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Richard_Head

Richard_Head

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Richard_Head's Latest Activity

  1. Yes you are overthinking it. The surgical interventions you described do not impair renal function. If a patient is on lopressor there is usually a good reason. Bad choice to DC, especially abruptly (due to receptor upregulation).
  2. Richard_Head

    NA's, Please tell me this isn't common practice!

    Just finished browsing through this thread and my 2 cents: When an anesthesia resident is in the process of intubating a patient, who is legally responsible for the outcome of that process? The anesthesia resident. If they tell you to zip it because they are working hard, accomodate them and do so. Continuing to announce VS during a difficult airway intervention is probably not helpful. Did the patient have an adverse outcome? As someone posted the audible that accompanies SPO2 has a tone that changes with SPO2 level, any one familiar with airway instrumentation knows this and makes note of the tone. As for the physiology questions, brief periods of desaturation/apnea are generally well tolerated. As someone pointed out the FRC can be a useful O2 reserve in the apneic patient if the patient received a 100% O2 pre-ox prior to induction. I have yet to see a patient tolerate 9 min of apnea depiste what the textbooks say.
  3. Richard_Head

    Lasix and CRF

    Lasix is not particularly helpful in this situation. Yeas lasix works in the Loop, if I recall it acts at the Na-K-2Cl cotransporter. It will not trick dead glomeruli into working. It is also probably not harmful. Nitroglycerin is a venodilator but a person in CRF has usually lost their ability to compensate via venous capacitance so NTG would be of minimal value. Dialysis with fluid removal is the is the answer to this problem.
  4. Big Clues: The pain is not exacerbated by deep breathing, coughing or movement
  5. Richard_Head

    Paradoxical Respirations in SCI?

    This is a good question. I am not certain but I think a non-obese patient with a T1 lesion in the supine position will have difficulty generating a diaphragmatic excursion (thus creating a tidal volume) because the abdominal viscera will pull down on the diaphragm (gravity pulling down the organs that are unsupported by any skeletal muscle tone will act like an anchor on the diaphragm). While the innervation of the diaphragm (C3-4-5) is intact and thus functional, the abdominal skeletal muscle inervation (T7 at the xyphiod process, T10 at the umbilicus) is absent leaving only the diaphragm to provide the work of breathing. I would think an abdominal binder would mitigate the effects of gravity on the abdominal viscera and subsequentally prevent the diaphragm from being anchored in largely immobile position. Placing the patient supine would make the problem with the abdominal viscera a non-issue, unless they were obese which would lead to a new set of problems.
  6. Richard_Head

    Edema question???????

    Hypervolemia does not cause edema. A change in the balance of net pressures between the tissue and the vascular system causes edema. Hypervolemia can contribute by increasing intravascular hydrostatic pressure (which favors fluid deposition into tissues) while not affecting intravascular oncotic pressure (which favors retention of vascular volume) resulting in a increased pressure gradient and net fluid movement into the interstitial space. If the hypervolemia was caused by iv administration of albumin instead of crystalloid, edema would be less likely to result because intravascular hydrostatic and oncotic pressure will have increased. In the case of CHF edema forms beacuse the heart is unable to keep up with venous return and venous capillary hydrostatic pressure increases thereby decreasing the arterial to venous pressure gradient. Edema in renal patients occurs due to a similiar mechanism, except actual fluid retention occurs and will eventually exceed compensatory increases in CO. Renal patients also typically have decreased serum oncotic pressure which also favors formation of edema. FYI if you bolus a liter of LR nearly 80% will leave the intravascular space by the time the bolus is complete (the % is less with subsequent boluses). With 5% albumin bolus only 25% of the volume administered will leave the vascular space initially. Osmosis has little to do with the fomation of edema in most clinical scenarios (except renal failure)...profound electrolyte derangement would have to exist (usually with other more important symptoms presenting first) for it be of significance.
  7. Richard_Head

    Autonomic drug help

    You are on the right track to a BASIC understanding of the ANS. It's easiest to think in terms of receptor and effect (affinity). Endogenous catecholamines often act different than exogenous ones (they can target receptors more specifically). Epi effects differently than norepi although there is a lot that is identical in the receptors they effect. Dopamine works on an entirely different set. Etc. The only way to know it is to read and re-read. Also, your last sentence is incorrect. A sympathetic agonist does not inhibit the parasympathetic branch, it just changes the clinical picture by emphasizing one branch of the ANS over another. Example: IV epinephrine effects Beta 1, 2, and Alpha 1 and 2 receptors. low doses can actually cause hypotension due to beta2 mediated skeletal muscle vasodilitation, high doses causes tachycardia, hypertension and a whole lot of other responses. Parasympathetic innervation is not blocked but progressivly overwhelmed as a result of exogenous epinephrine administration. Norepi acts nearly the same except there is no beta 2 agonism.
  8. Richard_Head

    Help!! I missed this question...why??

    I don't know. It is common practice to do it with neonates for a cappillary blood gas.
  9. Richard_Head

    lawsuit

    Lawyers add everyone they can get away with to the suit, that allows them the most felxibility.
  10. Richard_Head

    Toprol and MI?

    Toprol is not always indicated post-MI. It is useful in reducing cardiac O2 demand. If the ischemia/infarct is demand (tachycardia) related metop can be useful. The heart is unique in that it's tissue oxygen extraction is about 70-75% compared to 25-50% for other organs. Increased blood 02 extraction is not an option so your choicess for treating inadequate myocardial o2 are to increase supply (supplemental O2, coronary vasodilators) or decrease demand (beta 1 specific blockers like metop or esmolol). While morphine has historically been included as an adjunct in MI treatment (MONA) it causes significant histamine release and can cause a reflex tachycardia to compensate for decreased SVR.
  11. The simplest way to approach this is to re-read the autonomic nervous system chapter in your A&P book, if you don't have a good recall of the underlying systems it's not very effective to try and understand the pharmakokinetics/dynamics of the meds.
  12. Richard_Head

    Pericardial and Pleural Effusion??? HELP!!!!

    Always priortize every patient problem or scenario in terms of ABC, airway breathing circulation.
  13. Richard_Head

    What got you into school?

    3 Previous degrees adult and pediatric CCRN GPA 3.8 GRE 1390 3 years RN experience: Flight Nurse, STICU at level trauma center, PICU/peds TCV accepted on the spot at first interview
  14. Richard_Head

    Question regarding drug administration to an infant

    Be aware that if it a medicatio ordered as part of their hospital stay you will be the legally responsible party for any irregularities related to the administration of the med.
  15. Richard_Head

    Anyone know what happened to the CNL?

    It's always good to get additional education...but....degrees like MSN/CNL that don't specifically translate to revenue generation for a hospital are somewhat risky. I have worked at a place that went with the trend and hired several CNLs but as soon as the economy got a little shaky they fired all of them. They said the expense wasn't justifiable.
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