This chapter has tenuous relevance to Section G3(v) of the 2023 CICM Primary Syllabus, which asks the exam candidate to "describe and explain cardiac output curves, vascular function curves and their correlation". Though the words "venous return" were in fact used by the college in their syllabus document, it was only in the context of vasomotor regulation. The objective here is actually to answer the past paper questions on venous return. The discussion also by necessity touches on some of the details discussed in the chapter on cardiac and vascular function curves, hopefully without repeating most of those points.
Question 19 from the first paper of 2020 asked the candidates to "discuss the determinants of venous return to the heart", and the near-identical Question 6 from the second paper of 2018 asked the candidates to "outline" them. Functionally, there does not appear to have been any major difference in the college's expectations between these two questions, and the same answer is suitable for both.
- Venous return is the rate of blood flow into the heart from the veins.
- At a steady state, venous return and cardiac output are equal.
- Venous return can be expressed as VR = (MSFP - RAP) / VR = HR × SV
where MSFP is mean systemic filling pressure, RAP is right atrial pressure and VR is the venous resistance
- Factors which influence venous return include:
- Factors which affect cardiac output
- Factors which affect mean systemic filling pressure
- Total venous blood volume
- Venous smooth muscle tone (which affects the size of the "stressed volume"
- Factors which affect right atrial pressure
- Intrathoracic pressure (spontaneous vs. positive pressure ventilation)
- Pericardial compliance (eg. tamponade, open chest)
- Right atrial compliance (eg. infarct, dilatation)
- Right atrial contractility (i.e. AF vs sinus rhythm)
- Tricuspid valvular competence and resistance
- Factors which affect venous resistance
- Mechanical factors
- Intraabdominal pressure
- Skeletal muscle pump
- Obstruction to venous flow (eg. pregnancy, SVC obstruction)
- Hyperviscosity (polycythemia, hyperproteinaemia)
- Neuroendocrine factors
- Autonomic tone
- Vasoactive drugs (eg. noradrenaline, GTN)
If a diagram were ever called for, the exam candidate would probably have to reproduce something like this:
As there is a lot of material out there on this specific subject, the trainees would benefit from picking one single representative item of literature to guide their revision. The review paper by Beard & Feigl (2011) is that item. There is also some excellent material in Pappano & Weir (p. 200-208 of the 10th edition), but it is written and structured in a way which almost appears to be intentionally difficult. For a brief free review which contains some the same material, one may be directed to Bressack & Raffin (1987).
Venous return is usually defined as
"The flow of blood from the periphery back to the right atrium"
and perhaps there is no reason to refine or vary this simple statement even though it might appear in different forms among the different textbooks. Some authors will specify that it is venous blood (but what if fistula?) and others will insist on describing a volume of blood returning per minute instead of using the equivalent term "flow". Some might insist that the blood is returning to the right atrium specifically, which is discriminatory against individuals with TASVD. From a brief inspection of a series of well-respected textbooks, no life-changing differences in definition could be found. Arthur Guyton, who is probably the man who had the most to say about this topic, defined it as "rate of blood flow into the heart from the veins" which is probably the minimum amount of detail expected, the most economical form of this statement.
In short, venous return and cardiac output are equal, except for the briefest moments during the respiratory cycle and during large abrupt changes in intrathoracic pressure or posture. According to some acerbic comments from the college examiners, this relationship "appeared to elude some candidates", or at least they failed to explicitly state it in their written answer to Question 19 from the first paper of 2020. That may be because it is so completely obvious. Consider the scenario in which these two are not equal (one side of the circulation would rapidly empty while the other would dilate hideously, making for a very confusing autopsy).
A more interesting question is whether the cardiac output is the cause of the venous return, or the consequence of it. Is the heart a passive conduit which pumps everything presented to it (making the venous return the chief determinant of cardiac output), or is the cardiac output the main driver for venous return? This is discussed in greater detail elsewhere; in summary, no agreement has ever been reached over several decades of argument, and most authors - when pushed- either take a side or weasel out of the argument. For example, the official college textbook for cardiovascular physiology (Pappano & Weir, 10th edition being the most current at the time of writing) avoids the question by refusing to see a distinction between the two terms:
"The flow around the entire closed circuit depends on the capability of the pump, the characteristics of the circuit, and the total volume of fluid in the system... Whether one thinks of that flow as cardiac output or as venous return is irrelevant."
That may actually be the most sensible response, as realistically every aspect of it is accurate. However, it would not suit the purposes of the CICM First Part Exam to simply state that venous return is cardiac output, and then to give all the determinants of cardiac output as an answer to the question "what are the determinants of venous return". Clearly, the examiners expect us to consider venous return in Guytonian terms of mean systemic filling pressure, right atrial pressure and venous resistance.
The relationship of right atrial pressure, mean systemic filling pressure and venous return is best described by the vascular function curve:
This thing is discussed in greater detail elsewhere. In brief, the most important elements are:
So, if the right atrial pressure is a determinant of venous return, what are the determinants of right atrial pressure? It would serve nobody to get into a circular argument here, but some might say that venous return is itself the determinant of right atrial pressure. The defence of that statement is best left to the professionals (Bendjelid, 2005); suffice it to say that in order to discuss venous return in the way in which CICM clearly wanted us to, we must take the view that the right atrial pressure is a "back-pressure" on venous return, and that both are dependent variables of other factors such as resistance capacitance contractility and heart rate.
Thus, the determinants of right atrial pressure are:
The mean systemic filling pressure is a concept sufficiently interesting to merit its own chapter. In short, it is the pressure in the systemic circuit of the circulatory system which is measured in the absence of flow (with the heart stopped), and which consists of pressure exerted by the volume of fluid in the vessels on the walls of those vessels (which presumably have some sort of muscle tone, in spite of the organism being essentially dead). This pressure is thought to contribute to venous return by creating a pressure gradient between the peripheral circulation and the right atrium. In Guyton's dog experiments, this pressure was around 7-8 mmHg.
Logically, it follows that the mean systemic filling pressure should consist of two main components: the volume of blood and the vascular tone. As these variables change, so should the venous return change, all other things remaining equal. Indeed, this is what was observed by Arthur Guyton et al in a series of classical experiments from the mid-1950s. The diagram on the left from the original paper by Guyton (1955) is embellished and modernised on the left, which probably adds nothing to its explanatory potential:
It would be wasteful to invest much detail in the discussion of the determinants of volume (it's volume, surely), but some aspects need to be pointed out. The specific volume which contributes to the MSFP is the "stressed" volume, which is defined as the volume of blood which needs to be removed from the circulation in order for the MSFP to become zero. This ends up being about 15% of the total blood volume, whereas the rest of it is "unstressed", i.e. exerting zero pressure on the circulation (Young, 2010, and Magder, 2016). The relationship of blood volume and MSFP can therefore be described as follows:
So, the increase in mean systemic filling pressure by the addition of blood volume results in an increase in venous return. Clinically, this is said to correlate to fluid resuscitation. The same thing can be achieved by decreasing the resistance to blood flow (by altering vascular resistance). A decrease in resistance promotes flow even in the presence of a stable volume:
There are numerous factors which affect the resistance to venous blood flow. These can be loosely organised into "mechanical" and "neuroendocrine" factors, even though strictly speaking all of the neuroendocrine factors end up influencing resistance by producing a mechanical constrictor effect.