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    Heart FailureDr. Ibrahim Y Hachim

    The FrankStarling law

    states that the greater the

    volume of blood entering the

    heart during diastole (end-

    diastolic volume), the greater

    the volume of blood ejected

    during systolic contraction

    (stroke volume) and vice-

    versa.

    http://upload.wikimedia.org/wikipedia/commons/0/01/Starling_RAP_combined.svg
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    What is Heart Failure? I t i s a pathologic state in which impaired

    cardiac function renders the heart unable to

    maintain output sufficient for the metabolic

    requirements of the body.

    Common end point of many forms of heart

    disease .

    Heart Failure CHF is ccc by diminished cardiac output

    (forward failure) , accumulation of blood in thevenous system ( backward failure) , or both.

    cardiac output( forward failure)

    accumulation ofblood in the venoussystem ( backwardfailure)

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    Most instances of heart failure

    are the consequences of

    progressive detorioration of

    myocardial contractilefunction (systolic

    dysfunction).

    Frequently due to ischemic

    injury , pressure or volume

    overload , or dilated

    cardiomyopathy .

    Occasionally , failure results

    from inability of the heart

    chambers to relax

    sufficiently during diastole

    (diastolic dysfunction) .

    This can occur with massive

    left ventricular

    hypertrophy , deposition ofamyloid , or constrictive

    pericarditis.

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    Inadequate cardiac output in CHF

    Tachycardia Blood volumeexpansion bysalt and waterretension.

    Ventricular dilation ( improves contraction by myofiber stretchingaccording to the Frank-Starling law).

    LEFT-SIDED HEART FAILURE

    ischemic heart disease hypertension aortic and mitralvalvular diseases

    nonischemicmyocardialdiseases

    Involves the left ventricle (lower chamber) of theheart

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    Morphology.The findings in the heart vary depending on the cause of the

    disease process; abnormalities such as myocardial infarction or

    a valvular deformity may be present. This chamber is usually

    hypertrophied and often dilated, sometimes quite

    massively except with obstruction at the mitral valve or other

    processes that restrict the size of the left ventricle,

    Secondary enlargement of the left atrium with resultant atrial

    fibrillation (i.e., uncoordinated contraction of the atrium) may

    either compromise stroke volume or cause blood stasis and

    possible thrombus formation. A fibrillating left atrium carries a

    substantially increased risk of embolic stroke..

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    LungsPressure in the pulmonary veins mounts and is ultimately

    transmitted retrograde to the capillaries and arteries. The result

    is pulmonary congestion and edema, with heavy, wet lungs.

    LungsIt is sufficient to note here that the pulmonary changes include,in sequence:-(1) a perivascular and interstitial transudate, particularly in theinterlobular septa, responsible for Kerley's B lines on x-ray

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    (2) Progressive edematous widening of alveolar septa

    (3) Accumulation of edema fluid in the alveolar spaces.

    Moreover, hemosiderin-containing macrophages in the alveoli

    (called siderophages, or heart failure cells) denote previous

    episodes of pulmonary edema.

    Dyspnea (breathlessness), usually the earliest and thecardinal complaint of patients in left-sided heart failure.With further impairment, there is orthopnea, which isdyspnea on lying down that is relieved by sitting orstanding. Thus the orthopneic patient must sleep whilesitting upright. Paroxysmal nocturnal dyspnea is anextension of orthopnea. Cough is a commonaccompaniment of left-sided failure.

    Clinical manifestations

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    Decreased cardiac outputKidneys

    reduction in renal perfusion

    The renin-angiotensin-aldosterone

    THE RENIN ANGIOTENSIN ALDOSTERONE SYSTEM

    ACE

    ACE INHIBITORS

    JGA

    RENIN

    ADRENAL

    ALDOSTERONE

    ANGIOTENSINOGEN ANGIOTENSIN 1

    ANGIOTENSIN 2

    VASOCONSTRTICTS

    Na RETENTION

    INCREASED BP

    If the perfusion deficit of thekidney becomes sufficientlysevere, impaired excretionof nitrogenous productsmay cause azotemia, in thisinstance prerenal azotemia

    Poor renal perfusion is sensed by the

    juxtaglomerular apparatus, which secretesrenin. Renin converts angiotensinogen inthe blood to angiotensin1. This in turn isconverted by ACE (angiotensin convertingenzyme) to angiotensin2, which increasesblood pressure directly by vasoconstrictionand by increasing adrenal secretion ofaldosterone. ACE inhibitors are used totreat heart failure as well. as hypertension.Diuretic drugs are another mainstay oftreatment.

    BrainIn far-advanced CHF, cerebral hypoxia may give rise tohypoxic encephalopathy , with irritability, loss ofattention span, and restlessness, which may evenprogress to coma.

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    What is Right Heart Failure?

    Isolated right-sided heart failure occurs in only a few

    diseases. Usually it is a secondary consequence of left-

    sided heart failure because any increase in pressure inthe pulmonary circulation incidental to left-sided heart

    failure inevitably produces an increased burden on the

    right side of the heart.

    Cor pulmonale is the term given to heart failure due tolung disease, such as chronic obstructive airwaysdisease.

    The major morphologic and clinical effects of pure right-

    sided heart failure differ from those of left-sided heart

    failure in that pulmonary congestion is minimal,

    whereas engorgement of the systemic and portal venous

    systems may be pronounced.

    Right-sided HF

    Liver and Portal System

    Kidneys

    BrainPleural and Pericardial Spaces

    SubcutaneousTissues

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    1

    The liver is usually increased in size and weight (congestivehepatomegaly), and a cut section displays prominent

    passive congestion . Congested red centers of the liverlobules are surrounded by paler, sometimes fatty, peripheralregions (nutmeg liver).

    The liver

    Centralvein

    Right-sided heart failure also leads to elevated pressure inthe portal vein and its tributaries. Congestion produces atense, enlarged spleen (congestive splenomegaly).

    Kidneys

    Congestion of the kidneys is more marked with right-

    sided heart failure than with left-sided heart failure,

    leading to greater fluid retention, peripheral edema,

    and more pronounced azotemia.

    Brain

    Symptoms essentially identical to those described inleft-sided heart failure may occur, representing venous

    congestion and hypoxia of the central nervous system.

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    Subcutaneous Tissues

    Peripheral edema of dependent portions of the

    body, especially ankle (pedal)

    and pretibial edema, is a

    hallmark of right-sided heart

    failure. In chronically

    bedridden patients, the

    edema may be primarily

    presacral. Generalizedmassive edema is called

    anasarca.