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Two Interesting Situations: 5/03

1- A patient with pulmonary hypertension.

1-1: Nice pair of lungs.


1-2: How about this one?
1-3: A PA line.
1-4: These lungs are very stiff.
1-5: Blood is having a hard time getting through these stiff lungs.
1-6: A really impressive diagram of the closed foramen ovale.
1-7: A diagram of a patent foramen ovale.
1-8: Floating a swan.
1-9: Wedging the swan.
1-10: Doing an inhaled nitric oxide trial.
1-11: Pulmonary Vascular Resistance.
1-12: A whole lot of numbers with a yow!
1-13: The situation in a nutshell. Nice arrows.
1-14: What are the numbers telling us?

- Baseline numbers.
- Numbers after 15 minutes on 100% O2.
- Back to baseline.
- After 15 minutes on 20ppm inhaled nitric oxide.
- Back to baseline.

2: A patient with a right-ventricular MI.

2-1: A pretty cool 12-lead EKG.


2-2: What happens during an RV MI?
2-3: A whole lot more numbers. Different yow.
2-4: Following the stroke volume.
2-5: Two hours later.
2-6: Two hours after that.
2-7: Two more, plus the Starling curve, and setting goals for central pressures.
2-8: SVR comes down, and the pH does what?

Some nice hemodynamic numbers: These aren’t really discussions for beginners, although I
hope that I’ve been clear enough for anyone – I usually try new articles out on my kids (“Not
again!”), and if they seem to get it, I think I’m doing the right stuff. It may take a while getting used
to PA lines and “shooting numbers” before all this stuff makes sense.

A couple of scenarios that came up over the past week or so showed a really nice use of the PA
line numbers that we “shoot”: one was a pulmonary hypertension lady who was getting a nitric
oxide trial, and the other was a gentleman who was unfortunately having a big RV MI.

1- A patient with pulmonary hypertension.

Let’s take the pulmonary hypertension one first. This was a woman who came in short of breath –
a street person who had any number of social and life difficulties, but who now showed up with
dyspnea, which worried her enough to bring her into the ED. Turns out that as an alcoholic, her
portal hypertension had backed up pressures into her lungs, creating pulmonary hypertension –
anybody else ever heard of this? Not us – who knew? We wondered if a TIPS would help the
woman…anyhow, she came into the MICU as part of a protocol workup to see if inhaled nitric
oxide would help bring her pulmonary pressures down. She came to the MICU where the team
placed a PA line.

The purpose of the exercise: I guess the data show that if a patient like this is given inhaled nitric
oxide under controlled conditions, you can tell whether or not they’ll respond to oral calcium
channel blockers to help the PH or not – but you have to do the measurements first.

1-1: Nice pair of lungs:

Look familiar? So here’s the idea: lungs are like lots of other organs in the body – normally they’re
nice and soft, rather than stiff. The liver is like that: normally soft, but expose it to enough alcohol
and it becomes stiff – cirrhotic. Lungs that are soft are said to be “compliant” – stiff lungs are: big
surprise, “noncompliant”. A patient with stiff lungs will be obviously hard to “bag” with the ambu…
you’ll see new nurses looking at the bag in surprise, trying to figure out what’s wrong with it.

1-2: How about this one?

www.netdoctor.co.uk/focus/ heart/index.html
Who said “Liver!”?

So - there’s the problem: stiff lungs. Any idea how to measure just exactly how stiff they are?

1-3: A PA line.

Yes – a PA line, because why? Because when the balloon is down, remember, the transducer
“sees” what? The pressures all around it in the lung, very good. Also known as “ambient”
pressures. As opposed to what it sees when the balloon is up – when it can only see what’s
ahead of it, over there into the left side of the heart, right through the pulmonary capillaries and
all. How it does that I have no remote clue.

Anyhow. If you put a PA line in me, hopefully you’d see normal lung pressure numbers – that’s
what the PA numbers are, remember? They reflect the ambient pressures in the lung. Normal
would be something like 30ish over 12ish, right? Something like that. This lady had pressures of
about 105/60. In her lungs. Which means a couple of things:

1-4:These lungs are very stiff.

1-5: Blood is going to have a hard time getting through these stiff lungs – the pulmonary arterial
system is tight, right? So the pressures are high. So is the resistance to flow. Now let’s look at an
incredibly sophisticated cardiological-type diagram:

1-6: Closed Foramen Ovale

Atria:

Ventricles:

Wow – is that just some kind of really cool diagram or what? Now, anybody remember what it is
that babies have that goes between the atria, where the arrow is pointing? Remember that stuff?
The foramen ovale? (Not the same as the foramen O’Malley, which is where the beer goes…ow!
Editing doesn’t mean you have to hit, y’ know!) Otherwise known as an atrial septal defect – an
opening between the atria. Fetal blood flow.

It turns out that lots of people walk around with these, it’s just that they stay closed most of the
time. They have a “not-patent” foramen ovale.

Let’s ponder this a second. What pumps blood to the lungs? The right side of the heart, very
good. What if the lungs stiffen up over time? Well – you’re going to get hypertrophy on the right
side of the heart, that’s for sure, because it’s going to grow, just like any muscle will, if stressed.

Now – pumping against those stiff lungs, the pressure on the right side is going to go up. And up.
Eventually the pressure becomes high enough on the right side that if you still have a foramen
ovale that’s just sitting there being closed – well, it’s not going to stay closed if the RA pressure
gets high enough. See that?

So. Now the pressure in the lungs is so high that the blood doesn’t want to go through them any
more, not if it can find an easier route. And there it is: it’s going to go through that little opening,
from the right side of the heart to the left, taking the easy way, instead of going through those stiff
lungs.

But – does that blood pick up oxygen? No, it does not! Does it drop off carbon dioxide to get
exhaled? No, it does not! What it does do is stay de-oxygenated, and just goes right back around
into the arterial circulation. It gets shunted over there, from the right side to the left side, through
the foramen, which has been forced open by the pressure. Patent foramen ovale.
1-7: The patent foramen ovale.

Right side. Left side. As if you were looking at an x-ray.

Ha! Now you know what a right-to-left shunt is! Didn’t see that one coming, did ya!? And you
thought that was a big mystery…

Okay so far? So this person is going to be short of breath, probably even at rest, because some
significant part of their blood isn’t going through the lungs – instead, it’s being shunted across the
atria. That’s the “shunt fraction” – I would imagine that you’d want it to be something like zero,
normally.

1-8: Floating a swan.

So – what to do? Well – let’s float in our swan:

www.angelfire.com/folk/
tales6/marine.html

1-9: Wedging the swan.

Okay – now let’s wedge the swan:

Right. Anyhow – okay, here comes the swan. Sure enough, PA pressures are really high: almost
as high as the patient’s systolic pressures. Scary.

1-10: Doing an inhaled nitric oxide trial.

Now the nitric trial, which involves shooting a lot of numbers:

1- a set of numbers at baseline:


2- a set of numbers after 15 minutes at 100% mask oxygen
3- another set after 15 minutes back on room air
4- a set after 15 minutes on 20ppm of inhaled nitric oxide
5- another set back at baseline.

Let’s see if I can do a table without the kids:

1-11: Pulmonary Vascular Resistance

Just to be clear – everybody knows what these numbers are, right? Cardiac output, SVR, and so
forth? PVR turns out to be “Pulmonary Vascular Resistance” – everybody remembers that
Systemic Vascular Resistance is the number telling you how tight the arterial “bed” is – the
arterial system as a whole. High is tight, low is loose, and the SVR is the “afterload” for the left
ventricle – it’s what the ventricle has to push against to perfuse the body. Right?

1-12: A whole lot of numbers, with a yow!

So the right ventricle has an afterload too. Be smart now – if the arterial system is the afterload
for the LV, what’s the afterload for the RV? Well, what are we talking about here? Lungs! Very
good – yes, the RV pumps against the resistance created by the lungs. Tight pulmonary
vasculature – you get a high PVR. See that? So if I tell you that normal is about 100, and you
take a look over on the right there in the first row, what do you see? Yow! Eight and a half times
normal. Pretty tight lungs there, man!

PA pressures CO SVR CVP PCW PVR

- baseline 102/ 62 2.3 2400 26 13 855 (yow!)

- 100% O2 95/ 44 2.7 2050 22 16 745

- back to baseline 100/ 58 2.2 2480 26 12 875

- 20ppm NO 88/47 3.2 1900 16 18 655

- back to baseline 104/60 2.2 2450 25 14 845


1-13: The situation in a nutshell. Nice arrows.

Here’s the situation in a nutshell:

Stiff, high PVR. Think “Brillo pads.”


Or think of the lungs as a valve, a faucet
between the two sides of the heart
– either more open or more closed, with the PVR
as the indicator.

High CVP over here Low wedge pressure on


on the right, with a the left, because the
failing RV. blood isn’t getting through
the lungs. The result: low
cardiac output, with a
high compensatory SVR.

1-14: What are the numbers telling us?

So what we’re trying to do is see if we can open the valve with inhaled nitric. The numbers tell the
tale.

Baseline numbers:

Let’s flip pages back and forth now a little, going back to the chart. Everybody see that first row,
the baseline row? How’s the cardiac output? Kind of stinky. The SVR is really high – how come?
Because it’s the same kind of thing as cardiogenic shock – if the output is stinky, then the only
thing the body knows how to do is to squeeze the arterial bed to keep up the systemic blood
pressure. See that? How about the CVP? Really high, ain’t it? Why? It’s ‘cause that right side of
the heart can’t empty itself very well against those tight lungs, against that high PVR. Can’t empty
itself. Stays too full. CVP goes up.

How about the wedge pressure? Sort of low? Precisely the opposite volume problem, except on
the other side of the heart: instead of too much, as on the right side, the blood is just not getting
through to the left side, because it’s being held back by the stiff, high-PVR lungs. Low wedge.

Numbers on 100% O2:

A little better! It’s all about the PVR – see that? The PVR came down, so the resistance was less.
CVP came down – less resistance for the RV to empty against, right? PCW came up – better flow
through the lungs. Cardiac output – a little better.
Back to baseline:

Rats. Well, what did we expect? But do you see how the pattern works out? See how cool these
numbers are?

After 15 minutes on 20 ppm of inhaled nitric:

Whoa! Looks better to me! CVP is down, wedge is up, output is up, SVR is better because the LV
has a better supply and the CO is up. The PVR is much better. Bet she felt better too, and I bet
you could feel her peripheral pulses now for the first time. (Why?)

Back to baseline:

Rats. But it was a useful test.

Unfortunately for the patient, it wasn’t useful enough. I guess the data shows that the patient has
to have something like a 20% improvement in the PA mean for the study to indicate that the
patient can then go out and take calcium channel blockers on the outside and have them do any
good. As a street person, the patient was not a candidate for flolan.

2- A patient with a right-ventricular MI.

The second patient with cool hemodynamic things going on was an unfortunate lady who was
having an RV MI. By definition this means an extension of an inferior infarct (in Boston we say:
“She took an infahction!”) – Jayne says that something like 30% of people with IMIs infarct
enough inferior territory (RCA infarct – leads II, III and AVF) to produce an RV MI.

2-1: A pretty cool 12-lead EKG.

Everybody see those ST elevations


over there? These represent which
stage of an evolving IMI? For extra
credit: what’s up with the ST
depression in leads I and AVL? And
what the heck rhythm is this,
anyhow? That’s a rhythm strip down
there at the bottom.

http://www.netmedicine.com/img_ekg/ekg12.jpg
2-2: What happens during an RV MI?

So in an RV MI – what happens? You need to think about what each side of the heart is doing,
and what happens if it stops doing it.

Most of the time when we think of a patient taking an infahction we think of them having chest
pain, maybe having trouble breathing – things like that. That’s certainly true of almost all anginal
episodes, or chest pain associated with an MI. But there are specific differences that start to
make sense when you think of what each side is trying to do.

Left side of the heart: anterior and lateral territory, LAD and circumflex, respectively. The left
atrium and ventricle drain the volume arriving from where? The lungs – okay. Suppose the LV
takes a hit – and isn’t pumping so well. Now it can’t empty itself properly, and what happens to
the wedge pressure? Goes up. What happens to the lungs if the LV doesn’t empty? The pressure
backs up into the lungs from that over-full LV, and water begins to leak across the capillaries
around the alveoli: CHF.

So – left side ischemia or injury: CHF. Also hypotension maybe, from cardiogenic shock if the hit
is big enough.

How about the right side – inferior territory, RCA? These folks have just as much chest pain as
anybody else, but they probably aren’t going to get into CHF problems. Instead, they develop
bradycardias, maybe nausea and vomiting (apparently the innervation between the inferior part of
the heart is shared with the stomach). If they take a big enough hit, a significant part of the RV is
going to stop working and just sort of lie there, not moving much. “Inferior hypokinesis”, which I
believe translates as “just lying there, not moving much.”

The hypokinesis is the problem – remember that each side of the heart has a preload, a source of
incoming volume. Where does the LV get it’s preload, its volume from? The lungs – right, we just
said that. But what if the RV isn’t pumping blood into those lungs? Will there be enough blood
going through the lungs to get over there to the left side? No, there will not.

This can be a little hard to grasp, but important – bad push from the right side into the lungs,
means poor blood flow coming from the lungs into the left side of the heart. Poor left sided
preload. Low wedge pressure. Starting to sound familiar? Kind of like in pulmonary hypertension,
sorta kinda? Not for the same reason, but producing a similar effect – low wedge, low blood
pressure.

What to do? All other things being equal, it should be safe to give this person volume, right? They
shouldn’t go into ischemic CHF, or get easily pushed into CHF if the left side is working okay,
right? These people get the opposite treatment of left-side disease people, who get diuresed all
the time for failure – these RV folks get hydrated like mad. NS at 500cc/hour.
2-3: A whole lot more numbers; different yow.

So that’s what we did: and interesting things happened. First of all, a look at the numbers:

PA pressures CO SVR CVP PCW SV

Start of the shift: 24/10 1.9 2800 10 7 18 (yow!)

Two hours later: 30/12 2.1 2550 12 9 21

Two more: 34/12 2.2 2400 13 9 23

Two more, even: 35/12 3.1 1700 17 14 42

2-4: Following the stroke volume.

This time instead of looking at the PVR at the end there, we’re going to follow the stroke volume.
SV remember, is how much blood gets pumped out of the LV with every beat: you get the number
by dividing the CO in total cc’s per minute, by the heart rate. Quick example: patient has a CO of
8 liters, which is 8000cc/minute. Heart rate is 100 bpm. So the stroke volume is 80cc. See that?

So let’s look at the first set of numbers and try to interpret them. What’s low, what’s high? Cardiac
output is awful low – should be 4-6 liters/ minute. SVR is real high – sound like anything? Sound
like cardiogenic shock? Good try, especially since the patient’s having an MI. But wait a sec –
those central pressures are really kind of low, and what’s with that stroke volume? Normal is
something like 80-100cc/ beat. 18 sounds kind of low, like maybe super low. Yow!

Very good. This patient is dry. Or thinks he’s dry – I mean, he may be up a couple of liters, but
he’s not filling his LV very well. Wait – RV MI, right? Aha – see? Time for dobutamine to get his
output up? Nope – fluid. Why is his SVR so high?

2-5: Two hours later.

So we start NS at 500cc/hour after a liter bolus to get him going. Next set of numbers, a couple of
hours later. A little better. CVP is coming up a little, wedge up a little, SV up a tiny bit, output too,
and the SVR is coming down a little.

2-6: Two hours after that.

Two hours more: seems to be working. But slowly! Man, this patient is soaking up the volume!
She was, too. By the end of the night shift she was up 4.5 liters since midnight, and she’d been
up another 8 liters then! Hoo-wah!

2-7: Two more, plus the Starling curve, and setting goals for central pressures.

Two more: Now we’re getting someplace. Took long enough! Something seems to have optimized
here – suddenly things look a whole lot better: output and filling pressures are up, SV is up, SVR
is really coming down. Probably that Starling curve thing, which is where you take a bunch of
these little black birds, arrange them in a circle, and then do this sort of really cool nature dance
with the kindergarten kids…(What? What do you mean “No, stupid!”? I’ve always done the dance
with…what?)

Yeah, yeah. So: Starling says that at some point in filling up a ventricle, suddenly you hit a sweet
spot and everything looks better. Not too full, or things get crappy again – so the thing to do is to
make note of where you’re at: “Hey Chuck, he seems to really like a CVP of about 14!” So that
becomes your goal: “Titrate IV fluids to maintain a CVP of 14.”

2-8: The SVR comes down, and the pH does what?

A last point: see how her SVR came down? As we filled her up, she opened up, loosened up. If
the patient started the night with a pH of say 7.26 and a PCO2 of 40, what do you think might’ve
happened to her pH as her SVR came down, and how come?

So - I’ll tell you why: lactate. With a really high SVR like that, the distal perfusion can get really
poor – you may not be able to feel the person’s peripheral pulses as they clamp down so tightly.
Since the perfusion to the periphery is bad, they do what any other shock-state patient does: their
peripheral tissues switch from aerobic to anaerobic respiration, and instead of producing CO2,
they produce lactate. Metabolic acidosis. Loosen up that SVR, perfusion improves, everything
switches back to the aerobic thing, the lactate gets washed out, the pH gets better.

Now: wasn’t that just so cool?

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