Cardiac Pathophysiology II
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Cardiac Pathophysiology II. 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

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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


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

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) pressures

(nearly synonymous)

The failure „forwards“ and „backwards“ are connected vessels –

ability/unability to enhance filling pressures is decisive in both


Etiology – Fig. 1


Pathogenesis – Fig 2: A survey of some interconnections among the

components of cardiac failure.  = wall stress, Ø = Frank-Starling

mechanism ceases to work


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

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)

2. Pathological overload of the heart time

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

  • 1 time

    3 time

  • 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)

  • 4 time

    5 time

    1 time

    6 time

    7 time

    3. Systolic and diastolic dysfunction time

    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.)

    1 time

    3 time

    What should be known in a particular case: time

    - 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


    7 time

    8 time

    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

    1 time

    3 time

    Volume or pressure overload utilization of F-S = of diastolic


    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)

    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.)

    9 time

    Fig. 10 – a simple scheme of volume regulation time

    Already before manifest cardiac failure, plasma norepinephrine and

    atrial natriuretic factor levels are enhanced – physiological reactions

    merge smoothly into pathological ones

    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:


    unsufficient adaptation of vessel and capillary bed 

    coronary reserve compliance and contractility

    12 time