Author: Bryan Boling

I'm a critical care nurse practitioner and co-director of the Critical Care APP Fellowship Program at the University of Kentucky. I split my clinical time between the Neurocritical Care Service, the Surgical Critical Care Service, and the ECMO Service. I'm also an Adjunct Faculty Member in the Acute Care Nurse Practitioner Program at Georgetown University. I have a passion for education and #FOAM.

US Guided PIV

Thanks to Lakshman Swamy for the tip for this one! US guided peripheral IV placement is a game changer. If you’re not doing this, you should. In fact, a lot of the RNs in our hospital are trained to do this now as well! It certainly saves time and pain (for us and our patients) when it comes to placing PIVs. In many cases, this can seriously reduce the need for central access and/or PICC/midline catheters.

A lot of patients can get by with PIVs, but are “hard sticks,” keep blowing IVs, or need more reliable catheters for blood draws. Using US to place these allows for selection of better, deeper veins that aren’t readily visible to the eye or amenable to palpation. And, this is 100% within the scope of practice for RNs, so train the RNs in your ICU to do this as well (note, you may have to address some hospital policies first). I’ve found when I train new ICU NPs, those with experience placing PIVs with US often pick up arterial line, PICC/midline, and central line placement much faster.

Brown EM Blog has a great post offering tips for success in US PIV placement. Additionally, 5 Minute Sono has some great videos. And finally, a nice CME article on the process is available here.

POCUS Diagnosis of Aortic Dissection

Acute Aortic Dissection is a medical emergency and often a difficult diagnosis to make. The classic presentation is tearing, mid-scapular pain, but because the aorta runs the length of the thorax and abdomen, dissection can present in various ways. I learned POCUS diagnosis of dissection as part of the RUSH exam, but that specifically looks at the abdominal aorta.

Arthur Broadstock, an EM PGY-3 at University of Cincinnati presents a great case over at Taming the SRU and looks at identifying Type A dissections with bedside POCUS. His case focuses on using the PLAX view of the heart to evaluate the aortic root. The suprasternal view of the aortic arch can also be quite useful and it’s probably the most under-taught view of the heart in terms of bedside echo.

For more on how to use that view, and lot more detail on the diagnosis of aortic dissection (Types A and B), see this nice post on POCUS 101.

Cardiac Axis

Determining the cardiac axis from a ECG is an important skill. And it’s one that confused me initially when I first started reading ECGs. It is a topic that still confuses a lot of my students. But David Schaack has created a handy interactive tool to learn this skill. He and Mike Cadogan recently wrote a quick piece over at Life in the Fast Lane. It’s a neat little interactive tool where you can drag the axis around and watch the ECG change. It’s something I’m going to be sharing with my students next semester for sure.

Writing Notes

For better or for worse, a lot of our time in critical care in spent writing notes. in the US, these serve multiple purposes including communication, medico-legal documentation, and the basis for billing. But, I’ve found that the art of writing them is not really all that well taught. I can only speak of NP education first hand, first as a student and now as an educator, but anecdotally, I don’t think it’s much better in the MD/DO or PA worlds.

I was taught mostly by watching preceptors and reading their notes. That’s an OK strategy, except for 1) it places a lot of burden on the student to figure out why a note is good and how to adapt that to different situations, and 2) who’s to say that the preceptor is good at writing notes? I’ve had residents tell me before, “don’t worry about it. It doesn’t matter what you put in your note. No one really reads them.” But that’s wrong. On so many levels.

It does matter what your write (and how) and people do read your notes. for example, I read the notes of the people on my service who I’m following. I read the notes that consultants write, and I read the notes the primary service writes when I’m consulted on a patient. A well-written note is a great source of information and very helpful. A poorly written note can often me more of a hinderance than no note at all.

I’ve been wanting to write a Guide to Note Writing for a while, so I was really thrilled to see a great Twitter thread the other day from Robert Oubre covering this exact topic. I agree with everything he writes, so I’ll just let you read it for yourself. I will add this, your note is yours. There are right ways and wrong ways, but not one right way. The one constant I feel like I see (again, at least in NP education) is that people critiquing student notes often focus on the style points. The student doesn’t write the exact same way that they would. I’m always tempted to do this as well. I like the way I write and so I’d like if everyone else did the same. But, you’re a professional and should be able to find your own voice. But, this thread is gold.

Are Subclavian Lines Better than IJ Lines?

A friend of mine recently told me a story. He was told by someone that new best practice guidance was coming that the subclavian site is going to be the preferred site over the IJ. The reason for this is the decreased rate of infections at the subclavian site as compared to the IJ. I wasn’t able to verify this recommendation, but I can verify that subclavian lines have reduced rates of infection and clots. In a large, multi-center study in France, subclavian lines had a little fewer than half as many infections or clots (1.5 per 1000 catheter-days) as lines placed in the IJ (3.6 per 1000 catheter-days). And, IJ lines actually aren’t a lot better than femoral (4.6 per 1000 catheter-days). Additionally, you avoid several big problems (particularly in trauma and neuro patients) by not reducing venous drainage from the head or getting in the way of c-collars.

So, why don’t we all go for the subclavian as our first site of choice? Because we’re afraid of pneumothorax. That same French study found triple the rate of pneumothorax in subclavian lines (1.5%) as compared to IJ lines (0.5%). This is the reason we always hear for avoiding the subclavian site. But, I suspect that that pneumothorax rate is mostly related to technique. Whereas most IJ lines are placed with dynamic US guidance, most subclavian lines are placed using the old landmark technique. However, I had an attending teach me the US guided technique when I was a brand new NP and I regularly use it to place subclavian lines. Now, I still place far more IJ lines than subclavians, but I suspect that’s mostly habit.

It’s not a hard technique and I’ve had lots of success placing these lines with (so far, knock on wood) no pneumothoraces. How do you do it? Well, Josh Farkas over at PulmCrit has a great article detailing the use of US and the “shrug technique” for placing subclavian lines.

So, if the rate of infection and clots is so much lower (not to mention the other benefits) and we can reduce the rate of pneumothorax to an acceptable level, should subclavian be the site of choice? I mentioned that I wasn’t able to verify this rumor that the Best Practice guidelines were going to change, but, at least in Europe, there may be movement towards just that. The French Society of Intensive Care Medicine (SRLF), jointly with the French-Speaking Group of Paediatric Emergency Rooms and Intensive Care Units (GFRUP) and the French-Speaking Association of Paediatric Surgical Intensivists (ADARPEF) recently issued an expert consensus statement on management of intravascular catheters in the ICU. They make 2 interesting recommendations in this area: subclavian is the preferred site for central venous access, and IJ is probably not any better than femoral.

The American Society of Anesthesiologists, in Practice Guidelines for Central Venous Access 2020, cites the same data from the 2015 French study, but stops short of recommending subclavian over IJ, saying only, “in adults, select an upper body insertion site when possible to minimize the risk of infection.”

Where do you place your central lines? Do you use ultrasound? What are your thoughts on your current practice in light of this information?

Chest CT

I always have lots of students interested to learn to read radiology studies. In class, we typically only cover CXR. I occasionally do some special lectures on head CT, but it takes a lot of practice to really be able to read your own imaging studies. We don’t spend a whole lot of time in NP school teaching it. It’s something that is really better spent on the job. The fact is, with the exception of CXR, actually reading your own radiology studies is going to be highly dependent on the area in which you work.

But, I think it’s always good to be able to understand the basics. So, Dr Naveen Sharma (known on Instagram as theRadiologist) has some great posts to help. This is a really good one detailing the basic anatomy of the chest CT. Chest CT is a study that is used not infrequently in critical care, whether to evaluate for PE, look for pneumonia, or more advanced lung disease. So, check out this post with some really great teaching on the basics of reading chest CTs.

Bicarb in Metabolic Acidosis

The Resuscitationist has a great Instagram post about sodium bicarb in cardiac arrest, does it help or hurt? I’d expand this to just about any metabolic acidosis. IVP sodium bicarb used to be commonly given in these stations, especially during a cardiac arrest. It makes sense intuitively. Metabolic acidosis causes all sorts of cardiovascular problems including increased arrhythmias and poor contractility. Additionally, most vasopressors (vasopressin being the notable exception) won’t work in severe acidosis. So that just worsens things as the patient gets more hypotensive and you go up and up on the pressors to no effect.

So, it stands to reason that giving some bicarb would correct the acidosis (pH and HCO3 are inversely related in metabolic processes, after all) and fix all of our problems. So, why would you not want to give a couple of amps of bicarb?

Firstly, there isn’t any real evidence that it helps. Two studies mentioned in the IG post are pretty conflicting with one showing bicarbonate administration during cardiac arrest associated with earlier ROSC, but the other showing worse neurological outcomes. It may be beneficial in certain populations, including patients with severe metabolic acidosis and stage 2 or 3 AKI, some poisonings/overdoses (i.e. sodium channel blockers, TCA, salicylates, some toxic alcohols), and hyperkalemia (although a recent study question that as well).

So, there’s no real evidence it helps, but what’s the harm in trying? Well, firstly, I would argue that there’s always risk in medicine and so we shouldn’t be doing stuff “just because” if there is no evidence that it helps. But in the case of bicarb, it can actually hurt. Sodium bicarbonate (NaHCO3) gets metabolized and one of the byproducts is CO2. In a lot of cases, this isn’t really a big deal, but if your patient already has a respiratory acidosis (or is at risk for one), this is a really bad idea. It can also drop the ionized calcium, which again would be pretty bad in a critically ill patient.

So, no real evidence of benefit outside of certain situations. Possible harm. The better thing to do in most cases is to treat the cause of the metabolic acidosis. Having said that, I will sometimes give bicarb in a severe metabolic acidosis (pH < 7.2) in an unstable patient in order to buy some time. But, I’m cautious about it.

Resuscitate Before You Intubate

Critically ill patients will often “crump” following intubation. Why? There are various reasons, but probably the most common is that they are under-resuscitated to begin with. This is almost always in patients requiring emergent intubations. These patients are likely hemodynamically fragile and volume depleted. Intubation causes major hemodynamic changes, and it’s not all just because of the drugs we give. Normally, we breathe via negative pressure; the diaphragm moves down and decreases the intrathoracic pressure, sucking air into the lungs.

When we intubated a patient, we switch that over to a positive pressure process; the ventilator pushes air into the lungs. This increases the intrathoracic pressure, which, in a hypovolemic patient, can result in hemodynamic collapse. Add to that that we’ve paralyzed them and taken away their ability to respond to this sudden change (not to mention the potentially hypotensive effects of sedatives) and you can see why these people fall apart. But, it’s rarely sudden and usually totally predictable.

When time allows (and it almost always allows), resuscitate these patients before intubating them. But, don’t blindly flood people with fluid. A quick bedside echo can determine if they’re hypovolemic (and also evaluate their RV status, which is important before we intubate someone). In this great Instagram post, Obiajulu Anozie mentions using the Shock Index to evaluate patients as well. If you’re not familiar with the Shock Index, you just divide the heart rate by the SBP. A value ≥ 0.9 is indicative of need for further resuscitation. This is helpful if you find yourself without access to an ultrasound for some reason.

Spontaneous ICH

Spontaneous Intracranial Hemorrhage (ICH) is one of the more common things we see in the Neuro ICU. This is most commonly caused by hypertension, and so blood pressure management is usually a key part of ICU care in these patients. There is a fine line to walk between proper brain perfusion and increasing further bleeding. The other major pharmacological question involves reversal of oral anticoagulants that the patient may be taking. Although it’s not usually the cause of the bleed (again, hypertension, possibly in concern with anticoagulants is most likely; other causes include aneurysm rupture, vascular malformation, and malignancy), they can certainly exacerbate the bleeding.

@emergencymeded has a great post on Instagram covering the basics of pharmacological management of these patients. They point out that BP targets are controversial. I think controversial may be too strong, the guidelines generally recommend SBP < 140, but they do point out 2 large trials, INTERACT II and ATACH 2 both suggest that there is no increase in negative outcomes by allowing SBP up to 180. For management, labetalol and nicardipine are the mainstays of therapy. I generally start with 10-20mg labetalol IVP q1h PRN. If that is insufficient or if there are contraindications to beta blocker therapy, you can add 10-20mg hydralazine IVP q1h PRN (although this is rarely sufficient). If you’re still not able to get good control, or if you’re having to give lots of PRNs, a nicardipine gtt is the next best step. Although, be aware that due to it’s longer half-life, nicardipine isn’t really truly titratable. Once you get BP in range, it’s a good idea to back off a little on the dose to avoid overshooting. Clevidipine is probably a better option, but it’s pretty expensive so not as readily available. With a half-life of around 1 min, clevidipine is a truly titratable drug. Be aware that it is a lipid emulsion and can easily be confused with propofol in intubated patients.

When it comes to reversing oral anticoagulation drugs, the first question to ask is, “should we reverse?” Patients are on these drugs for a reason, after all. This is a decision that needs to be made after a careful risk:benefit assessment. In most cases though, you’ll end up reversing these drugs to prevent worsening of the bleed. There are 2 different strategies to reverse these drugs, targeted and non-targeted. Targeted involves giving an “antidote,” that is a specific reversal agent. Vitamin K for warfarin (although it doesn’t work fast enough and you’ll want to give FFP or 4-PCC as well), idarucizamab for dabigitran, and andexanet for the Xa inhibitors. Andexanet is not widely available due to cost and questions of efficacy. Non-targeted involves giving clotting factors that reverse all drugs. This is predominately 4-factor prothrombin complex concentrate (4-PCC) as FFP won’t reverse the Xa inhibitors and 4-PCC has been shown to do a better job of reversing warfarin than FFP. I’ll do a whole post soon on reversing anti-coagulation drugs.

Melatonin for the Prevention of ICU Delirium

Delirium is a common problem in the ICU. The reason is usually multi-modal, but sleep deprivation and alterations in the sleep-wake cycle are often a big part of it. so, if we ensure that patients get good sleep, that should prevent delirium, or at least SOME cases, right? to that end, we often will start patients who we deem at-risk for ICU delirium on melatonin in order to help them sleep and thereby prevent delirium. But does it actually work?

Pharmacy Joe looks at a recent study examining the efficacy of melatonin as a preventative strategy for ICU delirium and the results were not what I was hoping to see. The study was a multi-center RCT of around 800 patients in ICUs across Australia. Patients in the study group were all given 4mg of melatonin every night during their ICU stay. All patients were assessed twice daily using the CAM-ICU for delirium. There was no significant differences between the study group and the control group in terms of delirium.

One thing that isn’t clear is if 4mg might not be enough. Although I typically start with 3mg, I will often escalate it to 6mg pretty quickly if 3mg doesn’t seem to effective. I also typically don’t start melatonin until either the patient or the nurse complains of poor sleep. Further study is needed to determine if melatonin plays any role in delirium prevention.

For right now, it seems that the best strategy to prevent delirium (and we know that prevention is superior to treatment) is to focus on the nonpharmacological interventions. Maintaining a normal sleep-wake cycle is key. I encourage lights on during the day and having the TV on if there are no visitors to converse with the patient. It’s ok for patients to nap, but they shouldn’t be sleeping all day. If able, ambulation in the hallway or at least being up to the chair are beneficial as well.

Likewise, minimizing disturbances at night are important. Often patients are very ill and staff need to be in and out of the room frequently, but if possible, minimize these disturbances. Lights should be left off or low as much as possible. Don’t leave the TV on all night in the room. And, remember that sedation does not = sleep. I was a night shift ICU nurse for 10 years and often saw that the same care not to disturb day/night cycle was not observed in patients who were sedated.

The biggest pharmacological therapy you can do for prevention is to avoid the use of drugs known to cause or exacerbate delirium. The big offenders here are benzodiazepines. Benzo drips should almost never be used except in the case of status epilepticus. They were also found to be helpful in some cases of COVID back in 2020-2021 when nothing else would keep patients sedated, but they should be avoided in most cases.

The Critical Illness, Brain Dysfunction, and Survivorship (SIBS) Center has some great resources on delirium prevention and treatment.