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Physiology for Anaesthetists > Developmental - Fetal Physiology > Flashcards

Developmental - Fetal Physiology Flashcards

1
Q

Summarise and classify the functions of the placenta

A
  1. Respiratory gas exchange
  2. Nutritive and excretory
  3. Immunological barrier (allowing mother to tolerate fetus)
  4. Protein transfer of IgG = passive immunity
  5. Protective barrier against many infectious agents and drugs (except listeria, parvovirus B19, HIV)
  6. Endocrine function
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2
Q

From which cells does the placenta form

A

Maternal endometrial cells (= decidual cells in pregnancy)

AND

Trophoblastic cells from the fetus

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3
Q

What is a blastocyst?

A

The fetal cells form a ball of cells that implant within the endometrium. This is called a blastocyst.

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4
Q

From which part of the blastocyst does the placenta form?

A

The outer layer of the blastocyst. These outer cells form the trophoblast.

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5
Q

What is the trophoblast? From where is it derived, what does it form and what are the names of its various layers

A

Trophoblast forms from the outer layer of the blastocyst which is the ball of fetal cells implanted in the endometrium. The trophoblast cells develop into two layers forming the chorion. The layers within the chorion are:

  1. Inner chorionic layer = Cytotrophoblast cells
  2. Outer chorionic later = Syncytiotrophoblast cells

These two cell layers plus the fetal endothelium separate fetal blood circulation from maternal blood.

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6
Q

How is the interface between the chorion and the maternal blood formed

A

Outer layer of blastocyst –> trophoblast –> chorion (syncytiotrophoblast + cytotrophoblast) –> invades maternal decidua releasing enzymes which produce cavities within the decidua. When the maternal spiral arteries (which supply the decidua) are invaded, their blood fills these cavities.

Projections called chorionic villi form an extensive network of finger-like projections within these blood filled cavities, and then become vascularized.

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7
Q

When does the fetal heart become active and describe the fetal blood supply of the placenta

A

Fetal heart active at 5 weeks gestation

Fetal placental blood supply:
2 x umbilical arteries branch into the chorionic villi to form cappilaries here. The capillaries drain into venules which coalesce to form a single umbilical vein

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8
Q

What separates fetal and maternal blood

A
  1. Fetal endothelium
  2. Cytotrophoblast layer of chorion
  3. Syncytiotrophoblast layer of chorion

Normally, there is no mixing of fetal and maternal blood.

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9
Q

How does uterine blood flow change during pregnancy

A

Increases 10 fold

75 ml/min –> 750 ml/minute

85% of this increase to the placenta to match increasing nutritional demands of the developing fetus

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10
Q

Where are placental hormones produced? What types of hormones does the placenta synthesize

A

Syncytiotrophoblast.

Peptides

  1. Beta-hCG
  2. hPL

Steroids

  1. Oestrogen
  2. Progesterone
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11
Q

Describe the pathophysiology of pre-eclampsia

A
  1. Dysfunction of spiral arteries that constitute the sole blood supply to the placenta (?maternal/?fetal factors).
    –> INADEQUATE PLACENTAL PERFUSION
    |
    |
  2. This leads to hypoxia of syncytiotrophoblast
    |
    |
  3. Release of: cytokines, eicosanoids, vascular endothelial growth factor 1.
    |
    |
  4. Released placental factors lead to systemic inflammatory response in the mother with endothelial dysfunction
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12
Q

What mechanisms prevent a maternal immune response to the genetically distinct fetus? What is the down side of this

A
  1. Trophoblast cells lose most MHC molecules at implantation - Less immunogenic
  2. Chorionic cells act as an immune barrier, preventing maternal T cells and antibodies from reaching the fetal circulation
  3. Progesterone and alpha-fetoprotein
    - produced by the yolk sac at implantation act as maternal immunosuppressant agents, specifically damping down cellular immunity.

Downside –> risk of infection to mother

(especially Listeria monocytogenes)

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13
Q

Which important pathogens can cross the placenta

A
  1. Listeria monocytogenes
  2. Rubella
  3. Parvovirus 19
  4. HIV
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14
Q

How long until the fetal immune system is fully developed. What is the mechanism for the fetus to fight infection in utero?

A

6 months after birth

In-utero: Maternal IgG antibodies

Syncytiotrophoblasts have IgG receptors but no other Ig molecules can cross the placenta.

IgG can cross the placenta by endocytosis

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15
Q

What are the negative consequences of placental endocytosis of igG antibodies?

A
  1. Haemolytic disease of the newborn (anti-RhD IgG)
  2. Transient neonatal myasthenia gravis
  3. Neonatal lupus and Congenital heart block (anti-Ro IgG –> SLE)
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16
Q

How are the following molecules transported across the placenta

  1. O2 and CO2
  2. Glucose
  3. Amino acids
  4. Immunoglobulins
  5. Bulk flow
A
  1. O2 and CO2 - Simple diffusion
  2. Glucose - GLUT 1 and GLUT 3 facilitated transport proportional to maternal [glucose]
  3. Amino acids - Na+ dependent active transport
  4. Immunoglobulins - Transcytosis: IgG only
  5. Bulk flow - Water down conc. gradient between cells
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17
Q

Name and describe the drug properties that affect transfer of drugs across the placenta

A

Factor (favours transfer)

  1. Concentration gradient (High)
  2. Molecular weight (Low i.e. less 1000 Da)
  3. Charge/ionization/pKa/pH (unionized)
  4. Lipid solubility (high)
  5. Protein binding (Low)
  6. Placental efflux transporter proteins (P-glycoprotein) absent
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18
Q

Describe uterine blood flow at term?
What is the formula?
Is the vasculature responsive to respiratory gas tensions?

A

Its 10% of CO at around 750 ml/min (85% to placental)

Uterine blood flow = (P uterine artery - P uterine vein)
_________________________
Uterine Vascular Resistance

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19
Q

Is uterine flow autoregulated

A

No.

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20
Q

Describe fetal placental blood supply

A

2 x umbilical arteries (deox blood from fetus to placenta)

1 x umbilical vein (oxygenated blood from placenta to fetus)

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21
Q

What % of fetal CO supplies the umbilical arteries

A

50%

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22
Q

Are the umbilical arteries/veins of the fetus innervated or autoregulated

A

no

23
Q

What is umbilical flow at term in an undisturbed fetus

A

360 ml/min

24
Q

What is the mean BP in the umbilical arteries
What is the mean BP in the villous capillaries
What is the mean BP in the umbilical vein

A

arteries –> 50 mmHg
capillaries –> 30 mmHg
Vein –> 20 mmHg

always exceeds the intervillous space protecting fetal vessels from collapse

25
Q

How many times per minutes is the blood in the intervillous space exchanged

A

2 - 3 times per minute

26
Q

Is uterine blood flow to the placenta autoregulated

A

No

27
Q

Do volatile agents cross the placenta

A

Yes. Due to high lipophilicity

28
Q

Do induction agents cross the placenta.

A

Yes. Thiopental and propofol more than Etomidate as it is less lipophillic

29
Q

Do benzodiazepines cross the placenta

A

Yes. Concentrations are often higher in the fetus than in the mother, probably reflecting greater protein binding in the fetus.

30
Q

Do non-depolarizing muscle relaxants cross the placenta

A

These are quaternary ammonium salts that are fully ionized and do not cross the placenta readily

31
Q

Does succinylcholine cross the placenta, what are the effects of this

A

Maternal doses of 300mg succinylcholine are required before drug can be detected in umbilical venous blood.

32
Q

Does glycopyrrolate/atropine cross the placenta?

A

Glycopyrrolate –> no. (highly polar)

Atropine –> yes

33
Q

Do the anticholinesterase agents cross the placenta

A

Neostigmine and edrophonium are quaternary ammonium compounds that are ionized at physiological pH. They do not readily cross the placenta

34
Q

Do ephidrine and phenylephrine cross the placenta

A

Ephidrine –> yes

Phenylephrine –> unknown

These agents to not seem to impair uterine blood flow significantly when used at appropriate doses

35
Q

Does opioids cross the placenta?

A

Yes.
Morphinee crosses rapidly to a fetomaternal ratio of 0.92.

Fentanyl and its analogues cross less readily because protein binding to albumin is high and this offsets the high lipophilicity

Fentanyl Maternal Protein binding 90%

Morphine Maternal Protein binding 30%

36
Q

Describe the placental trasnfer of local anaesthetic agents

A

Lidocaine (70% protein bound) –> less protein bound, therefore greater transfer into fetus

Bupivacaine (95% % protein bound) –> limited placental transfer due to extensive protein binding

37
Q

What is ion trapping in the context of neonatal local anaesthetic toxicity?

A

Local anaesthetic agents are weak bases.
Bases ionize at physiological pH below their pKa

So in acidic environments, local anaesthetics become ionized.

A compromised fetus may become acidotic.

In this situation, more of the fetal local anaesthetic will be ionized and therefore will not be able to return back to the mother = ion trapping and can cause fetal toxicity

38
Q

Do warfarin, unfractionated heparin and low molecular weight heparin cross the placenta

A

Warfarin –> yes

Unfractionated heparin –> no

LMWH –>limited transfer with minimal functional significance to fetus

39
Q

List and describe the factors that aid the transfer of O2 from maternal HbA to fetal HbF across the placental barrier

A
  1. PaO2 gradient 6.7 (intervillous) to 2.7 (umbil. aa)
  2. Left shifted HbF curve (placenta makes 2,3 DPG which binds to Beta-globin chains not gamma-globin chains)
  3. The double Bohr affect
  4. higher fetal O2 carrying capacity (Hb 18 g/dL)
40
Q

What is the double Bohr affect?

A

The Bohr effect is the reduced affinity of haemoglobin for oxygen in the tissues (vs.lung) subsequent to a right shifted OHDC in the presence of CO2, H+, 2,3 DPG, increased temperature and exercise allowing for offloading of O2 from Hb at the tissue level

  1. PaCO2 (kPa) gradient: 6.7 (fetal umb. aa) to 4.9 (intervillous)

As CO2 moves out of fetal blood the fetal OHDC P50 shifts to the left because CO2 levels reduce.

As CO2 moves into intervillous blood maternal P50 of the OHDC shifts to the right because CO2 levels increase.

As CO2 reduces in fetal blood and increases in maternal blood a double bohr affect phenomenon is observed favouring the liberation of O2 from maternal haemiglobin and binding of O2 to fetal Hb.

41
Q

What is the double Haldane effect?

A

The Haldane effect is the increased ability of deoxygenated Hb to carry CO2.

As oxygen is offloaded from maternal to fetal blood PaO2 in maternal blood falls. Increased deoxyHb results. deoxyHb more readily forms carbamino compounds and binds CO2 exchanged with fetal blood more readily.

Additionally, O2 offloaded from maternal blood moves into fetal blood. Here it forms oxyHb and facilitates the release of CO2 from fetal Hb for transfer into maternal blood and removal

Together, these processes are known as the double Haldane effect.

42
Q

What happens to fetal oxygenation during labour

A

The placenta is supplied with maternal blood via spiral arteries which in turn arise from radial arteries. Radial arteries are supplied by the uterine artery. Importantly, uterine blood flow is not autoregulated and blood flow is pressure dependent.

During labour, uterine contractions occur which temporarily reduce blood flow to the placenta resulting in mild fetal hypoxia. The fetus can accommodate a degree of hypoxia without consequence.

43
Q

What causes severe fetal hypoxaemia during labour

A

Uterine contractions cause temporary radial artery compression and reduced placental blood flow, causing mild fetal hypoxia which can be accommodated by the fetus.

The following factors can cause severe fetal hypoxia

  1. Maternal factors - hypotension (sepsis / aortocaval compression)
  2. Fetal factors - Malpresentation
  3. Placental factors - praevia / abruption
  4. Umbilical cord factors - cord entaglement / true knots
44
Q

Summarise the differences between fetal and adult circulatory systmes

A
  1. The presence of umbilical vessels
  2. The vascular shunts: Ductus Arteriosus and Ductus Venosus
  3. Defect in the atrial septum: foramen ovale
45
Q

Describe the pattern of fetal blood flow including SaO2 and % flow through

A

UV (SaO2 80 - 90%, PaO2 4.0 - 5.0 kPa)
|
40% flow to Liver and 60% of flow bypass Liver to IVC in the Ductus Venosus
|
IVC –> RA
(Flap of tissue called eustachian valve directs flow through foramen ovale in LA
|
LA –> ascending aorta (PaO2 3.5 SaO2 65%)
|
Supplies upper half of body: heart, brain.
|
SVC (PaO2 2.5 kPA, SaO2 40%) –> RA
|
PA –> 90% into DA and 10% in R and L PA to lungs
(PVR is high due to HPV)
|
90% back into aorta (now descending) to lower half of body and
|
Umbilical arteries –> placenta
|
Umbilical vein (UV)

Repeat

46
Q

How does fetal heart differ from the adult heart?

A

LV pumps 1/2 VR to upper 1/2 body

RV pumps 1/2 VR to lower 1/2 body

Both pump into high pressure systems

  1. R and L heart usually similar size and thickness.
  2. Immature fetal myocardium
    - -> Cannot increase SV with increased preload
    - -> High proportion of non-contractile protein
    - -> SV is fixed and CO depends on HR (CO = SV x HR)
  3. Fetal heart is under autonomic control
    - -> PSNS: responsible for normal baseline variability
    - -> SNS: responsible for accelerations with fetal activity
47
Q

Discuss the physiology of an early versus a late deceleration

A

Early deceleration

  • -> Healthy fetus
  • -> Uterine contraction –> transient fall O2 delivery or compression of fetal head –>PSNS mediated fall in HR shortly after the onset of the uterine contraction.

Late deceleration

  • -> Severe fetal hypoxia
  • -> Peripheral chemoreceptors trigger peripheral vasoconstriction to redirect blood to vital organs –> resulting hypertension stimulates a baroreceptor reflex –> bradycardia. The deceleration of HR is late relative to the onset of Uterine contractions because time is taken in this two step reflex response
48
Q

At what gestational age are alveolar type 2 pneumocytes seen?

When are these cells fully mature and when do they produce adequate pulmonary surfactant

A

First seen: 24 weeks

Mature: 35 weeks

49
Q

What are the physiological changes that occur at birth in the respiratory system

A

Tactile/thermal/visual/auditory stimulation

Falling PaO2
Rising PaCO2
Falling pH
–> All stimulate central and peripheral chemoreceptors, stimulating the neonate to take its first breath.

First breath requires very high inspiratory work
–> lungs fluid filled and very poorly compliant

After first breath, PVR falls rapidly permitting pulmonary blood flow.

50
Q

What are the physiological changes that occur in the cardiovascular system at birth

A
  1. Umbilical arteries vasoconstrict in response to mechanical stimulation and exposure to cold air.
  2. Cord clamping (after 40 - 60 seconds) removes low resistance placenta from fetal circulation –> increase SVR –> reduction in RA venous return –> reduced blood flow through ductus venosus results in its closure within 1 - 3 hours
  3. Breathing rapidly reduces PVR. Blood flows through the lungs and venous return to LA increases. When LAP exceeds RAP, the foramen ovale closes.
  4. Physiological closure of the ductus arteriosus occurs over the next 10 hours, through a number of mechanisms: High PaO2 (unknown mechanism), reduced prostaglandins after birth, Bradykinin released from lungs
51
Q

Why do we delay cord clamping by 40 - 60 seconds

A

Allows additional venous return from placenta to fetus.

52
Q

How does the ductus venosus close after birth. How long does this take

A

Clamping of umbilical cord significantly reduces flow through umbilical vein and hence ductus venosus. The ductus venosus closes after 1 - 3 hours.

53
Q

Describe how the ductus arteriosus closes

A

Takes about 10 hours to close after birth via the following mechanisms

  1. high PaO2 (mechanism unknown)
    - -> high incidence of failed DA closure in neonates with significant hypoxaemia and those born at altitude
  2. Reduced prostaglandin production after birth (prostaglandins keep DA open)
  3. Bradykinin released from lungs afterbirth is implicated in DA closure too
54
Q

What are the most important reasons for reversion to a transitional circulation in the neonate

A

Hypoxia, hypercapnoea, acidosis, hypothermia

E.g. Neonatal Respiratory Distress Syndrome (formerly known as Hyaline Membrane Disease)

Hypoxaemia –> HPV –> Increased PVR –> Increased RAP –> patent foramen ovale.

Hypoxia –> patent ductus arteriosus.

Right to left shunting via PFO and PDA exacerbates hypoxia and acidosis and further increase PVR –> vicious cycle ensues.

TREATMENT
Surfactant
High FiO2
CPAP
Inhaled NO

Physiology for Anaesthetists (61 decks)

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