Module 2-Caitlyn Flashcards

1
Q

The fetus exists in a state of hypoxemia.

A

The fetus exists in a state of hypoxemia because the fetal pO2 is lower (17-19mmhg). This means when the blood oxygen levels are low, tissue oxygen levels are sufficient to meet the fetus’ low oxygen needs.

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2
Q

Right to left shunting, through the foramen ovale and ductus arteriosus, is a feature of fetal circulation.

A

Right to left shunting is normal and, in fact, desired characteristic of fetal circulation. Right to let shunting means that blood is normally headed for the lungs via the pulmonary artery is shunted through the ductus arteriosus to the aorta, thereby bypassing the lungs. Further, blood in the right atrium headed for the right ventricle is shunted through the foramen ovale to the left atrium, bypassing the lungs. Right to left shunting occurs due to patent shunts (foramen ovale + ductus arteriosus) and pressure gradients. Fetal pressure gradients are..pressure in the right heart is higher than the left; blood flows from path of least resistance –> flowing from high pressure areas to low pressure area.

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3
Q

Fetal lungs are high pressure, low volume organs.

A

The high pressure in the fetal lungs is due to pulmonary vasoconstriction, low blood oxygen and to the collapsed and fluid-filled nature of fetal lungs.

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4
Q

Fetal circulation functions to provide vital organs with sufficient oxygen.

A

Vital organs–> brain + heart
receive blood that is preductal.

Preductal blood:
is well oxygenated blood because it is blood through the foramen ovale rather than the ductus arteriosus.

Preductul blood is better oxygenated and the brain and the heart, due to the anatomic location, receive blood that arises from the coronary arteries and the carotid arteries. The coronary and carotid arteries are both preductal arteries. This is due the arteries being located on the aorta prior to the location of the ductus arteriosus.

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5
Q

What two perinatal events initiate transition?

A

The first breath:
The first breath causes the lungs to fill with air and expand, this helps to reduce pulmonary vascular resistance, allowing more blood to flow to the lungs.

Therefore more blood, in combination with the first few breaths means the lungs begin to function as organs of gas exchange.

Cutting the umbilical cord:

This eliminates the placenta as a reservoir for blood, causing a rise in bp and systemic vascular resistance.

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6
Q

What effect does rising pO2 have on transition?

A

Closure of the DA:

When the pO2 rises, it closes the Ductus Arteriosus which then also increases pulmonary perfusion.

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7
Q

What causes the DA to close?

A
  • rising P02

- decreasing levels of prostaglandin, this occurs during labour and delivery.

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8
Q

What must happen for the infant to make a successful transition from fetal to newborn circulation?

A
  • infant must breathe –> spontaneous or mechanically
  • lungs must inflate
  • cord must be cut
  • blood oxygen levels must rise
  • pulmonary vascular resistance must fall
  • fetal shunts (ductus arteriosus and foramen ovale must close)
  • pressure gradient must change
  • infant must be warm (cold stress uses lots of oxygen)
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9
Q

What can impede transition?

A
  • apnea at birth ( if not remedied will lead to asphyxia and PPHN)
  • lung diseases such as diaphragmatic hernia and pulmonary hypoplasia can prevent gas exchange from adequately occurring in the lungs immediately after birth.
  • Central nervous system depression can interfere with breathing at birth and this can be due to drugs, intrauterine hypoxia and congenital defects.
  • Mec. aspiration can block airways and can interfere with gas exchange at birth.
  • Hypothermia can lead to high oxygen utilization and, while hypothermia does not cause asphyxia, it does worsen it.
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10
Q

What does meconium consist of?

A
  • viscous dark green
  • water
  • intestinal epithelial cells
  • lanugo
  • mucous
  • intestinal secretions
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11
Q

How does meconium passage happen in utero?

A

in utero passage results from neural stimulation of the mature GI tract and usually results from fetal hypoxic stress.

as fetus approaches term , GI tract matures, and vagal stimulation from head or cord compression may cause peristalsis and relaxation of rectal sphincter leading to meconium passage.

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12
Q

Meconium stained amniotic fluid can be aspirated…

A

before or during labour and delivery.

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13
Q

Meconium aspiration chiefly affects which type of neonate?

A

term or post term infants.

meconium is rarely found in amniotic fluid prior to 34 weeks.

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14
Q

What are the effects of meconium in utero?

A
  • meconium directly alter the amniotic fluid, reducing antibacterial activity therefore increasing the risk of perinatal bacterial infection
  • meconium is irritating to fetal skin
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15
Q

Meconium aspiration effects pulmonary function in three ways:

A
  • airway obstruction
  • surfactant dysfunction
  • chemical pneumonitis
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16
Q

Meconium aspiration: airway obstruction effects

A
  • complete obstruction of the airways by meconium results in atelectasis
  • partial obstruction causes air trapping and hyperdistention of the alveoli, communly termed the ball valve effect.
  • hyperdistention of the alveoli occurs from airway expansion during inhalation and airway collapse around meconium in the airway, causing increased resistance during exhalation.
  • the gas that is trapped (hyperinflating the lung) may rupture into the pleura (pneumothorax), mediastinum (pneumomediastinum), or pericardium (pneumopericardium).
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17
Q

Meconium aspiration: Surfactant dysfunction effects

A

meconium deactivates the surfactant and results in diffuse atelectasis.

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18
Q

Meconium aspiration: Chemical pneumonitis effects

A

enzymes, bile salts and fats in meconium irritate the airways and parenchyma, causing a release of cytokines and resulting in a diffuse pneumonitis.

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19
Q

What is does PPHN stand for?

A

Persistent Pulmonary Hyptertension of the newborn.

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20
Q

What is PPHN?

A

It is a serious life threatening complication of perinatal asphyxia.

However not all babes with perinatal asphyxia will develop PPHN, they are at a higher risk.

It is defined as the failure of normal circulatory transition that occurs after birth. It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia and right-to-left shunting of blood through the ductus arteriosus and foramen ovale.

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21
Q

What are the causes of PPHN?

A
  • Acute pulmonary vasoconstriction
  • hypoplasia of the pulmonary vascular bed
  • Idiopathic pulmonary hypertension
22
Q

What can cause Acute pulmonary vasoconstriction?

A
  • most common cause of PPHN
  • Alveolar Hypoxia secondary to parenchymal lung disease
  • meconium aspiration syndrome
  • respiratory distress syndrome
  • pneumonia
  • Hypoventilation resulting from asphyxia or other neurologic conditions
  • Hypothermia
23
Q

What can cause Hypoplasia of the pulmonary vascular bed?

A
  • Congenital diaphragmatic hernia
  • Oligiohydraminios in utero may produce pulmonary hypoplasia and associated persistent pulmonary hypertension of the newborn
24
Q

What can cause Idiopathic pulmonary hypertension?

A
  • Constriction of the Fetal DA in utero, which can occur after exposure to NSAIDs such as Ibprofen and naproxen during the third trimester.
  • SSRI’s during late gestation is associated with PPHN
  • Parenchymal and vascular disease. An abnormally remodeled vasculature may develop in utero in response to prolonged fetal stress, hypoxia and pulmonary hypertension.
25
Q

Why does PPHN rarely occur in premature babes?

A

-Due to their relative lack of musculature in pulmonary arterioles and capillaries. This lack of musculature means that premature infants do not respond to perinatal asphyxia with the same degree of pulmonary vasoconstriction.

26
Q

PPHN is characterized by?

A
  • Increased pulmonary vascular resistance
  • Patent DA and FO
  • Vasocontriction of pulmonary vessels
  • Hypoxia
27
Q

In relation to PPHN explain (Increased pulmonary vascular resistance)

A

The normally high pulmonary vascular resistance, which was needed for fetal circulation, persists in the newborn period.

28
Q

In relation to PPHN explain (Patent DA and FO)

A

Increased pulmonary vascular resistance leads to right-to-left shunting of blood through the DA and possibly the FA. The FA will remain open as long as high right/low left pressure gradients exist.

29
Q

In relation to PPHN explain (Vasocontriction of pulmonary vessels)

A

Vasoconstriction leads to minimal amounts of pulmonary blood flow and this, in turn, leads to more hypoxia, acidosis and eventually lactic acidosis.

30
Q

In relation to PPHN explain (Hypoxia)

A

As the hypoxia continues, so does the pulmonary vasoconstriction. This state is considered the “vicious cycle” of PPHN

31
Q

To summarize PPHN

A

Hypoxia –>pulmonary vasoconstriction –>high pulmonary vascular resistance –> right to left shunting –>pulmonary hypoperfusion –> hypoxia

Hypoxia –> PDA–>shunting –> right to left shunting –> pulmonary hypoperfusion –> hypoxia

32
Q

How are the management of MAS and PPHN related?

A

Management of both MAS and PPHN overlap due to the interrelatedness of their etiology, sequelae, and clinical responses.

When MAS has accompanying PPHN, management is aimed at minimizing hypoxia and pulmonary vasoconstriction, both of which contribute to further hypoxemia, acidosis and increased pulmonary vascular resistance.

33
Q

What impact does cold stress have on the viscous cycle of MAS and PPHN?

A

Cold stress further compromises an infant with MAS and PPHN by worsening the hypoxia and acidosis that already exist.

Increases metabolic activity results in increased oxygen consumption of oxygen leads to anaerobic metabolism and eventually acidosis.

As a result, infants with cold stress have the viscious of MAS and PPHN further perpetuated adding to the hypoxia, acidosis and pulmonary vasoconstriction already in existence.

34
Q

What are the three umbilical vessels?

A

2 arteries and one vein

arteries are thick and round
vein is thin and oval

35
Q

How many lumens can be inserted into a umbilical venous catheter (UVC)?

A

single lumen
double lumens
triple lumens

36
Q

What is a uvc used for?

A
  • emergency drug administration
  • Iv fluid administration
  • central venous pressure monitoring
  • venous blood sampling
37
Q

What is the positioning for a UVC?

A

Low lying position - 2-4 cm (used for drug administration during resus)

Central position - catheter tip in the interior vena cava at the junction of the right atrium.

38
Q

How many lumens can be inserted into an Umbilical arterial catheter (UAC)?

A

single lumen

39
Q

What is UAC used for?

A
  • blood pressure monitoring
  • arterial blood sampling

** Umbilical arterial catheters can be used for administration of drugs, fluids, parenteral nutrition and blood products however as a general rule they are ONLY used for blood pressure monitoring and blood sampling unless with a doctors order***

40
Q

What is the positioning for a UAC?

A

low lying - between L3 and L4, catheter tip above the aortic bifurcation

high lying (preferred) - between T 6 to T 9, catheter tip above the diaphragm.

41
Q

A double lumen umbilical catheter can be used in an umbilical artery?

A

false

42
Q

A complication of UVC insertion is possible placement in the liver?

A

True

43
Q

Sepsis is a complication of both a UVC and UAC?

A

True

44
Q

An infant who has a UAC inserted should be assessed for blanching of the buttocks and legs?

A

True, a UAC can cause vasospasm of the artery, which can result in blanching or cyanosis or the lower body.

45
Q

Necrotizing enterocolitis is a potential complication of a UVC?

A

False – it is a potential complication of a UAC and is related to retrograde (reversing) blood flow

46
Q

Treatment for PPHN consists of…

A
  • optimizing lung expansion
  • Inhaled Nitric Oxide Therapy
  • Sedatives and Muscle relaxants
  • Cardiostimulatory therapy
47
Q

According to the Case Study How do we Optimize Lung Expansion?

A
  • Improving ventilation/perfusion matching
  • Recruitment of atelectatic alveoli while avoiding overdistention
  • Surfactant therapy to facilitate alveolar expansion
48
Q

What is High Frequency Ventilation?

A

High frequency Ventilation attempts to minimize ventilator-induced injury by using volumes that are smaller than the lung’s physiologic dead space (1-2 ml/kg), at very fast breathing rates. It is defined as “mechanical ventilation using tidal volumes less than or equal to the dead space volume and delivered at supraphysiologic rates. HFV devices are those that provide breathing rates greater than 150 breaths per minute”.

49
Q

High Frequency Oscillatory Ventilation (HFOV)

A
  • Rate is set in hertz (1 hertz = 60 cycles or breaths) - average hertz set at 10-15
  • E.g. Sensormedics 3100A
50
Q

High Frequency Jet Ventilation (HFJV)

A
  • Rate 100-600

- E.g. Bunnell Life Pulse Jet Ventilator