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"Starling curve" in heart failure


"Starling curve" in heart failure

المعلومة

What happens to "Starling curve" in heart failure?
And how could you make benefit out of it (in terms of treatment)?

ما هو التغير الذي يطرأ على مخطط ستارلنغ في قصور القلب ؟
ما التطبيق العملي لهذه المعلومة (عندما نتحدث على علاج القصور القلبي)؟

-الجواب بسيط-

المرجع

Davidson's Principles & Practice of Medicine

by
السنة السادسة

ok i am going to give you a little help,
this diagram:

OmHa
السنة السادسة

Quote:
sorry i'm the only one answered your question

there is no need to be sorry , actually you gave a nice try your answer is true >>>>Eye-wink

and here is the description for this image>

Figure 18.21 Starling's Law. Normal (A), mild (B), moderate (C) and severe (D) heart failure. Ventricular performance is related to the degree of myocardial stretching. An increase in preload (end-diastolic volume, end-diastolic pressure, filling pressure or atrial pressure) will therefore enhance function; however, overstretching causes marked deterioration. In heart failure the curve moves to the right and becomes flatter. An increase in myocardial contractility or a reduction in afterload will shift the curve upwards and to the left

.

AS for the second QUESTION i will leave it till further notice ,till our friends study the Heart failure thing.(:

OmHa
السنة السادسة

Quote:
ما التطبيق العملي لهذه المعلومة (عندما نتحدث على علاج القصور القلبي)؟
we should increase the contractility & decrease the afterload

contractility is increased by ionotropic agents as digoxin

afterload is decreased by decreasing volume i.e. diuretics
Rolling Eyes Rolling Eyes Rolling Eyes

lifespring
السنة الخامسة

Quote:
so to increase contractility we should reduce the Parasympathetic effects so we can give the patient
something to deactivate the m2 receptors in the heart(i dont know what it's called)

بس في شغلة أنو اللي عندو قصور قلب أصلا عندو زيادة تفعيل للجهاز الودي والجهاز نظير الودي موهو السبب بالمرض بس الشغلة اللي انت حكيت عنها الها تطبيق Eye-wink بغير شغلة (بالAsystole) هون القلب بيوقف ما بنعرف ليش ==>بس بنحاول يشتغل غصب عنه بالأتروبين (معاكس الاستيل كولين)

Quote:
afterload is decreased by decreasing volume i.e. diuretics

بس المدرات تنقص من الحمل القبلي ..... طيب هون الواحد بيسأل هيك حينقص نتاج القلب .....
بس الجواب هو أنو فرانك ستارلنغ بالقصور القلبي بتصير مسطحة ==> حتى لو نقص الحمل القبلي ماراح ينقص النتاج بشكل مؤثر ...
وهذا هو المصدر:Davidson's

Quote:
Although a fall in preload (ventricular filling pressure) tends to reduce cardiac output, the 'Starling curve' in heart failure is flat so there may be a substantial and beneficial fall in filling pressure with little change in cardiac output (Fig. 18.21, p. 543, and Fig. 18.25). Nevertheless, excessive diuretic therapy may cause an undesirable fall in cardiac output, with a rising blood urea, hypotension and increasing lethargy, especially in patients with a marked diastolic component to their heart failure.
OmHa
السنة السادسة


The effect of treatment on ventricular performance curves in heart failure. Diuretics and venodilators (A), angiotensin-converting enzyme (ACE) inhibitors and mixed vasodilators (B), and positive inotropic agents (C).
OmHa
السنة السادسة


هاد المخطط بيوضح آلية تخفيف أدوية قصور القلب للأعراض مربوطة مع مخطط فرانك ستارلنغ

OmHa
السنة السادسة

Quote:
afterload is decreased by decreasing volume i.e. diuretics

Embarrased Embarrased
it's the preload

but the afterload can be decreased by reducing the peripheral resistance
"but still there is a minor role of preload in afterloalRolling Eyes "

since the ionotropic agents're the best Rx: is there several types?
if 'yes' what 're the differences?

lifespring
السنة الخامسة

Actually Phantom I am glad that you are interested in this discussion ,
Ok if you noticed the diagram , inotropic drugs shift the curve upward so, the symptoms related to forward is relieved BUT the symptoms related preload “accumulation of fluids in lungs ==>causing dyspnea ) are not improved the same way diuretics do >> so, it is not the best drugs ,actually you are going to learn in Cardiology that Digoxin ”which is an inotropic agent” doesn’t decrease the mortality related to heart failure .
On the other hand the best drug of these, is the ACE inhibitors .
Because they shift the curve to the left & upward therefore improving (fatigue=afterload & dyspnea=preload) and the way they do this is related to the cycle that I posted earlier ,check it and you would see that it JUST stop this vicious cycle that keep on damaging the heart.
As for the issue that you raised about digoxin exhausting the heart ,I don’t have any idea ,but I know that it works by increasing intracellular Ca++ .
Quote:
since the ionotropic agents're the best Rx: is there several types?
if 'yes' what 're the differences?

Actually they are not, as mentioned above, but I looked for them in pharmacology book,
There are several types including : digoxin , B agonists , and Phosphodiestrase inhibitors (e.g: Amrinone) and others..
actually I just got the point that all of them are used on emergency situations (acute heart failure) except for digoxin which is used for chronic situations .

OmHa
السنة السادسة
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