the NTG dilates the blood vessels, and the CPAP pushes the fluid out of the lungs and back into the vessels, which can handle the additional fluid because they have been dilated by the NTG.
Somewhat. But not really.
In CHF, the neurohormonal responses (sympathetic, RAAS) kick into high gear to compensate for the reduced cardiac output. The side effects of this response are very high B/P (unless cardiogenic shock), increased HR, and increased afterload.
The APE comes from the failing LV which cannot handle the blood being returned to it and as a result it backs up into the left atrium and than the pulmonary vasculature. This creates a much higher pressure within the pulmonary system. This increased pressure is what forces fluid across the alveolar-capillary (AC) membrane and into the interstitial and alveolar spaces resulting in acute pulmonary edema (APE).
This fluid in the lungs has several negative effects with mainly being increased diffusion distance... gases have to travel further through the fluid to reach their destination... and atelectasis... the fluid causes the alveoli to collapse from surfactant washout. As a result, work of breathing goes way up as it takes more force to inflate a collapsed alveoli... this is where the beauty of CPAP comes in.
With CPAP, there is a continuous pressure applied to the airways on expiration which keeps the alveoli from collapsing. Since the alveoli are always partially inflated, it lessens the amount of work to expand them and have them take part in gas exchange.Think of a balloon. What is the hardest part of blowing up a balloon? It's always the initial blow right when the balloon is completely empty. Once you have a little air in the balloon you don't need to blow near as hard to inflate it. It's the same concept in the lung and this is what dramatically reduces the work of breathing. CPAP aids in recruitment of alveloi.
So the benefits of CPAP are: reduced atelectasis, reduced work of breathing, and increased surface area available for gas exchange. With the positive pressure induced within the chest, there is also reduced preload and a reduction in afterload which is a great thing. Reduced preload results in further reduction of B/P and reduced afterload makes it easier for the heart to eject blood.
Hopefully you can see there is no actual "forcing of fluid" out of the airways. The fluid leaves the airways mainly as a result of restoring the pressure gradient in the lungs by lowing the blood pressure.
The main goal of NTG in CHF is pressure reduction for reasons stated above. It's vital to get the B/P down to allow the fluid to retreat back across the AC membrane to where it belongs. Other main goals are to reduce the workload of the heart. To dilate is to reduce preload which makes the heart work less hard and reduces myocardial oxygen consumption. NTG also has effect on afterload especially with higher doses which makes the heart work less hard as it doesn't have near the resistance to pump against. A reduction in afterload is where ACE inhibitors come into play as that is what they do - some current evidence strongly recommend ACE inhibitors early.
A lot of patients in CHF are euvolemic (normal volume) or sometimes even dehydrated. Lasix isn't where the prize is. Along with diuresis effect, Lasix also relaxes blood vessels as well. But evidence doesn't hold Lasix real high anymore. And morphine has been shown to be bad in CHF. I like fentanyl personally. To treat with opiates helps to reduce the sympathetic response.
I just spewed this out but hopefully it helps to understand what is really going on and what the initial treatment goals are.
