Cardiovascular System PDF

The Cardiovascular System  Assessment HISTORY Heart disease in children =combination of genetic and environmental causes. The prenatal history : evidence of a maternal infection: ♥ early in pregnancy (possibly teratogenic) ♥ Later in p...

The Cardiovascular System  Assessment HISTORY Heart disease in children =combination of genetic and environmental causes. The prenatal history : evidence of a maternal infection: ♥ early in pregnancy (possibly teratogenic) ♥ Later in pregnancy (causing myocarditis or myocardial dysfunction in infants). A maternal history of medication, drug, or alcohol use or excessive smoking may contribute to cardiac and other systemic findings. Growth is an extremely valuable sign of cardiovascular health. ♥ Infants with congestive heart failure (CHF) grow poorly, with weight being more significantly affected than height and HC. CHF present with: 1. fatigue or diaphoresis with feeds 2. fussiness 3. tachypnea and dyspnea 4. feeding is difficult and prolonged 5. easy fatigability, shortness of breath on exertion, and orthopnea(Older children) 6. Exercise intolerance: by asking how well children keep up playing with their friends or in physical education class. 7. Before diagnosis of CHF, patients may have been diagnosed with recurrent "pneumonia," "bronchitis," wheezing, or asthma. A history of a heart murmur is important, but many well children have a normal or innocent heart murmur at some time in their life. Other cardiac symptoms include cyanosis, palpitations, chest pain, syncope, and near- syncope. A review of systems for possible systemic diseases or congenital malformation syndromes that may cause cardiac abnormalities. A history of drug use is important in older children and adolescents Family history for: 1. early atherosclerotic heart disease 2. congenital heart disease 3. sudden unexplained deaths 4. thrombophilia 5. rheumatic fever 6. hypertension 7. hypercholesterolemia Cardiac Manifestations of Systemic Diseases Systemic Disease Cardiac Complications Hunter-Hurler syndrome Valvular insufficiency, heart failure, hypertension Fabry disease Mitral insufficiency, coronary artery disease with myocardial infarction Pompe disease Short P-R interval, cardiomegaly, heart failure, arrhythmias Friedreich ataxia Cardiomyopathy, arrhythmias Duchenne dystrophy Cardiomyopathy, heart failure Juvenile rheumatoid arthritis Pericarditis Systemic lupus erythematosus Pericarditis, Libman-Sacks endocarditis, congenital AV block Marfan syndrome Aortic and mitral insufficiency, dissecting aortic aneurysm Homocystinuria Coronary thrombosis Kawasaki disease Coronary artery aneurysm, thrombosis, myocardial infarction, myocarditis Lyme disease Arrhythmias, myocarditis, heart failure Graves disease Tachycardia, arrhythmias, heart failure (hyperthyroidism) Tuberous sclerosis Cardiac rhabdomyoma Neurofibromatosis Pulmonic stenosis, coarctation of aorta Nelson Last Minute ۲٤٦ PHYSICAL EXAMINATION Information regarding the cardiovascular status can be gained by observation and inspection, which is supplemented by palpation and auscultation. The examination starts with vital signs: heart rate, respiratory rate, and blood pressure. The normal heart rate varies with age and activity. ♥ Tachycardia : 1. anemia 2. dehydration 3. shock 4. heart failure 5. dysrhythmia. ♥ Bradycardia : 1. normal finding in patients with high vagal tone (athletes) 2. atrioventricular block. The respiratory rate ↑: 1. left-to-right shunt 2. pulmonary venous congestion. The normal blood pressure also varies with age. ♥ A properly sized cuff: bladder width 90% of the arm circumference and a length that is 80% to 100% of the arm circumference. ♥ initially, blood pressure in the right arm is measured. If elevated, measurements in the left arm and leg are indicated  coarctation of the aorta. The pulse pressure ♥ Systolic pressure – diastolic pressure = < 50 mm Hg or half the systolic pressure. ♥ A wide pulse pressure is seen with: 1. aortopulmonary connections (PDA, truncus arteriosus) 2. arteriovenous malformations 3. aortic insufficiency 4. relative intravascular volume depletion (anemia, vasodilation with fever or sepsis). ♥ A narrow pulse pressure is seen with: 1. pericardial tamponade 2. aortic stenosis 3. CHF Many chromosomal abnormalities and syndromes associated with cardiac defects have dysmorphic features or failure to thrive. Skin color must be assessed for cyanosis and pallor. Perioral cyanosis is a common finding in pale infants or when infants and toddlers become cold. Chronic arterial desaturation results in clubbing of the fingernails and toenails. Inspection of the chest may reveal asymmetry or a prominent left precordium suggesting chronic cardiac enlargement. Pulses should be assessed for rate, regularity, intensity, symmetry, and timing between upper and lower extremities. The presence of a good pedal pulse effectively rules out coarctation of the aorta if the right arm blood pressure is normal. The precordium should be assessed for apical impulse, point of maximum impulse, hyperactivity, and presence of a thrill. Abdominal palpation is primarily for assessment of liver and spleen size. ♥ The liver size provides a good assessment of intravascular volume and is enlarged with systemic venous congestion. ♥ splenomegaly: rarely with heart failure, infective endocarditis. Nelson Last Minute ۲٤۷  Congenital Malformation Syndromes Associated with Congenital Heart Syndrome Cardiac Features Trisomy 21 (Down syndrome) Endocardial cushion defect, VSD, ASD, PDA Trisomy 18 VSD, ASD, PDA, PS Trisomy 13 VSD, ASD, PDA, dextrocardia XO (Turner syndrome) Coarctation of aorta, aortic stenosis CHARGE association (coloboma, heart, atresia TOF, aortic arch and conotruncal anomalies* choanae, retardation, genital and ear anomalies) 22q11 (DiGeorge) syndrome Aortic arch anomalies, conotruncal anomalies* VACTERL association† (vertebral, anal, cardiac, VSD P P tracheoesophageal, radial, renal, limb anomalies) Congenital rubella PDA, peripheral pulmonic stenosis, mitral regurgitation (in infancy) Marfan syndrome Dilated and dissecting aorta, aortic valve regurgitation, mitral valve prolapse Williams syndrome Supravalvular aortic stenosis, peripheral pulmonary stenosis Infant of diabetic mother Hypertrophic cardiomyopathy, VSD, conotruncal anomalies Holt-Oram syndrome ASD, VSD Asplenia syndrome Complex cyanotic heart lesions, anomalous pulmonary venous return, dextrocardia, single ventricle, single AV valve Polysplenia syndrome Azygos continuation of inferior vena cava, pulmonary atresia, dextrocardia, single ventricle Fetal alcohol syndrome VSD, ASD Ellis-van Creveld syndrome Single atrium Zellweger syndrome PDA, VSD, ASD Fetal hydantoin syndrome TGA, VSD, TOF *Conotruncal-tetralogy of Fallot, pulmonary atresia, truncus arteriosus, transposition of great arteries. Heart Sounds Abnormal Second Heart Sound Single S 2 R Pulmonary hypertension (severe) One semilunar valve (aortic atresia, pulmonary atresia, truncus arteriosus) Malposed great arteries (d-TGA, l-TGA) Severe aortic stenosis Widely split S 2 R Increased flow across valve (ASD, PAPVR) Prolonged flow across valve (pulmonary stenosis) Electrical delay (right bundle branch block) Early aortic closure (severe mitral regurgitation) Paradoxically split S 2 R Severe aortic stenosis Abnormal intensity of P 2 R Increased in pulmonary hypertension Decreased in severe pulmonary stenosis, tetralogy of Fallot S 1 = closure of the mitral and tricuspid valves, is usually single, and is best heard at the R R lower left sternal border or apex, if a split S 1 is heard: normal, ejection click or S 4. R R R R S 2 = closure of the aortic and pulmonary valves.S 2 normally split with inspiration and be R R R R single with expiration. S 3 is heard in early diastole and is related to rapid ventricular filling. It is best heard at the R R LLSB or apex, normal sound. A loud S 3 =dilated ventricles. R R Nelson Last Minute ۲٤۸  S 4 occurs late in diastole just before S 1. It is best heard at the LLSB/apex and is R R R R associated with decreased ventricular compliance. It is rare and is always abnormal. Clicks A click implies a valvular abnormality or dilated great artery Ejection or mid-systolic in timing. A mid-systolic click is associated with mitral valve prolapse. Ejection clicks early in systole. ♥ Pulmonary ejection clicks are best heard at the left upper sternal border and vary in intensity with respiration. ♥ Aortic clicks are louder at the apex, left mid-sternal border, or right upper sternal border. They do not vary with respiration. Murmurs Murmurs should be classified as systolic, diastolic, or continuous. Ejection murmurs are crescendo-decrescendo with a short time between S 1 and the R R onset of the murmur (isovolumic contraction). 1. aortic stenosis 2. pulmonic stenosis 3. atrial septal defects (ASDs) 4. coarctation of the aorta Holosystolic murmurs have onset with S 1 , and there is flow during isovolumic R R contraction. heard with: 1. ventricular septal defects (VSDs) 2. mitral regurgitation 3. tricuspid regurgitation A "late regurgitant" murmur may be heard after the mid-systolic click in mitral valve prolapse. Ejection murmurs usually are best heard at the base of the heart, whereas holosystolic murmurs are louder at the lower left sternal border and apex. Pulmonary ejection murmurs radiate to the back and axilla, whereas aortic ejection murmurs radiate to the neck. Early diastolic murmurs occur when there is regurgitation through the aortic or pulmonary valves. Mid-diastolic murmurs are heard when there is increased flow across the mitral or tricuspid valves (VSD, ASD), or when there is anatomic stenosis at these valves. The intensity or loudness of a heart murmur is graded I - VI. Heart Murmur Intensity Grade I Very soft, heard in quiet room with cooperative patient Grade II Easily heard but not loud Grade III Loud but no thrill Grade IV Loud with palpable thrill Grade V Loud with thrill, audible with stethoscope at 45-degree angle Grade VI Loud with thrill, audible with stethoscope off chest 1 cm Continuous murmurs: heard when there is flow throughout the entire cardiac cycle and are abnormal with one common exception, the venous hum A PDA is the most common abnormal continuous murmur. Continuous murmurs can also be heard with coarctation of the aorta when collateral vessels are present. Normal physiologic or innocent murmurs common, occurring in at least 80% of normal infants and children at some time in life. called benign, functional, vibratory, and flow murmurs. These normal murmurs are heard most often during the first 6 months of life, from 3 to 6 years of age, and in early adolescence. Nelson Last Minute ۲٤۹  Characteristic findings of innocent murmurs include: 1. the quality of the sound 2. lack of significant radiation 3. significant alteration in the intensity of the murmur with positional changes 4. the cardiovascular history and examination are otherwise normal. The presence of symptoms, including failure to thrive or dysmorphic features, should make one more cautious about diagnosing a "normal" murmur. Diastolic, holosystolic, late systolic, and continuous (except for the venous hum) murmurs and the presence of a thrill are not normal. Normal or Innocent Heart Murmurs Usual Murmur Timing/Location/Quality Age Still murmur/vibratory Systolic ejection murmur 3-6 yr murmur LLSB or between LLSB and apex Grade I-III/VI Vibratory, musical quality Intensity decreases in upright position Venous hum Continuous murmur 3-6 yr Infraclavicular region (right > left) Grade I-III/VI Louder in upright position Changes with compression of jugular vein or turning head Carotid bruit Systolic ejection murmur Any age Neck, over carotid artery Grade I-III/VI Adolescent ejection murmur Systolic ejection murmur 8-14 yr LUSB Grade I-III/VI Usually softer when upright position Does not radiate to back Peripheral pulmonic stenosis Systolic ejection murmur Newborn-6 mo Murmur of infancy Axilla and back, LUSB/RUSB Grade I-II/VI Harsh, short, high frequency Nelson Last Minute ۲٥۰  Pericarditis Pericarditis is inflammation of the parietal and visceral surfaces of the pericardium. ETIOLOGY It is most often viral in origin. A bacterial etiology is rare, S. aureus and Streptococcus pneumoniae are the most likely bacterial causes. causes a much more serious and symptomatic pericarditis Pericarditis is associated with: 1. collagen vascular diseases, such as rheumatoid arthritis. 2. uremia 3. Postpericardiotomy syndrome is common form of pericarditis follows heart surgery. Etiology of Pericarditis and Pericardial Effusion Idiopathic (Presumed Viral) Infectious Agents Bacteria Group A streptococcus Staphylococcus aureus Viral† P Coxsackievirus (group A, B), Hepatitis B Echovirus, Herpes simplex, Herpes zoster Mumps, Epstein-Barr, Cytomegalovirus, Influenza Fungal: Histoplasma capsulatum Parasitic Toxoplasma gondii, Entamoeba histolytica, Schistosomes Collagen Vascular-Inflammatory and Granulomatous Diseases Rheumatic fever, Mixed connective tissue disease, Reiter syndrome, IBD,SLE (idiopathic and drug- induced),Wegener granulomatosis,RA,Kawasaki disease,Scleroderma,Dermatomyositis,Stevens- Johnson syndrome Traumatic Cardiac contusion (blunt trauma),Penetrating trauma,Postpericardiotomy syndrome,Radiation Contiguous Spread Pleural disease,Pneumonia,Aortic aneurysm (dissecting) Metabolic Hypothyroidism,Uremia,Gaucher disease,Chylopericardium,Fabry disease Neoplastic Primary Contiguous (lymphoma),Metastatic Infiltrative (leukemia) Others Drug reaction,Pancreatitis,After myocardial infarction,Heart failure,Hemorrhage (coagulopathy),Biliary- pericardial fistula,Thalassemia CLINICAL MANIFESTATIONS The symptoms of pericarditis depend on the amount of fluid in the pericardial space and how fast it accumulates.The faster, the sooner the pt is hemodynamically compromised. symptoms: 1. Chest pain (worsened if lying down or with inspiration) 2. Patient assumes sitting position 3. Dyspnea & Malaise Signs: ♥ Nonconstrictive: 1. Fever, Tachycardia 2. Friction rub (accentuated by inspiration, body position) 3. Enlarged heart by percussion and x-ray examination 4. Distant heart sounds ♥ Tamponade : As above, plus: 1. Distended neck veins 2. Hepatomegaly 3. Pulsus paradoxus (>10 mm Hg with inspiration) 4. Narrow pulse pressure ,Weak pulse 5. poor peripheral perfusion Nelson Last Minute ۲٥۱  ♥ Constrictive Pericarditis: 1. Distended neck veins 2. Kussmaul sign (inspiratory increase of jugular venous pressure) 3. Distant heart sounds 4. Pericardial knock 5. Hepatomegaly 6. Ascites, Edema 7. Tachycardia. IMAGING AND LABORATORY STUDIES Echocardiography is the most specific and useful diagnostic test. A chest x-ray reveals cardiomegaly. A large effusion creates a rounded, globular cardiac silhouette. The ECG shows tachycardia, elevated ST segments, and changes in the QRS complex. blood tests & diagnostic testing of pericardial fluid : identify The causative organism. Laboratory Evidence of Pericarditis Test Evidence Seen ECG Elevated ST segments, T wave inversion (late), tachycardia, reduced QRS voltage, electrical alternans (variable QRS amplitudes) Chest radiograph Cardiomegaly ("water bottle heart") Echocardiogram Pericardial fluid Pericardiocentesis Gram and acid-fast stains, culture, PCR (virus, bacteria, mycobacteria, fungus), cytology, cell count, glucose, protein, pH Blood tests ESR, viral titers, ANA, ASO titers, EBV titers TREATMENT Pericardiocentesis is indicated for: 1. treatment of hemodynamically significant effusions 2. provides valuable information regards to the etiology of the pericarditis. There is no specific treatment for viral pericarditis other than anti-inflammatory medications. Rheumatic Fever ETIOLOGY AND EPIDEMIOLOGY most common in children 6 - 15 years old. It is due to an immunologic reaction that is a delayed sequela of group A betahemolytic streptococcal infections of the pharynx A family history of rheumatic fever and lower socioeconomic status are additional factors. CLINICAL MANIFESTATIONS Acute rheumatic fever is diagnosed using the revised Jones criteria, which consist of clinical and laboratory findings. ♥ The presence of either two major criteria or one major and two minor criteria, along with evidence of an antecedent streptococcal infection confirm the diagnosis e.g.: 1. scarlet fever 2. positive throat culture 3. elevated antistreptolysin O or other antistreptococcal antibodies The infection often precedes the presentation of rheumatic fever by 2 to 6 weeks. Streptococcal antibody tests, such as the antistreptolysin O titer, are the most reliable laboratory evidence of prior infection. Arthritis is the most common major manifestation. It involves the large joints and is migratory. ♥ Arthralgia cannot be used as a minor manifestation if arthritis is used as a major manifestation. Carditis occurs in 50% of pts. 1. Tachycardia 2. new murmur (mitral or aortic regurgitation) 3. pericarditis 4. cardiomegaly 5. Signs of CHF Nelson Last Minute ۲٥۲  Erythema marginatum, a serpiginous, nonpruritic, and evanescent rash, uncommon, occurs on the trunk, and is brought out by warmth. Subcutaneous nodules: predominantly with chronic or recurrent dz. firm, painless, non- pruritic, mobile nodules, on the extensor surfaces of large and small joints, scalp & spine. Chorea (Sydenham chorea or St. Vitus dance) consists of neurologic and psychiatric signs. It also is uncommon and often presents long after the infection. Major Criteria in the Jones System for Acute Rheumatic Fever Sign Comments 1. Polyarthritis Common; swelling, limited motion, tender, erythema Migratory; involves large joints but rarely small or unusual joints, such as vertebrae 2. Carditis Common; pancarditis, valves, pericardium, myocardium Tachycardia greater than explained by fever; new murmur of mitral or aortic insufficiency; Carey-Coombs mid-diastolic murmur; heart failure 3. Chorea (Sydenham Uncommon; presents long after infection has resolved; more common in disease) females; antineuronal antibody positive 4. Erythema Uncommon; pink macules on trunk and proximal extremities, evolving to marginatum (10%) serpiginous border with central clearing; evanescent, elicited by application of local heat; nonpruritic 5. Subcutaneous Uncommon; associated with repeated episodes and severe carditis; present nodules over extensor surface of elbows, knees, knuckles, and ankles or scalp and spine; firm, nontender Minor criteria : 1. fever ( [38.2°C - 38.9°C]) 2. leukocytosis 3. ↑ESR/CRP 4. arthralgias 5. Prolonged P-R interval 6. previous rheumatic fever TREATMENT AND PREVENTION Management of acute rheumatic fever consists of : 1. benzathine penicillin to eradicate the betahemolytic streptococcus, 2. anti-inflammatory therapy with salicylates after the diagnosis is established 3. bed rest. Long-term penicillin prophylaxis, preferably with IM benzathine penicillin G, 1.2 million U every 28 days, is required. Oral regimens for prophylaxis are not as effective. PROGNOSIS acute rheumatic fever depends on the degree of permanent cardiac damage. Cardiac involvement may resolve completely, especially if it is the first episode and the prophylactic regimen is followed. The severity of cardiac involvement worsens with each recurrence of rheumatic fever. Congestive Heart Failure ETIOLOGY AND EPIDEMIOLOGY As the preload (fiber length, left ventricular filling pressure or volume) increases, the myocardial performance (stroke volume and wall tension) increases up to a point (the normal Starling curve). Heart rate is another important determinant of cardiac work because the cardiac output equals stroke volume times the heart rate. CHF is defined as the pathophysiologic state in which the heart is unable to pump blood at a rate commensurate with the body's metabolic needs (oxygen delivery). may be due to: 1. Change in myocardial contractility  low cardiac output 2. abnormal loading conditions being placed on the myocardium. ♥ afterload (pressure overload, such as with aortic stenosis, pulmonary stenosis, or coarctation of the aorta) ♥ preload (volume overload, such as in VSD, PDA, or valvular insufficiency) Nelson Last Minute ۲٥۳  Volume overload is the most common cause of CHF in children. Etiology of Heart Failure Fetus Severe anemia (hemolysis, fetal-maternal transfusion, hypoplastic anemia) SVT,VT ,Complete heart block Atrioventricular valve insufficiency High-output cardiac failure (AV malformation, teratoma) Premature Neonate Fluid overload PDA, VSD Cor pulmonale (BPD) Full-Term Neonate Asphyxial cardiomyopathy AV malformation (vein of Galen, hepatic) Left-sided obstructive lesions (coarctation of aorta, hypoplastic left heart, critical aortic stenosis) Transposition of great arteries Large mixing cardiac defects (single ventricle, truncus arteriosus) Viral myocarditis Anemia SVT ,Complete heart block Infant-Toddler Left-to-right cardiac shunts (VSD) , Postoperative repair of congenital heart disease Hemangioma (arteriovenous malformation) Anomalous left coronary artery Metabolic cardiomyopathy Acute hypertension (hemolytic-uremic syndrome) SVT Kawasaki disease Child-Adolescent Rheumatic fever ,Viral myocarditis , Endocarditis Acute hypertension (glomerulonephritis) Thyrotoxicosis, Arrhythmias Hemochromatosis-hemosiderosis Cancer therapy (radiation, doxorubicin) Sickle cell anemia Cor pulmonale (cystic fibrosis ,Chronic upper airway obstruction) Unrepaired or palliated congenital heart disease Cardiomyopathy In the first weeks of life, CHF is most commonly due to an excessive afterload. CHF presenting around 2 months of age is usually due to increasing left-to-right shunts of congenital heart defects as the pulmonary vascular resistance decreases. Acquired heart disease, such as myocarditis & cardiomyopathy, can present at any age. CLINICAL MANIFESTATIONS Clinical presentation of CHF in infants includes: 1. poor feeding 2. failure to thrive 3. tachypnea 4. diaphoresis with feeding Older children may present with : 1. shortness of breath 2. easy fatigability 3. edema The physical examination findings depend on whether pulmonary venous congestion, systemic venous congestion, or both are present. Nelson Last Minute ۲٥٤  ♥ Tachycardia, a gallop rhythm, and thready pulses may be present with either cause. ♥ If left-sided failure is predominant, tachypnea,orthopnea,wheezing,Pulmonary edema. ♥ If right-sided failure is present, hepatomegaly, edema, distended neck veins IMAGING STUDIES chest radiography, are not specific, absence of cardiomegaly on a chest x-ray R/O CHF. An echocardiogram assesses the heart chamber sizes, measures myocardial function accurately, and diagnoses congenital heart defects when present. Treatment of Heart Failure Therapy Mechanism General Care Rest Reduces cardiac output Oxygen Improves oxygenation in presence of pulmonary edema Sodium, fluid restrictions Decreases vascular congestion; decreases preload Diuretics Furosemide Salt excretion by ascending loop of Henle; reduces preload; afterload reduced if hypertension improves; may also cause venodilation Combination of distal tubule Greater sodium excretion and loop diuretics Inotropic Agents Digitalis Inhibits membrane Na+, K+-ATPase and increases intracellular Ca2+, P P P P P P improves cardiac contractility, increases myocardial oxygen consumption Dopamine Releases myocardial norepinephrine plus direct effect on β-receptor, may increase systemic blood pressure; at low infusion rates, dilates renal artery, facilitating diuresis Dobutamine β 1 -receptor agent; often combined with dopamine R R Amrinone/milrinone Nonsympathomimetic, noncardiac glycosides with inotropic effects; may produce vasodilation Afterload Reduction Hydralazine Arteriolar vasodilator Nitroprusside Arterial and venous relaxation; venodilation reduces preload Captopril/enalapril Inhibition of angiotensin-converting enzyme; reduces angiotensin II production Other Mechanical counterpulsation Improves coronary flow, afterload Transplantation Removes diseased heart Extracorporeal membrane Bypasses heart oxygenation Carvedilol β-blocking agent Initial treatment is directed at improving myocardial function and optimizing preload and afterload. Long-term therapy is usually digoxin and diuretics. Depending on the etiology of failure, afterload reduction frequently is added. Long-term therapy with β-blockers is beneficial. CARDIAC DYSARHYTHMIAS ETIOLOGY AND DIFFERENTIAL DIAGNOSIS Cardiac dysrhythmias are uncommon in pediatrics, but may be caused by: 1. infection and inflammation 2. structural lesions 3. metabolic abnormalities 4. intrinsic conduction abnormalities Many pediatric dysrhythmias are normal variants that do not require treatment or even further evaluation. Nelson Last Minute ۲٥٥  Sinus rhythm originates in the sinus node and has a normal axis P wave (upright in leads I and AVF) preceding each QRS complex. sinus bradycardia and sinus tachycardia are defined based on age. Sinus arrhythmia is a common finding in children ♥ Represents a normal variation in the heart rate associated with breathing. ♥ The heart rate increases with inspiration and decreases with expiration, producing a recurring pattern on the ECG tracing. ♥ does not require further evaluation or treatment. Etiology of Arrhythmias Drugs Intoxication (cocaine, tricyclic antidepressants, and others) Antiarrhythmic agents (proarrhythmic agents [quinidine]) Sympathomimetic agents (caffeine, theophylline, ephedrine, and others) Digoxin Infection and Postinfection Endocarditis Lyme disease Diphtheria Guillain-Barré syndrome Rheumatic fever Metabolic-Endocrine Cardiomyopathy Electrolyte disturbances (↓↑K+, ↓↑Ca2+, ↓Mg2+) P P P P P P Uremia Thyrotoxicosis Pheochromocytoma Porphyria Mitochondrial myopathies Structural Lesions Mitral valve prolapse Ventricular tumor Ventriculotomy Pre-excitation and aberrant conduction system (Wolff-Parkinson-White syndrome) Congenital heart defects Arrhythmogenic right ventricle (dysplasia) Other Causes Adrenergic-induced Prolonged Q-T interval Maternal SLE Idiopathic Central venous catheter Atrial Dysrhythmias A wandering atrial pacemaker : ♥ change in the morphology of P waves with variable P-R interval & normal QRS. ♥ This is a benign finding, requiring no further evaluation or treatment. Premature atrial contractions: ♥ Relatively common prenatally and in infants. ♥ A premature P wave, with abnormal axis consistent with its ectopic origin, is present. ♥ The premature atrial activity may be: 1. blocked (no QRS following it) 2. conducted normally (normal QRS present) 3. Conducted aberrantly (a widened, altered QRS morphology). Premature atrial contractions are usually benign and, if present around the time of delivery, often disappear during the first few weeks of life. Nelson Last Minute ۲٥٦  Atrial flutter & atrial fibrillation are uncommon dysrhythmias in pediatrics 1. after surgical repair of complex congenital heart disease 2. myocarditis 3. drug toxicity. Supraventricular tachycardia (SVT) : ♥ the most common symptomatic arrhythmia in pediatric patients. ♥ The rhythm is a rapid, regular rate with a narrow complex QRS. ♥ SVT in infants is 280-300 beats/min with slower rates for older children & adolescents. ♥ The tachycardia has an abrupt onset and termination. ♥ In a child with a structurally normal heart, most episodes are relatively asymptomatic other than a pounding heart beat. ♥ If there is structural heart disease or the episode is prolonged (>12 hours), there may be alteration in the cardiac output and development of symptoms of CHF. ♥ most patients with SVT have structurally normal hearts and normal baseline ECGs, ♥ some children have Wolff-Parkinson-White syndrome or pre-excitation as A cause Ventricular Dysrhythmias Premature ventricular contractions : ♥ less common than premature atrial contractions in infancy but more common in older children and adolescents. ♥ not preceded by a P wave, and the QRS complex is wide and bizarre. ♥ benign and require no treatment If: 1. the heart is structurally normal 2. the premature ventricular contractions are singleton, uniform in focus, and disappear with increased heart rate. ♥ Any deviation from this presentation, ex: history of syncope or a family history of sudden death, requires further investigation and treatment with antiarrhythmic drugs. Ventricular tachycardia: ♥ defined as three or more consecutive premature ventricular contractions ♥ relatively rare in pediatric patients. ♥ usually is a sign of serious cardiac dysfunction or pathology. ♥ Rapid rate ventricular tachycardia results in decreased cardiac output and cardiovascular instability. ♥ Treatment in symptomatic patients is synchronized cardioversion. ♥ Medical management with lidocaine or amiodarone may be appropriate in a conscious asymptomatic patient. Classification of Drugs for Antiarrhythmia Class Action Examples I Depresses phase o depolarization (velocity of upstroke of action potential); sodium channel blockers Ia Prolongs QRS complex and Q-T interval Quinidine, procainamide, disopyramide Ib Significant effect on abnormal conduction Lidocaine, mexiletine, phenytoin, tocainide Ic Prolongs QRS complex and P-R interval Flecainide, propafenone, moricizine II β blockade, slows sinus rate, prolonged P-R interval Propranolol, atenolol, acebutolol III Prolonged action potential; prolonged P-R, Q-T intervals, Bretylium, amiodarone, sotalol QRS complex; sodium and calcium channel blocker IV Calcium channel blockade; reduced sinus and AV node Verapamil and other calcium pacemaker activity and conduction; prolonged P-R interval channel blocking agents Heart Block First-degree heart block is the presence of a prolonged P-R interval. It is asymptomatic and when present in otherwise normal children requires no evaluation or treatment. Second-degree heart block : ♥ When not all of the P waves are followed by a QRS complex. Nelson Last Minute ۲٥۷  ♥ Mobitz type I (also known as Wencke-bach) : characterized by a progressive prolongation of the P-R interval until a QRS is dropped. not progress to other forms of heart block & require no evaluation or treatment in otherwise normal children. ♥ Mobitz type II : when the P-R interval does not change, but a QRS is intermittently dropped. may progress to CHB and may require pacemaker placement. ♥ Third-degree heart block, which may be congenital or acquired, is present when there is no relationship between the atrial and ventricular activity. 1. Congenital complete heart block is associated with maternal collagen vascular disease (SLE) or congenital heart disease. 2. The acquired form most often occurs after cardiac surgery. TREATMENT Most atrial dysrhythmias require no intervention. In patients with a complaint of palpitations, it is important to document heart rate and rhythm during their symptoms before considering therapeutic options. Treatment of SVT depends on presentation and symptoms. ♥ Acute treatment of SVT in infants usually consists of vagal maneuvers, such as application of cold (ice bag) to the face. ♥ IV adenosine usually converts the dysrhythmia because the atrioventricular node forms a part of the reentry circuit in most patients with SVT. ♥ In patients with cardiovascular compromise at the time of presentation, synchronized cardioversion is indicated using 1 to 2 J/kg. Ongoing pharmacologic management with either digoxin or a β-blocker is usually the first choice. digoxin is contraindicated in patients with Wolff-Parkinson-White syndrome. Arrhythmias in Children Type ECG Characteristics Treatment SVT Rate >200 beats/min (180-320 beats/min); Increase vagal tone (bag of ice abnormal atrial rate for age; ventricular rate may water to face, Valsalva be slower because of AV block; P waves usually maneuver); adenosine; digoxin; present and are related to QRS complex; normal sotalol; electrical cardioversion if QRS complexes unless aberrant conduction is acutely ill; catheter ablation present Atrial flutter Atrial rate usually 300 beats/min, with varying Digoxin, sotalol, cardioversion degrees of block; sawtooth flutter waves Premature Premature, wide, unusually shaped QRS None if normal heart and if ventricular complex, with large inverted T wave premature ventricular contractions contraction disappear on exercise; lidocaine, procainamide Ventricular ≥3 Premature ventricular beats; AV dissociation; Lidocaine, procainamide, tachycardia fusion beats, blocked retrograde AV conduction; propranolol, amiodarone, sustained if >30 sec; rate 120-240 beats/min cardioversion Ventricular No distinct QRS complex or T waves; irregular Nonsynchronized cardioversion fibrillation undulations with varied amplitude and contour, no conducted pulse Complete heart Atria and ventricles have independent Awake rate