GAGAL JANTUNG/ DECOMPENSATIO CORDIS

MERUPAKAN SINDROMA KLINIK YANG TERDIRI DARI SESAK NAFAS DAN

RASA 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 RINGAN
DAN 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
dyspnea on e%ertion include reductions in pulmonary compliance, increased
airway resistance, respiratory muscle and+or diaphragm fatigue, and anemia.
,yspnea may become less fre-uent with the onset of right $entricular !./" failure
and tricuspid regurgitation.
*rthopnea
*rthopnea, which is defined as dyspnea occurring in the recumbent position, is
usually a later manifestation of HF than is e%ertional dyspnea. #t results from the
redistribution of fluid from the splanchnic circulation and lower e%tremities into
the central circulation during recumbency, with a resultant increase in pulmonary
capillary pressure. 0octurnal cough is a fre-uent manifestation of this process and
a fre-uently o$erlooked symptom of HF. *rthopnea is generally relie$ed by
sitting upright or by sleeping with additional pillows. Although orthopnea is a
relati$ely specific symptom of HF, it may occur in patients with abdominal
obesity or ascites and in patients with pulmonary disease whose lung mechanics
fa$or an upright posture.
1aro%ysmal 0octurnal ,yspnea !10,"
This term refers to acute episodes of se$ere shortness of breath and coughing that
generally occur at night and awaken the patient from sleep, usually 23' h after the
patient retires. 10, may be manifest by coughing or whee4ing, possibly because
of increased pressure in the bronchial arteries leading to airway compression,
along with interstitial pulmonary edema leading to increased airway resistance.
5hereas orthopnea may be relie$ed by sitting upright at the side of the bed with
the legs in a dependent position, patients with 10, often ha$e persistent coughing
and whee4ing e$en after they ha$e assumed the upright position. Cardiac asthma
is closely related to 10,, is characteri4ed by whee4ing secondary to
bronchospasm, and must be differentiated from primary asthma and pulmonary
causes of whee4ing.
CheyneStokes .espiration
Also referred to as periodic respiration or cyclic respiration, CheyneStokes
respiration is common in ad$anced HF and is usually associated with low cardiac
output. CheyneStokes respiration is caused by a diminished sensiti$ity of the
respiratory center to arterial 1
C*6
. There is an apneic phase, during which the
arterial 1
*6
falls and the arterial 1
C*6
rises. These changes in the arterial blood gas
content stimulate the depressed respiratory center, resulting in hyper$entilation
and hypocapnia, followed in turn by recurrence of apnea. CheyneStokes
respirations may be percei$ed by the patient or the patient7s family as se$ere
dyspnea or as a transient cessation of breathing.
Acute 1ulmonary 8dema
See Chap. 699.
*ther Symptoms
1atients with HF may also present with gastrointestinal symptoms. Anore%ia,
nausea, and early satiety associated with abdominal pain and fullness are fre-uent
complaints and may be related to edema of the bowel wall and+or a congested
li$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%cept
for 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<" 8%amination of the (ugular $eins pro$ides an estimation of
right atrial pressure. The (ugular $enous pressure is best appreciated with the
patient lying recumbent, with the head tilted at =>?. The (ugular $enous pressure
should be -uantified in centimeters of water !normal @ cm" by estimating the
height of the $enous column of blood abo$e the sternal angle in cm and then
adding > cm. #n the early stages of HF, the $enous pressure may be normal at rest
but may become abnormally ele$ated with sustained !A2 min" pressure on the
abdomen !positi$e abdomino(ugular reflu%". :iant v wa$es indicate the presence
of tricuspid regurgitation.
1ulmonary 8%amination
1ulmonary crackles !rales or crepitations" result from the transudation of fluid
from 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
'
!or protodiastolic 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 tricuspid
regurgitation 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$e been treated ade-uately with diuretics.
1eripheral edema is usually symmetric and dependent in HF and occurs
predominantly in the ankles and pretibial region in ambulatory patients. #n
bedridden patients, edema may be found in the sacral area !presacral edema" and
the scrotum. ;ongstanding edema may be associated with indurated and
pigmented skin.
Cardiac Cache%ia
5ith se$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.
Keluhan waktu kencing atau perubahan pada kencing
a. disuria B adalah rasa tidak enak yang bisa berupa rasa nyeri atau panas
pada waktu kencing. Ciasanya 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 F=<< ml+6= (am. #ni merupakan
tanda dari gagal gin(al.
c. anuria B yaitu bila $olume total urin F2<< ml+6= (am. Ciasanya disebabkan
oleh obstruksi ureter bilateral, atau karena adanya oklusi aorta atau a. .enalis
bilateral !Gogiantoro, et al, 6<<H".
Etiologi CKD
,iabetes melitus
Hipertensi
:lomerulonefritis
*bstruksi dan infeksi
Dista
1enyakit sistemik !S;8, $askulitis"
0eoplasma