Showing posts with label what I don't know. Show all posts
Showing posts with label what I don't know. Show all posts

Friday, May 1, 2015

Youtube: Intubation

*WARNING: PLEASE FOLLOW YOUR FACILITY POLICY AS INTUBATION IS NORMALLY NOT A NURSING SKILL.  WARNING: PLEASE FOLLOW YOUR FACILITY POLICY AS INTUBATION IS NORMALLY NOT A NURSING SKILL.  WARNING: PLEASE FOLLOW YOUR FACILITY POLICY AS INTUBATION IS NORMALLY NOT A NURSING SKILL.*


Neonatal Endotracheal Intubation
https://www.youtube.com/watch?v=23ArsJyJzvg




Endotracheal Intubation-an animated teaching movie
https://www.youtube.com/watch?v=0VGiBwyfuNI





Intubation and Mechanical Ventilation

Two studies on women's health service coverage...

... by independent insurance companies find that more than 50 insurance companies violate the ACA with discriminatory acts regarding maternity care, birth control, breast-feeding support, genetic testing, well-woman visits, prescription drug coverage, care related to gender transition, chronic pain, and pre-existing conditions.

http://www.nwlc.org/sites/default/files/pdfs/stateofcoverage2015final.pdf

http://www.nwlc.org/sites/default/files/pdfs/stateofbirthcontrol2015final.pdf

Thursday, April 30, 2015

Oxygen saturation

SpO2 >90% from periphery--pulse ox probe
SaO2 >95% from artery--ABG
PaO2 80-100mmHg--ABG

Thursday, April 23, 2015

Intraaortic balloon pump therapy for myocarditis--what is it?


"IABP Intraaortic Balloon Pump" by Doxacurium

CT or MRI? What's the difference?



"Difference between CT Scan and MRI" by KJ OM
https://www.youtube.com/watch?v=8mUaXmFi6Hc




And a super cool VOX vid on the power of the MRI:
"Life Looks Really Different Through an MRI Machine" by VOX
https://www.youtube.com/watch?v=l8xTVfs4FQ0

Wednesday, April 8, 2015

Thank God for Khan Academy: MultiFocal Atrial TachyCardia

"Multifocal Atrial Tachycardia (MAT)" by KhanAcademyMedicine

Thank God for Khan Academy: Atrial Flutter

"Atrial Flutter (AFL)" by KhanAcademyMedicine

Thank God for Khan Academy: Antiarrhythmics


"Antiarrhythmics" by KhanAcademyMedicine

Thank God for Khan Academy: EKG: Pulseless Electrical Activity and Asystole



"Pulseless Electrical Activity (PEA) and Asystole" by KhanAcademyMedicine

Thank God for Khan Academy: EKG III--Lead II, An Explanation of Normal Sinus Rhythm

"Normal Sinus Rhythm" on an EKG by KhanAcademyMedicine

  • Your typical EKG P-QRS-T complex figure is a Lead II EKG.  It records electrical activity from the SA node towards the bottom left part of your heart (your left leg, actually).
  • Tiny boxes=0.04sec
  • AV node cells are narrow=slow conduction.
  • Sodium channels are FAST at depolarizing.
  • ST segment=no net current =/= not active--it's when the ventricles are fully contracted--remember, the EKG is the electrical map and it actually precedes the actual contraction.
  • The PR wave is measured instead of the PQ wave because sometimes the Q doesn't show up.
  • The direction of which the waves and peaks go dictate whether it is the endocardium or epicardium depolarizes and repolorizes first.  (Cool--but not really necessary to understand.)

Thank God for Khan Academy: EKG II--Torsades De Pointes


"Torsades de Points" by KhanAcademyMedicine

Wednesday, March 18, 2015

Grapefruit Contraindication

Have you ever had one of those moments when the pieces fell into place?You knew the concept before but didn't really think much of it, and then suddenly realized that it was a critical piece of information, and you were just like:





Today I had one of those moments, and it all started when this NCLEX prep professor said: "What else do you have to remember to teach regarding statins?"  A student behind me chirped: "Don't drink grapefruit."  My brain said, "Oh yeah..." and remembered when I told my mom, "Ah, just wait an hour or drink it an hour before you take your medicine."  And just as that memory flashed in my mind the professor's voice zoomed back into the foreground with: "And you know, you can't just hold the medicine for an hour because the grapefruit stays in your system for 72 hours.**"

Thank God, my mom didn't listen to me.  And this totally explains why, even though I regularly take a sleep aid, some days I wake up and am fine, but other days, if I've had grapefruit juice (which I juice and drink for the benefits of vit C and ribavirin) I feel like I'm wobbling around in a haze all day.

**Now, I haven't been able to verify that grapefruit stays in the body for 72 hours, but I've read one primary article (admittedly with a rather weak sample size) and several secondary articles that says scientists have found evidence that the grapefruit's effect on increasing certain medication to toxic levels does last at least 24 hours.  [Edit: I've found an article that references studies supporting 72 hours as the upper threshold.]

Turns out, there's quite a few medications that interact with grapefruit.  The classification of anti-cancer medications, anti-diabetic medications, antibiotics, anti-inflammatory medications, anti-lipemics, heart medications, centrally activating medications, estrogen supplements, GI medications, and immunosuppressant medications each have several specific medications that are known to have some reaction with grapefruit.  I'm sure that's not a complete list, but, let's be honest, unless you have an eidetic memory you won't be memorizing all of those.

Now, as I said to my mentees, and as this professor said to us this morning, things are easier to remember if you understand why something happens.  I knew that grapefruit competed with these medications.  I knew that competing for binding sites meant the medication will reach a toxic level, but I didn't know that the enzyme responsible for the first pass effect was called "CYP3A4," and that it functioned both in the liver and in the small intestine.  CYP3A4's job is to remove some of the medication from the body.  But it has a high affinity for grapefruit so it will bind to the grapefruit juice first, allowing the medication to flow out of the liver and into the systemic circulation unaltered.

It is important to note, however, that I have read some clinicians are less inclined to be so stringent on withholding grapefruit juice because of debate on whether or the restrictions of patient lifestyle is necessary with less toxic medications when also taking into consideration the patient lifestyle.  For example, in the case of simvastatin, minor side effects of drinking grapefruit juice were joint and muscle aches, but if the levels of medication become toxic, it's possible that cells could begin to break down, resulting in rhabdomyolysis.  It should be stressed that this has only been reported once, and the prescription order of simvastatin is a dose that is now no longer standard practice.

Suffice it to say, per pharmacy warning and nursing teaching, we must teach our patients the risks--you're not just risking toxicity, you're also running the risk of amplifying any of those pesky side effects.  If the patient is a grapefruit juice worshipper, perhaps there should be a change in medication.  But if the patient normally abstains from grapefruit juice and accidentally forgets and drinks some, there's not likely a need for an ambulance.  After all the discovery of the effect of grapefruit juice on medication absorption was completely accidental, and patients had been taking their medications in conjunction with grapefruit juice for years.


References:

http://www.cmaj.ca/content/suppl/2012/11/26/cmaj.120951.DC1/grape-bailey-1-at.pdf
http://www.drugs.com/article/grapefruit-drug-interactions.html
http://spectrum.diabetesjournals.org/content/19/4/202.full
http://health.clevelandclinic.org/2013/08/do-statins-and-grapefruit-safely-mix/
http://www.fda.gov/downloads/ForConsumers/ConsumerUpdates/UCM292839.pdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873672/
http://www.ncbi.nlm.nih.gov/pubmed/11061578
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884539/
http://www.nature.com/ejcn/journal/v58/n1/full/1601736a.html
http://www.ncbi.nlm.nih.gov/pubmed/6362950
http://www.ncbi.nlm.nih.gov/pubmed/11009051

Monday, March 2, 2015

Diminished Breath Sounds: Story From the Trenches

The Leap.  It's what makes the difference between student and practitioner.  The Leap is when you see the theory in real life and recognize it, and apply the theory in practice, because you recognize it. I know I said "recognize it" twice in that last sentence, but seriously it's kind of the whole point of, well, everything.

Every student wants to make the leap.  And I totally, absolutely missed it.  Face planted like there was no tomorrow.  In front of two ex-paramedics turned into triage nurses in the ER--and thank God there were two ex-paramedic triage nurses to catch my absolute face plant because what I missed was pretty damn big.

The part that gets me is that I had just learned about it four days ago in lecture.  I learned about it, and every time my professor said it (and she said it at least once per lecture for 8 weeks) I could feel myself wanting to slam my own face into the table from the tedious repetition of it.  My professor was obsessed over airway.  Every day she would say: "If you have two patients--one, a man passing a kidney stone and screaming his lungs out with 10/10 pain, and the other a child in with exacerbated asthma and wheezing but now no longer wheezing, you better run in there and make sure that kid is breathing.  The guy next door has got very healthy lungs.  The kid is suffocating."

How many times did she say that?  And yet!

This was my very first, and only time, in the ER.  I didn't have an actual preceptor so I was just being bounced from one nurse to the next, from one case to the next--which isn't an excuse, I know.  Assessment is assessment, and it's the same no matter where you go, no matter which patient you're on.

I just didn't make the leap.  I don't know why.  I've been going over it again and again in my head.   Why didn't I see it?  Why didn't I stop and question when I heard what I heard?  What if I had been alone and triaged this man down?

This is what happened:

He was the third patient to come in.  I had just come back from delivering another patient to her bed, and the two triage nurses had already finished assessing, but they handed me a pair of stethoscopes and asked me to assess breath sounds.  The man was sitting with one hand braced on the table and one hand on his knee.  They had also already taken the pulse ox and bp cuff off so I had no vitals.  I know because I looked to see if his pulse ox would give me a hint.  And I had missed the intake so I didn't know what his complaint was.
http://e-safe-anaesthesia.org/sessions/06_03/gif/tripod.gif
"Okay, sir, sit up for me," I said, anticipating that if I was being instructed to auscultate lung sounds on a 25 year old male, the patient probably had asthma.  I expected to hear wretched crackling like the crumpling of a paper bag.

I chirped, "Deep breath please."

I didn't hear any wheezing or crackles on the back.  Nothing at all.  I had heard it in the front but not the back.  Puzzled, I stayed in the same spot.

"Breathe deep.  Please.  Deep."  (I mean, really, L.  SO OBVIOUS.)

I didn't hear anything, in fact, but I had a 15 dollar stethoscope, and I was listening through two layers of clothes and in a loud ER bay,  so I assumed I probably wasn't going to hear the most detailed of sounds.  Plus the man wasn't gasping for breath.  He didn't appear in distress as he was calm, and quiet.  Not just quiet.  Silent.  He didn't say a word.  (Which I didn't know was a big deal, but it seems so obvious to me now--the man was silent because he could barely supply himself with enough oxygen to keep from gasping like a fish out of water.)  And I did hear breath sounds in the front.  I also had no idea tripod was so subtle. It's subtle because the man can't breathe.  He's not exactly going to be making a lot of movement if he can barely breathe. Honestly, when I first saw the patient I thought to myself: "He's hunched over.  He looks tired."
So, like an excited, nervous puppy, I followed the pattern bilateral listening pattern, on his chest then on his back, and then took off the stethoscope and said, "Clear."

This is essentially what I heard: http://www.youtube.com/watch?v=O8OC7EiqBKQ&t=0m47s.  And, no, there wasn't even the faintest of crackles.  I didn't hear much, but there was some in and out, and there weren't crackles.  I've been kicking myself for over a week about missing this, because I swore there weren't crackled but dammit, L, that's the point!  You weren't thinking!

I didn't make the leap.

I just checked each part of his lungs like they were checkboxes, like they were tasks to overcome, not pieces of evidence to be examined and critically analyzed.

I was wrong.

I was so, so wrong.

"Clear," I said.
"Clear?" the first nurse asked, with the tiniest note of doubt.  Or maybe it was incredulity that I was as dumb as a brick.

Basically, the look he gave me.

"I don't hear crackles," I affirmed, a little less certain.
He gave me this look, then gestured to the other nurse.  "Take a listen," he said.  "Diminished?"
"Yeah," the other nurse said, nodding his head.  "Diminished."
The first nurse nodded and finished the paperwork, essentially dismissing me, and I, embarrassed but not really sure what had happened backed up against the supply table.  Silent.
The second nurse turned to me and said, "When people have really bad asthma, the bronchioles close up.  Wheezing means sound, just like when you blow through pursed lips you get a whistle.  When you open your mouth wide, there's still sound, it's loud and hollow.  When you close your lips.  There's no sound.  No sound is bad.  No sound is always bad."
"I'm sorry," I said after we had delivered the patient to the back for treatment.  "I messed up."
"No, you didn't mess up.  You're just new.  Next time, before you have the patient sit up, just step back and look.  He was tripoding, using accessory muscles--that's textbook respiratory distress--which you would have seen if you physically stepped back instead of standing right next to him.  It's not an emergency emergency, so, if the man isn't passed out or clutching his throat and turning blue, or hemorrhaging, you have time to look him over.  We'll just give him a neb treatment and refill his Albuterol, but, now you know.  Don't get sucked into just one part of the assessment.  Step back and look.  And if you don't hear anything it's not 'clear' it's 'diminished.'"

Saturday, December 20, 2014

Overview of the Hormones of the Female Reproductive Cycle: E, PG, GnRH, FSH, LH

The human female reproductive system is guided by an incredible coordination of hormones. This is the first of a series of posts reviewing the hormones involved in the ovarian and uterine cycles.  It is important to realize 2 things: 1) that the ovarian and uterine cycles operate on the same hormone signals: estrogen, progesterone, GnRH, LH, FSH.  The production of these hormones are intertwined. 2) These hormones are free flowing in the blood, so, if there is an increase GnRH, there will be an increase in FSH and LH systemically, which means there will be an increase in estrogen and progesterone systemically, which means that both the ovaries and the uterus will be fluctuating/reacting at the same time.


http://ib.berkeley.edu/courses/ib140/ovarian%20cycle,%20uterine%20menstrual%20cycle,%20menstruation_files/image016.jpg


Gonad/o/tropin Releasing Hormone: GnRH is a hormone released by the hypothalamus, that stimulates the anterior pituitary to release LH and FSH, which are hormones that act upon the sex organs, also known as "gonads" (hence the name GONAD-o-TROPIN.)  In most cases, the presence of both estrogen and progesterone in the bloodstream at the same time will inhibit the hypothalamus from releasing GnRH.  This is a type of negative feedback.  (However, during a part of the uterine and ovarian cycle, estrogen actually becomes a positive feedback loop--no one really knows how this happens, but I will attempt to explain how to identify when this happens in a later post.)

Follicle Stimulating Hormone: As the name implies, this hormone stimulates the follicles.  Follicles are a generic term for any type of little sac, or cavity.  In the case of ovarian follicles, we're talking about the little sack that surrounds a single egg before it is released from the ovary into the fallopian tube.  All of a woman's oocyte first starts off as primordial follicles-- primary oocytes surrounded by a single layer of squamous granulosa cells.  FSH is the hormone that helps each primary oocyte begin developing into a mature follicle with a gigantic fluid filled antrum.  The antrum builds up so much pressure it explodes, jettisoning the oocyte out of the ovary during ovulation.
https://classconnection.s3.amazonaws.com/427/flashcards/1500427/jpg/picture21335761453346.jpg

Luteinizing Hormone: This hormone causes the follicles to complete maturation and undergo ovulation in the "LH surge."  Right as the oocyte has exploded out of the ovary and into the waiting arms of the fimbriae, LH causes the leftover follicle bits (mostly granulosa cells) to crumple up into the corpus luteum (the fact that luteinizing hormone has the same root word as corpus luteum, should not escape your notice).  These granulosa cells change into luteal cells, and supports the corpus luteum in its task to secrete large amounts of progesterone and some estrogen.

Estrogen: Estrogen is secreted by granulosa cells.  The primary reason for granulosa cells secrete estrogen is for a positive feedback loop with LH to induce a ovulation.  The secondary reason for estrogen secretion is to increase the number of progesterone receptors in the uterine lining.  This is necessary to increase progesterone sensitivity in the uterine lining so that the uterine lining can proliferate, becoming thicker with more blood vessels to create nice, nutrient rich lining for the potential embryo.

Progesterone: The pregnancy hormone.  Progesterone is secreted by the corpus luteum, and later by the chorionic villi, and then, when the placenta finally becomes functioning, it is secreted by the placenta.  In order for a pregnancy to remain viable, there has to be a consistent, elevated level of progesterone.  Progesterone does many things, which I will cover in a different post, but the most important one is, it relaxes the muscles of the body, causing a decrease chance of uterine contraction (which would lead to spontaneous abortion).


https://courses.stu.qmul.ac.uk/smd/kb/microanatomy/humandev/placenta/index.htm

Human chorionic gonadotropin:  The pregnancy test hormone.  Human chorionic gonadotropin is only released by the syncytiotrophoblast of the blastocyst (see the picture above).  More specifically it is secreted by the most superficial epithelial layer of the embryonic placental villi, so there has to be an embryo mature enough to be embedding into the uterus for this hormone to appear.   (You should remember that embedding of the embryo occurs about 8 days after fertilization, so hCG would appear around day 22 of a standard menstrual cycle).  HCG is like the little brother of luteinizing hormone.  You know how sometimes there are two siblings who play the same sport but the little one not only plays at the same level as the older, he also seems to be able to land all the tricks the older one can't?  If LH were the older brother, hCG would be the little brother who can do the same thing as LH, except better, because it is secreted even in the presence of elevated estrogen (remember elevated levels of estrogen causes a negative feedback repression of GnRH, which would cut off the supply of LH from the pituitary).  Sometimes LH is referred to as the pituitary analogue.  As the analogue, hCG continues to support the corpus luteum after LH has faded from the blood stream, ensuring that there is a steady release of progesterone and estrogen even after the high concentrations of progesterone and estrogen have caused the pituitary to stop releasing LH.  Additionally, FSH is also suppressed, which is good, because the woman's body doesn't need to be wasting energy maturing extra oocytes when there's already a pregnancy underway.


References:

Perry, Shannon E., Marilyn J. Hockenberry, Deitra Leonard Lowdermilk, and David Wilson.  Maternal Child Nursing Care. St. Louis: Elsevier, 2014. 5th Ed.
Seeley, Rod, Cinnamon VanPutte, Jennifer Regan, Andrew Russo.  Seeley's Anatomy and Physiology. Boston: McGraw Hill, 2011. 9th Ed.
http://en.wikipedia.org/wiki/Syncytiotrophoblast


Wednesday, December 10, 2014

definition blast

It was brought to my attention recently that I had no idea what these were.

olanzapine: http://www.drugs.com/cdi/olanzapine.html
assertive community treatment: http://en.wikipedia.org/wiki/Assertive_community_treatment
dialectical behavior treatment: http://behavioraltech.org/resources/whatisdbt.cfm
adventitious crises: http://www.atitesting.com/ati_next_gen/focusedreview/data/datacontext/rm_mh_pn_8_chp_26.pdf

Magnesium sulfate and flushing

How I felt today:






Today was the OB ATI test.  70 questions in 70 minutes.  This was my question 68.  I was stumped, and tired, and frankly, by this point, didn't give two craps.  I just needed to get out of that room.  Now that I've finally got a few hours of sleep and had some time to think about it, I'm pretty sure I got it wrong, so I decided to do a post-mortem on it.

I'd like your input.

Here's the question:

A nurse is caring for a patient with preeclampsia with magnesium sulfate.  Which of these symptoms should you report to the provider?  Select all that apply.

a) Respiratory rate of 20 per minute
b) A urinary output of 400 mL/4hr
c) Epigastric pain
d) Facial flushing
e) Lack of deep tendon reflexes

I'm pretty confident I got this answer wrong, so what did you answer?  Why?  I'll give you a minute to think, and I'll explain my answer choices and reasonings below.

By the way, this is what a vial label for magnesium sulfate IM might look like:

http://dailymed.nlm.nih.gov/dailymed/image.cfm?id=59573&name=274e5d29-figure-02%2Ejpg

Ok, here's the question again:

A nurse is caring for a patient with preeclampsia with magnesium sulfate.  Which of these symptoms should you report to the provider?  Select all that apply.

a) Respiratory rate of 20 per minute
b) A urinary output of 400 mL/4hr
c) Epigastric pain
d) Facial flushing
e) Lack of deep tendon reflexes

I chose c) and e).  I think I should have chosen c), d), and e).

I had some confusion over this question for 2 reasons.  With the phrase "which of these symptoms" it was unclear to me whether the question was asking for the symptoms for preeclampsia progressing to eclampsia (essentially, the treatment was failing), or asking for the symptoms of magnesium sulfate overdose, or both.  In the moment my brain just thought: "Well, I'm going to report any potentially life threatening symptoms," because, you know, real life.  A good test taking tactic, if you don't know the answer to a question is to strike out the obviously WNL (within normal limits) answers.

a) Incorrect.  A respiratory rate of 20 breaths per minute is within normal range.
b) Incorrect.  An output of 30 mL/hour is "normal" on NCLEX questions.  30mL/hr x 4hrs = 120mL, so 400 mL/4hr is more than sufficient.
c) Epigastric pain.  Here's where it got a little confusing.  Was this question strictly about calling for signs of magnesium toxicity?  Or was it asking for what I should alert the doctor about in general?  Because epigastric pain, especially RUQ (right upper quadrant pain) is classic s/s of liver swelling, which happens with preeclampsia because the elevated blood pressure causes the blood to back up from the heart into the systemic circulation.  (The first organs to be affected by this systemic increase in blood pressure are your brain, heart, kidneys, and liver.)  This is why with preeclampsia and eclampsia, you'll see elevated liver enzymes.
d) Facial flushing.  I couldn't, for the life of me, remember with 100% certainty that facial flushing was a side effect of magnesium sulfate.  My gut said yes, but my brain was being a non-committing coward.  More on this later.
e) Magnesium sulfate classified as an anticonvulsant because it is a CNS depressant.  It blocks the transmission of Ach (acetylcholine), which decreases motor nerve impulse.  It would make sense, then, that if someone was given too much mag sulfate, that it would cause a cessation of motor nerve impulses, leading to a lack of deep tendon reflexes.  For a video explanation on how to perform deep tendon reflexes, click here.

So I got home and researched magnesium sulfate, and this is why I think I should have picked d):
http://www.healthline.com/health/pregnancy/preterm-labor-magnesium-sulfate#Overview1
Basically, it would have similar results to a calcium channel blocker.  It does not have the same mechanism of action, but if you think about it, calcium channel blockers block the calcium channels in smooth vascular muscles, prevent an influx of calcium, which causes vasodilation (hence, why a side effect of nifedipine is orthostatic hypotension).  Similarly, if you decrease the calcium blood levels by administering magnesium sulfate, there won't be an influx of calcium through channels on the smooth vascular muscles, so your body will be unable to vasoconstrict.  The vessels will remain vasodilated.  What else happens with vasodilation?  Flushing!  You get red.  When it's hot outside, or when you work out, or when you are embarrassed, your blood vessels dilate, causing flushing.

I'm not 100% sure, but it makes sense, right?  And, in the words of Ms. Soberano, "If you can defend your reasoning, then it's a good answer."

Now, if I could figure out why we use calcium gluconate as the antidote...

References:
http://www.drugs.com/sfx/magnesium-sulfate-side-effects.html
http://www.rxlist.com/magnesium-sulfate-side-effects-drug-center.htm
http://www.surgeryencyclopedia.com/La-Pa/Laxatives.html
http://en.wikipedia.org/wiki/Magnesium_sulfate
http://www.healthline.com/health/pregnancy/preterm-labor-magnesium-sulfate#Overview1
http://www.ncbi.nlm.nih.gov/pubmed/1331782
Mosby's 2013 Nursing Drug Reference
https://www.youtube.com/watch?v=0sqCIzuotWo
http://en.wikipedia.org/wiki/Calcium_channel_blocker
http://www.drugs.com/nifedipine.html