CHF ec OBESITAS

Presenter

: Ika Diamanda Apriano Amalia P Dewi

Day/Date Supervisor in charge

: Monday/ June 17th 2013 : Dr. Hj. Melda Deliana Sp.A(K)

INTRODUCTION Childhood obesity predisposes to insulin resistance and type 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/m2 at any age3. McGavock et al demonstrated that low cardiorespiratory fitness and reductions in fitness over time are significantly associated with

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 input 2. 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 :

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 Hypertension

Systolic 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 complete heart 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.

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 initiated by 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.

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.

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 and Prevention 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.

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.