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What is a normal CVP; 0-5 or 2-6?


While this question seems to be splitting hairs, it’s actually an interesting cross section of beliefs. To state a normal CVP is 0-5 mmHg you have to believe that a spontaneously breathing patient can have a perfectly acceptable cardiac output with a CVP of 0. Which also would mean you believe that a CVP does not need to be higher than zero to provide adequate preload.

Let’s take a look at two different pressures we need to become familiar with to properly interpret the data.

Central Venous Compartment:

This is the venous vasculature that is contained within the thorax and thus will be influenced by changes in thoracic pressure. This is measured with a transduced invasive line that sits in the central circulation (CVP).

Peripheral Vascular Compartment:

This is basically everywhere but the thoracic cavity, also known as the Mean Systemic Filling Pressure (MSFP).  This pressure is not easily measured although attempts have been made by plotting its relationship to CVP and cardiac output as intrathoracic pressure is increased.

In order for adequate venous return to be possible, the peripheral vascular compartment or MSFP needs to be higher than the CVC. As with all flow there needs to be a pressure gradient between these two compartments. In a spontaneously breathing patient, the inspiratory cycle will generate a negative intrathoracic pressure that will transpose a negative intravascular pressure within the central venous structures. This is why a CVP is measured at the end of exhalation when pressure is equal to atmospheric pressure (0).

In a mechanically ventilated patient the CVP will still be measured at the end of exhalation, however will fall victim to the amount of PEEP applied. A CVP of zero would not be normal in this scenario because the mere presence of an ET tube will generate a positive pleural pressure at the end of exhalation.


The blood returning to the right atrium will travel directly to the right ventricle during diastole. This means that the CVP will also be influenced by obviously the patency of the valves, but also the compliance of the ventricular walls. Just like in pressure control mechanical ventilation, the pressure to volume relationship is dependent upon compliance. In a study with healthy volunteers who had a CVP measured before and after a fluid bolus, the results were peppered all over the place.


So now that we accept that a normal CVP can be 0, we can understand that we are looking at the distal gradient to flow. The atmospheric pressure at the open end of a hose needs to be lower than the proximal pressure. This explains why a CVP of 8 mmHg suggested by the Surviving Sepsis Campaign does not make sense. If CVP is equal to or higher than MSFP, cardiac output is zero.

An increase in CVP should be viewed as a pathological condition and can have multiple negative effects. Let’s consider a few of these:

Decreased Micro-Circulatory Flow

As the arterioles gradually lose pressure and become capillaries, the micro-circulatory flow is considered a low-pressure system. This means that flow is mostly regulated by the venous pressure. If a CVP is elevated and the patient is still maintaining appropriate cardiac output, we can suspect that the MSFP is elevated as well. This means increased resistance for micro-circulation. It is postulated that micro flow is influenced more by venous congestion than mean arterial pressure.

Increased Capillary Permeability

As ventricular walls are distended, natriuretic peptides are released that breakdown the glycocalyx of the endothelial walls of vessels. This increases the permeability and increases edema.

Kidney Injury

A high CVP is transmitted backwards and can cause venous congestion. This increases the renal subcapsular pressure and decreases GFR.  This can also create an increased resistance to intra-renal collecting lymphatics and decrease lymphatic flow.

While none of this information is from my own experiments in the basement with my younger brother, it was my goal to try and break it down in a simple and digestible format for providers to become familiar with and understand why the CVP can be zero with perfectly acceptable cardiac output.

All photos are from the 4th Edition of the ICU Book by Paul Marino.

Peer Review #1:

 Thank you for challenging us with these interesting concepts!  The key takeaway here is the recognition that CVP values as transduced by a typical transport monitor may not tell us the entire story.  As a physicist - or even our friendly neighborhood plumber - would tell you, water (and blood) flows from high pressure to low.  Thus, low CVP values (including CVP = 0) may still be associated with adequate cardiac output if the upstream and downstream pressures are appropriate.  Similarly, high CVP values do not guarantee adequate cardiac output, and our efforts to increase CVP can "backfire" and result in effects that actually inhibit flow.

Now, let's challenge Tyler a bit! (Tyler will address these in his next blog article and podcast) – Stay Tuned!!

First, can you fill in the missing puzzle piece: the heart?  How do atrial and right ventricular pressures affect the equation?  Could we even have a negative CVP and still observe adequate cardiac output?  And how does the Frank-Starling curve fit into this discussion?

Second, do different monitors calculate the displayed CVP value differently?  Are there certain clinical scenarios where the displayed CVP value is misleading?

And finally, can you give us some general rules to help us negotiate these stormy waters as clinicians?  I've never measured systemic capillary pressure or even peripheral vascular venous pressures, but maybe I should start connecting my antecubital I.V. to the CVP transducer to see what I get?!?  Should we try a small fluid bolus, look at the CVP reaction, and then reassessing the clinical status of our patients to find the "optimal" CVP?  And what devices look promising to help us identify the optimal CVP for our patients?  Tissue oximetry?  Ultrasonographic stroke volume measurement?  Non-invasive cardiac output measurement using capnometry?

If you can answer these questions, you will upend the critical care apple cart...

Dr. Dan Davis, MD

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