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Fast Atrial Fibrillation

3 Aug

It is Atrial Fibrillation with a rapid ventricular response. The atrial rate can be more than 300 beats per minute followed by the ventricular rate of up to 170 beats. That is fast. I like to say in my mind Fast AFib. It just sounds cooler.

The intravenous cardizem is infusing giving a better control, or not.What about the or nots? I bet EPS Dr Wes, could give us the facts.

Why does it always have to be intravenous  cardizem?  I have seen Multaq post cardioversion sustain a nice sinus bradycardia. I have a love/hate relationship with Amiodarone.

I am a fan of the digoxin added to a beta-blocker.  I am starting to dig digoxin more and more because it does not drop the blood pressure.

 

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Cartwheels

14 Apr

Cartwheel by bobbipop

credit the artist on deviantART by clicking on the picture.

I like to do cartwheels. I do them all the time. Anywhere, anytime I feel like my heart needs it. On the grass, or on the black top, I am that 4 pointed object wheeling around the lot. Cartwheels are better in the grass. I like to take my shoes off when I do them so I can point my feet to the sky. Seriously, it is all about the heart. I bet when I do cartwheels it increases the venous return to my heart, and that makes me feel good.

I mock trend on my bed all the time too, but cartwheels are way more fun.

I want to go do cartwheels and round-offs right now, but I have to make sure that I know what it is that I do at work every week, and why I do it. I guess that is what certification is. I am already doing this, I already learned it, so I should just pass the test with pretty colors.

There is only 5 questions on the Endocrine system, and they will be about DKA and hypoglycemia.

Here is what I will remember!

When a DKA patient goes pee pee they will dump glucose and electrolytes out and that includes potassium. Insulin drives potassium into the cells. So the patient needs insulin and electrolyte replacement.

Hypoglycemia yikes. Half the time, hospitalized patients are not eating! Feed the patient. We do not have to run and push D50 all the time. That amp of D50 is caustic to the veins, if the patient is awake just feed them!

Hematology and Immunology have 3 questions, that is 2%.

Here is what I will remember!

The rule of 3s cake.

The RBCs x 3=the hemoglobin

The hemoglobin x3= the hematocrit.

If the Hb times 3 is less than the hematocrit the patient is dehydrated.

If the Hb times 3 is greater than the hematocrit there is fluid overload.

Platelets. Bleeding for nothing can happen with platelets less than 25.

For sure I am not inserting a rectal tube into a patient with super low platelets.

Gastrointestinal has 6 questions that is 5% of the exam. Yuck.

GI has lots of information for only 6 questions. Do you remember from nursing school that for acute pancreatitis, Dilaudid is the drug of choice for pain relief because Morphine may cause biliary colic or spasms of the sphincter of Oddi? Yeap, start laughing but I got that question right in nursing school.

There is Ranson’s Criteria to determine mortality and acuity. Acute pancreatitis patients just look sick, and they are sick. Imagine an organ eating itself.

Remember for the test that: Grey Turner’s sign bruising blue around the flank and that Cullen’s sign is around the umbilicus.

The GI hemorrhage, well it really smells bad and that is all I have to say about that. Most of these bleeds are caused by peptic ulcer disease, and next in line is the esophageal varices. Actually, I wonder why coumadin therapy is not on the top of this list, because certainly I care for lots of anemia for the coumadin patient!

Hepatic Failure, is ugly. The yellow, poopy, lactulose, change of mental status climbing out of the bed mess is just awful. The ascites, hypotension and tachycardia is nerve wrecking.

Yeah I am bored now, if you are bored too, well that makes this less painful for me somehow, sorry. I am not going to kill myself writing about portal hypertension, or the lovely memories of that first GI bleeder.  After this is over, I will write some poetry to make up for this pain.

Here are some practice questions. I am not going to write the multiple choice answers because well, I am out of time for that trickery.

1. What is the peak of rapid acting insulin?

60-90 minutes

2. A new diabetic should be closely monitored when taking which cardiac medication?

beta-blockers *can lower blood sugar

3. Treatment of metabolic acidosis from DKA consists of

a.insulin administration

b. bicarbonate

c. low salt diet

d. fluid volume resuscitation

* you can not mask the acidosis with HCO3

4. The patient has a blood glucose of 400, with lethargy and deep gasping resps. The ABG is pH 7.28, CO2 30, HCO3 14 (partially compensated metabolic acidosis) is most likely from:

diabetic ketoacidosis

5.Symptoms of thrombocytopenia include:

petecchiae

6. Ocreotide is often used to control bleeding from esophageal varices, the primary action of this drug is to:

decrease the blood flow.

*it also decreases gastric secretions.

7. An elderly patient is with severe abdominal pain. What should always be ruled out?

bowel infarction

8. Pulmonary complications from acute pancreatitis may include:

ARDS and elevation of the diaphragm and bilateral rales and atelectasis, especially in the left base.

9. Which lab finding is most specific for pancreatitis?

elevated serum and urinary amylase

10. I am not doing this anymore.

Tomorrow I will blast through the neurological section. I already know I have a whacked out limbic system, but I love it. I mean I love my limbic system.

I will go do cartwheels now.

Help!

13 Apr

Help by Fellow World

Click on the art to credit the artists.

Help me, I am stuck in that tree.  April 21 I will be taking the PCCN cert exam. I am a good test taker, I can eliminate the wrong answers. I can do that.

It is kind of like knowing what you do not want, but never knowing what you do want.

Somebody help me. It is cold and cloudy, and I just can’t sit any longer. Please tell me I am not all alone in this!

Just what does Potassium 3.5-5.0meQ/L do? it maintains intracellular water and acid/base balance.

Hyperkalemia is usually caused by renal failure. The symptoms of this may be bradycardia, tremors, twitching, tall peaked T waves. The treatment is: Kayexelate, dialysis, insulin/D50, or HCO3/Ca++.  It can take a while for the Kayexelate to work. I once had a patient NPO and the nephrologist actually wanted me to give the Kayexelate via rectal enema.When I asked him how was I supposed to keep the medicine in the rectum long enough for it to work, he told me to use a “butt cork”!  I bothered him till he cancelled that request and changed his mind to give HCO3.

Hypokalemia can be caused by inadequate intake or renal loss. NPO patients should be getting KCl 40meQ each day somehow. The symptoms are tachycardia, hypotension, flaccid muscles, and flat T waves. The treatment is: give KCl orally preferably, or IV.

Calcium 8.4-1.2mg/dL is needed for the contraction of the heart and blood vessels and coagulation.

Hypercalcemia is caused by bone loss or destruction. The symptoms are coma, flaccid muscles, short ST and QT interval. The treatment is IV fluids, diuretics and phosphate.

Hypocalcemia is caused by a low albumin, multiple blood transfusions. The symptoms are seizures, laryngeal spasm, hypotension, flat ST, and a small T wave. The treatment is calcium gluconate.

Magnesium 1.5-1.95meQ/L , my most favorite electrolyte of all! It is needed for the relaxation of the heart and blood vessels and it is NEEDED for the absorption and utilization of other electrolytes. Stop running those K riders, if the Mg is low you are wasting time and burning the veins if you do not replace the MG too! We like the Mg above 2! ❤

Hypermagnesemia is caused by renal failure. The symptoms are CNS depression, hypoactive reflexes, bradycardia, and hypotension. It is treated by giving IV calcium.

Hypomagnesemia is caused by inadequate intake. The symptoms include irritability, increased reflexes, ST depression, and T wave inversion. The treatment is Magnesium. I think I will go take some oral Mg right now.

Phosphorous 2.5-4.7mg/dL is essential for ATP production. Our cells need that energy.

Hyperphosphatemia is caused by renal failure. The symptoms are asymptomatic but you will see a low calcium. The treatment in Amphogel, Insulin/D50, Dialysis, Fluids.

Hypohosphatemia is caused by Mg deficiency, re-feeding syndrome, acute respiratory distress. The symptoms look like a decreased level of conciousness, respiratory distress, muscle weakness. The treatment is: phosphorus.

Sodium 135-145mEq/L is needed for water movement and the changes may cause cerebral edema.

Hypernatremia is caused by fluid loss. The symptoms are thirst, and CNS depression. The treatment is free water D5W. If they have a PEG tube you will be shoving in tap water bolus.

Hyponatremia is caused by overhydration with IV fluids sometimes. The symptoms are edema and mental status changes. The treatment is a fluid restriction, normal saline, or hypertonic saline. I was so afraid to run hypertonic saline the first time. The patients sodium was like 109.

The medications on the PCCN test with the desired effects!

Let’s make it easy!

All of the following medications increase the heart rate, the blood pressure and the cardiac output, these winners are:

Dopamine 2-20 ug/kg/min- Dobutamine 5-15ug/kg/min–Levophed 2-12 ug/kg.min–Epinephrine 1-10ug/min

Got that? OK give me some LOVaphed, will that be on the test? I know about that drug.

The next medication Digoxin 0.125-o.5mg will decrease the heart rate, actually increase the blood pressure (diastolic especially but don’t quote me on that) and increase the cardiac output.

The Nitroglycerine 5-20ug/min does nothing to the heart rate, it decreases the blood pressure and can either increase or decrease the cardiac output.

The Nitroprusside 0.1-10ug/kg/min increases the heart rate, decreased the blood pressure and cardiac output.

The Amiodarone Bolus 150-300mg followed by drip decreases the heart rate and blood pressure and increases the cardiac output. I have a love/hate relationship with Amiodarone.

Next!

Localizing the injury on the 12 lead EKG

Trouble: T wave inversion is ischemia. ST segment elevation is injury and Q waves indicate necrosis.

First find out if the changes are in more than 1 lead or every lead.

Next!

The vessels LCD and the LAD affect the anterior heart, the changes are in lead V3, V4

The vessel RCA affects the inferior heart and the changes are in lead II, II, AVF And remember with an inferior wall MI we are supposed to get a right-sided EKG which I have never even seen before!

The vessels LCA and the Circumflex affect the lateral heart and the changes are in V5, V6, I, aVL

The vessels LAD and PDA affect the posterior heart and the changes are reciprocal in leads V1-V4

The RCA vessel also affects the right ventricle and is present in V4R

Go memorize.

Now for my favorite part where all of you are going to pee pee in your panties!

H20+CO2=H2CO3=H+HCO3

Water and carbon dioxide equals carbonic acid equals hydrogen and bicarbonate! <giggles>

I loved chemistry in nursing school. I almost changed course on the ship of academia, but I held onto nursing steadfast.

It is just a balancing act this acid base balance and our lungs and our kidneys are working hard at it, even if you do not feel it.

Maybe I feel it. I like HCO3 in my mouth when I brush my teeth with baking soda like the old days when there was no toothpaste in the medicine cabinet. Just dip your brush into a box of Arm and Hammer and rinse it out with hydrogen peroxide. I bet you will have white teeth just like me, even if my teeth are slightly crooked. I like them that way, but I better stop licking them with my tongue, I do not want to get subacute bacterial endocarditis or something.

Anyway on with the ABGs

pH 7.35-7.45

pCO2 35-45mmHg

pO2 80-100mmHg

O2 sat 95-100%

HCO3 22-26mEq/L

Base Excess + or -2

Forget about the Anion gap-that better not be on the test! If it is I will punch the computer module and walk out. Just kidding!

So we have the lungs that remove CO2 that is made by cellular processes. That is what the lungs do to balance the pH. The kidneys balance by producing HCO3 and by getting rid of H+ ions. The way these organs interact is via the making of carbonic acid H2CO3, which is a constant thing. The water will attach to carbon dioxide, then when needed this breaks apart to make hydrogen ions and bicarbonate.

It is just a continuous, compensating balancing act to keep the pH normal.

I doubt that chemistry will be on the exam so here I will put it to use.

1. A 60 year old liver transplant patient with pneumonia, a room air ABG reveals: pH 7.46 (alkalosis) CO2 32 (alkalosis) pO2 77 (hypoxemia) O2 sat 96% (normal) HCO3 23 (normal)

The patient is mildly hypoxic with uncompensated respiratory alkalosis. From the low pO2 the patient might be breathing faster, blowing off the CO2 causing this problem. There will probably not be any treatment for this at this time.

2. A 22 year old has been fasting to lose weight. She is a diabetic. Noone is sure if the patient has been taking the insulin at home for a couple of days. ABG goes like this

pH 7.20(acidotic) CO2 28 (alkalosis) pO2 96 (normal) O2 sat 96% (normal) HCO3-11 (acidosis)

The patient has partially compensated metabolic acidosis from DKA. The treatment is to correct the glucose with insulin and IV fluids. If the internal medicine doctor tells you to give bicarbonate: don’t do it! It will not fix the pH and will mask the underlying problem.

3. 60 year old with chronic renal failure complaining of dizziness. ABGs are drawn.

pH 7.37 (normal) CO2 34 (alkalosis) pO2 94 (normal) O2 sat 97% (normal) HCO3 19 (Acidosis)

Common to renal failure this is fully compensated metabolic acidosis. No treatment.

Pt admitted for COPD. ABG

pH 7.33 (acidosis) paCO2 60 (acidosis) pO2 75 (hypoxemia) O2 sat 94% (low) HCO3 31 (alkalosis)

This is partially compensated respiratory acidosis and the patient will probably get a BiPAP on telemetry!

i hate asystole

14 Jan

epi epi epi

It is official, I have decided that I hate asystole or PEA codes.  Since my new nursling days that is almost 3 years ago today (I am still a nursling <3), I have been directly involved in a total of 4  code blues. I am not including respiratory distress with intubation etc because luckily in those situations intervention preceded cardiac arrest.

3 out of the 4 pulseless codes have been aystole or PEA and those 3 patients died. The only 1 that lived was the shockable ventricular fibrillation: so that is the kind of code I liked best, if “liking” a code were possible.

I am still feeling yucky about the last asystole code. The whole thing keeps playing over in my mind and I keep thinking of how it could have been better. I also can not stop thinking about: this code blue seemed different, maybe because it did not happen on my floor where I work. I was going over to a medical floor to pick the patient up to transfer to telemetry. I  had the feeling that something was not right because the nurse called me in a panic, requesting me to hurry and pick up the patient. While I was en-route 3/4 of the way there I heard the code blue announced to the very place I moving towards and I guessed that it was the patient I was supposed to be picking up.

I walked into the room and the medical nurses were doing chest compressions and nothing else. I am not trying to describe anything negative about the medical floor, I am just trying to express that the other code blues that I have been around on the telemetry floor where I work: the nurses just start working as if being moved by some invisible robotic arm. In fact the other codes on the tele floor that I have seen looks more like:  the defibrillator is hooked up, someone is ventilating till the RT gets there, CPR is performed, someone is checking the line, someone is getting the chart, someone is getting the doppler, someone is calling for an IV pump just in case, someone is recording, someone is printing out the morning labs. It helps that I work on a pretty big floor so there are lots of “someones” around to help. <giggle> And all these someones seem to just announce what they are doing without anyone asking or telling them what to do.  The nurse is telling everyone what is going on and then he/she repeats it all again when the doctor and the ICU nurse arrives.

All I can say is that I would rather see v fib on the monitor than asystole any day. This code was just lifeless, and actually I wonder how long the patient was dead before CPR was started. The latter part depresses me too.

So it makes me think about: I like to bitch and complain about the circus arena that I work in on telemetry. But here is an example of: I wished that patient was coding in my own area called telemetry. I am not intending to claim that the outcome would have been different for the patient, that patient was dead. I am just forming an early opinion that there might be a difference in atmosphere. The outcome for my emotions would be different. I bet I would of felt less hopeless afterwards.

And for me, for my sake who is going to lick my wounds and give me some understanding?

I started this blog in the summer of 2007 when my first patient died in a code 2 weeks off of my orientation. I was sad. It helped me to write my experiences and it still serves the purpose. I feel comforted reading medical and nurse blogs because it helps me to feel not so alone in this thing that we love to do: healthcare.

Alive after the code

1 Dec

I am being a lazy nurse blogger again. What can I say for myself? I have no legitimate excuses, I miss my blog so here I am with not much to say. I was going to write about my latest experience in a code blue situation, I was going to give everyone the step by step run down of ACLS initiated at the bedside on a telemetry floor and the awesome outcome, but I lost my drive as each day passed by after the event, till it seemed like routine. It was pretty darn amazing though: the teamwork, Fave Cardio, the RT, the nurses, the whine of the defibrillator charging.

Here is the scene without a minute by minute detail: I was just back from lunch, and the patient was being diaylized, I am walking down the hall and I hear the dialysis RN yelling we need help in here. She was talking to the patient when all of a sudden: nothing, no pulse, no response. At the same time at the monitor station the tech was saying: Ventricular Fibrillation in room # 13. By the time I get into the room I see the dialysis nurse un-hooking the permacath from her machine, there is water all over the floor, 2 nurses are already at the bedside, 1 calling for the backboard and 1 lowering the head of the bed and raising the bed at the same time.  It seemed like it took forever to hear the “code blue room telemetry room # 13”, in fact by the time I heard the announcement the patient was already being ventilated via ambu, the backboard was under and the patient was being compressed and had already been defibrillated with 200 joules and the first epinephrine was already prepared waiting to go in. Ten minutes in the patient was intubated, the House MD was there and one Fave Cardio showed up to collaborate with the House MD. Fave Cardio did a superb job demanding full charge on the defibrillator and he seemed to like to press the charge and shock button, he made everyone nervous charging that machine but kept saying every time, “Do not worry keep compressing, it is just charging.”  I took the position as recorder which I am comfortable doing and helped to keep everyone organized and aware of: how many shocks have been delivered, how much time has passed, reminding everyone to stop after the shock to check the rhythm and for pulse (it seems that it is natural and easy for everyone to get back on the chest quickly, forgetting to check pulse/rhythm) how many epinephrine have gone in, how many amiodarones have gone in, how many bicarbs have gone in etc. It was kinda amazing and long: over one hour this patient was being resuscitated related to the fact that the patient did get a pulse, rhythm, response several times but then kept losing it and we would start all over, and kept going till after about an hour and fifteen minutes the patient maintained pulse and rhythm to the point of moving the lower extremities, by the time we rolled the patient up to the unit the patient was trying to pull out the ET tube! It was neat to see not only ACLS but the differential being worked up at the same time to try and reverse the causation of the problem. ABG revealed severe acidosis and that being said it did seem that after dumping in amp after amp of HCO3 and running in the amiodarone gtt the whole intervention started to turn for the better, with maintenance of pulse and rhythm for longer periods. It was strange to watch the patient get defibrillated, hear the pulse via doppler, see a sinus rhythm on the monitor and then watch it go back to v fib again and then the scenario repeat time and again. The bottom line: the patient lived, early defibrillation improves the outcomes, and it does not always end badly. This was a patient on the younger side and we did not give up. Not to say that we would give up on the elderly patient though, it is just that in my 2 years and 10 months of being a registered nurse witnessing several code blues in the hospital setting, this is the only one that I actually witnessed a living outcome. All the rest died.

On a another note I have experienced many more rapid responses that prevent code situations before they develop, so I encourage the use of the rapid response system even if you are not sure what is going on with the patient, the point is to get help for the patient.

Other news: I am still spinning on telemetry. I am in a perpetual debate with myself over where I want to be in my career, so I just keep turning the telemetry packs. I kind of like tele nursing, the turnover rate is fast, the patient acuity has a huge range but at the same time I feel like I am doing the same thing everyday. Hmm, still thinking about  it.  The contest is between emerg vs critical care, we will see who the winner will be one day. ❤

itty bitty sepsis committee

20 Oct

It has been 2 years and 10 months since I graduated nursing school. I will not summarize that in one blog post do not worry. What I want to write about is sepsis and how I ended up on this sepsis committee at work.

I am anti-social Jane. (*gasps*) I was not interested in the performance and improvement committee, or the wound care task force (not my cup of tea), or anything that would bring me into the hospital on my days off (other than mandatory education requirements). Yeap, even during my first yearly evaluation, I got a raise but was informed by my director that I lack involvement. *sighs*

Involvement. I had this sepsis cloud following me for a while. It seemed that every week I would get report, assess the patient and end up with a septic shocker spiralling down the drain in front of my eyes. Working working  working never leaving the patient, and worrying about the stability of my other patients since I was unable to even get to them. I kept seeing it over and over: hypotension, febrile, tachycardia, infection and risk factors for sepsis.

I was such a new nurse and I knew the basics of what to do but it was always a long drawn out process. I mean: I knew to get the blood cultures and some fluids and antibiotics but the process was so unorganized and ineffective. My patients always ended up going to intensive care  eventually, after I tried the minimal interventions ordered by doctors and waited for progress that sometimes never came. The interventions were minimal because I was not pushing hard enough to present the clinical situation. And my heart always sank into my stomach after the patient was finally transferred to ICU: and I hear: code blue ICU: and call up later to find out: yeap, that was your patient.

My documentation would read something like this: Notified Attending MD that patient is hypotensive SBP 70s, sinus tachycardia,  admitted with pneumonia, yesterdays CXR showing infiltrates, febrile, lethargic, WBC doubled since yesterday. Attending (usually an internal med) would order 250ml saline bolus, Tylenol, blood cultures, antibiotics.

And new nurse would do all that not realizing that 250ml saline is not going to butter the bread at this point in her nursing career. And she would call back the MD, give another 250ml bolus and go round and round and round . It is just not working.

And then she found me, or I found her in desperation and she recruited me: to the sepsis committee to educate other nurses about this, how to treat it, and how to get your point across to the MD when they try to order the minimal interventions that are just not enough (usually because the nurse is not getting the whole clinical picture into that phone call).  And she is the critical care nurse educator for the hospital and she runs this committee trying to get everyone on the same page.

I mean I can not write about every single septic patient I ever had, that would be too much. Just know that there are nurses who have patients in early sepsis on the floors and if it is not turned around, the patient is eventually going to get worse. I can not say how many times I have received report from the night shift about a patient with a blood pressure in the 70s and febrile and they call the House MD and get Tylenol and a 250ml fluid bolus and then call it a night without even investigating the clinical situation.

My deal goes like this now:

Suspicion of sepsis when:

You assess your patient and find any of these new changes in status: hypothermia, hyperthermia, tachycardia (not on beta blockers) tachypnea, acute change in mental status, hypotension, hyperglycemia (without being diabetic), tachypnea, leukocytosis (or bands > 10%), or leukopenia.

AND

Your patient has an infection or risk factors: pneumonia, empyema, UTI, wounds, foley catheter, device infection, central line. risks: long term hospitalization, nursing home patients, immunosuppression, aspiration, etc…

If you find those clinical assessments and you know your patient has an infection or risks you can guess on sepsis AND get blood cultures times two, lactate level, cbc w/ diff, and coags (PT/PTT). Where I work it is protocol,  just do it.

AND you do not stop there.

Does your patient have evidence of ACUTE organ dysfunction? (not talking about chronic conditions).  Is the systolic blood pressure <90 or the MAP < 65 or a 40mmHg drop from the baseline?  Yessss.  I have been there with my patients.  What is on that chest x ray from yesterday?  Are there infiltrates?  Do you keep turning up the oxygen on the nasal cannula to maintain a SpO2 >90%?  What is the urine output?  Is it less than 0.5ml/kg/hr for more than 2 hours? *gasps* when the foley bag is empty!   What is the creatinine? Is the creatinine >2?   What are the platelets?   Are they less than 100,000?  You checked the lactate when you initially suspected sepsis right? If you are on a medical floor and the lactate is >2 or definitely >3 (but still maintaining blood pressure) the patient needs to be transferred to telemetry.  If you are on telemetry and the lactate is >4, or >3 with hypotension the patient needs to be transferred to ICU. All of the above criteria resemble suspicion of severe sepsis and organ dysfunction and guess what?

We have treatments for this do not worry, just get it done.

Here they are by standard protocol and clinical judgement,  it is the sepsis resuscitation bundle to be done withing the first six hours.

1. Mandatory diagnostics: lactate and repeat lactate in 6 hours, blood cultures prior to  a broad spectrum antibiotic within 1 hour.

2.Optional diagnostics (usually done): CXR, cardiac enzymes, cortisol level, urine culture and analysis, EKG, sputum if you got it.

If you and your patient are on telemetry and you are already waiting for an ICU bed to be available: you start initial fluid resuscitation and if there is no response to the initial resusc you apply vasopressors to maintain a mean arterial pressure >65.  AND you are finding out who is going to drop in the central line.

  If you are on a medical floor you call a rapid response and let them start resuscitation.

It goes like this: for hypotension SBP < 90, MAP < 65 or lactate >4 you deliver: minimum 20-30ml/kg of crystalloid–then, NSS 500ml bolus over 30 minutes repeating till getting an adequate urine output or if you have a central line and are in ICU you want a CVP 8-12mmHg. If this does not work you get on the vasopressors.

After getting all that going hopefully your patient will be in ICU receiving further treatments like steriods, drotrecogin alfa activated maybe, with tight glucose control among all the rest of whatever they do up there so well.

So now my phone call to the MD sounds more like this:

Attending MD (with this verbage)  your patient is hypotensive with a systolic pressure in the 70s, febrile on rectal temp, has new tachycardia, acute change in mental status revealed by lethargy and confusion and the patient was previously alert and orientated, the patient (your patient) admitted with infection, white blood cells are doubled since yesterday, I already drew lactate and it is greater than 4, blood cultures have been sent. I would like to start fluid resuscitation at 30ml/kg, administer a STAT broad spectrum antibiotic and transfer this patient to ICU where you can continue the sepsis protocol and monitor CVP? Does that sound ok to you?

 

It just kept happening to me over and over, this sepsis cloud following me. After awhile I just knew where to start and ended up helping every nurse that cries in the nurses station: I think my patient is septic. I would just go get the basin, start filling it with blood tubes, foley catheter, 18-20 gauge IV catheter, normal saline, and just start working.

That is how anti-social nurse Jane got on the itty bitty sepsis committee.

 

cat FIGHT?

15 Oct

I have been feeling this vibe throughout my patient care when it comes to certain internal medicine MDs and a certain cardiology group where I work, aka: the best place to work in the whole world. I thought at first that it was just me, that I was just imagining this rift due to an over active imagination and high tendencies towards drama. After last weeks shift work I have come to the conclusion: I am not imagining this, I am feeling it, seeing it, stuck in the middle of it, and my patients although safe, could have better outcomes if it were not for this rift going on. Can you imagine? Health care providers alert: this really is happening. I am not sure why or when it started but here is one example, that I am not even sure I should be blogging about. I mean it feels taboo to even write about. It feels like protected  going ons of inside hospital information. I have to get this off my mind though AND want to know if anyone else has experienced this AND how to best advocate for my patients during this what appears to be a cat fight.
(thinks about how to twist the facts and still provide an accurate description of what I am trying to describe)

This is not just one internal MD, it is a few of them and the cardiology group is a pretty big one and they stick together like a well trained military unit.

Example: Who is managing this patient?

Patient comes in for a urinary tract infection (besides the point really until the end of this example). IMD (internal medicine admitting MD)  admits this patient. The patient comes in with lethargy, and change of mental status from home. The patient is found on admission to be in a rapid Atrial fibrillation is started on Cardizem IV in the ED and admitted to telemetry. The urine sent from the ED reveals a UTI. So the patient also gets treated with antibiotics. IMD consults the cardiology group. Cardio does their job: Patient on Cardizem IV bridging to oral Cardizem, Heparin bridging to Coumadin all while checking diagnostics to determine perhaps why this patient has a new onset of atrial fibrillation, stroke risk, anti-coagulation risks versus benefits, etc… The IMD IMD “>presribes the antibiotics at a low dose for only 4 doses and then discontinued. The patient is well controlled on IV cardizem without any side effects or complaints. So the Cardio MD prescribes oral cardizem and discontinues the drip. (usual right? yes.) Unfortunately the patient who does not trust the medical profession does not want to take the cardizem pill. Why? Do not know, she just does not like it, does not want it. So the IMD comes in every day (after the cardiologist is long gone)  and takes the patient off oral cardizem because he knows the patient does not want it, and prescribes digoxin orally for the patient. The patient only trusts IMD and if IMD were to explain to the patient: “You did well on IV Cardizem the oral will be good for you and you are being treated by knowledgable experts of cardiology and I trust your care with their prescribed interventions for you.” Here is the problem. IMD does not load the patient with IV digoxin. The  pre=”The “>cardizem drip has been off for a while, then BAMM right back to Atrial fibrillation with a rapid ventricular response. Here we go…this is where it gets fun. RN calls Cardio right? Tells the Cardio MD:  uhhhggggg. I have to tell you that patient so and so of IMD that you are the cardio consulting specialist is back in rapid a fib….and….IMD discontinued the oral cardizem after you left today, started the patient on oral digoxin, the patient has gotten one dose. The patient is symptomatic, uncontrolled and now hypotensive and from shift report the nurses tell me that this is the third time this week for this same patient. RN says: what do you want me to give this patient to control this rate? Cardio MD says: I want this patient on Cardizem. UGHHHHHHHHHHHH! Cardio MD says: “call IMD and ask why he keeps discontinuing the cardizem or ask him why he consulted cardiology in the first place.”

 He then says, “Ask him if a cardiology consult just looks good on paper even though you rescind the prescribed intervention?”

NO. I am not getting in the middle of this. I am tired of it! (this is one example of a few just from lately from these doctors)

See in my humble nurse opinion:

3 times cardizem IV went up on the patient. The cardiology knew that IMD kept discontinuing the oral cardizem at the request of the patient who is not mentally intact by the way. IMD kept ordering digoxin orally. They both see this and know what is going on. They are both taking a stand against each other but no one is managing the patient. The IMD could of let the cardiologist manage this, the IMD could have called the cardiologist and said, “the patient does not like the cardizem, is there an alternative solution? (of course there is). The cardiologist could have seen that the IMD kept prescribing digoxin and could have written orders to load the patient with IV digoxin and maybe some atenolol on the side to go with it, but hey: I am just a sort of new nurse that notices the trends in what medications control heart rates. And guess what else the IMD did? Discontinued the IV antibiotics after four doses and 2 days later the patient is febrile probably exacerbating this fast heart rate even more. (RN cries for help) Why?

Can anyone believe this?

It is not all internal medicine MDs, just a few and they are only doing this to this one cardiology group (not to any of the other cardiology groups.) So I do not know what their problems are (well yeah I know) but it does not matter! My patients need better management and I am begging for it, stuck in the middle crying. I understand cardiology making their statement: “If you want us to manage on consult: LET us do our job.” I sort of understand the Internal Meds: but not when it gets this far out of hand and not when your patient comes in with a UTI and only 4 low doses of antibiotics are given, and the patient is febrile, with mental decline and hypotensive, and I ASK for orders for antibiotics and IV fluids and you tell me no AND the patient is in uncontrolled atrial fibrillation and you tell me let us just monitor the patient. Uh no no. Sorry. Not me today. I will get the Cardizem bolus and drip up per cardiology AND some IV fluids for hypotension  per cardiology AND I will not tell you that I am at this moment: Getting blood cultures times two, a urine sample (that we already know is positive!) a CBC, Chemistry, Lactate level, and coags!

And guess what! 2 hours later I call you with these results and interventions: Your patient has a lactate level >4, is hypotensive getting normal saline per the cardiologist, the heart rate rhythm is still uncontrolled (although a bit better thanx to cardio), the white blood cell count has doubled since yesterday! Your patient is febrile refusing tylenol because he thinks we are trying to slip him a cardizem pill (did someone tell this patient not to take oral cardizem or what?) and anyway the patient is probably to lethargic to take pills now,  AND the house physician has transferred the patient to the intensive care unit  AND would you like to consult a critical care MD for ICU management or are you coming in to see the patient?

Anyone out there understand  or relate ? because I am just shocked by this childish mis-managed behaviour. We are health care providers, not big egos waiting to be stroked! (or what ever the heck the problem is)

*Disclaimer: I feel better getting this off my mind but if any patients or future patients are reading this please note that this is not normal, not the usual, and not all MDs no matter what specialty.