Paediatrics Flashcards
Tachy
Tachycardia Tachycardia may result from physiological processes that alter the sympathetic/ parasympathetic tone, resulting in a sinus tachycardia. Such causes include: › Excessive activity. › Crying/ being upset. › Stress. It may also be caused by a secondary problem outside the heart, like fever, infection, hyperthyroidism, anaemia or any other problem causing a high metabolic rate. It is rarely due to a primary cardiac cause. A primary cause is more likely if tachycardia is particularly high or an isolated finding.
Brady
Bradycardia is commonly encountered in paediatrics and is usually physiological, occurring particularly in athletes and during sleep. Other causes include: › Drugs. e.g. beta blockers. › Cushing reflex. The combination of bradycardia, hypertension, reduced consciousness and irregular respiration is a sign of raised intracranial pressure. › Shock/ sepsis. › Heart block.
SVT
Supraventricular tachycardia (SVT) is a narrow complex tachycardia originating at or above the atrioventricular node. It is the most common tachyarrhythmia encountered by paediatricians and can be difficult to differentiate from a simple sinus tachycardia. Aetiology A re-entry mechanism is the most common cause of an SVT, and this can occur anywhere along the atrioventricular junction. This mechanism results in rapid acceleration of the heart rate, as it does not rely on a new impulse to be generated by the sino-atrial node. Children who develop re-entry tachycardia will generally have an anatomical abnormality or variant, such as an accessory conduction pathway or abnormal division of an existing conduction pathway. An example of this is the Bundle of Kent in Wolff-Parkinson-White syndrome.
SVT
Clinical Features Presentation of an SVT varies with the age of the child and the severity of the condition. It usually presents with palpitations, although some patients may present in heart failure, as moribund or in cardiorespiratory arrest. This is summarised in Table 4.
SVT
Differential Diagnoses Sinus tachycardia is the main differential diagnosis. The key features that distinguish SVT from sinus tachycardia are: › Sudden onset. › No rate variation. › Very fast rate (> 220 bpm in an infant and > 180 bpm in a child). › Not responsive to a fluid bolus. › No P waves visualised on the ECG reading.
SVT
Investigations
If the child is stable, elicit a history from them or their caregiver. The history will often indicate a certain diagnosis and can guide and focus further investigations. › ECG. This is the primary diagnostic test. The ECG will show narrow complex tachycardia. The rate will generally be above 220 bpm for an infant and above 180 bpm for an older child. There will be no discernible P-waves and there will be no rate variability (Figure 3). › Chest X-ray. This investigation can serve as a useful indicator of heart failure as it may show plethoric lungs. It can also help to exclude pulmonary causes of shortness of breath (e.g. consolidation, pneumothorax, pleural effusion). › Blood gas. This is a good investigation to do for an unwell child, as it can indicate how systemically compromised they are with lactate levels, carbon dioxide and base excess. Electrolyte levels, including potassium and calcium, are often available from the blood gas machine. › Blood glucose. It is very important to check this value in any unwell child, as hyper- or hypoglycaemia can cause or worsen many presentations.
SVT
Management Stable Child If the patient is relatively well, vagal manoeuvres can initially be attempted. These vary depending on the age of the patient. The child must be attached to a heart monitor/ ECG so that cardioversion can be captured and sent to the local tertiary unit. In infants, ice immersion can be attempted. This involves wrapping the infant and immersing its face into a basin of ice for approximately 10 seconds. This stimulates the diving reflex and can trigger the heart rate to return to normal. A variation of this is placing a bag containing crushed ice onto an infant’s face for 15– 30 seconds. In children, a Valsalva manoeuvre can be attempted. One way of getting children to successfully comply with this is by asking them to blow into an empty 10 mL syringe.
SVT
Unstable Child In patients that are more acutely compromised or in those in whom initial vagal manoeuvres don’t work, adenosine may be given or DC cardioversion may be needed. Complications In the acute setting, SVT can lead to cardiovascular compromise, insufficient cardiac output, shock and ultimately death. Treatment also has complications. Vagal manoeuvres and adenosine can lead to asystole and should be done under careful monitoring, with full resuscitation facilities available. Following resolution of SVT, further ECG abnormalities may be detected. An example of this would be Wolff-Parkinson-White syndrome (Figure 4). This is characterised by a slurred R wave, known as a delta wave, across all leads. The delta wave is caused by an accessory conduction system which bypasses the AV node, thereby shortening the PR interval and making the patient prone to episodes of re-entry tachycardia.
SVT
Prognosis In general, patients that have a single episode of SVT have a good prognosis, particularly with an uncomplicated presentation. SVT episodes may be recurrent. In the long-term, particularly if a patient has frequent episodes, prophylactic measures should be considered under the advice of a paediatric cardiologist. This would initially involve advice with regard to vagal manoeuvres and when to summon help. The patient may also be commenced on anti-arrhythmic medication. Those on longer term medications may suffer side effects, although SVTs can generally be well controlled, and medications are stopped after having an ablation. Patients may undergo radiofrequency ablation of their accessory pathway when they are teenagers, which renders that pathway nonfunctional.
VT
may also be commenced on anti-arrhythmic medication. Those on longer term medications may suffer side effects, although SVTs can generally be well controlled, and medications are stopped after having an ablation. Patients may undergo radiofrequency ablation of their accessory pathway when they are teenagers, which renders that pathway nonfunctional.
VT
Investigations It is important to review these patients frequently and to look for reversible causes of arrhythmia in their histories, examinations and biochemical evaluations. Investigations are similar to that for SVT. Figure 5 shows the ECG appearance of ventricular tachycardia. Management Any patient without a pulse requires cardiopulmonary resuscitation (CPR), cardiac defibrillation and possibly adrenaline/ amiodarone administration. Patients with a pulse are divided into those in shock and those who are not. › For patients not in shock, treatment with amiodarone is recommended. › For those in shock, synchronized DC cardioversion is preferred.
VT
Complications VT is associated with sudden death, and any suggestion of VT on ECG needs prompt evaluation by a senior clinician as the risks of cardiac arrest and further deterioration to ventricular fibrillation are high. Prognosis This is highly dependent on the aetiology and clinical situation. Short runs of asymptomatic VT could go unnoticed over an entire lifetime, whereas VT could also be first noted at a cardiac arrest.
HB
Heart Block As with adults, children can get first degree (slowed conduction of atrial impulses to ventricles, causing prolonged PR interval), second degree (some atrial impulses are conducted to the ventricles, causing “dropped beats”) or third degree heart block (complete dissociation between atrial and ventricular activity (Figure 6)).
HB
Treatment involves identifying and correcting any possible causes (e.g. Lyme disease), and focusing on maintaining a heart rate tolerated by the patient. Acutely, the most compromised patients might require isoprenaline (a β agonist that increases heart rate) or temporary pacing wires. The most severe cases may require a permanent pacemaker, but most patients require no active intervention.
Congenital HB
Congenital Heart Block Congenital heart block is most often encountered in a baby whose mother suffers from connective tissue disorders with anti-Ro or anti-La antibodies (e.g. systemic lupus erythematosus; SLE). These antibodies are thought to attack the conduction system within the developing heart and cause atrophy of the AV node. This faulty node causes heart block, or sometimes intrauterine death or a hydropic foetus. Whenever a maternal history of connective tissue disorder is encountered or when anti-Ro or anti-La antibodies are found, an ECG must be performed on the baby after birth. Zeshan Qureshi. The Unofficial Guide to Paediatrics: Core Curriculum, OSCEs, clinical examinations, practical skills, 60+ clinical cases, 200+MCQs 1000+ high definition colour clinical photographs and illustrations (p. 23). Qureshi Enterprises. Kindle Edition.
