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TCH APP Conference April 2019.keyCarolyn A. Altman Texas Children’s Hospital Advanced Practice Provider Conference Houston, TX April 6 , 2018 2 Some pearls on • General appearance • Physical exam beyond the heart 3 5 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 Chest wall development and symmetry
Palpation Auscultation Cardiac Palpation Consistent approach: palm of your hand, hypothenar eminence, or finger tips Precordium, suprasternal notch 10 • Abnormal sounds? Clicks, gallops 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 12 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 13 S2: normal splitting Single S2: Pulmonar Hypertension Wide, fixed splitting: ASD Paradoxical Splitting of S2: LBBB, severe LVOTO 14 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 15 Varies with respiration as does S2 Soft S1: low cardiac output, tachycardia Loud S1: hyperdynamic (fever, exercise), mitral stenosis 16 Abnormal ventricular function Mid way thru diastole Muscle tensing at end of rapid, early filling which occurs with ventricular relaxation Later than split S2 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 S1-Ej click S4 Heard best with bell since low pitched Can extinguish the sound by pressing too hard (turning bell into diaphragm) Usually heard over mitral area, if LV dysfunction Listen in left lateral decubitus position too If RV dysfunction-may hear best at LLSB S4 S3 Mid-systolic click: MVP Opening snap of MS 21 Innocent or pathologic 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 23 Ejection murmurs: Begins shortly after S1 Mid-systolic: MVP Often holosystolic Begin after valve opens, so hear S1 then murmur Should be able to hear S2 distinctly Early systolic ejection click if semilunar valve stenosis 26 Low pitched filling noise Louder in diastole: venous hums, coronary fistula PDA Coronary fistula AVM Helpful in figuring out what is generating the murmur URSB: Aortic stenosis ULSB: Pulmonary stenosis, pulmonary flow, ASD 31 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 32 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 33 35 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 36 v Size of defect v Differences in compliance between RV and LV- flow is usually left to right 37 38 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 39 Pulmonary flow murmur: v Large volume of blood crossing the pulmonary valve v ULSB to back v Ejection v Medium pitched 40 CHD: Atrial Septal Defect Diastolic Rumble: Consistent with at least 2:1 Qp:Qs Low pitched Listen with bell at LLSB 41 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 42 CHD: Patent Ductus Arteriosus Palpation RV impulse if pulmonary hypertension Hyperactive LV impulse if large volume of flow PDA 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 juxtarterial 45 Size of defect 46 CHD: VSD Palpation: Quiet precordium? RV impulse may be present with volume or pressure loading +/- thrill: cannot determine size by presence of thrill 47 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 48 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 49 (obscured) Ends with P2, S2 split normally Plateau shape The smaller the defect, the more high pitched 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 51 52 Compare right and lef chest 53 eventually Eisenmenger syndrome vCan be holosystolic, if any pressure restrichon v If no pressure restrichon, may be no murmur, or a pulmonary ouilow murmur 55 v Pulmonary valve click: dilated pulmonary root v Graham-Steele murmur: pulmonary insufficiency 56 Physiology: v Balance between VSD flow and pulmonary valve and sub valve stenosis v “Pink” tets have little pulmonary stenosis v Other extreme: pulmonary atresia with VSD v PS typically progresses over time 57 v Starts with S1, given subvalvar component v As subps worsens, murmur decreases in intensity: pop-off through VSD to systemic circulahon v Listen for murmur to decrease in hypercyanohc spell 59 60 not carry through S2-not continuous, not the diastolic component The diastolic murmur is of a different pitch 61 Physiology: usually slowly progressive obstruchon 62 v Thrill indicates more severe obstruchon 63 v Either at ULSB, or upstream from valve at LLSB v Increases in intensity with expirahon v Moves closer to S1 with increasing PS 64 v ULSB radiahng to back, axilla 65 Ofen bicommissural Exercise increases the relahve stenosis 66 v Thrills frequently presents vCan be along LVOT, ULSB, carohds, suprasternal notch 67 Ejechon click: vOpening of non-compliant valve v Moves earlier in systole with increasing severity of obstruchon, may become inaudible v Heard at apex (upstream) or URSB (downstream) 68 Murmur: v With increasing stenosis and normal cardiac output, murmur becomes louder, longer, later peaking vMay not have significant murmur if poor funchon (neonatal AS) v Heard at apex (upstream) or URSB (downstream) 69 Innocent Murmurs: Learn to recognize the three most common innocent murmurs of childhood: Venous hums, Still’s murmurs Physiologic pulmonary branch stenosis in infancy 70 I-III/VI SEM Vibratory, twanging 71 Subaortic stenosis can mimic Still’s: both can be musical 72 Use positional changes to help distinguish subAS from Still’s Dynamic obstruction in HCM accentuated with decrease in filling: murmur gets louder with stand Discrete sub AS will not usually get louder, but will also not diminish with stand 73 Venous Hum: innocent continuous murmur Turbulent flow merging from internal jugular and subclavian veins into SVC Louder in diastole Disappear when patient lies supine or turns head Audible along infraclavicular area, and low anterior neck (not the head) I-III/VI 75 PDA PPS in infant under 6 mos: same pitch as respirations As loud or loudest in back or axilla Systolic, high pitched, blowing Relatively small branch Pas arising at acute angle from large MPA 77 Tiny VSD: better heard at mid to LLSB, not back/axilla PS: has a click ASD: Has abnl S2 Position Changes Distinguish innocent Still’s murmurs from LVOTO Detect gallops: apex, left lateral decubitus Distinguish venous hums from non-innocent continuous murmurs Mitral valve prolapse 79 Worry if it goes away-valve thrombosis 81 Quiet room Recognize that naptime, stranger anxiety, hunger can adversely affect the situation Make the child as comfortable as possible: Silent distracters to entertain the child-flashlight, ID badge, toys, siblings Tips for Better Exams Tiny bodies: Use the right size stethoscope to minimize ambient noise and to accurately determine the presence and location of a murmur Change the order of the exam to fit the child Warm hands and scopes 83 Remember- Always not normal: RV impulse, thrills, apical murmurs, murmurs that increase with sitting or standing, murmurs with extra heart sounds, diastolic murmurs Need to have a normally split S2 to be normal If it does not sound innocent- needs further evaluation Thank you.