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Maternal Cardiac Disease Flashcards

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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
What happens to urinary Ca in preeclampsia
Decreases because there is increased tubular resporption
26
What causes renal sodium and water retention in preeclampsia
the intravascular depletion, vasoconstriction leads to decreased renal perfusion
27
What are some fetal consequences of preeclampsia and mechanism
Impaired uteroplacental blood flow -- fetal growth restriction, non-reassuring fetal status, oligohydramnios, abruption, preterm delivery, hypoxia-acidosis, neurologic injury, death
28
Mechanism of LDA in pree prevention
Inhibition of thromboxane A2
29
Magnesium decreases risk of seizure how much...decrease or increase anything else?
Decrease eclampsia by ~50% Reduced risk of placental abruption Maternal side effects in 25% 5% increased rate of CD
30
Rate of eclampsia in preeclampsia with severe features
4 in 200 without magnesium 1 in 200 with magnesium
31
Number needed to treat with Mag to prevent eclampsia
Pree with severe features - 129 Pree with severe features and symptomatic - 36
32
Contraindications to Mag
Myasthenia gravis Hypocalcemia Severe renal failure Cardiac ischemia Heart block Myocarditis
33
Mag therapeutic/toxic levels
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
34
Magnesium dosing
4g bolus over 20-30 minutes 1-2g/hr
35
IM dosing of magnesium
10g loading (5mg each buttock) then 5g every 4 hours
36
Mg dosing in renal dysfunction
Cr 1-1.5, oliguria (<30mL/hr x4 hrs) = normal load, followed by 1g/hr Cr >1.5 =
37
When to check mag levels
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
Treatment of Mg toxicity
Calcium gluconate 10% solution -- 10mL IV over 3 minutes Consider Lasix
39
Why treat severe HTN
to prevent ischemic/hemorrhagic stroke, renal injury/failure, myocardial ischemia, CHF
40
When to treat HTN
Severe BP sustained for 15 minutes or more Treat within 30-60 minutes
41
Labetalol max dose for PO regimen
2400mg/day
42
Labetalol max dose for acute IV regimen
300mg
43
Practice Labetalol/Nifedipine/Hydralazine acute treatment algorithms
44
Likelihood of CD in preterm preeclampsia
<28 weeks 97% 28-32 weeks 65%
45
Risks of general versus regional anesthesia
general = aspiration, failed intubation, stroke secondary to increased systemic and intracranial pressure during intubation/extubation
46
Effect of Mg on anesthesia
Prolongs duration of nondepolarizing muscle relaxants
47
Why no stop Mg for cesarean
1/2 life is 5hrs, so cessation only minimally reduces Mg concentration at time of delivery while possibly increased seizure risk
48
Steps to take during eclampsia
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
Treatment of recurrent eclamptic seizure
an additional 2-4 g of mag administered over 5 minutes
50
Treatment of refractory eclampsia (seizing 20 mins after bolus, more than 2 recurrences)
Amobarbital - 250mg IV in 3 minutes Phenytoin - 1250mg IV at rate of 50mg/minute Intubation, ICU admission, head imaging
51
HELLP labs that suggest increased mortality risk
LFT's > 2000 LDH > 3000
52
In HELLP the lowest observed platelet counts tend to be seen
23hours after delivery
53
What is the underlying pathophysiology of cardiovascular changes in pree
vasoconstriction -- imbalance between normal vasodilatory and vasoconstrictive substances hemoconcentration - due to intravascular volume depletion
54
Cause of thrombocytopenia in pree
microangiopathic hemolysis possibly
55
Profound renal insufficiency in pree can lead to what renal condition
acute tubular necrosis
56
Differential diagnosis in HELLP
TTP/HUS AFLP Lupus APLS
57
Labs to differentiate between HELLP, HUS/TTP, AFLP
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
ATN postpartum....signs/sx
Worsening renal dysfunction, not associated with a aHUS picture (hemolysis, thrombocytopenia)
59
Risk of recurrent eclamptic seizure while on magnesium
10%
60
When is head imaging indicated in cases of eclampsia
Recurrent or refractory seizures Focal neurological signs are persistent Coma Uncertain diagnosis
61
Why is the IM route for magnesium not preferred
Painful Gluteal abscess
62
Monitoring for magnesium toxicity is achieved how
DTR's Respiratory status Mental status Urine output
63
How does Ca gluconate work as an antidote for Mg toxicity
Calcium competitively inhibits magnesium at the neuromuscular junction
64
At what BP is hypertensive encephalopathy generally achieved
>220/120 However, women with typical normotensive values may develop at lower threshold as compared to someone with history of cHTN
65
Other systemic signs of HTN enecphalopathy
Retinal ischemia - vision changes Cardiac ischemia - MI or angina Renal ischemia - ATN or renal dysf
66
Drug of choice in hypertensive crisis
sodium nitroprusside alternatives - nitroglycerin, nifedipine, nicardipine, hydralazine
67
Aim of initial therpay for htn emergency
Reduce MAP by 25% in first hour, goal 155-160/100-110
68
Why is BP lowering done slower in htn emergency
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
MOA of sodium nitroprusside
Interferes with calcium influx and activation of intracellular calcium -- leads to arterial and venous relaxation
70
How is sodium nitroprusside administered
IV infusion short half life -- works quickly, stops working quickly when IV stopped (3-5 mins)
71
Risks of nitroprusside
Hypotension - quickly reversed with cessation Thiocyanate metabolite excreted in urine -- can accumulate if renal or liver dysfunction, large doses, prolonged administration (48 hrs)
72
Cyanide toxicity symptoms
Anorexia Disorientation Headache Fatigue Restless Tinnitus Delirium/hallucinations Nausea/vomiting Metabolic acidosis
73
Treatment if cyanide toxicity
sodium nitrite sodium thiosulfate
74
Nitroglycerin use with hypertensive encephalopathy?
contraindicated, it increased cerebral blood flow and intracranial pressure
75
MOA of magnesium
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
Adverse effects of Mg MOA
Also decrease smooth muscle contractibility of uterus and heart respiratory depression
77
Why not do intermittent bolus of Mg?
Leads to transient elevations in Mg level
78
Agents that can be used to terminate a seizure if already on magnesium
Valium - 5 or 10mg Lorazepam - 4mg General anesthesia
79
Hydralazine MOA
Dilation of arterioles
80
Labetalol MOA
alpha and beta-adrenergic blockade
81
Nifedipine MOA
Calcium channel blocker
82
Hydralazine effect on heart and uterus
Vasodilation leads to increased CO and increased uterine perfusion
83
Side effects of hydralazine
Headache and epigastric pain
84
CHAP trial demonstrates what findings for treatment of cHTN
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

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