PetERNurse

Even though your platelets are 65 or 50, they are still capable of forming a thrombus. This is why the doc ordered the hep drip. Heparin is not a "blood thinner", and does not decrease the viscosity of blood improving arterial flow. IT DOES potentiate ATIII causing increased binding to thrombin, decreasing the amount of thrombin available to form a clot, increasing coag times. While there may be less platelets circulating, you still need to anticoagulate the patient to prevent further blockages. Heparin will cause an initial drop in platelets, but they recover after discontinuation.

CVP, PAP, and wedge will all be elevated.

The answer to these depends on what the current vent settings are and full assessment of ABG taking disease process into account.

It's not as simple as saying the pH is X and the PCO2 is Y, therefore the disorder is N. It's not like a hemoglobin, where if it is low the disorder is anemia. You need a complete ABG to evaluate acid-base (pH, PCO2, HCO3, AnGap, PO2, lytes, and preferably an albumin level), looking at each value independently and the panel as a whole. The ICU Rounds podcast has an excellent lecture on ABG interpretation.

Ketamine causes increased HR and myocardial oxygen demand, while decreasing ventricular filling time. Don't fall into the trap of thinking it doesn't "stress out hemodynamics". Given that the patient needed RSI, a little transient hypotension was the least of your worries. I don't think propofol at the dose described above (2 mg/kg) would have the crashing down effect you describe when administered correctly, though each patient responds differently. Again, I stick with drugs that have the "best" side effect profile (fentanyl, midazolam, sux), and limit the use/dose of drugs with "worse" side effect profiles (propofol, ketamine, etomidate). It's all relative though.

"521 is a babysit. When he goes to bite you just toss the pill in the back of his mouth."

I think we can all agree that it increases morbidity and hemodynamic sequalae as it increases the likelihood of vasopressor dependence in the PO period. Yes jury is still out on if it increases mortality. And yes the ventilator study is when used as a maintenance agent (this study is probably why this is not practiced anymore today).

Controversies surrounding the use o... [Ann Pharmacother. 2010 Jul-Aug] - PubMed - NCBI Etomidate versus ketamine for rapid sequence intubati... [Lancet. 2009] - PubMed - NCBI Acute adrenal insufficiency aft... [J Intensive Care Med. 2007 Mar-Apr] - PubMed - NCBI http://www.ncbi.nlm.nih.gov/pubmed/20403156 [TABLE=width: 100%] [TR] [TD=width: 10]1.[/TD] [TD]Anaesthesia. 1984 Oct;39(10):973-81.[h=1]Mortality amongst multiple trauma patients admitted to an intensive therapy unit.[/h]Watt I, Ledingham IM.[h=3]Abstract[/h]A retrospective review of 428 severely injured patients admitted to an intensive therapy unit between 1969 and 1982 was performed. The patients' primary injuries were assessed using the injury severity score (ISS), and subsequent complications using the complications impact index and sepsis score. Between 1969 and 1980 mortality fluctuated between 19% and 29% but rose to 47% (p less than 0.05) during 1981-82 in spite of an unchanged ISS. The increased mortality was confined to ventilated patients surviving more than 5 days from injury and was associated with multiple organ failure and severe infection. The rapid and sustained increase in mortality could not be explained by any obvious change in severity of injury or referral pattern. The only deliberate change in management related to the combination of analgesic/sedative drugs used in ventilated patients. During 1979 to 1982 mortality was 28% in patients given morphine with or without benzodiazepines and 77% in those given morphine and etomidate (p less than 0.0005). After discontinuation of the latter regimen (May 1983) and resumption of the former analgesic/sedative combination, mortality fell to 25% (p less than 0.005). Possible mechanisms leading to increased mortality include adrenocortical insufficiency or depth of anaesthesia.[/TD] [/TR] [/TABLE] I try not to use it if I don't have to. Not worth the risk IMO. But I agree a large RCT would be nice.

People used to think the etomidate did not increase m+m, but that is not the consensus now. Even a single dose has been shown to cause prolonged adrenal supression that increases m+m, especially in septic shock. Use of etomidate during mechanical ventilation increased mortality from 28% (morphine + benzos) to 77% (morphine + etomidate). I prefer fentanyl/midazolam + micro propofol doses to facilitate intubation in critically ill patients.

Dipravan causes significant myocardial depression and decreased CO. Definitely can effect BP especially in a CV compromised patient. I agree you may need to up your sedation/look to other meds (fentanyl/midazolam as others have said). Additionally I have used dexmedetomidine, though I don't like the potential CV effects of that drug either (start low and work your way up). Dexmedetomidine has been shown to decrease ventilator days and ICU stays. Best bet is to use a multi-modal approach with a little of everything.

Morphine is also more vasodilatory than fentanyl and will provide more of an increase in myocardial oxygen delivery. Additionally the increase in mortality with morphine demonstrated by the CRUSADE study was in non-STEMI patients. It's also a non-randomized retrospective study, so who knows if the patients receiving morphine were just more sick (and therefore had a higher mortality rate). They make it look like morphine causes increased MI, CHF, death, etc. This may be because these patients were more painful and had worse disease. It may be because morphine DOES cause these things. You would need a large randomized controlled trial to determine this. Like Belgian said above, these folks need analgesia, and morphine is (probably) the best choice.

Your body wants to blow off the excess carbon dioxide so tachypnea is an early sign. Along with tachycardia as the heart tries to increase it's output to meet an inadequately supplied metabolic demand. You're mixing a couple different things here. Respiratory acidosis tends to result from hypoventilation, and often respiration will be decreased (hard to assess in a sleeping patient). If there is a diffusion impairment the patient may be tachypneic. The acidemia causes vasodilation, to which the heart responds by increasing CO (HR and SV). Remember one of the important things about blood pH is that it affects the oxyhemoglobin dissociation. when the blood becomes acidic, the RBC has an increased affinity for oxygen and won't exchange gas at the cellular level as effectively. So if you have a patient that is ventilating well and complaining of "smothering", one of the first things to consider is an ABG. these problems are often vicious circles and the patient will continue to decompensate until we intervene. Because of this, the O2 saturation is often of little use because the hemoglobin is well-saturated with oxygen but it doesn't release it to the cells in exchange for CO2. Hence the build up in the blood reflected in the ABG. Actually during acidemia the oxyhemoglobin dissocation curve shifts to the right and hemoglobin has a DECREASED affinity for oxygen (higher PO2 required for normal SaO2-hemoglobin gives O2 away). Alkalemia causes an INCREASED affinity (lower PaO2 required for normal SaO2-hemoglobin likes to keep O2), which causes a decrease in DO2 to the tissues (high ScvO2). In acidemia, the body tries to maintain by attempting to increase DO2 and decrease H+ ion concentration: vasodilation, increased CO, decreased hemoglobin affinity (RBCs release O2 more readily to tissues), increase RR (if possible), decrease buffer (bicarb) excretion, increase fixed acid excretion. Classic signs of mild acidemia are flushing of skin, tachycardia, feeling lightheaded, bounding pulses, sweating, etc. As the acidemia worses, you will have a decrease in CO due to negative inotropism (decrease SV), reflex vasoconstriction, cold clammy skin, tachycardia or bradycardia, and thready/weak pulses.

the problem here is that your answer to the op "original simple question" contains fundamentally incorrect material (see post 39 above). i'd be interested to see the clinician's reaction when you attempt to water/fluid restrict a hypovolemic patient (which is the case with the op patient). whether or not the patient has a low tbs depends on the underlying disease. if the patient is voiding sodium, but not taking in sodium (the body doesn't just "make" sodium), there will be a decrease in tbs. i'm having trouble thinking of a way a patient could be hypovolemic and hyponatremic, but not have a decreased tbs (if you can give me one i would love to be enlightened). these patients are unlikely to benefit from hypertonic saline, as there is not interstitial fluid to pull from to increase blood volume. treatment would be (is) ns or balanced solution (lrs, etc.) in order to raise the sodium ~1 meq/l/hr. in the case of hypervolemic hyponatremia, there may or may not be a decrease in tbs. then your logic is more likely to be applicable (hypertonic saline, water restriction, loop diuretics, etc.). (see post 18 above) back to the original issue... op- i believe that ns was a correct choice for treating your hypovolemic hyponatremic patient.

It's not so much that the kidneys separate Na, Cl, and H2O, but that it is an aqueous solution. NaCl does dissociate when in solution. It's just basic chemistry.

Right, 140, because that measurement is a measurement of CONCENTRATION, not a count of the absolute number of sodium molecules. Got that? If not, work on it, because you have to "get" it. If you have a concentration (140 meq/L) and a volume (blood volume, body weight, etc.) then you have a total count of sodium molecules. This is why you can estimate TB sodium and sodium deficit. Get it? As a matter of fact, you can pour quite a bit of NS into a body and not really influence the serum sodium that much at all. The way you change the serum sodium is by changing the amt of WATER. This is just not true. By this thought process, to bring up a patient's sodium you would water restrict them? No. You administer sodium containing fluid in order to increase TBS. YOU DON'T WANT the sodium to change very much very quickly. Slow is good. Saline is not sodium and water. Last I checked it was. Saline pretty much stays in its vascular place (unless you cut a blood vessel and spill some out). I think you need to review Na/K pump physiology and active transport. Sodium is the primary extracellular ion, but it doesn't "stay in the vascular space". OK. You are walking down the street with a perfectly good crit of 40 and a serum sodium of 140 (and normal other lytes). You are accosted by someone with a sharp thing and before you know it, a whole lot of your circulating volume is running into the storm drain. Fortunately, you are whisked into a nearby ER immediately, having had your bleeding stopped by a nearby Boy Scout with good First Aid Merit Badge training (ummmm, I teach that too). The ER nurse draws a baseline crit and lytes. What are they? OK, crit is still 40...because hct is a *percentage of the blood that is red cells*, not a count of the absolute number of red cells you have. So even if you lose a lot of your blood, your crit is unchanged. Until they start fluid-resuscitating you with.... normal (not half-normal) saline (or RL, which acts like it for purposes of this discussion). Na+ is still 140, because you have lost saline (serum counts as saline) but not water. This depends on how long before presentation to ED where crit and sodium are analyzed. RAS kicks in and body retains sodium, so serum sodium will increase. Why? The body is trying to autoresuscitate by raising serum sodium in an effort to draw fluid from EC space to IV space. This is why the crit drops, though not immediately. This is why if a GSW patient comes in you don't just administer WB or component therapy; you administer NS as well to resuscitate the ECF as well. But what happens to the crit of a tube of blood if you add water-- like D5W? Answer: Nothing. Why? Because the crit is a % of volume....and when you add water, the water travels into the cells too. So they swell up, and their %age size change means no change in the crit of the tube. They still take up (in this example) 40% of the volume. What happens if, instead of adding water to your original tube of hct=40 blood, you evaporate half of the water out of it? (The answer is NOT, "Make gravy." Shame on you.) No, the hct stays the same, because the cells lose water too, and they shrink as much as the liquidy part did. Same percentage of red cells in the resulting volume = no change in hematocrit. So. When you have someone dehyrated (as evidenced by their elevated serum Na+), you give him water (or D5W). This dilutes his serum Na+ back towards normal and allows his shrunken dehydrated cells to regain their girlish plumpness. Normal saline will not help, as it will not change the serum sodium level ("Saline is not sodium and water") and will not move into cells to restore their lost water content ("Saline stays, water travels.") Thankfully there is a huge difference between in vitro an in vivo. D5W will change the crit of a patient depending on water balance. Just because you have an elevated sodium doesn't mean you are dehydrated. NS WILL rehydrate a patient, and is the fluid of choice during hypovolemic hyponatremia. you give him saline, which goes into his vascular space where you want it for circulating volume but doesn't go anywhere else. D5W will not do the job, as it will travel into cells (not just RBC's, but all cells, and most of it will thus not be available in the vascular space to make blood pressure). Wow. OK. Saline does leave the IV space with only about 20-30% still remaining in the IV space after 1 hour. With D5W, even less remains, but some does remain in the IV space, as it equilibrates with the interstitium and the ICF. ) Serum Na+ 140, Hct 25, BP 110/60. OK, so this guy is relatively anemic, but his circulating volume is OK (as evidenced by an adequate BP) and his water balance is fine (as evidenced by his normal Na+). Just because you have a normal ABP doesn't mean you have adequate circulating volume (think compensatory shock-you need to lose 1/3 of blood volume before you see a drop in ABP), and just because you have normal sodium levels doesn't mean you have normal water balance (think DKA). Well, anemia can have many causes, but if he comes in with a hx of a recent bleed with fluid resuscitation, you could guess that he had a perfectly good crit until he lost some red cells out his GI bleed or stab wound or bloody ortho surgery or something, and we were stingy and just gave him NS back. His crit is called "dilutional," as in, "His red cells are floating in saline." This patient could present with these vitals and blood results before administration of any IVF, due to compensatory shock and autoresuscitation, which dilutes the crit in the same way (robbing the ICF and interstitium. 2) Serum Na+ 118, Hct 40, BP 110/60. This guy has 'way too much water on board, as evidenced by his Na+ that's 'way low ("dilutional" too). We call him hyponatremic, but it's not that he has lost sodium (in most cases), it's that he retained too much water. He hasn't lost saline, as evidenced by his decent BP This is so far off the mark. Just because you have a low sodium doesn't mean you are hypervolemic. You need to take into account pertinent history, other diesease processes, etc. There are 3 different types of hyponatremia, and this could be any of those 3. The patient MAY (probably does) have a decreased TBS. Again, ABP is not a reliable indicator of circulating volume, or "saline" as you say. "Syndrome of inappropriate antidiuretic hormone"? Lessee.... inappropriate, ummm, too much. Antidiuretic, ummmm, doesn't allow diuresis, holds onto water.... Bingo. Condescending much? However, for clinical purposes, saline pretty much sicks together as saline, and does not, for purposes of fluid management, dissociate. Yes, yes it does. That was the point I was trying to make. If someone is confused about how serum sodium and water are related and how IV water vs IV saline works, it is much more functional to think of saline as an entity, not as salt and water. Thus, "water moves, saline stays." Sorry I didn't make that clear enough. That is the WRONG way to think of saline, as it does redistribute in the body (large volume of distribution duh). Although I must say that in all the years I've been teaching this, you are the very first person to ask me this question! Thanks for the opportunity to clarify, and I hope that helps. I am so glad I wasn't a student of yours. I would go back and review basic fluid therapy and electrolyte homeostasis if I was you...