Chf and fluid boluses
- 0Jul 1, '13 by bug2621So I had a patient with CHF that hadn't eaten or drinken all day. There was a 1500cc fluid restriction but she was no where near that limit. That night her pressure dropped into the 70s and 60s. I asked the dr. for a 250cc bolus because she was symptomatic. He agreed but my preceptor said we should never give Chf patients boluses but encourage fluids. I understand the concept but what is the difference a small bolus given slowly vs. drinking the same amount? I agree I would never dump like 1000cc on a chf pt. In the end the chf patient was fine. Was I right to ask for the bolus or was my preceptor?
- 0Jul 1, '13 by nrsang97If BP was that low I would have asked for a bolus and given it slowly as well. Yes you could encourage oral fluids but it may take longer to correct a low BP. It the pt tolerated it then nothing wrong. Always when bolusing a CHF pt keep tabs on how they are tolerating the bolus.
- 0Jul 23, '13 by lilund27I work on an Acute Tele Unit and have given small bolus's to CHF pt's. Sometimes the benefit out ways the risk. Odds are your pt was on diuretics and that could have been partially to blame for a low bp too. The main thing to watch for is fluid overload, respiratory distress, O2 levels, ect. I am glad you asked the doctor for a small bolus. I prolly would have done the same thing.
- 4Jul 28, '13 by GrnTeaDo you understand the rationale for all this? Frank-Starling Law, preload and afterload and all that?
Ventricular filling pressure is just the pressure that is in the ventricles at the end of diastole (LVEDP, left ventricular end-diastolic presssure). For a given volume delivered to a ventricle, pressure can be lower if the ventricle is nice and soft and flexible and empty, ready to accept a new load, than if it's hard and scarred up or has leftover blood in it from the last systole because the AV is hard to open OR because its contractility was so lousy that it didn't empty well. Another term that is used could be "preload," pre- meaning "before systole," and load, well, being the load of blood delivered to the ventricle that it is gonna have to move out in systole. You can measure load as weight or volume, but the way we look at it is by measuring the pressure that occurs there. Pressure changes tell us what's going on in there. Think about a soft balloon (low pressure) and a hard one (high pressure). Which has more air in it?
Let's look at the blood flow in a linear fashion. I regret that I cannot give these in color so you can see the blue of venous, the red of arterial. But hey. Draw them on a piece of paper in color. The lungs are pink
Body > Veins > Vena Cava > Right Atrium > tricuspid valve > Right Ventricle > pulmonic valve > Pulmonary Artery > LUNGS >Pulmonary Vein > Left Atrium > mitral valve > Left ventricle > aortic valve > Arteries > Body
Think about when the valves between two chambers are OPEN. By definition, each chamber must be at the same pressure, right? So, at the end of diastole, just before systole, the pressure in the LV is the same as LA pressure is the same as the pressure in the pulmonary vein (no valve in the way there) and in the pulmonary capillary bed. And since there are no valves in the pulmonary capillary bed, tracking backwards, you can see that LV end diastolic pressure equals end-diastolic PULMONARY ARTERY PRESSURE, which is, conveniently, what we look at when we are wondering what's going on in the left heart. You can even follow it back all the way to the right atrium, and the vena cava-- central venous pressure! Wow!
OK. Now, why do we care about LV end-diastolic (filling) pressure? It's because that's where the work of supplying the whole body goes. For that, I wish I could draw you a nice little curve here. I can't, so I will describe it and YOU will draw it on a piece of paper to look at while we chat.
Horizontal axis: label this "preload" or any other term you like. Filling pressure, PA diastolic pressure is the same thing (see above) and you can even extrapolate all the way back to central venous pressure, for a rough trend-setting bit of data.
The vertical axis you will call "cardiac output," or "blood pressure," because the line we are going to draw is going to explain something really cool.
Start lowish on the left, near the vertical axis-- low filling pressure means low BP. Think: hemorrhage, hypovolemia, makes your BP low, right?
Slant the line upwards to the right, showing that blood pressure (cardiac output) increases the more blood you put into the heart. (Tank up that hypovolemic guy, and BP improves.) But at some point, that upward-going curve peaks, flattens out...and then it DROPS as the preload keeps increasing. This is because cardiac muscle is like a rubber band-- the more you stretch it, the harder it contracts...to a point, at which point it gets too stretched out and actually contracts less well. Draw a little asterisk at the top of that curve, where it starts to fall, then let it fall a little bit. That asterisk marks the best cardiac output you can get-- preload and output are optimal for that heart. Beyond that point, where the line slopes downwards, lies congestive heart failure- the heart is too full, has more than it can handle, and it fails. (This is, BTW, called the Frank-Starling Law of the heart, and you just drew the Frank-Starling curve) Pressure backs up into the pulmonary capillary bed making the lungs get wet and heavy. This is when people get diuretics (to decrease that excessive preload) AND drugs to improve their contractility.
Of course, if contractility is lousy because of coronary artery disease, previous MI, or whatever, this whole curvy line thing will kinda slide over to the left-- the myocardium will fail with lower pressures than it would if it had better contractility. Better contractility (a right shift) means it will handle more preload (higher filling pressures) and make better BP out of it. Draw a second curve to the right of the first one, parallel to it, to see that. With me so far?
I think you can see how CAD will give you higher filling pressures-- when the heart is failing a bit, it goes past the top of its curve more easily because its contractility is diminished.
Mitral STENOSIS will, in fact, decrease your LV preload, but it will increase pressures back into the lungs and, eventually, the right heart, because of the resistance to flow from the right side to the LV. Mitral REGURGITATION, on the other hand, will result in higher filling pressures because when the ventricle contracts in systole, some of the blood goes backwards, leaving excess sloshing around between the atrium and ventricle; the ventricle will have to accept a higher reload at diastole, and it doesn't like it. Over the top of the curve again.
Well, I hope this hasn't confused you. I used to tell my students they had to know this because we saw lots of people with all sorts of deficits, but if they didn't have hearts and lungs, they were dead and we didn't have to take care of them anymore. Works in every possible area you could work, except pathology. Please ask me if I've confused you anywhere.