EF in diastolic HF

[MudPhud20XX]

So FA says you get normal ejection fraction in diastolic HF. I am having difficult time understanding this. With diastolic HF, you can't really fill your Lt ventricle during diastole which decreases the stroke volume right? I guess the reasoning is you also get decreased EDV which will keep the EF value above normal right? Anyway, let me hear what you guys think. Many thanks in advance.

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[tasar1898]

Don't try to explain it mathematically , I had the same problem in understanding Diastolic Failure , but in the end it's really simple if you think like that..
Infiltration of ventricle with something that makes it ''stiffer''---> Ventricles can still fill with the same volume but at the ''cost'' of overtly increasing pressure ( the concept of compliance) --> EF/EDV/SV is normal/slightly subnormal --> Eventually , the ventricle ''thinks'' its gonna burst and over time tries to normalize the tension created by the increased pressure ( remember laplace --> T= Pressure/wall thickness) --> Concentric hypertrophy to increase wall thickness and thus decrease wall tension --> Concentric hypertrophy leads to restricted cavity size --> EDV falls and SV falls and symptoms start/get worse ( EF though stays the same)

 

[tasar1898]

Forgot to mention this , Increased pressure is ''transmitted'' backwards so you get symptoms of HF ( pulm or peripheral edema ) via increased Pc even at the initial stages with normal EDV

 

[Tajima]

EF is a ratio.
The ability of the heart to expel blood forward is technically preserved in textbook true diastolic dysfunction. The problem is that the heart cannot fill, but ejection is not affected.
Thus, the ratio of blood ejected to blood not ejected (the ejection fraction) is unchanged.

 

[deleted500612]

In early/compensated diastolic dysfunction (hypertrophic cardiomyopathy) the EDV and EF are both normally preserved, as is stated in first aid. This is because the left atrium will contract harder to fill the stiff LV in order to obtain a normal EDV, but at an increased end diastolic pressure. The way that I remember that EF is also not increased is simply that although hypertrophied LV may offer additional contractile force it is contracting against an increased afterload (usually why it underwent concentric hypertrophy in the first place) so the forces cancel out and EF is around normal.

Also interesting to note that in the physiologic myocardial hypertrophy due to cardiovascular exercise, there is no accompanying increase in afterload (as there normally is in hypertrophic cardiomyopathy) to counteract the contractility gained from myocardial hypertrophy and thus the EF, and therefore SV are actually increased here, allowing for the overall increase in cardiac output seen in trained athletes.

 

[gmbz]

Correct me if I am wrong, but doesn't diastolic dysfunction deal with a loss of lusitropy, not compliance?

 

[tasar1898]

I don't even know what lusitropy is… damn those cardiologists and their obscure terms … lusitropy ,chronotropy , isotropy .. who cares???

 

[gmbz]

I don't know what is to be expected on Step I as of yet so hopefully someone more knowledgeable can chime in on that.

Lusitropy seems to be a question of impaired removal of Ca++ which leads to decreased relaxation in the myocytes ect. So more of an "active" step as opposed to the "passive" step that is compliance?

 

[tasar1898]

Even though I wanted to ignore it I looked it up… Lusitropy refers to the rate of relaxation as influenced via intracellular calcium clearing via 1) SERCA , 2) Na/Ca ATPase , 3)Myocyte plasma membrane ATPase and it has nothing to do with passive properties of the ventricle i.e compliance etc..

Increased Lusitropy --> Catecholamines (more rapid clearing of Ca possibly to increase HR? , mediated via more SERCA activity)
Decreased Lusitropy --> Mutations/Dysfunction in these pumps , Digoxin or generally anything that increases intracellular Ca , except catecholamines

 

[walakin25]

wow tasar man why u gotta give me palpitations like that ... lusitropy wtf lol

 

[gmbz]

Now is this information fair game for Step I?

 

[tasar1898]

haha even I as a greek had no clue what these words mean , couldnt they use increased HR or w/e… intellectual crap...

 

[tasar1898]

@gmbz I guess you should know the Ca mechanisms , but i don't think anyone except pompous cardio researchers uses the term ''lusitropy''

 

[deleted500612]

Now is this information fair game for step I?

Just got a UWorld question 5 minutes ago that is EXACTLY what this thread is discussing, so I would assume yes it definitely is!

"Which of the following diagnostic findings would be most consistent with isolated diastolic heart failure?" Followed by an arrow table for left ventricular EDV, EF, and End diastolic pressure variables. Answer was EDP increased, EDV normal, EF normal. (Only 35% of people got it right)

 

[Daitong]

Don't try to explain it mathematically , I had the same problem in understanding Diastolic Failure , but in the end it's really simple if you think like that..
Infiltration of ventricle with something that makes it ''stiffer''---> Ventricles can still fill with the same volume but at the ''cost'' of overtly increasing pressure ( the concept of compliance) --> EF/EDV/SV is normal/slightly subnormal --> Eventually , the ventricle ''thinks'' its gonna burst and over time tries to normalize the tension created by the increased pressure ( remember laplace --> T= Pressure/wall thickness) --> Concentric hypertrophy to increase wall thickness and thus decrease wall tension --> Concentric hypertrophy leads to restricted cavity size --> EDV falls and SV falls and symptoms start/get worse ( EF though stays the same)

So is it that initially the SV, EDV are preserved, but it's only after concentric hypertrophy that occurs does SV and EDV decrease?

 

[Daitong]

Don't try to explain it mathematically , I had the same problem in understanding Diastolic Failure , but in the end it's really simple if you think like that..
Infiltration of ventricle with something that makes it ''stiffer''---> Ventricles can still fill with the same volume but at the ''cost'' of overtly increasing pressure ( the concept of compliance) --> EF/EDV/SV is normal/slightly subnormal --> Eventually , the ventricle ''thinks'' its gonna burst and over time tries to normalize the tension created by the increased pressure ( remember laplace --> T= Pressure/wall thickness) --> Concentric hypertrophy to increase wall thickness and thus decrease wall tension --> Concentric hypertrophy leads to restricted cavity size --> EDV falls and SV falls and symptoms start/get worse ( EF though stays the same)

I'm not sure this is correct- isn't it that the concentric hypertrophy CAUSES the diastolic dysfunction in the first place, not the opposite away around (though the symptoms could exacerbate on another, but diastolic dysfunc is still 2ndary to myocardial HF)

 

[Instatewaiter]

The traditional way this happens is that soneone has hypertension or AS and the increased afterload causes the ventricle to hypertrophy.

It thickens, this causes the heart to be less compliant. Your EF is always normal or low normal (50%ish) and your end diastolic volume is normal (at least initially) but to keep this volume you need a higher pressure. Thus your LVEDP rises.

Some people do experience enough hypertrophy that their end diastolic volumes do drop but this is rare and late.