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Heart Failure

 

It is a pathophysiological state in which abnormalities of the cardiovascular system (not just the heart) are responsible for the inability to deliver blood at a rate commensurate with the requirements of the metabolizing tissue.  Aka --- Supply does not equal demand

 

- May occur in association with systolic dysfunction (low ejection fraction) heart failure or diastolic dysfunction (normal ejection fraction) heart failure.  There are many reasons that lead to clinical presentation of dyspnea on exertion and fatigue.

Congestive Heart Failure epidemiology in US  the rest of the slides were skipped so read them if you want in the handout

 

          The only cardiovascular disease with a rising incidence and prevalence

          Nearly 1,000,000 annual hospital admissions (↑ 90% in past 10 years)

          Most common discharge diagnosis for patients older than 65 years

          Approximately 2.5 Million people have symptomatic Heart Failure,

          5.5 Million people have asymptomatic Heart Failure with 400,000 new cases diagnosed annually

 

Clinically on ECHO you can see two types of dysfunction leading to decreased CO.

 

ECHO of normal LV Ejection Fraction:

See mitral valve and normal opening and contractionà normal ejection fraction.

 

 
ECHO of Systolic dysfunction.- Hypocontractile dysfunction leading to decreased CO. The heart is dilated and a mobile round mass is present at the bottom of the heart(looks like the top of the image). This is a thrombus at the apex of the LV. This can embolize through the aortic valve and lead to further complications in the systemic circulation.
 

ECHO of Diastolic dysfunction:

Heart contraction is normal but there is an impaired relaxation so there is an impaired end diastolic volume which decreases the CO.



Acute vs. chronic Heart Failure  and Systolic vs. Diastolic Heart Failure

A patient that present with an acute anterior wall MI leading to acute Heart Failure. This is different than an elderly patient with a 35 year history of HTN who has Chronic Heart Failure.  The treatment, causes, and outcomes for each will be different.  Acute can be treated surgically and fixed.

 

Acute systolic dysfunction-  Ischemia and MI

Chronic systolic dysfunction -  HTN, DM, ischemic myopathy and MI

 

Diastolic Dysfunction:   Diastole is the energy consumption part of the cardiac cycle so it requires the most amount of oxygen. So an occluded coronary artery will lead to diastolic dysfunction

Causes:

Acute diasytolic dysfunction – ischemia, MI, tamponade

Chronic diastolic dysfunction- constriction, restriction, hypertrophic, HTN, DM

 

Heart Failure Abnormalities

  1. Impaired pump function / contractility best looked at in a pressure volume loop

Normal pressure volume loops

normal pressure volume loop

1.  Start 30ml initial diastolic volume and ventricle begins to fills.

2.  At end diastolic volume = 90 ml

3.  LV pressure increases until you begin systole and contract ventricles

4.  At end systole- volume is 30 ml

5.  Normal ejection fraction (60/90) = 66 %

 

2.  Mild to moderate Systolic dysfunction

moderate systolic dysfunction

1.  Early diastolic volume is going to be 50ml.  So you can only pump out 40 ml à ejection fraction is decreased to 40/90 = 40% = mild Heart Failure.

2. To compensate to maintain CO, there is an increase in end diastolic volume to 110ml and there is a slight here is an increase in LV end diastolic pressure.  There is a normal 60 ml stroke volume ejected to leave you with 50ml LV volume. This is basically Starling’s law, where you try to maintain CO by increasing end diastolic volume.

 

3. Severe dysfunction

severe systolic dysfunction

 

The contractility is so compromised that early diastolic volume 70ml so you can only compensate with a little increase in end diastolic volume.  There is impaired CO because there will be a decrease in ejection volume= SV

 

Starling curves

starling forces

Relates filling of ventricle to contractility. Normally as in exercise, as you fill the ventricle furtherà increased contractility àincreased CO.  

With impaired pump function you may get the same end diastolic volume but can’t increase contractility to increase CO.  With severely impaired contractility you can’t even get to the normal CO.

But these alone do not explain all the mortalities and exercise limitation in Congestive Heart Failure

 diastolic dysfunction

Diastolic dysfunction heart failure it is relaxation problem.   In the pressure -volume curve there normally is an increase in pressure with increase in volume.  But with increased chamber stiffness- the same volume increases there is a greater increase pressure.  So at low diastolic volumes you have high end diastolic pressure in the ventricles. This high pressure gets transmitted back to the pulmonary vasculature, leading to congestions and edema. 

 

B.  CHRONIC Heart Failure

Acute Heart Failure clinical syndrome is generally a hemodynamic problem that is isolated and severity is related to myocardial dysfunction . Whereas, chronic Heart Failure is  LV dysfunction but also with the following underlying problems.  Chronic Heart Failure is not only explained by pump function alone because if it were, then a CO vs Exercise capacity graph would be linear. However it is not linear, so there are more reasons to explain the clinical problems.

 

Other causes of Chronic Heart Failure

1.       Neurohormonal abnormalities- The consequences of a decrease in CO are equally important as myocardial dysfunction in causing symptoms

1.       Decrease in CO sensed by kidney by decreased renal perfusion àincrease renin secretion à increase Angiotensin II à increases release of Aldosterone, Endothelin and ADH.

2.       These mediators increase water and Na retention (ADH, Aldosterone) and cause vasoconstriction (Angiotensin II and endothelin)  à increase in afterload = wall stress increase, which aggravates the underlying pump dysfunction.

3.       Normally if you had a major hemorrhage and intervascular volume is decreased, these would be protective mechanism to conserve blood volume.

4.       Endogenous vasodilators and natriuretics exist but not enough to compensate for these elevated levels (ANF, NO, PG, dopamine)

2.       Adrenergic dysfunction – elevated NE levels

3.       Cytokine abnormalities

a.      TNFα  is elevated and mediates apoptosisà myocyte dysfunction but no current useful drug treatments available.

b.       IL-6

c.       IFN-g

4.       Impaired electrical function

 

Treatments

  1. 1. ACE inhibitor (Enalipril) improves survival of Heart Failure seen in hundreds of trials.
    1. But clinical trials show that there is still high mortality with use of ACE inhibitors. à Other drugs also needed at the same time a super complex diagram of Heart Failure came about. 
  2. Aldosterone inhibitor - added benefit in survival if used with ACE inhibitors.
  3. ADH inhibitors now being looked at
  4. *** Beta blockers -- MOST important development of therapy are now used to greatly improves survival b/c  elevation of NEpi levels in Congestive Heart Failure correlates with mortality

 

Systolic dysfunction Etiology from Myocyte loss (bold items are ones he said in lecture)

  1. MI= #1 reason
  2. Diabetes
  3. Myocarditis (coxsackie virus)
  4. Peripartum Cardiomyopathy (immunologic in women in 3rd tri-mester and persists after delivery
  5. alcoholic
  6.  idiopathic
  7. hypertension

 

Causes of Myocyte dysfunction:

  1. HTN
  2. valve diseases= aortic stenosis, aortic insufficiency, mitral insufficiency
  1. hypertrophic cardiomyopathy
  2. obesity
  3. DM
  4. ischemia
  5. congenital
  

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