Jugular Venous PRESSURE- so why do we use it to assess volume?

There is perhaps no physical exam sign more enthused about by consultants and more bluffed by students than the jugular venous pressure (JVP). While initially I was not a believer, I have come recently to appreciate its usefulness. This epiphany did not occur without significant time spent perusing the literature and finally coming to understand what the JVP does and does not tell you.

The first point to make abundantly clear is that JVP is simply a surrogate for central venous pressure (CVP). This roughly estimates the right atrial pressure. The obvious first question a sceptic would ask is how good a job it does at this?

Well, if we refer to the JAMA rational clinical exam series from 2009 (1), a systematic review of sorts on different examination findings, we see that the JVP, and hepatojugular reflux, correlates reasonably well with invasively measured CVP. The table of likelihood ratios below combines findings from the three studies addressing this question, including one where hilariously medical students were better at estimating CVP than staff physicians.

JVP
Credit: Reference (1)

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Plasmalyte is safe (and actually better) in hyperkalemia

In some indistinct corner of a ward somewhere where I spent the majority of my first house officer year, a laminated sign is blu-tacked to the wall which reads as follows:

“Normal Saline is the only fluid that should be used for patients with end stage renal failure”.

While on the face of it this serves to prevent some poor house officer charting fluid with 20mmol KCL in it to a patient on dialysis, normal saline is actually a poor choice for someone with renal failure or hyperkalemia.

While surgeons are known to sometimes insist on some bizarre things, their insistence on using plasmalyte as a resus fluid is well founded. This elegantly balanced crystalloid contains not only physiological amounts of Na and Cl (unlike NaCl which delivers an unphysiologic 150mmol/L of Cl) but also magnesium, acetate and gluconate. The latter two are converted into bicarbonate, and their metabolism provides 66kJ of energy per litre of fluid (1).

Plasmalyte also contains 5mmol per litre of potassium, hence the twitchiness of people to use it in hyperkalemia or renal failure. This worry, however, appears to be a misapplication of physiology.

If you take a second to think about it, there is no reason why addition of normokalemic fluid to plasma should make someone hyperkalemic (for a potassium of 5 is still a normal potassium). In fact, if you replaced all of someone’s plasma with plasmalyte, you could not get a potassium above 5. This is explained much more elegantly in this post on the veritable emcrit blog (2).

The second important point also explained in this post is that most potassium is intracellular and potassium levels are really largely dependent on cellular shifts more than anything else. Normal saline tends to cause a hyperchloremic metabolic acidosis because of the unphysiological quantities of chloride, which impair H+ excretion. Potassium will shift out of cells in response to buffer this. The end result is that potassium levels rise more with the administration of normal saline, even though  it contains no potassium in the bag, than with plasmalyte, which has a significant alkalinising effect (2).

Of course theory is no good without the studies to back it up, and the studies all strongly point in one direction. Three studies (3-5) looked at the perioperative administration of Ringers Lactate (LR) (a fluid similar to plasmalyte which contains 4 mmol/L of potassium) compared to Normal Saline in patients with end stage renal disease undergoing transplantation. Average potassium levels rose in the Normal Saline group in all three studies and fell or stayed the same in the LR groups. In fact, the first study had to be terminated early because 19% of the NS group developed hyperkalemia while none in the LR group did.

To satisfy you fully, let us turn to the evidence for plasmalyte directly. Adwaney and colleagues (6) demonstrated that, in the same setting of renal transplantation, recipients of plasmalyte had a significantly lower need for renal replacement therapy in days 1-3 post-op (OR of 0.15) and had a 2% incidence of hyperkalemia versus 17% in the NS group (despite pre-op potassium being the same).

Also recently Weinberg et al. (7) confirmed that NS caused significantly more hyperkalemia and acidosis in renal transplant recipients than plasmalyte.

Conclusion

The evidence is quite uniform and strong in a way that is uncommon for this type of topic. Not only does plasmalyte appear to be safe in renal failure/hyperkalemia, it is actually safer than normal saline. Understanding why this is the case delivers an important lesson in fluid physiology.

 

References

  1. http://www.medsafe.govt.nz/profs/Datasheet/p/plasmalytesol.pdf
  2. https://emcrit.org/pulmcrit/myth-busting-lactated-ringers-is-safe-in-hyperkalemia-and-is-superior-to-ns/
  3. Anesth Analg. 2005 May;100(5):1518-24, table of contents. A randomized, double-blind comparison of lactated Ringer’s solution and 0.9% NaCl during renal transplantation. O’Malley CM1, Frumento RJ, Hardy MA, Benvenisty AI, Brentjens TE, Mercer JS, Bennett-Guerrero E.
  4. Ren Fail. 2008;30(5):535-9. doi: 10.1080/08860220802064770. Effects of normal saline vs. lactated ringer’s during renal transplantation. Khajavi MR1, Etezadi F, Moharari RS, Imani F, Meysamie AP, Khashayar P, Najafi A.
  5. Saudi J Kidney Dis Transpl. 2012 Jan;23(1):135-7. A comparative study of impact of infusion of Ringer’s Lactate solution versus normal saline on acid-base balance and serum electrolytes during live related renal transplantation. Modi MP, Vora KS, Parikh GP, Shah VR.
  6. Perioperative Plasma-Lyte use reduces the incidence of renal replacement therapy and hyperkalaemia following renal transplantation when compared with 0.9% saline: a retrospective cohort study . Anamika Adwaney David W Randall  Mark J Blunden  John R Prowle Christopher J Kirwan. Clinical Kidney Journal, Volume 10, Issue 6, 1 December 2017, Pages 838–844, https://doi.org/10.1093/ckj/sfx040
  7. Effects of intraoperative and early postoperative normal saline or Plasma-Lyte 148® on hyperkalaemia in deceased donor renal transplantation: a double-blind randomized trial. BJA October 2017Volume 119, Issue 4, Pages 606–615. L. Weinberg, L. Harris, R. Bellomo, F.L. Ierino, D. Story, G. Eastwood, M. Collins, L. Churilov, P.F. Mount

 

What does atypical chest pain mean? Part 1

“I just had my dinner, this hospital food is terrible by the way, look at this, what is this?….anyway  a couple minutes later the pain just grabbed me here”, he says rubbing the back of four fat, tobacco stained fingers up and down from his throat to his epigastrium.

“And you were just sitting down in your chair, right?” – “Yeah. I get this all the time though at home though”.

You sit down to wearily write your note; ‘Impression: Atypical chest pain, probably GORD. Plan: Serial troponins to exclude cardiac’.

Of course, the pain only lasted 10 minutes, so your troponins will probably be negative. So is the pain atypical?

Atypical is another in a series of medical terms that we use all the time which don’t really mean anything- or rather mean different things for different people and should probably be abandoned (1). Some clinicians even use it in order to facilitate admitting the patient to hospital (1).

The question of what exactly is ‘typical’ for angina, or how frequent something needs to be in order to be considered typical, is an interesting one, which provides fodder for many future blog posts. Surely though, positional pain or pain related to food can’t be angina? At least this is kind of what I have been given to understand. Not so easy apparently.

We will run through 3 examples of chest pain presentations well described in the literature which are associated with severe CAD, which many people might consider to be atypical. They go to show that few patients read the medical school textbook. Or maybe the medical school textbook is incomplete.

Post-prandial angina

8.6% of patients with ischemic heart disease experience post prandial angina (angina after meals), with higher incidence of three vessel disease and left main disease, and lower ejection fractions on average. Such angina is more likely to occur after the dinner meal (2). The mechanism is unclear but is thought to be related to either redistribution of blood flow to the gut or increases in cardiac output following meals. Increases in heart rate, blood pressure and systemic vascular resistance are all observed at the onset of angina, which usually occurs within 25 minutes of the meal (2,3). Continue reading

Bowel obstruction is a clinical diagnosis

You: “Hello Mr/Mrs. Surgical Reg, I’ve got a patient up here on the ward who’s started vomiting tonight and he hasn’t passed flatus for 24 hours and he’s got a tender tummy and I’m worried about a bowel obstruction”

Surgical Reg: “What does his abdo Xray show?”

You: “Its normal”

Surgical Reg: “Well why do you think he has a bowel obstruction then? The Xrays normal!”

Unfortunately when you create work for people, they can sometimes be less than helpful.

Now if you knew the sensitivity of an abdominal Xray, you could answer this question with ease.

This 2007 study (1) showed the sensitivity and specificity to both be about 82%. Second year radiology registrars had sensitivities as low as 59%, while senior radiologists reached up to 93%. Only 29 out of 90 patients had CT proven SBO. CT was the gold standard.

This study (2) used enteroclysis as the gold standard. This involves injecting a contrast material through a NJ tube and taking Xrays. This showed a sensitivity and specificity of 69% and 57%. If you are observant, you might have realised the implication of the numbers going down when a different gold standard is used- CT must not be so great either. Indeed, in this study the sensitivity and specificity of CT were only 64% and 79%.

Part of the explanation for these numbers is that Xray did better at identifying high grade obstructions (86% sensitivity) than low grade obstructions (56% sensitivity). The usefulness of the CT was in showing the cause of the obstruction rather than being far more sensitive.

In contrast (pun intended) this 1999 study (3) showed CT to have a sensitivity and specificity of 93% and 100%, while plain films were 77% sensitive and 50% specific. The gold standard was diagnosis from operative findings (25/30 patients) or by contrast study or clinical follow up, whatever that means, in the remainder.

Lastly this 1997 (4) review article is very informative and worth a read. It describes how the term ‘non-specific gas pattern’ means different things to different people! For example 65% of radiologists use the term to mean ‘probably normal’, 22% mean ‘can’t tell’ and the remainder mean ‘abnormal but not sure if ileus or mechanical obstruction’. What useful terminology!

They identify another analysis (page 1173, paragraph 2) where the sensitivity of plain films was only 66% when read by experienced radiologists; 21% of patients with ’normal’ findings had low grade obstruction.

So we can see that the accuracy of Xrays in the diagnosis of SBO varies a lot depending on the study, but to me seems generally underwhelming. At most the sensitivity in the hands of an experienced radiologist is 93% when compared to CT. It is important to remember however that the usefulness of the sensitivity/specificity depends on the pre-test probability- if your patient is vomiting and not farting and distended, the pre-test probability is high, therefore even with a high sensitivity there will be a large number of false negatives.

Clinical suspicion is important- radiography is a diagnostic aid, not the final arbiter. Always be guided by your clinical findings.

 

References:

  1. William M. Thompson, Ramsey K. Kilani, Benjamin B. Smith, John Thomas, Tracy A. Jaffe, David M. Delong and Erik K. Paulson. Accuracy of Abdominal Radiography in Acute Small-Bowel Obstruction: Does Reviewer Experience Matter? American Journal of Roentgenology. 2007;188: W233-W238. 10.2214/AJR.06.0817
  2. Reliability and role of plain film radiography and CT in the diagnosis of small-bowel obstruction. D D Maglinte, B L Reyes, B H Harmon, F M Kelvin, W W Turner, Jr, J E Hage, A C Ng, G T Chua and S N Gage. American Journal of Roentgenology. 1996;167: 1451-1455. 10.2214/ajr.167.6.8956576
  3. Comparative Evaluation of Plain Films, Ultrasound and CT in the Diagnosis of Intestinal Obstruction. Sudha Suri, S. Gupta, P. J. Sudhakar, N. K. Venkataramu, B. Sood & J. D. Wig. Acta Radiologica. Volume 40, 1999 – Issue 4. Pages 422-428
  4. The role of radiology in the diagnosis of small-bowel obstruction. D D Maglinte, E J Balthazar, F M Kelvin and A J Megibow. American Journal of Roentgenology. 1997;168: 1171-1180. 10.2214/ajr.168.5.9129407

 

STEMI equivalents

It is another weary on call night, where annoyingly everyone has decided to have chest pain. As you sit down to scrutinise probably your tenth ECG, some ST elevation in lead AVR catches your eye. This jolts you from your torpor. Real pathology? You get your registrar to swing by and have a look. He furrows his brow as he looks down his nose at you, saying;

“ Remember, young padawan, one lead is no lead.” He reminds you of the STEMI criteria (1), which must be present in at least 2 anatomically contiguous leads:

  1. ≥1 mm (0.1 mV) of ST segment elevation in the limb leads
  2. ≥ 2 mm elevation in the precordial leads
  3. New LBBB

It turns out this teaching is not quite complete and will eventually cause you to miss some significant coronary occlusions. For you see, the classification of MIs into STEMI and NSTEMI is not some random division based on the aesthetic s of the ECG waveform. STEMI represents total occlusion of a coronary artery, therefore high risk of cardiogenic shock and death, and therefore benefit of immediate revascularisation. NSTEMI, on the other hand, an incomplete blockage, has failed to show benefit from immediate angiography (2).

The key point is that there are other ECG patterns that are also indicative of coronary occlusion which are simply not taught, mostly because they have only been described in the last decade or two, and unfortunately medicine can be slow to catch up. These “STEMI equivalents” cannot just be sat on, waiting for the troponin.

LBBB

To start with, new LBBB is not even considered a STEMI criterion anymore (3). You can however interpret ST segments in a LBBB, despite what you might have been told, by utilising the ‘Scarbossi Criteria’. These will be covered in a separate post.

De Winter’s Waves

de winter
[Image Credit: wikem.org/wiki/File:Dewinter.jpg]
ST depression indicating NSTEMI? Think again.

A decade ago, De Winter et al described the above ECG pattern consisting of  “1-to 3-mm upsloping ST-segment depression at the J point in leads V1 to V6 that continued into tall, positive symmetrical T waves. In most patients there was a 1- to 2-mm ST-elevation in lead aVR” (4). Continue reading