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.

Click here to read a more in-depth summary of the ACEP Clinical Policy on ALiEM. 

Interested in more of the ACEP-EQUAL Podcast?

Listen to more ACEP E-QUAL podcasts episodes on the ALiEM Soundcloud account.

By |2020-12-09T11:57:39-08:00Dec 7, 2020|Academic, ACEP E-QUAL, Cardiovascular|

LVAD Part V: The Coding LVAD Patient

Left ventricular assist devices (LVADs) have moved from being a bridge to a heart transplant to destination therapy for patients with severe heart failure. Although their use in the general public has increased, they still provide a challenge to the emergency medicine (EM) physician. This series aims to cover the basics of how the EM physician approaches the care of these patients.

(more…)

By |2020-04-20T09:48:07-07:00Apr 20, 2020|Cardiovascular, Emergency Medicine|

LVAD Part IV: Non-Device Pathology

Left ventricular assist devices (LVADs) have moved from being a bridge to a heart transplant to destination therapy for patients with severe heart failure. Although their use in the general public has increased, they still provide a challenge to the emergency medicine (EM) physician. This series aims to cover the basics of how the EM physician approaches the care of these patients.

(more…)

By |2020-04-13T13:16:03-07:00Apr 13, 2020|Cardiovascular, Emergency Medicine|

LVAD Part III: Complications

Left ventricular assist devices (LVADs) have moved from being a bridge to a heart transplant to destination therapy for patients with severe heart failure. Although their use in the general public has increased, they still provide a challenge to the emergency medicine (EM) physician. This series aims to cover the basics of how the EM physician approaches the care of these patients.

(more…)

By |2020-03-30T14:13:04-07:00Mar 30, 2020|Cardiovascular, Emergency Medicine|
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