Cardiac power output
CPO · Derived: CPO (W) = MAP × CO / 451
Normal range & thresholds
Resting CPO ≈0.8–1.0 W in healthy adults. CPO <0.6 W marks a critically low hydraulic output; in the SHOCK trial registry CPO was the strongest independent haemodynamic correlate of in-hospital mortality (threshold ≈0.53 W) [114].
Pathophysiology
Power is flow × pressure — the rate at which the heart does hydraulic work. A low CO with a high MAP (vasoconstriction) and a normal CO with a low MAP (vasodilation) can have the same CO or the same MAP but different power; CPO integrates both and reflects the reserve the ventricle has left [114].
Raised by
- Exercise and inotropes (a rise with dobutamine = contractile reserve)
- Hyperdynamic hypertensive states
Lowered by
- Cardiogenic shock, advanced heart failure
- Profound vasodilation with a failing ventricle
- Tamponade and massive PE (obstructive)
Technique & pitfalls
- Use the best MAP available (arterial line) and an averaged CO; report both inputs with the result.
- Echo CO in the ICU is acceptably accurate when LVOT technique is strict [170].
Pseudo-change & artefact
- Inherits every error of CO (LVOT diameter squared) and MAP.
- Mechanical circulatory support: device flow is not measured by LVOT VTI — do not calculate native CPO without accounting for it.
Treatment thresholds
- SCAI SHOCK staging and escalation — CPO <0.6 W with hypoperfusion supports escalation of inotropic or mechanical circulatory support in cardiogenic shock [154].
- Echo-derived haemodynamics at CICU admission, including SVI and CPO, independently predict in-hospital death [190].
Next step
- Next: find the mechanism (LV, RV, valve, mechanical complication, tamponade).
- Then: reassess after each intervention; a rising CPO is a treatment response.
Drugs
Inotropes and vasopressors raise it acutely; inappropriate vasodilators or negative inotropes lower it.
Reversibility
Tracks the underlying state — improves with recovery from stunning, revascularisation, relief of tamponade or PE.