Heart failure (neonatology)

Heart failure occurs when cardiac output is unable to meet the body's metabolic needs. A decline in cardiac output triggers a cascade of compensatory mechanisms to maintain organ and tissue perfusion. In newborns, it develops most often on the basis of myocardial dysfunction, left-sided obstructive lesions, tachyarrhythmias and large arteriovenous malformations. The consequence is tachycardia, tachypnea with retraction, hepatomegaly, cardiomegaly. In the later period, the most common cause of heart failure is a large left-right shunt (large ventricular septal defect (VSD) or large persistent Botall's aneurysm (PDA)), which manifests after a decline in pulmonary vascular resistance.

Causes

 * 1) heart malformations:
 * 2) * shunts: ventricular septal defect (VSD), patent ductus arteriosus of Botall (PDA), aortopulmonary window, atrioventricular septal defect, single ventricle (single ventricle) without pulmonary stenosis, rarely atrial septal defect;
 * 3) * Total/Partial Anomalous Pulmonary Venous Connection;
 * 4) * valvular regurgitation: mitral regurgitation, aortic regurgitation;
 * 5) * outflow obstruction: cor triatriatum, pulmonary stenosis, mitral stenosis;
 * 6) * outflow obstruction: aortic valve stenosis, subaortic stenosis, supravalvular aortic stenosis, aortic coarctation.
 * 7) cardiac causes in a structurally normal heart:
 * 8) * cardiomyopathy, myocarditis, arrhythmias; hypertension;
 * 9) non-cardiac:
 * 10) * anemia;
 * 11) * sepsis
 * 12) * hypoglycemia; diabetic ketoacidosis;
 * 13) * hypothyroidism, other endocrinopathies;
 * 14) * renal failure;
 * 15) * muscular dystrophies.

Clinical picture

 * acute cardiorespiratory collapse;
 * respiratory distress;
 * tachycardia (unless the cause of heart failure is a conduction system block);
 * hepatomegaly;
 * poor peripheral circulation, marbled skin, cold sweat;
 * oedema, pericardial, pleural and peritoneal effusion;
 * excessive or unexpected weight gain;
 * feeding difficulties, low weight gain.

Treatment of acute heart failure

 * ventilatory support according to the condition;
 * volume expansion, inotropic support;
 * catecholamines: dopamine, noradrenaline, adrenaline, dobutamine;
 * vasopressors are drugs that induce vasoconstriction and thus increase mean arterial pressure (dopamine, noradrenaline, adrenaline);
 * inotropics are drugs that increase cardiac contractility (dobutamine, milrinone);
 * some drugs have both vasopressor and inotropic effects;
 * the effect of these drugs is mediated by adrenergic and dopamine receptors, among others:
 * alpha-1 adrenergic receptors: in the vessel wall → vasoconstriction; in the heart → prolongation of contraction duration without increasing heart rate; (noradrenaline, adrenaline > dopamine);
 * beta-1 adrenergic receptors: in the heart → stronger contraction and faster heart rate (inotropic and chronotropic effect) with minimal vasoconstriction; (dobutamine, adrenaline > noradrenaline, dopamine in medium and higher doses);
 * beta-2 adrenergic receptors: in vessel wall → vasodilation; (dobutamine, adrenaline);
 * dobutamine: pure adrenergic agonist (β1 > β2 > α receptors); improves myocardial contractility; reduces end-diastolic pressure in the left ventricle and increases blood pressure by increasing cardiac output; may induce hypotension by peripheral vasodilation (β2 receptors);
 * dopamine: adrenergic and dopaminergic receptor agonist in a dose-dependent manner; low doses → vasodilation including coronary and renal arteries; medium doses → inotropic and chronotropic effect, but also increase in pulmonary capillary pressure; high doses → α-receptor-mediated vasoconstriction predominates, afterload increases;
 * noradrenaline: endogenous catecholamine; stimulates β and α adrenergic receptors → inotropic and chronotropic effect and peripheral vasoconstriction;
 * milrinone: phosphodiesterase inhibitor; inotropic effect (but not via β1 receptors) and peripheral vasodilation;
 * fluid restriction to about 2/3;
 * furosemide i.v. 1 mg/kg every 6-12 hours;
 * optimization of oxygenation, not hyperoxia;
 * correction of anaemia.

Treatment of chronic heart failure

 * normal amounts of fluids (not restriction) in an effort to maximize energy intake;
 * optimizing caloric intake (hypercaloric nutrition, supplements, nasogastric tube feeding);
 * oral diuretics: furosemide 2-6 mg/kg/day (up to 2-3 doses), potassium-sparing diuretics or potassium supplementation;
 * in myocardial dysfunction, ACEi and/or digoxin may be considered;
 * correction of anaemia.