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Park's Pediatric Cardiology for Practitioners: Expert Consult - Online and Print [ Myung K. Park MD FAAP FACC] on *FREE* shipping on qualifying . 6th edition, by Myung K. Park. Park's Pediatric Cardiology for Practitioners is the essential reference book for the ever-changing field of pediatric cardiology. Park Myung K. (ed.) Park's Pediatric Cardiology for Practitioners. Файл формата pdf; размером 27,35 МБ. Добавлен пользователем melrous.

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[Myung K Park] -- Park's Pediatric Cardiology for Practitioners is the essential medical reference book for the ever-changing field of pediatric cardiology. DOWNLOAD BOOK Park's Pediatric Cardiology for Practitioners By Myung K. Park Pdf books #pdf. Pediatric Cardiology for Practitioners 4th edition (February 15, ) by Myung K. Park, R. George, Md, Mph Troxler By Mosby. By OkDoKeY.

A spell frequently begins with an illness Figure , contd G, lead ECG demonstrating an irregularly irregular narrow complex tachycardia with an absence of true P waves. The second heart sound S 2 represents closure of the aortic A 2 and pulmonary P 2 valves at the end of systole, in that order. During inspiration, increased central venous return to the right heart takes longer to cross the right ventricular outflow tract. Rubs are usually best heard along the left sternal border and apex, often with better results with the patient in the sitting position, leaning forward. Feeding is the major activity of the infant, and exer- cise intolerance is marked by tiring during feeding, by increased respiratory effort, or by failure to continue eat- ing shortly after beginning, even though the baby still seems to be hungry. Is the patient developmentally delayed in motor skills, speech, or cognition? Pediatric Cardiology, 3rd ed.




Write a review Rate this item: Preview this item Preview this item. Park's pediatric cardiology for practitioners Author: Myung K Park Publisher: Philadelphia, PA: Sixth edition View all editions and formats Summary: Park's Pediatric Cardiology for Practitioners is the essential medical reference book for the ever-changing field of pediatric cardiology.



Easily grasp the latest techniques with helpful line drawings throughout. Select the best approaches for your patients with extensive coverage of special problems, including congestive heart failure and syncope. Read more Show all links. Allow this favorite library to be seen by others Keep this favorite library private. Another common obstacle to normal exercise tolerance is the presence of pulmonary disease, which most often relates to obstructive airway disease due to reactive airways, either in the case of true bronchospasm or with exercise-induced asthma.

Occa- sionally, pulmonary function tests will demonstrate restrictive lung disease. This can be seen in patients who have had thoracic surgery, or chest radiation ther- apy, and in patients with severe skeletal deformities such as scoliosis, pectus excavatum, or both. Primary pulmonary hypertension PPH is a rare but critical abnormality of the pulmonary vascular bed of unclear etiology, more common in females, often presenting in adolescence, and often first present as a change in exercise tolerance.

Finally, in patients with neuro- muscular diseases, including the muscular dystrophies and mitochondrial conditions, exercise capacity may be limited. Evaluation History The information obtained from a thorough history is a critical part of assessing exercise intolerance. The details of the patients or familys concerns regarding exercise performance need to be clarified. The onset of the exer- cise intolerance and its progression require delineation.

A differential of exercise intolerance is shown in Table In considering exercise intolerance in a pediatric patient, several points have to be considered: Is this a previously well child or a patient with a known cardiac condition?

Has the patient ever had surgery or other cardiac intervention? Is the patient medicated for a cardiac condition? Is there a history of cardiopulmonary disease in the family? Does the patient have any other medical problems, particularly of the respiratory system? Are there any known allergies? Is the patient age-appropriate for height, weight, and blood pressure? Does the patient complain primarily of shortness of breath or of easy fatigability with activity?

The details of the history should note the onset of symptoms, the frequency of occurrence, and the specific precipitating factors. Associated features such as palpita- tions, chest pain, dizziness, or syncope should increase the suspicion of a true cardiac etiology. Other features such as coughing, shortness of breath, color change e.

The history should include ques- tions about recent illness, fever, rash, joint swelling, sore throat, and insect bites, which could implicate an acquired form of cardiac disease e.

Park's The Pediatric Cardiology Handbook

Families with children who have Pediatric Evaluation of the Cardiac Patient 15 Figure , contd E, PA radiograph demonstrating the gastric bubble in the left upper quadrant.

Note that the apex of the heart is pointing to the right, consistent with dextrocardia. Table Exercise Intolerance Symptoms Possible Etiologies Easy fatuigability Deconditioning, obesity, anemia, low cardiac output, hypothyroidism, poor nutritional state, anorexia, hypoglycemia, dehydration, diabetes, neuromuscular disease, hypotonia, behavioral. Shortness of Reactive airway disease, smoking, breath cough pulmonary edema, chronic heart failure, restrictive lung disease, pulmonary hypertension atopic tendencies may be more prone to exercise- induced reactive airway disease.

A thorough review of prescription and nonprescription drug use, cigarette smoking in patients or family members, and illicit sub- stance use should be obtained from the patient. Physical Examination The physical examination of the patient presenting with exercise intolerance should be complete, including the vital signs and cardiac examination; the pulmonary, abdominal, and extremity examination; and a neurologic and a musculoskeletal exam.

Tachycardia for age, the presence of an irregular heart rate, a new or changing cardiac murmur, a gallop rhythm, or the presence of rales, hepatomegaly, and peripheral edema all strongly point to congestive heart failure.

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A loud, single S 2 sug- gests pulmonary hypertension. Careful auscultation for prolonged expiration is important, and if none is appreci- ated at rest, reassessment should be made after a period of exercise in the office. The reassessment should include resting and post-exercise pulmonary function testing. In the absence of any specific abnormalities of the general or cardiac examination, the health care providers attention should be directed to physical deconditioning.

The patients height and weight should be plotted on appropriate growth curves, and the body mass index BMI should be calculated and plotted for age. Many families are surprised to find the degree of extra weight being carried by their children. Dietary and activity his- tory should be reviewed in all cases, but especially when the height and weight are inappropriate. Diagnostic Tests Testing of the child or adolescent with a history of exer- cise intolerance should be guided toward the most likely etiologies, but it should include cardiac tests if there is a murmur or if the history suggests a potentially life- threatening cardiac issue, including exercise-related chest pain, palpitations, dizziness, or syncope.

Abnormalities of T waves can be seen in cardiomyopathies. Ambulatory ECG moni- toring Holter monitoring or event monitoring should be performed in patients with exercise-related palpita- tions, with use of the device during activities in which exercise intolerance is experienced. A chest x-ray CXR should be performed in any patient with exercise-related shortness of breath with or without a cardiac murmur , looking for hyperinflation, intrathoracic masses, or cardiomegaly. Attention should be paid to heart size, pulmonary vascular markings, and aortic arch sidedness.

Echocardiography in patients with exercise-related symptoms may be diagnostic and can allow the examiner to evaluate cardiac chamber size and contractility, to look for evidence of cardiac hyper- trophy or structural heart disease especially congenital or acquired coronary abnormalities , and to obtain esti- mates of intracardiac pressure.

This is particularly impor- tant in the evaluation of pulmonary hypertension. If no cardiac pathology is found by these preliminary tests, for- mal exercise stress testing may be indicated.

The goal of standard testing is to evaluate the patient at maximal exercise and to make objective assessments of exercise duration, heart rate and blood pressure response to exercise, and aerobic and physical working capacity, along with documentation of arrhythmias or ischemic changes.

Additional information can be obtained depending on the type of stress test performed. Metabolic testing includes noninvasive assessment of car- diac output at rest and with exercise, which differenti- ates primary cardiac dysfunction from pulmonary or neuromuscular conditions or from general decondition- ing.

Pulmonary stress testing assesses pulmonary func- tion at rest and with exercise, which is useful for exercise-induced asthma or other pulmonary conditions. Reproducing the patients symptoms with exercise stress testing allows the cardiologist to make a more accurate assessment of cause.

Treatment of Selected Conditions The primary roles of the evaluating cardiologist are to rule out the unlikely prospect of serious pathology and to provide reassurance and support to the patient and family.

Often, the cardiologist makes recommendations for further evaluation or treatment when a noncardiac cause is suspected because of the examination, history, or testing. Deconditioned patients without heart disease may benefit from an exercise prescription to improve physical fitness. Referral to a nutritionist may be helpful in patients with weight issues.

Referral to a pulmonary medicine specialist may be indicated for those patients with reactive airway disease. Judicious use of bron- chodilator inhalers prior to exercise, or other treatments of reactive airway disease, may relieve symptoms in young athletes. CHEST PAIN Background Chest pain is a common presenting complaint in patients seen by the general pediatrician and in the emergency department and is a common reason for referral to a cardi- ologist.

Extensive public education on the association of chest pain with ischemic heart dis- ease and myocardial infarction in the adult has led to an erroneous assumption that the same holds true for the pediatric patient. The least likely cause of chest pain in children is a cardiac origin. The differential diagnosis of pediatric chest pain is described in Box The neural fibers that convey pain stem from either cutaneous or visceral sources.

Cutaneous pain typically is described as sharp or stabbing in quality and is brief, well-localized, and easily reproduced by palpation. In contrast, visceral pain is diffuse and poorly localized.

The qualities ascribed to visceral pain are typically burning, gnawing, pressure, dull, or aching. Pain that recurs at night or after inges- tion of food or drink is suggestive of esophageal or gastric pathology.

Environmental factors or physical stress may provoke chest pain in asthmatics. Chest pain related to myocar- dial ischemia is often associated with exertion. Epidemiology Chest pain accounts for , physician visits per year in patients years of age. Noncardiac causes primarily arise from three sources: Often, a thorough his- tory delineates the cause without need for further testing or consultation.

Although cardiac causes of chest pain in children are decidedly rare, there are a few general cardiac causes to keep in mind. Lesions resulting in insufficient coronary perfusion either at rest or with exertion include the coro- nary aneurysm or stenosis associated with Kawasakis disease; congenital coronary anomalies; and moderate to severe left ventricular outflow tract obstruction, includ- ing valvar or subvalvar aortic stenosis and hypertrophic cardiomyopathy HCM.

Inflammatory lesions include pericarditis, postpericardiotomy syndrome, and rheu- matic fever. Other cardiac abnormalities associated with chest pain include cardiac neoplasms and arrhythmias. Aortic stenosis subvalvar, valvar, supravalvar , aortic aneurysm with dissection, ruptured sinus of Valsalva, coarctation of aorta, coronary anomalies, mitral valve prolapse, severe pulmonary stenosis, arrhythmogenic right ventricular dysplasia Acquired Lesions: Cardiomyopathy, endocarditis, myocarditis, rheumatic fever, Lyme, myocardial infarction, coronary vasospasm, Kawasaki disease, pericarditis, postpericardiotomy syndrome, pulmonary hypertension, Eisenmengers syndrome, Takayasus arteritis, cardiac tumors, pericardial neoplasm Arrhythmias: Chest pain in pediatrics.

Pediatr Clin North Am 46 2: Associated features that would heighten suspicion for a true cardiac etiology include exercise intolerance, palpitations or shortness of breath with activity, presyncope or syncope, or a family history of congenital heart disease or sudden cardiac death.

Physical Examination A complete cardiovascular, respiratory, and abdomi- nal examination should be performed. The physical examination of the patient presenting with chest pain should initially focus on the vital signs. After document- ing a stable regular heart rate and rhythm, respirations, and blood pressure, a thorough physical examination should focus on finding noncardiac causes.

Pediatric cardiology park pdf myung

The initial evaluation should include inspecting for evidence of trauma, bruises, or abrasions on the chest wall. Palpation should focus on bony abnormalities and local- ized chest swellings and on the site of the pain indicated by the patient.

There should be an attempt to reproduce the pain by palpation of the location indicated by the patient. Reproducible pain, particularly at the costo- chondral junction or over a rib, points to costochondri- tis as the etiology of the pain. Diagnostic Tests Although a broad array of tests exists Box to include or exclude various etiologies, a shotgun approach to the evaluation of chest pain is not advo- cated.

Often, the diagnosis can be made by history alone. In addition, the etiology of many cases of chest pain cannot be determined. Despite this, patients and families take great comfort when a clinician can exclude worrisome pathology, even though a definitive diagnosis cannot be made.

Treatment of Selected Conditions The primary role of the evaluating cardiologist is to rule out the unlikely prospect of serious cardiac pathol- ogy. An equally important role is to provide reassur- ance and support to the patient and family.

In addition, the cardiologist may need to begin definitive therapy for the cause of the pain. Most commonly, treatment takes the form of histamine blockers or pro- ton pump inhibitors PPIs for gastroesophageal reflux disease GERD or nonsteroidal anti-inflammatory drugs NSAIDs for costochondritis or other muscu- loskeletal disorders. In med- ical terms it is defined as the conscious, unpleasant awareness of ones own heartbeat. This includes the sen- sation of extra or missed beats, but the same sensation may be related to normal physiologic responses.

Evaluation of the patient complaining of palpitations becomes much easier when the clinician realizes that palpitations can be the subjective sensation of normal cardiovascular events. Etiology The majority of patients who complain of palpitations have no discernible pathologic process, or else the palpi- tations represent a physiologic variant with no risk of progression or sudden death.

Occasionally, palpitations are the initial manifestation of systemic disease or serious arrhythmia Box Pediatric Evaluation of the Cardiac Patient 19 Evaluation History It is important to determine the onset and duration of the symptoms.

The patient should be asked if the episodes begin and end gradually or abruptly, the latter of which is more characteristic of reentrant arrhythmias.

Association with factors such as activity or consumption of certain medications, including albuterol or other bronchodila- tors, decongestants, stimulants for attention deficit disor- der, certain psychotropic drugs, or foods that contain caffeine, such as chocolate, coffee, tea, sodas, and herbal stimulants, should be determined.

Symptoms of fever or systemic illness e. One should determine whether there are stressors that might point to a psy- chogenic etiology for these complaints. Physical Examination Palpation of the radial pulse is a part of the physical examination that can indicate abnormalities of cardiac rate or rhythm. The initial evaluation should determine whether there is a normal heart rate, bradycardia, or tachycardia.

Next, the clinician should determine whether the pulse is irregular and if there is a discernible pattern of irregularity. Finally, if irregularity is noted, one should determine if the patients symptoms correlate with the irregularity.

A complete cardiovascular examina- tion should be performed. In addition, the clinician should systematically evaluate the patient for evidence of noncardiac medical conditions that can be associated with alterations of heart rate e. Diagnostic Tests The extent of the cardiac evaluation depends on the impact that the symptoms have on day-to-day function- ing and the likelihood that the symptoms have a cardiac etiology.

If the history points to relatively infrequent, well-tolerated episodes that do not cause significant impairment and that appear to be secondary to an exter- nal cause, it may be prudent simply to monitor the patient closely and to instruct the patient to limit intake of possible stimulants e.

If episodes are prolonged and fre- quent without signs of systemic illness, a more extensive evaluation may be necessary. In either situation, a routine lead ECG and rhythm strip may be helpful to determine the origin of the rhythm, to determine the etiology of any irregularity, to assess the QT interval, and to look for evidence of any conduction abnormality or of preexcitation as seen in WPW syndrome or other arrhythmias.

Occasionally, documentation of premature beats of atrial or ventricu- lar origin or second-degree AV block occurs, even on asymptomatic recordings. Additional testing that may prove useful includes a variety of ambulatory electro- cardiographic monitoring devices. If the patients symptoms are frequent, one may choose to monitor him or her as an inpatient through continuous telemetry or as an outpatient with a hour ambula- tory Holter monitor three-lead ECG or an event monitor.

The patient is asked to keep a diary to correlate symptoms with objective electrocardiographic data. If the patients symptoms are relatively infrequent, the test of choice is a portable event monitor. This device can be activated when symptoms occur or can be of a continuous record- ing modality with activation of the device retaining a period of time before and after activation or with continu- ous monitoring through satellite technology.

The event monitor will document cardiac rate and rhythm during the seconds prior to activation and will record the ECG during or after symptoms; these ECG signals are transmitted by telephone for analysis.

For complicated cases in which no etiology has been found with event monitors but the index of suspicion is high, a subcutaneously implanted device may be used. If symptoms occur with exercise, exercise stress testing should be performed. In cases that appear to be poten- tially threatening, a cardiac catheterization using pro- grammed electrophysiologic testing may be warranted. The etiology of the arrhythmia and the need for interven- Box Causes of Palpitations Cardiac Primary Premature atrial contractions Premature ventricular contractions Supraventricular tachycardia Ventricular tachycardia Ventricular fibrillation Second-degree AV block Sinus arrest Secondary Systemic illness with cardiac effects hyperthyroidism neoplasm,pheochromocytoma Fever Anxiety Hyperventilation Exercise Muscle spasm tion with catheter ablation, pacemaker, or implantable cardioverter defibrillator can be determined.

Syncope in children causes great anxiety in parents, teachers, and school officials. These episodes result in a large number of visits to pediatricians, family physicians, and emergency departments and a surprising number of admissions to community and childrens hos- pitals nationwide.

The greatest concern regarding syncope is to discern which children might be at risk for sudden car- diac death. The overall incidence of sudden death in children and teenagers is 18 in , patient-years. The incidence of those seeking medical attention is about per , Air Force demonstrated an inci- dence of The single exception is the pallid breath-holding spell of the toddler.

There may be a sensation of an increased heart rate. Premonitory symptoms can occur without a true syn- copal event and are referred to as near syncope or pre- syncope. Presyncope is a sense that one is about to pass out. Patients often complain of an impending loss of consciousness accompanied by nausea and visual phenomena of blurring, dimming, or partial loss, and also by auditory symptoms of diminished hearing and lightheadedness, but without true syncope.

The approach to presyncope is essentially the same as that for syncope. Vertigo, dise- quilibrium, and seizures are often confused with syn- cope. Dizziness is a symptom that needs better defi- nition to distinguish it from lightheadedness or vertigo. The principal distinction is the description of the sensa- tion of motion. Swaying, whirling, and spinning of the environment or room are characteristics of vertigo. Alteration of balance or perception of the environment or a feeling of spinning often describes dizziness.

Park's Pediatric Cardiology for Practitioners, 6e

Hyper- ventilation can result in lightheadedness. Sensations of dizziness or lightheadedness may be frequently associ- ated with psychological distress, including anxiety, depression, and panic attacks.

This sensation is often unrelated to position or movement; the characteristic feature on history is diffi- culty ambulating. A fairly rare complaint among children, disequilibrium in the young is often caused by vestibular pathology or ataxia. Absence seizures and temporal lobe epilepsy can be described by younger patients and observers in a manner that appears to be syncope.

Both phenomena result in an impairment of consciousness. Seizures tend to occur and to resolve independent of position or posture; however, most pediatric syncope is related to position or volume status and is resolved quickly with supine posture without a postictal state. True vasodepressor syncope VDS does not occur in the supine position but may occur while sitting. Standing or rising to standing are the most common positional rela- tionships.

Etiology Categories of syncope include noncardiac, cardiac, and neurocardiogenic Box Syncope in most young patients will not be life-threatening, but the physicians aim must be to identify the patient at risk for a serious event. If a true syncopal event has occurred, an accurate description of the event is often sufficient to alert the physician to the likely cause.

Neurologic Etiology Certain neurally mediated or autonomic etiologies of syn- cope, such as breath-holding spells and VSD, can termi- nate with tonic-clonic movements, which can cause confusion with a true epileptic seizure. They may be referred to as convulsive syncope or anoxic seizures. Convulsive disorders are easily identified when they have an aura or prodrome, generalized tonic-clonic seizure activity, or a postictal phase with confusion and lethargy. Akinetic seizures or drop attacksare most common between 2 and 5 years of age.

TLE is associated with simple or complex semi-purposeful motor activity, also known as automatism. Loss of con- sciousness may be more gradual. Basilar artery migraine results in occipital headache, vertigo, visual symptoms, ataxia, confusion, or syncope, or a combination thereof. In the classic scenario, the headache and premonitory aura is severe enough to result in a vagally mediated syncope.

In atypical presen- tations, there is no premonitory headache, but vasocon- striction occurs in the vertebrobasilar arterial supply, leading to syncope without a change in heart rate or blood pressure. Diagnosis may be difficult to make with- out the input of a neurologist.

The sympathomimetic symptoms consist of tachycardia, mydriasis, and diaphoresis. The neuroglycopenic symptoms consist of irritability, emo- tional lability, confusion, lethargy, and syncope. Causes of hypoglycemia in children include diabetes, ketotic hypoglycemia, liver enzyme deficiencies, and inborn errors of metabolisms such as medium chain acyl- coenzyme A dehydrogenase MCAD deficiency.

Drug and Toxin Exposure Illicit drugs such as 3,4-methylenedioxy-N-methylam- phetamine MDMA or Ecstasy , cocaine, or others, as well as a variety of prescribed drugs, can result in syn- cope from a variety of causes, most commonly from arrhythmias triggered by the drugs or by increasing the likelihood of orthostatic hypotension. Psychogenic Etiology Hyperventilation, most commonly associated with unrecognized anxiety or distress, occasionally results in syncope.

Patients, who are usually adolescents, will rarely provide this aspect of the history and often present with the primary complaint of chest tightness or smothering. A detailed history may uncover frequent panic attacks, which result in hyperventilation episodes and syncope.

Hysterical syn- cope or conversion reaction mimics loss of conscious- ness and most commonly occurs in adolescents in the presence of an audience. Patients are typically calm when describing the episodes. The patient typically falls without injury. Frequently, an internalized stress can be uncovered by a psychiatrist or psychologist, and syncope can be resolved with therapy for the underlying issue. Cardiac Etiology Syncope without warning is more likely to be cardiac in origin, as is exertional syncope.

Such a history should always be of serious concern to the astute clinician. The catecholamine surge associated with exercise makes a vagally mediated phe- nomenon unlikely as an explanation for syncope that occurs during the period of exertion.

The exception is the volume-sensitive athlete who has maintained suboptimal hydration throughout exer- cise and develops hypotension in the face of the periph- eral vasodilatation associated with exercise. Such patients should receive the thorough evaluation war- ranted for exercise-induced syncope before the episodes can be attributed confidently to neurally medi- ated phenomena.

Causes of exercise-induced or cardiac syncope can be separated into three broad categories. First is low output on a primary cardiac basis from obstruction, including obstructed inflow, as in cardiac tamponade or from car- diac tumors external or internal , and obstructed out- flow, as seen in hypertrophic cardiomyopathy or aortic stenosis.

Symptoms from obstructive tumors, such as myxomas, may be paroxysmal and are often associated with changes in position. Another cause of cardiac syncope occurs with myocardial dysfunction with poor cardiac contractility associated with primary myopathy. Cardiomyopathy, associated with neuromuscular disorders such as Duchennes muscular dystrophy, can result in syncope.

Cardiomyopathies may be associated with low output, but more commonly, these patients have syncope from associated arrhythmias. Myocarditis from a viral etiology would be the most common in this category. Kawasaki disease is asso- ciated early with inflammation of coronaries and myocardium, and later with ischemic coronary disease from coronary aneurysms with stenosis or thrombosis.

Other causes of ischemia from coronary anomalies include abnormal-course or intramural coronary artery, anomalous origin from the pulmonary artery, and athero- sclerotic coronary disease, particularly with postcardiac transplant arteriopathy or with homozygous familial hypercholesterolemia.

A third major category of cardiac syncope occurs in association with a variety of arrhythmias that interrupt the cardiac output Fig. The corrected QT QTc in this patient is ms. B, Rhythm strip demonstrating a coarse wide complex tachycardia with a constantly twisting axisconsistent with torsades de pointes. C, lead ECG demonstrating a right bundle branch block pattern in an year-old and S-T segment elevation in the right precordial leads V 1 V 3 consistent with the diagnosis of Brugada syndrome.

Continued Pediatric Evaluation of the Cardiac Patient 25 too slow or too fast. Atrial tachyarrhythmias may result in syncope, as seen in the WPW syndrome, with atrial fibrillation and rapid ventricular response, which can lead to ventricular fibrillation. Atrial flutter with rapid AV conduction, seen after intraatrial repairs of D-TGA or after the Fontan repair for single ventricle physiology, can result in syncope and sudden cardiac death.

Syncope can be seen with supraventricular or ventricular tachycardia SVT or VT , more commonly in association with a struc- turally or functionally abnormal heart, although very rapid tachyarrhythmia can cause syncope in the presence of a normal heart.

Less frequently, slow rhythms, including high-degree atrioventricular block and sick sinus syn- drome with periods of asystole, can also be responsible for syncope. Hypercyanotic spellsmay be seen in conjunc- tion with an existing right-to-left shunt, most commonly described in TOF.

A spell frequently begins with an illness Figure , contd G, lead ECG demonstrating an irregularly irregular narrow complex tachycardia with an absence of true P waves. There are flutter waves with variable AV conduction. This represents atrial flutter with variable AV block. H, ECG of narrow complex tachycardia. There is evidence of retrograde P waves. This is consistent with a diagnosis of supraventricular tachycardia.

Increased resistance to pulmonary blood flow, combined with decreased resistance to systemic blood flow,can result in a spiraling cycle of cyanosis, hypoxemia, and syncope. Autonomic Nervous System Neurally Mediated Syncope Neurally mediated syncope, also referred to as auto- nomic, neurocardiogenic, vasovagal or vasodepressor syncope, common or emotional syncope, or reflex syn- cope, is the most common cause of syncope in the pedi- atric patient. Neurally mediated syncope is thought to be medi- ated by abnormal or heightened autonomic responses to various stimuli.

Peripheral vasodilatation occurs with a decrease in blood pressure and a slow heart rate. The prodromal symptoms often consist of lightheadedness, nausea, pallor and diaphoresis, and visual or auditory loss.

Usually the patient collapses suddenly and remains unconscious for less than 1 minute unless attempts are made to restore upright posture, which can result in exacerbation of symptoms or can prevent resolution of symptoms.

The patient may remain pale, weak or tired, and diaphoretic following the episode. A number of reflex and compen- satory neurocardiovascular mechanisms allow individuals to change position, to adjust to physical exercise, to digest food, and to respond to unexpected or unpleasant mental stresses.

These adaptive autonomic nervous system mechanisms preserve arterial blood pressure and cere- bral perfusion. Syncope can occur when afferent, cen- tral, or efferent portions of the autonomic reflex arc are impaired, myocardial contractility or vascular reactivity is suppressed, hypovolemia is present, hormonal responses are abnormal, or adaptive responses are inade- quate.

A decrease in venous return and, thus, decrease in cardiac output and blood pressure occur. The baroreceptors or stretch receptors detect these changes and relay information to the central nervous system with a resultant decrease in parasympathetic tone, allowing for an increase in heart rate.

There is a concomitant increase in sympathetic out- flow, which increases norepinephrine secretion and increases peripheral resistance. Blood pressure and cerebral perfusion are preserved.

Abnormalities can occur at one or several parts of this reflex arc. The traditional hypothesis regarding neurocar- diogenic syncope is that such episodes arise from vagally mediated hypotension vasodepressor type , bradycardia cardioinhibitory type , or both mixed type , in part associated with vigorous contraction of a relatively empty ventricle. The initial mechanism relates to a decrease in systemic venous return and excessive vagal stimulation associated with the decrease in ventricular filling.

Normal autonomic reflexes do not function nor- mally in these patients. The initial stimulus is venous pooling of blood within the vascular system, the vasodila- tor effects of adrenaline, decreased production of norepi- nephrine by the adrenal, an under-representation of receptors or over-representation or hypersensitivity of receptors, or else stimulus by a primary neurogenic process.

Although heart rate typically does increase prior to the syncopal episode, cardiac output does not increase sufficiently in response to the decrease in blood pressure. A poorly understood central nervous system reflex, in response to pain, fear, the sight of blood, or anxiety, triggers sympa- thetic inhibition with vasodilatation and parasympa- thetic activation with bradycardia, resulting in syncope. Reflex or Situational Syncope An amplified or inappropriate reflex response to a physi- ologic stressor can result in syncope.

Pallid breath-hold- ing spells are a common pediatric reflex phenomenon, usually beginning in infancy or early childhood. An unex- pected, startling stimulus elicits a sudden reflex increase in vagal tone and resultant asystole for up to 15 seconds.

As the episode nears conclusion, there may be accompa- nying tonic-clonic seizure activity. The more common type of breath-holding spell follows a period of crying, terminated with sustained exhalation often against a closed glottis and visible cyanosis. This is followed by vagally mediated hypotension and syncope.

Reflex syn- cope may be associated with swallowing, stretching, hair combing, sneezing, and diving. Cough, defecation, and micturition syncope are related to increased intratho- racic pressure, leading to vagally mediated reduction in cardiac output. Hypervagotonia Hypervagotonia, or excessive vagal tone, is primarily seen in 2- to 6-year-olds and is a result of an exaggerated vagal response that is not interrupted by normal reflexes.

Generally, there is a vagal stimulus, but not the type that elicits breath holding. Most children with this condition gradually have resolution, but they may require treatment with medication such as atropine for a period of time. They commonly develop vasodepressor syncope as ado- lescents. Both conditions are most likely manifestations of autonomic nervous system abnormalities or imbal- ance. Many individuals, especially in late childhood and early adolescence, have increased vagal tone that mani- fests as a low resting heart rate, junctional rhythm, or varying degrees of AV block, especially during sleep.

This is a physiologic variant found in healthy, asymptomatic children and adolescents. Rarely is it of sufficient magni- tude to be a cause for syncope.

Pediatric pdf cardiology park myung

Postural Orthostatic Hypotension and Syncope Postural neurally mediated syncope is more common than centrally mediated syncope. Syncope can result from orthostasis, defined as a decrease in systolic blood pressure of at least 20 mmHg within 3 minutes of stand- ing, or a lesser change in blood pressure but with associ- ated symptoms.

There is an exaggeration of the usual orthostatic pooling during the upright position. An increase in sympathetic activity occurs when the heart contracts vigorously with a relatively empty chamber. This exaggeration in the usual physiologic responses associated with a change in position is often a conse- quence of hypovolemia, anemia, or medications, or else of an autonomic nervous system ANS imbalance.

The role of the baroreceptors in maintaining a normal adap- tive process has suggested that malfunction of this reflex may be responsible for many instances of postural syn- cope. Normally, neurohormonal agents aid in blood vol- ume control and maintain peripheral vascular resistance. Postural orthostatic tachycardia syndrome POTS refers to a significant increase in heart rate of greater than 30 beats per minute bpm that occurs in some patients with positional change.

Although syncope may occur, the major symptom is that of tachycardia, which becomes disabling on its own. Post-Exercise Syncope VDS occurs after exercise in patients and is associated with extreme vasodilatation and hypovolemia, usually occurring once exercise stops and sympathetic with- drawal occurs.

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Other more serious causes of exercise- induced syncope must be excluded before this etiology can be entertained in this subset of patients. Dysautonomia Syncope can occur as a manifestation of familial dysau- tonomia, a sympathetic nervous system malfunction Riley-Day syndrome , in which the normal adrenergic responses do not occur due to a primary autonomic sys- tem disorder with abnormal control of heart rate and blood pressure.

Inheritance is an autosomal recessive pattern predominantly in children of Ashkenazi Jewish ancestry. Manifestations include sleep apnea, seizures, developmental delay, and temperature instability.

Evaluation History The history from the patient and eyewitness observers is invaluable in evaluating the patient with syncope. Of particular importance are the activity and position immediately prior to the episode, as well as sudden changes in position such as rising from supine to stand- ing. Associated symptoms such as dizziness, weakness, nausea, visual blurring or loss of vision, hearing loss, diaphoresis, or epigastric discomfort may be present.

Syncope during or immediately following exertion requires careful consideration and evaluation because it may be a harbinger of cardiac disease and a risk for sud- den death. Knowing the duration of loss of conscious- ness as well as the time to full recovery assists in forming the differential diagnosis.

Syncope of autonomic origin is usually brief in duration, whereas syncope due to neu- rologic, metabolic, or psychologic origin e. Syncope of cardiac cause is less commonly self-limited. A thorough family history should be obtained, particularly for family members with syncope, seizures, deafness, need for pacemaker or arrhythmia medication, or sudden early cardiac or acci- dental death.

If there is a strong family history for sud- den, unexplained early death, this may suggest a familial cardiomyopathy or LQTS.

Many patients with vasode- pressor syncope have a strong family history for similar episodes. In patients suspected of conversion reaction, family, school, or other stresses should be carefully sought in the history. A dietary history is important because those patients, particularly adolescents, with lim- ited fluid intake or salt restriction may be predisposed to orthostatic syncope.

Finally, a medication history may suggest drugsprescribed, over-the-counter, or illicit as a cause of syncope. In a standing adolescent, a systolic blood pres- sure of less than 80 mmHg, a decrease of 20 mmHg or more from the supine blood pressure measurement, or Pediatric Evaluation of the Cardiac Patient 27 an increase in heart rate of greater than 20 bpm is diag- nostic of orthostasis.

Try a Free Sample. List Price: Table of Contents Buy as you go Buy by the chapter and never pay more than the price of the full book. Chapter 1: History Taking. Chapter 2: Physical Examination. Chapter 3: Chapter 4: Chest Radiography. Chapter 5: Noninvasive Imaging Tools. Chapter 6: Other Noninvasive Investigation Tools. Chapter 7: Invasive Procedures. Chapter 8: