Okay, we're going to talk about hemodynamic terminology right now, try to clarify some terms for you so that when you hear these terms either in a chart, in the clinical setting, Monitoring a critically ill patient with these invasive hemodynamic monitoring devices that you'll know exactly what's being referred to. So let's think about preload. What is preload?
By definition preload is the amount of blood in the ventricles at n diastole. so it's the amount of volume that's kind of in there at end diastole so what patients have an elevated preload that we need to maybe manipulate those are the congestive heart failure patients so they're fluid volume overload, they're all kind of backed up. So we need to understand what a preload reducer is in that case. So what would lower that volume in that fluid volume overload patient?
The diuretic therapy. Another form of a preload reducer would be a venous vasodilator, something like nitroglycerin, which targets mainly the venous system, is going to dilate the vessel that's going into the right atrium. And so if...
if the vessel, if that tunnel, that pipe is bigger going into the right atrium, that's going to lower the amount of volume that's headed into that right atrium. So venous vasodilators are also preload reducers. Even morphine sulfate given for patients that have cardiac compromise, having an MI, morphine will not only satisfy pain as an opioid, but it will also dilate the venous system.
Would we ever want to increase preload? Do we know? how to do that. Absolutely, patients with low flow states, shock states, we definitely want to fill up the tank and we need to add more volume into their intravascular space so they have a higher preload.
Now how do we measure that preload? Well we can't measure volumes directly because we can't go in there with a little measuring cup and say how much volume is in here. So what we do is we extrapolate volume by measuring pressure and we do that with what's called the central venous pressure.
monitoring device. The central venous pressure or the right atrial pressure is the same thing. So CBP and RAP is interchangeable. Let's talk about afterload now. So what is afterload?
So by definition, afterload is the resistance that the ventricles must push against with their systolic ejection. So with afterload being resistance, do we ever have patients with resistance, that's too high. Who is that patient? That's the patient we treat kind of on an ongoing basis.
Those patients with hypertension have increased resistance, increased afterloads. So what do we do to intervene? We give afterload reducers with those ACE inhibitors. Those PRIL medications will prevent the conversion of angiotensin 1 to angiotensin 2, which is a vasoconstrictor, and it relaxes the vessel. That's an afterload reducer.
Now, would we ever want to increase resistance? Do we ever have patients with afterload that is way too high? Their resistance is absolutely not enough because it's not creating the pressures we want.
Absolutely. Those patients in those distributive type shock states, the anaphylactic and the septic and the neurogenic type shock has wide open vascular spaces. And we need to clamp it on down. vasopressor medications to increase afterload.
Now, can we measure afterload? Absolutely, we can with something called systemic vascular resistance, which is the measurement of afterload or SVR. We can only do that with invasive monitoring devices.
So with the PA catheter or the Swangans catheter, which we're going to talk about in a little while, you'll be able to get all these numbers pretty automatically because we have such sophisticated equipment now. Now we can also do it the long way, but you don't really need to know the formula for SVR. Again, you just need to know that it is via a formula that factors in an MAP, the CVP, cardiac output, in order to come up with this number that is measuring afterload, that SVR, that systemic vascular resistance.
Okay, let's talk about cardiac output. What's cardiac output? We're going to be talking about cardiac output all semester in all different context we want to increase it we want to decrease it you know in that hyper metabolic shock state of sepsis so what is it it's the amount of blood pumped in liters per minute so it's the amount of blood getting to the vital So obviously it's a big hot topic.
So what is normal? Normal is four to eight liters per minute. And how do we arrive at cardiac output? Stroke volume.
What's stroke volume? Stroke volume is the amount of blood pumped with each systolic ejection so just one time that's your stroke volume multiplied by how many times that happens in a minute that's the heart rate so stroke volume times the heart rate equals your cardiac output in liters per minute. Now the problem is that that cardiac output number in liters per minute sometimes doesn't give us really the whole picture. Now what do I mean by that? I mean that if you have somebody who's really large and let's say their cardiac output is four, let's say Arnold Schwarzenegger in my little example has a cardiac output of four.
I'm not so sure if that's gonna be adequate. Maybe yes, maybe no. We have Tom Cruise a little bit. bit of a smaller stature individual and his cardiac output is four.
Who's got a better cardiac output Arnold or Tom? Well let's get to the bottom of this by doing what's called the cardiac index and what the cardiac index does is that it factors in body surface area so you don't have to guess you can know precisely is this cardiac output sufficient to meet the needs of the system. So when we get the cardiac index for Arnold when we factor in their cardiac output of four with his body surface area we get a cardiac index of two now normal cardiac index is 2.5 to 4 liters per minute so his index is insufficient whereas the cardiac index of Tom when we factored in that cardiac output of four with his body surface area which is smaller his cardiac index is still four so it is much more accurate when you get an index.
In fact, any index that you get is going to be factoring in body surface area. Let's talk about something called the map. Not the map like you know you're traveling, car, going on vacay, unfortunately. But this map refers to blood pressure. Kind of a quick and dirty blood pressure is what I like to think of it as because it takes the three components of two components systolic and diastolic but it puts in the third component and it gives you you one number so it's actually easier to work with than systolic and diastolic.
So how do you arrive at a map? Systolic blood pressure plus two times the diastolic blood pressure divided by three. You have three numbers there on that numerator so therefore the denominator is going to be three.
So that's how I kind of remember one systolic plus two diastolics divided by three numbers and you should get one. So why don't you do a practice. Let's say we have a blood pressure for a patient with 104 over 60. What would be their MAP?
What would be their mean arterial pressure? The answer should be 74. Now what do we do with that number? We want patients to have a mean arterial pressure of at least 65 or greater. When do we use this?
We use this for patients who are having a low MAP. lot of circulatory compromise. Those patients in shock and we're kind of struggling to maintain that cardiac output and we need to follow that map to make sure that their organs are getting perfused.
Now let's look at contractility. What's contractility? Contractility refers to the force of a contraction.
Now another way we can think about it is eintropy, another term that we use to refer to contractility is called eintropy. So when we're talking about contractility, we want to know if we have something that's a positive eintrope or something that's a negative eintrope or do we need to administer a positive eintrope to improve contractility. So let's look at an example.
What would be an example of a medication that's a positive inotrope that improves contractility? Well, the gold standard for improving contractility of the myocardium is dobutamine. Dobutamine is pure cardiac output medication.
So it's going to be a positive inotropic drug. How about a drug that's a positive inotrope, but a negative chronotrope? Now, chronotrope... reverse heart rate. So something that improves contractility, but all the while decreasing heart rate.
We'll give you an example of that. Digitalis or digoxin. So we're always, you know, needing to know for patients who are compromised, what the effect is on contractility, what inotropic What properties does it have?
Let's talk about medications that are negative inotropes. And why would we ever want to decrease somebody's contractility? Well, let's think about somebody who's had a myocardial infarction. an infarct.
You know they have a tired myocardial muscle. They need to rest. So when we give them negative inotropes, we're preserving that energy. We're decreasing myocardial oxygen consumption by giving them a negative ion control.
So what would be a drug that does that? Does that kind of cardioprotective task? That would be the beta blockers.
So post-MI, we give patients beta blockers, not because their blood pressure is so high, but because it will be cardioprotective, because it will reduce contractility. But really what we want to do is... preserve myocardial oxygen consumption.
The last hemodynamic value or parameter that we're going to discuss is something called the pulmonary capillary wedge pressure, also called the pulmonary artery occlusive pressure. In order to get that value you need an invasive hemodynamic monitoring device. That device is called a Swann-Gans catheter. It was invented by two gentlemen, one named Swann and the other named Gans. It's also called the pulmonary artery catheter, so it's just good to be familiar with this terminology so you understand what's going on when it's discussed at the bedside.
So what happens with this swan gans catheter is that it is inserted into internal jugular all the way till it gets into the right atrium and then it continues to be threaded through the tricuspid valve to the right ventricle through the pulmonic valve and then into the pulmonary artery. So it sits there, it's got a proximal lumen, it's got a distal lumen, and it's able to get parameters like the pulmonary artery mean, or it's kind of like a pulmonary artery blood pressure, so the pulmonary artery systolic, the pulmonary artery diastolic. So these sophisticated numbers are used for patients that are so sick that you need such precise diagnostics in order to understand how to move forward and treat them.
And pulmonary capillary wedge pressure is... no different so it's used for patients when you really want to know the pressures on the left side of the heart so wait a minute I just told you that this this lumen that has a sensor on the end of it is threaded through the right side all the way from the RA to the RV and into the branch of this pulmonary artery when you are going to get this wedge pressure you inflate a balloon now there's a little arranged and normally the balloon is in a non-inflated state but when you want to get this wedge pressure you inflate the balloon at the bedside and that balloon enables this tip of the catheter to kind of float like balloons do when it's in fluid and then eventually it's wedged it gets stuck right here in the branch of a pulmonary artery and when that happens because it's wedged, it's not able to sense the right heart that is behind it. So the only thing it's able to sense are the pressures that are in front of it, which is the left side of the heart. So that is what we call a pulmonary capillary wedge pressure with normal being 6 to 12 millimeters of mercury. So it's just so you have that overview of what is a wedge pressure.
The only time that a wedge pressure is going to be considered kind of moot is when you've got pulmonary hypertension and then you're going to need to insert something directly into the left side of the heart called an la line or left atrial line because you the you need to bypass the right side of the heart so what i always like to show you is what the waveforms look like as this catheter is being threaded i think it's really interesting to watch at the bedside because with the little sensor on the end end of it, you know which chamber it's in just by looking at the pressures. Obviously the right atrium is a lower pressure chamber than the right ventricle. So when it's being threaded through the right atrium, you can see that waveform kind of low.
It's going to be a central venous pressure value. So it's going to be a two to six millimeters of mercury. So you can see the way forward down here.
And then as it gets into the right ventricle, you see the way of form kind of spike up. The pressures are higher in the right ventricle. It's a higher pressure chamber. we're going to the pulmonary circulation and then you see kind of a pulmonary artery waveform and then when it is wedged into a branch of the pulmonary artery then there's no more up and down there's no more systole and diastole it's now a flattened waveform and it'll sit right where that pulmonary artery occlusive pressure it needs to be you