CARDIAC FAILURE

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Last Updated : 1/10/2012
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N C Joshi
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Congestive heart failure (CHF) may be defined as that pathophysiological state in which an abnormality of cardiac function is responsible for the failure of heart to pump blood at a rate commensurate with the metabolic requirements.

Circulatory failure denotes an abnormal blood flow through the cardiovascular circuitry that compromises tissue perfusion with or without abnormal heart function.

Heart failure refers to abnormal cardiac pumping of blood with or without an abnormal heart muscle.

Myocardial failure denotes abnormal cardiac pumping of blood due to a defective heart muscle.

The major types of heart failure are
- Forward and Backwar
- Left sided and Right sided
- Acute and Chronic
- Low output and High output
- Systolic and Diastolic

Pathophysiology
The atria receives blood at low pressure (Left Atrium at 3 mm of Hg and Right Atrium at 6 mm of Hg) and pass it on to the ventricles. From ventricles it is propelled at a higher pressure in to the greater arteries. The right ventricle fills pulmonary arteries under relatively low pressure (30/12 mm of Hg) while the left ventricle generates higher aortic pressure (100/60 mm Hg).

The heart may fail if it is confronted with:
- An excessive preload i.e. increase in tension in ventricular cardiac muscle fibres. Ventricles expand excessively in diastole. It is seen in conditions with L - R shunt, mitral regurgitation and complete heart block (increased diastolic time.)
- When ventricles have to work against abnormally high afterload: hypertension and aortic stenosis.
- Impaired myocardial contractility: myopathy, myocarditis.
- Inadequate diastolic filling: Constrictive pericarditis, tachyarrhythmias.

Under these conditions, initially, various compensatory mechanisms come into play which have got salutary effects. But the same compensatory mechanisms if pressed into play indefinitely cause non-salutary effects and potentiates heart failure.

The compensatory increase in end-diastolic volume and pressure increase myocardial contractility force through Frank - Starling mechanism (Salutary effect). Yet when end diastolic pressure reaches high levels, pulmonary and peripheral congestion and edema develops (non-salutary action).

The compensatory increase in sympathetic tone augments myocardial contractility, which helps to maintain tissue perfusion pressure (salutary action). Yet when sympathetic action is intense, tachycardia and peripheral vasoconstriction (increased afterload) leads to substantial increase in myocardial oxygen consumption (non-salutary effect).

The compensatory stimulation of renin-angiotensin-aldosterone system causes renal retention of salt and water which increases diastolic filling pressure and causes vasoconstriction to maintain tissue perfusion pressure (salutary action). Yet when these effects are excessive, it causes systemic and pulmonary venous congestion on one hand and increases after load on the other hand (non-salutary effects).

The compensatory ventricular hypertrophy provides more contractile elements increasing myocardial contraction (salutary action). Yet progressive hypertrophy leads to abnormal diastolic relaxation leading to pulmonary and systemic congestion (non-salutary action).

Etiology
CHF is frequently encountered in the first year of life. During this period, CHF is caused by heart diseases resulting in
- Volume overload (L - R shunt: VSD,PDA)
- Pressure overload (Coarctation of aorta, Pulmonary Stenosis, Aortic Stenosis)
- Myocardial diseases (Endocardial fibroelastosis, cardiomyopathy)

Relatively common defects causing CHF are given in Table. It is helpful to be aware that specific cardiac lesions are likely to cause CHF at specific ages. More than 50% of pediatric patients with CHF are younger than 3 months.

Leading causes of CHF in relation to age

Birth to 1st week
  • Aortic atresia 

  • Transposition of great vessels 

  • Coarctation of aorta 

1 week to 1 month
  • Coarctation of aorta 

  • TGA 

  • Endocardial Fibroelastosis 

1 month to 2 months
  • TGA 

  • Endocardial Fibroelastosis 

2 months to 3 months
  • Coarctation of aorta 

  • Total Anomalous pulmonary venous return 

  • VSD 

3 months to 6 months
  • VSD 

6 months to 12 months
  • VSD 

  • ASD (Ostium Primum) 


CHF is rarely present in utero with exception of paroxysmal supraventricular tachycardia and anemia due to Rh incompatibility. It is often interpreted as intrauterine asphyxia and mother is subjected to Cesarean section.

After first year of life, CHF is much less frequent and it is due to variety of causes:
- Arrhythmias
- Viral myocarditis
- Acute rheumatic carditis
- Cardiomyopathy



Contributor Information and Disclosures N C Joshi
Consultant Pediatrician and Pediatric Cardiologist, Nanavati Hospital, Mumbai, India


First Created : 1/12/2001
References
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