BelgianRN

What's wrong with speaking to the RN herself? Why run to management. If you felt the need to spy on her patient care at least have the courtesy to go head on with her as well. There is too little direct communication nowadays.

"PEP", so i figured hmmm profylaxis. Turns out it stands for "poepen en pech" which is Dutch for "unfortunate sex", the guy had an STD. Or when the patients talk too much some secretaries summ it up to "sick". Also had "ITP (no clue what this is...)". Or "secretive patient".

The GCS was designed with the mindset of neurotrauma evaluation. It gained popularity for other usages and pathologies. But i think the point is moot as to what their GCS is if you have signs he is oriented. You can't properly use the GCS to determine consciousness in patients with disabilities influencing your GCS and the GCS as such has no value in the evaluation of these patients. Also get in the habit of reporting GCSs by their individual components. In my documentation I'll report a GCS like: GCS(EMV): 11(3-5-3) or if tubed/trached GCS(EMV): 9 (3-5-T).

You can only hear audible arterial pulses when the bloodflow is somehow obstructed. There are multiple reasons: pressure from your stethoscope on a superficial artery, partially clogged artery, aneurysmatic deformation, AV-malofrmation to name a few.

For every ABC-unstable patient we go 1:1, means the other nurses go up at the same time taking over your load. Medsurg anywhere from 3:1 to 6:1 depending on available staff. Peds generally 3:1. Small surgical cases: task oriented nursing, everyone with available time pitches in, assessment/primary diagnostics ordered by the triage nurse or dedicated ER physician. In general our patient load is very variable throughout our shift since we are involved in prehospital care as well. So if all other nurses have to go out on prehospital assignments and/or in-hospital codes, the ER falls back on 1 - 2 nurses for everything and everyone. All remaining patients fall under the responsibility of the remaining nurse, including ABC-unstable ones that get dropped off in the mean time. Luckily we have pretty amazing ER docs that will do many of our tasks themselves if we are too busy.

I used to do this for years, but somehow felt unrewarding as some members in my family can be really ungrateful. But last year I decided to work Christmas, escape from my extensive family (the easy part as they live abroad) and spent my entire christmas bonus on myself and a few selected people. And you know what I loved it, doing it again this year!

The only issue that we keep having with our new people is simple chemistry problems. Like you can't infuse potassiumphosphate and magnesiumsulphate together since it forms the insoluble magnesiumphosphate and things like sodiumbicarbonate and calciumchloride. It's easily overlooked when someone (esp. inexperienced residents) wants to supplement several electrolytes and is inexperienced with the solubility of different salts.

It is possible to have two ventricular spikes if your pacemaker activates the two ventricles separately and out of sync to some degree.

Indeed, an atrial ECG requires atrial pacing wires. The policy in my hospital is that we connect the extremity leads as they should and use V1 and V2 or V3 connected to both atrial wires. I generally use V3 if my complexes are too large and start overlapping with each other. The remaining precordial leads are not always connected. Just remember because your view point for the atrial leads is located in the atrium you'll probaly have large QRS-complexes but also very large P-waves that can easily be confused for QRS-complexes making atrial ECGs harder to interpret. I'm not sure which pacing ECGs you are taking. But when I have a temporary pacemaker (and I know there is an organized perfusing rhythm underneath) I disconnect the pacing wires from the external pacemaker unit and take an ECG without pacing spikes. I don't use the pause button because our pacemaker units just don't pause long enough to complete an entire ECG without pacing spikes and i'll end up with pacing spikes at the very end of my ECG. When we take ECGs on people with internal pacemakers we generally first take an ECG in the resting state (e.g. if the pacemaker is pacing we'll take an ECG of that if it isn't pacing we take one of that). Then the pacemaker technician will either mandate the pacemaker to start pacing or switch off so we can redo the ECGs and compare them. It gives great signs of failure to capture etc. But this takes coordination with a pacemaker technician and is not always needed for every pacemaker patient. Just remember when people have been paced for a while your unpaced ECG might still show abnormalities in repolarisation (e.g. altered T-waves) and can have ventricular conduction abnormalities just because the heart's own conduction system has been bypassed for so long by the pacemaker function.

Standard Practice in our ICUs is when spiking a temperature we draw at least one blood culture peripherally (or

It is a very common combination for our severe heart failure patients. Both drugs have a different pathway to stimulate the inotropy of the heart. Dobutamine works via your beta receptors stimulating the enzyme adenylate cyclase to promote formation of cAMP from ATP where cAMP will increase the intracellular calcium concentration that leads to inreased contractility. Milrinone is an PDE3-I (phosphodiesterase inhibitor class 3) that will inhibit the enzym phosphodiesterase so it no longer breaks down cAMP and as a result contractility increases. So both drugs can work synergistically. In my experience milrinone will cause more afterload reduction as compared to dobutamine therefore hypotension is more of an issue. At the same time milrinone is less proaritmogenic than dobutamine. And milrinone will have a more profound effect in decreasing pulmonary hypertension as compared to dobutamine. So usually the last two effects are what prompts preference for adding milrinone as opposed to increasing the dosage of dobutamine.

The thing that came to mind is that half sensitivity refers to 5 mm/1 mV instead of the standard 10 mm/1 mV. You'd change this value in the light of left ventricular hypertrophy or conduction abnormalities that cross into your other leads obscuring the view of those leads. This is generally most prominent in the precordial leads. If I translate roughly from Dutch we'd call it "half calibration" or "half gain".

As other posters have said preoxygenation is helpful. But you could see if you have orders to give a bolus of a sedative for an already intubated patient. This will decrease the oxygen consumption by avoiding anxiety altogether an also prevents excessive moving/struggling from the patient while turning him/her which in turn will help with minimizing oxygen consumption. I'd like to stress too that it's important to check all connections in your ventilatory circuit before turning a patient where derecruitment is a potential problem (e.g. ARDS) to prevent even greater desaturation when performing a manoeuver.

I remember a few years ago a colleague called around 22 pm she wouldn't be in for the nightshifft. She came home found her husband drowned in the tub together with her 1 year old. As she called us the EMTs were still coding her child. I'm still amazed she called in at that time. Long story short I stayed for her nightshift. Even though I had morning shift the day after, we decided the morning shift would do with one person less. I got chewed out by my manager even before asking how our colleague and her child were doing. Some people have just lost all compassion.

The thing that has bothered me with the OP's post is the first line where he/she mentions "turned in". It sounds so malignant. You don't turn your colleagues in via a report ever, you just report an error and preferably a solution to prevent it as well. I have the same problem with "writing someone up". Why not just report the situation and leave identification, naming, judging, branding and execution to management (they get payed more and some are great at executions). We have to work with most of our coworkers in the same space for hours at a time. In emergencies we have to rely on each other completely. How can you trust each other if you start turning people in and writing them up. I'm not saying you have to accept substandard performance from your colleagues but at least don't hand your colleagues over to the firing squad wrapped in a purple ribbon.

Bi-level is the competitor's name (I believe Maquet/Siemens) for Bipap from Evita

Hey, I'll give it a shot. CPAP is just continuous positive airway pressure. This means that the patients get a set amount of pressure (e.g. 5 cmH2O) applied to either his ETT or via mask. This 5 cm H2O gets applied regardless of inspiratory/expiratory efforts of the patient. There will always be 5 cm H2O applied. Conform the "rules" we speak of PEEP instead of CPAP when the patient has an ETT, and I will refer to PEEP after this. For this mode to work you need a conscious patient breathing in and out. CPAP or just giving PEEP is mostly used in non-invasive ventilation where your patient has impaired oxygenation but can ventilate on it's own. A prime example would be someone in cardiogenic pulmonary edema. It will augment your patients oxygenation by keeping alveoli from collapsing and at the same time forcing some of the pulmonary edema back into the interstitium and keeping the edema localized. These patients have only a moderate alleviation of their work of breathing, but if you can get rid of the edema quickly enough your patient won't have to be intubated. Pressure support is a mode where there is also a PEEP level set but the ventilator will deliver a preset pressure on top of this PEEP when it detects inspiratory efforts from the patient. This means for this mode you need to set at least two parameters (your PEEP and your pressure support level). And for it to work you need a breathing patient (so not heavily sedated). Pressure control is used in the weaning phase of your patient where he does a lot of work himself to prepare him for the big bad world of breathing unassisted without a tube. It's also used during non-invasive ventilation when the problem is mostly respiratory failure due to muscle fatigue, loss of functional alveoli. Prime example is a COPD exacerbation that you want to keep from getting intubated (non-invasive) because part of their work of breathing comes from the added pressure support their muscles can rest a bit and recover for later when you DC the non invasive ventilation. Or the recovering patient that you are preparing to extubate (invasive). Bipap stands for Biphasic positive airway pressure. When starting out I generally tell our newer colleagues to think of it as pressure control, but that's not completely right. I'll explain Bipap after explaining pressure control. Pressure control is a mode where you apply a PEEP and an inspiratory pressure. The difference with pressure support is that you also add settings that determine when your patient will breathe in and out (e.g. frequency, I:E-ratio, etc.). Benefit of this mode is your patient has to do even less/no work breathing on their own and you can be sure that the machine will deliver its pressures when you want them to be delivered. Down side is your patient either needs to be sedated very well to allow the machine to determine when to breathe in/out or the patient's own breathing pattern will conflict with your predetermined settings and the patient will possibly fight against the machine. An example would be your pneumonia patient that you intubated and you want to have him "rest" for a day (or two) as the antibiotics work their magic (you don't want to rest too long for fear of muscle wasting). Most modern ventilators combine some form of pressure support and pressure control together so your patients gets X times per minute their pressure control mode but they can also trigger their own breathing that gets supported via pressure support in between. This leads to less fighting and discomfort for our patients, but can tire them out as well. I wish I could give you the terms but all different ventilator brands seem to have come up with even more creative names of naming all their modes. I'm assuming you are using the Evita ventilator series. So Bipap in their system comes as either Bipap or Bipap/ASB. Bipap is a "pressure control like ventilation" but instead of just delivering the pressure you set X times per minute it will allow a patient to breathe in/out on it's own (unassisted) on top of this inspiratory pressure level but also during the expiratory phase when there is just PEEP applied. So the idea is your patient fights less against the machine and will have less muscle wasting because he/she keeps using their breathing muscles. Bipap/ASB is the same as Bipap but it will allow a pressure support (called ASB on an Evita) to be set as well. So when the ventilator detects inspiratory efforts from the patient it will give the ASB level of support instead of the inspiratory pressure you set for the pressure control part of the ventilator. During the expiratory phase when it gives its PEEP a spontaneous breathing attempt from the patient will also give them the ASB/pressure support level you set. So Bipap has more diversity to it than simple pressure control. And you have different options. If you heavily sedate your patient that doesn't have their own breathing attempts your bipap becomes pressure control (you set PEEP, inspiratory pressure and frequency, and some other shizzle...). Since there are no attempts at breathing from the patient. It's pressure control. If there is breathing but limited (and you didnt set an ASB/pressure support level) it will allow your patient to breathe in/out and regardless of this the machine will deliver its inspiratory pressure at X times per minute. If the patient is breathing a lot (and you did set an ASB/pressure support) your patient will fall into a pressure support mode of ventilation doing more work themselves. I hope this clears it up a bit. I can go on and on about vents but I'll keep it at that for now.

As a general rule you don't want to convert such a slow Afib you run the risk of going into cardiac arrest. As a PP stated such a slow Afib is usually secondary to excessive rate control (e.g. digoxin toxicity, beta blocker effect). It can also be due to a conduction abnormality (e.g. Afib with third degree AV block and an escape rhytm). In both circumstances you don't want to give any medication that decreases the ventricular response rate and run the risk of ending up with nothing left :) On top of that when treating an Afib you have to consider the benefit of converting. Comparing a slow Afib in the 40s - 50s to a sinus rhythm in the 40s-50s has very minimal differences in terms of hemodynamic consequences. At such a slow ventricular rate the ventricles have plenty of time to fill up already and the atrial kick from the sinus rhythm will add little or nothing of value to the filling of the ventricles.

What we sometimes do with VIPs or spectacular conditions/situations. Whenever someone calls claiming to be wife/husband/son/daughter we call them back on the listed telephone number in our PDMS to make sure it is indeed the person calling who they claim they are. As to what to tell them it's always difficult. I try to keep it simple and brief whenever talking to family. But some of my colleagues love going over every single lab, vent setting and monitor value. It usually turns contact with the family into a spanish inquisition and I'm the monster when I tell them that under corticosteroids you can't really rely on white blood cells and lab tests to rule out/in infection.

You have caths measuring it but if I don't have them in my patient I'll just draw blood from a central line or Swan Ganz and determine the SO2 myself via our blood gas analyzer.

I think your preceptor was indicating the oxygen hemoglobin dissociation curve. It's true that acidosis causes the curve to shift to the right thereby decreassing the "bond" between oxygen and the heme group in hemoglobin. In the lungs this isn't a real issue because you have ample time to saturate your hemoglobin fully in general terms. But on the tissue level this causes oxygen to come loose from the heme group much easier then in normo-pH states. The rational behind this is that acidosis caused by tissue hypoxia is a condition quickly leading to death so the body "designed" a mechanism to counter this. This wouldn't cause much of a change in paO2/saO2 due to the fact that in the arterial blood you are on the flat part of the curve. But in the tissues where the oxygen is used up you'll have noticably higher values for pO2 for a certain saturation level due to being on the steep part of the curve. And dissolved oxygen (pO2) is available for diffusion into the tissues/cells, where "bound" hemoglobin is not. There are certain other situations that cause right shift of this curve. And I love Wikipedia® for their "CADET, face right" indicating that increased CO2, Acidosis, 2,3-DPG, Exercise and increased Temperature cause right shift of the curve. I agree with with NBB2013 that failure of your proteins (read everything functional in your body) is a much more likely cause of death. Everything just stops functioning properly the more your pH deviates from 7,40 (wether it is up or down). Think about things like DIC, membrane destabilization, failure of your immune system that can be caused by pH abnormalities and you have your causes of death. And OP I like to stress the benefit of central venous/mixed venous blood gasses as well. An ABG shows you how well the lungs are capable of taking up oxygen and getting it into the arterial system. PaO2/SaO2 is basically what you are getting into the body, where I like to keep in mind that your hemoglobin carries your oxygen so saturation is much more indicative of the amount of oxygen available than paO2 is. For tissue hypoxia to be causing a drop in paO2/saO2 it would require such an depletion of oxygen in your tissues that your lungs don't have the diffusion capacity anymore to fill up nearly all your hemoglobin molecules with oxygen. Knowing that our body has about a 3 - 4 fold reserve capacity for diffusion capacity (in healthy lungs) you are looking at a (nearly) dead patient before you will see tissue hypoxia causing a normal paO2/SaO2 to drop. Central venous blood gasses or mixed venous blood gasses give you much more information. The blood collecting in your superior vena cava/right atrium is coming from the body (for the most part) if you determine the ScvO2 on that blood you can see exactly what's left over in terms of oxygen after it has been used by the body as a whole. Normally about 25% of our oxygen gets depleted so normal values are around 75%ish. Either it comes back as too high then there is decreased uptake due to decreased metabolism (usually not a problem), increased supply (hyperdynamic states) or due to a failure of oxygen to get into the tissues (problem, you will see other signs of tissue hypoxia like increased lactate levels). Or it comes back as way too low (much more common) which means the tissues take up more oxygen then usual. Increased metabolism (can be a problem especially when there isn't a lot of oxygen to begin with like ARDS patients breathing on their own), decreased supply (hydodynamic or hypovolemic or hypoxemic). Mixed venous gives you about the same information but in the mixed venous blood from the pulmonary artery there is also a big factor of venous blood coming from the heart itself. Keep in mind that venous blood is a pooling from all the tissues and it is entirely possible to miss signs of localized tissue hypoxia if your other tissues are receiving enough oxygen.

Since the 1950s we've come a long way in terms of condom use, birth control and birth planning as well. In the majority of cases having a child is a well balanced choice more than an accidental occurance or a consequence from lack of preventative measure. So I personally think that being pregnant and having a professional carreer can be combined but you need to plan this accordingly. Same way I fel that people shouldn't be having babies if you are not capable of caring for them emotionally, physically or financially. I come from a country where pregnant women are basically off for months. Since I have no kids nor do I ever intend to have them I never really bothered looking up the exact rules surrounding pregnancy. So as I read this thread I delved into the rules and regulations and will give you two examples in the end. We have different leaves for pregnant/delivered women: Maternity leave: 15 weeks (minimum of 9 weeks postnatal) - Standard for everyone. +4 weeks - For having more than one baby at a time. +1 week - For being unable to work during your pregnancy due to medical reasons. up to +24 weeks - For having medical issues with the baby that requires hospital/LTC admission. [*]Lactation leave: Up to the 5th month after the birth of the baby - If you are actively lactating (roughly 8 weeks added on top of the maternity leave). Only for professions with a medical risk factor like nursing. [*]Parenting leave: 17 weeks for a fulltime employee. You can take these 17 week all at once or spread them so you can work less every week. Is valid up to the point where your children's age is 12. counts per child, so duplicates in twins. [*]Medical Reasons The entire pregnancy duration one can be absent due to medical reasons. Up to a maximum of say 32 weeks. So for a regular mother they are gone for: 15 + 8 + 17 weeks = 30 weeks. For a twin bearing mom with medical issues prenatally from her 10th week of pregnancy with difficult twins in a NICU for 25 weeks this comes down to: 26 (prenatal) + 9 (standard postnatal) + 4 (for twins) + 1 (absent prenatal) + 24 (NICU issues) + 17 (twin #1) + 17 (twin #2) = 98 weeks. That's 1 year 10 months and a bit. I'm not talking about the financing of all this leave because that's not just the employer. But if I was to hire someone that's pregnant I'm looking for a potential gap of anywhere between 30 and 98 weeks that I need to fill up. I wouldn't hire either if i had a ton of non pregnant people to choose from. Probably if I was an employer I'd just hire men. Preferably men that sign a document they'll never adopt, get someone pregnant, fall sick, or hurt themselves while sporting ^^. While I hear from a lot of women that pregnancy and having children is wonderful, which is probably true. I do think there are quite a few women out there that plan their pregnancies very cunningly to coincide with being off all the nice periods and getting most benefit from all the different regulations surrounding pregnant women in my country. And I admit so far I haven't had one pregnant colleague that didn't exploit their pregnancy to get out of less popular tasks and assignments, so I'm very biassed. I'd like to stress I'm not against pregnancy but I consider it a choice more than a given these days. Do I try to keep pregnancy in mind when handing out work assignments? I certainly do by not giving them isolated patients with e.g. CMV. But I won't give them the patients closest to the nursing desk so they can take breaks in between of walking, or giving patients that are light as a feather all the time.

Working a general ICU in my hospital we frequently encounter this problem. Without knowing about your specific institution I can only comment on mine. For an empty bed in my ICU there are usually anywhere between 2 and 5 candidates waiting to be admitted. The problem for me isn't that they're on the floor receiving high flow oxygen. If the medical situation is under control and the patient is aggressively managed more often than not their oxygen demand will go down in the next 24 to 48 hours. E.g. if proper ABX has been started and inflammatory parameters are going down it is reasonable to expect that their pneumonia they came in with is resolving and their lungs will start improving. If they respond well to their diuretics the excessive fluid in the lungs will resolve as well. Etc. The problem is usually getting the floor MDs (in my hospial anyway) motivated to start aggressive management on these patients. Often there is a very expectant attitude towards these types of patients and they fail to improve in a proper timeframe and they end up in the ICU with MODS needing to be intubated basically because the patient used up all their reserves in the previous days with MDs considering 20 mg of furosemide aggressive diuretic therapy or thinking amoxicillin will cure anything! I agree completely with you if their oxygen demand doesn't go down and they remain with low sats for multiple days they need to be transferred to ICU and a place has to be created for these patients, room or not. That's generally when us poor general ICU's look angry towards our mixed trauma ICU/PICU or CTICU to get off their asses and admit the plebs patients as well. Or alternativey we start using our PACU as an overnight sleepover party for the more stable ICU patients awaiting discharge in the morning. It is true that oxygen has many toxic side effects. But these effects will just be as bad on the floor as in ICU. Only difference is that ICU has a few tricks up their sleeve to avoid giving this much oxygen and have ways of creating some CPAP wiithout need for intubation thereby decreasing oxygen toxicity. I completely agree that if patient keeps on needing this much oxygen and the problem isn't correctable sometimes sedating them and tubing them is the approprate action because it dramatically decreases oxygen consumption. I recently wrote a review on current guidelines/insights concerning ARDS for my department. Sadly it's in Dutch so you probably wouldn't be any wiser if I posted the section on oxygen toxicity here. Tried looking for a handy article on Medscape about oxygen toxicity but couldn't find it. If your facility has UpToDate® try looking it up there it has some great info. I agree that oxygen is very toxic but there is not a lot we can do about that except making sure the cause of their need for supplemental oxygen is removed ASAP by aggressive management.

My pockets contain: Pens (2 - 4 diff colors, totally unneeded but looks nice all the colors in a row), penlight, permanent marker (mostly for marking syringes during codes, has been used on foreheads during mass cass incidents), white board marker (sick of always looking for that one and makes for a nice marker on the mirror/window during codes when we lack paper ^^; bit nasty when I mix the two markers up :-( ), loads of stopcaps, alcohol/chlorhexidine spray, trauma shears, scissors, kocher (not sure what the english term is for these), pedi reference guide, ER pocket book (has all the standing orders for when we go into prehospital care), badges, cell phone (for calculations/apps), proper tourniquet for IV placement, keys, cash, beeper (depending on assignment), department telephone (depending on assignment). Good thing our uniforms come with seven pockets.

RNerd81 what's the point in increasing renal perfusion if it doesn't stop the patient from going into renal failure or from dieing? Especially if you look at the safety of the drug you're using. In very select patients it could make the numbers of my fluid balance look better, but that's about all it does.