🧵 Inlet impedance: the missing determinant of cardiac output 1/ What really limits cardiac output: the heart or the circulation delivering blood to it? This question has sparked heated arguments between physiologists for decades. To answer it, you first need to understand inlet
2/ Guyton taught venous return using resistance (as if the system were an electrical circuit). Anderson reframed it using inlet impedance (Zin) because veins and hearts are compliant, deformable, and state-dependent.
3/ Zin replaces venous resistance in the denominator: VR ∝ (Pms − RAP) / Zin Higher Zin means poorer conversion of pressure into flow.
4/ Think of venous return as blood entering the heart through a doorway. Pms is the push from behind. Zin describes how hard it is to get through the door.
5/ There are two fundamental ways inlet impedance (Zin) can increase – two ways the doorway can be affected. They often coexist, but the pressure signatures differ.
6/ 🚪 The door is small Flow is limited by a choke before the heart. Examples: • IVC compression • Abdominal hypertension • True Starling-resistor behaviour Pressure builds upstream of the door.
7/ 🔩 The hinges are stiff The heart is hard to open. Examples: • RV dilatation with septal shift • LV diastolic dysfunction • Pericardial constraint • High intrathoracic pressure (PEEP – constraint-dominant) Pressure rises inside the heart.
8/ ⚠️ Sometimes both are true The door is small and the hinges are stiff. Examples: • Very high PEEP • Tamponade physiology • Severe RV failure in a tight pericardium Here, inlet impedance skyrockets.
9/ 🔩 Stiff hinges Small increases in flow require large rises in filling pressure. At the new equilibrium: • RAP rises • congestion is central • fluids give pressure ≫ flow
10/ 🚪 Small door Flow is limited upstream. Pressure accumulates before the heart. At equilibrium: • RAP may be normal or low • congestion is extra-cardiac • fluids worsen pooling without meaningful CO gain
11/ This is why RAP is a dependent variable, not a cause. High RAP often reflects high inlet impedance – not “backpressure” opposing venous return.
12/ Increasing stressed volume (↑Pms) increases the driving pressure for venous return. But when Zin is high, the pressure-to-flow gain is poor. Most of the added volume appears as congestion, not flow.
13/ So the real clinical question isn’t: “Is the CVP high?” It’s: “Is venous return limited by a small door, stiff hinges or both?”
14/ Cardiac output depends on pressure (Pms), the pump (the heart), and how easily blood can enter it (Zin). High RAP in heart failure reflects impaired filling, not blocked flow. This sets up the real debate: what actually drives the circulation – the heart or the venous
16/ Start here 👇🏻
Thanks Stephen. I’m not 100% sure what question(s) you are asking. Can you clarify? Also apologies but those photos are too much effort to read 😆