Cardiovascular Disease in Pregnancy Part I: Normal Physiology

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Basic Heart Function

Right Heart

• Blood flows from the SVC + IVC → R atrium → tricuspid valve (3 leaflets) → R ventricle → pulmonary valve (3 leaflets) → pulmonary artery (or pulmonary trunk), which then divides to right and left pulmonary artery → lungs.

• What happens if the right heart fails?

  • R sided heart failure basically means that the right side of the heart is not pumping out as much blood to the lung that is coming in from the peripheral veins (blood in > blood out).

    • This leads to blood backing up into the systemic circulation → lower extremity edema, hepatomegaly, jugular venous distention.

    • One of the most common causes is left heart failure.

    • Other acute causes:: pulmonary embolism with large clot burden, adult respiratory distress syndrome, RV myocardial infarction, myocarditis.

    • Causes of chronic right heart failure: pulmonary hypertension, pulmonary arterial hypertension (which is different from PH!), COPD, OSA, congenital heart disease, cardiomyopathies, or right sided valve disease.

Left Heart 

• Oxygenated blood from lungs → left atrium → mitral valve (2 leaflets) → left ventricle → aortic valve (3 leaflets) → aorta & systemic circulation 

• What happens if the left heart fails?

  • Left heart failure again means that the left side of the heart is not pumping out as much blood to the body as is coming in (blood in > blood out).

    • This leads to blood backing up into the pulmonary circulation → pulmonary edema, which can lead to SOB, coughing, etc 

    • Causes of left heart failure: myocardial infarction, dilated cardiomyopathy, left sided valvular disease, hypertension, congenital heart disease 

How does the cardiovascular system change with pregnancy? 

Hemodynamic changes

• Antepartum 

  • Throughout pregnancy, there is a continuous increase in maternal cardiac output and plasma volume.

  • There is a decrease in maternal systemic vascular resistance.

  • Blood pressure will decrease initially, but will increase in 3rd trimester.

• Intrapartum and postpartum 

  • During labor and delivery, there is increase in cardiac output, heart rate, blood pressure, and plasma volume 

  • Immediately postpartum, there is a large fluid shift (500 cc of autotransfusion), as blood flow to the gravid uterus shifts back to maternal circulation 

  • Blood pressure may increase between days 3-6 because of fluid shifts 

  • All of these shifts will make women with cardiac disease more prone to fluid overload and pulmonary edema.

Structural changes 

• The heart itself will increase in size with pregnancy 

• The left and right ventricular mass increase by approximately 50 and 40% 

• LV end diastolic volumes increase by 10% 

• Approximately 20% of women have diastolic dysfunction at term → dyspnea on exertion 

• Structural changes return to baseline after 1 year postpartum 

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ACOG PB 212

Oxygen: Friend or Foe?

Shout out to Chelsea Jorgenson, nurse at UW Medical Center, for the episode idea! 

Oxygen is a drug.

The FDA regulates medical gases like oxygen as a drug, with the approved indications of hypoxia and hypoxemia. Did you know these are different?

• Hypoxemia: reduced partial pressure of O2 in the blood (low PaO2).

• Hypoxia: reduced tissue levels of O2 so that cellular metabolism is impaired.

  • Hypoxemia generally precedes hypoxia. 

    • You have less oxygen to deliver, so there’s less O2 in the tissues over time. 

  • Hypoxemia does not always result in hypoxia. 

    • For instance, those who live at high altitude can by hypoxemic, but not hypoxic. 

Like other drugs, oxygen has benefits, but also has potential harms. And for a quick review of the benefits/harms of oxygen medically, check out the Journal of Hospital Medicine’s series, “Things We Do For No Reason.”

Many studies have shown, mostly on animal models, that hyperoxygenation leads to lung injury, inflammation through free radical generation, and changes in perfusion that may actually be harmful:

• COPD: oxygen titrated to goal >88-92% is associated with 2x fold increased mortality risk.

  • Linked likely due to worsened ventilation-perfusion matching and poorer CO2 offloading as PaO2 rises (Haldane effect). 

• MI: 1976 RCT of O2 in suspected MI patients at 6L/min. Patients receiving for 24 hours or more had more episodes of tachycardia with no improvement in mortality, analgesic use, or infarct size. 

  • Subsequent trials have found similar outcomes, and actually have also demonstrated increased rate of MI recurrence with O2 use.

  • European Society of Cardiology has now actually recommended no O2 use unless SpO2 < 90% for MI patients! 

• Retinopathy of prematurity: hyper oxygenation of neonates increases risk of blindness.

• Other illness: trials in settings ranging from ICUs, strokes, TBIs, and cardiac arrest have also linked liberal O2 use (ranging from 2L NC upwards) to increased mortality and other adverse events.

  • A meta analysis demonstrated a dose-dependent toxicity: for every 1% increase of SpO2 above 94-96%, there was 25% relative increase in in hospital mortality!!! 

So when is oxygen helpful?

Importantly, these studies have mostly looked at normoxemic patients who receive supplemental oxygen. Patients who are significantly hypoxemic or hypoxic will certainly benefit from O2. 

Additionally, patients with conditions such as CO poisoning, cluster headaches, sickle cell crisis, and pneumothorax may all benefit from O2. These are actual indications for the drug.

OK, so what about pregnancy and labor?

O2 is most commonly administered in labor, in an attempt to improve fetal status. The thought being that, if we see significant decelerations that reflect fetal hypoxia, administration of supplemental oxygen through the mother/placenta will help to correct it. 

• Pro oxygen evidence:

  • Fetal pulse oximetry studies 2 small studies using a fetal pulse-oximeter in laboring women demonstrated increased fetal oxygenation of 5% with simple face masks, and 7-15% when using non-rebreathers, in non-hypoxic fetuses. In hypoxic fetuses, the observed benefit was greater, 20% with simple face mask and 26-37% with non-rebreather. 

    • Fetal pulse oximetry did not help to improve rates of cesarean delivery for fetal indications, and thus has not caught on as a routine technology in labor management. Thus critics would argue it’s hard to interpret these studies in context of whether O2 improves neonatal outcomes, or just makes the saturation numbers better.

• Anti-oxygen evidence:

  •  Fetal scalp pH study:a small study examining the effect of administering 50-10% oxygen during first stage of labor actually had no effect on fetal scalp pH, and trended towards a worsening base deficit with supplemental O2. Another study of primates administered O2 with acidotic fetuses by scalp pH demonstrated worsening of acidosis with O2 administration. 

    • These studies though, like the others, were small and nonrandomized. There is also criticism in the timing and application of O2 in each of these trials. 

  • Non-inferiority RCT: a 2018 RCT in JAMA used a non-inferiority approach to randomize 114 patients to supplemental O2 versus room air with category II EFM. They found no difference between groups in improving umbilical artery lactate, which was their primary marker for this trial.

    • There was also no difference in other cord gas components or rates of cesarean delivery for fetal indications. 

    • Umbilical artery lactate does have some ability to predict hypoxia-associated morbidity in neonates; however, it is not sensitive or specific for poor outcomes, a valid criticism. The trial was not powered for neonatal outcomes. 

  • A secondary analysis of this same RCT looked at umbilical venous O2 concentration and actually found lower O2 pressure in fetuses exposed to long periods of O2 than those exposed for short periods or on room air. 

The physiologic arguments for (or against) O2

Check out our fetal circulation episode for a quick review of how blood and oxygen travel in the fetus!

The maximum fetal PO2 (i.e., in the umbilical vein at the site of the placenta) cannot exceed maternal venous PO2. This is why fetal hemoglobin has to have a very high oxygen affinity, as it must extract O2 away from the venous side of maternal blood, which already is at a lower oxygen concentration. 

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An oxygen dissociation curve. Fetal hemoglobin maintains relatively excellent saturations, even at usual venous O2 pressures in maternal circulation (HbA). Source: WIKIPEDIA.

• A normal venous Po2 in adults is around 35-45 mmHg (arterial is around 100 mmHg). That would equate on a HbA dissociation curve to a saturation of around 65-75%. 

• A normal Po2 in a venous cord gas, by comparison, is on average around 35mmHg, again representing maternal venous O2 tension. 

  • But the fetal hemoglobin affinity for O2 powers this to about an 80-90% saturation! And that is considered normal -- most O2 saturation values at the 5 minute Apgar are in the mid-80%s.

• The question lies herein: by causing maternal hyperoxemia, will that result in fetal recovery if the fetus is hypoxic? 

  • By increasing the PaO2 in the mother with supplemental oxygen, theoretically there would be an increased oxygen gradient to diffuse downstream to the fetus. 

    • In effect, because there is more oxygen tension, the higher the maternal PvO2 and umbilical vein O2 pressure can become.

  • But as we discussed with ischemic events, sometimes oxygen may counterintuitively not improve outcomes, or mask worsening of the process! 

    • In this case, the fetus becomes hypoxic, or the “ischemic” tissue -- would the new O2 load in this case be detrimental? 

    • Or potentially, like in COPD, would the normoxemia actually mask worsening acidosis? 

    • Or finally, as demonstrated in the RCT we referenced, does the O2 even get to the fetus due to some placental transfer failure in the presence of hyperoxia?

What should the bottom line takeaway be?

That’s the other interesting thing about this -- in spite of the fact that there is little evidence supporting this practice, O2 is wildly popular as a resuscitative effort. It’s simple and quick to apply. 

Intrauterine resuscitation, defined as repositioning, oxytocin discontinuation, fluid administration, amnioinfusion, or oxygen administration in response to fetal heart rate tracing abnormalities, are all options. 

While we couldn’t identify any studies that shared the “natural history” of what’s done during a deceleration, anecdotally we know that reflexively, reaching for the facemask oftentimes will precede these other measures, despite the evidence on decelerations favoring these other options. In short, leave O2 for maternal hypoxia, or as a last-resort option for fetal resuscitation! 

Perinatal Depression

Depression is a major health disorder affecting around 10% of women, particularly in the perinatal and postpartum periods. Depression is twice as common in women as in men, and OB/GYNs should be familiar with its diagnosis and management, particularly in the perinatal period. You can read more with ACOG CO 757.

There are many different types of depression diagnoses, including: major depressive disorder, persistent depressive disorder, seasonal affective disorder, perinatal (postpartum) depression, premenstrual dysphoric disorder (PMDD), etc. According to the DSM-V, a major depressive episode is diagnosed when one has: 

• Five (or more) of the following symptoms have been present for a 2-week period and represent a change from previous functioning; at least one of the symptoms is either depressed mood or loss of interest/pleasure. 

• Symptoms cannot be explained by medications or another medical illness (i.e., hypothyroidism).

• The remaining (need 4+ from this list):

  • Depressed most of the day, nearly every day as indicated by subjective report or observation made by others;

  • Diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day;

  • Significant weight loss when not dieting or weight gain, or increase/decrease in appetite nearly every day;

  • Insomnia or hypersomnia;

  • Psychomotor agitation or retardation; 

  • Fatigue or loss of energy;

  • Feelings of worthlessness or inappropriate guilt;

  • Decreased ability to think/concentrate;

  • Recurrent thoughts of death/suicidal ideation.

Perinatal depression is defined separately as major and minor depressive episodes that occur during pregnancy or in the first 12 months after delivery. This is one of the most common medical complications during pregnancy and the postpartum period, affecting 1/7 women. 

Depression and other mood disorders can have devastating effects on women and their families: maternal suicide exceeds hemorrhage and hypertensive disorders as a cause of maternal mortality 

SO how do we screen for perinatal depression? ACOG recommends that obstetric care providers screen patients at least once during the perinatal period for depression and anxiety symptoms using a standardized tool, and again in the postpartum period during a comprehensive postpartum visit. There is evidence that screening alone can have clinical benefits for patients suffering with depression.

One of the most commonly used is the Edinburgh Postnatal Depression Screen, which is a 10 item survey that takes less than 5 minutes to complete. The sensitivity is estimated between: 59-100%, and specificity: 49-100%. A Spanish version is available.

The Patient Health Questionnaire 9 (PHQ-9) is another acceptable tool. Other items like the Postpartum Depression Screening Scale (PDSS) is more sensitive (91-94%) and specific (72-98%), but it is a 35 item survey and thus more time intensive.

Management of perinatal depression is a team sport, requiring multiple additional support members and medical team members. Medication prescription will vary for OB/GYNs and their comfort with this. In brief:

• Women with current depression/anxiety or a history of perinatal mood disorder should have close monitoring, evaluation, and assessment.

• Some OB/GYNs are comfortable starting antidepressant medication and following their patients, most commonly an SSRI. Psychiatry referral is also acceptable.

• Referral to social work and behavioral health - possibly for psychotherapy, which alone is a reasonable alternative to antidepressants if needed.

• For those with severe postpartum depression, another possibility is brexanolone.

  • Limited clinical experience and restricted availability 

  • Usually restricted to patients who do not improve with antidepressants 

Malposition and Malpresentation

We start off today with some news — for the foreseeable future, CREOGs Over Coffee will move to every-other-week Sunday episodes. It’s been a wild ride and now that we’ve moved across the country from each other, we want to make sure we deliver the same high-quality content we expect and want you to have! While you may hear less of us for now, we’re also working on some other projects, so stay tuned!

On to the episode! And for further reading, check out this review.

Malposition vs. Malpresentation

Fetal lie: the relationship between the fetal long axis and the mother (i.e., longitudinal, transverse, oblique).

Malpresentation: the fetal vertex is not the presenting part, or the part of the fetus closest to the pelvic inlet.

• Breech: 3-4/100 term pregnancies

• Face: 1/600-800 term deliveries

• Brow: 1/500-4000 term deliveries

• Compound: 1/1500 deliveries

• Shoulder: 1/200 deliveries

Malposition: the fetus is in vertex position, but the position of the fetal head is not optimal for delivery (i.e., rotated away from an occiput anterior, or OA, position in the pelvis).

• Occiput transverse (OT) or occiput posterior (OP).

  • These are given a direction based on rotation of the occiput 45 degrees from the direct position (i.e., right occiput posterior denotes rotation of the occiput to maternal right).

    • If occiput < 45 degrees from vertical, is OA or OP.

    • If occiput is > 45 degrees from vertical, is OT.

• Prior to labor, 15-20% of term fetuses in cephalic presentation are in OP position. At delivery, only 5% will persist this way, as they will often rotate spontaneously.

Action to take with various malpositions and malpresentations:

First, a word on “normal” vaginal deliveries 

• In OA position, the neck flexes to bring the chin to the chest → smaller diameter of the fetal head (about 9.5 cm), which is usually able to traverse the obstetric conjugate (average 10.5cm), which is the shortest anteroposterior pelvic diameter.

  • In other positions (ie. face or brow), the neck is extended and there is larger fetal cephalic head diameter that needs to traverse this area, making it more difficult to pass.

Breech, Transverse Lie, & Shoulder Presenations

• We have previously discussed breech vaginal delivery, but current recommendation for breech and shoulder presentation is cesarean section.

• Shoulder presentations cannot deliver vaginally. The shoulder is wedged into the pelvis, and the head will lie in one of the iliac fossa, and the breech in the other - the baby becomes wedged into the pelvic inlet and cannot get past.

• For shoulder, describe using location of the scapula: 

  • Left scapula anterior (LSA), and RSA. 

  • Left scapula posterior (LSP), and RSP. 

• With transverse lies, just like breech, can offer ECV prior to labor, but once labor occurs, usually versions become very difficult to do.

Face Presentation

• The fetal face from forehead to chin is the leading fetal body part descending into the birth canal. This is usually diagnosed by vaginal exam (can palpate the orbital ridge, nose, mouth, chin), not able to palpate the fontanelles.

• Described using location of the chin, or mentum.

  • At diagnosis, about 60% are mentum anterior and 26% are mentum posterior (ie. chin up or chin down); 15% are mentum transverse.

• Management varies depending on presentation:

  • Mentum anterior The fetal chin needs to pass under the symphysis pubis, and fetal neck may need to extend even more (though it is already extended).

    • After the chin clears the symphysis, it is possible for vaginal delivery, and women should be allowed to push during second stage.

    • Forceps can be used, but engagement doesn’t occur until the face is at +2 station, and the chin, rather than the occiput becomes the focal point for orientation.

    • Vacuums are contraindicated… because where would you put it?!?!

  • Mentum posterior In this case, the fetal neck is maximally extended and cannot extend further to allow the occiput to pass under the symphysis.

    • Will NOT deliver vaginally unless there is spontaneous rotation to mentum anterior. 

    • If discovered early in labor, can have expectant management in the hopes that the mentum will spontaneously rotate to anterior.

    • However, recommendation is for cesarean if persistent mentum posterior with abnormal labor progress.

    • What about attempting rotation? 

      • Not a lot of cases, and there have been case reports of successful internal and external manipulation.

      • Some case reports of uterine rupture, cord prolapse, and cervical spine trauma.

      • Overall: if cesarean is available, would favor cesarean.

Brow presentation

• A variant of face presentation, when presenting part is the anterior fontanelle to the brow (orbital ridge), which does not include the mouth and chin.

• Diagnosis is usually made with vaginal exam (you can feel the forehead, orbits, and nose).

• Management:

  • Can undergo trial of labor, as brow presentation may be transitional 

    • In one study, when brow presentation was diagnosed early, 67-75% of fetuses spontaneously converted to a more favorable presentation and delivered vaginally.

    • If diagnosed later:

      • 50% spontaneously converted and delivered;

      • 30% the neck extended further;

      • 20% the neck flexed and resulted in occiput posterior presentation. 

  • Rotational maneuvers, vacuum, and forceps are not recommended. 

Persistent occiput posterior 

• Most common malposition, encountered very frequently in clinical practice, and will often convert spontaneously.

• Manage expectantly in first stage of labor. In second stage of labor can also be expectant as long as fetal heart rate is reassuring and labor is progressing 

  • 50-80% of OP fetuses at beginning of second stage will rotate spontaneously to OA. 

  • If clinically adequate pelvis with a prolonged second stage - can attempt manual rotation to the OA position.

  • Prospective study - manual rotation vs. Expectant management of OP demonstrated higher likelihood of vaginal delivery and fewer cases of persistent OP presentation.

• Manual rotation techniques 

  • Digital - placing tips of index and middle fingers in the anterior segment of the lamboid suture near the posterior fontanelle, and then used to flex and slightly dislodge the head, and rotation to OA position with the operator’s hand and forearm.

  • Hand - placing operator’s four fingers behind the posterior parietal bone with palm up and thumb over the anterior parietal bone. Right hand for LOP, left hand for ROP.

    • Flex and slightly dislodge the head → rotate.

Obstetrical Analgesia and Anesthesia

Why do we care about labor anesthesia and analgesia? We’re obstetricians!

• Labor hurts!

  • Technically speaking, evolution of visceral pain to somatic pain in the second stage of labor when the fetus comes down to the perineum → pain through the pudendal nerve and S2-S4 distribution.

  • There is also a discrepancy with rating of pain and rating of satisfaction with pain relief in certain trials - possibly because there are varying expectations for pain control and labor experience 

What is available? 

• Parenteral or systemic analgesia 

  • IV opioids. Unfortunately, they have little effect on maternal pain scores, provide unreliable analgesia, and can have adverse effects, such as nausea or vomiting.

  • We usually use fentanyl, morphine or butorphanol (Stadol).

  • Cochrane review has not found the ideal parenteral opioid and though there is some pain relief with this, it’s poor overall.

  • Also, all opioids cross the placenta, and there can be some adverse effects on the fetus.

    • Drugs will take longer to eliminate in the newborn, and can cause respiratory depression if administered close to time of delivery. 

• Regional (Neuraxial) analgesia and anesthesia

  • More than 60% of women w/ singleton birth in the US get an epidural or a spinal 

    • Epidural - placement of a catheter into the epidural space; can have repeat or continuous administration of medication; usually a mixture of an opioid with a local anesthetic.

    • Spinal - single-injection of an opioid, local anesthetic, or both into the subarachnoid space; usually used for cesarean delivery and not for labor because it usually has a limited time frame.

    • Combined Spinal-Epidural Analgesia 

      • Inject into the subarachnoid space and also a placement of a catheter for ongoing analgesia 

      • This is usually used because of rapid onset of pain relief of spinal, combined with long-acting effect of epidural.

• Local anesthesetics 

  • Pudendal nerve blocks - local anesthesia that is injected transvaginally into the vicinity of the pudendal nerve below the ischial spines; usually just for second stage of labor or to help with lac repairs 

  • Local infiltration (usually for lac repair) 

• Inhaled agents 

  • Nitrous oxide - 50% of NO and 50% O2 with demand valve so only given when patients inhale using the mask.

  • Analgesia provided by NO is less effective than epidural when we look at pain scores; but NO is superior for mobility because patients can still move around, and also has quick termination of effect.

• General Anesthesia 

  • Exceptionally rare use for a vaginal delivery, and sometimes used for emergent cesarean sections.

  • The main issues is that these agents will transfer to the fetus → depression 

  • Also harder to manage airway of pregnant patient due to anatomic changes (increased airway edema).

Risks of Regional Analgesia and Anesthesia 

• Maternal 

  • Overall very low risk of maternal morbidity and mortality.

  • In a registry that was collected over 5 years (ended in 2009), in >300,000 recorded cases of anesthesia use, there were 157 complications.

    • There were 30 maternal deaths in this cohort, none of which were attributed to anesthesia.

    • There were 2 cardiac arrests attributable to anesthesia, 4 cases of epidural abscess or meningitis, 1 epidural hematoma, 10 failed intubations (no aspirations), 58 high neuraxial blocks

  • Minor complications can be things like pruritis, epidural headaches, hypotension, nausea/vomiting 

• Fetal 

  • Usually related to maternal effects of hypotension or transplacental passage of analgesic or anesthetic drugs 

  • Opioids can lead to neonatal depression (ie. respiratory depression, decreased muscle tone, decreased sucking) 

  • Alterations to FHT can also be seen; ie. minimal variability, bradycardia, prolonged deceleration in the first 15 minutes following spinal-epidural analgesia.

Who can’t get regional anesthesia? 

• Thrombocytopenia - relative contraindication, but safe lower limit for platelet count hasn’t been established.

  • One study stated that risk of epidural hematoma among obstetric patients was 0-0.6% when platelets were 70-100k, but stated that data was insufficient to assess risk when platelets were <70k.

  • So in most cases, epidurals/spinals can be considered same if platelets are 70K or above, as long as platelets are stable.

• Low dose aspirin - not a contraindication! 

• Anticoagulation 

  • Unfractionated heparin

    • Prophylactic dose (i.e., 5000u BID):

      • Not contraindication to neuraxial techniques

      • Place or remove catheter 4-6 hours after last dose.

    • Intermediate dose (7500-10000u BID):

      • Likely low risk to proceed with neuraxial anesthesia if > 12 hours after last dose 

    • High dose (>20,000u total daily):

      • Placement >24 hours after last dose and must have activated partial thromboplastin time within normal range or anti-factor Xa level undetected.

      • If taking unfractionated heparin >4 days, platelet count should be assessed for possible HIT.

    • Resume UF heparin >1 hour after catheter removal.

  • Low molecular weight heparin (ie. Lovenox)

    • Prophylactic dosing:

      • Stop medication at least 12 hours before placement or removal of epidural catheter 

    • Therapeutic dosing:

      • 24 hour delay in catheter placement.

    • Resume LMWH >4 hours after catheter removal 

• Space-occupying brain lesions - contraindication to neuraxial techniques because dural puncture can lead to increased intracranial pressure → hindbrain herniation.

  • However, not all space-occupying lesions result in increased ICP.

  • If imaging shows no mass effect, hydrocephalus, or other features suggestive of increased ICP, risk of herniation is minimal and epidural analgesia or anesthesia can be considered.