PEEP and blood pressure/other hemodynamics

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Hey all, I had a patient who cardiac arrested and they thought he was in ARDS given his Pa02 compared to his FiO2 and we were increasing his PEEP upwards to around 14 until he finally started oxygenating in the 90's (he was in the 80's before on 100% FiO2). I heard the RT discussing that his blood pressure would probably be affected. I have three questions:

1. How can adding PEEP drop a patient's blood pressure? He was already acidotic (so on a bicarb gtt) and on multiple pressors but vary labile with his blood pressures. The RT assumed that him being on this additional PEEP could make this situation worse. I've been reading and I read that adding PEEP decreases the venous return to the heart, but if that is so, then why is the CVP elevated (isn't CVP an indicator of the venous return to the heart-aka preload)?

2. I don't quite understand the relationship between PEEP and urine output. When I've called providers about a patient's low UO and their intubated, they ask me how much PEEP they are on. Does the extra pressure compress blood flow to the kidneys???

3. Also a side question, why the patient was dropping his O2 sat, the provider also wanted to know his peak inspiratory pressure. Once she knew that, she went up on the PEEP, so does that mean the PIP was low or high to make such a decision.

A little bit to unpack, but these are good questions.

You're on the right track when you say peep decreases venous return (VR). Really, any increase in intrathoracic pressure does that. CVP (RA pressure) is absolutely not an indicator of pre load as much as it is an IMPEDIMENT to venous return.

As the CVP rises less VR can fill the heart and the cardiac output (CO) FALLS, because less blood is making it thru the lungs to the left ventricle. Think of CVP/RA pressure as a dam that prevents VR. The higher it is, the lower the VR and, therefore the lower the CO because the relationship between VR and CO is LINEAR.

As CO falls so does end organ perfusion, so if the kidneys get less blood, they make less urine.

Specializes in ICU, CVICU, E.R..

Peak Inspiratory pressure is the total amount of pressure given during the inspiratory phase of the ventilator. PIP is the total inspiratory pressure + PEEP. PEEP helps the driving force of oxygen through the alveoli and prevents de-recruitment of alveoli. At 100% FI02, there's is no other way to increase saturations but to improve the driving force of oxygen accross the alveolar membrane.

Increasing the PEEP increases the driving force during inspiration (PIP) and expiration.

Specializes in ICU, CVICU, E.R..

PEEP not only increases intrathoracic pressures, but it also increases the venous pressure in the pulmonary vasculature. The increase in pulmonary vascular resistance increases the pressures in the right ventricle as the ventricle has to pump blood thru the higher pressures in the lungs.

So your CVP will be elevated.

So if CVP is not an indicator of preload, then how do we determine preload. I've been asked over and over again, "What's the patient's CVP" to see if they are dry or wet (whenever the number was too high, they wanted to give lasix or low, some fluid...) but if CVP isn't an indicator of fluid status then... what is?

Regarding the first response- I don't think it's accurate to describe high cvp as an impediment to venous return. But I think I get your point.

Cvp is often used as a measure of preload but lots of current info says it's inaccurate. People still use it.

the thing is cvp is a pressure measurement not volume measurement.

in a normal healthy person a cvp of 8 might reflect adequate preload.

put the same person in ARDS and add 14cm PEEP and 8 mm cvp is dry.

compliance will be down in ARDS and with peep so you will have less change on volume per mm of increase in cvp.

compliance is change in volume / change in pressure

http://www.cvphysiology.com/Blood%20Pressure/BP004.htm

Specializes in ICU, CVICU, E.R..

the thing is cvp is a pressure measurement not volume measurement.

There you go! You hit the nail on the head! Sunnybabe don't think of CVP only as preload. CVP measures pressure in the right ventricle on end diastole. So any condition that affects the pressures in the right ventricle will affect your CVP, and volume is only one of the many factors.

Same thing for wedge pressures

In order to determine if your patient has a volume deficit or excess you need to look at the whole picture. Patients clinical status, BNP, serum osmolarity, heart rate etc

You got a lot of answers to the first question. I'll take a stab at the other two.

2- The more obvious answer is that since increased intrathoracic pressures can impede cardiac output, you could theoretically hypoperfuse the kidneys, leading to lower urine output that way. On the other hand, your PEEP isn't a direct measure of this - the patient's blood pressure would be much more relevant.

I suspect the docs are actually asking because there are baroreceptors in the pulmonary arteries, atria, and vena cava that respond to increased venous/atrial wall stretching by limiting ADH and aldosterone, thus increasing urine output. Increasing intrathorascic pressure by increasing PEEP decreases this stretching and may encourage the body to produce more ADH and aldosterone lowering urine output.

Low pressure receptor zones - Wikipedia, the free encyclopedia

3- This one is tricky to answer, especially without being there. If the patient had a particularly high PIP, increasing the PEEP might lead to dangerously high mean airway pressures, which would increase the likelihood of your patient experiencing barotrauma. It is also possible that the MD was considering a trial of pressure controlled ventilation (rather than the volume-controlled setting I'm assuming he or she was on), in which case a particularly high PIP on volume control might indicate that the patient's lung compliance is poor (with a possible ventilation perfusion mismatch) in that setting and that pressure control is worthwhile.

Note that I could be wrong here - you might do well to ask a pulmonologist to explain.

Thank you all! You guys are awesome.

Regarding the first response- I don't think it's accurate to describe high cvp as an impediment to venous return. But I think I get your point.

Cvp is often used as a measure of preload but lots of current info says it's inaccurate. People still use it.

the thing is cvp is a pressure measurement.

Think of it this way.... if the CVP (really, the right atrial pressure) is higher than the mean systemic filling pressure (driving pressure behind venous return volume) it absolutely impedes venous return and therefore CO. You either need to cause the RAP to fall or the MSFP to rise for adequate forward flow to occur. We do that all of the time thru vasomotor tone, volume adjustments and contractility.

The confusion comes when conflating pressures and volumes, i.e. using CVP (a pressure) in relation to preload or venous return (a volume).

Sounds like you know more than I do about hemodynamics.

But my point was that I don't think it's clinically accurate to say that in all situations an increase in cvp = a drop in stroke volume. There are definite situations in which rising cvp and falling stroke volume occur (tamponade, too much peep, PE, etc). But there are also scenarios in which you might see the opposite relationship- cvp rises and stroke volume increases also (i.e: during blood transfusion to a bleeding patient or after you start norepinephrine and increase venous return on a septic patient).

Specializes in Anesthesia.

Simplest way to look at it: BP = Cardiac output(co) x systemic vascular resistance (SVR). In other words....BP = CO x SVR. PEEP adds additional pressure into the thoracic cavity which in turn decreases cardiac output. If CO decreases, according the equation BP is automatically decreased (unless SVR somehow increases to mathematically and physiologically compensate obviously). Also, urine output is a direct indicator of cardiac output. If cardiac output decreases, the kidneys may not be perfused and urine output can be decreased. Therefore, high PEEP can decrease CO which in turn decreases BP and renal perfusion which can subsequently decrease urine output since urine output is influenced directly by renal perfusion 2/2 cardiac output.

CVP is an okay measurement of preload. The problem is all of the factors that can affect the number (was the patient flat when the transducer was zeroed, did the last nurse have the transducer at the same level, PEEP, renal function, central line location, etc.) it is more of a number that should be looked at as a trend rather than an exact figure that precisely identifies preload.

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