Murmur Chart - Essentials Of Cardiology

Murmur What is it? Aortic Stenosis Obstruction of blood flow across the aortic valve (turbulence & afterload on LV) AS = increased afterload Murmurs Mitral Regurgitation Mitral valve fails to close fully in systole – blood regurgitates from LV to LA  volume overload on LV w/ subsequent dilation & hypertrophy Greatest need for intervention Preload dependent MR = increased preload Acute – post myocardial infarction with rupture of papillary muscle or chordae  Aortic Regurgitation Mitral Stenosis Leaflets of aortic valve fail to Narrowing of mitral valve impedes close completely during diastole flow from LA into LV during diastole  blood regurgitates from aorta (fails to open sufficiently in diastole) back into LV  volume overload on LV  Predominately younger Less common in adults than AS adults or MR  Leading cause of mitral stenosis in all age groups worldwide but rare in US  Trans mitral gradient affected significantly by s in HR which  filling time & thus SV and CO  Severe MS w/ mitral valve area <1.5 cm2 - correlates w/ significant LAE (ECK) & Pulmonary pressures (PH type 2) Dyspnea, hypotension (decreased CO) Chronic – secondary to MVP (MVP may have a murmur)   Dyspnea Volume overload of LA and LV MR is the MC murmur in adults >55 y/o Etiology Degenerative or calcific:  Calcification of congenital bicuspid aortic valve  50-70 y/o o Bicuspid aortic valve  MC congenital etiology o Thickens & calcifies  sx > 40 y/o (5th decade) o Male, autosomal dominant o A/w thoracic aortic dz – aneurysm o ACC – 1st degree relatives of pt w/ bicuspid aortic valve be screened for bicuspid and thoracic valve dz  Degenerative calcification of normal 3-valve aortic  > 70 y/o MR is the MC (middle aged)  Primary : organic intrinsic valve  Older pts : dilation of disease; MVP myxomatous ascending aortic secondary degeneration, pts >70 – flail HTN or primary aortic mitral leaflet, ruptured chordae disease, calcific aortic tendineae, calcific degen. sclerosis, rarely from  Secondary ischemia: MR d/t bicuspid aortic valve reversible ischemia or papillary  Acute AR : often d/t aortic mm. infarct +/- rupture, usually dissection or endocarditis a/w acute MI, pts > 70  Periprosthetic AR : after  Secondary non-ischemic: MR transcatheter aortic valve from papillary mm apical implantation (TAVI) displacement/annular dilation resulting in poor tolerance secondary to LV enlargement in volume overload and LV (HCM, LVH) HF   RHD – MC but rare in US (latency of 10-20 yrs) Other causes: MS, congenital MS, post mitral valve repair, atrial myxoma, radiation exposure Less common in adults than AS or MR Risk factors ASCVD, age, male, current cigarette smoking, HTN, dyslipidemia, aortic valve sclerosis Systolic or diastolic? Murmur description Systolic (mid systolic) Preload dependent  Harsh diamond shaped late peaking mid systolic (later the peak=more severe AS)  Harsh, late peaking, systolic murmur Location of auscultation Best @ right 2nd ICS (RUSB) Radiation Radiates to carotids (right>left) & cardiac apex Hand grip  murmur intensity Valsalva & standing Squatting Sx  murmur intensity Associated findings murmur intensity Extended latent period (>10-15 years) Classic triad=SAD (syncope w/ exertion, angina, & dyspnea) EKG: +/- LVH CXR: cardiomegaly, calcified valve, or prominent ascending aorta Helmet Cells (schistocytes): fragmented RBCs caused Acute – MI Chronic – MVP Secondary – IE, spontaneous rupture of chordae from degenerative valve disease, papillary mm. rupture from MI Scarlet fever (a/w GABHS)  RHD Systolic (holosystolic) Not preload dependent  Blowing, holosystolic  Constant intensity  not preload dependent  Apical S3 (ventricular gallop) indicates volume overload of LV (HF) Best @ apex w/ patient on L side (apical S3 reflects volume overload) +/- radiation to left axilla (posterior jet) or left sternal edge (ant. Jet)  RHD Diastolic Diastolic  Rumbling, low pitched, diastolic Loud opening snap after S2 High pitched, blowing, diastolic decrescendo – high gradient b/w aorta & LV  loudest at onset  Begins at S2 Best @ left 3rd or 4th ICS w/  pt leaning forward  Sometimes at apex (esp in   elderly)  If heard to right of sternum  suspect aortic root  Highest gradient b/w aorta & LV  murmur loudest at onset Sometimes at apex (esp. in elderly) murmur intensity (increased aorta-LV gradient)    Often asymptomatic early Widened pulse pressure LAH Best @ apex w/ pt in left lateral decubitus Use a bell Loud opening snap after S2 by AS d/t mechanical damage as they pass thru calcified valve Dx and monitoring Echocardiogram A: at risk – initial B (mild): q 3-5 years B (moderate): q 1-2 years Echocardiogram A: at risk – initial B (mild): q 3-5 years B (moderate): q 1-2 years C1 (asymp. severe): q 6-12 months C2: Dilating LV  more frequently C1 (asymp. severe): q 6-12 months   Progressive disease Worsening obstruction and afterload of the LV, eventually leading to LV dysfunction  Severe AS stage C (asymptomatic +/- LV dysfunction (hemodynamic effects on ventricle) and D (symptomatic)  Severe AS Monitor progression w/ serial echo in asymptomatic severe AR w/ preserved LV fxn & non dilated ventricles (stage C1)  Monitor until symptomatic  then refer for surgical repair (stages C2 or D) Echo Echocardiogram A: at risk – initial B (mild): q 3-5 years B (moderate): q 1-2 years C1 (asymp. severe): q 6-12 months Valve hemodynamics   C2: Dilating LV  more frequently peak transvalvular velocity or aortic Vmax > 4 m/s or aortic mean gradient > 40 mmHg or Anatomy  valve (open) area of <1.0 cm2 Grading Tx Surgical valve replacement for symptomatic pts or symptomatic severe AS -TAVR if not able to undergo open heart surgery Chronic MR  Vol. overload of LA and LV o Valve repair is curative  Secondary or functional MR – LVH with effect on mitral valve apparatus o Repair of valve does not resolve the underlying condition HTN management   GDMT Use BB w/ caution (d/t filling time  regurg volume & subsequent SV  systolic pressures Open AVR – no transcatheter technique currently approved Percutaneous balloon valvuloplasty is procedure of choice for favorable valve morphology   No significant MR No evidence of LA thrombosis  No indication for mitral annular calcification RHD – prophylaxis for AR  PCN, macrolide, sulfadiazine HR control (slowing to allow diastolic filling of LV)   B-blockers Anticoag w/ vit K antagonist d/t risk of thromboembolism from afib Open or transcatheter procedure – commissurotomy or valve surgery At risk and asymptomatic patients are monitored, may warrant treatment if LV dysfunction evident – C2 Symptomatic patients need intervention – D Preload dependent murmurs include:  AS  HCM  MVP Systolic Murmurs  Occur b/w S1 and S2 o S1 – closed mitral and tricuspid valves o S2 – closed aortic and pulmonic valves  AS, PS, MR, TR, MVP Diastolic Murmurs  Occur after S2 – b/w S2 and S1  MS, PR, AR, TS HEART BLOCKS Type of Block What is it? Key EKG Findings AV BLOCKS 1st degree  Delay in conduction @ AV node or Bundle of His  Common – may be normal finding or sign of pathology  Usually, benign  All beats are conducted through to ventricles 2nd degree  Only some beats are conducted through to ventricles Mobitz type 1 (Wenckebach)   Block WITHIN AV node Transient & benign – rarely progress to 3rd degree       Prolonged PR interval o > 0.2 sec (5 small boxes) 1:1 P wave: QRS Regular rhythm Narrow QRS Ratio of P waves to QRS > 1:1 on rhythm strip Both have irregular rhythm w/ variable P: QRS ratio  Progressive lengthening/prolongation of PR interval w/ each cycle until one QRS is dropped  Ratio of conducted to non-conducted e.g., 4:3 (4th PR impulse blocked after 3 beats conducted) EKG Mobitz type 2 3rd degree (Complete Block)  Block BELOW the AV node in Bundle of  Dropped QRS w/o progressive lengthening of the His PR interval  More serious although less common  Ratio of conducted to non-conducted beats often rd but may progress to 3 degree block variable (2:1, 3:2, etc.)  Pacemaker is tx  Each third P wave is not followed by QRS complex  see example  Block in AV node or lower  P waves & QRS are not associated  No atrial impulses make it through to  Regular rhythm at ventricular pace rate (30-45 bpm  brady) ventricles  Complete dissociation of P waves &  Wide QRS QRS complexes  atria & ventricles are driven by independent pacemakers o Atria contract 60-100 bpm o Ventricles contract own pace – ventricular escape beat  Pacemaker is tx BUNDLE BRANCH BLOCKS Right BBB  Delay in conduction of RBB o Delay in RV depolarization  wide QRS  Pathology in conduction but common in o/w normal beats  Precludes dx of RVH    Wide QRS (> 0.12 sec or 3 small boxes) RSR’ (“rabbit ears”) or tall R waves in V1 & V2 Reciprocal changes in left lateral leads (I, aVL, V5/6) w/ late deep S wave W/o bunny ears Left BBB  Delay in conduction of LBB o Delay in LV depolarization  Almost always reflects pathology – degenerative dz of conduction system or ischemic CAD  Precludes dx of LVH   Wide QRS (> 0.12 sec) Marked prolongation in rise of tall R waves  Broad or notched R waves in lateral leads (I, aVL, V5/6) o ST depression & T wave inversion  Deep S waves in V1/2 (reciprocal changes)  +/- LAD (d/t late LV depolarization)