Change
Clinical Implication
Core temperature
Unchanged
Fever should be investigated and treated; maternal fever is teratogenic in T1, and associated with adverse perinatal outcomes in T3
Upper airway
↑ edema and friability (hyperemia and glandular function)
Nasal congestion, epistaxis and snoring common.
Failed/difficult intubation more common than non-pregnant state
Thorax
↑ circumference, elevated diaphragm (~4 cm) but normal excursion
Anatomical landmarks for thoracentesis shifted.
ECG changes: QRS axis deviates to left in late pregnancy ± T-wave inversion ± ST depression in inferior and lateral leads
Tidal volume
↑ early in T1 at expense of FRC/RV
Expected PaO2 100–110 mmHg, PaCO2 28–32 mmHg (mild respiratory alkalosis), HCO3 18–21 mmol/L (compensatory reduction), arterial pH 7.40–7.45 (normal/slight alkalosis). An elevated RR should be investigated
Respiratory rate
Minimal increase by ~3–4 breaths/min at term
Minute ventilation
(RR × TV)
↑ by 50% at term
Oxygen consumption
↑ by 15–20%
Heart rate
↑ by 15–20 beats/min by T3
Pregnancy may unmask heart disease, especially obstructive lesions. Exacerbation of pre-existing tachyarrhythmias or de novo presentations also possible. Compression of IVC by gravid uterus in supine position may ↓ cardiac output by up to 25% left lateral decubitus position recommended
Greatest risk of cardiac decompensation between 28 and 32 weeks gestation (maximum increase in maternal blood volume), during labor (hemodynamic changes), and in post-partum period (fluid shifts)
Stroke volume
↑
Cardiac output
(HR × SV)
↑ by 30–50% (peaks ~28 weeks)
Ejection fraction
Unchanged
Systemic vascular resistance
↓
Blood pressure
↓ by 10–15 mmHg (nadir at ~20–24 weeks) with gradual increase back to baseline
↓↓ DBP > ↓ SBP → widened pulse pressure
Renin-angiotensin-aldosterone system
Upregulated
↑↑ renin, ↑ aldosterone, ↓ aldosterone/renin ratio in response to systemic vasodilation and ↓ SVR
Renal blood flow
↑ by 80%
Glomerular filtration rate
↑ by 40–50%
Hyperfiltration with ↓ in serum Cr to ~35–70 mmol/L [0.4–0.8 mg/dL]; higher levels suggest renal disease. Dose adjustments for renally-cleared drugs may be required
Plasma volume
↑ by 30–50% (1.1–1.6 L) by T3
JVP height remains normal
RBC mass
↑ by 40%
Iron requirements ↑ by 50%. Disproportionate ↑ in plasma volume results in physiologic anemia (hemoglobin ↓ by ~20 g/L [2 g/dL] by T3)
Coagulation system
↑ levels of coagulation factors, decreased fibrinolysis
10× ↑ risk for venous thromboembolism during pregnancy and up to 6 weeks postpartum
Gastric pH
↑
Impaired drug absorption, dose adjustments may be required
Lower esophageal sphincter pressure
↓ (progesterone effect)
GERD, nausea and vomiting common. ↑ risk of aspiration with intubation
GI motility
↓
Constipation and abdominal bloating common. Impaired drug absorption, dose adjustments may be required
Hepatic metabolism
Changes in drug metabolism (e.g., cytochrome P450 system enzymes may be ↑ or ↓)
Dose adjustments may be required for hepatically-metabolized medications (e.g., antiepileptics)
Biliary system
↓ motility, ↑ bile cholesterol secretion and saturation
↑ risk for gallstones during pregnancy
Thyroid
↑ thyroid gland size by 18%. ↑ estrogen → ↑ thyroxine-binding globulin → total T4 and ↑ total T3 (but free T4 and free T3 mostly remain normal)
Thyroid function tests should be interpreted using trimester-specific TSH and total T4 reference ranges for pregnant women. For those already on levothyroxine replacement, ~75% of women will require an increased dose during pregnancy. Homology between hCG and TSH can result in hCG mediated hyperthyroidism during pregnancy
Glucose metabolism
↑ insulin resistance (peak ~30 weeks gestation) from human placental lactogen and progesterone
Screen for gestational diabetes by 24–28 weeks gestation
Maternal Mortality and Resuscitation
MATERNAL MORTALITY
—defined as death during pregnancy or up to 1 year postpartum. Most common causes include cardiovascular disease, venous thromboembolism, amniotic fluid embolus, obstetric hemorrhage, infection (sepsis), suicide, and preeclampsia/eclampsia
MATERNAL RESUSCITATION
—follow ACLS algorithm for non-pregnant adult population including medications, dosages (for medications, defibrillation, cardioversion, pacing), compressions, and ventilation rate. Special considerations include: (1) obtaining venous access above the diaphragm (potential obstruction from gravid uterus below diaphragm); (2) chest compressions performed higher up on sternum; (3) left uterine displacement (first-line) or left lateral tilt (second-line) to relieve aorto-caval compression by gravid uterus; (4) difficult airway and ventilation requires expertise; (5) perimortem caesarean section if no return of spontaneous circulation within 4 min; (6) remove fetal monitors for defibrillation if possible (theoretical risk to fetus). Do not delay treatment: healthy baby requires healthy mother!
Preeclampsia/Eclampsia/HELLP Syndrome
JOGC 2014 36:5
SOGC Hypertensive Disorders of Pregnancy 2014 Guidelines
Differential Diagnosis of Hypertension in Pregnancy
PREEXISTING (CHRONIC) HYPERTENSION
—SBP ≥140 and/or DBP ≥90 mmHg prior to 20th week of gestation, complicates 1% of pregnancies: 20% risk of developing preeclampsia
PREECLAMPSIA SUPERIMPOSED UPON PREEXISTING HYPERTENSION
—preexisting (chronic) hypertension with new or worsening proteinuria (≥300 mg/day with 24-h urine collection or ≥30 mg/mmol on spot urine protein/Cr ratio), or resistant hypertension (i.e., resistance to ≥3 antihypertensive drugs), or development of adverse condition (see list below), or development of severe complication (see list below) at ≥20 weeks gestation. Diagnosis of preeclampsia does not require presence of proteinuria
GESTATIONAL HYPERTENSION
—new-onset hypertension ≥20 weeks gestation, complicates 5–6% of pregnancies. 35% risk of developing preeclampsia
PREECLAMPSIA SUPERIMPOSED UPON GESTATIONAL HYPERTENSION
—new-onset proteinuria, or development of adverse condition (see list below), or development of severe complication (see list below) after onset of gestational hypertension
PREECLAMPSIA
—occurring de novo, defined as gestational hypertension, with either proteinuria, adverse condition, or severe complication
Pathophysiology
MECHANISMS
—multifactorial involving immunologic, genetic and maternal factors that lead to uteroplacental mismatch and endothelial cell dysfunction
ADVERSE CONDITIONS OF PREECLAMPSIA
—headaches/visual symptoms, chest pain/dyspnea, oxygen saturation <97%, nausea, vomiting, elevated liver enzymes or creatinine, thrombocytopenia, hyperuricemia, oligohydramnios, IUGR, abnormal uterine artery or umbilical cord Doppler flow. SBP ≥160 mmHg most important predictor of fatal stroke among women with hypertensive disorders in pregnancy
SEVERE COMPLICATIONS OF PREECLAMPSIA
—generalized tonic-clonic seizures (eclampsia), PRES (posterior reversible leukoencephalopathy syndrome), cortical blindness/retinal detachment, altered level of consciousness, stroke, pulmonary edema, acute kidney injury, hepatic dysfunction/hematoma/rupture, hemolysis, placental abruption, fetal demise. HELLP (Hemolysis, Elevated Liver Enzymes, Low Platelets) syndrome = constellation of findings considered variant of severe preeclampsia
RISK FACTORS
—extremes of age (<18, >40), nulliparity, multiple gestations, prior preeclampsia, obesity, chronic hypertension, diabetes mellitus, chronic kidney disease, antiphospholipid antibodies, and inter-pregnancy interval ≥10 years
CAUSES OF DEATH
—hemorrhagic stroke from uncontrolled hypertension and eclampsia
Clinical Features
HISTORY
—inquire about headaches, visual disturbances, epigastric or RUQ pain, nausea, vomiting, swelling, decreased fetal movements
PHYSICAL
—check vitals, look for retinal vasospasm, heart failure, edema (facial, limbs), RUQ tenderness, hyperreflexia and clonus
Investigations
BASIC
labs—CBCD, Cr, spot urine for protein to creatinine ratio, AST, ALT, albumin, uric acid (hyperuricemia associated with preeclampsia)
SPECIAL
blood tests—peripheral smear, lytes, urea, bilirubin, INR, LDH if indicated
fetal effects—biophysical profile and fetal US
Management
ACUTE
—ABC, O2 to keep sat >95%, IV with judicious fluid
ACUTE LOWERING OF SEVERE HYPERTENSION
(SBP ≥160 mmHg or DBP ≥110 mmHg)—labetalol (start with 20 mg IV, repeat 20–80 mg IV q10–30 min, or infusion 1–2 mg/min, max 300 mg), nifedipine short-acting capsule 5–10 mg PO q30min, or hydralazine (start with 5 mg IV, repeat 5–10 mg IV q20–30 min, max 20 mg). Severe cases may require continuous infusion. Consider urgent delivery if not controlled
CHRONIC MANAGEMENT OF NON-SEVERE HYPERTENSION
(SBP 140–159 mmHg or DBP 90–109 mmHg)—target BP at 130–140/80–90 mmHg if renal disease, diabetes, cardiovascular disease, or cerebrovascular disease. Otherwise target BP 130–155/80–105 mmHg; tighter control (DBP 85 mmHg [vs. 100 mmHg]) results in less severe hypertension without significant ↑ risk of adverse fetal outcomes. Labetalol 100–400 mg PO BID–TID, max 1200 mg/day, nifedipine XL 20–60 mg PO daily, max 120 mg/day, or methyldopa 250–500 mg PO BID–TID, max 3 g/day are good first-line choices. Avoid ACE inhibitors, ARBs, atenolol and prazosin. Second-line: other β-blockers and hydralazine. Third line: other CCBs, clonidine, and thiazide diuretics
SEIZURE PREVENTION AND TREATMENT
—MgSO 4 4 g IV bolus, then 1–2 g/h × 24–48 h. Re-bolus for ongoing seizures. Monitor for magnesium toxicity (respiratory depression, hypotension, muscle weakness, hyporeflexia) and give calcium gluconate if toxic. MgSO4 is contraindicated in myasthenia gravis (may precipitate myasthenic crisis). Benzodiazepines, phenytoin and phenobarbital can be considered as adjunctive therapy if ongoing seizures despite MgSO4
DELIVERY
—the cure for preeclampsia, eclampsia, and HELLP. Administer steroids to promote fetal lung maturation prior to 34 weeks if early delivery
POSTPARTUM
—gestational hypertension, preeclampsia/eclampsia/HELLP syndrome can present de novo or worsen in the postpartum period. Blood pressure can increase on days 3–6 postpartum. Monitor and continue antihypertensive therapy. Gestational hypertension/hypertension related to severe preeclampsia expected to resolve within 6–12 weeks. Metabolic abnormalities (e.g., proteinuria) that do not resolve by 3–6 months require further work-up
RECURRENCE
—preeclampsia recurrence rate 10–40%. Consider antiphospholipid syndrome screen if preeclampsia or placental insufficiency <34 weeks. ASA 81 mg PO daily before 16 weeks gestation during next pregnancy and supplemental calcium 1000 mg/day (in women with dietary calcium intake <600 mg/day) recommended for prevention
LONG-TERM
—history of hypertensive disorders in pregnancy increases risk for chronic hypertension, cardiovascular events, cerebrovascular accidents, renal disease, type 2 diabetes, and hypothyroidism. Lifestyle changes and routine vascular risk factor screening essential. Women with history of preeclampsia may experience post-traumatic stress disorder; monitor and provide mental health support
Related Topics
Hypertension (p. 65)
Proteinuria (p. 85)
Seizures (p. 350)
Pulmonary Diseases in Pregnancy
Asthma
TREATMENTS
—similar to non-pregnant patients. β-agonists, anticholinergics, and glucocorticoids (inhaled, systemic) are safe. Leukotriene antagonists if refractory. Keep O2 sat >95% to prevent fetal hypoxia. Consider stress dose steroids during delivery if patient required moderate systemic steroids for >3 weeks in the preceding year
Venous Thromboembolism
PATHOPHYSIOLOGY
—increased risk of DVT/PE due to ↑ factors I, VII, VIII, IX, X, von-Willebrand factor, and fibrin, ↓ protein S and fibrinolytic activity, and increased resistance to activated protein C, especially during T3. Also stasis due to ↓ venous tone and flow. Similar risk of DVT/PE in each trimester but highest post-partum; 90% of DVT in pregnancies are left sided and majority are pelvic
DIAGNOSIS
—if suspect venous thromboembolism, consider initiation of LMWH while waiting for investigations. For DVT workup, perform compression US; if pelvic vein DVT suspected, consider MRV pelvis, Doppler study, or (postpartum) CT of pelvic veins. Otherwise, repeat compression US in 5–7 days if still symptomatic. For PE workup, perform V/Q scan if CXR normal (note: if Q normal, can skip V portion of scan). If CXR abnormal and/or V/Q scan non-diagnostic, proceed with CT chest. CT chest is associated with lower fetal radiation exposure than V/Q scan in T1–T2, but higher risk of maternal breast cancer (14% increased lifetime risk)
RADIATION RISKS
—fetal exposure of <5 cGy [5 rad] accumulatively in each pregnancy is acceptable, but oncologic effects controversial (e.g., childhood leukemia). Consider proximity of fetus to radiations site (i.e., radiation from CT chest > V/Q scan in T3) and limit where possible (i.e., abdominal shields)
FETAL RADIATION EXPOSURE FOR COMMON IMAGING MODALITIES
Imaging | Estimated fetal radiation exposure (rad) |
---|---|
Ultrasound | None |
CXR | <0.001 |
CT head | <0.001 |
V/Q scan | 0.01–0.02 ventilation (V) 0.01–0.03 perfusion (Q) |
CT chest (PE protocol) | 0.0003–0.002 (T1) 0.0008–0.0077 (T2) 0.005–0.013 (T3) |
Pulmonary angiogram | <0.05 via brachial route |
0.2–0.3 via femoral route | |
Cardiac angiogram | <1 |
AXR | 0.2–0.3 |
IVP | 0.8 (complete series) |
0.2 (limited series) | |
MRI/MRV/MRA | None |
Related Topics
Asthma (p. 1)
Pulmonary Embolism (p. 10)
TREATMENT
—LMWH dosed using current weight (not pre-pregnancy or ideal body weight). Consider monitoring of anti-Xa level (4–6 h after last dose, target 0.6–1.2 IU/mL). Duration of therapeutic anticoagulation 3–6 months, then transition to prophylactic dose of LMWH until end of 6 weeks postpartum. If neuraxial analgesia, hold therapeutic LMWH × 24 h and prophylactic LMWH × 12 h beforehand. If unable to hold anticoagulation (e.g., acute clot <4 weeks), consider bridging with IV unfractionated heparin (and hold when in active labor or 2 h prior to cesarean section), and/or consider IVC filter. Systemic thrombolysis generally contraindicated (risk of fetal demise). Warfarin not recommended during pregnancy (teratogenic in T1; associated with fetal CNS hemorrhage/malformations, miscarriage, stillbirth, neonatal demise). May consider warfarin as an alternative to LMWH in the postpartum period while breastfeeding
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