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.
I'm not sure if this has already been beat to death, but I think it might be helpful to clarify a few of the most important ideas that have been scattered among the other posts to explain this PEEP/CVP/CO relationship. I've seen a few of the comments with subtle, but important misunderstandings of this relationship.
First, as mentioned in another post CVP is a measure of RA PRESSURE, that we try to use as a stand-in for RV VOLUME because that is what we really want to know. The relationship between ventricular pressure and ventricular volume is known as compliance and varies between patients and is non-linear. There are circumstances where CVP is low, much volume is added, and RV volume increases to the benefit of the patient with modest increases in measured CVP (the compliant heart of an otherwise well trauma patient), circumstances where CVP is "normal" of high, relatively little volume is added and CVP rises disproportionately and CO falls (the non-compliant heart of CHF with ventricular hypertrophy), and there are also circumstances where CVP starts high, and patients need more volume to maintain driving pressures across the lungs (PE, valvular diseases, etc). Ultimately, we want to answer the question "will more volume increase this patient's cardiac output?" and unfortunately the answer is not as simple as if CVP low yes, if CVP high no because of the intricacies of compliance, where volume and pressure do not correlate directly.
Second, it is crucial to understand that the CVP/RA PRESSURE that you measure is a sum of forces on the catheter tip: it combines the pressure in the patient's venous system from their own hemodynamic status, PLUS any external forces impacting the RA. That would include positive pressure ventilation, referred pressure from abdominal compartment syndrome, compression from tamponade, or setting a pile of bricks on your patient's chest. So, all other things being equal anything that increases intrathoracic pressure will increase the measured CVP, so more PEEP=more measured CVP. But all we changed were the external contributors to CVP, not the internal ones.
At the same time, it is true that high intrathoracic pressures impede venous return, PLUS impact the dynamics of pulmonary blood flow, leading to decreased ventricular filling. So, as you continue to increase PEEP you will see an increase in the total measured CVP, but in reality, you are preventing blood volume from returning to the heart. So, your RT is correct, high PEEPs often lead to hypotension with high recorded CVPs-but now you know what the CVP is actually measuring.
Now, about this formula BP=COxSVR, which shows up on tests and whatnot. From a real life standpoint it is a bit problematic. First, if you think back to physics, you'll note it's just the formula for electrical resistance V=IR (Voltage = Current x Resistance) or conceptually, flow pressure= total flow x resistance. Physics majors speak up and correct me, but there is a fundamental difference in how resistance develops in an electrical system vs. a pulsitile fluid system, but it's the formula we use.
To get to the point, the other problem with this formula is that it mathematically couples CO and SVR. That is to say, that for a constant BP any increase in CO will result in a calculated decrease in SVR, and any decrease in CO will result in a calculated increase in SVR. Whether you use a PA catheter, PICCO, LiDCO or some other device I've never heard of, the calculated value is the CO, and the SVR is derived based on the formula we just saw. So, we tend to treat the CO as the independent variable because we calculated it directly, and the SVR as the dependent variable.
In reality, the vasculature isn't just sitting there, vascular squeeze (the real concept, not the number SVR) changes independently, BP fluctuates based on multiple factors including contractility, but this formula does not account for multiple independent variables. Again, this is called mathematical coupling because for a given value of any of BP, CO, and SVR, the other two values automatically move in opposition to each other in this formula. Mathematically, this effect becomes more pronounced at very high and low COs. So, it is important to look at changes in CO and SVR together, and trend in light of the interventions you've given. For example, you gave your septic patient with high CO, and low SVR a bunch of fluid. Subsequently, they have an increase in BP because you increased ventricular filling, and treated their relative hypovolemia. If you run these numbers again based on our formula, it will calculate an increased SVR, when in reality we actually did nothing to their vascular squeeze. I'm not saying this formula is useless, it's just important to think about your independent vs dependent variables and what aspects of hemodynamics are not accounted for in it.
About the kidney- much like in the brain (remember CPP=MAP-ICP anyone) renal perfusion requires a gradient between forces driving blood through the kidney, and forces working against it (from renal venous pressure). A large gradient exists when your patient's systolic pressures are high, and their venous resistance is low, so you get great blood flow and subsequently good UOP (assuming no intrinsic renal disease). As your patient's blood pressure decreases, if nothing affects venous pressure that gradient still exists, so you still get UOP. However, your critical patient just got hit with a double whammy. First, they are hypotensive which decreases driving forces. Second, as you turn up your PEEP, just like for the rest of the torso, renal venous PRESSURE rises, which causes a decrease in return of renal venous VOLUME. So in this case, your driving pressure has decreased, your resisting pressure has increased, so your total gradient for flow across the kidney is minimal leading to no UOP.
Hopefully that makes sense. If not start over and read again. The subtleties do matter.
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.)
Just to clarify, the position of the patient and transducer don't matter when you zero. You're referencing the transducer to atmospheric pressure - which doesn't vary significantly with a couple inches in height. When we measure pressure we're actually measuring the difference in pressure between the catheter tip inside the patient and atmospheric pressure outside the patient. When taking a measurement of the patient, position of the transducer matters because the pressure exerted by the weight of the fluid column in the line makes a relatively large difference in relation to the small pressures being measured.
CVP is PRESUMED to be a measure of the Right Ventricular End DIASTOLIC PRESSURE.
RIGHT ATRIAL PRESSURE= RVEDP
This is a huge problem with assumptions.
As an ICU nurse DO NOT DEPEND ONLY ON NUMBERS and ASSESS the patient's overall signs and symptoms.
You ask, what indicates fluid volume status of the patient?
Well there is A LOT of s/s that can give you an answer.
1. Urine output
2. Blood pressure
3. Cardiac output, SVV, CI, SV if you have a vigileo monitor
4. s/s of edema, crackles in the lungs
Do not just depend on the numbers and look at the overall picture of the patient.
decrease venous return (and other things) leads to decrease cardiac output that leads to low blood pressure because BP= cardiac output x resistance. Low cardiac output then lead to low blood pressure. Low cardiac output leads to decrease blood flow towards your kidneys thus leading to low urine output.
CVP is PRESUMED to be a measure of the Right Ventricular End DIASTOLIC PRESSURE.
RIGHT ATRIAL PRESSURE= RVEDP
This is a huge problem with assumptions.
As an ICU nurse DO NOT DEPEND ONLY ON NUMBERS and ASSESS the patient's overall signs and symptoms.
You ask, what indicates fluid volume status of the patient?
Well there is A LOT of s/s that can give you an answer.
1. Urine output
2. Blood pressure
3. Cardiac output, SVV, CI, SV if you have a vigileo monitor
4. s/s of edema, crackles in the lungs
Do not just depend on the numbers and look at the overall picture of the patient.
decrease venous return (and other things) leads to decrease cardiac output that leads to low blood pressure because BP= cardiac output x resistance. Low cardiac output then lead to low blood pressure. Low cardiac output leads to decrease blood flow towards your kidneys thus leading to low urine output.
A good summary... I encourage students to view RAP/CVP as more of a cardiac function indicator than indicator of adequacy of intravascular volume.
So I know this thread is a few months old at this point, but on the off chance you look at it again I figured I'd also give some RT insight on the whole urine output and PEEP thing. There were some good answers but one which was missed.
Muscle cells in the atria release atrial natriuretic peptide in response to blood volume (specifically triggered by atrial stretch -- so they are occasionally referred to as "atrial stretch receptors"). In essence when your right atrial volume is high ANP is released. ANP has the opposite effect of aldosterone in that ANP stimulates sodium loss, or urination.
Now, say you have a patient on the ventilator. Their PIP is 40, MAP is 26, and PEEP is 15. That's a lot of intrathoracic pressure yes? So you are going to have decreased venous return, but at the same time your right atrial volume will be less. In part from the pressure exerted on the IVC and SVC (though this one is not as important), but also simply due to the pressure the lungs will be exerting on the atria. This combination of increased pressure and lower IVC filling/return will lower the amount of atrial stretch/filling. Lower atrial filling = lower ANP production which = further depressed urine output!
So I know this thread is a few months old at this point, but on the off chance you look at it again I figured I'd also give some RT insight on the whole urine output and PEEP thing. There were some good answers but one which was missed.
Muscle cells in the atria release atrial natriuretic peptide in response to blood volume (specifically triggered by atrial stretch -- so they are occasionally referred to as "atrial stretch receptors"). In essence when your right atrial volume is high ANP is released. ANP has the opposite effect of aldosterone in that ANP stimulates sodium loss, or urination.
Now, say you have a patient on the ventilator. Their PIP is 40, MAP is 26, and PEEP is 15. That's a lot of intrathoracic pressure yes? So you are going to have decreased venous return, but at the same time your right atrial volume will be less. In part from the pressure exerted on the IVC and SVC (though this one is not as important), but also simply due to the pressure the lungs will be exerting on the atria. This combination of increased pressure and lower IVC filling/return will lower the amount of atrial stretch/filling. Lower atrial filling = lower ANP production which = further depressed urine output!
PEEP actually causes a rise in RAP which is the reason for the fall in venous return which means a fall in cardiac output and urine. But you're right about the fall in ANP with PEEP.
I think RAP/CVP is pretty helpful when combined with measurements like stroke volume variation. Swans are pretty useful in folks with severe PHTN too.
Based on what data? Both (CVP/Swans) have generally been proven ineffective as indices of volume responsiveness and fluid status in and of itself. They are static measurements. Unless of course you are following a trend. You are better then but still lagging behind in the game volume interpretation.
We need DYNAMIC indices. And more and more I am beginning to think a PLR and ETCO2 might be the best indicator. There are others. IVC ultrasound and svv and whatnot.
Based on what data? Both (CVP/Swans) have generally been proven ineffective as indices of volume responsiveness and fluid status in and of itself. They are static measurements. Unless of course you are following a trend. You are better then but still lagging behind in the game volume interpretation.
We need DYNAMIC indices. And more and more I am beginning to think a PLR and ETCO2 might be the best indicator. There are others. IVC ultrasound and svv and whatnot.
Based on what data? Using a PA catheter to manage severe PHTN with prostaglandins or NO or whatever? Google it.
I wrote that combined with svv/ppv, RA pressure is useful, and it is. A patient can be fluid responsive and not need fluid. Understanding the relationship of MAP and RAP when giving large amounts of volume is pretty important.
I think it has become vogue to dismiss the use of RAP (CVP) in hemodynamic management, which doesn't make any sense at all. Neither does qualifying that position by saying that it's only good for trending.
It is a real time, dynamic indicator that, when combined with ppv/svv appropriately, will prevent volume overload.
This is just classic Guytonian physiology that has been established since the 1960's. If you're interested in learning more, search Michael Pinsky, Manny Rivers et al for starters. They are part of an international group of CC folks that have articulated the use of these tools very well.
ETCO2 has no use at all in managing volume resuscitation.
frozenmedic
58 Posts
I'm not sure if this has already been beat to death, but I think it might be helpful to clarify a few of the most important ideas that have been scattered among the other posts to explain this PEEP/CVP/CO relationship. I've seen a few of the comments with subtle, but important misunderstandings of this relationship.
First, as mentioned in another post CVP is a measure of RA PRESSURE, that we try to use as a stand-in for RV VOLUME because that is what we really want to know. The relationship between ventricular pressure and ventricular volume is known as compliance and varies between patients and is non-linear. There are circumstances where CVP is low, much volume is added, and RV volume increases to the benefit of the patient with modest increases in measured CVP (the compliant heart of an otherwise well trauma patient), circumstances where CVP is "normal" of high, relatively little volume is added and CVP rises disproportionately and CO falls (the non-compliant heart of CHF with ventricular hypertrophy), and there are also circumstances where CVP starts high, and patients need more volume to maintain driving pressures across the lungs (PE, valvular diseases, etc). Ultimately, we want to answer the question "will more volume increase this patient's cardiac output?" and unfortunately the answer is not as simple as if CVP low yes, if CVP high no because of the intricacies of compliance, where volume and pressure do not correlate directly.
Second, it is crucial to understand that the CVP/RA PRESSURE that you measure is a sum of forces on the catheter tip: it combines the pressure in the patient's venous system from their own hemodynamic status, PLUS any external forces impacting the RA. That would include positive pressure ventilation, referred pressure from abdominal compartment syndrome, compression from tamponade, or setting a pile of bricks on your patient's chest. So, all other things being equal anything that increases intrathoracic pressure will increase the measured CVP, so more PEEP=more measured CVP. But all we changed were the external contributors to CVP, not the internal ones.
At the same time, it is true that high intrathoracic pressures impede venous return, PLUS impact the dynamics of pulmonary blood flow, leading to decreased ventricular filling. So, as you continue to increase PEEP you will see an increase in the total measured CVP, but in reality, you are preventing blood volume from returning to the heart. So, your RT is correct, high PEEPs often lead to hypotension with high recorded CVPs-but now you know what the CVP is actually measuring.
Now, about this formula BP=COxSVR, which shows up on tests and whatnot. From a real life standpoint it is a bit problematic. First, if you think back to physics, you'll note it's just the formula for electrical resistance V=IR (Voltage = Current x Resistance) or conceptually, flow pressure= total flow x resistance. Physics majors speak up and correct me, but there is a fundamental difference in how resistance develops in an electrical system vs. a pulsitile fluid system, but it's the formula we use.
To get to the point, the other problem with this formula is that it mathematically couples CO and SVR. That is to say, that for a constant BP any increase in CO will result in a calculated decrease in SVR, and any decrease in CO will result in a calculated increase in SVR. Whether you use a PA catheter, PICCO, LiDCO or some other device I've never heard of, the calculated value is the CO, and the SVR is derived based on the formula we just saw. So, we tend to treat the CO as the independent variable because we calculated it directly, and the SVR as the dependent variable.
In reality, the vasculature isn't just sitting there, vascular squeeze (the real concept, not the number SVR) changes independently, BP fluctuates based on multiple factors including contractility, but this formula does not account for multiple independent variables. Again, this is called mathematical coupling because for a given value of any of BP, CO, and SVR, the other two values automatically move in opposition to each other in this formula. Mathematically, this effect becomes more pronounced at very high and low COs. So, it is important to look at changes in CO and SVR together, and trend in light of the interventions you've given. For example, you gave your septic patient with high CO, and low SVR a bunch of fluid. Subsequently, they have an increase in BP because you increased ventricular filling, and treated their relative hypovolemia. If you run these numbers again based on our formula, it will calculate an increased SVR, when in reality we actually did nothing to their vascular squeeze. I'm not saying this formula is useless, it's just important to think about your independent vs dependent variables and what aspects of hemodynamics are not accounted for in it.
About the kidney- much like in the brain (remember CPP=MAP-ICP anyone) renal perfusion requires a gradient between forces driving blood through the kidney, and forces working against it (from renal venous pressure). A large gradient exists when your patient's systolic pressures are high, and their venous resistance is low, so you get great blood flow and subsequently good UOP (assuming no intrinsic renal disease). As your patient's blood pressure decreases, if nothing affects venous pressure that gradient still exists, so you still get UOP. However, your critical patient just got hit with a double whammy. First, they are hypotensive which decreases driving forces. Second, as you turn up your PEEP, just like for the rest of the torso, renal venous PRESSURE rises, which causes a decrease in return of renal venous VOLUME. So in this case, your driving pressure has decreased, your resisting pressure has increased, so your total gradient for flow across the kidney is minimal leading to no UOP.
Hopefully that makes sense. If not start over and read again. The subtleties do matter.