Cardiac Hemodynamic & Functional Indices

3.1 EPSS — operating-point clarification

EPSS is a continuous, target-specific variable. The 7-mm and 8-mm cut points are not nested severity categories; they arise from different diagnostic targets in different cohorts. Interpret EPSS with LV size, wall motion, IVC, image quality, and clinical context. Use caution in mitral stenosis or conditions that distort anterior mitral leaflet excursion.

EPSS less than 5.5 mm

This is a high-sensitivity negative test for LVEF less than 50%. If the negative result is accepted, LVEF less than 40% is also excluded or clinically unlikely because severe dysfunction is a subset of reduced EF. EF should be considered 50% or greater, not less than 40%. This is not a positive test for the 40–50% gray zone. In the Nuñez Ramos ED cohort, sensitivity was approximately 95% and negative likelihood ratio approximately 0.09 for EF less than 50%; for EF less than 40%, sensitivity was approximately 95.5% and negative likelihood ratio approximately 0.11. Negative predictive value is pretest-probability dependent. This is not an absolute rule-out.

EPSS less than 7 mm

High negative predictive value against severe LV systolic dysfunction, LVEF less than 30%, in the reported ED cohort. It does not fully exclude mild or moderate reduction. In McKaigney and colleagues, EPSS greater than 7 mm for LVEF less than 30% had sensitivity 100%, specificity 51.6%, positive likelihood ratio 2.07, and negative likelihood ratio 0.00. The severe subgroup was small, so 100% sensitivity is imprecise, and NPV is pretest-dependent.

EPSS greater than 7 mm

Abnormal. Do not interpret as normal. Interpretation is target-dependent: it may indicate severe dysfunction in some cohorts or mild-to-moderate dysfunction in others. McKaigney and colleagues used greater than 7 mm for LVEF less than 30%. Ucar and colleagues found EPSS 7.0 mm or greater with sensitivity 86.1% and specificity 81.5% for reduced EF. In Bahl and colleagues, greater than 7–20 mm corresponded to EF 30–55%, and greater than 20 mm to EF less than 30%.

EPSS 7–8 mm

Study-dependent transition zone. Interpret with LV size, wall motion, IVC, filling assessment, haemodynamics, and clinical context. This is not a universal gray zone.

EPSS greater than 8 mm

Supports reduced LVEF in some ED cohorts; specificity is modest. It is not specific for EF less than 50% or EF less than 40%. McKaigney and colleagues used an LVEF less than 55% target: sensitivity 83.3%, specificity 50%, positive likelihood ratio 1.67, negative likelihood ratio 0.33. State the target endpoint if applying it to EF less than 50%.

EPSS 11.5 mm or greater

Rule-in cutoff for LVEF less than 50% in the Nuñez Ramos ED cohort. High specificity and positive likelihood ratio; moderate sensitivity. Positive likelihood ratio approximately 12, specificity 95%, sensitivity approximately 66%. Useful for increasing post-test probability when pretest probability is moderate to high; not a high-sensitivity test.

EPSS 13.5 mm or greater

Rule-in cutoff for LVEF less than 40% in the Nuñez Ramos ED cohort. High specificity and positive likelihood ratio; moderate sensitivity. Positive likelihood ratio approximately 11, specificity 95%, sensitivity approximately 64%. Useful to strongly support severely reduced EF, but will miss a substantial proportion of cases if used alone.

EPSS greater than 20 mm

Severe dysfunction in the Bahl categorical scheme. Not a universal EPSS threshold. EPSS and fractional shortening limitations in real-world POCUS include poor image quality and operator-dependent measurement.

Bottom line

EPSS thresholds are target-specific statistical operating points, not a universal ordinal severity scale.

3.2 MAPSE

MAPSE is an M-mode or 2D displacement measurement, not tissue Doppler.

Approximately 15 mm or greater: generally normal.
Less than 15 mm: impaired longitudinal function.
Do not confuse MAPSE, measured in mm, with e′, measured in cm/s.

3.3 LVOT VTI, stroke volume, cardiac output

Acquire from the apical 5-chamber view with pulsed-wave Doppler at the LVOT. Align angle less than 20 degrees and average 3–5 beats.

LVOT area = 0.785 × diameter².
Stroke volume = LVOT area × VTI.
Cardiac output = stroke volume × heart rate.

Practical reference

LVOT VTI 16–22 cm: common adult range.
LVOT VTI 18 cm or greater: often adequate stroke volume in critical care.
LVOT VTI less than 16 cm: low.
Stroke volume 60–100 mL: typical adult.
Cardiac output 4–8 L/min: typical adult.

POCUS caveat: LVOT VTI requires spectral Doppler and training. It is more useful in serial monitoring than as a single snapshot. It is not a basic POCUS core measurement in most curricula.

3.4 Tricuspid regurgitation and estimated pulmonary pressure

Estimated RV systolic pressure, RVSP, is approximately:

RVSP ≈ 4 × TRV² + RAP

TR velocity depends on jet visibility; low flow may underestimate pulmonary pressure.

TR peak velocity

Less than 2.8 m/s: makes significant pulmonary hypertension less likely if image quality is adequate.
2.8–3.4 m/s: intermediate likelihood; correlate clinically.
Greater than 3.4 m/s: strongly suggests pulmonary hypertension.

Formal pulmonary hypertension is defined by mean pulmonary artery pressure greater than 20 mmHg in current criteria, or greater than 25 mmHg in older criteria. Systolic pulmonary artery pressure is not mean pulmonary artery pressure. Do not use “PASP less than 35 mmHg is normal” as a pulmonary hypertension criterion.

3.5 Diastolic function — advanced, load-dependent, revised to 2025 ASE framework

Scope: advanced cardiac POCUS. Requires adequate spectral and tissue Doppler. Interpret as a multiparametric pattern, not a single value. Assumptions for the standard algorithm include sinus rhythm, no significant mitral valve disease, adequate image quality, and no severe RV pressure overload or pericardial disease confounding annular velocities.

3.5.1 2025 ASE primary diagnostic algorithm

Step 1 — assess e′ as a marker of impaired LV relaxation

Impaired relaxation is suggested when any of the following is present:

Septal e′ less than or equal to 6 cm/s.
Lateral e′ less than or equal to 7 cm/s.
Average e′ less than or equal to 6.5 cm/s.

Step 2 — assess markers of LA/LV remodelling and elevated left atrial pressure

Relevant Step 2 markers include:

Average E/e′ greater than 14.
Left atrial longitudinal reservoir strain, LARS, less than or equal to 18%.
E/A less than or equal to 0.8 or E/A greater than or equal to 2.
LAVI greater than 34 mL/m².

Diagnosis rule

LV diastolic dysfunction is present if:

e′ is reduced and at least one Step 2 marker is present, or
e′ is preserved but at least two Step 2 markers are present.

Context notes

Age-specific e′ or E/A cutoffs may be considered after excluding LA enlargement in athletes and after excluding anaemia, atrial fibrillation, atrial flutter, and mitral valve disease.
LV mass index greater than 95 g/m² in women or greater than 115 g/m² in men may be accepted as an additional supporting finding after excluding athlete-related LV mass increase.
LARS may not be available at all sites. If unavailable, base interpretation on the remaining Step 1 and Step 2 variables.
The older v3 operating points of septal e′ less than 7 cm/s, lateral e′ less than 10 cm/s, and average E/e′ 15 or greater are demoted from primary diagnostic status in v4. The primary 2025 elevated-filling-pressure Doppler marker is average E/e′ greater than 14.
TR peak velocity greater than 2.8 m/s may remain as a practical bedside adjunct for elevated filling pressure or pulmonary pressure, but it is not a primary 2025 Step 2 diagnostic variable unless explicitly included in local algorithm.

3.5.2 Parameter interpretation in v4

Mitral E/A less than 0.8

Suggests impaired relaxation when supported by prolonged IVRT and reduced e′. It may also represent low LAP, hypovolaemia, tachycardia, or atrial arrhythmia.

Mitral E/A 0.8–2.0

Normal or pseudonormal. This is the critical gray zone. Requires average E/e′, LAVI, LARS when available, TR, pulmonary venous flow, or Valsalva.

Mitral E/A greater than 2.0

Usually restrictive when accompanied by short deceleration time and elevated filling pressures. Pseudonormalization usually produces E/A around 1.0, not greater than 2.0.

Average E/e′

Less than or equal to 8: normal filling pressure likely.
9–14: indeterminate.
Greater than 14: elevated LV filling pressure likely by the 2025 marker.

Septal e′

Less than or equal to 6 cm/s suggests impaired relaxation in the 2025 framework. It is affected by wall motion, mitral annular calcification, pericardial disease, and RV pressure overload. In RV pressure overload or ASD, septal e′ may be reduced from tethering; lateral e′ may be more useful.

Lateral e′

Less than or equal to 7 cm/s suggests impaired relaxation in the 2025 framework. It may be reduced by lateral wall abnormality or pericardial disease.

Mitral E-wave deceleration time

Less than 140–150 ms suggests elevated LAP or restrictive physiology, not impaired relaxation per se. Deceleration time is influenced by LA pressure and LV compliance/operating stiffness.

LAVI

Greater than 34 mL/m² indicates chronic elevated LAP. It is less specific for acute pressure elevation.

IVRT

Approximately 66–105 ms: normal range. Prolonged IVRT supports impaired relaxation in the appropriate context.

Restrictive pattern

E/A greater than 2.0 plus deceleration time less than 140–150 ms plus elevated average E/e′, often with LAVI greater than 34 mL/m². This is pattern recognition for very elevated LAP, not a precise quantitative estimator.

Multiparametric approach

Required. A single value is insufficient. Diastolic function is load-dependent and affected by atrial fibrillation, mitral valve disease, arrhythmia, ventilation, and vasoactive therapy.

3.5.3 Hemodynamic logic

Mitral inflow Doppler measures the LA–LV pressure gradient during diastole. The E wave is influenced by:

LA pressure and preload.
LV active relaxation and lusitropy.
LV passive compliance and operating stiffness.
Heart rate and cycle length.
Mitral valve morphology and function.
Arrhythmia and beat-to-beat variability.

Relative load dependence:

E/A: most load-dependent.
IVRT: load-dependent; influenced by relaxation and LA pressure.
E-wave deceleration time: influenced by LA pressure and LV compliance.
e′: less load-dependent but not load-independent.
Average E/e′: combines load-dependent inflow velocity with less load-dependent annular velocity.
LAVI: reflects chronic pressure exposure.
LARS: reflects LA reservoir function and chronic pressure/volume loading when available.
Pulmonary venous flow: reflects LA pressure, LA compliance, and atrial contraction.
TR velocity: indirect filling-pressure marker; interpret with lung disease and tricuspid valve disease in mind.

3.5.4 Grading in sinus rhythm

Normal diastolic function

Typical pattern:

E/A 0.8–2.0.
IVRT approximately 66–105 ms.
Septal e′ greater than 6 cm/s.
Lateral e′ greater than 7 cm/s.
Average e′ greater than 6.5 cm/s.
Average E/e′ less than or equal to 8, and not greater than 14.
LAVI 34 mL/m² or less.
TR velocity less than 2.8 m/s.
Pulmonary venous S/D greater than 1 with normal atrial reversal.
No Valsalva unmasking of relaxation abnormality.

Interpretation: normal E/A plus normal ancillary filling-pressure markers equals normal diastolic function.

Grade 1 — impaired relaxation

Typical pattern:

Reduced e′ by 2025 criteria: septal less than or equal to 6, lateral less than or equal to 7, or average less than or equal to 6.5 cm/s.
E/A less than 0.8.
Prolonged IVRT.
Average E/e′ low or normal, not greater than 14.
LAVI 34 mL/m² or less if not chronic.
TR velocity often normal.
Pulmonary venous S/D usually greater than 1.

Hemodynamic concept: delayed LV relaxation without elevated LA pressure. Early filling is reduced; the A wave is prominent.

Caveat: E/A less than 0.8 with normal IVRT and normal e′ may reflect low LAP, hypovolaemia, or tachycardia, not Grade 1 dysfunction.

Grade 2 — pseudonormalized filling

Typical pattern:

E/A 0.8–2.0.
Plus at least one elevated filling-pressure or remodelling marker:
- Average E/e′ greater than 14.
- LAVI greater than 34 mL/m².
- TR velocity greater than 2.8 m/s.
- Pulmonary venous S/D less than 1.
- Pulmonary venous Ar–A duration greater than mitral A by 30 ms or more.
- LARS less than or equal to 18% when available.
Often also reduced e′, indeterminate or elevated E/e′, and normal or shortened IVRT due to elevated LA pressure.

Hemodynamic concept: LV relaxation remains impaired, but LA pressure has risen, restoring the early transmitral gradient and making E/A appear “normal.”

Practical implication: E/A 0.8–2.0 may be normal or Grade 2 pseudonormalized dysfunction. Ancillary parameters are required.

Grade 3 — restrictive filling

Typical pattern:

E/A greater than 2.0.
E-wave deceleration time less than 140–150 ms.
Small mitral A wave.
Average E/e′ elevated, often markedly, greater than 14.
LAVI greater than 34 mL/m².
TR velocity often elevated.
Pulmonary venous D wave dominant over S wave.
Pulmonary venous Ar–A duration prolonged.
IVRT may be short.

Hemodynamic concept: severely reduced LV compliance with markedly elevated LA pressure. Early filling is prominent; rapid pressure equalization produces short deceleration time. Atrial contribution is reduced.

Some references divide restrictive filling into:

Reversible restrictive: unmasked or modified by Valsalva or volume challenge.
Fixed restrictive: persists despite maneuvers; worse prognosis.

3.5.5 Differentiating normal from Grade 2 pseudonormal dysfunction

If E/A is 0.8–2.0, the practical question is whether LAP is elevated.

Step 1 — average E/e′

Less than or equal to 8: normal filling pressure likely.
9–14: indeterminate; use LAVI, TR, pulmonary venous flow, LARS, or Valsalva.
Greater than 14: elevated LV filling pressure likely by 2025 marker.

If E/A is 0.8–2.0 and average E/e′ is greater than 14, consider Grade 2 pseudonormalized dysfunction with elevated filling pressures. If E/A is 0.8–2.0 and average E/e′ is less than or equal to 8 with normal ancillary markers, diastolic function is more likely normal. If E/A is 0.8–2.0 and average E/e′ is 9–14, the result is indeterminate.

Step 2 — LAVI and TR velocity

LAVI greater than 34 mL/m² suggests elevated filling pressure.
TR peak velocity greater than 2.8 m/s suggests elevated filling pressure.
If both are normal, filling pressures are more likely normal.
If either is abnormal, filling pressures are more likely elevated.
If results conflict, use pulmonary venous flow or Valsalva.

Caveat: TR greater than 2.8 m/s must be interpreted cautiously with primary pulmonary hypertension, severe tricuspid valve disease, or RV dysfunction.

Step 3 — pulmonary venous flow

Pulmonary venous S/D greater than 1: more consistent with normal or Grade 1.
Pulmonary venous S/D less than 1: suggests elevated LAP; Grade 2 or Grade 3.
Pulmonary venous Ar–A duration greater than mitral A by 30 ms or more: strong indicator of elevated LAP, especially markedly elevated LVEDP.
Not usable in atrial fibrillation.

Practical rules:

E/A 0.8–2.0 plus pulmonary venous S/D less than 1 equals pseudonormal or restrictive physiology until proven otherwise.
E/A 0.8–2.0 plus pulmonary venous Ar–A greater than mitral A by 30 ms or more equals elevated LAP.

Step 4 — Valsalva or unmasking maneuver

Valsalva reduces LA pressure and may unmask impaired relaxation.

Baseline E/A 0.8–2.0 falling to less than 0.8 or reduced by 50% or more: pseudonormalized diastolic dysfunction.
Baseline E/A 0.8–2.0 remaining 0.8–2.0 with no other abnormal filling markers: more likely normal, context-dependent.
Baseline E/A greater than 2.0 remaining greater than 2.0: fixed restrictive pattern, severe.
Baseline E/A greater than 2.0 falling into a lower grade: reversible restrictive pattern.

Adequacy matters. An inadequate Valsalva can produce a false “normal” result.

3.5.6 Practical examples

Normal

E/A 1.2, IVRT 90 ms, septal e′ 9 cm/s, lateral e′ 11 cm/s, average E/e′ 7, LAVI 28 mL/m², TR 2.5 m/s, pulmonary venous S/D 1.5. Interpretation: normal diastolic function.

Grade 1

E/A 0.6, IVRT 115 ms, septal e′ 5 cm/s, lateral e′ 8 cm/s, average e′ 6.5 cm/s, average E/e′ 8, LAVI 30 mL/m², TR 2.4 m/s, pulmonary venous S/D 1.8. Interpretation: impaired relaxation without clear elevated filling pressures.

Grade 2

E/A 1.1, IVRT 95 ms, septal e′ 5 cm/s, lateral e′ 7 cm/s, average E/e′ 17, LAVI 38 mL/m², TR 3.1 m/s, pulmonary venous S/D 0.8. Interpretation: pseudonormalized diastolic dysfunction with elevated LAP.

Indeterminate

E/A 1.3, average E/e′ 12, LAVI 31 mL/m², TR 2.6 m/s, IVRT 95 ms, e′ normal. Interpretation: indeterminate; use pulmonary venous flow, Valsalva, LARS if available, and clinical context.

Restrictive

E/A 2.6, deceleration time 125 ms, small A wave, average E/e′ 22, LAVI 48 mL/m², TR 3.4 m/s, pulmonary venous D greater than S, prolonged Ar–A. Interpretation: Grade 3 restrictive diastolic dysfunction with markedly elevated LAP.

3.5.7 Special situations modifying the algorithm

Atrial fibrillation

A wave is absent or unorganized.
E/A is unreliable.
Use average E velocity, IVRT, average E/e′, LAVI, TR velocity, LARS when available, pulmonary venous flow when feasible, and clinical/haemodynamic context.
No single parameter is sufficiently reliable in isolation.

Mitral stenosis

Inflow velocities are abnormal due to obstruction.
LV filling pressures may be normal unless coexisting myocardial disease is present.
E/e′ is generally not useful.
Short IVRT and high mitral A velocity may suggest elevated LA pressure.
Modify the standard algorithm.

Mitral regurgitation

Primary MR can increase chamber compliance and attenuate LAP elevation.
Severe MR can mimic advanced diastolic dysfunction.
Moderate or severe MR may increase mitral E velocity, reduce pulmonary venous S wave, lower S/D, or cause systolic pulmonary venous flow reversal.
Pulmonary venous Ar–A duration remains useful for elevated LVEDP.
E/e′ is less reliable in primary MR with preserved EF.

Mitral annular calcification

MAC can reduce mitral orifice area and annular excursion, producing increased E, reduced e′, increased E/e′, and false elevation of filling pressure.

Modified MAC approach:

E/A less than 0.8: filling pressure usually normal.
E/A greater than 1.8: filling pressure likely elevated.
E/A 0.8–1.8: measure IVRT.
IVRT 80 ms or greater: filling pressure usually normal.
IVRT less than 80 ms: filling pressure likely elevated.

Aortic stenosis

Diastolic dysfunction and elevated filling pressures worsen prognosis. The standard algorithm is usually applicable unless MAC or another confounder is present.

Aortic regurgitation

Severe AR jet may contaminate mitral inflow.
Chronic severe AR may produce early-peaking mitral inflow and short deceleration time.
Data are limited for precise filling pressure estimation.
Supportive findings: LA enlargement, average E/e′ greater than 14 in some contexts, reduced LA strain where available, TR greater than 2.8 m/s, and clinical context.
Acute severe AR with premature mitral closure and diastolic MR suggests very high LV filling pressure.

Pericardial constriction versus restrictive cardiomyopathy

Features favouring constriction:

Respirophasic septal motion.
Septal bounce.
Mitral inflow respiratory variation greater than 25%.
Tricuspid inflow respiratory variation greater than 40%.
Expiratory hepatic vein diastolic flow reversal.
Medial/septal e′ preserved or increased relative to lateral e′.
Annulus reversus: medial e′ greater than lateral e′.
Strain reversus: reduced lateral free-wall strain with relatively preserved septal strain.

In restrictive cardiomyopathy or advanced myocardial disease, septal and lateral e′ are often both reduced.

3.5.8 Simplified diastolic algorithm

Step 1 — mitral E/A

If E/A is less than 0.8:

Prolonged IVRT plus reduced e′: Grade 1 impaired relaxation.
No elevated filling markers: likely Grade 1.
Elevated filling markers present: reassess for mixed physiology, low LAP artifact, or confounders.

If E/A is 0.8–2.0:

Evaluate average E/e′, LAVI, TR, pulmonary venous flow, LARS, and Valsalva.
All normal: normal.
Any elevated filling or remodelling marker: Grade 2 pseudonormalized.

If E/A is greater than 2.0:

Check deceleration time and filling pressures.
Deceleration time less than 140–150 ms plus elevated filling pressures: Grade 3 restrictive.
Otherwise reconsider tachycardia, valve disease, artifact, high-output state, or technical error.

Step 2 — estimate filling pressure

Elevated LAP is supported by:

Average E/e′ greater than 14.
LAVI greater than 34 mL/m².
TR velocity greater than 2.8 m/s.
Pulmonary venous S/D less than 1.
Pulmonary venous Ar–A duration greater than mitral A by 30 ms or more.
LARS less than or equal to 18% when available.
Valsalva unmasking of impaired relaxation.
Late diastolic L wave, if present, as ancillary evidence.

Step 3 — assign grade

Normal: normal E/A plus normal filling parameters.
Grade 1: impaired relaxation without elevated filling pressures.
Grade 2: pseudonormal E/A with elevated filling pressures.
Grade 3: restrictive E/A with short deceleration time and elevated filling pressures.

3.5.9 Diastolic bottom line

E/A less than 0.8 suggests impaired relaxation only if supported by prolonged IVRT and reduced e′; it may represent low LAP.
E/A 0.8–2.0 is a gray zone, not automatically normal.
E/A greater than 2.0 is usually restrictive, not pseudonormal, when deceleration time is short and filling pressures are elevated.
Short E-wave deceleration time less than 140–150 ms suggests elevated LAP or restrictive physiology, not impaired relaxation.
Average E/e′ less than or equal to 8 is normal; 9–14 is indeterminate; greater than 14 is elevated filling pressure by the 2025 marker.
LAVI greater than 34 mL/m² indicates chronic elevated LAP.
The 2025 primary algorithm uses e′, average E/e′, LARS, E/A, and LAVI.
Diastolic function is a pattern diagnosis, not a single-number diagnosis.

3.5.10 LVDD in the perioperative and critical care setting

LVDD is common, often under-recognized, and clinically consequential in patients undergoing surgery and in critically ill patients. It independently associates with pulmonary oedema, major cardiac events, difficult weaning from cardiopulmonary bypass, failed spontaneous breathing trials, and increased mortality in sepsis. In acute pulmonary oedema, hypertensive crises, and heart failure with preserved ejection fraction, LVDD is often the dominant substrate even when LV systolic function is preserved.

The central therapeutic principle is to avoid the dangerous combination of tachycardia plus elevated LV filling pressure plus high afterload.

Preoperative optimization

Identify clinically significant LVDD.
Estimate baseline filling pressures and congestion risk.
Review risk factors: LVH, hypertension, coronary artery disease, valvular disease, known cardiomyopathy, advanced age, female sex, diabetes, CKD, obesity, and atrial fibrillation.
Consider echocardiographic diastolic assessment in high-risk patients or those with suggestive findings.
Assess volume status and chronic congestion.
Optimize blood pressure control when safe.
Assess heart rate and rhythm control.
Identify renal dysfunction and anaemia.
Plan invasive haemodynamic monitoring or TEE when the patient is high risk or the procedure is complex.

Intraoperative management

Avoid sustained tachycardia.
Treat supraventricular arrhythmias promptly.
In atrial fibrillation, rate control is essential; rhythm control should be considered when clinically indicated.
Loss of atrial contraction increases LA pressure and should prompt closer haemodynamic monitoring.
Avoid excessive systemic vascular resistance.
Hypertension increases LV filling pressure and myocardial oxygen demand.
Vasodilators may be useful when blood pressure permits, particularly in hypertensive LVDD with pulmonary congestion.
Maintain diastolic arterial pressure sufficient for coronary perfusion while avoiding excessive afterload.
In shock, vasopressor choice should be interpreted in the context of afterload, filling pressure, and oxygen delivery.
LVDD patients are sensitive to both underfilling and overfilling.
Cautious fluid administration is preferred.
Fluid challenges should be interpreted dynamically with frequent reassessment using echocardiography, lung ultrasound, and haemodynamic trends.
Persistent congestion should prompt early decongestion if haemodynamics allow.
Positive-pressure ventilation can reduce preload and pulmonary oedema but may increase PVR and worsen RV function.
Ventilator settings should be titrated while monitoring both LV and RV performance.
High-risk patients may benefit from arterial line monitoring, central venous access when indicated, and serial focused ultrasound.
TEE is valuable in the operating room when transthoracic windows are limited, although TDI alignment remains technically demanding.

ICU management: CHEOPS bundle

CHEOPS is a practical expert-opinion framework for optimization after initial resuscitation:

C — Chest ultrasound: combine cardiac and pulmonary ultrasound to assess filling pressures, congestion, and ventilation-related effects.
H — Haemodynamics: optimize heart rate, rhythm, afterload, vasoactive therapy, and oxygen supply/demand.
O — Optimization of ventilation and pulmonary circulation: adjust PEEP and ventilator settings with attention to right and left heart function.
S — Stabilization: manage volume status cautiously, avoid unnecessary fluids, and decongest promptly when safe.

Special situations

Sepsis and septic shock: LVDD is common and associated with higher mortality. Initial resuscitation follows standard sepsis principles, but with heightened vigilance for fluid overload. Once perfusion is restored, reassess filling pressures and congestion early. Decongestion should be pursued when haemodynamics permit. Lung ultrasound and venous congestion assessment are especially useful.
Atrial fibrillation: E/A is unreliable. Rely on E/e′, LAVI, LARS when available, TR velocity, and congestion assessment. Rate control is essential. Loss of atrial contraction increases LA pressure and can precipitate pulmonary oedema.
Weaning from mechanical ventilation: LVDD is a powerful predictor of failed spontaneous breathing trials. Before SBT, assess heart rate, rhythm, blood pressure, pulmonary oedema, volume status, and RV function. Treat tachycardia, AF, hypertension, pulmonary oedema, pain, and agitation. Diuresis may be beneficial if congestion is present and blood pressure allows.
Cardiac surgery and CPB: LVDD is associated with adverse postoperative outcomes, including difficulty weaning from bypass. Intraoperative monitoring should include careful assessment of filling pressures and congestion. Postoperative management should avoid prolonged elevated filling pressures. RV function and PVR should be monitored because LVDD-related pulmonary venous hypertension can contribute to RV strain.
Renal impairment: renal dysfunction is both a risk factor for LVDD and a common ICU complication. Fluid overload is common and may be difficult to manage. Diuretics may be ineffective or limited by hypotension. Renal replacement therapy may be required. Volume status assessment should integrate haemodynamics, lung ultrasound, IVC and venous congestion findings, urine output, and biomarkers when useful.

Biomarker adjunct

BNP and NT-proBNP have strong negative predictive value for acute heart failure in symptomatic patients. Approximate exclusion thresholds of BNP 35 pg/mL and NT-proBNP 125 pg/mL can help exclude acute volume overload in appropriate clinical contexts. Elevated values are nonspecific and may occur in renal impairment, tachyarrhythmia, sepsis, advanced age, and other acute illnesses.

3.6 Valvular and aortic — advanced

Aortic valve peak velocity 4 m/s or greater: severe AS.
Aortic valve mean gradient 40 mmHg or greater: severe AS.
Aortic valve area 1.0 cm² or less: severe AS.
MR vena contracta 7 mm or greater: significant MR.
Aortic root less than 40 mm normal; 40 mm or greater dilated; 50 mm or greater aneurysmal.

Basic POCUS should not definitively grade valvular disease. Detect gross abnormality and refer for formal echo.

3.7 Pericardium and tamponade

Pericardial effusion size

Less than 10 mm: small.
10–20 mm: moderate.
Greater than 20 mm: large.
Measure as maximal echo-free separation at end-diastole.
10 mm or greater may be reported as at least moderate or operationally significant in POCUS.
Size alone does not define tamponade.

RA collapse

RA collapse, typically in late diastole and systole, supports tamponade but is nonspecific if brief.
RA collapse persisting greater than one-third of the cardiac cycle is highly specific.
RA collapse is a supportive sign; sensitivity is variable.

RV diastolic collapse

Early diastolic RV collapse is the most specific chamber-collapse sign of tamponade.
It is more informative than RA collapse.

IVC plethora

Supports tamponade.
Formal elevated RAP: IVC greater than 2.1 cm with inspiratory collapse less than 50%.
Some POCUS/ICU protocols use IVC greater than 2.5 cm with collapse less than 50% as a marker of marked plethora.
Interpret with ventilation and volume status.
IVC greater than 3.5 cm is not a universal formal RAP cutoff.

Respiratory transvalvular variation

Greater than 25% variation in mitral and/or tricuspid inflow in spontaneously breathing patients supports tamponade physiology.
Less validated under positive-pressure ventilation.
Can be influenced by arrhythmia, severe LV dysfunction, low flow, and technical factors.

Size alone is not tamponade

Tamponade requires clinical and haemodynamic correlation: hypotension, tachycardia, elevated CVP, low cardiac output, chamber collapse, Doppler support. Effusion size alone is neither necessary nor sufficient.

Key refinements

Prolonged RA collapse greater than one-third of the cardiac cycle is highly specific; brief RA collapse is nonspecific.
Early diastolic RV collapse is the most specific chamber-collapse sign.
IVC greater than 2.1 cm with collapse less than 50% is the formal elevated-RAP criterion.
IVC greater than 2.5 cm with poor collapse is a POCUS/ICU operational marker of marked plethora.
Respiratory variation greater than 25% is best applied in spontaneous breathing.
Tamponade is a pressure-time-volatility phenomenon. Small acute or localized effusions can cause tamponade; large chronic effusions may not.
Post-cardiac-surgery localized collections may produce atypical presentations and may require TEE.

3.8 Cardiac-specific pitfalls

Confusing pleural fluid with pericardial fluid.
Misidentifying RV as LV in poor windows.
Overestimating LV function in a hyperdynamic state.
Underestimating RV dilation when chronically enlarged.
Failing to distinguish acute from chronic RV enlargement.
Applying adult EPSS to pediatric patients.
Using IVC collapsibility in mechanical ventilation without caution.
Treating EPSS 7 vs 8 mm as nested severity categories.
Using EPSS greater than 7 mm as universal severe dysfunction.
Not stating the EPSS target endpoint: EF less than 55%, less than 50%, or less than 40%.
Misreading EPSS less than 5.5 mm as suggesting EF less than 40%; the correct inference is EF 50% or greater.
MAPSE is displacement in mm; e′ is velocity in cm/s. Do not confuse them.
Diastolic function is load-dependent and requires multiparametric interpretation.
E/A 0.8–2.0 is not automatically normal.
E/A greater than 2.0 is not “pseudonormal”; it is usually restrictive when deceleration time is short and filling pressures are elevated.
Short E-wave deceleration time less than 140–150 ms suggests elevated LAP or restrictive physiology, not impaired relaxation.
TR velocity depends on jet visibility; low flow underestimates pressure.
Pericardial disease can mimic congestion.
POCUS does not definitively grade valvular disease.
Using aortic valve PSAX as the default basic POCUS short-axis view for LV assessment; mid-papillary PSAX is standard for rapid LV evaluation.
Applying older E/e′ 15 or greater as the primary 2025 threshold instead of average E/e′ greater than 14.
Using septal e′ less than 7 cm/s and lateral e′ less than 10 cm/s as the primary 2025 thresholds.
Ignoring LARS less than or equal to 18% when available.
Treating LVDD as a static echo label rather than a dynamic haemodynamic state.
Failing to reassess after fluids, diuresis, vasopressors, ventilator changes, or arrhythmia treatment.
Using CHEOPS as a substitute for initial resuscitation in unstable patients.