Electrocardiographic Changes of Sinoatrial Dysfunction in Hypoglycemia: A Case Report

INTRODUCTION

Hypoglycemia is a common complication in diabetic patients undergoing treatment with insulin or oral antidiabetics. Its clinical manifestations are diverse and potentially severe, and multiple electrocardiographic abnormalities have been associated with it.(1,2,3)

In 2016, approximately 26 million individuals in Latin America were diagnosed with diabetes. Among them, it is estimated that 10 % to 30 % of type 1 diabetics experience at least one severe hypoglycemic episode annually—similar rates are reported in type 2 diabetics treated with sulfonylureas or insulin.(4)

There is a widespread clinical belief that hypoglycemia in otherwise healthy or diabetic individuals is an acute, transitory condition with little long-term cardiovascular impact. However, scientific evidence increasingly suggests the contrary, presenting a growing body of support for its role as a significant cardiovascular risk factor due to its promotion of endothelial dysfunction and atherosclerosis—on par with hyperglycemia—and as a potential cause of both arrhythmic and ischemic sudden cardiac death.(5,6)

Chronic glycemic variability and abrupt glycemic drops act as independent noxious agents that impair endothelial function, with both short- and long-term cardiovascular consequences. Acute hypoglycemia produces profound pathophysiological changes that affect the cardiovascular system and several hematological parameters, mainly due to sympathetic-adrenal activation and the release of counterregulatory hormones.(7)

CASE PRESENTATION

Medical History and Physical Examination

We present the case of a 61-year-old female patient, fair-skinned and from an urban area, with a past medical history of grade II essential arterial hypertension of 10 years’ duration, treated with Enalapril (20 mg tablet) one tablet every 12 hours and Hydrochlorothiazide (25 mg tablet) one tablet daily. She also has type 1 diabetes mellitus, managed with long-acting insulin: 30 units in the morning and 15 units at night.

On this occasion, following the onset of fever (38,0°C), general malaise, and loss of appetite, she experienced an episode of near syncope, accompanied by cold sensation and profuse sweating. She was taken to the emergency department of the Manuel Fajardo Rivero Military Hospital in Santa Clara, where capillary blood glucose measurement revealed a value of 2,4 mmol/L. A 12-lead electrocardiogram (ECG) was performed, which showed sinus pauses lasting more than 3 seconds (Figure 1), followed by rapid recovery without loss of consciousness.

A consultation was made with the Cardiology and Endocrinology departments, and it was decided to initiate urgent administration of hypertonic dextrose, achieving complete resolution of the symptoms. A follow-up blood glucose measurement showed a value of 5,6 mmol/L, and a 12-lead electrocardiogram was performed, which showed no abnormalities (figure 2).

An echocardiogram was performed, which ruled out structural heart damage, revealing a left ventricular ejection fraction (LVEF) of 55,7 % and cardiac chambers with normal appearance, diameters, and configuration. The patient was subsequently transferred to the Cardiology ward, where she remained hemodynamically stable: heart rate (HR) 85 bpm, blood pressure (BP) 110/70 mmHg, respiratory rate (RR) 20 breaths/min, and regular rhythm on ECG and cardiac monitor. After completing the established observation period, hospital discharge was decided, with outpatient follow-up by the Arrhythmia and Endocrinology clinics.

DISCUSSION

Hypoglycemia may exert proarrhythmic effects through various mechanisms, generally related to the direct impact of low serum glucose levels on ion channels. Hypokalemia and catecholamine release prolong cardiac repolarization, increasing the risk of early afterdepolarizations and, consequently, ventricular arrhythmias.(8)

Experimental hypoglycemia has also been shown to prolong the QT interval in individuals with type 1 and type 2 diabetes, demonstrating a directly proportional relationship between the depth and duration of hypoglycemia and the degree of QT prolongation.(9,10)

The arrhythmogenic mechanism of hypoglycemia, in addition to repolarization changes such as QT prolongation and T wave flattening, is probably also linked to the exponential increase in plasma adrenaline concentration during hypoglycemic episodes, as documented in Marqués' publication.

Electrocardiographic changes attributed to adrenaline have been associated with serum potassium reduction mediated by direct stimulation of the Na/K ATPase pump.(11,12)

Regardless of its duration or severity, any hypoglycemic episode triggers a series of hematological and inflammatory alterations, including vasoconstriction, increased blood viscosity, elevated production and release of endothelin, increased synthesis and activation of factor VIII and von Willebrand factor, platelet activation, neutrophil activation, and elevated plasma C-reactive protein levels.(13)

Hypoglycemia also raises aldosterone levels in direct proportion to its severity. This elevation is attributed to activation of the renin-angiotensin-aldosterone system as well as increased ACTH levels.(14,15,16)

Furthermore, it has been demonstrated that prolonged cardiac repolarization caused by hypoglycemia results from sympathetic-adrenal stimulation acting directly on the myocardium and through decreased serum potassium. Cardioselective beta-blockers (BB) have been shown to prevent these effects in healthy individuals and may also have a therapeutic role in diabetic patients.(17,18)

In the present case, diagnosis was challenging with the initial ECG, due to the rarity of similar presentations in our emergency department. In type 1 diabetic patients, hypoglycemia provokes marked repolarization changes, mainly expressed as reduced T wave amplitude, decreased height and width of the T wave loop, and reduction of the R-to-T angular cosine.

Although there is no consensus regarding the clinical relevance of these repolarization changes in relation to outcomes such as mortality, they may increase the risk of cardiac arrhythmias during hypoglycemic episodes, including severe sinus bradycardia progressing to asystole, atrial fibrillation, and ventricular tachycardia.(19)

In this regard, further investigation is warranted into the potential contribution of hypoglycemia-induced repolarization abnormalities and autonomic neuropathy to sudden death in diabetic individuals.

This case demonstrates the need for a high index of suspicion in the presence of hypoglycemia and ischemic or non-ischemic electrocardiographic changes in patients treated in emergency services.

References

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