Maternal Physio - Cardiovascular Flashcards

1
Q

Cardiac output changes

  • AOG
  • Why
A
  • CO ↑ at 5th week AOG due to:
    • ↓ systemic vascular resistance plus ↑ heart rate
  • Memory aid:*
  • In Buntis, Both SVR and HR are affected
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2
Q

A pregnant woman’s CXR has a slightly enlarged cardiac silhouette. What is a possible explanation?

A

Some degree of benign pericardial effusion may increase the cardiac silhoutte

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3
Q

A pregnant woman has a diastolic murmur on auscultation. Is this normal?

A
  • No
    • Diastolic murmurs are never normal and should be evaluated by a cardiologist
    • Systolic murmur in 90% of pregnant patients due to ↑ flow across aortic and pulmonic valves
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4
Q

Plasma volume changes

  • AOG
  • Change
  • Effect
A
  • Between 10-20 weeks AOG
    • Plasma volume expands
    • ↑ preload

Note:

  • Increase preload due to plasma volume expansion
  • Decrease in afterload due to decreased vascular resistance
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5
Q

Heart position

  • Changes
  • CXR finding
A
  • Changes
    • Displaced to the left and upward
    • Rotated somewhat on its long axis
  • CXR finding
    • Apex is somewhat lateral from its usual position
    • Larger cardiac silhoutte on chest radiograph
      • some degree of benign pericardial effusion may increase the cardiac silhoutte
  • Note:*
  • This is best imagined!
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6
Q

ECG change

A

No characteristic ECG changes other than slight left-axis deviation as a result of the altered heart position

  • Note:*
  • Again, imagine and correlate!
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7
Q

Cardiac sounds

A
  • Exaggerated splitting of the 1st heart sound with increased loudness of both components
  • Systolic murmur in 90% of pregnant patients due to ↑ flow across aortic and pulmonic valves
    • intensified during inspiration
    • disappears shortly after delivery
  • Diastolic murmurs are never normal and should be evaluated by a cardiologist

Memory aid:

  • Splitting and
  • Systolic murmur are normal
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8
Q

BP changes

A
  • Arterial pressure usually decreases to a nadir at 24 to 26 weeks
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9
Q

How many percent of women experience supine hypotensive syndrome?

A

About 10%

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10
Q

RAA component changes and why

A
  • Increased on normal pregnancy
    • Renin
      • produced by kidney and placenta
    • Angiotensinogen
      • produced by maternal and fetal liver and influenced by estrogen
  • Memory aid:*
  • Vowels; so it is not progesterone
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11
Q

If angiotensin is increased, why is there no BP elevation in normal pregnancy?

A

Because of prostacyclin, which is implicated in the angiotensin resistance characteristic of normal pregnancy

  • Therefore:*
  • Prostacyclin is decreased in preeclampsia
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12
Q

Diastolic decreases ____ [less/more] than systolic

A

More

  • Memory aid:*
  • SBP/DBP → DBP decreased to a greater extent
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13
Q

Prostaglandin E2 synthesis

  • Where synthesized
  • Increased/decreased release and when
A
  • Where synthesized
    • Renal medulla
  • Increased/decreased release
    • Increased markedly in late pregnancy
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14
Q

Principal prostaglandin of endothelium

A

Prostacyclin

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15
Q

Potent vasoconstrictor in endothelial and vascular smooth muscle cells which also stimulates secretion of ANP, aldosterone and catecholamines

A

Endothelin

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16
Q

Fetal oxygen saturation is approximately ____% ____ (higher/lower) in a labouring woman

A

10% higher

17
Q

Potent vasodilator released by endothelial cells and have important implication for modifying vascular resistance during pregnancy

A

Nitric oxide