New Lecture Notes for 2017; Venous Excess.

 

To whet the appetites of fluidphysiologists everywhere, and to thank you for your Support in 2016 I offer Version 1 of my Lecture Notes on Venous Excess. Please please pretty please let me know what you think.

Learning points.

  1. Central venous pressure (CVP) measurement is invaluable in the differential diagnosis of acute low cardiac output shock.
  2. CVP monitoring is useful in the management of chronic heart failure.
  3. Metabolic demand for increased organ blood flow reduces peripheral resistance, and stroke volume increases to autoregulate arterial pressure…
    • … right ventricular stroke volume increases as impedance to ejection falls (pulmonary circulation interaction) and venous excess increases to create the additional venous flow needed to autoregulate CVP to a new haemodynamic equilibrium (higher blood volume, higher cardiac output).
  4. So-called optimization therapy to create a hypervolemic hyperdynamic equilibrium in the absence of metabolic demand is misguided and harmful.

Expert physiologists of the laboratory bench and expert physicians at the bedside provide differing accounts about the source of cardiac output more than a century after Otto Frank and Ernest Starling developed a much-quoted “law”; that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end-diastolic volume) when all other factors remain constant. The following “Guyton” diagram (fig 1) illustrates a commonly taught but very confusing narrative.

Physiologist CF Rothe taught that “A decrease in CVP by 1 cmH2O can reduce cardiac output by half.” J Rodney Levick boldly states in Introduction to Cardiovascular Physiology 5e that “CVP, not ‘venous return’, is the true regulator of stroke volume.” It is therefore unsurprising that clinicians became convinced that they should increase cardiac output by raising CVP by infusing intravenous fluid. Hence we find many major critical care resuscitation trial protocols requiring fluid to achieve a nominal CVP. A typical example is 8 cmH20 in spontaneous respiration, 12 in positive pressure ventilated patients.

How then do we reconcile physician M. Pinsky’s assertion that “data support the hypothesis that the normal human right ventricle fills at or below its unstressed volume, such that right ventricular end-diastolic volume changes occur without any change in diastolic wall stretch.” In the real patients who occupy our critical care beds there is observed to be no relationship between transmural right atrial pressure and right ventricular end-diastolic volume / stroke volume. It seems that the role of the venous system (including the right atrium and ventricle) is to sustain an effective cardiac output by assisting flow (veins) and minimising impedance (right ventricle) without limiting left ventricular filling. The right atrial pressure (let’s call it CVP) is kept constant and as low as possible in face of varying venous flow. CVP increases with fluid resuscitation from hypovolaemia, positive pressure ventilation at euvolaemia, or cardiovascular disease but maximal cardiac output responses to increased demand will be limited if CVP is raised above normal, in the extreme causing cardiogenic shock.

The flow of blood into the central venous volume is driven by the pressure drop between the capillaries and central veins. Reddi and Carpenter protest that labelling this flow ‘venous return’ is a common cause of confusion. In health CVP does not preload the right ventricle; the right ventricle distends as muscle fibres relax during diastole and will fill with blood so long as there is a sufficient flowing volume available to it. I shall restate this important point; in normal physiology right ventricular muscle fibres are not stretched (preloaded) by CVP.

It is a literally circular argument to consider whether venous return depends on cardiac output or vice-versa. I offer instead a Narrative that clinicians can share and which leads to more rational fluid and inotrope management.

First, you need to know that by measuring the changing volume under an upper-arm pressure cuff as it inflates to suprasystolic pressure and then deflates it is possible to construct volume/ pressure maps of the underlying blood vessels. On the venous side of the circulation one can identify separately the volume/ pressure characteristics of capillaries, venules, small veins and large veins (in the upper arm, brachial and cephalic). As there is almost no resistance between large veins and the intrathoracic point of CVP measurement, we can estimate CVP from large vein pressure. Coextensive volume and pressure mapping technology is patented and built by NIVasc Inc (Vancouver, WA) but at the time of writing is not commercially available.

Secondly, consider Figure 2 below. Though each venule is of very small diameter, there are very many of them in the pressure range 20-30 and at haemodynamic equilibrium they will be in the most elastic range of their volume/ pressure curve. There are fewer small veins, each of greater diameter than a venule but in their typical pressure range of 10-20 they exert less elastic recoil to assist flow.  The small veins do, however, have great capability to regulate venous excess by constriction/ relaxation. Large vein pressure is typically less than 10, in which pressure range compliance dominates and substantial changes in volume are possible with very little change in pressure. Anyone who has used 2D ultrasound to inspect a large vein knows that in health it may be almost collapsed while cardiac output is quite normal.

Consider now the relaxing right ventricle. As the ventricular capacity increases, a stroke volume’s worth of blood is drawn from the central venous (intrathoracic) volume of the atrium and vena cava because ’nature abhors a vacuum’.  Note that it is neither pushed from behind nor sucked from in front: CVP does not fall so long as there is sufficient volume of blood within the capacitance of the large veins to replace the central volume which has become right ventricular stroke volume and been ejected into the pulmonary artery behind a closed tricuspid valve. The large veins are in turn replenished by blood from the small veins, and the small veins are replenished from the venules. The venules are replenished by the open capillaries. (Capillaries can be open (“flow” condition) or closed (“stop” condition) according to local tissue metabolic needs, but at any time the open capillaries are distended by Pcap, the intraluminal hydrostatic pressure.)

The left ventricular stroke volume that exits the capillary bed and replenishes the venous compartments will be a little smaller or larger than the right ventricular stroke volume that empties them. This will lead to negative or positive venous accumulation of blood, distributed throughout the venous compartments according to their capacitance and elastance. The rolling sum of the accumulated volumes is the venous excess. The greater the venous excess, the greater the gradient of capillary to central venous pressure, and so the greater the venous flow. To emphasise; the effect of venous excess on the pressure gradient between Pcap and CVP is the major venous flow determinant, not CVP. CVP is kept almost constant across the regulatory range.

You may notice some similarity here with the fictional Guytonian concept of mean circulatory pressure (MCP), or mean systemic pressure (MSP) or some such, being the notional pressure within the not-yet-ischaemic circulation during asystole and no flow. I do accept that MSP should go up and down with the Pcap – CVP gradient, but see no reason to invent it if our narrative works using real and measurable dynamic parameters.

The rapidity of elastic recoil inherent in healthy venules and veins is attributable to collagen and elastin fibres within the basement membrane, a perivascular condensation of the interstitial biomatrix. This rapid recoil keeps the intravascular pressure needed to assist flow from one venous compartment to the next to a minimum. With age, in diabetes, and in systemic inflammation including sepsis this elasticity is diminished. One contributory factor seems to be the deposition of advanced glycation end-products (AGEs). The process may be one of the causes of heart failure with preserved ejection fraction, which was previously called diastolic heart failure, and is an early feature of cardiovascular dysfunction in sepsis.

DECLARATION. I hove provided unpaid Medical Advice to NIVasc Inc (Vancouver WA).

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