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  1. #1
    IMG SURVIVOR's Avatar
    IMG SURVIVOR is offline Moderator 536 points
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    Cardio#5

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    A 64-year-old woman is evaluated for acute dyspnea 3 days after discharge following an inferior myocardial infarction. When she was hospitalized, urgent coronary angiography showed single-vessel coronary artery disease with occlusion of her mid-right coronary artery. She underwent successful stenting of her right coronary artery, and was discharged on her third hospital day. Her ejection fraction was 50% with inferior wall hypokinesis before discharge.
    The patients dyspnea began 30 minutes ago. On physical examination, her pulse rate is 110/min, respiration rate is 34/min, and blood pressure is 100/60 mm Hg. Jugular venous pressure is elevated at 10 cm H2O, crackles are heard halfway up both lung fields, a parasternal lift is appreciated, and there is a new grade 3/6 systolic murmur at the left sternal border with an S3 gallop. The electrocardiogram shows sinus tachycardia with Q waves and T wave inversions in leads II, III, and aVF, and is unchanged from the discharge electrocardiogram.
    A pulmonary artery catheter is placed, which shows the following:
    Pressure (mm Hg) Oxygen Saturation (%)
    Right atrium 12 (normal 2-7) 49 (normal 60-75)
    Right ventricle 60/12 (normal 20-30/2-7) 78 (normal 60-75)
    Pulmonary artery 60/32 (normal 20-30/10-15) 80 (normal 60-75)
    Pulmonary capillary wedge 24 (normal <14) 98 (normal >93)


    Which of the following is the most likely diagnosis?
    A. Papillary muscle rupture
    B. Ventricular septal defect
    C. Pericardial tamponade
    D. Recurrent myocardial infarction
    E. Atrial septal defect

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    why even bother with the obvious. Just know where you are need it and where you can help the most.

  2. #2
    blackwolverine is offline Junior Member 510 points
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    Quote Originally Posted by IMG SURVIVOR View Post
    A 64-year-old woman is evaluated for acute dyspnea 3 days after discharge following an inferior myocardial infarction. When she was hospitalized, urgent coronary angiography showed single-vessel coronary artery disease with occlusion of her mid-right coronary artery. She underwent successful stenting of her right coronary artery, and was discharged on her third hospital day. Her ejection fraction was 50% with inferior wall hypokinesis before discharge.
    The patients dyspnea began 30 minutes ago. On physical examination, her pulse rate is 110/min, respiration rate is 34/min, and blood pressure is 100/60 mm Hg. Jugular venous pressure is elevated at 10 cm H2O, crackles are heard halfway up both lung fields, a parasternal lift is appreciated, and there is a new grade 3/6 systolic murmur at the left sternal border with an S3 gallop. The electrocardiogram shows sinus tachycardia with Q waves and T wave inversions in leads II, III, and aVF, and is unchanged from the discharge electrocardiogram.
    A pulmonary artery catheter is placed, which shows the following:
    Pressure (mm Hg) Oxygen Saturation (%)
    Right atrium 12 (normal 2-7) 49 (normal 60-75)
    Right ventricle 60/12 (normal 20-30/2-7) 78 (normal 60-75)
    Pulmonary artery 60/32 (normal 20-30/10-15) 80 (normal 60-75)
    Pulmonary capillary wedge 24 (normal <14) 98 (normal >93)


    Which of the following is the most likely diagnosis?
    A. Papillary muscle rupture
    B. Ventricular septal defect
    C. Pericardial tamponade
    D. Recurrent myocardial infarction
    E. Atrial septal defect
    the answer is B.
    here's why:
    first : of all the timing of the incident is 3 day post mi. this is the perfect time for interventricular rupture. also the chance for an interventricular rupture is increased due to an inferior mi
    second: the physical shows signs of volume overload in the right sided circulation and also a holosystolic murmur and a parasternal lift.
    third: the EKG rules out a reccurent MI ( although i would compliment it with a second CK_MB level... but that's just me!!!).
    fourth and most impo: the readings of the Right sided cath:
    A STEP UP IN BOTH O2 AND PRESSURE READING S IN THE RT VENTRICLE AND THE PULMONARY ART.====>LT TO RT SHUNT.
    so the answer is :B ventricular septal defect

  3. #3
    IMG SURVIVOR's Avatar
    IMG SURVIVOR is offline Moderator 536 points
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    I will tell you soon if you are right or wrong
    Moderator: USMLE AND Residency Forums.

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    why even bother with the obvious. Just know where you are need it and where you can help the most.

  4. #4
    thomasg2 is offline Newbie 510 points
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    ...and you never did as you typical never do...... Well I tell you later if you have right or wrong. And you never do!!!

  5. #5
    IMG SURVIVOR's Avatar
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    The correct answer is B
    Educational Objectives
    Recognize acute ventricular septal defect after myocardial infarction.
    Critique
    Mechanical complications usually occur 2 to 7 days after acute myocardial infarction (AMI). Ventricular septal defect (VSD) and papillary muscle rupture leading to acute mitral regurgitation are rare mechanical complications that occur in roughly 0.1% of cases of AMI. Both disorders usually lead to abrupt pulmonary edema and/or hypotension. Papillary muscle dysfunction, without rupture, can also cause severe mitral regurgitation after AMI. Early diagnosis is critical because survival 24 hours after a large VSD or papillary muscle rupture is roughly 25% with medical therapy.
    An emergent echocardiogram is indicated to help with the early diagnosis. Hemodynamic monitoring with a pulmonary artery catheter is usually necessary. An increased oxygen saturation between the right atrium and ventricle is seen with left-to-right shunting through a VSD. Both disorders may be associated with prominent v waves on the pulmonary capillary wedge tracing. Echocardiography is helpful in making the correct diagnosis.
    For both disorders, rapid treatment involves nitroprusside and/or intra-aortic balloon pump. Emergent surgical repair is usually considered for definitive therapy; however, the survival is still only 50% following repair.
    Pericardial tamponade from rupture of the left ventricular free wall usually leads to sudden hypotension and death. After heart failure, free wall rupture represents the second most common cause of death for patients who die in hospitals after myocardial infarction. Predisposing factors include advanced age as well as first myocardial infarction, probably due to lack of coronary collaterals. Ventricular free wall rupture is most commonly seen 1 to 4 days after a myocardial infarction, but can rarely occur up to 3 weeks afterward. The free wall rupture typically occurs in the junction of the infarction with normal myocardium, and less often within the center of the infarct. Patients usually present with cardiovascular collapse, tamponade, or pulseless electrical activity. Right heart catheterization in tamponade would demonstrate diastolic elevation and equalization of pressures from the right atrium, right ventricle, and pulmonary capillary wedge with reduced cardiac output. Atrial septal defect is not a complication following AMI.

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    why even bother with the obvious. Just know where you are need it and where you can help the most.

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