index

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Cardiac Pathophysiology II
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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
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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, hepato- megaly, jugulary
venous distention, pulmonary rales The term
congestive is too restricted and should be
avoided
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Types latent, manifest (cardiac
decompensation) chronic, acute (sudden, abrupt
more consequential)
Forwards Backwards Systolic dysfunction
unable to enhance filling able to enhance
filling pressures pressures
Diastolic dysfunction (unable to enhance
filling able to enhance filling pressures) pr
essures (nearly synonymous)
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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1
6
Pathogenesis Fig 2 A survey of some
interconnections among the components of cardiac
failure. ? wall stress, Ř Frank-Starling
mechanism ceases to work
2
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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, pre-
• supposes 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

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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, overshoot- ing and
detrimental later (vicious circles)
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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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1
11
3
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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 Anreps 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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4
14
5
15
1
16
6
17
7
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3. Systolic and diastolic dysfunction
8 of population asymptomatic left ventricle
dysfunction and manifest failure (11) ? 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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1
20
3
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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) balanc
ed (IACE) ?contractility by inotropic drugs
(cave arrhythmias and other side-effects!)
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7
23
8
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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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1
26
3
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3. Compensation mechanisms of the failing heart
Fig. 2
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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)
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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
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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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