Preload is defined as the volume in the ventricle at end-diastole. So far, so medical dictionary. But really, preload is better defined as the compliance of said ventricle–preload is, purely speaking, the length of a myocardial sarcomere immediately prior to contraction. It is the Frank-Starling curve in action.
We don’t have anything to measure it directly in a living person, though. We can’t see it. You’d have to catch at a living heart in the act of beating at a cellular level, and devise a way to measure the difference in length between systole and diastole, to directly measure preload. And then it would have to operate from beat to beat.
You see the problem. I mean, that’s not workable at all. So what do we use as a surrogate value for preload? CVP on the right side of the heart, PAWP on the left. I mean, I say this. I’m not convinced we should. In fact, I’m pretty sure we shouldn’t. These surrogate values are less impressive when you take into account the numerous physiologic mechanisms involved in the maintenance of hemodynamic stability, as well as the mechanical issues involved in obtaining them, as well as the larger, more philosophical (yet wholly applicable) question of whether said surrogacy is reliable in any given scenario…
Oh, my holy lungs. STOP. That was a ridiculous mouthful. What I meant to say was, our numbers–the PAs and the CVPs and the wedges–are dependent upon the way we obtain them, on how we interpret them, the trend, the scenario, and a hundred other factors. Some of these we can account for. Some of them we can’t. And that’s assuming–a proper large assumption–that the numbers are reflective of anything workable.
Look. We all grew up using the CVP/PAWP. The CSC, CMC, and CCRN still test you on them. I’m not ready to throw it all away just yet. But if you’re simply checking it willy-nilly every once in a while, and pinning everything on that single value, you are making a huge mistake. You need a shift in heuristics. Serving immediate goals (especially if those goals are numbers) will fail you.
If your ICU uses CVP & PAWP as surrogate measures for preload, I want you to understand what their intent is. I will do another post on the relative utility of CVP/PAWP, so watch for that.
How do we apply this information?
From a practical standpoint–that is, shooting from the hip at the bedside–preload is essentially these three things:
- Venous Return
- Venous Pressure
- Right Atrial Pressure
Other physiologic factors influence preload, but these are the big three.
Let’s look at venous return, first. No, scratch that. Let’s look at venous pressure, first, since that has a little to do with venous return.
Venous pressure refers to the pressure gradient between the venous bed and right atrium. Remember, blood flow isn’t solely dependent upon the force of contraction–it’s also dependent upon the pressure gradient of the system. The right atrium has a lower pressure than the venous vascular bed. This insures the forward flow of blood from the vena cavae and into the right atrium.
More than two-thirds of the body’s blood volume is within the venous system at any given time. Unlike the arterial system, the venous beds are extremely compliant, and able to hold three times the volume. This storage capacity–referred to as reserve volume–is maintained in the large sinuses of the liver and spleen, as well as in the veins.
Venous return is affected by baroreceptors found in the heart, the vena cavae, the carotids, and the aortic arch. These stretch receptors are very responsive to hypovolemia, and are capable of both SNS and PNS stimulation in order to increase or decrease heart rate, as well as augmenting flow via vasoconstriction or dilation. You know. Depending on what the body needs.
It’s also affected by changes in intrathoracic pressure.
The act of spontaneous inspiration is a pump to the circulation. When breathing in, pleural pressure creates a negative gradient in order to bring air into the lungs. The respiratory units aren’t the only structures affected by inspiration, though. Negative inspiratory pressure facilitates blood flow from the body (cerebral & abdominal vasculature) into the right atrium.
For years–since the sixties, in fact–the pressure of the right atrium, known as the “central venous pressure,” has been measured as a surrogate for the preload of the right ventricle. But surrogacy isn’t a direct value, and there is ample evidence that CVP is an inexact estimate of RV preload. That is not the only issue with its use, though.
In fact, the greater issue is the lack of a linear relationship between volume and pressure in the right atrium.
As if that wasn’t enough, we have the effects of positive-pressure ventilation. Intubation with mechanical ventilation raises intrathoracic pressure above atmospheric pressure during inspiration.
That’s worth saying again.
- Spontaneous inspiration is a negative-pressure state.
- Mechanically-vented inspiration is a positive-pressure state.
PEEP increases intrathoracic pressure throughout the entire ventilatory cycle. An increase in thoracic pressure causes a decrease in venous return. It artificially increases the CVP values, too.
When I was new in the ICU and still thought the CVP had some measure of utility, I was taught “for every five of PEEP above five, subtract three from the CVP.” And I’m going to leave it right there.
As far as the left ventricle is concerned (because we have two hearts, separated by the lungs, right?) we measure preload indirectly as a wedge (PAWP/PAOP). This is obtained from a pulmonary artery catheter, or Swan-Ganz. The left ventricle’s true end-diastolic volume can be assessed in cath lab from the contour of the ventricle wall, but we don’t have a bedside continuous direct measurement of the volume in the left ventricle. We have a surrogate–the wedge.
By now you know my feelings on surrogate values, right? And the relative utility of hemodynamic parameters derived from said surrogate values?
So ends Part One. More to follow…
We measure all hemodynamic variables (CVP, PAs, PAWP, CO/CI) at end-expiration, because exhalation is usually the longest period of the respiratory cycle. Inhalation increases systemic venous return, but also decreases pulmonary venous return, which in turn decreases flow to the left side of the heart.
Here is that mechanism at work with bolus thermodilution:
This image demonstrates the high degree of variability from respiratory artifact. Trials 1, 3, 5 were performed at end-exhalation. Trials 2, 4, 6 were performed during inhalation.