Advances in Hemodynamic Monitoring for Critically Ill Patients
Search Strategy: Searches performed via TRIP database (http://www.tripdatabase.com/index.html) entering the terms “fluid responsiveness” yielded 20 hits occurring via green color coding (“Highest yield evidence” i.e. Evidence Based Synopsis, Systematic Reviews, Guidelines). However after you open these none appear related to intravascular volume assessment. You scroll down to the MEDLINE summary and see hits for systematic reviews (14 hits), diagnosis (91 hits) and etiology (22 hits) selecting the PGY1/PGY2 articles (and narrative citations). The single search term of “USCOM” yielded several hits from which the MEDLINE filter yielded the PGY3 article. Search term “fluid responsiveness and inferior vena cava” yielded the PGY4 article (+narrative citation).
The Scenario: You’ve just barely caught up after seeing the last of the patients from a 3 room double booked TCC day when EMS brings the 4th double booked patient to TCC 5: “54 y/o male with h/o ESRD, IDDM, HTN, CHF/CAD/afib (on coumadin) with ‘shortness of breath’ the last few days….he was hypotensive 80/palp in the field and we weren’t able to get IV access, HR 120 sinus, FSBS 200, we put him on a NRB and he’s a full code”.
The Initial Evaluation: Sensing a broad differential of badness you quickly gather the following: +subjective chills (afebrile in the ED), +dry cough and unchanged bilat LE edema despite a sedentary lifestyle with legs usually elevated. He denies chest pain or h/o lung disease/PE/DVT. His lungs sound faintly coarse at the bases and clear a little with cough, no murmur, JVD indiscernible due to his obese neck, +bilateral LE edema w/o calf tenderness and skin feels euthermic with +thrill to left forearm fistula (no discharge/errythema), +oriented x3 but slightly slow to respond and reports no missed dialysis (anuric at baseline). He moves all 4 extremities w/o focal motor deficits. EKG is unchanged LBBB, CXR with “atelectasis and diffuse interstitial markings and perihilar fullness unchanged from prior exam”. Just as the motivated fourth year medical student is ready to put in an IO the nurse says she got a 22 gauge in his deltoid. His vitals recycle: 82/50, 117, 22, and pulse ox100% on non-rebreather. His POC lactate is 4.7 and the rest of the labs are pending.
The Dilemma: The off service junior resident (JR) had immediately requested an ICU bed when they walked out of the room and they were stunned to find that the other ICU boarders have already been waiting 5+ hours. After a 500ml bolus of NS his vitals are: 93/51 117. While the teaching resident is grabbing items for a central line, the junior resident expresses concerns for complications, vascular scarring/decreased HD access sites, coagulopathy, and limitations of CVP monitoring with another central line.
The Opportunity: The Teaching Resident (TR) looking to capitalize on yet another great teaching opportunity responds via the Socratic method asking the junior resident two questions:
- How sure are you of his intravascular volume status?
- Should we do more fluid, hemodialysis, inotropic support, afterload reduction or vasopressors? Just then the pagers go off for a Level 1 Trauma and the TR says, “We’ll talk more after the Level 1 (see page below “More to the story”) but for now here’s a quick way to start answering these questions”:
Patients: ED patients with unclear intravascular volume status or volume responsiveness
Intervention: Invasive or non-invasive measures of stroke volume or predictors of volume responsiveness
Control(s): Physical examination, heart rate, blood pressure, CVP, Pulmonary Artery Catheter
Outcome(s): Diagnostic accuracy (sensitivity/specificity/LRs) of intervention(s) or control(s) in predicting volume status or ponsiveness.
Second years: Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: A systematic review of the literature, Crit Care Med 2009; 37(9):2642-2647. (http://pmid.us/19602972)
Third years: Nurse-determined assessment of cardiac output. Comparing a non-invasive cardiac output device and pulmonary artery catheter: A prospective observational study, Int J Nurs Stud. 2009 Oct; 46(10): 1291-97. (http://pmid.us/19423107)
Fourth years: Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients, Intensive Care Med. 2004 Sep;30(9):1740-46. (http://pmid.us/15034650)
Article 1: Does Central Venous Pressure Predict Fluid Responsiveness? Chest 2008; 134:172-178
Article 2: Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: A systematic review of the literature. Crit Care Med 2009; 37:2642-2647
Article 3: Nurse-determined assessment of cardiac output. Comparing a non-invasive cardiac output device and pulmonary artery catheter: A prospective observational study, Int J Nurs Study 2009; 46:1291–1297
Article 4: Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients, Intensive Care Med 2004; 30: 1740–1746
More to the Story
Physical Exam, CVP & the Gold Standard
The TR mentions how physical exam (i.e. orthostatics, dry tongue/mucous membranes, sunken eyes, confusion, weakness) for non-hemorrhagic hypovolemia carries weak likelihood ratios with most hovering around 1 (range –LR 0.3 to +LR 3.4) [Evidence-based emergency medicine/rational clinical examination abstract. Clinical assessment of hypovolemia, Ann Emerg Med 2005; 45: 327-9]. The TR acknowledges CVP limitations citing the PGY1 article. The TR mentions the gold standard lies with dynamic changes in systolic pressure, pulse pressure, or stroke volume variations in conjunction with volume or pressure challenges and/or changes in mechanically ventilated/sedated patients with controlled/adequate tidal volumes (referencing the PGY2 article).
Pulse Contour Analysis
The JR is impressed thinking that the ED regularly places pulmonary artery catheters and the TR chuckles saying, “Well not really. We put in a regular radial or femoral arterial line, connect the ‘FloTrac’ tubing from that to our ‘Sepsis Monitors’ (Edwards Vigileo) and it gives us continuous cardiac output, stroke volume, and stroke volume variation via pulse contour analysis.” The TR mentions that it’s the same principles as printing off the a-line strip and taking the measurements, but the ‘FloTrac method’ provides a reading every 20-seconds. One study in 30 spontaneously breathing patients (7 with sepsis) using FloTrac and passive leg raise testing showed 85% sensitivity & 90% specificity (+LR=8.5;-LR=0.16) with a cut-off of ≥16% change in stroke volume to predict response to volume expansion [Changes in stroke volume induced by passive leg raising in spontaneously breathing patients: comparison between echocardiography and Vigileo TM/FloTrac TM device, Crit Care 2009;13:R195].
Ultrasonic Waveform Analysis
The JR having rotated in the MICU mentions, “isn’t this the same stuff that Drs. Thiel, Kollef, & Isakow were working on with the USCOM suprasternal notch ultrasound?” [Non-invasive stroke volume measurement and passive leg raising predict volume responsiveness in medical ICU patients: an observational cohort study, Crit Care 2009;13: R111]. The TR says, “Yes, exactly…. they used passive leg raise testing as an endogenous bolus and found it had 81% sensitivity & 93% specificity (+LR=11;-LR=0.2) in predicting volume responsiveness as defined by a stroke volume increase of ≥15%. Note that only 46% of the patients deemed to require volume expansion by the intensivists were truly volume responsive! One problem in applying this to our patient is that 65% of their patients were intubated and ours is not (yet). There is however another study showing reliability using these methods in spontaneously breathing patients compared to the Swan-Ganz catheter (PGY 3 article). The USCOM sits at the end of TCC in the ED and a group of nurses and several physicians are trained to obtain readings [Emergency physicians can reliably assess emergency department patient cardiac output using the USCOM continuous wave Doppler cardiac output monitor, Emerg Med Australas 2005 Jun;17: 193-9].
The JR says, “That’s all fine and good but I’ve heard that nearly 20% of the time USCOM readings are unable to be obtained for whatever reason and what if he’s one of them?” The TR says, “That’s a great question and luckily we have an ultrasound in every pod…..there’s some literature out there using IVC collapse to predict volume responsiveness. We could potentially look at that, too” [PGY4 article and similar results with The respiratory variation in inferior vena cava diameter as a guide to fluid therapy, Int Car Med 2004; 30: 1834-37].
Accurate assessment of volume responsiveness in any clinical setting is a challenge. Volume management decisions are frequently encountered in the ED. At times the decisions are not clear and can carry increased morbidity and mortality with either over- or under-volume resuscitation of patients. When encountering a hemodynamically unstable patient, it’s not always intuitively obvious to exactly know where they are on their Starling curve or if it’s a preload, afterload, contractility, or “another” problem.
This Journal Club was ameans to explore some approaches to help answer the “preload” part of the question. Traditional static hemodynamic indices (CVP, LVEDAI, CI, GEDVI, HR, Blood Pressure) do not appear to be reliable indicators for gauging volume responsiveness. Current evidence supports adynamic change of >/=10-15% in stroke volume (index) or cardiac output (index) as an accurate means of identifying volume responsiveness. Dynamic challenges can be performed viaanendogenous volume challenge (passive leg raise), exogenous volume challenge (crystalloid/colloid) or via intra-thoracic pressure changes (PEEP challenges or inspiratory/expiratory variations of pulse pressure/stroke volume/systolic pressure in sedated/mechanically ventilated patients).
A device capable of measuring continuous (or near-continuous) cardiac output or stroke volume is ideal. There are many devices/technologies on the market to measure these indices (arterial pulse contour analysis, thermo/chemical dilution, ultrasound [USCOM, Echo, IVC collapse, esophageal Doppler], bioreactance, bioimpedence, Fick) with more approaches to assessing preload responsiveness on the horizon.
So the next time you wonder if you should: bolus, diurese, or add vasopressors/dilators/inotropes hopefully you will have some additional tools to help steer you in a more confident direction regarding their preload status and what you might expect their heart will do with more or less fluid.