Catticus11

I'm a critical care nurse at this time, with a total of 3 years of bedside experience. My boyfriend and I want to take a roadtrip around the country. Maybe spending a week or two in different cities. We don't plan to take this trip for a year, so I have time to save. However, would also like to have some source of income while traveling as well. I like the idea of something that just requires me to need a phone and laptop, but I don't want to be required to stay by a laptop from 9-5 everyday considering that I do want to explore the sights on days other than the weekend. So I know this is incredibly specific, but i just want to know if there any options out there. Regardless of via distance-working or actual patient care.

No, he originally came in c/o dizziness, so he went to a cardiac telemetry unit where he fell and hit his head. He was transferred to CCU after that, where he began to become Apneic and developed a respiratory acidosis per ABG, so he was intubated. There was a question of ETOH use prior.

I responded to a code blue, MD was already at the bedside because he was responding for new symptomatic hypotension. Patient was admitted two days prior for NSTEMI, and there was plan for cardiac catherization but Cr was elevated so plan to cath when creatinine stabilzed. EKG was performed immediately prior to code which revealed a failure to sense from patient's PPM. Whenever we did a rhythm check, the rhythm was difficult to discern while the PPM was also firing irregularly. It looked like VT for a brief second, and then I would see a spike and then an irregular non-organized rhythm, and then a spike. Pulse was noted once, before it could no longer be palpated. Should I have placed a magnet over his pacemaker? Is there an indication for a magnet during a code?

I'm sorry, I forgot to include that his EF per the cath was 50%. Per the CXR the IABP looked like it was in the right place. But waveform could also be affected by inappropriate position? When I put it in a 1:2 it did change, his unassissted pressures were higher 170s, compared to assissted which was 150s-160s. But I assumed that was a normal response.

Hi! I love that an RT is on here. So yeah, when I was speaking with the cardiologist I asked the same thing, and he said his concern was from the fact that he has no history of COPD and that though compensated his CO2 was too high to just leave as is. He also assumed his sorta drowsiness was affecting his ability to blow it off and that's why needed to compensate. And I'm guessing his elevated CO2 was also contributing to the pulm htn/diastolic heart failure. But that lost part is just my conjecture based on what everyone has said so for.

Yay, I'm so glad! You're always learning in this field, and this website's a great resource for new nurses like myself to discuss things with the more experienced RN, NPs, etc. Best of luck! :)

Patient was admitted to cardiac telemetry unit s/p cardiac cath, 1 DES was placed and apparently she was Effient loaded in CCL, and on Plavix cath lab. No baseline CBC or BMP collected per the records, but a recent previous admission showed a Hgb was 9.4. She was on the floor, complained of some dizziness upon standing. VSS were stable on 2 L, but did c/o some SOB with exertion. She then had a small dark formed stool. Overnight covering cardiologist was made aware who ordered a CBC and Hgb/Hct was 5.9/19.1. He ordered for a 2 units of PRBCs and a move to CCU. I called the cardiologist to clarify whether the patient truly required a move, and he said that she symptomatic with the dyspnea and could crash at any moment, especially she's both on Effient and Plavix. When I asked what GI had said, they said they weren't going to scope her since she just had a cardiac cath. Patient arrived on a protonix gtt, and but we couldn't get a second IV access so called the MD for a central line. He instead just changed the Protonix gtt to IVP so we can use her current IV access for the blood. She had one small bowel black bowel movement since arrival to the unit. HR, BP, O2 all stable on 2 L of O2. I don't know, does anyone have any experience with a GIB following a cath? My charge RN didn't feel it was appropriate since the patient was stable with the exception of dyspnea on exertion, and we weren't going to do anything emergent asides from give blood, which they could do on the cardiac telemetry floor.

Thank you so much for the response. Would I treat seizures vs. diprivan induced myoclonus the same?

Thank you so much for your response! So a low diastolic pressure would merit the balloon pump sheerly for coronary perfusion? Is there a particular DBP value that they decide for that? Does the type and grade of lesion have anything to do for an IABP indication? I thought it was because he was a 95% left main. Otherwise, I don't believe he was experiencing chest pain when he went into the cath lab (I could be wrong), and he was having issues with hypertension since arrivng from the cath lab for which I was told in report they initiated Nitro for. He also did start experiencing chest pain the day and night after I had him, requiring titration of nitro and IVP morphine with complete relief.

So an equal assisted and unassisted diastolic is an indicator of poor offloading, in the setting of hypertension? Also, no I haven't tried manually timing. It was briefly reviewed to me by an older nurse (who also probably learned it in 1983 lol) but the waveforms appeared to be augmenting appropriately. I'm just still pretty new with balloon pumps maybe.

So I had a patient who was awaiting CABG after an outpatient cath revealed 95% Left main lesions, 90% RCA, and 60% LAD. He was on a Nitroglcyerin gtt and IABP. He started to complaining of chest pain and it revealed 0.7mm ST depression in lateral leads, and we adjusted the nitro and gave morphine with the MD at bedside. Then a couple hours later, the patient began to c/o chest pain again, we did a repeat EKG, let the MD know who came to the bedside. The EKG showed 0.7mm ST depression in the lateral leads, however the MD stated that it actually looked much worse then the previous EKG because the ST depression on the second EKG appeared slight coved compared to the ST depression on the first EKG which was straight, though both ST segments didn't deviate from a consistent 0.7mm depression. The patient's pain was resolved with the Morphine and Nitroglycerin titration, so no further intervention was taken. I just wanted to know if a coved ST-depression is in fact a negative sign, and if so, if there's any literature I can review to better understand it.

I had an IABP the other night on a patient awaiting CABG. 3VD, significant RCA and LMain involvement. The patient was slightly hypertensive on the IABP, he normally is on Lisinopril but they discontinued it prior to surgery. His pressures ranged from 110s-160s systolically on the IABP. Unassisted pressures ranged from 140s-170s. I had nitroglycerin up, which I was titrating as needed and he was bradycardic. We eventually gave IVP Hydralazine which brought his pressure down for a few hours. My arterial waveform was weird though, and I just wanted to know if it was because of the hypertension. My augmentation pressures were equal or less than my unassisted systolic pressures. And my diastolic unassisted and assisted were equal.

So I've had patients who have CHF and receive weekly Milrinone infusions. I've also had patients who are awaiting Heart Transplants but weren't on any inotrope, but did have lower-ish BP. I've had patients with new cardiogenic shock who were placed on an Impella with no inotrope. While I've had patients in a new acute cardiogenic shock with an IABP but on Dobutamine. So yeah, I'm having trouble understanding the key take-aways for inotrope use. I understand the desire to avoid increasing myocardial oxygen demand that goes with inotrope use, but I'm having a bad time understanding why they are used and why they're not. Sorry if this a dumb question!

Perfect, thank you so much!!

When I asked the nurse about the BP following Bipap placement, she said the BP remained normal. I don't think she was measuring the BP more frequently than q30min at the time, so I'm not sure how fast the BP dropped. So when the BP decreased, I should have asked to hold the Bumex gtt temporarily, and initiated vasopressin. That makes sense since he wasn't in much respiratory distress. I completely understand the thought behind the vasopressin, but would that cause any issues with the need to diurese him? Or would you say he was overdiuresed considering his BP dropped? Also, would the PaCO2 have the same effect (i.e. pulm HTN) considering that the HCO3 had compensated? Lastly, can you elaboate on "vasopressin to give a more pure systemic squeeze"...just so I can better understand the concept more.

Oh whoops, sorry about that typo. Thanks for the response!

I had a patient who needed bipap for an elevated pCO2 in the 80s but compensated. He was on a Bumex gtt for an elevated BNP, and CXR which showed bilateral pleurel effusions. Patient had history of diastolic CHF. Per the H&P, no history of COPD. Patient was transferred to the unit for possible precedex because he was agitated on the floor. No agitation witnessed by me upon initial assessment. We obtained an ABG, which showed compensated respiratory acidosis, pCO2 in 86. We started Bipap and he tolerated it fine, I believe the settings were (20/5). Bumex gtt still going with adequate urine output. BP was still stable after hte initial Bipap placement, no significant changes. BP dropped to 70s/50s. So the RN initiated a Neo gtt. I reviewed the patient's record, and he had a TEE that day or the previous day that showed severe pulmonary HTN. Could I have adjusted the Bipap settings somehow, or was pressors the most appropriate way to address the hypotension?

I had a patient who congenital LQT and was going into recurrent torsades. She initially on Amiodarone but was changed to Lidocaine after the cardiologist realized it was congenital. She had a temporary wire placed for overdriving pacing. She was on Lidocaine for several days before starting Mexilitine, and had a PPM placed. So yeah. This was my first Lidocaine gtt. I was told during report that she was "weird," and when I went into assess her, "weird" She was. She was forgetful, had hallucinations, but easily reoriented. Her Lithium level that was 7. One of the cardiologists was talking by, and I just casually asked him, "Hey, so is this normal to leave as is?" His words, "Well check it again tomorrow" I was kinda left hanging there.

St. Peter's Hospital in Albany, NY has a Critical Care Orientation Program that uses AACN ECCO model. You have the option of the Emergency Department, Medical ICU, Cardiac ICU, or CVICU.

I started in my hospital's critical care orientation with a bunch of CVICU nurses. They all had at least a couple years of experience, and came from either the OR, PACU, or cardiac telemetry floors. I was offered a position in our CVICU when I applied to the critical care program, and I had 2 years of cardiac tele experience--I ended up going to our CCU though. I do however know of a nurse who started in another hospital's CVICU right out of nursing school. Guess it depends on the hospital. The Cardiac telemetry experience provided a nice broad cardiovascular background before I started though.

I just recently went through the AACN ECCO program through my hospital; something that took me off guard was (either the program or my instructor) saying that it was unnecessary to let a provider know if a Troponin is elevated if the previous was one also elevated, regardless of whether or not it was trending up. The rationale was that the only diagnostic value was whether or not it was positive, not whether it was trending. Now, this is not taking into consideration other clinical signs or symptoms (c/o chest pain, hypotension, EKG changes, etc.) I was wondering about anyone else's take on that.

Thank you so much for explaining it so well! :)

Can you elaborate? I'm not familiar with the concept.

Just to clarify, are the numbers on the IABP machine reading the artifically high DBP as the SBP? And the artificially low SBP as the diastolic?

My charge nurse stated in passing, "during a code Epinephrine does nothing but vasoconstrict the coronary arteries, thus making compressions more effective." My mind was blown! And then after my mind put itself back together again, I realized that didn't sound right, and I didn't understand lol. Can someone help elaborate on that comment, and just give me a refresher on epi altogether if need be lol.