Quick viewing(Text Mode)

AUSCULTATION SKILLS for ATHLETIC TRAINERS

AUSCULTATION SKILLS for ATHLETIC TRAINERS

AUSCULTATION SKILLS for ATHLETIC TRAINERS

Dennis A. Cardone, DO, CAQSM Director, Sports Medicine and Sports Medicine Fellowship UMDNJ-Robert Wood Johnson Medical School New Brunswick, NJ

The Athletes (Athletic Heart Syndrome)

I. History a. Dietlen 1908: excessive and continued strain could lead to collapse of the cardiovascular system b. Medical community early 1900s: increased cardiac size in athletes was a pathologic response to the increased cardiac stress of exercise c. Frieberg 1972: cardiovascular changes noted among athletes were more a function of disease (acquired or congenital) than a physiologic response to the adaptations caused by the athlete’s training d. 2004: athletic heart syndrome represents normal physiologic adaptations to training that allows normal or improved cardiac function in contrast to the cardiac dysfunction of pathologic hypertrophy. II. Physiologic response of cardiovascular system to exercise a. Exercise training i. Peripheral response 1. increased number of capillaries, mitochondria, oxidative enzymes 2. improved uptake and utilization of O2 in skeletal muscles ii. Central response (Heart adaptations) 1. increased stroke volume due to cardiac dilation and hypertrophy 2. decrease in resting HR (CO=SV x HR) 3. maximal HRs are same in trained and untrained athletes 4. increased vagal tone III. History: negative IV. Physical examination a. b. Lower BP c. Laterally displaced PMI (because of LVH) d. i. Systolic ejection murmur (most intense supine b/c increased left ventricular filling; less intense standing or squatting b/c decreased left ventricular filling) ii. Sinus arrhythmia iii. Wide splitting first heart sound iv. Wide splitting second heart sound v. Filling sounds – S3 ventricular gallop vi. Venous hums vii. Systolic over carotid viii. Other innocent systolic murmurs ix. Diastolic murmurs are not associated with AHS V. EKG findings a. Bradycardia b. Sinus arrhythmia c. First-degree heart block (prolonged PR interval) d. Second-degree heart block (Wenckebach’s block, a sequential prolongation of PR interval with eventual dropped beat) e. Junctional rhythms f. Right axis deviation g. Incomplete RBBB h. LVH i. Minor ST-T wave changes j. Resolve with exercise VI. Echocardiography a. Increased left ventricular wall thickness b. Increased left ventricle chamber size c. Right ventricle and left atrium size may be increased VII. How much exercise to achieve anatomic and physiologic changes? a. Dynamic exercise b. 30-60 minutes c. 3-4 times per week d. 60-70% VO2 max

CARDIAC AUSCULTATION

I. Examine in different positions a. Sitting b. Supine c. Left lateral recumbent d. Standing e. Squatting II. Stethoscope a. Bell: low-frequency sounds b. Diaphragm: high-frequency sounds III. Sites for auscultation a. Lower left lateral sternal border (4th ICS): tricuspid valve and right side of heart b. Apex (5th ICS midclavicular line): mitral valve and left side of heart c. Right base (2nd ICS): d. Left base (2nd ICS): pulmonic valve IV. Sequence of auscultation V. Classification of sounds and murmurs a. I: very faint, heard after listener tunes in b. II: heard immediately but faint c. III: loud but without a thrust or thrill d. IV: loud with a thrust or thrill e. V: loud with a thrust or thrill and heard with chestpiece tilted on chest f. VI: loud with thrust or thrill and heard with chestpiece just off chest wall VI. Cardiac sound-cycle relationship a. First Heart Sound - S1 i. Beginning of ventricular ii. Closure of mitral and tricuspid valves iii. Split S1 b. Second Heart Sound – S2 i. Ventricular diastole ii. Closure of aortic and pulmonic valves iii. usually heard on inspiration c. – S4 i. Diastolic sound heard just before S1 ii. Low frequency iii. Result of decreased ventricular compliance or increased volume of filling iv. Sign of ventricular stress 1. normal in athletes <20 years (increased diastolic volume) 2. severe HTN, , CAD, Cardiomyopathy, pulmonary stenosis d. Third Heart Sound – S3 i. Diastolic sound that occurs during early rapid filling of ventricles ii. Low frequency iii. Heard just after S2 iv. Result of decreased ventricular compliance or increased ventricular diastolic volume 1. Normal in children and young adults 2. May be heard in athletes over 40 years 3. Pathologic conditions: CHF, CAD, Cardiomyopathy e. Murmurs i. Sustained noises audible during the time periods of systole, diastole, or both ii. Frequency: high, medium, low iii. Quality: blowing, harsh or rough, rumble iv. Timing 1. Systolic murmur: occurs between S1 and S2 2. Diastolic murmur: occurs between S2 and S1 f. Systolic murmurs i. May be normal in athletes (increased blood flow) ii. Produced from forward blood flow across aortic or pulmonic valves or regurgitant flow from mitral or tricuspid valve iii. Valves may be normal (but high rate of flow) or abnormal iv. Pathologic conditions: mitral insufficiency, aortic stenosis, pulmonic stenosis v. Early systolic murmurs 1. “innocent” murmurs 2. incompetent valve vi. Midsystolic murmurs 1. aortic or pulmonic stenosis vii. Late systolic murmurs 1. MVP viii. Pansystolic murmurs 1. Begins with S1 and ends with S2 2. mitral or tricuspid regurgitation, VSD g. Diastolic murmurs i. Not normal are PATHOLOGIC ii. Mechanisms: 1. aortic or pulmonic valve incompetence 2. mitral or tricuspid stenosis 3. increased blood flow across mitral or tricuspid valves iii. Early diastolic murmurs 1. aortic regurgitation 2. pulmonic regurgitation iv. Mid-diastolic murmurs 1. mitral stenosis 2. tricuspid stenosis v. Late diastolic murmurs 1. S1 is difficult to hear 2. mitral or tricuspid stenosis vi. Pandiastolic murmurs 1. S2 and S1 are difficult to hear 2. PDA h. Sounds around S1 i. Wide split S1 1. RBBB, ventricular , third degree heart block 2. mitral stenosis ii. Ejection sounds 1. High frequency “clicking” sounds that occur shortly after S1 2. Aortic or pulmonic origin a. Pulmonic stenosis b. Valvular aortic stenosis c. iii. Mid-systolic clicks 1. Usually occurs in middle of systole 2. MVP i. Sounds around S2 i. Paradoxical split S2 1. Closure of aortic valve is delayed 2. Severe aortic stenosis, severe aortic regurgitation ii. Wide split S2 1. Abnormal delay in pulmonic valve closure 2. ASD, VSD, pulmonary stenosis iii. Fixed split S2 1. Split doesn’t change with respiration 2. CHF, Cardiomyopathy, ASD, VSD iv. Narrow split S2 v. Opening snap 1. Opening of mitral valve 2. Occurs after S2 3. Mitral stenosis j. Friction rubs i. Pericardial inflammation: sound is a scratching, grating, or squeaking ii. Pleural inflammation: disappears if breath is held k. Common adult abnormalities i. Mitral regurgitation and tricuspid regurgitation 1. Systolic murmur 2. Wide split second sound 3. S3 if CHF present ii. Aortic stenosis 1. Aortic ejection sound 2. Systolic ejection murmur 3. Normal split S1 4. Physiologic split S2 iii. Pulmonic stenosis 1. Pulmonic ejection sound 2. Systolic ejection murmur iv. Aortic regurgitation 1. Aortic ejection sound 2. Early diastolic murmur v. Pulmonic regurgitation 1. Pulmonic ejection sound 2. Early diastolic murmur vi. Mitral stenosis and tricuspid stenosis 1. Louder than normal S1 2. Opening snap after S2 3. Mid-diastolic ejection murmur 4. Late diastolic accentuation of murmur l. Pediatric systolic murmurs i. Innocent murmurs 1. Still’s murmur 2. physiologic systolic ejection murmur 3. arterial supraclavicular 4. pulmonary flow murmur 5. cervical venous hum VII. When to refer a. 6-90% of school age children have innocent murmurs b. Innocent murmurs i. Normal history ii. Never solely diastolic iii. Area of maximal intensity well localized iv. Grade is less than III/VI v. Innocent systolic murmur decreases with standing c. Refer if: i. Murmur grade III/VI or higher ii. Harsh murmur iii. Diastolic murmur iv. Pansystolic murmur v. Diffuse area of maximal intensity vi. Murmur radiates to back or neck vii. Pathological murmur increases with standing or valsalva VIII. World Wide Web Links a. www.music.mcgill.ca/auscultation/the_heart.html b. http://medicine.osu.edu/exam/ c. www.medinfo.ufl.edu/year1/bcs/clist/cardio.html d. www.med.ucla.edu/wilkes/inex.htm