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Newborn Resuscitation
The Neonatal Heart
Spark of Life 2011
Newborn Resuscitation
Newborn resuscitation all about breathing
– Aeration of the lungs
Clears fetal lung fluid
Opens pulmonary capillary bed
Drives transition
– <1% of neonates require cardiac compression
The transitional heart
A most remarkable organ
– Rapid change from stable low demand fetal circulation
to more dynamic post natal circulation
– Organ specifically designed to cope with the
“asphyxia” of delivery while continuing to support the
rest of the body
Examine the current guidelines for cardiac support
Explore the physiology of the transitional heart
ARC 2010 Newborn Guidelines
Initial cardiac support with
ventilation
– Reverse hypoxia
– >90% reversal of bradycardia
ARC 2010 Newborn Guidelines
Initial cardiac support with
ventilation
– Reverse hypoxia
– >90% reversal of bradycardia
HR < 60 Chest compressions
– 3:1 ratio
The bradycardic newborn heart
Response to hypoxia induced energy
deficiency
– Need to increase blood oxygenation
– Poorly compliant lungs
– No effective ventilation during compressions
alone therefore need regular breaths
– 3:1 ratio
The bradycardic newborn heart
Response to hypoxia induced energy deficiency – Need to increase blood oxygenation
increase coronary blood flow Coronary arteries perfuse in diastole.
Flow dependent on gradient between diastolic BP and intra-luminal pressure
Responders
(n = 53)
Non-responders
(n = 9)
p
Median DBP during CPR
(mmHg)*
8 (6,10) 6 (3,9) NS
Max DBP during CPR
(mmHg)*
20 (16,20) 8 (7,11) <0.001
Mean DBP prior to HR >
60 bpm
20 ± 3
Time from DBP ≥
20mmHg to
HR > 60bpm (sec)
19 ± 12
Diastolic Blood Pressure Characteristics
During CPR
Compressions to raise diastolic BP
Diastolic pressure rises slowly over
sustained compressions.
Interruption of compressions drops
diastolic BP
– For auscultation every 30 seconds
use oximetry or endtidal CO2 to determine
ROSC
– Would an extended compression ratio help
ARC 2010 Newborn Guidelines
Initial cardiac support with ventilation
– Reverse hypoxia
– >90% reversal of bradycardia
Chest compressions HR < 60
– 3:1 ratio
HR remains <60
– Adrenaline
Adrenaline
Chronotrope and inotrope
Induces vascular constriction – Raises diastolic blood pressure
– Improves coronary perfusion
Route? Dose?
30 s compressions 3:1 Epi 0.01 mg/kg ROSC
Endotracheal Adrenaline
Longstanding clinical use
– Rapidity
Does it work
– Instances of babies responding to ET adrenaline
– Instances of babies only responding to a subsequent
IV dose
– Lower drug assays or radio-labelled recovery
– ? Need higher dose
– Slow sustained release a possible advantage
UVC Adrenaline
Preferred route
Can be rapid if UVC prepared before
delivery
Local Current Recommendation.
– First dose via ETT if UVC not placed
– Subsequent dosage via UVC
Adrenaline Dosage
Local Recommendation
– 1ml per dose of 1:10,000
– 0.5 ml per dose < 34 weeks
Consider Volume Expansion
Volumophobic
Volumophilic
Volume - The case against
Wyckoff MH, Perlman JM, Laptook AR. Use of volume expansion
during delivery room resuscitation in near-term and term infants.
Pediatrics. 2005 Apr;115(4):950-5.
Volume - The case against
Wyckoff M, Garcia D, Margraf L, Perlman J, Laptook A.
Randomized trial of volume infusion during resuscitation of
asphyxiated neonatal piglets. Pediatr Res. 2007 Apr;61(4):415-20.
Volume - The case against
Volume - The case against
In conclusion, the data in this prospective, randomized,
blinded, neonatal piglet trial support the concept that volume
infusion as part of intensive resuscitation for asphyxiainduced
hypotension and bradycardia increases pulmonary
edema, decreases pulmonary Cd, and does not improve blood
pressure either during the resuscitation or during a 2-h postresuscitation
interval compared with no SHAM.
Volume - The case for
In conclusion, the data in this prospective, randomized,
blinded, neonatal piglet trial support the concept that volume
infusion as part of intensive resuscitation for asphyxiainduced
hypotension and bradycardia increases pulmonary
edema, decreases pulmonary Cd, and does not improve blood
pressure either during the resuscitation or during a 2-h postresuscitation
interval compared with no SHAM.
Volume – the case for
Anecdotal evidence of response to acute volume after failure to respond to adrenalin alone
– increase in diastolic BP
Concept of functional hypovolaemia
Evidence from functional echocardiography
– Venous distension very rare
– Blood pressure a very poor determinant of CO or systemic flow
Volume – The case for P
eak P
BF
(m
L/k
g/m
in)
0
60
120
180
240
300
**
#
Time (min)
F 10 15 25 30 40 50 60 70 80 90
Min
after
systo
lic p
uls
e (
mL/k
g/m
in)
-75
-50
-25
0
25
50
75
100
*
Time (min)
F 10 15 25 30 40 50 60 70 80 90
Puls
atilit
y Index
0.6
0.9
1.2
1.5
*
*
*
**
*#
End D
iasto
lic P
BF
(m
L/m
in/k
g)
-40
-20
0
20
40
60
*
*
#
Pulmonary Waveform Analysis. Mean
systolic PBF (A), Peak systolic PBF (B), post
systolic minimum PBF (C) and Pulsatility
Index (D) in control (closed circles) and
volume load (open circles) lambs during
ventilation at different levels of PEEP (gray
bars). The black bar represents the period of
volume infusion. Statistically significant
differences are indicated by an asterisk
(p<0.05).
Polglase GR, Kluckow M, W GA, Allison BJ, Moss TJ,
Pillow JJ, et al. The effect of a volume load at birth on
cardiopulmonary haemodynamics in preterm lambs. .
Journal of Paediatrics & Child Health. 2010;46(S1):A125.
Volume
Local recommendations
– If an infant fails to respond to a dose of
adrenaline follow a second dose with a bolus
of 10 ml/Kg/NS
Physiology of the transitional heart
The fetal heart
– Combined ventricular work
– Relatively high volume low resistance circuit
– Little variability in demand
The heart at birth
– Possible “asphyxia” during delivery
– Repid decrease in RV preload and LV afterload
Post birth
– Increased load demand greater variability
Coping with delivery
How does the fetal heart withstand “asphyxia”
– Inbuilt fuel source, Glycogen Adult 2% Fetus 30%
In utero lactate
Transition glycogen / glucose
Post transition fat
– Resistant to arrhythmias
Fetal isoforms of the contractile unit
Glycogen stabilised sarcoplasmic Ca++
Adrenergic receptors not yet upregulated
Morphology of the heart
Fetal Isoforms
Metabolically efficient
Lesser contractility
Resistant to asphyxia
Resistant to arrhythmias
Adult Isoforms
Mechanically efficient
More contractility
Infarcts with asphyxia
Develops arrhythmias
Triggers for change
Metabolic environment
Mechanical demand
Hormonal
Inutero stress Chorio / LPS /
placental resistance
??????????
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