Could a kidney problems lead to lung problems?

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Just curious if a patient with kidney problems could have lung problems, or breathing problems?

My thinking was that with kidney issues, there could be less circulating blood volume -> less cardiac output -> less blood going to lungs -> respiratory difficulty

Is this case probable?

Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.

NO.....not this way. What makes you think that "kidney problems" is less circulating blood volume? What semester are you in?

Kidney problems lead to fluid over load which leads to lung congestion/fluid overload.

I think that you're thinking that decreased cardiac output will lead to decreased kidney perfusion which can then cause kidney failure. If the kidneys fail then you can go into fluid volume excess. I can understand how you think it effects the resp sys...

Respiratory changes can occur when the body is in fluid volume excess and the blood isn't getting pumped forward, but instead back up into the lungs.

I understand that with decreased cardiac output, the body would have to compensate by breathing faster to compensate for less oxygen in the body. So it seems that decreased cardiac output, could affect the lungs.

(For kidney issues there could be too much fluid or not enough fluid). In the case that, it is decreased fluid volume due to a kidney issue then that would mean that the heart has less pressure to pump out. Less volume less pressure. Which means there would be a decrease in cardiac output.

So what exactly is off.

My thinking was that with kidney issues, there could be less circulating blood volume -> less cardiac output -> less blood going to lungs -> respiratory difficulty

I understand that with fluid volume excess, this could cause fluid overload in the lungs, and end up in trouble breathing.

NO.....not this way. What makes you think that "kidney problems" is less circulating blood volume? What semester are you in?

Kidney problems lead to fluid over load which leads to lung congestion/fluid overload.

The kidneys help to requlate fluid volume through the renin-angiotensionogen system. Renin is released in the kidneys which eventually affects how much salt is retained in the kidneys. With salt goes water, and that affects fluid volume in the system.

I think that you're thinking that decreased cardiac output will lead to decreased kidney perfusion which can then cause kidney failure. If the kidneys fail then you can go into fluid volume excess. I can understand how you think it effects the resp sys...

Respiratory changes can occur when the body is in fluid volume excess and the blood isn't getting pumped forward, but instead back up into the lungs.

That part makes sense.

Less blood going through the lungs does not effect the respiratory system in that way. It just means less oxygenated blood being circulated.

Less blood going through the lungs does not effect the respiratory system in that way. It just means less oxygenated blood being circulated.

With less blood going through the lungs that must be where I get my respiratory difficulty coming in.

As there is less blood going to the lungs. So with less blood, the person needs to breath a little faster to keep the oxygen flowing in the right amount.

Is that it?

Decreased cardiac output causes shortness of breath and wet lung sounds and since there's less volume of blood there's decreased bp& decreased peripheral pulses. at least that's what I learned from hurst!

You're completely missing the very important aspect of compensation, the real meaning of how the heart "decides" how much to pump, and the concept of blood oxygen content. Things are very rarely that simplistic cut-and-dried, cause-and-effect you're thinking. There's a lot more going on.

I understand that with decreased cardiac output, the body would have to compensate by breathing faster to compensate for less oxygen in the body. So it seems that decreased cardiac output, could affect the lungs. With less blood going through the lungs that must be where I get my respiratory difficulty coming in.

As there is less blood going to the lungs. So with less blood, the person needs to breath a little faster to keep the oxygen flowing in the right amount.

No, it doesn't work like that.

Decreased cardiac output (CO) decreases the amount of blood per minute pumped into the aorta, but that may or may not result in tissue hypoxia. Besides, the lungs' first job, and the one it does most efficiently, is not getting oxygen in, it's getting CO2 out (you can look it up), and so resp rate would be expected to be that affected with decreased CO. Increased CO2 levels are what makes for tachypnea in most everyone. If someone is so hypoxic that the hypoxic drive is making him tachypneic, he (and you) have far worse problems.

(For kidney issues there could be too much fluid or not enough fluid). In the case that, it is decreased fluid volume due to a kidney issue then that would mean that the heart has less pressure to pump out. Less volume less pressure. Which means there would be a decrease in cardiac output.

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Not necessarily at all. That's another compensation you need to take into account. You learned about that in physiology.

You can be relatively hypovolemic (from any cause, including high-output renal failure) and still have a stable cardiac output. Why is that? Do you understand that CO = stroke volume (the amount of blood being pumped in every contraction) x heart rate? So, using exaggeration for effect, you could halve your stroke volume and double your heart rate and have a perfectly stable CO. As to BP (which you didn't mention, but comes in here), vascular contractions can stabilize BP in the face of decreased CO and hypovolemia too.

My thinking was that with kidney issues, there could be less circulating blood volume -> less cardiac output -> less blood going to lungs -> respiratory difficulty

I understand that with fluid volume excess, this could cause fluid overload in the lungs, and end up in trouble breathing.

You can't have less pulmonary blood flow and more pulmonary blood flow at the same time. Besides, pulmonary blood flow is not going to affect breathing itself.

Fluid overload is also a relative term, subject to the body's compensation ability. Let's look at that:

A normal heart will pump more blood out the more that comes into it, to a point. This makes sense if you figure that, for example, in exercise, the venous return is greatly increased. This tells the heart that more cardiac output would be a good idea, to support the exercise, so when it sees increased venous return in the form of diastolic s-t-r-e-t-c-h-i-n-g it contracts more forcefully, making a higher stroke volume. Rate goes up too, depending on other factors like increased blood CO2 level (from the working muscles). Result: higher cardiac output.

Now, let's look at what happens when the venous return is higher than the heart can accept-- the ventricle is s-t-r-e-t-c-h-e-d toooooo far, like an overinflated balloon. In that case, it's not able to increase its contractility any more to accommodate that increased volume (from whatever cause-- like renal failure or iatrogenic administration of fluids or **weakened cardiac muscle that has lost some of its compensation ability**). So it fails to pump it all out, and blood backs up into the lungs. This makes the lungs heavy and wet, increasing work of breathing and decreasing gas exchange as alveoli fill with fluid. This is why it's called congestive heart failure, and why you hear wet lungs with fluid overload.

Less blood flow in the lungs won't make them wet and heavy, so you won't get more trouble breathing. You would have to be very hypovolemic indeed to have so little oxygen-carrying ability to make you short of breath-- think exsanguination after major trauma. Not going to do that with a renal cause.

Hope this helps you think a little more about how these systems work together. They're critical concepts in many, many aspects of patient care, pharmacology, assessment, and teaching.

Decreased cardiac output causes shortness of breath and wet lung sounds and since there's less volume of blood there's decreased bp& decreased peripheral pulses. at least that's what I learned from hurst!

Exactly backwards. Or maybe sideways. :)

Decreased cardiac output from cardiac failure results in wet lung sounds, but that's not from hypovolemia. It's from relative fluid overload. The cardiac failure causes the decreased BP and weak pulses.

This is something to consider: Get out a piece of paper and follow along, because this is what you will need to understand about cardiac function related to fluid volume.

It's helpful if you can step back first and think of what the anatomy of the circulatory system is supposed to accomplish. It's supposed to move a fluid around in a bunch of blood vessels, pumped out at high pressure from the left side of the heart, returned to the heart by passive squeezing in the veins and kept from sloshing backwards by valves in the vessels. Then the right side of the heart is supposed to push it through the lungs (at a lower pressure, because it only has to perfuse the lungs right next door, not all the way down to the toes like the arterial system) to do the gas-exchange thing. Then the fluid goes back to the left side of the heart and out to the body again.

Ventricular filling pressure is just the pressure that is in the ventricles at the end of diastole (LVEDP, left ventricular end-diastolic pressure). 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 last time. 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?

Your instructor is partly right, but just didn't give you a very full explanation. 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.

I was wondering what could cause a person with kidney issues to have respiratory difficulty

Kidney issues, there could be less circulating blood volume -> (hypovolemic)less blood going into heart -> less oxygenated blood -> respiratory difficulty

Do I understand correctly that this case is very rare.

The kidney issues that have respiratory difficulty is most likely going to be due to fluid volume excess, fluid in the lungs, CHF.

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