mixed frequency sound
mixed frequency sound acoustics physics explanation
| Term | Meaning |
|---|---|
| Fundamental frequency | The lowest frequency in a complex sound; determines the perceived pitch |
| Harmonics / Overtones | Integer multiples of the fundamental (2f, 3f, 4f...) |
| Timbre | The quality/character of a sound determined by the mix of frequencies present |
| Spectrum | A plot of all frequencies and their amplitudes present in a sound |
| Fourier analysis | The mathematical technique used to decompose any complex sound into its individual frequency components |
ejection systolic murmur
ejection systolic murmur aortic stenosis heart sound diagram

This medical comparison chart and diagram illustrate the distribution patterns of systolic murmurs in isolated Aortic Stenosis (AS) and Mitral Regurgitation (MR) based on disease severity. The upper section focuses on Aortic Velocity (n=247), showing a progression of murmur localization as peak velocity increases from 1.3 to 4.0 m/sec. Visualized patterns include isolated base (cyan), isolated apical (green), small apical-base (purple), and broad apical-base (red). As AS severity increases, the murmur evolves from localized base or apex patterns to a broad apical-base distribution. The lower section depicts Mitral Regurgitation patterns (n=174) graded from trace to severe. Murmur patterns are categorized as isolated apical (green), broad apical (yellow), and broad apical-base (red). The bar graphs quantify the percentage of patients exhibiting each pattern at different severity levels, highlighting that severe cases of both AS and MR are characterized by broader, more extensive apical-base murmur distributions on the chest wall.

This diagnostic image displays a four-panel comparative analysis of cardiac acoustics in an 8-year-old patient with aortic stenosis. The top two panels, PCG1 and PCG2, show consecutive phonocardiogram waveforms plotted as amplitude over a 0.7-second interval. The third panel, labeled 'Murmurgram', illustrates the result of a signal subtraction method used to isolate abnormal heart sounds. The fourth panel is a Color Spectrogram (CSP), which provides a time-frequency analysis of the cardiac cycle. The CSP shows frequency components on the y-axis (kHz) and time on the x-axis, with color intensity indicating amplitude. Notably, the murmurgram demonstrates a non-flat, high-amplitude signal between S1 and S2, indicating a systolic murmur. The corresponding CSP highlights a concentration of frequency components extending up to approximately 400 Hz (0.4 kHz), peaking in mid-systole (0.1–0.2 seconds). This visual data characterizes the harsh mid-systolic murmur typical of aortic stenosis, localized between the first and second heart sounds.

This composite educational image illustrates the classification of patients with aortic stenosis based on Cardiac Magnetic Resonance (CMR) findings. Section A features a scatter plot correlating Left Ventricular Ejection Fraction (LVEF, %) on the y-axis with the presence or absence of Late Gadolinium Enhancement (LGE) on the x-axis. A horizontal threshold at 50% LVEF divides the cohort into normal and depressed systolic function. Sections B, C, and D provide representative short-axis CMR images in two rows: the top row shows cine images (anatomic structure) and the bottom row shows corresponding LGE-CMR images (tissue characterization). Panel B (Group 1) displays normal LV size and no LGE. Panel C (Group 2) shows normal LV size but mid-wall/patchy hyperintensities indicative of replacement fibrosis (LGE positive). Panel D (Group 3) demonstrates a dilated left ventricle with both depressed LVEF and extensive, bright signal areas representing significant myocardial LGE. This material is used to teach subclinical adverse LV remodeling and the prognostic value of myocardial fibrosis in valvular heart disease.

This composite diagnostic image features three panels representing a multimodal echocardiographic assessment of a patient with severe aortic stenosis. The left panel shows a grayscale 2D echocardiogram focusing on the aortic valve, demonstrating significant calcification and structural thickening. The central panel is an apical four-chamber view of the heart with an annotated Left Ventricular Ejection Fraction (LVEF) of 56%, indicating preserved systolic function. The right panel is a color-coded 'bullseye' polar plot illustrating speckle-tracking strain analysis. This plot maps regional longitudinal strain across segments of the left ventricle, including anterior (ANT), septal (SEPT), lateral (LAT), and posterior (POST) walls. A numerical value of -13.2% for Left Ventricular Global Longitudinal Strain (LVGLS) is displayed above the plot. The varying shades of red in the bullseye segments represent localized strain impairment, highlighting the clinical concept that global longitudinal strain can be significantly reduced even when the ejection fraction remains within normal limits. This visual is intended for cardiology and radiology education focusing on hemodynamic assessment and valvular heart disease.

This diagnostic image consists of two axial computerized tomography (CT) scans and a supporting schematic diagram illustrating a rare unicuspid aortic valve (UAV). The CT images represent the heart during diastole (left) and systole (right). In the systolic frame, the aortic valve is seen as a single, lunar-shaped (teardrop) leaflet with only one visible commissure attached to the aortic wall. This morphology results in a significantly restricted, eccentric orifice area, which is a classic visual finding of severe valvular stenosis. Key anatomical landmarks are labeled, including the right ventricular outflow tract (RVOT) and the left atrium (LA). A line diagram to the right summarizes the single-commissure 'uncommissural' architecture. This visual material is used in cardiovascular radiology and cardiology education to differentiate congenital unicuspid variants from more common bicuspid or tricuspid aortic valve morphologies and to demonstrate the anatomical basis for early-onset aortic stenosis.

This physiological waveform diagram displays a simultaneous recording of three cardiac parameters used for assessing cardiovascular hemodynamics. The top trace is an Electrocardiogram (ECG) showing standard QRS complexes representing ventricular depolarization. The middle trace is a Phonocardiogram (PCG) capturing acoustic vibrations of heart sounds, specifically the S1 and S2 sounds. The bottom trace is a Brachial Pulse Volume Waveform (bPVW) illustrating the peripheral arterial pressure pulse. Vertical markers indicate temporal relationships between these signals to calculate systolic time intervals. The 'QS2' interval is marked from the onset of the QRS complex on the ECG to the aortic component of the second heart sound on the PCG, representing the total electromechanical systolic interval. The 'bET' (Brachial Ejection Time) is delineated on the bPVW from the waveform foot to the dicrotic notch. An annotated formula shows the calculation of the Brachial Pre-ejection Period (bPEP) as the difference between QS2 and bET (bPEP = QS2 - bET). This diagram is an educational tool for understanding the non-invasive assessment of cardiac systolic function and arterial stiffness.
| Cause | Key Features |
|---|---|
| Aortic stenosis (AS) | Harsh, late-peaking, heard best at aortic area (2nd right ICS), radiates to carotids |
| Bicuspid aortic valve | Often quieter over precordium, best at suprasternal notch |
| Hypertrophic obstructive cardiomyopathy (HOCM) | Harsh murmur at left sternal border, crescendo-decrescendo, increases with Valsalva/standing |
| Aortic sclerosis | Same position as AS but no gradient; softer |
| High-flow states | Anemia, thyrotoxicosis, pregnancy - flow murmur without stenosis |
| Supravalvular/subvalvular AS | Rare; similar murmur profile |
| Cause | Key Features |
|---|---|
| Pulmonary stenosis (PS) | Best heard at left sternal border (pulmonic area, 2nd left ICS); radiates to left clavicle; associated with ejection click |
| Atrial septal defect (ASD) | Pulmonary ejection murmur from increased flow across pulmonary valve + fixed split S2 |
| Pulmonary artery stenosis | Murmur throughout the chest |

| Grade | Description |
|---|---|
| I | Barely audible (requires quiet room, experienced listener) |
| II | Soft but immediately audible |
| III | Moderately loud, no thrill |
| IV | Loud, associated with thrill |
| V | Very loud, thrill, audible with stethoscope edge |
| VI | Audible without stethoscope |
| Feature | Ejection Systolic | Pansystolic |
|---|---|---|
| Start | After S1 (gap present) | At S1 (no gap) |
| End | Before S2 | At or beyond S2 |
| Shape | Crescendo-decrescendo | Plateau/uniform |
| Causes | AS, PS, HOCM, flow states | MR, TR, VSD |
| Maneuver | AS/PS | HOCM |
|---|---|---|
| Valsalva (strain phase) | Decreases | Increases |
| Standing | Decreases | Increases |
| Squatting | Increases | Decreases |
| Amyl nitrite | Increases | Increases |
| Handgrip | Decreases | Decreases |
valve apparatus
mitral valve apparatus anatomy leaflets chordae tendineae papillary muscles diagram

This dual-panel educational material illustrates the normal anatomy of the mitral valve apparatus within the left ventricle. Panel A is an anatomical diagram in a vertical long-axis projection showing the anterolateral (AL) and posteromedial (PM) papillary muscles (green) originating from the ventricular wall. Blue lines represent chordae tendineae connecting the papillary muscles to the mitral valve leaflets (yellow). Panel B is an intraoperative clinical photograph providing a direct surgical view of these structures. It clearly demonstrates the fleshy heads of the anterolateral (AL) and posteromedial (PM) papillary muscles. Multiple thin, white fibrous strands—the chordae tendineae (indicated by black arrows)—extend from the papillary muscle heads to insert into the anterior (A) and posterior (P) mitral valve leaflets. The image highlights the mechanical tethering system essential for valvular competence during the cardiac cycle, specifically demonstrating how both papillary muscles contribute chordae to both leaflets to prevent valve prolapse into the left atrium during systole.

This medical illustration depicts a mitral valve repair utilizing artificial chordae tendineae (neochordae). The diagram shows a surgical view of the subvalvular apparatus, featuring the papillary muscles and mitral valve leaflets. Three sets of artificial chordal loops, represented as thin blue-grey lines made of PTFE, are anchored to the papillary muscle using white felt pledgets. The distal ends of these loops are sutured to the atrial aspect of the posterior mitral valve leaflet at the line of coaptation, visible as distinct black knots. Adjacent to the artificial cords, natural chordae tendineae are shown as thin, translucent string-like structures connecting the opposite leaflet to the papillary muscle. This illustration demonstrates a chordal replacement technique designed to treat mitral regurgitation—specifically for conditions like Barlow’s disease or fibroelastic deficiency—by restoring leaflet support and proper coaptation depth without the need for tissue resection.

This composite image illustrates the anatomy of a parachute mitral valve (PMV) through a schematic diagram and a diagnostic cardiac MRI. Panel A is an anatomical diagram showing the characteristic single papillary muscle (labeled 'P') within the left ventricle, from which all chordae tendineae (blue) originate. This configuration forces the mitral valve leaflets (yellow) into a restricted, funnel-like shape resembling a parachute. Panel B shows a four-chamber steady-state free precession (SSFP) cardiac MRI sequence. Red arrows indicate the convergent attachment of multiple chordae tendineae to a solitary, centrally located papillary muscle, rather than the typical distribution between anterolateral and posteromedial muscles. This rare congenital anomaly is a significant finding in pediatric and adult cardiology, often associated with mitral stenosis due to reduced leaflet mobility and restricted valve orifice area. It may also present as part of the Shone complex. The image serves as an educational tool for identifying atypical subvalvular apparatus morphology in congenital heart disease.

This clinical photograph of a porcine cardiac specimen (used as a model for human anatomy) illustrates the structural components of the mitral valve apparatus. The image highlights the anterior mitral valve leaflet and its associated chordae tendineae and papillary muscles. Key anatomical structures are labeled: the anterior leaflet appears as a translucent, pinkish-white fibrous sheet; the robust, reddish-purple papillary muscles serve as the inferior anchoring point. The description identifies three specific types of chordae tendineae based on their insertion points: the anterior marginal chord (attaching to the leaflet edge), the anterior basal chord (attaching to the leaflet base), and the anterior strut chord (thicker support structures attaching to the leaflet body). This specimen demonstrates the complex spatial relationship between the ventricular wall and the valvular leaflets, essential for understanding cardiac mechanics, valvular competence, and surgical repair techniques in cardiology and cardiothoracic surgery.

Anatomical photograph of a dissected human mitral valve apparatus, illustrating the subvalvular structures. The image features a detailed view of the anterior and posterior papillary muscles and their respective heads; specifically, the anterior papillary muscle is shown with two heads, while the posterior papillary muscle exhibits three heads. Multiple 'principal chordae' tendineae are clearly visible as fibrous cords connecting the papillary muscle heads to the mitral valve leaflets. The 'annulus fibrosus' (the fibrous ring of the valve) and the 'border of the mitral valve' are labeled at the superior portion of the specimen. A blue line indicates the 'measurement of chordae,' demonstrating the methodology for quantifying subvalvular dimensions. This clinical image is primarily used for anatomical study, surgical planning for mitral valve repair, and understanding the complex morphology of the left ventricular outflow tract and valvular support system.

A three-panel anatomical diagram (A-C) illustrating the step-by-step surgical implantation of artificial chordae using the CardioMech system for mitral valve repair. (A) Shows a transcatheter delivery system (blue catheter with a silver metallic distal tip) approaching the posterior mitral leaflet (PML) to perform a puncture. (B) Illustrates the deployment and anchoring of a blue ePTFE artificial chord into the papillary muscle within the left ventricle. (C) Depicts the final stage where the neochorda is tensioned to adjust the leaflet's position and ensure proper coaptation. The diagram highlights the interaction between the surgical instruments, the thin blue artificial chordae, and the cardiac anatomy, including the mitral leaflets and papillary muscles. This educational visual is designed to demonstrate minimally invasive, beating-heart techniques for correcting mitral regurgitation by replacing ruptured or elongated natural chordae tendineae.

| Feature | Anterior Leaflet | Posterior Leaflet |
|---|---|---|
| Annular attachment | ~1/3 of annular circumference | ~2/3 of annular circumference |
| Length | Longer | Shorter |
| Scallops | None | 3 scallops: P1 (lateral), P2 (central), P3 (medial) |
| Type | Insertion | Function |
|---|---|---|
| Primary (marginal) | Free edge of leaflet | Prevent prolapse |
| Secondary (strut chords) | Ventricular surface, body of leaflet | Structural support; maintain LV geometry |
| Tertiary (basal) | Base of posterior leaflet only | Anchor the leaflet base |
| Anterolateral (AL) | Posteromedial (PM) | |
|---|---|---|
| Heads | Usually 1 body/head | 2 or more bodies/heads |
| Blood supply | Dual - left anterior descending + circumflex (or marginal branches of LCA) | Single - terminal branch of posterior descending artery (from RCA or circumflex) |
| Vulnerability to ischemia | Lower (dual supply) | Higher - more commonly ruptured in MI |

factors affecting intensity of S1
| Factor | Mechanism | Clinical Example |
|---|---|---|
| Short PR interval | Mitral valve is wide open when systole begins; has to snap shut rapidly with great excursion, generating forceful vibration | WPW/pre-excitation, sinus tachycardia |
| Tachycardia / hyperdynamic states | Short PR + high contractility; most common cause of a loud S1 in clinical practice | Fever, anaemia, thyrotoxicosis, exercise, anxiety |
| Mitral stenosis (pliable leaflets) | Leaflets are held open throughout diastole by the pressure gradient; they are still held wide apart when systole begins, snapping shut with great force. The "tapping" S1 is often the only early sign of rheumatic involvement | Early/mild rheumatic MS with mobile, non-calcified leaflets |
| High-output states | Increased stroke volume and contractility | Pregnancy (S1 louder + more widely split in ~90% of pregnant women), anaemia, thyrotoxicosis |
| Ebstein's anomaly | Exceptionally large, sail-like anterior tricuspid leaflet produces a loud T1 component (an exception - most S1 abnormalities affect only M1) | Ebstein's anomaly |
| Factor | Mechanism | Clinical Example |
|---|---|---|
| Prolonged PR interval (1st degree AV block) | Mitral valve partially closes during the long PR interval before ventricular systole; by the time systole begins, the valve is nearly shut and the excursion is minimal | 1st degree heart block, digoxin toxicity |
| Long R-R intervals | Same mechanism - diastole is prolonged, valve drifts towards closure | Atrial fibrillation (long cycles have soft S1; short cycles have loud S1 - hence variable intensity S1 in AF) |
| Mitral stenosis (calcified, immobile leaflets) | Severely calcified/fibrotic valve cannot move freely; cannot generate forceful vibration on closure | Late/severe calcific rheumatic MS |
| LV systolic dysfunction / cardiomyopathy | Reduced contractility = less forceful valve closure | Dilated cardiomyopathy, acute MI |
| Acute severe aortic regurgitation | Markedly elevated LV end-diastolic pressure causes premature closure of the mitral valve during diastole; valve is nearly shut before S1 | Acute AR (e.g. endocarditis, aortic dissection) |
| Mitral regurgitation (primary) | Damaged, poorly coapting leaflets that cannot generate a normal closing force | Flail mitral leaflet, rheumatic MR |
| Beta-blocker therapy | Reduces contractility |
| Condition | Reason |
|---|---|
| Atrial fibrillation | Variable R-R intervals: short cycles (short diastole, valve open wide) → loud S1; long cycles (long diastole, valve partially closed) → soft S1 |
| Complete heart block (3rd degree AV block) | PR interval changes continuously as P waves "march through" - the S1 varies in intensity with each beat as the AV relationship changes; cannon a-waves in JVP are the jugular counterpart |
| Ventricular tachycardia / AV dissociation | Same principle - PR interval varies with each beat |
| S1 | Key Causes |
|---|---|
| Loud | Short PR, tachycardia/hyperdynamic state, mitral stenosis (pliable), Ebstein's anomaly |
| Soft | Long PR (1st degree block), cardiomyopathy/LV dysfunction, calcific MS, acute AR, beta-blockers |
| Variable | Atrial fibrillation, complete AV block, VT with AV dissociation |