podcast 2: how we care for each other

Hello there, Eve again. For my second podcast I decided to release a poem I wrote on the same theme, of caring for each other.

Resilience is now a buzzword in healthcare. It carries the idea of self-reliance on its shoulders, once again placing the full burden as a caregiver for others and a caregiver for self upon the person who is already carrying too much.

The song “Found / Tonight” with Ben Platt and Lin-Manuel Miranda: “Have you ever felt like you could disappear, like you could fall and no one would hear?” is playing as I write these words. “Even when the dark comes crashing through, and you’re broken on the ground, you will be found.” We carry each other. No one should walk this road alone.

Any “wellness package” for healthcare providers that doesn’t encourage and foster community is something either worthless or less than worthless. The idea that we can and should carry the weight alone is…it’s shameful.

Here is my story of how a small group of people cared for me when I was in crisis–how they insisted I needed help, and they provided it.

Blog post for the first podcast is here.

Podcast (available here and on iTunes)

Right Click and Choose Save-as to Download the Podcast.

a little rant


The podcast doesn’t contain any profanity, but it may be difficult for some people to hear. Be kind to yourselves.

Paralysis and PAD–pain, anxiety, and delirium–protocols have consumed me lately. Notice pain comes before anxiety on the scale. Address your patient’s need for analgesics prior to adding sedation, or you are merely hiding their need for pain control beneath a blanket of lethargy.

I know it’s easier to hang propofol than administer bolus fentanyl doses, especially when you’re initiating hypothermia or sending your patient emergently to cath lab, or running to CT, but consider the process that brought them to the point where they required intubation. Trauma, hypoxia, acidosis, CPR–painful states.

I notice with a lot of PAD protocols that while the sedation is ordered as a continuous drip, the pain medication requires a certain number of bolus doses to be administered in a certain narrow timeframe to justify initiation of a drip. This is, to my mind, fucking stupid. This shows a certain lack of good clinical judgment on the part of the people who designed the protocol. It’s the opposite of a delirium-avoidance approach. And while I am by no means insisting that every single patient requires pain medication and sedation while on a ventilator, I am most definitely suggesting that each paralysis requires adequate narcotizing prior to sedation, and prior to placement on a maintenance drip.

With the new guidelines for ARDS and the renewed emphasis on therapeutic paralysis, it is vital that we understand the difference between pain control, sedation, and paralysis.

Another concept, and to me, one of even greater importance, is the care we show people who are undergoing therapeutic paralysis. This is the subject of my podcast. It’s a short listen, but important.

This was hard for me to say. I know I pause a lot. I considered editing those pauses out but decided to let them stand, so you could hear what I felt, trying to explain what it was like.

something completely different

I’ve been intending to update for awhile, but haven’t. Sorry.

I’ve been depressed. I’m not talking about the kind of depression where you’re bored and vaguely dissatisfied. I’m talking about the kind where you can’t sleep, where you lose all interest in the things you love, where people you don’t even know can tell something is wrong. The kind where you break down sobbing while buying dinner for your family and the person at the checkout line calls 911 because she doesn’t know what else to do.

I was sleeping a few hours a night–broken, fitful sleep–waking to the same dream over and over. My mind couldn’t lay it down. I was carrying the problem with me everywhere I went.

The problem. It wasn’t a problem. It was a person.

I can’t tell you her name, or even promise the person is a she, because of the privacy restrictions we work under as medical professionals. But I wrote a thing about her, a thing I can’t share yet, and the writing did not have the effect I anticipated.

I thought it would be cathartic. I thought it would be like burning a memory, transferring the hurt to ash to be carried away by the wind. Instead the writing ensured that her name is burned on my heart.

So I don’t give two figs for the concept of preload. I have half an article written on something else and I simply cannot make myself write it. I do not care. The only thing I care about is finding some way to honor her memory. To do right by her and thousands like her.

Her memory haunts me. When I go to bed at night. When I rise in the morning. When I go throughout my day. She’s right there, at my shoulder, as I work and I think and I write and I start IVs. I missed two shifts on different floors because my mind is consumed with her.

If this story resonates with you, please–seek help. Find someone who can understand. Talk to them. Tell them your story. Don’t try to bear it alone. The weight can crush you, and you matter too much for that to happen.


preload: just enough to confuse us all

Preload is defined as the volume in the ventricle at end-diastole. So far, so medical dictionary. But really, preload is better defined as the compliance of said ventricle–preload is, purely speaking, the length of a myocardial sarcomere immediately prior to contraction. It is the Frank-Starling curve in action.

We don’t have anything to measure it directly in a living person, though. We can’t see it. You’d have to catch at a living heart in the act of beating at a cellular level, and devise a way to measure the difference in length between systole and diastole, to directly measure preload. And then it would have to operate from beat to beat.

You see the problem. I mean, that’s not workable at all. So what do we use as a surrogate value for preload? CVP on the right side of the heart, PAWP on the left. I mean, I say this. I’m not convinced we should. In fact, I’m pretty sure we shouldn’t. These surrogate values are less impressive when you take into account the numerous physiologic mechanisms involved in the maintenance of hemodynamic stability, as well as the mechanical issues involved in obtaining them, as well as the larger, more philosophical (yet wholly applicable) question of whether said surrogacy is reliable in any given scenario…

Oh, my holy lungs. STOP. That was a ridiculous mouthful. What I meant to say was, our numbers–the PAs and the CVPs and the wedges–are dependent upon the way we obtain them, on how we interpret them, the trend, the scenario, and a hundred other factors. Some of these we can account for. Some of them we can’t. And that’s assuming–a proper large assumption–that the numbers are reflective of anything workable.

Look. We all grew up using the CVP/PAWP. The CSC, CMC, and CCRN still test you on them. I’m not ready to throw it all away just yet. But if you’re simply checking it willy-nilly every once in a while, and pinning everything on that single value, you are making a huge mistake. You need a shift in heuristics. Serving immediate goals (especially if those goals are numbers) will fail you.

If your ICU uses CVP & PAWP as surrogate measures for preload, I want you to understand what their intent is. I will do another post on the relative utility of CVP/PAWP, so watch for that.

How do we apply this information?

From a practical standpoint–that is, shooting from the hip at the bedside–preload is essentially these three things:

  • Venous Return
  • Venous Pressure
  • Right Atrial Pressure

Other physiologic factors influence preload, but these are the big three.

Let’s look at venous return, first. No, scratch that. Let’s look at venous pressure, first, since that has a little to do with venous return.

Venous pressure refers to the pressure gradient between the venous bed and right atrium. Remember, blood flow isn’t solely dependent upon the force of contraction–it’s also dependent upon the pressure gradient of the system. The right atrium has a lower pressure than the venous vascular bed. This insures the forward flow of blood from the vena cavae and into the right atrium.

More than two-thirds of the body’s blood volume is within the venous system at any given time. Unlike the arterial system, the venous beds are extremely compliant, and able to hold three times the volume. This storage capacity–referred to as reserve volume–is maintained in the large sinuses of the liver and spleen, as well as in the veins.

Venous return is affected by baroreceptors found in the heart, the vena cavae, the carotids, and the aortic arch. These stretch receptors are very responsive to hypovolemia, and are capable of both SNS and PNS stimulation in order to increase or decrease heart rate, as well as augmenting flow via vasoconstriction or dilation. You know. Depending on what the body needs.

It’s also affected by changes in intrathoracic pressure.

The act of spontaneous inspiration is a pump to the circulation. When breathing in, pleural pressure creates a negative gradient in order to bring air into the lungs. The respiratory units aren’t the only structures affected by inspiration, though. Negative inspiratory pressure facilitates blood flow from the body (cerebral & abdominal vasculature) into the right atrium.

For years–since the sixties, in fact–the pressure of the right atrium, known as the “central venous pressure,” has been measured as a surrogate for the preload of the right ventricle. But surrogacy isn’t a direct value, and there is ample evidence that CVP is an inexact estimate of RV preload. That is not the only issue with its use, though.

In fact, the greater issue is the lack of a linear relationship between volume and pressure in the right atrium.

As if that wasn’t enough, we have the effects of positive-pressure ventilation. Intubation with mechanical ventilation raises intrathoracic pressure above atmospheric pressure during inspiration.

That’s worth saying again.

  • Spontaneous inspiration is a negative-pressure state.
  • Mechanically-vented inspiration is a positive-pressure state.

PEEP increases intrathoracic pressure throughout the entire ventilatory cycle. An increase in thoracic pressure causes a decrease in venous return. It artificially increases the CVP values, too.

When I was new in the ICU and still thought the CVP had some measure of utility, I was taught “for every five of PEEP above five, subtract three from the CVP.” And I’m going to leave it right there.

As far as the left ventricle is concerned (because we have two hearts, separated by the lungs, right?) we measure preload indirectly as a wedge (PAWP/PAOP). This is obtained from a pulmonary artery catheter, or Swan-Ganz. The left ventricle’s true end-diastolic volume can be assessed in cath lab from the contour of the ventricle wall, but we don’t have a bedside continuous direct measurement of the volume in the left ventricle. We have a surrogate–the wedge.

By now you know my feelings on surrogate values, right? And the relative utility of hemodynamic parameters derived from said surrogate values?

So ends Part One. More to follow…