Posts filed under Cardiovascular

ECMO Initiation in the ED

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Written by: Kaitlin Ray, MD (NUEM PGY-3) Edited by: Evan Davis, MD (NUEM Alum ‘18) Expert commentary by: Colin McCloskey, MD (NUEM Alum ‘16)


ECMO Initiation in the Emergency Department

Introduction:

Extracorporeal membrane oxygenation (ECMO) provides prolonged cardiopulmonary support in severe acute respiratory or cardiac failure. As the science behind ECMO continues to grow and with promising data regarding its use in acute hypoxemic respiratory failure, cardiac arrest, and cardiogenic shock, ECMO use in the United States has increased over 400% in the last ten years. This has stimulated an interest in earlier applications of ECMO both in the emergency department (ED) and even in the prehospital setting [1]. Initiation of ECMO in the ED is a relatively new development, with 65% of programs <5 years old and the majority of programs with <3 cases per year. However, this number continues to grow [2].

There two main types of ECMO: venoarterial (VA) and venovenous (VV). While VV ECMO provides respiratory support, only VA ECMO provides both respiratory and hemodynamic support. ECMO drains blood from the native vascular system, then circulates it outside of the body via a mechanical pump where it passes through an oxygenator and heat exchanger. Hemoglobin then becomes saturated with oxygen, CO2 is removed, and blood then reinfuses into the circulation [4]. Venoarterial ECMO is more commonly utilized in the emergency department as eligible ED patients often have concurrent hemodynamic and respiratory collapse.

Emergency medicine physicians have an increasing responsibility to initiate ECMO and/or make the decision to transfer to an ECMO capable facility. Knowing this, it is critical that we are familiar with the types of ECMO available, understand the indications, contraindications, risks, benefits, and logistics of initiating this form of extracorporeal life support.

 

Indications/Contraindications:

The specific criteria and contraindications to ECMO vary from institution to institution, often making the decision and ability to initiate ECMO challenging. The Extracorporeal Life Support Organization (ELSO) provides specific guidelines for ECMO initiation. These indications include cardiogenic shock as defined as (1) hypotension and low cardiac output with inadequate tissue perfusion despite adequate intravascular volume and (2) persistent shock despite volume, inotropes, pressors, and possibly an intraaortic balloon pump. The ELSO also provides guidelines for ECMO in acute respiratory collapse, as well as contraindications for ECMO including: unrecoverable heart failure and not a candidate for transplant or LVAD, advanced age, chronic multi-system failure, compliance issues, terminal malignancy and prolonged CPR without adequate tissue perfusion. 

As emergency physicians, which patients should we consider as candidates for ECMO? Generally speaking, consider younger and healthier patients who experience an acute but reversible insult leading to rapid cardiopulmonary collapse.  Recall that ECMO should only be considered as a bridge to more definitive therapy. Examples of scenarios that fit this criterion include:

  • Massive pulmonary embolism

  • Myocardial infarction causing V-Tach/V-Fib or cardiogenic shock

  • Acute myocarditis or cardiomyopathy causing cardiogenic shock

  • Drowning

  • Hypothermia

  • Drug overdose causing cardiovascular collapse (such as beta-blocker or Ca-channel blocker)

  • Massive smoke inhalation, pulmonary contusion, or pulmonary hemorrhage causing refractory hypoxemia

As mentioned above, generally those with more chronic conditions such as end-stage heart failure, end-stage COPD, or those with chronic multi-organ failure, do not make good ECMO candidates. Other patient populations to consider in an ICU rather than ED setting include those with septic shock and/or ARDS. Note that patients with traumatic injury leading to hemorrhagic decompensation, although acute in nature, typically are not good candidates for ECMO as ECMO does not prevent further blood loss.

Additionally, we must consider what an ECMO-eligible patient clinically looks like. The majority of the patients who present with one of the above conditions will either be responsive to conventional therapies (intubation, fluids, inotropes), or they will be dead on arrival. However it is the rare, in-between patient that should be considered for ECMO. The condition of a good candidate would include things like: 

  • Persistent hypotension despite maximum conventional therapy

  • Persistent hypoxemia despite maximum ventilator therapy

  • Patients brought in in cardiac arrest but achieve periods of unsustained ROSC

  • Patients brought in with vitals but arrest in the ED

Unfortunately patients who arrest in the field, are brought to the ED already in cardiac arrest, or who do not achieve ROSC despite 30-45 minutes of well executed ACLS are unlikely to be appropriate ECMO candidates. The critical ECMO population is truly those who are flirting with life vs. death, especially the patients with intermittent periods of ROSC. Key exceptions to this include drowning and/or hypothermic patients. Generally these patients are better candidates for ECMO even if there has not been a recorded pulse, with the caveat that they should have been pulled out of the water or other environment quickly.

 

Risks/benefits:

ECMO is unique in that it provides full cardiopulmonary support without the physical trauma of chest compressions, thereby decreasing trauma, stress, and number of interruptions. Additionally, it provides a higher flow state than would otherwise be provided by manual compressions [2]. VV ECMO also minimizes barotrauma, volutrauma, and oxidative stress. However ECMO is not without risks and complications. The risk of bleeding is significant in the context of continuous anticoagulation and platelet dysfunction. Thromboembolism may lead to stroke or limb ischemia [4]. Infection may also occur secondary to indwelling lines/tubes [1].

 

Logistics:

ECMO is a costly intervention that requires a multi-disciplinary approach and an organizational commitment in order to proceed. Consideration must be given to the required equipment, blood bank capabilities, cannulation, and personnel availability. In order for ECMO to be successfully initiated from the ED, coordination between EMS, emergency medicine physicians, the cath lab, nursing staff, neurocritical care, cardiothoracic surgery, and the ICU is required [3]. When cannulating for VV ECMO, one may use a two cannula approach (femoral vein and internal jugular/SVC), or a single dual-lumen cannula (right atrium/IVC via the IJ). VA ECMO typically involves cannulation through the femoral artery and femoral vein [1]. If CPR is ongoing during cannulation attempts, programs may use a modified ACLS algorithm with a continuous epinephrine infusion at 0.7 mg/kg/min and minimization of pulse checks by utilizing continuous TEE monitoring [3]. Aggressive anticoagulation is required with continuous infusion of either unfractionated heparin or direct thrombin inhibitor, and efforts should be made to maintain platelet counts >50K and hemoglobin >12 mg/dL6,7.

 

Recap:

While initiation of ECMO from the emergency department is still a relatively new endeavor for many certified ECMO centers, the ED is in a unique position to bridge select patients in acute respiratory or cardiac failure to recovery using ECMO.  While institutional criteria for ECMO varies, the ELSO guidelines may be used as a reference to guide decision making in the absence of formal criteria. Generally speaking, pursue ECMO for younger, healthier patients with acute hemodynamic and/or respiratory collapse that is potentially reversible and unresponsive to conventional therapies. Typically patients with massive PE, MI, hypothermia, drowning, acute cardiomyopathy are the best candidates for ED ECMO. Contraindications generally include severe neurologic injury, end stage malignancy, advanced age, and irreversible multi-organ failure. Knowing that the emergency physicians are often the first to receive patients in acute cardiac and respiratory failure, it is critical that we are familiar with the types of ECMO available, understand the indications, contraindications, risks and benefits, and logistics of initiating this form of extracorporeal life support.


Expert Commentary 

This is a thoughtful and thorough overview of ECMO within the emergency department. I will limit my commentary to VA ECMO for cardiopulmonary failure (ECPR), given the enthusiasm for the topic in the FOAM world and my experience within a ED based ECMO program. Some broad themes I would like to highlight: Evidence, Patient selection and Systems of Care.

Evidence: There is a signal that ECPR is better than conventional CPR. A systematic review and metanalysis found that those with cardiac arrest who received VA ECMO had an association with increased neurologically intact survival, with a number needed to treat of 7 [1]. However, most of the data is retrospective and from single centers, making it subject to a number of confounders, as well as selection bias. Further, those who received ECPR were more likely to receive therapeutic hypothermia and percutaneous catheterization, both interventions known to improve outcome following cardiac arrest.  Another single center experience has been promising, with 9/18 patients surviving to hospital discharge with good neurological outcome [2]. This protocol involved EMS bypassing the ED and taking the patient to the cardiac catheterization lab where they were placed on ECMO and underwent catheterization. Those who had good outcome all had concomitant intervenable coronary artery disease. There are several centers that have similar experiences with published case series [3,4], but it depends thus far on quality patient selection and a viable system of care.

Patient Selection:  All the above trials had strict inclusion and exclusion criteria. Most established protocols include an age cutoff (65-75 depending on center), initial shockable rhythm, and a time from arrest to cannulation between 30-60 minutes. Pertinent exclusions include advanced comorbidities, initial asystole or prolonged downtime. This is done with the intent of cannulating patients with the best chance of surviving their ECMO run; namely young patients with likely coronary artery disease who need ECMO as a bridge to cardiac catheterization. VA ECMO’s other successful ED applications, namely pulmonary embolism [5], drug overdose [6], and acute myocarditis [7] all share the commonality that ECMO provides time for recovery or as a bridge to a viable intervention. A bridge to recovery must exist prior to any cannulation scenario; this cannot be understated.

Systems of care: Cannulation is just one step in a VA ECMO patients hospital course. When conceptualizing a successful ED ECMO program, the institutional commitment should be visualized: A patient requiring 5-7 days in the ICU, formal neuroprognostication and continuous goals of care discussions with family. You rightly include a logistics session in your review, but this system of care is paramount to a successful ECMO program. Prehospital EMS systems must be designed for quick recognition and transport of ECMO candidates.  Emergency physicians need to be trained, and maintain competency in ECMO cannulation; interventional cardiology must be willing to catheterize appropriate patients; ICU consultants must have a standardized protocol for post-arrest care and neurology/ICU must have an institutionally accepted neuroprognostication scheme. In parallel to this, the family discussions regarding prognosis and any transition of care should include social work, case management and palliative care professionals. Cannulation is as exciting a procedure an emergency physician can perform, but without a thoughtful, multidisciplinary system of care, these patients will do poorly.

In closing, VA ECMO in the emergency department is an exciting development to tertiary ED practice. More experience, and more data, will help define the niche of patients and the necessities of post-arrest care that provide these patients with the best outcome.

1. Ouweneel DM, Schotborgh JV, Limpens J, et al. Extracorporeal life support during cardiac arrest and cardiogenic shock: A systematic review and meta-analysis. Intensive Care Med. 2016;42(12):1922-1934.

2. Yannopoulos D, Bartos JA, Martin C, et al. Minnesota resuscitation consortium's advanced perfusion and reperfusion cardiac life support strategy for out-of-hospital refractory ventricular fibrillation. J Am Heart Assoc. 2016;5(6):10.1161/JAHA.116.003732.

3. Stub D, Bernard S, Pellegrino V, et al. Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial). Resuscitation. 2015;86:88-94.

4. Bellezzo JM, Shinar Z, Davis DP, et al. Emergency physician-initiated extracorporeal cardiopulmonary resuscitation. Resuscitation. 2012;83(8):966-970.

5. Yusuff H, Zochios V, Vuylsteke A. Extracorporeal membrane oxygenation in acute massive pulmonary embolism: A systematic review. Perfusion. 2015;30(8):611-616.

6. Wang G, Levitan R, Wiegand T, et al. Extracorporeal membrane oxygenation (ecmo) for severe toxicological exposures: Review of the toxicology investigators consortium (toxic). Journal of Medical Toxicology. 2016;12(1):95-99.

7. Nakamura T, Ishida K, Taniguchi Y, et al. Prognosis of patients with fulminant myocarditis managed by peripheral venoarterial extracorporeal membranous oxygenation support: A retrospective single-center study. Journal of intensive care. 2015;3(1):5.

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Colin McCloskey, MD
NUEM Alum ‘16, Critical Care Anesthesiology fellow - University of Michigan Medical Center/University of Michigan Health System


How To Cite This Post

[Peer-Reviewed, Web Publication]  Ray K, Davis E (2018, November 12). ECMO Initiation in the ED  [NUEM Blog. Expert Commentary by McCloskey C]. Retrieved from http://www.nuemblog.com/blog/ECMO


Other Posts You May Enjoy


Resources

  1. Mosier, Jarrod M., et al. “Extracorporeal Membrane Oxygenation (ECMO) for Critically Ill Adults in the Emergency Department: History, Current Applications, and Future Directions.” Critical Care, BioMed Central, 17 Dec. 2015, ccforum.biomedcentral.com/articles/10.1186/s13054-015-1155-7.

  2. Tonna, Joseph E., et al. “Practice Characteristics of Emergency Department Extracorporeal Cardiopulmonary Resuscitation (ECPR) Programs in the United States: The Current State of the Art of Emergency Department Extracorporeal Membrane Oxygenation (ED ECMO).” Resuscitation, Elsevier Ireland Ltd, 10 Sept. 2016, experts.umich.edu/en/publications/practice-characteristics-of-emergency-department-extracorporeal-c.

  3. Tonna, Joseph E., et al. “Development and Implementation of a Comprehensive, Multidisciplinary Emergency Department Extracorporeal Membrane Oxygenation Program.” Annals of Emergency Medicine, Mosby Inc., 1 July 2017, cwru.pure.elsevier.com/en/publications/development-and-implementation-of-a-comprehensive-multidisciplina.

  4. Bartlett, Robert. Extracorporeal Membrane Oxygenation (ECMO) in Adults, 16 June 2017, www.uptodate.com/contents/extracorporeal-membrane-oxygenation-ecmo-in-adults.

  5. Extracorporeal Life Support Organization - ECMO and ECLS. “Guidelines for Adult Respiratory and Cardiac Failure.” Extracorporeal Life Support Organization - ECMO and ECLS > Resources > Guidelines, ELSO (Extracorporeal Life Support Organization), Dec. 2013, www.elso.org/Resources/Guidelines.aspx.

  6. Sklar MC, Sy E, Lequier L, et al. Anticoagulation Practices during Venovenous Extracorporeal Membrane Oxygenation for Respiratory Failure. A Systematic Review. Ann Am Thorac Soc 2016; 13:2242.

  7. Spinelli E, Bartlett RH. Anemia and Transfusion in Critical Care: Physiology and Management. J Intensive Care Med 2016; 31:295.

 

Posted on November 12, 2018 and filed under Cardiovascular.

Approach to Hypothermic Resuscitation

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Written by:  Luke Neil, MD (NUEM PGY-2) Edited by: Quentin Rueter, MD, (NUEM PGY-4) Expert commentary by: Kory Gebhardt, MD


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Expert Commentary

This is a good overview of the algorithmic approach to the hypothermic patient. Generally speaking, hypothermia can be divided into various categories of severity, but as you mention, it is really those patients with a core temperature of <32°C (90°F) with cardiac instability or cardiac arrest that will require especially aggressive care.

For any hypothermic patient, the most important initial intervention is to stop any further heat loss. This is especially important for those with damp or wet clothing. Any wet garments should be completely removed, the patient should be dried, and then covered with warm, dry blankets and possibly a forced air rewarming device (i.e. Bair Hugger). Recall that one of the most efficient ways to cool a HYPERthermic patient is with evaporative cooling (spraying with or submerging them in water and then using fans to circulate air over the wet surfaces). Similarly, this heat loss will strongly work against you in rewarming a hypothermic patient if they are not fully dry. After this simple intervention, the majority of mildly hypothermic and stable patients just need time to bring their core temperature back to normal and often can be discharged once this has occurred.

For those patients with a core temp >32°C with severe cardiac instability or in cardiac arrest, you should also consider alternative etiologies for their presentation rather than expect it solely caused by the hypothermia alone. Like you mention, if you are able to rewarm a cardiac arrest patient above this temperature and they remain in asystole, it is likely that irreversible damage has occurred and they are less likely to be able to be successfully resuscitated.

As you detail in the algorithm, those with a temperature less than 32°C (90°F) AND instability or arrest need aggressive and invasive rewarming. The best available means of doing this is ECMO. Much of the research surrounding accidental hypothermia and resuscitation comes from the Nordic countries where freezing temperatures are often combined with outdoor extracurriculars and results in a high “n” for the studies. Outcomes data from many of the expert centers in this area show major benefits of ECMO, including one showing survival post-arrest in nearly 60% of patients and, even more importantly, good neurologic outcomes in 38% compared to only 3% in those without extracorporeal rewarming!

Unfortunately, not all EM physicians will have quick or 24/7 availability of ECMO. While this should be the preferred means of rewarming if available, there are alternatives if it is not. Hemodialysis circuits can also be used to actively rewarm a patient. Generally these can achieve 2-4 degrees/hr of rewarming compared to the 4-6 degrees/hr of ECMO. Thoracic (bilateral chest tubes), gastric (NG tube), and bladder lavage (foley) with warm fluids can also provide several degrees per hour of rewarming if used appropriately. Use a ventilator that can warm and humidify air. Don’t forget about minimizing heat loss by fully drying the patient and keeping as much of them covered as possible.

Lastly, I want to say a word about prognostication. While the mantra is, “you’re not dead until you’re warm and dead”, you can imagine that these patients require a considerable amount of time, effort, and mobilization of resources when they present to the ED. There is information that can help guide which patients are likely to benefit from such aggressive care from those who are, unfortunately, unlikely to be resuscitated. While multiple markers have been studied, the one with the most evidence supporting it, is a potassium value. This value can serve as a sort of surrogate for “warm ischemia time”, or in other words, how long were they warm and dead. This should be obtained and sent early in the resuscitation of the patient. If the value is >12, there is nearly no chance of any meaningful recovery (still very unlikely at >10, and even a cutoff of >8). Conversely, if the potassium level is less than the 8-12 range, the patient still has a good chance at a meaningful recovery if resuscitated to ROSC and these are the patients that should receive everything we have to rapidly and efficiently rewarm them (they are also the patients that can have meaningful recoveries despite impressive downtimes of even hours).

Additionally, historical factors surrounding the hypothermia, if known, can provide valuable prognostic information. Immersion vs. Submersion, which you define in your algorithm, is one example that might influence your decision about whether a patient might have benefit from mobilizing ECMO or other aggressive/invasive rewarming.

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Kory Gebhardt, MD

Kaiser Permanente Emergency Medicine


How to cite this post

[Peer-Reviewed, Web Publication]   Neil L, Rueter Q (2018, June 4 ). Approach to Hypothermic Resuscitation.  [NUEM Blog. Expert Commentary by Gebhardt K]. Retrieved from http://www.nuemblog.com/blog/hypothermia


Posted on June 4, 2018 and filed under Cardiovascular.

Treatment of pSVT: A Case for Calcium Channel Blockers

Written by:  Amanda Randolph, MD (NUEM PGY-1) Edited by: Jim Kenny, MD, (NUEM PGY-4) Expert commentary by: Meghan Groth, PharmD - Emergency Medicine Clinical Pharmacist, UMass Memorial Medical Center 


The Case

A 37 year-old woman presents to the ED for palpitations. On the monitor, you see her heart rate is 190, but all other vitals are within normal limits. She feels anxious but is otherwise asymptomatic, breathing comfortably on room air. The rest of the physical exam is unremarkable. The patient tells you, “I think it’s my SVT again - I was just here for this last month!”

Her rhythm strip looks something like this:

https://lifeinthefastlane.com/ecg-library/svt/

SVT generally refers to any tachyarrhythmia generated above the His/Purkinje system. For simplicity, the term pSVT in this post will refer to only Atrioventricular Nodal Tachycardia (AVNRT), as it is the most common tachyarrhythmia in patients with normal cardiac structure [1].


SVT: Treatment Guidelines

You double-check the current ACLS protocol (2015) for the treatment of pSVT [2]: 

Figure 1. ACLS 2015 guidelines for treatment of AVNRT

This patient is stable, so you try some vagal maneuvers, including carotid massage and Valsalva. You even try the modified Valsalva maneuver you read about in the REVERT trial (straining followed by leg elevation and supine positioning), which is described to have a 43% success rate.

 

Despite your best efforts, the vagal maneuvers fail, so you ask the nurse to draw up some adenosine. 

 

At this point, the patient yells, “Absolutely no way! I’m not trying Adenosine - it makes me feel like I’m going to die! There has to be something else.” 

 

 

You know Calcium Channel Blockers (CCBs) are recommended as a second line drug if adenosine does not terminate the SVT, or if adenosine is contraindicated. But what does the data say? Is it ever reasonable to jump straight to CCBs?


The Problem with Adenosine

Adenosine administration is widely recognized to produce a variety of minor side effects, as listed below4. While not quantified in any studies to date, these “minor” side effects can be extremely traumatic for patients. This distress can have lasting psychological effects that may delay or even prevent patients from seeking care [5].

  •  Chest pain (7-40%)
  •  Facial flushing (18-44%)
  •  Nausea (13%)
  • Headache (2-18%)
  • Lightheadedness/Dizziness (12%)

The Problem with Calcium Channel Blockers

Current ACC/AHA guidelines give CCBs a class IIa recommendation for use in pSVT [2]. However, most EM practitioners continue to favor Adenosine, in part because of cultural dogma, but also due to concern about inadequate data to regarding the efficacy and safety for calcium channel blocker use. 

One pharmacologic difference between CCBs and Adenosine is the onset of action (100-400 seconds for CCBs compared with 21-34 seconds for Adenosine), which can create a delay to conversion [5]. However, because CCBs are only used in stable patients, this slightly longer onset is unlikely to be clinically significant [6].

More importantly, one of the most feared side effects of Calcium channel blockers is hypotension, as CCBs work by creating negative inotropy and peripheral vasodilation. In one study by Lim et al., the change in blood pressure after administration of adenosine was -2.6/-1.7, compared to -13.0/-8.1 with verapamil [9]. 

Of note, the duration of action is quite long for CCBs (2-5 hours), compared with adenosine (<10 seconds).7 This raises a concern that hypotension and other adverse effects of CCBs may be prolonged. For this reason, CCBs are contraindicated in patients with severe HFrEF.6,7 Additionally, CCBs are relatively contraindicated in patients taking beta blockers, as the combined effect can cause significant bradycardia and even heart block [6].

Theoretically, the use of CCBs via slow infusion instead of IV bolus may reduce the risk of hypotension,8 though there is limited data to support this. One randomized trial by Lim et al. compared the use of adenosine (n = 104) vs slow infusion of verapamil (n = 48) or diltiazem (n = 54), and reported no difference in outcomes between adenosine bolus and slow infusion of verapamil or diltiazem [9].


Calcium Channel Blockers vs. Adenosine - The Data

To date, there have been three meta-analyses comparing the efficacy and safety of CCBs to adenosine in patients with pSVT, including a recently published Cochrane review in October 2017.5,6,10 Note that the data described in these studies only refer to the use of Verapamil. Their findings are depicted below (table design inspired by a phenomenal ALiEM post) [8].

A Few Notes on Hypotension after Verapamil:

  • None of these metaanalyses specifically reported their definition of hypotension, nor did they clarify whether any of these patients had clinical signs of shock.
  • Holdgate and Foo reported two of three hypotensive patients subsequently reverted with adenosine and did not require any other specific treatment for their hypotension (the outcome and interventions for the third case were not reported). 
  • The study by Lim et al. using slow infusion of verapamil reported only one patient with clinically significant hypotension, with a drop in blood pressure from 122/81 mmHg to 74/61 mmHg after 7.5 mg of verapamil infusion. This patient’s SVT was terminated by synchronized cardioversion, after which his blood pressure improved to 103/69 mmHg.

Case Resolution

After the vagal maneuvers, you give 5mg IV Verapamil. The patient remains stable and converts to sinus tachycardia. She tells you she prefers Verapamil to Adenosine and will be “much less afraid” to come in next time. 


Conclusion

Overall, both Adenosine and Verapamil are reasonable choices for termination of SVT. Anecdotally, some patients prefer Verapamil; however, there is limited evidence to support this [6]. Given the current data, physicians should discuss the pros/cons of each drug with the patient and employ shared decision-making when possible. 


Take Home Points

  •  Start with vagal maneuvers, especially the modified Valsalva
  • Adenosine and Verapamil are equally effective for SVT 
    •  Moderate evidence by recent Cochrane review
    •  Class IIa by ACC/AHA
  •  Adenosine has a much higher incidence of minor side effects
    • chest pain, facial flushing, nausea, headache, and lightheadedness/dizziness
  • Verapamil has a slightly higher risk of hypotension
    • Verapamil: -13/-8 mmHg; Adenosine -2.6/-1.7 mmH
    • Rarely clinically significant - cases reportedly resolved with adenosine or synchronized cardioversion
  • Always employ shared decision-making when possible 

Expert Commentary

Thank you for your insightful post on this all-too-common conundrum we face in the ED. I think it’s incredibly important to remember, as you point out, that treatment of pSVT in the ED doesn’t have to be a “one size fits all” approach, and that we have more than just adenosine available as a treatment agent.

Most of the data for CCBs in this indication is with verapamil, but I’ve become comfortable recommending diltiazem in its place due to a lower risk of hypotension (see post for reference).

When attempting to mitigate the potential hypotension associated with calcium channel blockers, the study by Lim and colleagues that you mentioned is worth noting in more detail. Rather than the traditional 0.25 mg/kg diltiazem bolus (with 0.35 mg/kg repeat dose), subjects instead received diltiazem at a rate of 2.5 mg/min for up to 20 minutes (max dose 50 mg). This approach can optimize dose, reduce potential for hypotension, and spare the patient that “impending doom” feeling often experienced with adenosine (see further discussion on this here).

There are also some cases when adenosine should not be routinely administered, such as patients with reactive airway disease at risk of bronchospasm. A more thorough review of this topic is presented here but in such cases calcium channel blockers represent a reasonable alternative.

The strategy of using calcium channel blockers for pSVT can perhaps leave providers wanting in terms of the instant gratification that comes with adenosine administration, but agents like diltiazem or verapamil have demonstrated efficacy while avoiding some of the unpleasantries of adenosine.

For me, it comes down to recognizing that adenosine isn’t the only drug we have available for the treatment of pSVT. Calcium channel blockers like diltiazem may be used, and if we decide to try them, we can use different dosing approaches such as the slow bolus method outlined above to reduce some of the potential side effects.

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Meghan Groth, PharmD

Emergency Medicine Clinical Pharmacist 

UMass Memorial Medical Center

 


[Peer-Reviewed, Web Publication]   Randolph A,  Kenny J (2018, May 28 ). Treatment of pSVT: A case for calcium channel blockers.  [NUEM Blog. Expert Commentary by Groth, M]. Retrieved from http://www.nuemblog.com/blog/PSVT


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References

  1. Burns, E., Supraventricular Tachycardia (SVT), in Life in the Fast Lane, M. Cadogan and C. Nickson, Editors. 2012.
  2. Page R, Joglar J, Caldwell M, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2016;67(13):e27-e115.
  3. Appelboam, A., et al., Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. The Lancet, 2015. 386(10005): p. 1747-1753.
  4. Adenosine. Lexi-Drugs. Lexicomp. Wolters Kluwer Health, Inc. Riverwoods, IL.  Available at:  http://online.lexi.com.  Accessed November 12, 2017.
  5. Delaney, B., J. Loy, and A.-M. Kelly, The relative efficacy of adenosine versus verapamil for the treatment of stable paroxysmal supraventricular tachycardia in adults: a meta-analysis. European Journal of Emergency Medicine, 2011. 18(3): p. 148-152.
  6. Alabed S, Sabouni A, Providencia R, Atallah E, Qintar M, Chico TJA. Adenosine versus intravenous calcium channel antagonists for supraventricular tachycardia. Cochrane Database of Systematic Reviews 2017, Issue 10. Art. No.: CD005154. DOI: 10.1002/14651858.CD005154.pub4.
  7. [Peer Reviewed, Web Publication] S. Brubaker and B. Long (2017 Feb 1). Treatment of Refractory SVT: Pearls and Pitfalls. [EmDocs.net, Expert Commentary by A. Koyfman]. Retrieved from http://www.emdocs.net/treatment-refractory-svt-pearls-pitfalls/
  8. [Web Publication] S. Rappaport and M. Groth (2016 Mar 3).  Calcium channel blockers for stable SVT: A first line agent over adenosine? [AliEm Blog]. Retrieved from https://www.aliem.com/2016/03/calcium-channel-blockers-stable-svt-alternative-to-adenosine/ 
  9. Lim S, Anantharaman V, Teo W, Chan Y. Slow infusion of calcium channel blockers compared with intravenous adenosine in the emergency treatment of supraventricular tachycardia. Resuscitation. 2009;80(5):523-528.
  10. Holdgate, A. and A. Foo, Adenosine versus intravenous calcium channel antagonists for the treatment of supraventricular tachycardia in adults. The Cochrane Library, 2006. 
Posted on May 28, 2018 and filed under Cardiovascular.

The PESIT Trial: Do All Syncope Patients Need a PE Workup?

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Written by: Alex Ireland, MD (NUEM PGY-2) Edited by: Josh Zimmerman, MD,  (NUEM class of 2017) Expert Commentary by: D. Mark Courtney, MD


Syncope is defined as a transient loss of consciousness and postural tone caused by cerebral hypoperfusion. This chief complaint is familiar to most emergency physicians given it accounts for more than 1-2 million patient visits in the US annually.[1]  The differential diagnosis is broad and crosses multiple organ systems, including, but not limited to, cardiovascular, neurovascular,  and hemorrhagic/hematologic causes.  Pulmonary embolism (PE) is one cardiovascular cause that is considered to be infrequent. This is because when associated with syncope, it is often made more clinically apparent by signs and symptoms such as dyspnea, chest pain, tachycardia, hypotension, and hypoxemia.  The American Heart Association consensus statement on the evaluation of syncope gives little attention to diagnostics for PE, instead focusing on arrhythmia, ischemia, and structural heart disease. [2]  We know from a San Francisco Syncope Rule validation trial that when adverse events occur in the minority of patients with generalized syncope, they are related mostly to cardiac arrhythmias, followed by MI- not PE. [3] Previous studies have cited the prevalence of pulmonary embolism as a cause of syncope in hospitalized patients as low as 1.6%. [4]  But are we underestimating and under-diagnosing this potentially lethal condition? The PESIT study sought to systematically assess the prevalence of pulmonary embolism in patients admitted for syncope. [5] 


Prevalence of Pulmonary Embolism among Patients Hospitalized for Syncope. Paolo Prandoni, M.D., Ph.D., Anthonie W.A. Lensing, M.D., Ph.D., Martin H. Prins, M.D., Ph.D., Maurizio Ciammaichella, M.D., Marica Perlati, M.D., Nicola Mumoli, M.D., Eugenio Bucherini, M.D., Adriana Visonà, M.D., Carlo Bova, M.D., Davide Imberti, M.D., Stefano Campostrini, Ph.D., and Sofia Barbar, M.D., for the PESIT Investigators*. N Engl J Med 2016; 375:1524-1531. October 20, 2016

What was the PESIT trial? 

 Figure 1. Inclusion and Exclusion Flowchart

Figure 1. Inclusion and Exclusion Flowchart

    The PESIT trial was a cross-sectional study of patients older than 18 years of age who were hospitalized for a first episode of syncope. This was a multicenter trial, taking place in 11 hospitals (2 academic, 9 nonacademic) in Italy. There were several important exclusion criteria to this study including patients on anticoagulation, pregnant patients, and those with previous syncopal episodes.   Most importantly, however, the study excluded all patients discharged and solely focused on those admitted for an inpatient evaluation (Figure 1). 

 

    All included patients were subjected to a standardized history aimed at suggesting the cause of syncope and identifying risk factors for pulmonary embolism (Figure 2). They then underwent mandatory chest radiography, electrocardiography, arterial blood gas testing, and routine blood testing, including a D-dimer assay. Further diagnostic workup for causes other than pulmonary embolism was not standardized and varied between patients based on attending physician discretion.

Figure 2. Standardized History Questions

    The presence or absence of PE was assessed with a validated algorithm based on pretest clinical probability and the result of the D-dimer assay. The pretest clinical probability was defined according to the simplified Wells score, which classifies PE as being “likely” or “unlikely” (Table 1). In patients who had a high pretest clinical probability, a positive D-dimer assay, or both, computed tomographic pulmonary angiography or ventilation-perfusion lung scanning was performed.

 


Outcomes

    The primary outcome of the PESIT trial was to measure the prevalence of pulmonary embolism in patients admitted to the hospital for syncope. Secondarily, the thrombotic burden was assessed by measuring the most proximal location of embolus or the percentage of perfusion defect area.

    In 58.9% (339/560) of patients, PE was ruled out by low pre-test probability and a negative D-dimer. Of the remaining patients, 42.2% (97/229) had a pulmonary embolism. In the entire cohort, the prevalence of PE was 17.3% (97/560). Thus, the authors concluded that nearly one of every six patients hospitalized for a first episode of syncope has a pulmonary embolism (Figure 3, Table 2).

 Figure 3. Results Flowchart

Figure 3. Results Flowchart


Strengths and Weaknesses of the Study

    The major strength of the PESIT trial is the systematic approach with which PE's were diagnosed. ALL admitted patients underwent consideration of and testing for PE based on risk factors and pretest probability. Even if, for example, the initial ECG suggested an arrhythmia as the cause of syncope, if they did not rule out for PE, they went on to get a scan. This ensured a complete and thorough investigation. Furthermore, their results were internally valid, as the prevalence of PE was consistently 15-20% across all 11 centers.

    Additionally, the population studied is also fairly representative of those who most emergency medicine physicians would admit to the hospital with syncope. Reasons for admission included trauma, severe comorbidities, failure to identify a cause in the ED, and a high probability of cardiac syncope. While we don’t commonly site the EGSYS score that they used, the components such as palpitations, heart disease, and an exertional component to syncope, are all considerations that factor into our clinical gestalt for admission.

    A glaring problem with this study is the significant variation in diagnostic workup beyond PE. Other potential explanations for syncope were much more likely to be undetermined in those with confirmed embolism (see table 2). Because further workup was left to the discretion of individual physicians, alternative and perhaps more causative causes of syncope may have been under-diagnosed or underreported.

    Furthermore, this study has limited external validity when used to assess our ED population as a whole, given the exclusion criteria of all patients discharged from the ED. When recalculating the prevalence based on all patients who presented to the ED, only 1 in 26 (97/2584 = 3.8%) patients were diagnosed with a PE, far fewer than their conclusive 1 in 6. A major contributing factor is likely age. As expected, the mean age of patients discharged was much younger at 54 years (range 16 to 79). These patients are much less likely to develop PE based on currently available decision rules such as the PERC Rule.

    We commonly use tools such as the PERC Rule or the Wells score to quantify our pretest probability because they include characteristics known to be associated with PE. As seen in the clinical characteristics described in table 2, patients diagnosed with pulmonary embolism had a high prevalence of symptoms commonly associated with PE, such as hypoxemia and tachycardia, or clinical manifestations of DVT. They were also far more likely to have a history of previous venous thromboembolism or to have active cancer. A large proportion of PESIT patients diagnosed with PE presented exactly as we would expect patients with a PE to present. These  data strengthen support for current clinical practice, which for most physicians means only entering the diagnostic pathway for pulmonary embolism when history and physical exam suggests it as a potential diagnosis.

    Lastly, the PESIT trial spends significant effort quantifying radiographic burden of pulmonary embolism across all their positive cases. As mentioned earlier, all patients were evaluated for PE, regardless of clinical gestalt. However, we must remember that degree of radiographic filling defect does not necessarily correlate with clinically significant pulmonary embolism. In 40% of patients with PE, the extent of pulmonary vascular obstruction was at the segmental or subesegmental level or was less than 25% of total lung area. Some of these may have been clinically insignificant, not likely to have caused the syncopal event, and perhaps were discovered incidentally. A better predictor for the severity of PE might have incorporated factors such as heart rate, systolic blood pressure < 100 mmHg, elevated BNP, and elevated troponins, which are used in the simplified PE Severity Index and a subsequently developed composite score to predict mortality from PE. [6,7}


Take Home Message

    In summary, Pulmonary embolism is an important “must-not miss” cause of syncope, but it is likely an uncommon diagnosis in patients who pass out, recover, and appear well – the main way that most patients in the US with syncope present. Overall, 1 in 26 patients who present to the ED with first time syncope may have a PE. A large portion of these may be clinically insignificant and not causative of syncope. Those with symptoms and signs of PE are more likely to have a significant PE and should be evaluated as such. Thus, we should not change our current clinical practice based on the results of the PESIT trial.


Expert Commentary

Internal validity:

Dr. Ireland’s review of the Prandoni study reviews it’s methods and results quite well.  He also points out the important ways in which we as consumers of literature should address a study.  The first is with respect to internal validity (how well the authors measured what they in fact intended to measure).  This takes into account potential for bias, or systematic ways in which error could be introduced into the measurement.  Dr. Ireland does not seem to identify many problems with this study from that standpoint.   In general I agree with this, if the goal of measurement of this study was to exhaustively test all patients who are admitted largely at the discretion of their doctors after a first event of syncope.  If so, then the methods of this paper seem to have resulted in reasonable internal validity.  However if the goal of the paper is to identify the prevalence of symptomatically significant PE among ALL patients with first time PE, then it is quite possible that there is bias due to the methods of inclusion.  Specifically, the fact that only admitted patients were included, and those admitted had a fairly large degree of comorbid conditions may have resulted in a measurement of PE that is higher than what would be expected for in general “syncope.”

External validity:

The second key question for a consumer of medical literature to ask is, simplistically, “are these patients like mine?”  The answer to this is probably no.  The patients included are different than a typical US ED "undifferentiated passing out patient" not just because they are Italian, but also because they had a high prevalence of symptoms to suggest PE such as history of PE/DVT,  or history of malignancy. In the US, we would probably not consider many of these patients to be “undifferentiated syncope.” Rather, we would consider them to be possible symptomatic PE patients and simply test them.  Dr. Ireland points this out in his evaluation of table 2.  It is not a novel finding that many of the patients with these comorbidities, signs, and symptoms went on to have PE when tested (Courtney Annals of EM Annals of Emergency Medicine 2010;55(4):307–315).

Another way to examine generalizability is to examine the course of these syncope patients and ask if this is similar to the course that would be taken in the US. Of the 2584 ED syncope patients in this study, 1867 were discharged. Are we discharging 72% of our syncope patients?  Whether or not we should be is another question.  However,  it is likely that the US ED environment has a much lower threshold for admission for syncope than the Italian setting, similar to the way that the US ED environment has a much lower threshold for testing for PE than the European setting.  Therefore, it is highly likely that, at least to some extent, these Italian syncope patients are more ill than the average US ED syncope patient.  This is supported by the elderly median age in the Prandoni study of 80….meaning half of all their patients were over 80 years of age!  Also note that of the 717 remaining patients not discharged, a further 157 were excluded.  So this sample really is a unique selected group…..making it difficult to generalize this study to the average US ED patient with syncope.  

Dr. Jeff Kline and I explored the possible external generalizability of this report in a re-examination of the PERC dataset which included 7940 patients from 12 US emergency departments, all of whom had  symptoms prompting testing for PE.  Among 466 PE positive patients, 6.6% reported syncope, while among 7474 PE negative patients 6.0% reported syncope (95% CI for difference, -1.7 - 3.0).  This suggested syncope was not a predictor of PE. We also noted in the Prandoni study a mean age of 75 and a high prevalence of main pulmonary artery clot (42%), something we have not found in US studies of undifferentiated PE patients where median percent obstruction was 9%.

Bottom line: 

In elderly syncope patients with some combination of tachycardia, tachypnea, hypotension, active cancer, and perhaps especially those without a clear suspected cause of syncope, PE should be a consideration that warrants testing.  Perhaps this should be considered even when patients do not have the more traditional symptoms of PE such as dyspnea or chest pain.  However, we would caution clinicians NOT to interpret this study as rationale for widespread testing on all or nearly all US ED syncope patients.  The outcome of such a simplistic interpretation of this study would undoubtedly result in further radiation and contrast burden and harms for our patients.

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D. Mark Courtney, MD

Associate Professor of Emergency Medicine and Medical Social Sciences, Northwestern Emergency Medicine


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How to cite this post

[Peer-Reviewed, Web Publication] Ireland A,  Zimmerman J (2017, Sep 27). The PESIT Trial: Do All Patients Need a Syncope Workup?  [NUEM Blog. Expert Commentary By Courtney DM]. Retrieved from http://www.nuemblog.com/blog/PESIT


Resources

1. Syncope Evaluation in the Emergency Department Study (SEEDS): A Multidisciplinary Approach to Syncope Management. Win K. Shen, Wyatt W. Decker, Peter A. Smars, Deepi G. Goyal, Ann E. Walker, David O. Hodge, Jane M. Trusty, Karen M. Brekke, Arshad Jahangir, Peter A. Brady, Thomas M. Munger, Bernard J. Gersh, Stephen C. Hammill and Robert L. Frye. Circulation. 2004;110:3636-3645.

2. AHA/ACCF Scientific Statement on the evaluation of syncope: from the American Heart Association Councils on Clinical Cardiology, Cardiovascular Nursing, Cardiovascular Disease in the Young, and Stroke, and the Quality of Care and Outcomes Research Interdisciplinary Working Group; and the American College of Cardiology Foundation: in collaboration with the Heart Rhythm Society: endorsed by the American Autonomic Society. Strickberger SA, et. Al. American Heart Association Councils on Clinical Cardiology, Cardiovascular Nursing, Cardiovascular Disease in the Young, and Stroke; Quality of Care and Outcomes Research Interdisciplinary Working Group. American College of Cardiology Foundation.; Heart Rhythm Society.; American Autonomic Society. Circulation. 2006 Jan 17;113(2):316-27. No abstract available. Erratum in: Circulation. 2006 Apr 11;113(14):e697.

3. Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. Quinn J, McDermott D, Stiell I, Kohn M, Wells G.. Ann Emerg Med. 2006 May;47(5):448-54.

4. Etiology of syncope in hospitalized patients. Saravi M, Ahmadi Ahangar A, Hojati MM, Valinejad E, Senaat A, Sohrabnejad R, Khosoosi Niaki MR. Caspian J Intern Med. 2015 Fall;6(4):233-7.

5. Prevalence of Pulmonary Embolism among Patients Hospitalized for Syncope. Prandoni P, Lensing AW, Prins MH, Ciammaichella M, Perlati M, Mumoli N, Bucherini E, Visonà A, Bova C, Imberti D, Campostrini S, Barbar S; PESIT Investigators. N Engl J Med. 2016 Oct 20;375(16):1524-1531.

6. Jiménez D, Aujesky D, Moores L, et al. Simplification of the pulmonary embolism severity index for prognostication in patients with acute symptomatic pulmonary embolism. Arch Intern Med 2010; 170:1383.

7. Jiménez D, Kopecna D, Tapson V, et al. Derivation and validation of multimarker prognostication for normotensive patients with acute symptomatic pulmonary embolism. Am J Respir Crit Care Med 2014; 189:718.


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