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| we are approximately how much water? |
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[image]
Now, fluid shifts and intakes, we have about 30 liters. We're just going to use some general numbers here. We have about 30 liters intracellular. So a majority of our body water is locked within our cells. This is the intracellular compartment shown here in blue. Bathing our cells and occupying this interstellar space, such as the pleural cavity. This is then joint spaces and other locations. Our intravascular compartment holds the smallest amount of water. In this case, about 3 liters. About 2 liters of red cells makes up our total blood volume.
The interstitial and intravascular compartments make up our extra cellular space. Now, water moves freely between these compartments, but in our day to day use, fluids can only be given into or taken away from the vascular space. We can't go in and take away fluids intracellularly. Now, fluid loss occurs mainly from the vascular compartment as well. We lose water through our renal, and GI track, through urination, vomiting, bowel movements. And we can all see and record this. So this is one of the ways for us to measure our ins and outs on patients.
The ones we can't really measure, is the water we lose from our skin and respiratory tract. Those we can't measure. And it does make up what we call insensible losses. That's about 500cc's per day in a healthy person. Now, in sickness, or if you've got like, let's say, a fever, you increase your water loss through skin. And if you have an elevated respiratory rate and you're breathing fast, you're going to increase your insensible water loss through breathing. So there can be some changes there. But it's minimal because it's only about 500cc's per day anyway. |
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osmotic/oncotic pressure
Now why is this so important? Well, the distribution of water throughout the body is dictated early by the size of the compartments available. But mainly by its tonicity. Water balance is adjusted to maintain osmolality at a constant rate throughout all the compartments. We don't want water shifting rapidly from one location to another. Furthermore, this oncotic pressure generated by these large molecules like, plasma proteins, which stay in one location, add the force to maintain certain water in certain spots. If we didn't have our plasma proteins, and our blood vessels, and intravasculature, we would just have water moving back and forth throughout. And we'd probably all be swollen and edematous from all of our fluid.
Now sodium, as you can see here, moves freely between the vascular and interstitial spaces, but is actively extruded from interstellar space. So this actually takes energy or a pump to actually do this part. Sodium is the primary extracellular cation. And we've talked about that before when we talked about electrolytes and some other abnormalities, previously. This is why we give saline or sodium chloride. When we do this, we can increase our intra, or our extracellular tonicity and then water must move from our intracellular space to maintain this normal osmolality. And this is important, because what we're going to do is use these mechanisms to help us maintain fluid balance when we talk about giving people IV fluids. |
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| [ sodium x 2 ] + urea/2.8 + glucose/18 |
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• ADH = urinary concentration
• ADH = secreted in response to ⇑ osmo;
= secreted in response to ⇓ vol;
• ADH acts on DCT/CD to reabsorb water • Acts via V2 receptors and aquaporin 2
• Acts only on WATER |
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Definition
Now, anti-diuretic hormone, or ADH, has an issue here as well. This is important in urinary concentration. ADH is secreted in the response of an increase osmolality. So as you increase your osmolality, you secrete more ADH. So it's anti-diuretic hormone that is our main mechanism, our principal mechanism, for maintaining our osmolality in our bloodstream. ADH is secreted from the posterior pituitary. So this anti-diuretic hormone results in pure water re-absorption from the collecting ducts. So as our osmolality goes up, our body senses too many particles, we need more water, so anti-diuretic hormone is released. And that results in water being reabsorbed from the collecting ducts.
So, it acts at the distal convoluted tubules in the collecting ducts to reabsorb water. So anti-diuretic hormone only acts on water. But it helps us maintain our osmolar balance. So if we want to get rid of more water, we shut down our anti-diuretic hormone. If we want to maintain more water, we turn our anti-diuretic hormone on. |
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Definition
| Now, you can see certain things. Like if we change our sodium, if we dramatically increase our BUN, or dramatically increase our glucose, that can have an effect and raise our osmolality. If what we measure in the lab, OK, what the lab measures, differs by more than 10 from what we calculated, then we know we have what's called an osmolar gap. And that tells us that there's something else in the blood vessels, or in the vasculature, that's causing this difference. And this could be something like ethanol, methanol, or ethylene glycol. |
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Definition
Now, fluid shifts can occur from a number of reasons and disease you can lose fluids. There's numerous routes where you can have water or fluids lost or gained. We can have diarrhea and vomiting in the GI track. You can have NG tube suction. You put an NG tube down a patient and are constantly sucking out gastric secretions. You can have renal loss through diuretics that we give to lose water, or it can just be lost normal renal function. You can have it due to hemorrhage. People get cut, they get trauma, they get damage, that can cause renal loss, or vascular blood loss. And then skin-- burns. If you don't have the top surface or your skin to maintain the water inside our cells, burn patients lose huge amounts of water. That's why they get large amounts of fluid replacement. Now, you can have fluid gain, latrogenic, where we give you too much. Turn that IV on too fast, we give you too much fluids. But we can also retain fluids ourselves due to heart failure, liver failure, or kidney failure.
So you want to be very careful. You don't want to underestimate the potential for fluid movement and for fluid loss. And you want to make sure that in a lot of patients in the hospital who are critically ill we do what's called I & O's, where we want to measure ins and outs. How much fluid they're taken in, and how much they're losing. |
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Definition
• GI: diarrhea, vomiting, etc. • Renal: diuresis
• Vascular: hemorrhage
• Skin: burns |
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• Iatrogenic
• Heart / liver / kidney failure |
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• 0.9% saline—not “normal”! (normal is .85%)
• 5% dextrose
• 0.18% saline + 0.45% dextrose • Others |
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Now, we have certain fluids that we can use. We have therapeutic fluids that we can give intravenously. And they're divided into two sections, the crystalloids, and the colloids. OK? The most common crystalloids are the saline, we call it 0.9 normal saline. It's really not normal. Your actual percentage of sodium chloride in your blood is actually closer to 0.85%. But we call 0.9%, normal saline. 5% dextrose is another form. And then you have other combinations of saline percentages.
Colloids-- that's blood, and plasma, and albumin. Crystalloids can move freely in between compartments. OK? The colloids can't. Once you give somebody a blood transfusion it's going to stay in their blood. Once you give somebody plasma, or albumin, with all that protein, It's going to stay in their blood. So these will move, these stay in. And it's important with the movement. They don't all move the same. Sodium, normal saline, is going to move very little because it's fairly close to our tonicity in our bloodstream. Dextrose-- 5% dextrose, is mainly free water, and that's going to move.
So, 5%, means it contains about 5 grams of glucose per 100mls of water. It's roughly isotonic, but once the patient burns up the glucose, you're basically giving them free water. So this 5% dextrose solution, when you first give it, the body and the vascular system it maintains it, but as your body uses up that glucose, all that's free water is left and it just migrates between compartments. |
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| Rules of Fluid Replacement description |
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Definition
So there are some general rules when it comes to fluid replacement, and it depends on what you're losing. If you're losing blood, try to replace it with blood. Now, we know you can't always do that, but try. Maybe you can't get a unit of blood right away and you've got to give them IV solutions of normal saline first. But try to replace blood with blood. Try to replace plasma that they're losing with another colloid, or plasma, or blood. You try to resuscitate a patient with a colloid because you want to maintain that in their vascular system. Once again, we don't always have that option. You want to replace extracellular fluid depletion with saline. And you'd like to rehydrate a patient with dextrose because that free water will hydrate them back up, because they're dehydrated.
Now, there are some general rules, and we're going to go through some examples as we follow here, but there's some general rules. Someone with serious intravascular volume depletion, hypotension, and reduced cardiac output, is in shock. And that could be from blood loss, it could be from plasma loss, it could be from blood loss, or water loss. You want to make sure that you restore intravascular volume with fluid that remains there. So even while they're losing these things, you need to help them maintain blood pressure. And that's the most important.
So a fluid with a high iconic pressure will do the job. So blood would be a good choice or normal saline would be a good choice. You want something that's going to stay in the vasculature and help them maintain blood pressure. Our biggest damage-- or biggest concern with people who are losing fluids, and are intravascularly depleted, is that they can't maintain blood pressure. If you don't have the fluid to push around to oxygenate tissues, blood pressure drops, then oxygenation drops, and you have a whole cascade of effects. So you want do something that's going to help you maintain your blood pressure. |
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| Rules for fluid replacement bullet points |
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Definition
• Replace blood with blood
• Replace plasma with colloid
• Resuscitate with colloid
• Replace ECF depletion with saline • Rehydrate with dextrose |
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| So let's go through some examples here, now. Let's take a closer look here. So here we have our typical 30 liters, 9 liters, 3 liters. So this is our vascular system, right here, with the 3 liters. In this case, we're going to give somebody 2 liters of blood to someone. Now this will expand their compartment by 2 liters, so this will go up to 5 liters. And none of this is going to move anywhere else. None of this will escape across blood vessels or go. So this is the right treatment for blood loss. So we would go by increasing that intravascular area from 3 liters to 5 liters now. And that's ideally what we want to do. So this would all stay in and help us maintain our blood pressure. |
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Now if we add 2 liters of colloids, OK, in the vascular space, this will allow for immediate expansion of the volume. So we'll go to 5 liters. So you're giving this colloid into the vascular space. So we're going to add to this 3 liters. This will result in immediate expansion of the intravascular compartment by 2 liters, as it did with the blood. So we're going to go to 5 liters now. Now colloid does not escape from the vascular space, but now it's changed or increased the oncotic pressure in that vascular space markedly.
So then what happens is, this causes water to move from one compartment to the other. So you draw water into this vascular space from the interstitial and interstellar reserve. So what we're going to see happen, is we're going to move fluid from here, to there, to there, because it wants to try to balance these out. So giving colloids, therefore, only expands avascular space itself, but it does so by moving water from other spaces. So after you have this movement, what you're going to end up with is, 29 liters, 8 liters, and now 7 liters, as it tries to equalize the volumes between the two. |
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Definition
Now if we give saline-- let's say we have 2 liters of normal saline. Saline, being a crystalloid, does not remain within the vascular space. It will diffuse into the other spaces, especially interstitial space. The sodium it carries will not enter the intracellular space, however, because of this active transport of sodium I showed you early on, where it can actually be excreted out of the cell. So therefore, when I add 2 liters of saline, what I'm going to get is 5 liters. The will cause this immediate expansion. So I now got my 5 liters of fluid. Great for blood pressure maintenance. But what's going to happen next, is we're going to get movement to try to equilibrate this. We're going to get movement now. So some of this fluid is going to go into the interstitial spaces and you're going to have some of the fluid move this way. So this osmolalities are now going to be equal, which was equal, now is going to be slightly greater than what it was, than that of the intracellular space due to this increased sodium load.
So what happens here, is you get this water movement from intracellular space in order to equalize the osmolality throughout all three compartments. They all like to try to maintain the same osmolality in all three, and the body will do whatever it has to do to maintain those. So you can see the effect. So when he gave blood it all stays in this vascular system. When you give normal saline, fluids are going to shift around. Now we increased our vascular system to some degree. OK? So it helps maintain some blood pressure, but it's going to cause some other shifts as well. |
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Definition
Let's look at one other area. And this is giving somebody 2 liters of dextrose. So now we've given 5% dextrose. This is isotonic to plasma. So you give the 2 liters of 5% dextrose, and that causes an immediate expansion to 5 liters. But as that glucose is metabolized, it's rapidly metabolized, the remaining water now is going to be shifted and distributed throughout the different parts of the body. So you're giving free water. So very little-- when you give free water like this in the dextrose, very little of it stays intravascular, it's shifted into other compartments.
So if you wanted to resuscitate somebody to maintain blood pressure, giving somebody dextrose, or D5W, or dextrose in water, is the last choice you want to get for resuscitation, because it doesn't stay in the vascular system. It moves. It's great if I want to hydrate tissues and cells. But it's terrible if I want to maintain blood pressure. |
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Definition
Well you got to know where you're starting from. Are they euvolemic? Which means everything is normal. Are they hypovolemic? Which means they're dry. Or are they hypervolemic? Which means they're wet. If they're hypovolemic, or dry, you tend to see dry mucosal membranes in the mouth. You tend to see tenting of the skin. When you pinch up the skin it loses some of that skin integrity and dexterity. If they're hypovolemic it tends to be edema. You'll see swelling in the sacrum area, in the small of their back, ankle edema, swelling in the face. So that would be hypovolemia.
The other thing we have to ask ourselves is what are the expected losses, and what are the expected gains? Are we giving fluids? Are they having diarrhea? What kind of movement are we going to see? So once again, here's just some of the signs and symptoms that we might see with volume depletion or volume overload. They may have low blood pressure. Your body's response to low blood pressure is to become tachycardic, increase your heart rate to try to maintain that pressure. As I talked about, decreased skin turgor, dry mucosa. You shunt blood away from your kidneys, so you decrease your urine production. And you actually can shunt blood away from vital organs, because we want to perfuse our heart in our brain. So we can end up with other organ failure.
With overload, you end up with hypertension because there's too much fluid on board. JVP, Jugular Venous Pressure, can go up. That's how we measure that in the neck, looking for jugular venous distention. They can get edema. They can get fluid in their lungs. They get fluid in their belly or ascities. And once again, this can lead to fluid overload, can lead to organ failure as well, because you're not perfusing the organs as well.
The other thing we need to look at is what's coming in and what's going out. Now we have expected losses that are measurable. We can measure the urine. We can do it hourly if we need to. We can measure stool output from stomas, from drains, from tubes. But we really have trouble with sweat and exhaled air, which we talked about earlier. Potential gains, we have a pretty good chance of really controlling those. We can monitor their fluid intake, their oral intake with fluids, food, nutritional supplements, bowel preps. And we also know how much we're giving them exactly with IV intake, whether it's colloids or crystalloids, tube feedings, or even medications that may be an IV treatments. |
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| signs of volume depletion |
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Definition
• Postural hypotension • Tachycardia
• Decreased skin turgor • Dry mucosa
• Oliguria
• Organ failure |
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Definition
• Hypertension
• Tachycardia
• Elevated JVP
• Edema
• Pleural effusions
• Pulmonary edema
• Ascites
• Organ failure |
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Definition
-Measurable:
• Urine (measure hourly if
necessary)
• GI (stool, stoma, drains, tubes)
- Insensible: • Sweat • Exhaled |
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Definition
- Oral intake
• Fluids
• Nutritional supplements
• Bowel preparations
-IV intake
• Colloids and crystalloids
• Feeds
• Drugs |
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Term
| if you're trying to fluid resuscitate somebody |
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Definition
| giving them blood is great, giving them normal saline can be helpful, giving them D5, dextrose water, will not increase their vasculature. It will shift fluid into tissues and cells. Which may be something you want to do, but if you're trying to maintain blood pressure, it would be the wrong choice |
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Definition
-Sodium less than 130 mEq/l
-Signs/symptoms
• Nausea, headache, weakness, metal confusion • Seizures, lethargy, coma, death
-Labs
• Sodium low
• Serum osmolality <270
-Treat underlying cause
So the first one is hyponatremia. So this is just having a low sodium, less than 130. The symptoms here can include nausea, headache, weakness, some changes in mental status, seizures, coma, death. And these symptoms get more severe as you continue to drop your sodium. You get sodiums into the, you know, 110, one teen's area, they get much more severe symptoms.
So this is usually a diagnosis of laboratory. So what you're going to see on labs-- you're going to see a low sodium, of course, and you're going to see a low serum osmolality. Remember, most of this osmolality, the major component is two times the sodium. How do you treat this? We basically treat them underlying causes. And we'll get through that in one of the other lectures. |
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Definition
Now there are differential diagnosis here, working through hyponatremia. There can be hypovolemic hyponatremia, this can be due to thiazide diuretics, osmotic diuresis, vomiting, diarrhea. You can be hypervolemic, and have a low sodium. And you go, that makes a little more sense than being hypovolemic. But this can be due to heart failure, cirrhosis, renal failure, pregnancy. And then euvolemic hypothyroidism. And then, probably one of the more common things we see, is SIADH. This is the syndrome of inappropriate anti-diuretic hormone. and euvolemic- Addison's
There's also a condition called pseudohyponatremia, where the sodium really isn't abnormal, it's because of another substance. You can have markedly elevated triglycerides. If your triglycerides are, you know, up close to 1,000, that can give you an artificially low sodium. If your proteins are really high, say, somebody with multiple myeloma, and their total protein is up in the 13, 14, 15 range. That can lead to a pseudohyponatremia. And glucose-- the higher your glucose, the more that can make your sodium look artificially low. You correct all these things and the sodium will go back to normal. So don't be chasing the sodium abnormality thing, thinking, I've got to correct that. Correct the underlying etiology here and then the sodium will correct on its own. |
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Definition
Now if you have a low sodium, you must be a little high sodium, and that's hypernatremia. Usually severe thirst corrects this. We have the thirst mechanism. It's a very strong mechanism. So as long as we can get to water, we're OK. So typically, people who get hypernatremic have some type of mental confusion or mental disability that doesn't allow them to get to water. Now we can do this with patients who aren't mentally confused by withholding water from them. Making somebody NPO, or nothing by mouth, and then not giving them IV fluids. We can cause them to be dehydrated.
Lactulose was a substance we used in some patients, to remove substances or to treat people who have elevated ammonia levels. Mannitol, diabetes insipidus, DI, is another condition that can lead to hypernatremia. Here, the skin turgor, you can check their skin turgor, they'll be tachycardic, the skin turgor will be low. They'll be hypotensive, and they can have some mental status changes as well. Once again, those symptoms vary depending on how high your sodium is above normal. Once again, we typically only see this in the very old, the very young, or those that are neurologically impaired. And how do we treat this? We treat them by water replacement.
One of the things to watch for here, once again, if you're going to replace it, or correct it, whether you got to low a sodium or to high a sodium, you don't want to go up or down more than one milliequivalent per hour, or more than 24 milliequivalents per day. If you go too fast correcting hypernatremia, you'll end up with cerebral edema as water gets shifted into the brain. If you go too fast correcting a hyponatremia, you end up with a condition called central pontine myelinolysis. Where you basically start to destroy nerve cells (cerebral edema). labs • Sodium >145 mEq/L• Serum osmolality >300 (free water loss)
• Seen in the elderly, very young, or neuro impaired |
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Definition
| So hyperkalemia is an elevated potassium. These can present with weakness, paralysis, abdominal distension, diarrhea. And once again, symptoms vary as the potassium gets higher and higher. One of the things-- so any potassium over 5. Normal range for potassium is someplace between 3.5 to 5.0, or 3.5 to 5.5. EKG can be very helpful here. It'll show the peaked T waves, widening of this QRS complex, and flattening of the P waves. |
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Term
| hyperkalemia differential diagnosis |
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Definition
The differential diagnosis here includes renal failure. Renal failure and acidosis are probably two of the more common causes here. It can be elevated with certain artificial reasons. Increased platelets or white cells-- platelets and white cells have a lot of potassium in them. And if they release their potassium it can give you artificially elevated potassium. Also hemolysis-- sometimes when we draw blood, we actually draw traumatically, and we hemolize the patient's red blood cells in the tube of blood, that will release potassium into the sample, and that could cause. So if you see a blood sample and it says your potassium is 6, but they tell you that the blood is hemolyzed in the tube, you may need to redraw that to get a true potassium level.
• Renal failure
• Hypoaldosteronism
• K-sparing diuretics, ACE
inhibitors, adrenal disease
• Acidemia
• Burns, hemolysis
• Digitalis overdose
• Spurious—increase platelets or wbc |
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Definition
Treatment for this, I'm not going to go into a lot of detail, but emergency wise, if it's really elevated and you want to get it down, you can use calcium gluconate. I like giving somebody an amp of d50, and then giving them what I call, an insulin chaser. So you give them some insulin after giving them glucose. And what insulin does, is it takes the potassium and drives it into the cells. So it'll lower your serum potassium by driving the potassium into the cells. If it's not emergent, you've got some time to lower it, you can just stop the potassium that you've been giving them or that they've been taking. But we have this other substance called sodium polystyrene sulfonate. Otherwise known as Kayexalate. And this will actually bind up potassium in the system and lower your potassium level. Also, renal dialysis is a great way, but it's a little more complicated. But it would get rid of the potassium for sure.
- Emergency
• IV bicarbonate, calcium gluconate, glucose, insulin
- Nonemergent
• Potassium restriction, sodium polystyrene sulfonate, diuretics
- Dialysis |
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Definition
Of course, if you can have high potassium, you must be able to have low potassium. Most patients are asymptomatic. Once again, can develop muscle weakness, lethargy, paralysis. Once again, the symptoms vary as you become more and more severe. When it's severe, you end up with an ileus, muscle necrosis, and this classic ascending flaccid paralysis. So all of a sudden, they start getting weak, and not able to move, check their potassium. But we're talking potassium levels here, like, greater than 7.0.
EKG can be helpful. OK? You can see flattening of the T waves. U waves start to develop. And AV blocks can start to develop. The differential diagnosis here includes diuretic use. There are certain diuretics that cause potassium loss-- the thiazide diuretics and the loop diuretics. Alkalosis-- remember acidosis causes an elevated potassium, alkalosis causes a low potassium. Hypothyroidism-- probably one of the more common is diarrhea. And then you'll have another lecture where we talk about the renal tubular acidosis. And type 1 and type 3 actually present with low potassium levels. |
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Term
| Hypokalemia differential diagnosis |
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Definition
• Diuretic use
• Alkalemia
• Hyperaldosteronism
• Magnesium depletion
• Hyperthyroidism
• Diarrhea
• Renal tubular acidosis Type I and II |
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Term
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Definition
• Treat underlying cause • Potassium supplement
Treatment here, is replace it. Treat the underlying cause, and then give them potassium supplements. Is kind of rule of thumb if you want-- we usually give a drug called K-dur, it's a potassium supplement. Comes in a lot of different names. But for every 100 milliequivalents of potassium you give somebody, this should cause an increase in their serum potassium of 1.0 milliequivalents. So if their serum potassium was, let's say, 3 and you wanted to get them to 4, if you gave them potassium supplements equal to 100 milliequivalents of potassium, you should get their potassium up to that level. That's assuming you've corrected the reason they're losing it. If they're still losing potassium, that's not going to get it back up. But if you want to increase it by 1 milliequivalent, give them 100 milliequivalents orally. |
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Definition
Low calcium, this is hypocalcemia. Signs and symptoms here, can be included abdominal pain, muscle cramps, tetany, seizures. There are a couple of unique physical exam findings here. There's Chvostek sign, that's facial nerve spasm. If you tap the facial nerve on the side of their face it'll start to spasm. And then there's Trousseau sign, or spasm of the arm. You put a blood pressure cuff on their upper arm, and then what it does, is it causes their hand to spasm actually. It's called Trousseau sign.
This means that hypocalcemia is their calcium is below 8.5. Normal range is 8.5 to 10.5. This does have some EKG changes. It prolongs the QT interval, can lead to ventricular arrhythmias. And our differential diagnosis here includes vitamin D deficiency, malabsorption, hypothyroidism, is probably one of the more common causes here. But once again, the loop diuretics, aminoglycosides, and then an anti-viral agent called, foscarnet, can also lead to hypocalcemia. How do you treat it? Give them calcium supplements back. Treat the underlying disorder, and give them things like calcium gluconate. |
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Definition
signs and symptoms here-- so this is an elevated calcium greater than 10.5. They can present with polyuria, constipation, abdominal pain, thirst, dehydration, altered mental status. Once again, the higher your potassium goes, the more likely you are to see some of these more severe signs and symptoms. An EKG, this one shortens the QT interval. When we talked about hypocalcemia, we talked about prolonging the QT interval, now we're talking about shortening the QT interval.
Differential diagnosis-- the two main reasons for hypercalcemia are primary hyperparathyroidism and malignancy. These two together make up 80% of the causes of hypercalcemia. How do you treat it? Treat the underlying cause, of course. But then you try to get rid of the extra calcium. There's a couple of options. You can give IV fluids, and then give them things like Lasix, or furosemide as a diuretic to drive the potassium out. Because remember, loop diuretics can lead to hypocalcemia. The other thing, there's a drug, or a agent called, Calcitonin, which actually also helps you lower your serum calcium. So we have a couple of options there as well. |
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A 62-year-old man is 2 days postcolectomy. He is euvolemic and is allowed to drink 500 ml. His urine output is 63 ml/hour.
1. How much IV fluid does he need today? 2. What type of IV fluid does he need? |
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Definition
So back to case 1 here. Remember, we have a 62-year-old man. He's two days postcolectomy. He's euvolemic and allowed to drink 500 ccs of fluid or mls of fluid. His urine output is 63 mls or ccs per hour. So I asked you how much fluid does he need and what type of fluid. So let's go over this.
The first thing you've got to ask yourself is what's his status right now. And we know he's euvolemic. They told us that. So we're not dealing with any type of resuscitation here. We're just trying to help him maintain. He's actually able to drink some fluids already, so we have to take those into account, that he's able to take in 500 mls per day. So since we're trying to just maintain him, and he's got 63 mls per hour of urine output, if we do that per day, he's got about 1.5 loss of fluid per day liter-wise, 1.5 liters of urine loss.
Now, don't forget to add in the 500 ccs of insensible losses that these people can get. So we're really talking that this man-- what he's normally losing, everyday normal, is 2 liters. Now, he's able to take in 500 ccs, so we've got to make up the difference of that 1.5 liters that he's losing. So he's going to need 1.5 liters of IV fluid. So how much fluid does he need today? He's going to need the 1.5 liters divided up over 24 hours.
Now the question is what type of fluid does he need. So here, we want to give a mixed crystalloid. We don't want to give him just straight 5% dextrose, because if we do that, his osmolality is going to fall in his blood, and he's actually going to start to become hyponatremic. If we give him just normal saline, that may work for the short term, but he could gradually develop hypernatremia and then develop increased osmolality or hypertonicity. So we're going to have to give a combination of the two.
So the best thing that we could do for him, since he is taking some water in, 500 ccs per day, that will help. But what we're going to want to do is give him a combination of saline and dextrose. So we want to go saline plus the dextrose at a 2 to 1 ratio. That would be best to help him maintain his osmolaity and help him maintain his tonicity. So that's case one. |
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| Let's go now to case number two. This is case number two. Three days after her admission, a 43-year-old woman with diabetic ketoacidosis has a blood pressure of 88/46 and a pulse of 110. Her chart shows that her urine output over the last three days has been 26.5 liters with her total intake 18 liters. So now my questions to you are how much fluid does she need to regain a normal blood pressure and what fluids should you use. |
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Definition
OK, so let's get back to case 2 here. Remember, we have a 43-year-old woman. She's three days after her admission with diabetic ketoacidosis. So now we're looking at her at day 3. She has a blood pressure of 88 over 46, pulse of 110, and over those last three days, her urine output has been 26.5 liters with her total intake of 18 liters. So I asked you, how much fluid does she need to regain a normal blood pressure, and what fluids should you use?
So let's take a closer look at this. Now, because of her diabetes and her elevated blood sugars, what happens there is once the blood sugar gets high enough, it actually goes above the renal threshold. That means she's dumping glucose in her urine, which is going to lead to an osmotic diuresis, and it's just going to cause a water loss. Now, that water loss on all that fluid, we know that she's lost here, or those three days, her urine output has been 26.5 liters. That's the osmotic diaeresis, OK?
Now, remember, over those three days, she's also lost the 500 CCs, or MLs, of insensible losses. So she's had another 1.5 liters on top of that. So her 26.5 plus her 1.5, her total loss over those three days is really 28 liters. Now she's had 18 liters that she's taken in. So take away the 18 leaders, she has a 10 liter deficit that we have to catch up with that she needs.
Now, we know this is a resuscitation. She's 10 liters behind, and we know she has a low blood pressure, and she's tachycardic So this is more of a fluid resuscitation than a fluid maintenance or fluid balance issue, trying to maintain. So we know we're already 10 liters behind. We're going to need to give her colloids then to increase her blood pressure and to improve her pulse.
Now, we don't want to go that too far, because then we could cause some issues. If we only use colloid, this could cause intravascular overload and heart failure. So we want to increase fluids in her vascular system, but we don't want to do too much. So what fluids would we use? We'd start out with possibly 1 to 2 liters of colloids, and then we would switch her over to crystalloids. So we start with the colloids for a couple of liters, and then switch over to crystalloids.
Probably with crystalloids, we'd be mainly using dextrose. And you go, well, she's diabetic. Why would we want to add the dextrose? That's because she's going to need the free water. She's 10 liters down. She's going to need to hydrate her cells, as well, so we need some of this fluid to go into the cells. So the first 2 liters was to help with the blood pressure. The rest of the crystalloids is going to be to help the cells rehydrate over time.
Now, when we switch over to crystalloids, we've got to be very sure that we watch her sodium levels, because those could go out of whack with all the crystalloids. So she's going to need close monitoring over sodium. And remember, her sodium may already look abnormal because of her elevated glucose levels. |
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| So let's move on to case 3. In case 3, we have an 85-year-old man receiving IV fluids for three days following a stroke. He's not allowed to eat. He has some ankle edema and a JVP of 5 centimeters, which is elevated. His chart reveals a total intake of 9 liters and a urine output of 6 liters over these three days. So my questions now are, how much excessive fluid does he carry, and what would you do about his IV fluids? |
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Definition
So case 3 again. Here we go. 85-year-old man, remember receiving IV fluids for three days following a stroke. He's not been allowed to eat. He's got ankle edema and jugular venous pressure that's elevated at five centimeters. His chart reveals that he's had an intake of nine liters and a urine output of six liters over the last three days. And my questions to you were how much excess fluid is he carrying and what do we do about these fluids? So let's go review this one. Take a closer look here.
This man is hypervolemic. And he's been maintaining-- he's had more input than he has output. The reason we know he's hypervolemic is because he's got positive GVD or JVP and he's got the ankle edema.
Now we look and we see that his intake has been nine liters. He's had six liters of urine out. That leaves us with three liters extra. Don't forget though, once again, about those 500 CCs per day of insensible losses. So that's taking away another 1 and 1/2 liters. So he's really only 1.5 liters over. Not so bad. Not as bad as we thought. So all of that-- he's got all those losses so really 1.5 excess.
So what do we do about this excess? Do we need to keep maintaining fluids? In this case right now what do we do with his fluids? We stop them for a day. We stop them for a day and that will allow him to now become euvolemic. His edema should improve. His jugular venous pressure should drop, and he should be fine.
But don't forget then after maybe one day of no fluids, don't forget to restart the fluids, because he's not taking anything by mouth. OK. Not allowed to eat, which means that he's going to need to take in some fluids. So he's now going to have to be on that maintenance of 2 and 1/2 liters per day just to maintain, because we don't want to now go the other way and be dehydrated. |
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Five days after a liver transplant, a 48-year-old man has a pyrexia of 40.8 °C. His charts for the last 24 hours reveal:
• Urine output: 2.7 L
• Drain output:525 ml
• Nasogastric output: 1.475 L
• Blood transfusion: 2 units (350 ml each)
• IV crystalloid: 2.5 L
• Oral fluids: 500 ml
On examination he is tachycardic; his supine BP is OK, but you can’t sit him up to check his erect BP. His serum [Na+] is 140 mmol/l.
• How much IV fluid does he need? • What fluid would you use? |
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Definition
So let's review case number 4 briefly. There was a lot of information here before I give you the explanations. Remember, we are five days after a liver transplant, 48-year-old man with a high fever up to 40.8. His chart shows for the last 24 hours, he's had 2.7 liters of urine output, 525 MLs out of his drain, 1.475 liters out of his NG tube.
He's had two transfusions at 350 CCs each. He's had IV crystalloid solutions given to him at 2 and 1/2 liters. And he's been given some oral fluids at 500 CCs, or MLs. On exam, he's tachycardic-- his supine blood pressure is OK. We can't sit him up to check his erect blood pressure. And his serum sodium right now is 140.
So my questions to you were, how much fluid does he need and what fluid would you use? So let's take a closer look at this one. Now, this gentleman has had multiple fluid losses. So there's going to be some calculations we have to do here. When we look at his losses, he's had urine loss, he's had the drain loss, and he's had the NG loss.
So if we look at all of those, we have 2.7 in the urine liters, 500 CCs, or 0.525 liters of drainage fluid, and 1.475 CC, or liters from his NG tube. That gives us 4.7 liters of loss. Now, we also have to remember his insensible losses here. Now, he has a fever. Remember, I said early on, fever increases your insensible loss through the skin and through the breathing.
So instead of 500 CCs per day, he's probably losing about 800 CCs per day. So if we add in that 800, or 0.8, he really has 5.5 loss of liters per day. Now, he's been taking in some fluids. Remember, he's had the 2 and 1/2 liters of fluid per day, the 700 CCs of blood, and the 500 orally. So he's taken in 3.7 liters. So if we subtract these 2, he's actually deficient about 1.8 liters.
Now, if we assume-- we're going to make an assumption here-- that he's done this over the five days since he's been operated on, we multiply that by 5, we get 7.3 liters that he's probably down, give or take a little bit, over these last five days. So he's pretty deficit here. And this is a mixed issue. He's had to receive blood. He's received colloids. He's received lots of things and crystalloids. So this is going to be a complex correction.
He's going to need a couple of liters of colloids or blood again to help increase his intravascular volume. And we need to do that because we want to make sure that we maintain organ perfusion. So he's going to need maybe 2 liters of either a combination of blood products plus other colloids. And this will keep all of that stuff intravascular, and allow him to maintain his blood pressure, and perfuse his organs.
He's also going to need some saline replacement. This is to replace the water he's losing and to replace the solutes he's losing. He's also going to need some dextrose, or D5. And the reason he's going to need the D5 is this, so we can stop him or prevent him from losing sodium, preventing the hypernatremia, so to help us lose sodium and prevent the hypernatremia.
So this is a very complicated case. We're going to have to give him some more blood and colloids to maintain his intravascular volume. We're going to have to add some saline, and we're going to have to add some dextrose to it to help him maintain. So this is going to be a very complicated case.
So in real life, the thing I want you to walk away with here is in this man, you're going to need to monitor him. You're going to have to monitor electrolytes daily. You're going to have to monitor vital signs daily. You're going to have to monitor, monitor, monitor this patient, or you could run the risk of having hypo or hypernatremia, or having, once again, him dropping his blood pressure or going into fluid overload. |
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