Fetal And Neonatal Circulaation Flashcards

1
Q

What are the cardiovascular changes in pregnancy?

A
  1. Cardiac output is increased
  2. Systemic vascular resistance (decreased)
  3. Blood volume & RBC mass is increased
  4. Blood pressure is decreased

Satisfy the increased metabolic demands of mother and fetus

Ensure adequate uteroplacental circulation for fetal growth and development

Insufficient—> maternal & fetal morbidiity

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2
Q

How are cardiac output, stroke volume and heart rate affected in labor and delivery?

A

CO is about 70%
-increased stroke volume

  • heart rate due to pain and anxiety
  • increased stroke volume (SV) due to increased preload-due to venous return. (Autotransfusion of 300-500 ml of blood from uterus into systemic circulation immediately after each contraction)

Postpartum (after delivery )-
Temporary increase venous return (VR) —> increase SV and CO
Mean blood pressure & SV normal 24 hrs after delivery

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3
Q

What are the 4 shunts of fetal circulation?

A
  1. Umbilical/placenta
  2. Ductus venosus
  3. Foramen ovale
  4. Ductus arteriosus
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4
Q

Describe neonatal hypoxia

A

Hypoxia results in:

  • Pulmonary vascular resistance & pressure remains high
  • Ductus Arteriosus remains patent (open)

-Thus patent Ductus Arteriosus maintains a right to left shunt (or fetal circulation retained)

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5
Q

Describe the fetal cardiovascular response to acute hypoxia in early gestation

A

Early gestation-immature response to acute hypoxia. Tachycardia, no increase peripheral vascular resistance to maintain arterial blood pressure

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6
Q

Describe the fetal cardiovascular response to acute hypoxia in late gestation

A

Acute hypoxia-CV response to sustain perfusion and cardiac output (CO). Response is not all or none, but TITRATED to degree of hypoxia

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7
Q

Explain the symptoms of Acute hypoxemia

A

Vasoconstriction, hypertension, bradycardia

  • decreased blood oxygen levels (hypoxemia)
  • chemoreceptors reflex- constriction of blood vessels in non vital peripheral areas (kidney, GI, lower extremities)
  • this diverts moire blood flow to vital organs (adrenal glands, heart, and brain)

The peripheral vasoconstriction results in:

  • Increase blood pressure (hypertension). Maintain perfusion of vital organs.
  • Hypertension results in baroreceptor mediated vagal response which slows the heart rate (bradycardia)
  • Bradycardia- maintains cardiac output(increases EDV)
  • Fetal late heart rate decelerations (measured by ECG or HR)
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8
Q

Explain 3 important changes from fetal to neonate

A

At birth,
1 . Clamping of the umbilical cord: sudden massive increase in systemic vascular resistance with removal of placental circulation. Left ventricle has to pump against this new resistance. This resultant increase in left atrial (LA) pressure leading to the closure of the Foramen ovale

  1. Entry of air into the lungs: fall in the pulmonary vascular resistance and the lungs become the principal oxygenator. Initial ventilatory movements, lungs expand —pulmonary vasc. Resistance & pulmonary artery pressure decrease Right ventricle per fuses lungs
  2. Increased oxygen concentration: vasoconstriction and closure of the ductus arteriosus (DA). This causes systemic and pulmonary circulation to run in parallel. Increased oxygen to peripheral tissues causes vasoconstriction n most body organs (tissues are less hypoxic)

Overall the circulation changes to adult type

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9
Q

Describe the active agent of Ductus Arteriosus closure fetal vs neonate

A

Active agent: PGE1 regulates ductus arteriosus (DA) muscle sphincter (note: PGE1-is a prostaglandin)

Fetus: high levels of PGE1–> relax smooth muscle ductus arteriosus. (PGE1 is generated in response to a relative hypoxia)

Neonate: PGE1 levels decline as PO2 rises and the ductus arteriosus muscular wall constricts

In premature and abnormal mature infants, the DA fails to constrict—> Patent Ductus Arteriosus (PDA)

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10
Q

Describe the path o physiology of patent ductus arteriosus

A

Persistent shunt between descending aorta and left pulmonary artery

Blood flow is from aorta to the pulmonary artery(pressure gradient)—> Pulmonary circulation, LA and LV become volume overloaded

—> LV dilatation and left sided heart failure

Children with large left to right-shunts: congestive cardiac failure, tachycardia

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11
Q

What are the features of PDA?

A

Murmur heard during systole and diastole- continuous murmur (machinery) murmur

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12
Q

What is the treatment of patent ductus arteriosus?

A

Surgical closure

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13
Q

Explain the symptoms of patent ductus arteriosus

A

Symptoms 2-3 days after birth

Continuous blood flow into the pulmonary circulation —> continuous murmur(machinery sounding)and early onset PAH

Left—> right blood shunting of blood results in
-excessive blood flow through pulmonary circulation (aorta to pulmonary artery)

-hypoperfusion “ductal seal” of the systemic circulation

Moderate to large shunts
-pulmonary edema, hemorrhage , bronchopulmonary dysplasia

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14
Q

What is the clinical significance of the Foramen ovale?

A

Birth: Pressure reversal causes flap over Foramen ovale to close

Persistent left—> right shunting, frequent in first few weeks of life, and premature infants
About 70-75% septa with holes 3-8 mm fuse @ 2 years

Patent Foramen ovale: failure to close
-defects 1-10 mm maximum diameter

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15
Q

Describe the clinical manifestation of patent Foramen ovale

A
  • Most patients remain asymptomatic
  • Clinical presentation is ischemic stroke due to a paradoxical embolism
  • An increased prevalence of PFO in patients who have had a cardiogenic stroke, particularly in patients less than 55 years old

Cryptogenic stroke- a stroke in absence of identified cardioembolic or large vessel source and not consistent with small vessel disease.( Cryptogenic stroke accounts for approximately 20 to 40 percent of ischemia strokes)

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16
Q

What is persistent pulmonary hypertension ?

A
  • pulmonary vascular resistance (PVR) remains abnormally high after birth
  • Continuation of right to left shunting of blood through fetal circulatory pathways
  • Hypoxemia develops: may not respond to respiratory support
17
Q

Describe the clinical manifestations of persistent pulmonary hypertension

A
  • Initial Primary finding cyanosis, associated with tachypnea and respiratory distress
  • Cardiac examination: loud, single heart sound (S2) or a harsh systolic murmur secondary to tricuspid regurgitation
  • May also present systemic hypertension, symptoms of shock, and evidence of poor cardiac function and perfusion