Pressures in general
As previously emphasize, flows stem from pressures. It makes sense, therefore, for those interested in gauging flows to turn toward pressures for guidance. For clinicians interested in where blood is, where blood is going, how it is getting there, and what it is doing once there, knowing the pressures of the environment provides insight into flow and volume related phenomenon critical for hemodynamic monitoring and assessment. Researchers of volume status and responsiveness have used and are currently using many pressures in an effort to make diagnoses and guide treatment. What follows is a short review of a few of the key pressure based techniques used to assess intravascular volume status.
Central venous pressure
Perhaps the most familiar and most hotly debated parameter for guiding fluid management is central venous pressure, the pressure of blood in the vena cava near the right atrium. Famously proposed as one of the key parameters to which therapy should be targeted  and a staple of international guidelines for initial resuscitation while the treating severe sepsis and septic shock , the reasons for central venous pressures use or non-use or its use combined with other parameters in critical care hinge on what the pressure represents physiologically, what it does to influence fluid flow, and, most importantly, what it says about the volume status of the patient.
Venous pressures arise from arterial pressures being transmitted through the capillar- ies beds. As the heart cannot pump out any more blood than it receives, cardiac output is beholden to venous return. Going through the chain of causation previously outlined, we recognize that cardiac output is dependent on stroke volume which is dependent on preload which is determined by the preload, itself a factor of the filling time and venous return, which is a function between of the filling pressure and the right atrial pressure. Proponents of the metric contend that in many useful clinical settings right atrial pressure can be thought of directly through the surrogacy of central venous pressure, and therefore may considered a reliable indicator of right ventricular preload [26, 28]. Therefore, central ve- nous pressure is thought to give some measure of cardiac output, manifest through venous return.
Equating central venous pressure with right atrial pressure for a moment, the venous return function can be represented mathematically, first presented by Guyton , as
Venous Return = (f(MCFP)*f(D))/ν * (MCFP – RAP) * C
where f(MCFP) represents a function governing the filling pressure, f(D) is a function of the dimensions of the peripheral circulatory system, ν is the viscosity of the blood, RAP is the right arterial pressure, and C is a mathematical constant for scaling the other factors. We can see from equation 1.19 that there are only a few ways of increasing venous return: we can increase mean systemic pressure, decrease right atrial pressure, or increase the difference between them. (One could also alter the arterial and/or venous resistances or the viscosity of the blood, but these are strategies not implemented to any great clinical extent current and will not concern us here.) Evidence for the existence of relationship has shown that it is an effective means of predicting the results of a fluid challenge .
Here confusion of the matter may begin. As measured and reported, central venous represents the pressure within intrathoracic cranial or caudal the vena cava relative to the atmosphere [28, 31]. Central venous pressure is not only not equivalent to right atrial for a great many cases, but ventricular preload is actually determined by intrathoracic transmu- ral pressure, which is the difference between the intracardiac and extracardiac intrathoracic pressures. Transmural pressure is the more physiologically relevant parameter [31, 32] as it is actual pressure that distends the elastic structures of the heart and vessels and along whose gradients flows and forces act. Measuring the difference between the two components of transmural pressure is difficult and often not feasible in clinical practice and therefore, clinicians rely on central venous pressure as an approximation of much of the same information.
Adding further to the difficulty of the matter is the fact that the information central venous pressure is meant to represent lies at the intersection of two functions of cardiac performance: venous return and cardiac output (consider Figure 1.5). While the two functions are related, they can and do vary independently in a number of ways (as previously discussed).
Leaving to one side the difficulty in interpreting the bare signal of central venous pres- sure, a problem in consistently measuring it arises when different caregivers are asked to place the pressure transducer. Significant variability exists when different people are asked to place lines in different patients . The variability in the final measurement can be greater than the magnitude of the pressure signal itself, leading to wildly different clinical decisions. As patients with the most precarious fluid balance problems are those that are most likely to have their central venous pressure monitored, it is precisely those who need an accurate measurement most that are most susceptible to errors in measurement.
Finally, there many have demonstrated that central venous pressure poorly predicts the volume status [34, 18, 35, 36], demonstrating a power of prediction right around a coins. The reasons given for central venous pressures poor predictive power can be understood from the context in which it is extracted. As I have previously mentioned, though pressure and resistance are two very significant contributors to blood flow (and thus blood volume shifts), many other factors including venous return to the heart, right (and left) ventricular compliance, peripheral venous tone, and patient habitus and posture all factor into the pressure measured. Furthermore, in hypovolemic patients with a functioning sympathetic response system, CVP has actually been observed to fall in response to fluid with reduced compensatory venoconstriction. It is not merely hard to account for these various confounding factors, it makes such a measurement unusable in many disease states of the critically ill such as those with pulmonary vascular disease, right and left ventricular disease and failure, and many valvular heart diseases. Given these many factors, it is possible to be fluid responsive with a high CVP and to be non-responsive with low CVP, the opposite of intuition and theory.
Nevertheless, there are those who believe that if the limitations of such a measurement are respected, some relevant information can be gleaned [28, 37]. It is still used in many clinics globally.
Pulmonary artery occlusion pressure
Pulmonary artery occlusion pressure, variously known as pulmonary artery wedge pres- sure, pulmonary venous wedge pressure, pulmonary capillary wedge pressure, pulmonary wedge pressure, or simply wedge pressure, provides an indirect estimate of left atrial pressure. Pulmonary artery occlusion pressure is measured by inserting a small balloon-tipped catheter (known as a pulmonary artery or Swan-Ganz catheter) into a peripheral vein (usu- ally a jugular or femoral), feeding it through the right atrium, through the right ventricle, into the pulmonary artery. Once there, the distal end of the catheter measures pressure in the pulmonary artery (usually around 10-25 mmHg through diastole and systole). The catheter can also measure those pressures behind the pulmonary artery (from the right ventricle) and in front of the pulmonary artery (from the left atrium). Upon inflating the balloon, the pulmonary artery is obstructed, causing the pressure to drop rapidly, until it reaches a stable lower value (normally around 8-10 mmHg). All pressures behind the balloon are blocked and only those pressures from the left side of the heart are measured, specifically this occluded pressure is the left atrial pressure. During diastole when the mitral valve is open, the left atrium and the left ventricle become equally pressured. Thus, left ventricular end-diastolic pressure is equivalent to the pulmonary artery occlusion pressure. Theoretically, this left ventricular end-diastolic pressure should reflect left-ventricular end-diastolic volume (preload) and thereby was thought to be a good candidate for monitoring volume status.
Many studies have proven this untrue [4, 38, 39]. One of the assumptions about the use of pulmonary artery occlusion pressure to determine preload is that volume be proportional to pressure and that this proportionality can either be assumed or measured. Unfortunately, this pressure-volume relationship describing left ventricular compliance is often too complicated in practice for a physician to measure and too variable in context for one to simply assume. Left ventricular compliance is affected by preload, afterload, left ventricular wall thickness, elasticity, and stiffness [40, 41, 42], all of which can be radically altered in dialysis, diabetes, obesity, aging, myocardial ischemia, sepsis, etc.
Though still widely used, cardiac filling pressures do not appear to reliably predict fluid responsiveness . Some contend that mean systemic filling pressure would be the most accurate measure of volume status  because of its roles in venous return. Even here, some will hedge by contending that such a measurement is not possible clinically. Others, going further, challenge this notion.