Pre-Arrest Acidemia and the Effect of Sodium Bicarbonate on ROSC

Background

Sodium bicarbonate during a cardiac arrest is widely debated and used in many cases. In a 2018 PULMCrit post, Dr. Josh Farkas reviews much of the data and concludes that use of sodium bicarbonate is a “source of eternal disagreement.” A 2013 EMCrit article and podcast by Dr. Scott Weingart also details some of the controversy. The 2020 ACLS Guidelines state that routine use of sodium bicarbonate is not recommended in cardiac arrest [1]. Despite this recommendation, sodium bicarbonate is still often administered during resuscitations if a metabolic (or respiratory) acidosis is suspected or after a prolonged downtime. A recent study evaluated the effect of pre-arrest acid-base status on response to sodium bicarbonate and achievement of return of spontaneous circulation (ROSC) [2].

Evidence

This was a retrospective review of in-hospital cardiac arrests (IHCA) in patients with pre-arrest serum bicarbonate levels ≤21 mmol/L compared to >21 mmol/L. Pre-arrest bicarbonate levels were obtained <24 hours prior to the arrest. Similarly, post-arrest bicarb levels were obtained <24 hours following the arrest. Bicarbonate levels were recorded from basic chemistry panels rather than blood gases. All patients received a median sodium bicarbonate dose of 100 mEq. The groups were relatively well-matched, with the only major difference being the time to first bicarb administration was faster in the ‘acidotic’ group (6.9 vs. 9.2 minutes). Initial ECG rhythms were similar between the groups.

  • 102 patients in ‘acidotic’ group with a median pre-arrest bicarb level of 17 mmol/L
  • 123 patients in ‘non-acidotic’ group with a median pre-arrest bicarb level of 27 mmol/L
  • There was no difference in ROSC (53.9% vs 48.8%, p=0.44) or survival to discharge (8.8% vs 5.7%, p=0.36) between the acidotic group versus the nonacidotic group

Thoughts and Limitations

  • A meta-analysis found no difference in sustained ROSC or survival to discharge with sodium bicarbonate (Alshahrani 2021).
  • In the current study, prearrest bicarb levels could have resulted up to 24 hours prior to the arrest and the authors don’t comment on when exactly they were drawn. The timing limits the ability to know true acid-base status just prior to the arrest. And, that really limits applying this to out-of-hospital cardiac arrest where patients may have more significant acidemia if resuscitation is delayed.
  • A median bicarbonate concentration of 17 mmol/L isn’t really that low, relatively speaking, to indicate a potential impact from administering sodium bicarbonate.
  • Retrospective cardiac arrest studies are challenging. Many interventions happen around the same, making it impossible to connect any one of them with a specific outcome.
  • The study that would be more helpful is taking patients with metabolic/respiratory acidosis and giving have bicarb and the other placebo.

Bottom Line

  • In this cohort of IHCA patients, sodium bicarbonate administration did not improve the chances of ROSC or survival to hospital discharge, irrespective of pre-arrest acid-base status. In other words, attempting to correct ‘acidosis’ does not seem to change rate of ROSC.
  • Sodium bicarbonate use in cardiac arrest should be targeted (e.g., hyperkalemia with metabolic acidosis, sodium channel blockade secondary to an overdose).

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References

  1. Panchal AR, Bartos JA, Cabañas JG, et al. Part 3: adult basic and advanced life support: 2020 american heart association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2020;142(16_suppl_2):S366-S468. doi: 10.1161/CIR.0000000000000916. PMID: 33081529.
  2. Mclean H, Wells L, Marler J. The effect of prearrest acid-base status on response to sodium bicarbonate and achievement of return of spontaneous circulation. Ann Pharmacother. Published online August 5, 2021:10600280211038392. doi: 10.1177/10600280211038393. PMID: 34353142.

SAEM Clinical Image Series: Pulseless and Painful Blue Leg

painful blue leg

A 57-year-old male who works as a truck driver with a history of hypertension, type 2 diabetes, and recent COVID-19 infection presents with right lower extremity pain for two hours. He reports experiencing one day of dull aching of the right leg, then being suddenly awakened with the abrupt onset of severe right leg pain and shortness of breath. He denies chest pain. EMS reports a pulseless and painful blue leg en route. The patient denies any history of trauma, irregular heartbeat, or anticoagulation.

Vitals: T 97.5°F; BP 120/78; HR 102; RR 20; oxygen saturation 100%

General: Writhing and moaning in pain

Cardiovascular: Tachycardic; 2+ pulses in all extremities except for the right lower extremity

Pulmonary: No respiratory distress

Hemoglobin: 12.9 g/dL

INR: 1.02

Phlegmasia cerulea dolens

When a patient presents with a painful, pulseless extremity, acute limb ischemia, with etiologies including aortic dissection, arterial thromboembolism, and phlegmasia dolens, is of the highest concern. Unlike a typical deep venous thrombosis (DVT), phlegmasia dolens is a DVT that causes complete occlusion, resulting in venous congestion and hypoperfusion. Risk factors for phlegmasia dolens and DVT are the same; this patient had both a sedentary occupation and recent COVID-19 as risk factors.

Phlegmasia is usually characterized early on with pale discoloration (alba) due to patency of collaterals and later with blue/cyanotic discoloration (cerulea) after complete occlusion of the venous system. It is important to remember this exam finding might be limited in pigmented skin. Venous gangrene and compartment syndrome can be delayed exam findings. The exam should include immediate evaluation of pulses with doppler and compartment checks. Imaging modalities are controversial and should not delay vascular surgery consultation. Bedside ultrasound can be rapidly performed for clot evaluation, but CT venogram would be the preferred method for surgical planning. A common femoral vein DVT can be seen on the accompanied ultrasound and CT images. The limb should be elevated, and heparin infusion should be initiated. Surgical consultation should include a discussion of thrombectomy or catheter-directed thrombolysis.

Take-Home Points

  • Phlegmasia cerulea dolens is an uncommon complication of DVT that presents with a discolored, painful, pulseless extremity, and is associated with high morbidity and mortality.
  • Initial management includes vascular surgery consultation, elevation of the extremity, and heparinization.
  1. Baker, William, and Samuel Kim. “Risking Life And Limb: Management Of Phlegmasia AlbaAnd Cerulea Dolens”. Emra.Org, 2020, https://www.emra.org/emresident/article/risking-life-and-limb-management-of-phlegmasia–alba-and-cerulea-dolens/.
  2. Gardella L, Faulk J. Phlegmasia Alba And Cerulea Dolens. 2020 Oct 12. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. PMID: 33085284.

 

 

Diagnosis on Sight: “I have a rapid heart rate”

A 31-year-old male presented to the emergency department with palpitations. The patient stated that he thinks his symptoms began “last night” and felt like he had “a rapid heart rate.” He said that prior to last night he felt fine. He did admit to drinking alcohol with his friends 2 nights prior. The patient estimated that he “must have drunk about 30 beers.” On review of systems, he reported feeling anxious. He denied illicit drug use, headache, chest pain, cough, shortness of breath, fevers, nausea, vomiting, abdominal pain, dysuria, or increased urinary frequency. He reported that he was unaware of any family history of early heart disease or sudden death. His initial EKG is shown below.

After consultation with cardiology, the decision was made to cardiovert the patient given the wide complex tachycardia.  After cardioversion, the resulting EKG is shown below:

On review of previous records, the patient had a recent ED visit 2 months ago with the EKG shown below:

What is the diagnosis?

Preexcited atrial fibrillation with underlying Wolf-Parkinson-White syndrome

Explanation:

Wolf-Parkinson-White (WPW) syndrome and the WPW pattern on EKG are rare disorders. Only 0.13 – 0.25% of the population have a WPW pattern on EKG [1,2]. However, only a small fraction of these people will develop WPW syndrome. WPW syndrome is defined as a symptomatic arrhythmia with a WPW pattern on EKG.

The patient’s initial EKG showed a wide complex tachycardia that was ultimately determined to be preexcited rapid atrial fibrillation. After cardioversion, the patient’s underlying baseline EKG tracing showed findings of Wolf-Parkinson-White with:

  • A shortened PR interval
  • Widened QRS complex
  • Delta wave: Slurred upstroke of the QRS complex

The most common arrhythmias associated with WPW syndrome are:

  • AV Reentrant Tachycardia (AVRT): Seen in over 90% of patients with WPW syndrome [3,4]
  • Atrial Fibrillation: 10-30% [5,6]
  • Atrial Flutter: Less than 5%

As in this case, AVRT (i.e. SVT) is often followed by atrial fibrillation in patients with WPW. Although the pathophysiology is unclear, up to 35% of instances of atrial fibrillation were preceded by AVRT [5,7,8].

Fortunately, fatal dysrhythmias such as ventricular fibrillation and ventricular tachycardia are very rare with WPW.

Case Conclusion:

Following cardioversion, the patient remained stable in sinus rhythm. After consultation with cardiology, the patient was discharged on Flecainide and Metoprolol and a referral for outpatient cardiology was placed for follow-up care. Soon after, the patient had an electrophysiology study that showed a left posterolateral accessory conduction pathway. He then underwent successful ablation of his orthodromic AVRT.

Want more visual stimulation? Check out the Diagnose on Sight archives!

 

References:

  1. Krahn AD, Manfreda J, Tate RB, et al. The natural history of electrocardiographic preexcitation in men. The Manitoba Follow-up Study. Ann Intern Med 1992; 116:456. PMID: 1739235
  2. Kobza R, Toggweiler S, Dillier R, et al. Prevalence of preexcitation in a young population of male Swiss conscripts. Pacing Clin Electrophysiol 2011; 34:949. PMID: 21453334
  3. Josephson ME. Preexcitation syndromes. In: Clinical Cardiac Electrophysiology, 4th, Lippincot Williams & Wilkins, Philadelphia 2008. p.339.
  4. Chugh A, Morady F. Atrioventricular reentry and variants. In: Cardiac electrophysiology from cell to bedside, 5th edition, Zipes DP, Jalife J (Eds), Saunders/Elsevier, Philadelphia 2009. p.605-614.
  5. Campbell RW, Smith RA, Gallagher JJ, et al. Atrial fibrillation in the preexcitation syndrome. Am J Cardiol 1977; 40:514. PMID: 910715
  6. Sharma AD, Klein GJ, Guiraudon GM, Milstein S. Atrial fibrillation in patients with Wolff-Parkinson-White syndrome: incidence after surgical ablation of the accessory pathway. Circulation 1985; 72:161. PMID: 4006127
  7. Sung RJ, Castellanos A, Mallon SM, et al. Mechanisms of spontaneous alternation between reciprocating tachycardia and atrial flutter-fibrillation in the Wolff-Parkinson-White syndrome. Circulation 1977; 56:409. PMID: 884796
  8. Fujimura O, Klein GJ, Yee R, Sharma AD. Mode of onset of atrial fibrillation in the Wolff-Parkinson-White syndrome: how important is the accessory pathway? J Am Coll Cardiol 1990; 15:1082. PMID: 2312962
By |2021-08-27T09:10:41-07:00Aug 25, 2021|Cardiovascular, Diagnose on Sight, ECG|

Beta-Blockers for Inhalant-Induced Ventricular Dysrhythmias

Background

There are a few unique scenarios when beta-blockers may be indicated for patients in cardiac arrest. Use of esmolol for refractory ventricular fibrillation was summarized in a 2016 PharmERToxGuy post with an accompanying infographic. Another potential use for beta-blockers is in the rare case of a patient with inhalant-induced ventricular dysrhythmias. The term ‘sudden sniffing death’ refers to acute cardiotoxicity associated with inhaling hydrocarbons. Check out this ACMT Toxicology Visual Pearl for more information about the background and diagnosis of inhalant abuse.

It is thought that inhalants causes myocardial sensitization via changes in various cardiac channels (e.g., sodium channels, potassium channels, calcium channels, or gap junctions) leading to prolonged repolarization and conduction [1, 2]. Additionally, chronic inhalant use can lead to structural heart damage. When the above alterations are combined with a sudden increase in catecholamines (e.g., exercise, caught sniffing), a dysrhythmia can develop which is often fatal [2-4].

Evidence

There are no case reports to support the use beta-blockers to treat inhalant-induced dysrhythmias. However, the case reports below include patients that ingested various hydrocarbons who developed ventricular dysrhythmias and improved following the initiation of beta-blockers. As the adverse cardiac effects should be similar between inhaled and ingested hydrocarbons, we can potentially extrapolate this data to patients with inhalant-induced dysrhythmias.

DemographicsAgent(s) Ingested Cardiac EffectsInterventionsResolution of dysrhythmia following BB?
39 yo M [5]TrichloroethylenepVT/VF arrestDefibrillation, Propranolol bolus and infusion

Y

70 yo F [6]TrichloroethyleneBigeminy, Junctional rhythmEsmolol bolus and infusion

Y

23 yo F [7]Chloral hydrateVF arrestEsmolol bolus and infusion

Y

27 yo M [8]Chloral hydrate, Loxapine, FluoxetineStable VTPropranolol bolus and infusion

Y

3 yo M [9]Chloral hydrateSinus tachycardia, Bigeminy, Trigeminy, NSVTEsmolol bolus and infusion

Y

44 yo M [10]Chloral hydrateStable VTPropranolol bolus, Labetalol infusion

Y

BB=beta-blocker; pVT=polymorphic ventricular tachycardia; VT=ventricular tachycardia; VF=ventricular fibrillation; NSVT=non-sustained ventricular tachycardia

Bottom Line

  • Patients presenting to the ED with cardiopulmonary manifestations of inhalant use should have routine electrolytes and an ECG to assess cardiac status
  • A quiet environment is important to decrease stimulation and minimize catecholamine surges
  • For both stable and non-perfusing dysrhythmias, propranolol or esmolol are reasonable choices to counteract the catecholamine effects, in addition to standard care [5-10]
    • Consider avoiding epinephrine and other catecholamines unless necessary, as they may worsen the dysrhythmia

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References

  1. Nelson LS. Toxicologic myocardial sensitization. J Toxicol Clin Toxicol. 2002;40(7):867–79. doi: 10.1081/clt-120016958. PMID: 12507056.
  2. Tormoehlen LM, Tekulve KJ, Nañagas KA. Hydrocarbon toxicity: A review. Clin Toxicol (Phila). 2014 Jun;52(5):479–89. doi: 10.3109/15563650.2014.923904. PMID: 24911841.
  3. Bass M. Sudden sniffing death. JAMA. 1970 Jun 22;212(12):2075–9. PMID: 5467774.
  4. Baydala L. Inhalant abuse. Paediatr Child Health. 2010 Sep;15(7):443–54. doi: 10.1093/pch/15.7.443. PMID: 21886449.
  5. Gindre G, Le Gall S, Condat P, Bazin JE. [Late ventricular fibrillation after trichloroethylene poisoning]. Ann Fr Anesth Reanim. 1997;16(2):202–3. doi: 10.1016/s0750-7658(97)87204-8. PMID: 9686084.
  6. Mortiz F, de La Chapelle A, Bauer F, Leroy JP, Goullé JP, Bonmarchand G. Esmolol in the treatment of severe arrhythmia after acute trichloroethylene poisoning. Intensive Care Med. 2000 Feb;26(2):256. doi: 10.1007/s001340050062. PMID: 10784325.
  7. Shakeer SK, Kalapati B, Al Abri SA, Al Busaidi M. Chloral hydrate overdose survived after cardiac arrest with excellent response to intravenous β-blocker. Oman Med J. 2019 May;34(3):244–8. doi: 10.5001/omj.2019.46. PMID: 31110633.
  8. Zahedi A, Grant MH, Wong DT. Successful treatment of chloral hydrate cardiac toxicity with propranolol. Am J Emerg Med. 1999 Sep;17(5):490–1. doi: 10.1016/s0735-6757(99)90256-5. PMID: 10496517.
  9. Nordt SP, Rangan C, Hardmaslani M, Clark RF, Wendler C, Valente M. Pediatric chloral hydrate poisonings and death following outpatient procedural sedation. J Med Toxicol. 2014 Jun;10(2):219–22. doi: 10.1007/s13181-013-0358-z. PMID: 24532346.
  10. Wong O, Lam T, Fung H. Two cases of chloral hydrate overdose. Hong Kong Journal of Emergency Medicine. 2009 Jul;16(3):161–7. doi: 10.1177/102490790901600307.

Safety and Efficacy of Clevidipine for Acute Blood Pressure Control

Background

Rapid and precise control of blood pressure is vital for patients with a hypertensive emergency or an acute stroke. Commonly, nicardipine is utilized in these situations, with nitroprusside being a less appealing alternative. The most recent AHA/ASA Acute Ischemic Stroke Guidelines, updated in 2019, also recommend clevidipine as a first-line antihypertensive option [1]. Clevidipine is a dihydropyridine calcium channel blockers, similar in mechanism to nicardipine and amlodipine. The main advantage of clevidipine over nicardipine is related to its pharmacokinetics (Table 1). Given its shorter half-life of elimination, clevidipine can be titrated every 1-2 minutes. Additionally, if hypotension does occur, stopping the clevidipine infusion allows blood pressure to rebound quickly.

MedicationOnsetDurationHalf-Life
Clevidipine2-4 mins5-15 mins1-15 mins
Nicardipine10-20 mins1-2 hours2-4 hours
Nitroprusside1-2 mins1-10 mins2 mins

Table 1: Pharmacokinetics of Common Antihypertensive Infusions [Micromedex; Lexicomp]

Evidence

Most studies demonstrate equivalent outcomes between clevidipine and other agents (e.g., nicardipine, nitroprusside, nitroglycerin) [2-5]. The ECLIPSE trial is the largest to assess the safety and efficacy of clevidipine [6]. The authors randomized cardiac surgery patients to clevidipine, nicardipine, nitroprusside, or nitroglycerin and found no difference in the incidence of myocardial infarction, stroke, or renal dysfunction. They noted that mortality was higher in patients receiving nitroprusside vs clevidipine, but equivalent compared to the the other medications. Additionally, clevidipine treated patients had significantly fewer excursions outside the prespecified blood pressure range than patients treated with any of the other agents.

Safety

Clevidipine is formulated in a 20% lipid emulsion and packaged in a glass vial. This causes clevidipine to appear similar to propofol, which could lead to safety issues. Also, care should be taken when using both clevidipine and propofol concomitantly, especially at high doses, as both provide clinically significant amounts of lipids, so triglycerides should be monitored.

Bottom Line

Clevidipine is a safe and effective antihypertensive to use in patients that require rapid and strict blood pressure control, specifically in patients with an aortic dissection or an acute ischemic/hemorrhagic stroke.

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References

  1. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the early management of patients with acute ischemic stroke: 2019 update to the 2018 guidelines for the early management of acute ischemic stroke: a guideline for healthcare professionals from the american heart association/american stroke association. Stroke. 2019;50(12):e344-e418. doi: 10.1161/STR.0000000000000211. PMID: 31662037.
  2. Allison TA, Bowman S, Gulbis B, Hartman H, Schepcoff S, Lee K. Comparison of clevidipine and nicardipine for acute blood pressure reduction in patients with stroke. J Intensive Care Med. 2019;34(11-12):990-995. doi: 10.1177/0885066617724340. PMID: 28820038.
  3. Rosenfeldt Z, Conklen K, Jones B, Ferrill D, Deshpande M, Siddiqui FM. Comparison of nicardipine with clevidipine in the management of hypertension in acute cerebrovascular diseases. J Stroke Cerebrovasc Dis. 2018;27(8):2067-2073. doi: 10.1016/j.jstrokecerebrovasdis.2018.03.001. PMID: 29627171.
  4. Ulici A, Jancik J, Lam TS, Reidt S, Calcaterra D, Cole JB. Clevidipine versus sodium nitroprusside in acute aortic dissection: A retrospective chart review. Am J Emerg Med. 2017;35(10):1514-1518. doi: 10.1016/j.ajem.2017.06.030. PMID: 28669696.
  5. Brehaut SS, Roche AM. Abstract W P65: Clevidipine Outperforms Other Agents in Emergent Acute Hypertension Treatment in Ischemic Stroke Pre-rt-PA. 2015;46:AWP65. doi: 10.1161/str.46.suppl_1.wp65.
  6. Aronson S, Dyke CM, Stierer KA, et al. The ECLIPSE trials: comparative studies of clevidipine to nitroglycerin, sodium nitroprusside, and nicardipine for acute hypertension treatment in cardiac surgery patients. Anesth Analg. 2008;107(4):1110-1121. doi:10.1213/ane.0b013e31818240db. PMID: 18806012.

2020 ACLS Guidelines on Medications for Management of Specific Arrhythmias

ACLS 2020 arrhythmias

The 2020 ACLS guidelines provide recommendations on the medication-specific management for arrhythmias including wide-complex tachycardia, regular narrow-complex tachycardia, atrial fibrillation/flutter, and bradycardia [1]. There are also our 2020 ACLS guideline summaries on vasopressor and non-vasopressor medications used during cardiac arrest and toxicology-related conditions.

Wide-complex tachycardia (WCT)

Wide-complex tachycardiaMedication(s)Evidence
Hemodynamically stableAdenosineCOR 2b, LOE B-NR
Amiodarone, procainamide, or sotalolCOR 2b, LOE B-R
NOTE: Verapamil is harmfulCOR 3, LOE B-NR
Polymorphic VT with long QT (torsades de points)MagnesiumCOR 2b, LOE C-LD
Polymorphic VT without long QTLidocaine or amiodaroneCOR 2b, LOE C-LD

Regular narrow-complex tachycardia

  1. Vagal maneuvers (COR 1, LOE B-R)
  2. Adenosine (COR 1, LOE B-R)
  3. Diltiazem or verapamil (COR 2a, LOE B-R)
  4. Beta-blockers (COR 2a, LOE C-LD)

Atrial fibrillation/flutter with rapid ventricular rate

  1. Beta-blocker or diltiazem or verapamil (COR 1, LOE B-NR)
  2. Amiodarone (COR 2a, LOE B-NR)


Bradycardia

  1. Treat reversible causes (COE 1, LOE C-EO)
  2. Atropine if hemodynamic compromise (COR 2a, LOE B-NR)
  3. Epinephrine or transcutaneous pacing if unresponsive to atropine (COR 2b, LOE C-LD)

Reference

Panchal AR, Bartos JA, Cabañas JG, et al; Adult Basic and Advanced Life Support Writing Group. Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020 Oct 20;142(16_suppl_2):S366-S468. doi: 10.1161/CIR.0000000000000916. Epub 2020 Oct 21. PMID: 33081529.

ACEP E-QUAL: ACEP Non-STEMI Clinical Policy

Clinical Policy

In 2018, the American College of Physicians (ACEP) released a Clinical Policy with management recommendations for patients presenting to the emergency department (ED) with concern for non-ST-elevation myocardial infarction (NSTEMI). Dr. Jason Woods hosted an episode of the ACEP E-QUAL Network podcast highlighting key aspects of the new policy. Dr. Woods was joined by lead writer Dr. Christian Tomaszewski from the University of California San Diego, and Dr. Michael Ross, Director of the Chest Pain Center at Emory University. Below are show notes reviewing the recommendations and the process involved in creating the clinical policy.

 

How is a clinical policy different than a practice guideline?

The National Guideline Clearinghouse (NGC), a public resource initiative of the Agency for Healthcare Research and Quality (AHRQ), provides rules and frameworks for evidence-based clinical practice guidelines. ACEP refers to clinical practice guidelines in Emergency Medicine (EM) as policies to denote the more prescriptive design process.

What was the process of drafting the policy?

Development of the 2018 ACEP NSTEMI Clinical Policy was a 2-year “labor of love.” Writers, methodologies, and committee members were required to be free from both financial and intellectual conflict of interest.

The clinical policy is a result of a systematic review and critical analysis of available medical literature. Clinical studies were graded on robustness, design, and class of evidence according to the ACEP policy development process which includes internal and external review.

Recommendations were categorized as reflecting high clinical certainty (Level A), moderate clinical certainty (Level B), or mixed clinical certainty (Level C) due to the heterogeneity of results, unclear effect magnitude, bias, among other factors.

What questions did the policy address?

Four critical questions were decided by consensus methods to address the evaluation and management of adult patients presenting to the ED with concern for NSTEMI.

1) If ST-elevation myocardial infarction is excluded, can a combination of bedside and laboratory evaluation in the ED identify patients at low risk for major adverse cardiac events (MACE)?
Level B recommendation: History, ECG, Age, Risk Factors, Troponin (HEART) score < 3 can be used as a clinical prediction tool for a 30-day MACE miss rate between 0-2%.
Level C recommendation: Thrombolysis in Myocardial Infarction (TIMI) score can be used to predict risk of 30-day MACE.

2) Can repeat Troponin testing in the ED be used to identify patients at low risk for MACE?
Level C recommendations:

    • Conventional troponin testing at hour 0 and 3 in low risk (HEART score < 3) patients can predict and acceptable low risk for 30-day MACE.
    • A single high-sensitivity troponin less than the detectable limit on arrival to the ED or negative serial high-sensitivity troponin at hour 0 and 2 is predictive of a low rate of MACE.
    • Patients deemed to be low risk with a non-ischemic ECG and negative high-sensitivity troponin at 0 and 2 hours can be considered low risk for 30-day MACE, allowing for accelerated discharge from the ED.

3) In patients who have been ruled out for acute coronary syndromes (ACS), does advanced cardiac provocative testing prior to discharge from the ED reduce MACE?
Level B recommendation:  Do not routinely use advanced cardiac testing in low-risk patients who have been ruled out for ACS to further reduce 30-day MACE.
Level C recommendation: Arrange follow-up in 1-2 weeks for low-risk patients in whom ACS has been ruled out. If unable to arrange follow-up, consider observation and advanced testing prior to discharge.

4) Should patients with NSTEMI receive antiplatelet therapy in addition to aspirin in the ED?
Level C recommendation: P2Y12 inhibitors and glycoprotein IIb/IIIa inhibitors can be given in the ED or delayed until cardiac catheterization.

What questions remain?

  1. The clinical policy does not address the “delta factor” involved in assessing changes to the cardiac marker levels that may be seen with repeat testing at set time points.
  2. Duration of pain was not discretely addressed, and differences in real-world practice can exist depending on whether the time of onset or time of presentation is considered for defining repeat testing and observation length.
  3. Shared decision-making was not factored into the selection of management steps.

Important points for consideration:

The 2018 ACEP Clinical Policy for NSTEMI was written for the evaluation of patients with suspicion for ACS who presented with chest pain. It does not apply to those presentations of ACS that are considered atypical in nature.

Read a more in-depth summary of the ACEP Clinical Policy on ALiEM. 

Interested in more of the ACEP-EQUAL Podcast?

By |2021-09-15T11:34:21-07:00Dec 7, 2020|Academic, ACEP E-QUAL, Cardiovascular|
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