Chapter 7 — Left Ventricular Systolic Function

📚 Guideline basis

ASE/EACVI 2015 chamber quantification (Lang et al., JASE 2015;28:1–39); ASE 2019 comprehensive TTE examination; ESICM PRICES consensus on CCE reporting (Intensive Care Med 2021); EACVI/ASE strain standardisation task force.

Pathophysiology & Mechanisms

Ejection fraction is not contractility. It is the ratio of stroke volume to end-diastolic volume, and therefore a composite of preload, afterload, heart rate, synchrony, and intrinsic inotropic state. Three consequences dominate ICU interpretation:

Afterload dependence. In vasoplegic shock, systemic vascular resistance falls, ejection becomes easy, and EF rises even when intrinsic contractility is depressed. Restoring perfusion pressure with noradrenaline then "unmasks" a low EF that was present all along. The EF changed; the myocardium did not.
Preload dependence. A hypovolaemic ventricle with a small end-diastolic volume ejects a small absolute stroke volume at a high fractional shortening — the "hyperdynamic, kissing" ventricle. EF is 75%; cardiac output is 2.4 L/min.
Geometric assumption dependence. Every volumetric method assumes a shape. Regional wall motion abnormalities, aneurysm, or a foreshortened image break the assumption.

The mechanical substrate: subendocardial longitudinal fibres shorten first and are the most vulnerable to ischaemia, elevated wall stress, and inflammatory injury. Circumferential mid-wall fibres, which contribute most to ejection fraction, are relatively preserved until later. This anatomy is why longitudinal function (GLS, MAPSE, s′) falls before EF falls — the earliest detectable systolic abnormality in sepsis, in cardiotoxicity, and in infiltrative disease is longitudinal, and EF is normal at that point.

Clinical Phenotypes

Phenotype	EF	SV / CO	LV size	Typical setting
Hyperdynamic, underfilled	>70%	Low	Small, end-systolic cavity obliteration	Hypovolaemia, haemorrhage, early distributive shock
Hyperdynamic, high-output	>65%	High	Normal or small	Sepsis with vasoplegia, thyrotoxicosis, liver failure, severe anaemia
Depressed, acute, non-dilated	20–45%	Low	Normal cavity size	Sepsis-induced cardiomyopathy, stress cardiomyopathy, myocarditis
Depressed, chronic, dilated	<35%	Low	Dilated, spherical, with secondary MR	Chronic dilated cardiomyopathy decompensated by the acute illness
Regional	Variable	Variable	Segmental	Acute coronary syndrome, stress cardiomyopathy (apical ballooning)
Normal EF, abnormal longitudinal	>55%	Variable	Normal	Early septic cardiomyopathy, amyloid, HFpEF

Quantification methods

Biplane method of discs (Simpson's)

The reference echocardiographic method. Trace the endocardial border at end-diastole and end-systole in A4C and A2C; the software sums stacked elliptical discs.

EF = ((EDV - ESV) / EDV) × 100

Requirements: unforeshortened apical views; endocardium visualised in ≥80% of the border (otherwise use an ultrasound enhancing agent); papillary muscles and trabeculae included in the cavity, not the wall; end-diastole and end-systole defined by ECG and valve motion.

Normal LVEF (ASE/EACVI 2015): 52–72% in men, 54–74% in women. Values below these define abnormal; severe dysfunction is conventionally <30%.

Visual (eyeball) estimation

Validated against volumetric methods when performed by trained operators, and the practical default in the ICU. Its accuracy is category-level, not point-level: reporting "moderately impaired" is defensible; reporting "EF 42%" from visual estimation is not. Categories: hyperdynamic (>70%), normal (52–72%), mildly reduced (41–51%), moderately reduced (30–40%), severely reduced (<30%).

Fractional shortening and Teichholz

FS = ((LVIDd - LVIDs) / LVIDd) × 100

Normal FS ≈ 25–45%. Do not use the Teichholz or Quinones formulas to derive EF from linear dimensions in the ICU: they cube a single basal measurement, and in the presence of regional dysfunction, septal flattening from RV overload, or post-cardiotomy septal motion, the result is arbitrary. ASE 2015 explicitly recommends against volumetric estimation from linear dimensions.

E-point septal separation (EPSS)

M-mode distance from the anterior mitral leaflet E-point to the interventricular septum in PLAX. EPSS > 7 mm suggests reduced EF; the correlation is strongest at the extremes.

Invalid when: aortic regurgitation (the AR jet holds the anterior leaflet away from the septum), mitral stenosis (restricted leaflet excursion), severe LVH or a small cavity, and marked septal hypertrophy. Useful as a rapid corroborative sign in a poor window, never as a stand-alone measure.

MAPSE and mitral annular s′

MAPSE (mitral annular plane systolic excursion, M-mode at the lateral or septal annulus in A4C): normal ≥ 10–12 mm; values < 8 mm indicate longitudinal dysfunction. Tissue Doppler s′ at the mitral annulus: normal ≥ 6–7 cm/s (septal), lower values indicating longitudinal impairment.

Both are load-dependent, angle-dependent, and reflect basal segments only — they miss apical disease entirely (which is precisely why they are normal in apical-ballooning stress cardiomyopathy while EF is markedly depressed).

Global longitudinal strain (GLS)

Speckle-tracking measurement of myocardial deformation. Reported as a negative number; more negative is better. Normal is approximately −20% or more negative, with vendor-specific variability that makes cross-vendor comparison invalid.

GLS is the most sensitive routine measure of systolic function and detects abnormality when EF is normal. In septic shock it is abnormal in a large fraction of patients with preserved EF. Its relationship to outcome in sepsis is contested — it identifies myocardial involvement reliably, but whether that involvement independently predicts mortality remains unresolved across cohorts.

⚠️ Evidence quality

GLS thresholds are derived from ambulatory populations and are vendor-dependent. In the ICU, GLS is load-dependent in the same direction as EF: it improves with vasodilatation and worsens with vasoconstriction. Serial GLS across a large change in noradrenaline dose is not comparing like with like.

dP/dt from the mitral regurgitant jet

When MR is present, the rate of pressure rise during isovolumic contraction is derived from the CW MR envelope, measuring the time interval between 1 m/s and 3 m/s:

dP/dt = 32 mmHg / Δt (s)

(The 32 mmHg comes from 4(3²) − 4(1²) = 36 − 4.) Normal > 1200 mmHg/s; < 800 mmHg/s indicates significant systolic dysfunction. Less afterload-dependent than EF, which is its attraction in vasoplegia — but it requires a measurable MR jet with a clean early envelope.

Diagnostic Synthesis

Parameter	Normal	Mildly abnormal	Moderately	Severely
LVEF, men	52–72%	41–51%	30–40%	<30%
LVEF, women	54–74%	41–53%	30–40%	<30%
Fractional shortening	25–45%	—	—	—
MAPSE	≥10 mm	—	—	<8 mm
Septal s′	≥7 cm/s	—	—	<5 cm/s
GLS (vendor-dependent)	≤ −20%	−16 to −20%	−12 to −16%	> −12%
EPSS	<7 mm	—	—	>13 mm
dP/dt	>1200 mmHg/s	1000–1200	800–1000	<800

ICU-Specific Limitations

Confounder	Direction of error	Management
Vasoplegia / low SVR	EF overestimates contractility	Report EF with the concurrent MAP and vasopressor dose; consider dP/dt or GLS
High-dose vasoconstrictor	EF underestimates contractility	Same; re-assess after weaning
Hypovolaemia	Small EDV, high EF, low SV	Always report SV or VTI alongside EF
Tachycardia >120/min	Foreshortened filling, degraded tracing	State the heart rate; interpret cautiously
Atrial fibrillation	Beat-to-beat variation	Average ≥5 beats or use index-beat method
RV pressure overload	Septal flattening violates geometric assumptions	Use biplane Simpson's, not linear methods
Post-cardiotomy	Paradoxical septal motion, normal for weeks	Judge by lateral/posterior wall and longitudinal indices
Poor endocardial definition	Over-gain worsens it; borders drift outward	Use an ultrasound enhancing agent — ASE-endorsed when ≥2 contiguous segments are non-diagnostic

Therapeutic Logic

An EF value alone changes nothing. The action follows from the combination:

Pattern	Interpretation	Action
Low EF + low VTI + dilated IVC + B-lines	Cardiogenic failure with congestion	Inotrope/afterload reduction; avoid fluid; consider MCS if lactate rising
Low EF + low VTI + small LV + collapsing IVC	Hypovolaemia superimposed on chronic cardiomyopathy	Cautious small-volume challenge with reassessment of VTI
High EF + low VTI + small LV	Underfilled/hyperdynamic	Volume, then vasopressor; exclude dynamic LVOT obstruction (Chapter 28)
High EF + high VTI + low MAP	Vasoplegic high-output shock	Vasopressor; fluid will not fix the pressure deficit
Normal EF + abnormal GLS/MAPSE	Early myocardial involvement	Prognostic flag; avoid escalating inotropes on this finding alone

🛑 Critical pitfall: Starting an inotrope on the basis of a low EF in a patient with a high stroke volume and a low SVR. The problem is arterial, not ventricular; inotropes worsen vasodilatation and arrhythmia. Always measure flow before treating a number.

🛑 Critical pitfall: Reporting "normal LV systolic function" in a patient with a hyperdynamic, cavity-obliterating ventricle. This is not normal function — it is a specific and actionable finding (hypovolaemia or vasoplegia, with a risk of dynamic LVOT obstruction).

💡 Clinical pearl: EF answers "how well does this ventricle empty at this afterload?" Stroke volume answers "how much blood is the patient receiving?" Only the second correlates with organ perfusion.
💡 Clinical pearl: Longitudinal indices fall first. A normal EF with MAPSE 6 mm and s′ 4 cm/s is an abnormal ventricle, and a normal-EF report is misleading.
💡 Clinical pearl: Record vasopressor dose and MAP in the report body, not the notes. It converts a snapshot into an interpretable data point for the next operator.

References

Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults. J Am Soc Echocardiogr 2015;28:1–39.
Sanfilippo F, Huang S, Herpain A, et al. The PRICES statement. Intensive Care Med 2021;47:1–13. PMID 33275163.
Porter TR, Mulvagh SL, Abdelmoneim SS, et al. Clinical applications of ultrasonic enhancing agents in echocardiography: 2018 ASE guidelines update. J Am Soc Echocardiogr 2018;31:241–74.
Mitchell C, Rahko PS, Blauwet LA, et al. Guidelines for performing a comprehensive TTE examination in adults. J Am Soc Echocardiogr 2019;32:1–64.