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Scientific letter
Transient electrocardiographic abnormalities during hypoglycemia
Alteraciones electrocardiográficas transitorias durante un episodio de hipoglucemia
Manuel José Fernández Anguita
Corresponding author
, Virgilio Martínez Mateo, Laura Cejudo del Campo Díaz, Miguel Ángel Villanueva Terrazas, Antonio Jesús Paule Sánchez
Servicio de Cardiología, Hospital General La Mancha Centro, Alcázar de San Juan, Ciudad Real, Spain
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She was also being treated with pravastatin 10<span class="elsevierStyleHsp" style=""></span>mg and Eutirox<span class="elsevierStyleSup">&#174;</span> 50<span class="elsevierStyleHsp" style=""></span>&#956;g for dyslipidemia and hypothyroidism respectively&#46; At admission&#44; the patient was unconscious&#44; with no response to verbal or painful stimuli and mydriatic&#44; nonreactive pupils&#46; She was breathing spontaneously&#46; Her blood pressure was 110&#47;75<span class="elsevierStyleHsp" style=""></span>mmHg&#44; and heart rate 56<span class="elsevierStyleHsp" style=""></span>bpm&#46; Heart auscultation revealed cardiac rhythmic sounds&#44; with no murmurs&#44; and pulmonary auscultation found no pathological sounds&#46; The initial capillary blood glucose level was 35<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#46; Intravenous infusion of hypertonic glucose resulted in the recovery of consciousness and increased the blood glucose level to 280<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#46; Laboratory test results included&#58; chemistry&#58; urea&#44; 49<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#59; creatinine&#44; 1&#46;2<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#59; sodium&#44; 141<span class="elsevierStyleHsp" style=""></span>mEq&#47;L&#59; potassium&#44; 3&#46;9<span class="elsevierStyleHsp" style=""></span>mEq&#47;L&#59; chloride&#44; 112<span class="elsevierStyleHsp" style=""></span>mEq&#47;L&#59; troponin Ic &#40;peak value&#41;&#44; 2&#46;1<span class="elsevierStyleHsp" style=""></span>&#956;g&#47;dL&#59; baseline arterial blood gases&#58; pH 7&#46;42&#44; <span class="elsevierStyleItalic">p</span>CO<span class="elsevierStyleInf">2</span> 35<span class="elsevierStyleHsp" style=""></span>mmHg&#44; <span class="elsevierStyleItalic">p</span>O<span class="elsevierStyleInf">2</span> 75<span class="elsevierStyleHsp" style=""></span>mmHg&#44; HCO<span class="elsevierStyleInf">3</span> 22<span class="elsevierStyleHsp" style=""></span>mmol&#47;L&#59; complete blood count&#58; WBCs&#44; 8760&#47;&#956;L&#59; hemoglobin&#44; 11&#46;8<span class="elsevierStyleHsp" style=""></span>g&#47;dL&#59; and platelets&#44; 316&#44;000&#47;&#956;L&#46; The ECG at admission &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41; showed sinus rhythm at 62<span class="elsevierStyleHsp" style=""></span>bpm with signs of left ventricular hypertrophy&#44; 1<span class="elsevierStyleHsp" style=""></span>mm ST segment elevation in aVR&#44; and 1<span class="elsevierStyleHsp" style=""></span>mm ST segment depression in <span class="elsevierStyleSmallCaps">II</span>&#44; <span class="elsevierStyleSmallCaps">III</span>&#44; aVF&#44; and V4&#8211;6 with generalized asymmetrical negative T waves&#44; and a QTc interval of 510<span class="elsevierStyleHsp" style=""></span>ms&#46; The ECG performed after the correction of hypoglycemia with intravenous hypertonic glucose &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41; showed a normalization of changes in the ST segment and repolarization&#44; and the persistence of left ventricular hypertrophy &#40;a pattern of diastolic overload with asymmetrical negative T wave in <span class="elsevierStyleSmallCaps">I</span>&#44; aVL&#44; and V5&#8211;6&#41;&#46; While the patient reported no chest pain&#44; the slightly elevated troponin Ic level prompted the performing of an echocardiogram which showed moderate concentric hypertrophy and normal LVEF&#44; and a treadmill exercise test which was electrically and clinically negative&#46; The course of the patient in the ward was favorable&#44; with good blood glucose control&#46; She was discharged on Lantus<span class="elsevierStyleSup">&#174;</span> insulin 46<span class="elsevierStyleHsp" style=""></span>IU at lunch time&#44; and a rescue regimen of rapid-acting insulin based on the blood glucose level &#40;less than 80<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#58; none&#59; 81&#8211;130<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#58; 4<span class="elsevierStyleHsp" style=""></span>IU&#59; 131&#8211;200<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#58; 7<span class="elsevierStyleHsp" style=""></span>IU&#59; 201&#8211;250<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#58; 8<span class="elsevierStyleHsp" style=""></span>IU&#59; 251&#8211;300<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#58; 10<span class="elsevierStyleHsp" style=""></span>IUI&#59; over 300<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#58; 14<span class="elsevierStyleHsp" style=""></span>IU&#41;&#44; with the discontinuation of metformin&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">Various electrocardiographic changes associated with hypoglycemia have been reported&#46; Their incidence is unknown&#44; as most data found in the literature come from isolated case reports&#46; ST segment and repolarization changes&#44; T-wave flattening and inversion&#44; QT interval prolongation&#44; as well as sinus tachycardia and bradycardia&#44; various degrees of atrioventricular block&#44; atrial fibrillation or supraventricular or ventricular extrasystole&#44;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">2</span></a> and even the induction of fatal arrhythmia have been seen&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a> The mechanisms of the electrocardiographic changes associated with hypoglycemia have not been fully elucidated&#46; However&#44; the direct effect of hypoglycemia&#44; increased epinephrine secretion&#44; secondary hypokalemia&#44; and autonomic dysfunction have been suggested&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> Glucose is vital for myocardial metabolism&#44; and hypoglycemia may be associated with deficient energy provision to the cell&#46; On the other hand&#44; secondary sympathoadrenal discharge increases oxygen consumption&#44; and may also decrease the oxygen supply by vasoconstriction&#46; All these factors may cause a significant impairment in cell metabolism The decrease in serum potassium levels that may occur with hypoglycemia could explain the changes in the ST segment&#44; T wave&#44; and QT interval&#44;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a> favored by excess circulating epinephrine levels&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">5</span></a> In an experimental study reported in 1975&#44; Libby et al&#46; stated that in hypoglycemia&#44; ST depression occurred in territories without coronary artery disease&#44; while elevation occurred in those supplied by obstructed coronary arteries&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">6</span></a> Maroto et al&#46;&#44; however&#44; reported the case of a young patient with ST segment elevation concurrent with hypoglycemia and with normal coronary arteries&#44; and suggested that these changes resulted from a maximum degree of diastolic depolarization of cardiac myofibril caused by changes in intracellular potassium concentrations&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">7</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">It may be concluded that in any patient with diabetes who experiences ECG&#44; hypoglycemia should be suspected as a cause&#46;</p></span>"
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