Thank you very much Dr Miller for this. I don’t think any one / any book would give this sort of an account on venous congestion. And thanks for simplifying this🙏🙏🙏🙏
Regarding case 2, where forward flow is maintained but filling pressures are elevated. If we think of the circulatory system as "one tube" (as a simplification, analogous to how we can analyze an electrical circuit "globally" even though it contains parallel elements), when we increase CVP while maintaining relatively constant MAP and CO, then "globally" SVR must decrease. We also know that in edematous tissues, conductance decreases anyway, so local flow also decreases.
Where does the "rest" of global flow (understood as volume over time) go? Is it true that in the remaining tissues, precapillary resistance decreases, and we are dealing with shunting and excess flow that are inadequate to tissue demand? Is it also the case that due to the increase in Pc secondary to CVP, excess fluid circulates in the lymphatic system - then it would be a parallel branch with a large conductance range?
Yes if cardiac output is preserved despite a higher CVP and similar MAP, then the calculated global SVR must be lower. But that global number is only the aggregate result of many vascular beds in parallel. It does not mean resistance has fallen everywhere.
If an oedematous organ becomes externally constrained, its local conductance may fall. It becomes a less favourable pathway for flow. The remaining flow is then redistributed through other lower-resistance pathways. Some of that flow may be excessive relative to local demand, poorly matched to exchange, or effectively shunt-like.
I would be cautious about saying all remaining tissues have reduced precapillary resistance. Some may. Others may autoregulate, while some congested or oedematous beds may have increased effective resistance. The global fall in SVR is the summed result of all those local changes.
The lymphatic system is slightly different. It can increase lymph flow substantially when capillary filtration rises, so it is an important compensatory drainage pathway. But it is not a major parallel branch for cardiac output. The lymphatics handle filtered fluid, not the “missing” blood flow. Once filtration exceeds lymphatic reserve, oedema develops, tissue pressure rises, and local external constraint can further reduce microvascular conductance.
I'm asking about lymph because in one of your threads regarding "capillary leak" in sepsis, you wrote that the lymphatic system becomes a hyperdynamic circulation. So, reasoning according to Kirchhoff's First Law, we have flow flowing into the capillaries, from which it flows into the venous bed, and some flows into the lymphatic system (not blood per se, but fluid nonetheless). And if we have a greater flow to such a "node," couldn't we treat the lymphatic system as buffering this "excess"?
Blood flow through the organ is one thing. Fluid filtering out of capillaries and returning through lymphatics is another. Most blood entering a capillary bed still leaves through the venous side. But some plasma water and protein filters into the interstitium. The lymphatics then return that filtered fluid to the circulation.
So yes: when filtration increases in sepsis or congestion, the lymphatics can become a high-flow drainage system. They buffer the excess filtered fluid and help defend plasma volume.
But they are not really where the cardiac output “goes”. Preserved cardiac output is still blood moving through vascular pathways. If one organ becomes a worse pathway for blood flow, that flow is mainly redistributed through other vascular beds.
Lymphatics buffer xs filtration not xs cardiac output.
The cardiovascular system does not transport pressure; it transports mechanical energy. The heart therefore does not generate pressure per se, it generates mechanical energy. Pressure is simply one of the macroscopic forms in which that energy is stored within the circulation.
From this perspective, it is correct to say that a pressure gradient is not an independent “motor” of flow. However, it remains the generalized driving force governing flow through a dissipative system. As blood traverses the vascular tree, the available mechanical energy is progressively dissipated through viscous and structural losses, which are manifested macroscopically as pressure loss. Therefore, the argument that the pressure gradient merely describes the final state of the circulation is incomplete. In physics, the pressure gradient participates causally in determining flow, even though, in a closed cardiovascular system, that gradient simultaneously emerges from the interaction between cardiac energy generation, stressed blood volume, vascular resistance, vascular compliance, and transmural pressure.
Rather than viewing the pressure gradient as an isolated pump, it is more accurate to regard it as the macroscopic expression of the mechanical energy available to be dissipated through a vascular pathway with a given conductance.
Ultimately, venous congestion should not be interpreted simply as an elevation in venous pressure. Instead, it represents a shift in the thermodynamic operating state of the cardiovascular system, increasing exergy destruction within specific vascular beds and reducing the useful mechanical energy ultimately delivered to the tissues, even when global cardiac output is preserved.
We mostly agree then. I’d be careful with your casual language though. A pressure gradient is not an independent physical actor. It is the macroscopic expression of an energy state across a pathway.
That state is produced by energy input interacting with the fundamental properties of the system: resistance, compliance/elastance and inertance.
Pressure gradients therefore appear in the equations of flow, but the measured gradient is not a free-standing cause. It’s the signature not the mechanism.
I think we are distinguishing between two different levels of causality.
I completely agree that a pressure gradient is not an independent source of energy. It emerges from the interaction between cardiac work, stressed volume, vascular elastance, resistance, compliance and boundary conditions.
However, once that energy state exists, continuum mechanics treats the pressure gradient as the generalized force acting on the fluid. In the Navier–Stokes equations -∇P is not merely a descriptor of the final state, it is the force density that accelerates a fluid element. In that sense, the pressure gradient is not the ultimate source of energy, but it is the immediate mechanical mechanism by which stored mechanical energy is converted into blood motion.
So I would distinguish between the origin of the pressure gradient (system energetics) and its local dynamical role (fluid acceleration). Both statements are true, but they address different questions.
Continuum mechanics uses pressure gradients as an efficient local description of stress imbalance. That is valid. But it can become misleading shorthand if we then treat the gradient as the independent cause of flow. The pressure field itself is generated by energy input interacting with system properties. So the gradient describes how the generated field behaves locally; it does not explain why the field exists.
I think the distinction you’re making is between the origin of the field and the mechanism of interaction, and I agree those shouldn’t be conflated.
The pressure field certainly requires an energetic origin. Without those no pressure gradients would exist.
However, in continuum mechanics, the momentum balance is formulated locally. Once the pressure field exists, the force acting on a fluid element is:
>f = -∇P,>
which is why the Navier–Stokes equations contain the pressure-gradient term explicitly as the source of fluid acceleration.
More fundamentally, the pressure gradient is not merely descriptive. It arises directly from applying Newton’s second law to an infinitesimal fluid element. The net force produced by the normal stresses on the surfaces of that element is exactly what gives rise to the term -∇P. In other words, the pressure gradient is not simply a linguistic shorthand or a signature of the pressure field, it is the mathematical representation of the net mechanical force due to normal stresses acting on the fluid.
So I would distinguish between the origin of the pressure field (system energetics) and the proximate mechanical cause of motion (the local stress imbalance represented by -∇P). The former explains why the field exists; the latter explains why a fluid element accelerates.
A uniform pressure field, regardless of how much energy it represents, produces no acceleration because -∇P = 0. This illustrates that continuum mechanics attributes fluid acceleration not to pressure itself, nor directly to its energetic origin, but to the spatial imbalance of pressure, the pressure gradient.
More broadly, I think venous return remains one of the most fascinating and least completely understood problems in cardiovascular physiology. Despite decades of elegant work by Guyton, Levy, Brengelmann, Rothe and many others, we probably have more sophisticated models today, but also more unanswered questions. That is precisely why these discussions remain so valuable.
Thank you very much Dr Miller for this. I don’t think any one / any book would give this sort of an account on venous congestion. And thanks for simplifying this🙏🙏🙏🙏
A pleasure Chamin
Regarding case 2, where forward flow is maintained but filling pressures are elevated. If we think of the circulatory system as "one tube" (as a simplification, analogous to how we can analyze an electrical circuit "globally" even though it contains parallel elements), when we increase CVP while maintaining relatively constant MAP and CO, then "globally" SVR must decrease. We also know that in edematous tissues, conductance decreases anyway, so local flow also decreases.
Where does the "rest" of global flow (understood as volume over time) go? Is it true that in the remaining tissues, precapillary resistance decreases, and we are dealing with shunting and excess flow that are inadequate to tissue demand? Is it also the case that due to the increase in Pc secondary to CVP, excess fluid circulates in the lymphatic system - then it would be a parallel branch with a large conductance range?
Yes if cardiac output is preserved despite a higher CVP and similar MAP, then the calculated global SVR must be lower. But that global number is only the aggregate result of many vascular beds in parallel. It does not mean resistance has fallen everywhere.
If an oedematous organ becomes externally constrained, its local conductance may fall. It becomes a less favourable pathway for flow. The remaining flow is then redistributed through other lower-resistance pathways. Some of that flow may be excessive relative to local demand, poorly matched to exchange, or effectively shunt-like.
I would be cautious about saying all remaining tissues have reduced precapillary resistance. Some may. Others may autoregulate, while some congested or oedematous beds may have increased effective resistance. The global fall in SVR is the summed result of all those local changes.
The lymphatic system is slightly different. It can increase lymph flow substantially when capillary filtration rises, so it is an important compensatory drainage pathway. But it is not a major parallel branch for cardiac output. The lymphatics handle filtered fluid, not the “missing” blood flow. Once filtration exceeds lymphatic reserve, oedema develops, tissue pressure rises, and local external constraint can further reduce microvascular conductance.
I'm asking about lymph because in one of your threads regarding "capillary leak" in sepsis, you wrote that the lymphatic system becomes a hyperdynamic circulation. So, reasoning according to Kirchhoff's First Law, we have flow flowing into the capillaries, from which it flows into the venous bed, and some flows into the lymphatic system (not blood per se, but fluid nonetheless). And if we have a greater flow to such a "node," couldn't we treat the lymphatic system as buffering this "excess"?
Blood flow through the organ is one thing. Fluid filtering out of capillaries and returning through lymphatics is another. Most blood entering a capillary bed still leaves through the venous side. But some plasma water and protein filters into the interstitium. The lymphatics then return that filtered fluid to the circulation.
So yes: when filtration increases in sepsis or congestion, the lymphatics can become a high-flow drainage system. They buffer the excess filtered fluid and help defend plasma volume.
But they are not really where the cardiac output “goes”. Preserved cardiac output is still blood moving through vascular pathways. If one organ becomes a worse pathway for blood flow, that flow is mainly redistributed through other vascular beds.
Lymphatics buffer xs filtration not xs cardiac output.
The cardiovascular system does not transport pressure; it transports mechanical energy. The heart therefore does not generate pressure per se, it generates mechanical energy. Pressure is simply one of the macroscopic forms in which that energy is stored within the circulation.
From this perspective, it is correct to say that a pressure gradient is not an independent “motor” of flow. However, it remains the generalized driving force governing flow through a dissipative system. As blood traverses the vascular tree, the available mechanical energy is progressively dissipated through viscous and structural losses, which are manifested macroscopically as pressure loss. Therefore, the argument that the pressure gradient merely describes the final state of the circulation is incomplete. In physics, the pressure gradient participates causally in determining flow, even though, in a closed cardiovascular system, that gradient simultaneously emerges from the interaction between cardiac energy generation, stressed blood volume, vascular resistance, vascular compliance, and transmural pressure.
Rather than viewing the pressure gradient as an isolated pump, it is more accurate to regard it as the macroscopic expression of the mechanical energy available to be dissipated through a vascular pathway with a given conductance.
Ultimately, venous congestion should not be interpreted simply as an elevation in venous pressure. Instead, it represents a shift in the thermodynamic operating state of the cardiovascular system, increasing exergy destruction within specific vascular beds and reducing the useful mechanical energy ultimately delivered to the tissues, even when global cardiac output is preserved.
We mostly agree then. I’d be careful with your casual language though. A pressure gradient is not an independent physical actor. It is the macroscopic expression of an energy state across a pathway.
That state is produced by energy input interacting with the fundamental properties of the system: resistance, compliance/elastance and inertance.
Pressure gradients therefore appear in the equations of flow, but the measured gradient is not a free-standing cause. It’s the signature not the mechanism.
I think we are distinguishing between two different levels of causality.
I completely agree that a pressure gradient is not an independent source of energy. It emerges from the interaction between cardiac work, stressed volume, vascular elastance, resistance, compliance and boundary conditions.
However, once that energy state exists, continuum mechanics treats the pressure gradient as the generalized force acting on the fluid. In the Navier–Stokes equations -∇P is not merely a descriptor of the final state, it is the force density that accelerates a fluid element. In that sense, the pressure gradient is not the ultimate source of energy, but it is the immediate mechanical mechanism by which stored mechanical energy is converted into blood motion.
So I would distinguish between the origin of the pressure gradient (system energetics) and its local dynamical role (fluid acceleration). Both statements are true, but they address different questions.
Continuum mechanics uses pressure gradients as an efficient local description of stress imbalance. That is valid. But it can become misleading shorthand if we then treat the gradient as the independent cause of flow. The pressure field itself is generated by energy input interacting with system properties. So the gradient describes how the generated field behaves locally; it does not explain why the field exists.
I think the distinction you’re making is between the origin of the field and the mechanism of interaction, and I agree those shouldn’t be conflated.
The pressure field certainly requires an energetic origin. Without those no pressure gradients would exist.
However, in continuum mechanics, the momentum balance is formulated locally. Once the pressure field exists, the force acting on a fluid element is:
>f = -∇P,>
which is why the Navier–Stokes equations contain the pressure-gradient term explicitly as the source of fluid acceleration.
More fundamentally, the pressure gradient is not merely descriptive. It arises directly from applying Newton’s second law to an infinitesimal fluid element. The net force produced by the normal stresses on the surfaces of that element is exactly what gives rise to the term -∇P. In other words, the pressure gradient is not simply a linguistic shorthand or a signature of the pressure field, it is the mathematical representation of the net mechanical force due to normal stresses acting on the fluid.
So I would distinguish between the origin of the pressure field (system energetics) and the proximate mechanical cause of motion (the local stress imbalance represented by -∇P). The former explains why the field exists; the latter explains why a fluid element accelerates.
A uniform pressure field, regardless of how much energy it represents, produces no acceleration because -∇P = 0. This illustrates that continuum mechanics attributes fluid acceleration not to pressure itself, nor directly to its energetic origin, but to the spatial imbalance of pressure, the pressure gradient.
More broadly, I think venous return remains one of the most fascinating and least completely understood problems in cardiovascular physiology. Despite decades of elegant work by Guyton, Levy, Brengelmann, Rothe and many others, we probably have more sophisticated models today, but also more unanswered questions. That is precisely why these discussions remain so valuable.