disease. If coughing is productive and persistent, diagnoses such as bronchiectasis should be considered. PHYSICAL EXAMINATION Inspect the chest for bony abnormalities such as kyphoscoliosis and pectus excavatum, both of which may lead to exercise limitation, and for symmetry of the posterior chest wall during a normal inspiration as deviation of the chest wall excursion may suggest advanced pleural filling process. Also, inspect the hands for clubbing and cyanosis for evidence of chronic cardiopulmonary conditions. Auscultate for expiratory wheezing that suggests asthma. The episodic nature of asthma makes this examination finding poorly sensitive. Focal findings may indicate localized airway abnormalities such as bronchiectasis or obstruction of the airway lumen by a foreign body. Inspiratory squeaks should be differentiated from upper airway inspiratory stridor by listening over the trachea, as the former typifies bronchiolitis, while the latter, paradoxical VCD. CASE EXAMPLES Case 1: An Amateur Male Cyclist A 33-year-old cyclist presents with excessive dyspnea while exercising over the last 6 months. He notes that his symptoms have progressed since moving to a new location because of his job as an information technology consultant. He has no personal history of allergy. His symptoms are most pronounced shortly into his cycling routine but seem to plateau as he continues to ride, and his return rides are seemingly less symptomatic. Office spirometry is normal; however, exercise spirometry reveals 15% reduction in Forced Expiratory Volume (FEV1) during the first 10 min of cycling and the diagnosis of EIB is made. Key Point: The presence of a refractory period wherein dyspnea is mitigated within 4 h of symptoms onset suggests EIB; most importantly, exercise spirometry that reveals a drop in FEV1 from a normal baseline confirms the diagnosis. Case 2: Teenage Football Player A 16-year-old adolescent male presents with worsening dyspnea during his football tryout routines at high school. The symptoms have been slowly progressive over the preceding years despite utilization of both an inhaled shortacting bronchodilator and inhaled corticosteroid. His symptoms are particularly pronounced at peak exercise and gradually resolve as he stands on the sidelines. His physical examination result is normal, but postexercise office spirometry exhibits and inspiratory flow ‘‘cutoff.’’ Referral to an otolaryngologist for direct laryngoscopy confirms the diagnosis of paradoxical vocal cord movement with inspiration. Key Point: VCD can mimic EIB, and the diagnosis should be confirmed before using bronchodilators for extended periods. A referral to speech pathology is warranted. Case 3: Adult Male Marathon Runner A 43-year-old marathon runner is referred for excessive dyspnea while running. His symptoms have progressed for over 3 years; he notes following an admission for a severe pneumonia. While not exercising, he has complained of 260
Volume 14 & Number 3 & May/June 2015
productive cough with yellow sputum but no fevers and no chills. He has attributed the cough to his severe postnasal drip that is exacerbated by seasonal allergies. Physical examination result is remarkable for right lower lobe rhonchi with localized inspiratory squeaks. A subsequent chest computerized tomography confirms an area of focal right lower lobe bronchiectasis, and he is referred to a pulmonologist for further evaluation. Key Point: Associated productive cough with localized physical examination findings suggest focal airway disease. Case 4: Young Female Physician Who Works Out A 27-year-old medicine resident is referred for worsening dyspnea during her normal exercise routine along the beach. The dyspnea has worsened as the days have become short in the fall months; her inability to exercise generates a considerable amount of frustration. Her dyspnea begins almost immediately as she runs and does not abate although she notes no wheezing. She has no history of allergy. Her examination, spirometry, and exercise spirometry results are all normal. She is referred for cardiopulmonary exercise testing, and she is noted to have the onset of rapid shallow breathing in anticipation of the test, which continues throughout testing. Her minute ventilation on exercise testing is dramatically elevated. She is referred to a counselor for anxiety management. Key Point: Anxiety can present with asthma-like symptoms. Reference 1. Crapo RO, Casaburi R, Coates AL, et al. Guidelines for methacholine and exercise challenge testing-1999. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999. Am. J. Resp. Crit. Care. Med. 2000; 161:309Y29.
Heart Murmurs in Athletes: From Personal History and Physical Examination Sections Shirin Zarafshar, MD and Vic Froelicher, MD 4A. PERSONAL HISTORY: HAVE YOU BEEN TOLD THAT YOU HAVE A HEART MURMUR? To determine the importance of a positive answer to this question, the following questions should be asked: 1. Has the murmur been present since birth, and is it still present? Athletes with congenital murmurs may remain asymptomatic for life, particularly if there is no associated pathologic condition. However, ventricular or atrial septal defects, patent ductus arteriosus (PDA), bicuspid aortic valves, and other causes of heart murmur may have long-term consequences and require correction. 2. Has anyone told you that the murmur is physiologic or pathologic? A documented prior medical evaluation, particularly if imaging has been performed, can facilitate decisions regarding athletic participation. If the studies are of questionable quality or not available, reevaluation may be necessary. Cardiovascular Preparticipation Evaluation
Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
3. Are there other associated symptoms such as chest pain, shortness of breath, dyspnea on exertion, and/or palpitations? The presence of cardiovascular symptoms such as chest pain, dyspnea, and palpitations can be indicative of an underlying cardiac pathology. Chest pain due to microvascular disease is a feature of HCM. 5. Does anyone in your family have a heart murmur? Familial HCM is an autosomal-dominant trait and one of the most common causes of sudden death in athletes. Other congenital abnormalities that cause murmurs such as Marfan syndrome can cluster in families as well.
PHYSICAL EXAMINATION: IS A HEART MURMUR PRESENT ON PHYSICAL EXAMINATION? The Cardiovascular Examination of the Athlete Setting The cardiac examination should be performed in a stable state and not in the recovery period from an extended period of exercise or competition and in a quiet, comfortable setting with attention given to privacy and room temperature. The examination should be conducted sitting and supine with maneuvers like the Valsalva maneuver, standing, and squatting added if a significant murmur is detected. Normal findings Physiologic and morphologic adaptations of the aerobically trained athlete’s heart include slow heart rate, systolic ejection flow murmur at the upper, left sternal border, a third heart sound, lateral displacement of point of maximal impulse, and hyperdynamic carotid pulses. Athletes predominantly engaged in isometric training (weightlifters) will not exhibit these changes. The examination of the athlete can be challenging because of these physiologic adaptations. Cardiac enlargement by visual examination (apical movements) and palpation (lateral displacement) can simulate the examination of patients with cardiomyopathies or heart failure. The loudest third heart sounds you will ever hear will be in athletes, and they are physiologic when occurring at low heart rates. This contrasts to the third heart sounds in patients with heart failure where they occur at fast heart rates (called ‘‘gallops’’ because of the cadence). Furthermore, third heart sounds in athletes are not related to position, while in patients with heart disease, the S3 gallop is loudest in the supine position. Even in the resting state, systolic flow murmurs can be appreciated in athletes, but they are soft, occur early in systole, and radiate upward rather than laterally toward the apex. While fixed splitting of the heart sounds can be appreciated in the supine position in nonathletes, this splitting is particularly noticeable in athletes. Thus, the finding of fixed splitting should only be considered abnormal if heard in the sitting or standing position. Abnormal findings Any diastolic murmur is abnormal whether or not there is an accompanying systolic murmur. The most common cause is aortic insufficiency (or regurgitation, abbreviated AI or AR). Early AR is best appreciated at the upper left of the sternum, with the athlete in the seated www.acsm-csmr.org
position, during forced expiration and leaning forward. A trick is to carefully listen after the second heart sound to focus attention at the correct time. Since AR can be difficult to appreciate, it is helpful to listen even more carefully when the following occur:
1. A systolic murmur. 2. Wide pulse pressure (950 mm Hg) or a diastolic pressure of 50 mm Hg or less. 3. Hyperdynamic carotid pulse. While AR is the most common cause of a to-and-fro (systolic/diastolic) murmur in athletes, another cause is PDA. This is a congenital abnormality more often encountered than other congenital abnormalities in athletes because athletic performance can be quite normal if the shunt is small. Characteristics that increase the likelihood of systolic murmurs being pathologic include the following:
1. Greater than grade 2/6 intensity 2. Lateral rather than upward radiation 3. Occurrence in mid-systole or late systole rather than in early systole 4. Accompanied by a click in mid-systole or late systole 5. Any murmur that becomes louder with the Valsalva maneuver (best performed supine with your hand on abdomen and telling the athlete to push against your hand while continuing to breathe) Other auscultation abnormalities include a third heart sound during tachycardia or fixed splitting of the second heart sound in the seated position. Sinus tachycardia at rest is abnormal in an aerobically trained athlete, and if not easily explained (recent workout, fever, etc.), further workup may be indicated, particularly if accompanied by any symptoms. CASE EXAMPLES Case 1: Tennis Player with Unexplained Sinus Tachycardia A 20-year-old White female tennis player presented with tachycardia and shortness of breath while going to classes. She normally performed at the top level of competitions but was out of season at the time. She had been symptomatic for nearly a week and presented late in the day after classes. An examination yielded unremarkable results, and she was afebrile, with blood pressure 120/70 and HR of 100 bpm, although S2 seemed to be louder than S1 even at the apex. She was on birth control pills and had just recovered from a leg injury. There was no leg tenderness or swelling. Blood tests were ordered (complete blood count, thyroid function), and a Holter monitor, placed. The Holter was read the next day and was unremarkable except for an average heart rate of 100 bpm with maximum of 140 bpm during light exercise. Laboratory test results were normal. An echocardiogram showed a dilated right ventricle (RV), elevated pulmonary artery (PA) pressures, and normal left ventricle (LV) function. Primary pulmonary hypertension was considered, but she was sent for a computerized tomography chest angiogram lung scan, which revealed pulmonary embolus. She was started on heparin and then treated with Current Sports Medicine Reports
Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
261
Coumadin with gradual recovery. She was found to have factor V Leiden genotype. Key Point: Sinus tachycardia may be the only finding with a pulmonary embolus. Case 2: Baseball Player with Continuous Murmur During mass screening, a cardiology fellow noted a systolic murmur while examining a 19-year-old White male baseball player. The athlete was asymptomatic and had normal ECG. The fellow performed screening echocardiogram on site, which was considered normal, and the athlete was cleared for participation. As formality, the supervising cardiologist auscultated the athlete and noted a toand-fro continuous murmur. Echocardiogram and cardiac catheterization revealed PDA with significant right-to-left
shunting. The athlete was offered surgical or percutaneous correction. Key Point: Continuous (systolic and diastolic) and diastolic murmurs are always due to cardiac pathologic lesions. The continuous murmur of PDA is described as a continuous ‘‘washing machine’’ type murmur; best appreciated in the second left intercostal space. A scanning echocardiogram will miss it. Case 3: Soccer Goalie with Fixed Split of Second Heart Sound (S2) A 21-year-old African transfer student complained that he could not ‘‘keep up’’ with his peers during his PPE for collegiate soccer. Upon examination, he had a fixed split S2 while sitting and standing. His ECG results exhibited right axis deviation and incomplete right bundle branch block.
Figure: Major systolic and diastolic murmurs.
262
Volume 14 & Number 3 & May/June 2015
Cardiovascular Preparticipation Evaluation
Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
His echocardiogram results appeared to be normal, but a bubble study was added, showing a secundum atrial septal defect permitting an interatrial left-to-right shunt. A rightto-left shunt would have suggested significant pulmonary hypertension and Eisenmenger syndrome. He also had a systolic ejection murmur at the left upper sternal border from increased flow across the pulmonary valve. Catheterization revealed significant shunting with high risk of developing pulmonary hypertension. He was offered surgery or percutaneous closure and opted for the latter. Key Point: Secundum atrial septal defects are the most common type of atrial septal defect (ASD) and the only defects amenable to percutaneous closure. Case 4: Football Lineman with Chest Pain and Systolic Murmur A 20-year-old African-American freshman football lineman was noted to have systolic murmur during PPE. The murmur increased with Valsalva maneuver; his carotid pulse was brisk, and his apical impulse laterally displaced. Upon further questioning, he reported vague exertional chest pain. Echocardiogram results showed mild septal hypertrophy (14 mm), but a magnetic resonance imaging (MRI) demonstrated significant asymmetric hypertrophy at the distal septum. Key Point: The Valsalva maneuver can decrease LV volume and increase mitral flow obstruction to make the diagnosis of HCM with obstruction. Care must be taken to do it properly without breath holding. HCM can be present without such obstruction, and a systolic murmur only be due to hyperdynamic flow not affected by Valsalva. HCM without obstruction can be missed with echocardiography as much as 50% of the time due to focal hypertrophy that is best seen with MRI.
Heart Murmur and Physical Examination in Athletes with a Focus on Congenital Heart Disease George K. Lui, MD; Fahad Al Sindi, MD; and Ami B. Bhatt, MD Congenital heart disease (CHD) is the most common birth defect, occurring in 1 in 100 live births. There is a wide spectrum ranging from small ventricular septal defects (VSD), which spontaneously close before adulthood to complex disease states that require lifelong cardiac care. Children with history of CHD were restricted from exercise until studies demonstrated how exercise can have cardiovascular and quality of life benefits for individuals with surgical repairs (1,2). Because of the advances in diagnosis and surgical repair, the prevalence of adult survivors with CHD continues to grow at a pace of 5% per year, so that there are more than 1 million adults with CHD in the United States (4). These patients often perceive themselves to be ‘‘cured’’ because of surgical repair at a young age. As these individuals become adolescents and adults, they often seek medical advice regarding exercise and sports. Some individuals, however, continue to have reduced exercise www.acsm-csmr.org
capacity from residual abnormalities, and others live with fear and anxiety regarding physical activity. They are often lost to cardiac follow-up and present in adulthood with complications related to their prior repair. It is important to evaluate any patient with history of surgical repair before prescribing exercise. Remember that there are many forms of CHD that present initially in adulthood. KEY POINTS IN THE HISTORICAL ASSESSMENT Simple Defects Simple types of CHD include repaired and unrepaired problems shown in the Table. Patients with repaired defects without residual shunt or pulmonary hypertension can participate in all sports without restriction. Patients with unrepaired defects such as a small-to-moderate atrial septal defect (ASD) or patent ductus arteriosus (PDA) are typically asymptomatic. Late symptoms include dyspnea on exertion or palpitations, and these patients will have history of a murmur. Arrhythmia, heart failure, and pulmonary hypertension are late complications. These patients will need to be referred for further imaging and closure of the shunt before participation in physical activity. Moderate/Complex Defects Moderate-to-complex types of CHD are outlined in the Table. Initial presentation of these lesions in adulthood is rare. Athletes may complain of dyspnea on exertion, dizziness with exertion, palpitations, or syncope. They may have history of a heart murmur, cyanosis, or clubbing. Heart failure, arrhythmias, and sudden cardiac death are shared complications of all these defects. For instance, an athlete may complain of dizziness with exertion and be found to have atrioventricular (AV) block with exercise secondary to AV conduction disease commonly seen in congenitally corrected transposition of the great arteries. In this defect, the patient has atrioventricular and ventriculoarterial discordance whereby the morphologic right ventricle is the systemic ventricle. These patients are prone to complete heart block later in life. Another example of de novo presentation of CHD in adulthood includes hypertension in the adolescence or young adult. Coarctation of the aorta is a narrowing of the aortic isthmus at the proximal descending thoracic aorta, which results in hypertension and late complications of aortic aneurysms, heart failure, and sudden death. These patients will need to be referred for further imaging and surgical/percutaneous repair before participation in sports activities. Individuals with repaired coarctation of the aorta and no residual obstruction or aortic dilation can participate in all sports. More commonly, patients with moderate-to-complex CHD will present having been repaired in early childhood. These individuals will seek recommendation regarding the safety of physical activity. It is important to inquire about symptoms and auscultate for heart murmurs. The history assessment should focus on residual abnormalities that are often present in this patient population such as pulmonary regurgitation in patients with repaired tetralogy of Fallot. Patients with no residual shunting, no significant right ventricular volume overload, and no arrhythmias can participate in all sports. Patients with residual right ventricular Current Sports Medicine Reports
Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
263
Volume 14 & Number 3 & May/June 2015
productive cough with yellow sputum but no fevers and no chills. He has attributed the cough to his severe postnasal drip that is exacerbated by seasonal allergies. Physical examination result is remarkable for right lower lobe rhonchi with localized inspiratory squeaks. A subsequent chest computerized tomography confirms an area of focal right lower lobe bronchiectasis, and he is referred to a pulmonologist for further evaluation. Key Point: Associated productive cough with localized physical examination findings suggest focal airway disease. Case 4: Young Female Physician Who Works Out A 27-year-old medicine resident is referred for worsening dyspnea during her normal exercise routine along the beach. The dyspnea has worsened as the days have become short in the fall months; her inability to exercise generates a considerable amount of frustration. Her dyspnea begins almost immediately as she runs and does not abate although she notes no wheezing. She has no history of allergy. Her examination, spirometry, and exercise spirometry results are all normal. She is referred for cardiopulmonary exercise testing, and she is noted to have the onset of rapid shallow breathing in anticipation of the test, which continues throughout testing. Her minute ventilation on exercise testing is dramatically elevated. She is referred to a counselor for anxiety management. Key Point: Anxiety can present with asthma-like symptoms. Reference 1. Crapo RO, Casaburi R, Coates AL, et al. Guidelines for methacholine and exercise challenge testing-1999. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999. Am. J. Resp. Crit. Care. Med. 2000; 161:309Y29.
Heart Murmurs in Athletes: From Personal History and Physical Examination Sections Shirin Zarafshar, MD and Vic Froelicher, MD 4A. PERSONAL HISTORY: HAVE YOU BEEN TOLD THAT YOU HAVE A HEART MURMUR? To determine the importance of a positive answer to this question, the following questions should be asked: 1. Has the murmur been present since birth, and is it still present? Athletes with congenital murmurs may remain asymptomatic for life, particularly if there is no associated pathologic condition. However, ventricular or atrial septal defects, patent ductus arteriosus (PDA), bicuspid aortic valves, and other causes of heart murmur may have long-term consequences and require correction. 2. Has anyone told you that the murmur is physiologic or pathologic? A documented prior medical evaluation, particularly if imaging has been performed, can facilitate decisions regarding athletic participation. If the studies are of questionable quality or not available, reevaluation may be necessary. Cardiovascular Preparticipation Evaluation
Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
3. Are there other associated symptoms such as chest pain, shortness of breath, dyspnea on exertion, and/or palpitations? The presence of cardiovascular symptoms such as chest pain, dyspnea, and palpitations can be indicative of an underlying cardiac pathology. Chest pain due to microvascular disease is a feature of HCM. 5. Does anyone in your family have a heart murmur? Familial HCM is an autosomal-dominant trait and one of the most common causes of sudden death in athletes. Other congenital abnormalities that cause murmurs such as Marfan syndrome can cluster in families as well.
PHYSICAL EXAMINATION: IS A HEART MURMUR PRESENT ON PHYSICAL EXAMINATION? The Cardiovascular Examination of the Athlete Setting The cardiac examination should be performed in a stable state and not in the recovery period from an extended period of exercise or competition and in a quiet, comfortable setting with attention given to privacy and room temperature. The examination should be conducted sitting and supine with maneuvers like the Valsalva maneuver, standing, and squatting added if a significant murmur is detected. Normal findings Physiologic and morphologic adaptations of the aerobically trained athlete’s heart include slow heart rate, systolic ejection flow murmur at the upper, left sternal border, a third heart sound, lateral displacement of point of maximal impulse, and hyperdynamic carotid pulses. Athletes predominantly engaged in isometric training (weightlifters) will not exhibit these changes. The examination of the athlete can be challenging because of these physiologic adaptations. Cardiac enlargement by visual examination (apical movements) and palpation (lateral displacement) can simulate the examination of patients with cardiomyopathies or heart failure. The loudest third heart sounds you will ever hear will be in athletes, and they are physiologic when occurring at low heart rates. This contrasts to the third heart sounds in patients with heart failure where they occur at fast heart rates (called ‘‘gallops’’ because of the cadence). Furthermore, third heart sounds in athletes are not related to position, while in patients with heart disease, the S3 gallop is loudest in the supine position. Even in the resting state, systolic flow murmurs can be appreciated in athletes, but they are soft, occur early in systole, and radiate upward rather than laterally toward the apex. While fixed splitting of the heart sounds can be appreciated in the supine position in nonathletes, this splitting is particularly noticeable in athletes. Thus, the finding of fixed splitting should only be considered abnormal if heard in the sitting or standing position. Abnormal findings Any diastolic murmur is abnormal whether or not there is an accompanying systolic murmur. The most common cause is aortic insufficiency (or regurgitation, abbreviated AI or AR). Early AR is best appreciated at the upper left of the sternum, with the athlete in the seated www.acsm-csmr.org
position, during forced expiration and leaning forward. A trick is to carefully listen after the second heart sound to focus attention at the correct time. Since AR can be difficult to appreciate, it is helpful to listen even more carefully when the following occur:
1. A systolic murmur. 2. Wide pulse pressure (950 mm Hg) or a diastolic pressure of 50 mm Hg or less. 3. Hyperdynamic carotid pulse. While AR is the most common cause of a to-and-fro (systolic/diastolic) murmur in athletes, another cause is PDA. This is a congenital abnormality more often encountered than other congenital abnormalities in athletes because athletic performance can be quite normal if the shunt is small. Characteristics that increase the likelihood of systolic murmurs being pathologic include the following:
1. Greater than grade 2/6 intensity 2. Lateral rather than upward radiation 3. Occurrence in mid-systole or late systole rather than in early systole 4. Accompanied by a click in mid-systole or late systole 5. Any murmur that becomes louder with the Valsalva maneuver (best performed supine with your hand on abdomen and telling the athlete to push against your hand while continuing to breathe) Other auscultation abnormalities include a third heart sound during tachycardia or fixed splitting of the second heart sound in the seated position. Sinus tachycardia at rest is abnormal in an aerobically trained athlete, and if not easily explained (recent workout, fever, etc.), further workup may be indicated, particularly if accompanied by any symptoms. CASE EXAMPLES Case 1: Tennis Player with Unexplained Sinus Tachycardia A 20-year-old White female tennis player presented with tachycardia and shortness of breath while going to classes. She normally performed at the top level of competitions but was out of season at the time. She had been symptomatic for nearly a week and presented late in the day after classes. An examination yielded unremarkable results, and she was afebrile, with blood pressure 120/70 and HR of 100 bpm, although S2 seemed to be louder than S1 even at the apex. She was on birth control pills and had just recovered from a leg injury. There was no leg tenderness or swelling. Blood tests were ordered (complete blood count, thyroid function), and a Holter monitor, placed. The Holter was read the next day and was unremarkable except for an average heart rate of 100 bpm with maximum of 140 bpm during light exercise. Laboratory test results were normal. An echocardiogram showed a dilated right ventricle (RV), elevated pulmonary artery (PA) pressures, and normal left ventricle (LV) function. Primary pulmonary hypertension was considered, but she was sent for a computerized tomography chest angiogram lung scan, which revealed pulmonary embolus. She was started on heparin and then treated with Current Sports Medicine Reports
Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
261
Coumadin with gradual recovery. She was found to have factor V Leiden genotype. Key Point: Sinus tachycardia may be the only finding with a pulmonary embolus. Case 2: Baseball Player with Continuous Murmur During mass screening, a cardiology fellow noted a systolic murmur while examining a 19-year-old White male baseball player. The athlete was asymptomatic and had normal ECG. The fellow performed screening echocardiogram on site, which was considered normal, and the athlete was cleared for participation. As formality, the supervising cardiologist auscultated the athlete and noted a toand-fro continuous murmur. Echocardiogram and cardiac catheterization revealed PDA with significant right-to-left
shunting. The athlete was offered surgical or percutaneous correction. Key Point: Continuous (systolic and diastolic) and diastolic murmurs are always due to cardiac pathologic lesions. The continuous murmur of PDA is described as a continuous ‘‘washing machine’’ type murmur; best appreciated in the second left intercostal space. A scanning echocardiogram will miss it. Case 3: Soccer Goalie with Fixed Split of Second Heart Sound (S2) A 21-year-old African transfer student complained that he could not ‘‘keep up’’ with his peers during his PPE for collegiate soccer. Upon examination, he had a fixed split S2 while sitting and standing. His ECG results exhibited right axis deviation and incomplete right bundle branch block.
Figure: Major systolic and diastolic murmurs.
262
Volume 14 & Number 3 & May/June 2015
Cardiovascular Preparticipation Evaluation
Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
His echocardiogram results appeared to be normal, but a bubble study was added, showing a secundum atrial septal defect permitting an interatrial left-to-right shunt. A rightto-left shunt would have suggested significant pulmonary hypertension and Eisenmenger syndrome. He also had a systolic ejection murmur at the left upper sternal border from increased flow across the pulmonary valve. Catheterization revealed significant shunting with high risk of developing pulmonary hypertension. He was offered surgery or percutaneous closure and opted for the latter. Key Point: Secundum atrial septal defects are the most common type of atrial septal defect (ASD) and the only defects amenable to percutaneous closure. Case 4: Football Lineman with Chest Pain and Systolic Murmur A 20-year-old African-American freshman football lineman was noted to have systolic murmur during PPE. The murmur increased with Valsalva maneuver; his carotid pulse was brisk, and his apical impulse laterally displaced. Upon further questioning, he reported vague exertional chest pain. Echocardiogram results showed mild septal hypertrophy (14 mm), but a magnetic resonance imaging (MRI) demonstrated significant asymmetric hypertrophy at the distal septum. Key Point: The Valsalva maneuver can decrease LV volume and increase mitral flow obstruction to make the diagnosis of HCM with obstruction. Care must be taken to do it properly without breath holding. HCM can be present without such obstruction, and a systolic murmur only be due to hyperdynamic flow not affected by Valsalva. HCM without obstruction can be missed with echocardiography as much as 50% of the time due to focal hypertrophy that is best seen with MRI.
Heart Murmur and Physical Examination in Athletes with a Focus on Congenital Heart Disease George K. Lui, MD; Fahad Al Sindi, MD; and Ami B. Bhatt, MD Congenital heart disease (CHD) is the most common birth defect, occurring in 1 in 100 live births. There is a wide spectrum ranging from small ventricular septal defects (VSD), which spontaneously close before adulthood to complex disease states that require lifelong cardiac care. Children with history of CHD were restricted from exercise until studies demonstrated how exercise can have cardiovascular and quality of life benefits for individuals with surgical repairs (1,2). Because of the advances in diagnosis and surgical repair, the prevalence of adult survivors with CHD continues to grow at a pace of 5% per year, so that there are more than 1 million adults with CHD in the United States (4). These patients often perceive themselves to be ‘‘cured’’ because of surgical repair at a young age. As these individuals become adolescents and adults, they often seek medical advice regarding exercise and sports. Some individuals, however, continue to have reduced exercise www.acsm-csmr.org
capacity from residual abnormalities, and others live with fear and anxiety regarding physical activity. They are often lost to cardiac follow-up and present in adulthood with complications related to their prior repair. It is important to evaluate any patient with history of surgical repair before prescribing exercise. Remember that there are many forms of CHD that present initially in adulthood. KEY POINTS IN THE HISTORICAL ASSESSMENT Simple Defects Simple types of CHD include repaired and unrepaired problems shown in the Table. Patients with repaired defects without residual shunt or pulmonary hypertension can participate in all sports without restriction. Patients with unrepaired defects such as a small-to-moderate atrial septal defect (ASD) or patent ductus arteriosus (PDA) are typically asymptomatic. Late symptoms include dyspnea on exertion or palpitations, and these patients will have history of a murmur. Arrhythmia, heart failure, and pulmonary hypertension are late complications. These patients will need to be referred for further imaging and closure of the shunt before participation in physical activity. Moderate/Complex Defects Moderate-to-complex types of CHD are outlined in the Table. Initial presentation of these lesions in adulthood is rare. Athletes may complain of dyspnea on exertion, dizziness with exertion, palpitations, or syncope. They may have history of a heart murmur, cyanosis, or clubbing. Heart failure, arrhythmias, and sudden cardiac death are shared complications of all these defects. For instance, an athlete may complain of dizziness with exertion and be found to have atrioventricular (AV) block with exercise secondary to AV conduction disease commonly seen in congenitally corrected transposition of the great arteries. In this defect, the patient has atrioventricular and ventriculoarterial discordance whereby the morphologic right ventricle is the systemic ventricle. These patients are prone to complete heart block later in life. Another example of de novo presentation of CHD in adulthood includes hypertension in the adolescence or young adult. Coarctation of the aorta is a narrowing of the aortic isthmus at the proximal descending thoracic aorta, which results in hypertension and late complications of aortic aneurysms, heart failure, and sudden death. These patients will need to be referred for further imaging and surgical/percutaneous repair before participation in sports activities. Individuals with repaired coarctation of the aorta and no residual obstruction or aortic dilation can participate in all sports. More commonly, patients with moderate-to-complex CHD will present having been repaired in early childhood. These individuals will seek recommendation regarding the safety of physical activity. It is important to inquire about symptoms and auscultate for heart murmurs. The history assessment should focus on residual abnormalities that are often present in this patient population such as pulmonary regurgitation in patients with repaired tetralogy of Fallot. Patients with no residual shunting, no significant right ventricular volume overload, and no arrhythmias can participate in all sports. Patients with residual right ventricular Current Sports Medicine Reports
Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
263
