AND CARDIOVASCULAR DISEASE



Cardiovascular Changes in Pregnancy


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 liver.


• ↑ 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% ↑ CO. 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



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 edema. 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 Preg. 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.


CHRONIC HYPERTENSION (CHTN)


Definitions


CHTN in Preg: Use of antihypertensive medication prior to Preg, OR onset of HTN before Preg, prior to 20 w gest, or that persists beyond 12 w postpartum


Epidemiology and Etiology


Nonpregnant: 10–15% Caucasian adults, 25% AA adults


Pregnant: Occurs in up to 5% of pregnant women. Hypertensive disorders overall represent the most common medical complications of Preg (incid 6–8%)


• Essent (95%)


Secondary:


Renal (4%): Renal artery stenosis, parenchymal


Endocrine (0.5%): Pheo, primary hyperaldo, Cushing’s


Coarct of the aorta (0.2%)


Other: Collagen vascular dz, sleep apnea





Workup


H&P: Including fundoscopic, cardiac, abdominal, vascular, & neurologic exams


Studies: Electrolytes, BUN/Cr, gluc, Hgb/Hct, UA, lipids, ECG


W/u for secondary causes: Age <20 or >50, sudden onset, sev, refrac


Additional w/u for Preg: Baseline HELLP labs including Hgb, Plt, Cr, AST/ALT, uric acid, 24-h urine prot


Complications


Nonpregnant: Mostly long term, including TIA/CVA, CAD, CHF, CKI


↑ of 20 mmHg SBP or 10 mmHg DBP doubles CV complications (Lancet 2002;360:1903)


Pregnant: Additional mat risks: Pulm edema, hypertensive encephalopathy, retinopathy, cerebral hemorrhage, acute renal failure


Additional fetal risks: Perinatal mortality ↑ 3–4×


Rx goal: <140/90 mmHg (<130/80 mmHg w/ DM or renal dz) (NEJM 2003;348:610)



Additional Management in Pregnancy (Obstet Gynecol 2002;100:369)


• Lifestyle modifications preconception (each ↓ SBP by 5 mmHg)


Weight loss, diet (low saturated & total fat, low sodium), exercise, ↓ EtOH


Low risk: No antihypertensive drugs. US at 16–20 w, rpt at 28–30 w then monthly for growth assessment till term. Deliver at 38–39 w.


High risk: Antihypertensive meds to keep BP <140/90 mmHg. US at 16–20 w, rpt at 28 w, then every 3–4 w until deliv. Serial fetal testing (NST, AFI) beginning at 28–32 w. Deliver at 39 w if BP controlled & no fetal growth restriction, otherwise deliver at 37–38 w.


HYPERTENSIVE CRISIS


Definition


Hypertensive emergency: Elevated BP w/ target organ damage


Hypertensive urgency: SBP > 210 or DBP > 120 w/ minimal or no target organ damage


Treatment


Hypertensive emergency: ↓ MAP by 25% in minutes to 2 h using IV agents


Hypertensive urgency: ↓ BP in hours using oral agents



PREGNANCY-RELATED HYPERTENSION


Definitions (And see chapter 11; For up to date details, Hypertension in Pregnancy, ACOG Task Force, 203)



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



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 mod- to 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 prot. Rpt if ↑ clinical concern.


• Fetal eval: NST/AFI, growth US


Management/Treatment




Figure 12.1 Algorithm for management of sPEC <34 weeks


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Jul 2, 2016 | Posted by in OBSTETRICS | Comments Off on AND CARDIOVASCULAR DISEASE

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