don’t CHEAT a heart

Hey, there. It’s been awhile.

This post is for nurses who care for patients immediately following open-heart surgery, but most of it applies to any patient. I mean, since they all have hearts. Or so I assume.

The top six concerns for patients following open-heart surgery…


Cold. Cold is the first problem with open-heart surgery. Cold hearts are bradycardic hearts. What do we see in induced hypothermia? Exactly. Bradyarrhythmias.

Open heart surgeries come back to us with epicardial leads–often both atrial and ventricular, but sometimes they will only have a V lead. Keep your patient connected to the pacemaker, ensuring both capture and sensitivity are appropriate for your patient.

While you’re at it, mark the end of the V cable with a piece of tape. Do not mark both. In an emergency it’s really hard for someone under stress to see the difference between an A and a V.

Mark the V lead only.

If you’re having difficulty maintaining cardiac output and your patient’s heartrate is less than 80, consider turning on the pacer to 90 bpm. Definitely will not work on everyone, particularly if you only have a V lead. Pesky atrial kick, amirite?

Cold doesn’t just increase the odds your patient will be bradycardic. It also increases the odds of atrial and ventricular arrhythmias, and could lower the vfib threshold.

It also causes vasoconstriction. What happens to your hands when you go outside in cold weather? Peripheral vasoconstriction, right? That’s increased afterload (SVR) in action, as well as elevated filling pressures. Another thing cold does–reduces the clearance of anesthetic and sedative medications.

Warm your patient up. Remember, if they aren’t 36 degrees C when they hit the door anesthesia loses their 5%, so they want to hit that mark. Warm blankets or the forced-air warmer are available.

Cold does another thing. It influences coagulopathy. Hypothermic patients bleed more, right?

*Really has no effect down to 35C. Below 35C but above 33C you may see some mild platelet dysfunction. Below 33C the coagulation cascade is affected, but rarely will you ever see an open heart patient come back this cold.

It also precipitates shivering. Shivering increases lactic acid production, CO2 production, and O2 consumption, which brings us to H.


Hypoxia–tissue ischemia–is the next consideration. This may or may not be reflected in the ABG alone due to the way oxygen dissociates from the hemoglobin, the amount of circulating hemoglobin, or the presence of methemoglobin.

Here’s where I reference that horrible oxyhemoglobin dissociation curve we all remember being dense about in physiology.

No, it’s not that bad. In fact, I’m not even going to bring it up. How about that. Important thing to understand is that hypoxic patients are more prone to dysrhythmias. An ischemic heart is an unhappy one.


No, it’s not exanguination. Although that would be bad. Everyone remember the old saying, “Surgical bleeding is bleeding you can hear”? It rushes, dumping in the chest tubes.

If you hold the chest tubes level with the insertion point and blood fills them, that’s an indication for urgent return to the OR. All roads lead rapidly to a resternotomy.

Electrolytes. The heart simply adores magnesium and potassium and calcium. Typical goals in a post-op heart surgery:

K+ >4.2 mEq/L

Mg++ >2.2 mEq/L

ionized Ca++ >4.7 mg/dL.

Low-normal levels of potassium and magnesium predispose an irritated heart to dysrhythmias, which is why our goals for replacement are a touch supratherapeutic, but not high.

Ionized calcium is the amount of circulating calcium not bound to albumin, which means it’s the bit of the electrolyte that’s free to do work–clotting, muscle relaxation, contractility–and this last function is the one we’re interested in.

Most open-heart protocols require you to check these electrolytes with an ABG and CBC fifteen to twenty minutes after arrival and four hours later. Because things change, yeah? Sometimes quite unexpectedly. If your open-heart protocol doesn’t require ionized calcium, check one anyway. Tell ’em Eve said so.

Nah. Tell them that, in light of blood product administration and relative tenderness of the myocardium following surgical manipulation, you wanted to ensure there were adequate amounts of calcium ions to do the work. Tilt your head to the side, wink and smirk as you say it. Or not.


This next one is a biggie. Acidosis. Obviously acid-base balance affects heart function. Acidosis impairs contractility. As it turns out, the body requires the blood supply to be a certain pH for proper functioning. Even oxygen…oh. Yes. There we are again, at the oxyhemoglobin dissociation curve. Yes. I promised I wouldn’t bring it up. Ok, fair.

Let’s not be acidotic. Query me this: what is the fastest way to correct an acid-base imbalance safely?

Did you say by increasing the respiratory rate? DING DING DING. Yes. And the tidal volume. Which is…what Kussmaul respirations are. You guys remember those, right? The deep, rapid respirations of metabolic acidosis? Oh, DKA is the classic example. But our patients, our immediate cardiac post-op patients, the ones who are anesthetized and chemically paralyzed, they are unlikely to be capable of mustering said response, correct? Which means we must help them.

Except maybe not blow their lungs with high tidal volume. So. Rate is the way to go.

Oh, and by the way–let’s not give a ton of sodium bicarbonate. I mean, every amp you give you’ll pay for later. It dissociates in the serum to make NaCl and CO2…so…yeah…


Touch. We fiddled with that heart. Hearts don’t like to be touched. Just sayin. And yes, it’s almost Valentine’s Day. Take it from the twice divorced mom of five. Hearts are tender. They can’t take a lot of rough handling. Most post-ops experience myocardial depression for 6-12 hours after surgery, with a drop in ejection fraction of 10-15% even when hyperdynamic on pre-op TEE.

You think the LV is the whole story?

Got another think coming. If the LV is occasionally fussy, the RV is a straight bitch. Any intervention on the right side, affecting the right side, and you need to consider primacor or dobutamine for forward flow. Low-dose epinephrine will also work, say, 0.02-0.05 mcg/kg/min.

Know your surgeon and your patient.

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…

breathe in, breathe out

We measure all hemodynamic variables (CVP, PAs, PAWP, CO/CI) at end-expiration, because exhalation is usually the longest period of the respiratory cycle. Inhalation increases systemic venous return, but also decreases pulmonary venous return, which in turn decreases flow to the left side of the heart.

Here is that mechanism at work with bolus thermodilution:


This image demonstrates the high degree of variability from respiratory artifact. Trials 1, 3, 5 were performed at end-exhalation. Trials 2, 4, 6 were performed during inhalation.