Have you ever seen a CHF patient who is fluid overloaded and in shock?


I have recently.

When I started writing this blog I thought I would stick with the philosophical aspects of medicine, but sometimes I feel compelled to speak out about poor medical care. I am especially apt to speak out when I kindly offer my observations and suggestions only to be called “stupid” by people who have mastered medical guidelines instead of medicine, and haven’t updated their practice since before I was born.

                So here is how it goes, patient is admitted to a monitored bed with CHF exacerbation. You don’t have to look too hard to see the edema nor do you need a stethoscope to hear his lung sounds. It seems rather simple, decide this patient has a fluid overload problem and begin treatment.

                We assume with treatment that works…But some have decided that furosemide is still in vogue because some guideline somewhere still lists it.

                For those of you who have been hanging out in Emergency Medicine of some form, you know this practice for acute exacerbation has been out of favor for the better part of a decade. This illustrates the critical problem of “specialists” not knowing why they are doing something AND not talking to other specialists.

                In medical science there is a secret code. The word “novel,” which is the code for “I actually understand pathophysiology and came up with a treatment based off of it instead of the expert opinion that no amount of scientific evidence will ever convince you to change your practice.”

                Now there are several “novel” ways of treating CHF patients. One of them involves renal replacement therapy, continuous or for a short period. Yet another that I recently explored is the use of hypertonic saline.

                This is where McMedicine falls apart. For the longest time it was believed restricting sodium intake was critical to success of managing a range of cardiovascular issues. A quick Pubmed search will reveal that most of the evidence produced after 1980 shows it doesn’t really make a difference. Further research might also lead you to the problems of hyponatremia in a majority of hospitalized patients and all the consequences arising from that. But if you are still practicing bloodletting and cautery, the idea of adding salt to this wound seems like madness or as I was accused of “stupidity.”

                But let me tell you something about the theory that has produced that. The story starts off with an extremely boring meeting, one where my mind was wandering through the various pathological mechanisms of the patients I was helping to care for. A few were CHF patients who were being diuresed with furosemide per the guidelines.

                A thought that struck me was that in the emergent setting, furosemide was removed from the guidelines because the problem with CHF isn’t actually water overload, it is water distribution.

                Under the concept of increased afterload, in CHF, blood “pools” in the vascular system. But there is also the consideration of inflammatory and kinin changes evoked by local ischemia, rendering the capillary beds permeable. You can find the exact same type of permeability in sepsis and anaphylaxis. The long and short of it is that the Starling’s forces cause a net movement of water out of the intravascular space and into the interstitial compartment.

                In a brief review of Starling’s forces, there is osmotic pressure and hydrostatic pressure. In the CHF patient there is an increase in hydrostatic pressure out of the vessels at the capillary. By adding furosemide, you eliminate electrolytes in the loop of Henle, and water follows. However, these electrolytes, particularly sodium, also normally increase intravascular osmotic pressure in the later part of the capillary and venous system. So when you reduce them, you would have less movement of water from the extravascular space into the vascular compartment. (General Chemistry 101, you don’t even need medical school) The net result is a decrease in fluid shift from the extravascular space into the vascular system. With so little fluid shift, the only logical explanation is water goes nowhere.

                So I started to ponder how to move water from the extravascular compartment to the intravascular compartment, and because many of these patients have diabetes, I instantly ruled out dextrose, glucose, and mannitol, as they are all sugars, even though mannitol is not absorbed. But I also hypothesized since it isn’t so great for cerebral edema, a systemic effect would not be likely anyway.

                The only logical conclusion I was left with was a hypertonic saline. I must qualify I was working on the assumption of 3% NACL. But after I proposed this and was very publically and ceremoniously degraded, I did the only thing a scientist can do… I looked it up on Pubmed expecting to find studies on why it didn’t work in order to postulate a new hypothesis for treatment.

                What I found was quite the opposite. Not only does it work, it works very well in all of the studies I found, including a handful of respected reviews. Not only does it work in CHF, but in a number of fluid balance pathologies, including shock states. I even learned the technique on how to do it. My hypothesis on 3% saline was grossly underpowered. But I would like to qualify I was thinking on using it as a more prolonged treatment than acute treatment.

                The technique is thus, using a bolus of 10-12% NACL, 40mg of furosemide is added to prevent renal reuptake of the sodium, ensuring sodium’s unopposed action as an osmotic diuretic. This salt bolus ensures increased intravascular osmotic pressure, pulling water into the vascular system. The furosemide prevents reabsorption, but the low dose ensures there is not a complete absence of reabsorption, furosemide does not inhibit sodium uptake in the proximal tubule. This has the side effect of insuring there is not “salt wasting” and consequent hyponatremia, which is an independent predictor of all-cause morbidity and mortality.

                It was a few days later when the particular patient that inspired this post was admitted and his McMedicine treatment started. While I was explaining the case to students, while going over obvious clinical findings, I pointed out, he had obvious gross dependent edema, difficulty breathing, low urine output which was dark yellow from his catheter, on the monitor his BP was 88/60, with a heart rate of 136. I didn’t have the benefit of a lactate measurement at the time, but clinically, he was full of water and in shock. I SWAGed what the American college of surgeons would describe as class I. (<15% total volume loss, and would be responsive to fluid therapy) He was not hemorrhaging, so clearly this was a “distributed shock.” I later did find lab values in his chart of increased lactate, decreased PH, and base deficit.

                Following the McMedicine guideline, this patient was medicated to a shock state! Some clinicians may dismiss this as early shock and not extremely significant, but I would like to point something out. (I know a considerable bit about shock, I spent years researching and writing my PhD on it) Cited in several texts, shock is the final common pathway before death. All diseases decompensate to shock. It affects every organ and system in the body, from the biochemical level to gross clinical level. It potentiates inflammatory response. While there are some demonstrated benefits to leaving patients in low levels of shock, I cannot think of any benefit of actually purposefully causing it. Even when managing traumatic brain injury or stroke, the purpose of therapy is to normalize pressure, not to reduce it to the point of negative fluid balance and impaired oxygen delivery! Inducing shock is not even done in diabetes insipidus.

                One of my university General Chemistry professors back in the States, Dr. Shupe, professed every class, it doesn’t matter how many PhDs come up with the most convoluted equations to explain the value of a chemical formula, if it doesn’t meet the basic fundamentals of the most basic scientific knowledge, the concept will always result in failure. In medicine and education it is often professed that if you do not understand the basic concepts, you can never work with advanced ones. But yet 90% of all clinical studies and clinical guidelines do not meet this basic burden! It is why I believe clinical studies, without basic laboratory studies that demonstrate that it does meet the basic science test are at best useless and at worst, harmful. Yet there is no shortage of medical doctors putting out hundreds of these studies a year. It is simply bad science and bad medicine.

                They defend this crap by calling the people who understand it “stupid.” These same people call the studies of other researches, particularly nurses, garbage because the experiments are inherently biased to prove what you are currently doing works. But what they are doing is absolutely no different!

                “Consensus” guidelines… Utterly useless… Consensus doesn’t make anyone right, it just makes them part of a herd.  Is a herd of medical providers hurting people right? You will have to decide that for yourself.

                In the meanwhile, I am going to continue to be stupid.   


3 thoughts on “Have you ever seen a CHF patient who is fluid overloaded and in shock?

  1. Adam

    An excellent article. Solely for the sake of education, once the HSS+furosemide is administered and the fluid shift moves from extravascular to intravascular space, what would keep the fluid from leaking back into the extravascular space? Will the increase in osmolar pressure render the capillaries less permeable? Just trying to learn a bit more about this, it makes a hell of a lot of sense.

    • To answer your questions, “What would keep the fluid leaking back into the intravascular space?” Good question, I don’t think it has been answered. In normal physiology, hydrostatic pressure is mostly responsible for the fluid shift out of capillaries. Oncotic pressure is responsible for re-uptake into the intravascular space. The purpose behind this treatment is to amplify the movement of water from the extravascular space back into the intravascular space. Edema reduces capillary blood flow, which is the supposed mechanism for the increased hydrostatic pressure locally. (certainly a CHF patient does not have an increase in hydrostatic pressure from increased cardiac output.)

      A reduction in edema would facilitate a local decrease in hydrostatic pressure. In effect rebalancing the normal physiologic Starling forces.

      That is local balance, but osmotic diuretics action of water removal is in the nephron tubule. (the location is still debated, but there is good evidence pointing to the loop of Henley.) But the ultimate net effect is the same, Na cannot be reabsorbed, urine is diluted and salt and water excreted.

      As I mentioned in the article, the trick then is to prevent hyponatremia, because then you are simply back where you started.

      It may even be that to maintain therapeutic effect, a relative hypernatremia may be required. Which completely calls into question any benefit from a low sodium diet.

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