CARDIOPULMONARY CHANGES AT BIRTH AND PRINCIPLES OF NEWBORN RESUSCITATION Flashcards
T/F: Before birth the lungs take no part in gas exchange
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Before birth the future airways of the lungs are liquid-filled and the lungs take no part in gas exchange, which instead occurs across the placenta
Pulmonary blood flow (PBF) is low because pulmonary vascular resistance (PVR) is high, redirecting the majority of right ventricular output (RVO) through the — and into the systemic circulation
ductus arteriosus (DA)
Conversion of the fetal to adult circulation requires —, — and —
Elimination the umbilical – placental circulation
Increase of pulmonary blood flow to a level necessary for adequate gas exchange
Separation of the left sides of the heart by the closure of fetal channels
T ventilation comprises two components —- and —
Physical expansion of the lungs with gas
Elimination of fluid in the alveoli and increase in alveolar concentration associated with breathing air
T/F: Removal of placental circulation facilitates closure of the foramen ovale and causes a small decrease in right atrial pressure
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T/F: Removal of placental circulation enables functional closure of ductus arteriosus resulting in elimination of flow from the pulmonary trunk to the aorta
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T/F: In fetal life small pulmonary arteries have a thick MEDIAL layer composed predominantly of smooth muscle cells
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T/F: In fetal life the pulmonary vessels constrict markedly with hypoxia and dilate with an increase in PO2
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T/F: Following the immediate fall in pulmonary vascular resistance following birth, morphologic changes in the pulmonary vessels result in a PERMANENT fall in pulmonary vascular resistance
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T/F: The decrease in the thickness of the smooth muscle layer in the small arteries results in a gradual further decrease in pulmonary vascular resistance and pulmonary arterial pressure within 2-3 weeks after birth
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T/F: Within 2 -3wks after birth there a gradual further decrease in pulmonary vascular resistance and pulmonary arterial pressure
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4 conditions that can result from persistence of any fetal shunts/physiology
- Persistent Ductus Arteriosus
- Patent Foramen Ovale
- Persistent Pulmonary
hypertension of the Newborn - Transient Tachypnea of the newborn
After birth functional closure of the ductus arteriosus occurs when
10 -15 hrs after birth by constriction of the medial smooth muscle
T/F: Both functional and anatomic closure of the DA occur at the same time
F
Anatomic closure is completed by 2-3 weeks of age by permanent changes in the endothelium and the sub-intimal layers of the ductus
Anatomic closure of the DA is completed at — wks after birth
2 -3 wks
What causes the anatomic closure of the DA
permanent changes in the endothelium and the sub-intimal layers of the ductus
Permanent changes in the – and – causes the anatomic closure of the DA
Endothelium and sub-intimal layers of the ductus
% of PDA seen in all CHD
5 - 10%
T/F: PDA can be asymptomatic
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Usually asymptomatic when DA is small
Persistent patency of the DA leaves a communication between the DA and —
Left pulmonary artery
T/F: Large shunt PDA may cause CHF and recurrent pneumonia
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— disease may develop if large PDA with pulmonary hypertension is left untreated
Pulmonary vascular obstructive disease
% of newborns with failure of functional closure of the foramen ovale
75%
T/F: Patent foramen ovale causes a left-to-right shunt
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T/F: ASD is commoner in males
F.
Has a female preponderance
The 3 types of ASD
Primum defect
Secundum defect
Sinus venosus defect
The most common of the ASDs
Secundum defect
Location of the primum defect
Antero-inferior atrial septum
Location of the secundum defect
Middle portion of atrial septum
Location of the sinus venosus defect
Postero-superior atrial septum
Defect in the middle portion of atrial septum
Secundum defect
Defect in the antero-inferior atrial septum
Primum defect
Defect in the postero-superior atrial septum
Sinus venosus defect
% of children with PFO/ASD that will experience spontaneous closure in the first 4 years of life
40%
T/F: If a large PFO/ASD defect is untreated, CHF and pulmonary HTN may develop in the 1st decade of life
F
2nd or 3rd decade of life
If a large PFO/ASD defect is untreated, — and —may develop in the 2nd or 3rd decade of life
CHF and pulmonary HTN
Incidence of persistent pulmonary hypertension of the newborn
I in 1500 live births
What type of shunt is seen in persistent pulmonary hypertension of the newborn
right to left shunt through PFO or PDA causing varying degrees of cyanosis
3 causes of persistent pulmonary hypertension of the newborn
Pulmonary vasoconstriction in presence of normally developed pulmonary vascular bed
Hypertrophy of pulmonary vascular smooth muscle
Developmentally abnormal pulmonary arterioles with decreased cross sectional area of pulmonary vascular bed
T/F: Symptoms of persistent pulmonary hypertension of the newborn manifest one week after birth
F.
Symptoms begin 6-12 hours after birth
5 signs and symptoms of persistent pulmonary hypertension of the newborn
- Cyanosis
- Retractions
- Grunting
- A gradient of 10% or more in sat between preductal/postductal ABG
- Cardiomegaly on CXR
T/F: A gradient of 10% or more in sat between preductal/postductal ABG is seen in persistent pulmonary hypertension of the newborn
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Transient tachypnea of the newborn is caused by —
Retention of fetal lung fluid
When do symptoms of tachypnea of the newborn appear in the newborn
2 hours after birth
T/F: Transient tachypnea of the newborn is self-limiting
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T/F: Transient tachypnea of the newborn is a diagnosis of exclusion
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Treatment of transient tachypnea of the newborn involves – and –
Oxygen therapy and non-invasive respiratory support
T/F: Prenatal administration of steroids 48hrs before elective C- section @ 37- 39 weeks gestation reduces TTN but this has not become a common practice
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4 principles of neonatal resuscitation
- Anticipation
- Adequate Preparation
- Accurate evaluation – Algorithm- Based
- Post-resuscitative Care
% of babies that will require some assistance at birth for normal transition
10%
5 initial steps in resuscitation
Provide warmth
Head position “ sniffing position”
Clearing the airway, if necessary
Drying the baby
Tactile stimulation for breathing
T/F: Stimulation of the posterior pharynx during the first minutes after birth can produce a vagal response leading to bradycardia or apnea
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T/F: Wet skin increases evaporative heat loss.
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T/F: All babies must be dried regardless of GA at birth
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Drying is not necessary for very preterm babies less than 32 weeks’ gestation because they should be covered immediately in polyethylene plastic.
Contraindication to drying a baby immediately after birth
Very preterm babies less than 32 weeks’ gestation because they should be covered immediately in polyethylene plastic.
T/F: Very preterm babies less than 32 weeks gestation should be covered in polyethylene plastic immediately after birth
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T/F: Babies require vigorous stimulation during resuscitation
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Gently rub the newborn’s back, trunk, or extremities.
Overly vigorous stimulation is not helpful and can cause injury
T/F: If a newborn remains apneic despite rubbing the back or extremities for several seconds, begin PPV
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T/F: Initiate PPV when there is poor respiratory effort
F
Needed when there is no improvement in HR
Rate of PPV delivery
40-60 breaths /min to achiece and maintain HR>100 /min
Devices for PPV
BMV
ET (endotracheal tube), LMA(laryngeal mask airway)
Pulse oximetry
Technique for positioning of facemask in neonatal resuscitation
E-C clamp technique
Describe the E-C technique of mask positioning
The hand is positioned so that the little, ring and middle fingers are spread over the mandible from the angle of the jaw forward towards the chin in the configuration of the letter ‘E’. The jaw is then lifted, pulling the face into the mask. The thumb and forefinger are placed are placed over the mask in the shape of the letter “C”. The mask is squeezed onto the face and a seal is formed between the mask and the face.
Targeted SPO2 1 minute after birth
60 - 65%
Targeted SPO2 10 minutes after birth
85 - 90%
Targeted SPO2 5 minutes after birth
80 - 85%
Targeted SPO2 in the 2nd, 3rd and 4th minutes of life
65 - 70%
70 - 75%
75 - 80%
T/F: If heart rate is less than 100beats per minute, but greater than 60 beats per minute consider alternate airway
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Size of laryngoscope for preterm infants
No. 0
Size of laryngoscope for term infants
No. 1
Endotracheal tube size 3.5 to 4 is used for which babies
> 38wks
3000g
Size 3.5 endotracheal tube is used for which babies
34 to 38wks
2000 to 3000g
Size 3 endotracheal tube is used for which babies
28 to 34 wks
1000 to 2000g
Size 2.5 endotracheal tube is used for which babies
< 28 wks
< 1000g
What are the various sizes of endotracheal tubes
2.5,
3
3.5
4
When do you start chest compressions in neonatal resuscitation
Started when HR<60 per minute despite adequate ventilation with 100% oxygen for 30 sec
Site and depth of neonatal chest compressions
lower third of sternum
depth 1/3 of AP diameter of chest
2 techniques for chest compression
2 thumb-encircling hands technique
Compression with 2 fingers and second hand supporting the back
compression/ventilation ratio
3:1
90 comp : 30 ventilations
T/F: In neonatal chest compressions, the area of the xiphoid process should be avoided
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To prevent injury to the liver, spleen and stomach
T/F: With the 2 finger method, the fingers should be perpendicular to the chest and straight
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The most sensitive indicator of a successful resuscitation is —
Increase in heart rate
T/F: Most important step to treat bradycardia is establishing adequate ventilation
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Route, dose and concentration of epinephrine used in neonatal resuscitation
IV
0.01 - 0.03mg/kg/dose
1:10,000 (0.1 mg/ml)
Fluid dose for volume expansion
10ml/kg
T/F: Post resuscitation care is required for those who needed PPV
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Oxygen flow rate in neonatal resuscitation
up to 10L/min
T/F: Laryngeal mask and stylet are optional intubation equipments
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Sizes for oropharyngeal airways
0, 00, 000 and
30, 40 and 50mm lengths
T/F: For very preterm babies, use compressed air source in neonatal resuscitation
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Use O2 blender to mix oxygen and compressed air
