cardio exam 2

Card Set Information

Author:
crazysupermedic
ID:
246030
Filename:
cardio exam 2
Updated:
2013-11-24 21:59:09
Tags:
cardio exam
Folders:

Description:
cardio exam
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user crazysupermedic on FreezingBlue Flashcards. What would you like to do?


  1. which systolic murmur is heard at the RUSB
    aortic stenosis
  2. which systolic murmurs are heard at the LUSB
    • pulmonic stenosis
    • PDA
  3. which systolic murmur is heard at ERBs point
    HoCM
  4. which systolic murmurs are heard at LLSB
    • tricuspid regurg
    • VSD
  5. which systolic murmurs are heard at the apex
    • mitral regurg
    • mitral valve prolapse
  6. which diastolic murmurs are heard at LUSB
    • Pulmonary insufficiency (PI)
    • spilt S2
  7. which diastolic murmur is heard of Erbs point
    aortic insufficiency (AI)
  8. which diastolic murmur is heard at LLSB
    tricuspid stenosis
  9. which diastolic murmur is heard at the apex
    mitral stenosis
  10. what is a delayed, non-suppurative sequelae of a pharyngeal infection with group A streptococcus
    acute rheumatic fever
  11. what is the most common age group for acute rheumatic fever
    5-15 years old
  12. what is the latent period before initial s/s appear for acute rheumatic fever
    2-3 weeks
  13. what are some specific symptoms that pts will complain about with rheumatic fever
    • arthritis that affects numerous joints but emerges one joint at a time
    • abnormal heart beat
    • CP
    • red patches on skin
    • small painless lumps beneath skin
    • rapid, involuntary movements in muscles of extremities or face
  14. what are the major criteria of Jones criteria
    • J= joints (migratory polyarthritis)
    • O= carditis (heart involvement)
    • N= nodules (subcutaneous)
    • E= erythema marginatum
    • S= Sydenham's chorea
  15. this is a neurologic disorder, that has abrupt/rapid, involuntary, nonrhythmic movements, emotional disturbances and muscle weakness, and it ceases during sleep
    sydenhams chorea
  16. what are the minor Jones criteria in rheumatic fever
    • other arthralgias (without arthritis)
    • fever: 101-104 degrees f
    • elevated acute phase reactants (ESR and CRP)
    • prolonged PRI on ECG
  17. what are the diagnostic tests for diagnosis group A strep pharyngitis infx
    • positive throat culture
    • positive rapid streptococcal antigen test
    • elevated (especially rising) streptococcal antibody testing:
    • - ASO (antistreplysin O)
    • - Anti-DNase B
    • - ASTZ (antistreptozyme)
  18. what are the 3 circumstances that be used to make a presumptive dx for ARF
    • chorea is the only manifestation
    • indolent carditis may be the sole manifestation in pt who fail to seek early medical tx
    • recurrent RF individuals with a hx of ARF should be presumed to have recurrence with any manifestations
  19. how long should antibiotic therapy with PCN be started and maintained for in ARF
    at least 10 days regardless of presence or absence of pharyngitis at time of dx
  20. what meds can be used in a pt who is allergic to PCN but has ARF
    • azithromycin
    • clarithromycin
    • clindamycin
  21. when does rheumatic heart disease occur after the original illness
    10-20 years after
  22. what is the major cause of valvular heart dz world wide
    ARF
  23. what is the most commonly affected valve in ARF
    mitral valve (mitral stenosis)
  24. what is the most common cardiac valve lesion in the US
    aortic stenosis
  25. what are the etiologies behind aortic stenosis
    • congenital (bicuspid, unicuspid)
    • degenerative (calcific/"wear and tear")
    • Rheumatic heart dz
  26. what are the cardinal sxs of advanced AS and average survival after onset
    • angina (5 years)
    • exertional syncope (3 years)
    • CHF (2 years)
    • AFIB precipitates overt HF and can increase mortality rates
  27. why is there angina with aortic stenosis
    because there is an imbalance between myocardial supply and demand. the increased LVDP reduces coronary perfusion pressure gradient between the aorta and myocardium
  28. why is there syncope with aortic stenosis
    LV cannot increase cardiac output during exercise which leads to decreased cerebral perfusion pressure then syncope
  29. why is there CHF with aortic stenosis
    LV develops contractile dysfunction due to increased afterload which leads to increased LV diastolic volume/pressure.

    The increased LA pressure backs up into the pulmonary vasculature, then there is increased alveolar congestions and that leads to CHF
  30. what type of pulse will a pt with aortic stenosis have
    pulses parvus et tardus
  31. what are the clinical features of aortic stenosis
    • pulsus parvus et tardus (weak and late)
    • displace PMI
    • narrow pulse pressure
    • AFib
  32. this type of murmur is harsh, has a crescendo-decrescendo "diamond shape", it is a systolic murmur. It is best heard at the RUSB with either the bell or diaphragm and radiates to the carotids
    aortic stenosis
  33. what will the EKG show is aortic stenosis
    LVH
  34. what will a CXR show with aortic stenosis
    • LVH
    • CHF in advanced dz
  35. what will an echo show with aortic stenosis
    • increased LV wall thickness
    • determine the severity of dz
    • increased valve pressure gradient (Doppler)
    • reduced valve area
  36. what is recommend for the initial diagnosis and assessment for aortic stenosis severity
    Echo (class 1)
  37. which diagnostic test is used in the assessment of LV wall thickness, size and function
    echo (class 1)
  38. if you have a pregnant pt with AS, which diagnostic testing do you want to use
    echo (class 1)
  39. what is recommended for re-evaluation of asymptomatic pts with aortic stenosis
    transthoracic echo (TTE)
  40. how often is severe AS re-evalutated with a TTE
    every year
  41. how often is moderate AS re-evaluated with a TTE
    every 1-2 years
  42. how often is mild AS re-evaluated with a TTE
    every 3-5 years
  43. what is the only effective therapy for adults with severe AS
    aortic valve replacement
  44. what type of treatment may be considered in young pts with congenital AS
    balloon aortic valvuloplasty
  45. what are the etiologies of aortic insufficiency (regurg)
    • abnormalities of the valve leaflets (congenital; bicuspid valve, rheumatic; RA or rheumatic fever, infective endocarditis)
    • dilation of the aortic root
    • aortic aneurysm
    • inflammation/CT dz (marfan syndrome, ehlers-danlos, IBD)
    • trauma- aortic dissection
    • syphilis
    • annuloaortic ectasia
  46. this is typically associated with rapid decompensation due to the inability to accommodate to increase end diastolic pressure (acute or chronic AR)
    acute AR
  47. this may be compensated for by ventricular dilation which leads to hypertrophy eventually leading to CHF (acute or chronic AR)
    chronic AR
  48. high LV stroke volume + reduced diastolic pressure = ??
    widened pulse pressure
  49. what is the hallmark sign of AR
    widened pulse pressure
  50. what are the s/s of acute AR
    acute pulmonary edema
  51. what are the s/s of chronic AR
    • prolonged asymptomatic period
    • widened pulse pressure (bounding pulse, "water hammer" pulse)
    • CHF sxs
    • angina
    • atypical CP ("uncomfortable awareness of a forceful heart beat)
  52. if you are examining a pt with AR and you notice they have head bobbing with systole, what is that sign called
    De Musset's sign
  53. if you are examining a pt with AR and you notice they have a water hammer pulse, what is the name of that oulse
    Corrigans pulse
  54. what is the name of the pulse is the pt has capillary pulsations in the nail beds
    Quincke's pulse
  55. what is the name of the sign if a pt has pistol shot sounds over the radial or femoral artery
    Traube's sign
  56. what is the name of the sign is the pt has a to and fro femoral murmur
    Duroziez's sign
  57. this type of murmur has a high-pitched, blowing diastolic murmur, is heard best with the diaphragm in the 3rd left intercostal space (Erbs point) with the pt sitting up, leaning forward and exhaling
    aortic regurg
  58. this murmur is a low-pitched rumbling mid-diastolic sound attributed to normal diastolic blood flow from the left atrium hitting the anterior leaflet of the mitral valve
    Austin-flint murmur
  59. what can an ECG show if a pt has aortic regurg
    • LVH
    • strain pattern (chronic ischemia)
    • LBBB
    • LAE
    • LAD
    • Atrial fibrillation
  60. what is used to confirm the presence and severity of acute or chronic AR
    echo
  61. this diagnostic testing is used for the dz and assessment of the cause of chronic AR
    echo
  62. this diagnostic testing is indicated in pts with an enlarged aortic root to assess regurg and the severity of aortic dilation
    echo
  63. this diagnostic testing is used for the re-evaluation of mild, moderate, or severe AR in pts with new or changing sxs
    echo
  64. this diagnostic testing is indicated for the initial and serial assessment of LV volume and function at rest in pts with AR and suboptimal echos
    radionuclide angiography or MRI
  65. this diagnostic testing is used when the noninvasive tests are inconclusive or to provide discrepant results from clinical findings with pts that have AR
    cardiac cath
  66. this diagnostic testing is used for chronic AR, it is reasonable for assessment of functional capacity and symptomatic response in pts with a hx of equivocal sxs
    exercise stress
  67. this diagnostic testing is used to assess sxs/functional capacity prior to athletic activity in a pt with AR
    exercise stress
  68. which medications benefit asymptomatic pts with severe AR with preserved LV function or pts with sxs or reduced LV function who are not surgical candidates
    • ACE-I
    • dihydropyridine CCB
    • hydralazine)
  69. what is the most common etiology of mitral stenosis
    rheumatic fever/heart dz
  70. what can worsen mitral stenosis
    • A-fib
    • tachycardia
    • pregnancy (increased preload)
  71. this type of pulmonary HTN is an increase in pressure due to backward transmission of elevated left atrial pressure
    passive pulmonary HTN
  72. this type of pulmonary HTN is due to pulm arterial/arteriolar vasoconstriction, hypertrophy of pulmonary artery
    reactive pulmonary HTN
  73. this murmur is low pitched, rumbling, decrescendo, diastolic murmur, it is associated with an opening snap, is best heard at the apex in the left lateral decubitus position with the bell
    mitral stenosis
  74. this type of murmur is seen on an EKG that has LAE (p-mitral) and/or RVH/RAD
    mitral stenosis
  75. which diagnostic testing is used for the diagnosis of MS
    echocardiogram
  76. this diagnostic test is used for the re-evaluation of pts with known MS and changing symptoms or signs
    echocardiogram
  77. this diagnostic study for MS should be performed to assess the presence or absence of left atrial thrombus and to further evaluate the severity of MS in pts considered for percutaneous mitral balloon valvotomy
    TEE
  78. how often is severe MS evaluated
    every year with echo
  79. how often is moderate MS evaluated
    every 2 years with an echo
  80. how often is mild MS evaluated
    every 3-5 years with an echo
  81. when is pharmacologic therapy appropriate for mitral stenosis
    • stabilization prior to intervention
    • to treat decompensation due to intercurrent illness
    • for persistent symptoms after intervention
  82. which medications may improve symptoms of mitral stenosis
    diuretics and beta blocks
  83. what are the etiologies of mitral regurg
    • mitral valve prolapse (most common cause)
    • congenital cleft leaflets
    • left ventricular dilation (CHF, DCM, myocarditis)
    • infective endocarditis
    • Marfans
    • acute MI
    • myxoma
    • MV annulus calcification
    • chordae/papillary muscle/ischemia/rupture
    • rheumatic fever
  84. which leaflet is most often affected in mitral regurg
    posterior leaflet
  85. the severity of MR is based on what 5 things
    • 1) size of the opening during regurg
    • 2) the systolic pressure gradient between the LA and LV
    • 3) systemic vascular resistance opposing the LV forward outflow
    • 4) LA compliance
    • 5) duration of regurg
  86. what are the clinical features/signs and symptoms of mitral regurg
    • dyspnea
    • paroxysmal nocturnal dyspnea (PND)
    • orthopnea
    • palpitations
    • peripheral edema
    • arrhythmia (A fib)
  87. acute mitral regurg will show what type of clinical signs in a pt
    pulmonary edema
  88. chronic mitral regurg will show what type of clinical signs in a pt
    low cardiac output
  89. what will your PE show in a pt with mitral regurg
    • apical thrill (if severe MR)
    • soft S1
    • loud P2 and RV heave
  90. this murmur is loud, high pitched, holosystolic at the apex that radiates to the axilla, will have a loud S2 and best heard at the apex/LLSB in the left lateral decubitus position with the diaphragm
    mitral regurg
  91. mitral regurg intensifies with what activity
    should intensify with hand grip
  92. what will an ECG show if a pt has mitral regurg
    • Afib
    • LAE
    • LVH
  93. what is used for baseline evaluation of LV size and function, RV and left atrial size, pulmonary artery pressure, and severity of MR in any pt suspected of have MR
    TTE
  94. which diagnostic testing is used for annual or semiannual surveillance of LV function in asymptomatic pts with moderate to severe MR
    TTE
  95. which diagnostic testing is used to evaluate the MV apparatus and LV function after a change in signs or symptoms
    TTE
  96. this diagnostic test is reasonable in asymptomatic pts with severe MR to assess exercise tolerance and the effects of exercise on pulmonary artery pressure and MR severity
    exercise Doppler echo
  97. this is the most common cause of isolated MR requiring surgical repair
    mitral valve prolapse
  98. what are the etiologies of mitral valve prolapse
    • congenital (associated with Ebsteins anomaly, ASD)
    • Marfan, Ehlers-Danlos syndrome
    • Rheumatic Heart Dz
    • sequel of cardiomyopathy or MI
  99. what is the hallmark macroscopic valvular lesion of MVP
    excessive mitral leaflet tissue leading to folding and hooding
  100. what are the signs and symptoms of mitral valve prolapse
    asymptomatic

    *key to clinical manifestations are ausculatory findings
  101. what are the S/S of MVP syndrome
    • stabbing chest pain
    • dyspnea
    • palpitations
    • fatigue
    • dizziness
    • anxiety of panic disorder
  102. what accentuates/alters mitral valve prolapse
    bedside maneuvers that increase/decrease volume of LV
  103. this diagnostic imaging is indicated for the diagnosis of MVP
    echo
  104. this diagnostic imaging can be effective for risk stratification in asymptomatic pts with physical signs of MVP or known MVP
    echo
  105. what are the etiologies of pulmonic stenosis
    • rare
    • congenital (most common)
    • carcinoid syndrome (rare):
    •      - tumor with mets to the liver releases serotonin metabolites into the bloodstream forming endocardial plaques on the right side of the heart
  106. what are the signs and symptoms of pulmonic stenosis
    • asymptomatic
    • exertional dyspnea
    • symptoms of right HF
    • exercise induced fatigue, syncope or CP
  107. what will a PE show if a pt has pulmonic stenosis
    • S2 split
    • prominent right ventricular systolic impulse with a left para-sternal lift
  108. this murmur is a crescendo-decrescendo, systolic murmur, it is heard best with either the bell or the diaphragm at the LUSB, is often accompanied by an early systolic ejection click
    pulmonic stenosis
  109. what is the management for pulmonic stenosis
    • balloon valvuloplasty via catheterization
    • treat the underlying RHF
  110. what are the etiologies of pulmonic stenosis
    • pulmonary HTN (most common)
    • infective endocarditis
    • rheumatic disease
    • tetralogy of fallot
  111. what are the signs and symptoms of pulmonary insufficiency
    • asymptomatic
    • exertional dyspnea
    • exertional chest pain
    • exertional syncope
    • fatigue
    • peripheral edema
    • anorexia/adb pain
  112. this murmur is an early diastolic ejection murmur with an ejection click heard at the pulmonic area
    pulmonic regurg
  113. this murmur is a high-pitched, decrescendo, diastolic murmur heard along the left sternal border
    graham steel murmur
  114. what are the etiologies of tricuspid stenosis
    • rare
    • rheumatic disease (most common)
    • congenital
    • carcinoid syndrome
    • right atrial or metastatic tumors
  115. what are the signs and symptoms of tricuspid stenosis
    • peripheral edema
    • abd distention/hepatomegaly
    • fatigue
    • palpitations
    • JVP with giant "a" waves
    • +/- kussmauls sign
  116. this is a low-pitched, rumbling diastolic murmur that is best heard with the bell at the LLSB
    tricuspid stenosis
  117. what accentuates and diminishes tricuspid stenosis
    inspiration, diminished with valsalva and expiration
  118. what will an EKG show with tricuspid stenosis
    RAE

    * the absence of RVH in the presence of sxs of right-sided failure should suggest the diagnosis
  119. what is the management of tricuspid stenosis
    • preload reduction (diuretics)
    • sx is usually reserved for pts undergoing other valve or CT sx
    • valvulotomy/commissurotomy or valve replacement is indicated with diastolic pressure gradients >5mmHg or orifice <1.5-2 cm2
  120. what are the etiologies are tricuspid regurg
    • largely functional vs primary valve disease
    • - dilated right atrium and right ventricle
    • - pressure or volume overload
    • rheumatic dz
    • - rheumatic MS leads to TR due to pulmonary HTN with right ventricular enlargement
    • infective endocarditis (IV drug use)
    • congenital
    • - ebstein anomaly is most common form
    • carcinoid (rare)
    • connective tissue d/o (marfan)
  121. what are the signs and symptoms of tricuspid regurg
    • peripheral edema
    • fatigue
    • palpitations
    • Afib is usually present
  122. what are the PE associated with TR
    • RV heave
    • ascites and peripheral edema
    • ** severe TR pt may appear cachetic or chronically ill***
  123. this murmur is a blowing holosystolic murmur, is best heard with the diaphragm along the LLSB
    TR
  124. what intensifies and diminishes TR
    • intensifies with inspiration
    • diminished by valsalva or standing
  125. what is the most common congenital disorder in newborns
    congenital heart disease
  126. this syndrome is the development of pulmonary vascular disease due to chronic large left-to-right heart shunt
    eisenmenger syndrome
  127. what are the acyanotic lesions in congenital heart disease
    • atrial septal defect (PFO- not a true ASD)
    • VSD
    • PDA
    • Coarctation of the aorta
    • aortic stenosis
    • pulmonic stenosis
  128. what are the classifications of ASD
    • ostium secundum (75%)
    • ostium primum (15%)
    • sinus venosus (10%)
  129. this is not a true ASD, it is significant in the context of increased right-to-left shunts which can lead to a paradoxical embolism
    patent foramen ovale (PFO)
  130. what are the 3 factors that shunt volume is dependent on
    • size of defect (determined severity)
    • pressure gradient between atria
    • peripheral outflow resistance
  131. if an infant has a large ASD, how may they present
    • HF
    • recurrent respiratory infections
    • failure to thrive
  132. what are the clinical features of ASD
    • fatigue
    • dyspnea on exertion or decreased stamina
    • palpitations
    • fixed spilt S2
    • murmur
    • increased frequency of atrial arrhythmias, especially atrial flutter and fibrillation (most frequent presenting symptom)
  133. what are the causes of a RV heave in ASD
    • hyperdynamic right ventricular impulse, most pronounced along the LSB
    • precordial bulge due to atrial enlargement (large left-to-right shunt)
  134. this is a soft, mid-systolic ejection murmur heard at the ULSB OR it can be a mid-diastolic murmur that may be also present at the LLSB due to increased flow across the tricuspid valve
    ASD
  135. a fixed S2 split is associated with what type of congenital heart disease
    ASD
  136. what will an ASD show on an EKG
    • RAD (exception is it will be LAD with ostium primum type due to LAFB)
    • RVH
    • incomplete RBBB or complete RBBB
  137. what is the treatment for an ASD
    if volume of shunted blood is large or when the ration of pulmonary to systemic flow is 1.5 or greater, treatment is via surgical repair even is asymptomatic
  138. how is surgical closure of an ASD completed
    • cardiopulmonary bypass
    • percutaneous transcatheter device closure
  139. this is the most common congenital heart defect in infants and children
    VSD
  140. what are the classifications of VSD
    • membranous (70%)
    • muscular (20%)
    • other (10%) near the aortic valve or mitral-tricuspid junction
  141. how will a pt with a large VSD present
    • secondary pulmonary HTN
    • CHF by 2 years of age
  142. how do adults present with VSD
    • arrhythmias or sxs of right HF
    • pulmonary HTN
    • dyspnea on exertion
    • peripheral edema
    • fatigue
  143. this is a harsh holosystolic/early systolic murmur best heard at the LLSB, mid-diastolic "rumble" heard at the apex (increased flow across the mitral valve) and is associated with a systolic thrill over the area of defect
    VSD
  144. how will infants with a VSD present within the first months of life
    • FTT, delayed growth, poor feeding
    • develop early symptoms of CHF
    • tachycardia, tachypnea, hyperdynamic precordium, displaced PMI
  145. which diagnostic study is used to see the location of the VSD and the shunts magnitude
    echocardiogram with doppler
  146. what will an ECG show in a pt with a VSD
    • LAE
    • LVH
    • RVH (if pulmonary vascular dz)
  147. how are large VSD's treated
    • dietary interventions to facilitate weight gain
    • diuretics are first line pharmacologic therapy (Furosemide is well tolerated)
    • ACE inhibitors
    • can add digoxin
  148. what are the indications for surgical repair in the first few months of life
    • CHF or pulmonary vascular dz
    • pulmonary artery pressure >50mmHg
    • LAE or LVH
    • deteriorating left ventricular function
  149. a PDA is common in which pt population
    • premature births (most common)
    • exposure to maternal rubella infx 1st trimester
  150. what is the most common cause of CHF in premature newborns
    PDA
  151. a PDA that is associated with this syndrome will show as lower extremity cyanosis (feet), and upper extremities remain acyanotic
    Eisenmenger's syndrome
  152. how do large PDAs manifest
    • fatigue
    • dyspnea
    • poor feeding
    • recurrent lower respiratory tract infxs
    • accessory muscle use
    • apneic spells or symptomatic bradycardia
  153. what is the most common finding with a PDA
    the murmur
  154. this murmur is a continuous machine-like murmur best head at the left infra-clavicular area
    PDA
  155. what does the exam show with PDA
    • tachycardia
    • bounding pulses
    • wide pulse pressure
    • hyperactive precordium (lifts, heaves)
    • lower extremity cyanosis
    • increased risk of endocarditis
  156. what will the EKG show on a pt with a PDA
    • LAE
    • LVH
  157. which diagnostic study is used to show the PDA location and flow and gives the estimation of right-sided systolic pressures
    echocardiogram with doppler
  158. what is the treatment of PDA in preterm infants
    initial intervention is indomethacin or ibuprofen
  159. how is a PDA treated in an older infant
    • percutaneous device closure is recommended
    • surgical ligation is an alternative
  160. how long are antibiotics indicated for after percutaneous PDA closure (to prevent endocarditis)
    6 months
  161. what are the cyanotic lesions associated with congenital heart diseases
    • tetralogy of fallot
    • transposition of the great arteries
    • ebsteins anomaly
  162. what are the 4 primary abnormalities that develop in response to a single abnormal development of the outflow tract of the intra-ventricular septum
    • VSD (caused by malalignment of the intraventricular septum)
    • RV outflow obstruction (in effect pulmonic stenosis)
    • RVH (due to high pressure load from PS)
    • overriding aorta (receives blood from both ventricles)
  163. this is the most common cyanotic heart defect diagnosed after infancy or age 1
    tetralogy of fallot
  164. what are the clinical features of tetralogy of fallot
    • dyspnea on exertion
    • - "tet spells" or "tet fits"
    • - poor feeding, cyanosis during feeding
    • - fussiness, tachypnea, cyanosis, agitation
    • - hyperventilation, syncope
    • - learn to squat after exercise or when symptomatic
    • growth retardation
    • development, puberty may be delayed
  165. what are the consequences of chronic cyanosis assoc with tetralogy of fallot
    • perioral and mucosal cyanosis
    • - mild cyanosis noted around lips, mucus membranes and digits
    • clubbing of digits- chronic hypoxemia
    • erythrocytosis (aka polycythemia)
    • hyperviscosity- stroke risk
  166. this murmur is a mild systolic murmur related to right ventricular outflow obstruction, is best hear LUSB, may hear a single loud S2, and/o a possible holosystolic VSD murmur
    tetralogy of fallot
  167. what will an ECH show on a pt with tetralogy of fallot
    • RVH
    • RAD
  168. what will an CXR show on a pt with tetralogy of fallot
    "boot-shaped heart" (right heart enlargement/prominent RV)
  169. this diagnostic study defines the expected anatomy of tetralogy of fallot, it makes the dx, and it estimates the severity of the RVOTO
    echocardiogram
  170. what is the treatment for "tet spells"
    • O2
    • knee chest position
    • fluid bolus
    • morphine sulfate
    • propranolol or esmolol
  171. what type of repair do pts go under for tetralogy of fallot
    intracardiac repair
  172. what is the unoxygenated systemic circuit that is assoc with transposition of the great arteries
    body ⇨ RA ⇨ RV ⇨ aorta ⇨ body
  173. what is the oxygenated pulmonary circuit assoc with transposition of the great arteries
    lungs ⇨ LA ⇨ LV ⇨ pulmonary artery ⇨ lungs
  174. what is the most common cyanotic heart defect in the neonatal period
    transposition of the great arteries
  175. what are the clinical features associated with transposition of the great arteries
    • "blue baby"
    • generalized cyanosis first day of life which progresses (PDA closes)
    • tachypnea
    • palpable RV impulse
  176. what may a CXR show on a pt with transposition of the great arteries
    base of heart may narrow giving an "egg shaped" heart
  177. what makes the dx of transposition of the great arteries
    echocardiogram
  178. what is the treatment for transposition of the great arteries
    • rapid surgical correction is required, medical emergency
    • - arterial switch)

    PGE1 infusion alprostadil and/or balloon atrial septostomy
  179. what are the histologic changes that occur with Eisenmenger syndrome
    • pulmonary artiolar media hypertrophies
    • intima proliferates
    • vessels become thrombosed
  180. what are the clinical features of Eisenmenger syndrome
    • chronic cyanosis, digital clubbing
    • prominent "a" wave when left to right shunt
  181. which diagnostic test is used to identify the underlying defect and quantify the pulmonary artery pressure
    echocardiogram with doppler
  182. what is the treatment for Eisenmenger syndrome
    • activity restriction and other interventions to reduce cardiovascular demands
    • end stage sx in terminal pts
  183. this is a congenital defect of the tricuspid valve in which the septal and posterior leaflets are malformed and displaced into the right ventricle leading to variable degrees of right ventricular dysfunction
    ebsteins anomaly
  184. this congenital heart disease may be associated with maternal lithium during the 1st trimester
    ebsteins anomaly
  185. what are the clinical features of ebsteins anomaly
    • intrauterine demise
    • incidental finding
  186. when is endocarditis prophylaxis suggested for pts with ebstein anomaly
    • it is suggested in cyanotic pts
    • pts with prosthetic cardiac valves or with prosthetic material used for cardiac valve repair
  187. what are the treatments for ebsteins anomaly
    • endocarditis prophylaxis
    • tricuspid repair or replacement with severe sxs
    • arrhythmia treatment, if afib warfarin is recommended
  188. in infective endocarditis, what causes the leaflet vegetation
    platelet-fibrin thrombi, WBCs and bacteria (or other pathogens)
  189. what are the 3 ways to classify infective endocarditis
    • 1) by clinical course: acute (aggressive) and subacute (insidious in onset)
    • 2) by host: native valve (MC), prosthetic valve, IV drug user
    • 3) specific infectious organism ("bug")
  190. which pathogen is more common found on native valve infective endocarditis
    streptococcus
  191. which pathogen is more commonly found with IVDU infectious endocarditis
    S aureus
  192. which pathogen is more commonly found with prosthetic valves with a recent sx < 1yr infective endocarditis
    s. epidermidis
  193. which pathogen is more commonly found with prosthetic valves with a remote surgery > 1 yr infective endocarditis
    streptococcus
  194. for community acquired infectious endocarditis, which valve is most commonly affected
    MV
  195. for IV drug uses what is the most common valve affected with infectious endocarditis
    TV
  196. what are the risk factors for infective endocarditis (7 risk factors)
    • acquired valvular dz
    • prosthetic valve
    • CHD
    • hypertrophic cardiomyopathy
    • indwelling catheter
    • IV drug use
    • previous endocarditis
  197. what changes are associated with/ within the heart that is affected by infective endocarditis
    • endocardial surface injury (turbulent blood flow from valvular dz)
    • thrombus formation at the site of injury
    • bacterial entry into circulation (bacteremia)
    • bacterial adherence to the injured endocardial surface
  198. what are the acute sxs of infective endocarditis
    • aggressive, high fever, shaking chills
    • occurs and worsens over days
    • typical IE causing organisms
  199. what are the subacute sxs of infective endocarditis
    • develops over weeks
    • much less specific sxs
    • may be easily overlooked or confused with less aggressive dz process (viral syndrome)

    ** more CHF type sxs
  200. what are some common symptoms of infective endocarditis
    • fever
    • chills
    • anorexia
  201. what are some common signs of infective endocarditis
    • fever
    • murmur
    • neurological abnormalities
    • embolic event
  202. which criteria is used to help dx infective endocarditis
    duke criteria
  203. what is the initial test of choice that detects large vegetations, quantifies valvular dysfxn, non-invasive and easy to obtain
    TTE
  204. which diagnostic study is more sensitive for the detection of small vegetaions and is useful for the evaluation of prosthetic valves
    TEE
  205. what are the major Duke criteria's
    • positive blood cultures for IE
    • evidence of endocardial involvement (+ echo for IE, new valvular regurgiation
  206. what are the minor Duke criteria's
    • predisposition- predisposing heart condition or IV drug use
    • fever- 100.4
    • vascular phenomena- major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, janeway lesions
    • immunologic phenomena- glomerulonephritis, osler's nodes, roth spots, RF
    • microbiologic evidence- + blood culture but not meeting major criteria
    • echocardiographic minor criteria eliminated
  207. how many major and minor Duke criteria need to be present for definite IE
    • 2 major
    • 1 major and 3 minor
    • 5 minor
  208. how many major and minor Duke criteria need to be present for possible IE
    • 1 major and 1 minor
    • 3 minor
  209. what are the different treatments for IE
    • antibiotics 4-6 weeks of high dose IV abx therapy
    • sx
    • anti-coag
    • prophylaxis
  210. what is the appropriate initial therapy most pts will receive until cultures results are back for IE
    vancomycin
  211. if a pt has IE what is the treatment for strep
    high dose PCN-G (12 million units daily)
  212. if a pt has IE what is the tx for staph
    nafcillin IV
  213. what are some complications to be aware of in IE
    • emboli
    • CHF
    • abscess formation
    • intracranial hemorrhage
    • immune complex glomerulonephritis
  214. what are the indications for sx in IE
    • mod-severe CHF caused by valvular dysfxn
    • unavailable effective antimicrobial therapy:
    • - fungi
    • - brucella spp
    • - pseudomonas aeruginosa
  215. how much fluid is required for clinically evident cardiomegaly on CXR
    200-250ml
  216. this serves as a barrier to limit spread of infection from adjacent lungs to the heart
    pericardium
  217. a pt presents to the ER with acute pleuritic CP. You do an EKG and notice distinctive EKG changes and upon auscultation you hear a pericardial friction rub, what is your presumptive dx
    acute pericarditis

    * may or may not also have a fever
  218. what is the most common infectious cause of acute pericarditis
    idiopathic/viral (coxsackie, CMV, HIV)
  219. a pt reports to the ER stating that he is having pleuritic CP, upon getting his past hx he tells you he had a MI about 2 weeks ago. You listen to his heart and you hear a pericardial friction rub, what syndrome is associated with these sxs
    dresslers
  220. the highest mortality is associated with which type of pericarditis
    purulent
  221. which type of pericarditis is associated with PMNs, lymphocytes, histocytes (thin exudate)
    serous acute pericarditis
  222. which type of pericarditis has yellow exudate protein/fibrinogen which appears rough/shaggy. Is the most common type of pericarditis. The pericardium becomes thick, sometimes scar causing restriction of diastolic filling
    serofibrinous ("bread and butter")
  223. which type of pericarditis has purulence and an intense inflammatory response to bacteria
    suppurative (bacterial)
  224. which type of pericarditis has gross blood associated with it
    hemorrhagic (TB/Ca)
  225. what are the major clinical manifestations of acute pericarditis
    • CP (sharp and pleuritis and exacerbated by position or coughing)
    • friction rub (scratchy or squeaking sound best heard with diaphragm over the LSB
    • ECG changes (new widespread ST elevation with/without PR depression)
    • pericardial effusion
  226. what will an ECG show on a pt with pericarditis
    • diffuse ST elevation
    • PR segment depression
    • concave upsloping ST segment
  227. what will a CXR show on a pt with pericarditis
    water bottle heart with large effusion
  228. when would you order a STAT echo
    if tamponade is suspected
  229. how much pericardial fluid must accumulate before the cardiac silhouette enlarges
    200 mL
  230. when do you need to get blood cultures on a pt with pericarditis
    if fever great than 100.4 or signs of sepsis
  231. what is the treatment for acute pericarditis
    • viral or idiopathic pericarditis is self-limiting, lasts 1-3 weeks (rest and pain relief: combo colchicine + NSAIDS)
    • NSAIDS are the maintstay of therapy, unless CI then use ASA
  232. when would you not use NSAIDS on a pt with acute pericarditis
    post MI--- use ASA instead
  233. the likelihood of the this is determined primarily by the pressure-volume relationship
    tamponade
  234. what are some clinical features of pericardial effusion
    • dyspnea
    • dysphagia
    • hoarseness
    • hiccups
    • increased JVP with dominant "x" descent
    • arterial pulse normal to decreased
    • decreased pulse pressure
    • rub
    • atypical CP
  235. what are some clinical features of cardiac tamponade
    • Becks triad (distant heart sounds, JVD, HoTN)
    • atypical CP
    • "small quiet heart"
    • compression of surrounding structures
    • tachycardia
    • loss of "y" descent on JVP
    • pulsus paradoxus
    • shock
    • death
  236. what will an EKG show on a pt with an effusion
    • flat T waves
    • low voltage
  237. what will an EKG show on a pt with a tamponade and large effusion



    • electrical alternan (pathognomonic)
    • low voltage
  238. this diagnostic test can identify fluid collections as small as 20ml, it assists in quantifying the volume and if ventricular filling is compromised, and can help direct placement of pericardiocentesis needle if needed
    echo (effusion)
  239. this diagnostic test can tell if a pericardial effusion led to the tamponade, can see if there is compression of the cardiac chambers, and assists with a differential dx
    echo (tamponade)
  240. if you suspect a pt has a tamponade, what can be used to get the direct measurement of intracardiac and intrapericardial pressures
    cardiac cath
  241. what is the tx for effusions
    • mild: frequent observation with serial echos
    • mod to severe: pericardiocentesis, definitive tx should it persist, is sx removal of part/all of the pericardium
  242. what is the tx for a tamponade
    • pericardiocentesis
    • pericariotomy is recurrent
  243. what are the etiologies of exudative effusion
    • malignancy
    • infectious/parainfections
    • postpericardiotomy syndrome
    • collagen vascular dz
  244. what are the etiologies of transudative effusion
    • radiation
    • uremia
    • hypothyroidism
    • trauma
  245. this is a serious physiological state that develops as a consequence of chronic inflammatory changes to the pericardium (fibrosis, thickening, adherence, calcification)
    constrictive pericarditis
  246. what is the MC etiology of constrictive pericarditis
    idiopathic/post viral
  247. this type of pericarditis impairs diastolic filling without impairment of systolic filling
    constrictive pericarditis
  248. when do abnormalities occur with constrictive pericarditis
    diastole
  249. what are s/s of constrictive pericarditis
    • dyspnea
    • fatigue
    • HoTN
    • tachycardia
    • abd pain
    • right failure sxs (ascites, hepatosplenomegaly, peripheral edema, JVD)
  250. what will an ECG show on a pt with constrictive pericarditis
    • non specific ST and T wave changes
    • tachycardia common
    • low voltage
    • AFib
  251. what is the essential diagnostic test for constrictive pericarditis
    TTE
  252. which diagnostic study is superior for assessment of pericardial anatomy and thickness
    CT scan
  253. what is the normal consideration for pericardial thickness
    <2mm
  254. which diagnostic study confirms elevation and equalization of diastolic pressures, shows a dip and plateau from ventricular tracings with a prominent "y" descent, and is necessary to distinguish between constrictive pericarditis and restrictive cardiomyopathy
    cardiac cath
  255. what is the tx for constrictive pericarditis
    the ONLY effective tx of severe constrictive pericarditis is sx removal of the pericardium
  256. what type of pulse with cardiac tamponade have that constrictive pericarditis will not have
    pulsus paradoxus
  257. what sign can be visualized on a pt that can help you differentiate between constrictive pericarditis and cardiac tamponade
    kussmaul's sign
  258. what characteristics will be present with a pt that has constrictive pericarditis but wont be present with a pt that has tamponade
    • kussmauls sign
    • pericardial knock
    • HoTN (variable)
  259. what characteristics will be present with a pt that has tamponade but wont be present in a pt with constrictive pericarditis
    • pulses paradoxus
    • HoTN (severe)
  260. which phase is when rapid Na+ channels open (-85mv), slow Ca++ channels open (-40mv)
    phase 0
  261. which phase is when the Na+ channels close which causes the Na+ flux to cease (outflow rectifier K+ channels open transiently)
    phase 1
  262. which phase is when the K+ channels open, Ca++ influx continues (plateau phase--responsible for prolonging the cardiac action potential, making it longer than a nerve action potential)
    phase 2
  263. which phase is the repolarization phase where the Ca++ channels close, K+ outflow continues (delayed rectifier K+ channel)
    phase 3
  264. which phase is when K+ channels are closed, active transport of Na+ and K+ to return to resting state concentrations. (inward rectifier K+ channels)
    phase 4
  265. what is the pulse rate of the SA node
    60 to 100 bpm
  266. what is the pulse rate of the AV junction
    40-60 bpm
  267. what is the pulse rate of the purkinje system
    20 to 40 bpm
  268. what are the 2 issues that cause arrhythmias
    • altered impulse formation
    • altered impulse conduction
  269. what can cause altered impulse formation
    • altered normal automaticity
    • increased sinus node automaticity (sympathetic; PAC,PJC, PVC)
    • decreased sinus node automaticity (parasympathetic)
    • escape rhythms
    • enhanced automaticity of latent pacemakers
    • ectopic beats and rhythms
    • abnormal automaticity
    • triggered activity
    • early after depolarizations (torsades de pointes)
    • delayed after depolatizations (digoxin-toxic rhythms)
  270. what can cause altered impulse conduction
    • conduction block
    • transient versus permanent
    • unidirectional versus bidirectional
    • functional versus fixed
    • reentry (WPW, Afib, Aflutter, VFib, Vflutter)
    • primarily unidirectional (fixed path)
    • include accessory pathways (WPW)
    • multidirectional (unstable path)
  271. how can you recognize a SVT arrhythmia


    • appears as a narrow complex
    • may be regular or irregular
    • rate depends upon underlying arrhythmia mechanism
    • are there any discernible P waves
    • sinus tachycardia
  272. what is the most frequent cause of a compensatory pause


    PAC
  273. this rhythm is a macro-re-entrant atrial rhythm, typically occurs in pts with pre-existing heart disease, will have atrial structural abnormalities, PE dz, TR, TS, hyperthyroidism, alcoholism, percarditis


    atrial flutter
  274. what will an EKG show for a pt with atrial flutter
    • saw toothed pattern
    • atrial rate up to 350
    • variation in conduction at AV node
    • 2:1, 3:1, 4:1
  275. this arrhythmia has symptoms that are rate related, can be paroxysmal or permanent, increased thromboembolic events, can lead to high output heart failure
    atrial flutter
  276. how is atrial flutter managed
    • rate control- through atrial flutter rate is difficult to control:
    • - CCB (verapamil/diltiazem)
    • - BBB
    • - Digoxing
    • rhythm control/conversion:
    • - synchronized cardioversion preferred for unstable  or stable (internal or external DC)
    • - rapid atrial pacing
    • - chemical cardioversion (ibutilide DOC)

  277. what is the definitive treatment for a stable pt with AFlutter
    EP intervention, radiofrequency cath ablation
  278. this arrhythmia is chaotic, uncontrolled atrial contractions with similar etiologies to aflutter
    • AFIB
  279. what are the etiologies of Afib
    • VHD (MS, MR)
    • coronary heart dz
    • HTN heart dz
    • lone A-Fib
  280. what is the most common arrhythmia requiring treatment
    AFIB
  281. what are the clinical features of AFIB
    • sxs are rate related (rapid ventricular rate)
    • range from asymptomatic pts to disabling sxs
    • paroxysmal or permanent
    • absent "a" waves on JVP or monitoring
    • NO S4 heart sounds
  282. what will an EKG show on a pt with AFIB
    • no discernible P-waves, irregular RR intervals
    • Irregularly irregular
    • evaluate for rapid ventricular response
  283. for AFIB, when will you know if a pt is unstable and how is it treated
    • HoTN
    • ongoing ischemia
    • severe heart failure
    • cerebrovascular event

    cardioversion
  284. for AFIB, when will you know if a pt is stable and how is it treated
    H&P and diagnostics

    determine underlying etiology and treat
  285. what are the three major therapeutic strategies in managing AFIB
    • prevention of stroke
    • rate control
    • rhythm control
  286. what is the preferred management as an initial approach for the majority of older pts with AFIB
    rate control
  287. what is the approach the is usually pursed in younger pts (<60) with AFIB
    rhythm control
  288. what are the 2 ways that rate control manages AFIB
    • Pharmacological therapy:
    • influenced by underlying cardiac condition
    • pharmacologically we block the AV node with BB, CCBs (verapamil or diltiazem)
    • Dig is used with those with systolic HF
    • Electrically:
    • anticoagulation required prior if pt is stable
    • 3 weeks prior and 4 weeks after to decrease stroke risk
  289. if you have a pt with AFib and there is no structural heart dz, what meds can be used for rhythm control
    flecainide or propafenone
  290. how soon should AFIB be cardioverted
    within 48 hrs
  291. a pt who has severe clinical instability due to Afib is less likely to have been in Afib for more than how many hours
    48 hrs
  292. what should be given to a pt with Afib prior to cardioversion
    heparin
  293. for pts with AFIB, what are the stroke risk determinants
    • C- CHF
    • H- HTN
    • A- Age >75
    • D- DM
    • S- stroke or TIA

    • * CHAD worth 1 pt for each letter
    • * S worth 2 pts
  294. what class of medications are usually tried first in pts with AFIB
    beta blockers
  295. what is the most common type of paroxysmal SVT
    AVNRT
  296. this represents a self sustaining electrical circuit that repeatedly depolarizes a region of cardiac tissue, unidirectional block, slowed conduction through a loop tissue, and MOST COMMON cause of narrow QRS complex tachycardia
    re-entry
  297. what is the most common cause of narrow QRS complex tachycardia
    re-entry paroxysmal SVT
  298. which type of PSVT will show a PAC on the EKG
    AVNRT
  299. which type of PSVT will show a delta wave, short PR, prolonged QRS (orthodromic or antidromic) or a concealed pathway
    AVRT
  300. which type of disease is more commonly seen if a pt has a MAT arrhythmia
    lung dz
  301. this type of WPW is usually associated with the bundle of kent left side of the heart, impulse travels down the bundle of kent and back up the AV node, can give a wide complex tachycardia difficult to distinguish between VT
    type A: antidromic

    * can be very dangerous because the AV node no longer can pause the impulse
  302. which type of WPW has impulse that travels down the AV node and back up through the bundle of kent
    type B: orthodromic

    * less dangerous because the AV nod still influences the physiological block
  303. explain the adult tachycardia ACLS algorithm
  304. how is unstable AVNRT treated
    cardioversion or adenosine
  305. how is stable AVNRT treated
    vagal maneuvers then adenosine
  306. how is antidromic AVRT PSVT treated
    IV procainamide-- remember this rhythm can be a wide QRS and look like Vtach
  307. how is orthodromic AVRT PSVT treated
    vagal maneuvers, IV adenosine
  308. if a pt has an EKG done and they have a WPW and the are unstable how are they treated
    cardiovert
  309. what is recommended for pts with symptomatic arrhythmias (WPW)
    catheter ablation
  310. how is a pt with attach (ectopic and MAT) treated
    • treat underlying cause
    • rate control: verapamil used in MAT and slows AV nodal conduction used in pts with bronchospasm/advance COPD otherwise use BB
    • ablation: those that can't tolerate pharmacologic therpay
  311. this is a cariac beat arising from the ventricle usually with a wide complex QRS reflecting the ventricular origin
    PVC
  312. if a pt complains of palpitations or "skipped beats" and you do an EKG, what may be a finding on the EKG
    PVC
  313. how are PVCs treated
    • asymptomatic= benign neglect
    • symptomatic without underlying disease= BB
    • treat underlying cardiac dz
  314. what does an EKG look like if a pt has VTach
    • wide QRS complexes
    • rate >120
    • regular rhythm with slight irregularity
    • RAD, even extreme RAD
  315. this type of Vtach is an abberant conduction associated with alternating R-R interval, and has an underlying A-fib
    ashmans phenomenon
  316. what are some causes of Vtach
    • superimposed cardiac insult, previous MI more like to have Vtach
    • ischemia
    • electrolyte disturbance
    • drug/medication toxicity
    • prolonged QT
  317. how is asymptomatic and non-sustained Vtach treated
    • diagnostic eval:
    • - potential unrecognized cardiac dz
    • - treat underlying dz
  318. how is acute sustained unstable vtach treated
    • ACLS, immediate synchronized cardioversion
    • if pulseless-- DFIB
  319. how is acute sustained stable vtach treated
    • consider urgent or elective cardioversion
    • procainamide or amiodarone
  320. how is acute sustained vtach torsade treated
    defibrillation
  321. how can vtach be prevented
    ICD
  322. how is primary vtach treated
    • BB
    • amiodarone
    • ICD
  323. how is secondary vtach treated
    • amiodarone
    • ICD
  324. this arrhythmia is a disordered, uncoordinated, ventricular contractions leading to a pulseless state with no effective cardiac output that is invariably fatal without treatment
    Vfib
  325. this arrhythmia is the most common rhythm leading to SCD
    Vfib
  326. what is the ACLS protocol for adult cardiac arrest
  327. what are the 5 H's that are reversible causes of Vtach/VFib/PEA
    • hypovolemia
    • hypoxia
    • H+ (acidosis)
    • hypo/hyperkalemia
    • hypothermia
  328. what are the 5 T's that are reversible causes of Vtach/Vfib/PEA
    • tension pneumothorax
    • tamponade
    • toxins
    • thrombosis, pulmonary
    • thrombosis, coronary
  329. what is the ACLS protocol for bradycardia

What would you like to do?

Home > Flashcards > Print Preview