Hypotension in the Newborn Infant
|Publication: 01/10/2002 --|
|Last review: 27/11/2018|
|Next review: 27/11/2021|
|Copyright© Leeds Teaching Hospitals NHS Trust 2018|
This Clinical Guideline is intended for use by healthcare professionals within Leeds unless otherwise stated.
Hypotension in Newborn Infants
Newborn babies undergo a period of profound physiological change during the transition period after birth. The pulmonary vascular resistance (PVR) is high, but falling rapidly and there may be persistent pulmonary hypertension. The systemic vascular resistance (SVR) has increased markedly from fetal levels (when the circulation was connected to a low resistance placenta). The left ventricle has taken over from the right ventricle in being the dominant ventricle contributing to cardiac output and there may be multiple shunts present at the level of the foramen ovale, the arterial duct or within the lungs.
In addition there may be hypovolaemia and myocardial dysfunction and there may be positive pressure ventilation, all of which will affect cardiac output. For all these reasons it is important to make an overall assessment of the circulation and of adequate tissue perfusion rather than just focus on the blood pressure.
Cardiac output (CO)= Heart Rate (HR) x Stroke volume (SV)
Stroke volume is proportional to:
- Preload (cardiac filling- affected by dehydration, blood loss including IVH and third spacing)
- Myocardial contractility (affected by asphyxia and extreme prematurity)
- Afterload (SVR)- (determined by vascular bed size and function- affected by sepsis, capillary leak, vasodilatation)
The cardiac output and need for intervention can be considered using the following graph
Evidence base: there are very few RCTs on the use of different inotropes and none have looked at long term outcomes. In some studies hypotension was associated with IVH and adverse developmental outcome but in others there was no association between treatment and outcome or hypotension (defined as blood pressure (BP) less than gestational age) and adverse outcome. In the ELGAN (extremely low GA newborn) study of 945 infants with a GA <28 weeks, logistic regression analysis adjusted for potential confounding factors demonstrated no association between the lowest recorded BP and developmental outcome at 24 months corrected age. The drug with the most neonatal research evidence is Dopamine, which is shown to increase blood pressure, but there is little evidence that it improves cardiac output, cerebral or tissue perfusion. Hence any treatment must be based on the overall clinical picture (see scenarios below) and not just BP alone.
Blood pressure is related to gestational age and birth-weight and rises with post natal age. Normal levels of BP are difficult to define. The graph below shows the 95th confidence intervals for systolic and diastolic BP in 329 infants on day 1 of life:
From Zubrow AB1, Hulman S, Kushner H, Falkner B.
Determinants of blood pressure in infants admitted to neonatal intensive care units: a prospective multicenter study. J Perinatol. 1995 Nov-Dec;15(6):470-9.
Graph below shows 10th centile for MBP in the first 72 hrs
Ref: 12. H. William Taeusch, M.D., Roberta A. Ballard, M.D., and Christine A. Gleason, M.D. Avery's Diseases of the Newborn (Eighth Edition) Elsevier 2005
The American Accademy of Paediatrics recommends a target mean BP of >30mmHg in extreme preterm infants. In many units a mean BP > gestational age in weeks is regarded as acceptable. Since this is the easiest to use in practice we generally adopt this rule, but remember that babies can have normal tissue and crebral perfusion despite a low BP or can have reduced perfusion despite a BP above this threshold.
- Consider treatment if Mean BP < GA in weeks.
- Target BP should be >30mmHg in extreme preterm (<28 weeks) and >50-60mmHg in term infants with PPHN
Assessment of the circulation should include:
- History of blood or fluid loss (including feto-maternal , twin to twin)
- Heart rate (tachycardia in absence of inotropes may suggest hypovolaemia)
- Pulse volume especially femoral pulses
- Blood pressure (ideally invasive- see figures for normal values) and pulse pressure (systolic-diastolic). Low diastolic BP may represent a large PDA.
- Urine output (normal >1ml/kg/hr)
- Capillary refill time (normal <2 sec)
- pH, Lactate and base excess
- Evidence of sepsis (clinical and laboratory) including NEC.
- Functional echocardiography (if available) to assess filling, contractility and cardiac output (MPA peak velocity<0.35m/sec is suggestive of reduced cardiac output, >0.45m/sec is normal)
There are several recognisable clinical scenarios. However, an individual baby may not fit the scenario exactly and difficult cases should always be discussed with a senior neonatologist. When starting inotropes always purge the line to prevent delay in effect. Once running do not interrupt the infusion, even briefly.
1. The extreme preterm infant (<28 weeks) in the first 24-48 hrs of life
These babies are usually adapting to a sudden increase in SVR and the myocardium may not be fully adapted. In addition there are left to right shunts present and high PVR due to RDS/ventilation. These babies are in a low flow state.
- Consider reducing/stopping or avoiding morphine unless in pain
- Start with inotrope: Dobutamine 10 micrograms/kg/min and titrate (5-20 micrograms/kg/min. Ideally via a central line but may be given peripherally with caution.
- Review effect over next 30 mins (unless in shock)
- Consider 10ml/Kg saline bolus
- Only exceed 10ml/kg if known hypovolaemia or reduced CRT or urine output or evidence of underfilling.
- If anaemic (<120 g/L) give blood transfusion as per protocol.
- If no response to maximum dobutamine (20micrograms/Kg/min) start dopamine (5 micrograms/kg/min) and titrate to max 20 micrograms/kg/min)
- If no response (i.e. both dopamine and dobutamine ≥15 micrograms/kg/min) then add hydrocortisone 2.5mg/kg every 4-6 hours until BP stable and then wean.
2. Any preterm baby after 24-48 hrs or (non-asphyxia) term baby with hypotension and potential shock. IUGR babies are often in this category.
These babies are likely to be in a high flow, low resistance state due to sepsis, fluid/blood losses or capillary leak (e.g. NEC). If tissue perfusion is adequate (good urine output, CRT<2 sec) there may be no immediate need for treatment. If there are signs of shock or BP is very low then treat:
- Give 10ml/kg bolus of saline
- If clear evidence of acute blood loss give blood 20ml/kg over 30min-1 hr
- Start with vasopressor : Dopamine 10 micrograms/kg/min and titrate (5 - 20micrograms/kg/min). Dopamine must be given by central line. Discuss with consultant before giving peripherally.
- Consider further 10ml/kg bolus of saline and observe for response (fall in heart rate, improved CRT or rise in BP).
- If no response consider adding Noradrenaline 0.2 micrograms/kg/min via a central line (titrate to max 1 microgram/kg/min)
- If resistant to inotropes consider adding hydrocortisone 2.5mg/kg every 4-6 hours until BP stable and then wean.
- If NEC and have given >20ml/kg saline consider use of colloid (HAS 4.5%)
- Dobutamine is an inodilator and may make shock worse. Reducing dobutamine (if it has been used) can sometimes paradoxically improve BP in high flow shock states.
3. Post asphyxia (any gestation)
These babies are likely to have poor or very poor myocardial contractility.
- Start with dobutamine 10 micrograms/kg/min and titrate (5-20 micrograms /kg/min)
- Only give 10ml/kg saline bolus with caution and do not repeat unless clear response in BP. This may make cardiac output worse.
- Consider early echo to assess contractitlity and filling and guide further management.
- If no response to maximum dobutamine and filling is optimal then consider adding a pressor agent (dopamine or noradrenaline)
4. PPHN at term
These babies should be managed according to the PPHN protocol.
- Optimize ventilation and consider nitric oxide at 20ppm.
- If on HFOV be aware that a very high MAP can impair cardiac filling leading to reduced stroke volume and cardiac output. Discuss with senior neonatologist.
If hypotension and reduced cardiac output are significant then:
- Echocardiography to confirm pulmonary hypertension and assess right ventricular function.
- Do not give fluid boluses without evidence of hypovolaemia.
- Consider ‘offloading’ the right ventricle by using prostin to open the duct (Alprostadil 12.5 nanograms/kg/min)
- Consider Milrinone 250 nanograms/kg/min (range 100-750 nanograms/kg/min). If blood pressure falls add in adrenaline 0.1-1.5 micrograms/kg/min (increasing dose until BP responds) .
- If no response add in Dobutamine 10-20 micrograms/kg/min
In any scenario if no response to treatment consider:
- Technical problem with BP measurement- check cuff/ transducer etc.
- Prescription /administration error- check all infusions
- High Mean airway pressure (especially on HFOV)
- Pericardial tamponade
- Extreme hypovolaemia
- Hidden blood loss- IVH/ Scalp/ Bowel/ Twin to twin or feto-maternal
- PPHN (check pre and post ductal saturation)
- Congenital heart defect
- Drug side effect
Main inotropes and mode of action:
Dopamine- acts on dopamine receptors and β1,β2 agonist. Increases contractility and SVR (by vasoconstriction). May be vasodilator at very low doses.
Dobutamine- β1 agonist. Increases contractility without increasing SVR. May cause vasodilatation and tachycardia.
Adrenaline - α1,α2, β1,β2 agonist. Proportionally greater? β effect. Increases contractility (with increased SVR at high doses) May cause tachycardia. More potent than dopamine.
Noradrenaline- α1,α2, β1agonist- proportionally greater effect on alpha receptors causing vasoconstriction.
Milrinone- phosphodiesterase III inhibitor. Improves myocardial function and has positive inotropic and vasodilator effects. Used in low cardiac output
post cardiac surgery and increasingly for low flow states such as PPHN.
Hydrocortisone- unknown mode of action but has been shown to reduce need for inotropes in preterm babies. May address borderline cortisol insufficiency or improve inotrope receptor activity. Avoid concurrent use with ibuprofen as risk of intestinal perforation.
Hypotension and shock
|Target patient group:||Neonatal patients|
|Target professional group(s):||Secondary Care Doctors
Secondary Care Nurses
1. UpToDate: L. Adcock. Etiology, clinical manifestations, and evaluation of neonatal shock.
2. Cox DJ,Groves AM. Inotropes in preterm infants- Evidence for and Against. Acta Pediatrica 2012:101:17-23
3. Evans N. Which inotrope for which baby? Arch Dis Child Fetal and Neonatal 2006;91:213-220
4. Evans N. Management of circulation in Neonatal period. Neonatal haemodynamics and cardiology conference, Middlesborough Sept 2015.
5. Addenbrookes hypotension Guideline 2013
6. North Trent Neonatal Network Guideline Oct 2014
7. Leeds hypotension guideline 2006-2015
8. Anderson RH et al. Pediatirc Cardiology, 3rd edition 2010. Churchill Livingstone
9. Martin RJ, Fanaroff AA. Neonatal-Perinatal medicine. 10th ed.2015. Elsevier saunders.
and Evidence levels:
A. Meta-analyses, randomised controlled trials/systematic reviews of RCTs
B. Robust experimental or observational studies
C. Expert consensus.
D. Leeds consensus. (where no national guidance exists or there is wide disagreement with a level C recommendation or where national guidance documents contradict each other)
LHP version 1.0
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