Frank Starling’s Curve

OK, it’s not actually Frank Starling’s curve, it’s the Frank-Starling curve, named for Otto Frank and Ernst Starling. But for some reason, a lot of people refer to it as if it is named for some guy named Frank Starling. It’s a pedantic pet peeve of mine. But, I digress…

The Frank-Starling Curve, often referred to just as the Starling Curve is a super-duper important (of you’ll forgive the technical jargon) concept in cardiac physiology. Understanding it is key to resuscitation of critically ill patients. Fortunately, Rishi Kumar does a great job of explaining it.

Vasopressor Receptors

Different vasopressors have different functions and these functions dictate why we choose certain pressors at certain times. We’re all familiar (hopefully) with the fact that epinephrine is a positive inotrope as well as a vasopressor while phenylephrine is pure vasoconstrictor. This is why we choose epi over phenylephrine when we need inotropy and why phenylephrine will actually make hypotension secondary to cardiogenic shock worse.

These differences in function are dictated by the different receptors on which the pressor drugs act. In addition to different functions, some vasopressors with the same general effect (vasoconstriction) act on different targets (catecholamine vs non-catecholamine) and so can have a synergistic effect. Adding vasopressin to norepinephrine for a patient in septic shock, for example, can help even beyond the fact that norepi is at its limit. This is why adding vasopressin before maxing out norepi is often beneficial. Additionally, vasopressin is less affected by blood pH, so it will work in patients with extreme acidosis where norepi will not.

Eddy Joe Gutierrez has a great Instagram post on this with a nice slide showing how the different pressors work.

Calcium in MTP

Transfusing a lot of blood presents a lot of problems (not the least of which being that the patient needs a lot of blood to begin with!). Chief among those is likely the coagulopathy that results from a depletion of coagulation factors due to losing whole blood (PRBCs, plasma, and platelets) but only getting PRBCs back. Massive transfusion protocols (MTP) helps to address this by transfusing additional products in some sort of “proper” ratio (what that ratio IS is up for debate), but even if you transfuse PRBCs, FFP, and platelets in proper balance, you can still run into another life threatening complication. And I’m not talking about TACO (although that certainly is a problem). It’s one that may not be as readily recognized or remembered, but one that can wreak havoc with your resuscitation. Hypocalcemia.

Banked blood contains citrate as a preservative for storage. Citrate binds calcium and renders it inactive. Giving lots of banked blood can result in hypocalcemia. Hypocalcemia can cause all sorts of problems including hypotension (probably ALREADY a problem in someone requiring MTP) and seizures.

Pharmbythegram has a really nice post summarizing the role of calcium administration during MTP. Hopefully, you’ll now always remember to give calcium along with PRBCs, FFP, and platelets.

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.

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?

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.

Lactic Acidosis

Every student learns the mnemonic “MUDPILES” for the diagnosis of anion gap metabolic acidosis (AGMA), but I think the one on that list that is the most misunderstood is lactic acidosis. In and of itself, “lactic acidosis” is more of a problem than a diagnosis. I’ve never yet had a patient who had spontaneous hyperlactatemia, yet we often want to just says that the patient has “lactic acidosis” and leave it at that.

When approaching the patient with an AGMA, if there is an elevated lactate, we can’t just jump to the conclusion that “lactic acidosis” is the cause, and even if it is, we need to dig in to determine WHY the lactate is elevated. and it turns out, that’s a complex question. There are a number of things than can cause an elevated serum lactate, it’s not just tissue ischemia, and despite the idea of “trending lactates” in sepsis, elevated lactate doesn’t always = sepsis.

Obiajulu Anozie (@icuexplained) has a great post over on Instagram that goes over the basics of classifying and further diagnosing a lactic acidosis. Once the cause has been identified, then you can get to work treating the cause, rather than just bolusing IVF until the “lactate clears.”

So, what’s the deal with therapeutic hypothermia?

Therapeutic hypothermia following cardiac arrest was a strategy to improve neurological outcomes first explored in 2002 following the publication of the publication of a trial by Bernard and colleagues in the NEJM. The theory was that metabolic demand slowed when the patient was placed in a hypothermic state. This would improve neurologic outcomes by reducing cerebral oxygen demand. It’s similar to the practice of cooling the patient during deep hypothermic circulatory arrest in the operating room for complex cardiac surgeries such as repair of the aortic arch.

The downside is, there are a number of major consequences and potential complications from hypothermia, as anyone who has treated environmental injuries associated with prolonged cold exposure can tell you. In the intervening 20 years since the initial Bernard study, a number of other studies have been published showing the benefit of cooling, but more than likely, no need for true hypothermia.

Bottom line, it seems that prevention of hyperthermia is probably just as beneficial and hypothermia, with far fewer deleterious effects. The University of Kentucky ICU Pharmacy recently did a great tweetorial summarizing the data surrounding hypothermia. Check it out for more details.

If You’re Going to Bolus Fluid…Bolus It!

A pet peeve of mine is when a fluid bolus is given, but it’s given over an extended period of time. There is a term for that, “maintenance fluid.” And maintenance fluid is not generally helpful at all, and it certainly isn’t helpful to the patient who needs a bolus. Dr Obiajulu Anozie has a great Instagram post detailing why this is and how to address fluid boluses in your patient. It should go without saying, make sure that your patient needs a fluid bolus first. But, then, if you’re going to give a bolus, give a bolus.