cardio exam 3

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  1. the abrupt and transient loss of consciousness associated with absence of postural tone, followed by complete and usually rapid spontaneous recovery is known as what
  2. which etiology of syncope is neutrally-mediated; this includes vasovagal
    reflex (~58%)
  3. which etiology of syncope will cause bradyarrhythmia or tachyarrhythmia, can be due to a structural heart dz leading to abrupt episodic drops in cardiac output by various mechanisms, poorly tolerated supraventricular and ventricular tachycardias and bradycardias
    cardiac disease
  4. what is common among the cardiovascular causes of syncope
    • transient cerebral hypoperfusion
    • alteration in systemic blood pressure which leads to rapid drop in BP
  5. what are the etiologies of syncope (PASS OUT)
    • Pressure
    • Arrhythmias
    • Seizures
    • Sugar
    • Output
    • Unusual
    • Transient
  6. what is the most common reflex mediated syncope
    vasovagal syncope
  7. this etiology of syncope is when pts usually have no apparent cardiac or neurological dz
    vasovagal (neurocardiogenic) syncope
  8. this type of syncope is when there is an episode after eating, coughing, emotional event, hunger, or pain
    situational vasovagal syncope
  9. a postural decrease in systolic BP of at least 20mmHg or greater or a postural increase in HR greater than 20bpm with standing is known as what
    orthostatic HoTN
  10. what are the causes of pressure caused syncope
    • decreased intravascular volume
    • primary autonomic insufficiency or failure (Parkinson Dz)
    • secondary autonomic insufficiency (DM, amyloidosis)
    • alcohol consumption
    • aging
    • drug effects
  11. this test is commonly performed to evaluate syncope, LIMITED specificity/sensitivity and reproducibility, can be used for pts with recurrent episodes of syncope in the absence of heart dz, unexplained single syncopal episode in high risk settings
    tilt test
  12. what are the etiologies of arrhythmias
    • brady-dysrhythmia
    • tachy-dysrhythmia
    • SVT
    • non-sustained Vtach
    • Afib
    • pacemaker malfunction
  13. who do you admit with arrhythmias
    • cardiac sxs
    • cardiac risk factors
    • abn ECG
    • no support network
    • seizure sxs
    • injury with syncope
  14. which diagnostic test is recommended for pts at risk or with CAD; abn ECG or those with syncope during or shortly after exertion
    exercise test (stress test)
  15. what is the diagnostic test that should be completed prior to a stress test (exercise test)
  16. which diagnostic test is indicated in selected pts with unexplained syncope, especially if they have structural heart dz
    EPS (electrophysiology study)
  17. what are some prodromes associated with seizures
    • auditory or visual phenomena
    • olfactory phenomena
    • nausea
  18. what are the gold standards for dx of a seizure
    • witnessed
    • sxs (aura)
    • + EEG
  19. a partial or complete LOC but without global cerebral hypoperfusion and is usually caused with low glucose is known as what
  20. what cardiac sxs are associated with output syncope
    • CP
    • tachypnea
    • dyspnea
  21. what are some cardiac causes of output syncope
    • valvular (MS, MS, PS)
    • HoCM
    • restrictive or dilated cardiomyopathy
    • atrial myxoma
    • cardiac tamponade
    • aortic dissection
    • MI
    • CHF
  22. what are the pulmonary causes of output syncope
    • PE
    • pulmonary HTN
    • carbon monoxide
    • COPD exacerbation
  23. what is the initial testing for the workup of output syncope
    • SaO2
    • ABG
    • CXR
    • ECG
  24. when would you get an echo with output syncope
    • structural heart disease
    • murmurs
    • exertional syncope
    • Hx of cardiac output impairment sxs (DOE)
  25. when would you get a lung scan with output syncope
    • dyspnea
    • pleuritic CP
    • Hx of DVT
  26. what are the causes of unusual syncope
    • anxiety
    • panic d/o
    • somatization d/o
    • major depressive d/o
    • hyperventilation syndrome
  27. what are the causes of transient syncope
    • strokes
    • TIA
    • subarachnoid hemorrhage
    • subdural hematoma
    • basilar artery migraine
    • subclavian steal
    • CNS mass effect (tumor, edema, AV malformation)
  28. how is transient syncope dx'd
    • neuroimaging (head trauma, focal neurological signs)
    • US carotid or vertebral (hx of neurovascular sxs)
  29. what is the most common cardiac cause of syncope
  30. what type of hx would suggest cardiac etiology
    • syncope following CP
    • syncope preceded by palpitations
    • exertional syncope
    • syncope without warning or aura
  31. for the evaluation of syncope, when would you order an echo
    • pre-cardiac stress testing
    • exertional syncope
    • r/o cardiac obstruction
  32. for the evaluation of syncope when would you order a stress test
    • pts at risk for/or hx of CAD
    • pts with syncope during or shortly after exertion
    • echo performed PRIOR to testing
  33. which criteria can we use to evaluate high risk syncope pts
  34. what is the ROSE criteria used to evaluate a high risk syncopal pt
    • B-B type natriuretic peptide >300
    • B- bradycardia of <50bpm
    • R- rectal exam with positive FOB test
    • A- anemia (Hb <9g/dL)
    • C- CP with syncope
    • E- EKG with Q waves
    • S- Sat <94% on room air
  35. if the pt is at a high risk for syncope, when should the be admitted
    • age >65
    • known structural heart dz or CAD
    • SOB
    • syncope in supine position or during exertional without prodrome
    • palpitations associated with syncope
    • Fmhx of sudden cardiac death
    • abn EKG
    • HCT <30%
  36. the inability of the heart to pump blood forward at a sufficient rate to meet the metabolic demands of the body (forward failure), or the ability to do so only if cardiac filling pressures are abnormally high (backward failure), or both is known as what
    heart failure
  37. about half of pts who have HF die within how many years
    5 years
  38. this is most commonly due to conditions that lead to impaired left ventricular function, particular CAD and HTN
  39. this is caused when the heart is unable to maintain adequate cardiac output to meet demands and/or able to do so only by elevating filling pressure
    forward heart failure
  40. this is caused when the heart is unable to accommodate venous return resulting in vascular congestion (systemic or pulmonary)
    backward HF
  41. severe pulmonary congestion secondary to backwards left heart failure is known as what
    pulmonary edema
  42. ineffective ventricular filling is known as what
    diastolic dysfunction
  43. ineffective ventricular emptying is known as what
    systolic dysfunction
  44. poor cardiac output is known as what
    low output
  45. increased metabolic demand is known as what
    high output
  46. if there is a pressure overload, what is the compensatory response
  47. if there is a volume overload, what is the compensatory response
    cardiac dilatation
  48. this type of HF (systolic/diastolic) is 2/3 of all HF cases, CAD is the underlying etiology, there is impaired myocardial contractile function which leads to decreased EF and SV, and blood backs up into the pulmonary system
    systolic dysfunction
  49. this type of HF (systolic/diastolic) is 1/3 of all HF cases, will have a normal EF, decrease compliance (transient by ischemia, permanently by severe hypertrophy, restrictive cardiomyopathy, MI), and has increased LV filling pressures that produce venous congestion upstream
    diastolic dysfunction
  50. what are the causes of L HF
    • CAD
    • HTN
    • idiopathic
    • valvular (AS, AR, MR)
    • alcohol (toxic cardiomyopathy)
  51. what are the pure forms of right sided HF
    • RV has increased compliance in order to handle wide differences in volume return to the heart
    • RV ejects into the low-pressure pulmonary vascular bed and may be susceptible to acute failure with sudden increases in pulmonary pressures
  52. what are the causes of right HF
    • pulmonary parenchymal dz
    • COPD
    • interstitial lung dz
    • ARDS
    • chronic pulmonary infx
    • pulmonary vascular dz
    • thromboembolic dz
    • pulmonary HTN
  53. this is associated with conditions that prevent the heart from meeting the body's cardiac output needs
    low output failure
  54. this is associated with conditions that initially cause increased cardiac output, is caused by demand for increased cardiac output, often exacerbates existing HF or decompensates a pt with other cardiac pathology
    high output failure
  55. what are the neuro-hormonal alterations that are compensatory mechanisms for HF
    • adrenergic nervous system (baroreceptors, alpha-receptors)
    • RAAS
    • antidiuretic hormone (Produced in posterior pituitary gland)
    • Natriuretic peptides
    • endothelin
  56. which neuro-hormonal alteration is a positive compensatory effect, and are produced in response to atrial and ventricular stress
    natriuretic peptides
  57. which remodeling compensatory mechanism is due to chronic volume overload  ⇨ chronic chamber dilation  ⇨ synthesis of new sarcomeres in series with old ⇨ myocytes elongate ⇨ proportional increased ventricular chamber radius and wall thickness
    eccentric hypertrophy
  58. which remodeling compensatory mechanism is due to chronic pressure overload ⇨ chronic chamber hypertrophy ⇨ synthesis of sarcomeres in parallel with old ⇨ myocytes thicken ⇨ wall thickness increases without proportional chamber dilation ⇨ significant decreased wall stress
    concentric hypertrophy
  59. what are the precipitating factors of HF
    • increased metabolic demands
    • increased volume
    • increased afterload
    • impaired contractility
    • non-compliance
  60. what are some precipitants of HF (HEARTFAILED)
    • Hypertension
    • Endocarditis/environment (heat)
    • Anemia
    • Rheumatic heart dz (other valvular dz)
    • Thyrotoxicosis
    • Failure to take medications (non-compliance)
    • Arrhythmias
    • Infection/ischemia/infarction
    • Lung problems (PE, pneumonia, COPD)
    • Endocrine (pheo, hyperaldosteronism)
    • Dietary indiscretion
  61. what are some s/s of L sided HF
    • dyspnea
    • orthopnea
    • paroxysmal nocturnal dyspnea
    • nocturnal cough and wheezing
    • fatigue, exercise intolerance
    • chest discomfort
  62. what are some s/s of R sided HF
    • lower extremity edema
    • RUQ discomfort
    • abd discomfort, nausea
  63. what are the L sided physical findings
    • diaphoresis
    • tachycardia
    • tachypnea
    • pulmonary rales
    • loud P2
    • S3 gallop
  64. what are the R sided physical findings
    • JVD
    • hepatomegaly
    • peripheral edema
    • ascites
  65. what are the labs studies ordered during the work up of HF
    • CBC
    • metabolic panel
    • LFT, renal function
    • TSH
    • iron studies
    • cardiac enzymes
    • BNP
    • UA
  66. this lab is extremely sensitive for atrial and ventricular stress with great variability in serially measured values even in one pt
  67. what are the average values for CHF pts by NYHA
    • Class I: 244 +/- 286 pg/mL
    • Class II: 389 +/- 374 pg/mL
    • Class III: 640 +/- 447 pg/mL
    • Class IV: 817 +/- 435 pg/mL
  68. what is the TOC for diagnosing HF
  69. this diagnostic study may be useful in circumstances requiring precise EF
  70. what is the simplest and most widely used method to gauge symptom severity of HF
  71. this is a classification system that is a well-established predictor of mortality and can be used at diagnosis and to monitor treatment response of HF
  72. this NYHA classification is when ordinary physical activity does not cause symptoms of HF
    class I
  73. this NYHA classification is when the pt is comfortable at rest, ordinary physical activity results in symptoms
    Class II
  74. this NYHA classification is when there is marked limitation of ordinary activity, less than ordinary physical activity that results in symptoms
    class III
  75. this NYHA classification is when the pt has the inability to carry out any physical activity without symptoms, symptoms present at rest
    class IV
  76. In systolic HF, what is a powerful predictor of mortality
    reduced LVEF
  77. if Framingham criteria are not met or BNP level is normal, _________ is essentially ruled out
    systolic HF
  78. if angina is present with HF what is a recommended diagnostic study
    coronary angiography
  79. what type of HF is when the EF ≥ 50%, there is elevated LA pressure, decreased LV compliance, and impaired LV relaxation
    diastolic HF
  80. what type of HF is when the EF is < 50%
    systolic HF
  81. which co-morbidities may be present when there is HF with a preserved EF
    • HTN
    • ischemic heart disease
    • DM
    • thyroid dysfxn
    • COPD
    • obstructive sleep apnea
  82. which class of medications are offered first for pts with HF caused by left ventricular systolic dysfunction
    • loop diuretics
    • - furosemide 20-40mg daily
  83. what is the treatment of HF caused by left ventricular systolic dysfunction
    • loop diuretics
    • ACE-I (or ARB)
    • BB
    • Aldosterone antagonists (if pt is with NYHA class II-IV and LVEF ≤ 35%)
    • Digoxin
    • ICD (when appropriate)
  84. what needs to be monitored if you Rx aldosterone antagonists to pts with HF
    renal function and plasma potassium concentration
  85. If you have an African American with HF and you have Rx'ed a loop diuretic, ACE-I (or ARB), BB, and an aldosterone antagonist and they still have persistent sxs, what medication is added
    hydralazine plus oral nitrate therapy
  86. what are some s/s of pulmonary edema
    • cough, dyspnea, fatigue which is rapidly worsening
    • may/may not have chest discomfort
  87. what is the acute treatment of a pulmonary edema
    • OMI
    • Lasix (IV 40mg start)
    • Nitroglycerine (initial dose 5-10 mcg IV)- for pts withouth HTN
    • positive pressure airway
    • position- sitting upright with legs hanging down CI in pts that are HoTHN
  88. what vasodilators are used if the pt is not hypotensive, is combined with diuretics, and need close hemodynamic monitoring for HF pts
    • nitropusside
    • nitroglycerine
  89. which inotropes are used in hypotensive pts with systolic dysfunction who remain in pulmonary edema despite all previous treatments for HF
    • dobutamine
    • phosphodiesterade inhibitors (milrinone)
    • dopamine (recommended for hypotensive STEMI pts with clinical evidence of shock)
  90. when would you consider pulmonary artery catheterization in HF pts
    • to monitor PCWP
    • unstable pt
    • PCWP >18 indicates cardiac etiology
  91. what are the life saving last resort measures in HF pts
    • intra aortic balloon pump
    • ventricular assist device
  92. which co-morbidities are at a high risk for HF but are without structural heart disease or sxs of HF (stage A)
    • HTN
    • atherosclerotic disease
    • DM
    • obesity
    • metabolic syndrome
    • pts using cardiotoxins
    • Fmhx of co-morbidities
  93. if a pt has had a previous MI, LV remodeling including LVH and low EF, or asymptomatic valvular disease, which stage of at risk heart failure are they
    stage B- structural heart disease but without signs or symptoms of HF
  94. if a pt has known structural heart and SOB and fatigue (including exercise intolerance), what stage of HF are they
    stage C- structural heart disease with prior or current symptoms of HF
  95. for pts who have marked symptoms at rest despite maximal medical therapy, what stage of HF are they
    stage D- refractory HF requiring specialized interventions
  96. if a pt is NYHA class I and stage A HF risk, what meds are they given
    • ACE-I
    • BB for selected pts
  97. if a pt is  NYHA II to IIIa and a stage B risk for HF, what meds are they given
    • ACE-I
    • BB
    • aldosterone antagonist (after MI)
    • hydrazaline (selected pts)
    • diuretics (PRN congestion)
  98. if a pt is NYHA IIIb to most IV and stage C HF, what meds are they given
    • ACE-I
    • BB
    • aldosterone antagonist
    • hydrazaline (select pts)
    • diuretic
  99. if a pt is NYHA IV and stage D HF, what meds are they given
    • ACE-I
    • BB
    • aldosterone antagonist
    • hydrazaline (selected pts)
    • diuretics
  100. what are the factors that most clinicians place increased emphasis on in pts with diastolic dysfunction
    • preventing and/or controlling volume overload
    • preventing and/or controlling factors that negatively impact atrial contraction and heart rate
  101. what are the goals in diastolic HF management
    • reduce congestive state
    • maintain atrial contraction prevent tachycardia or control ventricular rate
    • treat and prevent myocardial ischemia
    • control HTN
    • promote regression of hypertrophy and prevent myocardial fibrosis
  102. how is edema controlled in pts with diastolic heart failure
    • low salt diet (<2g Na+/day)
    • diuretics (furosemide of HCTZ)
    • ACE-I (enalapril or lisinopril)
    • angiotensin II receptor blocker (candesartan, valsartan, or losartan)
    • aldosterone antagonist (spironolactone)
  103. how is rate controlled with diastolic heart failure
    • CCB (diltiazem or verapamil)
    • BB (atenolol, metoprolol)
    • radiofrequency modifications of atrioventricular node and pacing
  104. how do you maintain and restore atrial contraction in pts with diastolic HF
    • medical management:
    • - nitrates (isosorbide dinitrate or mononitrate)
    • - BB (atenolol, metoprolol)
    • - CCB (diltiazem or verapamil)
    • percutaneous coronary intervention
    • coronary artery bypass surgery
  105. how do you control atrial HTN in pts with diastolic HF
    • diuretics (chlorthalidone or HCTZ)
    • BB (atenolol, metoprolol)
    • CCB (amlodipine or felodipine)
    • ACE-I (enalapril or lisinopril)
    • ARB (candesartan, valsartan, or losartan)
  106. if the pt has classic sxs of HF with a normal LVEF, what are the recommended solutions
    consider diastolic HF, valvular heart dz, HTN heart dz, and ischemia)
  107. if the pt has HoTN: when is the systolic pressure to low and what is the recommended solution
    asymptomatic pts with dilated cardiomyopathy often tolerate a SBP of 90mHg. if no lightheadedness or undue fatigue, peripheral perfusion is adequate, and BUN and Cr are unchanged, continue the same doses of medications

    symptomatic pts, decrease the dose of diuretic. if sxs persist, adjustment of the timing of concomitant medications may be helpful. Decreasing the dose of the ACE-I, BB, ARB or vasodilator is indicated
  108. if the pt is hyperkalemic, what are the recommended solutions
    ensure that the pt is taking no exogenous potassium supplement or potassium-containing salt substitute. Avoid hypovolemia. Consider decreasing the dose of a potassium-sparing diuretic. Concomitant use of an ACEI or ARB and spironolactone may increase the risk of hyperkalemia. Avoid high doses of ACEI and ARBS in pts receiving spironolactone. Avoid use of spironolactone in pts with renal failure, and use low doses of ACEI and ARBS
  109. if the pt has increasing azotemia while taking ACE-I, what is the recommended solution
    decrease the dose of diuretic. Consider renal-artery stenosis if azotemia persists
  110. if the pt has a cough while taking an ACEI what is the recommended solution
    R/O worsening CHF and change to ARB if severe cough persists
  111. should the dose of the ACEI be increased or should the BB therapy be initiated in a symptomatic pt
    start BB therapy if there are no CI
  112. should an ARB be added to an ACEI therapy or should a BB be added in a symptomatic pt
    start BB therapy if there are no CI
  113. the pt has worsening sxs of CHF after starting BB therapy, what are the recommended solutions
    increase the dose of diuretic and slow the titration of the BB
  114. the pt has worsening bronchospasms after starting BB therapy, what are the recommended solutions
    decrease the dose of the BB. Consider a beta-selective agent. Discontinue treatment with the drug if the problem persists
  115. if a pt has persistent paroxysmal nocturnal dyspnea or orthopnea or daytime fatigue despite absence or fluid retention on PE, what are the recommended solutions
    evaluate the pt for central or obstructive sleep apnea
  116. if the pt requires repeated hospitalization for HF, what are the recommended solutions
    a multidisciplinary approach should be initiated, with a visiting nurse in the home. Referral for HF is indicated
  117. what are the conservative measures for symptomatic pts with HF
    • oxygen if hypoxic
    • bed rest
    • elevation of head of bed
  118. what are the lifestyle measures in for HF pts
    • diet
    • exercise
    • DM control
    • smoking cessation
    • alcohol control
    • sodium and fluid restrictions
    • pneumococcal vaccine and annual influenza vaccine
  119. which medications control systolic and diastolic HTN for pts with HF
    • individualized to the pt with comorbid dz, DM, or COPD
    • Diuretic, BB, CCB, ACEI or ARB
  120. what medications control ventricular rate for pts with HF
    • CCB (diltiazem or verapamil* improves LV diastolic function, increases LV diastolic filling rate)
    • BB (atenolol or metoprolol) increases LV filling and coronary flow, reduces myocardial oxygen supply and demand, lower BP
  121. what medications control pulmonary congestion/peripheral edema in pts with HF
    • diuretic (furosemide or HCTZ)
    • ACEI
    • ARB
    • aldosterone antagonist
  122. what medications are used for antiischemic therapy
    BB and CCBs are preferred
  123. what is recommended in the presence of atherosclerotic cardiovascular dz and what meds are used
    intense lipid lowering

  124. what meds are CI or used with caution for pts with HF
    • NSAIDS
    • class I and III antiarrhythmic agents
    • metformin
    • thiazolidinediones (TZD's, rosiglitazone)
    • cGMP phosphdiesterase inhibitors (silendafil, vardenafil, tadalafil) with borderline low BP
  125. when is resynchronization therapy is recommended when
    • QRS >120ms
    • LVEF < 35%
    • severe symptoms despite optimal therapy
  126. what type of pt heart problems have the greatest benefit of resynchronization therapy
    • marked LV enlargement
    • mitral regurgitation
    • QRS >120ms
    • high diuretic requirement
  127. systolic dysfunction of the heart leads to which cardiomyopathy
    dilated cardiomyopathy
  128. diastolic dysfunction of the heart leads to what cardiomyopathies
    • HCM
    • restrictive cardiomyopathy
  129. what is the hallmark of dilated cardiomyopathy
    • dilation and impaired systolic (contraction)  function of one or both ventricles
    • - dilation out of proportion to hypertrophy
    • - marked enlargement of all chambers
  130. what are the common recognized causes of dilated cardiomyopathy
    • viral myocarditis (parvo B19, HHV6, coxsackie)
    • alcohol toxicity
    • specific gene mutation
  131. what are the reversible causes of dilated cardiomyopathy
    • alcoholic cardiomyopathy
    • toxin exposure
    • metabolic (hypothyroid)
    • sarcoidosis
  132. what are the most common symptoms of low forward output in dilated cardiomyopathy
    • fatigue
    • DOE
    • feeling lightheaded
  133. what is the workup of dilated cardiomyopathy
    • echo
    • CXR
    • ECG
    • labs
    • cardiac cath
  134. what can an Echo show if a pt has dilated cardiomyopathy
    • four chamber enlargement
    • global hypokinesis
    • depressed LVEF ≤ 40%
    • MR/TR
    • mural thrombi
  135. what will an CXR show if a pt has dilated cardiomyopathy
    • global cardiomegaly
    • CHF
  136. what will an ECG show if a pt has dilated cardiomyopathy
    • variable ST-T wave abnormalities
    • LAD
    • conduction defects (1st degree heart block, LBBB, RBBB)
    • arrhythmias (re-entrant SVT, AFib, Vtach)
  137. this diagnostic study determines co-existent CAD, previous MI, elevated left/right diastolic pressures, measures CO, degree of LV dysfunction in pts with dilated cardiomyopathy
    cardiac cath
  138. what is obtained when the etiology needs clarification for dilated cardiomyopathy
    endomyocardial biopsy
  139. how is dilated cardiomyopathy treated
    • tx with conventional HF meds
    • treat Afib if present
    • L sided HF tx includes: exercise, decreased weight/ETOH intake, tobacco cessation
    • if after 1 week of no clinical improvement, consider bx
  140. unexplained ventricular hypertrophy (not due to systemic HTN or AS) is known as what
    hypertrophic cardiomyopathy
  141. what is the most common pattern of hypertrophy in HCM
    septal hypertrophty
  142. this can heart dz can cause sudden death in athletes
  143. what is the wall thickness measurement is HCM
    >15mm (normal is 11mm)
  144. what type of pulse is associated with HCM
    bifid carotid pulse
  145. this murmur is a harsh systolic crescendo-decrescendo murmur heard at the LLSB, it is increased with valsalva and squat to stand, decreased with squatting or sitting, handgrip, passive elevation of legs
  146. why does the valsalva maneuver increase HCM
    it increases intrathoracic pressure, decreases venous return, reduces LV size. The septum and MV anterior leaflet are brought closer together, increasing the murmur
  147. why does squatting decrease HCM
    it increases preload, increases LV size, decreases LV outflow tract obstruction which decreases the murmur
  148. what is the work-up for HCM
    • ECG
    • 24 hr or event monitor
    • CXR
    • echo (TTE is TOC)
    • cardiovascular magnetic resonance (CMR)
    • treadmill exercise testing
    • cardiac cath
  149. what will an ECG show if a pt has HCM
    • LVH
    • high voltage across precordium
    • prominent q waves in leads looking away from septum (I, aVL, V4-V6)
  150. which diagnostic study should be done if a pt complains of palpitations or lightheadedness, it can identify ventricular arrhythmias, risk for sudden cardiac death or if the pt is a candidate for ICD
    24 hr or event monitor
  151. what is the diagnostic test of choice for the workup of hypertrophic cardiomyopathy
  152. this diagnostic study is used in the assessment of LVOT gradient, determines functional capacity, and determines response to therapy
    treadmill exercise testing
  153. if the diagnosis of hypertrophic cardiomyopathy is uncertain or if the pt is being considered for invasive therapy, which diagnostic study is considered
    cardiac catheterization
  154. what is the treatment of HCM
    • avoidance of:
    • volume depletion
    • overexertion
    • vasodilators, diuretics, digoxin
  155. which negative inotropic drugs used in the treatment of HCM slow the heart rate and prolong diastole, allowing increased ventricular filling
    Beta blockers and verapamil
  156. which device is usually placed in pts with at least one major risk factor for sudden cardiac death or multiple (3 or more) minor risk factors
  157. what are the major risk factors of HCM
    • cardiac arrest (VFib)
    • spontaneous sustained Vtach
    • family history of sudden death
  158. what are the minor risk factors for HCM
    • unexplained syncope
    • left ventricular wall thickness >30mm
    • abnormal BP on exercise
    • nonsustained vtach
    • left ventricular outflow obstruction
    • microvascular obstruction
    • high-risk genetic defect
  159. this type of cardiomyopathy is when there is restricted ventricular filling in a non-dilated, non-hypertrophied ventricle secondary to myocardial abnormality (stiffening, fibrosis, decreased compliance)
    restrictive cardiomyopathy
  160. what are the infiltrative etiologies of restrictive cardiomyopathy
    • amyloidosis (most common)
    • sarcoidosis
  161. what are the non-infiltrative etiologies of restrictive cardiomyopathy
    • scleroderma
    • idiopathic myocardial fibrosis
  162. what are the storage diseases of restrictive cardiomyopathy
    • hemochromatosis
    • fabry's disease
    • glycogen storage disease
  163. what are the endomyocardial etiologies of restrictive cardiomyopathy
    • endomycardial fibrosis
    • loefflers endocarditis
    • eosinophilic endomyocardial disease
    • radiation
    • carcinoid syndrome
  164. what are the helpful historical clues to suggest a diagnosis of constrictive vs restrictive cardiomyopathy
    • constrictive:
    • prior history of acute pericarditis
    • history of active TB
    • prior cardiac surgery
    • prior mediastinal radiation therapy
  165. what are the s/s of restrictive cardiomyopathy
    • CHF usually with preserved LV systolic function
    • arrhythmias (dilated atria)
    • elevated JVP with prominent x and y descents
    • +/- kussmauls sign
    • S3 is common
    • S4 early in disease, disappears with Afib or true atrial systolic failure (advanced amyloidosis)
  166. what is the workup of restrictive cardiomyopathy
    • EKG
    • CXR
    • Echo
    • cardiac cath
    • endomyocardial biopsy
    • CT scan
    • MRI
  167. what will an ECG show on a pt with restrictive cardiomyopathy
    • low voltage
    • non-specific, diffuse ST-T wave changes
    • +/- non-ischemic q waves
    • heart blocks, A-fib
  168. what will an echo show on a pt with restrictive cardiomyopathy
    • biatrial enlargement
    • normal or decreased ventricular volume
    • normal wall thickness
    • normal systolic function
    • impaired ventricle filling
    • "starry night" or "speckled" pattern seen (due to infiltrative d/o)
  169. what is the essential test in the etiology of restrictive cardiomyopathy (esp with infiltrative disease)
    endomyocardial biopsy
  170. what is the test of choice for differentiating restrictive cardiomyopathy from constrictive pericarditis
    ct scan
  171. what drugs are used to manage the diastolic dysfunction of restrictive cardiomyopathy
  172. what drugs are used to treat the rhythm disturbances of restrictive cardiomyopathy
    • flecainide
    • amiodarone
    • propafenone
    • digoxin (with great caution)

    *also treated with a pacemaker
  173. what is used to treat/prevent thromboembolic events of restrictive cardiomyopathy
    anticoagulation therapy
  174. what is the normal measurement of mean pulmonary arterial pressure
    8 to 20 mmHg at rest
  175. what measurement of mean pulmonary artery pressure at rest has uncertain clinical implications
    21 to 24 mmHg
  176. what is the mean pulmonary arterial pressure at rest for pulmonary HTN
    >25 mmHg
  177. what is the mean arterial pulmonary arterial pressure with exercise for pulmonary HTN
    > 30 mmHg
  178. what is the systolic pulmonary artery pressure in pulmonary HTN
    >40 at rest
  179. what is pulmonary HTN characterized by
    • elevated pulmonary arterial pressure
    • secondary right ventricular failure (ie. cor pulmonale)
  180. what is the definition of Cor pulmonale
    • altered structures (eg hypertrophy or dilatation)
    • impaired function of the right ventricle
  181. what diseases can cause cor pulmonale
    • lung: COPD
    • vasculature (ie idiopathic pulmonary arterial HTN)
    • upper airway (ie obstructive sleep apnea)
    • chest wall (kyphoscoliosis)
    • acute: massive PE
    • chronic: pulmonary HTN
  182. when is right sided heart disease not considered cor pulmonale
    when the right-sided heart disease is due to left-sided heart disease or congenital heart disease
  183. any factor that significantly increases either pulmonary blood flow or resistance will likely lead to pulmonary hypertension is known as what law
    Ohms law
  184. what are some sxs of pulmonary HTN
    • dyspnea at rest and/or exertion (95% of pt)
    • fatigue
    • CP
    • exertional syncope
    • cough or hemoptysis
    • anorexia, RUQ fullness or pn if hepatic vascular congestion is present
    • hoarseness (ortners syndrome)
    • peripheral edema
  185. what will a PE show in a pt with pulmonary HTN
    • tachypnea
    • elevated JVP
    • loud and sometimes palpable pulmonic component of P2
    • hepatomegaly, ascites
    • pulsatile liver
    • peripheral edema
  186. what are the different diagnostic tests used for pulmonary HTN
    • echo (preferred initial test)
    • CXR
    • EKG
    • CT
    • PFT
    • VQ scan
    • right heart cath
  187. if there is a high clinical suspicion for pulmonary HTN and the echo does not suggest this diagnosis, what diagnostic study should be done
    right heart cath
  188. what will a CXR show on a pt with pulmonary HTN
    enlargement of pulmonary arteries ("pruning")
  189. what will an ECG show on a pt with pulmonary HTN
    • RVH:
    • - peaked p-wave in lead II (p-pulmonale)
    • - RAD
    • - RV strain pattern (usually inverted T wave in V1-V3 and the inferior leads)
    • - large R wave in V1
    • RBBB
  190. Image Upload 1
    what does this EGC show?
    A) restrictive cardiomyopathy
    B) LBBB
    C) HCM
    D) pulmonary HTN
    D) pulmonary HTN
    (this multiple choice question has been scrambled)
  191. this diagnostic study may detect previously unrecognized pulmonary parenchymal diseases as well as thrombotic/embolic vascular disease
    spiral CT scan
  192. this diagnostic study shows that the measurement of the main PA trunk diameters may correlate to the presence of PH, especially in COPD pts
    spiral CT scan
  193. this diagnostic test has a highly sensitive and specific means of assessing the presence of chronic thrombotic/embolic vascular disease
    lung scintography ventilation/perfusion (V/Q) scan
  194. what is the gold standard for diagnosing sleep breathing disorders like OSA
    sleep study
  195. which diagnostic study is used in the predictability of survival in idiopathic PH
    exercise testing
  196. this diagnostic study is necessary for a definitive diagnosis and accurately determines the severity and guides treatment
    right-heart catheterization
  197. what is the coag of choice in the treatment of PH
    warfarin (therapeutic goal INR of 2.0)
  198. which class of the WHO functional classification for PH is when the pts with PH but without resulting limitations of physical activity. Ordinary physical activity does not cause undue fatigue or dyspnea, CP, or heart syncope
    class I
  199. which class of the WHO functional classification for PH is when the pts with PH results in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in undue fatigue or dyspnea, CP, or heart syncope
    class II
  200. which class of the WHO functional classification for PH is the pts with pulmonary HTN results in marked limitation of physical activity. They are comfortable at rest/ Less than ordinary physical activity causes undue fatigue or dyspnea, CP, or heart syncope
    class III
  201. which class of WHO functional classification for PH is when the pts with pulmonary HTN results in inability to carry on any physical activity without sxs. These pts manifest signs of right heart failure. Dyspnea and/or fatigue may be present even at rest. Discomfort is increased by physical activity
    class IV
  202. what are the indication for referral to a pulmonary HTN center
    • unexplained dyspnea or CP on exertion with evidence of PH by transthoracic echo
    • evidence of moderate to severe pulmonary arterial HTN
    • clinical or echo evidence of RV dysfunction
    • parenchymal lung disease
    • known pulmonary arterial HTN with worsening disease despite therapy
  203. what are the 3 basic mechanisms leading to peripheral vascular disease
    • structural changes (degenerative conditions, infection, inflammation)
    • luminal narrowing (atherosclerosis, thrombosis, inflammation)
    • smooth muscle spasm
  204. this is a life threatening tear in the aortic intima allowing blood to dissect between the aortic intima and media
    aortic dissection
  205. what is the normal width of the aorta
    • 3cm at the origin/base of the heart root
    • descending aorta 2-2.5cm in healthy adults
  206. what is the anatomy of the media vessel
  207. what is the anatomy of the adventitia layer of vessels
    • collagen fibers
    • accessory tissues: nerve fibers and tiny blood vessels within the vasa vasorum
  208. what are the 3 factors that determines aortic pressure
    • volume of blood that enters it during systole
    • compliance of the vessel wall
    • resistance (cumulative resistance or more distal vessels, mild effect from the column of blood in the vascular system)
  209. what are the chronological effects of aortic disease
    • increased pulsatile pressure
    • shear stress
    • degeneration of CT characteristics with aging
  210. this is an increased diameter but less than 50% increase from normal (aortic aneurysm or ectasia?)
  211. this is an increased diameter that is at least a 50% increase from normal (aortic aneurysm or ectasia?)
  212. what are the true aortic aneurysms
    • fusiform
    • saccular
  213. what are the aortic pseudoaneurysms (false aneurysm)
    • contained rupture
    • pseudoaneurysm formation in the femoral artey is a known complication of cardiac cath
  214. what mostly affects the segment of the aorta between the renal and inferior mesenteric arteries
  215. what is the most common location for an aortic aneurysms
    abdominal (AAA)
  216. what are the different locations of aortic aneurysms
    • abdominal (AAA)- most common
    • thoracic (TAA)- ascending (~60% ascending, ~40% descending)
    • thoracoabdominal
  217. what are the high risk groups for thoracic aortic aneurysms
    • 65 and older
    • male>>female
    • HTN ++ risk factor
  218. what are the high risk groups for abdominal aortic aneurysms
    • advancing age... 65 and older
    • male gender*, caucasian
    • smokers*
    • atherosclerosis and its risk factors (HTN*, dyslipidemia)
    • family hx of AAA
    • presence of other peripheral aneurysms
  219. what is the predominant process of ascending TAA
    cystic medial necrosis (aging, HTN, inherited DO: marfans, ehler-danlos)
  220. what is the predominant process of descending TAA and AAA
    atherosclerosis (smoking, HTN, hyperlipidemia, DM, male gender, advanced age, inherited D/O)
  221. what are the common presentation of aortic aneurysms
    • majority are asymptomatic
    • pain (chest, abd, flank, back)
    • syncope
    • HoTN
    • palpable mass above umbilicus (in two directions)
    • airway or esophageal obstruction
  222. what are the clinical findings associated with aortic aneurysms
    • hoarseness (left recurrent laryngeal nerve)
    • hemoptysis
    • hematemesis
    • distal pulse may be intact
  223. what are the associated diseases with aortic aneurysms
    • HTN
    • PVD
    • CAD
    • COPD
    • renal insufficiency
  224. what will a CXR show on a pt with a TAA (thoracic abdominal aneurysm)
    • widened mediastinum (usually ~8cm at a minimum)
    • enlargement of the aortic knob
    • loss of the AP window
  225. if the entire aorta needs to be examined and it is an emergent situation, which diagnostic study should be considered
  226. what is the procedure of choice for the diagnosis of aortic aneurysms in most centers
    CT with contrast/ MRA
  227. what are the clinical findings of an abdominal aneurysm
    • majority are asymptomatic
    • pain (atypical abd, back, leg, groin, or flank)
    • palpable mass above the umbilicus
    • anorexia, nausea, vomiting
  228. what is the size of most pulsatile abd masses in most adults when it is generally considered aneurysms
  229. what diagnostic study is up too 100% sensitive for AAA
    abd U/S
  230. what is the imaging TOC for non-ruptured AAA
    abd U/S
  231. what is the imaging TOC for the diagnosis of ruptured AAA
    CT scan
  232. what is the USPSTF screening guidelines for an AAA
    • recommendation for one-time screening for AAA with US in males aged 65-75 with any smoking hx
    • no recommendation for or against screening for AAA with US in males who have never smoked
    • recommendation against screening females of any age for AAA with US
  233. what is the surgical threshold for a TAA (ascending)
  234. what is the surgical threshold for pts with a TAA (descending)
  235. what is the surgical threshold for pts with a AAA
    ~5.5 cm
  236. what are the CI to surgical repairs
    • life expectancy <1 year
    • terminal dz
    • recent MI
    • UA
  237. what are the risk factors for aortic dissection
    • HTN
    • atherosclerosis
    • pre-existing aortic aneurysm
    • inflammatory d/os
    • bicuspid aortic valve
    • aortic coarctation
    • crack cocaine
  238. which Stanford classification type is a proximal aortic dissection, is about 2/3 of pts, and the ascending aorta is involved
    type A
  239. which Stanford classification type is a distal aortic dissection, is about 1/3 of pts, and typically is the descending aorta only
    type B
  240. what are the clinical findings of an aortic dissection
    • sudden onset of CP radiating to the back
    • - tearing or ripping... type A- anterior chest...type B- between the scapula, back and abd
    • - asymmetric BP or pulse between arms (>20mmHg)
    • - ischemic sxs (occlusion of coronary arteries, aortic branches, carotids, or splanchnic arteries)
  241. which present sxs if associated with an aortic dissection is associated with a worst outcome
  242. what will the PE show on a pt with an aortic dissection
    • HTN
    • UE BP differential
    • neurological abnormalities (syncope, AMS)
    • new diastolic murmur if associated AR present
    • physical signs of pericardial tamponade in some type A dissections
  243. what is the TOC for an aortic dissection
  244. what are the 3 sxs that can help you clinically dx an aortic dissection
    • pain- described as abrupt onset of thoracic/abd pn with sharp, tearing, or ripping sensation
    • mediastinal widening on CXR
    • a variation in pulse or BP (>20 mmHg between L and R arm)
  245. what is the acute tx of an aortic dissection
    • pain control (morphine)
    • BP control
    • hemodynamically unstable or airway compromise intubate
    • obtain a bedside TEE in an unstable pt to comfirm the dx
    • stable pt CT or MRI/MRA to confirm dx
    • ADMIT
  246. a type A aortic dissection requires what type of treatment
    emergent sx
  247. type B aortic dissection requires what type of tx
    can be managed medically
  248. which beta blockers are used in the treatment of an aortic dissection
    • esmolol IV (fastest onset, short half life, easy to titrate)
    • propranolol IV or labetalol
    • IV vasodilators (nitroprusside)
  249. this is a spectrum of disorders typically characterized by abnormal venous dilatation ranging from varicose veins to venous stasis and ulcerations, it is occasionally associated with a discrete etiology, and most cases are related to the progressive degenerative changes in venous structure and function with aging
    peripheral venous disease
  250. this is the most important sequelae of DVTs
    • pulmonary embolism (50%) of untreated cases
    • chronic venous insufficiency
  251. what is virchows triad
    • endothelial/vascular damage
    • venous stasis
    • hypercoagulability
  252. what are the inherited etiologies of hypercoagulability in a DVT
    • activated protein C resistance (Factor V leiden)
    • prothrombin gene mutation
    • protein C&S deficiency
    • antithrombin III deficiency
    • antiphospholipid antibody syndrome
  253. if there is a proximal vein thrombosis, what arteries are/can be involved
    • popliteal
    • femoral
    • iliac
  254. which type of DVT is more commonly associated with the development of a PE
    proximal vein thrombosis
  255. if a pt presents with unilateral leg edema, erythema, warmth and tenderness, what is your suspected dx
  256. what are the most useful test for DVTS
    • US (Doppler)
    • D-dimer tests
  257. what score is commonly used for the dx of a DVT
    wells score
  258. which diagnostic study provides a definitive diagnosis for a DVT
    venography (invasive)
  259. what is the initial therapy for a DVT
    • LWMH
    • unfractionated heparin
    • fondaparinux (arixtra) factor Xa inhibitor
    • coumadin
  260. when are fibrinolytics used for a pt with a DVT
    • limb/life threatening thrombosis
    • very recent sxs
    • low bleeding risk
  261. what are the different methods for primary prophylaxis for a DVT
    • intermittent pneumatic compression
    • graduated compression stockings
    • unfractionated heparin
    • LMWH
    • fondaparinux
    • warfarin
  262. this is a benign disorder of erythema, induration, and tenderness along a superficial vein, usually is spontaneous, but can follow venous cannulation
    superficial thrombophlebitis
  263. what are the risk factors for superficial thrombophlebitis
    • venous stasis
    • abnormal coagulation/fibrinolysis
    • endothelial dysfunction
    • infection
    • IV therapy
    • IV drug use
  264. this is a recurrent migratory superficial thrombophlebitis, associated with adneocarcinomas
    trousseau syndrome
  265. which vein is most common for getting superficial thrombophlebitis
    greater saphenous
  266. what are some conservative treatments for superficial thrombophlebitis
    • bed rest and elevation of limb PRN for pain/swelling (otherwise ambulation is encouraged)
    • moist heat
    • compression
    • analgesia
    • anti-inflammatory
    • anti-coag
  267. when is a surgical excision indicated in a pt with superficial thrombophlebitis
    • failure of conservative tx
    • symptoms > 2 weeks or recurrent sxs
    • suppurative thrombophlebitis
  268. distention of tortuous superficial veins resulting from incompetent valves in the deep, superficial, or perforator systems is known as what
    varicose veins
  269. where is the most common development of varicose veins
    greater saphenous vein
  270. what is the most common form of venous disorders of the lower extremity
    varicose veins
  271. this is known as a chronic elevation of deep venous pressure and blood pooling in lower extremities
    chronic venous insufficiency
  272. what is the most common vascular disorder
    chronic lower extremity venous disease
  273. the clinical features of this disorder is when the pt complains of tired or heavy legs, it gets worse with standing or seated with feet dependent for long period of time that IMPROVES with limb elevation and walking
    chronic venous insufficiency
  274. what is the test of choice for chronic venous insufficiency
    duplex (Doppler and B-mode) US
  275. what are the systemic agents used to treat chronic venous insufficiency
    • ASA therapy appears to accelerate the healing of chronic venous ulcers
    • Anbx only when s/s of acute cellulitis or clinically infected ulcer
  276. obstruction of lymphatic drainage resulting in edema with high protein content is known as what
  277. what is the most common cause world wide of lymphedema
  278. what is the most common cause of lymphedema within the US
    radiation/surgery (axillary or groin lymph node removal)
  279. formation of atherosclerotic plaques in large and medium sized arteries that results in chronic occlusive arterial disease is known as what
    peripheral arterial disease
  280. if there is a delay in treatment of acute peripheral arterial disease of greater than 6 hours, what can this result in
  281. chronic impairment of under-perfused structures in PAD, can lead to what
    • muscular atrophy
    • ischemic non-healing ulcerations
    • gangrene
  282. what are the traditional risk factors for PAD
    • smoking (highest risk)
    • DM (highest risk)
    • age
    • hyperlipidemia
    • HTN
    • Fmhx
  283. what are the 6 "P"s in acute PAD
    • Pain
    • Pallor- within a few hours progresses to mottled cyanosis
    • Paresthesia
    • Paralysis/power loss- heralds impending gangrene
    • Poikilothermia- cool extremity
    • Pulselessness- least reliable
  284. what are the sxs of chronic PAD
    • claudication
    • - pain with exertion (calves most common)
    • - relieved by rest (2-5 minutes without postural changes)
    • - reproducible (same distance, same location, same recovery)
    • fatigue
    • paresthesias
    • extremity weakness
    • erectile dysfunction (Leriche syndrome)
    • recurrent extremity infection/ulcerations (esp cellulitis)
    • rest pain
  285. what is the most common complaint of chronic PAD
    calf claudication
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