Heart murmurs. Timing, pressure and bedside decisions
Identify heart murmurs by timing, location and physiology, distinguish valve disease from mimics, and practice evidence-based clinical decisions.
A faint murmur can accompany a dangerous valve lesion. A loud one can come from a small septal defect. First locate the sound in the cardiac cycle, then ask what pressure difference could produce it. Loudness alone cannot answer how sick the valve is.
Place the sound between the valves closing
Find S1 and S2 before naming the murmur. S1 marks mitral and tricuspid closure at the start of ventricular systole. S2 marks aortic and pulmonic closure at its end. A palpable carotid upstroke helps locate systole when the rhythm is difficult to follow. A murmur is sustained sound from disturbed flow, unlike an isolated click, snap or extra heart sound. [2]
Two phases, opposite valve jobs
S1 → S2
Ventricular systole
Exit valves open during ejection, after isovolumic contraction. Aortic or pulmonic stenosis obstructs forward ejection.
Filling valves closed. Mitral or tricuspid regurgitation permits backward flow.
S2 → next S1
Ventricular diastole
Filling valves open after isovolumic relaxation. Mitral or tricuspid stenosis obstructs filling.
Exit valves closed. Aortic or pulmonic regurgitation permits backward flow.
This valve map describes ejection and filling. All valves are closed during the intervening isovolumic phases. It does not include every cause of a murmur. Septal defects and increased flow through normal valves also produce sound. [13]
An ejection murmur builds and fades as ventricular outflow accelerates and decelerates. A holosystolic murmur occupies the interval from S1 to S2 because a pressure difference persists across an incompetent AV valve or a ventricular septal defect. Aortic regurgitation starts after S2 and fades as aortic and ventricular pressures approach one another. A continuous murmur crosses S2 without a silent gap because its driving pressure persists into diastole. [2][3]
Systolic does not mean stenosis. Diastolic does not mean regurgitation. Name the valve and the phase together.
Describe timing, contour, pitch, loudest location, radiation and response to maneuvers. Record intensity on the six-grade systolic scale. Grade 1 is barely audible, 2 is soft but readily heard and 3 is moderately loud without a thrill. Grade 4 adds a palpable thrill. Grade 5 remains audible with only the stethoscope edge touching; grade 6 can be heard with it just off the chest. These descriptors localize a problem; Doppler echocardiography establishes its anatomy and hemodynamic importance. New symptoms, syncope or a diastolic murmur warrant investigation even when the sound is soft. [1][2]
Try it here · Checkpoint 1 of 3
Make your prediction before reading the choices. A first attempt is just a starting point.
Case 9
Show answer and explanations for case 9
A. A large LV-to-RV pressure difference creates a high-velocity jet (Best answer)
A restrictive opening maintains the ventricular pressure difference, which can produce a loud jet despite a small shunt.
B. High pulmonary vascular resistance increases RV pressure toward LV pressure (Why this does not fit)
Rising RV pressure reduces the pressure difference across a VSD and can soften its murmur; loudness does not prove pulmonary hypertension.
C. A large shunt volume produces marked pulmonary overcirculation (Why this does not fit)
The normal chamber sizes and restrictive defect do not indicate a large shunt. Jet velocity can be high even when shunt volume is small.
D. A low-resistance opening permits near-equal ventricular pressures (Why this does not fit)
That describes a nonrestrictive defect. This small restrictive opening maintains a substantial systolic pressure difference.
Takeaway: A loud VSD may be small and restrictive; quantify the shunt and chamber response.
Auscultation sites are listening windows, not the anatomical coordinates of the valves. Begin with the diaphragm, compare all four windows, then use the bell lightly for low-frequency sounds. Pressing the bell firmly filters out the rumble you are trying to hear.
Right second interspace
The aortic window. A harsh ejection murmur transmitted to the neck suggests aortic stenosis. Check carotid amplitude and timing, not just radiation.
Left second interspace
The pulmonic window. Pulmonic stenosis produces an ejection murmur here. A flow murmur with a wide, fixed split S2 suggests an atrial septal defect.
Lower left sternal border
Compare tricuspid regurgitation, tricuspid stenosis and VSD. Inspiration accentuates many right-sided murmurs, especially TR.
Cardiac apex
MR often transmits toward the axilla. Left lateral positioning brings the apex closer to the chest wall and helps expose the low rumble of MS.
For suspected AR, listen along the left sternal border with the patient leaning forward at end-expiration. Aortic root disease can make AR more prominent along the right sternal border. Anatomy and jet direction vary, so an atypical location is a reason to image, not a reason to discard a coherent clinical picture. [2][3]
S2 adds a second layer of information. A soft A2 or delayed aortic closure can accompany severe AS. Fixed splitting suggests persistent right ventricular volume loading from ASD; its systolic sound is increased pulmonic flow, not flow across the atrial opening. S3 can reflect volume loading and S4 reduced compliance, but neither identifies a particular valve lesion alone. [2]
Separate the systolic patterns
Aortic stenosis versus dynamic outflow obstruction
AS narrows the valve opening. Calcific degeneration and bicuspid valve disease are common settings. Its crescendo-decrescendo sound is usually strongest at the right upper sternal border and often transmits to the carotids. A delayed, low-amplitude upstroke is pulsus parvus et tardus. Exertional dyspnea, angina and syncope are warning symptoms, not a required sequence. Late peaking can suggest advanced obstruction, but low output may make a severe lesion quiet. [8]
Obstructive HCM narrows the outflow tract during contraction. Septal and mitral apparatus anatomy allow systolic anterior motion, or SAM, of the mitral leaflet toward the septum. The typical ejection murmur is left parasternal. A smaller ventricular cavity usually increases obstruction. Carotid radiation favors AS, but location alone is insufficient. Echo distinguishes a fixed valve lesion from a dynamic gradient. HCM can exist without obstruction or an audible murmur. [4]
Mitral regurgitation versus mitral valve prolapse
MR classically produces a blowing holosystolic apical murmur with axillary radiation. Primary MR arises from the valve apparatus, including degenerative leaflet disease, rheumatic damage or chordal rupture. Secondary MR arises when ventricular or atrial remodeling prevents otherwise relatively intact leaflets from coapting. Their treatments differ because the source of the leak differs. [7]
MVP often announces itself with a midsystolic click followed by a late systolic murmur. The click marks abrupt tension as prolapsing tissue and chordae become taut. A reduced LV volume makes prolapse occur earlier, lengthening the murmur. With substantial MR, a prolapsing valve can produce holosystolic sound. Do not require the classic click in every case. [2]
Tricuspid regurgitation versus VSD
Both can sound holosystolic at the lower left sternal border. An inspiratory increase, large jugular systolic waves and a pulsatile liver favor TR. Secondary TR may reflect RV dilation from pressure loading or right atrial and annular dilation associated with atrial fibrillation. AF does not automatically mean pulmonary hypertension. Endocarditis and carcinoid disease instead damage the leaflets themselves. [7]
A restrictive VSD can be strikingly loud because the LV-to-RV pressure difference drives a high-velocity jet through a small opening. A large defect with severe pulmonary vascular disease can become quieter as ventricular pressures approach one another. The volume of the sound cannot substitute for shunt assessment. [2]
Soft ejection murmurs can also accompany anemia, fever or pregnancy. Pulmonic stenosis is an obstructive lesion, usually congenital, rather than an innocent flow state. A click, abnormal S2, thrill, symptoms or abnormal pulses should prevent reflex reassurance. [2]
Diastolic and continuous sounds need their own map
Aortic regurgitation
Blood returns from the aorta into the LV after aortic closure, producing an early diastolic decrescendo. Chronic significant AR may widen pulse pressure because increased total stroke volume raises systolic pressure while diastolic runoff lowers diastolic pressure. A bounding, collapsing pulse fits that mechanism. Wide pulse pressure also occurs with arterial stiffness and high-output states. No pulse-pressure cutoff diagnoses AR or establishes its severity. [3][8]
Leaflet injury from endocarditis and dilation of the aortic root are different routes to failed closure. Bicuspid valve disease, heritable aortopathy and, less commonly, syphilitic aortitis belong in the cause list. An Austin Flint rumble is apical diastolic sound in severe AR that can imitate MS without rheumatic commissural fusion. Look for the accompanying AR and confirm the mitral anatomy on echo. [3][5]
Mitral and tricuspid stenosis
MS restricts atrial emptying during diastole, raising left atrial and pulmonary venous pressures. Listen for a low apical rumble and, with sufficiently mobile leaflets, an opening snap. Higher LA pressure can open the valve sooner after A2, shortening the A2-to-snap interval. The snap is abrupt opening tension, not valve closure. Heavily calcified valves may lack a snap. Presystolic accentuation depends on atrial contraction and disappears in AF. [3]
Rheumatic commissural fusion remains a major worldwide cause. Rheumatic damage can cause both stenosis and regurgitation. An apical diastolic rumble plus a new apical holosystolic sound warrants imaging of both opening and coaptation; chronic scarring can impair closure, while new symptoms also require assessment for other causes of MR. Older adults can have degenerative MS from mitral annular calcification, which does not offer fused commissures for a balloon to separate. TS produces a similar filling rumble lower along the left sternal border, often accentuated by inspiration. [7]
Pulmonic regurgitation and PDA
PR is an early diastolic sound in the pulmonic region. In pulmonary hypertension, the high-pressure regurgitant sound is called a Graham Steell murmur. An inspiratory increase and other evidence of right-sided pressure loading help distinguish it from AR. [3]
A PDA connects the aorta and pulmonary artery. When aortic pressure exceeds pulmonary pressure through both phases, the murmur continues across S2, often near the left infraclavicular region. Prematurity is a familiar setting, but sound alone does not establish a need for closure. Echo and clinical effects determine hemodynamic significance. For preterm infants, the 2025 AAP report advises against prophylactic or early medical closure before 2 weeks of age.
Beyond 2 weeks, a hemodynamically significant PDA requires individualized assessment of observation, medication or procedural closure because comparative benefits remain uncertain. This preterm guidance does not define treatment for every term infant or older child. [10]
Try it here · Checkpoint 2 of 3
Make your prediction before reading the choices. A first attempt is just a starting point.
Case 16
Show answer and explanations for case 16
A. Rheumatic mitral stenosis (Why this does not fit)
The mitral anatomy and opening are normal; the accompanying severe AR provides another mechanism for a rumble.
B. Tricuspid stenosis (Why this does not fit)
Its rumble would be lower parasternal and linked to right-sided filling.
C. Mitral valve prolapse (Why this does not fit)
MVP produces systolic rather than diastolic sounds.
D. Austin Flint murmur (Best answer)
Severe AR can disturb mitral inflow and create an apical rumble that resembles MS without anatomical mitral stenosis.
Takeaway: A diastolic apical rumble does not prove anatomical MS when severe AR is present.
Standing or Valsalva strain → less venous return → smaller cavity → greater dynamic obstruction → usually louder ejection murmur.
Mitral valve prolapse
Standing or Valsalva strain → smaller cavity → prolapse begins earlier → click nearer S1 and a longer late systolic murmur.
Both respond to reduced LV volume. The click and murmur contour separate them. A maneuver alone cannot choose the diagnosis.
Squatting increases venous return and systemic resistance. AS commonly becomes louder; obstructive HCM becomes softer; MVP prolapse begins later.
Passive leg raising increases venous return without reproducing every afterload effect of squatting. It commonly reduces dynamic HCM obstruction.
Sustained handgrip primarily raises systemic vascular resistance. MR and AR often intensify, and many VSD murmurs do too. HCM obstruction usually decreases. It is not simply another preload maneuver.
Inspiration increases right-sided venous return. An increase in TR is useful, though severe RV failure can blunt the response.
Valsalva strain reduces filling. Release restores return, so always specify the phase when interpreting a reported response.
Maneuvers are physiologic experiments with variable responses, not infallible diagnostic rules. Avoid using them to provoke symptoms in an unstable patient. Amyl nitrite is historical examination material rather than a required bedside test. Phenylephrine can support pressure in selected monitored patients with dynamic obstruction because it increases vascular resistance without direct beta-agonist stimulation. That is a treatment decision, not a home auscultation maneuver. [2][4]
Turn the sound into a clinical decision
New murmur with shock, pulmonary edema, chest pain or suspected infection needs urgent assessment and echocardiography. Acute severe MR or AR can have a short, soft murmur because pressures equalize rapidly. Chronic bounding pulses and chamber dilation may be absent.
After an MI, acute MR from papillary muscle rupture and a new VSD are competing mechanical complications. Echo identifies the failed structure. Abrupt chest or back pain with new AR raises concern for proximal aortic dissection. A prosthetic mitral valve with newly impaired opening can cause diastolic obstruction from thrombosis or pannus; paravalvular mitral regurgitation is systolic. TTE, TEE and, when needed, CT or fluoroscopy resolve the mechanism. Afebrile presentation or negative cultures alone does not exclude endocarditis. [1][5][9]
Symptoms plus confirmed severe AS → valve-team evaluation for replacement. High-gradient severe AS generally has peak velocity at least 4 m/s or mean gradient at least 40 mmHg, with valve area usually 1.0 cm² or less. A low mean gradient with a small valve area needs flow assessment, measurement review and often stress echo or CT calcium assessment.
Severe primary MR → use symptoms, LV response and repair feasibility. Under ACC/AHA criteria, LVEF 60% or less or LV end-systolic diameter at least 40 mm indicates LV dysfunction even without symptoms. An EF of 58% is not reassuring in severe MR.
Severe secondary MR → optimize heart-failure therapy and resynchronization when indicated, then assess persistent symptoms and suitability for intervention.
Symptomatic severe rheumatic MS, usually valve area at most 1.5 cm² → consider balloon commissurotomy with suitable anatomy, less than moderate MR and no left atrial thrombus. Calcific MS and unfavorable anatomy need a different valve-team strategy.
These are US guideline anchors, not a complete intervention algorithm. The 2025 ESC/EACTS update further emphasizes integrated imaging, individualized timing and Heart Team decisions. TAVR versus surgery depends on anatomy, age, expected longevity, other surgical needs and patient preferences, not age alone. [1][6][7][8]
For stable asymptomatic isolated AS or MR with normal LV function, ACC/AHA echo intervals are generally 3 to 5 years for mild disease, 1 to 2 years for moderate disease and 6 to 12 months for severe disease. New symptoms, mixed disease or ventricular changes shorten that schedule. No medicine has been established to reverse calcific AS. Sports advice requires assessment of lesion severity and exercise response. [1][11]
With Marfan aortic dilation, maximally tolerated beta blocker or ARB therapy is recommended; combination therapy can be reasonable. Root surgery is generally recommended at 5.0 cm and can be appropriate at 4.5 cm with high-risk features. Body size, growth, family history and pregnancy plans can change the decision. A mandatory drug addition based on one diameter is not an adequate plan. [5][12]
For each case, decide in this order. Is the patient unstable? When is the sound? What structure and pressure difference explain it? What test or treatment changes the outcome?
Try it here · Checkpoint 3 of 3
Make your prediction before reading the choices. A first attempt is just a starting point.
Case 23
Show answer and explanations for case 23
A. Every 3 months (Why this does not fit)
This intensity is not routinely needed for stable isolated mild AS.
B. Every year even if symptoms and LV function remain unchanged (Why this does not fit)
Annual imaging may be appropriate with progression or additional disease, but it is more frequent than the routine interval for stable isolated mild AS.
C. Every 3 to 5 years, with earlier reassessment for new symptoms (Best answer)
This is the general interval for stable mild AS with normal LV function; a clinical change overrides the schedule.
D. Every 6 to 12 months (Why this does not fit)
This is the usual range for severe AS with preserved LV function, rather than stable mild disease.
Takeaway: Surveillance follows severity and clinical change, not the murmur label alone.
A narrowed aortic valve explains an ejection murmur, delayed arterial upstroke and symptoms when cardiac output must increase.
B. Mitral regurgitation (Why this does not fit)
MR usually produces an apical holosystolic murmur and does not explain the delayed carotid upstroke.
C. Obstructive hypertrophic cardiomyopathy (Why this does not fit)
Dynamic obstruction can cause exertional symptoms, but the combined late-peaking aortic-area sound and delayed pulse favor valvular AS. Echo distinguishes them.
D. Aortic regurgitation (Why this does not fit)
The characteristic regurgitant sound is after S2; chronic AR more often gives a bounding than a delayed low-amplitude pulse.
Takeaway: Combine timing, radiation and pulse contour before naming AS.
A. Emergency stabilization with urgent cardiac surgical and valve-team assessment (Best answer)
Acute severe MR after MI suggests papillary apparatus failure. Shock and pulmonary edema require urgent definitive assessment despite a soft murmur.
B. Treat pulmonary edema and defer surgical assessment until the infarct has healed (Why this does not fit)
Medical stabilization is necessary, but shock from an acute mechanical valve complication requires urgent surgical assessment rather than waiting for infarct healing.
C. Repeat coronary revascularization alone as definitive treatment for the MR (Why this does not fit)
Coronary management may also be needed, but restoring flow does not repair a ruptured papillary apparatus with a flail leaflet.
D. Use diuresis alone and reassess the need for repair after several days (Why this does not fit)
Diuresis alone cannot correct the structural failure and can be difficult in hypotension. Stabilization and urgent surgical evaluation must occur together.
Takeaway: Acute severe MR is an emergency even without a loud holosystolic sound.
A. Exercise treadmill testing to determine severity from symptom onset (Why this does not fit)
Exercise testing cannot distinguish true severe from pseudo-severe AS as directly in reduced-EF low-flow disease; low-dose dobutamine assesses flow-dependent valve opening.
B. Use the resting mean gradient alone to classify moderate AS (Why this does not fit)
Low stroke volume can lower the gradient despite severe obstruction. Integrating flow and valve measurements is essential.
C. Repeat resting valve-area planimetry without assessing flow (Why this does not fit)
Another resting anatomical estimate alone may not resolve low-flow discordance. Measurement review and flow augmentation or valve calcium assessment address the uncertainty.
D. Review measurements and perform low-dose dobutamine stress echo, with CT calcium assessment if needed (Best answer)
Assessing the valve response to increased flow helps distinguish true severe from pseudo-severe AS; CT is useful when uncertainty remains.
Takeaway: A small valve area plus a low gradient is a question to resolve, not an automatic severity label.
A. Immediate mitral replacement before treating the ventricle (Why this does not fit)
Secondary MR may improve when LV loading and synchrony improve; untreated HF should be addressed first unless an acute emergency changes priorities.
B. Optimize guideline-directed HFrEF therapy and assess CRT eligibility (Best answer)
The leak follows ventricular remodeling, so treating the ventricle is foundational before assessing persistent severe MR for intervention.
C. Proceed directly to transcatheter edge-to-edge repair before optimizing HF therapy (Why this does not fit)
TEER may help selected persistently symptomatic patients after optimized therapy; receiving only a loop diuretic leaves major treatable ventricular dysfunction unaddressed.
D. Increase loop diuresis as the sole long-term treatment (Why this does not fit)
Diuresis can relieve congestion, but it omits disease-modifying HF therapy and assessment for resynchronization that may reduce secondary MR.
Takeaway: Secondary MR demands treatment of its ventricular or atrial driver.
A. Normal flow through a mechanical prosthesis (Why this does not fit)
The new restriction and increased gradient with symptoms are not routine prosthetic findings.
B. Isolated paravalvular mitral regurgitation (Why this does not fit)
A paravalvular leak occurs during systole and does not primarily explain restricted diastolic opening.
C. Prosthetic valve thrombosis causing mitral obstruction (Best answer)
Subtherapeutic anticoagulation and new impaired mechanical opening strongly suggest thrombosis, requiring urgent valve-team imaging and management.
D. Slowly progressive pannus ingrowth restricting the prosthesis (Why this does not fit)
Pannus is a genuine alternative cause of obstruction, but the short course and subtherapeutic anticoagulation favor thrombosis. Multimodality imaging distinguishes them.
Takeaway: New prosthetic obstruction is an urgent imaging and management problem, not a murmur-only diagnosis.
A. Carcinoid leaflet fibrosis (Why this does not fit)
That would produce structural leaflet thickening and restricted retraction, absent here.
B. Ventricular secondary TR from pulmonary hypertension and RV remodeling (Why this does not fit)
That mechanism requires the relevant RV pressure and geometric changes; the stem instead describes predominant RA and annular dilation without significant pulmonary hypertension.
C. Rheumatic commissural fusion (Why this does not fit)
The leaflets are structurally normal without fusion.
D. Atrial secondary TR from annular dilation (Best answer)
Atrial remodeling associated with longstanding AF can widen the annulus and prevent normal leaflets from coapting.
Takeaway: Distinguish atrial secondary TR from RV pressure-loading and primary leaflet disease.
A. Continue individualized aortic surveillance and maximally tolerated beta blocker or ARB therapy; combination may be reasonable (Best answer)
His diameter alone does not mandate surgery or one mandatory drug addition. Growth, body size, family history and tolerance guide care.
B. Schedule root replacement now using the usual 4.5-cm high-risk threshold (Why this does not fit)
He is below that threshold and lacks the listed high-risk features. Even the lower threshold is conditional; surveillance and individualized medical treatment fit this stem.
C. Stop aortic medication because moderate AR has preserved EF (Why this does not fit)
Marfan aortic therapy targets aortic risk, not only LV systolic dysfunction. Preserved EF does not remove its indication.
D. Base follow-up only on the murmur and omit serial aortic imaging (Why this does not fit)
Aortic enlargement may progress without a useful change in murmur. Serial measurements and clinical risk assessment remain necessary.
Takeaway: Marfan management integrates aortic risk and medication tolerance rather than one diameter alone.
A. Isolated leaflet injury explains the AR; assess valve replacement without addressing the aorta (Why this does not fit)
Leaflet pathology can cause AR, but a 6.1-cm root also requires aortic surgical evaluation. A valve-only plan misses major aortic disease.
B. Root enlargement impairs leaflet coaptation; refer for aortic and valve surgical assessment (Best answer)
Aortic enlargement can separate leaflet coaptation. A root this large and severe AR with LV dysfunction warrant specialist intervention planning.
C. Root dilation explains AR; defer surgery until symptoms occur at rest (Why this does not fit)
He is already symptomatic with severe AR, reduced EF and marked root dilation. Rest symptoms are not required for surgical assessment.
D. Use medical afterload reduction as definitive treatment for the root aneurysm (Why this does not fit)
Blood-pressure treatment can be appropriate, but it does not replace aortic and valve surgical assessment at this diameter and degree of valve dysfunction.
Takeaway: Root pathology can cause AR without primary leaflet destruction.
