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“Everybody gets so much information all day long that they lose their common sense. They listen so much that they forget to be natural. This is a nice story.”
It was my great honour and pleasure to speak, virtually, at the Congresso Nacional de Medicina Intensiva hosted by the Sociedade Portuguesa de Cuidados Intensivos in January of this year. I gave an introduction to the physiology of right atrial pressure just before my friend and colleague Dr. Phillipe Rola spoke about the VExUS score, that is, the venous excess in ultrasound score. The VExUS score is being deployed in post-operative cardiac surgery patients, and in the ICU as an ultrasonographic assessment of ‘venous congestion’ which is integrated within clinical context to help direct hemodynamic optimization [e.g., right heart afterload reduction, volume management, etc.].
While venous congestion, volume overload, right atrial pressure, cardiac function and tissue perfusion are intertwined sometimes used interchangeably, I hoped to provide some physiological foundation for thinking about these disparate terms and their rough approximation at the bedside. My lecture is posted below for viewing, pro re nata.
Right atrial pressure
As an approach to right atrial pressure, I employ the Guytonian model. From first principles, this approach is appropriate, I believe, because both smooth muscle within the peripheral vasculature [e.g., veins] and cardiac muscle within the heart may add energy to blood – a moveable tissue. Not all agree with this supposition – holding that only the heart adds energy to the system. This topic has been covered previously and a recent mathematical model proposed. I have exchanged correspondence with Dr. Brengelman on these positions; I encourage an open-mind – science and medicine never cease to be humbling.
Though as Tyberg mentions in his excellent criticism, the venous vasculature has a ‘capacitance’ that acts analogous to a ‘spring’ that may be tightened or loosened. Thus, considering ‘venous return’ as an independent energy source seems appropriate. As previously described, the unification of pressure, volume, energy and mechanical power may tie biological damage across the lungs and the cardiovascular system. The Guytonian perspective holds that pressure within the right atrium – or the central venous pressure – forms as the energetic nexus of the peripheral vasculature and cardiac function.
Finally, on the formation of right atrial pressure and blood flow in the steady state, no one captures the circular scientific exacerbation as well as Guyton himself – reported in a classic review by Rothe:
“We would be arguing in circles to say which is more important, venous return or cardiac output. They are interdependent and except transiently, are equal to each other. Nevertheless, when the venous return changes before the cardiac output changes, physiologists often say that the change in venous return changes the cardiac output. When the cardiac output increases before venous return changes, it is often said that the increase in cardiac output caused an increase in venous return. It is mainly factors in the peripheral circulation that cause the venous return to change ahead of cardiac output, and it is mainly cardiac factors that cause the cardiac output to change ahead of venous return.”
Right atrial pressure by ultrasound
Thereafter, the talk very briefly describes how right atrial pressure is transduced by changes in great vein diameter. These topics have been covered before; in fact, the underlying meaning of inspiratory collapse of the inferior vena cava was my first entry on pulmccm.org. For a dedicated video on IVC collapse, please see this post from a few years ago.
Yet beyond b-mode imaging, right atrial pressure can also be assessed by venous Doppler. This too has been covered here at pulmccm.org and literature dating back to the late 1970s support the use of venous Doppler as an index of right heart function. Importantly, from a very basic, ‘Frank-Starling’ perspective, both IVC size and great vein Doppler lay themselves out along the x-axis of the cardiac preload-output relationship. In other words, a plethoric, unvarying great vein diameter with monophasic D-wave Doppler pattern gives the clinician good reason to believe that the central venous pressure is elevated. In other words, the x-axis of the Starling mechanism is elevated. However, this does not tell you with certainty the slope of the Starling curve. Ask yourself why low right heart filling pressure is observed in patients intolerant of additional preload?
One final model
Finally, I try to link macrohemodynamic parameters such as central venous pressure [CVP], cardiac output and mean arterial pressure to individual tissue perfusion. This too is a complicated concept and definitely not as simple as commonly taught. We often learn that ‘CVP is the back pressure for tissue perfusion’ but this ignores the concept of tissue closing pressure and the unique and dynamic resistance properties of each tissue and organ bed. Thus, raising cardiac output may or may not augment MAP which, in turn, may or may not improve perfusion through a particular tissue bed. These are functions of local closing pressure, resistance and whether or not auto-regulatory mechanisms are intact. Accordingly, tissue oxygen demand, consumption and arteriolar dys-regulation in shock remain key links between macro and micro-hemodynamics.
In summary the relationship between ‘right atrial pressure’ and ‘tissue perfusion’ is complex and depends upon the following CVP co-variates: cardiac output, arterial impedance, individual tissue closing pressure, resistance and the robustness of local auto-regulation. Hemodynamics can be confusing; all models belie its complexity. In no way should these models be considered authority; I present them only to encourage engagement with the primary literature. I try to keep with me what Carl Sagan taught us:
“Try not to get overly attached to a hypothesis just because it’s yours. It’s only a way station in the pursuit of knowledge. Ask yourself why you like the idea. Compare it fairly with the alternatives. See if you can find reasons for rejecting it. If you don’t, others will.”