CARDIOVASCULAR DISEASE IN PREGNANCY
• CVD = leading cause of death in women in US. 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 0.2–4% of pregnancies (in western countries).
Maternal Cardiac Risk Estimation
• Prepregnancy counseling: Risk of Preg depends on specific heart dz & current clinical status. Risk assessment should be performed prior to Preg, including medication review.
• Mat risk assessment: WHO risk classification integrates all known mat CV risk factors
Cardiovascular Changes in Pregnancy
• 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
• 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)
• 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%)
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
• 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
• 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 emergency: Elevated BP w/ target organ damage
• Hypertensive urgency: SBP > 210 or DBP > 120 w/ minimal or no target organ damage
• Hypertensive emergency: ↓ MAP by 25% in minutes to 2 h using IV agents
• Hypertensive urgency: ↓ BP in hours using oral agents
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
• 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)
• ≠ 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
• 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
Figure 12.1 Algorithm for management of sPEC <34 weeks
• 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
• Continue to monit BPs closely. 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 Gynecol2005;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 vs. 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
CORONARY ARTERY DISEASE/ACUTE CORONARY SYNDROME
Definition and Epidemiology (Circulation 2012;125:188; Clin Cardiol 2012;35(3):141)
• CAD → MI, angina pectoris (AP), or both
• ACS: Atherosclerosis → plaque rupture → thrombosis → acute myocardial ischemia. Other causes of ischemia: Coronary artery spasm, embolism, aortic dissection, vasculitis, myocarditis.
• Risk factors: Age, smoking, HTN, hyperlipidemia, DM, FHx
• Prevalence: CAD: 8.3%, 6.1%. MI 4.3%, 2.2%. AP: 3.8%, 4%
• 1 of 6 deaths in US in 2008 due to CAD; ↑ mortality in women <55 yo
Presentation and Physical Exam
• Angina + dyspnea, diaphoresis, N/V, palps, lightheadedness
• Women often present w/ nonclassic sx (eg, GI distress)
• Signs of ischemia or heart failure: S3, S4, new murmur, ↑ JVP, crackles
• ECG: ST segment deviation or T wave inversion
• Cardiac enzymes: Troponin = most sensitive & specific. Detectable 4–6 h after injury, peaks 24 h after injury, ↑ up to 10 d. CK-MB = less sensitive/specific.
• NSTEMI: Meds – Anti-ischemic (nitrates, β-blockers, CCBs) & antithrombotic (ASA, clopidogrel, heparin, LMWH, GPIIb/IIIa inhibitors); angiography generally only w/ recurrent ischemia
• STEMI: Primary PCI by 90 min; antifibrinolytics if no PCI; meds same as NSTEMI
Pregnancy Considerations (Eur Heart J 2011;32:3147)
• Risk of MI 3–4× higher compared to nonpregnant women. ACS: 3–6/100000 deliveries → mortality 5–10%. All stages of gest, but more common in 3rd trimester. Most commonly involves anter wall.
• Preg can be considered if CAD & no residual ischemia or LV dysfxn
• Rx: PCI for STEMI. AVOID ACEI & ARB. Clopidogrel or GPIIb/IIIa no data.
• Intrapartum mgmt: SVD generally preferred. AVOID methergine for postpartum hemorrhage: May induce coronary artery vasospasm.
Definition and Epidemiology
• Mean PA pres > 25 mmHg at rest or >30 mmHg w/ exertion
• Idiopathic pHTN: 1–2 per million. Mean age of onset: 36 (men older than women). Female:male 1.7–3.5:1.
Etiology (JACC 2003;43:5S)
• Pulmonary arterial HTN: Idiopathic, familial, or related to risk factors or assoc conditions (collagen vascular dz, portal HTN, HIV, congen systemic-to-pulm shunts → Eisenmenger syn). A/w left heart dz, lung dz, hypoxemia, chronic thrombotic/embolic dz, sarcoidosis, histiocytosis X, lymphangiomatosis, pulm vessel compression, drugs (cocaine, appetite suppressants).
• Dyspnea, syncope or chest pain on exertion, sx of right-sided heart failure
• Prominent P2, right-sided S4, RV heave, PA flow murmur, PR, TR
• Signs of RV failure: JVD, periph edema, ascites, hepatomegaly
• Definitive dx w/ cardiac cath: ↑ RA, RV, & PA pres, ↑ PVR, ↓ CO, nml PCWP
• W/u: CXR, ECG, PFTs, ABG, echocardiogram
• Oxygen, diuretics, dig, anticoagulation
• Vasodilators: CCB, prostacyclin, prostacyclin analogues, endothelin-1 receptor antag
• Lung xplant if refrac
• Preconception counseling: Women w/ pHTN should be discouraged from Preg; if Preg occurs, termination should be offered
• Antepartum mgmt often requires hospitalization
• L&D: RV filling is important; modest elevations in CVP → increasing RV dysfxn & rapid deterioration
• Nonpregnant: 2.5-y median survival if untreated; if respond to nifedipine: 95% 5-y survival; nifedipine nonresponder (requiring prostacyclin): 54% 5-y survival; lung xplant: 45–55% 5-y survival
• Pregnant pop: 17–33% mortality w/ sev pHTN & Eisenmenger syn (Eur Heart J 2009;30:256); mod pHTN (PAP <40 mmHg) up to 30% develop cardiac failure or die w/i 3 mo postpartum (Eur Heart J2009;30:256); death occurs in last trimester & in 1st months after deliv from hypertensive crisis, pulm thrombosis, refrac right heart failure. 75% mortality occurs postpartum.
VALVULAR HEART DISEASE
Clinical Manifestations and Diagnostic Studies
• Dyspnea, pulm edema, Afib
• ECG, CXR, echocardiogram, cardiac cath
Pregnancy Considerations/Prognosis (Eur Heart J 2011;32:3147)
• MS: Decompensation depends on severity, heart failure ↑ w/ mod or sev MS. Mortality: 0–3%. W/ mod or sev MS, counsel against Preg. Offer termination in early Preg. Avoid signif tachy.
• AS: Morbidity related to severity, heart failure in 10% & arrhythmias in 3–25% of women w/ sev AS, mortality low. Get preconception exercise testing. Peak gradient < 60 mmHg → typically Uncomp prenatal courses.
• Mitral regurg or aortic regurg: Prepregnancy eval for sx, echo, LV dimension & fxn; exercise testing for mod to sev; preconception Surg for sev regurg, sx, or LV dysfxn due to ↑ heart failure risk
Labor and Delivery Considerations
• Pain → tachy that can exacerb valvular pathology
• Contractions → ↑ venous return therefore pulm congestion
• Abrupt elevation of PAPs in the immediate postpartum period from autotransfusion
• Cesarean deliv for obstetric indications only
Endocarditis Prophylaxis (Circulation 2007;116:1736)
• Cardiac conditions a/w infxn that warrant abx ppx: Prosthetic cardiac valve; prev infective endocarditis; CHD; unrepaired cyanotic CHD; completely repaired CHD w/ prosthetic material during 1st 6 mo after procedure; repaired CHD w/ residual defect at adj to the site of a prosthetic patch or device
Types of prosthetic valves (Obstet Gynecol 1994;83:353)
• Mechanical: Durable but require anticoagulation; ↑ miscarriage & thromboembolic events
• Bioprosthetic: Less durable, but do not require anticoagulation; Preg seems to adversely impact life of a porcine valve
Definition and Epidemiology
• Heart failure w/i the last month of Preg to 5 mo postpartum
• Diagnostic criteria based on risk for idiopathic DCM (Obstet Gynecol 1999;94:311): Absence of prior heart dz; no alternative cause; echocardiographic evid of LV dysfxn (EF <45% or fractional shortening <30%, LVED dimension > 2.7m2)
• Incid 1 in 3000–4000 live-births (JAMA 2000;283:1183); ↑ risk w/ multiparity & age
• Cause unk; dev of pulm edema 2/2 LV dilation & dysfxn
Clinical Manifestations and Diagnostic Studies
• S/sx of pulm edema: Dyspnea, cough, orthopnea, tachy, hemoptysis, elevated JVP, S3 present
• CXR: Cardiomegaly, pulm edema, pleural effusions
• ECG: Look for Afib, bundle branch block
• Echocardiogram: LV dilation, ↓ EF, regional or global LV HK, poss RV HK, poss mural thrombi
• β-blockers improve cardiac fxn & survival in stable, euvolemic pts
• OK to use implantable defibrillators in Preg (Circulation 1997;96:2808)
Labor and Delivery Management
• Pain control w/ epidural: ↓ cardiac work & ↓ tachy
• Cesarean for obstetric indications only
• Peripartum: Mortality 6–10%; cardiac xplantation 4–7% (Circulation 2005;111(16):2050; N Engl J Med 2000;342(15):1077); w/i 6 mo, ½ of pts demonstrate resolution of LV dilation → good prog, the other ½ → 85% 5-y mortality
• Subseq Preg: Recurrence up to 50% (Circulation 1995;92 (Suppl 1):1; N Engl J Med 2001;344(21):1567; Ann Intern Med 2006;145(1):30)
>8% mortality if LV dysfxn has not resolved → discourage Preg; <2% mortality if LV dysfxn has resolved