UBP 3.1 (Short Form): Obstetrics – Aortic Stenosis

Question 1

What do you think of her aortic transvalvular gradient?

(A 28 yo, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery. Her history includes multiple sclerosis, migraine headaches, asthma, and aortic stenosis with a mean transvalvular gradient of 50 mmHg. She is receiving albuterol for asthma, digoxin for aortic stenosis, methylprednisolone for multiple sclerosis, antibiotics for suspected chorioamnionitis, and 80 mg of enoxaparin BID for deep vein thrombosis that developed during this pregnancy. BP = 146/88 mmHg; Temp = 38.8 C; Platelets = 115,000.)

Answer 1

Her transvalvular gradient of 50 mmHg is very concerning since it may represent severe, or even critical, aortic stenosis.

Recognizing that the hyperdynamic circulation associated with pregnancy can lead to an increased aortic transvalvular gradient and overestimate of the severity of her aortic stenosis, I would also review the echocardiographic estimation of the aortic valve area (a superior method of assessing the severity of aortic stenosis in pregnant patients).

Likewise, I would keep in mind that a failing or dysfunctional left ventricle can lead to a decreased aortic transvalvular gradient as compared to a normally functioning left ventricle, potentially leading to an underestimate of the severity of her aortic stenosis

Question 2

Does this patient require bacterial endocarditis prophylaxis?

(A 28 yo, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery. Her history includes multiple sclerosis, migraine headaches, asthma, and aortic stenosis with a mean transvalvular gradient of 50 mmHg. She is receiving albuterol for asthma, digoxin for aortic stenosis, methylprednisolone for multiple sclerosis, antibiotics for suspected chorioamnionitis, and 80 mg of enoxaparin BID for deep vein thrombosis that developed during this pregnancy. BP = 146/88 mmHg; Temp = 38.8 C; Platelets = 115,000.)

Answer 2

According to the revised American Heart Association guidelines from 2007,

aortic stenosis is no longer an independent indication for endocarditiis antibiotic prophylaxis.

The new guidelines now emphasize prophylaxis for those conditions associated with the highest risk for adverse outcomes from infectious endocarditis (IE) versus those associated with the highest lifetime risk of acquisition of IE.

(see below)

Therefore, prophylaxis is more reasonably reserved for patients with the following conditions:

1. a prosthetic cardiac valve or prosthetic material used for valve repair;
2. a previous IE;
3. Congenital heart disease (CHD):
   
   • unrepaired cyanotic congenital heart disease;
   • the 6 month postoperative period following a repaired congenital heart defect using prosthetic material or a device;
   • repaired congenital heart disease with residual defects at the site or adjacent to the site of a prosthetic patch or device (which inhibits endothelialization); and
4. cardiac transplantation recipients who develop cardiac valvulopathy.

Although aortic stenosis is not an independent indication for antibiotic prophylaxis, I would continue any current antibiotics she is receiving to treat chorioamnionitis.

• Previous AHA guidlines categorized underlying cardiac conditions associated with the risk of IE as those with high risk, moderate risk, and negligible risk and recommended prophylaxis for patients in the high- and moderate-risk categories.*
• For the present guidelines on prevention of IE, the Committee considered three distinct issues:*

1. What underlying cardiac conditions over a lifetime have the highest predisposition to the acquisition of endocarditis?
2. What underlying cardiac conditions are associated with the highest risk of adverse outcome from endocarditis?
3. Should recommendations for IE prophylaxis be based on either or both of these two conditions?

• In a major departure from previous AHA guidelines, the writing group NO longer recommends IE prophylaxis based SOLELY on an increased ilfetime risk of acquisition of IE.*
• Rather, prophylaxis is reocmmended for patients with highest risk of adverse outcome from endocarditis (See Table Listings above).*
• It is noteworthy that patients with the conditions listed above are also among those patients with the highest lifetime risk of acquisition of endocarditis.*
• No published data demonstrate convincingly that the administration of prophylactic antibiotics prevents IE associated with bacteremia from an invasive procedure.*
• We cannot exclude the possibility that there may be an exceedingly small number of cases of IE that could be prevented by prophylactic antibiotics in patients who undergo an invasive procedure.*
• However, if prophylaxis is effective, such therapy should be restricted to those patients with the highest risk of adverse outcome from IE who would derive the greatest benefit from prevention of IE.*

Question 3

Would you agree to a labor block?

(A 28 yo, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery. Her history includes multiple sclerosis, migraine headaches, asthma, and aortic stenosis with a mean transvalvular gradient of 50 mmHg. She is receiving albuterol for asthma, digoxin for aortic stenosis, methylprednisolone for multiple sclerosis, antibiotics for suspected chorioamnionitis, and 80 mg of enoxaparin BID for deep vein thrombosis that developed during this pregnancy. BP = 146/88 mmHg; Temp = 38.8 C; Platelets = 115,000.)

Answer 3

While I recognize there are some concerns about providing neuraxial anesthesia to a patient with multiple sclerosis, maternal fever, severe aortic stenosis, and preeclampsia,

I would agree to a labor block in this case as long as her enoxaparin had been discontinued for at least 24 hours

(therapeutic dosing requires a 24 hour delay prior to neuraxial block placement).

Neuraxial blockade would be desirable because it would more reliably prevent pain-induced tachycardia in this patient with severe aortic stenosis.

Moreover, should a cesarean section be required, it would preclude the necessity for providing general anesthesia to this patient who is at increased risk for difficult airway management

(the physiologic changes of pregnancy along with her obesity, preeclampsia, and asthma increase the risk of difficult airway management).

• In regards to the previously mentioned concerns, the evidence suggests that neuraxial anesthesia may be safely provided for patients at increased risk for bacteremia (fever and chorioamnionitis), despite concerns that dural puncture and vascular disruption could lead to increased incidence of epidural abscess and meningitis in these patients.
• Also, while neuraxial anesthesia has been associated with an exacerbation of multiple sclerosis, this has been most significant with spinal anesthesia and epidural anesthesia utilizing higher concentrations of local anesthetic.
  
  • Therefore, most practitioners consider it safe to provide epidural anesthesia using dilute solutions of local anesthetics for patients in labor.
• Furthermore, while preeclampsia often affects both platelet number and function, the risk of bleeding in the epidural or spinal space should be minimal with her platelet level of 115,000.
• And, finally, even with severe aortic stenosis, an epidural anesthetic can be safely provided by slowly administering small doses of local anesthetic without epinephrine (epinephrine could lead to tachycardia), allowing for adequate fluid replacement and compensatory vasoconstriction above the level of neuraxial blockade.

Question 4

Wouldn’t the drop in SVR often associated with neuraxial anesthetics improve her cardiac output?

(A 28 yo, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery. Her history includes multiple sclerosis, migraine headaches, asthma, and aortic stenosis with a mean transvalvular gradient of 50 mmHg. She is receiving albuterol for asthma, digoxin for aortic stenosis, methylprednisolone for multiple sclerosis, antibiotics for suspected chorioamnionitis, and 80 mg of enoxaparin BID for deep vein thrombosis that developed during this pregnancy. BP = 146/88 mmHg; Temp = 38.8 C; Platelets = 115,000.)

Answer 4

While a decrease in afterload often promotes increased cardiac output,

this is not the case in severe aortic stenosis where the stenotic valve, rather than systemic vascular resistance, creates most of the afterload on the left ventricle.

Therefore, a significant drop in systemic vascular resistance is poorly tolerated by these patients with a relatively fixed stroke volume and an inability to adequately increase cardiac output.

The subsequent diastolic hypotension and compensatory tachycardia places this patient with a likely hypertrophied myocardium at increased risk for subendocardial ischemia.

Question 5

Assuming you were willing to place an epidural for labor, how long would you have to wait following her last dose of enoxaparin?

(A 28 yo, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery. Her history includes multiple sclerosis, migraine headaches, asthma, and aortic stenosis with a mean transvalvular gradient of 50 mmHg. She is receiving albuterol for asthma, digoxin for aortic stenosis, methylprednisolone for multiple sclerosis, antibiotics for suspected chorioamnionitis, and 80 mg of enoxaparin BID for deep vein thrombosis that developed during this pregnancy. BP = 146/88 mmHg; Temp = 38.8 C; Platelets = 115,000.)

Answer 5

NOTE – See updated ASRA Consensus guidelines – saved on Google Drive

Based on recommendations of the 2nd ASRA consensus conference on neuraxial anesthesia and anticoagulation, I would wait at least 24 hours following her last therapeutic dose of enoxaparin before initiating neuraxial blockade.

While a delay of only 10-12 hours is recommended with patients receiving low-dose LMWH for thromboprophylaxis, a longer delay of 24 hours is recommended for those receiving high-dose LMWH for DVT treatment.

Of course, in addition to considering the guidelines, I would weigh all risks and benefits before making a definitive decision.

My considerations in this regard would include –

• airway management (i.e., the anticipated difficulty of airway management; and the likelihood that she will require a cesarean section where airway management would be necessary in the absence of neuraxial blockade),
• the importance and urgency of providing neuraxial anesthesia (i.e., cesarean section rather than just labor; the importance of more effective pain control for a patient with aortic stenosis), and
• the risks associated with alternative anesthetic options (i.e. PCA for labor; or general anesthesia for cesarean section).

Question 6

If it had not been enough time yet, could you check an anti-Xa level or administer protamine to reverse the effects of enoxaparin?

Answer 6

I would NOT check an anti-Xa level as a means of weighing the risk of epidural or spinal hematoma because, while it may be used to guide therapeutic dosing, the anti-Xa level is NOT predictive of hemorrhagic complications.

Likewise, I would NOT administer protamine, since it does not reliably reverse the anti-factor Xa activity of LMWH and is NOT recommended for the reversal of LMWH.

Question 7

Would you require any special monitoring at this point?

(A 28 yo, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery. Her history includes multiple sclerosis, migraine headaches, asthma, and aortic stenosis with a mean transvalvular gradient of 50 mmHg. She is receiving albuterol for asthma, digoxin for aortic stenosis, methylprednisolone for multiple sclerosis, antibiotics for suspected chorioamnionitis, and 80 mg of enoxaparin BID for deep vein thrombosis that developed during this pregnancy. BP = 146/88 mmHg; Temp = 38.8 C; Platelets = 115,000.)

Answer 7

Considering this patient’s –>

• aortic stenosis,
• the increased risk for bleeding (due to preeclampsia and the acquired von Willebrand syndrome associated with moderate to severe aortic stenosis), and
• the potential for hemodynamic changes during vaginal delivery (pain-induced sympathetic stimulation, bleeding, and auto-transfusion during uterine involution),

I would employ:

1. fetal heart rate monitoring (the mother’s aortic stenosis and preeclampsia increase the risk of inadequate uterine perfusion),
2. a 5-lead EKG (increased risk for arrhythmia and/or myocardial ischemia), and
3. an arterial line for labor and delivery (peripartum invasive arterial monitoring is recommended in the setting of moderate to severe aortic stenosis).

If her enoxaparin had been discontinued at least 24 hours prior, I would consider placing a central venous pressure line to facilitate fluid management.

Finally, I would ensure the availability of transthoracic echocardiography to help with determining the cause of any hypotension (e.g., heart failure, hypovolemia, or myocardial ischemia).

Question 8

Would you place a pulmonary artery catheter?

(A 28 yo, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery. Her history includes multiple sclerosis, migraine headaches, asthma, and aortic stenosis with a mean transvalvular gradient of 50 mmHg. She is receiving albuterol for asthma, digoxin for aortic stenosis, methylprednisolone for multiple sclerosis, antibiotics for suspected chorioamnionitis, and 80 mg of enoxaparin BID for deep vein thrombosis that developed during this pregnancy. BP = 146/88 mmHg; Temp = 38.8 C; Platelets = 115,000.)

Answer 8

Although a pulmonary artery catheter could prove useful for fluid management, identifying the cause of any hypotension (hypovolemia vs. heart failure), and providing a means for pacing should it become necessary, I would not employ it in this situation.

• First, in the setting of aortic stenosis, the monitor may overestimate the left ventricular end-diastolic volume due to the decreased compliance of the often hypertrophied left ventricle.
• Second, there is no evidence that utilizing a pulmonary artery catheter improves outcome.

Rather, I would utilize a central venous pressure line and transthoracic echocardiography to facilitate fluid management and more accurately diagnose the cause of any cardiovascular instability.

Moreover, I would ensure the presence of a defibrillator, adenosine, diltiazem, a B-blocker, and amiodarone in order to treat the development of any supraventricular tachycardia (e.g. atrial fibrillation).

Question 9

You decide to place a central line for fluid management.

During placement she develops atrial fibrillation with a pulse of 130.

Does this concern you?

(A 28 yo, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery. Her history includes multiple sclerosis, migraine headaches, asthma, and aortic stenosis with a mean transvalvular gradient of 50 mmHg. She is receiving albuterol for asthma, digoxin for aortic stenosis, methylprednisolone for multiple sclerosis, antibiotics for suspected chorioamnionitis, and 80 mg of enoxaparin BID for deep vein thrombosis that developed during this pregnancy. BP = 146/88 mmHg; Temp = 38.8 C; Platelets = 115,000.)

Answer 9

This does concern me because – atrial fibrillation significantly increases the risk of myocardial ischemia in patients with aortic stenosis, who already have increased myocardial oxygen demand secondary to concentric hypertrophy (increased muscle mass) and increased afterload.

1. First, the rapid ventricular rate often associated with atrial fibrillation leads to – increased myocardial oxygen demand while, at the same time, reducing the time for ejection of stroke volume, coronary perfusion, and left ventricular filling (the latter two occur during diastole).
2. Second, atrial fibrillation eliminates the atrial contribution to ventricular filling

• (which normally accounts for up to 30-40% of left ventricular filling in the setting of aortic stenosis due to the decreased compliance of the left ventricle),
• leading to a significant reduction in left ventricular filling and cardiac output.

Question 10

You decide to place a central line for fluid management.

During placement she develops atrial fibrillation with a pulse of 130.

What will you do?

(A 28 yo, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery. Her history includes multiple sclerosis, migraine headaches, asthma, and aortic stenosis with a mean transvalvular gradient of 50 mmHg. She is receiving albuterol for asthma, digoxin for aortic stenosis, methylprednisolone for multiple sclerosis, antibiotics for suspected chorioamnionitis, and 80 mg of enoxaparin BID for deep vein thrombosis that developed during this pregnancy. BP = 146/88 mmHg; Temp = 38.8 C; Platelets = 115,000.)

Answer 10

I would immediately treat her dysrhythmia, recognizing that atrial fibrillation places this patient with aortic stenosis at increased risk for myocardial ischemia.

To this end, I would:

1. pull back the central line, recognizing that the line may have induced the dysrhythmia, and
2. get a 12-lead EKG to confirm a narrow QRS (a QRS <0.12 seconds confirms a supraventricular tachycardia), verify the absence of P-waves (multifocal atrial tachycardia is often mistaken for atrial fibrillation), and identify any myocardial ischemia.

Assuming this represented atrial fibrillation and she were stable, I would:

• administer diltiazem or a B-blocker to slow her ventricular rate.

If at any point she developed hypotension, pulmonary edema, or signs of myocardial ischemia (ST-segment elevation or depression), I would:

• proceed with cardioversion (biphasic defibrillator – 100-200 joules; monophasic defibrillator – 200 joules).

Clinical Notes:

• Treatment Priorities in the Stable Patient (In Order):
  
  • Find the cause
  • Fix the cause
  • Slow the rate
  • Convert the rhythm
• Common causes of Afib:
  
  • Heart failure
  • Cardiomyopathy
  • Acute MI
  • Longstanding Hypertension
  • Valvular Heart Disease
  • Hyper/Hypothyroidism
  • Drugs (cocaine, sympathomimetics)
  • Pulmonary Embolus
  • Hypoxemia
  • Sick Sinus Syndrome
    *

Question 11

Assume it has been an appropriate amount of time since her last dose of anticoagulant.

How would you provide neuraxial anesthesia to control her labor pain?

(A 28 yo, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery. Her history includes multiple sclerosis, migraine headaches, asthma, and aortic stenosis with a mean transvalvular gradient of 50 mmHg. She is receiving albuterol for asthma, digoxin for aortic stenosis, methylprednisolone for multiple sclerosis, antibiotics for suspected chorioamnionitis, and 80 mg of enoxaparin BID for deep vein thrombosis that developed during this pregnancy. BP = 146/88 mmHg; Temp = 38.8 C; Platelets = 115,000.)

Answer 11

Given this patient’s maternal fever and suspected chorioamnionitis, severe aortic stenosis, and multiple sclerosis, I would:

1. ensure this patient with possible bacteremia was receiving the appropriate antibiotics to reduce the risk of epidural abscess and meningitis;
2. ensure adequate hydration to maintain adequate preload;
3. utilize epidural anesthesia for pain control (as opposed to a spinal anesthetic), slowly raising the level of blockade to T10 with small doses of local anesthetic without epinephrine, to avoid the rapid drop in SVR and/or tachycardia that is so poorly tolerated by patients with severe aortic stenosis (epinephrine could lead to tachycardia, which can lead to cardiac ischemia in patients with severe aortic stenosis); and
4. administer a low concentration local anesthetic (0.125% or 0.0625% Bupivacaine), recognizing that the use of higher concentration local anesthetics for neuraxial anesthesia may be associated with an increased risk of exacerbating her multiple sclerosis.

Question 12

How does aortic stenosis affect the heart?

Answer 12

Progressive stenosis of the aortic valve leads to –

concentric ventricular hypertrophy

(increased left ventricular wall thickening without ventricular dilation),

which occurs in response to increased intraventricular systolic pressure.

Concentric ventricular hypertrophy results in –>

1. diastolic dysfunction (“stiff” ventricle),
2. increased left ventricular end-diastolic pressures (the atrial contribution to end-diastolic volume increases from the normal 20% to 30-40%), and
3. increased myocardial oxygen requirements (placing the patient at increased risk for subendocardial ischemia).

Eventually, eccentric left ventricular hypertrophy may develop, leading to decreased cardiac output.

Clinical Note:

• Concentric Ventricular Hypertrophy:
  
  • Usually results from pressure overload.
  • Sarcomeres are added in parallel (thickening rather than lengthening).
  • Ventricular volume is not increased.
• Eccentric Ventricular Hypertrophy:
  
  • Usually results from volume overload.
  • Sarcomeres are added in series (lengthening rather than thickening).
  • Ventricular volume is increased.