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Neonatal Pathophysiology > Fetal Circulation > Flashcards

Fetal Circulation Flashcards

1
Q

What are unique structures to fetal circulation?

A

1) placenta
2) umbilical arteries and veins
3) fetal shunts: ductus venosus, foramen ovale and ductus arteriosus

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2
Q

What are the functions of the placenta?

A

1) respiratory function- instead of lungs
2) metabolic function- instead of intestines
3) provides O2, nutrients and H20 to fetus
4) transfers CO2 and other wastes to MOB for elimination

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3
Q

How many umbilical arteries are there?

A

2

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4
Q

What is the function of the umbilical arteries?

A

to carry Deoxygenated blood in utero

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5
Q

What is the reaction of arteries in a hypoxic environment?

A

vasoconstrict

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6
Q

How do umbilical arteries present in the cord?

A

muscular, smaller vessels

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7
Q

What is the range of PaO2 available in the umbilical arteries?

A

15-25%

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8
Q

What central line should be placed in an emergent situation if no vascular access is previously in place?

A

UVC, never arterial

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9
Q

What type of medications should never be run through an arterial line?

A

RX with vasocontricting effects: Epi, caffeine, insulin, dopamine, norepi

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10
Q

How many umbilical veins are there?

A

1

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11
Q

What is the function of the umbilical vein?

A

to carry oxygenated blood in utero

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12
Q

What is the range of PaO2 available in the umbilical vein?

A

32-35%

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13
Q

How does the umbilical vein present in the cord?

A

larger, thinner walled vessel

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14
Q

What is the ductus venous?

A

structure that allows blood to bypass the liver and empty into the IVC

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15
Q

When is closure of the ductus venous expected?

A

within the first week of life

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16
Q

What becomes of the ductus venous after anatomical closure?

A

eventually becomes the hypogastric ligament

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17
Q

What is the foramen ovale?

A

structure preferentially allows blood to flow from the RA into the LA

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18
Q

Where is the foramen ovale located?

A

in the central portion of the atrial septum

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19
Q

What mechanism facilitates the closure of the foramen ovale?

A

increasing LA pressure

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20
Q

When is anatomic closure of the FO achieved?

A

approximately 1 month

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21
Q

Where is the PDA?

A

connects the pulmonary artery and the aorta; can be a site of shunting especially in the preterm infant

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22
Q

What mechanism facilitates the closure of the PDA?

A

in response to readily available pO2

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23
Q

When is functional and anatomic closure of the PDA achieved?

A

functional: 2-4 dol; anatomic: during the next month

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24
Q

What becomes of the PDA after anatomical closure?

A

persists as the ductus ligament

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25
Q

What percentage of total cardiac output goes to the lungs in utero for tissue nourishment?

A

8-12%

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26
Q

What is the effect of acidosis on the vasculature?

A

vasoconstriction

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27
Q

Where is the site of greatest vascular resistance in fetal circulation?

A

PVR>SVR

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28
Q

Where is the site of O2/CO2 exchange in fetal circulation?

A

intervillous spaces; placenta is nourished from maternal venous system

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29
Q

Where is the site of greatest vascular resistance in postanatal circulation?

A

SVR>PVR

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30
Q

Where is the site of O2/CO2 exchange in postnatal circulation?

A

alveolus/capillary

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31
Q

In fetal circulation, where is the point of highest pO2 concentration?

A

from the point of entering the placenta and ascending the umbilical vein

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32
Q

What is the route of hepatic blood circulation?

A

the UV branches into the portal vein that perfuses the liver and into the DV which bypasses the liver and empties into the IVC

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33
Q

The IVC empties into what structure?

A

the RA

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34
Q

As blood streams into the LA through the FO, it mixes with blood that has returned from where?

A

blood returning from the collapsed fetal lungs through the pulmonary vein

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35
Q

Blood that moves from the LA to the LV has to move through what valve?

A

mitral

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36
Q

What structures are perfused by blood that leaves the LV through the ascending sort to the aortic arch?

A

the brain, heart and upper torso

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37
Q

What is the first vessel that branches off from the aortic arch?

A

the right subclavian artery (why pre ductal probe is placed on right arm)

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38
Q

What arteries are located on the aortic arch?

A

1) brachiocephalic (branches into right subclavian and right common carotid) 2) left common carotid 3) left subclavian

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39
Q

What happens to the blood that perfused the liver?

A

it mixes with the blood that perfused the brain, heart and upper torso in the SVC. This blood will go to the RA into the RV

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40
Q

Blood that moves from the RA to the RV has to move through what valve?

A

tricuspid

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41
Q

In the defending aorta, what percentage of blood will perfuse the lower extremities?

A

1/3

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42
Q

What happens to the remaining 2/3 of blood that has left the fetal heart?

A

will be sent to the placenta for reoxygenation

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43
Q

What is a R>L shunt?

A

(PFO) shunting results in deoxygenated blood in systemic perfusion, hypoxemia and cyanosis

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44
Q

What is a L>R shunt?

A

(PDA) shunting results in oxygenated blood returning to the lungs (leading to pulmonary edema, increasing PVR and PPHN)

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45
Q

Which organs receive the most oxygen?

A

the brain and heart (pO2 25-28%)

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46
Q

What is the first challenge that a newborn faces?

A

cardiorespiratory transition; life without placental support

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47
Q

What occurs with cardiopulmonary adaptation?

A

1) onset of ventilation with a decrease in PVR and an increase in pulmonary blood flow, 2) rise in blood O2 and saturation further decreases PVR, 3) loss of placental circulation with resultant increase in SVR

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48
Q

Approximately how much of fetal lung lung fluid is reabsorbed during labor?

A

35%

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49
Q

How does labor affect the excretion of alveolar fluid?

A

decreases the excretion of alveolar fluid and increases excretion of surfactant

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50
Q

What occurs with the first breath of an infant?

A

establishes alveolar surface tension, increases alveolar pO2, establishes negative pressure and decrease the PVR- all contributing to improving pulmonary blood flow

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51
Q

How does endothelium derived relaxing factor affect on the cardiopulmonary system?

A

exactly like nitric oxide

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52
Q

What is an indication of an unsuccessful transition to extrauterine life?

A

if PVR remains elevated

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53
Q

What is the incidence of CHD in live born infants?

A

~ 1%

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54
Q

What percentage of all CHD cases are diagnosed within the first week of life?

A

50%

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55
Q

In infants with complex CHD, what is the rate of hospital mortality?

A

as high as 7%

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56
Q

Infants with CHD have a high frequency of what related risk factors?

A

multiple congenital anomalies, syndromes, LBW and prolonged LOS

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57
Q

What are the most frequently occurring CHD anomalies seen within the first week of life?

A

PDA, transposition of the great arteries, HLHS, TOF and pulmonary atresia

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58
Q

How do you conduct a hyperoxia test?

A

1) determine PaO2 while the infant is on RA
2) give 100% O2 for 10-20 min by mask, hood or ETT
3) obtain PaO2 while infant is breathing 100%

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59
Q

What are the implications of the hyperoxia test?

A

because of intracardiac R>L shunting, the newborn with cyanotic CHD (in contrast to the infant with pulmonary dz) is unable to raise arterial saturation, even in the presence of increased ambient oxygen.

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60
Q

How are CHD classified?

A

s/s of newborns with CHD permit grouping according to levels of arterial oxygen saturation based on the hyperoxia test. Further classification based on physical findings & labs, facilitates delineation of the exact cardiac lesion

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61
Q

What is cyanotic CHD?

A

infants are usually unable to achieve a PaO2>100mmHG after the hyperoxia test

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62
Q

What is acyanotic CHD?

A

infants achieve a PaO2>100mmHG after the hyperoxia test

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63
Q

Why is cyanosis a potential confounding factor in the physical assessment of an infant with CHD?

A

because polycythemia, jaundice, racial pigmentation or anemia can make clinical recognition of cyanosis difficult

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64
Q

Why is a murmur or absence of a murmur a potential confounding factor in the physical assessment of an infant with CHD?

A

an infant with CHD often does not have a distinctive murmur. the most serious of anomalies may not be a/w a murmur at all

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65
Q

What is the most common cardiac cause of cyanosis in the first year of life?

A

D-transposition of the great arteries

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66
Q

What is the male to female ration of D-TGA?

A

2:1 male:female

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67
Q

What is the pathophysiology of D-TGA?

A

the aorta ascends from the RV and the pulmonary ascends from the LV, with resultant separate systemic and pulmonary circuits

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68
Q

With modern medical interventions, what is the 1 year survival rate of infants with D-TGA?

A

90%

69
Q

What is observed in the physical examination of an infant with D-TGA?

A

typical infant is large and vigorous with cyanosis but little to no respiratory distress. there may be no murmur or a soft, systolic ejection murmur

70
Q

What does the CXR of an infant with D-TGA look like?

A

CXR may be normal but typically reveals a very narrow upper mediastinal shadow (“egg on a stick”)

71
Q

What does the EKG of an infant with D-TGA look like?

A

there are no characteristic EKG findings

72
Q

What is revealed by an Echo done on an infant with D-TGA?

A

diagnostic; typical findings include branching of the anterior great vessel into the innominate, subclavian and carotid vessels and branching of the posterior great vessel into the right and left pulmonary arteries

73
Q

What treatment is indicated for an infant with D-TGA?

A

if severe hypoxia or acidosis occurs, urgent balloon atrial septostomy can be done under ECHO guidance. cardiac cath with balloon septostomy and subsequent atrial switch operation are methods of treatment. PGE MAY INCREASE SHUNTING

74
Q

What 4 anomalies characterize a TOF?

A

1) pulmonary stenosis
2) overriding aorta
3) VSD
4) right ventricular hypertrophy

75
Q

What is the male to female ration of TOF?

A

there is a slight male predominance

76
Q

What does cyanosis in an infant with TOF signify?

A

complete or partial atresia of the right ventricular overflow tract or extreme pulmonary stenosis with hypo plastic pulmonary arteries.

77
Q

How does the right ventricular outflow tract relate to pulmonary blood flow and the degree of cyanosis in infants with CHD?

A

the degree of right ventricular outflow obstruction is inversely proportional to pulmonary blood flow and directly proportional to the degree of cyanosis

78
Q

In an infant with TOF, how will an absent pulmonary valve present?

A

with respiratory distress or poor feeding (bc of compression of the esophagus or bronchi by the large pulmonary arteries

79
Q

What is observed in the physical examination of an infant with TOF?

A

the patient is cyanotic with a systolic ejection murmur along the left sternal border. loud murmurs are a/w more flow across the right ventricular outflow tract and milder degrees of desaturation. Softer murmurs are a/w less flow and more hypoxia.

80
Q

What does the CXR of an infant with TOF look like?

A

CXR film reveals a small, often “boot shaped” heart with decreased pulmonary vascular markings. A right aortic arch is seen in ~ 20% of these infants

81
Q

What does the EKG of an infant with TOF look like?

A

EKG may be normal or may demonstrate RVH. the only sign of RVH may be an upright T wave in V4R or V1, after 72 hours of age

82
Q

What is revealed by an Echo done on an infant with TOF?

A

usually diagnostic, with an overriding aorta, ventricular septal defect and small right ventricular outflow tract

83
Q

What treatment is indicated for an infant with TOF?

A

pulmonary blood flow may be ductal dependent with severe cyanosis and may respond to ductal dilation using PGE. This measures allows more flexibility for planning cardiac catheterization and surgical correction.

84
Q

In an infant with an acyanotic CHD, how will a murmur present?

A

the infant who is NOT cyanotic will have wither a heart murmur or symptoms of congestive heart failure

85
Q

What is the most common congenital heart abnormality with equal sex distribution?

A

VSD

86
Q

When do murmurs a/w VSDs appear?

A

can be present at birth but typically appear between 3 days and 3 weeks of age

87
Q

In infants with congestive heart failure secondary to a VSD, when do symptoms typically present?

A

congestive heart failure is unusual before 4 weeks of age but may develop earlier in premature infants

88
Q

What treatment is indicated for VSDs?

A

spontaneous closure occurs in 50%, surgical correction is reserved for large, symptomatic VSDs only

89
Q

What are the clinical implications of an ASD?

A

not an important cause of morbidity and mortality in infancy, occasional congestive heart failure can occur (rarely in neonatal period)

90
Q

What defects are included in there term endocardiacl cushion defects?

A

ostium primum type ASD with or without a cleft mitral valve and an atrioventricular canal

91
Q

What are the clinical implications of marked AV valve insufficiency?

A

the patient may have congestive heart failure at birth or in the neonatal period

92
Q

What is observed in the physical examination of an infant with an endocardial cushion defect?

A

a systolic murmur resulting from AV valve insufficiency may be heard, cyanosis may be present but not severe, infants with severe pulmonary artery hypertension may have little to no murmur

93
Q

What does the CXR of an infant with and endocardial cushion defect look like?

A

varibale findings may include a dilated pulmonary artery or a large heart secondary to atrial dilation

94
Q

What does the EKG of an infant with an endocardial cushion defect look like?

A

left axis deviation (left superior vector) is ALWAYS found, the PR interval may be long, or there may be an RSR pattern

95
Q

What is revealed by an Echo done on an infant with an endocardial cushion defect?

A

usually diagnostic, demonstrates a common AV valve with inlet VSD or a defect in the septum primum with an abnormal mitral valve

96
Q

What treatment is indicated for an endocardial cushion defect?

A

congestive heart failure is treated with diuretics and digoxin. early cardiac cath with corrective surgery may be need to prevent pulmonary vascular obstructive disease

97
Q

How do infants with HLHS present with cyanosis?

A

in 15% of infants, there is a persistent PFO and this prevents atrial mixing causing cyanosis

98
Q

How do infants with HLHS present with acyanosis?

A

infants with adequate atrial mixing will not have cyanosis

99
Q

HLHS accounts for what percentage of cardiac deaths within the first week of life?

A

25%

100
Q

What is observed in the physical examination of an infant with HLHS?

A

the infant is typically pale and tachypneic with poor peripheral perfusion and poor to absent peripheral pulses. A loud, single S2 is present, usually with a gallop and no murmur. There is hepatomegaly and metabolic acidosis by 48h of life

101
Q

What does the EKG of an infant with HLHS look like?

A

demonstrates small or absent left ventricular forces

102
Q

What does the CXR of an infant with HLHs look like?

A

moderate cardiomegaly, often with a large main pulmonary artery shadow

103
Q

What is revealed by an Echo done on an infant with HLHS?

A

a diagnostic study demonstrates a small or slit like left ventricle with a hypo plastic ascending aorta

104
Q

What are the undesired effects of supplemental oxygen administration to an infant with HLHS?

A

resultant dilation of the pulmonary vessels increases pulmonary blood flow. Respiratory compromise and subsequent RV dilation and reduced right ventricular function

105
Q

What are the treatment implications for an infant with HLHS?

A

1) Norwood 2) hemi Fontan or bi direction Glenn 3) Fontan

cardiac transplant and compassionate care

106
Q

What is intended outcome of the Norwood procedure?

A

palliation; redirecting blood flow so that the right ventricle serves as the “systemic ventricle” and a surgically constructed shunt provides pulmonary good flow

107
Q

What affects the successful outcome of an infant having undergone a Norwood procedure?

A

GA and the presence of other major anomalies

108
Q

What is intended outcome of the bi-direction Glenn procedure?

A

routes blood from the SVC to the lungs and closes the systemic to pulmonary artery shunt

109
Q

What is intended outcome of the Fontan procedure?

A

directs remaining systemic venous return directly to the pulmonary circulation

110
Q

If an infant is diagnosed with thoracic and abdominal situs, what is the likelihood that the infant also has a CHD?

A

> 90%

111
Q

What is the optimal GA to perform an ECHO?

A

18-24 weeks when structural abnormalities and arrhythmias can be detected

112
Q

What are some maternal indications for a fetal Echo?

A

diabetes, collagen vascular dz, maternal drug use/teratogen exposure, family h/o chromosomal/genetic dz, or previous children with CHD

113
Q

What are some fetal indications for a fetal Echo?

A

abnormal HR, suspected cardiac malformation on screening ultrasound, presence of other malformations on ultrasound, oligo or polyhydramnios, evidence of hydrops or IUGR

114
Q

What is a common cause of hydrops and intrauterine death?

A

arrhythmias; can result from congenital complete heart block

115
Q

What are the most common arrhythmias in utero and at delivery?

A

a rapid SVT with a 1:1 ventricular response, occasionally, atrial flutter with 2:1 heart block will present before or just after birth

116
Q

How can arrhythmias be treated in utero?

A

some anti-arrhythmia medications given to MOB can cross the placenta enabling fetal treatment

117
Q

What medication is contraindicated in Wolff-Parkinson-White syndrome?

A

digitalis

118
Q

Why are MRIs of limited diagnostic utility for the neonate with CHD?

A

the rapid heart rate makes gaiting for image acquisition very difficult

119
Q

What medications manipulate PVR and have a favorable influence on cardiac output?

A

NO, sildenafil, O2

120
Q

What are the indications for milirnone administration?

A

an afterload reducer that is often used and can be transitioned to oral enalapril, used after surgical ductal ligation treats hemodynamic instability, facilitating CNS and gut perfusion

121
Q

What are the indications for levosimendan administration?

A

calcium sensitizing agent with inotropic and vasodilator effects

122
Q

What are the indications for Nesiritide administration?

A

a recombinant form of human B type natriuretic peptide with both vasodilation and diuretic properties

123
Q

Describe the DA.

A

a large vessel that connects the main pulmonary trunk, or proximal left pulmonary artery with the descending aorta, 5-10mm distal to the origin of the left subclavian artery

124
Q

What are the potential consequences to fetal closure of the DA?

A

fetal demise or pulmonary hypertension

125
Q

What is the rate of DA closure in full term infants?

A

final fx closure occurs in almost half of full-term infants by 24h of age, in 90% by 48h and in all by 96h post birth

126
Q

What are some of the factors a/w a PDA?

A

1) prematurity
2) RDS and surfactant tx
3) Fluid administration
4) Asphyxia
5) high altitude
6) CHD
7) congenital syndromes

127
Q

What is the incidence of a PDA in premature infants?

A

~45% in babes <1000g ~80%

128
Q

What is the association between a PDA and RDS?

A

the presence of RDS is a/w increased risk of PDA and is correlated with the severity of RDS. After surfactant tx, there is an increased risk of a clinically symptomatic PDA; moreover, surf may lead to an earlier clinical presentation of a PDA

129
Q

What is the correlation bw a PDA and IVF tx?

A

an increased IVF load in the first few days of life is a/w an increased incidence of PDA

130
Q

What is the correlation bw a PDA and infants born at high altitudes?

A

infants born at high altitudes have an increased risk of PDA

131
Q

What congenital syndromes increase the risk of PDA?

A

present in 60-70% of infants with congenital rubella. Additional syndromes include: trisomy 13 & 18, Rubinstein-Taybi syndrome and XXXXX

132
Q

What factors decrease an infant’s risk of PDA?

A

antenatal steroids, IUGR and PROM

133
Q

What is the patency of the DA dependent upon?

A

balance bw the various constricting effects and relaxing effects of substances

134
Q

What is the correlation between oxygen and GA?

A

oxygen has less of a constricting effect with decreasing GA

135
Q

What is the correlation between prostaglandin E2 and GA?

A

the sensitivity of the ductus to the relaxing effects of prostaglandin E2 is greatest in premature infants and decreases with advancing GA. In term infants, responsiveness is lost shortly before birth.

136
Q

How are the effects of indomethacin altered dependent upon GA?

A

indomethacin constricts the immature ductus more than it does the close-to-term ductus

137
Q

What is the magnitude and direction of the shunt related to?

A

vessel size- diameter and length, the pressure difference between the aorta and the pulmonary artery and the ratio bw the SVR and PVR

138
Q

What are the clinical features of a L>R PDA shunt dependent upon?

A

the magnitude of the shunt and the ability of the infant to handle the extra volume

139
Q

How does a PDA lead to congestive heart failure?

A

LV output is increase by extra col return, increase in plum venous return causes an increase in ventricular diastolic vol (preload). LV dilation will result, c an increase in LV end diastolic pressure and a 2ndary increase in LA pressure. this will lead to left sided heart failure c pulmonary edema. eventually these changes will lead to RV failure.

140
Q

When is the typical presentation of a PDA?

A

initial presentation may be at birth but is usually on day 1-4

141
Q

Describe a PDA associated heart murmur.

A

usually systolic and heard best in the 2nd/3rd intercostal space at the L sternal border. may be continuous or intermittent

142
Q

Can a PDA present with a hyperactive precordium?

A

the increased left ventricular stroke volume may result in a hyperactive precordium

143
Q

What is the etiology of bounding peripheral pulses and a wide pulse pressure a/w a PDA?

A

increased stroke volume with diastolic runoff through the PDA

144
Q

What is a silent PDA?

A

a PDA is a/w a decreased MAP. in ELBW infants, hypotension may be the earliest clinical manifestation of a PDA, sometimes without a murmur

145
Q

How does a hemodynamically significant PDA present in pulmonary symptoms?

A

respiratory deterioration after an initial improvement in a small premature infant with RDS should arouse suspicion of a PDA. The deterioration may be gradual or brisk, but is usually not sudden (like a pneumo).

146
Q

What are other non specific signs of PDA presentation?

A

tachypnea, crackles or apenic spells. if the PDA is not treated, the L>R shunt may lead to heart failure with frank pulmonary edema and hepatomegaly.

147
Q

What is the most sensitive means of diagnosing a PDA?

A

a 2d Echo combined with a doppler ultrasound

148
Q

How does a PDA present on CXR?

A

on initial presentation, the CXR may be unremarkable, especially if p/w RDS. later, pulmonary plethora and increased interstitial fluid may be noted with subsequent florid pulmonary edema. Cardiomegaly is a later sign.

149
Q

What are some typical strategies in PDA mgmt?

A

ventilatory support, fluid restriction and increasing HCT

150
Q

What is the effect of a central HCT level >40-45% on a PDA?

A

increasing the HCT will decrease the L>R shunt. frequently, an increase in HCT abates some of the signs of the PDA

151
Q

What is indomethacin and what is its primary indication?

A

a prostaglandin synthetase inhibitor that has proven to be effective in promoting ductal closure

152
Q

What is the timeframe for indomethacin efficacy in patients with a PDA?

A

efficacy is limited to premature infants and decreases with postnatal age (limited effects beyond 3-4weeks)

153
Q

What is the major disadvantage of prophylactic indomethacin therapy?

A

up to40% of these infants probably would never have had a symptomatic PDA

154
Q

What are the indications for early symptomatic indomethacin therapy?

A

given if there are any clinical signs of a PDA before there are overt signs of failure

155
Q

What is the problem with the late symptomatic indomethacin therapy approach?

A

if indomethacin fails to constrict the ductus significantly, there is less opportunity for a second trial and the infant is more likely to require surgery

156
Q

What is the rate of PDA reopening after the first course of indomethacin?

A

20-30%; in such cases, a second course of indomethacin may be worthwhile bc a significant proportion of these infants will have their PDA closed with this course

157
Q

What are factors that are known to increase the risk for ductus reopening?

A

very preterm and those who received a greater ant of fluids previously, infix and NEC

158
Q

What are the renal complications a/w indomethacin?

A

causes a transient decrease in the GFR and UOP. in these cases, TF should be reduced to correct for decreased UOP which should improve within 24h

159
Q

What are the GI bleeding complications a/w indomethacin?

A

stools may be heme-positive after tx; this is transient and usually of no clinical significance. it is a mesenteric vasoconstrictor (but so is a PDA) in most trials, there is not increased incidence of NEC

160
Q

What are the spontaneous intestinal perforation complications a/w indomethacin?

A

has been a/w spont perts, especially when the drug was given early or when given together with postnatal corticosteroids

161
Q

What are the platelet function complications a/w indomethacin?

A

impairs plt fx for 7-9d regardless of pot count; no increased incidence of IVH and no evidence that it extends the degree of pre-existing IVH

162
Q

What are contraindications for indomethacin therapy?

A

serum crt >1.7, frank renal or GI bleeding or generalized coagulopathy, NEC and sepsis

163
Q

What is ibuprofen?

A

another nonselective cyclooxygenase inhibitor that closes the ductus

164
Q

How does ibuprofen compare to indomethacin?

A

it does not reduce mesenteric and renal dblood flow as much and is a/w fewer renal s/e; no evidence of differences in incidence of significant clinical side effects

165
Q

When is surgical ligation indicated?

A

patients with a hemodynamically significant PDA in whom medical treatment has failed or pharm intervention was contraindicated; at the earliest signs of significant congestion; before 1 yr of age to prevent endocarditis and pulmonary HTN

166
Q

What is the surgical mortality risk of PDA ligation?

A

<1%

167
Q

What are possible long term consequences of a PDA ligation?

A

increased risk of chronic lung dz and neurodevelopmental/neurosensory impairment in extremely preterm babes

168
Q

What is the prognosis for infants with a PDA?

A

excellent with an isolated PDA, preterm infants <30 wk have a spontaneous closure (72%) & conservative treatment with medications has a closure rate of 94%

Neonatal Pathophysiology (17 decks)

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