CONTENTS

GENERAL APPROACH

• History & symptoms
  • Dyspnea
  • Chest pain
  • Cough
  • Hemoptysis ➡️
  • Palpitations
  • Peripheral edema
• Physical examination
• Laboratory tests
  • Common laboratory tests
  • ABG interpretation
• Radiology
• Pharmacologic issues in pregnancy
  • Antibiotic ➡️
  • Anticoagulation & antiplatelets
  • Cardiac medications
  • Steroid
  • Uterotonic medications

SPECIFIC DISEASE STATES

• Airway
  • Asthma
• Cardiac
  • Acute coronary syndrome (ACS)
  • Aortic dissection
  • Arrhythmias
    • SVT (supraventricular tachycardia)
    • Atrial fibrillation
    • Ventricular tachycardia
  • Heart failure & cardiogenic pulmonary edema
    • Peripartum cardiomyopathy (PPCM)
  • Valve disease
    • Mitral stenosis
    • Aortic stenosis
• Pulmonary vascular
  • Amniotic fluid embolism
  • Air embolism
  • PE in pregnancy
  • Pulmonary hypertension
• Neuromuscular & sleep
  • Sleep-disordered breathing
  • Myasthenia gravis in pregnancy ➡️
• Pleural
  • Pleural effusion
• Parenchymal lung disease
  • Pulmonary edema:
    • ARDS
    • Tocolytic pulmonary edema
    • Cardiogenic pulmonary edema
    • Preeclampsia ➡️
  • Choriocarcinoma ➡️
  • Pulmonary infections
    • Influenza
    • Pneumonia
    • Tuberculosis

Landmarks in pregnancy:

• 1st trimester: 1-12 weeks.
• 2nd trimester: 13-27 weeks.
• 3rd trimester: 28-40 weeks.
• Fetal viability: ~23-24 weeks. (31376394)
• Term pregnancy: ≧37 weeks.

abbreviations used in the pulmonary section: 6

• ABPA: Allergic bronchopulmonary aspergillosis 📖
• AE-ILD: Acute exacerbation of ILD 📖
• AEP: Acute eosinophilic pneumonia 📖
• AFB: Acid fast bacilli
• AIP: Acute interstitial pneumonia (Hamman-Rich syndrome) 📖
• ANA: Antinuclear antibody 📖
• ANCA: Antineutrophil cytoplasmic antibodies 📖
• ARDS: Acute respiratory distress syndrome 📖
• ASS: Antisynthetase syndrome 📖
• BAL: Bronchoalveolar lavage 📖
• BiPAP: Bilevel positive airway pressure 📖
• CEP: Chronic eosinophilic pneumonia 📖
• CF: Cystic fibrosis 📖
• COP: Cryptogenic organizing pneumonia 📖
• CPAP: Continuous positive airway pressure 📖
• CPFE: Combined pulmonary fibrosis and emphysema 📖
• CTD-ILD: Connective tissue disease associated interstitial lung disease 📖
• CTEPH: Chronic thromboembolic pulmonary hypertension 📖
• DAD: Diffuse alveolar damage 📖
• DAH: Diffuse alveolar hemorrhage 📖
• DIP: Desquamative interstitial pneumonia 📖
• DLCO: Diffusing capacity for carbon monoxide 📖
• DRESS: Drug reaction with eosinophilia and systemic symptoms 📖
• EGPA: Eosinophilic granulomatosis with polyangiitis 📖
• FEV1: Forced expiratory volume in 1 second 📖
• FVC: Forced vital capacity 📖
• GGO: Ground glass opacity 📖
• GLILD: Granulomatous and lymphocytic interstitial lung disease 📖
• HFNC: High flow nasal cannula 📖
• HP: Hypersensitivity pneumonitis 📖
• IPAF: Interstitial pneumonia with autoimmune features 📖
• IPF: Idiopathic pulmonary fibrosis 📖
• IVIG: Intravenous immunoglobulin 📖
• LAM: Lymphangioleiomyomatosis 📖
• LIP: Lymphocytic interstitial pneumonia 📖
• MAC: Mycobacterium avium complex 📖
• MCTD: Mixed connective tissue disease 📖
• NIV: Noninvasive ventilation (including CPAP or BiPAP) 📖
• NSIP: Nonspecific interstitial pneumonia 📖
• NTM: Non-tuberculous mycobacteria 📖
• OHS: Obesity hypoventilation syndrome 📖
• OP: Organizing pneumonia 📖
• OSA: Obstructive sleep apnea 📖
• PAP: Pulmonary alveolar proteinosis 📖
• PE: Pulmonary embolism 📖
• PFT: Pulmonary function test 📖
• PLCH: Pulmonary Langerhans cell histiocytosis 📖
• PPFE: Pleuroparenchymal fibroelastosis 📖
• PPF: Progressive pulmonary fibrosis 📖
• PVOD/PCH Pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis 📖
• RB-ILD: Respiratory bronchiolitis-associated interstitial lung disease 📖
• RP-ILD: Rapidly progressive interstitial lung disease 📖
• TNF: tumor necrosis factor
• UIP: Usual interstitial pneumonia 📖

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history & symptoms

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dyspnea in pregnancy

differential diagnosis is broad, including

• Pulmonary vascular disease:
  • PE.
  • Pulmonary hypertension.
• Pulmonary edema:
  • Cardiogenic pulmonary edema:
    • Cardiomyopathy.
    • Chronic mitral or aortic stenosis, exacerbated by pregnancy.
    • Preeclampsia.
  • Noncardiogenic pulmonary edema:
    • Tocolytic pulmonary edema. ⚡️
    • Pneumonia.
    • Interstitial lung disease.
• Anemia.
• Thyrotoxicosis.
• Asthma (suggested by chest tightness, wheeze, cough, prior history).
• Neuromuscular weakness (e.g., Guillain-Barre syndrome, myasthenia gravis).
• Benign dyspnea in pregnancy:
  • Up to two thirds of women report some dyspnea during pregnancy (most often in the first two trimesters, with improvement towards the end of the third trimester).
  • Normal physiological causes of dyspnea in pregnancy include:
    • Progesterone elevation stimulates the respiratory drive.
    • Normal anemia seen during pregnancy.
    • Restrictive physiology due to gravid uterus.

red flags suggesting pathology

• 🚩 Dyspnea is combined with additional symptoms (e.g., wheezing, cough, chest pain, fever).
• 🚩 Dyspnea is severe (e.g., impairs the ability to perform normal activities).
• 🚩 Dyspnea is present at rest.
• 🚩 Dyspnea is acute in onset (may suggest pulmonary embolism, pulmonary edema, or pneumothorax). (Lapinsky 2020)
• 🚩 Vital sign abnormalities (e.g., tachypnea, desaturation, fever, abnormal blood pressure).
• 🚩 Abnormal physical examination (e.g., wheezing, rales that don't clear, moderate to severe peripheral edema).
• 🚩 Dyspnea substantially worsens after ~31 weeks of gestation. (Lapinsky 2020)

initial evaluation might include:

• Physical examination (focusing on wheezing, systemic congestion).
• Chest radiograph.
• EKG and echocardiography.
• Laboratory studies:
  • Basic metabolic panel.
  • Complete blood count (to exclude anemia).
  • BNP (brain natriuretic peptide).
  • Thyroid stimulating hormone.
• Evaluation for pulmonary embolism if clinically warranted: ⚡️

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chest pain in pregnancy

differential diagnosis includes

• Pulmonary embolism.
• Pneumothorax or pneumomediastinum.
• Myocardial infarction (including spontaneous coronary artery dissection).
• Aortic dissection.
• Gastroesophageal reflux disease.
• Costochondritis or musculoskeletal pain.

concerning features

• Severe chest pain.
• Radiation.
• Exertional chest pain.
• Pressure-like in quality.
• Association with other symptoms (e.g., diaphoresis, emesis, dyspnea, dizziness).

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cough in pregnancy

common causes

• Infection (most common cause of cough lasting <4 weeks).
  • Respiratory viruses.
  • Bacterial pneumonia.
  • Tuberculosis or pertussis may cause cough >4 weeks. (Lapinsky 2020)
• Asthma.
• Allergic rhinosinusitis or possibly pregnancy rhinitis.
• Gastroesophageal reflux.

indications to consider imaging include:

• Hemoptysis or substantial sputum production.
• Fever.
• Dyspnea.
• Chest pain (aside from expected costochondritic chest pain).
• Failure to gain weight during pregnancy. (Lapinsky 2020)

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palpitations in pregnancy

causes of palpitations include: 

• Benign feature of pregnancy.
• Structural heart disease:
  • Cardiomyopathy.
  • Valvular heart disease.
  • Pulmonary embolism with right ventricular strain.
• Arrhythmia (~10% of palpitations in pregnancy). (Hameed 2020)
• Thyrotoxicosis.
• Sepsis.
• Hypoglycemia.
• Anemia.
• Medications or illicit substances, e.g.:
  • Sympathomimetics.
  • Vasodilators.
  • Anticholinergics.
  • Substance use (e.g., cocaine, amphetamine). (Hameed 2020)

less worrisome features:

• Self-limited.
• Occur for short duration of time.
• Not associated with physical exertion.
• No other symptoms of cardiac disease.

more likely cardiac:

• Persistent palpitations.
• Worsening of palpitations with exertion.
• Other associated symptoms (e.g., dyspnea, orthopnea, paroxysmal nocturnal dyspnea, chest pain, fatigue, dizziness, syncope). (Hameed 2020)

investigation may include:

• EKG.
• Echocardiogram.
• Laboratory studies (basic metabolic panel, magnesium level, complete blood count, thyroid stimulating hormone).
• Holter monitor or loop recorder to capture occasional events.

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peripheral edema in pregnancy

differential diagnosis includes

• Physiologic edema related to pregnancy.
• Deep vein thrombosis.
• Heart failure.
• Preeclampsia.

worrisome signs

• Acute onset.
• Severe.
• Asymmetric edema (DVT in the context of pregnancy is usually on the left side).
• Associated symptoms (e.g., dyspnea, fatigue, palpitations). (Hameed 2020)

evaluation may include:

• Venous ultrasonography to exclude DVT.
• Evaluation for heart failure (e.g., BNP level, echocardiography).
• Evaluation for preeclampsia (e.g., protein/creatinine ratio, urinalysis, basic metabolic panel, liver function tests).

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physical examination

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vital signs in pregnancy

• Temperature: Unchanged.
• Blood pressure:
  • Blood pressure normally decreases, reaching a nadir at ~16-28 weeks.
  • Diastolic pressure decreases more (~15 mm) than systolic pressure (~5-10 mm). This reflects systemic vasodilation.
  • Blood pressure returns to normal shortly after delivery.
  • ⚠️ Hypertension should always raise concern for the possibility of preeclampsia: 📖
• Heart rate:
  • Heart rate increases steadily throughout pregnancy.
  • Normally, heart rate increases by ~15-20 b/m by weeks 32-36.
  • Heart rates >100 b/m should be regarded as abnormal. (Hameed 2020)
  • Heart rate >120 b/m is a red flag that requires prompt evaluation. (Hameed 2020)
  • Heart rate typically normalizes within 6 hours postpartum. (Hameed 2020)
• Respiratory rate:
  • There is normally no change in respiratory rate, or only a minimal increase (1-2 breaths/min). (Lapinsky 2020)
  • Pregnancy normally induces a reduction in CO2 due to increased tidal volumes, not an increased respiratory rate.
• Oxygen saturation:
  • Normal value in pregnancy is >96%. (Lapinsky 2020)
  • For pregnant women with respiratory failure, a reasonable target saturation might be ~94-98% (although there is unfortunately not high-quality evidence regarding this). (Lapinsky 2020)

general examination findings of note

• Cardiac examination:
  • Prominent S2?
  • Murmurs?
• Pulmonary examination:
  • Wheezing?
  • Rales that persist with coughing?
• Abdomen:
  • Right upper quadrant tenderness?
• Extremities:
  • Peripheral edema?
  • Clubbing?

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laboratory tests

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commonly utilized laboratory tests in pregnancy 

• Blood count with differential.
  • Hemoglobin normally decreases in pregnancy, with normal values as follows: (19935037)
    • 1st trimester: 11.6 – 13.9 g/dL.
    • 2nd trimester: 9.7 – 14.8 g/dL.
    • 3rd trimester: 9.5 -15 g/dL.
• Electrolytes including Ca/Mg/Phos.
• INR, PTT, fibrinogen, D-dimer, LDH, haptoglobin.
• Liver function tests, ammonia.
• BNP (brain natriuretic peptide).
  • BNP doesn't normally change substantially during normal pregnancy. (38197818)
  • Elevated BNP suggests preeclampsia, congenital heart disease, pulmonary vascular disease, or cardiomyopathy.
• TSH (if thyroid disease is a concern).
• If infection suspected: appropriate cultures.
• Urinalysis and spot protein/creatinine ratio.
• Troponin elevation may suggest MI or PE.
• (Useful reference on normal lab values in pregnancy: Perinatology.com)

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ABG interpretation in pregnancy

pH, bicarbonate, PaCO2

• Normal values:
  • PaCO2 is normally ~27-32 mm.
  • pH is normally ~7.40-7.47 (Murray 2022)
  • Bicarbonate is normally ~18-21 mEq/L.
  • Base excess may decrease by as much as -5 mEq/L. (Lapinsky 2020)
• PaCO2 >35 mm may indicate respiratory fatigue.
• PaCO2 >42 may be an indication to consider intubation (although this will obviously be dictated primarily by the clinical assessment).

oxygenation

• The A-a gradient should not generally be elevated due to pregnancy. (Lapinsky 2022)
• An elevated minute ventilation with a reduced PaCO2 will elevate the PaO2 slightly:
  • Room air PaO2 in normal nonpregnant people is ~75-100 mM
  • Room air PaO2 in pregnancy is often ~95-105 mm.
  • Late in pregnancy, PaO2 may decrease somewhat (especially in a supine position), but values remain relatively elevated. (Lapinsky 2022)
• PaO2 >70 mm is often targeted to establish adequate fetal oxygenation (in the absence of any rigorous evidence).

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radiology

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fetal radiation exposure due to different radiologic studies

• Chest radiograph: 0.0005 – 0.01 mGy.
• Perfusion scan only: 0.1 – 0.37 mGy (with maternal breast exposure of 0.25 mGy).
• Chest CT scan: 0.1 – 0.66 mGy (and maternal breast exposure of 10-70 mGy).
• Ventilation-Perfusion (VQ scan): 0.32 – 0.74 mGy.
• PET/CT scan: 9-20 mGy. (Lapinsky 2020, Hameed 2020)

chest radiograph

• Chest radiograph is safe and rapidly available.
• The radiation exposure is negligible. (Murray 2022) A chest radiograph should never be deferred due to pregnancy.
• Benefits from chest radiograph in the evaluation of pulmonary embolism:
  • Chest radiograph may reveal an alternative diagnosis.
  • Chest radiograph may guide the selection of a CT scan versus perfusion scan (abnormalities on chest radiograph predict a nondiagnostic perfusion scan).

ventilation-perfusion scan (V/Q scan) & perfusion scan

• Ventilation-perfusion scans are most useful for patients without underlying lung disease. Fortunately, this scenario is commonly encountered among pregnant women.
• Perfusion-only scanning is generally preferable for women with a normal chest radiograph. A normal perfusion scan has the same clinical significance as a normal V/Q scan, in terms of excluding pulmonary embolism. For patients with a normal chest radiograph, the ventilation component of the test is unlikely to provide useful information (it's generally normal). An isolated perfusion scan reduces radiation exposure to both the fetus and the mother, while avoiding lung irritation from inhaled radiotracer (e.g., in patients with asthma).
• In patients undergoing perfusion scanning, radiotracer will be cleared by the kidneys. Adequate hydration and placement of a Foley catheter may accelerate excretion of radiotracer out of the body. (A Foley catheter prevents accumulation of radiotracer in the bladder, which is close to the fetus).

CT angiography

• CT angiography is generally safe in pregnancy. The amount of radiation exposure to the fetus is low (and similar to that involved in ventilation/perfusion scanning). The primary concern with regard to radiation is exposure of radiosensitive maternal breast tissue (although that risk is also low).
• Pregnant patients are more likely to have suboptimal CT angiography, due to increased cardiac output. Protocols to increase the volume and injection rate of contrast may improve study quality. (35792687)

choice of perfusion scanning versus CT angiography 

• The selection of perfusion scanning vs. CT angiography is controversial.
• In most cases, either test is fine.
• CT angiography may be preferable under the following circumstances:
  • (1) Abnormal chest radiograph (which often causes perfusion or V/Q scanning to be nonspecifically abnormal).
  • (2) Sicker patients (CT scan may be performed quickly, allowing for global evaluation of numerous potentially life-threatening disorders).
• Perfusion scanning may be useful under the following circumstances:
  • (1) Normal chest radiograph increases the likelihood of a diagnostic study (i.e., “normal perfusion scan”).
  • (2) Patients who are relatively well – where the goal is purely to exclude pulmonary embolism.
  • (3) Younger patients (in whom the radiation exposure to breast tissue may cause a greater lifelong cancer risk).
  • (4) Prior anaphylactoid reaction to IV contrast dye.

EKG: normal changes that may occur in pregnancy

• Left axis deviation (due to high-riding diaphragm which causes a horizontal heart configuration).
• ST segment and T-wave flattening.
• Inverted T-waves in III, V1-V3.
• Prominent Q-waves in II, III, and aVF. (Hameed 2020)

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pharmacology in pregnancy

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pharmacokinetic changes in pregnancy

• Increased GFR (glomerular filtration rate). GFR often increases by 50% by the end of the first trimester and then may continue to rise as high as 85% above baseline toward the end of the third trimester. (Hameed 2020)
• Hepatic metabolism is often increased:
  • Drugs with a high hepatic extraction ratio (ER) are cleared based on hepatic perfusion, which may increase during pregnancy (e.g., propranolol, verapamil, nitroglycerine). (30704579)
  • Clearance of low extraction ratio (ER) drugs is less affected. However, if low albumin causes an increased free fraction of drug, then hepatic metabolism may be increased.
  • Some cytochrome P450 enzymes are induced in pregnancy (e.g., CYP3A4 and CYP2C9, which metabolize metoprolol). (30704579)
• Increased volume of distribution by ~50%.
  • Increased plasma volume.
  • Increased fat accumulation.
• Decreased albumin and plasma binding proteins.
• Enteral absorption might theoretically be impaired:
  • Delayed gastric emptying.
  • Prolonged small bowel transit time. (Hameed 2020)
  • However, studies on sotalol and propranolol haven't shown different bioavailability. (30704579)

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anticoagulation & antiplatelets in pregnancy 

Warfarin or DOACs (direct-acting oral anticoagulants) are contraindicated prior to delivery. Consequently, treatment generally involves either unfractionated heparin or low molecular-weight heparin. Following delivery, therapeutic options are broader (e.g., heparin, low molecular-weight heparin, or warfarin are all safe during lactation).

LMWH (low molecular weight heparin)

• DVT prophylactic dose:
  • Initially 40 mg/day s.q. for patients weighing 50-90 kg.
  • As the patient's weight increases during pregnancy, the dose should be increased (e.g., 0.25 mg/kg enoxaparin q12 hours; see the table below).
• Therapeutic dose:
  • Enoxaparin 1 mg/kg q12 hours should be used initially. (Fishman 2023)
  • The precise dosing weight is unclear. The weight utilized to dose enoxaparin might ideally be a weight obtained during the 1st-2nd trimesters. (Lapinsky 2020)
  • Pharmacokinetics of LMWH in pregnancy may be altered. Thus, monitoring of anti-Xa levels is prudent, four hours after the third dose (especially in the context of obesity plus pregnancy). 📖
• Prior to delivery or procedures, LMWH should be held. In occasional cases, an unfractionated heparin infusion may be utilized as bridging therapy.

unfractionated heparin

• Patients may be switched to a heparin drip as they approach delivery.
• Heparin drip may be stopped 4-6 hours prior to epidural anesthesia. (Hameed 2020)

other anticoagulants 

• Fondaparinux doesn't cross the placenta, so it might be the preferred agent for patients who cannot receive heparin (e.g., due to heparin-induced thrombocytopenia). It is class B in pregnancy. (34405872)
• Argatroban may penetrate the placenta, but it also seems reasonably safe.

antiplatelet agents

• Aspirin:
  • Low-dose aspirin is generally safe (e.g., 81 mg/day). It is commonly used in the prevention of preeclampsia. (30704579)
  • High-dose aspirin should be avoided, due to the risk of premature closure of the ductus arteriosus. (30704579)
• Clopidogrel is the preferred P2Y12 inhibitor in pregnancy (Class B). However, it should be used for the shortest duration possible. Clopidogrel should be held for a week prior to epidural anesthesia. (30704579)

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cardiac medications in pregnancy

diuretics

• Furosemide is the mainstay of therapy in pregnancy.
• Thiazides may be utilized if needed. Hydrochlorothiazide is class B in pregnancy and may be supported by the most experience. There is some concern regarding the possibility of inducing electrolyte imbalance within the fetus, so caution is required. Randomized trials involving hydrochlorothiazide for the treatment of hypertension in pregnancy detected a reduced risk of preeclampsia and no evidence of harms. (3917318) 
• 🚫 Mineralocorticoid receptor antagonists aren't well investigated in pregnancy, so they aren't generally used.

antiarrhythmics

• Adenosine: Generally safe.
• Amiodarone:
  • Class D; may cause congenital goiter, bradycardia, and QT prolongation. (33832606) Fetal thyroid abnormalities may impair neurocognitive development. (30704579)
  • Amiodarone can be utilized, but only if truly necessary.
• Atropine is generally safe. (Hameed 2020)
• Beta-blockers are generally safe:
  • Beta-1 selective agents are often preferred (e.g., metoprolol – which has a track record for efficacy and safety). (Hameed 2020) Selectivity for the beta-1 receptor may avoid fetal hypoglycemia and also avoid alteration of beta-2 mediated uterine relaxation and peripheral vasodilation. (30704579)
  • Labetalol is safe.
  • Propranolol is generally considered safe.
  • 🚫 Atenolol is contraindicated (it's an undesirable drug regardless, due to renal clearance with a tendency to accumulate).
• Calcium channel blockers: Diltiazem is generally preferred over verapamil in atrial fibrillation (based on greater hemodynamic stability). However, verapamil may be preferred for treatment of SVT (supraventricular tachycardia). (30704579) Calcium channel blockers may have a tocolytic effect. (Griffin 2022)
• Digoxin is generally safe, but requires close monitoring of levels. Accelerated drug metabolism and higher circulating volume in pregnancy may require the use of higher doses than usual.
• Dofetilide: Class C in pregnancy; arguably preferable to amiodarone.
• Ibutilide.
• Lidocaine is generally safe (Class B). There may be a risk of neonatal CNS depression. (Griffin 2022)
• Magnesium.
• Sotalol is Class B (potential risks of fetal bradycardia or intrauterine growth restriction). (Griffin 2022)

vasodilators & other antihypertensives

• Hydralazine is commonly utilized for afterload reduction (but avoid IV hydralazine if possible).
• IV nitroglycerine or oral isosorbide dinitrate are safe.
• Calcium channel blockers are safe: amlodipine, nifedipine.
• Clonidine seems safe, but may require shorter dosage intervals. (30704579) There is a rare risk of neonatal hypertension. (Griffin 2022)
• 🚫 ACE inhibitors / ARBs / renin inhibitors are contraindicated due to teratogenicity.
• 🚫 Nitroprusside can cause fetal cyanide poisoning.
• Further discussion of antihypertensives in the chapter on preeclampsia: 📖

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systemic steroid

• Risk?
  • Systemic steroid use in the first trimester was previously thought to associate with a very small risk (~0.2%) of cleft palate in the fetus. However, newer studies have found that there is actually no risk. (24777675, 21482652, 23011170)
  • Steroid does increase the risk of gestational diabetes mellitus and preeclampsia.
  • If genuinely indicated (e.g., uncontrolled asthma), the benefit of steroid outweighs the risks.
• Different steroids carry varying risk:
  • 🏆 Prednisone, prednisolone, and methylprednisolone have limited fetal uptake due to active retrograde transport by P-glycoprotein and metabolism to inactive metabolites by placental 11-beta-hydroxysteroid dehydrogenase. (26590298) By using these agents, benefits may be achieved while minimizing effects on the fetus.
  • Dexamethasone and betamethasone cross the placenta.
• Steroid to induce lung maturity:
  • This is often utilized in preterm gestation, if there is a risk of early delivery (with a goal of reducing neonatal respiratory distress syndrome).
  • The dose is 6 mg dexamethasone twice daily for 48 hours.
• ⚠️ Patients on prolonged courses of systemic steroid should consider stress-dose steroid during labor. (Fishman 2023)

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uterotonic medications: cardiopulmonary consequences

• 1st line agent: Oxytocin
  • Causes reduced blood pressure with a slight elevation in pulmonary pressures.
  • Most effective uterotonic agent.
  • Avoid bolus administration in patients with cardiac disease.
  • Vasodilation may need to be counteracted with the use of a vasopressor agent.
• 2nd line agent in unstable patients: misoprostol
  • This is the least effective agent but seems to be hemodynamically stable.
• Methylergonovine
  • Can cause profound elevation of systemic vascular resistance, pulmonary vascular resistance, and coronary vasospasm.
  • Generally avoided in cardiac patients. (Hameed 2020)
• Carboprost
  • Causes profound elevation in pulmonary artery pressure.
  • May cause bronchospasm with ventilation/perfusion mismatch.
  • Avoid in patients with asthma or patients unable to tolerate increased pulmonary pressure. (Hameed 2020)

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asthma in pregnancy

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epidemiology & disease course

• Asthma is the most common respiratory disease seen in pregnancy (affecting ~6% of women).
• During pregnancy, asthma control may improve in ~25% of women, deteriorate in ~25% of women, or remain stable in ~50%. (Murray 2022)
• Disease course:
  • Weeks 17-32: exacerbations are increased. (Fishman 2023) 
  • Final weeks of pregnancy: higher levels of endogenous cortisol tend to improve asthma control. (Fishman 2023) Thus, problems during delivery are rare.
  • Immediate postpartum period: asthma control may deteriorate.

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asthma control in pregnancy

aggressive asthma control is important:

• Uncontrolled asthma poses numerous risks to mother and fetus, including:
  • Preeclampsia.
  • Fetal mortality.
  • Congenital malformations.
  • Prematurity.
  • Low birth weight. (Lapinsky 2020)

assessment of asthma control

• Neither spirometry nor peak expiratory flow rate (PEFR) are affected by pregnancy. Thus, these tests may be used to monitor and manage asthma as per usual. 📖 (Fishman 2023)
• The ACT (Asthma Control Test) has been found to be reliable in pregnant women. (Lapinsky 2020)

usual inhaled medications are safe

• Inhaled short-acting and long-acting beta-2 agonists are safe (including albuterol, salmeterol, and formoterol). (Murray 2022) 
• Budesonide might be the preferred inhaled steroid, as there is more data available to support its use in pregnancy. Substantive safety data support the use of beclomethasone and fluticasone as well. (Murray 2022) However, any inhaled steroid is probably safe.
  • If the patient is well controlled on an inhaled steroid, the steroid shouldn't be switched solely because of pregnancy.
  • If the patient isn't well controlled, budesonide-formoterol might be a good choice (as a component of SMART therapy, discussed further here: 📖).
• Intranasal steroids are also safe (especially intranasal budesonide).

other controller medications & therapies

• Montelukast is probably safe in pregnancy, but there is an FDA warning related to reports of limb reduction defects. In total there are six reported cases of limb reduction defects, but causality is unknown. (28398707, Fishman 2023)
• Gastroesophageal reflux disease should be treated aggressively (as this is often exacerbated by pregnancy). Famotidine is safe in pregnancy. Proton pump inhibitors are likely safe as well.
• Pregnancy-induced rhinitis may worsen asthma control, so this should be treated aggressively if present.
• Omalizumab is generally considered safe for patients who are already initiated on this therapy and tolerating it well. However, omalizumab therapy shouldn't be initiated during pregnancy, since this carries a risk of anaphylaxis.

agents to avoid:

• ⚠️ Theophylline may cause fetal toxicity. Theophylline isn't a preferred agent for asthma anyway. 📖
• ⚠️ Zileuton should be avoided in pregnancy. (Lapinsky 2020)

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management of an asthma exacerbation in pregnancy

• Treatment is generally the same as for other patients with acute exacerbation of asthma.
• Some diagnostic differences:
  • Pregnant women normally display hypocapnia, so normocapnia (e.g., PaCO2 >35 mm) may indicate ventilatory failure. More on ABG interpretation in pregnancy above: ⚡️
• Some therapeutic differences:
  • Mild hypoxemia should be treated aggressively.
  • IV beta-agonists may inhibit labor, if administered near term.
  • Systemic steroid is discussed further above. 📖

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planning for labor and delivery

• For patients on prolonged systemic steroid during pregnancy, stress-dose steroid may be considered.
• Oxytocin and prostaglandin E2 are safe. However, other prostaglandins used for induction of labor and morphine may cause bronchospasm. (Fishman 2023)

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acute coronary syndrome (ACS)

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Pregnancy associated MI (PAMI) is defined as an MI occurring during pregnancy or within 3 months postpartum. (Hameed 2020)

causes of pregnancy associated MI

• ~43% SCAD (spontaneous coronary artery dissection) – discussed below.
• ~27% Atherosclerotic coronary artery disease.
• ~17% Coronary artery thrombosis (without atherosclerosis; for example antiphospholipid antibody syndrome).
• ~2% Takotsubo cardiomyopathy.
• ~1% Suspected coronary artery spasm. (Hameed 2020)

risk factors for pregnancy associated MI

• Higher maternal age is a strong risk factor.
• Most patients lack risk factors for atherosclerosis.

differential diagnosis

• Myocardial infarction.
• Pulmonary embolism.
• Aortic dissection (+/- coronary artery occlusion).
• Preeclampsia.

management

• Generally similar to other patients with MI.
• Aspirin, nitrates, beta-blockers, and heparin are considered safe. (Griffin 2022)

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SCAD (spontaneous coronary artery dissection) 

basics

• SCAD is the most common cause of pregnancy-associated myocardial infarction.
• Anatomy:
  • Usually a single coronary artery is involved, but multiple arteries can be involved simultaneously.
  • The left anterior descending artery is most often involved (>70%), followed by the left main coronary artery, the circumflex, and finally the right coronary artery. (Hameed 2020) 

epidemiology

• SCAD most often occurs in late pregnancy or early postpartum (with a peak in the first week postpartum). (Hameed 2020)
• Risk factors for SCAD may include a history of fertility therapy, multiparity, and preeclampsia. (33832606)

management

• Beta-blockers may be useful if tolerated. They could serve to reduce the risk of malignant arrhythmia, while also reducing coronary arterial wall stress. (Hameed 2020)
• Heparin use is controversial, since anticoagulation could promote extension of the dissection. (Hameed 2020) Heparin should be discontinued once SCAD has been identified. (33832606)
• Percutaneous coronary intervention is challenging. Coronary arteries are fragile, so instrumentation may risk propagation of the dissection.
• ⚠️ Thrombolysis should be avoided, as this may cause extension of the intramural hematoma and worsen the dissection.

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aortic dissection

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risk factors for aortic dissection

• Hypertension is the most common risk factor.
• Bicuspid aortic valve.
• Genetic/congenital:
  • Marfan syndrome.
  • Ehlers-Danlos syndrome type IV.
  • Turner syndrome.
  • Fibromuscular dysplasia.
• Exposures:
  • Cocaine use.
  • Trauma.

presentation of aortic dissection

• Timing:
  • First trimester (5%)
  • Second trimester (10%)
  • Third trimester (50%)
  • Postpartum (20%). (Hameed 2020)
• Chest pain (typically: sudden onset, tearing pain, may radiate to the back).
• Occlusion of aortic branches may cause additional symptoms (e.g., stroke, limb ischemia, mesenteric ischemia).

diagnostic studies may include:

• POCUS/echocardiography may reveal:
  • Aortic dilation.
  • Aortic valve regurgitation.
  • Pericardial effusion (+/- tamponade).
  • Dissection flap involving the aorta or carotid arteries.
• Blood pressure differential between arms of >20 mm (performance may be better in pregnant women who generally don't have substantial underlying vascular disease).
• EKG may show occlusive myocardial infarction (if dissection involves a coronary artery).
• CT angiography is generally the diagnostic test of choice.

management

• Target heart rate <60 b/m and systolic blood pressure <100-120 mm with:
  • Analgesia (e.g., IV fentanyl).
  • Beta-blockade (e.g., esmolol infusion).
  • Vasodilator (e.g., nicardipine).
• Immediate consultation with vascular surgery and obstetrics.
  • Surgical intervention is indicated for type A dissections as well as some type B dissections (e.g., with leakage, rupture, progressive aortic dilation, ischemia).
  • Before 28 weeks, surgery may be required with the fetus in utero. However, if the fetus is viable, then it may be preferable to proceed with a STAT C-section followed immediately by aortic repair.

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arrhythmias

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The management of arrhythmias is largely the same as for any patient. The main difference is that amiodarone should be avoided if possible. Cardioversion is safe and effective at any stage of pregnancy. 

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narrow-complex supraventricular tachycardia (SVT)

basics

• SVT is the most common sustained arrhythmia in pregnancy.
• The prognosis is generally fine.

acute treatment options include: 

• [#1] If unstable: cardioversion.
• [#2] Vagal maneuvers.
• [#3] Adenosine.
• [#4] Beta-1 selective beta-blockers, other than atenolol (e.g., IV metoprolol).
• [#5] Other options include:
  • Nondihydropyridine calcium channel blockers (if hemodynamics allow).
  • DC cardioversion. (34405872)

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AF (atrial fibrillation)

epidemiology

• AF usually occurs in the context of underlying structural heart disease. However, pregnant women may also have lone AF (i.e., atrial fibrillation in the absence of other structural heart disease).
• Risk factors for AF include:
  • Older age.
  • Obstructive sleep apnea.
  • Underlying congenital heart disease.
  • Hypertension. (Hameed 2020)

treatment

• General approach:
  • Identify and treat any underlying causes of AF.
  • For stable patients, rate control is often utilized initially. Among patients with structurally normal hearts, atrial fibrillation will generally revert to sinus rhythm. If symptoms persist despite rate control, rhythm control may be attempted. (Hameed 2020)
• Rate control:
  • Beta-blockade (usually first-line therapy; e.g., 5 mg IV metoprolol, dosed up to 15 mg total if needed, followed by a transition to oral metoprolol if successful 💉).
  • Calcium channel blockers.
  • Digoxin.
• Rhythm control:
  • Medical options include flecainide, propafenone, sotalol, or ibutilide.
  • DC cardioversion may be used for unstable patients.
• Anticoagulation: Aspirin may be adequate for patients with CHADSVASC 1-2, whereas anticoagulation may be considered for selected patients with CHADSVASC 2 or higher. (Hameed 2020)
• General discussion of AF: 📖

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VT (ventricular tachycardia) & VF (ventricular fibrillation)

basics

• These usually occur in the context of underlying structural heart disease.
• Causes may include: (34405872)
  • Peripartum cardiomyopathy.
  • Right ventricular infundibular tachycardia (the most common type of ventricular tachycardia in young pregnant women with a structurally normal heart).
  • Long QT syndrome.
  • Brugada syndrome.
  • Thyrotoxicosis.
  • Hyperemesis gravidarum with electrolyte abnormality.

treatment options include:

• Prompt DC cardioversion is generally preferred.
• Treat any underlying disorder, e.g.:
  • Active myocardial ischemia.
  • Electrolyte abnormalities.
• Medical therapies may include:
  • Beta-blockers (including metoprolol, propranolol).
  • Lidocaine.
  • Procainamide.
  • Amiodarone (relatively contraindicated, but use it if needed to sustain life).
• (Treatment of VT storm: 📖)

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heart failure & cardiogenic pulmonary edema

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potential causes

• Preeclampsia.
• Valvular heart disease:
  • Exacerbation of chronic valvular disease (especially mitral stenosis, aortic stenosis).
  • Acute valvular heart disease (e.g., endocarditis).
• Iatrogenic volume overload.
• Coronary artery disease (including spontaneous coronary artery dissection).
• Arrhythmia (e.g., atrial fibrillation).
• Dilated cardiomyopathy – see the differential diagnosis of peripartum cardiomyopathy below.

symptoms of cardiogenic pulmonary edema

• Dyspnea with orthopnea.
• Cough may occur (in severe cases, pink frothy sputum may occur as a reflection of diffuse alveolar hemorrhage).

treatment

• Treat any underlying cause, e.g.:
  • Preeclampsia management with calcium channel blockers to reduce afterload will improve heart failure.
  • Arrhythmia treatment.
• Pulmonary support (e.g., using noninvasive ventilation).
• Optimization of volume status: Furosemide is safe in pregnancy. However, note that pregnant women may be quite sensitive to furosemide (especially in comparison to other populations of ICU patients). (Fishman 2023) 
• Optimization of afterload (e.g., using nitroglycerin, nicardipine, or nifedipine). (Lapinsky 2020) ACE inhibitors are teratogenic, but the combination of isosorbide dinitrate plus hydralazine may be used in their place. (Fishman 2023)
• Inotropic support if needed. Pregnancy itself causes reduced systemic vascular resistance, so dobutamine or milrinone alone may cause excessively low systemic vascular resistance in some cases (which may require the addition of norepinephrine). (34405872)
• Mechanical support, if refractory to other interventions.
• Additional information:
  • Cardiac medications in pregnancy: ⚡️
  • Chapter on cardiogenic shock and severe heart failure: 📖

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peripartum cardiomyopathy (PPCM)

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epidemiology

• PPCM occurs in ~1/2,000 births, with substantial geographic variation.
• PPCM accounts for 60% of cardiogenic shock during pregnancy and early postpartum period. (38197818)

risk factors

1. Hypertensive diseases of pregnancy (especially preeclampsia).
2. Higher maternal age (1/270 risk for women >40 years old). (37163197)
3. Multifetal pregnancy.
4. African American race (in the United States, this increases risk fourfold). (Hameed 2020; 38197818)

clinical presentation

• Timing: PPCM usually occurs within the last month of pregnancy or first five months following delivery. The greatest incidence is the first week after delivery. (38197818)
• Presentation is similar to that of other forms of systolic heart failure:
  • Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, crackles on pulmonary examination.
  • Peripheral edema.
• Patients can present with cardiogenic shock.
• Complications may include:
  • Thromboembolism from the left ventricle to the systemic circulation (e.g., stroke).
  • Arrhythmia (including ventricular tachycardia).

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diagnostic evaluation

differential diagnosis: causes of systolic failure in pregnancy

• Peripartum cardiomyopathy (PPCM).
• Exacerbation of preexisting cardiomyopathy (e.g., idiopathic or familial dilated cardiomyopathy).
• Chemotherapy (e.g., anthracyclines, doxorubicin, trastuzumab).
• Toxin/substance abuse:
  • Alcoholic cardiomyopathy.
  • Sympathomimetic use (e.g., cocaine).
• Myocarditis, including:
  • Viral cardiomyopathy.
  • Giant cell myocarditis.
  • Chagas disease.
  • HIV.
• Takotsubo cardiomyopathy.
• Tachycardia-induced cardiomyopathy.
• Hyperthyroidism.
• Myocardial infarction (e.g., SCAD, MINOCA).

diagnostic criteria for PPCM

• [1] Nonischemic cardiomyopathy with ejection fraction <45%.
• [2] Develops in the last month of pregnancy or first five months following delivery.
• [3] No alternative diagnosis or previously known structural heart disease.

diagnostic evaluation for PPCM

• Basic imaging:
  • EKG (often normal in PPCM, but may have nonspecific abnormalities). (37163197)
  • Echocardiogram.
  • Chest radiograph.
• Laboratory tests:
  • Troponin, BNP (brain natriuretic peptide), lactate, liver function tests.
  • Laboratory evaluation for alternative diagnoses (e.g., HIV screening, thyroid stimulating hormone, testing for respiratory viruses as clinically indicated).
• Cardiac MRI may be helpful, especially if echocardiogram images are limited (but note that gadolinium is contraindicated in pregnancy).
• Endomyocardial biopsy usually isn't needed and is rarely performed. (38197818)

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management

general supportive care for heart failure

• General management of heart failure
  • Prior to delivery: Management as discussed above ⚡️.
  • After delivery: Treatment with more standard approach for heart failure: 📖
• Advanced therapies: may involve mechanical support, cardiac transplantation.

bromocriptine

• Bromocriptine therapy remains controversial. There is some evidence supporting bromocriptine, but it is of low quality. Bromocriptine may promote thrombosis, so anticoagulation should be utilized in patients receiving bromocriptine. (30704579) Bromocriptine will suppresses lactation. 
• American sources are less enthusiastic about bromocriptine, recommending that it be considered if the ejection fraction is <35%. (38197818)
• European Society of Cardiology 2018 guidelines state the following regarding bromocriptine: “Addition of bromocriptine to standard HF therapy may improve LV recovery and clinical outcome in women with acute severe PPCM. Bromocriptine (2.5 mg once daily) for at least
  1 week may be considered in uncomplicated cases, whereas prolonged treatment (2.5 mg twice daily for 2 weeks, then 2.5 mg once daily for 6 weeks) may be considered in patients with EF <25% and/or cardiogenic shock. Bromocriptine treatment must always be accompanied by anticoagulation with heparin (LMWH or UFH), at least in prophylactic dosages. The essential therapies for patients with acute PPCM have been summarized under the BOARD label: Bromocriptine, Oral heart failure therapies, Anticoagulants, vasoRelaxing agents, and Diuretics.” (30165544)

anticoagulation

• Pregnancy is a hypercoagulable state, so the risk of apical left ventricular thrombosis may be higher than other heart failure patients. (38197818) Thromboembolic complications in PPCM are reported in ~7-20% of patients.
• Anticoagulation is generally recommended for patients with:
  • [1] Substantial LV dysfunction (e.g., <30-35%).
  • [2] Known left ventricular or left atrial thrombus.
  • [3] Atrial fibrillation. (Hameed 2020, 38197818) 

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prognosis

general prognosis

• About half of women recover normal cardiac function.
• About half of women experience stable cardiac dysfunction, or worsening cardiomyopathy. (Griffin 2022)

poor prognostic factors

• Echocardiographic parameters:
  • More severe LV dilation (LV end-diastolic diameter >6 cm).
  • Lower ejection fraction (<30%).
  • Right ventricular dysfunction.
• Abnormal cardiac biomarkers.
• Late gadolinium enhancement on MRI. (38197818)
• Family history of heart failure. (Hameed 2020)

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valve disease in pregnancy

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basics

• Stenotic lesions are more problematic than regurgitant lesions, given the increase in cardiac output and heart rate during pregnancy.

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mitral stenosis 

basics

• One of the most poorly tolerated valvular disorders in pregnancy.
• Moderate to severe mitral stenosis (valve area <1.5 cm2) carries a substantial risk of arrhythmia and/or heart failure during pregnancy. Ideally this should be corrected prior to conception. (Griffin 2022)

clinical presentation

• Heart failure may occur in previously asymptomatic patients.
• Sustained atrial fibrillation occurs in up to 10% of women with moderate or severe mitral stenosis. Atrial fibrillation may cause acute decompensation in the context of mitral stenosis.

echocardiographic grading of mitral stenosis

• Mild: valve area >1.5 cm2, mean gradient <5 mm.
• Moderate: valve area 1-1.5 cm2, mean gradient 5-10 mm.
• Severe: valve area <1, mean gradient >10 mm.

management may include:

• Diuretics are generally needed to avoid volume overload.
• Beta-blockers may reduce heart rate and thereby improve diastolic filling.
• Management of comorbid atrial fibrillation:
  • Rhythm control may be required if AF precipitates hemodynamic instability (e.g., cardioversion).
  • Rate control: beta-blockers are front-line therapy. Digoxin may be used in patients with AF and heart failure who don't respond sufficiently to beta-blockers.
  • Anticoagulation is recommended for paroxysmal or permanent AF.
• Management of the valve:
  • (1) PMBV (percutaneous mitral balloon valvuloplasty) may be considered. (Hameed 2020)
  • (2) Surgical mitral valve repair is most safely performed in the second trimester. (Griffin 2022)

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aortic stenosis

basics

• In developed countries, aortic stenosis in pregnancy will usually be due to a congenital bicuspid aortic valve.
• Mild-moderate aortic stenosis with preserved left ventricular systolic function is usually tolerated. Severe aortic stenosis with left ventricular dysfunction is the most worrisome constellation of findings.

echocardiographic grading of aortic stenosis

• Mild:
  • Aortic Valve Area >1.5 cm2.
  • Indexed aortic valve area >0.85 cm2/m2.
  • Mean pressure gradient <20 mm.
  • Aortic jet velocity 2-2.9 m/s.
• Moderate:
  • Aortic Valve Area 1-1.5 cm2.
  • Indexed aortic valve area 0.6-0.85 cm2/m2.
  • Mean pressure gradient 20-39 mm.
  • Aortic jet velocity 3-3.9 m/s.
• Severe:
  • Aortic Valve Area <1 cm2.
  • Indexed aortic valve area <0.6 cm2/m2.
  • Mean pressure gradient >40mm.
  • Aortic jet velocity >4 m/s.

clinical presentation

• Presentations mimic those of atrial stenosis in general (e.g., dyspnea, angina, or syncope).
• Symptoms usually arise in the second or early third trimester. (Griffin 2022)

management may include

• Diuresis may be needed for management of heart failure.
• Heart rate control may be considered (e.g., beta-blocker or non-dihydropyridine calcium channel).
• Percutaneous valvuloplasty or surgical intervention may be needed in severely symptomatic patients.

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amniotic fluid embolism (AFE)

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epidemiology of amniotic fluid embolism (AFE) 

AFE is rare, yet has a high mortality. AFE may be roughly the fourth leading cause of maternal death (following thromboembolism, hemorrhage, and sepsis).

timing

• Common timing:
  • During labor.
  • During Caesarean delivery.
  • Immediately following vaginal delivery. (33456838)
• May also occur following uterine manipulation (e.g., amniocentesis, blunt trauma, pregnancy termination, spontaneous abortion).

risk factors

• Induction of labor by any method. (33456838)
• Premature rupture of membranes, turbulent labor, trauma, C-section, forceps delivery.
• Placental abnormality (previa, abruption, accreta).

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clinical manifestations of amniotic fluid embolism (AFE)

• Early symptoms may be nonspecific (e.g., anxiety, restlessness, dyspnea, hypoxia, and chest pain). (Baxter 2023)
• Dyspnea, with rapidly worsening severe hypoxemia:
  • Bronchospasm may occur.
  • ARDS usually develops.
• Cardiovascular collapse
  • Hypotension is nearly universal.
  • Cardiac arrest is common.
• Neurologic symptoms may vary widely:
  • Anxiety, paresthesias, agitation, or encephalopathy may be seen.
  • Seizures may occasionally be the initial presentation. (Lapinsky 2020)
  • Coma and even brain death may result in some cases.
  • ⚠️ Neurologic abnormalities including seizure should always lead to a consideration of the possibility of (pre)eclampsia.
• Other features:
  • Nausea, vomiting may occur.
  • DIC with subsequent hemorrhage may occur in women who survive the initial phases of AFE. However, rare cases of AFE are described with DIC as a predominant or even sole manifestation. (33456838)
  • Fetal distress is almost always present (prior to delivery).

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differential diagnosis of amniotic fluid embolism (AFE) 

more commonly encountered possibilities

• Pulmonary embolism.
• Obstetric hemorrhage (e.g., uterine rupture, placenta previa, placental abruption).
• Sepsis (including bacterial or viral pneumonia).
• Aspiration pneumonitis causing SIRS (Mendelson syndrome).
• Anaphylaxis.
• Tension pneumothorax.

additional considerations

• Heart failure (may be unmasked during delivery):
  • Peripartum cardiomyopathy.
  • MI (including spontaneous coronary artery dissection).
  • Chronic pulmonary hypertension.
• Tocolytic-induced pulmonary edema.
• Preeclampsia or eclampsia.
• Transfusion reaction.
• Air embolism.
• Fat embolism.
• Toxicologic:
  • High spinal/epidural anesthesia.
  • Local anesthesia systemic toxicity (LAST).

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diagnostic study results in amniotic fluid embolism (AFE)

lab panel

• ABG/VBG.
• Electrolytes including Ca/Mg/Phos, ionized calcium (iCal).
• Lactate.
• Complete blood count.
• INR, PTT, fibrinogen, D-dimer.
• Liver function tests.
• Microbiological studies: Blood cultures x2, sputum culture if applicable.

POCUS

• AFE may cause right ventricular failure, thereby mimicking pulmonary embolism.
• POCUS may help direct resuscitation in terms of fluid responsiveness.
• Cardiopulmonary POCUS may help exclude alternative diagnoses (e.g., tension pneumothorax). If hypovolemia is seen, consider the possibilities of anaphylaxis or hemorrhage.

EKG

• Right ventricular strain may be seen.
• EKG may help evaluate for alternative diagnoses (e.g., spontaneous coronary artery dissection).

chest radiograph

• The primary utility is to help exclude alternative diagnoses (e.g., tension pneumothorax).
• Initially, the chest radiograph may be normal. Later in the disease course, diffuse airspace opacities consistent with cardiogenic or non-cardiogenic pulmonary edema are commonly seen. (Lapinsky 2020)

CT scan

• CT angiography may be desirable to evaluate for pulmonary embolism, if stability allows for this.

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diagnostic criteria for AFE 

There is no gold-standard diagnostic test for AFE (even autopsy results may be equivocal). Consequently, it's impossible to construct any validated diagnostic criteria. Nonetheless, the following criteria may be useful: (27372270)

• Sudden onset of cardiorespiratory arrest, or both hypotension (systolic blood pressure <90 mm Hg) and respiratory compromise (dyspnea, cyanosis, or oxygen saturation <90%).
• Clinical onset during labor or within 30 min of delivery of placenta.
• No fever (≥38.0°C) during labor.
• Documentation of overt DIC following appearance of these initial signs or symptoms, based on the ISTH criteria that have been modified for pregnancy:
  • Platelet count:
    • 50,000-100,000 = 1 point
    • <50,000 = 2 points
  • INR:
    • INR 1.3 – 1.7 = 1 point
    • INR >1.7 = 2 points
  • Fibrinogen <200 mg/dL = 1 point
  • Score of 3 or more indicates overt DIC.
  • Coagulopathy must be detected prior to loss of sufficient blood to itself account for dilutional or shock-related consumptive coagulopathy. (27372270)

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treatment pathway for probable amniotic fluid embolism (AFE) 

Definitive diagnosis of AFE is frequently impossible to determine in real time. When in doubt, an array of supportive measures should be provided immediately. If DIC worsens over time, this supports the diagnosis of AFE.

hemodynamic support for right ventricular failure

• Volume resuscitation can be counterproductive (dysfunction of the left and/or right ventricle are common features). Fluid resuscitation should ideally be guided by POCUS.
• Epinephrine infusion may be an optimal front-line inopressor (beta-agonist effects provide inotropic support for the right ventricle and also promote pulmonary vasodilation). Epinephrine also provides therapeutic coverage for the possibility of anaphylaxis.
• Inhaled pulmonary vasodilators may improve oxygenation and right ventricular function:
  • Inhaled nitroglycerine or milrinone may be provided immediately (e.g., 5 mg of nebulized cardiac nitroglycerine, or 5 mg milrinone via endotracheal tube). 📖 (Baxter 2023)
  • Inhaled epoprostenol or nitric oxide may be utilized for longer time periods. The combination of both inhaled epoprostenol plus nitric oxide together may be more effective than either alone, if needed for management of refractory right ventricular failure.
• Vasopressin may be useful to support systemic blood pressure without impairing right ventricular function. For refractory shock, doses may be increased beyond the typical dose range (e.g., 0.08 U/min). (Baxter 2023)
• Intravenous calcium may be utilized for transient relief from refractory hypotension, especially among patients who have received substantial blood product support that increases risk for hypocalcemia.
• VA ECMO may be utilized (if available).
• Intravenous epoprostenol: This might be used for refractory right ventricular failure if other measures are ineffective and ECMO is unavailable. (31376394, 33417901) Potential risks include worsening of hypoxemia (due to deterioration in ventilation-perfusion matching), worsening of cardiogenic pulmonary edema (due to increased preload on the left ventricle), and hypotension (due to systemic vasodilation). Therefore, intravenous epoprostenol should be initiated only with meticulous monitoring of systemic hemodynamics and oxygenation. Epoprostenol has a short half-life, so if it causes deterioration it may be rapidly discontinued. An initial dose of 2 ng/kg/min may be utilized, with up-titration by 2 ng/kg/min every 15 minutes until hemodynamic improvement or side effects occur. More on epoprostenol dosing here: 📖 (19332472)
• ⚠️ Later in the course of AFE, left ventricular failure may develop. Some therapies for right ventricular failure (e.g., pulmonary vasodilators) may be counterproductive in the presence of left ventricular failure. (Baxter 2023)

respiratory support

• Aggressive oxygen support (e.g., high-flow nasal cannula) may support oxygenation and reduce pulmonary vascular resistance.
• Intubation will generally be required. Ideally, there will be sufficient time to stabilize the patient's hemodynamics prior to intubation. Severe hypoxemic respiratory failure commonly evolves over the disease course, so if the patient is showing signs of deterioration then prompt intubation may be reasonable.

delivery (pre-delivery AFE)

• If AFE occurs prior to delivery, urgent/emergent delivery is generally required.
• If your hospital has a protocol or code for an obstetric emergency (e.g., to simultaneously engage anesthesiology, obstetrics, neonatal ICU, and adult ICU) – consider activating this.
• If cardiac arrest occurs, follow standard ACLS protocols (including resuscitative hysterotomy).

hemorrhage management / DIC

• If DIC with hemorrhage occurs, this should be managed with blood product support.
  • Fibrinogen target >200 mg/dL may be beneficial in the context of peripartum hemorrhage with DIC.
  • Tranexamic acid has been demonstrated to reduce mortality in the context of postpartum hemorrhage. (33456838)
• Postpartum hemorrhage should be managed using standard protocols, as directed by obstetrics.
  • ⚠️ Some uterotonic medications (methylergonovine and carboprost) may worsen pulmonary pressure, so these are generally contraindicated in the context of right ventricular failure. Discussed further here: ⚡️

seizure management

• Benzodiazepine followed by levetiracetam (loading dose of 60 mg/kg up to 4.5 grams total) are generally the preferred antiepileptic agents for status epilepticus in pregnancy.
• Further discussion of status epilepticus management: 📖

steroid

• Methylprednisolone 125 mg IV may be considered for patients progressing to multiorgan failure.
  • Steroid may be beneficial for ARDS, sepsis, and/or anaphylaxis – all of which are often diagnostic possibilities early on.
• Ongoing steroid therapy may be reconsidered the following day, depending on diagnostic studies and patient stability.

antibiotic

• If sepsis is a possibility, administration of antibiotic may be reasonable.
• Depending on the context, single-coverage with a beta-lactam is generally adequate (e.g., ceftriaxone 2 grams IV, or initiation of piperacillin-tazobactam).

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air embolism

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causes & epidemiology

• Percutaneous procedures, especially:
  • Central line insertion and removal.
  • Hemodialysis catheter insertion and removal (large bore catheters may allow rapid entrainment of air).
  • Lung biopsy (note that if air enters a pulmonary vein, it can cause systemic emboli immediately).
  • Intra-aortic balloon rupture.
• Endoscopy.
• Surgical procedures:
  • Neurosurgery (especially seated craniotomy).
  • Cardiac surgery, ECMO.
  • Laparoscopic surgery.
• Obstetric-gynecologic procedures:
  • Childbirth.
  • Cesarean delivery.
  • Laparoscopic procedures.
  • Vacuum abortion.
  • Hysteroscopy, intrauterine gas insufflation.
  • Placenta previa/abruption.
  • Uterine surgery in Trendelenburg position (reduces venous pressure).
• Trauma.

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clinical manifestations 

• Cardiopulmonary: may mimic pulmonary embolism:
  • Dyspnea, coughing.
  • Chest pain.
  • Hypotension, shock.
  • Cardiopulmonary arrest.
• Neurological injury may result from arterial and/or venous infarction:
  • Seizures.
  • Altered mental status, loss of consciousness.
  • Stroke with focal neurologic symptoms (e.g., hemiplegia).

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diagnosis

Small amounts of air often enter the venous system without clinical effects. Consequently, the detection of some intravascular gas may not necessarily indicate a clinically significant air embolism.

• Echocardiography:
  • Test of choice for bedside diagnosis of air embolism.
  • Sensitive for detection of air in the right ventricle.
  • Specificity is limited.
  • May detect right ventricular failure.
• CT scan:
  • Chest CT scan may reveal moderate-large amounts of air in the heart.
  • Head CT may show large air bubbles in the vasculature and/or evidence of infarction (but this has relatively poor sensitivity).
• EKG may reveal right ventricular strain (similar to acute pulmonary embolism).

differential diagnosis includes:

• Pulmonary embolism.
• Pneumothorax.
• Myocardial infarction or stress cardiomyopathy.
• Stroke.
• Medication side effect following a procedure.
• Mesenteric ischemia or intra-abdominal pathology may release small amounts of gas into the venous circulation.

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management

eliminate additional air embolization

• If a central line has been recently removed, ensure that the site is covered by an occlusive dressing.
• Eliminate any disconnections in intravenous lines.

positioning

• Venous air embolism:
  • Left lateral decubitus positioning (left side down).
  • Head-up positioning (Trendelenburg) may prevent obstruction of the right ventricular outflow tract (with improvement in hemodynamic stability). However, upright position could also encourage venous bubbles to travel into the cerebral vasculature, which could theoretically promote venous infarction of the brain.
• Arterial embolism: Patient may be maintained in a flat position. (27809224)
• (Note that after bedside echocardiography indicates that there is no residual air within the cardiac chambers, then positioning is no longer important.)

aspiration of air

• If a central venous catheter is present, efforts should be made to aspirate air from the distal port.
• Insertion of a catheter solely to aspirate air is controversial and has low yield. (28802790)

100% FiO2 administration

• Immediate administration of 100% oxygen is essential (the goal is to de-nitrogenate the blood and thereby accelerate embolism reabsorption). This may be achieved in various ways:
• (1) For intubated patients, FiO2 is easily set to 100%.
• (2) High-flow nasal cannula set to 100% FiO2 with a flow rate well above the patient's inspiratory flow rate (e.g., 40-60 L/min).
• (3) BiPAP or CPAP using an orofacial mask, set to 100% FiO2.
• (4) A combination of a nonrebreather facemask at 15 liters/min plus a nasal cannula underneath it at 15 liters/minute.
• ⚠️ A non-rebreather facemask alone does not provide 100% FiO2. By itself, a non-rebreather facemask is not adequate.

hemodynamic stabilization

• Large air embolism may cause acute right ventricular dysfunction, similar to PE.
• Management may involve:
  • Fluid resuscitation (if there is evidence of intercurrent hypovolemia – which often is present among patients with air embolism).
  • Inopressor infusion (e.g., epinephrine).
  • Inhaled pulmonary vasodilators.

hyperbaric oxygen therapy

• Hyperbaric therapy is likely effective if provided very rapidly (ideally within 4-6 hours).
• It is unclear whether hyperbaric therapy provided at later time-points could be helpful. Delayed application of hyperbaric therapy could theoretically increase reperfusion oxidative injury to the brain, aggravating injury.

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PE in pregnancy

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epidemiology

general risk:

• PE is a leading cause of maternal mortality (with a rate of 0.3-1 per thousand deliveries).
• Risk of PE may be highest from the third trimester through six weeks postpartum. The risk is especially high following a C-section.

specific risk factors:

• Preeclampsia.
• C-section.
• Postpartum hemorrhage.
• Bed rest / immobility.
• Age >35 years old.
• Obesity.
• Smoking.
• Known thrombophilia, e.g.:
  • Sickle cell disease.
  • Lupus.
  • Inflammatory bowel disease.
• Prior venous thromboembolic disease.

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clinical presentation

• Various presentations of PE are discussed here: 📖
• In the context of pregnancy, common features include: (Hameed 2020)
  • Dyspnea (73%).
  • Pleuritic chest pain (66%).
  • Tachypnea (54%).
  • Cough (36%), hemoptysis (13%).
  • Arrhythmia/tachycardia (24%).
  • Wheezing (21%).

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diagnosis

extremity ultrasonography

• Ultrasonography of the leg veins has the advantages of being safe and often being rapidly available.
• If a DVT is diagnosed, then the patient has been diagnosed with venous thromboembolic disease (VTE). Unless the patient has a submassive/massive PE, the treatment of DVT and PE are the same. A positive DVT ultrasound is therefore sufficient to initiate therapeutic anticoagulation (without further investigation).
• If DVT is not diagnosed, this is nonspecific (it doesn't exclude PE).
• (~90% of DVT in pregnancy occurs on the left side, due to the anatomic relationship of the inferior vena cava and the uterus.) (Fishman 2023)

D-dimer in pregnancy

• Normally, the D-dimer rises during the course of pregnancy. By the 20th week of pregnancy, only half of women have a normal D-dimer. Following delivery, the D-dimer falls over a period of weeks.
• A normal D-dimer has the same/greater ability to exclude DVT/PE, as compared to other patients. Unfortunately, pregnant women often have an elevated D-dimer (which is nonspecific).
• A higher D-dimer threshold (1000 FEU or ~500 DDU) may be utilized within the context of the YEARS algorithm (which has been validated in pregnant women).

radiologic studies are discussed above: ⚡️

diagnostic algorithms

• The same general approaches may be used in pregnancy, as are used in most situations (figure below). However, a few nuances are worth discussing.
• There may be an expanded role for performing DVT ultrasonography immediately, with a goal of avoiding further diagnostic studies. Some sources recommend DVT ultrasound for all patients, whereas others recommend them selectively for patients with symptoms of DVT. Either approach is reasonable. However, if DVT ultrasound isn't available, this shouldn't delay evaluation.
• The Wells score and YEARS algorithm seem to be safe to use in pregnancy, with the cutoff parameters shown below. (21854126, 35792687) Nonetheless, clinical judgement is required (indeed, it is built into these decision tools).

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management

anticoagulation is discussed further above: ⚡️

management of massive PE

• Thrombolysis with alteplase is FDA-approved and recommended for massive pulmonary embolism in the context of pregnancy (in the absence of the usual contraindications listed here 📖). Thrombolytic therapy won't cross the placenta. The risk of intracranial hemorrhage is generally low in women of childbearing age.
• If thrombolysis isn't an option, other treatments may include ECMO, percutaneous embolectomy, and/or surgical embolectomy.

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pulmonary hypertension (PH) in pregnancy

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natural history of PH in pregnancy

• Mild-moderate PH is usually well tolerated, but severe PH carries a high mortality.
• PH in pregnancy is usually due to type-1 or type-4 PH (which is the focus of the following discussion).
• Decompensation is most frequent beginning 20-24 weeks gestation, in the third trimester, and postpartum. (33406332)
• (Decision-making surrounding contraception and abortion in PH are extremely important, but these topics are beyond the scope of this chapter.)

diagnosis of PH in the context of pregnancy

• PH is newly diagnosed among about half of women with PH in pregnancy or postpartum. (33406332)
• Symptoms of PH in pregnancy reflect the symptoms of PH in general 📖 (e.g., dyspnea, presyncope/syncope, anginal chest pain, systemic congestion).
• Pulmonary hypertension may also be revealed by detecting right ventricular dilation (e.g., on CT scan, chest radiograph, or POCUS).
• Echocardiography is the front-line test to evaluate for pulmonary hypertension (as discussed here 📖). However, elevated cardiac output may lead to an increased false-positive rate during pregnancy.
• PAC (pulmonary artery catheterization) 📖 is the test of choice if there is a high index of suspicion for moderate/severe PH. The initial evaluation of patients with a new diagnosis of PH additionally involves a battery of tests to evaluate for any underlying etiology: 📖

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optimization of PH in pregnancy

drugs for pulmonary arterial hypertension (PAH) in pregnancy

• Drugs that are considered safe in pregnancy: (36017548)
  • Calcium channel blockers (e.g. amlodipine, nifedipine XR) may be utilized for a very small minority of patients with group 1.1-1.3 PH who demonstrate vasoreactivity during their pulmonary artery catheterization.
  • Phosphodiesterase-5 inhibitors (sildenafil or tadalafil; greater experience with sildenafil). (30704579)
  • Prostacyclin analogues (including inhaled, IV, or subcutaneous):
    • 🏆 IV epoprostenol has the longest record of efficacy and safety in pregnancy.
    • Treprostinil (IV/sc) or inhaled iloprost may be acceptable alternatives. However, iloprost is teratogenic in animals. (Fishman 2023)
• Drugs that should be stopped due to potential teratogenicity: (36017548)
  • Endothelin receptor agonists (e.g., ambrisentan, bosentan, macitentan) are high-grade teratogens that are absolutely contraindicated.
  • Riociguat (absolutely contraindicated).
• Selexipag: evidence is limited.

optimization of chronic PH therapy 

• Women with moderate/severe PH should receive aggressive therapy to optimize their PH as early as possible during their pregnancy (e.g., intravenous epoprostenol plus sildenafil for Group I and also Group IV pulmonary hypertension). (Lapinsky 2020)
• Ideally, treatment will allow women to achieve a WHO functional class of I-II 📖 early in the course of pregnancy (e.g., asymptomatic or mild symptoms only with activity). It's extremely important to achieve a good functional class early in pregnancy, because a WHO functional class of III-IV correlates with significantly elevated mortality and morbidity. (Hameed 2020)
• Close monitoring should be performed throughout pregnancy. PH therapies and volume status should be optimized (e.g., with serial monitoring of weight, brain natriuretic peptide, and transthoracic echocardiography).
• More on basic supportive care in PH: 📖

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decompensation, delivery, and post-delivery plan

management of decompensation

• The management of decompensated right ventricular failure is discussed here: 📖
• Severe decompensation early in pregnancy may require consideration of pregnancy termination to prevent maternal death. (Lapinsky 2020) Decompensation at later time points may require expedited delivery. 

delivery

• Mode of delivery: Both vaginal delivery and C-section have risks and benefits. An unplanned, emergent C-section probably has the highest risk. This will be determined by the obstetric team.
• Timing of delivery: Planned delivery at ~34-36 weeks is recommended, with earlier delivery in cases of symptomatic decline. (33406332)
• Hemodynamic monitoring: placement of a central line to monitor right atrial filling pressures throughout the delivery and post-delivery period may help track and manage fluid shifts. In the most tenuous patients, a pulmonary artery catheter could be considered.
• Anticoagulation plan:
  • For patients requiring systemic anticoagulation (e.g., chronic thromboembolic pulmonary hypertension), there should be a plan to interrupt this prior to delivery.
  • Post-delivery DVT prophylaxis is generally advisable.
• In high-risk patients, delivery should occur at a hospital capable of performing high-level critical care interventions for both the mother and the baby.

post-delivery management

• ⚠️ Mortality is greatest during the week following delivery. (Hameed 2020)
• Risks include:
  • (1) Hemorrhage or epidural anesthesia may reduce venous return, causing cardiovascular collapse. Note that some uterotonic medications utilized for peripartum hemorrhage exacerbate pulmonary hypertension and must be avoided: ⚡️
  • (2) Right ventricular decompensation. Blood autotransfusion from the uteroplacental bed may cause volume overload, which is poorly tolerated in severe PH.
  • (3) Acute pulmonary embolism (risk is especially high following C-section).
• Management following delivery includes close monitoring, with:
  • Early diuretics may help avoid volume overload due to autotransfusion of blood and volume following delivery. If right ventricular failure occurs, it may be managed with escalation in pulmonary vasodilators and inotropes. 📖
  • Aggressive DVT prophylaxis.
  • Continuation and optimization of pulmonary hypertension therapies. For example, if teratogenic therapies were held prior to delivery, these may be restarted.

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sleep-disordered breathing in pregnancy

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types of OSA (obstructive sleep apnea) in pregnancy

• Chronic OSA that is exacerbated by pregnancy.
• Gestational OSA that arises de novo during pregnancy.

consequences of OSA in pregnancy may include:

• Uncontrolled hypertension, preeclampsia.
• Cardiomyopathy, heart failure, pulmonary edema.
• Fetal growth restriction.

screening for OSA in pregnancy

• Clinical features that suggest a risk of OSA: (Lipinsky 2022)
  • BMI >30 kg/m2.
  • Chronic hypertension or history of gestational hypertension or preeclampsia.
  • Neck circumference >40 cm.
  • Snoring or witnessed apneas.
  • Daytime somnolence.
• The STOP-BANG risk stratification tool has a sensitivity of ~55% and a specificity of ~88%. (Lapinsky 2022)
• (More on clinical features and assessment of OSA: 📖)

testing for OSA in pregnancy

• Full polysomnography is the gold standard, but this frequently suffers from unacceptable delays in scheduling studies.
• Home sleep apnea testing (HSAT) isn't perfect, but will likely detect moderate to severe OSA. (Lapinsky 2022)
• (More on the diagnosis of OSA: 📖)

management of OSA in pregnancy

• Auto-titrating CPAP devices may be ideal, as these will automatically up-titrate the pressure level if needed as the pregnancy progresses.
• Patients with OSA may be at increased risk for hypoventilation following C-section. Risk may be reduced by avoidance of respiratory suppressive medications and ongoing adherence to CPAP therapy.
• (More on treatment of OSA: 📖)

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pleural effusion in pregnancy

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pleural effusions associated with pregnancy

• Transudate:
  • Benign postpartum effusion.
  • Preeclampsia.
  • Heart failure (e.g., peripartum cardiomyopathy).
  • Urinothorax due to urinary obstruction or ureteral injury.
• Exudate:
  • Pneumonia.
  • Pulmonary embolism.
• Hemothorax:
  • Choriocarcinoma.
  • Neurofibromatosis. (Lapinsky 2020)

benign postpartum effusion

• Small effusions may be a benign finding in the immediate postpartum period.
• Studies disagree on the incidence of this finding.
• Red flags to consider an alternative process: (Lapinsky 2020)
  • Failure to resolve within days.
  • Moderate to large size.
  • Complexity/septations on ultrasonography.
  • Other worrisome signs or symptoms suggesting active cardiopulmonary disease.

Further discussion about pleural effusion: 📖

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ARDS in pregnancy

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causes of ARDS in pregnancy

• Pneumonia, most often:
  • Bacterial pneumonia.
  • Viral pneumonia.
• Extrapulmonary sepsis:
  • Pyelonephritis.
  • Toxic shock syndrome.
  • Necrotizing fasciitis.
  • Abdominal sepsis (e.g., appendicitis).
  • Obstetric infection:
    • Septic abortion.
    • Chorioamnionitis.
    • Postpartum endometritis.
• Aspiration.
• Trauma.
• TRALI (transfusion related acute lung injury).
• Pancreatitis.
• Other obstetric causes:
  • Preeclampsia and eclampsia.
  • Amniotic fluid embolism. ⚡️
  • Tocolytic pulmonary edema. ⚡️
  • Retained products of conception.

management

• Management is similar to ARDS in general 📖, with a few additional concerns.
• BiPAP may be less desirable, given increased risk of aspiration in pregnancy.
• Proning may not be possible in the context of a gravid uterus.

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tocolytic pulmonary edema

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basics

• Pulmonary edema may be caused by beta-2 selective agents used to prevent premature labor, such as terbutaline, albuterol, and ritodrine. (Similar effects have been reported during tocolysis with calcium antagonists and atosiban). (Murray 2022)
• The etiology of pulmonary edema is unclear (potentially reflecting altered vascular permeability and fluid retention). (Murray 2022)

epidemiology

• Tocolytic pulmonary edema occurs in up to 9% of patients treated with beta-agonist tocolytics.
• This develops 24-48 hours after starting tocolytic therapy (but may also develop within 24 hours of discontinuation).
• Risk factors:
  • Intercurrent volume overload, including steroid use (which promotes fluid retention).
  • Prolonged use of tocolytics.
  • Preeclampsia, magnesium administration.
  • Multiple gestation.

symptoms

• Dyspnea.
• Cough.

differential diagnosis

• Cardiogenic pulmonary edema.
• Pulmonary embolism.
• Amniotic fluid embolism.
• Gastric acid aspiration.
• (See above: other causes of ARDS ⚡️.)

evaluation

• Echocardiogram should be obtained to exclude cardiac dysfunction.

treatment

• Discontinue beta-agonists. Resolution usually will occur within <12-24 hours.
• Supportive care (e.g., oxygen supplementation).
  • <10% of patients require intubation.
• Diuretics may be appropriate for patients with volume overload.

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pulmonary infections in pregnancy

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influenza in pregnancy 

• Pregnant women are at increased risk from influenza; however, most cases are self-limited.
• Primary life-threats from influenza:
  • (1) Exacerbation of underlying illness (e.g., asthma).
  • (2) Post-influenza bacterial pneumonia may be severe (associated with Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes, and Haemophilus influenzae). (Lapinsky 2020)
  • (3) Rarely, influenza pneumonia may itself cause ARDS (especially influenza H1N1).
• Prevention: Vaccination against influenza is recommended to protect mother and baby. Breast feeding may transfer antibodies to the baby, providing protection over the early months of life.
• Treatment:
  • Oseltamivir is safe and recommended in pregnancy. (32068576) The most common side effect is nausea and vomiting. However, the benefit of oseltamivir if initiated >48 hours after symptom initiation is dubious. 
• Further discussion of influenza here: 📖

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pneumonia in pregnancy 

• Pneumonia is generally similar to pneumonia in non-pregnant patients, with a few minor modifications.
• Diagnosis: CRP (C-reactive protein) increases in pregnancy, so it may be unhelpful.
• Management:
  • Antibiotic selection in pregnancy is discussed here: 📖
  • Risk stratification scores haven't been validated in pregnancy. The threshold for admission in pregnancy is generally lower than usual, given limited oxygenation reserve of the fetus.
• Further discussion of community-acquired pneumonia here: 📖

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tuberculosis in pregnancy 

• Suppression of Th-1 immunity in pregnancy may increase susceptibility to tuberculosis. Following delivery, immunity improves (which may cause increased symptoms from tuberculosis, analogous to immune reconstitution inflammatory syndrome).
• Investigation and management of tuberculosis are generally similar to that of nonpregnant patients.
• Further discussion of tuberculosis is here: 📖

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questions & discussion

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