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The Physiologic Based Approach to Hypoxemic Respiratory Failure Dr. Yasser Elsayed, MD, PhD Associate Professor Integrated Hemodynamics Program International POCUSNEO University of Manitoba

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Page 1: The Physiologic Based Approach to Hypoxemic Respiratory ...neokw.com/presentations/yaser/physiologic-based-approach-in-HRF.… · The Physiologic Based Approach to Hypoxemic Respiratory

The Physiologic Based Approach to Hypoxemic Respiratory Failure

Dr. Yasser Elsayed, MD, PhD

Associate Professor

Integrated Hemodynamics Program

International POCUSNEO

University of Manitoba

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Objectives

This presentation is aiming to demonstrate :

• Basic pathophysiology of hypoxemia

• Management of critically ill infants at risk of hypoxemia orwith pulmonary hypertension

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Important Definitions

• Hypoxemia:

SpO2< 80%, or PaO2 < 50 mmHg

• Hypoxia:

Low oxygen delivery (Low SpO2, blood flow, or Hb)

< 18 of oxygen ml/kg/min

• Hyperoxemia

SpO2 higher than the upper limit of target saturation,

or PaO2 > 90 mmHg (infant on oxygen)

• Hyperoxia:

High oxygen delivery and PaO2 at the tissues (infant on oxygen)

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PHYSIOLOGY OF:VENTILATION PERFUSION MISMATCH AND R-L SHUNT

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Decreasing VentilationDecreasing Perfusion

VA/Q=1/0

VA/Q=0/1

VA/Q=0.8

Pulmonary hypertension (PH)Massive pulmonary embolism ShockBPD with PH Lung collapse

Pneumonia BPD with no PHLung congestion

Ventilation –Perfusion Mismatch and Right to Left shunt

0.6 0.4 0.21.8 1.4 1.2

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SevereV-Q mismatchR-L shunt is 50% (assumed example)

INOO2

R

L

75%

100%

75%

87%

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0.21 0.3 0.4 0.5 0.6 0.7 0.8 0.9

Oxy

hae

mo

glo

bin

satu

rati

on

%7

5

80

8

5

9

0

9

5

10

0

FIO2

1020

30

40

Oxygen reduction test

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0.21 0.35 0.45 0.55 0.65

Oxy

hae

mo

glo

bin

satu

rati

on

%7

5

80

8

5

9

0

9

5

97

FIO2

0.8

0.4

0.2

0.15

Oxygen reduction test

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PHYSIOLOGY OF PULMONARY HYPERTENSIONAND FACTORS AFFECTING PVR

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High Pulmonary hypertension

BP α F (CO) X PVRPPHN

Pulmonary Congestion

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Circulatory Changes During Transition

16Rudolph AM. Circulation. 1970;61:343-359.

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Types of Pulmonary Hypertension in Neonates

18

1 Hypoxic Vasoconstriction1

2 Abnormal Vasoconstriction (Idiopathic)1

eg. Premature Closure of the Ductus Arteriosus, Alveolar Capillary Dysplasia

3 Pulmonary Vascular Hypoplasia1-3

eg. Congenital Diaphragmatic Hernia, Oligohydramnios, Potter Sequence

4 Excessive Pulmonary Blood Flow1

eg. Congenital Heart Defects With Left-to-Right Shunting

5 Pulmonary Venous Hypertension1

eg. Congenital Heart Defects With Left Atrial Hypertension, Mitral Valve Disease, Aortic Valve Disease

1 Lakshminrusimha S. Clin Perinatol. 2012;39(3):655-683. 2 Bohn D. Am J Respir Crit Care Med. 2002;166:911-915. 3 Gubler MC. Pediatr Nephrol. 2014;29:51-59.

PVR

PVR

PVR

FLOW V-Q mismatch

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Pathological Effects of High PVR on the Newborn’s Heart

When pulmonary vascular resistance (PVR) does not decrease appropriately during the transition from a fetus to a newborn, a condition called persistent pulmonary hypertension of the newborn, or PPHN, results.1,2

191 Levin DL, et al. Pediatrics. 1975;56:58-64.2 Lakshminrusimha S. Clin Perinatol. 2012;39:655-683.

Intracardiac Shunting

Ventricular Dysfunction

a. RV dilation and decreased functionb. Decreased LV preload and

contractility c. Bowing of interventricular septum

into the LV

1

High PVR during PPHN can cause:1,2

2

Reduced Oxygen Delivery to Tissues.

High PVR

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Elevated PVR Promotes Shunting Through the Intracardiac Fetal Channels

High PVR promotes shunting of deoxygenated blood through the fetal channels, DA and FO, reducing the oxygen saturation of the blood feeding the body.1,2

201 Levin DL, et al. Pediatrics. 1975;56;58-64.2 Lakshminrusimha S. Clin Perinatol. 2012;39:655-683.

Shunting Through the FO

Shunting Through the DA

Deoxygenated Blood to Body

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Elevated PVR Affects Heart FunctionHigh PVR affects heart function in several ways:1,2

211 Levin DL, et al. Pediatrics. 1975;56;58-64.2 Lakshminrusimha S. Clin Perinatol. 2012;39:655-683.

Decreased Contractility

Increase Pooling of Blood in the RV and the RA:

Decreased RA Emptying

RV Dilation and Decreased Contractility

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Elevated PVR Causes Distention of the Right Ventricle That Affects Left Ventricular Output

22Bronicki RA, et al. Pediatr Crit Care Med. 2016;17:S182-S193.Animation adapted from Constantino J, et al. Am J Physiol Heart Circ Physiol. 2013;305:H1265-H1273.

High PVR causes a bowing of the interventricular septum into the LV which can:

• Decrease the ability of the LV to contract appropriately (reduces oxygen delivery)

• Decrease the LV volume and the LV stroke volume (reduce oxygen delivery)

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Distention of the Right Ventricle Obstructs Blood Flow From the Left Ventricle

231 Levin DL, et al. Pediatrics. 1975;56;58-64.2 Lakshminrusimha S. Clin Perinatol. 2012;39:655-683.

Bowing of interventricular septum into the left ventricle becomes an impediment to the LV outflow tract (reduces oxygen delivery).

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Effect of lung volume on resistance

FRC

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In the CINRGI Study, Clinical Evidence of

PPHN Was Defined as One of the Following1:

a The attending physician must attribute the desaturation events to PPHN and not to changes in lung disease or

ventilator strategy.

SaO2=arterial oxygen saturation.

1. Clark RH, et al. N Engl J Med. 2000;342:469-474. 2. INOMAX [package insert]. Hampton, NJ: Ikaria, Inc; 2013.]

• Differential oxygenation in

preductal and postductal areas

(ie, 5% difference in preductal

and postductal saturations by

pulse oximetry or arterial blood

gases)

A

Differential Oxygenation

Preductal

Postductal • Marked clinical lability in

oxygenation despite optimized

treatment of the neonate’s lung

disease

• Marked clinical lability is defined as

more than 2 desaturation (SaO2

<85%) events occurring within a

12-hour perioda

B

>2 Desaturation Events

in 12 hours

2

1

3

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Integration

Diffusion limitation

V/Q mismatch

Pulmonary BF

Effect on MV on PBF

Evidence of Hypoxia

Step 1

Step 2

Step 3

Evaluate for the mechanism of

hypoxemia

Formulated medical recommendation

Effect on systemic circulation

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Case scenario

• Baby girl born at 26 weeks, PMA is 35 weeks

• With VAP, FIO2 :0.9-1 to maintain saturation between 90-95 % for last 10 days before assessment of oxygen physiology

• HFJV with MAP of 14

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Pulmonary hypertension was wrong clinical assumption

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Gradual oxygen reduction with pulse oximetry and NIRS

Time (minutes) FIO2 SpO2 % Cerebral oxygen Saturation (NIRS)Normal 60-80%)

Fractional oxygen extractionNormal (0.15-0.33)

0 0.85 93 88 0.05

5 0.83 93 88 0.05

10 0.8 92 84 0.08

15 0.78 92 81 0.12

20 0.75 91 80 0.12

25 0.7 89 77 0.13

30 0.6 88 77 0.13

35 0.55 78 66 0.15

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Software assessment of V-Q mismatch and R-L shunt