19 Heart Failure



10.1055/b-0035-121514

19 Heart Failure



19.1.1 Basics



Definition


Heart failure is defined as the inability of the heart to pump sufficient cardiac output to meet the metabolic needs of the body and supply it with enough oxygen. Depending on the section of the heart affected, a distinction is made between left heart, right heart, and global failure. Heart failure is also divided into acute and chronic heart failure according to the course of the disease.



Epidemiology


No precise epidemiological data are available on heart failure in children and adolescents. Congenital heart defects in neonates occur with a frequency of 8 to 11 per 1,000 live births—that is, about 1% of all live births. Only a fraction of these individuals develop symptoms of heart failure, estimated to be 0.1–0.2% of all live births.



Etiology


Heart failure is a result of congenital or acquired heart disease that leads to a volume or pressure overload of the heart or to myocardial insufficiency (Table 19.1). Furthermore, arrhythmias can lead to insufficient cardiac output.


















































Table 19.1 Causes of acute and chronic heart failure

Pathological preload




  • Shunt defects




  • Valve regurgitations


Pathological afterload




  • Valve stenosis




  • Outflow tract obstructions




  • Arterial hypertension




  • Pulmonary hypertension, pulmonary embolism, bronchial obstruction


Diminished myocardial contractility or restricted ventricular filling




  • Cardiomyopathies




  • Myocarditis




  • Pericarditis




  • Myocardial ischemia




  • Kawasaki disease




  • Endocarditis




  • Sepsis




  • Acidosis




  • Severe hypoxia, peripheral asphyxia




  • Metabolic disorder




  • Toxic myocardial damage (e.g., anthracycline)


Pathological heart rate




  • Tachycardia and bradycardia


In childhood, congenital heart defects that lead to volume or pressure overload of the heart are the most common causes of heart failure. Examples of volume overload are a large ventral septal defect (VSD), patent ductus arteriosus (PDA), or atrioventricular septal defect (AVSD). Pressure overload develops in aortic stenosis, coarctation of the aorta, or mitral stenosis, for example.


The clinical symptoms of heart failure in the various congenital heart defects typically manifest at certain times (Table 19.2). Congenital heart defects with a large left-to-right shunt, for example, usually lead to heart failure when pulmonary resistance drops at the age of 6 to 8 weeks. An atrial septal defect (ASD) usually does not lead to heart failure until adulthood. In most cases, children with tetralogy of Fallot do not develop heart failure, as they are protected from a large shunt volume and corresponding volume overload due to pulmonary stenosis.













































Table 19.2 Typical manifestation times of congenital heart defects

Heart disease


Remark


Manifestation in the fetal period




  • Fetal tachyarrhythmia



  • Complete AV block



  • Severe valve regurgitation (e.g., severe form of Ebstein anomaly)



  • Large AV anomalies



  • Severe anemia


Clinical manifestation: hydrops fetalis


Manifestation at birth




  • HLHS with restrictive foramen ovale



  • Severe valve regurgitation (e.g., Ebstein anomaly)



  • Severe AV anomalies


Clinical manifestation: cardiogenic shock


Manifestation in the 1st week of life




  • TGA



  • Total anomalous pulmonary venous connection with pulmonary venous obstruction



  • Critical aortic or pulmonary stenosis



  • HLHS


Clinical manifestation: cyanosis and cardiogenic shock




  • PDA in premature infants


Premature infants do not compensate volume overload as well as mature neonates


Manifestation in the 1st month of life




  • High grade coarctation of the aorta

 



  • VSD in premature neonates


Premature infants do not compensate volume overload as well as mature neonates


Manifestation in the 2nd–4th month of life




  • AVSD



  • Large VSD



  • Large PDA



  • Truncus arteriosus


Heart defects with a large left-to-right shunt usually manifest at the age of 6–8 weeks when the pulmonary vascular resistance drops




  • Bland–White–Garland syndrome, ALCAPA


A steal phenomenon develops when the pulmonary vascular resistance drops



Pathophysiology


The body reacts to the decreased pumping capacity of the heart with various compensatory mechanisms that initially improve the blood supply to the body, but over time contribute considerably to deterioration of cardiac condition.


Neuroendocrine activation


The increase in the sympathetic tonus, and thus the increased release of catecholamines initially leads to an increase in the heart rate and contractility. However, over time, downregulation of the beta-adrenergic receptors occurs so that the effectiveness of the catecholamines in the heart decreases. Because of an increase in systemic vascular resistance, the afterload increases.


The activation of the renin–angiotensin–aldosterone system (RAAS) leads to an increase in the afterload due to vasoconstriction and to an increase in the preload due to sodium and water retention. Increased secretion of antidiuretic hormone (ADH) results in excessive water retention.


The increased pressure and volume load also leads to activation of the NO and the natriuretic peptides ANP (atrial natriuretic peptide), BNP (brain natriuretic peptide), and CNP (C-type natriuretic peptide). They cause vasodilatation and an inhibition of the RAAS as well as natriuresis, in effect a counter-regulatory mechanism.


NT-pro-BNP (N-terminal pro brain natriuretic peptide), a precursor of BNP, is also used as a laboratory chemical marker of heart failure. The serum levels of the natriuretic peptides rise with increasing heart failure.


The recombinant form of BNP, nesiritide, is currently used in clinical trials for the treatment of acute heart failure due to its vasodilator properties.


Frank–Starling mechanism


An increase in the preload (e.g., through activation of RAAS and increased secretion of ADH) initially causes an improvement in contractility and an increase in stroke volume, but over time, the increases in end-diastolic pressure and afterload (also consequences of the neuroendocrine compensatory mechanisms) lead to a decrease in cardiac pump function.


Myocardial hypertrophy


Chronic volume overload leads to dilatation and thus to eccentric hypertrophy. By contrast, pressure overload leads to concentric hypertrophy with an increase of heart wall thickness. These remodeling processes initially improve the pumping function of the heart, but with increasing hypertrophy, the oxygen demand of the myocardium increases disproportionately.



19.1.2 Diagnostics



Symptoms


Most affected children have global heart failure; it is rarely possible to distinguish between right heart failure and left heart failure.


Infants and younger children have a history of poor feeding, failure to thrive, tachypnea (especially under exertion, such as drinking), and increased sweating (especially on the forehead). In older children, the main symptoms are dyspnea or shortness of breath under stress, rapid fatigability, and eyelid or foot edema.


On clinical examination, the following findings are indicative of heart failure:




  • Tachycardia: due to increased sympathetic tone.



  • Gallop rhythm: A third or fourth heart sound is probably a sign of rapid filling of a relatively stiff ventricle.



  • Cool limbs, pallor, prolonged capillary refill time: signs of peripheral vasoconstriction and reduced peripheral perfusion in sympathetic activation.



  • Tachypnea, dyspnea, subcostal and intercostal retractions, orthopnea: Tachypnea is the clinical manifestation of the excessive pulmonary blood flow and pulmonary edema. With advancing heart failure, ventilation function is increasingly impaired. Dyspnea with subcostal and intercostal retractions develops. Manifest pulmonary edema causes fine bubbly crackles. Frequent pulmonary infections are also a result of excessive pulmonary blood flow. A dry cough can also be a sign of excessive pulmonary blood flow or pulmonary congestion.



  • Pulsus tardus: Arterial pulses weak on palpation.



  • Pulsus paradoxus



  • Cyanosis: Sign of increasing oxygen utilization in the periphery or deterioration of gas exchange as a result of pulmonary edema. Cyanosis may also be indicative of an increasing right-to-left shunt.



  • Hepatomegaly: Sign of systemic venous congestion in the context of right heart failure or global failure.



  • Jugular vein distention: Occurs mainly in older children and adults as a sign of a systemic venous congestion. It is rarely observed in younger children.



  • Edema: Mainly eyelid edema in children. Peripheral edema is less common than in adults.


Similar to adults, the clinical severity of heart failure is divided in four NYHA classes. The criteria have been modified for children (Table 19.3).























Table 19.3 New York Heart Association (NYHA) classification of heart failure in children

NYHA class


Symptoms


I


No limitation of physical activity




  • Ordinary physical activity does not induce symptoms (undue fatigue, sweating, shortness of breath)


II


Slight limitation of physical activity




  • No discomfort at rest



  • Greater physical activity (depending on age: drinking, crawling, walking, climbing stairs) causes symptoms (fatigue, sweating, shortness of breath)


III


Marked limitation of physical activity




  • Still no discomfort at rest



  • Slight physical activity leads to symptoms (fatigue, sweating, dyspnea)


IV


Discomfort during all physical activity and at rest




  • Symptoms such as sweating, dyspnea, or cyanosis from all physical activity and at rest



  • Bedridden, cardiac dystrophy or cachexia

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Jun 13, 2020 | Posted by in CARDIOLOGY | Comments Off on 19 Heart Failure
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