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SCORE School Organ System Dysfunction, Part 2
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SCORE School Organ System Dysfunction, Part 2
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AMIT JOSHI: Hi, everyone. It's Amit Joshi from SCORE. Happy New Year to everyone joining us for our first session in 2021. Today, we'll be covering derangements of electrolytes and acid/base balance. I'm delighted to introduce our speaker, Dr. Ford Flippin. He's a trauma and acute care surgeon at MetroHealth Medical Center and Case Western Reserve University in Ohio.
AMIT JOSHI: Dr. Flippin did his residency at Cleveland Clinic, Florida, after getting his medical degree from LSU. He's done a fellowship in surgical critical care and acute care surgery at Rutgers Robert Wood Johnson Medical Center in New Jersey. Dr. Flippin's an acute care trauma surgeon currently. He has a particular clinical interest in disaster medicine and disaster surgery, and from chatting with him just before this, it sounds like after five days of on-call around New Year's, he's done a lot of disasters, so thank you, Dr. Flippin, for taking the time.
AMIT JOSHI: He's got a really interesting background, is involved in entrepreneurship, helps to run three companies and has multiple patents. Thanks, Dr. Flippin, and take it away, please.
FORD FLIPPIN: Amit, thank you so much for the introduction, and thank you, everyone, for joining us here for the SCORE lecture. So our goals and objectives today are fairly broad, electrolytes and their derangements, as well as disorders of acid/base status is a very large topic. So we're going to try to break things up into manageable parts, so that we can ultimately achieve these goals.
FORD FLIPPIN: Initially, we're going to identify the essential electrolytes of human plasma and their normal physiologic ranges. That's going to also allow us to describe some common IV fluids and their composition, and their proper usage. Thereafter, we'll identify major electrolyte derangements, their causes, and their treatments. Then we're going to shift to disorders of acid/base status which hopefully will allow us to be able to use pH, serum bicarb level, and PCO2 to properly diagnose acid/base disorders, and ultimately to be able to diagnose the causes and management of acid/base disorders.
FORD FLIPPIN: This quote from Paul Dirac is going to guide us, "You can never solve all difficulties at once." So we're going to take things in sequence and build on our understanding as this lecture goes along. So let's start with some basic human chemistry. Any discussion of electrolytes has to begin with the solvent in which they're present. In humans, this is water. Total body water, and derangements therein, is essential to understanding, diagnosing, and correcting abnormalities in electrolytes and in acid/base disorders.
FORD FLIPPIN: Humans are more than half water, and it's different between men and women. Males tend to be about 60% water, females a little less, around 50%. The normal total body water is the above fraction multiplied by ideal body mass, yielding a volume in liters. The current total body water is calculated by multiplying the normal total body water by the ratio of the normal sodium, which we will calculate as 140, to the current sodium.
FORD FLIPPIN: And free water deficit is the absolute value of the difference of the two above equations. So that's how it looks in words. This is how it looks as equations. Again, normal total body water is the ideal body weight times 0.6 in men or 0.5 in females. Current total body water is the normal total body water times 140 normal serum sodium over the current serum sodium in your patient.
FORD FLIPPIN: Free water deficit is the difference of the two. To find the necessary volume of infusion to correct a free water deficit, you must know the sodium concentration of the fluid you intend to use. For us, this is most often either lactated Ringer's solution or normal saline. And the volume to be infused, measured in liters, is the free water deficit times 140, again, your desired serum sodium, over the sodium concentration of the fluid you're going to use.
FORD FLIPPIN: So let's talk about some of these fluids. If body water has been lost, which is to say, the patient is hypovolemic or dehydrated, we're often asked, what is the best choice for replacement? Some people have very strong opinions on this and always use the same fluid, but the answer usually isn't that straightforward. This table expresses the concentrations of different electrolytes and components of the three most commonly used resuscitative fluids.
FORD FLIPPIN: Normal saline, lactated Ringer's, and Plasma-Lyte, which you're less likely to run into because it's more expensive and has never shown survival benefits but it's listed here for reference. When you look at normal saline, it only has three components. Water, sodium, and chloride. And you'll see here that sodium and chloride are present in higher concentrations than they are in the plasma.
FORD FLIPPIN: And indeed, the pH is actually fairly acidotic. Normal human pH is around 7.4. Normal saline pH is 5.5. As we move to the right, lactated Ringer's looks a little bit more like what we're familiar with. Sodium is a little hypotonic to normal plasma, but chloride and potassium are pretty close. There is some lactate as well, and the pH is much closer to human pH.
FORD FLIPPIN: So it's a little acidemic at 6.75. Plasma-Lyte, on the other hand, achieves a normal pH by the addition of acetate as a buffer and has relatively normal sodium and chloride concentrations, though no calcium or lactate is present here. Obviously, these fluids are very different. The best guidance that I can give is to consider the individual application and parameters of a patient.
FORD FLIPPIN: Lactated Ringer's is probably inappropriate for patients with renal failure, owing to its potassium and calcium content. The relative hypernatremia of normal saline is actually beneficial in many neurosurgical patients, and it's also often a good choice to replace gastric losses owing to the metabolic alkalosis present in these patients due to chloride loss. And for plasma re-expansion and replacement of insensible losses, lactated Ringer's or Plasma-Lyte are probably very good choices because they pretty accurately reflect the actual composition of human plasma.
FORD FLIPPIN: So having discussed these broad strokes, let's proceed to electrolyte disorders and discuss each of these electrolytes in a sequence. We're going to start with sodium. Sodium is the most abundant electrolyte in plasma. Indeed, there's more sodium than all of the other electrolytes combined. Sodium concentration is inextricably linked to volume status, in that sodium follows water in all cases, even when volume status is normal.
FORD FLIPPIN: Normal plasma sodium, we've already discussed, is around 140 but ranges from 135 to 145 milliequivalents per liter. We're going to start with hypernatremia. The initial evaluation of sodium derangements, both hypernatremia and hyponatremia, is an evaluation of volume status. So to evaluate volume status, ask yourself some basic questions.
FORD FLIPPIN: What are the patient's vital signs? Is the patient tachycardic? Are they hypertensive or hypotensive? If you have adjunctive measurement devices present like an arterial line, do they indicate a change in volume status such as high pulse pressure variability? Once you've gotten a sense of the patient's volume status, you can sort them into either hypovolemic, euvolemic, or hypervolemic hypernatremia.
FORD FLIPPIN: And this allows you to proceed down one of these pathways. In hypovolemic hypernatremia, the loss of free water is the main culprit. They may also have lost substantial quantities of sodium, but the free water loss is significantly greater than the sodium loss. In euvolemic hypernatremia, the net loss of free water is the cause here. It's most commonly due to diabetes insipidus, and if it's untreated, it can eventually progress to hypovolemic hypernatremia as well.
FORD FLIPPIN: And hypervolemic hypernatremia is almost always iatrogenic, from the infusion of hypertonic saline solutions. Remember, that as we just discussed normal saline is hypertonic in sodium terms to the normal plasma. The treatments, you can see down here below. In hypovolemia, free water replacement is the key, but because sodium losses may also be a component of this pathology, additional isotonic saline may be required.
FORD FLIPPIN: In euvolemic hypernatremia, the treatment is vasopressin for diabetes insipidus or one of its analogues. Free water replacement is also often required as is the removal of causative agents, which we'll talk about on the next slide. In hypervolemic hypernatremia, diuresis is required, often with partial free water replacement if needed with more dilute solutions. Again, in hypovolemic hypernatremia, there are many causes.
FORD FLIPPIN: Diuretics are one of them, which cause free water loss greater than sodium loss though they do cause both. Another very common cause, especially in our patients in surgery, is GI losses, whether it's from vomiting, elevated ileostomy output, or diarrhea. Heat related and sweating can also cause hypovolemic hypernatremia, especially in people who are doing long-distance, high-impact sports, especially in high temperatures.
FORD FLIPPIN: You're losing both, sodium and free water, but again free water loss is greater than the sodium loss. The final cause here, that is fairly common, is impaired thirst. This is often found in the chronically ill or elderly patients where failure to thrive is a significant problem. It can also be part of the hospital course if we fail to replace losses adequately in these patients. As you can see, the pathology includes both free water loss and, in most cases, sodium lost too.
FORD FLIPPIN: So replacement must take both into account. You need to calculate the free water deficit as we previously discussed and replace with normal saline in more severe cases. Replacement should never exceed 0.5 mEq's per liter per hour due to the risk of central pontine myelinolysis, and this is true for all forms of both, hypernatremia and hyponatremia. As we discussed, euvolemic hypernatremia is almost always caused by diabetes insipidus.
FORD FLIPPIN: Central DI is the impaired release of antidiuretic hormone from the posterior pituitary which is often caused by traumatic brain injuries. Alternatively, diabetes insipidus can originate in the kidney where it's termed a nephrogenic DI, and there's an impaired response to antidiuretic hormone in the kidney. This is most often drug related.
FORD FLIPPIN: Some common medications that can cause this include amphoterecin, aminoglycosides, lithium, dopamine, radio contrast dyes, and it can also occur in the polyuric phase of acute tubular necrosis. Any type of nephrogenic diabetes insipidus tends to be less severe than the central form described above. If you're uncertain about the diagnosis, it can be confirmed by urine osmolality. In diabetes insipidus, the urine osmolality is almost invariably less than 200 milliosmoles per liter, whereas the normal is 200 to 500.
FORD FLIPPIN: As discussed before, treatment is the removal of any potentially causative agent in either intermittent desmopressin or vasopressin infusions. Finally, hypervolemic hypernatremia is almost universally due to iatrogenic saline administration. This may be due to hypertonic infusions for brain-injured patients with the goal of reducing cerebral edema or the inappropriate administration of normal saline.
FORD FLIPPIN: Remember, normal saline is isotonic overall to plasma, but in sodium and chloride terms individually, it's hypertonic to the normal concentrations of these ions in a plasma. The treatment is diuresis, which promotes sodium loss, but as previously discussed, it may initially worsen the hypernatremia due to the loss of hypotonic urine. And therefore, gentle fluid replacement with hypotonic fluids, usually quarter-normal saline, is often required.
FORD FLIPPIN: Let's move on to hyponatremia now. As with hypernatremia, evaluation of volume status is the initial step, as we've already discussed. Further evaluation with urine sodium and urine osmolality is also often helpful. Symptoms range from headache and nausea to vomiting, progressing to encephalopathy, and even coma. And the more precipitous the drop in the sodium, the more severe the symptoms tend to be.
FORD FLIPPIN: In some patients, which we'll discuss soon, this hyponatremia can be quite chronic, and they will have minimal symptoms. Other patients will have a precipitous drop, and they'll be the ones where you see severe symptoms. As with hypernatremia, hyponatremia is sorted based on volume status. Hypo-, eu-, and hypervolemic hyponatremia. In hypovolemic, the sodium loss is greater than the free water loss, and this tends to be caused either by cerebral salt wasting or primary adrenal insufficiency.
FORD FLIPPIN: Euvolemic hyponatremia tends to be because of either free water retention or excess free water intake as in SIADH, the syndrome of inappropriate antidiuretic hormone excretion, or primary polydipsia, respectively. And hypervolemic hyponatremia is due to free water retention greater than sodium retention. These patients tend to have chronic illnesses, such as severe cirrhosis, heart failure or oliguric or even anuric renal failure.
FORD FLIPPIN: As you see in the next row, urine sodium and urine osmolality are key to making these diagnoses. In a hypovolemic patient, a urine sodium greater than 20 demonstrates a renal sodium loss as with other conditions, such as acute tubular necrosis. And urine sodium less than 20 demonstrates extrarenal losses. In euvolemic hyponatremia, the urine osmolality is generally greater than 100 in the case of excess water retention as with SIADH.
FORD FLIPPIN: Or in the case of excess water intake, as with primary polydipsia, urine osmolality tends to be very low, less than 100 even. Hypervolemic hyponatremia shows, again, urine sodium greater than 20 with renal losses and a urine sodium less than 20, if there are extrarenal losses. The treatment for these include fluid restriction and normal saline or even hypertonic saline administration if symptoms are especially severe.
FORD FLIPPIN: And a reminder, sodium correction should not exceed 0.5 mEq's per liter per hour. We're going to move on to potassium physiology now, and conversely to what we saw with sodium, the vast majority of potassium is actually intracellular. In the average 70 kilogram adult, about 3,500 milliequivalents of potassium exist inside the cells, but only about 70 milliequivalents exist in the serum.
FORD FLIPPIN: And this serum potassium is very tightly regulated. The normal serum potassium ranges from 3.5 to 5 mEq's per liter. Most potassium is excreted through the kidney with smaller losses in the stool and sweat. However, we'll see the derangements in these systems can result in serious abnormalities. We'll start with hypokalemia, where the causes include renal losses, most commonly with loop diuretics like Lasix or furosemide, NG suctioning, .
FORD FLIPPIN: where hypovolemia and alkalosis promote potassium loss in urine, diarrhea, magnesium depletion, and transcellular shifts caused by such drugs as insulin and beta agonists, as well as hypothermia. The manifestations of hypokalemia include muscle weakness as well as EKG changes such as prominent U waves, T-wave flattening and inversion, QT prolongation as well. These are relatively non-specific changes and hypokalemia rarely leads to cardiac instability unless there is another underlying condition.
FORD FLIPPIN: With that said, many of our patients are in the hospital because they have underlying conditions. So hypokalemia does have to be taken seriously. So what do you do about it? The repletion of hypokalemia, in general, requires you to raise the serum potassium by 1 milliequivalent which requires about 100 milliequivalents of infused potassium chloride. The usual maximum rate of infusion is about 20 mEq's per hour, though this can be raised in critical situations but only with central venous access because potassium-containing solutions are very caustic to the vasculature.
FORD FLIPPIN: There are some important exceptions. These include patients on tacrolimus, most of which are transplant patients. Tacrolimus inhibits potassium excretion in the kidney, and the administration of significant loads of potassium can raise the potassium very precipitously, even leading to cardiac arrest. Replacement of potassium also has to be done carefully in patients with renal failure, but this is uncommon as these patients are rarely hypokalemic.
FORD FLIPPIN: Indeed, often they're hyperkalemic. Any patient in whom you are trying to replete potassium without a response that you're expecting should prompt an evaluation for hypomagnesemia. Let's move on to hyperkalemia. The causes of hyperkalemia include impaired renal secretion, as we've just discussed with CKD and tacrolimus, as well as transcellular release as with tumor lysis syndrome, especially with non-Hodgkin's lymphoma, crush injuries, and some medications including succinylcholine and digitalis.
FORD FLIPPIN: Of note, cardioplegia solutions in cardiac surgery, which are the solutions used to stop the heart, can raise the serum potassium to as high as 20, which stops the heart in seconds. But you're not going to interact with that unless you decide to go down the route of cardiac surgery. The manifestations of hyperkalemia pretty much all happen in the heart and they're very serious. At milder hyperkalemias, you'll find peaked T waves, and that is, the hyperkalemia worsens.
FORD FLIPPIN: The cardiac manifestations can worsen to heart blocks and even cardiac arrest. These are due to impaired conduction of the polarization currents between the cardiac myocytes. The treatment of hyperkalemia goes down three steps. The first and most immediate priority is stabilization of the cardiac membrane. This is achieved with 1 gram of calcium gluconate or, in the cases of shock, 1 gram of calcium chloride.
FORD FLIPPIN: We'll discuss the differences next when we discuss calcium. This must be re-dosed every 60 minutes until the hyperkalemia has been resolved. The next most immediate course of action is to force potassium into the cells. This is done with insulin and dextrose administration. In general, '10 units of regular insulin plus 25 grams of 50% dextrose, and the effects of this cocktail lasts about 60 minutes.
FORD FLIPPIN: Especially in non-diabetic patients, we must be extremely vigilant of the blood glucose level as these patients can get hypoglycemic very quickly. Beta agonists can also be a useful adjunct, but they're not a first-line treatment for pushing potassium into cells. These measures, the first two, will temporize the situation, but ultimately, the goal must be to remove potassium. Kayexelate is a medication given orally or rectally which can draw potassium into the GI tract and remove it, but it's slow acting and can take as much as two to four days to have real effect.
FORD FLIPPIN: In emergent situations, dialysis is the gold standard for removing potassium. Next, we're going to discuss calcium as promised. Plasma calcium exists in two states. The first is bound to proteins, mostly albumin, or ionized, which is the biologically active form. When calcium stores are low, the bound fraction will decrease as albumin releases calcium to replete the ionized fraction.
FORD FLIPPIN: The ionized fraction may indeed remain normal but repletion is still indicated. Ionized calcium is essential for numerous processes in the body, including vasomotor tone and as a clotting factor. For those of you who don't remember, calcium is clotting factor IV. We'll start with hypocalcemia. And causes of hypocalcemia can include magnesium depletion, where it suppresses parathyroid hormone release and decreases the tissue responsiveness to parathyroid hormone.
FORD FLIPPIN: It can also be present in blood transfusion and the risk for this increases with the volume of blood transfusion, pancreatitis, renal failure due to phosphate retention, and impaired vitamin D production, as well as alkalosis where the increased bicarb can bind to calcium. Manifestations of hypocalcemia include tetany, hyperreflexia, and in severe cases, paresthesias and seizures.
FORD FLIPPIN: You may remember from medical school, Chvostek's and Trousseau's signs. These are useful but rarely diagnostic. Chvostek is a very non-specific sign in that it is present in 25% of normal patients, and Trousseau's sign is relatively insensitive in that it is absent in at least 30% of patients who have hypocalcemia. There are also cardiac manifestations including hypotension, decreased cardiac output, and ventricular ectopy.
FORD FLIPPIN: But all of these require very severe hypocalcemia to be present. The repletion in hypoglycemia is done either with calcium chloride or calcium gluconate. Per unit volume, calcium chloride contains three times as much elemental calcium, and the resultant osmolarity is three times higher. Calcium chloride's osmolarity is fully 2 osmoles per liter, meaning that it can really only be infused via central line except in emergencies.
FORD FLIPPIN: Both are generally supplied as 10% solutions. 200 milligrams of elemental calcium, which is usually supplied as two grams of calcium gluconate solution, would be expected to raise the serum ionized calcium by about half a milligram per deciliter, though the individual response will vary, especially in relation to the patient's serum albumin. Additionally, in patients with significant total serum calcium depletion, some of the ionized calcium will be absorbed by plasma proteins, so further repletion is often required.
FORD FLIPPIN: Refractory hypocalcemia, as with refractory hypokalemia, should raise concern for hypomagnesemia, which we'll talk about after we talk about hypercalcemia. Most cases of hypercalcemia that require immediate treatment are related to malignancy due to parathyroid hormone related peptide release. Other cases of significant hypercalcemia are usually due to primary hypoparathyroidism. The manifestations of hypercalcemia include GI manifestations like nausea, vomiting, constipation, ileus, and pancreatitis, as well as cardiac symptoms like hypovolemia due to hypercalciuria and the resultant osmotic diuresis, hypotension, and shortened QT intervals.
FORD FLIPPIN: There are renal manifestations as well, such as polyuria and nephrocalcinosis, and in severe cases, neurological manifestations such as confusion and depressed level of consciousness including, in severe cases, coma. The treatment is rehydration. As we just mentioned, most patients, who are hypercalcemic, are also relatively volume depleted. In order to reduce the serum calcium total, bisphosphonates are the first-line treatment.
FORD FLIPPIN: These usually have a fairly slow onset though of about two days. Diuresis can be helpful in promoting calciuria, but should only be used once the volume status is relatively normal. Historically, calcitonin has been used, however it has fallen out of favor because of the severe tachycardia that it can cause. Its rapid onset is of benefit, but the effect is only modest.
FORD FLIPPIN: And in tumor syndromes, steroids may be a useful adjunct, especially with lymphomas and myelomas. Next, let's talk about magnesium. Magnesium's essential functions in the body include energy metabolism where it is a cofactor for many ATPases, as well as an important regulator of electrical activity. It's required for the proper function of the sodium/potassium exchange pump which charges cell membranes, and this explains why magnesium deficiency also affects potassium deficiency.
FORD FLIPPIN: Magnesium also regulates calcium movement across cell membranes, especially smooth muscle, affecting the contractility of vascular and cardiac musculature. Most magnesium in the human body exists in bone, muscle, and soft tissue, and serum magnesium is tightly regulated to a level of about 1.4 to 2 milliequivalents per liter.
FORD FLIPPIN: The most common derangement in magnesium is hypomagnesemia, and that's what we're going to talk about first. The most common causes include diuretics and other medications, especially platinum-containing chemotherapeutics, diarrhea, chronic alcoholism, which is mostly due to malnutrition, but also affects thiamine conversion, and uncontrolled diabetes. The osmotic diuresis due to glucosuria carries not only magnesium but calcium and phosphorus as well along with it.
FORD FLIPPIN: The manifestations of hypomagnesemia are usually found in other electrolyte abnormalities as we've already discussed with hypokalemia and hypocalcemia, as well as hypophosphatemia, which we'll discuss next. In severe cases, cardiac rhythm instability can be a manifestation, but this requires pretty severe hypomagnesemia. You'll remember torsade de pointes is something that you treat with magnesium and this is why.
FORD FLIPPIN: Seizures can also be a manifestation of severe hypomagnesemia. To replete magnesium, it's important to take into account that some half of whatever you replete is going to be excreted in the urine. Magnesium is generally supplied as magnesium sulfate salt. In mild hypomagnesemia, where the magnesium is between 1 and 1.4, the total deficit most often amounts to 1 to 2 milliequivalents per kilogram of ideal body weight.
FORD FLIPPIN: One milliequivalent per kilogram should be infused the first day with further repletion guided by blood levels. But in severe or symptomatic hypomagnesemia, an initial infusion of 2 grams of magnesium sulfate can be infused over as little as two minutes. This would be the treatment for torsade de pointes. Further repletion will be required, and indeed some patients require as much as 50 grams of repletion in the cases of severe malnutrition, but this further repletion should also be guided by blood values.
FORD FLIPPIN: Hypermagnesemia is significantly less common clinically but warrants discussion. Its causes include iatrogenic infusions, especially in the setting of eclampsia in the obstetrics and gynecology world, renal failure, and massive hemolysis. As previously stated, clinically significant hypermagnesemia in any of these conditions is still very rare. The first sign of clinically significant hypermagnesemia is hyporeflexia, which occurs somewhere above 4 milliequivalents per liter.
FORD FLIPPIN: More severe manifestations include first-degree AV block which occurs around 5 milliequivalents per liter, complete heart block, which requires a magnesium level of 10 milliequivalents per liter, and even cardiac arrest at 13 milliequivalents per liter. Again, these manifestations are rare, and you can imagine why. It would take a lot of magnesium to get someone to 10 milliequivalents per liter of blood volume and magnesium. Let's finally discuss phosphate and hypophosphatemia.
FORD FLIPPIN: Most phosphate is located intracellularly, and here, it's part of the glycolysis pathway that forms ATP, the major energy molecule within cells. It also participates in numerous second messenger systems within the cell. The causes of hypophosphatemia include glucose loading or refeeding syndrome, which is common in chronic alcoholics and the severely malnourished. Other causes can include prolonged hyperglycemia.
FORD FLIPPIN: As we discussed, in hyperglycemic states such as diabetic ketoacidosis, the osmotic diuresis causes urinary phosphate loss as well as the other electrolytes that we've discussed before. Respiratory alkalosis can also cause hypophosphatemia. Glycolysis is accelerated in an alkalotic environment, and thus increases the demand for phosphate, and the body may end up running low. The manifestations of hypophosphatemia include impaired cardiac function, hemolytic anemia, a shift in the oxygen dissociation curve to the left, meaning that hemoglobin holds onto oxygen more strongly than usual, a decrease in overall available energy, and this leads to muscle weakness.
FORD FLIPPIN: To treat hypophosphatemia, the daily requirement is some 800 milligrams if given IV or about 1,200 milligrams PO. Replacement is mandatory for any patient with any symptoms or known severe depletion by laboratory values. The replacement is supplied either as sodium or potassium phosphate. To choose which one you should give the patient, evaluate the patient's other serum electrolytes.
FORD FLIPPIN: If the patient is hypokalemic, potassium phosphate is the best choice. Otherwise, sodium phosphate should be used because the body is more able to eliminate sodium. Hyperphosphatemia is most commonly due to renal failure, either chronic or acute. And the manifestations include hypocalcemia because calcium binds phosphate and its deposition into soft tissues, which is termed calciphylaxis.
FORD FLIPPIN: Calciphylaxis though is a fairly rare clinical entity. The treatment of hyperphosphatemia includes reducing phosphate absorption in the GI tract with phosphate binders. But more commonly, patients require dialysis, though this is not usually an independent indication in and of itself for dialysis. So we've had a lengthy discussion already about the electrolytes in the human body, and now, we're going to build on that to look at acid/base disorders.
FORD FLIPPIN: One of my favorite quotes is from H. L. Mencken, and reminds us that life is a struggle, not against sin, neither against money or power, but against hydrogen ions. And acid/base disorders are a great manifestation of this quote. Let's start with a discussion of how to use acid/base analysis because I think this is really important.
FORD FLIPPIN: The identification of an acid/base disorder is only a first step. An acid/base disorder, whether it's metabolic acidosis, respiratory alkalosis, or the others, is not a diagnosis in and of itself. It's a symptom of an underlying condition. And that's really what you're after because that's what you have to treat in order to correct the acid/base problem.
FORD FLIPPIN: But by determining the imbalance, you're enabled to then identify and treat that underlying causative condition, so keep those things in mind. We're going to start with the primary disorders. The initial physiologic alteration, which is caused by the underlying condition which changes the serum pH, is denoted the primary acid/base disorder. These can be due to respiratory derangements, causing either respiratory acidosis or alkalosis, or metabolic derangements causing either a metabolic acidosis or alkalosis.
FORD FLIPPIN: These primary changes then provoke a secondary or sometimes termed compensatory response. As you see in the table below, for example, a respiratory acidosis has the primary change with an increase in the partial pressure of carbon dioxide, but the secondary change will be an increase in serum bicarbonate to compensate for the decrease in pH. The same logic applies to respiratory alkalosis and the metabolic derangements as well.
FORD FLIPPIN: Secondary responses, as I just mentioned, are the body's attempt to balance the pH change which are caused by the primary disorder. The response pathway to metabolic disorders is through the lungs, and it is pretty rapid in onset. Observable changes occur within 30 minutes, and the response will be complete within 24 hours. This response is mediated by the chemoreceptors of the carotid body in the neck.
FORD FLIPPIN: Metabolic acidosis will provoke a respiratory alkalosis through increased minute ventilation, and metabolic alkalosis provokes the opposite response, a respiratory acidosis through reduced minute ventilation. But this response is much less vigorous than the respiratory response to metabolic acidosis. And indeed, in most cases, it's pretty hard to detect. The response pathway to respiratory disorders is through the kidneys and it's relatively slow.
FORD FLIPPIN: You may be able to observe some changes within 12 to 18 hours, but a complete response can take two to three days to take effect. Respiratory disorders may also be divided into acute or chronic types. Chronicity affects the magnitude of the anticipated secondary response. Respiratory acidosis provokes a metabolic alkalosis with the goal of retaining bicarbonate by resorption at the proximal tubule to buffer the serum pH.
FORD FLIPPIN: And respiratory alkalosis produces the opposite, a metabolic acidosis, a decreased serum bicarb, by decreasing the resorption of bicarb in the kidney. Acute responses by themselves, as we discussed above, are rarely of sufficient magnitude to be clinically recognized. However, chronic responses are usually measurable, and we'll talk about this a little bit more. This slide shows a table giving the expected responses secondarily to primary disorders.
FORD FLIPPIN: You can see that in the respiratory acidoses and alkaloses, it's divided into acute and chronic responses. The expected change in serum bicarb, as you can see in the acute respiratory acidosis and alkalosis, is of very small magnitude, whereas it's much larger with chronic respiratory conditions. We'll talk a little bit more about these equations later. But you already made it through med school, so I'm pretty sure you can read and I'm not going to read this all to you.
FORD FLIPPIN: So your ultimate question is, how do you know which response is primary and which is secondary? And we're going to go through a stepwise function to figure that out. Step 1 requires you to ask the question, is there a disorder at all? If the pH, which is usually between 7.36 and 7.44 or the PCO2, which is usually between 35 and 45, is out of the normal range, then there is a disorder, and you're going to proceed to step 2.
FORD FLIPPIN: In step 2, if the PCO2 and the pH are both abnormal, then you'll compare the direction of the change to determine which aberration is present. But if this doesn't apply, you'll go to step 3. If the direction change is the same, which is to say, the primary and secondary changes are either going up or down, then the primary disorder is metabolic. If the direction change is the opposite, then the primary disorder is respiratory.
FORD FLIPPIN: Remember this table from a couple of slides ago, and now it has the pH added. For example, in the third row, metabolic acidosis will show a total decrease in serum bicarb. It also shows a decrease in pH. Therefore, you know that the primary disorder is metabolic. The secondary change will be a decrease in the PCO2, hyperventilation or compensatory respiratory alkalosis.
FORD FLIPPIN: If you skip step 2, then we'll go to step 3, and this applies only if the pH or PCO2 is abnormal. The derangement then is a mixed process. If the PCO2 is abnormal, then the direction change in the PCO2 indicates the type of respiratory disorder and the converse metabolic disorder. For example, in a patient with a normal pH and a high PCO2, this would indicate-- for those of you thinking ahead-- a respiratory acidosis and a metabolic alkalosis.
FORD FLIPPIN: Conversely, if only the pH is abnormal, the direction of change of the pH indicates the metabolic disorder and the converse respiratory disorder. For example, a low pH with a normal PCO2 would indicate-- again, for those of you reading ahead-- a metabolic acidosis and a respiratory alkalosis. At the end of step 3, you will have identified the primary disorder, but now you have to evaluate the secondary response.
FORD FLIPPIN: If it's not as expected, it's either incomplete or there is another disorder working that hasn't been identified in steps 1 through 3. So we're going to move on to step 4 now. In metabolic disorders only, which is what step 4 applies to, if the PCO2 is greater than expected, there is a concurrent respiratory acidosis, and if PCO2 is lower than expected, there is a concurrent respiratory alkalosis.
FORD FLIPPIN: Now we'll move to step 5, which allows us to evaluate acuity. This applies to primary respiratory disorders only. If the serum bicarb is normal or nearly so, then the disorder is necessarily acute. If this doesn't apply, you'll proceed to step 6, but before we do that, ask yourself if the serum bicarb is normal or nearly so, why is the disorder acute?
FORD FLIPPIN: The answer is because the secondary response to the renal system takes two to three days to take real clinical effect. So in acute disorders, you're not going to see a significant change in serum bicarb, and therefore, it'll be normal or at least nearly so. The final step, and I'm sure you're glad to hear it's the final step, is step 6.
FORD FLIPPIN: In respiratory disorders where the bicarb is abnormal, determine the expected bicarb for the disorder using the equations that you saw in the slides before for chronic conditions. For a chronic respiratory acidosis, if the bicarb is lower than expected, then there's an incomplete renal response, but if it's higher than expected, there's a concurrent metabolic alkalosis.
FORD FLIPPIN: Or for chronic respiratory alkaloses, if the bicarb is higher than expected, there is an incomplete renal response, but if lower than expected, there's a concurrent metabolic acidosis that needs to be identified. So let's review the causes of acid/base disorders, and keep in mind, this isn't an exhaustive list, but it's going to be as complete as possible, and I'm going to highlight the things that you're most likely to see.
FORD FLIPPIN: Respiratory acidosis tends to be because of hyperventilation or minute ventilation less than physiologic requirements. There are central causes like brain injury and spinal cord trauma, as well as intrinsic lung diseases such as restricted lung diseases, as well as obstructive pulmonary diseases, of which COPD is, of course, the most common. Respiratory alkaloses, or hyperventilation with minute ventilation greater than the physiologic requirement, is common in postsurgical patients and some preop patients as well due to anxiety and pain causing hyperventilation.
FORD FLIPPIN: Another, not uncommon cause, is aspirin overdose. And finally, let's talk about metabolic alkaloses. Metabolic alkalosis can be subdivided into chloride responsive, or chloride resistant pathologies. In general, chloride responsive pathologies are ones where chloride has been lost from the body, and this includes vomiting, prolonged NG suction, volume depletion, laxative abuse, and chloruretic diuretics, especially loop diuretics and thiazide diuretics.
FORD FLIPPIN: Chloride resistant metabolic alkalosis is somewhat less common and manifests either as primary hyperaldosteronism or severe hypokalemia. You can differentiate the two by measuring the urine chloride. If the urine chloride is less than 15 mEq's per liter, then the likelihood is that the metabolic alkalosis will be chloride responsive, and can be treated, for example, with normal saline.
FORD FLIPPIN: If urine chloride is greater than 25 milliequivalents per liter, it is likely that it's chloride resistant. And these above causes, primary hyperaldosteronism or severe hypokalemia, have the obvious treatments there. We're going to talk about metabolic acidosis next because it's probably the most common thing you're going to encounter in clinical practice, and it has a lot of different manifestations. But before we discuss the root causes of metabolic acidosis, we have to add one more equation to our toolkit, and that is gaps.
FORD FLIPPIN: So we're going to help identify metabolic acidoses, and this is why calculating gaps is useful. So metabolic acidosis, as discussed, has numerous potential causes, some of which cause an excess of acids, which is termed an anion gap metabolic acidosis and some cause the loss of bicarbonate, which manifests as a non-anion gap metabolic acidosis. Therefore, you can see that calculating the anion gap can eliminate numerous potential culprits and lead one closer to the ultimate diagnosis or problem.
FORD FLIPPIN: So how do you calculate an anion gap? The basic anion gap is calculated by subtracting the most numerous anions from the most abundant cations in the serum. The most abundant cation is sodium, and the most abundant anions are chloride and bicarbonate, yielding the equation that you see in the center of the screen. The normal value for anion gap is usually around 12, plus or minus 4, give or take.
FORD FLIPPIN: Once you've calculated this gap, then you can use it to differentiate between anion gap or non-anion gap metabolic acidosis. Anion gap metabolic acidoses have many different mnemonics that have been used. The one I learned in medical school was mud piles, but it's been expanded since then into cat mud piles, which includes things such as carbon monoxide and cyanide poisoning, aminoglycosides, toluene, which is an intoxicant from huffing glue, methanol, metformin, uremia, diabetic ketoacidosis, propylene glycol, P here is also for paracetamol, which Americans know better as Tylenol or acetaminophen, I for isoniazid, inborn errors of metabolism and iron, lactic acidosis, ethylene glycol and ethanol, as well as salicylates.
FORD FLIPPIN: You probably remember this list from medical school, or at least some components of it. Non-anion gap metabolic acidoses are also common, especially in surgical patients. Diarrhea, excess administration of normal saline, hyperalimentation, the use of certain diuretics like acetazolamide or spirinolactone, or ureteroenterostomy or ileal conduit, as well as hyperparathyroidism and even hyperalimentation can all be causes of non-anion gap metabolic acidosis.
FORD FLIPPIN: So we're going to finally move on to a scenario to test your understanding of what we've talked about here today. So imagine a 55-year-old female patient with a long-term history of peptic ulcer disease, who presents to the emergency department with a three-day history of severe vomiting and weakness. She's been unable to tolerate anything orally and has noticed that her urine is both scant and dark.
FORD FLIPPIN: Ask yourself, what do you expect her electrolyte profile to be? If you said that her vomiting is expected to cause losses, both of hydrogen ions and chloride, then you're right because that's what's in her stomach. She's likely to be hypochloremic. She's also likely to be alkalotic, specifically metabolically alkalotic, possibly with a secondary respiratory acidosis.
FORD FLIPPIN: But ask yourself, are there any other potential electrolyte abnormalities that you need to take into account? If you answered yes, you're right. And the question is, which ones? Vomiting can also lead to hypokalemia as well as hyponatremia. This patient is likely to have a hypovolemic hyponatremia. So how would you treat this patient?
FORD FLIPPIN: She obviously needs volume resuscitation, but what fluid would you use? Would you use lactated Ringer's in this patient or Plasma-Lyte? I would say, no. The best IV fluid for her is probably normal saline because you're trying to replace both sodium and chloride in this patient, and she's alkalotic, meaning that a somewhat acidemic solution might actually be a good thing for her.
FORD FLIPPIN: She's going to need guided potassium supplementation as well, but that should be guided by her lab values as well as other clinical history. This will allow you to stabilize the patient enough to do further workup to understand the cause of her nausea and vomiting. This lecture wouldn't be complete without an acknowledgment of sources.
FORD FLIPPIN: I have used, for years, Paul Marino's The ICU Book which is currently in its fourth edition, and many of the tables and other information that you've seen in this lecture come from Dr. Marino's excellent text. And if you're ever looking for a source to understand acid/base disorders, electrolytes, and volume status, I think that his book is second to none. Another excellent book is the Textbook Of Critical Care that you see here.
FORD FLIPPIN: I appreciate you staying engaged for this lecture. I know this topic is tedious, especially for surgical residents. You want to hear me talk about scalpels and sutures and other cool devices and procedures, and this topic can seem boring, but it underlies almost everything that we do. The vast majority of your practice is not going to be spent in the operating room.
FORD FLIPPIN: It's going to be spent caring for patients, both before surgery and after surgery, and if you don't master these concepts, I can assure you that you will struggle to adequately manage these patients. So thank you for paying attention. I'm going to go to the end of the slide here and turn it back over to Dr. Joshi.
AMIT JOSHI: Thanks so much. That was so comprehensive and as you were going through it, I was thinking to myself exactly what you just said, that this is basic science that is used at the bedside every single day, whether you're in the ICU, whether you're caring for any patient who has any kind of derangement. Actually, I think the sources you cited are really classic sources but even I would say that this lecture will be-- it will become a pretty popular lecture, I think, on the SCORE portal, particularly as it's going to be linked to the individual module within SCORE, so thank you so much for this.
AMIT JOSHI: I hope the rest of your call weekend is somewhat better than it has been, and we'll see everyone next week for the next addition of SCORE School. Thanks, everyone.
FORD FLIPPIN: Thank you.
Segment:0 .
AMIT JOSHI: Hi, everyone. It's Amit Joshi from SCORE. Happy New Year to everyone joining us for our first session in 2021. Today, we'll be covering derangements of electrolytes and acid/base balance. I'm delighted to introduce our speaker, Dr. Ford Flippin. He's a trauma and acute care surgeon at MetroHealth Medical Center and Case Western Reserve University in Ohio.
AMIT JOSHI: Dr. Flippin did his residency at Cleveland Clinic, Florida, after getting his medical degree from LSU. He's done a fellowship in surgical critical care and acute care surgery at Rutgers Robert Wood Johnson Medical Center in New Jersey. Dr. Flippin's an acute care trauma surgeon currently. He has a particular clinical interest in disaster medicine and disaster surgery, and from chatting with him just before this, it sounds like after five days of on-call around New Year's, he's done a lot of disasters, so thank you, Dr. Flippin, for taking the time.
AMIT JOSHI: He's got a really interesting background, is involved in entrepreneurship, helps to run three companies and has multiple patents. Thanks, Dr. Flippin, and take it away, please.
FORD FLIPPIN: Amit, thank you so much for the introduction, and thank you, everyone, for joining us here for the SCORE lecture. So our goals and objectives today are fairly broad, electrolytes and their derangements, as well as disorders of acid/base status is a very large topic. So we're going to try to break things up into manageable parts, so that we can ultimately achieve these goals.
FORD FLIPPIN: Initially, we're going to identify the essential electrolytes of human plasma and their normal physiologic ranges. That's going to also allow us to describe some common IV fluids and their composition, and their proper usage. Thereafter, we'll identify major electrolyte derangements, their causes, and their treatments. Then we're going to shift to disorders of acid/base status which hopefully will allow us to be able to use pH, serum bicarb level, and PCO2 to properly diagnose acid/base disorders, and ultimately to be able to diagnose the causes and management of acid/base disorders.
FORD FLIPPIN: This quote from Paul Dirac is going to guide us, "You can never solve all difficulties at once." So we're going to take things in sequence and build on our understanding as this lecture goes along. So let's start with some basic human chemistry. Any discussion of electrolytes has to begin with the solvent in which they're present. In humans, this is water. Total body water, and derangements therein, is essential to understanding, diagnosing, and correcting abnormalities in electrolytes and in acid/base disorders.
FORD FLIPPIN: Humans are more than half water, and it's different between men and women. Males tend to be about 60% water, females a little less, around 50%. The normal total body water is the above fraction multiplied by ideal body mass, yielding a volume in liters. The current total body water is calculated by multiplying the normal total body water by the ratio of the normal sodium, which we will calculate as 140, to the current sodium.
FORD FLIPPIN: And free water deficit is the absolute value of the difference of the two above equations. So that's how it looks in words. This is how it looks as equations. Again, normal total body water is the ideal body weight times 0.6 in men or 0.5 in females. Current total body water is the normal total body water times 140 normal serum sodium over the current serum sodium in your patient.
FORD FLIPPIN: Free water deficit is the difference of the two. To find the necessary volume of infusion to correct a free water deficit, you must know the sodium concentration of the fluid you intend to use. For us, this is most often either lactated Ringer's solution or normal saline. And the volume to be infused, measured in liters, is the free water deficit times 140, again, your desired serum sodium, over the sodium concentration of the fluid you're going to use.
FORD FLIPPIN: So let's talk about some of these fluids. If body water has been lost, which is to say, the patient is hypovolemic or dehydrated, we're often asked, what is the best choice for replacement? Some people have very strong opinions on this and always use the same fluid, but the answer usually isn't that straightforward. This table expresses the concentrations of different electrolytes and components of the three most commonly used resuscitative fluids.
FORD FLIPPIN: Normal saline, lactated Ringer's, and Plasma-Lyte, which you're less likely to run into because it's more expensive and has never shown survival benefits but it's listed here for reference. When you look at normal saline, it only has three components. Water, sodium, and chloride. And you'll see here that sodium and chloride are present in higher concentrations than they are in the plasma.
FORD FLIPPIN: And indeed, the pH is actually fairly acidotic. Normal human pH is around 7.4. Normal saline pH is 5.5. As we move to the right, lactated Ringer's looks a little bit more like what we're familiar with. Sodium is a little hypotonic to normal plasma, but chloride and potassium are pretty close. There is some lactate as well, and the pH is much closer to human pH.
FORD FLIPPIN: So it's a little acidemic at 6.75. Plasma-Lyte, on the other hand, achieves a normal pH by the addition of acetate as a buffer and has relatively normal sodium and chloride concentrations, though no calcium or lactate is present here. Obviously, these fluids are very different. The best guidance that I can give is to consider the individual application and parameters of a patient.
FORD FLIPPIN: Lactated Ringer's is probably inappropriate for patients with renal failure, owing to its potassium and calcium content. The relative hypernatremia of normal saline is actually beneficial in many neurosurgical patients, and it's also often a good choice to replace gastric losses owing to the metabolic alkalosis present in these patients due to chloride loss. And for plasma re-expansion and replacement of insensible losses, lactated Ringer's or Plasma-Lyte are probably very good choices because they pretty accurately reflect the actual composition of human plasma.
FORD FLIPPIN: So having discussed these broad strokes, let's proceed to electrolyte disorders and discuss each of these electrolytes in a sequence. We're going to start with sodium. Sodium is the most abundant electrolyte in plasma. Indeed, there's more sodium than all of the other electrolytes combined. Sodium concentration is inextricably linked to volume status, in that sodium follows water in all cases, even when volume status is normal.
FORD FLIPPIN: Normal plasma sodium, we've already discussed, is around 140 but ranges from 135 to 145 milliequivalents per liter. We're going to start with hypernatremia. The initial evaluation of sodium derangements, both hypernatremia and hyponatremia, is an evaluation of volume status. So to evaluate volume status, ask yourself some basic questions.
FORD FLIPPIN: What are the patient's vital signs? Is the patient tachycardic? Are they hypertensive or hypotensive? If you have adjunctive measurement devices present like an arterial line, do they indicate a change in volume status such as high pulse pressure variability? Once you've gotten a sense of the patient's volume status, you can sort them into either hypovolemic, euvolemic, or hypervolemic hypernatremia.
FORD FLIPPIN: And this allows you to proceed down one of these pathways. In hypovolemic hypernatremia, the loss of free water is the main culprit. They may also have lost substantial quantities of sodium, but the free water loss is significantly greater than the sodium loss. In euvolemic hypernatremia, the net loss of free water is the cause here. It's most commonly due to diabetes insipidus, and if it's untreated, it can eventually progress to hypovolemic hypernatremia as well.
FORD FLIPPIN: And hypervolemic hypernatremia is almost always iatrogenic, from the infusion of hypertonic saline solutions. Remember, that as we just discussed normal saline is hypertonic in sodium terms to the normal plasma. The treatments, you can see down here below. In hypovolemia, free water replacement is the key, but because sodium losses may also be a component of this pathology, additional isotonic saline may be required.
FORD FLIPPIN: In euvolemic hypernatremia, the treatment is vasopressin for diabetes insipidus or one of its analogues. Free water replacement is also often required as is the removal of causative agents, which we'll talk about on the next slide. In hypervolemic hypernatremia, diuresis is required, often with partial free water replacement if needed with more dilute solutions. Again, in hypovolemic hypernatremia, there are many causes.
FORD FLIPPIN: Diuretics are one of them, which cause free water loss greater than sodium loss though they do cause both. Another very common cause, especially in our patients in surgery, is GI losses, whether it's from vomiting, elevated ileostomy output, or diarrhea. Heat related and sweating can also cause hypovolemic hypernatremia, especially in people who are doing long-distance, high-impact sports, especially in high temperatures.
FORD FLIPPIN: You're losing both, sodium and free water, but again free water loss is greater than the sodium loss. The final cause here, that is fairly common, is impaired thirst. This is often found in the chronically ill or elderly patients where failure to thrive is a significant problem. It can also be part of the hospital course if we fail to replace losses adequately in these patients. As you can see, the pathology includes both free water loss and, in most cases, sodium lost too.
FORD FLIPPIN: So replacement must take both into account. You need to calculate the free water deficit as we previously discussed and replace with normal saline in more severe cases. Replacement should never exceed 0.5 mEq's per liter per hour due to the risk of central pontine myelinolysis, and this is true for all forms of both, hypernatremia and hyponatremia. As we discussed, euvolemic hypernatremia is almost always caused by diabetes insipidus.
FORD FLIPPIN: Central DI is the impaired release of antidiuretic hormone from the posterior pituitary which is often caused by traumatic brain injuries. Alternatively, diabetes insipidus can originate in the kidney where it's termed a nephrogenic DI, and there's an impaired response to antidiuretic hormone in the kidney. This is most often drug related.
FORD FLIPPIN: Some common medications that can cause this include amphoterecin, aminoglycosides, lithium, dopamine, radio contrast dyes, and it can also occur in the polyuric phase of acute tubular necrosis. Any type of nephrogenic diabetes insipidus tends to be less severe than the central form described above. If you're uncertain about the diagnosis, it can be confirmed by urine osmolality. In diabetes insipidus, the urine osmolality is almost invariably less than 200 milliosmoles per liter, whereas the normal is 200 to 500.
FORD FLIPPIN: As discussed before, treatment is the removal of any potentially causative agent in either intermittent desmopressin or vasopressin infusions. Finally, hypervolemic hypernatremia is almost universally due to iatrogenic saline administration. This may be due to hypertonic infusions for brain-injured patients with the goal of reducing cerebral edema or the inappropriate administration of normal saline.
FORD FLIPPIN: Remember, normal saline is isotonic overall to plasma, but in sodium and chloride terms individually, it's hypertonic to the normal concentrations of these ions in a plasma. The treatment is diuresis, which promotes sodium loss, but as previously discussed, it may initially worsen the hypernatremia due to the loss of hypotonic urine. And therefore, gentle fluid replacement with hypotonic fluids, usually quarter-normal saline, is often required.
FORD FLIPPIN: Let's move on to hyponatremia now. As with hypernatremia, evaluation of volume status is the initial step, as we've already discussed. Further evaluation with urine sodium and urine osmolality is also often helpful. Symptoms range from headache and nausea to vomiting, progressing to encephalopathy, and even coma. And the more precipitous the drop in the sodium, the more severe the symptoms tend to be.
FORD FLIPPIN: In some patients, which we'll discuss soon, this hyponatremia can be quite chronic, and they will have minimal symptoms. Other patients will have a precipitous drop, and they'll be the ones where you see severe symptoms. As with hypernatremia, hyponatremia is sorted based on volume status. Hypo-, eu-, and hypervolemic hyponatremia. In hypovolemic, the sodium loss is greater than the free water loss, and this tends to be caused either by cerebral salt wasting or primary adrenal insufficiency.
FORD FLIPPIN: Euvolemic hyponatremia tends to be because of either free water retention or excess free water intake as in SIADH, the syndrome of inappropriate antidiuretic hormone excretion, or primary polydipsia, respectively. And hypervolemic hyponatremia is due to free water retention greater than sodium retention. These patients tend to have chronic illnesses, such as severe cirrhosis, heart failure or oliguric or even anuric renal failure.
FORD FLIPPIN: As you see in the next row, urine sodium and urine osmolality are key to making these diagnoses. In a hypovolemic patient, a urine sodium greater than 20 demonstrates a renal sodium loss as with other conditions, such as acute tubular necrosis. And urine sodium less than 20 demonstrates extrarenal losses. In euvolemic hyponatremia, the urine osmolality is generally greater than 100 in the case of excess water retention as with SIADH.
FORD FLIPPIN: Or in the case of excess water intake, as with primary polydipsia, urine osmolality tends to be very low, less than 100 even. Hypervolemic hyponatremia shows, again, urine sodium greater than 20 with renal losses and a urine sodium less than 20, if there are extrarenal losses. The treatment for these include fluid restriction and normal saline or even hypertonic saline administration if symptoms are especially severe.
FORD FLIPPIN: And a reminder, sodium correction should not exceed 0.5 mEq's per liter per hour. We're going to move on to potassium physiology now, and conversely to what we saw with sodium, the vast majority of potassium is actually intracellular. In the average 70 kilogram adult, about 3,500 milliequivalents of potassium exist inside the cells, but only about 70 milliequivalents exist in the serum.
FORD FLIPPIN: And this serum potassium is very tightly regulated. The normal serum potassium ranges from 3.5 to 5 mEq's per liter. Most potassium is excreted through the kidney with smaller losses in the stool and sweat. However, we'll see the derangements in these systems can result in serious abnormalities. We'll start with hypokalemia, where the causes include renal losses, most commonly with loop diuretics like Lasix or furosemide, NG suctioning, .
FORD FLIPPIN: where hypovolemia and alkalosis promote potassium loss in urine, diarrhea, magnesium depletion, and transcellular shifts caused by such drugs as insulin and beta agonists, as well as hypothermia. The manifestations of hypokalemia include muscle weakness as well as EKG changes such as prominent U waves, T-wave flattening and inversion, QT prolongation as well. These are relatively non-specific changes and hypokalemia rarely leads to cardiac instability unless there is another underlying condition.
FORD FLIPPIN: With that said, many of our patients are in the hospital because they have underlying conditions. So hypokalemia does have to be taken seriously. So what do you do about it? The repletion of hypokalemia, in general, requires you to raise the serum potassium by 1 milliequivalent which requires about 100 milliequivalents of infused potassium chloride. The usual maximum rate of infusion is about 20 mEq's per hour, though this can be raised in critical situations but only with central venous access because potassium-containing solutions are very caustic to the vasculature.
FORD FLIPPIN: There are some important exceptions. These include patients on tacrolimus, most of which are transplant patients. Tacrolimus inhibits potassium excretion in the kidney, and the administration of significant loads of potassium can raise the potassium very precipitously, even leading to cardiac arrest. Replacement of potassium also has to be done carefully in patients with renal failure, but this is uncommon as these patients are rarely hypokalemic.
FORD FLIPPIN: Indeed, often they're hyperkalemic. Any patient in whom you are trying to replete potassium without a response that you're expecting should prompt an evaluation for hypomagnesemia. Let's move on to hyperkalemia. The causes of hyperkalemia include impaired renal secretion, as we've just discussed with CKD and tacrolimus, as well as transcellular release as with tumor lysis syndrome, especially with non-Hodgkin's lymphoma, crush injuries, and some medications including succinylcholine and digitalis.
FORD FLIPPIN: Of note, cardioplegia solutions in cardiac surgery, which are the solutions used to stop the heart, can raise the serum potassium to as high as 20, which stops the heart in seconds. But you're not going to interact with that unless you decide to go down the route of cardiac surgery. The manifestations of hyperkalemia pretty much all happen in the heart and they're very serious. At milder hyperkalemias, you'll find peaked T waves, and that is, the hyperkalemia worsens.
FORD FLIPPIN: The cardiac manifestations can worsen to heart blocks and even cardiac arrest. These are due to impaired conduction of the polarization currents between the cardiac myocytes. The treatment of hyperkalemia goes down three steps. The first and most immediate priority is stabilization of the cardiac membrane. This is achieved with 1 gram of calcium gluconate or, in the cases of shock, 1 gram of calcium chloride.
FORD FLIPPIN: We'll discuss the differences next when we discuss calcium. This must be re-dosed every 60 minutes until the hyperkalemia has been resolved. The next most immediate course of action is to force potassium into the cells. This is done with insulin and dextrose administration. In general, '10 units of regular insulin plus 25 grams of 50% dextrose, and the effects of this cocktail lasts about 60 minutes.
FORD FLIPPIN: Especially in non-diabetic patients, we must be extremely vigilant of the blood glucose level as these patients can get hypoglycemic very quickly. Beta agonists can also be a useful adjunct, but they're not a first-line treatment for pushing potassium into cells. These measures, the first two, will temporize the situation, but ultimately, the goal must be to remove potassium. Kayexelate is a medication given orally or rectally which can draw potassium into the GI tract and remove it, but it's slow acting and can take as much as two to four days to have real effect.
FORD FLIPPIN: In emergent situations, dialysis is the gold standard for removing potassium. Next, we're going to discuss calcium as promised. Plasma calcium exists in two states. The first is bound to proteins, mostly albumin, or ionized, which is the biologically active form. When calcium stores are low, the bound fraction will decrease as albumin releases calcium to replete the ionized fraction.
FORD FLIPPIN: The ionized fraction may indeed remain normal but repletion is still indicated. Ionized calcium is essential for numerous processes in the body, including vasomotor tone and as a clotting factor. For those of you who don't remember, calcium is clotting factor IV. We'll start with hypocalcemia. And causes of hypocalcemia can include magnesium depletion, where it suppresses parathyroid hormone release and decreases the tissue responsiveness to parathyroid hormone.
FORD FLIPPIN: It can also be present in blood transfusion and the risk for this increases with the volume of blood transfusion, pancreatitis, renal failure due to phosphate retention, and impaired vitamin D production, as well as alkalosis where the increased bicarb can bind to calcium. Manifestations of hypocalcemia include tetany, hyperreflexia, and in severe cases, paresthesias and seizures.
FORD FLIPPIN: You may remember from medical school, Chvostek's and Trousseau's signs. These are useful but rarely diagnostic. Chvostek is a very non-specific sign in that it is present in 25% of normal patients, and Trousseau's sign is relatively insensitive in that it is absent in at least 30% of patients who have hypocalcemia. There are also cardiac manifestations including hypotension, decreased cardiac output, and ventricular ectopy.
FORD FLIPPIN: But all of these require very severe hypocalcemia to be present. The repletion in hypoglycemia is done either with calcium chloride or calcium gluconate. Per unit volume, calcium chloride contains three times as much elemental calcium, and the resultant osmolarity is three times higher. Calcium chloride's osmolarity is fully 2 osmoles per liter, meaning that it can really only be infused via central line except in emergencies.
FORD FLIPPIN: Both are generally supplied as 10% solutions. 200 milligrams of elemental calcium, which is usually supplied as two grams of calcium gluconate solution, would be expected to raise the serum ionized calcium by about half a milligram per deciliter, though the individual response will vary, especially in relation to the patient's serum albumin. Additionally, in patients with significant total serum calcium depletion, some of the ionized calcium will be absorbed by plasma proteins, so further repletion is often required.
FORD FLIPPIN: Refractory hypocalcemia, as with refractory hypokalemia, should raise concern for hypomagnesemia, which we'll talk about after we talk about hypercalcemia. Most cases of hypercalcemia that require immediate treatment are related to malignancy due to parathyroid hormone related peptide release. Other cases of significant hypercalcemia are usually due to primary hypoparathyroidism. The manifestations of hypercalcemia include GI manifestations like nausea, vomiting, constipation, ileus, and pancreatitis, as well as cardiac symptoms like hypovolemia due to hypercalciuria and the resultant osmotic diuresis, hypotension, and shortened QT intervals.
FORD FLIPPIN: There are renal manifestations as well, such as polyuria and nephrocalcinosis, and in severe cases, neurological manifestations such as confusion and depressed level of consciousness including, in severe cases, coma. The treatment is rehydration. As we just mentioned, most patients, who are hypercalcemic, are also relatively volume depleted. In order to reduce the serum calcium total, bisphosphonates are the first-line treatment.
FORD FLIPPIN: These usually have a fairly slow onset though of about two days. Diuresis can be helpful in promoting calciuria, but should only be used once the volume status is relatively normal. Historically, calcitonin has been used, however it has fallen out of favor because of the severe tachycardia that it can cause. Its rapid onset is of benefit, but the effect is only modest.
FORD FLIPPIN: And in tumor syndromes, steroids may be a useful adjunct, especially with lymphomas and myelomas. Next, let's talk about magnesium. Magnesium's essential functions in the body include energy metabolism where it is a cofactor for many ATPases, as well as an important regulator of electrical activity. It's required for the proper function of the sodium/potassium exchange pump which charges cell membranes, and this explains why magnesium deficiency also affects potassium deficiency.
FORD FLIPPIN: Magnesium also regulates calcium movement across cell membranes, especially smooth muscle, affecting the contractility of vascular and cardiac musculature. Most magnesium in the human body exists in bone, muscle, and soft tissue, and serum magnesium is tightly regulated to a level of about 1.4 to 2 milliequivalents per liter.
FORD FLIPPIN: The most common derangement in magnesium is hypomagnesemia, and that's what we're going to talk about first. The most common causes include diuretics and other medications, especially platinum-containing chemotherapeutics, diarrhea, chronic alcoholism, which is mostly due to malnutrition, but also affects thiamine conversion, and uncontrolled diabetes. The osmotic diuresis due to glucosuria carries not only magnesium but calcium and phosphorus as well along with it.
FORD FLIPPIN: The manifestations of hypomagnesemia are usually found in other electrolyte abnormalities as we've already discussed with hypokalemia and hypocalcemia, as well as hypophosphatemia, which we'll discuss next. In severe cases, cardiac rhythm instability can be a manifestation, but this requires pretty severe hypomagnesemia. You'll remember torsade de pointes is something that you treat with magnesium and this is why.
FORD FLIPPIN: Seizures can also be a manifestation of severe hypomagnesemia. To replete magnesium, it's important to take into account that some half of whatever you replete is going to be excreted in the urine. Magnesium is generally supplied as magnesium sulfate salt. In mild hypomagnesemia, where the magnesium is between 1 and 1.4, the total deficit most often amounts to 1 to 2 milliequivalents per kilogram of ideal body weight.
FORD FLIPPIN: One milliequivalent per kilogram should be infused the first day with further repletion guided by blood levels. But in severe or symptomatic hypomagnesemia, an initial infusion of 2 grams of magnesium sulfate can be infused over as little as two minutes. This would be the treatment for torsade de pointes. Further repletion will be required, and indeed some patients require as much as 50 grams of repletion in the cases of severe malnutrition, but this further repletion should also be guided by blood values.
FORD FLIPPIN: Hypermagnesemia is significantly less common clinically but warrants discussion. Its causes include iatrogenic infusions, especially in the setting of eclampsia in the obstetrics and gynecology world, renal failure, and massive hemolysis. As previously stated, clinically significant hypermagnesemia in any of these conditions is still very rare. The first sign of clinically significant hypermagnesemia is hyporeflexia, which occurs somewhere above 4 milliequivalents per liter.
FORD FLIPPIN: More severe manifestations include first-degree AV block which occurs around 5 milliequivalents per liter, complete heart block, which requires a magnesium level of 10 milliequivalents per liter, and even cardiac arrest at 13 milliequivalents per liter. Again, these manifestations are rare, and you can imagine why. It would take a lot of magnesium to get someone to 10 milliequivalents per liter of blood volume and magnesium. Let's finally discuss phosphate and hypophosphatemia.
FORD FLIPPIN: Most phosphate is located intracellularly, and here, it's part of the glycolysis pathway that forms ATP, the major energy molecule within cells. It also participates in numerous second messenger systems within the cell. The causes of hypophosphatemia include glucose loading or refeeding syndrome, which is common in chronic alcoholics and the severely malnourished. Other causes can include prolonged hyperglycemia.
FORD FLIPPIN: As we discussed, in hyperglycemic states such as diabetic ketoacidosis, the osmotic diuresis causes urinary phosphate loss as well as the other electrolytes that we've discussed before. Respiratory alkalosis can also cause hypophosphatemia. Glycolysis is accelerated in an alkalotic environment, and thus increases the demand for phosphate, and the body may end up running low. The manifestations of hypophosphatemia include impaired cardiac function, hemolytic anemia, a shift in the oxygen dissociation curve to the left, meaning that hemoglobin holds onto oxygen more strongly than usual, a decrease in overall available energy, and this leads to muscle weakness.
FORD FLIPPIN: To treat hypophosphatemia, the daily requirement is some 800 milligrams if given IV or about 1,200 milligrams PO. Replacement is mandatory for any patient with any symptoms or known severe depletion by laboratory values. The replacement is supplied either as sodium or potassium phosphate. To choose which one you should give the patient, evaluate the patient's other serum electrolytes.
FORD FLIPPIN: If the patient is hypokalemic, potassium phosphate is the best choice. Otherwise, sodium phosphate should be used because the body is more able to eliminate sodium. Hyperphosphatemia is most commonly due to renal failure, either chronic or acute. And the manifestations include hypocalcemia because calcium binds phosphate and its deposition into soft tissues, which is termed calciphylaxis.
FORD FLIPPIN: Calciphylaxis though is a fairly rare clinical entity. The treatment of hyperphosphatemia includes reducing phosphate absorption in the GI tract with phosphate binders. But more commonly, patients require dialysis, though this is not usually an independent indication in and of itself for dialysis. So we've had a lengthy discussion already about the electrolytes in the human body, and now, we're going to build on that to look at acid/base disorders.
FORD FLIPPIN: One of my favorite quotes is from H. L. Mencken, and reminds us that life is a struggle, not against sin, neither against money or power, but against hydrogen ions. And acid/base disorders are a great manifestation of this quote. Let's start with a discussion of how to use acid/base analysis because I think this is really important.
FORD FLIPPIN: The identification of an acid/base disorder is only a first step. An acid/base disorder, whether it's metabolic acidosis, respiratory alkalosis, or the others, is not a diagnosis in and of itself. It's a symptom of an underlying condition. And that's really what you're after because that's what you have to treat in order to correct the acid/base problem.
FORD FLIPPIN: But by determining the imbalance, you're enabled to then identify and treat that underlying causative condition, so keep those things in mind. We're going to start with the primary disorders. The initial physiologic alteration, which is caused by the underlying condition which changes the serum pH, is denoted the primary acid/base disorder. These can be due to respiratory derangements, causing either respiratory acidosis or alkalosis, or metabolic derangements causing either a metabolic acidosis or alkalosis.
FORD FLIPPIN: These primary changes then provoke a secondary or sometimes termed compensatory response. As you see in the table below, for example, a respiratory acidosis has the primary change with an increase in the partial pressure of carbon dioxide, but the secondary change will be an increase in serum bicarbonate to compensate for the decrease in pH. The same logic applies to respiratory alkalosis and the metabolic derangements as well.
FORD FLIPPIN: Secondary responses, as I just mentioned, are the body's attempt to balance the pH change which are caused by the primary disorder. The response pathway to metabolic disorders is through the lungs, and it is pretty rapid in onset. Observable changes occur within 30 minutes, and the response will be complete within 24 hours. This response is mediated by the chemoreceptors of the carotid body in the neck.
FORD FLIPPIN: Metabolic acidosis will provoke a respiratory alkalosis through increased minute ventilation, and metabolic alkalosis provokes the opposite response, a respiratory acidosis through reduced minute ventilation. But this response is much less vigorous than the respiratory response to metabolic acidosis. And indeed, in most cases, it's pretty hard to detect. The response pathway to respiratory disorders is through the kidneys and it's relatively slow.
FORD FLIPPIN: You may be able to observe some changes within 12 to 18 hours, but a complete response can take two to three days to take effect. Respiratory disorders may also be divided into acute or chronic types. Chronicity affects the magnitude of the anticipated secondary response. Respiratory acidosis provokes a metabolic alkalosis with the goal of retaining bicarbonate by resorption at the proximal tubule to buffer the serum pH.
FORD FLIPPIN: And respiratory alkalosis produces the opposite, a metabolic acidosis, a decreased serum bicarb, by decreasing the resorption of bicarb in the kidney. Acute responses by themselves, as we discussed above, are rarely of sufficient magnitude to be clinically recognized. However, chronic responses are usually measurable, and we'll talk about this a little bit more. This slide shows a table giving the expected responses secondarily to primary disorders.
FORD FLIPPIN: You can see that in the respiratory acidoses and alkaloses, it's divided into acute and chronic responses. The expected change in serum bicarb, as you can see in the acute respiratory acidosis and alkalosis, is of very small magnitude, whereas it's much larger with chronic respiratory conditions. We'll talk a little bit more about these equations later. But you already made it through med school, so I'm pretty sure you can read and I'm not going to read this all to you.
FORD FLIPPIN: So your ultimate question is, how do you know which response is primary and which is secondary? And we're going to go through a stepwise function to figure that out. Step 1 requires you to ask the question, is there a disorder at all? If the pH, which is usually between 7.36 and 7.44 or the PCO2, which is usually between 35 and 45, is out of the normal range, then there is a disorder, and you're going to proceed to step 2.
FORD FLIPPIN: In step 2, if the PCO2 and the pH are both abnormal, then you'll compare the direction of the change to determine which aberration is present. But if this doesn't apply, you'll go to step 3. If the direction change is the same, which is to say, the primary and secondary changes are either going up or down, then the primary disorder is metabolic. If the direction change is the opposite, then the primary disorder is respiratory.
FORD FLIPPIN: Remember this table from a couple of slides ago, and now it has the pH added. For example, in the third row, metabolic acidosis will show a total decrease in serum bicarb. It also shows a decrease in pH. Therefore, you know that the primary disorder is metabolic. The secondary change will be a decrease in the PCO2, hyperventilation or compensatory respiratory alkalosis.
FORD FLIPPIN: If you skip step 2, then we'll go to step 3, and this applies only if the pH or PCO2 is abnormal. The derangement then is a mixed process. If the PCO2 is abnormal, then the direction change in the PCO2 indicates the type of respiratory disorder and the converse metabolic disorder. For example, in a patient with a normal pH and a high PCO2, this would indicate-- for those of you thinking ahead-- a respiratory acidosis and a metabolic alkalosis.
FORD FLIPPIN: Conversely, if only the pH is abnormal, the direction of change of the pH indicates the metabolic disorder and the converse respiratory disorder. For example, a low pH with a normal PCO2 would indicate-- again, for those of you reading ahead-- a metabolic acidosis and a respiratory alkalosis. At the end of step 3, you will have identified the primary disorder, but now you have to evaluate the secondary response.
FORD FLIPPIN: If it's not as expected, it's either incomplete or there is another disorder working that hasn't been identified in steps 1 through 3. So we're going to move on to step 4 now. In metabolic disorders only, which is what step 4 applies to, if the PCO2 is greater than expected, there is a concurrent respiratory acidosis, and if PCO2 is lower than expected, there is a concurrent respiratory alkalosis.
FORD FLIPPIN: Now we'll move to step 5, which allows us to evaluate acuity. This applies to primary respiratory disorders only. If the serum bicarb is normal or nearly so, then the disorder is necessarily acute. If this doesn't apply, you'll proceed to step 6, but before we do that, ask yourself if the serum bicarb is normal or nearly so, why is the disorder acute?
FORD FLIPPIN: The answer is because the secondary response to the renal system takes two to three days to take real clinical effect. So in acute disorders, you're not going to see a significant change in serum bicarb, and therefore, it'll be normal or at least nearly so. The final step, and I'm sure you're glad to hear it's the final step, is step 6.
FORD FLIPPIN: In respiratory disorders where the bicarb is abnormal, determine the expected bicarb for the disorder using the equations that you saw in the slides before for chronic conditions. For a chronic respiratory acidosis, if the bicarb is lower than expected, then there's an incomplete renal response, but if it's higher than expected, there's a concurrent metabolic alkalosis.
FORD FLIPPIN: Or for chronic respiratory alkaloses, if the bicarb is higher than expected, there is an incomplete renal response, but if lower than expected, there's a concurrent metabolic acidosis that needs to be identified. So let's review the causes of acid/base disorders, and keep in mind, this isn't an exhaustive list, but it's going to be as complete as possible, and I'm going to highlight the things that you're most likely to see.
FORD FLIPPIN: Respiratory acidosis tends to be because of hyperventilation or minute ventilation less than physiologic requirements. There are central causes like brain injury and spinal cord trauma, as well as intrinsic lung diseases such as restricted lung diseases, as well as obstructive pulmonary diseases, of which COPD is, of course, the most common. Respiratory alkaloses, or hyperventilation with minute ventilation greater than the physiologic requirement, is common in postsurgical patients and some preop patients as well due to anxiety and pain causing hyperventilation.
FORD FLIPPIN: Another, not uncommon cause, is aspirin overdose. And finally, let's talk about metabolic alkaloses. Metabolic alkalosis can be subdivided into chloride responsive, or chloride resistant pathologies. In general, chloride responsive pathologies are ones where chloride has been lost from the body, and this includes vomiting, prolonged NG suction, volume depletion, laxative abuse, and chloruretic diuretics, especially loop diuretics and thiazide diuretics.
FORD FLIPPIN: Chloride resistant metabolic alkalosis is somewhat less common and manifests either as primary hyperaldosteronism or severe hypokalemia. You can differentiate the two by measuring the urine chloride. If the urine chloride is less than 15 mEq's per liter, then the likelihood is that the metabolic alkalosis will be chloride responsive, and can be treated, for example, with normal saline.
FORD FLIPPIN: If urine chloride is greater than 25 milliequivalents per liter, it is likely that it's chloride resistant. And these above causes, primary hyperaldosteronism or severe hypokalemia, have the obvious treatments there. We're going to talk about metabolic acidosis next because it's probably the most common thing you're going to encounter in clinical practice, and it has a lot of different manifestations. But before we discuss the root causes of metabolic acidosis, we have to add one more equation to our toolkit, and that is gaps.
FORD FLIPPIN: So we're going to help identify metabolic acidoses, and this is why calculating gaps is useful. So metabolic acidosis, as discussed, has numerous potential causes, some of which cause an excess of acids, which is termed an anion gap metabolic acidosis and some cause the loss of bicarbonate, which manifests as a non-anion gap metabolic acidosis. Therefore, you can see that calculating the anion gap can eliminate numerous potential culprits and lead one closer to the ultimate diagnosis or problem.
FORD FLIPPIN: So how do you calculate an anion gap? The basic anion gap is calculated by subtracting the most numerous anions from the most abundant cations in the serum. The most abundant cation is sodium, and the most abundant anions are chloride and bicarbonate, yielding the equation that you see in the center of the screen. The normal value for anion gap is usually around 12, plus or minus 4, give or take.
FORD FLIPPIN: Once you've calculated this gap, then you can use it to differentiate between anion gap or non-anion gap metabolic acidosis. Anion gap metabolic acidoses have many different mnemonics that have been used. The one I learned in medical school was mud piles, but it's been expanded since then into cat mud piles, which includes things such as carbon monoxide and cyanide poisoning, aminoglycosides, toluene, which is an intoxicant from huffing glue, methanol, metformin, uremia, diabetic ketoacidosis, propylene glycol, P here is also for paracetamol, which Americans know better as Tylenol or acetaminophen, I for isoniazid, inborn errors of metabolism and iron, lactic acidosis, ethylene glycol and ethanol, as well as salicylates.
FORD FLIPPIN: You probably remember this list from medical school, or at least some components of it. Non-anion gap metabolic acidoses are also common, especially in surgical patients. Diarrhea, excess administration of normal saline, hyperalimentation, the use of certain diuretics like acetazolamide or spirinolactone, or ureteroenterostomy or ileal conduit, as well as hyperparathyroidism and even hyperalimentation can all be causes of non-anion gap metabolic acidosis.
FORD FLIPPIN: So we're going to finally move on to a scenario to test your understanding of what we've talked about here today. So imagine a 55-year-old female patient with a long-term history of peptic ulcer disease, who presents to the emergency department with a three-day history of severe vomiting and weakness. She's been unable to tolerate anything orally and has noticed that her urine is both scant and dark.
FORD FLIPPIN: Ask yourself, what do you expect her electrolyte profile to be? If you said that her vomiting is expected to cause losses, both of hydrogen ions and chloride, then you're right because that's what's in her stomach. She's likely to be hypochloremic. She's also likely to be alkalotic, specifically metabolically alkalotic, possibly with a secondary respiratory acidosis.
FORD FLIPPIN: But ask yourself, are there any other potential electrolyte abnormalities that you need to take into account? If you answered yes, you're right. And the question is, which ones? Vomiting can also lead to hypokalemia as well as hyponatremia. This patient is likely to have a hypovolemic hyponatremia. So how would you treat this patient?
FORD FLIPPIN: She obviously needs volume resuscitation, but what fluid would you use? Would you use lactated Ringer's in this patient or Plasma-Lyte? I would say, no. The best IV fluid for her is probably normal saline because you're trying to replace both sodium and chloride in this patient, and she's alkalotic, meaning that a somewhat acidemic solution might actually be a good thing for her.
FORD FLIPPIN: She's going to need guided potassium supplementation as well, but that should be guided by her lab values as well as other clinical history. This will allow you to stabilize the patient enough to do further workup to understand the cause of her nausea and vomiting. This lecture wouldn't be complete without an acknowledgment of sources.
FORD FLIPPIN: I have used, for years, Paul Marino's The ICU Book which is currently in its fourth edition, and many of the tables and other information that you've seen in this lecture come from Dr. Marino's excellent text. And if you're ever looking for a source to understand acid/base disorders, electrolytes, and volume status, I think that his book is second to none. Another excellent book is the Textbook Of Critical Care that you see here.
FORD FLIPPIN: I appreciate you staying engaged for this lecture. I know this topic is tedious, especially for surgical residents. You want to hear me talk about scalpels and sutures and other cool devices and procedures, and this topic can seem boring, but it underlies almost everything that we do. The vast majority of your practice is not going to be spent in the operating room.
FORD FLIPPIN: It's going to be spent caring for patients, both before surgery and after surgery, and if you don't master these concepts, I can assure you that you will struggle to adequately manage these patients. So thank you for paying attention. I'm going to go to the end of the slide here and turn it back over to Dr. Joshi.
AMIT JOSHI: Thanks so much. That was so comprehensive and as you were going through it, I was thinking to myself exactly what you just said, that this is basic science that is used at the bedside every single day, whether you're in the ICU, whether you're caring for any patient who has any kind of derangement. Actually, I think the sources you cited are really classic sources but even I would say that this lecture will be-- it will become a pretty popular lecture, I think, on the SCORE portal, particularly as it's going to be linked to the individual module within SCORE, so thank you so much for this.
AMIT JOSHI: I hope the rest of your call weekend is somewhat better than it has been, and we'll see everyone next week for the next addition of SCORE School. Thanks, everyone.
FORD FLIPPIN: Thank you.
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