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 effectsSite of actionDOSENAME 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/minDOBUTAMINE
Inotropic effects decrease SVR
Vasopressor 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 receptors0.1 -1 mic/kg/minNOREPINEPHRINE
UNCERTAINEnhance sensitivity to
catecholamines
1-2.5 mg/kg 4-6 hourlyHYDROCORTISONE
Incease SVR no inotropic effV1 receptors0.018-0.12 u/kg/hVASOPRESSIN
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 (Dmin) and (B) expansion
during expiration (Dmax). 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

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11-Elsayed Y FD. Integrated Evaluation of Neonatal Hemodynamics, Part 2: Systematic Bedside