22 ABSITE 2024 Fluids and Electrolytes - edited

All right. We are back for our ab site review. This is Patrick here with John. Hello. And we're gonna be covering a mundane topic here, fluids and electrolytes. Okay. We know this isn't fun, but if you want to get a few questions right in your ab site, you want to listen in. It's gonna be lots of numbers, lots of quick answers.

We apologize in advance, but we're gonna give you the information that you need. So John, what is the percentage of total body water by weight in an adult? So in males, it's body weight in kilograms times 0. 6 equals your total body water. And females, it's body weights in kilograms times 0. 5, that equals your total body water in liters.

So total body water can be intracellular, extracellular, or intravascular. What is the breakdown? So two thirds of your total body water is intracellular. Of the one third of your total body weight that's extracellular, one quarter of that is intravascular, and three quarters of that is extravascular. So with that, what is the average blood volume of an average size adult?

So about five liters. Okay, now

pediatric patients though, how would you calculate average blood volume? So about 80 cc's a kilogram. Okay what are some of the commonly used maintenance fluids for patients? Let's give how about adult? When we say maintenance fluids, what comes to mind? Yeah, the traditional maintenance float is D5 half normal saline with 20 milliquins, a milliequivalence of potassium.

Okay. How about in a pediatric population? So D5 normal saline with 20 milliequivalence of potassium. Okay. And how about neonates? It's D5 quarter normal saline with 20 mg of potassium. Okay, so for adults we have half normal saline, pediatric normal saline, and neonates one quarter normal saline. What about the most commonly used resuscitative fluids?

Yeah, this is pretty, you know, generic, but isotonic crystalloids and colloids. Yeah, isotonic crystalloids are? They're LR and normal saline. Okay, and what are the component electrolyte concentrations within normal saline? So of normal saline, you have 154 milliequivalents of sodium and

154 milliequivalents of chloride.

Yeah, so that's not normal. So a tie, right? Yeah, yeah. Versus LR? So you have 130 milliequivalents of sodium, 4 milliequivalents of potassium, 2. 7 milliequivalents of calcium, 109 milliequivalents of chloride, and 28 milliequivalents of bicarbonate. Right, so more physiologic, that's the favored resuscitative.

fluid in most but not all circumstances. So, how would you calculate an appropriate maintenance fluid? Yeah, I use the 4 2 1 rule to calculate hourly fluid rate. So it's 4 cc's a kilogram for the first 10 kilograms, kilogram for the second 10 kilograms, and 1 cc for every kilogram over 20 kilograms.

Sure, and there's a simplified formula too, you could add the patient's weight in kilograms plus 40. And that's their hourly rate of fluids. All right. High yield alert. You're almost guaranteed to have a question on FINA. So John, what is the FINA, the formula for FINA?

How's it calculated? So it's the result of your urine sodium divided by your cerium sodium.

which is then divided by the result of your urine keratinine divided by your serum keratinine times a hundred. Right, and how do you interpret that? So, it can help determine the etiology of your acute kidney injury. So pre renal, if the result of that is less than one, then you have a pre renal cause of your AKI.

If it's greater than two, then it's a renal cause. And if it's as high as over four, it's post renal. Right. So you have urine sodium divided by serum sodium over urine creatinine divided by serum creatinine. So sodium is on top, creatinine is on bottom. You can have US over US. So for urine and sodium, or excuse me, urine and serum.

So if a patient has used a diuretics, we can't use the FINA formula. We have to use the FE urea formula. What is that? That is the result of your serum creatinine divided by your urine creatinine, which is then divided by the

result of your urine urea divided by your serum ureta times a hundred. Okay, so that is serum creatinine divided by urine creatinine over urine urea.

divided by serum urea. Alright John, let's talk hyponatremia. What are some simple steps to evaluating this kind of confusing problem? Yeah, so we want to start with calculating our serum osmolality. I'm not going to go into the calculations for this but just know that's what you have to do. And then we want to measure your urine osmolality.

So using those two things in hyponatremic patients you can kind of narrow your differential. So when your serum osmolality is low and your urine osmolality is high, So overly concentrated urine, right? Right, yes. Then you have to be considering SID, SIDH renal losses, diarrhea and vomiting, overdiuresis, adrenal insufficiency, CHF and cirrhosis.

When you have a serum osmolality that's low and your urine osmolality is low, then it most likely causes

excess free water. And so when it comes to hybronatremia, we want to decrease free water intake, so restrict the water. If we suspect it's secondary to SIADH, we're going to fluid restrict, add sodium supplementation, and if needed consider VAPTANs, or vasopressin receptor antagonist.

Another formula, John, how do you calculate a sodium deficit? So that's your desired sodium, which is usually 140, minus actual sodium. Times total body water and that equals your sodium deficit in milo equivalents. Okay. What are some of the common etiologies of hypernatremia in surgical patients? Yeah, so hypovolemia hypovolemic hypernatremia You can consider water loss insensible or insensible GI losses Uvolemic hypernatremia, you must consider nephrogenic or neurogenic diabetes insipidus and you can suspect this if there's a head injury and hypervolemic hypernatremia You consider hypertonic fluid resuscitation or mineral corticoid

excess.

Okay, so you mentioned for a euvolemic patient you can have nephrogenic di or neurogenic DB di. So if you have a patient on the exam who has a head injury, they have excess urine output and hypernatremia. How do we confirm that diagnosis of di? You wanna compare your serum osmolality to your urine osmolality.

So if your serum osmolality is high and your urine osmolality is low. You would suspect DI. Right, and this is all about, again, this is the failure to concentrate urine. And so, that's really important. If you're getting confused on the exam, think about is the urine concentrated or is it not, and that can help you start your differential.

Okay, we have a patient with hypernatremia and nephrogenic DI. How are they treated? So nephrogenic DI is treated with free water supplementation and a thiazide diuretic. Okay, we have a hypernatremic patient with neurogenic DI. How do we treat them? We can treat them with low dose vasopressin or use

DDAVP.

Okay. All right. So let's talk about free water deficit because this is actually something really common. We see ICU often and we have to calculate how much to resuscitate that patient. How do you calculate that? So that's your total body water times your actual sodium minus your desired sodium. So about 140 divided by your desired sodium.

And that equals your free water deficit in liters. Right. You remember that total body water equals the weight in kilograms times percent total body water, which is 0. 6 in males and 0. 5 in females. All right, let's move on to potassium abnormality. So what are the EKG findings that are present in hyperkalemia?

Yeah, this is the classic peak T waves. Yeah, how is this managed? We want to stabilize the myocardium and we can do that with calcium. We want to push the potassium intracellularly with insulin D5 and albuterol. We want to increase the urinary excretion by use of

Lasix. We want to bind the potassium within the intestine using K exolate.

And if we need a rapid reduction or if renal failure is present, then we consider hemodialysis, right? We should note that that intestinal cat eye exchange with catch slate to slow, much slower process, right? All right. What EKG abnormality is commonly seen in patients with hypocalcemia. So here you would have a prolonged QT interval.

Okay. And what symptoms might you see in a patient with hypocalcemia? So from a neuromuscular standpoint, you see weakness, paresthesias, anxiety, muscle cramping, and seizures. Yeah. And there's this thing called Chostek sign, right? Which is when you tap on the facial nerve and this evokes perioral twitching or trousseau sign, which is when you have a carpal pedal spasm with blood pressure cuff inflation on the arm and what cardiovascular issues might arise with hypocalcemia?

Yeah, we could see hypotension torsades de points and heart block. Okay. How you gonna manage hypocalcemia? So, IV calcium and vitamin

D and magnesium supplementation. Alright, what are some of the most common causes of hypercalcemia? So how about adult in the outpatient setting? Yep. So hyper prepared thyroidism.

How about an adult That's hospitalized and malignancy. Okay. What are the common symptoms that are associated with hypercalcemia? Yeah, we talked about this. This is hypercalcemia. And we talked about this previously in another chapter, but it's stones, bones, groans, thrones, and psychiatric overtones.

Yeah. And these patients may have a kidney stones. They can have bone pain, abdominal issues or GI distress and polyuria as well as psychosis. So how is acute symptomatic hypercalcemia managed? So volume resuscitation you want to use normal saline theoretically. You want to avoid LR as it contains calcium, but relatively small amounts.

You want to start loop diuretics, bisphosphonates. You can do calcitonin, glucocorticoids, or dialysis if you have renal failure. All right. Let's talk magnesium. So what EKG findings

are common in hypomagnesemia? So the most common is prolonged QT interval, but this can progress the TifSOD to point. Okay.

And what medications are associated with the development of hypomagnesemia? So diuretics are the number one. There's antibiotics. Yeah, like immunoglycosides, Amphotericin B. Yep. And then platinum based chemotherapy and PPIs are also associated with hypomagnesium. Great. Alright, moving on to acid based abnormalities.

Patrick, what are the components of a standard ABG and their normal values? Yeah, so pH should be between 7. 35 and 7. 45. PaCO2 should be between 35 and 45. PAO2 greater than 80 and bicarb of 22 to 26. So Patrick, using an ABG, how can you quickly differentiate between the four main acid base abnormalities in the most simple way possible?

Sure. So you can certainly have mixed picture by keeping it very simple. A low pH of the patient is

acidotic. You're going to either have a respiratory or a metabolic acidosis. If the PACO2 is high, that's a respiratory acidosis. If the bicarb is low, that's a metabolic acidosis. If the patient's pH is high, they are alkalotic.

If the PaCO2 is low, they have a respiratory alkalosis. If the bicarb is high, they have a metabolic alkalosis. How is the anion gap calculated and what constitutes an elevated anion gap? Sure. So an anion gap is the sodium plus the potassium minus chloride plus bicarb. Again, that's sodium plus potassium minus chloride plus bicarb.

Normal is less than 12. An elevated anion gap would be greater than 12. All right, what are the common ideologies of an elevated anion gap or anion gap metabolic acidosis? And there's a, is there a mnemonic we can use? Yeah. Mud piles. This is a good one, right? Mud piles. Methanol, uremia, DKA, propylene

glycol, isoniazide, lactic acidosis, ethanol and salicylates.

Yeah. Good. And then what are the common ideologies of a non anion gap metabolic acidosis? As this would be intestinal losses from diarrhea or fistulas renal tubular acidosis or iatrogenic things like giving acetazolamide or too much normal saline resuscitation. Alright, to finish this out, what are the most common ideologies of metabolic alkalosis?

Yeah, so this would be gastric losses from excessive vomiting or NG tube suctioning. You can also get a contraction alkalosis from over diuresis. All right, so I know it's a lot. You should definitely reference the chart in the text. It's common electrolyte abnormalities in treatment It really kind of dies everything down to a nice like organized manner.

All right, Patrick, you wanna do some quick hits? I do. All right, let's go through these. What cation primarily determines cerium osmolality? Sodium. What is the primary intercellular cellular

cation? Potassium. What is the standard volume of a pediatric fluid bolus? Yeah. For fluid or crystalloid, we're going to give 20 cc's per kg for blood products.

10 cc's per kg. All right. And this was asked before were the three most common electrolyte abnormalities seen in refeeding syndrome. This is a highly testable, a little nugget of information. So hypophosphatemia is most common. You may also see hypokalemia and hypomagnesemia. All right. What causes hypophosphatemia and refeeding, refeeding syndrome?

And how does this present in critically ill patients? Yeah. Another good another good one. So the phosphate will shift from extracellular to intracellular, and this can present with failure to wean from the ventilator. Okay. You have a patient with a potassium is 6. 7 peak T ways on EKG. What is the next best step?

The next best step, right? We're gonna do multiple things, but first and foremost, I'm giving some calcium to stabilize the myocardium. All right. A patient is on the liver transplant list and was started on a

water pill by his PCP. His potassium is 2. 5. What drug is most likely the culprit? Yeah, that'd be a loop diuretic like Lasix.

All right. A patient is on the liver transplant list and was started on a quote unquote water pill by his PCP. His potassium is 5. 5. What drug is most likely the culprit? Yeah, in this case, spironolactone. All right, Patrick, a baby with pyloric stenosis will present with What electrolyte acid base abnormality was a good one to hypochloric hypokalemic metabolic alkalosis Alright, what is the mechanism of the metabolic alkalosis?

Yeah, this is paradoxical acid urea And so the kidney in this case is putting a priority on maintaining volume and it does that by absorbing sodium ions In exchange for hydrogen ions Therefore despite the fact that the patient has a metabolic alkalosis. The urine is actually acidic All right. Next one.

What is the impact of acidosis on the oxygen hemoglobin dissociation curve? This is a right

shift and there's more unloading of oxygen. All right. You have a patient with marked metabolic alkalosis and now has decreased respiratory drive. What could, what drug could you get? Yeah. Acetazolamide. What is the electrolyte acid base abnormality seen with diarrhea?

Hypokalemic metabolic acidosis. All right. What is the acid base abnormality seen in high altitude? Respiratory alkalosis. Right. A postoperative patient has pinpoint pupils and is unresponsive. What would the ABG likely show? Yeah. Respiratory acidosis is likely due to opiates resulting in decreased respiratory drive.

What is the acid base abnormality seen in a patient with high output ileal conduit? This is a non anion gap metabolic acidosis. All right. Last one. What EKG findings are most commonly seen in hypermagnesemia? Yeah, that's a good one. Peak T waves, PR prolongation, and QRS widening. All right, we got through it.

We got through it. On to the

next.