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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 Neonatal cardiac failure
• Unique anatomic and physiologic factors
• Different etiologies of cardiac failure
• Functional and structural differences between mature and immature
myocardium
6. Postnatal transition and congenital 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
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
12. Counterregulatory neurohormones in Cardiac 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
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 in cardiac 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
25. Diuretics
• Initial treatment 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
26.
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 babies less 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
29.
30. Afterload in cardiac failure 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- as early 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 transport mechanism – ? 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??
36. Fluid management
Left ventricular 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- concept of 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
• Respiratory support – CPAP
• Anticipation of increased oxygen requirement
• Intravenous diuretics
• Nasogastric tube for venting
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
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
45.
46. Summary
• Neonatal Myocardium anatomically different
• Complex pathology
• Pathophysiological understanding to direct treatment
