UBP 4.4 (Long Form): Obstetrics – Ischemic Cardiomyopathy Flashcards Preview

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Flashcards in UBP 4.4 (Long Form): Obstetrics – Ischemic Cardiomyopathy Deck (16)
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1

Intra-operative Management:

Would you recommend a cesarean section for this patient?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

I would if there were an obstetric indication (i.e. severe preeclampsia), or if immediate delivery was indicated secondary to maternal hemodynamic instability.

While a cesarean section has the advantage of avoiding the prolonged stress of labor and the profound hyperdynamic circulatory changes that occur at delivery,

the cardiovascular stress of delivery is not entirely avoided since cardiac output increases by up to 50% even with cesarean section.

In addition, cesarean section is associated with increased blood loss, a higher risk of infection, delayed ambulation, and increased pain following delivery.

---

However, this patient's high blood pressure and urinary protein suggest she may be preeclamptic,

in which case, a cesarean section may be indicated should her condition become severe (i.e. headache, visual disturbances, epigastric pain, HELLP, intrauterine growth restriction, oliguria, pulmonary edema, BP >/= 160/110 mmHg, proteinuria > 5 g/24 hr) or should she become eclamptic.

2

Intra-operative Management:

The patient begins to complain of right upper quadrant pain and the obstetrician decides to perform a cesarean section secondary to severe preeclampsia.

Should this patient be receiving magnesium sulfate?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

While the administration of magnesium sulfate would be beneficial for seizure prophylaxis in this patient with severe preeclampsia, it would likely be contraindicated in this patient with ischemic cardiomyopathy and a recent myocardial infarction less than one month ago.

This contraindication is based on the potentially deleterious cardiac effects associated with magnesium administration, such as -- hypotension, bradycardia, complete heart block, and cardiac arrest.

EKG signs of magnesium toxicity include --

  • a prolonged PR interval, prolonged QT interval, and a widened QRS.

The risk of cardiotoxicity secondary to hypermagnesemia is increased in the setting of --

  • hypocalcemia, hyperkalemia, renal insufficiency, and digitalis therapy.

Other relative contraindications to magnesium sulfate administration include --

  • myasthenia gravis (magnesium decreases the presynaptic release of acetylcholine and decreases motor end-plate sensitivity to calcium),
  • impaired renal function (magnesium is renally excreted), and
  • concomitant calcium channel blocker therapy (potentiates cardiotoxic effects).

-----

Clinical Notes:

  • Treatment of magnesium toxicity?
    • The treatment of hypermagnesemia involves --
      • diuretic administration, to increase renal excretion and
      • calcium gluconate administration to antagonize the neurologic and cardiac effects of magnesium.
  • Magnesium Toxicity Levels --
    • Serum Magnesium Level (mEq/L) // (mg/dL) -- Physiologic Effect:
      • 1.5-2.5 // 1.8-3.0 -- Normal
      • 4.0-7.0 // 4.8-8.5 -- Therapeutic Range
      • 7.0-10.0 // 8.5-12.2 -- Loss of Patellar Reflexes; Hypotension; Significant CNS Depression
      • 13-15.0 // 15.8-18.2 -- Respiratory Paralysis
      • 16-25 // 19.4--30.4 -- EKG Changes (prolonged PR interval; widened QRS; prolonged QT interval)
      • 20-25 // 24.3-30.4 -- Cardiac arrest

3

Intra-operative Management:

How will you provide anesthesia?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

Given the potential difficulty of airway instrumentation in this obese, obstetric patient with preeclampsia (airway edema) and a Mallampati III airway, and considering the risk that the hemodynamic changes associated with laryngoscopy and intravenous induction pose to a patient with coronary artery disease and severe preeclampsia,

I would prefer to provide regional anesthesia.

However, since this patient's preeclampsia and low platelet place her at increased risk for developing an epidural or spinal hematoma following neuraxial anesthesia, I would look for any signs of coagulopathy (excessive bruising, bleeding at IV sites, etc.) and consider the trend of her thrombocytopenia before proceeding with regional anesthesia.

Assuming no signs of coagulopathy and a reasonably stable platelet count, I would place an epidural.

Given the risk of inadeqaute cardiac or uterine perfusion with rapid sympathectomy, and considering the risk of maternal tachycardia and myocardial ischemia with the absorption of epinephrine, I would provide a judicious fluid bolus and slowly raise the level of blockade using plane local anesthetic

(the rapid sympathectomy often associated with spinal anesthesia would make this form of neuraxial blockade less desirable).

If the patient became hypotensive despite my precautions, I would treat with phenylephrine, which is less likely to result in maternal tachycardia than ephedrine.

4

Intra-operative Management:

Do you have any concerns about performing a regional anesthetic?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

I am concerned that the sympathectomy caused by neuraxial anesthesia may result in significant hypotension,

which could compromise uteroplacental perfusion and maternal coronary perfusion pressure

(uteroplacental perfusion is probably already compromised in the setting of preeclampsia).

I am also concerned about a potential decrease in maternal platelet number and function, placing the mother at increased risk of epidural hematoma with neuraxial anesthesia.

Therefore, I would --

  • confirm an adequate platelet count,
  • ensure that there are no physical signs of coagulopathy,
  • place the appropriate monitors (i.e. arterial line, pulmonary artery catheter),
  • ensure adequate intravascular volume,
  • place an epidural catheter, and
  • slowly raise the anesthetic levels to T4 using plain local anesthetic.

5

Intra-operative Management:

Would you place a neuraxial block if her platelets were 92,000?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

I would place a neuraxial block, assuming there were no signs of coagulopathy, such as bleeding at IV sites, mucosal bleeding, and marked or easy bruising.

While I am concerned about the effects of preeclampsia on platelet number and function, and the associated risk of epidural or spinal hematoma,

I must weight this risk against the risks of airway instrumentation in this patient with a potentially difficult airway, significant coronary artery disease, and severe preeclampsia.

As I mentioned earlier, significant hemodynamic changes or inadequate ventilation during laryngoscopy and intubation could place this patient with coronary artery disease and severe preeclampsia at increased risk of further cardiac injury and/or cerebral ischemia

(severe preeclamptic patients may have cerebral edema and elevated ICP).

However, when weighing the risks of proceeding with regional anesthesia, I would consider the trend of the platelet number in addition to the absolute number.

6

Intra-operative Management:

What if they were 74,000?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

While a lower platelet value, such as 74,000, is even more concerning,

my decision to perform a regional anesthetic would still be made by weighing the risks of epidural hematoma against the risks of general anesthesia.

In other words, my decision would be based on more than a specific lab value.

If there were no clinical signs of coagulopathy and I was very concerned about the management of this patient's airway, then I would place an epidural for the procedure.

However, recognizing the increased risk of epidural hematoma, I would take specific precautions to prevent hematoma-induced neurologic injury, such as delaying catheter removal until lower extremity motor function had returned

(this allows for subsequent evaluation of motor function following catheter removal -- a time of increased risk of epidural bleeding) and,

following the catheter removal, performing hourly neurologic examinations to ensure that the symptoms of spinal cord compression were quickly identified to allow for timely treatment.

7

Intra-operative Management:

Assume the platelets were still at 92,000 and you decide to perform a regional anesthetic.

How will you prepare the patient and what lines and monitors will you use?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

Given this patient's recent myocardial infarction combined with peripheral edema, pulmonary edema, and increasing shortness of breath, I would --

order a CXR and echocardiogram if not already done.

I would also consider additional beta-blocker to reduce her heart rate to about 80 beats/minute.

After taking these steps, I would provide supplemental oxygen and place the standard monitors, a Foley catheter, an arterial line, and a pulmonary artery catheter before induction

(keep in mind that there is some increased risk when placing a pulmonary artery catheter in a patient with coagulopathy).

Computer ST-segment analysis would also be of benefit if it were available.

Finally, I would provide regional anesthesia with the goal of avoiding significant hypotension, which could compromise uteroplacental and/or coronary artery perfusion.

To this end, I would ensure adequate intravascular volume with the guidance of the pulmonary artery catheter, place an epidural catheter, and slowly raise the anesthetic levels to T4 using plain local anesthetic.

-----

*** My additional note -- may not place PA catheter. May consider Flotrac arterial line ***

8

Intra-operative Management:

You are raising the epidural and notice ST-segment depression on the EKG.

What are you going to do?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

I would cease any epidural injections, and attempt to optimize the myocardial oxygen supply/demand relationship.

To this end, I would continue supplemental oxygenation, ensure adequate left uterine displacement, and treat any tachycardia, hypotension, hypertension, and/or dysrhythmia using my intra-arterial catheter and pulmonary artery catheter for guidance.

In the absence of significant hypotension, I would consider administering nitroglycerine to achieve coronary dilation.

However, I would avoid administering this drug if I felt the subsequent venodilation would result in inadequate cardiac filling

(Note: Venodilation and reduced venous return may be beneficial in reducing myocardial wall tension. On the other hand, an excessive reduction in venous return may result in inadequate cardiac filling.)

9

Intra-operative Management:

During your assessment you determine that the ST-segment depression was possibly the result of hypotension secondary to the sympathectomy induced when raising the epidural.

You have just begun to treat the hypotension when she develops ventricular tachycardia, loses consciousness, and then progresses to asystole.

What are you going to do?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

I would immediately:

  1. call for help and a defibrillator (in case a shockable rhythm developed during resuscitation).
  2. I would then -- secure the airway,
  3. provide positive pressure ventilation with 100% oxygen,
  4. ensure left uterine displacement, and
  5. start chest compressions.
  6. Next I would attempt to -- confirm true asystole (make sure all cables are connected properly, ensure adequate monitor gain, check another lead, check for pulse -- very fine ventricular fibrillation can look like asystole), and
  7. administer 1 mg of epinephrine intravenously.
  8. I would then -- continue to monitor the patient for the development of a shockable rhythm,
  9. attempt to identify and treat the underlying cause of the arrest (which in this case is most likely myocardial ischemia and/or infarction), and
  10. give additional 1 mg doses of epinephrine every 3-5 minutes until the patient moved out of asystole or until resuscitative efforts were discontinued (one dose of vasopressin 40 U can be substituted for the first or second dose of epinephrine).
  11. If she did not respond to resuscitative efforts within the first few minutes, I would ask the obstetrician to deliver the baby to improve the chances of survival for both the mother and her baby.

-----

Clinical Note:

  • Atropine and pacing are no longer recommended because they are unlikely to be beneficial -- especially when asystole occurs out-of-hospital. These modalities may be beneficial if promptly initiated in the setting of witnessed asystole.

10

Intra-operative Management:

What is your differential for her cardiac arrest?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

Given her recent myocardial infarction and cardiac history, the most likely cause of cardiac arrest in this patient is --

  1. myocardial ischemia and/or infarction.

However, other causes to be considered would include --

  1. amniotic fluid embolism
    • (she is at higher risk of placental abruption since she is preeclamptic),
  2. pulmonary embolism
    • (she is at increased risk of DVT secondary to the hypercoagulable state of pregnancy and the inactivity likely associated with her obesity and extreme shortness of breath),
  3. rupture of a subcapsular hematoma
    • (a known life-threatening complication of HELLP syndrome),
  4. intracranial hemorrhage
    • (higher risk in severe preeclampsia),
  5. local anesthetic toxicity
    • (her epidural block was being raised at the time of arrest),
  6. hypovolemia,
  7. hypokalemia
    • (patient is taking a loop diuretic), and
  8. tension pneumothorax
    • (a central line was placed for the case).

-----

Clinical Notes:

  • Most frequent causes of asystole (5 "H's" and 5 "T's"):
    • Hypovolemia
    • Hypoxia
    • Hydrogen Ion (Acidosis)
    • Hyper-/Hypokalemia
    • Hypothermia
    • Tablets/Toxins (Drugs)
    • Tamponade (Cardiac)
    • Tension Pneumothorax
    • Thrombosis (Coronary -- acute MI)
    • Thrombosis (Pulmonary embolism)

11

Intra-operative Management:

Will you deliver the baby before starting cardiac compressions?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

Initially, I would NOT delay cardiac compressions for delivery of the baby.

However, if resuscitative efforts were not successful within the first couple of minutes, I would ask the obstetrician to perform an immediate cesarean section.

Delivery of the baby within 5 minutes of maternal cardiac arrest may improve the chances of survival for both the mother and the infant by:

  1. relieving aortocaval compression, which improves venous return to the heart,
  2. decreasing metabolic demands, and
  3. allowing for more effective chest compressions.

12

 Intra-operative Management:

The baby is delivered and you note that the patient now has a pulse, but is in ventricular tachycardia.

What will you do?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

Assuming there were a pulse and the patient were stable (no change in mental status, chest pain, hypotension, or signs of shock), I would --

  1. attempt to determine if the rhythm is monomorphic, polymorphic, WPW, Torsades, or of uncertain etiology.

Assuming this were monomorphic ventricular tachycardia -- I would:

  1. consult a cardiologist;
  2. administer adenosine, recognizing that this would convert 5-10% of ventricular tachycardia rhythms;
  3. administer procainamide or amiodarone (amiodarone is preferred in the presence of known impaired left ventricular function); and
  4. identify and correct any contributing factors such as hypoxemia, hypovolemia, hypercapnia, hypo/hyperkalemia (taking HCTZ), hypomagnesemia (taking HCTZ), hypothermia, hypoglycemia (diabetic), pulmonary embolism (long bone fracture), and acid-base derangements.

If at any time the patient became unstable despite the presence of a pulse (i.e unstable due to the fast rate), I would --

  1. perform immediate synchronized cardioversion (assuming this was monomorphic VT - polymorphic VT usually requires unsynchronized shock).

13

Intra-operative Management:

The patient is successfully resuscitated. The surgeon is working and you determine that she has lost about 1,100 mL of blood.

Do you think a transfusion is necessary?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

If there were no signs of cardiac ischemia, bleeding was reasonably controlled, and I believed the 1,100 mL of blood loss was accurate (no occult blood loss), I would NOT transfuse at this time.

However, considering this patient's severe cardiac disease, I would want to maximize her oxygen carrying capacity by maintaining a hemoglobin level of at least 10 mg/dL, placing her estimated allowable blood loss at around 1,300 mL.

However, if I believed there were any signs of ischemia, occult blood loss was potentially significant, there were any signs of coagulopathy, or that adequate hemostasis was not yet achieved, I would begin transfusing blood products as indicated.

-----

Clinical Note:

  • Estimated Blood Volume (EBV) = Weight (kg) x Average blood volume (mL/kg)
  • Average Blood Volume:
    • Premature Neonates = 90-100 mL/kg
    • Pregnant Female = 90 mL/kg
    • Full Term Neonates = 80-90 mL/kg
    • Child 3-12 months of age = 70-80 mL/kg
    • Child > 1 year = 70-75 mL/kg
    • Obese Child = 60-65 mL/kg
    • Adult Men = 75 mL/kg
    • Adult Women = 65 mL/kg
  • Estimated Allowable Blood Loss = [ EBV x (Hi - Hf) ] / Hi

14

Post-operative Management:

The newborn's respiratory effort is weak.

What do you think is going on?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

With the mother's cardiac arrest and the lower than normal perfusion that occurs during resuscitation, combined with the impaired uteroplacental perfusion often associated with preeclampsia,

it is likely that acute uteroplacental deficiency has led to neonatal depression (i.e. metabolic acidosis, persistent pulmonary hypertension, and persistent fetal circulation).

However, there are other possible causes and contributing factors that should be considered such as:

  1. transient tachypnea of the newborn, secondary to retained fetal lung fluid
    • (a condition often associated with small preterm babies and babies delivered by cesarean section who experience less chest compression during delivery);
  2. hypoglycemia, secondary to an abrupt discontinuation of the uteroplacental transfer of excessive maternal plasma glucose from the neonate's diabetic mother following delivery
    • (the newborn's pancreas continues to secrete an excessive amount of insulin despite the loss of exposure to the mother's high glucose load following placental separation);
  3. meconium aspiration, secondary to stress-induced intrauterine passage of meconium followed by inhalation of meconium-stained amniotic fluid
    • (stress often induces fetal gasping and inhalation of amniotic fluid); and
  4. an undiagnosed congenital anomaly affecting airway patency, such as --
    • choanal atresia/stenosis, laryngeal or subglottic webs, Pierre Robin syndrome, or Beckwith-Wiedemann syndrome.

15

Post-operative Management:

The mother has been moved to recovery and you are preparing to remove the epidural catheter.

The nurse reports that lab taken just before entering the OR has returned and her platelets were 76,000.

The measurement upon admission earlier that day was 92,000.

Will you still remove the catheter?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

Considering this rapid decline in her platelet level over just a few hours I would be very concerned that a further decline had occurred since the last measurement, increasing her risk for epidural hematoma.

Given this uncertainty, I would NOT pull the catheter and risk initiating bleeding even if there were no current signs of coagulopathy such as oozing at the surgical incision or IV sites

(the two times when the risk of initiating epidural bleeding is highest are during placement and removal of the epidural catheter).

Rather, I would delay removal of the catheter until complete epidural regression had occurred, so that the symptoms of epidural hematoma with spinal cord compression would not be masked by the analgesia of a working epidural

(in this way the patient and medical staff are better able to monitor any decline in function and alert the appropriate medical professionals if intervention is required.)

Following complete regression, I would remove the catheter after verifying an adequate platelet count.

16

Post-operative Management:

When would you remove the catheter?

(A 44-year-old 5'3" 265 lb, G3P2 female at 38 weeks gestation presents to the obstetric floor with ruptured membranes. Her history includes ischemic cardiomyopathy and a recent myocardial infarction (MI).

HPI: The patient had a myocardial infarction 4 weeks ago. Cardiac catheterization immediately following the MI showed a 50% occlusion of the right coronary artery and a 30% occlusion of the left anterior descending artery. Her coronary artery disease has been medically managed since her myocardial infarction, and she reports progressively increasing shortness of breath throughout this pregnancy. Currently, she is short of breath even at rest. The obstetrician informs you that her blood pressures have been elevated for the past few weeks.

PMI: History of severe preeclampsia with first pregnancy, tobacco use for 28 years, and insulin dependent diabetes mellitus.

PE: Vital Signs: HR = 98, BP = 156/93

Airway: Mallampati III, adequate thyromental distance and neck ROM

Cardiovascular: RRR

Lungs: bilateral fine crackles heard in the lung bases

Extremities: pitting peripheral edema

ECG: NSR, Q waves in leads II, and III, left axis deviation

Meds: furosemide, NPH, and regular insulin

Lab: Hgb = 11.4; Hct = 34; Platelets = 92,000; Urine = 3+ protein)

My plan would be to remove the epidural catheter as soon as her epidural wore off, her lower extremity motor function returned to normal, and her platelet count was at an acceptable level.

After removing the catheter, I would make the patient aware of the symptoms of epidural hematoma and make her aware of the importance of immediate treatment should any of these symptoms develop.

In addition, I would order neurologic examinations every hour to facilitate early detection of spinal cord compression and allow for immediate intervention within the recommended six-hour window.