Nigerian Journal of Cardiology

: 2020  |  Volume : 17  |  Issue : 1  |  Page : 71--75

Supraventricular tachycardia complicating pneumonia in a resource-poor setting

Ujuanbi Amenawon Susan1, Uche-Ajunwa Prisca Ijeoma1, Mankwe Abaram Chesa2,  
1 Department of Paediatrics, Federal Medical Centre, Yenagoa, Nigeria
2 Department of Internal Medicine, Federal Medical Centre, Yenagoa, Nigeria

Correspondence Address:
Dr. Ujuanbi Amenawon Susan
Department of Paediatrics, Federal Medical Centre, Yenagoa


Pneumonia is a common condition in children, especially among the under-fives and a leading cause of morbidity and mortality. Cardiac complications, including congestive heart failure, arrhythmias, myocarditis, and myocardial infarction, are a significant burden among patients hospitalized for pneumonia. Supraventricular tachycardia (SVT) is the most common cardiac arrhythmia in children requiring therapy. We present a 6-week-old Nigerian female child admitted into our children emergency with clinical features suggestive of pneumonia who subsequently developed SVT confirmed by electrocardiogram without an underlying cardiac defect. The child improved on antibiotics, propranolol, and digoxin and was discharged home for follow-up. SVT is a life-threatening clinical condition. High index of suspicion is required as recognition could be made difficult by its nonspecific symptoms.

How to cite this article:
Susan UA, Ijeoma UAP, Chesa MA. Supraventricular tachycardia complicating pneumonia in a resource-poor setting.Nig J Cardiol 2020;17:71-75

How to cite this URL:
Susan UA, Ijeoma UAP, Chesa MA. Supraventricular tachycardia complicating pneumonia in a resource-poor setting. Nig J Cardiol [serial online] 2020 [cited 2021 May 15 ];17:71-75
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Full Text


Pneumonia is a leading cause of morbidity and mortality among children worldwide, especially in developing countries where the greatest burden of the disease is among the under-fives.[1],[2],[3] Patients with pneumonia are at increased risk of cardiac complications, including congestive heart failure, arrhythmias, myocarditis, myocardial infarction, and pericardial effusion, which may contribute to their mortality.[4],[5],[6],[7]

Supraventricular tachycardia (SVT) is the most common cardiac arrhythmia in children, especially requiring therapy.[8] This arrhythmia is usually the manifestation of an accessory conduction pathway that allows the atrioventricular (AV) impulses to reenter the normal pathway, thus completing a circuit and stimulating atrium and ventricle at a fast rate.[8],[9] Infants and young children generally present with poor feeding and tachypnea, whereas palpitation and chest discomfort are prominent symptoms in older children. Electrocardiogram (ECG) shows a narrow complex tachycardia at a rate >220/min, and together with the clinical picture, helps in making a firm diagnosis in the majority of patients.[8],[10] Recognition is made difficult by the nonspecific symptoms, and short-term and long-term management continues to be a major challenge.[10] This is especially the case in resource-poor countries where facilities for effective medications are not readily available.

Hypoxia, underlying heart conditions, local (pulmonary) and systemic (cytokines) inflammation, and medications all contribute to the pathophysiology of cardiac complications in patients with pneumonia.[6] However, the main mechanism responsible for SVT in infants and children with pneumonia is unclear. With advances in antiarrhythmic therapy, there are now many therapeutic options for the treatment of SVT. In this article, we present a recently encountered case of SVT in a child with pneumonia from the Niger Delta region of Nigeria and discuss the diagnosis, as well as challenges in treatment options for the infant with SVT in a resource-poor country like ours.

 Case Report

A 6 week-old female child who was admitted to the children emergency ward of a tertiary institution of Niger Delta, Nigeria, with a history of cough, vomiting, fever, poor feeding, irritability, and fast breathing of 4 days' duration. On general examination, she was in respiratory distress, tachypneic (respiratory rate = 72), mildly pale, and chest examination showed evidence of pneumonia with widespread coarse crepitations. Her pulse rate was 170b/min; the rest of the cardiovascular system and other systems were normal. Oxygen saturation was 95%, and chest X-ray revealed multiple mottled opacities in the lung parenchyma in keeping with pneumonia, and there was no cardiomegaly. Full blood count showed leukocytosis with absolute neutrophilia and a packed cell volume of 38%. Two days into admission, her pulse rate increased >220 b/min, and an urgent ECG revealed narrow complex tachycardia at 260 b/min, thus confirming SVT [Figure 1], and there were abnormal P-waves following the QRS complexes. Carotid sinus massage and application of ice packs to the face failed to change the heart rate; intravenous digoxin and oral propranolol were given since adenosine was not available. Rhythm, however, reverted to sinus in a few seconds and a simultaneously running ECG documented the change [Figure 2]. A 12-lead ECG at that time failed to show any preexcitation pathway, and echocardiography showed a structurally normal heart. The child was maintained on digoxin, and antibiotics were for pneumonia. Thyroid function tests yielded normal results. The child was discharged on maintenance digoxin, and follow-up was advised.{Figure 1}{Figure 2}


SVT is a rapid, paroxysmal regular tachyarrhythmia that commonly involves the AV conduction system and an accessory AV pathway.[11] This is the most frequent sustained arrhythmia in children. Infants and young children are more commonly affected; however, a child may experience the first episode at a higher age also.[11] Our patient was a 6-week-old infant.

Cardiac disorders could be serious complications of pneumonia and may also contribute to mortality. Although the exact pathophysiology of SVT in patients with pneumonia is not clear, its being found that acute lower respiratory tract infections could alter the cardiovascular performance in several ways, including hypoxia and invasion of microorganisms, resulting in myocarditis and other potentially life-threatening cardiac complications such as arrhythmias.[6] Our patient had pneumonia and subsequently developed SVT, and it was difficult to ascertain if myocarditis initiated the SVT as this was not confirmed on ECG or echocardiography. Ko et al. showed that in 90% of infants and about 50% of older children, an AV reentrant pathway initiates SVT.[11] This accessory pathway normally conducts impulses from atrium to ventricle, giving rise to the delta wave on the surface ECG, as in Wolff–Parkinson–White syndrome (WPW syndrome).[8] When the accessory pathway is nonconducting and does not appear on surface ECG, it is referred to as concealed.[12] SVT could be triggered when for some reason the accessory pathway is refractory to the impulse it receives from the atrium, but later conducts the impulse in the reverse direction from the ventricle to atrium, in turn, initiating a second quick forward impulse that reenters the ventricle through AV node and normal conduction pathway.[12] The initiating event may be an episode of premature supraventricular or ventricular beat, sinus pause, sinus tachycardia, or myocarditis.[12] Another common mechanism of SVT in children involves an accessory pathway in or around the AV node (AV nodal reentry).[8] Ectopic atrial tachycardia, atrial flutter, and junctional tachycardia are the other varieties of SVT. Atrial flutter forms a significant proportion of fetal and 5%–10% of neonatal tachycardias.[8] These were not demonstrated in our patient.


Regardless of the mechanism of origin, SVT has a common mode of presentation. Symptoms are nonspecific in infants and young children and include poor feeding, tachypnea, irritability, and excessive crying.[8] Our index patient was an infant and had poor feeding, tachypnea, irritability, and other features of pneumonia.

Palpitation and chest discomfort are more often complained of in older children;[13] our patient was an infant, and these features were not present. Patients usually manifest acutely without any identifiable precipitating factor;[13] however, our patient had pneumonia at the time of admission. The diagnosis of SVT is based on history, physical examination, and ECG.[13] Tachycardia is obvious on the examination which was present in our patient. The elevated heart rate and the narrow QRS complexes are most helpful in cases of SVT.[13] It is to be known that 10% of SVT cases have a wide QRS secondary to aberrant conduction, our patient had a narrow complex pattern.[8] P-waves are generally not visible on the surface ECG in SVT and if present are abnormal, and these abnormal P-waves can be better appreciated if a rhythm strip is recorded at 50 mm/s rather than the usual 25 mm/s.[8] Our patient had abnormal P-waves seen on 25 mm/s rhythm strip.


Unremitting SVT in children requires intervention because of the risk of hemodynamic deterioration. In infants like our patient, it is often a medical emergency as they go rapidly into a state of shock. Vagal stimulation by carotid sinus massage, Valsalva maneuver, application of ice cubes to the face (diving reflex), or a combination of these is attempted initially in the stable child, and these have a role even in the unstable patient while awaiting more definitive therapy.[8],[14] Our patient had the application of ice cubes to the face, which was not helpful in reverting the SVT to sinus rhythm.

The universal drug of choice in all patients with SVT is adenosine.[15] Adenosine acts by inducing transient block of AV node, thereby interrupting the reentrant pathway. It has an extremely short half-life (10–15 s) and is effective in aborting an attack in most patients. Adenosine should be administered as a bolus into good venous access in the upper limb, using a three-way connection. The initial dose is 0.1 mg/kg and repeat doses 0.2 mg/kg with a maximum of 0.3 mg/kg.[15] Adenosine loaded syringe and a second syringe with 3–5 ml normal saline are both connected to the three-way catheter. The physician administers the adenosine as a bolus push and just as he completes it, an assistant pushes in the saline, after changing the direction of the three-way catheter. A running ECG rhythm strip monitors the effect of adenosine reaching the heart. There is a period of cardiac asystole lasting 5–15 s followed by the return of sinus rhythm.[15] However, episodes of junctional and ventricular complexes may be seen during the period of asystole with an additional risk of immediate recurrence of SVT.[15] Usual side effects are confined to autonomic disturbances such as a feeling of impending doom, excessive salivation, abdominal pain, vomiting, flushing, and headache (10%–25%).[8],[15] More recently, major side effects of the drug have also been reported, such as apnea, prolonged asystole, accelerated ventricular rhythm, atrial fibrillation, and wide complex tachycardia.[16] Therefore, resuscitation equipment should be kept ready before administering adenosine. Adenosine was not available in our center, and hence, our patient did not benefit from its usage. Other antiarrhythmic agents such as amiodarone, flecainide, and verapamil, which are other options in the management of SVT were also not available in our center, though they are often not recommended in infants due to risk of hypotension and shock. The only available drugs in our center were digoxin and propranolol, which were used for our patient with good response and conversion of SVT to sinus rhythm after a brief period of asystole. For digoxin, the loading dose was 30 μg/kg, and it was given in three divided doses as infusion over 20 min each at an interval of 8 h. The initial dose was half the total dose (15 μg/kg) and the subsequent doses one fourth (7.5 μg/kg). The maintenance dose was 10 μg/kg daily in two divided doses administered orally. These drugs act by inducing AV block.[8] They have longer-lasting effects than adenosine and repeat doses can be administered orally. Resistant or frequently recurring SVT are other indications for the use of digoxin. Our patient did not have recurrence of SVT. In the immediate steps after conversion to sinus rhythm, patients require continued monitoring to identify and treat recurrences. A 12-lead ECG was taken to look for evidence of preexcitation (WPW syndrome) in our patient which was not present. Recurrences are treated in the same manner with adenosine using increasing doses and taking care to optimize the mode of administration.

Where available, in critically ill patients with difficulty securing an intravenous access, a direct current electrical cardioversion has to be resorted to.[8] The recommended dose of energy is 0.5–2 J/kg. Pediatric paddles are used for infants; children >10 kg require adult-size paddles.[14] This again was not available in our center. In selected patients when all other measures fail, there is a role for transesophageal atrial pacing to terminate the tachyarrhythmia which was also not available in our center.

Radiofrequency (RF) catheter ablation is another treatment option. The major advantage of this mode of therapy is the prospect of a cure. Data on RF catheter ablation of the accessory pathway in SVT have shown an initial success rate of 94%, and freedom from the recurrence of 85%, 77%, and 66% at 1 year, 2 years, and 3 years, respectively, after the procedure.[17],[18] However, it can be performed only in specialized centers, and there is a major complication rate of 2.9% even in the best of centers.[19]


SVT can complicate pneumonia in children with structurally normal heart and can be life-threatening. Early recognition and prompt treatment will reduce associated morbidity and mortality. In resource-poor countries like ours, using available anti-arrhythmic drugs when adenosine is not accessible can be lifesaving.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


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