In Podcast 64, Paul Marik and I discussed the concept of Fluid Responsiveness, and then we had the amazing Jean-Francois Lanctot discussing his four-part assessment with ultrasound to determine fluid use in sepsis. After that talk, I definitely felt I needed to discuss some of these issues further. If you have not listened to those two podcasts, it may be beneficial to go back before listening to this one.
and what has come to me is that perhaps we have been conflating two concepts:
Can the RV take it?
Can the LV use it?
Perhaps the problem we have been having is that we are trying to blend these two questions into 1. Let's use that as our path to discuss this morass of volume-responsiveness
Fluid Challenge or PLR with CO measurements
Stress the System with PLR or Fluid Challenge
Passive Leg Raise
Worth mentioning, though it should be obvious, PLR demonstrates how ridiculous the practice of Trendelenberg Position for resuscitation
500 ml crystalloid or colloid
10-Second Mini-Fluid Challenge
50 ml bolus over 10 seconds through a central line (Critical Care 2014;18:R108) change in VTI measured immediately afterwards
Then Measure the Response
Can Changes in MAP Predict Fluid Responsiveness?[cite source='pubmed']22278593[/cite], [cite]20111858[/cite], [cite]22464162[/cite]
Most recent analysis states changes in MAP don't predict CI increase from fluid load in septic shock (Intensive Care Med (2012) 38:422–428)
The Cardiac Output Monitors
and my buddy Seth Manoach wrote a nice review as well [cite source='pubmed']22537573[/cite]
NICOM – Bioreactance
- Marik studied 34 patients in the ICU with PLR, NICOM, SVV, and Carotid Flow (The use of NICOM (Bioreactance) and Carotid Doppler to determine volume responsiveness and blood flow redistribution following passive leg raising in hemodynamically unstable patients (Chest 2012 Marik et al.)
- Big validation study showed good accuracy (Intensive Care Med (2007) 33:1191–1194)
- There were a couple of small studies indicating inaccuracy, but when I looked into these–the authors may have had some conflicts
USCOM – Aorta Ultrasound
- Anaesthesia. 2012 Nov;67(11):1266-71.
- PCA + thermodilution
Pulse Contour Analysis Alone
- Bunch of studies keep going back and forth in the lit. I'm not sure if these track changes in afterload. They don't accurately track pressors/inopressors (Anesth Analg. 2011 Oct;113(4):751-7.)
- A PLR-induced increase in EtCO2 >5 % predicted a fluid induced increase in CI >15 % with sensitivity of 71 % (95 % confidence interval: 48–89 %) and specificity of 100 (82–100) %. (Intensive Care Med (2013) 39:93–100)
- Passive leg raise to etco2 (CCM 2014;42:1585)
Carotid and Brachial Artery Analyses
- Search for the evidence on pubmed, it is emerging now
LVOT velocity time integral (VTI)
- Accurate in the hands of experts–kind of annoying to obtain
Can the LV use it?
Dynamic changes can be false if there is RV dysfunction (will yield false positives) as the PPV means the LA needs more fluid but giving it in the face of the RV failure will not get the fluid to the LA. (CCM 2009;37(9):2642)
Pulse Pressure and Stroke Volume Variation
- Predicting fluid responsiveness in the OR (Br J Anaes 2007;98(4):545)
- Editorial on pulse pressure variation
- Original PPV Study
- Dynamic Arterial Waveform Changes[cite source='pubmed']19602972[/cite]
Proposed checklist before performing volume expansion suggested by PPV[cite source='doi']10.1186/cc13109[/cite]
- Is the patient ventilated with IPPV without spontaneous efforts?
- Is the patient ventilated in non-protective ventilation (tidal volume at least 8 ml/kg)? (EMCrit says 10)
- Is the patient in sinus rhythm?
- Is chest wall compliance normal (thorax closed, no flail chest, no binding)?
- Is the patient unaffected by valvular disease?
- Is the patient unaffected by right ventricle and/or left ventricle dysfunction (for example, as assessed by an echocardiographic examination including measurement of peak systolic velocity of tricuspid annular motion assessed by tissue Doppler echocardiography)?
- Does the patient have normal abdominal pressure?
- Have you decided or have you performed a calibration to decide which threshold value (6 to 20.5%) should be used for the binary decision of volume responsiveness?
- Have you established the compliance of the patient’s vascular capacitance in order to standardize the VE?
- Have you established that the patient’s heart rate/respiratory rate ratio is 3.6?
- Can you safely establish a baseline, perform a volume challenge and remeasure without any factors affecting heart efficiency and/or vasomotor tone during the assessment?
When the percentage of patients who would meet these criteria were evaluated in an ICU, it was achingly small (BJA 2014;112(4):681)
- A Critical Challenge to the accuracy of SVV during mech vent both for absolute and as a trend (Crit Care Med 2012;40:1186)
- Put the patient on 10 ml/kg and sedate them. (CCM 2009;37(9):2642) Driving pressure > 20 is probably necessary to get good PPV (Inten Care Med Volume 36, Number 3 / March, 2010:1432)
- Slow the arterial line trace to 6.25mm/second to synch with the capnograph. Makes it easy to identify systolic pressure variation (twitter anesthesia tips)
- anesthesia study
Can the RV take it?
I was just thinking about it the wrong way
I think this is the only ? CVP may be able to indicate, and probably not as well as IVC
Easy-Peezy for Quick ?s of Squeezy
End-Expiratory Occlusion Test
(Crit Care Med. 2012;40:152–157)
15 sec end-exp occlusion, look for pulse pressure >=5% during the end-expiratory occlusion with a sensitivity and a specificity of 87% and 100%, respectively, and by an increase in cardiac index >=5% during the end-expiratory occlusion with a sensitivity and a specificity of 91% and 100%, respectively
Works even with high PEEPS (Crit Care Med 2013;41:1692)
End-exp occlusion was good in pts with poor resp compliance; PPV was not (Crit Care Med 2012;40(1):151)
Expiratory Hold to Predict Volume Responsiveness
(Crit Care Med 2009;37(3):951)
15 second expiratory hold, maximal change during last five seconds=test. If the patient is spont breathing, change the trigger settings to make it hard to take a breath. 5% change in arterial pulse pressure predicts volume expansion as does increase in CI.
And even more controversies and thoughts
In Critical Care Medicine, an editorial by Hilton and Bellomo questioning whether fluids should be given in sepsis in any amount greater than a couple of liters; they want to know where the evidence is…
An article seems to indicate that the best predictor for development of pulmonary edema during fluid loading is reaching plateau of CI, indicated by no additional increase with fluids (CCM 2012; 40:793) as shown graphically by the Marik-Phillips Curves
See this great Meta
What do you think? Comment below
Now on to the Podcast…
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