Its Leaky...

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Its Leaky...

• MITRAL REGURGITATION
• Rami Khouzam, MD

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Mitral Regurgitation

• Anatomy3 basic mechanisms of MR
• 1- Alteration of Mitral leaflets, commissures, or
  annulus
• 2- Defective tensor apparatus
• 3- Alterations of LV and LA size function

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1- Alteration of Mitral leaflets, commissures, or
annulus

• MVP most common cause of isolated MR. Posterior
  leaflet more frequent and severe. Greater in men.
  Increases with age.
• Rheumatic fever
• Mitral annulus calcification age-related
• Infective endocarditis
• Congenital cleft of anterior MV associated with
  primum ASD

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2- Defective tensor apparatus

• Abnormal chordae tendineae Idiopathic/
  endocarditis/ MVP/ Trauma
• Papillary muscle dysfunction
• Posteromedial gt anterolateral (vulnerability to
  ischemia infarction) single blood supply

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3- Alterations of LV and LA size function

• Alteration of position and axis of papillary
  muscle
• Mitral ring dilatation

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Key points...

• Mitral prolapse is the most common cause of
  isolated MR
• Ischemia ? dysfunction/rupture of papillary
  muscle. Posteromedial gt anterolateral
• LV enlargement abnormal contractile function
  are common causes of MR

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Pathophysiology of MR

• 1. Acute Stage
• 2. Chronic Compensated Stage
• 3. Chronic Decompensated Stage

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Key points...

• Acute severe MR is characterized by normal-sized
  chambers, high EF, pulmonary congestion.
• Chronic compensated severe MR is typified by few
  symptoms, enlargement of the LV LA, and high EF
• Chronic decompensated severe MR is typified by
  enlargement of the LV LA, pulmonary congestion,
  and normal to low EF
• A normal range EF in the setting of severe MR
  usually implies LV systolic dysfunction

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Clinical syndrome of MR

• Acute MR
• If severe pulmonary congestion
• S3 S4
• Systolic murmur short, soft or absent

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• Chronic MR
• Prolonged asymptomatic interval.
• Fatigue/ generalized weakness
• Laterally displaced, enlarged apical impulse
• Severe MR apical thrill
• Early aortic closure
• Holosystolic murmur intensity does not correlate
  with severity of regurgitant flow
• Anterior leaflet MR Radiates to axilla
  frequently
• Posterior leaflet abnormality ? regurgitant flow
  anteriorly ? radiation to aortic area, and all
  precordium
• Short diastolic apical rumble in the absence of
  MS high diastolic transmitral flow severe MR

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Key points...

• Acute severe MR short or soft murmur because of
  low LV-LA pressure gradient
• Nonspecific fatigue weakness may represent
  early symptoms of chronic severe MR
• Duration of apical impulse in chronic severe MR
  is related to LV systolic function
• Posterior leaflet prolapse murmur to aortic area
• Amyl nitrite distinguishes diastolic rumble of
  mixed MS MR (?) from that due to isolated
  severe MR (?)

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Evaluation of MR

• EKG
• LAE
• Atrial fibrillation
• LVH
• Nonspecific ST-T changes
• CXR
• LVE
• LAE (straightening left border, atrial double
  density, elevation of left main-stem bronchus)
• Pulmonary venous congestion

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Echocardiography

• In some cases, TEE is better to assess the
  anatomy of the MV, to rule out atrial thrombus,
  gather supplemental data in quantitative
  qualitative measures of regurgitation severity
  (but not always necessary).

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Determination of severity

• Over 20 variables described.
• Color flow Doppler
• Atrial side
• Small jet occupying lt 20 of LA mild
• 20- 40 moderate
• Large jet gt 40 and extending into the pulmonary
  veins) severe
• Ventricular side PISA proximal flow acceleration
  (proximal isovelocity surface area) concentric
  series of hemispheric rings of alternating
  colors, each ring denoting an isovelocity of
  aliasing. The diameter of the ring closest to the
  regurgitant orifice is measured and, in severe
  mitral regurgitation, usually approaches
• 1 cm.

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• Pulsed and continuous wave Doppler of mitral
  inflow
• E gt 1.4 m/sec
• E/A ratio gt 2
• (Finding an A-wave dominant pattern of mitral
  inflow makes severe mitral regurgitation very
  unlikely).
• Uniformly dense jet throughout its duration,
  well-defined envelope
• ? TR peak velocity pulmonary hypertension.
• Doppler of pulmonary veins show systolic flow
  reversal

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• Doppler of pulmonary veins
• (pulse Doppler of the left and right upper
  pulmonary veins from the apical four-chamber
  view). Normal pulmonary venous flow is antegrade
  during both ventricular systole and diastole
  (ventricular systolic component dominates), with
  slight retrograde flow during atrial systole. In
  hemodynamically severe mitral regurgitation, the
  flow in one or more pulmonary veins (depending
  upon the direction of the jet) will show systolic
  flow reversal

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Index of severity

• Based on 6 variables, each scored on a scale of 0
  to 3 then averaged
• 1- Color Doppler regurgitant jet width and
  penetration2- Color Doppler PISA diameter3-
  Continuous wave Doppler characteristics of the
  regurgitant jet4- Continuous wave Doppler TR
  derived PAP
• 5- Pulse wave Doppler pulmonary venous flow
  pattern6- Left atrial size by 2D-
  echocardiography
• (Mild MR index 1.7, Severe MR (regurgitant
  fraction gt40 percent) index 1.8, A value 2.2
  identified patients with severe mitral
  regurgitation with a sensitivity, specificity,
  and positive predictive value of 90, 88, and 79
  percent, respectively).

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Cardiac catheterization

• Right heart cath Prominent V wave on PCWP
  tracing
• Left heart cath/ Ventriculogram Only when -
  noninvasive data are discordant or
• - technically limited or
• - differ from the clinical perception of the
  severity of MR or ventricular function.
• Angiographic grading many variables..

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Sellars criteria
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Key points...

• No EKG or CXR findings pathognomonic of MR
• Echo is invaluable for assessing cause severity
  of MR, size and function of LV, LA, RV
• Left ventriculography is most useful when
  noninvasive data discordant or technically
  limited or differ from clinical impression of the
  severity of MR, or ventricular function

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Mitral valve prolapse

• Click systolic billowing of a portion of mitral
  leaflet into LA
• Maneuvers that ?ventricular preload (Valsalva,
  standing) prolapse, click murmur earlier in
  cardiac cycle.
• Progression to severe MR more in men, and
  advancing age
• MVP severe MR managed as severe MR
• Antibiotic prophylaxis when?
• - Click murmur, or
• - Click echo significant leaflet thickening or
  regurgitation
• B-Blocker for MVP/palpitations/atypical
  CP/anxiety
• ASA TIA in the setting of MVP

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Natural history of MR

• Depends on its cause
• Time course of progressive LV dysfunction in
  chronic MR is variable unpredictable
• Acute worsening of MR suggests chordal rupture,
  infection, new arrhythmia, or ischemia

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Outcome after surgical correction of MR (The
unnatural history)

• Current surgical practice is to operate on
  patients with severe MR before the development of
  heart failure or ventricular dysfunction, if
  possible
• Preoperative EF best predictor of long-term
  mortality, CHF, postoperative LV function
• End-systolic dimension significant predictor
• A. fib more than 3 months preoperatively
  associated with high risk of postoperative
  arrhythmia persistence and need for long-term
  anticoagulation

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Treatment of Acute severe MR

• i.v. vasodilators (Na nitroprusside),
• i.v. inotropes, IABP
• Mitral valve Repair or Replacement
• Endocarditis delay surgery if possible (risk of
  recurrence), unless progressive heart failure,
  unresponsive to antibiotics, intracardiac
  abscess, recurrent systemic embolization

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Treatment of Chronic Nonischemic MR

• Dental hygiene/ Antibiotic prophylaxis
• Treat contributing underlying disease
• No data to indicate diuretics or vasodilators (or
  both) provide morbidity or mortality benefit
• Every patient should be considered for surgery

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Indications for surgery for chronic mitral
regurgitation
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MV REPAIR

• Who gets it??
• Repair should be performed preferentially
  whenever possible favorable predictor of
  operative mortality, late survival, postoperative
  EF.
• High risk patients severe LV dysfunction (EF lt
  35 ,
• CI lt 1.5 L/min per m2)
• MR posterior leaflet, non-rheumatic,
  noninfective, noncalcific, nonischemic most
  amenable to repair

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Treatment of MR d.t. Ischemia or Cardiomyopathy

• Maximal medical therapy FIRST
• MVR (Mitral annular rings)

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Key points...

• Patients with acute severe MR hemodynamic
  instability require rapid evaluation, aggressive
  stabilization, early valve operation
• Patients with acute severe MR hemodynamic
  stability semielective surgery
• Indications for valve surgery in endocarditis
  progressive heart failure, resistance to
  antibiotics, intracardiac abscess, recurrent
  systemic embolization despite therapy
• Severe chronic MR NYHA class III or IV, EF lt 60
  , End-systolic diameter gt 45 mm, or end-systolic
  volume gt 50 mL/m2 Definite Surgery

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Key points...

• Emerging indications for MV Replacement Flail
  leaflet, paroxysmal or recent A. Fib, pulmonary
  HTN
• Impaired LV function Valve repair preferred
• NO Repair in
• rheumatic, ischemic, endocarditis, anterior or
  bileaflet prolapse, significant calcification

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• QUESTIONS

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• Question 20 of 264
• Which one of the following statements about
  mitral valve prolapse is incorrect?
• A. The degree of echocardiographic thickening of
  the mitral valve is related to long-term
  prognosis.
• B. Clinical auscultatory phenomena as well as
  echocardiographic documentation should be present
  for the diagnosis of mitral valve prolapse.
• C. Most symptoms in patients with the mitral
  valve prolapse syndrome are related to the
  severity of mitral regurgitation.
• D. Echocardiographic mitral valve prolapse may be
  seen in normal individuals after volume depletion.

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• The correct answer is C.
• Several clinical and autopsy studies have
  demonstrated that patients with mitral valve
  prolapse and thick mitral valve leaflets are at
  high risk for the development of complications.
  The diagnosis of mitral valve prolapse as a
  general rule should be based on auscultatory and
  confirmatory echocardiographic findings, and not
  on "soft" echocardiographic or nonspecific
  auscultatory findings. Echocardiographic mitral
  valve prolapse may be seen in normal individuals
  after volume depletion or a decrease in
  intravascular volume. Symptoms in patients with
  mitral valve prolapse may be directly related to
  the severity of regurgitation. Certain patients
  with mitral valve prolapse, however, may have
  symptoms related to autonomic dysfunction (mitral
  valve prolapse syndrome). For the diagnosis of
  mitral valve prolapse syndrome, mitral valve
  prolapse should be present.

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• A 55-year-old African-American man is referred to
  you for evaluation of a murmur. The murmur was
  first noted five years ago. He denies any
  symptoms, but admits that he has always done
  little physical activity. He states that he no
  longer walks to the office, and does not have to
  walk stairs to the third floor because there is
  an elevator. Family history Both his 78-year-old
  father and his 48-year-old brother have heart
  murmurs, but are doing well.Physical
  examination BP 110/70 mm Hg, pulse 80/minute,
  respirations 15/minute. Neck veins 5 cm. Carotid
  upstroke is normal without bruits. Lungs are
  clear to auscultation and percussion. Point of
  maximal impulse is diffuse in the 5th intercostal
  space in the midclavicular line and forceful.
  First and second heart sounds are normal. There
  is a grade III/VI systolic murmur crescendo to
  the second sound, best heard at the apex, but
  radiating well to the base. There are no S4 or S3
  gallops and no other abnormalities.Laboratory
  Chest X-ray Prominent LV, normal lung fields.
  ECG LV hypertrophy by voltage, no ST-T wave
  changes. Valve 2D echo-Doppler Floppy mitral
  valve, severe posterior leaflet prolapse,
  moderately severe mitral regurgitation (MR) with
  the jet directed anterior-medially. LV
  end-diastolic diameter is 5.8 cm and LA diameter
  4.5 cm. His EF is estimated at 45-50.
• What is the most appropriate recommendation for
  treatment for this patient?
• A. Follow medically with close observation and
  repeat echo if there is a clinical change.
• B. Start enalapril and repeat echo in four
  months.
• C. Send to surgery for mitral valve replacement.
• D. Send to surgery for mitral valve repair.
• E. Start long-acting nifedipine and repeat echo
  in one year.

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• The correct answer is D.
• This man has MR and has the best pathology for
  successful mitral valve repair. To require mitral
  replacement would be very unusual with posterior
  leaflet prolapse and would be a harder decision
  to make in this man who claims to be
  asymptomatic, if it were necessary. Both options
  B and E are incorrect because this man has an EF
  at the lower limits of normal or mildly
  decreased, indicating a decreased myocardial
  contractility in the presence of moderately
  severe MR.

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• Question 51 of 264
• A 36-year-old woman presents with sudden severe
  dyspnea. She had mitral valve replacement five
  years ago with a St. Jude valve and ran out of
  warfarin two weeks ago. Physical examination
  shows signs of pulmonary edema and right heart
  failure. She is afebrile, BP is 130/86, and pulse
  is 95 with sinus rhythm. TEE shows a large mass
  impairing the mobility of one of the bileaflets.
  
• The best initial management strategy would be
  which one of the following?
• A. Immediate valve replacement.
• B. High-dose IV antibiotics.
• C. A loading dose of heparin.
• D. IV thrombolytic therapy.
• E. IV enalapril.

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• The correct answer is D.
• Acute valve thrombosis is a catastrophic
  complication of prosthetic valve replacement and
  is almost always a result of inadequate chronic
  anticoagulation. Because of the rarity of this
  problem (0.2 per patient-year), there is not a
  great deal of experience with any form of
  management. When clinical suspicion is high,
  cinefluoroscopy or TEE should be done to confirm
  the diagnosis. If thrombus is believed to be
  present and the patient is hemodynamically
  stable, thrombolytic therapy should be tried
  first followed by heparin, provided there are no
  contraindications to this approach. If there are
  contraindications to thrombolytics but not
  heparin, the latter can be tried first. If there
  is no improvement in 48-72 hours or if the
  patient decompensates, surgery is indicated.

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• Question 101 of 264
• In which of the following diseases is pregnancy
  difficult, but not highly risky to the mother and
  fetus?
• A. Eisenmenger's syndrome.
• B. Primary pulmonary hypertension.
• C. Mitral prolapse with significant mitral
  regurgitation. D. Prior peripartum
  cardiomyopathy with heart failure. E. The Marfan
  syndrome with dilated aortic root.

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• The correct answer is C.
• The CV system must be able to handle a doubling
  of cardiac output during pregnancy. Thus,
  cardiopulmonary diseases that obstruct blood flow
  are usually contraindications to pregnancy
  because both the mother and fetus get inadequate
  blood flow. Thus, obstruction to pulmonary flow
  due to the Eisenmenger reaction or primary
  pulmonary hypertension fits into this category,
  but hypertrophic cardiomyopathy does not. The
  increased cardiac output increases venous return
  to the left heart, resulting in LV enlargement
  and less obstruction. In fact, during pregnancy,
  the murmur of hypertrophic obstructive
  cardiomyopathy may lessen or even disappear,
  causing the diagnosis to be missed.Prior
  peripartum cardiomyopathy with heart failure is a
  contraindication to pregnancy because of the high
  incidence of recurrent failure and
  death.Hormonal changes during pregnancy alter
  vascular walls, making them more distensible.
  This is a normal mechanism to adapt to higher
  cardiac output however, in the patient with the
  Marfan syndrome and an enlarged aortic root, it
  can lead to increased wall stress and aortic
  rupture or dissection.

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• Question 153 of 264
• A 52-year-old woman goes into acute pulmonary
  edema after an auto accident. She has a mild
  concussion and bruises on her upper body. ECG
  shows sinus tachycardia and nonspecific ST-T wave
  changes. Physical exam shows BP 123/72, pulse 110
  regular, diffuse pulmonary rales, a grade 2 early
  systolic murmur, and a third heart sound.
• What is the most likely diagnosis?
• A. Ruptured papillary muscle.
• B. AMI.
• C. Cardiac contusion.
• D. Noncardiogenic pulmonary edema.
• E. Pulmonary contusion.

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• The correct answer is A.
• Cardiac problems discovered following an auto
  accident raise the question of whether the
  cardiac condition caused the accident or vice
  versa. In this case, there is no cardiac history
  preceding or during the accident, but only later.
  The ECG is not suggestive of AMI, but it cannot
  be eliminated based on the information given. The
  physical examination is consistent with CHF
  (i.e., rales and third heart sound), and
  myocardial contusion or ruptured papillary muscle
  could lead to pulmonary edema. The early systolic
  murmur is characteristic of severe acute mitral
  regurgitation due to papillary muscle rupture
  since the resultant severe regurgitation rapidly
  eliminates the gradient between the LV and atrium
  during systole, shortening what would ordinarily
  be a holosystolic murmur. Thus, the best answer
  is ruptured papillary muscle.

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• Question 163 of 264
• A referring physician treating a patient with an
  inferior wall MI calls you. The patient received
  thrombolytic therapy and seemed to be stabilizing
  nicely. On the third day after the infarction,
  the patient became acutely short of breath and is
  now in pulmonary edema with a BP of 80 mm Hg
  systolic. On examination, the jugular venous
  pressure is normal and auscultation of the heart
  reveals no murmur or gallop. The ECG is
  unchanged.
• The correct diagnosis in this case is
• A. Ruptured ventricular septum.
• B. Papillary muscle rupture with severe mitral
  regurgitation.
• C. Massive pulmonary embolism.
• D. Infarct extension.
• E. RV infarction.

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• The correct answer is B.
• This is a typical presentation of a patient with
  inferior wall MI and rupture of a papillary
  muscle several days after the initial event. This
  complication can be treated with great success if
  recognized and surgery to replace/repair the
  valve is accomplished without delay. The lack of
  a murmur is not unusual and probably relates to
  prompt equilibration of LV and LA pressures.
  Involvement of the posterior papillary muscle is
  more common as a result of a more common single
  artery supplying this structure. Infarct
  extension is unlikely in view of the unchanged
  ECG. An RV infarction is unlikely in view of the
  normal jugular venous pressure.

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• A 68-year-old Caucasian male has been a patient
  of yours for 10 years. He has had insulin-treated
  diabetes mellitus for 14 years, known CAD with an
  MI 12 years ago, and CABG 12 years ago. He
  follows his regimen of diet and exercises
  moderately, including playing golf. In the past
  six months he has noted new bilateral ankle edema
  toward the end of the day, as well as mild
  dyspnea on exertion. He denies chest discomfort.
  His medications have been furosemide 40 mg daily,
  atorvastatin 40 mg daily, metoprolol 6.25 mg bid,
  isosorbide mononitrate 60 mg daily, ezetimibe 10
  mg daily, aspirin 325 mg daily,
  losartan/hydrochlorothiazide combination 100
  mg/25 mg daily, dixogin 0.125 mg qd, and
  rosiglitazone metformin combination 2/500 mg
  daily.Laboratory work has shown total
  cholesterol 177 mg/dl, LDL cholesterol 77 mg/dl,
  HDL cholesterol 48 mg/dl, and triglyceride 92
  mg/dl. Renal, hepatic, and hematologic functions
  were normal. Two-hour postprandial glucose was
  134 mg/dl.His ECG shows an old anterior MI and
  left anterior hemiblock an echocardiogram shows
  an LVEF of 0.38. The LA is mildly enlarged. There
  is moderate mitral regurgitation. You should, as
  your first strategy
• A. Refer for mitral valve surgery.
• B. Refer for biventricular pacing.
• C. Increase his furosemide to 80 mg daily.
• D. Begin spironolactone 25 mg daily.
• E. Increase his losartan to 200 mg daily.

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• The correct answer is D.
• The therapeutic issue is deciding what is maximum
  medical therapy in this man with left- and now
  right-sided heart failure. There is little to be
  gained by doubling his dose of losartan. While
  you may need to increase his furosemide for
  comfort due to fluid retention, the best first
  step is to add spironolactone, which should not
  only affect diuresis, but contribute to
  improvement in LV systolic performance through
  its renin-angiotensin effects. The device
  interventions may be considered after maximum
  medical therapy has been achieved in reference to
  both the number and dosage of the drugs. Mitral
  valve surgery is possible in many patients with
  advanced failure, but in this case, the degree of
  mitral regurgitation may lessen considerably with
  optimal medical therapy, and additional
  evaluation including catheterization is needed to
  make the decision if severe mitral regurgitation
  persists. He does not currently meet accepted
  indications for ICD placement with his EF above
  35.

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• Question 197 of 264
• Which one of the following conditions is not
  considered a contraindication to pregnancy?
• A. Eisenmenger's syndrome.
• B. Moderate primary pulmonary hypertension.
• C. The Marfan syndrome with aortic root
  dilatation.
• D. Moderately severe mitral regurgitation.

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• The correct answer is D.
• The risk of pregnancy to the patient with
  pulmonary hypertension is so great that pregnancy
  is not considered an option. Similarly, the risk
  of aortic dissection is quite high in those
  patients with the Marfan syndrome and aortic root
  dilatation, so that pregnancy is contraindicated.
  So long as LV function is normal, patients with
  mitral regurgitation tolerate the hypervolemia of
  pregnancy.

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• Question 116 of 264
• A 30-year-old black woman suddenly develops
  severe tachypnea and tachycardia two days after
  open reduction of a comminuted fracture of the
  right femur. You are called to see her in the
  recovery room. Physical exam BP is 85/40 mm Hg.
  Pulse is 120/minute and irregular. Respiratory
  rate is 28/minute. Neck veins are 15 cm. Lungs
  No rales. Cardiac Left anterior precordial lift.
  S2 widely split. A grade II/VI short systolic
  ejection murmur is heard loudest at the third
  intercostal space left sternal border. There is
  an S3 that increases with inspiration. Liver is
  palpable 35 cm below the right costal margin. No
  pedal edema. Lab Chest X-ray Decreased vascular
  markings in the right lower lobe and left upper
  lobe. Small pleural effusion right costophrenic
  angle. ECG Right axis deviation, RBBB, AF. Echo
  Doppler dilated poorly contracting RV. Dilated
  RA. Normal size LA and LV.
• The Doppler jet of tricuspid regurgitation is
  most likely to be
• A. 1 m/sec.
• B. 2 m/sec.
• C. 3 m/sec.
• D. 4 m/sec.
• E. 5 m/sec.

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• The correct answer is C.
• The case is that of a patient with a fracture who
  develops the classical picture of acute massive
  pulmonary embolism. Such a patient with extreme
  increase in RV afterload has no opportunity to
  hypertrophy to compensate, dilates the RV, then
  fails. Such a ventricle cannot generate systolic
  pressures much above 50 mm Hg. The tricuspid jet
  by the modified Bernoulli equationP (m Hg)
  4x Vcm/sec2Where P the pressure drop across
  the tricuspid value And V the maximum jet
  velocity that can be used to estimate the
  pulmonary artery systolic pressureP maximal RA
  pressure reflected by the jugular venous pressure
  estimated RV systolicpressure, which in the
  absence of pulmonic infundibular and/or valvular
  stenosis equals thesystolic pressure of the
  pulmonary artery.

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• Question 142 of 264
• Abnormal septal motion can be seen in patients
  with each of the following except
• A. CABG, postop.
• B. A pacemaker.
• C. LBBB.
• D. Severe mitral regurgitation.
• E. Constrictive pericarditis.

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• The correct answer is D.
• Abnormal septal motion can be seen in CABG
  patients or valve patients and is considered a
  "postop" septum. In addition, the septum has
  abnormal motion when it is electrically activated
  in an unusual fashion, as would be the case for a
  patient with an LBBB or a pacemaker (when the
  septum is activated right to left). Also,
  patients with constrictive pericarditis typically
  have an abnormal septal bounce. Patients with
  severe mitral regurgitation do not have abnormal
  septal motion unless they have one of the
  previously listed conditions (or severe pulmonary
  hypertension or right-sided volume overload as
  well) in addition to their mitral regurgitation.

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Formulas for evaluation of MR

• RV PISA x Velocity
• (PISA determined as the aliasing velocity)
• PISA 2 ?r2
• RV ROA x VTI
• ROA RV/VTI
• RV Regurgitant Volume, PISA Proximal
  Isovelocity Surface Area, ROA Regurgitant
  Orifice Area or ERA Effective Reugurgitant Area,
  VTI Velocity Time Integral