Stroke volume, cardiac output & index

SV, SVi, CO, CI · LVOT diameter (zoomed PLAX, mid-systole) and LVOT VTI (PW, A5C/A3C, 0.5–1 cm below the valve); heart rate from the same beats

Normal range & thresholds

SV 60–100 mL · SVi 35–65 mL/m² · CO 4–8 L/min · CI 2.5–4.0 L/min/m² · LVOT VTI 18–22 cm. SV = 0.785 × LVOT d² × LVOT VTI; CO = SV × HR; CI = CO / BSA ^[33].

• SVi <35 mL/m² defines the low-flow state that reorganises aortic-stenosis grading ^[5].
• LVOT VTI <15 cm marks low forward flow; in advanced heart failure and cardiac-ICU cohorts it carries higher mortality independently of ejection fraction ^[190,191].
• CI <2.2 L/min/m² with hypoperfusion defines cardiogenic shock (SCAI stage C and beyond) ^[154].

Pathophysiology

Stroke volume is the product of how full the ventricle is (preload), how hard it contracts (contractility) and what it ejects against (afterload); heart rate multiplies it into output. In a failing ventricle SV is afterload-limited; in hypovolaemia it is preload-limited; in tachyarrhythmia it is filling-time-limited. Because the LVOT diameter does not change within a patient over hours, VTI alone tracks SV — the reason serial VTI is the workhorse of haemodynamic echo ^[171].

Raised by

• High-output states: sepsis (early), anaemia, thyrotoxicosis, pregnancy, arteriovenous fistula, beri-beri, cirrhosis
• Inotropes, exercise, fever
• Significant aortic regurgitation (total LVOT SV is high; forward SV may not be)
• Bradycardia raises SV (longer filling) while CO may fall

Lowered by

• LV systolic dysfunction of any cause; acute myocarditis; stunning; takotsubo
• Hypovolaemia, haemorrhage, vasodilated under-filling
• Obstruction to filling: tamponade, constriction, mitral stenosis, massive PE with RV failure (interdependence)
• Significant MR or VSD (forward SV reduced), dynamic LVOT obstruction
• Tachyarrhythmia, severe bradycardia (CO), high-dose β-blockade

Technique & pitfalls

• LVOT diameter: zoomed PLAX, mid-systole, inner edge to inner edge at the hinge points — the same level as the PW sample volume ^[5].
• PW sample volume in the LVOT 0.5–1 cm proximal to the valve; clean envelope with a closing click; trace the modal velocity.
• Average 3 beats in sinus rhythm, 5–10 in AF; report the heart rate with the VTI.
• In the ICU, if the diameter is uncertain, report VTI itself and follow it serially — the diameter error is squared, the VTI error is not ^[171].
• Echo CO agrees acceptably with thermodilution when technique is strict, and is precise enough to track change ^[170].

Pseudo-change & artefact

• A 1 mm diameter error ≈10% SV error (squared).
• Sampling in the zone of flow acceleration overestimates VTI; sampling too deep underestimates.
• Poor alignment (>20°) underestimates.
• Dynamic LVOT obstruction or subaortic membrane produces a late-peaking dagger envelope that is not LVOT stroke distance.
• Irregular rhythm: a single beat after a long pause overstates SV.

Treatment thresholds

• Shock phenotyping: low SVi/CI with poor LV function (cardiogenic) vs preserved/high output with low SVR (distributive) vs small hyperdynamic LV (hypovolaemic) vs RV failure/tamponade (obstructive) directs fluids, vasopressors, inotropes or drainage ^{[151,152,153]}.
• SCAI SHOCK staging uses CI and CPO to escalate to mechanical support ^[154].
• Low-flow AS (SVi <35) triggers dobutamine stress or calcium scoring before severity is decided ^[5,6].
• Qp:Qs, volumetric regurgitant volume and AVA all start from this SV ^[4,33].

Next step

• Next: combine with blood pressure → SVR and cardiac power output (cards 43, 44).
• Then: dynamic fluid-responsiveness test if hypoperfused (card 45).
• Then: find the mechanism — LV/RV function, valves, pericardium, LVOT obstruction; lung ultrasound for congestion.
• Repeat after every intervention: VTI is the fastest response marker available at the bedside.

Drugs

• Raise SV: inotropes (dobutamine, milrinone, levosimendan), afterload reduction in a failing LV, fluids in a preload-responsive patient, rate control in tachyarrhythmia.
• Lower SV: β-blockers and non-dihydropyridine calcium blockers (acutely), vasopressors in a failing LV (afterload), positive-pressure ventilation with high PEEP (preload), over-diuresis.

Reversibility

Minute-to-minute — the most dynamic number in echocardiography. Chronically, SV rises with reverse remodelling on GDMT and after correction of valve lesions; in septic cardiomyopathy it typically recovers within days to weeks.