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Challenge Accepted: Tyler's follow up on "What is a normal CVP?"

the strategy win champion the championship

Dr. Dan Davis posed some great questions in response to my last blog/podcast on CVP. Here is my feeble attempt at answering them. 

Question #1: First, can you fill in the missing puzzle piece: the heart?  How do atrial and right ventricular pressures affect the equation?  

 In my first post on this topic we stated that a plethoric IVC and elevated CVP is a pathological condition. A increase in right ventricular pressure will therefore increase right atrial pressure. This congestion can not only cause decreased coronary perfusion of the right ventricle, but also stretch the RV and RA releasing BNP & ANP.  This cascade will cause a break down of endothelial glycocalyx.

Question #2: Could we even have a negative CVP and still observe adequate cardiac output?  And how does the Frank-Starling curve fit into this discussion?

During normal physiological respiratory swings you will and should see a negative value for your CVP during inspiration. A negative value at the end of exhalation may be seen with a right ventricular assist device. Otherwise, your CVP at the end of exhalation should be equal to relative atmospheric pressure (0).

Frank-Starling curve shows the relationship between preload and cardiac output. The healthy heart curve shows early escalations in cardiac output with increased preload. However the relationship is not linear and does meet a point of diminishing returns. The curve plateaus even earlier in patients with heart failure. This is because increased preload and stretching of the ventricle does not equate to increase in contractility due to diseased myocardium.

Question #3: Do different monitors calculate the displayed CVP value differently?  Are there certain clinical scenarios where the displayed CVP value is misleading?

  1. The CVP should be marched out against a capnography waveform tracing. This will give the best location of measuring end of exhalation. This should be done regardless of the device.
  2. There are several situations that can provide false high CVP’s. The most common is positive pressure ventilation. Instead of looking for collapsibility, we look for expansion with respiration variability.

Question #4: Finally, can you give us some general rules to help us negotiate these stormy waters as clinicians?  

Rule #1 - Do not use CVP to guide fluid therapy.

Rule #2 - CVP can be used as a surrogate of RV performance.

Rule #3 - Many things can increase the CVP regardless of volume status.

Rule #4 - Never let Mike Verkest control the audio for your portion of a debate. 😉

Question #5: 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?!?

We will do this live at FAST19 and see the effects escalating PEEP has on PVVP. 🤙

Question #6: 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?

See Rule #1 - Do not use CVP to guide fluid therapy.

Question #7: 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?

The question really isn’t how to find optimal CVP, but how to assess whether or not a fluid bolus will increase cardiac output. The passive leg raise with pulse pressure variation at this time is the most reliable test.

Reference: 

1. Monnet, X., Marik, P. & Teboul, JL. Intensive Care Med (2016) 42: 1935. https://doi.org/10.1007/s00134-015-4134-1

Dr. Davis challenged Tyler by stating - "If you can answer these questions, you will upend the critical care apple cart..." - Dr. Dan Davis, MD

Tyler's Response - ...
Image 4 4 18 at 1.22 PM

Tyler Christifulli

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