IM Case #4

[Kalel]

Pre-Case Disclaimer: Let me just forewarn case-participants that due to one of my attendings going on vacation next week, I may not be able to order extra labs or make management reccomendations based on user reccomendations. Also, due to a clerical error, an important test that probably would have helped us conclude this case was not done correctly today and I don't know if it will be corrected over the weekend or ever. As of right now, the ultimate answer/diagnosis to this case may never be known based on the information that I have. However, I still think that that this case presents some really interesting points that are worth discussing. And as always, I will just add the usual disclaimer that this is an actual patient and I am only a medical student, therefore, my thoughts on management and diagnosis may not be correct. Anyways, with that much out of the way:

Case #4:
A 31 yo AAF s/p C-section 1.5 weeks ago for fetal distress and poorly dilated cervix comes to the ER on 4/1 with complaints of persistent b/l LE swelling. The swelling became progressively worse towards the end of her pregnancy, and has not changed since her c-section. There is no pain associated with the LE edema. She reports that the LE edema is worse when she stands for prolonged periods of time, and better when puts her leg up.

Her pregnancy course was also complicated by increasing dypsnea on exertion over the past month, but she was d/ced prematurely from the hospital before a complete w/u was done because she states that she was "tired of being" in the hospital. Her w/u of this SOB includes venous dopplers that were read as negative, and a CXR done on 3/25 (the day that she had to leave). She still feels slightly SOB, with minor sx of orthopnea and a cough, but no PND or nocturia. She estimates that she can climb 1-2 flights of stairs, and walk 2-3 blocks, before becoming SOB now, but reports that her DOE was worse last week.

PMHx: Irritable Bowel Sydrome, Mitral Valve Prolapse (for which she states that she experiences no symptoms, but was diagnosed by echo for a heart murmur), iron deficient anemia, GERD controlled with diet and lifestyle modifications.
Ob/gyn Hx: She has had one uncomplicated vaginal birth and one spontaneous aborition. She also has a hx of genital HSV, and was on valtrex while pregnant.

Current meds: None

All: NKDA

FHx: Significant for DM, htn, breast ca.

SHx: Unemployed, single. Denies any tobacco, alcohol, or illicit substance abuse.

PE:
Vitals: P:44, BP: 170/70, R: 8, T: 99.4
On review of her computer record through prior visits, you note that she was normotensive to pre-hypertensive throughout her pregnancy.
HEENT: PERRL, EOMi
CVS: bradycardia, with a II/VI systolic ejection murmur best heard on the upper sternal borders. No carotid bruits, no JVD noted. Peripheral pulses normal.
Resp: Clear to auscultation bilaterally.
Abd: Obese, soft/non-tender/non-distended; no organomegaly.
Ext: +1-+2 pitting edema noted on lower extremities over pretibial areas b/l.

Initial labs:
CBC: WBC: 9.6, Hgb: 9.6, Hct: 28.8, Plt: 430
Chem-7: Na:141, K: 4.5, Cl: 106, CO2: 28, BUN: 12, Cr: 1.1, Glucose: 77
Chest x-ray taken on 3/25, when the patient was discharged (not actually patient's, but representative of what was found on patient's chest x-ray):

Questions:

-What labs/tests would you order now?
-What is on your differential?
-Feel free to make any comments or to discuss the patient's management thus far. Thanks for participating.

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[Renovar]

One quick question about the vitals... A pulse of 44 and BP of 170's just doesn't make sense (and makes me worried... VERY worried )


There are a couple things in my mind that stands out about this case. Basically an otherwise healthy woman came in 2 wks post-partum with hypertension, swelling and peripartum complaint of CP and SOB and decreased exercise tolerance. CXR basically showed normal sized heart with very generous pulmonary vasculature. I did not see any infiltrative process or any pleural fluid collection. The mediastinal width is normal and does not suggest fluid overload, however.

hmm...

My differential at this time would be:

-post-delivery pre-eclampsia (supported by her current BP... As far as I know, pre-eclampsia is caused by a vaso-constrictive state and can happen up to 4 weeks after pregnancy. She meets 2 criteria for PIH - from your post we dont know if the patient has proteinuria. PLT are fine, but not sure whether LFT's, or the presence of hemolysis for the presence of the HELLP syndrome.)

-CHF (pregnancy state requires significantly increased cardiac output, and her peripartum/postpartum symptoms, and her CXR is very consistent with the clinical presentation)

-anemia from various sources (not sure her baseline - plus, if the HCT of 28 accurately reflects her post-pregancy state, what would her HCT be before her delivery? 22? Could this be causing her CHF-symtpoms because of tissue underperfusion? Can this be hemolytic anemia caused by HELLP making her having CHF symptoms?)

-PE (can never be exactly sure without PAgram especially in pregnancy, although the hypercoagulable state should correct itself right after pregnancy, and having DVT's present as purely LE edema is not very classic.)

I would like to know a more complete pregnancy course and her labs during pregnancy (ie. UA, urine protein/cr ratio, LFT's, glucose, BP during pregancy and fetal outcome) as well as her baseline blood levels.

Test that I would want to order at the start:

UA, spot urine lytes/protein (or 24 hour collection), Echo, liver function tests with bilirubin fraction and a manual diff and retic on that CBC.

Other tests to consider would be a BNP level, haptoglobin.

 

[Kalel]

Thanks for participating Renovar. Those are some excellent thoughts, and I guess that I will reveal now that I am currently doing a cardiology elective and we were called to see the patient by ob/gyn as a cardiology consult. That's why there is some concern with me over the attending who is following the patient going away on vacation next week in terms of me being able to ask to order any labs or make any additional management recc's, I'm doing my card's elective at a private hospital with private attendings who sometimes see patients at odd hours (I'm there for the free food and nicer hours ). Anyways, I will reveal some of your requested studies, but I don't know many of the labs that the patient had while she was in the hospital for her c-section.

U/A: Small leukocyte esterase, pH: 6.5, specific gravity: 1.011, moderate amount of blood, no protein (one study 1 week ago showed trace protein in u/a, otherwise, has always been negative), no glucose.
Urine macro analysis: WBC: 5-10, RBC: 5-10, occasional epithelial cells, moderate amount of bacteria.

Chest x-ray on 3/25(remember that the film showed wasn't her actual film, sorry, couldn't scan it at this private hospital): Read as having pulmonary congestion with interstitial infiltrates and kerley B lines noted. Heart appears mildly enlarged.
Chest x-ray on 4/1: Read as improved pulmonary congestion and decreased interstitial infiltrates.

Liver enzymes:
Total protein: 6.7
Albumin: 3.0 (low)
Total Bili: 0.5
Direct Bili: 0.1
AST: 20
ALT: 28
Alk Phos: 160 (high)

Sorry, no differential of the cbc was ordered. Other CBC values include an RDW of 17.8 H, and MCV of 90 though.

BNP: 268.4 (high)

Other labs ordered by ob/gyn:
LDH: 747 (high, upper limit is 618)
Urate: 8.3

A transthoracic echo was ordered, and here's where the clerical mistake comes in. For some reason, TTE orders require a doppler note in the order to be attached in order for the tech to do the doppler. So, a doppler was not completed as of today (which is absolutely ridiculous, for someone to write suspect cardiomyopathy based on the chest x-ray and for the tech to not take an extra 5 minutes to do the doppler study . One attending told me that it might have to do with billing). Anyways, hopefully, the doppler will be ordered this weekend and I can look up the result and post it. As of now, TTE showed:
TTE: normal chamber sizes, normal wall motions, normal LV function with an EF estimated to be 75-80%. No pericardial effusions. However, without doppler studies, no comment can be made about any valvular dysfunction.

Urine lytes: not ordered, and I doubt that I could convince ob/gyn or my cardiology attending to order this, even though creatinine does suggest chronic renal insufficiency with a non-prenal origin (BUN/Cr ratio is only ~10).

Anyways, I have attached an ECG too.

New questions:
-With a TTE showing a normal EF, have we ruled out heart failure as an etiology?
-The BP of 170/70 with a pulse of 40's is quite remarkable. Why does the patient have such a wide pulse pressure?
-What is your differential now?
-With these new labs, how would you begin to treat your patient?
-What is your interpretation of the ECG I have attached? Does it account for the patient's symptoms/presentation?

P.S. Sorry for the poor quality of the ECG, I photocopied it at the nursing station using a fax machine and kept it folded up in my pocket all day . The three leads on the very left are I, II, and III, from top to bottom; and the very bottom one is a continuous tracing of lead II.

 

[Surfer75]

Sorry, I won't be able to contribute much cuz I'm post-call and feel like al;sjda, but I was just browsing this and from what I can see on EKG there are TWI V1-V2. Did she have a set of trops drawn? This wide pulse pressure is new then? TTE revealed normal chamber sizes, EF... hrmm.. acute AI given the wide PP, but no audible diastolic m, ... CHF as a result of diastolic dysfxn (is BNP higher in systolic v. diastolic dysfxn?)... uM, the anemia could certainly be an exacerbating factor... and this was proven to be Fe deficient v. hemolytic v. acute loss (?MCV)? LDH is increased.. bili normal, no retics/hapto..etc. Increased ALP,... is that more because of placental alk phos or? I'm not sure how rapidly it decreases post-partum, but I guess it could be double/triple normal in third trimester? K, time for bed. Sorry this note's so jumbled.

 

[Renovar]

First a couple questions: an EF of 75-80% is not normal. Normal EF is more in the line of 45-50%. Do you mean 75-80% of the expected value?

A couple things that can cause a widened pulse pressure are AI and high CO CHF. Too bad the echo cannot comment on the valvular function. I was going to put down AI on my original differential of that big pulse pressure, but you did mention a systolic murmur - AI have diastolic murmurs. Other than that murmur, AI would fit perfectly with the case description, with pumonary vascular congestion, right heart strain, and edema.

The other possibility is in the case of high output cardiac failure. Not sure whether or not that's going to give us a systolic murmur, but it can also cause a widened pulse pressure as LV is trying so hard to compensate for what it considered as a high tissue oxygen requirement. This may be from anemia (which the patient has, still not sure why), sepsis (urosepsis in ths patient?), or hyperthyroidism. This is why I am wondering if that EF (defined as SV/EDV is REALLY 80%.

That EKG is crappy indeed. From what I can see, the precordial and limb leads looks ok. Axis looks ok. May have some high voltage in V2 that may qualify the patient for LVH. T waves are kind of tall, so would recheck a K level. The money is obviously going to be at the rhythm strip, which has 2 stragetically placed crease over it ... But from what I can see, it is slow and very irregular narrow complex QRS's. I can see some P's and those appear regularly marching out to me. From what I can see (which isn't too much, mind you), I am inclined to call it a 3rd degree AVB, which would be consistent with the slow rate.

 

[ERMudPhud]

My best guess on a diagnosis would be peripartum cardiomyopathy which is now resolving. This is a well known but rare disease which can be quite severe but can also be self limited and result in return to completely normal cardiac function after a short period. The rythym looks like second degree heart block to me and I think I can see gradually increasing PR intervals thus wenkebach. At this point the doppler study would be great to have and I would keep a close eye on her rythym to make sure her heart block doesn't get worse. The only other lab I can think of is a TSH. In terms of treatment I wouldn't do anything yet as she appears to be getting better on her own.

 

[sanfilippo]

myriad issues here:
anemia, normocytic: baseline? modestly elev LDH with nl bilirubin makes me think hemolysis is unlikely. expanded volume in pregnancy, a baseline high output state itself, right?, can cause a mild anemia, too.

peripheral edema, pulm edema, high CO, h/o MVP: we now have an audible murmur (worsening of MVP, right? clicks can fade if the regurg flow becomes bad) according to the exam and an inconclusive echo. has the pregnancy state worsened her cardiac fxn and MVP? In an obese woman with MVP, I am wondering if this is secondary to rheumatic heart dz (prior hx? h/o IVDA?), thyroid disorder or CM as someone has pointed out. MVP can be associated with dysautonomia as part of syndrome to explain unexpected bradycardia of 44?

I really can't read the EKG but do see some TWI as someone mentioned already. what was the official rhythm?

finally, dyspnea in the post-partum state will make anyone think of PE, which I think can happen even up to a few months after delivery.
i know LE dopplers have been done but you have thought about it, which probably means ordering PE coag labs, right? i am not sure i would even proceed to imaging at this point if this patient is moderately stable.

Also, SaO2 and/or ABG if persistently dyspneic???
-s.

 

[Kalel]

Regarding the official read of the ECG (since it's tough to read): Those of you who called it a second degree AV block were correct, specifically, it's a wenchebach, or Morbitz type I. It's tough to tell, but if you look at the continuous tracing of lead two on the very bottom, you can see a gradual increase of the PR interval until 3/4 of the way over, when you can clearly see one P with no QRS following it. Rhythm is sinus rhythm too; for some reason the computer read it as "a fib with slow ventricular responses"; I suspect that it was because the PR intervals were too long for it ot read. Note that the rhythm does not have to be a classic 2:1 pattern for it to be called a type II block, as the rhythm often fluctuates between a 1:1 and a 2:1 pattern.

Regarding the ejection fraction, a normal ejection fraction is actually considered to be 50-75%. I didn't realize this before, but a lot of those readings on echo reports (eg mild to moderate to severe, and EF's) are pretty rough approximations and subject to interpreter opinion and how good the tech is at placing the probe in the right directions. The computer calculates an ejection fraction, but it's value is sometimes off because most computers fail to take into account the assymetrical cylider shape of the heart chamber. Some cardiologists just call everything 65% and higher normal. There are certainly different diseases associated with a high EF though (eg hypertrophic cardiomyopathy), so I'm not discounting her EF as being "normal". Her TTE, without the doppler study, was interpreted by the cardiologist (a different one who knew nothing about the patient) as a "normal" echo though.

SaO2 was 100%, and no ABG was ordered. I'm certain that coags were ordered before, but I don't have access to them right now. I'm also going to look for a TSH when I get back on Monday, in addition to trying to figure out if the doppler was done.

Pt had no hx of IVDA, and an attempt to hear AI was made by having the patient hold her breath while leaning forward and listening to the right upper sternal border. No diastolic murmur was heard in this position. The murmur of MVP, a mid-systolic click, sometimes better heard while doing the valsalva or standing at the apex of the heart, was also not audible to my ears but my attending claimed that he heard a soft one.

Anyways, I'm going to keep looking stuff up and wait for more people to post before I post what I think is going on. I agree with many of your thoughts though.

 

[Kalel]

Here are my thoughts on this very interesting case:

Similar to Renovar, my first thoughts when we were called about this consult (LE edema, new hypertension) was that this may be a case of severe pre-eclampsia associated with pulmonary edema or possibly a coagulopathy with an associated myocardial infarction. Unfortunately, I remembered almost nothing about pre-eclampsia; so I first had to look that up. Pre-eclampsia can occasionally first ?appear? or be detected in the first few days postpartum, and although delivery is the ultimate therapy, the disease process can sometimes last for several weeks post-delivery. Although 30% of normal pregnancies are associated with a lower extremity edema, the edema in pre-eclampsia is secondary to endothelial damage rather then a general volume overload and can involve a sudden change in edema, and edema into non-dependent places (like the face, hands); generalized edema is considered a highly specific physical finding for pre-eclampsia. However, the diagnostic criteria for meeting pre-eclampsia includes a blood pressure of over 140/90 and proteinuria (usually greater then +1 on urine dipstick, and always greater then 0.3 g on 24 hr urine collection); which our patient did not have. Therefore, our patient does not have pre-eclampsia. With no proteinuria, our patient met diagnostic criteria for gestational hypertension instead of pre-eclampsia. Incidentally, I believe that ob/gyn ordered the LDH, LFT?s, and uric acid as part of their work up of pre-eclampsia or severe pre-eclampsia. I don?t think that any of these results (even the slightly elevated LDH) were very remarkable.

I agree with ERMudPhud in what diagnosis is highest on my differential. Peripartum cardiomyopathy is a rare form of heart failure that occurs in 1 in 3,000-4,000 live births every year. The cause is unknown, but inflammatory cytokines are thought to play some role in the pathogenesis, perhaps as some sort of myocarditis. Risk factors include being over 30 yrs old, multiparity, being African American, pregnancy with multiple fetuses, history of pre-eclampsia or post-partum hypertension, cocaine abuse, or long-term oral tocyltic therapy with beta agonists (eg terbutiline). It usually presents during the first 4-5 months post-partum, and patients complain of symptoms similar to CHF symptoms. Diagnosis is essentially made ruling out other causes of heart failure (which we haven?t been able to do yet without the Doppler study), and by documenting systolic dysfunction (which we were not able to do, but this may be secondary to the time course with her symptoms resolving as observed with her CXR and decreasing dypsnea in history over the past week). An elevated BNP though, is highly suggestive of some sort of cardiomyopathy despite our inability to observe it on echo. So essentially, I haven?t been able to confirm my diagnosis, but this is what is highest on my differential. Most patients with peripartum cardiomyopathy recover heart function by 6 months, therefore, if she did have peripartum cardiomyopathy, I believe that she would have had a mild form. Treatment is essentially the same as the treatment of congestive heart failure, with diuretics, blood pressure control, and beta blockers (beta blockers would not be indicated when the patient was acutely decompensating though, similarly to how you wouldn?t want to give a patient with a CHF more beta blockade). We ended up recommending (before seeing the echo) that the patient be started on furosemide 40 mg IV and Hctz 20 mg IV in order to further diurese the patient of whatever was left of her pulmonary edema and to help rid her of her LE edema. When I left on Friday, the patient?s blood pressure had dropped to 150/80.

Regarding other points:
Mitral Valve Prolapse and pregnancy: Unless complicated by mitral regurgitation, these patients typically tolerate pregnancy quite while. Cardiovascular changes typical in pregnancy include an increase and blood volune and a decrease in peripheral resistance (although not the case in our patient), which usually improves mitral vavle function. I?m not certain if our patient received antibiotic prophylaxis during her c-section, but MVP is considered a moderate risk factor for endocarditis, and antibiotic prophylaxsis is indicated for patients with regurgitation or valve thickening during the perioperative period.

Surfer75: Thanks for posting while post-call! Mean BNP levels are on average, lower in diastolic dysfunction patients then systolic dysfunction heart failure patients (a plasma BNP of greater then 62 has a sensitivity of 85% in detecting diastolic dysfunction, while a plasma level of BNP of greater then 75 was shown to be necessary to achieve a sensitive of 85% in all heart failure patients in a different study); however, studies haven?t been shown that BNP values can be used alone to discriminate between the two types of heart failure. I imagine that part of the problem with conducting a study examining the difference between BNP in systolic versus diastolic dysfunction is because the diagnosis of diastolic dysfunction is oftentimes a presumptive one in patients with heart failure symptoms and a normal EF. I?m glad that somebody brought up diastolic dysfunction though, that answers the question that I posted regarding how a normal EF does not rule out heart failure. Doppler studies can help establish a diagnosis of diastolic dysfunction by demonstrating things like poor or slow diastolic filling of the ventrical or slow mitral valve inflow velocity, but Doppler studies haven?t been done yet in our patient. I?m not certain why her alkaline phos was slightly elevated, but it may have just been an incidental finding.

Wenckebach (Morbitz type I) block: Can occur in otherwise healthy patients, particularly athletes at rest with a high vagal tone (seen in 2-10% of long distance runners). Usually is asymptomatic (particularly when the conduction ratio is high); however, given our patient?s bradycardia, a known precipitatant of heart failure, her abnormal rhythm is probably contributing to her pathophysiology. Therapy for symptomatic (particularly bradycardic) Wenckebach blocks include atropine to decrease the vagal response, and pacing; neither of which we elected to do at the time because the patient was improving. The point that I wanted to make about her high pulse pressure was that it is likely due to her bradycardia. With a large preload, the heart is able to produce a significant cardiac output that can explain her elevated systolic pressure. With the slow conduction rate though, the aortic valve remains close for an abnormally long period of time with bradycardia, allowing the arterial pressure time to drop as blood flows into the venous system, giving us the low diastolic pressure and wide pulse pressure.

Pulmonary Embolism: Glad sanfillipo and Renovar brought this diagnosis up. Physicians always must be consider PE in the differential of a dyspnic patient, particularly a pregnant one. Pregnancy is a risk factor for developing venous thromboembolisms secondary to an increase in coagulation factors, venous stasis, and decreased fibrinolytic activity. The overall incidence of thromboembolic disease in pregnant women range from 1 in 200 to 1 in 1,400 deliveries. Using ultrasound to ?rule out? DVT?s as a way to diagnose PE?s is not acceptable; in patients who have no symptoms of DVT (which our patient did not have), the sensitivity of this test falls to less then 30% for even picking up a proximal DVT. Also, only ~1/3 of patients with a proven PE will have a positive venous ultrasound for DVT. Our patient was not tachycardic (23% sensitivity) or tachypnic (70% sensitivity), so physical findings were not enough to rule her out of having a PE as well. We ultimately decided against a further work up of looking for a PE though, because her chest x-ray showing pulmonary congestion would account for her dypsnea and is not consistent with a PE.

Thanks again for participating in my case everybody. I will try to follow up with the patient this week, and feel free to continue posting thoughts about the case/comments made about the case as well.

 

[Kalel]

Well, I tried my best to get some follow up to this case today. Unfortunately, the patient was discharged on Friday night, presumably because her symptoms had resolved, and her pulse and blood pressure returned to normal levels (P: 60-90, BP: 150-110/70-80 recorded in the computer). She did not have color dopplers done before being discharged, and there no evidence that anyone had ever ordered a TSH on her in this hospital. Here CBC while pregnant included a Hgb that was running around 11-12. I'd like to know how she was when she was discharged, but she was never really my patient and the attending cardiologist who was taking care of her is going to be away all week. I really think that she needed a doppler study before being discharged to further work up her elevated BNP and cardiomyopathy (and a TSH would have been indicated too), but this is a private hospital where the case-managers are very agressive about patient turn-around time and profit. The requiring "doppler" to be written specifically on the order, with a reason for ordering it, is apparently a medicare/insurance universal requirement according to one of my attendings. I will ask the attending when he returns next week what sort of follow up plans he has for this patient.

 

[ClassSwitch]

Kalel, Renovar, et. al.: thanks for posting and discussing this very interesting case!

Only thing I would've added to the initial DDx is primary pulmonary HTN (PPH) -- this would've been ruled out by some of the initial studies (eg, ECHO and EKG), but given the urgency of this condition in gravid women, it might have been worth considering among the initial diagnoses. Major sx include dyspnea, fatigue, CP, all of which can arise in the 2nd trimester. Sx become worse as the hemodynamic demands of pregnancy continue to increase. Early spontaneous labor is common, so delivery may be planned at 32-36 wks GA. Major complication is maternal death, which occurs in the first week postpartum from CHF or other cardiac abnormalities. If dx'd early in pregnancy, abortion is recommended; otherwise, elective delivery is recommended under strict hemodynamic monitoring.

 

[Kalel]

ClassSwitch: Pulmonary hypertension is an interesting diagnosis that I had not considered. There does not appear to be a reason for our patient to develop secondary pulmonary hypertension (no COPD, no PE's, no ASD, etc), but I was able to find case reports of primary pulmonary hypertension being exacerbated by the cardiovascular changes associated with pregnancy and delivery (when CO increases and systemic and pulmonary blood pressure rises). On chest x-ray, central pulmonary arteries are typically enlarged while peripheral vessels are attenuated. This is not what we saw in our CXR. ECG does oftentimes show RVH, but the ECG is specific, but not very sensitive, for RVH. TTE can be normal in these patients as well, although one typically sees the findings of RVH (thickened RV wall, RA enlargement). The best test (besides right-sided heart cath, the gold standard) is actually a doppler study, the one study that was not done. Anyways, because we were not able to find any secondary causes of pulmonary hypertension, and primary pulmonary hypertension is rare; and because her CXR was not consistent with pulmonary hypertension, I agree with you in that I would not put it highest on my differential. A doppler would have been nice to confirm this though, as the CXR can be confusing. Thanks for the extra differential though.

 

[Tenesma]

sounds like mitral prolapse worsening to mitral regurg (due to LV distention from increased volume due to pregnancy) leading to mild right heart failure with a background of mild LVH (possibly due to hx of HTN).

This would explain all of her symptoms. A heart rate of 44 is not unusual in somebody who has a combination of type II heart block and high systolic pressures... and the mild LVH and MR would dictate a higher recorded EF... if her EF were lower then she would be in big doo-doo.

she needs a proper Echo and proper hypertensive management... more than likely as she starts redistributing fluid her MR will resolve and her right heart will hopefully recuperate... if not, she is in a for a whole lotta hurting at her age...

 

[Kalel]

Originally posted by Tenesma
sounds like mitral prolapse worsening to mitral regurg (due to LV distention from increased volume due to pregnancy) leading to mild right heart failure with a background of mild LVH (possibly due to hx of HTN).

This would explain all of her symptoms. A heart rate of 44 is not unusual in somebody who has a combination of type II heart block and high systolic pressures... and the mild LVH and MR would dictate a higher recorded EF... if her EF were lower then she would be in big doo-doo.

she needs a proper Echo and proper hypertensive management... more than likely as she starts redistributing fluid her MR will resolve and her right heart will hopefully recuperate... if not, she is in a for a whole lotta hurting at her age...

Hmmm. I feel rather stupid, different attendings have been telling me all week while reading echo's how reading those EF's is subjective and things like MR can cause a miscalculation of an actual EF to occur. I discussed the case with the cardiology director here at this hospital, and he didn't think that it sounded like a case of peripartum cardiomyopathy because it resolved so quickly and there wasn't any systolic dysfunction observed on the TTE. It all comes down to doing that damn doppler that was never done. This is actually applicable to everybody reading this forum since it's a stupid medicare rule, but when you order an TTE, you must write in "DOPPLER" too! There are very few indications for ordering a TTE without a doppler (looking for thrombus, pericardial fluid), but medicare and therefore insurance co's still require that the physician ordering the test write "doppler" out specifically in order for the test to be done and the echo center to be paid. Anyways, I'm not saying that your diagnosis is the right diagnosis because usually patients with MVP without previously documented MR tolerate pregnancy fine, but now that I read your post and I think about it more, your diagnosis would be highest on my differential too.

 

[Tenesma]

if you like cardiology or are interested in cardiology - a good thing during an elective month would be to spend time doing intra-operative TEE on the cardiac anesthesia service... not only will you learn a LOT about ECHO, but you will also see things that most cardiologists don't often get an opportunity to see: how the echo exam changes in the same person with the same pathology based on changes in blood pressure, heart rate, volume filling, opening of the pericardial sac, and the list goes on... it is really neat...