Pathophysiology of CHF

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Chewy20

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Am curious to see how paramedics try and explain it. You don't need to get all technical if you decide to answer. I know what it is and how to treat it etc...I am just digging more into the patho side of things and Google is not doing it for me on this one.
 
Cardiac failure is, in simple terms, where the heart is unable to eject the amount of blood that is returned to it from the pulmonary circulation.

The most common causes of this are (a) worsening of existing myocardial ischaemia, (b) acute myocardial infarction - particularly lateral or anterolateral infraction as these normally involve a portion of the left ventricle or (c) tachydysrhythmia - particularly VT.

As the heart is unable to eject the volume of blood being returned to it then the hydrostatic pressure in the pulmonary venous bed exceeds that of the interstitial fluid and the natural place for the excess fluid to go is down the osmotic gradient to an area of lesser pressure (concentration).

It is the fluid within the alveoli that impairs gas exchange.

Most people have left ventricular failure but it is also possible to have right ventricular failure too, either in isolation (although I understand this is quite rare) or in conjunction with LVF; i.e. bilateral cardiac failure. I know some older Doctors and Nurses refer to "high output" and "low output" cardiac failure but I'm not sure exactly what these mean as these terms are no longer used.

Briefly - the best prehospital treatment for acute pulmonary edema is GTN and non invasive ventilation. We no longer carry frusemide (and in fact haven't done so for about five years I think, it was just on the way out when I started). Morphine is not an effective treatment although I know some people still use very small doses of morphine to treat anxiety and severe respiratory depression. Alas, we do not have CPAP in NZ, we have poor man variety which is holding bag mask over their face with a PEEP valve attached; which is messy and a pain in the bottom to be totally honest.

Oh, and do a good 12 lead ECG to exclude MI and/or VT.

Hope that helps :)
 
I'll add on a little to what Clare said.

As the left ventricle continues to fill with more blood than it knows what to do with, you lose the Frank-Starling effect (contractility - the heart is a muscle, and can be overworked just like any other muscle, becoming hypertrophic, or from those pathological failures Clare mentioned). This excess blood return results in an increase in preload and afterload. Our goals in the field are to decrease that preload and afterload, and if they're at a point of cardiogenic shock, an inotropic drug may be given to support contractility.

Right sided failure secondary to chronic pulmonary conditions is called cor-pulmonale. Essentially, chronic pulmonary hypertension (think COPD, for example) secondary to chronic hypoxia brings on the same 'over-filling' effect with the right ventricle, and over time a now hypertrophic right ventricle can no longer support the increase in preload and right ventricular pressure. A much lesser of an issue than left sided failure w/ pulmonary edema.
 
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Don't forget about the RAAS. That's an important cascade of events that further worsens the problem.
 
Thanks guys

Feel free if others want to explain it the way they understand it.
 
It's like when the sump pump under the house cannot keep up with the volume being added to it... The liquid will back up and get into the house.

For CHF, the 'house' is your lungs.
 
There are better ways to describe CHF. Are we talking about acute failure or chronic failure, or acute on chronic failure (acute exacerbation)? Is it systolic dysfunction (low ejection fraction) or diastolic dysfunction (low filling volume) or both? Is it ischemic or non-ischemic?
 
Heart Failure is one of those conditions that you can keep digging more into; it's incredibly complex.
gotshirtz001 said:
It's like when the sump pump under the house cannot keep up with the volume being added to it... The liquid will back up and get into the house.
Click to expand...
Not all Failures are fluid overloaded. Something like 40% of acute failure patients are actually hypovolemic, which is why pre-hospital lasix is falling out of favour. Almost half of the patients we were diuresing in the field we were actually harming.

This is a good website that breaks down CHF a little more without going too far down the rabbit hole ;)
[ur]http://www.pathophys.org/heartfailure/[/ulr]
 
Heart failure = the inability of the heart to meet the demands of the organs. It could be pump failure or increased metaboliic demand.

I think for prehospital EMS, we can boil it down to an acute exacerbation, which is a vicious cycle.

Acute L ventricular systoloc (pumping) dysfunction (for whatever reason) >
Decreased cardiac output >
Sympathetic response increases pre- and after-load >
Increased workload of L ventricle against increased afterload >
diastolic (filling) dysfunction >
Increased pulmonary artery and capillary pressures >
fluid being pushed into alveoli >
Hypoxia >
Increased myocardial demand ischemia >
Increased systolic dysfunction


That being said, there are many ways to get to HF, and the physiologic effects are mucho complicated, both acutely and chronically...I didn't even mention the kidneys ;)
 
to add, furosemide is out for most places for treatment. Here we give nitro and a CPAP. Look it at as fluid misplacement, rather than "overload". not saying overload can't be a cause, but it's not left to us prehospital to determine that
 
Pulmonary edema will cause surfactant washout, which results in atelectasis, and the fluid also impairs gas exchange in the alveoli. That atelactasis can cause what you may have been told was "cardiac asthma," or "cardiac wheezing." CPAP does not only just "push lung water," it also helps splint open the alveoli, to reverse the atelectasis. The increased intra-thoracic pressure from CPAP (and also PPV) can impede venous return, and drop blood pressure. Consider a small fluid bolus, or a pressor depending on what side the failure is believed to be, to support the pt's B/P while the CPAP begins to work. #savethemfromETI
 
46Young said:
Pulmonary edema will cause surfactant washout, which results in atelectasis, and the fluid also impairs gas exchange in the alveoli. That atelactasis can cause what you may have been told was "cardiac asthma," or "cardiac wheezing."
Click to expand...
Atelectasis causes the crackles or rales. The wheezing of "cardiac asthma" is caused by accumulation of perivascular edema in the interstitial space of the alveolar and bronchial walls. This engorgement causes a constriction of the small airways which produces wheezing.
 
46Young said:
Pulmonary edema will cause surfactant washout, which results in atelectasis, and the fluid also impairs gas exchange in the alveoli. That atelactasis can cause what you may have been told was "cardiac asthma," or "cardiac wheezing." CPAP does not only just "push lung water," it also helps splint open the alveoli, to reverse the atelectasis. The increased intra-thoracic pressure from CPAP (and also PPV) can impede venous return, and drop blood pressure. Consider a small fluid bolus, or a pressor depending on what side the failure is believed to be, to support the pt's B/P while the CPAP begins to work. #savethemfromETI
Click to expand...

Can you expand on that?
 
This article is excellent. Great review, thanks for posting it.
 
Clare said:
I know some older Doctors and Nurses refer to "high output" and "low output" cardiac failure but I'm not sure exactly what these mean as these terms are no longer used.
Click to expand...

You may be thinking of systolic versus diastolic failure. True "high output heart failure" is not very common and comprises an heterogeneous collection of oddities like wet beri beri, AV malformations, etc... basically where the heart is pumping fine (neither systolic nor diastolic failure) but that's still not cutting it. Not what we have in mind when we talk about cracklin' granny.
 
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