Download - Contekan Ika
-
8/13/2019 Contekan Ika
1/7
CHF ec OBESITAS
Presenter : Ika Diamanda Apriano
Amalia P Dewi
Day/Date : Monday/ June 17th 2013
Supervisor in charge : Dr. Hj. Melda Deliana Sp.A(K)
INTRODUCTION
Childhood obesity predisposes to insulin resistance andtype 2 diabetes,hypertension,hyperlipidemia, liver and renal disease, and reproductive dysfunction. This condition also
increases the risk of adult-onset obesity and cardiovascular disease.1
Obesity in children is a complex disorder. Its prevalence has increased so significantly
in recent years that many consider it a major health concern of the developed world. The
National Health and Nutrition Examination Survey (NHANES) indicates that the prevalence
of obesity is increasing in all pediatric age groups, in both sexes, and in various ethnic and
racial groups. Many factors, including genetics, environment, metabolism, lifestyle, and
eating habits, are believed to play a role in the development of obesity. However, more than
90% of cases are idiopathic; less than 10% are associated with hormonal or genetic causes.
The BMI is a continuous, although imperfect, measure of body fatness. Calculated as
weight (kg) divided by height (m2), BMI corrects for body size and can be readily and
reliably quantified in clinical settings. The BMI correlates closely with total body fat (TBF),
which is estimated using dual-energy x-ray absorptiometry (DEXA) scanning in children who
are overweight and obese.
Normal values for BMI vary with age, sex, and pubertal status, and standard curves
representing the 5th through the 95th percentiles for BMI in childhood and adolescence were
generated using data from the 1988-1994 NHANES2. Consensus committees have
recommended that children and adolescents be considered overweight or obese if the BMI
exceeds the 85th or 95th percentiles, on curves generated from the 1963-1965 and 1966-1970
NHANES, or exceeds 30 kg/m2at any age3. McGavock et al demonstrated that low
cardiorespiratory fitness and reductions in fitness over time are significantly associated with
http://emedicine.medscape.com/article/925700-overviewhttp://emedicine.medscape.com/article/889877-overviewhttp://emedicine.medscape.com/article/889877-overviewhttp://emedicine.medscape.com/article/925700-overview -
8/13/2019 Contekan Ika
2/7
weight gain and the risk of being overweight in children aged 6-15 years. Analysis on a
cohort of 902 schoolchildren showed higher waist circumference and disproportionate weight
gain over a 12-month follow-up period in those children with low cardiorespiratory fitness.
The 12-month risk of overweight classification was 3.5-fold higher in youth with low
cardiorespiratory fitness, relative to fit peers4. Reductions in cardiorespiratory fitness were
significantly and independently associated with increasing BMI. Low levels of
cardiorespiratory fitness have also been associated with elevated depressive symptoms in
obese adolescents4.
One study suggests that a lack of adequate sleep time in young children is associated
with increased BMI; this observation is independent of other confounding variables (eg,
physical activity)5
. Furthermore, data indicate that over a 5-year period an increase in BMI
among overweight children 6 to 11 years of age is associated with increases in both systolic
and diastolic blood pressure, as well as with a decrease in sleep time6.
The most likely causes of pediatric congestive heart failure depend on the age of the c
hild. Congestive heart failure in fetus, or hydrops, can be detected by performing fetal echoca
rdiography. In older children, congestive heart failure may be caused by left sided obstructive
disease (valvar or subvalvar aortic stenosis or coarctation), myocardial dysfunction (myocard
itis or cardiomyopathy), hypertension, renal failure, or, more rarely, arrhythmias or myocardi
al ischemia. Illicit drugs such as inhaled cocaine and other stimulants are increasingly precipit
ating causes of congestive heart failure in adolescents; therefore, an increased suspicion of dr
ug use is warrantened in unexplained congestive heart failure7.
Congestive heart failure occurs when the heart can no longer meet the metabolic dema
nds of the body at normal physiologic venous pressures. Typically, the heart can respond to i
ncreased demands by means of 1 of the following :
1. Increasing the heart rate, which is controlled by neural and humoral input2. Increasing the cintractility of the ventricels, secondary to circulating
catecholamines and autonomic input.3. Augmenting the preload, medicated by constriction of the venous capacitate
vessels and the renal preservation of intravascular volume.Many classes of disorders can result in increased cerdiac demand or impaired cardiac
function. Cardiac causes include arrythmias (tachicardia or bradycardia), structural heart dise
ase, and myocardial dysfunction (systolic or diastolic).Cardiac rhythm disorders may caused by following :
-
8/13/2019 Contekan Ika
3/7
Complete heart block Supraventricular Tachycardia Ventricular Tachycardia
Sinus node dysfunction
Volume overload may be caused by the following :
Structural heart defect Anemia Sepsis
Pressure overload may be caused by the following :
Structural heart defect
HypertensionSystolic ventricular dysfunction or failure may be caused by the following :
myocarditis
dilated cardiomyophaty
malnutrition
ischemia
Diastolic ventricular dysfunction or failure may be caused by the following :
hypertropic cardiomyophaty
restrictive cardiomyophaty
pericarditis
cardiac tamponade (pericardial effusion)8
Thorough history taking and physical examination, including an assessment of the up
per-extremity and lower-extremity blood pressures, are crucial in the evaluation of an infant o
r child with congestive heart failure.
Regardless of the etiology, the first manifestation of congestive heart failure is usually
tachycardia. An obvious exception to this finding occurs in congestive heart failure due to a
primary bradyarrhythmia or completeheart block.
As the severity of congestive heart failure increases, signs of venous congestion
usually ensue. Left-sided heart failure is generally associated with signs of pulmonary venous
congestion, whereas right-sided heart failure is associated with signs of systemic venous
congestion. Marked failure of either ventricle, however, can affect the function of the other,
leading to systemic and pulmonary venous congestion.
http://emedicine.medscape.com/article/151597-overviewhttp://emedicine.medscape.com/article/151597-overview -
8/13/2019 Contekan Ika
4/7
Later stages of congestive heart failure are characterized by signs and symptoms of
low cardiac output. Generally, congestive heart failure with normal cardiac output is called
compensated congestive heart failure, and congestive heart failure with inadequate cardiac
output is considered decompensated.
Signs of congestive heart failure vary with the age of the child. Signs of pulmonary
venous congestion in an infant generally include tachypnea, respiratory distress (retractions),
grunting, and difficulty with feeding. Often, children with congestive heart failure have
diaphoresis during feedings, which is possibly related to a catecholamine surge that occurs
when they are challenged with eating while in respiratory distress.
Right-sided venous congestion is characterized by hepatosplenomegaly and, less
frequently, by edema or ascites. Jugular venous distention is not a reliable indicator of
systemic venous congestion in infants, because the jugular veins are difficult to observe. In
addition, the distance from the right atrium to the angle of the jaw may be no more than 8-10
cm, even when the individual is sitting upright.
Uncompensated congestive heart failure in an infant primarily manifests as a failure to
thrive. In severe cases, failure to thrive may be followed by signs of renal and hepatic failure.
In older children, left-sided venous congestion causes tachypnea, respiratory distress, and
wheezing (cardiac asthma). Right-sided congestion may result in hepatosplenomegaly,
jugular venous distention, edema, ascites, and/or pleural effusions. Older children with
uncompensated congestive heart failure may have fatigue or lower-than-usual energy levels.
Patients may complain of cool extremities, abdominal pain, nausea/vomiting, exercise
intolerance, dizziness, or syncope9.
If the underlying cause of the congestive heart failure cannot be immediately
corrected in a patient who is hemodynamically stable, outpatient management can be initiatedby using several agents. Afterload reduction using an ACE inhibitor is indicated in the
presence of left ventricular (LV) dysfunction, regardless of symptoms.
Afterload reduction is indicated in patients who have large left-to-right shunts at the
ventricular or arterial level (ventricular septal defect or patent ductus arteriosus), left-sided
regurgitant lesions (aortic insufficiency or mitral regurgitation), or poor systolic function
(myocarditis or dilated cardiomyopathy). ACE inhibitors are the medications of choice.
-
8/13/2019 Contekan Ika
5/7
Alternatively, an angiotensin receptor blocker (ARB), such as losartan, may be used in
patients in whom ACE adverse effects (particularly cough) may be unacceptable10.
In addition to afterload reduction (ACE inhibitor), low-dose furosemide (1
mg/kg/dose PO bid) may be initiated, with or without the addition of another agent for
inotropic effect (digoxin), or beta-blockade (carvedilol) to treat mild symptoms of congestive
heart failure The dose of digoxin (0.005-0.010 mg/kg/day PO divided twice daily, not to
exceed 0.125-0.250 mg PO qd) is almost never increased, either for effect or according to
digoxin levels, which are notoriously unreliable. However, the dose may be decreased in the
presence of signs of toxicity. The suspicion of digoxin toxicity should increase if an infant is
uninterested in feedings, gags, or vomits frequently. These symptoms are typically due to an
overdose or renal failure.
For more severe congestive heart failure, diuretic therapy with oral furosemide may
be increased to 2 mg/kg/dose orally 3 times daily or a second agent, such as
hydrochlorothiazide or metolazone, can be added. To be most effective, hydrochlorothiazide
and metolazone are best administered simultaneously with furosemide to achieve their
synergistic effect11.
-
8/13/2019 Contekan Ika
6/7
Reference
1. Ogden CL, Yanovski SZ, Carroll MD, Flegal KM. The epidemiology of
obesity. Gastroenterology. May 2007;132:2087-2102.
2. Fiore H, Travis S, Whalen A, Auinger P, Ryan S. Potentially protective factors
associated with healthful body mass index in adolescents with obese and non
obese parents: a secondary data analysis of the third national health and nutrition
examination survey, 1988-1994.J Am Diet Assoc. Jan 2006;106(1):55-64; quiz
76-9.
3. Flegal KM, Ogden CL, Wei R, et al. Prevalence of overweight in US children:
comparison of US growth charts from the Centers for Disease Control andPrevention with other reference values for body mass index. Am J Clin Nutr. Jun
2001;73(6):1086-93
4. McGavock JM, Torrance BD, McGuire KA, Wozny PD, Lewanczuk RZ.
Cardiorespiratory fitness and the risk of overweight in youth: the Healthy Hearts
Longitudinal Study of Cardiometabolic Health. Obesity (Silver Spring). Sep
2009;17(9):1802-7
5. Carter PJ, Taylor BJ, Williams SM, Taylor RW. Longitudinal analysis of sleep in
relation to BMI and body fat in children: the FLAME study.BMJ. May 26
2011;342:d2712.
6. Archbold KH, Vasquez MM, Goodwin JL, Quan SF. Effects of Sleep Patterns and
Obesity on Increases in Blood Pressure in a 5-Year Period: Report from the
Tucson Children's Assessment of Sleep Apnea Study.J Pediatr. Jan 25 2012
7. Rajagopal SK, et al. Pediatric heart failure and worsening renal function: Associat
ion with outcomes after heart transplantation.J Heart Lung Transplant. Oct 18 20
11
8. Kaza AK, et al. Surgical interventions for anterioventricular septal defect subtypes
: The pediatric heart network experience. Ann Thorac Surg. Oct 2011; 92 (4) : 14
68-75
9. Erickson LC. Medical issues for the cardiac patient. Critical Care of Infants and
Children. 1996:259-62.
-
8/13/2019 Contekan Ika
7/7
10.Konstam MA, Neaton JD, Poole-Wilson PA, Pitt B, Segal R, Sharma D, et al.
Comparison of losartan and captopril on heart failure-related outcomes and
symptoms from the losartan heart failure survival study (ELITE II).Am Heart J.
Jul 2005;150(1):123-31.
11.Rosenthal D, Chrisant MR, Edens E, Mahony L, Canter C, Colan S, et al.
International Society for Heart and Lung Transplantation: Practice guidelines for
management of heart failure in children.J Heart Lung Transplant. Dec
2004;23(12):1313-33.