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Neonatal cardiac failure
This document discusses neonatal cardiac failure, including the pathophysiology of atrioventricular septal defect. It notes that the neonatal myocardium is anatomically different from the mature heart, with less organized myofibrils and contractile efficiency. This makes the neonatal heart more dependent on compensatory mechanisms like neurohormonal activation and the Frank-Starling response. Medical management aims to reduce afterload and preload on the heart through diuretics and ACE inhibitors while providing respiratory support. Surgical intervention may be needed to correct underlying structural defects.
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Neonatal cardiac failure
- 1. Neonatal cardiac failure- Pathophysiological basis Dr.Gopakumar Hariharan Senior Registrar, Neonatal and Paediatric Intensive care
- 2. Neonatal cardiac failure • Case scenario • Fetal circulation and neonatal heart • Pathophysiology • Basis of Management
- 3. Case scenario •Ex 31 weeker, now corrected age 38 weeks • Holt Oram syndrome – Hypoplastic radius and Cardiac defect – Large AVSD • Initial management for respiratory distress syndrome • Prolonged non invasive respiratory support • Cardiac failure – Frusemide and Captopril • Transfer to Melbourne for definitive surgery
- 4. Challenges with Neonatalcardiac failure • Unique anatomic and physiologic factors • Different etiologies of cardiac failure • Functional and structural differences between mature and immature myocardium
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- 6. Postnatal transition andcongenital heart defects Cord clamping – increase in SVR PVR decreases PDA shunts from left to right ( functionally closes by 12 hours of life – Mediated by oxygen, bradykinins and nitric oxide) Blood flow to the left atrium increased substantially through the pulmonary veins. Left atrium pressure increases - septum primum apposes the crista, resulting in closure of foramen ovale Heyman MA,RudolphAM. Effects of congenital heart diseaseon fetal and neonatal circulations.Prog Cardiovasc Dis.1972;15:115-143
- 7. Reduction in PVR • Fall in PVR- contributed by improved ventilation and oxygenation • Increase in oxygenation - modest increase in pulmonary blood flow and decrease in mean pulmonary artery pressure. • Oxygen modulates the production of the vasoactive substances nitric oxide and prostacyclin
- 8. Neonatal cardiac failure- etiology • Systolic Vs Diastolic • Right sided Vs Left sided • Low output Vs High output
- 9. Pathophysiology – Atrioventricularseptal defect •
- 10. Atrioventricular septal defect Large VSD • Equalisation of Right and left ventricular pressures • Left to right shunt • Large pulmonary blood flow into lungs • Pulmonary hypertension Primum ASD • Left to right shunt • Volume load on right ventricle AV valve regurgitation • Volume loading of left atrium and left ventricle • Decreased left ventricular compliance • Increase in left to right shunting at atrial level Normal physiologic nadir of the infant hematocrit first 30-60 days of life, - further decrease in the pulmonary vascular resistance causes additional left to right shunting and the resulting pulmonary overcirculation. Cardiac failure
- 11. Compensatory mechanisms Neurohumeral Cardiac failure compensatory mechanisms Myocardial hypertrophy Frankstarling law
- 12. Counterregulatory neurohormones inCardiac failure – Vicious cycle in impaired heart Renin-Angiotensin aldosterone mechanism • Retain sodium and water • Increase intravascular volume and preload Increased sympathetic activation • Vasoconstriction of arteries • Increased afterload Incraesed sympathetic activation • Increased contractility
- 13. Frank Starling Principle If the initial (resting) length of (i) Either an individual myocardial cell (or ) (ii) Whole of ventricle Is incr. WITH IN LIMITS The force generated by the contractile Fibers (or) cardiac output as a whole increases
- 14. Frank starling forces Kirkpatrick SE, Pitlick PT, Naliboff J, Friedman WF (1976) Frank-Starling relationship as an important determinant of fetal cardiac output. Am J Physiol 231:495-500.
- 15. Neonatal myocardium •Left ventricular mass increase in postnatal period – initially hyperplasia and later hyperplastic • Myocyte proliferation occurs more rapidly in the left than the right – due to increased demands of a high vascular resistance • myocyte hypertrophy accounts for most of the increase in ventricular mass subsequently ( mediated by increased work load, circulating growth factors and catacholamines). • Acidic fibroblast growth factors and transforming growth factors produced by the cardiac myocyte may mediate cellular proliferation and differentiation.
- 16. Neonatal myocyte Rounded,relatively short and quite disorganized intracellulary Myofibrils- contractile proteins Mature cells- myofibrils densily concentrated and are aligned in parallel with the axis of the cell, organized into alternating rows of mitochondria Neonates- myofibrils less dense and more likely to be situated along the periphery of the cell . The more central portion is made up of disorganized clumps of mitochondria and nuclei
- 17. Inefficient Myocardial contractility • Less complaint • Generate less contractile force • Inefficiently shaped and less organized myofibrils • Greater ratio of noncontractile elements to contractile units
- 18. So.. Why isour baby working hard
- 19. Contributory Factors •Premature lungs • Preterm infants develop symptoms earlier as their PVR is lower due to inadequate mascularisation of the pulmonary arteries • Increased preload from Neurohumeral mechanisms • Increased afterload from high Sympathetic activity • Insufficient ventricular contractility
- 20. Circulatory adaptation incardiac failure ( in context of pulmonary overcirculation) • Activation of sympathetic nervous system – increase in plasma norepinephrine • Stimulation of renin- angiotensin- aldosterone system • Increase in plasma arginine vasopressin • Increased atrial natriuretic peptides – from atrial stretch from volume/ pressure overload • Peripheral vasoconstriction • Increased heart rate • Water retension
- 21.
- 22. Goals of management • Provide symptomatic relief • Correct metabolic abnormalities • Reverse haemodynamic derangements
- 23. Decreased myocardial contractility • Unload myocardium with diuretics • Reduce afterload
- 24.
- 25. Diuretics • Initialtreatment in decompensated cardiac failure • Diuretic resistance – add intravenous thiazide diuretics( chlorthiazide) • Continuous loop diuretic infusion Monitoring • Electrolyte disturbance – profound urinary loss of potassium, magnesium and calcium due to immature renal secretory control in neonates • Renal insufficiency • Hypotension
- 27. • 117 •premature infants • 20 had intrarenal calcification • 2 required nephrolithotomy • 4 had recurrent UTI • Discontinuation- results in resolution of calcification • Continued treatment with Frusemide- Associated with renal morbidity
- 28. • 27 babiesless than 1500 grams.3 groups A) No Frusemide and no calcification B) Frusemide and no calcification C) Frusemide and calcification • No abnormalities in renal function in group A and B • Higher calcium creatinine ratios, increased fractional excretion of sodium and lower tubular absorption of Phosphate in group C • Possible glomerular and tubular dysfunction
- 30. Afterload in cardiacfailure Afterload – Little effect on normal ventricle systolic failure – even small increases in afterload have significant effects. Small reductions in afterload in a failing ventricle can have significant beneficial effects on impaired contractility
- 31. ACE inhibitors •Inhibits formation of Angiotensin II ( Potent vasoconstrictor, promotes aldosterone release and facilitates sympathetic activity) • Inhibition results in accumulation of kinins like bradykinin- promotes vasodilator activity
- 32. Age range- asearly as 6 days Initial median dose – 0.1mg/kg(0.05to 0.55mg/kg/day) Additionally treated with Frusemide Sideeffects in 17 patients of 43 a) Renal impairement/ failure b) Hypotension All side effects reversible Side effects not dose related
- 33. Deficient Calcium transportmechanism – ? Role for calcium • Cardiac myocyte membrane(sarcolemma) – has ion channels and pumps-allows transport of calcium and other ions • Immature heart- more dependent on extracellular calcium for myocardial contraction • Sarcoplasmic reticulum of fetal sheep- low density of calcium channels and decreased pump activity • Importance- Frusemide and calcium loss??
- 35.
- 36. Fluid management Leftventricular filling volume is reduced beyond a particular pressure( lesser in magnitude than adult)- smaller boluses SpotnitzWD, Spotnitz HM, Truccone NJ (et al) (1979) Relation of ultrastructure and function. Sarcomere dimensions, pressure-volume curves, and geometry of the intact left ventricle of the immature canine heart. Circ Res 44:679-691
- 37. Fluid management- conceptof ventricular interdependence Filling of one ventricle reducing the distensibility of the opposite ventricle More profound in fetus than adults Little change in cardiac output when the immature ventricle is volume loaded Romero T, Covell J, Friedman WF (1972) A comparison of pressure-volume relations of the fetal, newborn, and adult heart. Am J Phys 222:1285-1290.
- 38. NETS • Respiratorysupport – CPAP • Anticipation of increased oxygen requirement • Intravenous diuretics • Nasogastric tube for venting
- 39. Surgical management Amedical perspective
- 40. Evaluation TAR –hematology for thrombocytopenia Holtoram- Kidneys , heart scans Vateryl
- 41.
- 42. Thumb hypoplasia •Pollicisation - converts index finger into thumb – prehensile hand with a thumb and three fingers – improved function and appearance • Toe to hand transfer( second toe) – excellent improvement in function and appearance • Role for physiotherapist and occupational therapist • Therapy ideally started in the neonatal period- especially with restricted interphalangeal joint extension • Gain in length – distraction techniques
- 43. (A) Child withpollicisation of the index finger to make a thumb. Watson S Arch Dis Child 2000;83:10-17 Copyright © BMJ Publishing Group Ltd & Royal College of Paediatrics and Child Health. All rights reserved.
- 44. Radial club hand • Therapy, splints and stretching should start in the neonatal period • Distal radial hypoplasia responds well to treatment • Severe from- absence with forearm at right angles – no major respose • Hypoplastic thumbs- stabilized and given more movements by tendon transfers
- 46. Summary • NeonatalMyocardium anatomically different • Complex pathology • Pathophysiological understanding to direct treatment
- 47.