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Flashcards in obstetric cardiac disease Deck (35):

what leads correspond to which walls of the heart and which arteries?

II, III, aVF - inferior - RCA
V5, V6, I - lateral - left circ
V1-4 - anterior/septal - LAD


a patient presents with ROM at 38 weeks gestation. h/o MI last month and ischemic CM, IDDM, smoker, severe preeclampsia with last pregnancy. 6'3", 120 kg.

HR 98
BP 156/93
HgB 11.4

what do you want to know about this patient?

1. obstetric plan
2. thorough H & P. review chart, talk to patient, records from cardiologist. would like to know extent of damage, if there is more myocardium at risk, any procedural or pharm intervention that was taken. current EF. past/present symptomatology.
3. airway - given her height/weight and changes with pregnancy, elevated BP (may suggest preeclampsia) - any history of difficult airway with anesthesia
4. condition of baby
5. is elevated BP due to preeclampsia and are there any other associated complications? renal insufficiency, coagulopathy, cerebral edema
6. h/o tobacco use/pulm disease
7. accucheck and severity/stability of current therapy and any end-organ damage


what are you specifically looking for on physical exam?

1. airway exam
2. CV exam - HR, rhythm, signs of CHF (JVD, pulm edema, hepatomegaly, peripheral edema)
3. pulm exam - auscultate lungs, CXR
4. volume status - urine output, cap refill, skin turgor
5. signs of coagulopathy - bleeding around iv site, gums, excessive bruising
6. lab work - urine protein, h/h, blood glucose, electrolytes, platelets


what about PFTs?

I would consider PFTs if there were any signs or symptoms of advanced pulmonary disease (like wheezing, baseline SOB, low RA SpO2). they could provide additional information regarding the type and severity of disease, baseline pulm fxn, and the presence of a reversible component. she is at increased risk of periop pulm complications due to her obesity, smoking, poss preeclampsia (pulm edema), cardiac diease, and the depression of resp ms after neuraxial anesthesia


what do you think about the ECG findings?

this indicates an inferior infarct, most likely in the distribution of the RCA. i would also keep in mind, however, that some normal findings in pregnancy include LAD, ST depression, and a Q wave in lead III.


how would you optimize the patients cardiac condition?

i would develop a plan with her cardiologist, given the complicated nature of her history. some of my goals would include:
1. ensure adequate intravascular volume to prevent significant hypotension with the initiation of regional anesthesia, while at the same time avoiding fluid overload (h/o CM, possibly, preeclampsia-induced increases in capillary permeability
2. if LV fxn is suboptimal, i would consider afterload reduction or inotropes
3. ensure continuation of B-blocker if already on B-blocker (Class I recommendation)


she is not currently on a B-blocker, would you start one?

i would only initiate a beta-blocker in consultation with her cardiologist. therapy could potentially be recommended due to her unstable condition, because the routine administration of high-dose beta-blockers without titration.

perioperative initiation of beta-blockers in the absence of titration may reduce DV morbidity/mortality, it also leads to increased risk of hypotension, bradycardia, CVA, and increased overall mortality


what are the current ACC/AHA guidelines regarding perioperative beta-blocker initiation?

can carefully titrate beta-blockers at least 2-7 days prior to surgery:
- continue beta-blockers if patient is currently on one
- preop initiation without titration may reduce CV morbidity/mortality but increases overall orbidity (increased hypotension, bradycardia, stroke, death)
- it may be reasonable to begin perioperative BB 2-7 days preop in patients with 3 or more RF (DM, CHF, CAD, renal insuff, CVA) or intermediate to high risk myocardial ischemia identified on preop testing
- if compelling long-term indication for BB, but no other RF, BB intiation is of uncertain benefit in perioperative period
- if BB therapy is initiated, preferable to start more than 1 day before surgery (if started


would you order a CXR or echo?

yes, to more accurately assess the patients cardiac condition because of her recent MI (this is an unstable coronary sydnrome). CXR to look for cardiomegaly or pulm edema and echo to assess regional wall abnormalities and LVEF.


what are the active cardiac conditions according to the ACC/AHA?

1. unstable coronary syndromes - unstable/severe angina, recent MI (>7 days, but


who is appropriate to asses LV function perioperatively?

- dyspnea of unknown origin
- current or prior HF who have worsening dyspnea, other change in clinical status
- no evaluation of LV in past 12 months with previous documentation of LV dysfunction


should this patient have a c-section?

i would not recommend a c-section solely based on her cardiac condition, because although it avoids the prolonged stress of labor, CO still increases by up to 50% during c-section. it as also a/w increased blood loss, infection, delayed ambulation, pain.

however, her high bp and urinary protein suggest preeclampsia, in which case, a csection may be indicated if her condition becomes severe (HA, vision changes, epigastric pain, HELLP, IUGR, oliguria, pulm edema, BP>160/110, proteinuria >5g/24 hr) or eclampsia.


pt begins to experience RUQ and ob decides to proceed with c-section. should pt receive mag?

no i would not recommend mag for this patient with ischemic CM and recent MI. it would be relatively contraindicated due to the negative effects associated with its administration (hypotension, bradycardia, complete heart block, cardiac arrest). i do recognize it would be beneficial for seizure prophylaxis in the setting of severe eclampsia, so i would discuss and weight the benefits and risks with the obstetrician and cardiologist.


what are the signs of mag toxicity?

- loss of patellar reflexes
- hypotension
- CNS depression
- resp depression
- prolonged PR
- widened QRS
- prolonged QT


how do you treat mag toxicity?

1. d/c administration
2. check mag level
3. administer a diuretic (to increase renal excretion)
4. give calcium gluc to antagonize neurologic and cardiac effects of mag


what conditions increase the risk of cardiotoxicity secondary to hypermagnesemia?

renal insufficiency


what are the levels and signs associated with magnesium toxicity?

1.5-2.5 mEq/L - normal
4.0-7.0 mEq/L - therapeutic range (at 4 can see hyporeflexia, at 5 can see delayed of AV conduction)
7.0-10.0 - loss of patellar relfex, hypotension, CNS depression
13-15 - resp paralysis
16-25 - prolonged RP, widened QRS, prolonged QT
20-25 - cardiac arrest


would you place neuraxial block for c-section?

given the concerns i have for difficult airway (obesity, preeclampsia) and risk of HD changes associated with IV induction/laryngoscopy. i am concerned however about her thrombocytopenia and history of preeclampsia and potential increased risk for spinal/epidural hematoma. i would carefully question her regarding increased bleeding/bruising to assess developing coagulopathy. i would also take into consideration the platelet trend and be concerned about any sudden downturns.


which neuraxial block would you perform?

i would prefer epidural catheter with a slow titration to T4 level to avoid the rapid sympathectomy and subsequent hypotension associated with intrathecal injection that would put her at risk of myocardia/placental hypoperfusion and ischemia.


patient becomes hypotensive, what is your first line therapy?

phenylephrine, as it is not associated with tachycardia (only alpha agonist)


what if platelets were 74,000?

in the absence of signs of coagulopathy, i would still proceed.


any special considerations postoperatively?

i would not remove the catheter until the patient regained LE motor function so that hourly neuro checks could performed after the catheter was removed (the time the patient is at most risk for bleeding).


platelets are still 92,000. how will you prepare the patient for neuraxial block and what lines and monitors would you like?

given the history of recent MI combined with peripheral edema, pulmonary edema, and increasing SOB, i would:
1. order a CXR and Echo to further assess her cardiac function.
2. consult her cardiologist about the efficacy of high-dose BB therapy to reduce her HR to goal of 60-80 bpm. this is not routinely recommended, however it may benefit this patient with an acute cardiac condition.
3. provide supplemental O2
5. place a 5-lead ECG with ST segment analysis
6. foley catheter to assess UOP and volume status
7. arterial line for close BP monitoring
8. consider PAC or TTE to monitor cardiac function
9. ensure adequate IV volume (either hypo or hypervolemia may be poorly tolerated due to her CAD, preeclampsia, and CM)
10. slowly titrate epidural anesthesia by slowly raising to a T4 level using plain local anesthetic (no epi to avoid tachycardia)


you are raising the epidural and notice ST depression on the EKG. what will you do?

stop epidural infusion/injection. attempt to optimize myocardial supply/demand:
- treat tachycardia, hypo/hypertension, dysrhythmia
- if no significant hypotension, administer NTG for coronary dilation


you believe the ST depression is due to hypotension secondary to sympathectomy from the epidural. you are starting to treat the hypotension when she develops v tach, loses consciousness and then asystole. what do you do?

1. call for help and crash cart including defibrillator
2. LUD
3. start chest compressions while waiting for drugs/ett
4. mask ventilate as necessary with cricoid pressure to attenuate risk of aspiration
5. secure ETT
6. ventilate with 100% FiO2
7. confirm asystole
8. administer 1 mg epinephrine IV every 3-5 minutes while continuing chest compressions with a goal of 100 compressions/minute
9. if no response to resuscitation, ask OB to deliver baby to improve chances for both survival

***for witnessed asystole, atropine/pacing may be considered even though they are no longer part of the ACLS guidelines***


what is your differential diagnosis for her cardiac arrest?

1. myocardial ischemia
2. amniotic fluid emobolism (possible placental abruption - high risk bc of preeclampsia)
3. pulmonary embolism (increased risk due to hypercoagulability of pregnancy and sedentary lifestyle wiht obesity and extreme SOB)
4. subcapsular hematoma rupture - life-threatening HELLP complication
5. ICH - increased incidence with severe preeclampsia
6. LA toxicity
7. hypovolemia
8. hypokalemia (on a loop diuretic)
9. tension PTX if CVL placed


what are the most common causes of asystole?

5 Hs:
hydrogen ion (acidosis)

5 Ts
tension ptx
thrombosis (coronary, acute MI)
thrombosis (PE)


should the baby be delivered prior to starting chest compressions?

no! chest compressions should begin immediately to provide end-organ perfusion and help circulate the administered epinephrine or vasopressin. however, delivery needs to proceed quickly to improved chances of survival for both mother and baby (relieves atrocaval compression, decrease metabolic demands, allow more effective compressions)


the baby is delivered and you note a pulse in the mother but she is in vtach. what will you do?

i would assess if the patient was stable or unstable and the morphology of the VT. signs of instability would be hypotension, mental status changes, chest pain, signs of shock, or acute HF. if unstable and monomorphic, i would perform synchronized cardioversion. if unstable and polymorphic, i would perform unsynchronized cardioversion.

if stable, i would consult cardiology and assess the morphology. if monomorphic and regular, i would consider 6 mg and then 12 mg IV push of adenosine. if polymorphic, i would start an antiarrhythmic infusion, such as amiodarone (150mg over 10 min, then 1mg/min for 6 hours) or procainamide (20-50mg/min then 1-4 mg/min; must turn dose down when 50% of max dose reached - 17mg/kg) amiodarone would be first choice in the setting of impaired LV fxn.
i would also attempt to allay any contributing factors - hypoxemia, hypovolemia, hypercapnia, hypo/hyperkalemia, hypomagnesemia, hypothermia, hypoglycemia, PE, acid-base derangements


how does amiodarone work?

works on both SA and AV nodes and increases the refractory period


how does procainamide work?

increases refractory period directly on cardiac myocytes


what are the recommedations of joules to apply for the various types of v tach?

narrow regular: 50-100 J
narrow irregular: 120-200 J biphasic, 200 J monophasic
wide regular: 100 J
wide irregular: defibrillation dose


resuscitation works. the surgeon is working and you determine there is approximately 1,100 mL blood loss. is transfusion necessary?

assuming the bleeding was controlled, i would not transfuse. however, considering her severe cardiac disease, i would want to maximize her oxygen carrying capacity an keep Hgb around 10 mg/dL. her ABL is around 1300 mL. as her BL is approaching her ABL, i would be vigilant about monitoring for signs of ischemia, occult bleeding, coagulopathy, and adequate hemostasis and transfuse as indicated

EBV: 90 mL/kg (pregnant woman) x weight
EBV: 10,840

ABL: 10840(34-30)/34 = 1275


the neonate exhibits poor respiratory effort. why?

the lower than normal perfusion that resulted from cardiac arrest and resuscitation in combination with the uteroplacental insufficiency associated with preeclapmsia likely led to metabolic acidosis, persistent pulm htn and persistent fetal circ that is causing the neonatal depression.

other ddx:
1. transient tachypnea (retained fetal lung fluid due to small preterm babies or babies delivered via c-sxn - less chest compression during delivery)
2. hypoglycemia due to abrupt d/c of uteroplacental transfer of excessive maternal glucose and the neonate's pancreas persistently secreting insulin
3. magnesium toxicity
4. meconium aspiration
5. undiagnosed congenital anomaly (choanal atresia, laryngeal/subglottic webs, pierre robin, beckwith wiedemann)


you are about to remove the epidural catheter and the nurse reports that the platelet count just before entering the OR was 76k (down from 92k earlier that day). will you still remove the catheter?

i would not pull the catheter because the rapid decline in her platelet count in just a few hours and possible platelet dysfunction place the patient at higher risk of developing epidural hematoma. even in the absence of signs of coagulopathy, i would delay removal until a current plt count was obtained. if still inadequate, i would wait until platelet count had rebounded. also of note, i would like complete epidural regression so that signs/symptoms of epidural hematoma would not be mistaken for working epidural.