re: a-line waveform interpretation

[toughlife]

It's my understanding that fluctuations in an a-line waveform due to mechanical ventilation can be used to guesstimate hemodynamic response to a fluid challenge.

Would this also be the case in a spontanously-breathing, non-intubated patient?

I heard from a fellow that it also does but I am not buying it. Can someone enlighten me here?

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[BIS]

Upstoke on wave form = Contractility
Dicrotic Notch Height= Vol Status
Urea under Curve = Stroke Volume
Respiratory variability = Vol. status
Down stroke = SVR & Vol status

Try reading Miller Anesthesia, have a pretty good section on Aline wave form analysis.

I believe you can have resp variability w/ spontaneous breathing pt though its not going to be a prominent b/c when on Mech vent w/ PPV your pressures are normally going to be much higher. Eg. PMax set on 30 on Volume mode causing decreases in preload with that higher pressure breath. Your nml pt spontaneous ventilating is not gonna be generating these higher pressures which isnt gonna effect preload and SV as much. Just observe it for yourself and make your own judgement.

 

[ZA_Gasman]

OK. Here goes. Fluctuations in the a-line trace CAN be used as a surrogate for estimating fluid status when the patient is ventilated. The explanation is as follows.

PPV causes incr. intrathoracic pressure which will decr venous return leading to a drop in Cardiac output during the positive pressure portion of the ventilator cycle. In addition, alveolar expansion causes compression of the peri-alveolar blood vessels in West's Zones 1 and 2, which results in decreased Left atrial filling and consequently decr. LV preload and resultant decreased apmlitude of your a-line trace. These are all normal physiological responses to PPV. When the fluid status is borderline, however, they are exaggerated, particularly the decreased alveolar blood flow. This results in the characteristic swing, which may be exacerbated by the use of PEEP.

In terms of spontaneously breathing patients, inspiration will lead to incr. venous return, leading to increased cardiac output. In terms of the peri-alveolar blood vessels, they are opened further by inspiration due to radial traction applied across the trans-pulmonary unit, which should also serve to increase preload to the LV. I don't believe that expiration is essentially different in vented or spontaneously breathing patients, so LV preloading in both groups should be essentially the same.

The upshot of this long argument is that I agree with you toughlife. I don't buy it either in the spontaneously breathing patient. WIll check today with our resident genius physiologist attending. anyone disagree?

 

[Noyac]

Your explanation is good Gasman.

I don't think the mechanics are changed all that much however, unless the right heart (ventricle) is weakened. Once the right heart is weakened then the PPV mechanics have a greater effect. The same thing can be observed when you have had a pt with an RCA lesion/infarct and you allow the EtCO2 rise. These guys may not respond well to increased pulmonary pressures.

 

[ZA_Gasman]

OK. Have checked with the resident Guru. Apparently if the fluid status is marginal to poor, the effect will still be seen on spontaneously breathing patients, but the pathophysiology is a little different. When they breathe in, the peri-alveolar vessels dilate due to the traction being applied across them. As I understand it, blood could then conceivably pool in these vessels during inspiration, also resulting in decreased preload to the LV, causing a drop in BP during inpiration that would be seen as a swing on the A-line. I believe that one would need to be more fluid deplete to see this in the sponatneously breathing patient than in the patient who is being ventilated.

The other thing is that when said patient breathes out the compression of the intra-pulmonary vessels obviously shunt (probably not a good term) the blodd out of the lung into the LV again, causing a transient increase in output.

I thus retract my earlier statment about not buying the sponatneously breathing theory. Hope this helps....

 

[Carm]

Great explanation. Very well thought out.

The quick answer for most situations requires two things to be present for A-line variation to be a fairly accurate indication of fluid status. In general, the patient should be mechanically ventilated, and should have a regular rhythm. Obviously there are situations beyond this that variations may be helpful, but in general these two things should be in place to put much stock into decision making. A patient with PPV and a regular rhythm and a 15% variation in A-line tracing may (and I say may depending on other clinical indicators) benefit from a fluid bolus.

 

[Antibiotix2006]

More on this over here


http://anesthesiology.org/pt/re/ane...ovft&results=1&count=10&searchid=1&nav=search

 

[ZA_Gasman]

Thanks for that link, looks like a great explanation. Reading the abstract, I can't help wondering what the difference between 'fluid-responsiveness' and hypovolaemia is. Surely, to my mind, if a patient's haemodynamic status and cardiac performance would benefit from a fluid bolus, he is, by definition, relatively hypovolaemic? This is probably a matter of semantics, but I think it may be unnecessarily confusing the issue.

 

[cchoukal]

I've occasionally noticed the pulse oximetry tracing fluctuate with the respiratory cycle in patients undergoing PPV. Presumably, this reflects a similar underlying physiology. Anyone study this or seen literature?

 

[Bougie]

There is an article in this month's issue of Anesthesia and Analgesia (Volume 103, number 5) on page 1182 about ABP variability on the pleth. Interesting topic; plan to test it out next time I'm twiddling my thumbs during an ankle ORIF. Anyone use this consistently in their practice?

 

[Noyac]

Anyone use this consistently in their practice?

Sure do.

 

[ZA_Gasman]

Yep, must agree that I also use the pleth trace as a surrogate of the A-line trace. Of course this requires a really good pleth trace, which, like an honest politician, is often the exception rather than the rule.

 

[IceDoc]

I've occasionally noticed the pulse oximetry tracing fluctuate with the respiratory cycle in patients undergoing PPV. Presumably, this reflects a similar underlying physiology. Anyone study this or seen literature?

Yes this has been studied. While the variation is also seen on pulse ox, it has not been as reliable (i.e. not statistically significant) as the systolic variation.