Congestive heart failure

Congestive Heart Failure . It is defined as the state in which the heart cannot produce the cardiac output necessary to satisfy the metabolic needs of the organism.

Summary

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  • 1 Pathophysiology
    • 1 Factors that make the heart work like a pump
    • 2 Situations that alter these factors
    • 3 Classification of Heart Failure
  • 2 cardiovascular reserve factors
    • 1 Cardiac
  • 3 Clinical manifestations
  • 4 Etiology by age
    • 1 Fetal
    • 2 Premature newborn
    • 3 Newborn at term
    • 4 Infant-preschool
    • 5 Child-adolescent
  • 5 Etiology according to the factor affected
  • 6 Diagnosis
    • 1 Signs of predominance of right cavities
    • 2 Signs of predominance of left cavities
  • 7 Complementary exams
  • 8 Differential diagnosis
  • 9 Treatment
    • 1 Treatment objectives
  • 10 General measures
  • 11 Source

Pathophysiology

The healthy heart increases cardiac output linearly until it reaches a maximum (Frank-Starling principle). Systemic oxygen transport (TSO) is calculated as the product of cardiac output (GC) and systemic oxygen content (CaO2).

Cardiac output can be calculated as the product of heart rate and stroke volume (HR x VS). The main determinants of stroke volume are afterload (working pressure), preload (working volume), and contractility (intrinsic myocardial function).

Heart rate disturbances can also compromise cardiac output, such as bradyarrhythmias and tachyarrhythmias that decrease the diastolic time interval for ventricular filling.

One of the main compensatory mechanisms for increased cardiac output is increased sympathetic tone secondary to increased adrenal secretion of circulating epinephrine and neural release of norepinephrine. The initial beneficial effects of sympathetic stimulation are increased heart rate and myocardial contractility, which serve to increase cardiac output. Due to localized vasoconstriction, blood flow can be redistributed from the cutaneous, visceral, and renal beds to the heart and brain.

Factors that make the heart work like a pump

Pre-load: depends on the degree of elasticity, stretching of the muscle fiber during end-diastole. It is determined by blood volume, atrial pressure, and venous return.

Post-load: they are the forces that oppose ventricular emptying. It is determined by: peripheral and aortic resistance. Structures with different contraction and expansion capacities intervene.

Contractility: it is a property of the heart. It is the force generated during the contraction of the heart muscle, it depends in part on the flow of calcium ions during the depolarization of the membrane.

Heart rate: when the frequency increases, cardiac work increases and therefore oxygen consumption.

Situations that alter these factors

Pre-load

  1. a) Increased

Heart disease with high pulmonary flow.

Overhydration

Treatment: diuretics

  1. b) Decreased

Dehydration

Blood loss Plasma loss

Treatment: replenish blood volume.

Post-loading

  1. a) Increased

Peripheral vasoconstriction.

Treatment: vasodilators.

  1. b) Decreased

Aortic coarctation.

Treatment: surgical

Contractility.

  1. a) Decreased.

Dilated cardiomyopathies.

Restrictive cardiomyopathies.

Treatment: inotropic.

Distensibility.

  1. a) Decreased.

Tumors: intra or extracardiac.

Cardiosclerosis.

Classification of Heart Failure

  • According to the claudicant ventricle:

– Right IC.

– IC left.

– Global, mixed or cebgestive HF.

  • According to ventricular dysfunction:

– IC with systolic dysfunction (myocarditis).

– HF with diastolic dysfunction (aortic coarctation).

  • According to the etiology:

– Congenital.

– Acquired.

  • According to evolution:

– Acute.

– Chronicle.

  • According to cardiac output:

– With high cardiac output.

– With low cardiac output.

Cardiovascular reserve factors

Cardiac

  • Tachycardia (release of catecholamines): When there is an increased need, the heart responds by increasing heart rate and stroke volume through more vigorous contraction. Its compensatory action is limited because it reduces ventricular filling, which ultimately decreases minute volume.
  • Dilation: When the tachycardia is very marked, the cardiac output decreases again, which causes resistance that prevents adequate ventricular emptying, while the venous return continues normal or increased, this brings with it an increase in diastolic volume. Therefore it results in cardiac dilation.
  • Hypertrophy: the dilated myocardium performs a greater task but it also has to bear a greater load and expend more energy to achieve the same volume per minute as before, causing an increase in the volume and thickness of the cardiac muscle fibers.
  • Biochemical mechanisms related to heart coupling (increased contractility converting chemical energy into mechanical).
  • Extracardiac
  1. Secondary aldosteronism.
  2. Peripheral vasoconstriction.
  3. Erythrocyte-dependent mechanism.
  4. Mechanism of increase with lung dynamics.
  5. Decrease in nutritional requirements.

However, when the compensatory mechanisms fail to maintain adequate cardiac output, there is a decrease in renal plasma flow and therefore glomerular filtration with retention of dio and water that produces edema. The insufficient heart cannot expel the blood that comes to it during diastole and it collects behind the cavities and in the lungs, as well as in the great circulation, causing venous and arterial hypertension, which further reduces cardiac output.

Clinical manifestations

Symptoms: A seriously ill infant or child who has exhausted its compensatory mechanisms to the point that it is no longer reaching sufficient cardiac output to meet the basal needs of its body will present symptoms of rest. Other patients may be comfortable at rest, but are unable to increase their cardiac output in response to even light activity without significant symptoms. On the other hand, children with less severe heart disease will require intense exercise to alter their heart function.

Cyanosis can be considered merely as “an intense coloration” and not be recognized as a pathological finding. The story from the parents of a young infant should focus on the feeding process. An infant with congestive heart failure often ingests less volume per feeding, has dyspnea on suckling, and may sweat heavily. Uncovering a history of fatigue in an older child requires specific questions about their activity.

In children, the symptoms and signs of congestive heart failure are similar to those in adults. They consist of fatigue, exertion intolerance, anorexia, abdominal pain and cough. Dyspnea is a reflection of pulmonary congestion. The elevation of systemic venous pressure can be calibrated by measuring jugular venous pressure and hepatomegaly. There may be orthopnea and basal rales; there is usually detectable edema in the sloping parts; there may also be anasarca. There is always cardiomegaly. Gallop rhythm is frequent; Other auscultatory findings are those produced by the basic injury.

In infants, congestive heart failure may be more difficult to identify. Its most prominent manifestations are tachypnea, feeding difficulties, little weight gain, excessive sweating, irritability, weak crying and noisy and labored breathing with rib and subcostal retractions, as well as nasal flutter and sternal retractions.

Pulmonary congestion may be impossible to distinguish from the signs and symptoms of bronchiolitis, including wheezing as the most striking. Pneumonitis is common, with or without partial atelectasis of the lung, especially in the middle and lower right lobes and due to bronchial compression by the enlarged heart. Hepatomegaly is almost always present, and cardiomegaly is always present. Despite pronounced tachycardia, a gallop rhythm is often recognized. Edema can be generalized affecting both the eyelids and the sacrum, legs and foot. Differential diagnosis depends on age.

Etiology by age

Fetal

  • Severe anemia (hemolysis, fetal-maternal transfusion, parvovirus B19-induced anemia, hypoplastic anemia).
  • Supraventricular tachycardia.
  • Ventricular tachycardia.
  • Complete heart block.

Premature newborn

  • Fluid overload.
  • Patent ductus arteriosus.
  • Ventricular septal defect.
  • Cor pulmonale (bronchopulmonary dysplasia).

Term newborn

  • Asphyctic cardiomyopathy.
  • Arteriovenous malformation (Galen vein, liver).
  • Obstructive lesions on the left side (coarctation of the aorta, hypoplastic left hemicardias).
  • Large mixed heart defects (single ventricle, truncus arteriosus).
  • Viral myocarditis.
  • Left cardiac hypoplasia syndrome.
  • Total anomalous drainage of the pulmonary veins transposition of great vessels plus CIV.
  • Common trunk.
  • AV channel.
  • Septal defect: multiple CIV.
  • Coarctation of the aorta.
  • Tricuspid atresia.
  • Arrhythmias: paroxysmal supraventricular tachycardia.

Infant-preschool

  • Cardiac shunts from left to right (ventricular septal defect)
  • Hemangioma (arteriovenous malformation)
  • Abnormal left coronary artery.
  • Metabolic cardiomyopathy.
  • Acute hypertension (hemolytic-uremic syndrome).
  • Supraventricular tachycardia.
  • Kawasaki disease.
  • Obstructive lesions: coarctation, aortic stenosis.

Child-adolescent

  • Rheumatic fever.
  • Acute hypertension (glomerulonephritis).
  • Viral myocarditis.
  • Hemochromatosis-hemosiderosis.
  • Cancer treatment (radiation, Adriamycin).
  • Sickle-cell anaemia.
  • Cor pulmonale (cystic fibrosis).
  • Cardiomyopathy (hypertrophic, dilated, post-viral)

Etiology according to the factor affected

  • Volume overload (increased preload):
  1. a) Short circuit from left to right:
  • Atrium-ventricular septation defect.
  • Common trunk.
  • Pulmonary aortic window.
  • Transposition of large vessels + large IVC or PCA.
  • DEVD without PE (double emergence of the right ventricle).
  • Fallot tetralogy + agenesis of the pulmonary sigmoid. (if it represents only the thetalogy, no)
  • Severe valve insufficiencies.
  1. b) Arterio-venous fistulas. c) Severe anemia. d) Hypervolemia.
  • Pressure overload (increased afterload):
  • Systemic circulation:
  • Aortic stenosis.
  • Aortic arch insufficiency.
  • Hypoplasia of the aortic arch.
  • Aortic coarctation.
  • Pulmonary circulation:
  • Pulmonary stenosis.
  • Branch stenosis.
  • Pulmonary hypertension.
  • Contractility disorders:
  • Myocardial ischemia.
  • Metabolic disturbances.
  • Arrhythmias (Fc disorders)
  • Tachyarrhythmias

Diagnosis

In childhood, cottony lung signs suggestive of venous congestion and acute lung edema are rarely observed, except in the most extreme circumstances of heart failure. Low-voltage QRS morphology with ST-T abnormalities may suggest myocardial inflammatory disease, although they can also be seen in pericarditis. An electrocardiogram is the best means of evaluating rhythm disorders as a potential cause of heart failure.

Echocardiographic techniques are very useful in determining ventricular function. The most used parameter is the shortening fraction. Doppler studies are also useful in calculating cardiac output. Arterial oxygen concentration may be decreased when impaired ventilation / perfusion occurs secondary to lung edema. Infants with congestive heart failure often have hyponatremia due to water retention.

Signs of predominance of right cavities

Signs of predominance of left cavities

  • Pulmonary edema.
  • Decreased urine output, nocturia (due to increased renal flow).
  • Nocturnal cough, polypnea.
  • Bloody sputum.

Complementary exams

  • Differential blood count: anemia, leukocytosis.
  • Gasometry: metabolic acidosis.
  • C reactive protein.
  • Enzymatic studies.
  • EKG: signs of ventricular-atrial overload, rhythm disturbances
  • Telecardiogram: cardiomegaly.
  • Echocardiography: determines the type of alteration, whether there is a effusion or not, assesses the degree of ventricular dysfunction.
  • Urine: transient albuminuria with increased urine density.
  • Pharyngeal exudate.
  • Ionogram: Dilutional hyponatremia, hypochloremia, hyperkalemia due to tissue release as tissue perfusion decreases.

Differential diagnosis

  1. Hypoxic crisis: it occurs with irritability, cyanosis, respiratory distress. There is a history of cyanotic heart disease.
  2. Pneumopathy.
  3. CAAB.
  4. Foreign body in the airways.
  5. Bronchiolitis.
  6. Large circuits from left to right: there is a murmur from birth and the presence of IRA on repeat.
  7. Pericarditis with effusion: muffled heart sounds, paradoxical pulse and friction.
  8. In cases of edema, edema and nephritic and nephrotic syndromes are also differential diagnoses.

Treatment

Treatment goals

  1. Improve heart rate and rhythm.
  2. Improve preload.
  3. Improve contractility.
  4. Decrease post-load.
  5. Decrease cardiac work.
  6. Control sodium and water retention.

General measures

– Flower position.

– Oxygen therapy: 8-10 liters / minute. It is recommended to use tents because the masks irritate the child.

– Venous approach, if it is deep better.

– Diet: Infants with congestive heart failure may have growth retardation due to increased metabolic demands and decreased calorie intake.

It may be useful to do this by increasing the number of calories per 30 grams of bottle (or breastfeeding supplementation). The use of bottle formulas with very low sodium levels is not recommended as a routine treatment for infants with congestive heart failure, because these formulas are often very poorly tolerated by patients.

The administration of more powerful diuretics allows the elaboration of conventional bottle formulas with a more pleasant flavor. Most older children can be treated with salt-free diets and abstinence from foods that contain large amounts of sodium. A strict diet with extremely low amounts of sodium is usually not necessary.

 

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