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VOLUME 18 NUMBER 1 • JULY 2021
Case Report
SA JOURNAL OF DIABETES & VASCULAR DISEASE
Severe bradycardia caused by diabetic ketoacidosis
João Ferreira, João Martins, Lino Gonçalves
Correspondence to: João Ferreira
Cardiology Department, Coimbra Hospital and University Centre, Portugal
e-mail:
joaoaferreira29@gmail.comLino Gonçalves
Cardiology Department, Coimbra Hospital and University Centre;
Faculty of Medicine, University of Coimbra, Portugal
João Martins
Intensive Care Unit, Coimbra Hospital and University Centre, Portugal
Previously published in
Cardiovasc J Afr
2021
;
32
: 108–110
S Afr J Diabetes Vasc Dis
2021;
18
: 10–12
Abstract
Atrial standstill is an uncommon but serious clinical entity
that is often unrecognised in the clinical setting. Its diagnosis
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 educatione
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, Pa
CO
2
21.5 mmHg and HCO
3
10.6
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 rhythm
2,3
(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 electrophysiological
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 is present, a sign nowadays
rarely searched for, is also proof of absent atrial contraction.
However, in the emergency setting, a rapid approach to this patient
is needed, and diagnosis must be confirmed with ECG, jugular
venous pulse observation and transthoracic echocardiography,
tools readily available in the majority of emergency departments.
AS can be a serious condition as the loss of active atrial
contraction and profound bradycardia can lead to markedly
decreased cardiac output. Cardiac arrest can also occur, not only
because the escape mechanism can be unstable but also because
the bradycardia can be extreme, and pause-related ventricular
arrhythmias such as polymorphic ventricular tachycardia can arise.
6
Moreover, blood stasis, originating with no atrial activity, can cause