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ResTech

ResTech

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While reading up on CPAP and CHF today I came across sources that appeared to conflict with the physiology of how CPAP can induce hypotension.

One source states that CPAP reduces both preload and afterload by causing an INCREASE in intrathoracic pressure, of which can cause hypotension in some cases.

And than, when looking at pulsus paradoxus, that source states that a decrease in blood pressure can be noted as a result of the DECREASED intrathoracic pressure. Whereas the pressure inside the chest is more negative in comparison to atmospheric.

Which is it? Im confused ???? Can someone in simple terms to start with explain how the pressures play a role in reducing preload and afterload. I been Google'ing and am frustrated... cant find the answer.
 
ResTech said:
While reading up on CPAP and CHF today I came across sources that appeared to conflict with the physiology of how CPAP can induce hypotension.

One source states that CPAP reduces both preload and afterload by causing an INCREASE in intrathoracic pressure, of which can cause hypotension in some cases.

And than, when looking at pulsus paradoxus, that source states that a decrease in blood pressure can be noted as a result of the DECREASED intrathoracic pressure. Whereas the pressure inside the chest is more negative in comparison to atmospheric.

Which is it? Im confused ???? Can someone in simple terms to start with explain how the pressures play a role in reducing preload and afterload. I been Google'ing and am frustrated... cant find the answer.
Click to expand...
The main reason for hypotension associated with CPAP use is that it decreases preload by putting additional pressure on the right ventricle and reducing the filling causing the RV stroke volume to be reduced. The effect is particularly seen in patients who have lost the atrial filling kick (such as in atrial fibrillation) or when you turn the pressures up too high. The comparatively thinner walls of the right ventricle make it more prone to this. As for its effect on afterload, I would imagine it has some effect, but believe the reduction in RV stroke volume is primarily responsible for this effect.

A similar effect can be seen in patients who are on a ventilator and have the PEEP (positive end expiratory pressure; physiologically the same thing as CPAP) turned up to high or the rate of ventilation is excessive causing breath stacking due to insufficient ability to exhale which produces what has been termed "auto-PEEP". The way to fix either of these problems rapidly (and diagnose the problem at the same time) is to disconnect the patient from the bag/vent/CPAP and let them passively exhale. Reduction of the rate of ventilation (increasing the expiratory time in other words) and/or the PEEP/CPAP setting once you resume mechanical ventilation- and CPAP is a mechanical ventilation mode- should fix the problem if that is what is producing the hypotensive event.

Any further questions? Anything I need to clarify?
 
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Im still confused as to why in one condition with CPAP, its the INCREASED intrathoracic pressure causing a drop in B/P... and in another condition... Pulsus Paradoxsus... its the DECREASED intrathoracic pressure causing the drop in B/P.

That isnt making sense still.

I guess most importantly for now, as long as I know and understand that CPAP causes an increase in intrathoracic pressure which causes an overall reduction in myocardial workload by reducing preload and afterload... Im good. And also, I understand that its best to start with the lowest PEEP setting (usually 5cm/H2O) and titrate up to maximum of 10cm.H20 and be watchful as more PEEP can induce the hypotension by reducing preload too much.

Is this correct?

My brain is overloaded and can hardly think from studying/worrying about this stuff today. Time to walk away and take a break!
 
Im still confused as to why in one condition with CPAP, its the INCREASED intrathoracic pressure causing a drop in B/P... and in another condition... Pulsus Paradoxsus... its the DECREASED intrathoracic pressure causing the drop in B/P.
Click to expand...

OK....how to explain this....basically it is the effect of the decreased intrathoracic pressure causing the pulmonary vasculature to expand slightly which basically causes the intravascular space to increase slightly while the intravascular volume remains fixed. So while normally a drop in intrathoracic pressure would INCREASE the amount of blood reaching the right side of the heart, in certain cases (COPD, tamponade, pericardial effusions, severe asthmatic exacerbations, etc) the drop in pressure actually causes blood to "pool" momentarily in the vessels feeding and draining the lungs so the BP drops slightly. Normally it is only really noticeable if you have a patient with either very compliant lungs (COPD) or something putting pressure on the right ventricle already (pericardial tamponade or effusion, or the overinflated lungs seen in severe asthma) or a depleted intravascular volume to begin with. In cases where there is a dramatic compression of the right ventricle associated with normal or increased intravascular fluid volume, the intraventricular septum can also be pushed over towards the left ventricle reducing the LV stroke volume. This feature is something I've seen a couple of occasions while performing echocardiograms on patients with large pericardial effusions.
 
I'm going to throw USAF off of his game.


Why is CPAP and PEEP measured in cm/H2O, but suction in mmHG?


Riddle me that batman!^_^
 
Linuss said:
I'm going to throw USAF off of his game.


Why is CPAP and PEEP measured in cm/H2O, but suction in mmHG?


Riddle me that batman!^_^
Click to expand...
I recall being told the reason once, but that was many moons ago. In other words, I can't remember off the top of my head and don't want to be accused of simply looking around for the answer online.
 
I would never accuse you of such. I can't find the answer my self.
 
Linuss said:
I would never accuse you of such. I can't find the answer my self.
Click to expand...
I vaguely recall it having something to do with historical BS. Beyond that, I'm stumped.
 
mmh20

Due to the extremely fine adjustment the respiratory world necessitates, they needed a smaller delineation. Not to mention 3 A.M math is way easier with a number like 15 rather than 1.103. Suction in the other hand… …is a game of brute force. No one in the back of an ambulance cares about a tenth of a mmHg. Chest tubes notwithstanding, but now you’re using suction in the respiratory world.

PS, for grins I did the math. Your range of 6-30 mmH20 Cpap would give you a range of .441-2.2 mmHg.

1 mmH2O = .074 mmHg

I’m a fan of whole numbers while bouncing down the highway at or above 75 MPH
 
The reason BP drops in pulses paradoxes is that when you increase venous return to the heart, like during inspiration, the right ventricle fills more, and you get bowing of the septum, which can occlude the aortic outflow tract. Normal doesn't have much of an effect but when you have a condition like pericardial effusion, which prevents the ventricle from expanding outward, you get more bowing and more obstruction and more blood pressure drop.

In artificial ventilation like intubation or Bipap during inspiration there is an increase in pressure, decreasing preload. Especially if the person is already intravascularly depleted this can decrease BP.
 
That makes a lot of sense thanks Doc.
 
ResTech said:
While reading up on CPAP and CHF today I came across sources that appeared to conflict with the physiology of how CPAP can induce hypotension.

One source states that CPAP reduces both preload and afterload by causing an INCREASE in intrathoracic pressure, of which can cause hypotension in some cases.

And than, when looking at pulsus paradoxus, that source states that a decrease in blood pressure can be noted as a result of the DECREASED intrathoracic pressure. Whereas the pressure inside the chest is more negative in comparison to atmospheric.

Which is it? Im confused ???? Can someone in simple terms to start with explain how the pressures play a role in reducing preload and afterload. I been Google'ing and am frustrated... cant find the answer.
Click to expand...

If you look at the hemodynamic normal pressure readings you'll see that the CVP normals are, according to the 2010 ACLS guidelines, are 2-6 mmHg or 2.5-12 cmH2O.

How do they come up with these measurements? Back in the day all of this was invented they didn't have all of the new fangled thangs called computers. What they did have were pressure cuffs that had mercury and would measure how many millimeters the mercury would be displaced. They also had sterile water and buckets and would stick corrugated tubing in them and would measure how many centimeters the water would be displaced.

Now if you think about it, 5 -10 cmH2O of CPAP or PEEP is right smack dab in the middle of those CVP measurements. And if you begin to add more (15 or 20), you need to be real careful. Because that much is automatically more than the normal CVP ranges. When your CPAP exceeds that much it can and will begin to push the blood back upstream and out of the RA and back into the Vena Cavae which will drop the blood pressure.
 
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