Cardiology

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Mat
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61242
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Cardiology
Updated:
2011-08-10 13:27:19
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Heart
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Heart disease
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  1. What are indications for dobutamine stress echo or nuclear imaging?
    • bronchospasm
    • 20 AV block
    • theophylline dependent
    • valvular dysfunction
  2. What are contraindications for dobutamine stress echo or nuclear imaging?
    What would be indicated instead?
    • Prior symptomatic arrhythmia (particularly VT)
    • Low blood pressure
    • Marked HTN
    • Poor echo window

    Do adenosine perfusion instead, but if they have bronchospasm, 20 AV block, theophylline dependent, valvular dysfunction -- then do other modes such as Holter or angiography.
  3. Discuss noncontrast CT cardiac risk evaluation :
    • Mainly for detection of coronary calcification
    • A high calcium score (> 100) indicates an increased risk of cardiac events
    • Lack of coronary calcification is predictive of a very low risk of a cardiac event.
  4. Uses of Cardiac MR in cardiac evaluation:
    • LV function
    • Tissue characterization (infiltrative cardiomyopathies)
    • Myocardial masses
    • Myocardial viability
  5. What is a normal PCWP?
    <12 mm Hg
  6. What conditions can increase PCWP?
    • LVH
    • LV failure
    • MR
    • AR
    • Tamponade
    • Constrictive pericarditis
  7. For the following PCWP pressures, state the associated symptoms:
    1. > 12
    2. 15-20
    3. 25-35
    4. >35
    • 1. Mild dyspnea on exertion
    • 2. DOE
    • 3. Dyspnea at rest
    • 4. Pulmonary edema
  8. What is the normal RA pressure?
    7 cm H2O
  9. Normal RA pressure
    0-5
  10. Normal PA pressure
    13-28/3-13
  11. Normal PCWP
    3-11
  12. Normal BP
    110/70
  13. If RA > PCWP and systemic BP is low, what would be the most possible diagnosis?
    RV infarction
  14. Describe the Swan Ganz reading in a pt with cardiogenic shock
    RA pressure is high, but the PCWP is higher (extremely elevated), BP is low.
  15. Describe the Swan-Ganz finding in mitral stenosis
    Pulmonary systolic pressure and PCWP are very high, systemic BP is normal.
  16. Swan-Ganz finding in Pulmonary HTN
    PA systolic and diastolic pressures are very high, but the PCWP is normal.

    Chronic multiple PE may also show something similar.
  17. What are causes of "inspiratory fall in systolic BP" (pulsus paradoxus)?
    • pericardial tamponade
    • asthma
    • tension pneumothorax
  18. Two causes of bifid pulse with 2 aortic peaks:
    • Aortic regurgitation
    • Hypertrophic cardiomyopathy
  19. Causes of "alternating arterial pulse."
    • Bigeminal PVC
    • Severe LV dysfunction
    • Severe AS
  20. Cause of "decreased rise time and volume of the arterial pulse."(Pulsus parvus et tardus)
    • Aortic stenosis
    • May not be present in the elderly in spite of severe AS
  21. What causes distended neck veins with no pulsatile activity?
    • Tension Pneumothorax
    • SVC obstruction
  22. What causes regular cannon a waves?
    Large "a" waves are of considerable diagnostic value (figure 203-b ). When giant "a" waves are present with each beat,the right atrium is contracting against an increased resistance. This may result from obstruction at the tricuspid valve( tricuspid stenosis or atresia,right atrial myxoma or conditions associated with increased resistance to right ventricular filling. A giant "a" wave is more likely to occur in patients with pulmonary stenosis or pulmonary hypertension in whom both the atrial and right ventricular septa are intact. Cannon "a" waves occur when the right atrium contracts while the tricuspid valve is closed during right ventricular systole. Cannon waves may occur either regularly or irregularly and are most common in the presence of arrhythmias
  23. What causes rapid x and y descents?
    It is pathognomonic for constrictive pericarditis.
  24. What causes large a waves and a slow y descent?
    Tricuspid stenosis
  25. Discuss the jugular wave forms:
    • a wave = RA systole
    • x descent = atrial relaxation and dropping of TV annulus during RV systole
    • v wave = rise in RA pressure with inflow to the RA during RV systole
    • y descent = RA emptying following RA systole
  26. Causes of large a waves:
    • Tricuspid stenosis
    • Severe pulmonic stenosis
    • Severe noncompliant RVH
    • Mitral stenosis

    Severe RV dysfunction of any sort.
  27. Discuss Irregular Cannon a waves
    • Indicate A-V dissociation
    • Occur in:
    • --70% of VT
    • --Third degree AV block
    • --Ventricular pacing in a patient with sinus rhythm and complete heart block
  28. Irregular large pulsations on the neck means?
    V-tach
  29. 2nd heart sound does not vary with respiration. What is the diagnosis?
    ASD
  30. What causes decreased intensity of S1?
    • Caused by closure of the mitral valve leaflets when they are close together
    • Prolonged PR interval
    • AR
    • Severely calcified MV
  31. What causes increased intensity of S1?
    • Caused by closure of the mitral valve leaflets when they are wide open or stiffened:
    • Short PR interval
    • Hyperdynamic LV function
    • MS
  32. What causes a "Persistently split S2?"
    • Or "widened S2", caused by delayed RV emptying:
    • Pulmonic stenosis
    • PE
    • Ectopic LV rhythm
    • RBBB
    • Early closure of the aortic valve (as in severe MR) may also cause a wide S2
  33. What causes Paradoxically split S2?
    • Caused by delayed LV emptying:
    • Severe AS
    • Paced rhtym in the RV
    • Ectopic RV rhythm
    • LBBB
    • HCM
  34. What is the significance of S3?
    • Indicates poor LV function and therefore poor prognosis indicator.
    • It is usually normal in children and in pregnant women
    • Abnormal over age 40
    • May be described as "early diastolic sound at the apex."
  35. A single second heart sound is associated with what pathology?
    Critical AS
  36. Absolute contraindications to thrombolytic therapy:
    • Previous hemorrhagic stroke
    • CVA within 1 year
    • Intracranial neoplasm
    • Active internal bleeding
    • Suspected aortic dissection
  37. Explain the effectiveness of various fibrinolytics:
    • Mortality is decreased the earlier fibrolysis is given, particularly first hour
    • In the GUSTO trial, the combination of tPA and the IV heparin had a slight mortality advantage over other agents.
  38. Does VT or VF within 48 hours of an MI imply a worse prognosis?
    No. However, arrhythmias that occur after 48 hours imply a bad prognosis.
  39. Suspect RV infarction with the triad of :
    • Hypotension
    • Clear lung fields
    • Elevated JVP (Kussmaul's sign)
  40. Discuss treatment of ventricular tachyarrhythmias
    • Cardiovert VF and unstable VT
    • Stable VT can be treated with:
    • Amiodarone 150 mg infused over 10 minutes repeated every 10-15 minutes
    • Or, 360 mg over 6 hours (1 mg/min), then 540 mg over next 18 hours (0.5 mg/min ), not to exceed 2.2 g in 24 hours.
  41. What is the treatment for papillary muscle rupture
    Urgent surgery
  42. Discuss VSD
    • Large anterior MI
    • Loud holosystolic murmur along the left lower sternal border
    • There is an oxygen step-up (>10%) from RA to PA on right heart cath
    • Mortality is 50%
    • Tx is urgent surgery
  43. Discuss the benefits of Smoking cessation
    • decreases mortality and decreases reinfarction rate by 50%.
    • benefits of smoking cessation begin within 48 hours
  44. Discuss the role of nitrates in angina
    Post ACS patients should be instructed to take 1 NTG for ischemic-like pain, and to call 911 if the pain is not relieved within 5 minutes.
  45. Medications that prolong survival in post-MI:
    beta-blockers, ACE-I, ARB
  46. Medications that prolong survival in HF
    beta-blockers, nitrates (with hydralazine), ACE-I, ARB, Spironolactone/Eplerenone
  47. Discuss the diagnosis for Peripheral Arterial Disease:
    What is the best test for functional impairment?
    How do you define the location of the disease?
    • Brachial and ankle blood pressures before and after exercise is the best test of the degree of functional impairment
    • Angiography is the best test for defining the location of the disease
  48. What are the risk factors for PAD?
    • In order of importance:
    • Smoking
    • Diabetes
    • HTN
    • Hypercholesterolemia
    • Hyperhomocysteinemia
    • C-Reactive protein (not a risk factor but a marker for ongoing inflammation)
  49. Medical therapy for PAD
    What is the goal LDL?
    What medication can improve symptoms and increase walkig distance?
    When is this medication contraindicated?
    • Smoking cessation
    • Treatment of HTN to JNC-7 goals
    • Beta-blockers are not contraindicated
    • Decrease LDL < 100, perhaps to 70 mg/dl (typically with a statin)
    • Treat diabetes aggressively
    • ASA for all patients
    • Clopidogrel is an effective alternative
    • Cilostazol (100 mg bid) improves symptoms and increases walking distance (contraindicated in heart failure)
    • Pentoxifylline is a second-lie alternative with less effectiveness.
  50. What is the best med combination in the treatment of aortic dissection
    Nitroprusside and Beta-blocker
  51. What are the Jones criteria?
    Major criteria?
    Minor criteria?
    Criteria for diagnosis?
    • Major
    • Carditis
    • Polyarthritis
    • Chorea
    • Erythema marginatum
    • Subcutaneous nodules

    • Minor
    • Previous rheumatic fever
    • Arthralgias
    • Increased seed rate, WBC, C-reactive protein
    • Prolonged PR interval

    • Diagnosis
    • 2 major criteria or
    • 1 major and 2 minor criteria
    • AND positive Strep test or elevated ASO titers
  52. Discuss Bicuspid Aortic Valve
    What is it associated with?
    • Commonest congenital cardiac anomaly (1 in 50)
    • By age 45, half will have significant AS
    • May be associated with ascending aortic aneurysm or dissection
  53. In aortic stenosis, when do symptoms occur?
    When orifice size is reduced to ≤ 25% (orifice area < 0.7 cm2; normal 2-4 cm2)
  54. What are the physical examination findings in Aortic Stenosis?
    • 1. Decreased rise time and volume in the carotid pulses (pulsus parvus et tardus)
    • 2. Systolic thrill or shudder in the carotids or the suprasternal notch
    • 3. Second heart sound paradoxically split or A2 absent completely
    • 4. Murmur peaks after mid systole
  55. State Bernoulli's equation.
    Pressure = 4(peak velocity)2
  56. Indications for surgery in Severe AR?
    • 1. Symptomatic patients
    • 2. Asymptomatic patients but with LVEF > 50%, LVESD > 55 mm, or LVEDD > 75 mm
    • -- LVEF < 50%
  57. Endocarditis organisms in native valve
    • Streptococcus viridans -- 50%
    • Staph aureus -- 20%
  58. Endocarditis organisms in addicts
    • Staphylococcus is most common (80%), particularly the tricuspid endocarditis
    • Fungi (Candida)
  59. Endocarditis organisms of prosthetic valve
    • Early (< 2 months) Staphylococcus epidermis
    • Late ( > 2months) similar to native valve
  60. Discuss the Duke Endocarditis Criteria:
    • Major criteria:
    • --Positive blood cultures
    • --Evidence of endocardial involvement (echo, new regurgitant murmur)

    • Minor Criteria:
    • -- Predisposing cardiac lesion
    • -- Fever
    • -- Vascular phenomena
    • -- Immunological phenomena
    • -- < 2 positive blood cultures
    • -- mild echo abnormalities

    Diagnosis is by 2 major criteria, or 1 major plus 3 minor criteria, or 5 minor criteria
  61. What are Janeway lesions?
    • They are flat, painless lesions on the palms and soles seen on endocarditis.
  62. What are Osler nodes?
    • Painful raised lesions on the hands and feet.
    • Seen in endocarditis
  63. What immunologic phenomena is seen in endocarditis?
    • Glomerulonephritis
    • Janeway lesions
    • Osler nodes
    • Roth spots
    • (+) Rheumatoid factor
  64. What are Roth spots?
    • Retinal hemorrhages with white centers seen in endocarditis
  65. What are the indications for surgery in endocarditis?
    • Heart failure
    • Annular involvement or abscesses
    • Fungal endocarditis
    • Antibiotic-resistant organism
    • Vegetation > 10 cm
  66. Who needs antibiotic prophylaxis for endocarditis?
    • 1. Prosthetic cardiac valve
    • 2. Previous infective endocarditis
    • 3. Congenital heart disease
    • -- Unrepaired cyanotic CHD
    • -- Completely repaired CHD with prothetic material or device
    • 4. Cardiac transplantation recipients who develop valvular disease
  67. What is the most important test in valvular disease?
    Echo
  68. What is the treatment for Aortic Stenosis?
    • Surgery is indicated in symptomatic patients with severe AS
    • Most patients who have gradients of > 50 mm Hg are symptomatic
    • Almost all sudden deaths occur in symptomatic patients
    • AVR is often followed by dramatic improvement in LV function and symptoms.
  69. What needs to be done prior to Aortic Valve surgery for AS?
    Heart catheterization due to the high prevalence of CAD in those with AS ( > 33% in those over 69 years old).
  70. What group of medications are contraindicated in patients with AS?
    Beta- blockers
  71. What are the common causes of Chronic Aortic Regurgitation?
    • Congenital deformities
    • Endocarditis
    • Aortic root dilation (Marfan's, HTN)
    • VSD
    • Giant cell arteritis, relapsing polychondritis
    • Syphilis
    • Trauma
  72. What is the usual course of Chronic Aortic Regurgitation?
    • Long asymptomatic latent period
    • Exercise is well tolerated ( as opposed to every other valvular disease ) because of:
    • -- peripheral vasodilation
    • -- increased heart rate shortens diastole
  73. What is the physical finding in Chronic AR?
    High-pitched, blowing, decrescendo murmur at the lower left sternal border best heard leaning forward at exhalation.
  74. What is the significance of a low-pitched, apical, mid-diastolic rumble?
    • Austin-Flint murmur found in Severe AR
    • Caused by the AR jet hitting the anterior MV leaflet and forcing it into the posterior leaflet, causing functional mitral stenosis
    • A systolic outflow murmur may occur, caused by the high velocity of blood through the aortic valve.
  75. What are the causes of Acute Aortic Regurgitation?
    • Caused by: "T-E-A"
    • -- Endocarditis
    • -- Trauma
    • -- Aortic dissection
  76. What are the physical examination findings in Acute Aortic Regurgitation?
    • Tachycardia, hypotension, pulmonary edema, signs of vasoconstriction
    • The murmur, if heard at all, is short, high-pitched, and decrescendo.
    • The bounding pulse pressure of chronic AR is not present.
  77. How do you diagnose Acute AR?
    Echo, especially TEE
  78. Treatment for acute AR?
    • Urgent Cardiothoracic surgical consult
    • Temporizing measures include positive inotropic therapy (dobutamine) and peripheral vasodilation (nitroprusside)
  79. What is the pathognomonic triad on CXR for mitral stenosis?
    • The CXR features of:
    • 1. Pulmonary vascular congestion
    • 2. Large left atrium
    • 3. Normal sized ventricle

  80. Mitral stenosis
    What sex is mostly affected?
    How do they often present?
    What are the common signs?
    • 2/3 are females
    • Often present with sudden onset of symptoms when atrial fibrillation occurs
    • Hemoptysis is fairly common in MS because of the very high pulmonary pressures
    • Peripheral emboli, particularly stroke, occurs in 20% of patients
  81. What are the physical exam findings in mitral stenosis?
    • opening snap heard at the apex
    • S1 may be loud
    • A low-pitched diastolic rumble is heard at the apex with the bell.
  82. How do you treat a pregnant patient with mitral stenosis?
    • May present with pulmonary edema at the onset of atrial fibrillation
    • Digoxin probably indicated in all patients
    • Warfarin is teratogenic
    • Cardioversion, procainamide, and verapamil are all safe during pregnancy
  83. Treatment in Severe Mitral Stenosis
    Tx in patients with Class II-IV symptoms?
    How about asymptomatic patients?
    • Patients with class II-IV symptoms should have percutaneous balloon valvuloplasty (PBV) or surgery ( only if PBV is not possible)
    • Asymptomatic patients should have PBV if PA pressure is > 50 mmHg.
  84. Do patients with mitral stenosis need angioplasty prior to surgery? (like in AS patients)
    No, because these are mostly young women and chances of CAD is low.
  85. In a patient with known mitral stenosis, what is the usual cause of sudden deterioration?
    Onset of atrial fibrillation
  86. Physical exam findings in Chronic Mitral Regurgitation
    • Soft S1
    • Holoystolic murmur
    • In severe MR, the aortic valve may close early, resulting in a widely split S2
    • An S3 is common in severe MR
  87. Indications for Surgery in severe MR:
    • Symptomatic
    • -- LVEF > 30% and LVESD < 55 mm

    • Asymptomatic patients
    • -- LVEF < 60% and LVESD > 40 mm
    • -- LVEF > 60% ad LVESD < 40 mm in the presence of pulmonary HTN as long as the valve can be repaired (not replaced).
  88. Physical exam findings in Mitral Valve Prolapse
    • There may be a mid-systolic ( not diastolic) click, which may be followed by a murmur
    • The click becomes louder and moves earlier in systole with maneuvers that decrease LV volume, such as Valsalva or standing.
  89. Discuss the Severe Form of MVP:
    • Congenital myxomatous degeneration of the chordae and mitral valve leaflets
    • Some degree of chronic MR virtually certain
    • Risk of acute MR from chordal rupture
  90. Causes of Acute Mitral Regurgitation:
    • T-E-A-R
    • Trauma
    • Endocarditis
    • Acute ischemia of the papillary muscle
    • Rupture of a myxomatous chord

    Patients present with shock similar to acute AR
  91. Physical exam findings in Acute Mitral Regurgitation:
    • Tachycardia, hypotension, pulmonary edema, signs of peripheral vasoconstriction
    • The murmur, if heard at all, is short, early systolic, and decrescendo
  92. Treatment of Acute Mitral Regurgitation:
    • Urgent cardiothoracic surgical consult
    • Temporizing measures include inotropic therapy (dobutamine) and peripheral vasodilation (nitroprusside)
  93. Physical exam findings in Tricuspid Regurgitation
    • Usually overshadowed by findings of MS
    • A diastolic rumble is heard along the LLSB, which increases with inspiration
    • All right-sided murmurs and sounds increase with inspiration, except the pulmonic ejection sound (heard in PS)
    • The neck veins show a large a wave and a slow y descent
    • There is systemic venous congestion
  94. Causes of Tricuspid Stenosis
    • Rheumatic heart disease
    • Congenital
    • Carcinoid causes TS/TR and any other right-sided valvular lesions
  95. Treatment of severe Tricuspid Stenosis
    Valvuloplasty
  96. Physical exam findings in Tricuspid Regurgitation
    • Large v waves in the neck
    • Pulsatile liver
    • Holosystolic murmur at the LLSB that increases with inspiration
    • Other signs of pulmonary HTN are frequently present
  97. Discuss Pulmonic Stenosis
    • Virtually always congenital
    • Does not progress
    • Usually not seen with other congenital defects except Noonan syndrome
    • May be seen in adults
  98. Physical exam findings in Pulmonic stenosis
    • There may be a faint systolic murmur heard at the upper left sternal border
    • Usually, there is a pulmonic ejection sound
    • Prominent a wave in the JVP
  99. Describe Ebstein's abnormality
    What would the echo show?
    What would the ECG show?
    What kind of murmur would you hear?
    What are its associations?
    • Echo shows a redundant tricuspid septal leaflet arising lower in the ventricle than normally
    • The RA, therefore, appears to be huge
    • A TR murmur and a "sail" sound may be heard
    • ECG shows signs of right atrial enlargement or tall and broad 'Himalayan' P waves, 1st degree block
    • Frequently associated with PSVT or the WPW syndrome
    • Associated with other cardiac abnormalities such as an ASD or PFO

  100. Systolic murmur increases post PVC
    AS, HOCM
  101. Systolic murmur increases during Valsalva
    HOCM
  102. Systolic murmur increases during handgrip
    MR
  103. Systolic murmur increases during standing
    HOCM
  104. Systolic murmur increases during squatting
    AS, MR
  105. Systolic murmur increases during Mueller
    AS, MR
  106. Describe the systolic murmur response of HOCM to maneuvers
    • Increase in Post-PVC, valsalva, and standing.
    • Decrease in Mueller, Handgrip, Squatting
  107. Describe the systolic murmur response of AS to maneuvers:
    • Increase in Post-PVC, mueller, squatting
    • Decreae in Valsalva, handgrip, standing
  108. Describe the systolic murmur response of MR to maneuvers:
    Increased in Mueller, handgrip, and squatting
  109. What is the Mueller maneuver?
    • After a forced expiration, an attempt at inspiration is made with closed mouth and nose, whereby the negative pressure in the chest and lungs is
    • made very subatmospheric; the reverse of Valsalva manoeuvre
  110. What valvular disease causes hemoptysis?
    Mitral stenosis -- because of the extraordinary valvular pressures
  111. Decreased rise time and volume in the carotid pulses?
    AS
  112. Low-pitched diastolic rumble at the apex
    • AR
    • This is the Austin-Flint murmur
  113. Late-peaking systolic ejection murmur in the second right intercostal space
    AS
  114. Slow y descent in the jugular pulse
    Tricuspid stenosis
  115. Paradoxically split S2
    AS
  116. What are the four findings of a critical AS?
    • 1. Decreased rise time and volume in the carotid pulse
    • 2. Systolic thrill or shudder in the suprasternal notch or on the carotids
    • 3. Late-peaking systolic ejection murmur in the 2nd right intercostal space
    • 4. Paradoxically split S2 or absence of A2 altogether
  117. Which of the following cardiac disease tolerates exercise well?
    AR
  118. What is the best predictor of prognosis in Heart Failure?
    • LVEF
    • Exercise tolerance does not predict outcome
  119. What are the markers of poor outcome in Heart Failure?
    • Poor LVEF
    • Low serum sodium
    • High BUN
    • Low Potassium
    • High or low magnesium
    • High catecholamine levels
  120. Discuss Peripartum Dilated Cardiomyopathy
    • Occurs from the beginning of the third trimester to 6-months postpartum
    • Predilection for older women and African-Americans
    • About 2/3 resolve spontaneously
    • Increased risk of recurrence with subsequent pregnancies
  121. Discuss Dilated Cardiomyopathy and Embolization
    • About 2% of patients form mural thrombi and can have arterial embolization
    • Pulmonary emboli can arise from the RV
    • Anticoagulation is indicated even if no mural thrombi can be detected
  122. Discuss Restrictive Cardiomyopathy
    • Caused by infiltrative diseases, such as amyloid and sarcoidosis
    • Presents with signs of left and right heart failure, initially from diastolic dysfunction, but later from systolic failure
  123. An echo appearance of "enlarge atria, normal ventricles" is suggestive of?
    Restrictive cardiomyopathy
  124. "Segmental wall motion abnormalities" on TTE suggests what?
    • Ischemic cardiomyopathy
    • -- the ventricles are infiltrated so can't dilate, but have huge ventricular pressures which dilate the upper chambers resulting in "Mickey Mouse" heart on echo.
  125. Discuss Hypertrophic Cardiomyopathy
    • Disordered myocytes in the region of the hypertrophy, especially in the upper ventricular septum
    • Other areas than the septum can be affected; Asians frequently have an apical form
    • Occasionally presents as concentric LVH
    • Symptoms include dyspnea, chest pain, or exercise-induced syncope
    • Echo is diagnostic
    • The severity of the LV outflow gradient is not related to the risk of sudden death
    • Associated with sudden cardiac death (VT/VF), especially in exercising young people
    • An ambulatory ECG that shows VT indicates a high risk for sudden death
    • Atrial fibrillation is common because of high LVEDP
  126. Physical findings in HCM:
    • Harsh nonradiating midsystolic aortic murmur
    • Murmur is louder with maneuvers which decrease LV volume. e.g. Valsalva
    • Carotid pulse has a rapid upstroke and is bifid in 2/3 of patients (as opposed to AS)
    • Apical pulse ay be double or triple
  127. Discuss ECG of HCM:
    • If patients have septal hypertrophy, there may be inferolateral Q waves because of the thick septum
    • The precordial lead voltage is usually high in the area of the hypertrophy
  128. Discuss therapy of HCM:
    • Beta-blockers, verapamil
    • Resynchronization therapy (biventricular pacing)
    • Septal myomectomy
    • Antiarrhythime therapy (amiodarone) for symptomatic VT or atrial fib
    • No drugs prolong survival
    • Decreasing ventricular volume (diuretics, nitrates, dehydration) is potentially dangerous
    • Implantable defibrillators have been shown to reduce the incidence of sudden death
    • No ultimate cure except for heart transplant
  129. In Hypetrophic Obstructive Cardiomyopathy, what prolongs survival?
    • AICD
    • Heart transplant
  130. Discuss Stage A classification in heart failure:
    • Patients at risk for heart failure but without structural heart disease, including:
    • HTN
    • Atherosclerotic disease
    • Diabetes
    • Metabolic syndrome
    • Using cardiotoxins
    • Family history of cardiomyopathy
  131. What is the drug therapy for Stage A heart failure?
    ACE inhibitors or ARBs
  132. Discuss Stage B heart failure:
    • Patients with structural heart disease but without symptoms or signs of heart failure:
    • Previous MI
    • LV remodeling including LVH and low LVEF
    • Asymptomatic valvular heart disease
  133. Therapy in Stage B heart failure:
    • ACE inhibitors or ARBs
    • Implantable defibrillators
  134. Discuss Stage C heart failure
    • Pts with structural heart disease with prior or current symptoms of heart failure.
    • Known structural heart disease and dyspnea fatigue, and decreased exercise tolerance
  135. Review the precipitating causes of CHF exacerbation:
    • Inappropriate reduction of therapy
    • Dietary indiscretion
    • Ischemia or infarction
    • Arrhythmias
    • Systemic infection
    • PE
    • Physical, environmental, or emotional stress
    • High output states (anemia)
    • Poorly controlled HTN
    • A new, unrelated illness
    • Administration of a cardiac depressant drug
    • Acquiring a second form of heart disease
    • Surgical procedure
  136. What are the medication known to prolong survival in HF?
    • ACE-I
    • ARB
    • Hydralazine/Nitrates
    • Beta-blockers
    • Spironolactone or eplerenone (for all patients with increased preload and create < 2.5
  137. When is resynchronization therapy indicated?
    • EF < 30%
    • Wide QRS > 120 msec
  138. What two medications are known to cause pericarditis?
    • Procainamide
    • Hydralazine
  139. Discuss acute pericarditis
    • Present with severe, usually pleuritic, chest pain, relieved by sitting forward
    • fever and tachycardia are common
    • If present, a friction rub is diagnostic
    • ECG usually shows diffuse ST elevation and PR segment depression, particularly in lead II
  140. When differentiating between acute pericarditis and acute MI, how do you differentiate between the two?
    An echo would show a segmental wall motion abnormality in acute MI
  141. What are causes of Constrictive Pericarditis?
    • 50% of cases in the US are idiopathic, presumably post viral
    • TB is the most common cause in developing countries
    • Other causes include cardiothoracic surgery, radiotherapy, and coccidiomycosis
    • -- > 4,000 rads increase the risk of pericarditis
  142. How do you diagnose Constrictive Pericarditis?
    (how to differentiate from restrictive pericarditis)
    • Inspiratory rise in the jugular venous pulse (Kussmaul sign)
    • Rapid x and y descents in the JVP
    • Pericardial knock in early diastole
    • Calcification of the pericardium on CXR (particularly if TB is the cause)
    • Thickened pericardium on CT or MR
  143. Discuss the diagnosis of Tamponade
    • Echo shows pericardial effusion, diastolic collapse of the RA and perhaps the RV
    • Physical exam shows pulsus paradoxes and JVD with a single rapid x descent
  144. Discuss Secundum ASD
    • 70% of ASDs
    • Second most common adult congenital heart disease (after bicuspid aortic valve)
    • Atrial fibrillation is common
    • Does not require antibiotic prophylaxis
  145. What are the physical exam findings of Secundum ASD?
    • Systolic ejection murmur at the left sternal border due to increased pulmonary flow
    • A diastolic murmur is possible due to increased tricuspid blood flow
    • Fixed splitting of the second heart sound.
    • ECG shows right axis deviation and/or RBBB
  146. Treatment of Secundum ASD
    When is surgery indicated?
    When is surgery contraindicated?
    • Surgery is indicated if there is more than a 2:1 left-to-right shunt, even in asymptomatic patients n (this is figured by echo).
    • If the pulmonary resistance is > 15 U/m2, surgery cannot be performed
  147. When is surgery contraindicated for Secundum ASD
    If the pulmonary resistance is > 15 U/m2, surgery cannot be performed
  148. Discuss Ostium Primum ASD
    Where is it located in the interatrial septum?
    What kind of murmur would you hear?
    What would the ECG show?
    What is the treatment?
    • A defect low in the interatrial septum which may affect the mitral and tricuspid valves
    • Systolic murmurs because of MR or TR
    • ECG shows left axis deviation and RBBB
    • Treatment is the same as for secundum ASD
  149. Discuss Sinus Venosus ASD
    Where is the defect located?
    What is it associated with?
    • Defect is high in the intertribal septum
    • Associated with anomalous pulmonary venous return
  150. Discuss Patent Ductus Arteriosus
    What sex is it most common?
    What is the usual presentation?
    Characteristic murmur?
    Intervention?
    • More common in females
    • May have differential cyanosis, with the hands affected but not the feet
    • Usually has a continuous murmur
    • Surgical or percutanous closure should be done in symptomatic patients of any age
  151. Discuss VSD
    Intervention and treatment?
    • Most common congenital defect in children
    • 80% os small defects close spontaneously
    • Large VSDs require surgical closure
  152. Discuss Coarctation of the Aorta
    What is it usually accompanied with?
    Typical physical exam finding?
    What syndromes are associated with it?
    • Accompanied by a bicuspid aortic valve 70% of the time
    • Other left-sided defects are common
    • Delay in the femoral pulses
    • Upper extremity HTN
    • Rib notching on CXR
    • Turner syndrome is associated with coarctation and a bicuspid aortic valve
  153. Discuss Eisenmenger Syndrome
    What is it?
    Treatment?
    What is the usual picture on CXR?
    • A large intracardiac shunt eventually causes pulmonary vascular resistance to exceed systemic resistance
    • The shunt becomes right-to-left and causes cyanosis
    • All of the intracardiac shunts can cause this except secundum ASD
    • Treatment is heart-lung transplant
    • CXR shows dilated pulmonary a. and prominent RA
  154. What intracardiac shunt cannot cause Eisenmenger syndrome?
    • Secundum ASD
  155. What are three causes of severe pulmonary HTN?
    • Primary pulmonary HTN
    • Multiple pulmonary emboli
    • Mitral stenosis
  156. If a pregnant patient presents with new-onset pulmonary edema, what can be the cause?
    They usually has mitral stenosis or a secundum ASD
  157. What causes BNP to become elevated?
    • Anything that stretches myocardium such as:
    • LV systolic and diastolic dysfunction
    • Acute PE
    • Cor pulmonale
  158. What is the most common finding on autopsy in asymptomatic young people who died during athletic activity?
    • No cause is the most common finding
    • Second most common is anomalous coronary artery
  159. What are the criterias for a RBBB?
    • Delayed intrensicoid deflection time n V1
    • rSR' in V1
    • wide S-wave in Lead I and V6
  160. Criteria for LBBB
    • QRS delay more than 120 sec in Leads I and V6
    • Monophasic R-wave in lead I and V6
    • rS or Q in Lead V1
  161. What is contraindicated in severe aortic regurgitation?
    An intra-aortic balloon pump is absolutely contraindicated in patients with severe aortic regurgitation because diastolic inflation of the balloon would exacerbate aortic regurgitation.
  162. In severe aortic valve stenosis, when do you intervene?
    • Patient is symptomatic
    • EF < 50%
    • Patient needs other cardiothoracic surgery
  163. When do you intervene in Severe Mitral Stenosis
    • If pt symptomatic or
    • Abnormal hemodynamic response to exercise (PAP increases by 25 mm Hg)
  164. What kind of intervention would you recommend in mitral stenosis, if needed?
    Percutaneous valvotomy if anatomy amenable and if less than moderate mitral regurgitation and no left atrial appendage clot by TEEa; otherwise, mitral valve replacement
  165. When do you intervene in Chronic Aortic Regurgitation?
    • Patient symptomatic, or
    • Ejection fraction <50%, or
    • End-systolic dimension >55 mm or end-diastolic dimension > 70 mm, or
    • Abnormal hemodynamic response to exercise (PAP increases by 25 mm Hg)
  166. Intervention is indicated in Chronic Mitral Regurgitation if:
    • Patient symptomatic, or
    • Ejection fraction <60%, or
    • End-systolic dimension >40 mm, or
    • (Consider if) pulmonary hypertension or atrial fibrillation
  167. Describe findings in Lyme carditis
    manifested by acute onset, high-grade av conduction defects that may occasionally be associated with myocarditis
  168. EKG changes showing left axis deviation and first-degree AV-block are typically seen in what heart defect?
    ostium primum ASD
  169. What are the indications for biventricular pacemaker-defibrillator placement?
    • NYHA class III or IV heart failure
    • an ejection fraction less than or equal to 35%
    • QRS width greater than 120 msec.
  170. How do you recognize complications that occur after repair of tetralogy of Fallot?
    What is the most common residua after repair?
    Describe the murmur of pulmonary valve regurgitation.
    Describe the murmur of tricuspid regurgitation
    • Tetralogy of Fallot repair involves placement of a transannular pulmonary outflow tract patch. This causes severe pulmonary valve regurgitation, which is confirmed by the presence of a diastolic murmur that increases with inspiration, a parasternal impulse (right ventricular enlargement), and elevated central venous pressure. The holosystolic murmur at the left lower sternal border that increases with inspiration is characteristic of tricuspid regurgitation. Long-standing pulmonary valve regurgitation causes right ventricular enlargement and tricuspid annular dilatation with resultant regurgitation. The tricuspid regurgitation causes right atrial enlargement and increases the risk of atrial arrhythmias.
    • Aortic valve regurgitation may occur in patients with repaired conotruncal abnormalities, such as tetralogy of Fallot. These patients may demonstrate progressive enlargement of the aorta and, eventually, aortic valve regurgitation may occur.
    • The murmur of aortic regurgitation does not vary with respiration and is best heard in the second left intercostal space and down the left sternal border and would not cause right ventricular enlargement with a parasternal impulse.
    • In a patient with aortic regurgitation, a wide pulse pressure would be expected.
    • Residual or recurrent ventricular septal defect also occurs in patients with prior tetralogy of Fallot repair. A ventricular septal defect causes a loud systolic murmur that obliterates the S2 and is often associated with a palpable thrill. A displaced apical left ventricular impulse and mitral diastolic flow rumble would suggest a hemodynamically important ventricular septal defect causing volume overload.
    • Right ventricular outflow tract obstruction occurs commonly after repair of tetralogy of Fallot. However, the primary features include right ventricular hypertrophy rather than right heart enlargement.
    • The murmur of pulmonary stenosis is an early systolic murmur that increases with inspiration and is heard best at the second left intercostal space. It is associated with a loud P2 heart sound that is sometimes palpable.
  171. When is exercise stress testing not recommended?
    When is it recommended?
    Exercise stress testing is not recommended for the estimation of cardiovascular risk in an asymptomatic patient. In patients with diabetes mellitus who are beginning an exercise program, exercise testing has been recommended.
  172. When is CABG recommended?
    • Significant left main coronary artery stenosis
    • Left main coronary artery equivalent disease: ≥70% stenosis of proximal LAD and proximal left circumflex artery
    • Three-vessel disease
    • Two-vessel disease with significant proximal LAD stenosis and either ejection fraction <50% or demonstrable ischemia on noninvasive testing
  173. When is CABG beneficial?
    • One- or two-vessel disease without significant proximal LAD stenosis but with a large area of viable myocardium and high-risk criteria on noninvasive testing
    • Developed disabling angina despite maximal noninvasive therapy, when surgery can be performed with acceptable risk (if angina is not typical, objective evidence of ischemia should be obtained)
  174. What are the physical findings consistent with severe aortic valve regurgitation?
    • wide pulse pressure
    • rapidly collapsing pulse
    • pulsating nailbeds
    • brief systolic and long diastolic murmur
    • features of left ventricular enlargement
  175. What are physical findings that in a pt with history of aortic coarctation that may point toward aortic aneurysm?
    • Patients with coarctation of the aorta are prone to aneurysm formation.
    • Hoarseness due to left vagus or left recurrent laryngeal nerve compression
    • Dysphagia due to esophageal compression
    • Recurrent pneumonia due to bronchial compression
    • Superior vena cava syndrome
  176. How do you manage anticoagulation during pregnancy in a patient with a mechanical prosthetic valve?
    Warfarin use throughout pregnancy until near term provides the lowest risk for maternal complications and death in women with mechanical heart valves.
  177. Cilostazol

    What is its use?
    What is it recommended for?
    What is its contraindication?
    Medical treatment with cilostazol, a phosphodiesterase inhibitor, is effective in increasing pain-free and overall walking distance and is recommended for patients with lifestyle-limiting claudication. However, cilostazol is contraindicated in patients with heart failure or left ventricular systolic dysfunction. Chronic use of oral phosphodiesterase inhibitors (not specifically cilostazol) for inotropic therapy in patients with heart failure has been associated with increased mortality.
  178. What is the effect of obesity on BNP levels?
    BNP levels are generally lower in obese pts, even those with acute heart failure.
  179. What is the Brugada syndrome?
    • The Brugada syndrome is characterized by a pseudo right bundle branch block pattern with ST-segment elevation on the electrocardiogram and ventricular arrhythmias.
    • It is genetic, with ventricular fibrillation as the cause of death
  180. What is the Short QT Syndrome?

    What is the usual clinical presentation?
    What is the appropriate intervention?
    • Another inherited arrhythmic disorder is the short QT syndrome, which carries a high risk of sudden cardiac death. The syndrome is characterized by an autosomal dominant pattern of inheritance, a short QT interval (<300 msec), atrial fibrillation occurring at a young age, and an increased risk of death due to ventricular fibrillation.
    • Other clinical presentations include polymorphic VT or VF, unexplained syncope
  181. How do you diagnose long QT syndrome?
    • It is suggested by recurrent syncope triggered by activity, a prolonged QT interval > 580 msec, and a family history of early sudden death.
    • Pts can be misdiagnosed with a seizure disorder.
    • Cardiac events in LQTS patients include syncope and cardiac arrest due to torsade de pointes.
    • Corrected QT intervals are considered abnormal if greater than 440 msec in men and 450 to 460 msec in women, but there is substantial overlap among normal patients and abnormal LQT gene carriers.

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