As easy as … airway and breathing

Given that the new batch of house officers have just started, it seemed like a good time to update this blog. Today’s post is the first in a two part series about the ABCs. When called to the bedside of an unwell patient, the advice given is to “attend to the ABCs” first. Without further explanation of what the ABCs actually entail, this is only minimally helpful. Today we shall focus on the first two letters.

The best way to start is to make explicit that the lung really only has two functions. The first is to maintain an appropriate blood level of oxygen. Appropriate can be considered to be an oxygen saturation somewhere in the 90s. Now, an oxygen saturation of 92% may not be normal, but it is generally sufficient for the purposes of oxygen delivery to organs. The second is to get rid of CO2. More specifically, to maintain a CO2 of 40mmHg (around 5kpa).

These two processes proceed very differently. To get oxygen into blood one needs an open alveolus and a capillary that supplies it. The blood flow through that capillary must be appropriately matched to the amount of oxygen in the alveolus- if the blood flow is too much for the amount of oxygen in the alveolus, the blood in that capillary will be desaturated. This explains why you can have patients who are much more hypoxic than you might expect from looking at their chest xray. Collapse of alveoli occurs on a microscopic level and is not necessarily visible on chest Xray. Many patients are on vasodilatory medications (antianginal or antihypertensives) that impair their ability to match capillary blood flow with the amount of oxygen in the alveolus. It can also be easy to miss collapse of an entire lobe on xray unless you know what you are looking for. The relevance of this is that it is easy to go on a wild goose chase of other causes of hypoxia if you believe that the Xray must correlate with the patient’s clinical condition. Consider the following case.

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How to assimilate information accurately and why aortic dissections and PEs get missed- the pretest probability

Medical school and medical training teaches us that we do tests to confirm the presence or absence of disease. This is the wrong way to think about things. A better concept is to realise that we start with a certain pre-test probability of a disease, which is determined by the base rates of that disease in the population and the patient’s clinical history. Tests can only ever modify this pre-test probability into becoming more or less likely. At a certain point the disease may become so unlikely that testing for it causes more harm than good. This greater harm may come from radiation, reactions to things such as contrast dyes, harmful therapy that might be initiated as a result of a false positive result e.g. antibiotics for a blood culture result that is a contaminant, or simply the fact that time is wasted not pursuing the most likely diagnosis. Other times the disease remains so likely that you may have to pursue repeat testing (take for example the high false-negative rate of COVID swabs).

Consider this scenario. You are the on call house officer. You get paged to the ward to review a 35 year old patient who is having abdominal pain. He was admitted 6 hours ago with severe central chest pain that came on over a matter of seconds and lasted 2 hours. His troponins and ECG have been normal. He has now developed abdominal pain of the same severity and also reaching its peak over a matter of seconds. Concerned about the possibility of aortic dissection you look for mediastinal widening on the chest Xray, pulse defecits, or any neurological symptoms as you know these are the things to look for in a dissection. None of these things are present. Satisfied, you order further ECGs and troponins. The next day you find out he died overnight of an aortic dissection. The next day your consultant tells you “it just shows you how useless clinical exam findings are for aortic dissection- you can’t rely on them. Most dissections have a normal Xray!”

Is this correct? Are these clinical exam findings useless? Is the chest Xray normal in most dissections, as commonly quoted? Well, not quite. They are actually reasonably good tests, including the chest Xray (1,2). The problem is not taking into account the pre-test probability of an aortic dissection, which in this case is high based on the clinical history. Continue reading

The test is not the disease

When I was a trainee intern we had a patient on my general medical placement present with 2 days of right arm swelling and tenderness, with dilated superficial veins over her arm and upper chest. Her d-dimer was normal. She had an ultrasound of the upper limbs looking for a DVT. This was negative. With a negative d-dimer and USS we were all ready to discharge the patient home (who was otherwise well), however the consultant, a mentor of mine, insisted on a CT venogram. We all rolled our eyes. Eye rolling turned into eye widening as the scan showed the subclavian vein thrombosis we had all been missing. Continue reading

Why does hypoxia happen?

It is hard to avoid anything covid related in medicine at the moment. This pesky virus does raise an important point about pathophysiology however. There has been a collective surprise at the degree of hypoxia these patients can have despite a chest X-ray that doesn’t look that bad and at how comfortable these patients can appear despite their severe hypoxia.
Except there is nothing particularly new about this and it has long been a pitfall for the intern seeing hypoxic patients on the ward. Often one comes across a patient with post operative atelectasis (or viral pneumonia!) who has some opacities on chest X-ray (such as the one pictured above) but a degree of hypoxia seemingly unexplained by the chest X-ray. These patients are often sent for unnecessary CTPAs looking for PE.
Firstly, the sensitivity of chest X-ray for pneumonia and atelectasis is not as great as we think it is. Changes to the lung parenchyma are often more extensive than what is visualized on X-ray. Secondly the hypoxia is occurring on a microscopic level. Hypoxia occurs when there is mismatch between ventilation and perfusion i.e. blood flow to an alveolus is in excess of the lowered oxygen tension in that diseased alveolus. The larger volume of hypoxic blood that mixes with ‘good blood’, the worse it is. This is called shunting. Hypoxic pulmonary vasoconstriction is the reflex that protects against this mismatch but this reflex becomes less efficient with age, the presence of vasodilator drugs (pretty much antihypertensive or antianginal drug you care to mention), and a whole host of other physiological factors some of which may be specific to the disease itself.
Unwell septic patients with their high cardiac outputs will have a large volume of blood rushing through their pulmonary circulation which further decreases ventilation perfusion matching. The end result is that the degree of hypoxia is related much more to things occurring at microscopic level that we can’t see on an X-ray (on top of the fact that X-ray doesn’t tell us the true extent of parenchymal changes anyway). It is not uncommon to have post operative patients with a chest X-ray that looks like the one above but that are on 50-60% inspired oxygen.
These patients are tachypneic (because hypoxia contributes to the ventilatory drive) but they may not appear overly distressed because the work of breathing is more mediated by lung mechanics and the stiffness of the lung rather than the degree of hypoxia. If you’ve ever seen congenital cardiac babies with right to left cardiac shunts and resting saturations of 75% you’ll know what I mean. They can look blue but pretty happy.
So if you have a good reason for shunting (a high pre-test probability) such as being immediately postoperative or having a diagnosis of a viral pneumonia, that probability remains high despite what the chest X-ray might show you, and there is not necessarily a reason to go chasing a PE or invoking the presence of an unknown hemoglobinopathy (as many people are speculating with Covid). Of course, this doesn’t mean that looking for a PE is never indicated and clinical judgement in the individual situation is paramount. But you have to evaluate the patient in front of you, and not a computer screen, and if you understand the pathophysiology you’ll have a much better chance of doing this.
Till next time…

Hyponatremia Part 2: Managing it

The first step when confronted with a low sodium is to ask yourself if it is real. There are two interpretations of the word “real”. Firstly the machine at the lab may have spat out an incorrect result. This occurs if there is excess protein or lipid in the sample, because it affect the calculations made when the sample is diluted. This is not true of blood gas analysers- the blood gas sodium is accurate on a blood gas.

The other is to ask does this actually reflect a low serum osmolarity. We don’t care about hyponatremia so much because of the low sodium itself, but because we assume it reflects low serum osmolarity overall. It is this that actually causes all the troubles of cerebral oedema etc. Most of the time this is a correct assumption because serum osmolarity is


Most of the time the other components don’t play a huge role. But if the glucose is sky high, or you have another osmotically active particle such as mannitol, water will be sucked out of the cells, diluting the sodium. The sodium in this case is “real” however is doesn’t really matter because the overall plasma osmolarity is raised due to the presence of mannitol or craploads of sugar.

An easy way to eliminate this possibility is to check a serum osmolarity.

At the end of the first section we discussed people who had excessive sodium losses. Now, even though these patients might be losing a lot of sodium from the GI tract or the respiratory tract the sodium concentration of these losses is still always LESS than plasma sodium concentration. The total amount of sodium being lost is high but the sodium concentration of lost fluid is still low. So how do these patients become hyponatremic?

Well firstly one of the responses of the kidney to hypovolemia is to activate vasopressin and hold onto free water. However patients with hypovolemia also tend to hold onto sodium – a urine sodium < 20mmol/L fits with hypovolemic hyponatremia. So this doesn’t fully explain it. Even when urinary sodium reabsorption is inhibited, as you might see if the cause of hypovolemia is diuretics, the urine sodium rarely gets above 100mmol/L. So the renal response to hypovolemia of holding onto free water does not fully explain why the sodium drops.

It’s because people continue to drink water, usually from the tap, and the thirstier they feel the more they drink.  In short water and sodium are both lost, the water is replaced, the sodium is not, and the renal response prevents the free water from being excreted. Voila, low sodium levels. However without an ongoing exogenous source of water, hyponatremia will not develop.

So hypovolemic hyponatremia presents with low urine sodium levels, unless the cause is diuretics, or some other form of renal loss, such as acute tubular necrosis where the tubules are damaged, cannot retain sodium and put out vast quantities of urine. One could of course examine the patient and determine that they are hypovolemic as the textbooks advise, but anyone who has worked in clinical medicine for more than 2 minutes will realise that when it comes to differentiating between hypovolemia and euvolemia, one might as well do a rain dance, summon the gods, and ask them what they think. People who are confident in their ability to clinically differentiate between the two are probably deluded.

So the treatment is to expand the plasma volume with a resuscitation fluid and remove the stimulus for vasopressin secretion. Free water will be able to be excreted and the sodium will rise. You should probably do this cautiously- dumping a lot of fluid into someone often removes the vasopressin stimulus quite rapidly and an alarming diuresis can result, one that raises the sodium by more than the 8mmol/24 hours that safety recommends.

It would actually make complete sense to volume expand someone intravenously while at the same time restricting their oral fluid intake. Given that salt water tastes disgusting we tend to drink mostly free water, so expanding someone with salty water while limiting their free water intake is perfectly logical. Maybe best avoided however as people will give you weird looks and if you’ve already induced a diuresis adding on a free water restriction might overcorrect the sodium.

The classic cause of euvolemic hyponatremia is SIADH. The same pathophysiology that we already discussed applies, except this time vasopressin release is stimulated in the absence of hypovolemia, so the kidneys will not be holding onto sodium, and the urine sodium will be > 40mmol/L. However as mentioned, renal losses of sodium from diuretics or ATN will give the same urine chemistry, and this is a common pitfall. SIADH is actually not that common in patients presenting from home. It is more common is postsurgical patients where vasopressin is released due to the surgical stimulus and in little kids who become sick.

Hypervolemia should be more obvious clinically. The pathophysiology here is once again the same except the stimulus for vasopressin release is the sympathetic response to a failing heart. Diuresis is the treatment of choice here. It probably works because frusemide induces a loss of “salty water” and “free water”, but more “free water” and the patient is prevented from taking excessive free water because we usually fluid restrict people who are overloaded. Reducing atrial stretch and the neuroendocrine response to this also probably plays a part.

In all of these conditions the urine osmolarity will be higher than serum because the kidney is reabsorbing water. If the urine osmolarity is low the patient is likely to have psychogenic polydipsia.

If your patient has acute neurological symptoms a bolus of hypertonic saline is in order, and you should ask for help on how to do this.

Lastly you may wonder why the chloride is low- given that chloride is the main anion that balances the cations in the plasma, it is inevitable that a low Na+ leads to a low Cl-.

Hopefully this gives some better understanding of why hyponatremia develops and how to manage it. The key is really understanding the difference between salty water and free water.

Hyponatremia Part 1: Salt versus free water

Hyponatremia is difficult to understand. So I’ve decided to devote two whole posts to unravelling this enigma. The first part deals with normal salt physiology and the often forgotten difference between salty fluids and free water, while part 2 will deal more with the management.

It is important to distinguish between salty water and free water. Salty water refers to your resuscitation fluids like normal saline, Hartmann’s and plasmalyte, which contain 140-150mmol/L of Na. Because they are isotonic with body fluids, these fluids will be confined to the EXTRACELLULAR space, which you might recall is about 15L in a 70kg male. Turns out having fluid that stays in the extracellular space is a good thing if your goal is to expand the blood volume.

In contrast free water is solute free fluid which is hypotonic. Therefore it will distribute itself among TOTAL BODY WATER, which again you might recall is about 40L in a 70kg male. Now, we don’t often give pure water intravenously, but we do give fluids like 5% or 10% dextrose. This essentially functions as free water because the glucose will be taken up by cells leaving the free water component. From the point of view of the blood compartment, this free water is a muddy pig- it slips its way out of your grasp and disappears into the vast expanse of total body water, which is why it is wholly useless for resuscitating someone. The commonly used fluid dex-saline (which is 4% dextrose plus 0.17% saline) contains some salt but one can kind of think of it as free water also.

Herein the questions arises of what kind of fluid do we lose everyday? Most people will remember that the daily requirement for fluid is about 2-3L per day. But what is the composition of this fluid? Does it matter?


Of course it does. A human’s daily requirement for Na is about 70mmol. Read that again. That’s not 70mmol/L. That’s 70mmol TOTAL. So you are losing far more water than you are sodium (relative to normal body concentrations). This is from sweat, respiratory losses, the GI tract and the kidneys. Even though the kidneys can produce highly concentrated urine, they still lose more water than they do sodium. Another factoid you might recall is that the normal urine sodium concentration is 20mmol/L. Even if you are being hammered with a diuretic and losing lots of sodium in the urine, the urine sodium might get up to 80-90mmol/L, but this still falls far short of normal plasma sodium concentrations.

Given the above information it reasons that the function of the 2L of maintenance fluid we chart patients who are nil by mouth should be to maintain plasma osmolarity (given that salt is the main determinant of this). Therefore one should prescribe a maintenance fluid that achieves this, which is the reason that dextrose saline is favoured. Going without maintenance fluid will steadily raise your plasma osmolarity/sodium.

The purpose of 2L of maintenance fluid is not really to maintain blood volume (assuming your patient is euvolemic to begin with). Of course it fulfils this purpose to a degree but the more important determinant of blood volume is the solute load. A sodium load activates vasopressin which allows us to reabsorb water in the kidneys. Water follows sodium in the kidneys and this “sodium attached water” stays in the extracellular space, allowing maintenance of blood volume. As mentioned however the daily sodium load required to achieve this is only 70mmol/day (pretty much what you get with two bags of dex-saline).

The last two paragraphs may be confusing, so let me recapitulate. To maintain blood volume your kidneys must reclaim a certain amount of “water attached to sodium” or “salty water”, and this reclamation is dependent on an adequate sodium load and adequate water intake. However most of the fluid lost by your kidneys is actually “sodium free water” which must be replaced orally or intravenously to maintain serum osmolarity. Of the 2-3L a day of “fluid” one loses (not just from the kidneys), most of it is in the form of “sodium free water”, while “salty water” is a smaller component.

So what happens if I give a euvolemic patient normal saline as maintenance? In order to cope with the solute load (one bag already has twice the daily sodium requirement) and maintain a normal serum sodium concentration the kidneys will activate vasopressin and hold onto more water. The amount of “salty water” will increase, while the amount of “sodium free water” the kidneys can excrete is reduced. The serum osmolarity will be maintained, but at the expense of an expanded extracellular fluid volume. This may not be so much of an issue in healthy patients but you can bet it will significantly increase tissue oedema in those with heart failure, or with inflamed leaky capillaries. People with good kidney function will be able to increase the sodium loss in their kidneys, but remember even when they are losing heaps of sodium in the urine they are still losing more water than they are sodium. The effect will be worse in those with impaired kidney function who are less able to increase urinary sodium losses.

Of course such a maintenance regime may be appropriate in those with ongoing sodium losses. Those with ongoing sodium losses will have trouble maintaining their extracellular fluid volume (and therefore their blood volume) so ongoing sodium replacement will be appropriate. These patients may have vomiting, diarrheoa, losses from stomas or fistulae or renal losses from diuretics or acute tubular necrosis. Which brings us to managing hyponatremia in Part 2…

The hypoxic drive myth

It was difficult to go through any single month in medical school without being reminded that giving oxygen to chronic CO2 retainers abolishes their respiratory drive (which in these patients is apparently dependent on hypoxia).

This is taught with similar vigour in nursing schools.

There is one small problem with this elegant concept. To quote Blackadder; “it is complete bollocks”.

The concept was developed in 1949 and we have held onto it with fervour ever since. I would not wish to minimise the efforts of physicians who precede us, but for context the year 1949 predates the invention of CPR.


This graph (1) from 1980 shows what happens when patients with COPD and acute respiratory failure are given uncontrolled high flow oxygen for 15 minutes. The first thing to note is that the ventilatory drive (minute ventilation – VE) is supranormal to begin with (normal is about 5L/min). The graph is produced here with no permission whatsoever.

The second thing is that after a brief, not particularly significant, drop in the minute ventilation in the first few minutes, it pretty much returns to baseline. The last is the lack of correlation between minute ventilation and the rise in CO2 (which has been confirmed in subsequent studies).

So how does uncontrolled oxygen result in worsening hypercapnia in chronic CO2 retainers? It seems two main mechanisms are at play. The first is that oxygen displaces CO2 off of haemoglobin- the Haldane effect. The second is that usually the blood flow in the lungs is directed away from crappy hypoxic alveoli to healthy alveoli where the CO2 can be properly eliminated (hypoxic pulmonary vasoconstriction). Supplying crappy alveoli with excess oxygen reverses this process.

So, yes, uncontrolled oxygen can make respiratory failure worse, but it will not make your patient stop breathing. Which is important to know. If the patient has a respiratory arrest it is likely because they were tiring out and heading there anyway, not because you weren’t stingy enough with the oxygen.

It is also important to realise that the patient saturations give a good indication of how much oxygen their alveoli are seeing (it is this that determines how much hypoxic pulmonary vasoconstriction goes on). People obsess about the flow rate on the wall, but really the flow rate does not tell you how much oxygen is getting into crappy alveoli. As long as you are hitting a more conservative oxygen saturation target of 88-92%, you are fine.


  1. Crit Care. 2012; 16(5): 323. Published online 2012 Oct 29. doi: 10.1186/cc11475. PMCID: PMC3682248 PMID: 23106947. Oxygen-induced hypercapnia in COPD: myths and facts. Wilson F Abdo  and Leo MA Heunks

The folly of chasing urine output with fluid in sepsis

Through medical school and house office years it is easy to develop many ‘reflex’ responses to certain conditions. Treating low urine output with fluid is one of these.

This makes sense in certain conditions. Hypovolemia leads to reduced renal perfusion. Correcting hypovolemia is therefore a good thing. Aggressive fluid resuscitation to restore renal perfusion makes sense in conditions where the patient is significantly fluid deplete, like enteritis or DKA, or where diuresis is helpful to prevent nephrotoxicity such as rhabdomyolysis or tumour lysis syndrome.

Unfortunately this has been extrapolated to every condition associated with AKI, resulting in massive fluid volumes being given to patients in the hope that the fluid will somehow drive the kidneys to work better. This is entirely devoid of physiological sense. This is most apparent in septic conditions. I particularly recall patients on the surgical ward with pancreatitis, who were given fluids for their oliguria and renal failure until they were swollen like the Michelin Man.

Chest Journal has published an article this month (1) addressing fluid management in acute kidney injury. This narrative is supported by a 2017 article of the same name. There are a few things to note.

Firstly, there is really no scientific evidence that macrovascular renal blood flow is routinely compromised in sepsis. Septic patients may be hypovolemic due to fluid shifts into the extracellular space but generally the problem is one of vasodilatation. The pathophysiology of acute kidney injury in sepsis is complex and involves tubular apoptosis and dysfunction at the cellular level.


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Why is hypoxia not part of the Wells Criteria?

Whether you have done medical or surgical runs you will have spent plenty of time trying to figure out whether a patient has a pulmonary embolism. Many clinicians will hang their hat on the presence or absence of hypoxia. You may then wonder why hypoxia is not actually part of the esteemed Wells criteria.

Well, it turns out the presence of hypoxia in PE is quite variable. In fact, not uncommonly patients with massive PE may have normal oxygen saturations, a phenomenon confirmed both by the literature (1) and my own observations. To understand why, we have to understand why hypoxia might occur in the first place.

It has actually taken a while for people to figure out why hypoxia occurs in PE, although it is still not 100% transparent. Many people assume that the problem is V (ventilation)/Q (perfusion) mismatching, where Q is decreased due to the obstruction. This is not quite correct. V > Q results in hypercarbia, but not hypoxia. The problem is that Q is redistributed to other lung units, without a matching rise in V. This results in regions of lung with low V/Q, away from the embolism (2,3). This seems to be the most likely cause of hypoxia.

This explains why massive pulmonary embolism may not cause hypoxia. Remember that massive pulmonary embolism is defined by the presence of RV strain and cardiogenic shock. If most of the pulmonary arterial tree is obstructed there is nowhere for the blood to be redistributed, minimizing the ability for areas of low V/Q to form. Additionally, if the patient has cardiogenic shock, low cardiac output reduces Q, reducing the inequality. Therefore, paradoxically, improving oxygen saturations may be a sign of worsening shock (4).

Hypoxia is therefore not correlated with the severity of pulmonary embolism. Patients with severe PE may not be hypoxic. If your patient appears shocked, or just looks terrible, you cannot use the absence of hypoxia to rule out PE.

On the other hand, small PEs may also not cause hypoxia, if they are too small for significant redistribution of pulmonary blood flow to occur.

All of this leads onto the next point, which is the utility of ABGs when you suspect PE. No doubt at some point you will have been asked to obtain an ABG in a patient where PE is suspected. The origins of this were some small, flawed studies suggesting that a normal A-a gradient on an ABG could rule out PE in combination with other features. This has been proven false in a more rigorous study (5) – a normal A-a gradient is equally likely in patients with or without PE initially suspected of having PE. This study concluded that ABGs had limited diagnostic value in the investigation of PE. Hopefully now you understand why.

Additionally most of these ABGs are requested on patients in whom it is clearly obvious from the end of the bed that there is an elevated A-a gradient. If you are on 5L of oxygen to maintain normal saturations and there is no clinical reason for hypoventilation, then you will have an elevated A-a gradient.

Till next time…


  1. Intensive Care Medicine. June 1977, Volume 3, Issue 2, pp 77–80| Cite as Massive pulmonary embolism without arterial hypoxaemia Pathophysiology in two cases. F. Jardin, J. Bardet, A. Sanchez, F. Blanchet, J. P. Bourdarias, A. Margairaz.
  2. Pulmonary Circulation. Gas Exchange and Pulmonary Hypertension following Acute Pulmonary Thromboembolism: Has the Emperor Got Some New Clothes Yet? John Y. C. Tsang, James C. Hogg First Published June 1, 2014 Review Article.
  3. Journal of Applied Physiology. Pulmonary embolization causes hypoxemia by redistributing regional blood flow without changing ventilation. William A. Altemeier, H. Thomas Robertson, Steve McKinney, and Robb W. Glenny. 01 DEC 1998
  4. Hemodynamic Factors Influencing Arterial Hypoxemia in Massive Pulmonary Embolism with Circulatory Failure FRAN(OIS JARDIN, M.D., FRANCIS GURDJIAN, M.D., PIERRE DESFONDS, M.D., JEAN-LUC FOUILLADIEU, M.D., AND ANDRI MARGAIRAZ, M.D. Circulation 59, No. 5, 1979.
  5. Diagnostic Value of Arterial Blood Gas Measurement in Suspected Pulmonary Embolism. MARC A. RODGER , MARC CARRIER , GWYNNE N. JONES , PASTEUR RASULI , FRANÇOIS RAYMOND , HELENE DJUNAEDI , and PHILIP S. WELLS.   PubMed: 1111212 Received: April 24, 2000

How to properly interpret the creatinine (Cr)

The house officer wades through a swamp of daily creatinines. Unfortunately there is poor example setting on what to do with these. The classic example is the 90 year old with a “normal” creatinine of 90.

Nobody likes formulae, but it is important to refer to a couple here in order to understand what is to come.

Cr Clearance = (Urine volume x urine concentration of Cr) / Plasma Cr

The exact formula is irrelevant for your purposes but it is important to take home the concept that from this formula we can say that Cr clearance is inversely proportional to serum Cr.

Of course we don’t calculate Cr clearance by taking samples of everybody’s piss. That would be far too unwieldy. Instead we estimate Cr clearance using formulae, such as Cockgrauft- Gault, which takes sex, age and weight and spits out a result.

Of course it would be foolish to think we can accurately determine someone’s muscle mass and rate of Cr production even with fancy maths, so these formulae are estimates only, especially at the extremes of age and weight.

What this really boils down to is that I’m more likely to win the lottery than a 90 year old is to have “normal” renal function with a Cr of 90. This, at least, is commonly accepted, although commonly ignored, probably because we all have a habit of only looking at the exact number if it appears in red.

The nephron deepens

There are more interesting conclusions we can come to just from looking at the Cr clearance formula. Consider the graph that plots the function y = 1/x (CrCl being proportional to 1 / Cr)


If the y axis is Cr clearance and the x axis is Cr, what you can see is that

  • On the first part of the graph a fairly significant fall in Cr clearance is accompanied by only a small increase in Cr
  • Towards the end of the graph a fairly small drop off in Cr clearance is accompanied by a large increase in Cr

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