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    GAGAL JANTUNG/ DECOMPENSATIO CORDIS

    MERUPAKAN SINDROMA KLINIK YANG TERDIRI DARI SESAK NAFAS DANRASA CEPAT LELAH YANG DISEBABKAN OLEH KELAINAN JANTUNG.

    KLASIFIKASI FUNGSIONAL GAGAL JANTUNG (NYHA

    1. TIMBUL GEJALA SESAK NAFAS ATAU CAPAI PADA KEADAAN FISIK

    YANG BERAT

    2. TIMBUL GEJALA PADA KEGIATAN FISIK YANG SEDANG

    3. TIMBUL GEJALA PADA KEGIATAN FISIK YANG RINGAN

    4. TIMBUL GEJALA PADA KEGIATAN FISIK YANG SANGAT RINGANDAN PADA WAKTU ISTIRAHAT

    5. SEBAB GAGAL JANTUNG

    PENYAKIT JANTUNG KORONER DAN

    PASCA IMA

    HIPERTENSI

    PENYAKIT KATUB JANTUNG

    KARDIOMIOPATI SERTA MIOKARDITIS

    PENYAKIT JANTUNG BAWAAN

    PENYAKIT PARU KRONIS CPC

    Clinical Manifestations

    Symptoms

    The cardinal symptoms of HF are fatigue and shortness of breath. Although

    fatigue has been traditionally ascribed to the low cardiac output in HF, it is likely

    that skeletalmuscle abnormalities and other noncardiac comorbidities !e.g.,

    anemia" also contribute to this symptom. #n the early stages of HF, dyspnea is

    obser$ed only during e%ertion& howe$er, as the disease progresses, dyspnea occurs

    with less strenuous acti$ity, and ultimately may occur e$en at rest. The origin of

    dyspnea in HF is likely multifactorial !Chap. ''". The most important mechanism

    is pulmonary congestion with accumulation of interstitial or intraal$eolar fluid,

    which acti$ates (u%tacapillary ) receptors, which in turn stimulate rapid, shallow

    breathing characteristic of cardiac dyspnea. *ther factors that contribute to

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    See Chap. 699.

    *ther Symptoms

    1atients with HF may also present with gastrointestinal symptoms. Anore%ia,

    nausea, and early satiety associated with abdominal pain and fullness are fre-uent

    complaints and may be related to edema of the bowel wall and+or a congested

    li$er. Congestion of the li$er and stretching of its capsule may lead to rightupper

    -uadrant pain. Cerebral symptoms, such as confusion, disorientation, and sleep

    and mood disturbances, may be obser$ed in patients with se$ere HF, particularly

    elderly patients with cerebral arteriosclerosis and reduced cerebral perfusion.

    0octuria is common in HF and may contribute to insomnia.

    1hysical 8%amination

    A careful physical e%amination is always warranted in the e$aluation of patients

    with HF. The purpose of the e%amination is to help determine the cause of HF, as

    well as to assess the se$erity of the syndrome. *btaining additional information

    about the hemodynamic profile and the response to therapy and determining the

    prognosis are important additional goals of the physical e%amination.

    :eneral Appearance and /ital Signs

    #n mild or moderately se$ere HF, the patient appears in no distress at rest, e%ceptfor feeling uncomfortable when lying flat for more than a few minutes. #n more

    se$ere HF, the patient must sit upright, may ha$e labored breathing, and may not

    be able to finish a sentence because of shortness of breath. Systolic blood pressure

    may be normal or high in early HF, but it is generally reduced in ad$anced HF

    because of se$ere ;/ dysfunction. The pulse pressure may be diminished,

    reflecting a reduction in stroke $olume. Sinus tachycardia is a nonspecific sign

    caused by increased adrenergic acti$ity. 1eripheral $asoconstriction leading to

    cool peripheral e%tremities and cyanosis of the lips and nail beds is also caused by

    e%cessi$e adrenergic acti$ity.

    )ugular /eins

    !See also Chap. 66 cm. #n the early stages of HF, the $enous pressure may be normal at rest

    but may become abnormally ele$ated with sustained !2 min" pressure on the

    abdomen !positi$e abdomino(ugular reflu%". :iant vwa$es indicate the presence

    of tricuspid regurgitation.

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    1ulmonary 8%amination

    1ulmonary crackles !rales or crepitations" result from the transudation of fluidfrom the intra$ascular space into the al$eoli. #n patients with pulmonary edema,

    rales may be heard widely o$er both lung fields and may be accompanied by

    e%piratory whee4ing !cardiac asthma". 5hen present in patients without

    concomitant lung disease, rales are specific for HF. #mportantly, rales are

    fre-uently absent in patients with chronic HF, e$en when ;/ filling pressures are

    ele$ated, because of increased lymphatic drainage of al$eolar fluid. 1leural

    effusions result from the ele$ation of pleural capillary pressure and the resulting

    transudation of fluid into the pleural ca$ities. Since the pleural $eins drain into

    both the systemic and pulmonary $eins, pleural effusions occur most commonly

    with bi$entricular failure. Although pleural effusions are often bilateral in HF,

    when unilateral they occur more fre-uently in the right pleural space.

    Cardiac 8%amination

    8%amination of the heart, although essential, fre-uently does not pro$ide useful

    information about the se$erity of HF. #f cardiomegaly is present, the point of

    ma%imal impulse !1M#" is usually displaced below the fifth intercostal space

    and+or lateral to the midcla$icular line, and the impulse is palpable o$er two

    interspaces. Se$ere ;/ hypertrophy leads to a sustained 1M#. #n some patients, a

    third heart sound !S'" is audible and palpable at the ape%. 1atients with enlarged or

    hypertrophied right $entricles may ha$e a sustained and prolonged left parasternal

    impulse e%tending throughout systole. An S'!orprotodiastolic gallop" is most

    commonly present in patients with $olume o$erload who ha$e tachycardia and

    tachypnea, and it often signifies se$ere hemodynamic compromise. A fourth heart

    sound !S=" is not a specific indicator of HF but is usually present in patients with

    diastolic dysfunction. The murmurs of mitral and tricuspid regurgitation are

    fre-uently present in patients with ad$anced HF.

    Abdomen and 8%tremities

    Hepatomegaly is an important sign in patients with HF. 5hen present, the

    enlarged li$er is fre-uently tender and may pulsate during systole if tricuspidregurgitation is present. Ascites, a late sign, occurs as a conse-uence of increased

    pressure in the hepatic $eins and the $eins draining the peritoneum. )aundice, also

    a late finding in HF, results from impairment of hepatic function secondary to

    hepatic congestion and hepatocellular hypo%ia, and is associated with ele$ations

    of both direct and indirect bilirubin.

    1eripheral edema is a cardinal manifestation of HF, but it is nonspecific and

    usually absent in patients who ha$e been treated ade-uately with diuretics.

    1eripheral edema is usually symmetric and dependent in HF and occurs

    predominantly in the ankles and pretibial region in ambulatory patients. #n

    bedridden patients, edema may be found in the sacral area !presacral edema" and

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    the scrotum. ;ongstanding edema may be associated with indurated and

    pigmented skin.

    Cardiac Cache%ia

    5ith se$ere chronic HF, there may be marked weight loss and cache%ia. Although

    the mechanism of cache%ia is not entirely understood, it is likely multifactorial

    and includes ele$ation of the resting metabolic rate& anore%ia, nausea, and

    $omiting due to congesti$e hepatomegaly and abdominal fullness& ele$ation of

    circulating concentrations of cytokines such as T0F& and impairment of intestinal

    absorption due to congestion of the intestinal $eins. 5hen present, cache%ia

    augers a poor o$erall prognosis.

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    Keluhan waktu kencing atau perubahan pada kencinga. disuria B adalah rasa tidak enak yang bisa berupa rasa nyeri atau panas

    pada waktu kencing. iasanya disebabkan oleh adanya infeksi pada bulibuli

    !cystitis" atau uretra !urethritis".

    b. Stranguria B adalah rasa amat nyeri pada waktu kencing dan kencing yang

    dikeluarkan hanya beberapa etes. #ni bisa disebabkan oleh infeksi berat pada buli

    buli.

    c. frekuensi B yaitu meningkatnya frekuensi kencing sehingga penderita

    kencing berkalikali melebihi kebiasaan normalnya.

    d. 0okturia B yaitu bila penderita bangun pada malam hari untuk buang air

    kecil sampai beberapa kali. #ni bisa disebabkan oleh #SD atau pembesaran prostat.

    Perubahan jumlah kencing

    a. poliuria B bila $olume total urin meningkat !E' l+6= (am". 1enyebabnya

    antara lain karena adanya gangguan mekanisme konsentrasi urin atau karena

    (umlah air yang diminum berlebihan.

    b. *ligouri B yaitu bila $olume total urin =

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    Etiologi CKD

    iabetes melitus

    Hipertensi

    :lomerulonefritis

    *bstruksi dan infeksi

    Dista

    1enyakit sistemik !S;8, $askulitis"

    0eoplasma