EchoCompass

ASE 2025: the simplified script

Check three things: e′ (septal 6 or less, lateral 7 or less, or average 6.5 or less), E/e′ (average 14 or more), TR 2.8 m/s or more (or PASP 35 or more).
All three abnormal: LAP elevated. Grade with E/A: below 2 is Grade 2, 2 or more is Grade 3.
All three normal: normal diastolic function.
Only e′ reduced: E/A 0.8 or less is Grade 1. Above 0.8, go to step 5.
Anything else (one or two abnormal): check LAVI above 34, LARS 18% or less, pulmonary vein S/D 0.67 or less, or IVRT 70 ms or less. Any one positive means LAP is elevated; grade with E/A.
None positive: LAP is normal (Grade 1 if e′ is reduced).
No additional markers: use supplemental signs (PR end-diastolic velocity, L-wave, Ar minus A, Valsalva).

Grade 1 in a symptomatic patient: the guideline recommends a diastolic exercise echo.

What changed from 2016

One algorithm for every EF. The A and B split is gone.
The first step is e′, E/e′ and TR, not mitral inflow.
e′ cutoffs are lower (6, 7 and 6.5), with optional age-specific values.
E/e′ and TR thresholds now include equality: 14 or more and 2.8 or more.
LAVI moved to the second line, joined by LA strain, pulmonary vein S/D and IVRT.
E/A grades the dysfunction after LAP is decided.
Supplemental signs reduce indeterminate results.
Separate approaches for AF, MAC, MR, MS, PH, transplant and LVAD.

2016 script (for older exams)

Normal EF and myocardium: count e′, E/e′ above 14, TR above 2.8, LAVI above 34. More than half abnormal is dysfunction; half is indeterminate.
Then, or if EF is reduced or the myocardium is abnormal: E/A 0.8 or less with E 50 or less is Grade 1; E/A 2 or more is Grade 3.
Otherwise count E/e′, TR and LAVI. Majority decides Grade 1 or 2; a two-criteria split is indeterminate.

Traps: septal and lateral e′ count once, E/A 0.8 or less needs E 50 or less to stop, a 1:1 split is never Grade 1.

Fluids: three questions, kept apart

Need: is there hypoperfusion? Without it, a positive responsiveness test is just normal physiology.
Respond: use a dynamic test. PLR with VTI (10% or more) works in most patients. PPV needs strict conditions.
Tolerate: elevated LAP, diffuse B-lines, VExUS 2 or 3, or RV dysfunction make the patient likely intolerant. So do two or more clinical overload signs.

There’s no validated fluid tolerance score. The tool combines markers the way you would at the bedside and says so.

Systolic function and shock

Separate pump from flow: EF tells you contractility, LVOT VTI tells you output. A weak LV can still deliver enough flow.
RV by ASE 2025: TAPSE above 17 mm, s′ above 9.5 cm/s and FAC above 35% are normal; TAPSE below 10 mm, s′ below 5 cm/s and FAC 22% or less are severe.
Always look for dynamic LVOT obstruction before starting an inotrope.
MAP first with norepinephrine, then preload, then an inotrope if hypoperfusion persists with low flow.
Choose dobutamine or milrinone by patient factors: AKI, tachyarrhythmia, hypotension, beta-blockade, RV failure.
RV failure: avoid fluid when the RV is dilated, keep MAP up with norepinephrine (vasopressin as an adjunct), optimize ventilation, keep sinus rhythm, treat the cause (thrombolysis for high-risk PE, revascularization for RV infarction), and escalate early to the shock team.
Set a working diagnosis, but let the echo challenge it: the tool flags findings that don’t fit.

About the action tiers: the cut points that separate “Do now” from “Consider” (LVOT VTI below 15 cm, cardiac index below 2.2 L/min/m², lactate above 4 mmol/L, ScvO₂ below 60%) are pragmatic bedside thresholds chosen for teaching. They are not validated decision rules, and they should always be read alongside the trend and the clinical picture. Capillary refill uses the 3-second threshold from ANDROMEDA-SHOCK.

Where the board answer and current evidence differ

Topic	Traditional board answer	Current evidence
Diastolic grading	2016 algorithm: inflow first, EF decides the pathway	2025 ASE supersedes it: one algorithm starting with e′, E/e′, TR
CVP	Target CVP 8 to 12 mmHg	CVP doesn’t predict fluid responsiveness; EGDT trials (ProCESS, ARISE, ProMISe) showed no benefit
IVC	Collapse above 50% means fluid responsive	Weak accuracy, especially spontaneously breathing. Specific at high values, poorly sensitive
PPV	Above 13% means responsive	Valid only with controlled ventilation, sinus rhythm, Vt 8 mL/kg or more. Grey zone 9 to 13%. With low Vt, use a tidal volume challenge
Initial volume	30 mL/kg for everyone	SSC 2021 downgraded it to a weak suggestion. CLASSIC and CLOVERS found no mortality difference between restrictive and liberal strategies
Perfusion target	Lactate clearance	ANDROMEDA-SHOCK: capillary refill targeting was not inferior to lactate, with fewer interventions
VExUS	Rarely tested	Observational data link grade 3 with AKI; not yet shown to improve outcomes when used to guide therapy
Milrinone vs dobutamine	Milrinone causes hypotension; dobutamine causes arrhythmias	DOREMI: no difference in death, major complications, arrhythmias or hypotension-related outcomes
Vasopressor in cardiogenic shock	Dopamine is acceptable	SOAP II: dopamine caused more arrhythmias and higher mortality in the cardiogenic subgroup. Norepinephrine is first line; OptimaCC linked epinephrine to more refractory shock
IABP	Routine IABP in MI shock	IABP-SHOCK II: no mortality benefit. DanGer Shock: a microaxial pump lowered mortality in selected STEMI shock
Levosimendan in sepsis	Inotrope option	LeoPARDS: no benefit, more arrhythmias. Surviving Sepsis 2026 keeps the recommendation against it
Oxygen delivery	Push DO₂ high and target ScvO₂ of 70% or more	Supranormal DO₂ didn’t help (Hayes, Gattinoni), and ScvO₂ targeting fell with the EGDT trials. Aim for adequate delivery and look at the CO₂ gap
Transfusion	Keep Hb above 10 g/dL	TRICC and TRISS support 7 g/dL for most ICU patients, including septic shock. In acute MI, MINT found no significant difference with a liberal strategy
RV infarction	Give fluid to maintain preload	Fluid helps only when the RV isn’t dilated and filling pressures are low; excess volume worsens septal shift and lowers LV output
Fractional shortening	Estimate EF from M-mode	ASE 2015 advises against linear EF methods, especially with regional wall motion abnormalities

References

Nagueh SF, et al. Recommendations for the evaluation of LV diastolic function by echocardiography and for HFpEF diagnosis: an update from the ASE. J Am Soc Echocardiogr 2025;38:537-69.
Nagueh SF, et al. Recommendations for the evaluation of LV diastolic function by echocardiography. J Am Soc Echocardiogr 2016;29:277-314.
Monnet X, et al. Passive leg raising for predicting fluid responsiveness: a systematic review and meta-analysis. Intensive Care Med 2016;42:1935-47.
Muller L, et al. An increase in aortic blood flow after an infusion of 100 mL colloid over 1 minute can predict fluid responsiveness. Anesthesiology 2011;115:541-7.
Monnet X, et al. Predicting volume responsiveness by using the end-expiratory occlusion in mechanically ventilated patients. Crit Care Med 2009;37:951-6.
Michard F, et al. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients. Am J Respir Crit Care Med 2000;162:134-8.
Cannesson M, et al. Assessing the diagnostic accuracy of pulse pressure variations: a gray zone approach. Anesthesiology 2011;115:231-41.
Myatra SN, et al. The changes in pulse pressure variation or stroke volume variation after a tidal volume challenge. Crit Care Med 2017;45:415-21.
Barbier C, et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Intensive Care Med 2004;30:1740-6.
Airapetian N, et al. Does inferior vena cava respiratory variability predict fluid responsiveness in spontaneously breathing patients? Crit Care 2015;19:400.
Beaubien-Souligny W, et al. Quantifying systemic congestion with point-of-care ultrasound: development of the venous excess ultrasound grading system. Ultrasound J 2020;12:16.
Marik PE, Cavallazzi R. Does the central venous pressure predict fluid responsiveness? Crit Care Med 2013;41:1774-81.
Hernández G, et al. ANDROMEDA-SHOCK randomized clinical trial. JAMA 2019;321:654-64.
Meyhoff TS, et al. Restriction of intravenous fluid in ICU patients with septic shock (CLASSIC). N Engl J Med 2022;386:2459-70.
NHLBI PETAL Network. Early restrictive or liberal fluid management for sepsis-induced hypotension (CLOVERS). N Engl J Med 2023;388:499-510.
Mathew R, et al. Milrinone as compared with dobutamine in the treatment of cardiogenic shock (DOREMI). N Engl J Med 2021;385:516-25.
De Backer D, et al. Comparison of dopamine and norepinephrine in the treatment of shock (SOAP II). N Engl J Med 2010;362:779-89.
Levy B, et al. Epinephrine versus norepinephrine for cardiogenic shock after acute myocardial infarction (OptimaCC). J Am Coll Cardiol 2018;72:173-82.
Thiele H, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock (IABP-SHOCK II). N Engl J Med 2012;367:1287-96.
Møller JE, et al. Microaxial flow pump or standard care in infarct-related cardiogenic shock (DanGer Shock). N Engl J Med 2024;390:1382-93.
Gordon AC, et al. Levosimendan for the prevention of acute organ dysfunction in sepsis (LeoPARDS). N Engl J Med 2016;375:1638-48.
Prescott HC, et al. Surviving Sepsis Campaign: international guidelines for management of sepsis and septic shock 2026. Crit Care Med 2026;54:725-812.
Evans L, et al. Surviving Sepsis Campaign: international guidelines for management of sepsis and septic shock 2021. Crit Care Med 2021;49:e1063-e1143.
Naidu SS, et al. SCAI SHOCK stage classification expert consensus update. J Am Coll Cardiol 2022;79:933-46.
Konstantinides SV, et al. 2019 ESC guidelines for the diagnosis and management of acute pulmonary embolism. Eur Heart J 2020;41:543-603.
Harjola VP, et al. Contemporary management of acute right ventricular failure: a statement from the Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the ESC. Eur J Heart Fail 2016;18:226-41.
Hayes MA, et al. Elevation of systemic oxygen delivery in the treatment of critically ill patients. N Engl J Med 1994;330:1717-22.
Gattinoni L, et al. A trial of goal-oriented hemodynamic therapy in critically ill patients. N Engl J Med 1995;333:1025-32.
Mekontso-Dessap A, et al. Combination of venoarterial PCO₂ difference with arteriovenous O₂ content difference to detect anaerobic metabolism. Intensive Care Med 2002;28:272-7.
Hébert PC, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care (TRICC). N Engl J Med 1999;340:409-17.
Holst LB, et al. Lower versus higher hemoglobin threshold for transfusion in septic shock (TRISS). N Engl J Med 2014;371:1381-91.
Carson JL, et al. Restrictive or liberal transfusion strategy in myocardial infarction and anemia (MINT). N Engl J Med 2023;389:2446-56.
Lang RM, et al. Recommendations for cardiac chamber quantification by echocardiography in adults. J Am Soc Echocardiogr 2015;28:1-39.
American Society of Echocardiography. Guidelines for the echocardiographic assessment of the right heart in adults. J Am Soc Echocardiogr 2025.

Working diagnosis

1. Patient and vitals

2. Perfusion

3. Current support

4. Clinical context

5. LV function

6. Forward flow

7. LVOT obstruction

8. RV function (optional)

9. Oxygen delivery and extraction (optional)

1. Do they need fluid?

2. Will they respond?

3. Will they tolerate it?

Case 1