i am a shell

I am a shell. From me you shall not hear

A strident voice, fierce and clear,

Hanging in the air once I’ve spoken.

My timbre is the merest token

Of tones light, barren, scrubbed clean.

I am not heavy with authority—

I am a whisper. No sonorous tones, mine.

My voice far too rapidly declines,

Drifting among the stones of the shore

Until it fades. There is no more

Except as the beats of the seas endure,

So shall my echoing song waft pure.

As suffering of the waves resides in me,

My hollows roar dimly with the passion of the sea.

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…

getting sick

a poem, for something completely different

I referred to it as “getting sick,”

as though she went to the market

and picked up cancer with a loaf of good bread,

a nice red, and some figs.

“Try the small-cell carcinoma, it’s divine.”

“Aplastic anemia, just wonderful what they’re

doing with Chilean varietals lately.”

As though she brought it home

in a paper bag, nestled with the bread

and the wine and the figs,

seasoned it and roasted it,

plated it with rosemary and au jus,

ate it, sighing over its robust flavor,

a meal she reminded me of later,

sunken eyes shadowed waxen flesh

stretched tight over high cheekbones

describing how she consumed it,

and how it now feasts on her,

on her lungs, on her liver,

the spongy marrow of her bones,

and all along I thought it was something

she could get, something she could catch,

something in the air, universal as breathing,

when the truth is that it caught her.



Today’s #CCRN, #CMC, #CSC education tip: VASOPRESSIN.


Today we’re going to talk about vasopressin.

Those of you who have been nursing a bit will remember when vasopressin, 40 units, IV as a bolus dose was the ACLS recommendation for the second medication to give during a cardiac arrest. The first? Epinephrine, as always. “All dead people get epi,” at least if we’re following the recommendation of the AHA. As I said before, there’s some controversy.

But we aren’t here to talk about epinephrine. Let’s look at vasopressin. The chart I posted over catecholamines is useful, but vasopressin wasn’t on it. That’s because vasopressin isn’t an alpha-1/beta-1/beta-2 drug. Nor does it metabolize into a drug that accesses those receptor sites.

Vasopressin is anti-diuretic hormone. It is necessary for life in humans and animals, and it works on the V1 and V2 receptor sites. The first is located on the membrane of a vascular smooth muscle cell and mediates vasoconstriction in much the same way as angiotensin II. The second receptor regulates water excretion by increasing water reabsorption.

Vasopressin is used to restore vascular tone in vasodilatory shock. We usually use it in sepsis, but also in vasoplegic syndromes and advanced heart failure. It’s the drug we reach for when shock is resistant to catecholamines.

There are several ways vasopressin performs its magic. We mentioned vasoconstriction and increasing water reabsorption. Other effects include modulating endrogenous nitric oxide and potentiating adrenergic agents to promote vasoconstriction.

Platelets are affected by stimulation of the V1 receptor site to provoke an increase in intracellular calcium levels. This facilitates thrombosis, but the amount of variability in aggregation response is so large it’s not possible to point to vasopressin as a cause of coagulopathy.

V1 receptor agonism doesn’t affect every part of the kidney in the same way, but selectively affects the inner (but not the outer) medulla blood flow rate, and contracts the efferent arterioles but not the afferent arterioles.

DDAVP is a selective form of vasopressin which affects only the V2 receptors, causing a release of von Willebrand factor and vasodilation in the kidney alone. Although V2 receptors are found elsewhere, for reasons most mysterious it doesn’t seems to have effects outside the renal circulation.

The vasopressin receptors are relatively resistant to downregulation. The interaction of vasopressin with arrestins, when combined with this resistance, allows vasopressin to (purportedly) bypass the downregulated myocardial adrenergic receptors.

Vasopressin is dosed in 0.01-0.04 units per minute or 0.1-0.4 units per hour. Either way, it’s particularly helpful in hypoxic/acidotic states, as well as those resistant to sympathomimetics. It’s not generally titrated–for sepsis or vasoplegic syndromes, we generally place it at 0.03 units/min and leave it. It increases MAP without affecting inotropy, as a general rule.

Although the cardiac effects of vasopressin are complex and conflicting, a few common uses have emerged over the last ten years. One is the pairing of milrinone and vasopressin. In cases of severe advanced heart failure requiring the use of inotropic agents, plus the necessity to bypass downregulated receptor sites, added to the need for diuresis in the presence of relative hypotension, vasopressin has emerged as a superior agent for maintaining vascular tone and perfusion.

It’s also an excellent choice for blood pressure support in PAH, as it avoids vasoconstriction in pulmonary circulation.

Consider adding vasopressin to levophed in refractory hypotension, particularly in septic shock. In those patients the levophed dose can get so high it blocks perfusion of the capillary beds. Starting vasopressin in these patients can allow you to reduce the rate of levophed infusions to much more reasonable levels.

Another use is in post-operative cardiac surgery patients. Maintenance on bypass circuitry for surgery has multiple effects on a patient’s physiology, which can evidence themselves in a vasoplegic scenario post-operatively. Vasopressin can prevent cardiovascular collapse in this patient population without adversely affecting inotropy.


levophed descriptionLevophed, also known as norepinephrine, is another stress hormone, and the topic for today. We’ve mentioned norepinephrine in the posts on dopamine and epinephrine, but now we’re going a little deeper.

“Levophed will leave ’em dead,” I was taught as a new nurse in the ICU, and definitely it can. Norepinephrine is a powerful alpha-1-agonist, producing intense vascular vasoconstriction. High doses of this medication will clamp the vascular system, both arterial and venous, to the extent no perfusion occurs in the capillary beds.

In other words, it increases afterload. In fact, it can increase afterload so much that it causes metabolic acidosis. Because of its venous activity it diminishes preload. At the same time, cardiac output drops as the heart rate falls. This mechanism makes it a poor choice as an inotrope.

Wait a minute…heart rate falls?

Let’s look at this. Norepinephrine has beta-1 agonist activity comparable to epinephrine, but it has NO effect on beta-2 receptor sites. But didn’t I say that beta-1 agonists increase contractility and heart rate? Yes, I did.

The increase in mean arterial pressure levophed induces will cause baroreceptor-mediated drop in heart rate, which the beta-1 stimulation of norepinephrine is often too weak to overcome. Not always, though.

We use levophed as a first-line vasoactive agent, directly behind or in conjunction with crystalloid, for hypotensive patients in the presence of infection. This state is what we refer to as “septic shock,” and I’m not going into SIRS criteria in this post. In these patients it’s unlikely to see the drop in heart rate, as the pathophysiology of sepsis results in tachycardia.

Norepinephrine doesn’t affect the alpha-2 receptor sites, which are found in the cerebral circulation. Since it lacks beta-2 activity, it also will not dilate the bronchioles, making it less than ideal in anaphylaxis or status asthmaticus. Incidentally, it’s also a poor choice in cardiogenic shock or advanced heart failure patients since it increases afterload.

The higher the dose of levophed, the more profound the effect on systemic vascular resistance. A pet peeve of mine? Receiving a patient on levophed with a MAP greater than 75. Unless of course you are a neuro nurse, in which case you are titrating for an appropriate CPP (cerebral perfusion pressure) and you should ABSOLUTELY continue, please and thank you, carry on.

PRIMARY CONSIDERATIONS: The development of tachycardia (worse in septic patients, which is our primary use of levophed), dysrhythmias (as all beta-1 agonists do), myocardial ischemia, colitis, and other effects of decreased organ perfusion.

It doesn’t really contribute to hyperglycemia like epinephrine does.

Here’s an interesting tip about norepinephrine: it must be mixed in D5W in order to provide enough acidity to prevent oxidation. Oxidation makes levophed ineffective by inactivating it.

The lungs are responsible for clearing endogenous catecholamines, and can extract about 25% of circulating norepinephrine in a single go. This clearance is diminished by halothane & nitrous oxide in animal studies, so it may be that anesthetic agents interfere with the process in our patients, too.