Document Type : Case Report


Ankara Training and Research Hospital


Introduction: The cardiovascular effects of alcohol consumption are variable. In addition to its protective effects, it may also result in mortality. In this study, we presented a case, who developed cardiac arrest after excessive ethanol intake.
Case Report: A 68-year-old patient, who was brought to the emergency room due to out-of-hospital cardiac arrest, showed ST elevation in the electrocardiogram after returning to spontaneous circulation, and no vascular occlusion was detected in the coronary angiography. The patient’s blood ethanol level was found to be 605 mg/dl and he had cardiac arrest again in the follow-up. He did not respond to cardiopulmonary resuscitation (CPR) for 30 minutes and died.
Discussion:  Acute alcohol intoxication causes various metabolic changes, cardiovascular side effects, gastrointestinal side effects, and respiratory depression. It has been stated that coronary vasospasm can occur even when ethanol levels reach a basal level after 9 hours of excessive alcohol intake. We believe that ST-segment elevation developed as a result of vasospasm and respiratory depression emerged after ethanol intake and that the patient had a cardiac arrest.
Conclusion: We contend that ST-segment elevation after spontaneous return to circulation in out-of-hospital cardiac arrest patients may be caused by excessive ethanol intake, besides acute coronary syndromes.



       Alcohol consumption is responsible for 3.8% of mortality and 4.6% of morbidity worldwide [1]. Although it is known that moderate alcohol use has a protective effect on cardiovascular diseases, there is an increased risk of myocardial infarction in the 24 hours following a heavy drinking period, especially in elderly patients [2].  In this research, we aimed to present a rare case that developed cardiac arrest after high-dose ethanol intake in which we detected ST-segment elevation after spontaneous return to circulation and resulted in death.




Case Report

       A 68-year-old male patient developed an out-of-hospital witnessed cardiac arrest, and cardiopulmonary resuscitation protocol was started by emergency medical technicians. The patient's blood sugar was 189 mg/dl. He was resuscitated by the guideline protocols and was brought in approximately 20 minutes after the development of cardiac arrest. Throughout the cardiopulmonary resuscitation process, asystole rhythm was observed in the patient, and a pulse was detected 6 minutes after his arrival. The patient, who returned to spontaneous circulation, had no known additional disease and had a history of chronic alcohol use. Arterial blood pressure was 110/60 mm/Hg, heart rate was 90/min, oxygen saturation was 95%, and body temperature was 36°C. Glasgow Coma Score was E1M1V1 (intubated). Electrocardiogram revealed 1 mm ST-segment elevation in leads D2, D3, and AvF, and ST-segment depression in lead AvL. (Figure 1)

In the laboratory, WBC: 19.000/mcgL (4-10.5) Hgb: 14.7 g/dl (13.5-18) platelet 202 103 u/L (150-450), glucose: 201 mg/dl (75-99) urea: 35 mg /dl (18-55) creatinine: 1.04 mg/dl (<1.20) alanine aminotransferase 24 U/L (0-41 U/L) , aspartate aminotransferase 33 U/L (0-37 U/L), Sodium: 148 mmol/L(136-145), Potassium: 5.1 mmol/L (3.5-5.5) hs-Troponin T: 13.7 ng/L (<14) CKMB: 6.42 mcg/L (<14) ethanol: 605 mg/dl In blood gas: pH:7.00 pCO2: 62.3 mmHg (35-48) PO2:80 mmHg HCO3: 14.6 mmol/L (24-28) lactate: 10.6 mmol/L (0.9-1.7). Cranial and thoraco-abdominal CT angiography images of the patient were evaluated as normal. In echocardiography, EF was measured to be normal and there was no wall motion defect. Coronary anjiography showed coronary arteries with plaques with no significant stenosis.

Due to the presence of metabolic acidosis, the patient was accepted as cardiovascular unstable and 1 mEq/kg/h NaHCO3 infusion was started. The patient's blood pressure was 60/40 mmHg and noradrenaline infusion was started. Cardiac arrest developed in the follow-up of the patient, who did not respond to cardiopulmonary resuscitation for approximately thirty minutes, was accepted as exitus approximately 3 hours after his admission.



The annual incidence of Out-of-Hospital Cardiac Arrest (OHCA) in Europe is 67-170 /100.000. The average rate of hospital discharge is 8% (0-18) [3]. Acute coronary syndromes are responsible for 60-80% of OHCA causes. Approximately 5-10% of them are electrolyte disorders, metabolic disorders, drug intoxications, and non-cardiac causes [4].  Emergency coronary angiography is recommended if the patient's electrocardiogram after OHCA has ST-segment elevation and cardiac origin was suspected or in high-probability acute cardiac occlusions without ST-segment elevation. [5]   In a study, it was reported that ST-segment elevation after the return of spontaneous circulation (ROSC) in OHCAs was 95% specific for a significant coronary lesion [6].   A low perfusion index was found in patients with false positivity with STEMI after ROSC [7].   It has been stated that patients with age>85, non-VF initial rhythm, unwitnessed arrest, ROSC after 30 minutes, end-stage renal failure, cancer disease, pH<7.2, lactate>7 in patients with ST-segment elevation, and Non-ST myocardial infarction after ROSC will benefit less from coronary angiography [8].   

Acute alcohol intoxication causes various metabolic changes, cardiovascular side effects (causing tachycardia, peripheral vasodilation, and volume reduction, which induces hypothermia and hypotension), gastrointestinal side effects (nausea, vomiting, alcoholic hepatitis), and respiratory depression [9].   After ethanol intake, impairment in situations requiring skills and increase in talkativeness are observed in blood alcohol concentration below 50 mg/dl, while above 100 mg/dl relaxation, ataxia, hyperreflexia, lack of coordination, personality and behavioral changes, nystagmus, speech disorder are seen. Above 200 mg/dl, amnesia, diplopia, dysarthria, hypothermia, nausea, and vomiting are observed, while over 400 mg/dl results in respiratory failure, coma, and death. [9]  

It is known that many intoxications such as carbon monoxide, cocaine, and cannabis cause acute myocardial infarction [10-12].   Cases of myocardial infarction have been reported as a result of ethanol intoxication. After excessive intake of ethanol, the increase in plasmogen activator inhibitor and the decrease in tissue plasmogen activator causes a decrease in fibrinolysis [13].   Repeated doses of excessive ethanol intake accelerate the progression of atherosclerosis and pose a risk for myocardial infarction. It has also been reported that excessive alcohol intake accelerates blood flow with tachycardia and causes thrombocyte activation [14-15].   

         Hypovolemia, hypoxia, acidosis, hypo/hyperkalemia, hypothermia, tension pneumothorax, cardiac tamponade, pulmonary and cardiac thrombosis, and toxins should be considered in return to spontaneous circulation (known as 5H-5T) [16]. Diagnoses of hypovolemia, tension pneumothorax, cardiac tamponade, pulmonary, and cardiac thrombosis were excluded by echocardiography, thoracoabdominal CT angiography, and coronary angiography in our case. Body temperature was normal in his vitals. There was no hypo/hyperkalemia in his laboratory. We believe that ST-segment elevation developed as a result of vasospasm and respiratory depression emerged after ethanol intake and that the patient had a cardiac arrest. It has been stated that coronary vasospasm can occur even when ethanol levels reach a basal level after 9 hours of excessive alcohol intake [17].

        As a result, it has been published that excessive alcohol intake accelerates atherosclerosis, decreases fibrinolysis, increases platelet activation, and increases vascular tone. Thus, it poses a risk for acute myocardial infarction, while moderate and mild alcohol intake reduces the myocardial incidents as it slows atherosclerosis, accelerates fibrinolysis, decreases platelet activation, and decreases vascular tone[15-18-19]. Treatment of acute alcohol intoxication includes ensuring airway safety, providing mechanical ventilation support and sedation if necessary, controlling hypoglycemia and electrolyte disorders, and the administration of metadoxin to increase ethanol elimination [9].



       Based on the results of this study, it can be concluded that ST-segment elevation after spontaneous return to circulation in out-of-hospital cardiac arrest patients may be caused by excessive ethanol intake, besides acute coronary syndromes.


Funding and Support: None to be declared

Conflict of interest: None

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