Question Of The Day #59

question of the day
38 - atrial fibrillation

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

This patient presents to the Emergency Department with palpitations, generalized weakness, and shortness of breath after discontinuing all her home medications.  She has hypotension, marked tachycardia, and pulmonary edema (crackles on lung auscultation).  The 12-lead EKG demonstrates atrial fibrillation with a rapid ventricular rate.  This patient is in a state of cardiogenic shock and requires prompt oxygen support, blood pressure support, and heart rate control. 

Pulmonary embolism (Choice A) can sometimes manifest as new atrial fibrillation with shortness of breath and tachycardia, but pulmonary embolism initially causes obstructive shock.  If a pulmonary embolism goes untreated, it can progress to right ventricular failure, pulmonary edema, and cardiogenic shock.  This patient has known atrial fibrillation and stopped all her home medications.  The abrupt medication change is a more likely cause of the patient’s cardiogenic shock.  Dehydration (Choice D) and systemic infection (Choice D) are less likely given the above history of abruptly stopping home maintenance medications.  Untreated cardiac arrythmia (Choice B) is the most likely cause for this patient’s pulmonary edema and cardiogenic shock. 

The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.  

 

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #59," in International Emergency Medicine Education Project, October 15, 2021, https://iem-student.org/2021/10/15/question-of-the-day-59/, date accessed: October 17, 2021

Question Of The Day #56

question of the day

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

This trauma patient arrives with hypotension, tachycardia, absent unilateral lung sounds, and distended neck veins. This should raise high concern for tension pneumothorax, which is a type of obstructive shock (Choice C). This diagnosis should be made clinically without X-ray imaging. Bedside ultrasound can assist in making the diagnosis by looking for bilateral lung sliding, if available. Treatment of tension pneumothorax should be prompt and includes needle decompression followed by tube thoracostomy. Other types of shock outlined in Choices A, B, and D do not fit the clinical scenario with information that is given.

Recall that shock is an emergency medical state characterized by cardiovascular or circulatory failure. Shock prevents peripheral tissues from receiving adequate perfusion, resulting in organ dysfunction and failure. Shock can be categorized as hypovolemic, distributive, obstructive, or cardiogenic. The different categories of shock are defined by their underlying cause (i.e., sepsis, hemorrhage, pulmonary embolism, etc.) and their hemodynamics which sometimes overlap. The diagnosis of shock is largely clinical and supported by the history, vital signs, and physical exam. Additional studies, such as laboratory investigations, bedside ultrasound, and imaging tests help narrow down the type of shock, potential triggers, and guide management. The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.

 

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #56," in International Emergency Medicine Education Project, September 24, 2021, https://iem-student.org/2021/09/24/question-of-the-day-56/, date accessed: October 17, 2021

Question Of The Day #55

question of the day
738.2 - STEMI
Which of the following is the most likely cause for this patient’s condition?  

This patient presents with chest pressure at rest and an anterior ST segment elevation myocardial infraction (STEMI) seen on 12-lead EKG.  This patient should be given aspirin, IV fluids to increase the preload status, and receive immediate coronary reperfusion therapy.  This patient’s hypotension is likely due to infarction of the left ventricle causing poor cardiac output (Choice D).  This is known as cardiogenic shock.  The patient has been vomiting, but the acute onset of symptoms and STEMI on EKG make poor cardiac output (Choice D) more likely than hypovolemia (Choice A) as the cause for the patient’s condition.  Systemic infection (Choice B) and pulmonary embolism (Choice C) are also less likely given the clinical information in the case and the STEMI on EKG.  The best answer is Choice D.  Please see the chart below for further detailing of the different types of shock.   

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #55," in International Emergency Medicine Education Project, September 17, 2021, https://iem-student.org/2021/09/17/question-of-the-day-55/, date accessed: October 17, 2021

Acute Atrial Fibrillation in the ED: Almost all goes home

Atrial fibrillation (AF) is the most common dysrhythmia presenting to ED. The management options depend on patient stability, presence of underlying causes and factors in the patient history. In stable patients presenting in AF with a rapid ventricular response, both rate and rhythm control are acceptable approaches. Physicians often tend toward rate control because evidence has shown no mortality benefit between the two approaches. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial contributed to this trend when it concluded no survival advantage and higher risk of adverse drug effects with rhythm control. However, rhythm control is the preferred approach for the management of acute stable AF in Canadian guidelines. The advantages are a higher rate of symptom resolution, restoration of sinus rhythm and avoiding the need for rate control prescriptions, decreased ED length of stay, and hospital admissions.

In the electrical versus pharmacological cardioversion for emergency department patients with acute atrial fibrillation (RAFF2) trial, it was found that both drug–shock and shock-only strategies were effective, rapid, and safe with 96% of patients discharged home in sinus rhythm. The drug infusion worked for 50% of patients avoiding procedural sedation.

The evidence that supports the management of acute AF in the ED without hospital admission is increasing. Implementing practices to achieve that will markedly decrease the burden on the health care system.

ED Management

Approach of Atrial fibrillation

AF might be secondary to variable causes, including ACS, Heart failure, PE, sepsis and bleeding. In patients with secondary AF, cardioversion might be harmful, and the mainstay of treatment is tackling the underlying cause. Those patients will require hospital admission. For primary AF, if the patient is unstable, electrical cardioversion should be done without delay. Stable primary AF may be managed with rate or rhythm control.

Rate control can be achieved with the following:

CCB: Diltiazim 0.25 mg/kg over ten mins, repeat q15-20 mins, up to three doses (avoid in heart failure)

BB: Metoprolol 2.5-5 mg q15-20 mins

Digoxin: 0.25-0.5 mg loading dose then 0.25 mg q4-6 hs (if hypotension or acute HF occur)

Target is HR <100 at rest or <110 walking

Rhythm control is safe with the following according to The CAEP AF best practice guidelines:

  1. Anticoagulated for three or more weeks.
  2. No valvular heart disease, prior stroke or TIA plus: 
  • Onset in 12 hours or less
  • Onset more than 12 hours but less than 48 hours plus less than two of :
    • Age less than 65, DM, HTN, HF.
  • Cleared by TOE

Methods:

  • Procainamide 15mg/kg in 500 ml of NS over an hour.

Other agents: Amiodarone, Ibutilide, flecainide, etc.

  • Electrical: 150-200 J synchronized. Requires sedation.

Anticoagulation:

If CHADS positive then discharge on DOAC or Warfarin.

Disposition:

Almost all patients can be discharged home after cardioversion or effective rate control with appropriate follow up: within a week if warfarin or rate control agent prescribed, otherwise in 4 weeks.

Patients will require admission if one of the following:

  • Highly symptomatic after treatment.
  • ACS
  • Acute heart failure not improved in the ED

References and Further Reading

  1. Stiell, I. G., Macle, L., & CCS Atrial Fibrillation Guidelines Committee (2011). Canadian Cardiovascular Society atrial fibrillation guidelines 2010: management of recent-onset atrial fibrillation and flutter in the emergency department. The Canadian journal of cardiology27(1), 38–46. https://doi.org/10.1016/j.cjca.2010.11.014
  2. Wyse, D. G., Waldo, A. L., DiMarco, J. P., Domanski, M. J., Rosenberg, Y., Schron, E. B., Kellen, J. C., Greene, H. L., Mickel, M. C., Dalquist, J. E., Corley, S. D., & Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators (2002). A comparison of rate control and rhythm control in patients with atrial fibrillation. The New England journal of medicine347(23), 1825–1833. https://doi.org/10.1056/NEJMoa021328
  3. Baymon, D. E., & Baugh, C. E. (2020). Patients with Atrial Fibrillation in the Emergency Department: Strategies to Achieve Best Outcomes. https://www.hmpgloballearningnetwork.com/site/eplab/patients-atrial-fibrillation-emergency-department-strategies-achieve-best-outcomes
  4. Martín, A., Coll-Vinent, B., Suero, C., Fernández-Simón, A., Sánchez, J., Varona, M., Cancio, M., Sánchez, S., Carbajosa, J., Malagón, F., Montull, E., Del Arco, C., & HERMES-AF investigators (2019). Benefits of Rhythm Control and Rate Control in Recent-onset Atrial Fibrillation: The HERMES-AF Study. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine26(9), 1034–1043. https://doi.org/10.1111/acem.13703
  5. Stiell, I. G., Sivilotti, M., Taljaard, M., Birnie, D., Vadeboncoeur, A., Hohl, C. M., McRae, A. D., Rowe, B. H., Brison, R. J., Thiruganasambandamoorthy, V., Macle, L., Borgundvaag, B., Morris, J., Mercier, E., Clement, C. M., Brinkhurst, J., Sheehan, C., Brown, E., Nemnom, M. J., Wells, G. A., … Perry, J. J. (2020). Electrical versus pharmacological cardioversion for emergency department patients with acute atrial fibrillation (RAFF2): a partial factorial randomised trial. Lancet (London, England)395(10221), 339–349. https://doi.org/10.1016/S0140-6736(19)32994-0
  6. Ian G. Stiell, et al. (2021). 2021 CAEP Acute Atrial Fibrillation/Flutter Best Practices Checklist.https://caep.ca/wp-content/uploads/2021/06/2021-CAEP-AAF-Checklist-FINAL-6-June-2021.pdf
Cite this article as: Israa M Salih, UAE, "Acute Atrial Fibrillation in the ED: Almost all goes home," in International Emergency Medicine Education Project, September 13, 2021, https://iem-student.org/2021/09/13/acute-atrial-fibrillation-in-the-ed-almost-all-goes-home/, date accessed: October 17, 2021

Defibrillator: Clear!

Defibrillator clear

So, this is your first day at your internship rotation in the Emergency Department. You see some movement in the resuscitation room, and someone shouts: CODE!

Then, you approach the team, excited to learn and help with cardiopulmonary resuscitation (CPR). The attending physician looks at you and asks: Do you know how to use the defibrillator?

What would your answer be?

Knowing the main functions of the defibrillator is essential but not enough; you need to get used to the model in your hospital to be able to help safely with an emergency.

Defibrillators are devices used to apply electrical energy manually or automatically. Their use is indicated for electrical cardioversion, defibrillation or as a transcutaneous pacemaker.

Later that day, another patient presents with unstable atrial fibrillation (AFib).

The attending suggests cardioverting the patient. Do you know how to prepare the defibrillator?

Defibrillation versus cardioversion

Both defibrillation and cardioversion are techniques in which an electrical current is applied to the patient, through a defibrillator, to reverse a cardiac arrhythmia.

Defibrillation

Defibrillation is a non-synchronized electrical discharge applied to the chest, which aims to depolarize all myocardial muscle fibres, thus literally restarting the heart, allowing the sinoatrial node to resume the generation and control of the heart rhythm, and reversing the severe arrhythmias. It is indicated for pulseless ventricular tachycardia and ventricular fibrillation during CPR.

Electrical Cardioversion

Electrical cardioversion is the application of shock in a synchronized way to ensure the electric discharge is released in the R wave, that is, in the refractory period because accidental delivery of the shock during the vulnerable period, that is, the T wave, can trigger VF. It is reserved for severe arrhythmias in unstable patients with a pulse. It can usually be an elective procedure.

Special Situations

Digital Intoxication

Digital intoxication can present with any type of tachyarrhythmia or bradyarrhythmia. Cardioversion in this situation is a relative contraindication, as digital makes the heart sensitive to electrical stimulation. Before considering cardioversion, correct all electrolyte imbalances, otherwise, the cardioversion can degenerate the rhythm to a VF.

Pacemaker / Implantable cardioverter-defibrillator (ICD)

Cardioversion can be performed, but with care. The inadequate technique can damage the generator, the conductive system, or the heart muscle, leading to dysfunction of the device. The blades must be positioned at least 12 cm away from the generator, preferably in the anteroposterior position. The lowest possible electrical charge must be used.

Pregnancy

Cardioversion can be used safely during pregnancy. The fetal beat should be monitored throughout the procedure.

Things To Consider

Keep your devices tested!

Working in the ED is not easy. This is the place where organization and preparation should be routine. Constant checking of materials and operation of the equipment must be the rule because the smallest detail can cause a difference in saving a life.

During adversity, it is necessary to remain calm, trying to not affect the reasoning and disposition of the team. It is an arduous job, it takes practice and a lot of effort. Errors can only be corrected after they are recognized and must have the right time to be exposed. It happens.

There is no time for despair, yelling and stress when it comes to CPR.

No conductive gel, what can we do?

The main guidelines regarding the use of the conductive gel used in the defibrillator paddles are:

  • Using the proper gel for this purpose is essential. The gel is an electrically conductive material that decreases the resistance to the flow of electric current between the paddle and the chest wall. The absence of conductive material can lead to the production of an arc that causes burns in the patient and the risk of explosion if there is an oxygen source very close, among others.
  • Avoid the use of gauze soaked in saline solution, as the excess serum can cause burns on the patient’s skin, but it is a reasonable option, in an emergency
  • Do not use the ultrasound gel
  • The preference is to use adhesive paddles that already come with their own conductive gel (but this is rare in Brazil).

Location recommended by Advanced Cardiac Life Support (ACLS)

Antero-lateral

One paddle is placed on the right side of the sternum, right below the clavicle and the other laterally where the cardiac appendix would be in the anterior or medial axillary line (V5-V6).

Adhesive paddles can also be placed in an anteroposterior position: The anterior one is placed in the cardiac appendage or precordial region, and the posterior one is placed on the back in the right or left infrascapular region.

During the shock, the provider must ensure that no one is in contact with the patient. A force of approximately 8k must be used to increase the contact of the paddles with the chest. Do not allow a continuous flow of oxygen over the patient’s chest to avoid accidents with sparks.

Complications

  • Electric arc (when electricity travels through the air between the electrodes and can cause explosive noises, burns and impair current delivery)
  • Electrical injuries in spectators
  • Risk of explosion if there is a continuous flow of oxygen during the shock
  • Burning of the skin by repeated shocks
  • Myocardial injury and post-defibrillation arrhythmias and myocardial stunning
  • Skeletal muscle injury
  • Fracture of thoracic vertebrae

References and Further Reading

  1. Sunde, K., Jacobs, I., Deakin, C. D., Hazinski, M. F., Kerber, R. E., Koster, R. W., Morrison, L. J., Nolan, J. P., Sayre, M. R., & Defibrillation Chapter Collaborators (2010). Part 6: Defibrillation: 2010 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Resuscitation81 Suppl 1, e71–e85. https://doi.org/10.1016/j.resuscitation.2010.08.025
  2. Panchal, A. R., Bartos, J. A., Cabañas, J. G., Donnino, M. W., Drennan, I. R., Hirsch, K. G., Kudenchuk, P. J., Kurz, M. C., Lavonas, E. J., Morley, P. T., O’Neil, B. J., Peberdy, M. A., Rittenberger, J. C., Rodriguez, A. J., Sawyer, K. N., Berg, K. M., & Adult Basic and Advanced Life Support Writing Group (2020). Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation142(16_suppl_2), S366–S468. https://doi.org/10.1161/CIR.0000000000000916
  3. Ionmhain, U. N. (2020). Defibrillation Basics. Life in The Fastlane. Retrieved April 26, 2020, from https://litfl.com/defibrillation-basics/
  4. Paradis, N. A., Halperin, H. R., Kern, K. B., Wenzel, V., & Chamberlain, D. A. (Eds.). (2007). Cardiac arrest: the science and practice of resuscitation medicine. Cambridge University Press.
  5. Nickson, C. (2020). Defibrillation Pads and Paddles. Life in The Fastlane. Retrieved April 26, 2020, from https://litfl.com/defibrillation-pads-and-paddles/
Cite this article as: Jule Santos, Brasil, "Defibrillator: Clear!," in International Emergency Medicine Education Project, August 9, 2021, https://iem-student.org/2021/08/09/defibrillator-clear/, date accessed: October 17, 2021

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: October 17, 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: October 17, 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: October 17, 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: October 17, 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: October 17, 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: October 17, 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: October 17, 2021