new approach to Hypotension in neonates

ppt about the pathophsiologic approach to neonatal hypotension

1. Hypotension in neonates By Dr Tarek Kotb SPECIAL THANKS FOR Dr. Yasser Elsayed , MD, PhD Director of the Targeted Neonatal Echocardiograph, Hemodynamics, and neonatal ultrasound Programs Staff Neonatologist, Health sciences Centre-Winnipeg

2. background Compromise of the neonatal circulation should be suspected in any infant who has hypotension , tachycardia or poor tissue perfusion. 1-hypotension…… no consensus for definition 2-tachycardia ……..? 3-impaired issue perfusion: # capillary refil time…….? # lactate or base excess…….? # low measured cardiac output (LVO or RVO)…..? Is it accurate ..? # SCVO2 ……. From where we will get the blood sample…? # Persistent oliguria,,,,,?

3. The pathophysiologic mechanisms of compromised systemic circulation Category I : issues with blood flow (risk of ischemic shock) 1- low preload 2-high afterload 3- poor myocardial performance 4-low systemic vascular resistance 5-left to right shunt 6-obstructive or restrictive systemic blood flow

4. Pathophysiologic mechanism of hypoxemia Categroy 2: infant is requiring high FIO2 1- HYPOVENTILATION 2- LIMITED DIFFUSION 3-VENTILATION PERFUSION MISMATCH(V/Q MISMATCH) 4- INTRAPUMONARY RIGHT TO LEFT SHUNT 5- HIGH PULMONARY VASCULAR RESISTENCE 6- LUNG CONGESTION 7- OBSTRUCTIVE LUNG HYPOPERFUSION

5. Conclusion Understanding the pathophysiologic mechanism early -before worsening of hemodynamics or progression to anaerobic metabolism –is helpful in targeting the management,

6. SCENARIO I Preterm 26 weeks GA admitted to NICU with BW 600 gms APGAR score was 7 at 1 minute and 9 at 5 minutes the attending physician apply delaed cord clamping after 1 minute there were no maternal risk factors patient was intubated in DR 1 hour after admission presented with low blood pressure ,poor perfusion and blood gas showing metabolic acidosis. What I the relevant pathophysiologic mechanism ? 1- high after load 2- poor myocardial performance 3- left to right PDA shunt 4- low systemic vascular resistance 5- low preload

7. SCENARIO II Preterm 28 weeks D12 was initially tolerating OGT feeding formula milk presented with abdominal distension , dilated bowel loops with pneumatosis intestinalis in the x ray his blood pressure is low with delayed CRT and metabolic acidosis. What is the relevant pathophysiologic mechanism for his hypotension 1- low systemic vascular resistance 2-low preload 3- poor myocardial performance 4- suprarenal dysfunction 5- 1 & 2

8. SCENARIO III Full term 39 weeks delivered by emergency LSCS due to history of decreased foetal movements and bad CTG baby born flat with cord blood gas pH 6.8 PCO2 80 HCO3 6 with base deficit – 16 APGAR score 1 at first minutes and 5 at 10 minutes patient shifted to NICU intubated few hours after delivery patient running metabolic acidosis ,poor perfusion , hypotension and desaturation What is the pathophysiologic mechanism ? 1- poor myocardial performance 2- low systemic vascular resistance 3- low preload 4- relative adrenal insufficiency 5- all of the above 6- 1,2 & 3

9. SCENARIO IV Full term with meconium stained liquor born via LSCS due to fetal distress intubated in OR due to Laboured breathing shifted to NICU and connected to ventilator , There was too uch difference between upper limp and LL SPO2 ,ECHO done showed severe pulmonary hypertension .Patient was hypotensive ,CRT prolonged , high lactate What is the relevant pathophysiologic mechanisms 1- low preload 2- low systemic vascular resistance 3- poor myocardial performance 4- all of the above

10. Scenario v Preterm 31 weeks who was hypotensive with poor perfusion and high lactate started Started on high dose inotropic support currently his HR is 190 / min Blood pressure is not improving What is the pathophysiologic mechanism ? 1- low preload 2- poor myocardial performance 3- drug induced or wrong CVS support 4- low systemic vascular resistance

11. Systolic and diastolic pressures Systolic blood pressure: 1.Pressure created by ventricular contractile function to exceed vascular resistance (afterload) 2 . To push SV through CVS VR Myocardial performance SV Diastolic blood pressure: 1.Resistance by contractile property of arterioles (SVR) 2.To maintain higher pressure gradient at arterial side (proximal > distal ( resistance and intravascular volume) SVR Overall vascular volume

12. Commonly used inotropes and vasopressor drugs in neonatal shock. Hemodynamic effects Site of action DOSE NAME OF DRUG Renal & mesenteric dilatation Inotropic effect Vasopressor , increase SVR& PVR Dopaminergic receptors 1&2 @ receptors B receptors 1-4 mic/kg/min 4-10 mic/kg/min 11-20 mic/kg/min DOPAMINE Inotropic effects decrease SVR increase CO B1&B2 On @ receptors 5-20 mic/kg/min DOBUTAMINE Inotropic effects decrease SVR V asopressor eff increase SVR @1receptors B1&B2 receptors 0.02-0.3 mic/kg/min 0.3-1 mic/kg/min EPINEPHRINE Vasopressor effects increase SVR @1&@2 receptors 0.1 -1 mic/kg/min NOREPINEPHRINE UNCERTAIN Enhance sensitivity to catecholamines 1-2.5 mg/kg 4-6 hourly HYDROCORTISONE Inc ease SVR no inotropic eff V1 receptors 0.018-0.12 u/kg/h VASOPRESSIN Inodilator eff,lusitropic effects increase contractility and decrease SVR Phosphodiesterase III inhibitor and produce effect at B1&B2 50-75 mic/kg/min bolus followed by 0.25-0.75 mic/kg/min MILRINONE

13. Pulse pressure vs MAP in prediction of death

14. CATEGORY I low peripheral vascular resistance Blood pressure components are low (SBP/DBP and MAP )

15. CATEGORY II High ventricular afterload (high svr WITH low co) Low to normal SBP with high DBP and narrow pulse pressure(PP ) Pathognomonic marker is narrowing of the pulse pressure (<10mmHg for preterm infants<24 hours old and <20mmHg for> 24 hours old)

16. scenario

17. Milrenone started

18. Category three Low cardiac output or myocardial dysfunction with normal or low systemic vascular resistance Blood pressure trends: Low all BP components SBP,DBP and MBP) with narrow pulse pressure(PP )

19. scenario

20. ROLE OF ECHOCARDIOLOGY IN SHOCK Assessment on cardiac filling on visual inspection “eyeballing.” Images (A,B) show under-filled heart in apical 4 chamber (A4C) and parasternal long axis (PLAX) views. Images (C,D) show volume overloading of left atrium (LA) and left ventricle (LV) in A4C and PLAX views.

21. ROLE OF ECHOCARDIOLOGY IN SHOCK Physiological variation in inferior vena cava (IVC) diameter. Normal collapsibility of (A) IVC during inspiration ( D min ) and (B) expansion during expiration ( D max ). In hypovolemia, IVC may be collapsed while in hypervolemia there is minimal or no collapsibility

22. ROLE OF ECHOCARDIOLOGY IN SHOCK Pericardial effusion in (A) subcostal and (B) apical 4 chamber views. In large pericardial effusion and cardiac tamponade, there may be collapse of cardiac chambers—first seen collapse of right atrium followed by right ventricle

23. ROLE OF ECHOCARDIOLOGY IN SHOCK Interventricular septum (IVS) and left ventricle (LV) shape in pulmonary hypertension on visual inspection. Image (A) shows normal circular LV and IVS shapes. Image (B) shows right ventricular dilatation and hypertrophy of right ventricle, flattening of IVS and “D” shaped LV in pulmonary hypertension

24. conclusion 1- look at the TREND of systolic ,diastolic and pulse pressures before and after any deterioration and intervention 2- Compare the values to the normalized centile curves for PMA 3- Integrate the impression from systolic and diastolic pressure with other parameters (UOP, acidosis ,MAP, fluids status , Hb ,oxygen requirement, and peripheral perfusions) 4- Change your formulated recommendation If there is no improvement after 1-2hours, or worsening after any time 5- Consider echocardiography by an expert person if the case is worsening despite multiple strategies

25. REFRENCES 1. Evans N. Which inotrope for which baby? Arch dis Child 2006; 91: F213-F220 2. Miall Allen et al, Arch Dis Child 1987;62:1068-9 3. Kluckow & Evans. Arch Dis Child 2000; 82: F188-94 4. Mortality Statistics: Childhood, infant and perinatal. Review of the Registrar General on deaths in England and Wales, 2005. Series DH3 no.38. London: Office for National Statistics 2007. 5. Cochrane Database of Systematic Reviews 2007 Issue 6 . Wolff CB. Normal cardiac output, oxygen delivery and oxygen extraction. Adv Exp Med Biol . 2008;599:169-182 . doi:10.1007/978-0-387-71764-7-23 . 7 . Azhan A, Wong FY. Challenges in understanding the impact of blood pressure management on cerebral oxygenation in the preterm brain. Front Physiol . 2012;3 DEC(December):1-8 . doi:10.3389/fphys.2012.00471. 8 . de Boode WP. Clinical monitoring of systemic hemodynamics in critically ill newborns. Early Hum Dev . 2010;86(3):137-141. doi:10.1016/j.earlhumdev.2010.01.031. 9 . Sehgal A. Haemodynamically unstable preterm infant: an unresolved management conundrum. Eur J Pediatr . 2011;170(10):1237-1245. doi:10.1007/s00431-011-1435-4. 10. Vutskits L. Cerebral blood flow in the neonate. Paediatr Anaesth . 2014;24(2):22-29. doi:10.1111/pan.12307 . 11- Elsayed Y FD. Integrated Evaluation of Neonatal Hemodynamics, Part 2: Systematic Bedside