Pediatrics 5th year, 20th lecture/part one (Dr. Jamal)
Cardiac Arrhythmias "C. A."Abnormal rate and rhythm of the heart can be physiological or pathological, congenital oracquired, transient or chronic, self-limited or life threatening. For all of which ECG isessential to make a diagnosis.I. Tachyarrhythmia (increased H.R.):1) Sinus tachycardia: a physiological compensatory mechanism due to rapid discharge from S.A. node in response to: a. Certain physiological events as crying, pain, anxiety and exercise. b. Certain pathological events as fever, shock, hypoxia, H.F. , anemia or c. Due to certain drugs as atropine, adrenaline or theophylline.ECG shows tachycardia with normal "P", normal 1:1 AV conduction and normal QRS.2) Supra ventricular tachycardia "S.V.T."; the discharge is from an abnormal mechanism proximal to the bifurcation of "His" bundle. It is of 3 types: a. Paroxysmal S.V.T.: caused by "Re-entery" phenomenon through the AV node or through other conducting pathways. SVT affects all ages from fetal life onward. The paroxysm occurs suddenly without an event cause or follows an infection or a physical factor and usually occurs at rest. The H.R. is between 180 and 300 /min. short attacks for minutes or hours may be tolerated but prolonged and severe forms may lead to C.C.F. The attack may spontaneously terminate as suddenly as it began. Polyuria may occur due to release of atrial nitriuretic peptide. Maneuvers that increase vagal tone (unilateral carotid sinus massage, valsalva maneuver, abdominal pressure, pressure on the eye ball [not in young infants] and ice pack on the face) may successfully terminate the attack. SVT may be precipitated by nasal decongestants (sympathomimetics). ECG reveals a very fast rate, normal "P", normal 1:1 AV conduction and normal QRS. Some patients with SVT have WPW syndrome and are at higher risk for sudden death from WPW syndrome. During the paroxysm the ECG misses WPW picture which is in the form of short P-R and slow upstroke QRS (delta wave). If the above measures fail I.V adenosine 0.05 mg/kg bolus repeated every 2 min for several times. When available DC cardioversion Other drugs used in SVT include; Phenylphrine, Edrophonium, Amiodarone, Quinidine, Procainamide, propranolol and Verapamil (not used in infants). After cessation of the acute paroxysm maintenance drugs as Digoxin (not in presence of WPW), Propranolol, Amiodarone, Verapamil, etc….should be used for 1 year. Recurrences are common in older children and may indicate for radiofrequency ablation therapy.
b. Atrial flutter: a very uncommon form of tachyarrhythmia, caused by an abnormal atrial focus discharging at a very high rate (300-500/min) producing atrial "sawtooth" flutter waves on ECG. As the AV node can not transmit all these impulses a degree of AV block occurs. ECG shows a regular sawtooth "P" waves and a regular QRS complexes but there is one QRS for each 2 or 3 P waves. This conduction is rare in normal heart. Treatment includes vagal maneuvers, adenosine and synchronized DC cardioversion. c. Atrial fibrillation: mostly seen in older children with chronic rheumatic heart disease, usually mitral stenosis. Thyrotoxicosis may be the cause. It is characterized by irregular discharges from atrial foci resulting in an irregular disorganized atrial rate of 350-600/min. patients are liable to have thromboemboli and stroke. The ventricular response is variable, resulting in a very irregular beating. ECG shows: Absent "P" waves (irregular base lines) Irregular P-R intervals (irregular ventricular contractions) Normal shapes QRS complex. Treatment is by digitalization which restores the ventricular rate to normal although the atrial fibrillation usually persists, followed by Amiodarone± Warfarin.3) Ventricular tachyarrhythmia: the rapid heart rate originates from abnormal ventricular mechanisms. Two main forms are known: o Ventricular tachycardia; a serious condition which may change to fatal ventricular fibrillation, predisposed by myocarditis, cardiomyopathy, digoxin toxicity, hypoxia or severe electrolyte imbalance. Clinically there is tachycardia ± syncope and sudden death may occur. ECG shows rapid wide QRS not preceded by P waves. I.v. lidocaine is essential to prevent fibrillation and death. o Ventricular fibrillation: a potentially fatal dysrhythmia which cause death within few minutes unless immediate resuscitative measures ere provided. Clinically the patient suddenly loses consciousness with no detectable heart beat and the ECG shows total disorganization with absent QRS. Immediate cardiac massage, i.v. amiodarone or lidocaine,intracardiac adrenaline and artificial ventilation + cardioversion when available.
II. Bradyarrhythmia:Bradycardia is considered to be present when the heart rate is less than the lower normallimit for age.The lower limit of heart rate in awake state is: } − Newborn 90/min. − Infant 100/min. − Young children 80/min. Some what less during sleep − Older children 60/min.Bradyarrhythmias include: 1) Sinus bradycardia (S.B.); characterized by abnormally slow heart rate caused by discharge from S.A. node. Sinus bradycardia may be physiological (during sleep and in athletes), pathological (syncope or raised intra cranial pressure) or caused by drugs (Digoxin or propranolol) Clinically there is bradycardia which increases with exertion (crying), a point which differentiates sinus bradycardia from AV block. ECG shows a slow rate but normal P-QRS-T complexes. 2) Atrioventricular block; it is of three types: a. First degree AV block: prolonged P-R interval but all the atrial impulses are conducted to the ventricle. b. Second degree; failure of conduction of some of the atrial impulses to the ventricle. It is subdivided in to two forms: − Mobitz type I (wenckebach); in which the P-P interval remains constant, but there is progressive increase of the P-R interval until a "P" wave is not conducted. After this dropped beat the cycle starts again with a short P-R interval. − Mobitz type II; P-R interval remains constant, but an occasional atrial beat does not conduct to the ventricle. Syncope may occur and the conduction may change to complete AV block. c. Third degree (complete heart block): no atrial impulse reaches the ventricles. The cause may be; − Congenital, usually associated with maternal SLE. − Acquired; digixin, post cardiac surgery, or bacterial endocarditis. Clinically; most are asymptomatic, heart rate is around 50/min, may increase by 10-20 on exercise or atropine. Symptoms include fatigue, exercise intolerance, syncope (stokes- Adams attacks) and rarely sudden death may occur. Systolic murmurs are commonly heared. Cardiomegaly and elevated blood pressure may be detected. ECG: QRS duration may be prolonged. Prognosis of the congenital complete heart block is good. Some who have exercise intolerance,progressive cardiomegaly or Stokes-Adams attacks need implantation of the permanent cardiac pace maker.
3) Sick Sinus Syndrome "SSS" This form of Bradyarrhythmia usually follows cardiac surgery, myocarditis,myocardial ischemia or cardiomyopathy. SSS is characterized by profound unresponsivesinus bradycardia with or without periods of tachycardia (bradycardia- tachycardiasyndrome) manifests as dizziness and syncope. In symptomatic cases drugs as digoxin orventricular pacemaker are necessary. 4) Asystole; complete cessation of cardiac contraction, (flat ECG) may follow bradycardias or results from sever hypoxia, acidosis, shock, hypothermia, electrolyte disturbances or hypovolemia. Stressful procedures as lumber puncture, intubation or intra venous canulation may cause cardiac arrest.Extrasystoles (premature beat): these are mostly benign and occur in normal children.They may also accompany various organic (inflammation, ischemia, fibrosis) heartdisease or be drug induce (digoxin)They result from isolated discharge from an ectopic atrial or ventricular focus.The atrial extrasystoles are shown on ECG as; − Abnormally shaped "P" wave − Normal QRS − No compensatory pauseThe ventricular extrasystoles are shown on ECG by: − Wide bizarre QRS, inverted "T" and a compensatory pause. Long Q-T Syndrome "LQTS"This is a rare condition characterized by prolonged QT interval, syncopal attacks. Nervedeafness, hemiplegia, petit-mal may be present. LQTS may be a cause of SUIDS.There may be an abnormality in the sympathetic innervation of the myocardium.LQTS may be familial (both A.R. and A.D. are known) or acquired due to: − Drugs as phenothiazine − Hypokalemia, hypocalcemia or hypomagnisemia − Hypothermia − Cerebrovascular diseases − Neck surgery.Treatment includes propranolol, di-phenyl hydantoin and left satellate ganglionectomy.The mortality is high (75%) without treatment.