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Systolic Murmurs Murmurs and the Cardiac Physical Exam Carolyn A. Altman Texas Children’s Hospital Advanced Practice Provider Conference Houston, TX April 6 , 2018 The Cardiac Physical Exam Before applying a stethoscope….. Some pearls on • General appearance • Physical exam beyond the heart 2 Jugular Venous Distention Pallor Cyanosis 3 Work of Breathing Normal infant breathing Quiet Tachypnea Increased Rate, Work of Breathing 4 Beyond the Chest Clubbing Observed in children older than 6 mos with chronic cyanosis Loss of the normal angle of the nail plate with the axis of the finger Abnormal sponginess of the base of the nail bed Increasing convexity of the nail Etiology: ? sludging 5 Chest ❖ Chest wall development and symmetry ❖ Long standing cardiomegaly can lead to hemihypertrophy and flared rib edge: Harrison’s groove or sulcus 6 Ready to Examine the Heart Palpation Auscultation General overview Defects Innocent versus pathologic 7 Cardiac Palpation ❖ Consistent approach: palm of your hand, hypothenar eminence, or finger tips ❖ Precordium, suprasternal notch ❖ PMI? ❖ RV impulse? ❖ Thrills? ❖ Heart Sounds? 8 Cardiac Auscultation Where to listen: ★ 4 main positions ★ Inching ★ Ancillary sites: don’t forget the head in infants 9 Cardiac Auscultation Focus separately on v Heart sounds: • S2 normal splitting and intensity? • Abnormal sounds? Clicks, gallops v Murmurs v Rubs 10 Cardiac Auscultation Etiology of heart sounds: Aortic and pulmonic valves actually close silently Heart sounds reflect vibrations of the cardiac structures after valve closure Sudden deceleration of retrograde flow of the column of blood in the aorta and pulmonary artery when the elastic limits of the tensed valve leaflets are met 11 Cardiac Auscultation S2 ❖ Physiologic splitting of S2: Increased systemic venous return and increased pulmonary capacitance during inspiration causes delayed closure of the pulmonary valve ❖ S2 cannot be considered “normal” unless physiologic splitting is heard 12 S2: normal splitting Single S2: Pulmonar Hypertension Wide, fixed splitting: ASD Paradoxical Splitting of S2: LBBB, severe LVOTO 13 S2 HInts ❖ If splitting persists while patient supine, try sitting position- less volume in heart may normalize splitting ❖ Listen for splitting at mid to ULSB in kids ❖ Infants: Mid to LLSB ❖ Splitting of S2 if the HR is over 160 hard to hear: gently blowing a breath in the baby’s face will slow HR 14 Cardiac Auscultation: S1 ❖ Physiologic splitting of S1: ❖ Can be heard in children with slower heart rates. ❖ Varies with respiration as does S2 ❖ Soft S1: low cardiac output, tachycardia ❖ Loud S1: hyperdynamic (fever, exercise), mitral stenosis 15 Cardiac Auscultation Gallops: S3 or S4 ❖ Short, low pitched diastolic sounds ❖ Abnormal ventricular function 16 Auscultation: S3 Gallop ❖ Mid way thru diastole ❖ Muscle tensing at end of rapid, early filling which occurs with ventricular relaxation ❖ Later than split S2 ❖ Earlier than S4 17 Auscultation: S4 Gallop ❖ If impaired ventricular relaxation, less filling of the ventricles during during early diastole and more during atrial contraction ❖ Hypertrophic cardimyopathy, eg ❖ S4 is thus a sound generated late in diastole ❖ Very close to S1, can mistake for split S1 or S1- ejection click 18 S1-Ej click S4 S3 and S4 Gallops ❖ Heard best with bell since low S3 pitched ❖ Can extinguish the sound by pressing too hard (turning bell into diaphragm) S4 ❖ Usually heard over mitral area, if LV dysfunction S1-Ej click ❖ Listen in left lateral decubitus position too ❖ If RV dysfunction-may hear best at LLSB 19 Other Extra Heart Sounds ❖ Ejection Click: opening of the aortic or pulmonary valve ❖ Mid-systolic click: MVP ❖ Opening snap of MS ❖ Listen for difference in timing, cadence 20 How to Characterize Murmurs ❖ Timing ❖ Site of maximum intensity ❖ Intensity ❖ Radiation ❖ Pitch: ❖ Associated findings: clicks, rumbles, precordial activity ❖ Different from previous in your patient ❖ Innocent or pathologic 21 Timing of Murmurs Systolic ? Diastolic? or Continuous ? ❖ Systolic occurs as the heart contracts ❖ Diastolic as the heart relaxes ❖ Continuous murmurs continue from systole into diastole ❖ Find S2 and listen to whether the murmur comes before it, after it, or through it ❖ Inching the stethoscope can help with timing 22 Murmurs: Timing Systolic murmurs: ❖ Regurgitant murmurs: Begin with S1 ❖ Ejection murmurs: Begins shortly after S1 ❖ Mid-systolic: MVP 23 Regurgitant Systolic Murmurs ❖MR, TR, VSD ❖Begin with S1: “coincident with S1” ❖Often holosystolic 24 Systolic Ejection Murmurs ❖ AS/PS, Still’s, pulmonary flow ❖ Begin after valve opens, so hear S1 then murmur ❖ Should be able to hear S2 distinctly ❖ Early systolic ejection click if semilunar valve stenosis 25 Mid Systolic Murmurs ❖Mitral valve prolapse ❖Click ushers in murmur 26 Diastolic murmurs Aortic or pulmonary regurgitation: ❖High pitched ❖Decrescendo 27 Diastolic murmurs Diastolic rumbles: ❖ Increased volume across MV or TV ❖ Low pitched filling noise ❖ Absence of silence 28 Continuous Murmurs ❖ Start during systole, continue past S2 Venous Hum ❖ Louder in systole: PDA, AVM, shunts ❖ Louder in diastole: venous hums, coronary fistula PDA Coronary fistula AVM 29 Murmurs by location of greatest intensity: Helpful in figuring out what is generating the murmur ❖ URSB: Aortic stenosis ❖ ULSB: Pulmonary stenosis, pulmonary flow, ASD ❖ LLSB: VSD, Still’s, TR ❖ Apical: Mitral 30 Characterize Murmurs: Grading system allows accurate communication between caretakers ❖ Grade I: is there something there? ❖ Grade II: Ok, I can hear it ❖ Grade III: Boy, that’s loud ❖ Grade IV: Associated with a thrill, knock your socks off loud ❖ Grade V: Audible with scope off chest ❖ Grade VI: Audible without stethoscope 31 Characterize Murmurs: Important to follow trends: ❖ Is an aorto-pulmonary shunt murmur getting softer? A shunt may be getting obstructed, outgrown, or PVR elevated ❖ Is the outflow tract obstruction getting worse in a patient with new chest pain? ❖ Is the patient with TOF spelling or just colicky: the outflow murmur will get softer during a spell as less flow traverses the RVOT 32 Characterize Murmurs by Pitch: ❖ High ❖ Low ❖ Harsh (multitonal) 33 Congenital Heart Defects ❖ Atrial Septal Defect ❖ Patent Ductus Arteriosus ❖ Ventricular Septal Defect ❖ Pulmonary Stenosis ❖ Aortic Stenosis 34 CHD: Atrial Septal Defect ❖ Anatomy: described by location in the septum Secundum Primum Coronary Sinus Sinus Venosus ❖ Physiology and physical signs the same, regardless of location of ASD 35 CHD: Atrial Septal Defect Physiology: Amount of shunting depends on v Size of defect v Differences in compliance between RV and LV- flow is usually left to right 36 CHD: Atrial Septal Defect Palpation: right ventricular impulse from increased RV volume 37 CHD: Atrial Septal Defect ❖ Widely split S2: v Persistent separation of A2P2 components of S2 throughout respiratory cycle v Increased pulmonary capacitance or v Reciprocal changes in flow into the right atrium from the defect or systemic veins 38 CHD: Atrial Septal Defect ❖ Pulmonary flow murmur: v Large volume of blood crossing the pulmonary valve v ULSB to back v Ejection v Medium pitched 39 CHD: Atrial Septal Defect Diastolic Rumble: Consistent with at least 2:1 Qp:Qs Low pitched Listen with bell at LLSB 40 CHD: Patent Ductus Arteriosus Physiology: v In the setting of low pulmonary vascular resistance, flow is continuous, left to right v If large PDA, PA pressures may be high: flow can be •Left to right •Bidirectional •All right to left 41 CHD: Patent Ductus Arteriosus Palpation ❖ RV impulse if pulmonary hypertension ❖ Hyperactive LV impulse if large volume of flow PDA 42 CHD: PDA Murmur v Continuous if low pulmonary vascular resistance v Machinery like v Accentuated at end systole v Left infra-clavicular area, back, and left supraclavicular areas 43 CHD: Ventricular Septal Defect Anatomy described by location Perimembranous Inlet Muscular Doubly committed- juxtarterial 44 CHD: VSD Physiology: amount of shunting depends on ❖ Size of defect ❖ Pulmonary resistance: more shunting with decreasing resistance 45 CHD: VSD Palpation: ❖ Quiet precordium? ❖ RV impulse may be present with volume or pressure loading ❖ +/- thrill: cannot determine size by presence of thrill 46 CHD: VSD S2 in VSDs can be ❖ Normally split (typical) ❖ Widely split if very generous amount of flow crossing to fill RV ❖ Single: if pulmonary hypertension with elevated resistance 47 CHD: VSD Auscultation Murmur ❖ Usually along LSB ❖ Very small defects do not radiate ❖ Subpulmonary VSDs follow the RV outflow to the pulmonary arteries ❖ “Blowing” quality ❖ Start with S1 48 CHD: VSD murmurs Holosystolic murmur: ❖ Starts with S1 (obscured) ❖ Ends with P2, S2 split normally ❖ Plateau shape ❖ The smaller the defect, the more high pitched 49 CHD: VSD murmur Short systolic murmur consistent with very small defect v Starts with S1 v Ends before S2, as defect closed by ventricular contraction v Usually very localized, may only hear in certain positions 50 CHD: VSD Mitral Rumble vIndicates at least 2:1 Qp:Qs vLow pitched vUse bell at apex 51 CHD: VSD Diastolic rumble Can be quite subtle Listen for absence of diastolic silence Compare right and lef chest 52 CHD: VSD Very Large VSDs vAllow high pressure and high flow v If lef unrepaired: elevated PVR develops, eventually Eisenmenger syndrome Palpahon v RV impulse v Palpable S2 53 CHD: VSD Large VSDs: Systolic Murmur vCan be holosystolic, if any pressure restrichon v If no pressure restrichon, may be no murmur, or a pulmonary oulow
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