Cardiovascular Journal of Africa: Vol 32 No 2 (MARCH/APRIL 2021)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 32, No 2, March/April 2021 108 AFRICA
Case Report
Severe bradycardia caused by diabetic ketoacidosis
João Ferreira, João Martins, Lino Gonçalves
Abstract
Atrial standstill is an uncommon but serious clinical entity
that is often unrecognised in the clinical setting. Its diagno-
sis and treatment should be swift as malignant arrhythmias
and thromboembolic complications can arise. We present a
79-year-old man brought to our emergency department with
acute confusion, heart failure and severe bradycardia in the
context of diabetic ketoacidosis, and discuss the diagnosis
and management of this arrhythmic condition.
Keywords: atrial standstill, electrocardiogram, transthoracic
echocardiogram, emergency, bradycardia, diabetic ketoacidosis,
medical education
Submitted 9/9/19, accepted 14/7/20
Cardiovasc J Afr 2021; 32: 108–110
DOI: 10.5830/CVJA-2020-026
Case report
A 79-year-old man with a history of hypertension, type 2
diabetes mellitus and known poor therapeutic compliance was
brought to our emergency department with acute confusion. A
physical examination revealed normal blood pressure (144/65
mmHg), a heart rate of 30 beats/min and tachypnoea on ambient
air with normal peripheral oxygen saturation (95%). Lung
auscultation showed bilateral basal crackles with concomitant
jugular venous distention.
Arterial blood gas analysis showed partially compensated
metabolic acidosis (pH 7.312, PaCO 2 21.5 mmHg and HCO310.6
mmol/l), severe hyperkalaemia (7.89 mmol/l), high serum lactate
level (2.5 mmol/l) and hyperglycaemia (849 mg/dl; 47.12 mmol/l).
High-sensitivity cardiac troponin was negative (27.9 ng/l). Blood
tests also showed acute kidney injury (serum creatinine 3.89 mg/dl).
The initial electrocardiogram (ECG) revealed no discernible P
waves with a slightly irregular bradycardic junctional rhythm (Fig.
1A). Bedside transthoracic echocardiography revealed a preserved
left ventricular ejection fraction, moderate mitral regurgitation,
mild left atrial enlargement and confirmed absent atrial contraction
as there were no A waves on transmitral pulsed-wave Doppler flow
(Fig. 2). These findings were suggestive of atrial standstill (AS).
The patient was quickly started on calcium gluconate,
furosemide, inhaled salbutamol, intravenous saline and insulin
perfusion, restoring normal glycaemic levels. While the metabolic
and electrolyte changes were being corrected, and because he had a
supra-hissian escape rhythm, the patient was put on isoproterenol
infusion in order to treat acute heart failure, mainly caused by
new severe bradycardia. The patient successfully returned to sinus
rhythm 82 minutes after the first ECG (Fig. 1B).
After the emergency presentation, the patient was hospitalised
in the endocrinology ward, where treatment was continued and
antidiabetic drugs were optimised. He was discharged symptom
free and referred for a cardiology and endocrinology consultation,
where he has been followed up with good glycaemic control and no
further rhythm disturbances.
Discussion
AS was first described in 1946 by Chavez et al.,1 and is
characterised by the complete absence of electrical and
mechanical atrial activity. Therefore, the most common ECG
pattern associated with this entity is the absence of atrial
depolarisation with bradycardic regular junctional or ventricular
escape rhythm2,3 (Fig. 1A). Recognising this ECG pattern is
important because secondary causes must be excluded, avoiding
unnecessary interventions and non-priority therapies. 4
AS is usually transient, occurring with digitalis or
quinidine intoxication, hypoxia, hyperkalaemia or myocardial
infarction. Persistent AS is rare, being reported in association
with some types of muscular dystrophies, cardiomyopathies,
valvular diseases, congenital heart diseases, Ebstein’s anomaly,
amyloidosis, acute myocarditis, following open cardiac surgery
or after longstanding atrial fibrillation.4 In this specific case, as
the patient did not present any other major causes of AS, severe
hyperkalaemia was most likely responsible for the transient AS.
The mainstay of diagnosis of this entity is an electrophysiolog-
ical study, capable of proving the bilateral absence of atrial
electrical activation, and transthoracic echocardiography,
through spectral Doppler, showing lack of atrial contraction by
the absence of an A wave in transmitral or transtricuspid flow,
the absence of atrial contraction in tissue Doppler imaging or the
absence of telediastolic mitral valve opening.5 Also, the lack of
an A wave during jugular venous pulse when jugular distension
Cardiology Department, Coimbra Hospital and University
Centre, Portugal
João Ferreira, MD,
Lino Gonçalves, MD, PhD
Intensive Care Unit, Coimbra Hospital and University
Centre, Portugal
João Martins, MD
Faculty of Medicine, University of Coimbra, Portugal
Lino Gonçalves, MD, PhD