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Flashcards in Pulmonary Hypertension Deck (32)
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1

What is hypoxia?

a relative deficiency of oxygen in arterial blood

2

What is the clinical significance of OI?

to determine the severity of hypoxemia

3

What is the OI calculation?

OI= (FiO2 x MAP)/ PaO2

4

What are the mechanisms by which decreased delivery of oxygen to the tissues can occur?

1) decreased amount of O2 in the blood
2) anemia
3) decreased perfusion

5

What is the expected OI of an infant with HMD?

8-10

6

What sustained OI is an indication for ECMO?

>40

7

What is one of the most common reasons to require ECMO?

pphn

8

What are the causes of pulmonary hypertension as categorized by primary disease process?

1) lung dysfunction (MAS, RDS, PNA, CDH, pulmonary hypoplasia)
2) pulmonary vascular (idiopathic- pulmonary arteries can constrict all by themselves w/o comorbid lug dz- rare)
3) cardiac dysfunction

9

How can cardiac dysfunction cause pulmonary hypertension?

poor contractility (or development) of LV, causes blood to back up creating LA hypertension and back up into the pulmonary vasculature

10

What is the definition of PPHN?

a clinical, pathologic syndrome a/w various lung dz or idiopathic; previously referred to as persistent fetal circulation

11

What is the incidence of pulmonary hypertension?

2 per 1,000 live births

12

What is the associated mortality with pulmonary hypertension?

11%-48%; mortality is bad if you don't have access to iNO or ECMO

13

What is the clinical presentation of pulmonary hypertension?

1) marked pulmonary hypertension and vasoliability
2) labile hypoxemia (caused by extrapulmonary R>L shunting at PFO or PDA)- independent of FiO2
3) tachypnea
4) respiratory distress- rtx. nasal flaring
5) progressive cyanosis
* clinically at the bedside what you will see is marked sat lability with an inability to oxygenate

14

Why did PPHN used to be called persistent fetal circulation?

in utero, pulmonary HTN is an expected developmental mechanism; pHTN after birth is apathological process as a failure to transition to extrauterine life; clinical symptoms reflect underlying pulmonary dz

15

Regardless of etiology, what are the common threads underlying PPHN?

1) elevated pulmonary resistance
2) pulmonary vasoconstriction
3) altered pulmonary reactivity

16

What is the end result of altered vascular reactivity?

*results in high pulmonary pressure, which may lead to:
- R>L shunting across FO
- R>L shunting across DA
- tricuspid regurg

17

What is the key finding with PPHN?

increased pulmonary vascular resistance; blood is not having trouble at the alveolar level, but difficulty accessing the alveoli

18

What is the effect of PPHN on the right side of the heart?

b/c blood can't get out of the heart to the lungs, there will be a back up of blood and will follow the path of least resistance. increased RV pressure and subsequently RA, perpetuating R>L intracardiac shunt (PFO) into LA.

19

What is the clinical presentation in the cardiac exam of PPHN?

because the RV is working so hard, you frequently have a murmur as blood regurgs across the tricuspid valve. persistent condition may lead to RV dilation.

20

How is CO affected by intrauterine stress?

only 7% of combined CO goes to the lungs and when stressed, can be reduced to 1%

21

How does the mechanism of intrauterine stress manifest?

the more stressed a fetus is, the better they are at "clamping down" and preventing blood from flowing into the pulm vasculature- this is a protective, evolutionary mechanism
*PPHN babes usually have a h/o stress prior to birth

22

What type of intrauterine stressors contribute to PPHN post delivery?

1) the sicker the MOB
2) the worse intrauterine environment
3) the lower available O2
4) high altitude
5) meconium stress
6) post dates
all contribute to the infant's ability to R>L shunt; the longer the baby has been stressed, the more hypertrophied the vessels

23

What is an extrapulmonary shunt?

R>L shunting across fetal channels: FO or DA

if an infant has a h/o stress and has concomitant lung dz, infant will try and persist in fetal circulation

24

Why is prophylactic PDA closure not helpful in the PPHN course?

ligation of the ductus doesn't change pressure in the lungs and therefore doesn't force blood into the right side. the end result was right side dilation and right sided heart failure, which can lead to death

25

What should be the aim of PPHN interventions?

opening the pulm veins and arteries to limit R>L shunting. the problem is not the ductus, the problem is the elevated pressures in the pulmonary beds.

26

How is PPHN diagnosed?

- hyperoxia test
- ECHO
- Differential PaO2 or SaO2
- cardiac cath
- hyperventilation

27

What is an infant with PPHN's response to the hyperoxia test?

not responsive; they have a large V/Q mismatch- make sure the lungs are inflated and its not the lungs fault that the baby is not responding to O2; differential is PPHN v CHD

28

What are the interventions that can improve intrapulmonary shunting?

surf, good CXR, good expansion, gentle mechanical ventilation, increased PEEP

29

What ECHO findings are c/w PPHN?

1) elevated PA pressure reliably estimated, compared with simultaneous systemic pressure
2) R>L or bidirectional PDA shunting
3) R>L or bidirectional PFO shunting

30

What is intrauterine PA pressure?

65-50mmHg