Pocket ObGyn – Cardiovascular Changes and Disease in Pregnancy / Pregnancy-Related Hypertension

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Pocket ObGyn – Cardiovascular Changes and Disease in Pregnancy /  Pregnancy-Related Hypertension 
See Abbreviations

Epidemiology
  • CVD = leading cause of death in women in More women than men die from CVD annually (Circulation 2011;123:e18)
  • ­ incid of CVD in Preg due to ­ age at 1st Preg & ­ prevalence of risk factors (DM, HTN, obesity) (Eur Heart J 2011;32:3147)
  • Hypertensive disorders occur in 6–8% of pregnancies. Other CVD complicates 2–4% of pregnancies (in western countries).
Maternal Cardiac Risk Estimation
  • Prepregnancy counseling: Risk of Preg depends on specific heart dz & current clinical Risk assessment should be performed prior to Preg, including medication review.
  • Mat risk assessment: WHO risk classification integrates all known mat CV risk factors

 

WHO maternal cardiac risk classification
WHO class Definition & mgmt Example
1 Low risk, limited cardiology followup in Preg MV prolapse, isolated ectopic atrial or ventricular beats
2 Low or mod risk, cardiology follow-up every trimester Most arrhythmias, repaired tetralogy of Fallot, unrepaired ASD/VSD
3 High risk, frequent cardiology follow-up Mechanical valve, cyanotic heart dz
4 Very high risk, Preg “contraindicated.” Recommend termination of Preg, otherwise frequent cardiology follow-up. Pulm arterial HTN, sev ventricular dysfxn (NYHA III–IV), sev MS or AS, prev peripartum cardiomyopathy w/ residual impairment
From Thorne S, MacGregor A, Nelson-Piercy C. Risks of contraception and pregnancy in heart disease. Heart.

2006;92(10):1520–1525.

 

Cardiac disease in pregnancy score (CARPREG)
1 point earned for each of the following:
NYHA functional class >II or cyanosis
Left heart obst w/ MV area <2 cm2, AVA <1.5 cm2, or L ventricular outflow tract gradient

>30 mmHg
LVEF <40%
H/o prior cardiac event or arrhythmia
Risk of cardiac complication (eg, pulm edema, tachy/bradyarrhythmia req rx, MI, stroke, cardiac death): 0 points = 5%; 1 point = 27%; >1 point = 75%
From Siu SC, Sermer M, Colman JM, et al. Prospective multicenter study of pregnancy outcomes in women with heart disease. Circulation. 2001;104(5):515–521.
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Cardiovascular Changes

Blood Volume
  • Plasma vol ­ 45% from 6–32 w gest to 4700–5200 mL
  • RBC mass ­ by 20–30% (from ­ production of RBCs)
  • Plasma vol ­ more than RBC vol, causing physiologic hemodilution ® anemia

­ erythrocyte 2,3-diphosphoglycerate conc, ¯ affinity of mat Hgb for O2 ®

facilitates dissociation of oxygen from Hgb ® preferential xfer of O2 to fetus

Hemodynamic Profile
  • CO ­ 30–50% during Preg (50% of that during 1st 8 w)

Turning from supine to left lateral recumbent position ® release of vena caval compression by gravid uterus can ­ CO by 25–30%

  • Uterine bld flow ­ 10-fold to 500–800 mL/min (17% of total CO at term)
  • Renal bld flow ­ by 50%. No change in perfusion to brain or

 

  • ­ HR at 5 w ® max ­ 15–20 beats/min by 32 w to term (Am J Physiol 1989;256:H1060)
  • ¯ BP from 7 w to nadir 5–10 mmHg systolic & 10–15 mmHg diastolic by 24–32 w, then ­ toward nonpregnant values at term (Am J Med 1980;68:97)

Heart Sounds (Am Heart J 1966;71:741)

  • Benign systolic flow murmur develops in more than 95% of pregnant women: ­ CO ®

turbulent flow over pulmonic or aortic valve

Audible 1st btw 12 & 20 w w/ regression usually by 1 w postpartum

Intrapartum Hemodynamic Changes
  • 1st stage labor: 12–31% ­ 2nd stage: 49% ­ CO. »2-fold ­ from nonpregnant.
  • Contractions cause 300–500 mL xfer of bld from uterus to general circulation SBP & DBP ­ by 35 & 25 mmHg respectively

 

Maternal hemodynamic profiles in the 3rd trimester
  Nonpregnant Pregnant Change
CO (L/min) 4.3 ± 0.9 6.2 ± 1 +43%
HR (beats/min) 71 ± 10 83 ± 10 +17%
SVR (dyne-sec cm−5) 1530 ± 520 1210 ± 266 -21%
PVR (dyne-sec cm−5) 119 ± 47 78 ± 22 -34%
CVP (mmHg) 3.7 ± 2.6 3.6 ± 2.5 —
COP (mmHg) 20.8 ± 1 18 ± 1.5 -14%
PCWP (mmHg) 6.3 ± 2.1 7.5 ± 1.8 —
COP–PCWP (mmHg)* 14.5 ± 2.5 10.5 ± 2.7 -28%
*Important factor in dev of pulm edema throughout Preg.

From Clark SL, Cotton DB, Lee W, et al. Central hemodynamic assessment of normal term pregnancy. Am J Obstet Gynecol. 1989;161:1439.
Postpartum Hemodynamic Changes
  • 60–80% ≠ CO w/i 10–15 min of vaginal deliv: Release of venocaval obst, autotransfusion of uteroplacental bld, rapid mobilization of extravascular fluid ® watch for pulm CO returns to prelabor value by 1-h postpartum.
  • Important to monit women w/ CVD closely until at least 24 h after deliv
  • CV measurements (SV, SVR, CO) take up to 24 w to return to prepregnancy values
ECG Changes in Pregnancy
  • Majority of pregnant pts have a nml ECG (Eur Heart J 2011;32:3147)
  • Change in heart position (rotated to left) ® 15–20º L axis deviation; mimics LV hypertrophy
  • Common ECG changes: Transient ST segment & T wave changes; Q wave & inv T wave in lead III; attenuated Q wave in lead AVF; inv T wave in leads V1, V2, & occ V3
  • Premature beats & sustained tachyarrhythmia ­ in Ventricular & atrial ectopy in

up to 50–60% of pregnant women. Symptomatic exacerbation of paroxysmal SVT in Preg in 20–44% of cases. 15% of pregnant women w/ CHD develop arrhythmia. Most palps are benign, but warrant a Holter monit. Limited data on antiarrhythmic meds: Weigh mat risk against potential fetal teratogenicity.

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Pregnancy-Related Hypertension

Definitions (And see chapter 11; For up to date details, Hypertension in Pregnancy, ACOG Task Force, 2013)

 

Gestational hypertensive disorders
Dz BP Proteinuria* Notes
gHTN SBP ³ 140 or DBP ³

90

Sev: SBP ³ 160 or DBP

³ 110

On 2 occasions at least 4 h apart & no more than 7 d apart

 <300 mg prot in 24-h urine 1st diagnosed beyond 20 w gest
Mild

(nonsevere) PEC

 SBP ³ 140 or DBP ³

90

On 2 occasions at least 4 h apart & no more than 7 d apart

 ³300 mg prot in 24-h urine

OR

At least 1+ on 2 random urine samples collected at least 6 h apart & no more than 7 d apart

 1st diagnosed beyond 20 w gest

gHTN plus proteinuria

*Newest guideline does NOT use proteinuria to r/o PEC
sPEC SBP ³ 160 or DBP ³

110

On 2 occasions at least 4 h apart while the pt is on bed rest. BP should be measured seated upright.

 Not used.

Evaluate for Severe Features such as: thrombocytopenia (<100,000/uL) or serum Cr >1.1 mg/ dL or elevated LFTs (2´ upper limit normal) or pulmonary edema or cerebral/visual symptoms

 Criteria for nonsevere PEC plus: Sev-range BP or proteinuria or 1 of the following:

Oliguria: <500 mL in 24 h Cerebral or visual

disturbances Pulm edema or

cyanosis

Epigastric or RUQ pain Impaired liver fxn: AST >

2´ nml Thrombocytopenia: Plt < 100000/mm3

New guidlines do not use fetal growth as dx criterion

Epidemiology (Obstet Gynecol 2003;102:181)

  • Risk factors for Preg-related HTN: Nulliparity, multifetal gest, obesity, AMA, prior PEC, CHTN, renal dz, DM, vascular & CTD, antiphospholipid Ab syn, AA race
  • gHTN: 6–17% in nulliparous & 2–4% multiparous women
  • PEC: 4–8% of all pregnancies; up to 18% in women w/ a h/o PEC
  • Eclampsia: 1 in 2000–3448 pregnancies

 

Other disorders associated with HTN in pregnancy
Dz Definition
Superimposed PEC CHTN + PEC: New onset proteinuria (³300 mg 24-h urine) in a woman w/ CHTN but no proteinuria prior to 20 w gest OR sudden ­ in proteinuria, BP, or evid of multiorgan system involvement in a woman w/ known HTN & proteinuria prior to 20 w gest
Eclampsia Seizures not attributed to another cause in a woman w/ PEC
HELLP Hemolysis, Elevated Liver enzymes, Low Platelets (sev PEC variant)
AFLP Acute Fatty Liver of Pregnancy.Very elevated LFTs, low gluc.

 

Etiology/Pathophysiology
  • Poorly understood. Potential causes:Abn trophoblast invasion of uterine bld vessels, immunologic intolerance btw fetoplacental & mat tissues, maladaptation to the CV/ inflamm changes of Preg, dietary deficiencies, genetic abnormalities (Obstet Gynecol 2003;102:181)
Prevention
  • ≠ risk: H/o PEC, other hypertensive d/o, DM, abn uterine artery dopplers, nulliparity, multi gest ® therefore, reduce risk factors early
  • Low-dose ASA in modto high-risk pts (Obstet Gynecol 2010;116:402)

Prior PEC: Start ASA by 16 w: RR 0.47 (95% CI 0.34–0.65); NNT 9

Prior sPEC: Start ASA by 16 w: RR 0.09 (95% CI 0.02–0.37); NNT 7

Starting after 16 w ® no benefit. Stop ASA ~1 w prior to deliv.

Clinical Manifestations of PEC
  • Cerebral: HA, dizziness, tinnitus
  • Visual: Diplopia, scotomata, blurred-vision, amaurosis
  • GI: Nausea, vomiting, epigastric/RUQ pain, hematemesis
  • Renal: Oliguria, anuria, hematuria
Initial Workup
  • Collect baseline bld work at 1st prenatal visit or at time of dz presentation Hgb, Plt, Cr, AST/ALT, uric acid, 24-h urine Rpt if ­ clinical concern.
  • Fetal eval: NST/AFI, growth US
Management/Treatment

 

Management & treatment of PEC
  Mat surveillance Fetal surveillance Deliv
gHTN No hospitalization or bedrest

Monit for sev gHTN or PEC

 Daily kick counts Serial NST/AFI or BPP

(1–2´/w)

Serial fetal growth US (q4w)

 37–38 w gest

Sev gHTN managed as sPEC
Nonsevere PEC Hospitalization per provider

No bedrest Monit for sPEC

Evaluate for organ dysfxn

Weekly labs

 Daily kick counts Serial NST/AFI or BPP

(1–2´/w)

Serial fetal growth US (q3–4w)

 37–38 w gest
Sev PEC

(expectant mgmt)

OR

Superimposed PEC w sev features

 Evaluate organ dysfxn Serial labs (q6h ® daily

if stable) MgSO4 sz ppx

Antihypertensive meds

for BPs

 Daily fetal assessment Serial NST/AFI (2´/w) Serial fetal growth US (q3w)

Betamethasone for fetal lung maturity <34 w gest

 Expectant mgmt if

<32 w gest & nml labs/growth/ assessment

Deliv by 34 w
Eclampsia Stabilize mother Rx:

IM: “Give 2 high fives”

– 5 mg MgSO4 IM

to each buttock IV: MgSO4 4–6 g

loading dose ®

2 g/h

 Fetal brady frequently occurs during eclamptic sz ® managed by mat resusc

Continuous monitoring

 Deliv “in timely fashion”

Method dependent on gestational age, presentation, cervical dilation, & mat stability

Cesarean NOT always indicated
HELLP/AFLP Stabilize mother MgSO4 for sz ppx Supportive therapy

postpartum

 Continuous monitoring  
NOT ELIGIBLE for expectant mgmt: Imminent eclampsia (persistent sev sx), suspected placental abruption, nonreassuring fetal testing, HELLP or AFLP, abn mat labs or end-organ damage.

From Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia. Obstet Gynecol.

2003;102(1):181–192.

 

Figure 12.1 Algorithm for management of sPEC <34 weeks

(From Sibai BM. Evaluation and management of severe preeclampsia before 34 weeks’ gestation. Am J Obstet Gynecol.

2011;205(3):191–198)

 

Intrapartum Management
  • sPEC/Eclampsia is not an indication for cesarean deliv; IOL by obstetric indications
  • Mat precautions: Frequent BP monitoring, sz precautions
  • Fetal precautions: Continuous fetal monitoring
  • MgSO4 to prevent sz (Clin Obstet Gynecol 2005;48:478)

MgSO4 superior to other antiepileptics (diazepam, phenytoin, or lytic cocktail) in PEC. Lower rate of recurrent seizures (RR = 0.41 [95% CI, 0.32–0.51]). Lower rate of mat death (RR = 0.62 [95% CI, 0.39–0.99]). Use intrapartum & 12–24 h postpartum. NNT for sPEC: 71; NNT for nonsevere PEC: 400.

Magnesium tox: Monit closely throughout rx. Lower dose (eg, 1 g/h) if mat renal impairment. Therapeutic level: 4–6 mEq/L. Loss of patellar reflexes: 8–10 mEq/L. Respiratory depression: 12 mEq/L. Mental status changes: >12 mEq/L. Cardiac arrest: >24 mEq/L.

Rx of magnesium tox: D/c magnesium, obtain serum level, give calcium gluconate:

1 g IV over 5 min, supportive therapy & close monitoring

 

Dosing magnesium sulfate
IM Loading dose 5 g IM each buttock
  Maint dose 5 mg IM q4h
IV Loading dose 4–6 g IV over 10–20 min
  Maint dose 1–2 g/h IV
Postpartum Management
  • Continue to monit BPs BP decreases w/i 48 h, but may ­ 3–6 d postpartum. Monitor 72 h postpartum in hospital, then check at home daily, and 1 w postpartum BP check in clinic.

 

  • If magnesium initiated intrapartum, continue until 12–24 h postpartum or until adequate diuresis has been documented (fluid balance net negative). Consider furosemide diuresis daily ´ 5 d (Obstet Gynecol 2005;105(1):29).
  • Follow labs daily until clinically stable & trending toward nml
  • Postpartum HTN (Am J Obstet Gynecol 2012;206(6):470): Persistence of gHTN, PEC, CHTN de novo dev. Treat w/ magnesium sulfate ´ 24 h or until clinical improv w/ PEC. Prevalence: 0.3–27.5%.

Ddx for postpartum HTN includes PEC spectrum, pre-existing or undiagnosed HTN, hyperthyroidism, primary hyperaldo, pheo, renal artery stenosis, cerebral vasoconstriction syn, cerebral venous thrombosis/stroke, thrombotic thrombocytopenic purpura/hemolytic uremic syn

Management of Maternal Complications/Sequelae
  • Convulsions: See Eclampsia in Chap. 18
  • Pulm edema: Diurese w/ furosemide (10–40 mg IV) ® monit urine output, intubation if necessary
  • Acute renal or liver failure, liver hemorrhage, DIC, stroke: Supportive therapy ® consider xfer to ICU
Complications/Sequelae

 

Progression to preeclampsia with mild gHTN
Weeks’ gest % who developed PEC
34–35 37.3
32–33 49.3
30–31 50
<30 52.1
From Barton JR, O’brien JM, Bergauer NK, et al. Mild gestational hypertension remote from term: Progression and outcome. Am J Obstet Gynecol. 2001;184(5):979–983.

 

Pregnancy outcomes in women with PEC
Outcome Nonseverea Sevb (%)
Preterm deliv 14–25.8% 33–66.7
SGA infant 4.8–10.2% 11.4–18.5
Placental abruption 0–3.2% 1.4–6.7
Perinatal death 0–1% 1.4–8.9
Mat mortality Rare 0.2
Mat morbidityc Rare 5
aRates similar to normotensive & gHTN pregnancies.

bRates similar to sev gHTN.

cConvulsions, pulm edema, acute renal or liver failure, liver hemorrhage, DIC, stroke.

From Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia. Obstet Gynecol.

2003;102(1):181–192.
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See Abbreviations

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