Transcript Cardiac failure

1. Cardiac failure – a survey
2. Pathological overload of the heart
2.1 Volume overload
2.2 Pressure overload
3. Systolic and diastolic dysfunction
3.1 Systolic dysfunction
3.2 Diastolic dysfunction
4. Compensation mechanisms of the failing heart
5. Frank-Starling mechanism
6. Neurohumoral activation
7. Wall stress and hypertrophy
8. Hypertrophy  dilation and manifest failure
9. Cellular and molecular mechanisms
10. Neurohumoral hypothesis and vitious circles
11. Organismic consequencies of the heart failure
1.Cardiac failure – a survey
Definition:
Pathophysiologic: Condition in which the heart is not able to
pump blood adaquately to the metabolic needs of the body
under normal filling pressures
Clinical: Syndroma in which a ventricular dysfunction is
connected with lowered capacity to cope with physical
loading, encompassing dyspnea, venostatic edema, hepatomegaly, jugulary venous distention, pulmonary rales
The term „congestive“ is too restricted and should be avoided
Types: latent, manifest („cardiac decompensation“)
chronic, acute (sudden, abrupt – more consequential)
Forwards
Backwards
unable to enhance filling
pressures
able to enhance filling
pressures
(unable to enhance filling
pressures)
able to enhance filling
pressures
(nearly synonymous)
Systolic dysfunction
Diastolic dysfunction
The failure „forwards“ and „backwards“ are connected vessels –
ability/unability to enhance filling pressures is decisive in both
conditions
Etiology – Fig. 1
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Pathogenesis – Fig 2: A survey of some interconnections among the
components of cardiac failure.  = wall stress, Ø = Frank-Starling
mechanism ceases to work
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Systolic and diastolic dysfunction represent an early stage of later
manifest failure and its immediate hemodynamic mechanism
Neural and endocrine compensatory reactions are originally useful
physiological feedback reactions; their effectivity, however, presupposes the functioning „regulatory organ“ = heart and vessels.
If the regulatory organ is not able to respond properly the SAS and
RAS reactions overshoot and become detrimental:
peripheral resistance & fluid retention & myocardial hypertrophy
vicious circles  pathological reversal  myocardial dysfunction
  SAS  RAS
Both dysfunction and compensatory reactions are stretched in time
just from the action of etiological factors to the definitive failure.
The role of compensatory reactions is, however, different in different
phases: compensatory and advantageous at the beginning, overshooting and detrimental later (vicious circles)
2. Pathological overload of the heart
1/3 of all failures
2.1 Pathological volume overload
Causes see Fig. 1
Stages:
- acute volume overload, F-S  end-systolic volume maintained
- slippage of myocardial fibers  compliance of myocardium
(not dilation)
- excentric hypertrophy
- (lasting overload   and hypertrophy)  internal
irreversible changes of the myocardium  systolic and
diastolic function (Fig. 3)
ESV, ejection fraction = emptying
EDV  , coronary perfusion  ischemia 
fibrotization  active relaxation (diastolic dysfunction)
Disruption of aortal valve in endocarditis, mitral regurgitation with
disruption of papillary muscle  acute volume overload  no
compliance  acute pulmonary edema
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2.2 Pathological pressure overload
Stroke volume declines linearly with the afterload (Fig. 4)
Systolic work, effectivity (Fig. 5)
Causes see Fig. 1
aortic or pulmonary stenosis, coarctation of aorta, hypertrophic
cardiomyopathy, systemic or pulmonary hypertension
right ventricle: persisting ductus arteriosus, mitral stenosis
Stages:
- acute pressure overload: Anrep´s phenomenon + F-S 
maintaining of stroke volume (SV)
- sympaticus  contractility (Fig. 6)
- concentric hypertrophy
- hypertrophy  compliance  systolic and diastolic
dysfunction (Fig. 7)
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3. Systolic and diastolic dysfunction
8% of population: asymptomatic left ventricle dysfunction and
manifest failure (1:1)  cardiac failure from inherent cause
2.3 Systolic dysfunction
Systolic dysfunction  contractility
Etiology see Fig. 1
Overload  hypertrophy  contractility (mechanisms
known only partially)
Working diagram: Fig. 3
Failure forwards: tissue perfusion (calm and sticky skin),
renal perfusion (oliguria), cerebral perfusion (confusion)
Failure backwards: pressure in pulmonary veins (left v.) or
in systemic veins (right v.)
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What should be known in a particular case:
- preload (EDV or EDP)
- afterload (arterial pressure)
- contractility (SV and EF)
A compromise between forward and backward failure (Fig. 7)
Therapy see Fig. 8
 preload by volume expansion (cave pulmonary congestion
and edema!)
 afterload by vasodilators (cave hypotension!)
arteriolar (hydralazine)
„balanced“ (IACE)
contractility by inotropic drugs (cave arrhythmias and other
side-effects!)
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2.4 Diastolic dysfunction
Diastolic dysfunction  compliance
Etiology see Fig. 1
Pressure overload  mainly diastolic dysfunction (possibly
with intact systolic function)
Working diagram: Fig. 3
Although the pathogenesis of systolic and diastolic dysfunction is
different, the consequences for the pumping function (and
for the patient) are the same – forward or backward failure
Moreover, EDP  pressure gradient ventricle – aorta 
coronary perfusion  ischemia
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3. Compensation mechanisms of the failing
heart
Fig. 2
3.1 Frank-Starling mechanism
Volume or pressure overload  utilization of F-S = of diastolic
reserve
diastolic reserve: the work which the heart is able to perform
beyond that required under the ordinary circumstances of daily
life, depending upon the degree to which the cardiac muscle
fibers can be stretched by the incoming blood during diastole
contractility  utilization of F-S
Dilation  utilization of F-S (strongly limited)
3.2 Neurohumoral activation
Fig. 9 – regulation of blood pressure
Cardiac failure  CO  lowered pressure is indicated 
sympatoadrenal system  generalized vasoconstriction 
 venous return  F-S (stops later)
 maintaining of blood pressure (and cutting off kidneys,
skin, GI etc.)
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Fig. 10 – a simple scheme of volume regulation
Already before manifest cardiac failure, plasma norepinephrine and
atrial natriuretic factor levels are enhanced – physiological reactions
merge smoothly into pathological ones
3.3 Wall stress and hypertrophy
Definition of cardiac hypertrophy: left ventricle muscular mass
per unit of the body surface
Presupposes protein synthesis (dilation not so!)
Pathogenesis: wall stress ()
Important compensatory mechanism normalizing the wall
stress. Risiko factor of morbidity and mortality at the same time
Fig. 12
muscle mass, but contractility/gram of tissue not changed
There probably is a qualitative difference between physiological and
pathological hypertrophy (Tab. 1)
A „fine“ must be paid for hypertrophy:
EDP
unsufficient adaptation of vessel and capillary bed 
coronary reserve  compliance and contractility
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