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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