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Oral MFM Boards > Maternal Cardiac Disease > Flashcards

Maternal Cardiac Disease Flashcards

1
Q

Define gHTN

A

BP >/= 140/90 >/= 20 weeks on 2 occasions at least 4 hours apart
AND
-No history of hypertension
-No history of proteinuria
-No severe features of preeclampsia

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2
Q

Define preeclampsia and what features are severe

A

BP >/= 140/90 >/= 20 weeks at least 4 hours apart
AND
-Proteinuria (P/C >/= 0.3 or >/=300mg/24hr)
—— severe features—–
-Thrombocytopenia, < 100k
-Renal insufficiency, Cr >1.1mg/dL or 2x baseline
-Impaired liver function, 2x upper limit normal AST or ALT
-Pulmonary edema
-Cerebral or visual symptoms
-Refractory RUQ/epigastric pain

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3
Q

Incidence of hypertensive disease of pregnancy

A

4% pregnancies in US

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4
Q

Those recommended to use prophylactic LDA and dosing

A
  • 1 or more high risk factors (=8% risk of pree)
    OR
    -2 or more moderate risk factors

81mg daily >/=12 -28 weeks-, ideally before 16 weeks

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5
Q

High risk factors for LDA therapy

A
  1. History of preeclampsia
  2. Multifetal gestation
  3. Renal disease
  4. Chronic hypertension
  5. Pregestational diabetes
  6. Autoimmune disease (SLE, APS)
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6
Q

Moderate risk factors for LDA therapy

A
  1. Age >35
  2. Nulliparity
  3. BMI >30 kg/m2
  4. Black race
  5. Mother or sister with preeclampsia
  6. Low income
  7. IVF pregnancy
  8. History – SGA, adverse pregnancy outcome, pregnancy interval >10years
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7
Q

LDA reduces the rate of

A
  1. Preeclampsia ~50%
  2. Fetal growth restriction~60%
  3. Medically indicated preterm birth before 35 weeks
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8
Q

Contraindications to expectant management of preeclampsia

A
  1. uncontrolled severe range BP
  2. refractory headache
  3. refractory RUQ/epigastric pain
  4. visual disturbances
  5. pulmonary edema
  6. HELLP
  7. eclampsia
  8. Renal dysfunction
  9. MI
  10. Stroke
  11. placental abruption
  12. abnormal fetal testing
  13. fetal death or lethal anomaly
  14. REDF
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9
Q

Long term health risks of preeclampsia

A

-2-3x risk of developing CVD (CAD, MI, HF and stroke)
-Offspring effects (DM, HTN, neurodevelopmental)

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10
Q

Time frame for BP check after preeclampsia discharge

A

within 72hrs

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11
Q

Risk of gHTN developing preeclampsia

A

50%

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12
Q

HELLP diagnsosi

A
  1. Hemolysis - LDH >600 IU/L
  2. LFT dysfunction - AST/ALT 2x upper limit of normal
  3. Thrombocytopenia - <100k

15% without HTN or proteinuria

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13
Q

Typical main symptoms with HELLP

A

RUQ pain, generalized malaise, nausea, vomiting

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14
Q

Define eclampsia

A

new onset, tonic-clonic/focal/multifocal seizures in the absence of other causative conditions (epilepsy, cerebral ischemia/infarct, ICH, drug use)

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15
Q

Cause of maternal mortality with eclampsia

A

maternal hypoxia, trauma, aspiration pneumonia

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16
Q

Is there residual neuro damage after eclampsia

A

Rarely – some women have short and long term memory and/or cognitive impairment

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17
Q

Are there usual premonitory signs of eclampsia

A

Yes – headache, blurred vision, photophobia, altered mental status

Some cases without htn or proteinuria or any premonitory signs

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18
Q

Cause of headache in htn disorder/eclampsia

A

elevated cerebral perfusion pressure, cerebral edema, hypertensive encephalopathy

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19
Q

Define PRES

A

Posterior reversible encephalopathy syndrome

abnormal nervous system manifestations vision loss or deficit, seizure, headache, altered sensorium or confusion

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20
Q

How is diagnosis of PRES made

A

vasogenic edema and hyperintensities in the posterior aspect of the brain on MRI

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21
Q

Treatment of PRES

A

same as preeclampsia

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22
Q

Which LFT is usually more elevated first in preeclampsia and why

A

AST due to periportal necrosis

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23
Q

In general, evaluation of coagulation factors in preeclampsia is indicated when

A

Thrombocytopenia, significant liver dysfunction, placental abruption

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24
Q

Cause of proteinuria in preeclampsia

A

increased tubular permeability to proteins

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25
Q

What happens to urinary Ca in preeclampsia

A

Decreases because there is increased tubular resporption

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26
Q

What causes renal sodium and water retention in preeclampsia

A

the intravascular depletion, vasoconstriction leads to decreased renal perfusion

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27
Q

What are some fetal consequences of preeclampsia and mechanism

A

Impaired uteroplacental blood flow – fetal growth restriction, non-reassuring fetal status, oligohydramnios, abruption, preterm delivery, hypoxia-acidosis, neurologic injury, death

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28
Q

Mechanism of LDA in pree prevention

A

Inhibition of thromboxane A2

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29
Q

Magnesium decreases risk of seizure how much…decrease or increase anything else?

A

Decrease eclampsia by ~50%
Reduced risk of placental abruption

Maternal side effects in 25%
5% increased rate of CD

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30
Q

Rate of eclampsia in preeclampsia with severe features

A

4 in 200 without magnesium
1 in 200 with magnesium

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31
Q

Number needed to treat with Mag to prevent eclampsia

A

Pree with severe features - 129
Pree with severe features and symptomatic - 36

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32
Q

Contraindications to Mag

A

Myasthenia gravis
Hypocalcemia
Severe renal failure
Cardiac ischemia
Heart block
Myocarditis

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33
Q

Mag therapeutic/toxic levels

A

5-9 mg/dL therapeutic
> 9 loss of DTR
>12 respiratory compromise
>30 cardiac arrest

toxicities due to its action as a smooth muscle relaxant

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34
Q

Magnesium dosing

A

4g bolus over 20-30 minutes
1-2g/hr

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35
Q

IM dosing of magnesium

A

10g loading (5mg each buttock)
then 5g every 4 hours

36
Q

Mg dosing in renal dysfunction

A

Cr 1-1.5, oliguria (<30mL/hr x4 hrs) = normal load, followed by 1g/hr

Cr >1.5 =

37
Q

When to check mag levels

A

Renal dysfunction (every 4 hours, if >9.6 then stop infusion and check q2hrs, restart at lower infusion rate when <8.4))
Suspected Mg toxicity

38
Q

Treatment of Mg toxicity

A

Calcium gluconate 10% solution – 10mL IV over 3 minutes

Consider Lasix

39
Q

Why treat severe HTN

A

to prevent ischemic/hemorrhagic stroke, renal injury/failure, myocardial ischemia, CHF

40
Q

When to treat HTN

A

Severe BP sustained for 15 minutes or more
Treat within 30-60 minutes

41
Q

Labetalol max dose for PO regimen

A

2400mg/day

42
Q

Labetalol max dose for acute IV regimen

A

300mg

43
Q

Practice Labetalol/Nifedipine/Hydralazine acute treatment algorithms

A
44
Q

Likelihood of CD in preterm preeclampsia

A

<28 weeks 97%
28-32 weeks 65%

45
Q

Risks of general versus regional anesthesia

A

general = aspiration, failed intubation, stroke secondary to increased systemic and intracranial pressure during intubation/extubation

46
Q

Effect of Mg on anesthesia

A

Prolongs duration of nondepolarizing muscle relaxants

47
Q

Why no stop Mg for cesarean

A

1/2 life is 5hrs, so cessation only minimally reduces Mg concentration at time of delivery while possibly increased seizure risk

48
Q

Steps to take during eclampsia

A
  1. call help
  2. ensure maternal safety
  3. lateral decubitus position
  4. administer oxygen
  5. monitor vitals and o2 saturation
  6. magnesium to prevent additional seizures
49
Q

Treatment of recurrent eclamptic seizure

A

an additional 2-4 g of mag administered over 5 minutes

50
Q

Treatment of refractory eclampsia (seizing 20 mins after bolus, more than 2 recurrences)

A

Amobarbital - 250mg IV in 3 minutes
Phenytoin - 1250mg IV at rate of 50mg/minute

Intubation, ICU admission, head imaging

51
Q

HELLP labs that suggest increased mortality risk

A

LFT’s > 2000
LDH > 3000

52
Q

In HELLP the lowest observed platelet counts tend to be seen

A

23hours after delivery

53
Q

What is the underlying pathophysiology of cardiovascular changes in pree

A

vasoconstriction – imbalance between normal vasodilatory and vasoconstrictive substances

hemoconcentration - due to intravascular volume depletion

54
Q

Cause of thrombocytopenia in pree

A

microangiopathic hemolysis possibly

55
Q

Profound renal insufficiency in pree can lead to what renal condition

A

acute tubular necrosis

56
Q

Differential diagnosis in HELLP

A

TTP/HUS
AFLP
Lupus
APLS

57
Q

Labs to differentiate between HELLP, HUS/TTP, AFLP

A

Ammonia - elevated AFLP
Anemia - severe TTP/HUS
ATIII - decreased AFLP, may be elevated HELLP
AST - normal in TTP/HUS
Fibrinogen - decreased AFLP
Glucose - decreased AFLP
LDH - elevated in all

58
Q

ATN postpartum….signs/sx

A

Worsening renal dysfunction, not associated with a aHUS picture (hemolysis, thrombocytopenia)

59
Q

Risk of recurrent eclamptic seizure while on magnesium

A

10%

60
Q

When is head imaging indicated in cases of eclampsia

A

Recurrent or refractory seizures
Focal neurological signs are persistent
Coma
Uncertain diagnosis

61
Q

Why is the IM route for magnesium not preferred

A

Painful
Gluteal abscess

62
Q

Monitoring for magnesium toxicity is achieved how

A

DTR’s
Respiratory status
Mental status
Urine output

63
Q

How does Ca gluconate work as an antidote for Mg toxicity

A

Calcium competitively inhibits magnesium at the neuromuscular junction

64
Q

At what BP is hypertensive encephalopathy generally achieved

A

> 220/120

However, women with typical normotensive values may develop at lower threshold as compared to someone with history of cHTN

65
Q

Other systemic signs of HTN enecphalopathy

A

Retinal ischemia - vision changes
Cardiac ischemia - MI or angina
Renal ischemia - ATN or renal dysf

66
Q

Drug of choice in hypertensive crisis

A

sodium nitroprusside

alternatives - nitroglycerin, nifedipine, nicardipine, hydralazine

67
Q

Aim of initial therpay for htn emergency

A

Reduce MAP by 25% in first hour, goal 155-160/100-110

68
Q

Why is BP lowering done slower in htn emergency

A

Esp in cHTN the cerebral autoregulation may be shifted. Lowering too quickly could clear to cerebral ischemia, stroke, coma in additional to reduced flow to other organs (coronary, placenta, renal)

69
Q

MOA of sodium nitroprusside

A

Interferes with calcium influx and activation of intracellular calcium – leads to arterial and venous relaxation

70
Q

How is sodium nitroprusside administered

A

IV infusion

short half life – works quickly, stops working quickly when IV stopped (3-5 mins)

71
Q

Risks of nitroprusside

A

Hypotension - quickly reversed with cessation
Thiocyanate metabolite excreted in urine – can accumulate if renal or liver dysfunction, large doses, prolonged administration (48 hrs)

72
Q

Cyanide toxicity symptoms

A

Anorexia
Disorientation
Headache
Fatigue
Restless
Tinnitus
Delirium/hallucinations
Nausea/vomiting
Metabolic acidosis

73
Q

Treatment if cyanide toxicity

A

sodium nitrite
sodium thiosulfate

74
Q

Nitroglycerin use with hypertensive encephalopathy?

A

contraindicated, it increased cerebral blood flow and intracranial pressure

75
Q

MOA of magnesium

A

Elevated concentrations of Mg act on cell membranes to slow or block neuromuscular and cardiac conducting system transmission

decrease smooth muscle contractility

depress CNS irritability

76
Q

Adverse effects of Mg MOA

A

Also decrease smooth muscle contractibility of uterus and heart
respiratory depression

77
Q

Why not do intermittent bolus of Mg?

A

Leads to transient elevations in Mg level

78
Q

Agents that can be used to terminate a seizure if already on magnesium

A

Valium - 5 or 10mg
Lorazepam - 4mg
General anesthesia

79
Q

Hydralazine MOA

A

Dilation of arterioles

80
Q

Labetalol MOA

A

alpha and beta-adrenergic blockade

81
Q

Nifedipine MOA

A

Calcium channel blocker

82
Q

Hydralazine effect on heart and uterus

A

Vasodilation leads to increased CO and increased uterine perfusion

83
Q

Side effects of hydralazine

A

Headache and epigastric pain

84
Q

CHAP trial demonstrates what findings for treatment of cHTN

A

BP <140/90 associated with decreased risk of preeclampsia w/ severe features, medically indicated birth <35 weeks, placental abruption/fetal/neonatal death

No change in SGA

85
Q
A

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