Blood Pressure Fluctuations Due to Lurasidone Reversal: A Case Report

Abstract

Background of study: Although catecholamine medications are frequently employed to promote circulation, in certain circumstances they may unexpectedly result in hypotension. Here, we report the first instance of hypotension that was unanticipated in response to catecholamine drugs.

Case presentation: A 36-year-old guy from Addis Ababa,Ethiopia was brought to our emergency room due to schizophrenia. He was unconscious and in shock. We administered catecholamine agents after fluid resuscitation, however the catecholamine infusion caused his blood pressure to drop to 62/45 mmHg. However, his blood pressure significantly improved once we started vasopressin, and he eventually became stable. He acknowledged taking a lot of lurasidone on day two, and we determined that he had overdosed on the medication. We surmise that the lurasidone-induced a-adrenergic blockade was the reason for this unanticipated hypotension in response to catecholamine infusion. Research on animals demonstrated that concurrently administering adrenaline and a-adrenergic inhibition caused a drop in blood pressure, a phenomenon known as “adrenaline reversal.” We refer to this occurrence as “catecholamine reversal” since in our situation, catecholamine infusion under the a-adrenergic blocking effect of lurasidone may have induced a drop in blood pressure through the same mechanism. Since vasopressin functions differently in some situations than catecholamines, we advise using it to keep blood pressure stable.

Conclusions: We presented the first documented clinical instance of “catecholamine reversal” and emphasized that we should be suspicious of the use of a-adrenergic antagonists if unexpected hypotension results from a catecholamine infusion. Instead, we ought to think about giving vasopressin in these circumstances.

Keywords: Cardiovascular; Emergency medicines; Cardiac shock; Electrocardiogram; Intensive care units

Introduction

Often used to promote circulation, catecholamines act differently on various receptors depending on the agent [1]. Catecholamine activity improves chronotropic and inotropic effects on β1 adrenergic receptors, increases vasodilation on β2-adrenergic receptors, and promotes peripheral vasoconstriction on a-adrenergic receptors [2]. We often employ catecholamine drugs, such as dopamine and noradrenaline, to enhance vasoconstriction in distributive shocks like septic shock since they primarily impact the a-adrenergic receptor [3]. Nonetheless, in some circumstances, these catecholamine medications may result in unanticipated hypotension [4]. Here, we report a case of unanticipated hypotension brought on by the use of catecholamine medications.

Presentation of Case Study

A 36-year-old guy from Addis Ababa, Ethiopia was brought to our emergency room due to schizophrenia. He arrived in a state of shock and unconsciousness. His body temperature was 36.6°C, his heart rate was 140 beats per minute (bpm), his respiratory rate was 40 breaths per minute, and his blood pressure was 62/45 mmHg. (E1V1M1) was his Glasgow Coma Scale score. Due to his shock and unconsciousness, we conducted intubation right away. His blood pressure rose to 75/30 mmHg after receiving 3000 ml of crystalloid fluid resuscitation, but his shock remained. We tentatively started dopamine infusion at 5μg/kg per minute, then raised it to 10μg/kg per minute before inserting a central venous line; nonetheless, his hypotension deteriorated with time to 50/30 mmHg. After arriving for seventy minutes, we started the infusion of noradrenaline at 0.1 μg/kg per minute and then raised it to 0.3 μg/kg per minute by inserting the central venous line. Furthermore, we started dobutamine at 5 μg/kg every minute 95 minutes after arriving. His blood pressure suddenly dropped to 50/35 mmHg, though. The etiology of the coma and hypotension was not found using head computed tomography, improved chest-abdominal computed tomography, point of care sonography, or laboratory data (Table 1). He had an extremely low Systemic Vascular Resistance Index (SVRI) of 430 dynes/second/cm/m2, which is within the normal range of 1970 to 2400 dynes/second/cm/m2. We thus suspected an unknown distributive shock that was resistant to a significant infusion of catecholamines. Thus, 165 minutes after arrival, we started vasopressin infusion at 3 U/hour in addition to catecholamine infusion. Due to an improvement in his metabolic acidosis: pH is 7.36; partial pressures of carbon dioxide and oxygen in arterial blood are 39.2 and 73.6 mmHg, respectively; bicarbonate (HCO-) is -1.2 mmol/l, lactate (Lac) is 1.6 mmol/l, and the Fraction of Inspired Oxygen (FiO2) is 0.4. We stopped the vasopressin injection on day two. His status was stable upon extubation: BP of 124/78 mmHg and HR of 100 bpm. We moved him to our general ward. He acknowledged taking about 150 mg of lurasidone in an effort to end his life. His blood sample had a very high concentration of lurasidone upon admission; on day two, that value had dropped to 3.58 ng/ml. As a result, we identified a lurasidone overdose. After that, nothing happened to his condition, and on day five, he was sent to a psychiatric facility for mental health treatment.

  


    
Blood CP

    
Clotting

  

  


    
WBC

    
5700/μl

    
PT-INR

    
1.06

  

  


    
RBC

    
450×104/μl

    
APTT

    
22.6

  

  


    
Hb

    
12.1 g/dl

    
Fib

    
220 mg/d

  

  


    
Chemical    lab values

    
ABGs

  

  


    
ALT

    
17 U/L

    
pH

    
7.31

  

  


    
AST

    
20 U/L

    
pCO2

    
37.7 mmHg

  

  


    
CPK

    
134 U/L

    
pO2

    
482 mmHg

  

  


    
Cr

    
1.20 mg/d

    
HCO-

    
20.1    mmol/l

  

  


    
Na

    
145 milli    Eq/l

    
- 

    
- 

  

  


    
K 

    
2.5 milli    Eq/l

    
- 

    
- 

  

  


    
Cl

    
106 milli    Eq/l

    
- 

    
- 

  

Table 1: Findings on arrival.

  


    
Agents

    
Values

  

  


    
Partial pressure of CO2 

    
35.8 mmHg

  

  


    
Partial pressure of O2 

    
216 mmHg

  

  


    
Bicarbonate ions

    
14.7    mmol/l

  

  


    
Base excess

    
-11.2    mmol/l

  

  


    
Sodium

    
142 mmol/l

  

  


    
Potassium

    
2.6 mmol/l

  

  


    
Chloride

    
106 mmol/l

  

Table 2: ABGs in ICU.

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Citation: Priyatha V, Guna SDS, Reddy JV, Elkhalifa ATF, Geleta ST, et al. Blood Pressure Fluctuations Due to Lurasidone Reversal: A Case Report. Austin J Pharmacol Ther. 2024; 12(1): 1186.

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