"JVP not appreciated"
"On physical exam patient was alert and oriented, tachycardic but no murmurs, JVP not appreciated..." is a commonly heard phrase on the wards when presenting a patient.
What exactly does "not appreciated" mean?
Is the patient overweight and the vein cannot be visualized (here on referred to as Double Chin Obstruction Syndrome, DCOS)? Or is the pressure in the venous system low enough that the JVP does not rise above the clavicle to be seen? Or did the clinician just not look and say it wasn't appreciated due to his or her own negligence?
Unfortunately, our current methods don't offer any certainly. The reason we even care about the JVP is because it is a correlate for the venous pressure and can help us determine if the patient is volume overloaded or not. But how well correlated is it? To answer these often overlooked questions, we must travel back in time to understand cardiac physiology.
Dr. J Ward Kennedy, a pioneer in cardiovascular research at the University of Washington published The Normal Left Ventricle in Man in 1966, measuring the volume and mass of normal hearts in 22 men and women. He and his co-authors showed that if you take the difference between when the heart is at its fullest (end diastolic volume) and subtract the volume when it is least full (end systolic volume),
you can calculate what fraction of blood is ejected, hence the term ejection fraction:
"The stroke volumes and stroke indices were calculated, and the ratio of stroke volume to end-diastolic volume, hereafter referred to as systolic ejection fraction, is given...The systolic ejection fraction showed a narrow range of variation with a mean of 0.67 + 0.08."
Dr Kennedy et al showed (in Table 2) that the end diastolic volume (EDV) - end systolic volume (ESV) is equal to the stroke volume. On average, a normal heart ejects ~65% of the end diastolic volume as the stroke volume. They also estimated that the average end diastolic volume was 70 cc/m2.
We also know from later studies that as hearts become weaker, they eject less blood with each beat, resulting in a larger volume left over (left ventricular end diastolic volume, which directly relates to elevated pressures in the left ventricle, LVEDP).
Since the cardiovascular system is like a circuit in series, if there is less blood ejected and more blood present in the left ventricle with each heart beat, fluid will accumulate upstream into the pulmonary veins and then into the lungs. This excess fluid is thought to cause interlobular septa thickening which causes a reverberation artifact we see as B-lines.
LVEDP, The Gold Standard
The gold standard of the cardiovascular volume exam is to know what the LVEDP is, and then adjust diuresis based on this value. If it is high, diurese; if it is low, stop diuresing. However getting this value can only be done with a left heart catheterization by placing a pressure sensor in the left ventricle. We can also measure it indirectly using pulmonary capillary wedge pressure (PCWP) via a right heart catheterization as a surrogate, or elevated JVP as a more distant, back-of-the-envelope-calculation surrogate. However this assumes concordance between right and left sided filling pressures, which is not always the case.
Researchers at Brigham and Women's hospital compared left and right sided pressures in 537 patients undergoing heart transplant evaluation. They compared right atrial pressure (RAP, less than 10 or greater than 10) with PCWP less than or greater than 22 (as a surrogate for LVEDP). The mean ejection fraction was 21%, about half the time due to coronary artery disease. They demonstrated a concordance of right and left sided filling pressures 72% of the time, noting that:
"the presence of rales or edema is of limited value with sensitivities under 30%. Pulsatile hepatomegaly and positive hepatojugular reflux can be useful, but these too are strongly reflective of right sided pressures...[t]his study validates the reliance on JVP to guide therapy aimed at reducing congestion for the majority of patients."
The results are impressive, however they conclude saying "1 in 3 patients with elevated filling pressures cannot be identified readily from clinical information [JVP]", and that other measurements in addition to JVP are needed to identify mismatch.
This also does not address the discrepancy between PCWP and LVEDP, which can be very important when diagnosing pulmonary arterial hypertension, which requires an elevated pulmonary artery pressure in setting of a normal PCWP.
Researchers in Philadelphia compared right and left heart catheterization data on 12,744 patients. Among 4,320 patients (37.5%) with pulmonary hypertension, [mean pulmonary artery pressure, ≥ 25 mm Hg], hemodynamic data were complete for 3,926 patients (90.9%). Of these, 580 patients (14.8%) met the criteria for PAH with a PCWP ≤ 15 mm Hg, but over half of them (53%) had an LVEDP > 15 mm Hg.
This means they were incorrectly diagnosed with PAH due to the the discordance between PCWP and LVEDP, results consistent with other studies.
They conclude that "PCWP frequently underestimates LVEDP, that it is poorly calibrated to LVEDP, and that it has a moderate ability to discriminate between patients with normal or elevated LVEDP. Perhaps most importantly, these results suggest that approximately half of all patients who meet the hemodynamic criteria for PAH on the basis of PCWP measurements may, in fact, have elevated left ventricular filling pressures."
So while our circuit in series analogy works in many cases, it cannot be relied on with certainty. Elevated JVP is a reasonable estimate of right and left sided filling pressures....until it's not.
Can ultrasound improve these estimates?
As we discussed in our last post, using ultrasound to determine JVP is simple and 100% sensitive for visualizing the internal jugular vein. This is the only non-invasive way to confirm that the "not appreciated" JVP is in fact not present above the clavicle, or if there is just DCOS.
Using ultrasound, the level of the JVP can be accurately determined by detecting the meniscus of the blood in the IJ. It can also be corroborated with other techniques, such as the JVD rest:valsalva ratio, to confirm that the RAP is in fact elevated.
However can we take it a step further and use POCUS to estimate PCWP or LVEDP?
If we recall, as LVEDP increases, as in the case of heart failure, fluid will back up into the pulmonary veins and further into the lungs, causing pulmonary edema and presumably B-lines when looking with ultrasound.
Using B-lines To Assess PCWP AND LVEDP
In 2009, Dr. Lichenstein looked at this clinical question comparing anterior interstitial edema detected by lung ultrasound the degree of pulmonary artery occlusion pressure (synonymous with PCWP). They categorize the lung US findings into 4 categories:
- A profile: A lines with lung sliding
- A' profile: A lines, no lung sliding
- B profile: Bilateral B-lines and lung sliding
- B' profile: B lines, no lung sliding
The PCWP was assessed using a Swan-Ganz catheter in 102 patients and they looked at the PCWP cutoffs of 12 and 18 mmHg. 87 patients had PCWP < 18, of which the A profile was found in 31 cases, A' in 7 cases, A/B in 6 cases, B profile in 22 cases.
Out of the patients with elevated PCWP ( > 18), all except for 1 patient had a B-profile. For diagnosing PCWP < 13, A-profile predominance was 90% specific and and 67% sensitive.
These results suggest A-predominance is highly specific for diagnosing low PAOP, however B-predominant pattern was not sensitive or specific in this patient population of ICU patients.
Another study in 2012 performed 8-zone lung ultrasound in 100 subjects prior to a scheduled right heart catheterization. Median ejection fraction was 58%, and 35 of them had a history of heart failure. They found that the number of B-lines on ultrasound was linearly associated with rising right atrial pressure (RAP), pulmonary artery diastolic pressure, pulmonary artery systolic pressure, mean pulmonary artery pressure but notably NOT with PCWP. As the B-line score went from 0.3 B-lines to >8, the PCWP stayed in the 15-16 range. This relationship was unchanged using an 8-zone Lung protocol or a more limited 2-zone lung protocol (only scanning the lower lateral chest zones).
A few years later in Torino, Italy, a group of intensivists enrolled 73 ICU patients and compared PCWP with B-line prevalence and ejection fraction. They looked at 8 antero-lateral lung views with ultrasound and defined "B-line pattern" as at least 3 B-lines in a single scan on at least 2 areas per lung. They then performed a cardiac ultrasound to estimate LVEF and visually determine if it was reduced or not reduced.
Of patients with PCWP less than 18 mmHg, A-pattern was detected in 18/21. However the A-line pattern was also seen in 12 patients with high PCWP over 18, showing sensitivity of 85% but specificity of only 40%.
In contrast, the combination of B-line pattern and reduced EF was 100% specific to patients with PCWP > 18. It was never found in patients with low PCWP.
In contrast a normal LVEF and absence of B lines (A-line pattern) has 100% sensitivity for PCWP of 18 or less, specificity of 72%, and therefore a 100% negative predictive value for elevated PCWP, an extremely useful finding for estimating the PCWP at the bedside.
In 2019, another study looked at 93 adults with dyspnea who needed an ischemic evaluation with a left heart catheterization. They underwent a standard echo measuring systolic and diastolic parameters, and then performed a lung ultrasound 8-zone method (measuring 8 zones and quantifying B-lines from 0-10 in each). The LVEDP was then calculated on the cath and defined as elevated if LVEDP was > 20.
A large difference in B-lines was observed when comparing high to low LVEDP. The high group had a median B-line count of 17, where the low LVEDP group had a median count of 1.0, and this was highly significant (p < 0.0001).
This correlation was higher than all echocardiographic parameters!
B-line count was most strongly correlated with LVEDP. "Strikingly, none of the left sided recorded echocardiographic parameters correlated well with LVEDP or were associated with a similarly important increase in diagnostic accuracy for elevated LVEDP." They also note that IVC diameter significantly increased the accuracy further.
Putting it all together
These results are in fact striking as the authors state. B-line evaluation takes 1-3 minutes and is better correlated than complex diastolic dysfunction measurements on echo. Looked at as a whole, B-line pattern overall is highly suggestive of elevated LVEDP and PCWP, especially in the setting of a reduced EF.
In our opinion, when evaluating a patient who is overweight, has DCOS, or who is thin with perfect JVP-friendly anatomy, unless you ultrasound their IJ, heart and lungs, you will not know what is going on.
If they have a very elevated JVP but no evidence of pulmonary edema and normal EF, then pulmonary hypertension or right sided heart disease should be first on your differential diagnosis.
If you see a pulsation on the lateral neck but aren't confident it is in fact the JVP, the only way to know for sure at the bedside is with ultrasound. When this becomes universal, we can eradicate the phrase "JVP not appreciated" from the medical lexicon, and replace it with phrases like "JVP is not present above the clavicle and I know that for a fact!"