Set yourself up to hear and see

• Explain the examination and obtain permission; provide appropriate exposure, draping and chaperone support. Warm hands and stethoscope; reduce background noise.
• Use tangential light for neck veins. Change the bed angle until the venous top is visible. Listen on skin, with the patient supine, left lateral and sitting forward as tolerated.
• Describe what you observe before naming the disease. Repeat after a meaningful change in position, rhythm, breathing or treatment.
• A stethoscope examines sounds; echocardiography quantifies anatomy and hemodynamics. Their roles are complementary.

History before the eponym

• Ask about valve disease, rheumatic fever, congenital repairs, prostheses, coronary disease, prior radiation and chemotherapy, pregnancy, infection, injection drug exposure and implanted devices.
• Family history: premature coronary disease, cardiomyopathy, sudden unexplained death, drowning, unexplained vehicle crashes, pacemakers at a young age, aortopathy. Ask age and relationship.
• Review diuretics, vasodilators, beta-blockers, anticoagulants, adherence, OTC decongestants, supplements and substances; these change the examination.
• Record function concretely: “previously two flights without stopping; now breathless crossing a room” is more useful than an unsupported NYHA class.

Both photographs are source-described Osler lesions. Pain cannot be inferred from an image; no photograph here is presented as a definitive Janeway lesion.

The 2023 Duke-ISCVID criteria explicitly integrate modern microbiology and imaging. Skin lesions are pieces of that assessment; they do not substitute for it.

Measure legs when coarctation or relevant vascular disease is suspected; interpret arm–leg comparisons with the correct cuff and technique. A pulse deficit or arm BP difference in abrupt severe chest/back pain supports urgent aortic assessment but is often absent.

Original schematic: contour is not a calibrated arterial tracing.

Count a full minute when irregular. Compare simultaneous apical and radial rates for a pulse deficit: some ventricular beats may not produce a palpable pulse, particularly with AF or ectopy. Confirm rhythm with ECG. Compare bilateral radial, femoral and pedal pulses; new painful, pale, cool or neurologically impaired limbs require urgent vascular assessment.

Example: 120 − 108 = 12 mmHg; thresholds are illustrative, not a patient measurement.

Manual cuff technique

• Use quiet spontaneous breathing, a correctly sized cuff and a slow controlled deflation. Observe respiration directly. Do not ask for exaggerated breaths.
• Inflate above systolic pressure. Record the first pressure at which Korotkoff sounds occur only during expiration.
• Continue deflating until sounds are audible throughout inspiration and expiration. The difference between these pressures estimates pulsus paradoxus.
• Repeat if respiration, rhythm or sounds are irregular. Document technique, respiratory state and the actual difference.

Mechanism in tamponade: constrained total cardiac volume amplifies ventricular interdependence. Inspiratory RV filling competes with LV filling, reducing LV stroke volume. The “paradox” historically refers to an inspiratory arterial pulse that may disappear despite continuing heartbeats.

It may be absent or less prominent with regional tamponade, high LV filling pressures, severe AR, ASD or positive-pressure ventilation. Arrhythmia, tachypnea and mechanical ventilation make conventional cuff interpretation difficult. An absent sign does not exclude tamponade.

A routine automated BP cuff does not reliably measure pulsus paradoxus. Respiratory variation on a pulse-ox plethysmogram can raise suspicion but does not replace paired manual cuff pressures or a properly interpreted arterial tracing.

Use the vertical distance above the sternal angle; the conventional +5 cm is an estimate of the atrial reference.

• Begin semi-recumbent, often 30–45°, head supported and slightly turned left. Avoid excessive rotation or neck muscle tension. Use tangential light over the right neck.
• Identify the internal jugular oscillation; inspect between/around sternocleidomastoid heads. If too high, sit the patient up; if too low, lower the head of bed. You cannot declare “normal JVP” when the top was never seen.
• At quiet end-expiration, measure vertical height from the sternal angle to the highest venous oscillation. Document height and bed angle.
• Conventionally add about 5 cm to estimate pressure above the right atrium in cm H₂O; the distance varies with posture and body habitus. To convert cm H₂O to mmHg, divide by about 1.36.

A venous top roughly ≤3–4 cm above the sternal angle is commonly considered within the normal bedside range. Avoid false precision. Obesity, tachypnea, tricuspid disease and positive-pressure ventilation complicate assessment. The external jugular can help locate a column but local valves/obstruction may mislead.

With very large a or v waves, describe peak height separately from estimated mean venous level. JVP estimates right atrial pressure. Right- and left-sided pressures can diverge, so a normal JVP does not exclude elevated left-sided filling pressure.

Schematic venous timing; the c wave is often not separately visible at the bedside.

Compare timing as well as amplitude. These drawings illustrate patterns rather than diagnostic cutoffs.

Abdominojugular test (hepatojugular reflux)

• First identify the jugular venous top; adjust bed angle to keep it in view. Ask the patient to breathe normally with an open glottis.
• Apply firm, steady mid-abdominal or right-upper-quadrant pressure for about 10–15 seconds. Stop for discomfort; avoid a painful abdomen or a site of recent surgery.
• A brief rise that settles is expected. A sustained rise around ≥3 cm for the duration of pressure is commonly considered positive; published protocols use slightly different cutoffs. Watch the column fall after release.
• Document duration and approximate rise. Straining, breath-holding, loss of the visible column and local venous obstruction invalidate the inference.

Kussmaul sign

The JVP rises, or fails to fall appropriately, during inspiration. Suspect impaired right-heart filling accommodation: constrictive pericarditis, restrictive cardiomyopathy, RV infarction/failure or tricuspid stenosis. Interpret while the patient breathes spontaneously.

A double apical impulse can reflect a palpable presystolic atrial component in a stiff LV; HCM may produce a prominent double or triple impulse. Obesity, emphysema and chest-wall deformity reduce sensitivity. A nonpalpable apex is a limited examination, not evidence of normal LV size.

Patient right is viewer left. Listen beyond the standard windows when sound radiates.

Identify S1/S2 before searching for disease. The carotid upstroke follows S1; S1-to-S2 is systole. Tachycardia can make silence intervals unreliable. Avoid prolonged breath-holding in dyspnea; a few quiet end-expiratory beats are sufficient.

The diagram illustrates timing. Component loudness and audibility also depend on the chest and valve state.

Diastolic intensity: a common four-grade convention is 1/4 faint, 2/4 readily audible, 3/4 loud and 4/4 very loud. Some clinicians use a six-grade scale instead. State the denominator and describe the sound; do not assume that 4/4 and 4/6 mean the same thing.

The complete murmur sentence

• Time: early/mid/late/holosystolic; early/mid/late diastolic; continuous across S2.
• Shape, pitch and quality: ejection diamond, plateau, decrescendo, rumble, musical, blowing or machinery-like.
• Location, radiation, respiratory/positional response, maneuver response, associated sounds and pulse.

Read systolic shape with the clinical examination; peak timing is not an echo severity grade.

Gallavardin phenomenon: the higher-frequency component of an AS murmur may be prominent at the apex and mimic MR. Time the ejection shape and correlate the basal murmur, carotids and A2. A late-peaking murmur can suggest more severe obstruction but cannot determine valve area or gradient.

Smaller LV cavity tends to increase obstructive HCM intensity and move the MVP click earlier.

Isometric handgrip increases afterload and typically reduces an obstruction murmur while increasing regurgitant flow murmurs. In MVP, the relation of click timing, cavity volume and associated MR is more nuanced than a single “louder/softer” rule.

MR versus AS at the apex

• MR is typically holosystolic and plateau-like; AS has a crescendo–decrescendo envelope beginning after S1. Severe AS may extend late in systole and obscure A2; do not require an audible terminal gap.
• Search the base and neck, palpate the carotid and characterize A2. Gallavardin radiation can create two seemingly different sounds from one aortic lesion.
• Echo defines primary versus secondary mechanism, regurgitant burden and chamber response.

A restrictive muscular VSD may have a short systolic murmur if the defect functionally narrows/closes during contraction. Large shunts can add an apical mid-diastolic flow rumble. With severe pulmonary vascular disease, the murmur can attenuate as the LV–RV pressure difference falls.

For a pulsatile liver, distinguish expansile systolic pulsation from transmitted aortic movement. Tender hepatomegaly indicates congestion in context but has a broad differential.

Supravalvar/branch pulmonary artery stenosis may be best heard in the axillae or posterior chest. Congenital repairs and conduits change the sound map. Ask which operation was performed and listen over the actual anatomy.

In cyanotic congenital disease, murmur intensity may fall as effective pulmonary flow falls. A quieter sound in a deteriorating patient is not improvement. Adult congenital anatomy should be reconciled with prior imaging and operative history.

Abrupt chest/back pain plus new AR raises concern for a proximal aortic syndrome. Acute endocarditis-related AR is another emergency phenotype. Bedside findings can trigger urgent imaging; their absence cannot exclude these conditions.

Rheumatic commissural fusion and degenerative mitral annular calcification are different mechanisms. The classic snap-and-rumble examination is most closely tied to a mobile rheumatic valve; do not transplant its acoustic severity rules to every calcific lesion.

If safe, a modest increase in flow can accentuate the rumble, but exertional provocation is inappropriate in an unstable or markedly symptomatic patient. Position and focused listening are usually the practical first maneuvers.

A murmur after congenital pulmonary-valve repair or replacement must be judged against baseline anatomy, prosthesis type and prior imaging. The stethoscope cannot distinguish every conduit obstruction, paravalvular leak or regurgitant mechanism.

Pericardial rubs, pleural rubs, breath sounds and venous hums can all mimic valve disease. Move the stethoscope, time with the pulse and respiration, and use safe position changes. A prosthetic valve click is a discrete sound rather than a murmur.

Use supported positions and stop for dyspnea, pain or presyncope. Pharmacologic amyl-nitrite maneuvers are historical/specialized and are not part of this routine bedside guide. Never trade patient stability for a more memorable sound.

Normal phases versus an illustrative square-wave response. This is arterial BP over time, not JVP or ventricular diastolic pressure.

A classic bedside sphygmomanometer method holds cuff pressure slightly above baseline systolic pressure while the patient performs standardized strain; persistence of Korotkoff sounds during strain suggests maintained pressure. Beat-to-beat BP is much clearer for waveform teaching. Unstandardized effort or a routine cycling oscillometric cuff cannot reliably resolve all phases.

This is an advanced physiologic observation for a stable, cooperative patient, not an invitation to provoke symptoms in shock, severe symptomatic valve obstruction or a patient unable to strain safely. Autonomic dysfunction, medications, strain pressure and volume status alter the response.

The square-root sign is an invasive ventricular diastolic pressure pattern; restriction can share it.

Early rapid filling followed by abrupt restraint produces the dip-and-plateau contour. Equalized diastolic pressures and this shape can overlap with restriction. Respiratory LV/RV systolic discordance during properly obtained simultaneous catheterization is more discriminating for constrictive physiology. Effusive-constrictive disease combines features.

Congestion and perfusion are separate bedside axes; the scheme is descriptive, not a treatment algorithm.

The guide includes deliberately illustrative recordings and drawings as well as clinical photographs. Synthetic sounds and schematic waveforms teach timing and shape; they cannot reproduce the full acoustic or hemodynamic range encountered at the bedside.

First identify S1 and S2. Then locate the added sound: systolic or diastolic, continuous or discrete? Describe what you hear before opening the teaching note. A recording is a selected example; it cannot establish diagnostic accuracy or severity for a new patient.

Further free listening

University of Washington: heart sounds and murmurs provides additional freely accessible examples of S3, S4, mitral regurgitation, mitral stenosis, aortic regurgitation and pericardial rub. Stanford Medicine 25: cardiac examination adds bedside technique demonstrations. These are links to the original teaching sites; their material is not relicensed by this guide.

A copy-ready descriptive structure

Example: “Comfortable at rest. Regular pulse with delayed carotid upstroke. JVP 3 cm above sternal angle at 45°. Sustained apical impulse; 3/6 late-peaking systolic ejection murmur at RUSB radiating to both carotids, soft A2, no palpable thrill. Findings raise concern for AS; TTE requested.” This is a constructed documentation example, not a real patient record.

Jugular or carotid?

From an image to a bedside measurement

Locate pulsation in real time, distinguish venous from arterial motion, adjust inclination until the top is visible, measure vertically above the sternal angle, and report the reference and respiratory state. Neck-vessel prominence alone does not quantify right atrial pressure.

Severe TR may make the external jugular visibly pulsatile. Infer the systolic c-v pattern only after timing it against S1/S2 or the carotid. A single still image cannot establish that timing.

Eight heart-sound excerpts

Vladimir Kudriavtsev, Vladimir Polyshchuk and Douglas L. Roy. Heart energy signature spectrogram for cardiovascular diagnosis. BioMedical Engineering OnLine 6, 16 (2007). Unmodified publisher WAV supplements 1–3 and 5–9. License CC BY 2.0: https://creativecommons.org/licenses/by/2.0/. Source: https://link.springer.com/article/10.1186/1475-925X-6-16. File-specific titles, supplement numbers and checksums are in the linked media manifest. Simulated S2 splitting is explicitly identified.

Added photograph: Steinberg thumb-sign sequence, Rollcloud, CC0 1.0. Source and license are linked beside the image in chapter 31.
12 original schematics: Cardiology Guide, 2026. Chapter 10 adds an original animated timing cursor to the normal JVP schematic. Available under MIT or CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/); see full original-diagram license. No third-party photograph is relicensed under MIT. CC BY-SA applies to the respective source image and adaptations, not automatically to the whole guide.