Böttiger, B. W., Herlitz, J., … & Zeng, T. (2016). EuReCa ONE-27 Nations, ONE Europe, ONE Registry: A prospective one month analysis of out-of-hospital cardiac arrest outcomes in 27 countries in Europe. Resuscitation, 105, 188–195.
  5. Grunau, B., Reynolds, J., Scheuermeyer, F., Stenstom, R., Stub, D., Pennington, S., … & Christenson, J. (2016). Relationship between time-to-ROSC and survival in out-of-hospital cardiac arrest ECPR candidates: when is the best time to consider transport to hospital?. Prehospital Emergency Care, 20(5), 615-622.
  6. Hutin, A., Abu-Habsa, M., Burns, B., Bernard, S., Bellezzo, J., Shinar, Z., … & Lamhaut, L. (2018). Early ECPR for out-of-hospital cardiac arrest: best practice in 2018. Resuscitation, 130, 44-48.
  7. Hutin, A., Loosli, F., Lamhaut, L., Mantz, B., & Corrocher, R. (2017). How Physicians Perform Prehospital ECMO on the Streets of Paris. Accessed Feb 26, 2021, from https://www.jems.com/patient-care/how-physicians-perform-prehospital-ecmo-on-the-streets-of-paris/
  8. Inoue, A., Hifumi, T., Sakamoto, T., & Kuroda, Y. (2020). Extracorporeal Cardiopulmonary Resuscitation for Out‐of‐Hospital Cardiac Arrest in Adult Patients. Journal of the American Heart Association, 9(7), e015291.
  9. Kim, S. J., Jung, J. S., Park, J. H., Park, J. S., Hong, Y. S., & Lee, S. W. (2014). An optimal transition time to extracorporeal cardiopulmonary resuscitation for predicting good neurological outcome in patients with out-of-hospital cardiac arrest: a propensity-matched study. Critical Care, 18(5), 1-15.
  10. MacLaren, G., Masoumi, A. & Brodie, D. (2020). ECPR for out-of-hospital cardiac arrest: more evidence is needed. Critical Care24, 7
  11. Nickson, C. (2020). Extracorporeal Membrane Oxygenation. Accessed Feb 26, 2021, from https://litfl.com/ecmo-extra-corporeal-membrane-oxygenation/
  12. Singer, B., Reynolds, J. C., Lockey, D. J., & O’Brien, B. (2018). Pre-hospital extra-corporeal cardiopulmonary resuscitation. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 26(1), 1-8.
  13. Tan, B. K. K. (2017). Extracorporeal membrane oxygenation in cardiac arrest. Singapore Medical Journal, 58(7), 446.

The Future of Resuscitation in the ED: ECMO-CPR (Part 1)

ecmo-cpr 1

As a junior emergency department (ED) physician, I clearly remember my first code -first cardiopulmonary resuscitation (CPR) attended- and the mixed feelings of sorrow and helplessness for not being able to bring that soul back to life despite our best efforts. After a couple of more codes, listening to the sounds of the hearts slowly fading away, my mind started to question: How effective is the current standard Advanced Cardiac Life support (ACLS) protocol we follow?

I remember admitting to one of my attendings how desperate I felt about the ACLS during every code, expecting very abysmal neurological and overall outcomes, even if the patient was lucky enough to achieve the return of spontaneous circulation (ROSC). It almost felt that what we did was completely futile. A couple of weeks later, during my cardiology rotation, I had a field trip in the cardiac intensive care unit (ICU) with one of the cardiologists who introduced me to different advanced mechanical support devices, including extracorporeal membrane oxygenation (ECMO), intra-aortic balloon pump (IABP) and others. While he explained the basic concepts behind how they functioned, it almost immediately occurred to me: “Well! That’s what we need in cardiac arrest patients!”

While certainly, it was not a very novel idea, it did urge me to search into the available evidence and where we stood in terms of bringing this idea into more practical terms. This is how I was introduced, as a postgraduate year one (PGY-1) ED resident, to the concept of ECMO-CPR.

What is ECMO?

Extracorporeal membrane oxygenation (ECMO) is the use of a blood pump and an oxygenator to support either pulmonary or both pulmonary and cardiac function. An ECMO circuit is usually made of a centrifugal pump and a membrane oxygenator for oxygen delivery, CO2 removal, and temperature management.

What are the types of ECMO?

There are two main types of ECMO circuits:

Veno-venous (V-V) ECMO

Veno-venous (V-V) ECMO provides lung support only so it requires a functional heart. Venous cannulae are usually placed in the right or left common femoral vein (for drainage) and right internal jugular vein (for infusion). The tip of the femoral cannula should be maintained near the junction of the inferior vena cava and right atrium, while the tip of the internal jugular cannula should be maintained near the junction of the superior vena cava and right atrium.

Veno-arterial (V-A) ECMO

Veno-arterial (V-A) ECMO provides both cardiac and pulmonary support. The drainage (access) cannula is placed into the inferior vena cava via the femoral vein, and the “return” cannula is inserted into the femoral artery to the level of the common iliac artery.

We will focus on V-A ECMO given its relation with E-CPR.

How does V-A ECMO work?

Venous blood (blue) drained via a cannula positioned at the inferior vena cava to the right atrial junction passes through the extracorporeal membrane where oxygenation and CO2 removal occurs. The oxygenated blood (red) is returned via a “return” cannula positioned in the common iliac artery or descending aorta. After ECMO support is established, the distal perfusion catheter is inserted into the superficial femoral artery distal to the insertion point of the femoral return cannula, and it supplies oxygenated blood to the distal limb to prevent distal limb ischemia (Figure 1).

ecmo-cpr
Figure 1: V-A ECMO Configuration (Ref: 3 - Dennis, M., Lal, S., Forrest, P., Nichol, A., Lamhaut, L., Totaro, R. J., Burns, B., & Sandroni, C. (2020). In-Depth Extracorporeal Cardiopulmonary Resuscitation in Adult Out-of-Hospital Cardiac Arrest. Journal of the American Heart Association, 9(10), e016521.)

What are the indications for VA-ECMO?

  • Cardiac arrest
  • Low Cardiac Index (<2L/min/m2) and hypotension despite inotropic support and an IABP.
  • Failure to wean from cardiopulmonary bypass
  • Cardiogenic shock or severe cardiac failure, caused by:
    • Acute coronary syndrome
    • Ventricular tachycardia storm or refractory arrhythmias.
    • Sepsis
    • Drug overdose/toxicity
    • Myocarditis
    • Massive pulmonary embolism
    • Cardiac trauma
    • Acute anaphylaxis

What are the contraindications for VA-ECMO?

The list below includes both absolute and relative contraindications:

  • Patients with non-recoverable cardiac dysfunction who are not candidates for left ventricular assist device (LVAD) or transplantation
  • Chronic organ dysfunction
  • Prolonged CPR without adequate tissue perfusion
  • Disseminated malignancy
  • Known severe brain injury
  • Unwitnessed cardiac arrest
  • Contraindications to therapeutic-dose anticoagulation
  • Severe aortic regurgitation
  • Aortic dissection
  • Existent multiorgan failure
  • Mechanical ventilation >7–10 days
  • Advanced age

We will continue with the use of ECMO during CPR in the part 2. Stay tuned!

Cite this article as: Amani Khalouf, UAE, "The Future of Resuscitation in the ED: ECMO-CPR (Part 1)," in International Emergency Medicine Education Project, March 22, 2021, https://iem-student.org/2021/03/22/ecmo-cpr-part-1/, date accessed: July 28, 2021

References and Further Reading

  1. Berdowski, J., Berg, R. A., Tijssen, J. G., & Koster, R. W. (2010). Global incidences of out-of-hospital cardiac arrest and survival rates: systematic review of 67 prospective studies. Resuscitation, 81(11), 1479-1487.
  2. Bougouin, W., Dumas, F., Lamhaut, L., Marijon, E., Carli, P., Combes, A., … & Jouven, X. (2020). Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest: a registry study. European Heart Journal, 41(21), 1961-1971.
  3. Dennis, M., Lal, S., Forrest, P., Nichol, A., Lamhaut, L., Totaro, R. J., Burns, B., & Sandroni, C. (2020). In-Depth Extracorporeal Cardiopulmonary Resuscitation in Adult Out-of-Hospital Cardiac Arrest. Journal of the American Heart Association, 9(10), e016521.
  4. Gräsner, J. T., Lefering, R., Koster, R. W., Masterson, S., Böttiger, B. W., Herlitz, J., … & Zeng, T. (2016). EuReCa ONE-27 Nations, ONE Europe, ONE Registry: A prospective one month analysis of out-of-hospital cardiac arrest outcomes in 27 countries in Europe. Resuscitation, 105, 188–195.
  5. Grunau, B., Reynolds, J., Scheuermeyer, F., Stenstom, R., Stub, D., Pennington, S., … & Christenson, J. (2016). Relationship between time-to-ROSC and survival in out-of-hospital cardiac arrest ECPR candidates: when is the best time to consider transport to hospital?. Prehospital Emergency Care, 20(5), 615-622.
  6. Hutin, A., Abu-Habsa, M., Burns, B., Bernard, S., Bellezzo, J., Shinar, Z., … & Lamhaut, L. (2018). Early ECPR for out-of-hospital cardiac arrest: best practice in 2018. Resuscitation, 130, 44-48.
  7. Hutin, A., Loosli, F., Lamhaut, L., Mantz, B., & Corrocher, R. (2017). How Physicians Perform Prehospital ECMO on the Streets of Paris. Accessed Feb 26, 2021, from https://www.jems.com/patient-care/how-physicians-perform-prehospital-ecmo-on-the-streets-of-paris/
  8. Inoue, A., Hifumi, T., Sakamoto, T., & Kuroda, Y. (2020). Extracorporeal Cardiopulmonary Resuscitation for Out‐of‐Hospital Cardiac Arrest in Adult Patients. Journal of the American Heart Association, 9(7), e015291.
  9. Kim, S. J., Jung, J. S., Park, J. H., Park, J. S., Hong, Y. S., & Lee, S. W. (2014). An optimal transition time to extracorporeal cardiopulmonary resuscitation for predicting good neurological outcome in patients with out-of-hospital cardiac arrest: a propensity-matched study. Critical Care, 18(5), 1-15.
  10. MacLaren, G., Masoumi, A. & Brodie, D. (2020). ECPR for out-of-hospital cardiac arrest: more evidence is needed. Critical Care24, 7
  11. Nickson, C. (2020). Extracorporeal Membrane Oxygenation. Accessed Feb 26, 2021, from https://litfl.com/ecmo-extra-corporeal-membrane-oxygenation/
  12. Singer, B., Reynolds, J. C., Lockey, D. J., & O’Brien, B. (2018). Pre-hospital extra-corporeal cardiopulmonary resuscitation. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 26(1), 1-8.
  13. Tan, B. K. K. (2017). Extracorporeal membrane oxygenation in cardiac arrest. Singapore Medical Journal, 58(7), 446.

Dead on Arrival, What Should We Do?

Dead on Arrival, What Should We Do

If you have worked long enough in the emergency department (ED), you probably have seen several patients with cardiac arrest on arrival during your shifts. The question is: Would you consider your patient already dead or still alive? It seems an easy enough question but another question follows: Are you sure about that?

I had many night shifts in the ED. I remember a night when an unconscious 55-year-old gentleman came with mydriatic pupils and no pulse. His wife’s cries broke my heart! Suddenly, my mind went so blank that I couldn’t even recall the basic life support! I needed to resuscitate him, but what was next Epinephrine or cardioversion? In my perplexity, I felt to my bones that everything I learnt and memorised was in vain. The nurses were waiting for my instructions, but I was petrified myself. Why couldn’t I think systematically? At that point in time, I swore to myself that I would try again, harder and harder, to learn -and implement- life support better. And, I had to be quick about it, because soon this year, I would be handling patients myself (even though I still have to report each case to the staff).

Long after that moment, I came to realise that death means different things to different people. Even for the same people, it will be different from each perspective -Biologically, spiritually, medically, metaphorically, metaphysically, existentially, chemically, anatomically, ethically, legally, or on a cellular basis. So, now that I am about to take more responsibility of my patients, the fundamental question remains: How do we make sure that the patient without a pulse on arrival is positively dead? Or more importantly, how should we act?

Between 10% and 50% of deaths occur before reaching hospitals (1-2). Death on arrival (DoA) can refer to two different patient groups: those who were declared dead upon arrival to an ED with no resuscitation attempt or those who died after failed resuscitation, usually within the first hour of arrival (3). The studies show that in addition to prehospital and hospital care, basic life support by laypeople plays a crucial role in reducing deaths (4).

lay person CPR

Do you know this?

Sometimes, when we put the defibrillator paddles on an arrest patient, the first rhythm we see is ventricular fibrillation (VF). It’s an easy call – which means if we quickly resuscitate the patient, we can save him or her. At other times, the patient arrives with mydriatic pupils, no breathing, and no pulse, and a flat line. This decision is more challenging because the patient might have passed the critical period for resuscitation or what causes pupils to be mydriatic could be a recent amphetamine or cocaine overdose. What is the best course of action in this scenario

  1. American Heart Association realised that this is a worldwide problem (5). Therefore, they made a statement about this very situation. According to it:
    At the time of cardiac arrest, there is no way to assess reliably brain death or neurologic outcome.
  2. From an ethical perspective, withholding resuscitation during resuscitation and discontinuation of life-sustaining treatment after are equivalent.
  3. If the prognosis is not clear, starting resuscitation without delay is reasonable so that more information can be gathered about the situation to predict the clinical course and the outcome, and learn the patient’s end-of-life preferences.

In other words, not being able to diagnose a patient with DoA at the first glance is OK. Once we don’t feel the pulse, we start CPR! We should learn more about the situation to be sure. In this way, we avoid any adverse outcomes, which might be associated with the delay of treatment.

What steps should we take to save the patient?

My Opinion

Personally, I find pronouncing someone DoA difficult. Dead on arrival diagnosis is an irreversible verdict. Devastating news for families who lost their loved ones forever.

Of course, we can declare someone dead if obvious clinical signs of irreversible death (eg, rigour mortis, dependent lividity, decapitation, transection, decomposition) are present. Otherwise, I feel that we should try and give patients the best possible chance for survival.

The key to a good doctor is three-pronged: comprehensive knowledge, mastery of skills, and proper attitude. Ever doctor, especially those who are dealing with emergencies, must know the process of death, master skills to provide help to those who can benefit, and remain dedicated to serving.

Take-home messages

  • Don’t memorise the algorithm, understand it clearly.
  • Try not to panic even though it’s your first time. There is a first time for everything.
  • Little acts of help can save someone’s life.

References and Further Reading

  1. Arreola-Risa, Carlos, et al. “Low-cost improvements in prehospital trauma care in a Latin American city.” Journal of Trauma and Acute Care Surgery 48.1 (2000): 119.
  2. Roudsari, Bahman S., et al. “Emergency Medical Service (EMS) systems in developed and developing countries.” Injury 38.9 (2007): 1001-1013.
  3. Khursheed, Munawar, et al. “Dead on arrival in a low-income country: results from a multicenter study in Pakistan.” BMC emergency medicine 15.2 (2015): 1-7.
  4. Calland, James Forrest, et al. “The effect of dead-on-arrival and emergency department death classification on risk-adjusted performance in the American College of Surgeons Trauma Quality Improvement Program.” Journal of Trauma and Acute Care Surgery 73.5 (2012): 1086-1092.
  5. Panchal, Ashish R., et al. “Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.” Circulation 142.16_Suppl_2 (2020): S366-S468.
Cite this article as: Cicilia Evajelista, "Dead on Arrival, What Should We Do?," in International Emergency Medicine Education Project, March 15, 2021, https://iem-student.org/2021/03/15/dead-on-arrival/, date accessed: July 28, 2021

Question Of The Day #30

question of the day
qod30

Which of the following is the most appropriate next step in management for this patient?

This patient arrives to the Emergency department with the return of spontaneous circulation (ROSC) from a ventricular fibrillation cardiac arrest. His regaining of pulses was likely due to his limited downtime, prompt initiation of CPR, and prompt diagnosis and treatment of ventricular fibrillation with electrical defibrillation. Important elements of emergency post-ROSC care include avoiding hypotension, hypoxia, hyperthermia, and hypo or hyperglycemia. Maintaining proper perfusion to the brain and peripheral organs is crucial in all ROSC patients. A 12-lead EKG should always be obtained early after ROSC is achieved in order to look for signs of cardiac ischemia. Cardiac catheterization should be considered in all post-ROSC patients, but especially in patients with cardiac arrest from ventricular fibrillation or ventricular tachycardia.

Patients who achieve ROSC can vary markedly in terms of their clinical exam. Some patients may be awake and conversive, while others are comatose and non-responsive. The neurological exam immediately post-ROSC does not predict long-term outcomes, so decisions on prognosis should not be based on these factors in the emergency department. For this reason, resuscitation efforts should not be considered medically futile in this scenario (Choice A). Vasopressors (Choice B) are medications useful in post-ROSC patients who have signs of hemodynamic collapse, such as hypotension. This patient is not hypotensive and does not meet the criteria for initiation of vasopressors. A CT scan of the head (Choice D) is a study to consider in any patient who presents to the emergency department with collapse to evaluate intracranial bleeding (i.e., subarachnoid bleeding). Although not impossible, the history of chest pain before collapse makes brain bleeding a less likely cause of death in this patient. Targeted Temperature Management (Choice C), also known as Therapeutic Hypothermia, is the best next step in this patient’s management.

Targeted Temperature Management involves a controlled lowering of the patient’s body temperature to 32-34ᵒC in the first 24 hours after cardiac arrest. This treatment has been shown to improve neurologic and survival outcomes. The theory behind this treatment is that hypothermia post-ROSC reduces free radical damage and decreases cerebral metabolism. Data behind targeted temperature management shows the greatest benefit in cardiac arrest patients due to ventricular fibrillation, but arrest from ventricular tachycardia, pulseless electrical activity, and asystole may also show benefit. Adverse effects of this treatment include coagulopathy, bradycardia, electrolyte abnormalities (i.e., hypokalemia), and shivering. Important contraindications to this treatment are an awake or alert patient (post-ROSC GCS >6), DNR or DNI status, another reason to explain comatose state (i.e., intracranial bleeding, spinal cord injury), age under 17 years old, a poor functional status prior to the cardiac arrest (i.e., nonverbal, bedbound), or an arrest caused by trauma. Correct Answer: C

References

 

Cite this article as: Joseph Ciano, USA, "Question Of The Day #30," in International Emergency Medicine Education Project, March 12, 2021, https://iem-student.org/2021/03/12/question-of-the-day-30/, date accessed: July 28, 2021

Question Of The Day #29

question of the day
qod29
842 - Wide QRS complex tachycardia

Which of the following is the most appropriate next step in management for this patient?

This patient presents to the emergency department with seven days of severe vomiting, diarrhea, tachycardia, and borderline hypotension. The clinician should be concerned about dehydration and potential electrolyte derangements induced by the vomiting and diarrhea. Certain electrolyte derangements can put a patient at risk for cardiac dysrhythmias, so ordering a 12-lead EKG is an important step in evaluating any patient with a potential electrolyte disturbance. Dangerous electrolyte disturbances that can predispose a patient to cardiac dysrhythmias include hyperkalemia, hypokalemia, hypomagnesemia, and hypocalcemia. Signs of hyperkalemia on the EKG include peaked T waves, absent or flattened P waves, widened QRS complexes, or a sine wave morphology. Low potassium, magnesium, and calcium can all prolong the QT interval and predispose the patient to polymorphic ventricular tachycardia (Torsades de Pointes). Hypokalemia on EKG may also be associated with a U wave, which is an upward wave that follows the T wave.

This patient’s 12-lead EKG shows a wide-complex tachycardia with QRS complex “twisting” around the isoelectric line and varying QRS amplitudes. These EKG signs, along with the inferred history of severe electrolyte abnormalities, support a diagnosis of Torsades de Pointes (TdP). Another risk factor for TdP is a history of congenital prolonged QT syndromes. Similar to monomorphic ventricular tachycardia, TdP should always be treated with electrical cardioversion if there are any signs of instability (i.e., altered mental status, SBP <90mmHg). A pulseless patient with TdP always necessitates unsynchronized cardioversion, also known as defibrillation. This patient may have briefly syncopized or potentially underwent cardiac arrest. Intravenous Amiodarone (Choice A) and Procainamide (Choice B) are contraindicated in TdP as both of these agents can further prolong the QT interval. These agents can be used in a stable patient with monomorphic ventricular tachycardia. Intravenous Ciprofloxacin (Choice C) is a quinolone antibiotic that is useful for treating infections from gram-negative bacteria. This may be beneficial for this patient, especially if there is a concern for bacterial gastroenteritis. However, quinolone antibiotics also can prolong the QT interval, and this medication will not acutely stabilize this patient. Intravenous Magnesium Sulfate (Choice D) shortens the QT interval and is the preferred therapy for a TdP patient with a pulse. Correct Answer: D

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #29," in International Emergency Medicine Education Project, March 5, 2021, https://iem-student.org/2021/03/05/question-of-the-day-29/, date accessed: July 28, 2021

Question Of The Day #28

question of the day
qod28

EKG#1

710 - hyperkalemia

EKG#2

855 - bradycardia

Which of the following is the most likely underlying cause for this patient’s condition?

This patient presents to the emergency department with vague and nonspecific symptoms of nausea, fatigue, and palpitations. The initial EKG (EKG #1) demonstrates a wide-complex tachycardia (QRS >120msec) with a regular rhythm. The differential diagnosis for wide-complex tachyarrhythmias include ventricular tachycardia (monomorphic ventricular tachycardia), torsades de pointes (polymorphic ventricular tachycardia), coarse ventricular fibrillation, supraventricular tachycardias with aberrancy (i.e. underlying Wolf Parkinson White Syndrome or Ventricular Bundle Branch Block), electrolyte abnormalities (i.e., Hyperkalemia), and from medications (i.e., Na channel blocking agents). If the history is unclear or the patient shows signs of instability, Ventricular tachycardia should always be the assumed tachyarrhythmia. This is managed with electrical cardioversion or with medications (i.e., amiodarone, procainamide, lidocaine), depending on the patient’s symptoms and hemodynamic stability.

The prior EKG for the patient (EKG #2) is helpful in showing that the patient does not have a wide QRS complex at baseline. There also are no EKG signs of Wolf Parkinson White Syndrome (Choice B) on EKG #2, making this choice incorrect. Signs of this cardiac pre-excitation syndrome on EKG include a shortened PR interval and a delta wave (slurred upstroke at the beginning of the QRS complex). Anxiety (Choice D) can cause sinus tachycardia and be a symptom associated with any arrhythmia, but it is not the underlying cause for this patient’s bizarre wide-complex tachydysrhythmia. On a closer look, the patient’s EKG (EKG #1) demonstrates tall, peaked T waves in the precordial leads. This supports a diagnosis of hyperkalemia. Other signs of hyperkalemia on EKG include flattened or absent P waves, widened QRS complexes, or a sine wave morphology. A common underlying cause of hyperkalemia is renal disease (Choice C). Ischemic heart disease (Choice A) is a common underlying cause for ventricular tachycardia. Ventricular tachycardia is less likely in this case given the presence of peaked T waves and the lack of fusion beats, capture beats, or signs of AV dissociation on the 12-lead EKG. Correct Answer: C 

References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685
  • Burns, E. (2020). Ventricular Tachycardia – Monomorphic VT. Life in The Fast Lane. Retrieved from https://litfl.com/ventricular-tachycardia-monomorphic-ecg-library/

Cite this article as: Joseph Ciano, USA, "Question Of The Day #28," in International Emergency Medicine Education Project, February 26, 2021, https://iem-student.org/2021/02/26/question-of-the-day-28/, date accessed: July 28, 2021

Question Of The Day #27

question of the day
qod27
756.1 - palpitation - SOB

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient has a narrow-complex, regular tachycardia that is causing the sensation of palpitations. The clinical history, rapid heart rate, and 12-lead EKG provide enough information to diagnose this patient with supraventricular tachycardia, also known as “SVT.” Supraventricular tachycardias refer to a broad range of arrhythmias, including sinus tachycardia, atrial fibrillation, atrial flutter, multifocal atrial tachycardia, and AV nodal re-entry tachycardia. This scenario specifically depicts an AV nodal re-entry tachycardia (AVNRT). AVNRT is a common type of SVT that can occur spontaneously or is triggered by sympathomimetic agents (i.e., cocaine, amphetamines), caffeine, alcohol, exercise, or beta-2 agonists using in asthma treatment (i.e., albuterol, salbutamol). AVNRTs are narrow-complex tachycardias with rates that range from 120-280bpm. P waves are typically absent in AVNRTs, but rarely they may be present as retrograde inverted P waves located immediately before or after the QRS complex. Symptoms experienced by the AVNRT patient may include pre-syncope, syncope, dizziness, palpitations, anxiety, or mild shortness of breath. Patients with AVNRTs are more likely to be young and female over male.

QRS complexes in AVNRTs are often narrow (<120msec), however, wide QRS complexes may be present in AVNRTs if there is a concurrent bundle branch block or Wolff-Parkinson White Syndrome. AVNRTs are often stable and do not require electric cardioversion. Signs that indicate instability and necessitate cardioversion are hypotension (SBP <90mmHg), altered mental status, or ischemic chest pain (more common if known history of ischemic heart disease). This patient lacks all of these signs and symptoms.

Treatment of AVNRT focuses on restoring the patient to normal sinus rhythm, which leads to resolution of symptoms. First-line medications for AVNRTs are short-acting AV nodal blocking agents, like adenosine (Choice A). Beta-blockers or calcium channel blockers act as second-line agents for patients who do not respond to adenosine. Metoprolol is a beta-blocker (Choice C) and Diltiazem is a calcium channel clocker (Choice D). Prior to any medications, vagal maneuvers should always be attempted first in a stable patient with AVNRT. The Valsalva maneuver (Choice B), or “bearing down,” is a commonly used vagal maneuver in the termination of AVNRTs. Other vagal maneuvers include the carotid massage or the Diving reflex (place bag of ice and water on face). Correct Answer: B

References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685
  • Burns, E. (2020). Supraventricular Tachycardia (SVT). Life in the Fast Lane. Retrieved from https://litfl.com/supraventricular-tachycardia-svt-ecg-library/

Cite this article as: Joseph Ciano, USA, "Question Of The Day #27," in International Emergency Medicine Education Project, February 19, 2021, https://iem-student.org/2021/02/19/question-of-the-day-27/, date accessed: July 28, 2021

Question Of The Day #26

question of the day
qod26
38 - atrial fibrillation

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient presents to the emergency department with palpitations, a narrow complex tachycardia (<120msec), and an irregularly irregular rhythm. A close look at this patient’s EKG reveals the absence of discrete P waves and QRS complexes that are spaced at varying distances from each other (most apparent in lead V6). These signs support a diagnosis of Atrial Fibrillation, or “AFib.” Atrial Fibrillation is an arrhythmia characterized by an irregularly irregular rhythm, the absence of P waves with a flat or undulating baseline, and narrow QRS complexes. Wide-QRS complexes may be present in AFib if there is a concurrent bundle branch block or Wolff-Parkinson White Syndrome. AFib is caused by the electric firing of multiple ectopic foci in the atria of the heart. This condition is triggered by a multitude of causes, including ischemic heart disease, valvular heart disease, dilated or hypertrophic cardiomyopathies (likely related to this patient’s congestive heart failure history), sepsis, hyperthyroidism, excess caffeine or alcohol intake, pulmonary embolism, and electrolyte abnormalities.

The main risk in AFib is the creation of thrombi in the atria as they fibrillate, resulting in emboli that travel to the brain and cause a stroke. The CHA2DS2VASc scoring system is used to risk stratify patients and determine if they require anticoagulation to prevent against thrombo-embolic phenomenon (i.e. stroke). This patient has a high CHA2DS2VASc score, so she would require anticoagulation. In addition to anticoagulation, A fib is treated with rate control (i.e. beta blockers or calcium channel blockers), rhythm control (i.e. anti-arrhythmic agents), or electrical cardioversion. Electrical cardioversion (choice A) is typically avoided when symptoms occur greater than 48 hours, since the risk of thrombo-emboli formation is higher in this scenario. An exception to this would be a patient with “unstable” AFib. Signs of instability in any tachyarrhythmia are hypotension, altered mental status, or ischemic chest pain. This patient lacks all of these signs and symptoms. Although this patient lacks signs of instability, this patient’s marked tachycardia should be addressed with medical treatment. General observation (Choice C) is not the best choice for this reason. Intravenous adenosine (Choice D) is the best choice for a patient with supraventricular tachycardia (SVT). This is a narrow-complex AV nodal re-entry tachycardia with rates that range from 120-280bpm. SVT also lacks discrete P waves. A key factor that differentiates A fib from SVT is that SVT has a regular rhythm, while AFib has an irregular rhythm. Intravenous metoprolol (Choice B) is the best treatment option listed in order to decrease the patient’s heart rate.

References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685
  • Burns, E. (2020) Atrial Fibrillation. Life in The Fast Lane. Retrieved from https://litfl.com/atrial-fibrillation-ecg-library/

 

Cite this article as: Joseph Ciano, USA, "Question Of The Day #26," in International Emergency Medicine Education Project, February 12, 2021, https://iem-student.org/2021/02/12/question-of-the-day-26/, date accessed: July 28, 2021

Question Of The Day #25

question of the day
qod25
835 - 3rd degree heart block

Which of the following is the most likely diagnosis of this patient’s condition?

This patient has marked bradycardia on exam with a borderline low blood pressure. These vital sign abnormalities are likely the cause of the patient’s dizziness. Bradycardia is defined as any heart rate under 60 beats/min. The most common cause of bradycardia is sinus bradycardia (Choice A). Other types of bradycardia include conduction blocks (i.e. type 2 or type 3 AV blocks), junctional rhythms (lack of P waves with slow SA nodal conduction), idioventricular rhythms (wide QRS complex rhythms that originate from the ventricles, not atria), or low atrial fibrillation or atrial flutter. About 80% of all bradycardias are caused by factors external to the cardiac conduction system, such as hypoxia, drug effects (i.e., beta block or calcium channel blocker use or overdose), or acute coronary syndromes.

ecg qod25Sinus bradycardia (Choice A) occurs when the electrical impulse originates from the SA node in the atria. Signs of sinus bradycardia on EKG are the presence of a P wave prior to every QRS complex. This EKG shows P waves prior to each QRS complex, but there are extra P waves that are not followed by QRS complexes. Some P waves are “buried” within QRS complexes or within T waves. The EKG below marks each P wave with a red line and each QRS complex with a blue line.

 

First-degree AV Block (Choice B) is a benign arrhythmia characterized by a prolonged PR interval. This patient’s EKG has variable PR intervals (some prolonged, some normal). This is a result of a more severe AV conduction block. Second-Degree AV Blocks are divided into Mobitz type I and Mobitz Type II. Mobitz type I, also known as Wenckebach, is characterized by a progressive lengthening PR interval followed by a dropped QRS complex. This can be remembered by the phrase, “longer, longer, longer, drop.” Wenckebach is a benign arrhythmia that does not typically require any treatment. Mobitz type II (Choice C) is characterized by a normal PR interval with random intermittent dropping of QRS complexes. This patient’s EKG has consistent spacing between each QRS complex (blue lines) and consistent spacing between each P wave (red lines). However, the P waves and QRS complexes are not associated with each other. This phenomenon is known as AV dissociation. These EKG changes are signs of a complete heart block, also known as Third-Degree AV Block (Choice D). Both Second-Degree AV block- Mobitz type II (Choice C) and Third-Degree AV Block (Choice D) are more serious conduction blocks that require cardiac pacemakers. Correct Answer: D

References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685
  • Nickson, C. (2020). Heart Block and Conduction Abnormalities. Life in the Fast Lane. Retrieved from https://litfl.com/heart-block-and-conduction-abnormalities/

 

Cite this article as: Joseph Ciano, USA, "Question Of The Day #25," in International Emergency Medicine Education Project, February 5, 2021, https://iem-student.org/2021/02/05/question-of-the-day-25/, date accessed: July 28, 2021

Question Of The Day #24

question of the day
qod24
738.1 - Prior ECG before 738.2 - STEMI

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient is suffering from severe bradycardia with signs of poor cardiac output, shock, and diminished perfusion to the brain. Bradycardia is defined as any heart rate under 60 beats/min. Many individuals may be bradycardic at rest with no danger to the patient (i.e. young patients or athletes). Bradycardia in these scenarios is physiologic and is not associated with difficulty in perfusing the brain and other organs. This patient’s 12-lead EKG shows sinus bradycardia since there is a P wave prior to every QRS complex. Sinus bradycardia is the most common type of bradycardia. Other types of bradycardia include conduction blocks (i.e. type 2 or type 3 AV blocks), junctional rhythms (lack of P waves with slow SA nodal conduction), idioventricular rhythms (wide QRS complex rhythms that originate from the ventricles, not atria), or slow atrial fibrillation or atrial flutter. About 80% of all bradycardias are caused by factors external to the cardiac conduction system, such as hypoxia, drug effects (i.e. beta block or calcium channel blocker use or overdose), or acute coronary syndromes.  

For any patient with a bradyarrhythmia or tachyarrhythmia, it is crucial to determine if the arrythmia is “stable” or “unstable”. Signs that an arrhythmia is unstable include altered mental status, hypotension with systolic blood pressure under 90mmHg, chest pain, or shortness of breath. Patients with a stable arrhythmia can be managed supportively with observation and less invasive medical management. Patients with unstable arrhythmia are managed more aggressively with the use of electricity, often in combination with other medical treatments. This patient has an unstable bradyarrhythmia, given her altered mental status and hypotension. Intravenous metoprolol (Choice D) would make the patient more bradycardic since this medication blocks beta-adrenergic receptors of the heart that control heart rate and contractility. Intravenous Amiodarone (Choice C) is an antiarrhythmic agent used often in wide complex tachyarrhythmias (i.e. Ventricular Tachycardia). Intravenous atropine or epinephrine are agents that can be used in this patient prior to preparing for electric pacing. Transcutaneous pacing (Choice A) should always be attempted prior to Transvenous pacing (Choice B), as Transcutaneous pacing is less invasive and quicker to set up. If Transcutaneous pacing does not result in electrical “capture” or change the heart rate, the next step is Transvenous pacing. Correct Answer: A 

References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685
  • Burns, E. (2020). Sinus Bradycardia. Life in the Fast Lane. Retrieved from https://litfl.com/sinus-bradycardia-ecg-library/
Cite this article as: Joseph Ciano, USA, "Question Of The Day #24," in International Emergency Medicine Education Project, December 11, 2020, https://iem-student.org/2020/12/11/question-of-the-day-24/, date accessed: July 28, 2021

Hypertrophic Cardiomyopathies

Hypertrophic Cardiomyopathies

Hypertrophic cardiomyopathy is an inherited cardiovascular disease [1]. The condition can lead to sudden death in young adults and other problems such as heart failure, arrhythmias and stroke. It is prevalent in the world, with cases reported in over 50 countries and in people of all sexes, ethnicities and races. In diverse regions including the USA, Europe and East Africa, the prevalence of hypertrophic cardiomyopathy is 1 in 500 in the general population [2]. While considered a common and possibly fatal disease, most affected individuals remain undiagnosed in their lifetime and do not experience symptoms or reduced life expectancy [1].

Hypertrophic cardiomyopathy is passed on by an autosomal dominant fashion through mutations in more than 12 genes that encode for thick and thin myofilament proteins. However, sporadic cases caused by de-novo mutations in the predisposing genes can also occur [3]. Genetic testing for the identification of causative mutations can be conducted via DNA sequencing; however, pathogenic mutations are identified in roughly fewer than 50% of clinically affected patients [1].

Clinical Presentation, Signs and Symptoms

Clinical diagnosis of hypertrophic cardiomyopathy entails a hypertrophied but non-dilated left ventricle without evidence of any other disorders, such as cardiac or systemic diseases that may cause cardiomyocyte hypertrophy [4]. Often, patients with hypertrophic cardiomyopathy do not have any symptoms, and diagnosis is made either incidentally or through familial genetic screening. However, symptomatic patients may experience chest pain with exertion and varying rates of dyspnoea on a daily basis. Chest pain may also present at rest and can be caused by large meals. Some patients can also experience syncope [5]. Dyspnoea, chest pain and syncope are common symptoms that we faced in the emergency department. Although there are more common and deadly presentations with those symptoms, hypertrophic cardiomyopathy should always be in our differential diagnoses, particularly in cases with additional findings explained below.

Clinical Exam and Investigations

Clinical examination of patients with hypertrophic cardiomyopathy often reveals little information. In patients with dynamic left ventricular outflow tract obstruction, a systolic murmur may be heard with auscultation at the left sternal edge, radiating to the aortic and mitral areas [5]. However, if hypertrophic cardiomyopathy is suspected, either due to familial screening, the presence of a murmur or an abnormal 12-lead electrocardiogram (ECG), its diagnosis needs to be confirmed with either echocardiography and/or cardiovascular MRI [1].

Natural History and Clinical Course of Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathies can present at any age from infancy to adulthood. Many patients with this cardiovascular disease are expected to have a normal life expectancy without any major complications or even therapeutic interventions [6]. However, complications may occur in some patients and can include a range of events. Sudden death may occur in patients who are mildly symptomatic or even asymptomatic. Progressive heart failure with possible obstructive outflow obstruction and normal systolic function can occur, which may slowly lead to systolic dysfunction [4]. Cardiac arrhythmias may also develop – most commonly atrial fibrillation. This can lead to symptoms of heart failure and embolic stroke in 20% of the patients [7].

Sudden Death

Sudden death is the most unpredictable and devastating consequence of hypertrophic cardiomyopathy and is the most common cause of sudden death in young patients (under the age of 30) and young athletes [1,4,8]. However, the risk of sudden death falls gradually with older age. Although sudden death from mild physical activity or even inactivity can occur, death due to vigorous exertion amongst this patient population is more common [1]. Sudden death from hypertrophic cardiomyopathy usually occurs due to ventricular fibrillation and tachycardia. Risk stratification of high-risk patients for sudden death is important and can lead to the prevention of sudden death using various approaches, such as an implantable defibrillator [1,9]. Additionally, young professional athletes should be screened to detect silent signs of cardiovascular disorders that may lead to sudden death. Unfortunately, if young athletes are found to have hypertrophic cardiomyopathy, implementation of a cardiovert-defibrillator is not sufficient to grant athletes to return to competing. Athletes are often advised to stop participating in competitive sports, unless it is of low intensity such as golf [8].

Heart Failure

Symptoms of heart failure associated with preserved left-ventricular systolic function most often occur in middle-aged patients but can occur at any age [13]. Functional limitations can occur at differing rates but are often gradual and involve day to day variability. Women with hypertrophic cardiomyopathy have been shown to experience more severe symptoms of heart failure later in life compared to male patients. Frequently, these symptoms experienced in women have been associated with left-ventricular outflow-tract obstruction [14]. Some causes of heart failure in hypertrophic cardiomyopathy patients include left-ventricular outflow-tract obstruction, atrial fibrillation and diastolic dysfunction [1,4]. Treatment strategies include drugs and surgical myectomy or alcohol septal ablation for relief of symptoms of heart failure and outflow obstruction, and pharmacological strategies to treat atrial fibrillation and prevent stroke (such as blood thinners).

Hypertrophic Cardiomyopathy Management in the ED

Patients with hypertrophic cardiomyopathy exacerbation may present to the ED with a range of symptoms including syncope, chest pain, dyspnea, cardiac arrhythmia and worst of all, sudden cardiac death [10]. Diagnosis of hypertrophic cardiomyopathy patients presenting with these symptoms to the ED may be difficult as most of these patients are not aware of their underlying cardiovascular disease. Therefore, ED staff should keep this differential in mind and should be aware of certain diagnostic tools and approaches for acute management of hypertrophic cardiomyopathy.

Primarily, ED staff should conduct a complete history of the patients, including family history of relatives with early cardiovascular disorders or sudden death at a young age. Physical examination of the patient may be inconclusive, as patients usually don’t present with any specific cardiovascular symptoms, unless their disease has progressed to having left-ventricular outflow obstruction tract. An electrocardiogram (EKG) should be conducted, as most patients with hypertrophic cardiomyopathy will have abnormal EKGs. Specifically, their EKGs will show signs of left ventricular hypertrophy through large amplitude QRS, and deep, narrow Q waves particularly in the lateral leads if the patient has septal hypertrophy [11]. Physical examination should be coupled with EKG to rule out other cardiac problems.

HCM-pattern-with-asymmetrical-septal-hypertrophy
Adopted from - Ed Burns. Hypertrophic Cardiomyopathy (HCM). https://litfl.com/hypertrophic-cardiomyopathy-hcm-ecg-library/

Deep narrow Q waves in chest leads are typical ECG finding of the hypertrophic cardiomyopathy patients. For more ECG information please visit – https://litfl.com/hypertrophic-cardiomyopathy-hcm-ecg-library/

In managing hypertrophic cardiomyopathy patients, following the ACLS algorithm if the patient is hemodynamically unstable is first priority. Otherwise, the goal of acute treatment of hypertrophic cardiomyopathy is to restore normal sinus rhythm or control the ventricular rate. Appropriate vasopressors should be given if patients are experiencing volume fluctuations due to diarrhea or other consequences of their disease. If patients present with a new onset of atrial fibrillation, approach of rate versus rhythm control and thromboembolism risk management should be considered [10]. If acute pharmacological treatment of hypertrophic cardiomyopathy patients is required, caution should be taken considering the state of their disease. For example, caution must be exercised when giving diuretics to patients with severe heart failure, as reduction in left ventricular preload can exacerbate obstruction and lead to hypotension [12]. The same considerations must be applied to any other treatment and guidelines should be followed closely. In conclusion, quick identification of the patient’s underlying cardiovascular problem and acute pharmacological management in the ED is critical to help the patient until a specialist can see them.

References and Further Reading

  1. Maron, B. J., & Maron, M. S. (2013). Hypertrophic cardiomyopathy. The Lancet381(9862), 242-255.
  2. Maron, B. J., Gardin, J. M., Flack, J. M., Gidding, S. S., Kurosaki, T. T., & Bild, D. E. (1995). Prevalence of hypertrophic cardiomyopathy in a general population of young adults: echocardiographic analysis of 4111 subjects in the CARDIA study. Circulation92(4), 785-789.
  3. Alcalai, R., Seidman, J. G., & Seidman, C. E. (2008). Genetic basis of hypertrophic cardiomyopathy: from bench to the clinics. Journal of cardiovascular electrophysiology19(1), 104-110.
  4. Maron, B. J. (2002). Hypertrophic cardiomyopathy: a systematic review. Jama287(10), 1308-1320.
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Cite this article as: Maryam Bagherzadeh, Canada, "Hypertrophic Cardiomyopathies," in International Emergency Medicine Education Project, December 9, 2020, https://iem-student.org/2020/12/09/hypertrophic-cardiomyopathies/, date accessed: July 28, 2021