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The Effect of Lipid Emulsion durıng Advanced Cardiac Life Support for Bonzai (Tetrahydrocannabınol) Cardiovascular Toxicity

Demet Doğan Erol

Department of Anaesthesiology and Reanimation, Yıldırım Beyazıt Hospital, Ankara, Turkey

E-mail : bhuvaneswari.bibleraaj@uhsm.nhs.uk

Can Erdoğan

Department of Anaesthesiology and Reanimation, Yıldırım Beyazıt Hospital, Ankara, Turkey

Cem Koray Çataroğlu

Department of Anaesthesiology and Reanimation, Yıldırım Beyazıt Hospital, Ankara, Turkey

Süleyman Sürer

Department of Cardiovascular Surgery, Yıldırım Beyazıt Hospital, Ankara, Turkey

Zeynep Uluşan Özkan

Department of Cardiovascular Surgery, Yıldırım Beyazıt Hospital, Ankara, Turkey

DOI: 10.15761/JIC.1000233

Article
Article Info
Author Info
Figures & Data

Key words

Bonzai, Tetrahydrocannabinol, Cardiovascular disorders, Lipid resuscitation

Objective

Worldwide, bonzai tetrahydrocannabinol is among the most widely used illicit drugs. The current wave of decriminalization may lead to more widespread use, and it is important that cardiologists be made aware of the potential for marijuana-associated adverse cardiovascular effects that may begin to occur in the population at a greater frequency. The main active substance, tetrahydrocannabinol, affects cannabinoid receptor 1 in the brain and cannabinoid receptor 2 in the periphery, with predominantly psychoactive effects [1]. There are several well-recognized complications associated with tetrahydrocannabinol use, including psychiatric, respiratory system, and cardiovascular disorders [2]. Published reports describe a temporal relation between tetrahydrocannabinol use and the development of acute myocardial infarction, cardiomyopathy, and sudden cardiac death. The mechanism underlying the association between tetrahydrocannabinol use and myocardial infarction is currently unknown. It is possible that cannabis has a deleterious effect on coronary microcirculation. Dahdouh, et al. reported the case of a 20 years old patient who abused tobacco and marijuana and developed cardiac arrest and massive myocardial infarction [3]. 

Lipid resuscitation refers to the use of an intravascular infusion of a lipid emulsion to treat severe, systemic drug toxicity or poisoning. Increasing evidence suggests that the intravenous (IV) infusion of lipid emulsions can reverse the cardiac and neurologic effects of local-anesthetic toxicity [4]. The role of lipid emulsion has expanded to treatment of cardiac toxicity due to other lipophilic drugs. Indeed, case reports support the early use of lipid emulsion at the first sign of arrhythmia, prolonged seizure activity, or rapid progression of toxic manifestations in patients with suspected local anesthetic toxicity. The similarity of several subsequent reports suggests that underlying ischemic heart disease or cardiac conduction defects may predispose to local anesthetic cardiac toxicity [5].

Case-Report

23 years old man reported heart fluttering and near syncope a few hours after bonsai tetrahydrocannabinol, heroin smoking. In the emergency department, he was found to have a right bundle-branch–type ventricular tachycardia and had failed more than 40 mins of standard life support therapy including ventilation with oxygen, vasopressors, and force diüuresis. Current guidelines suggest that 20% lipid emulsion initially be administered as a bolus of 1.5 mL/kg over 1 min. Following completion of the bolus, a continuous infusion of 0.25 mL/kg/min should be started. Followed 20% lipid infusion at 16 hours rapidly restored normal cardiac markers and hemodynamic parameters. The patient recovered completely with no evidence of myocardial damage after 96 hours. (Table 1)

Table 1. Cardiac markers

 

4. hour

8. hour

12.hour

16. hour

 20.hour

After lipid

 24.hour

After lipid

48.hour

After lipid

 72.hour

After lipid

96.hour

After lipid

Creatinin kinaz (U/L)

1384

2576

3137

4065

2324

1215

266

117

 

CKMB (U/L)

64

78

99

95

55

60

19

22

6.6

Troponin I(ng/ml)

 

1.11

1.49

2.5

0.67

 

0.08

0.05

0.03

AST (U/L)

109

161

160

157

115

75

27

33

28

ALT (U/L)

85

134

138

135

129

105

71

56

48

Conclusions

While the exact mechanism of action is not known, several hypotheses exist as to how lipid emulsion works in the setting of local anesthetic toxicity. The first is the ‘lipid sink’ hypothesis that suggests that lipid-soluble local anesthetic molecules in the aqueous phase are extracted by the injected lipid. The lipid sequesters the local anesthetic and reduces the concentration of tissue bound local anesthetic. Alternatively, the metabolic hypothesis postulates that lipid impedes local anesthetic’s inhibition of acyl carnitine, thereby improving mitochondrial metabolism. Finally, it has been proposed that lipid emulsion increases calcium concentrations in myocytes thereby improving contractility [6].

References

  1. Thomas G, Kloner RA, Rezkalla S (2014) Adverse cardiovascular, cerebrovascular, and peripheral vascular effects of marijuana inhalation: what cardiologists need to know. Am J Cardiol 113: 187–190. [Crossref]
  2. Jouanjus E, Leymarie F, Tubery M, Lapeyre-Mestre M (2011) Cannabisrelated hospitalizations: unexpected serious events identified through hospital databases. Br J Clin Pharmacol 71: 758-765. [Crossref]
  3. Dahdouh Z, Roule V, Lognoné T, Sabatier R, Grollier G (2012) Cannabis and coronary thrombosis: what is the role of platelets? Platelets 23: 243-245. [Crossref]
  4. Neal JM, Bernards CM, Butterworth JF 4th, Di Gregorio G, Drasner K, et al. (2010) ASRA practice advisory on local anesthetic systemic toxicity. Reg Anesth Pain Med 35: 152-161. [Crossref]
  5. Weinberg GL (2010) Treatment of Local Anesthetic Systemic Toxicity (LAST). Reg Anesth Pain Med 35: 188-193. [Crossref]
  6. Toledo P (2011) The role of lipid emulsion during advanced cardiac life support for local anesthetic toxicity. Int J Obstet Anesth 20: 60–63. [Crossref]

Editorial Information

Editor-in-Chief

Massimo Fioranelli
Guglielmo Marconi University

Article Type

Case Report

Publication history

Received date: January 10, 2018
Accepted date: January 26, 2018
Published date: January 30, 2018

Copyright

© 2018 Erol DD. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation

Erol DD, Erdoğan C, Çataroğlu CK, Sürer S, Özkan ZU (2018) The effect of lipid emulsion durıng advanced cardiac life support for Bonzai (Tetrahydrocannabınol) cardiovascular toxicity. J Integr Cardiol 4: DOI: 10.15761/JIC.1000233

Corresponding author

Demet Doğan Erol

Department of Anaesthesiology and Reanimation, Yıldırım Beyazıt Hospital, Ankara, Turkey

E-mail : bhuvaneswari.bibleraaj@uhsm.nhs.uk

Table 1. Cardiac markers

 

4. hour

8. hour

12.hour

16. hour

 20.hour

After lipid

 24.hour

After lipid

48.hour

After lipid

 72.hour

After lipid

96.hour

After lipid

Creatinin kinaz (U/L)

1384

2576

3137

4065

2324

1215

266

117

 

CKMB (U/L)

64

78

99

95

55

60

19

22

6.6

Troponin I(ng/ml)

 

1.11

1.49

2.5

0.67

 

0.08

0.05

0.03

AST (U/L)

109

161

160

157

115

75

27

33

28

ALT (U/L)

85

134

138

135

129

105

71

56

48