• Cardiac preset: the screen marker is on the right of the screen (echocardiography convention).
• Abdominal / radiology preset: the screen marker is on the left.
• If you scan the heart with an abdominal preset, the image comes out mirrored left to right. Either switch to the cardiac preset, or rotate the probe 180° from the positions on this page. Don't do both.
• On this page, all probe-marker directions assume the cardiac preset: PLAX to the right shoulder (about 10 o'clock); PSAX to the left shoulder (about 2 o'clock); A4C and subcostal 4C to the patient's left (3 o'clock); IVC to the head (12 o'clock).

• Depth: start deep (about 16–20 cm) so you can see the descending aorta and any pleural fluid behind the heart. Then reduce depth until the heart fills about two-thirds of the sector.
• Gain: blood in the cavities should be black. Too much gain fills the cavities with speckle and can mimic thrombus or smoke. Too little loses endocardial borders and the edges of an effusion.
• Focus / sector width: narrow the sector to raise the frame rate when you are judging motion.
• Cine loop: always review the last few beats. Freeze to measure, then scroll.
• ECG lead: if the machine has one, attach it. Tamponade timing and diastolic measurements depend on it.

Pencil grip, with the heel of the hand resting on the chest to stop drift. Use small movements. The four movements: slide (move along the skin), rotate (turn about the probe's long axis), tilt (rock towards or away from the marker, in the imaging plane), fan (angle across the imaging plane).

Left sternal edge, 3rd–5th intercostal space; left lateral decubitus if possible.

• PLAX: marker to the right shoulder.
• PSAX: from PLAX, rotate 90° clockwise so the marker points to the left shoulder.

Point of maximal impulse, usually 5th intercostal space at about the anterior axillary line; further lateral in a big heart or in left lateral decubitus.

• A4C: marker to the patient's left, beam aimed at the right shoulder.

Just below the xiphoid; supine; knees flexed relaxes the abdomen.

• Subcostal 4-chamber: probe almost flat on the abdomen, marker to the patient's left, aimed at the left shoulder, looking through the liver.
• IVC long axis: from the subcostal 4C, centre the RA, then rotate anticlockwise until the marker points to the head (12 o'clock). Follow the IVC into the RA.

• Ventilated, COPD or obese patients: parasternal and apical windows are often poor. The subcostal window is often the best and is reachable without moving the patient.
• Post-laparotomy, distended or painful abdomen: subcostal is limited, so go parasternal.
• Breath-hold at end-expiration, or a brief end-expiratory pause on the ventilator, if safe.

Chest wall → RV / RVOT → interventricular septum → LV cavity → posterior LV wall → pericardium (bright line) → descending thoracic aorta in cross-section, behind the LA. On screen-right: the aortic root with the aortic valve, and the LA beneath it. The anterior mitral leaflet is continuous with the posterior aortic root.

• LV systolic function: eyeball, EPSS, fractional shortening.
• Pericardial versus pleural effusion. The descending aorta is the landmark.
• Gross aortic and mitral valve red flags.
• RVOT size: compare the RVOT with the aortic root. In normal hearts they are similar.

Aortic valve level (the 'Mercedes sign', with RVOT and pulmonary valve) → mitral valve level (the 'fish mouth') → mid-papillary level, the FoCUS standard → apical level.

• Global LV function: concentric inward motion and thickening. The best single view for 'how is it squeezing'.
• Regional wall motion at mid-papillary level: LAD anterior and anteroseptal; RCA inferior and inferoseptal; LCx inferolateral and anterolateral. Territories overlap; this is approximate.
• The septum: a round 'O' LV is normal. A D-shaped LV means RV overload: systolic flattening suggests pressure overload (it may persist into diastole); isolated diastolic flattening suggests volume overload.
• Hyperdynamic, empty LV: papillary muscles touch at end-systole ('kissing papillary muscles').

LV on screen-right, RV on screen-left, atria below. Mitral and tricuspid valves are visible. The tricuspid annulus sits slightly closer to the apex than the mitral annulus.

• RV:LV size comparison: the key view for RV size.
• TAPSE: M-mode through the lateral tricuspid annulus.
• Global and regional LV function (septal and lateral walls).
• Pericardial effusion: lateral to the LV, and around the RA.
• Gross valve red flags.
• LVOT VTI: tilt anteriorly to get the apical 5-chamber view.

• Supine, knees flexed. Probe just below the xiphoid, almost flat (10–30° to the skin), marker to the patient's left. Aim at the left shoulder through the liver.
• On screen: liver at the top, then RV free wall, RV, septum, LV. In the cardiac preset the atria lie on the left of the screen and the apex points to the right.
• Press firmly and wait for the patient to exhale. Don't fight the liver: use it as the window.
• Best view for: pericardial effusion (between the liver and the RV free wall), RV free-wall diastolic collapse, cardiac arrest pulse checks, ventilated or COPD patients.

• From subcostal 4C, centre the RA. Rotate anticlockwise until the marker points to the head (12 o'clock). Fan slightly to the patient's right.
• Confirm it is the IVC: it enters the RA; a hepatic vein drains into it; it has a thin wall; its size changes with respiration.
• The aorta lies more to the left and deeper. It has thick walls, does not enter the RA, and pulsates with arterial timing.
• Measure perpendicular to the IVC long axis, about 1–2 cm from the cavo-atrial junction, just caudal to where the hepatic vein joins, at end-expiration. M-mode can help but beware of translational movement.

EF depends on the starting volume.

A 40 mL ventricle with EF 70% ejects 28 mL. A 200 mL ventricle with EF 30% ejects 60 mL. The lower EF does not necessarily mean the lower stroke volume. These are constructed examples, not normal reference volumes.

Ejected volume may not all travel forward.

With isolated mitral regurgitation (MR), total LV stroke volume includes blood returning to the LA. Forward stroke volume is the remainder. This model assumes no aortic regurgitation or shunt; it does not grade MR severity.

At the bedside

• Use good, non-foreshortened views. Formal EF usually uses biplane Simpson volumes or an appropriate 3D method.
• Preload, afterload and valve disease affect EF. A hyperdynamic appearance does not establish adequate perfusion.
• Measure forward flow when it changes the decision; interpret it with pressure, perfusion, valve findings and clinical context.

• Pulmonary pressures are about one-sixth of systemic pressures, so the RV wall is thin.
• Thin wall plus a low-resistance circuit means the RV is very sensitive to afterload. A sudden rise (PE, hypoxia, acidosis, high airway pressure) can make it dilate and fail. It copes with extra volume much better than with extra pressure.
• It shares the septum with the LV. Normally the LV indents the RV, and LV contraction helps the RV eject. So LV function affects RV function, and the reverse.

When the RV dilates, the septum moves towards the LV, LV filling falls and cardiac output falls. Low systemic pressure then reduces RV coronary perfusion, and the RV gets worse. Positive-pressure ventilation raises RV afterload. With a big, poorly contracting RV: support the blood pressure first, avoid reflex fluid boluses, and get senior help before you induce.

• The RV normally appears smaller than the LV, roughly no more than two-thirds its size. A basal RV:LV diameter ratio ≥1 is concerning in acute PE. Do not apply area-ratio cut-offs to diameter measurements.
• ESC 2019 PE guideline: an RV/LV diameter ratio ≥1.0 is a marker of RV dysfunction. The 2026 AHA/ACC PE guideline includes RV size, RV/LV ratio, TAPSE and TR velocity. In confirmed acute PE with an elevated clinical severity score but no persistent hypotension or shock (categories C–D), it favours echo over CT for short-term risk stratification. This is not a preference for diagnosing PE. Echo signs of RV strain do not diagnose PE: confirm it with dedicated PE imaging.
• Use an RV-focused A4C at end-diastole for size: the 2025 ASE normal basal diameter is <41 mm. Include the whole free wall; foreshortening changes the measurement.
• Check the RV apex: a normal LV forms the cardiac apex. An RV that reaches the apex is dilated.

• D-sign in systole, sometimes persisting into early diastole → pressure overload (PE, pulmonary hypertension, ARDS/high PEEP).
• D-sign in diastole only → volume overload (e.g. ASD, severe TR).
• Flat in both systole and diastole → combined pressure and volume overload. See real clips →
• Paradoxical septal motion towards the LV.

• TAPSE: M-mode at the lateral tricuspid annulus in A4C; longitudinal excursion of the annulus. Normal >17 mm (ASE 2025). Borderline values need context. Angle- and load-dependent; measures basal longitudinal motion, not global RVEF.
• S′ >9.5 cm/s; FAC >35% are the 2025 ASE normal references. S′ samples lateral annular systolic velocity. FAC = (end-diastolic area − end-systolic area) / end-diastolic area × 100; it needs a complete RV contour and omits the RVOT.
• Integrate size, free-wall thickening, septal shape and multiple function measures. Preserved TAPSE or S′ alone does not prove a normal RV.
• McConnell sign: akinesis of the mid RV free wall with preserved apical motion. Reported with acute PE, but also RV infarction and other RV disease. Neither this sign nor a normal FoCUS confirms or excludes PE.

• In PLAX, pericardial fluid lies anterior to the descending aorta and usually tapers at the posterior AV groove; it rarely tracks far behind the LA (oblique sinus).
• Pleural effusion lies posterior to the descending aorta, extends beyond the heart, and may contain a 'jellyfish' of collapsed lung.
• Epicardial fat: commonly anterior, grainy or speckled, and moves with the heart. Location alone cannot distinguish fat from fluid or clot; inspect texture and multiple views.
• Size (end-diastole, ESC 2015): small <10 mm, moderate 10–20 mm, large >20 mm.
• Circumferential or loculated? Loculated effusions are common after cardiac surgery and can compress only one chamber.

• RA systolic collapse (inversion at end-diastole to early systole): the earliest and most sensitive sign. Collapse lasting more than one-third of the cardiac cycle is more specific.
• RV diastolic collapse (free wall pushed in during early diastole): less sensitive but more specific.
• Plethoric IVC (>2.1 cm, <50% respiratory change): very sensitive (present in >90% of tamponade), poorly specific. A small or collapsing IVC does not exclude low-pressure or localised tamponade.
• Swinging heart (electrical alternans on ECG) with large effusions.
• Advanced: exaggerated respiratory variation in mitral (>25%) and tricuspid (>40%) inflow on pulsed-wave Doppler.

• Pulmonary hypertension or RV hypertrophy: the RV may not collapse.
• Hypovolaemia: 'low-pressure tamponade' with a non-plethoric IVC.
• After cardiac surgery, localised fluid or clot may compress one chamber without a circumferential effusion or classic right-sided collapse. A reassuring limited TTE does not exclude tamponade: seek urgent expert assessment, often TOE when TTE is inadequate.
• Positive-pressure ventilation alters respiratory variation.
• Use the ECG or M-mode to time collapse to systole or diastole.
• If tamponade is likely, prepare for drainage (echo-guided pericardiocentesis or surgery). Avoid induction and positive-pressure ventilation if at all possible. Give a modest fluid bolus as a bridge only.

• Heavily calcified, immobile aortic valve with restricted opening, ± LV hypertrophy: suspect severe aortic stenosis. This matters before a spinal or induction (keep SVR and sinus rhythm; avoid tachycardia).
• Flail mitral leaflet / ruptured papillary muscle: leaflet tip prolapses into the LA, with a new murmur after MI. Also look for a new VSD (septal defect with flow on colour Doppler).
• Dynamic LVOT obstruction with SAM: the anterior mitral leaflet moves towards the septum in systole, in a small, hyperdynamic, hypertrophied LV. Inotropes, tachycardia and hypovolaemia make it worse.
• Large, mobile mass: vegetation, LV apical thrombus, thrombus in transit in the RA/RV.
• Dilated aortic root (>about 4 cm in PLAX) or an intimal flap with pericardial effusion: suspect type A dissection.
• Colour Doppler: a big, wide regurgitant jet filling much of an atrium is a red flag, not a grade.
• Prosthetic valve that looks rocking or immobile.

• Get the probe on (subcostal) during compressions. Record a clip at the pulse check and review it after CPR restarts; keep each pause under 10 s, with someone counting aloud.
• Look for organised wall motion (pseudo-PEA: treat as profound shock), standstill, a large effusion, or an empty heart. A dilated RV is common after any arrest, so it does not prove PE on its own.
• Ultrasound must not lengthen pauses in compressions; if it does, stop scanning.

• An off-axis or foreshortened view makes structures look the wrong size or shape.
• Grading the LV on one view.
• Calling a D-sign on an oval PSAX.
• Fat called as effusion; pleural fluid called as pericardial.
• Aorta called as IVC.
• Anchoring: the scan looked 'normal', so the shock must be distributive.
• Vasopressors and inotropes change what you see, so rescan after a change.

• Mechanically ventilated, fully passive: the IVC distends with each positive-pressure breath. Distensibility index (Dmax − Dmin)/Dmin >18% predicted response (Barbier 2004). ΔIVC (Dmax − Dmin)/mean >12% predicted response (Feissel 2004). Overall accuracy of IVC variation is only moderate (meta-analysis in ventilated shocked patients: pooled sensitivity 69%, specificity 80%, AUROC 0.82; Huang 2018); use it as one input, not a test.
• Valid only with no spontaneous breathing effort, tidal volume about ≥8 mL/kg predicted body weight in the original studies and no raised intra-abdominal pressure; a regular rhythm helps. Do not increase tidal volume solely to make this test applicable.
• Spontaneously breathing: much weaker. A large collapse (e.g. ≥40–50%) makes response likely, but a small collapse does not rule it out (high specificity, low sensitivity; Airapetian 2015). Breathing effort varies breath to breath.

• A small, collapsing IVC may support low right-sided filling pressure. It does not establish hypovolaemia, fluid responsiveness or fluid tolerance; assess the heart, lungs and response to a reversible preload test.
• A plethoric, minimally varying IVC raises concern for elevated right-sided pressure. Seek the cause (RV failure, obstruction, TR, positive-pressure ventilation or congestion); it cannot by itself determine whether fluid will help.
• The middle ground is uninformative. Use a passive leg raise with VTI (next slide).

Raised intra-abdominal pressure compresses the IVC. RV failure, TR or tamponade distend it whatever the volume status. High PEEP dilates it. Forceful breathing exaggerates collapse. The cylinder effect and translational movement fake collapse. Athletes can have a large IVC. Being fluid-responsive is not a reason to give fluid. It must also be needed and safe.

• Take an apical 5-chamber view (tilt anteriorly from A4C). Place the pulsed-wave gate in laminar LVOT flow just proximal to the aortic valve, aligned with flow. Avoid the valve acceleration zone and trace the dense modal envelope, excluding faint spectral noise. Average representative beats.
• VTI is the 'stroke distance' (cm). Stroke volume = VTI × LVOT area (π × (LVOT diameter/2)²).
• VTI is a distance, not a volume. Interpret it with LVOT area and heart rate; a low VTI suggests low stroke volume only in the relevant geometry. Significant aortic regurgitation can make systolic LVOT flow exceed net systemic flow.
• Use trends in VTI. Keep the same gate position and angle for repeat measurements.

• Start semi-recumbent at 45°. Lower the trunk flat and raise the legs to 45° in one movement. This returns about 300 mL of venous blood, reversibly.
• Capture the maximum flow change promptly, usually within about a minute; the response can fade. Return to the original position and confirm recovery towards baseline.
• A rise of ≥10% predicts fluid responsiveness. Pooled sensitivity 85%, specificity 91%, AUROC 0.95 for cardiac output changes (Monnet 2016 meta-analysis). In spontaneously breathing patients, a PLR-induced rise in stroke volume (from LVOT VTI) ≥12.5% predicted response: sensitivity 77%, specificity 100% (Lamia 2007).
• Measure flow, not blood pressure: pulse pressure changes after PLR are much less sensitive.
• Pitfalls: pain, coughing or waking increase sympathetic tone and give a false positive. Raised intra-abdominal pressure can give a false negative. Not suitable with raised ICP or with unstable spine or leg fractures. Start from semi-recumbent: starting supine recruits less volume.

• Fluid responsiveness: stroke volume rises with a fluid challenge (previous two slides). It tells you fluid could help.
• Fluid tolerance: the patient can take more fluid without harm from venous congestion or oedema (Kattan 2022). A patient can be both responsive and intolerant, for example a septic patient with ARDS or capillary leak, or with intra-abdominal hypertension, whose stroke volume still rises with fluid. A congested, failing RV is usually neither responsive nor tolerant.
• High right atrial pressure is transmitted back to the liver, gut and kidneys. Venous congestion lowers the organ perfusion gradient, and the kidney is especially vulnerable.
• VExUS (venous excess ultrasound; Beaubien-Souligny 2020) grades how far that pressure reaches the organs, using the IVC plus three venous Doppler waveforms.

Grading as published (VExUS 'C' prototype, Beaubien-Souligny 2020). Only severe patterns raise the grade above 1.

• Atrial fibrillation: no A wave and a small S wave, so S < D is common at baseline. Interpret the hepatic vein with care.
• Severe tricuspid regurgitation: the regurgitant jet itself reverses the hepatic S wave. The finding reflects the TR more than overall venous pressure, so grade on the portal and renal veins and the IVC too.
• Cirrhosis or portal hypertension: a stiff liver flattens the hepatic vein waveform (often monophasic) and can damp or even reverse portal flow, whatever the RAP. Both hepatic and portal signals are unreliable; lean on the IVC, the renal vein and the echo.
• Fit, thin, young people: portal pulsatility can be a normal variant. A pulsatile portal vein with a small IVC is grade 0.
• CKD and renal parenchymal disease: intrarenal venous patterns are less reliable. This is also the hardest window; check you are not sampling the main renal vein.
• Raised intra-abdominal pressure compresses the IVC and can alter the waveforms. High PEEP and chronic pulmonary hypertension raise RAP without volume excess.
• VExUS shows pressure, not volume. It cannot tell RV failure from fluid overload: the echo does that.

• Derivation (145 patients after cardiac surgery): grade 3 predicted AKI, HR 3.69 (95% CI 1.65–8.24), 2.82 after adjustment. At ICU admission grade 3 was highly specific (96%) but insensitive (about 27%) (Beaubien-Souligny 2020).
• General ICU (145 patients, multicentre): VExUS ≥2 in about one in five at admission and not associated with AKI or 28-day mortality (Andrei 2023). In sepsis (108 patients, four ICUs), VExUS ≥2 was not independently associated with AKI: adjusted OR 1.82 (0.62–5.31) (Song 2025).
• Meta-analysis (9 observational studies, 1036 patients): VExUS ≥2 associated with AKI, OR 2.63 (1.06–6.54) with high heterogeneity; strongest after cardiac surgery (OR 3.86). No association with mortality (Melo 2025).
• Physiology: grade correlated with right atrial pressure at catheterisation, better than IVC size alone (pilot study; Longino 2023).
• Guiding treatment: in cardiorenal syndrome type 1 (RCT, 140 patients), VExUS-guided diuresis achieved decongestion more often, but kidney function recovery and 90-day survival did not differ (Islas-Rodríguez 2024). No trial yet shows better hard outcomes.