Cardiology 1

  1. Amiodarone (Pacerone, Cordarone)
    Considered class III but has properties of all three classes
  2. Digoxin (Lanoxin)
    Inhibits the sodium potassium ATPase pump
  3. A system of classifying antiarrhythmic medications based on simplified electrophysiologic actions
  4. Procainamide (Procan SR, Procanabid)
    Vaughan-Williams Type IA
  5. Modulation/blockade of sodium channels
    Vaughan-Williams Type I antiarrhythmics
  6. The class that exhibits slow conduction velocity and prolongs action potential duration
    Vaughan-Williams Type IA
  7. Quinidine (Quinidex)
    Vaughan-Williams Type IA
  8. Disopyramide (Norpace)
    Vaughan-Williams Type IA
  9. Lidocaine (Xylocaine)
    Vaughan-Williams Type IB
  10. Mexiletine
    Vaughan-Williams Type IB
  11. Class that has no effect on conduction velocity, May shorten action potential duration
    Vaughan-Williams Type IB
  12. Flecainide (Tambocor)
    Vaughan-Williams Type IC
  13. Propafenone (Rhythmol)
    Vaughan-Williams Type IC
  14. Moricizine
    Vaughan-Williams Type IC
  15. Slows coduction velocity and may prolong action potential duration (mildly)
    Vaughan-Williams Type IC
  16. Mexiletine
    Oral analog of Lidocaine
  17. Lidocaine
    unlike other class I antiarrhytmics it can be used in patients with active ischemia
  18. Beta blockers
    Vaughan-Williams Type II
  19. Beta blockers
    Inhibit phase IV (depolarizing current) and prolong repolarization
  20. Beta blockers
    decrease sympathetic stimulation of myocardium
  21. Beta blockers
    slow the sinus rate
  22. Amiodarone (Pacerone, Cordarone)
    Vaughan-Williams Type III
  23. Sotalol (Betapace)
    Vaughan-Williams Type III
  24. Dofetilide (Iikosyn)
    Vaughan-Williams Type III
  25. Ibutilide
    Vaughan-Williams Type III
  26. Blockade of potassium channel
    Vaughan-Williams Type III
  27. Prolongation of action potential plateau, repolarization, and refractor period
    Vaughan-Williams Type III
  28. Verapamil
    Vaughan-Williams Type IV
  29. Diltiazem
    Vaughan-Williams Type IV
  30. Calcium channel blockers
    Vaughan-Williams Type IV
  31. Blockade of calcium channel
    Vaughan-Williams Type IV
  32. slows conduction velocity through AV node and prolongs refractory period
    Vaughan-Williams Type IV
  33. Sets of the initial depolarization
    Phase IV
  34. Does not increase mortality in high risk patients-has a higer safety level than the other classes
    Type III
  35. Ibutilide
    IV administration only -one time use for conversion-no long term treatment
  36. Anticipated ECG change for this type is prolongation of the QT interval
    Type IA
  37. Usually no ECG changes in therapeutic doses
    Type IB
  38. Anticipated ECG changes for this type is prolongation of the PR and QRS intervals
    Type IC
  39. Anticipated ECG change for this type is prolongation of the QT interval
    Type III
  40. This type is used for atrial and ventricular tachyarrhythmias
    Type IA
  41. This type is used for ventricular arrhythmias
    Type IB
  42. This type is used for atrial and ventricular arrhythmias
    Type IC
  43. Procainamide (Procan SR, Procanabid)
    Used for WPW
  44. This type is used for atrial and ventricular arrhythmias
    Type II
  45. This type is used for atrial and ventricular arrhythmias
    Type III
  46. This type is used for atrial arrhthmias
    Type IV
  47. Procainamide (Procan SR, Procanabid)
    SE-lupus like syndrome, torsades
  48. Disopyramide (Norpace)
    SE-anticholinergic symptoms, heart failure, torsades (QT prolongation)
  49. Lidocaine (Xylocaine)
    SE-seizures, CNS
  50. Amiodarone (Pacerone, Cordarone)
    SE-many toxic side effects (Pulmonary fibrosis, hypo/hyperthyroidism, photophobia, liver toxicity, blue staining of skin.
  51. Amiodarone (Pacerone, Cordarone)
    Has a very large volume of distribution
  52. Amiodarone (Pacerone, Cordarone)
    Has a half life of 15-180 days
  53. Amiodarone (Pacerone, Cordarone)
    If patient is on Warfarin at the time of prescription, cut the Warfarin dose by 30-50%
  54. Procainamide (Procan SR, Procanabid)
    Used for hemodynamically stable VT
  55. Procainamide (Procan SR, Procanabid)
    Limited role in a-fib/a-flutter
  56. Quinidine (Quinidex)
    SE-include chinchonism, hypotension, torsades, hemolytic anemia
  57. Quinidine (Quinidex)
    Use with digoxin leads to increased digoxin concentration
  58. Disopyramide (Norpace)
    Indicated for conversion/maintenance of sinus rhythm in patients with a-fib/a-flutter
  59. Lidocaine (Xylocaine)
    Used for management of VT or pulseless VT/Vfib
  60. Lidocaine (Xylocaine)
    Dose determined by liver function
  61. Flecainide (Tambocor)
    used in a-fib/a-flutter for maintenance of sinus rhythm
  62. Flecainide (Tambocor)
    Avoid in patients with structural heart disease or history of CAD
  63. Propafenone (Rhythmol)
    Indicated for conversion/maintenance of sinus rhythm in patients with a-fib/a-flutter
  64. Dofetilide (Tikosyn)
    Indicated for conversion/maintenance of sinus rhythm in patients with a-fib/a-flutter
  65. Dofetilide (Tikosyn)
    Starting dose based on estimated creatinine clearance. Contraindicated in patients with CrCl <20 ml/min.
  66. Sotalol (Betapace)
    used in a-fib/a-flutter for maintenance of sinus rhythm
  67. Stroke risk index based on a point system, integrating risk based on various co-morbidities
  68. The C in CHADS2 stands for
    Cardiac failure (one point)
  69. The H in CHADS2 stands for
    Hypertension (one point)
  70. The A in CHADS2 stands for
    Age >75 years (one point)
  71. The D in CHADS2 stands for
    Diabetes (one point)
  72. The S2 in CHADS2 stands for
    Sroke or TIA (you get 2 points for this one)
  73. CHADS2 score of 0-1
    Low risk-treat with full dose asa
  74. CHADS2 score of 2 and above
    High risk-treat with Warfarin
  75. Most common arrhythmia
  76. Characterized by rapid and disorganized atrial activation with ventricular responses of 120-180 bpm
  77. A-fib management in the hemodynamically stable patient
    Ventricular rate control with beta blocker, calcium channel blocker, or digoxin
  78. A-fib management in the hemodynamically stable patient
    Anticoagulation therapy
  79. A-fib management in the hemodynamically unstable patient
  80. When a-fib is symptomatic, recurrent and failed response of greater than or equal to 1 AAD plus rate contrel
    consider ablation
  81. Beta blockers
    safe and effective treatment for Ventricular Premature Beat suppression
  82. Lidocaine (Xylocaine)
    Sustained monomorphic V-tach with LVEF <40% and expected ischemia/MI
  83. Movement of ions across the cell membrane resulting in activation of cardiac cells and a transient depolarization.
    Action Potential
  84. Impulse generation; the property of a cardiac cell that causes it to depolarize spontaneously during phase 4 of the AP
  85. The speed of impulse propagation through cardiac tissue.
    Conduction Velocity
  86. the period of recovery cells require after being discharged before they can be re-excited by a stimulus.
    Refractory Period
  87. All antiarrhythmic agents have the potential to cause arrhythmias
  88. Risk factors including ischemic heart disease, left ventricular dysfunction and underlying ventricular arrhythmias
    predispose patients to proarrhythmia
  89. Procainamide; Quinidine; Disopyramide
  90. Modulation/blockade of Na+ channels inhibiting phase 0 depolarization
    IA; IB & IC
  91. Slow conduction velocity and prolongs action potential duration (APD). Intermediate association/dissociation
  92. No effect on conduction velocity; may shorten APD. Fast association/ dissociation
  93. Slow conduction velocity and may prolong APD (mildly). Slow association/dissociation
  94. Lidocaine; Mexiletine
  95. Flecainide; Propafenone; Moricizine
  96. Inhibition of phase IV (depolarizing current) and prolongation of repolarization; ↓ sympathetic stim, slow sinus rate
    Beta blockers (type II)
  97. Blockade of potassium channelProlongation of action potential plateau, repolarization, and refractory period
    Type III: Amiodarone; Sotalol; Dofetilide; Ibutilide; Dronedarone
  98. Blockade of calcium channel; slows conduction velocity through AV node and prolongs refractory period
    Type IV:Verapamil; Diltiazem
  99. Prolongation of the QT interval
    Type IA: Procainamide; Quinidine; Disopyramide
  100. None (Possible increased QRS and PR intervals with toxic concentrations)
    Type IB: Lidocaine; Mexiletine
  101. Prolongation of the PR and QRS intervals
    Type 1C: Flecainide; Propafenone
  102. Prolongation of the QT interval
    Type III: Amiodarone; Sotalol; Dofetilide; Ibutilide; Dronedarone
  103. Atrial and ventricular tachyarrhythmias
    Type IA: Procainamide; Quinidine; Disopyramide: Use/Indication
  104. Ventricular arrhythmias
    Type IB: Lidocaine; Mexiletine; Use/Indication
  105. Atrial and ventricular arrhythmias
    Use/Indication: Type IC: Flecainide; Propafenone
  106. Atrial and ventricular arrhythmias
    Use/Indication: Beta blockers
  107. Atrial and ventricular arrhythmias
    Use/Indication: Type III:Amiodarone; Sotalol; Dofetilide; Ibutilide; Dronedarone
  108. Atrial arrhythmias
    Use/Indication: Type IV: Verapamil; Diltiazem
  109. Fatigue, bradycardia, exercise intolerance, erectile dysfunction, exacerbation of pulmonary d/o’s
    AE Beta blockers: Type II
  110. AV block, bradycardia, HF exacerbation, hypotension
    Verapamil; Diltiazem: Type IV
  111. Limited role in management of afib/flutterRole in WPW, hemodynamically stable VT
  112. Elimination/metabolismHepatic: acetylation forms less active (but toxic) metabolite NAPARenal: NAPA primarily elim. Renally
  113. Side effects include drug-induced lupus, torsades, vent arrhythmias, aggravation of underlying heart failure
  114. Side effects include GI, cinchonism, hypotension (IV), torsades, vent arrhythmias, hemolytic anemia
  115. Eliminated by hepatic metabolism (3A4) and renal elimination
  116. Indicated for conversion/maintenance of sinus rhythm in patients with afib/flutter.
  117. Significant negative inotropic effects
  118. Side Effects include: GI, anticholinergic symptoms, heart failure, worsening of underlying conduction abnormalities, ventricular arrhythmias, torsades (QT prolongation)
  119. Class 1B antiarrhythmic agent; Used in management of ventricular tach or pulseless VT/Vfib; Dose determined by hepatic function/cardiac output (LVEF)
  120. Normal half-life extends to up to 12 hrs in patients with cirrhosis/CHF; Side-effects include CNS (confusion,tremor,paresthesias), seizures
  121. Used to manage ventricular arrhythmias; esp when responsive to lidocaine. Significantly hepatically metabolized, 1º to inactive metabolites
  122. Substrate for CYP 2D6 and 1A2; Inhibitor of CYP 1A2; Half-life 8-15 hours
  123. Side-effects: CNS, psychosis, GI, aggravation of underlying conduction disturbances or ventricular arrhythmias, rarely blood dyscrasias
  124. Used in afib/flutter for maintenance of sinus rhythmAvoid in patients with structural heart disease or history of CAD
  125. Side-effects: EKG (prolongation of QRS and PR), ventricular arrhythmias, GI, blurred vision; Elimination: renal and hepatic (CYP2D6)
  126. Used for conversion/maintenance of sinus rhythm in patients with afib/flutter.Potent negative inotropic agent (avoid in patients with systolic dysfunction)
  127. Side-effects: GI, worsening of underlying CHF, ventricular arrhythmias; Elimination: hepatic metabolism
  128. Prescribers must complete training program; Requires hospitalization for at least 3 days to initiate (due to risk of proarrhythmias)
  129. Baseline QTc should be less than 440 msec (500 msec if baseline ventricular conduction abnormalities)
  130. Class III antiarrhythmic with beta-blocking activity. Indicated for maintenance of sinus rhythm. May chemically convert patientsContraindicated if baseline QTc > 450 msecCareful monitoring of electrolytes
    Sotalol (Betapace®, Betapace AF®
  131. Mechanism of Action: Class III anti-arrhythmic with properties of all classes:inhibition of adrenergic stimulation; decreased AV node conduction and sinus node function; prolongation of action potential and; refractory period of myocardial tissue
  132. Cardiac: QT prolongation, monitor EKG daily during initiation and q 3 months
    Amiodarone Side Effects
  133. Pulmonary toxicity: Pulmonary fibrosis (3-10%), check baseline pulmonary function tests
    Amiodarone Side Effects
  134. Thyroid disturbances: hypothyroidism (~20%), hyperthyroidism (~5-10%), monitor thyroid function tests at baseline and q 6 months
    Amiodarone Side Effects
  135. Ocular: optic neuritis (1%), photophobia (75-90%) eye exam at baseline and every year thereafter
    Amiodarone Side Effects
  136. Liver: elevated hepatic transaminases (5-20%), monitor liver function at baseline and q 6 m
    Amiodarone Side Effects
  137. Indicated to reduce CV hospitalization in patients with PAF or AF or aflutter with recent episode and associated risk factors who are in sinus rhythm or who will be cardioverted.
  138. Effective for both conversion and maintenance of NSR in Afib pts. Use only in persons without coronary artery disease or left ventricular dysfunction.
    Propafenone and Flecainide
  139. Symptoms precede LV dysfunctionTypically, intervene for symptoms
  140. LV dysfunction may precede symptomsMonitor LV functionIntervene for symptoms AND to preserve cardiac function
  141. Narrowing or obstruction to forward flow while valve is openChronic – slow progression of disease
  142. Backward leakage during time when valve is closedAcute vs chronic
    Regurgitation / Insufficiency
  143. thickness is < 12 mm
    Normal LV wall
  144. Who: Older, calcific or younger, bicuspid
    Aortic Stenosis
  145. Sx: Angina, syncope, CHF
    Aortic Stenosis
  146. PE findings: Harsh, systolic ejection murmur at RUSB with radiation to neck, subclavian; sit patient forward, exhalation
    Aortic Stenosis
  147. Dx: Echo, cardiac cath
    Aortic Stenosis
  148. Management: Surgery for symptoms
    Aortic Stenosis
  149. Marfan syndrome, syphilis, ankylosing spondylitis, cystic medial necrosis, aortic dissection, trauma
    Aortic root disease
  150. Wide pulse pressureLarge difference between systolic and diastolic pressuresDiastolic murmur – soft, high pitched and localized to left sternal border‘Water-hammer’ or ‘Corrigan’s’ pulseQuincke’s pulse – nail bedMusset’s sign – head bob
    • Chronic Aortic Regurgitation--
    • Physical Findings
  151. nail bed
    Quincke’s pulse
  152. head bob
    Musset’s sign
  153. Who: No classic patient, think bicuspid or Marfan syndrome
    Aortic Regurgitation
  154. Sx: CHF symptoms – dyspnea, fatigue
    Aortic Regurgitation
  155. PE findings:Wide pulse pressureSoft, decrescendo diastolic murmurBounding pulses - ‘Water-hammer’, Musset’s head bob, Quincke’s pulse
    Aortic Regurgitation
  156. Dx: Echo
    Aortic Regurgitation
  157. Management: Medical therapy; surgery for acute AI, symptoms, or evidence of LV changes
    Aortic Regurgitation
  158. Think rheumatic heart disease first
    Mitral Stenosis
  159. PathophysiologyFibrosis, scarring and thickeningCommissural fusionChordae fusion and shorteningDecrease in orifice size
    Mitral Stenosis
  160. Who: History of rheumatic fever
    Mitral Stenosis
  161. Symptoms: Dyspnea/orthopnea and fatigue
    Mitral Stenosis
  162. PE findings: Low pitched, diastolic rumble near apex with opening snapHeard best in left lateral decubitus position
    Mitral Stenosis
  163. Diagnosis: Echo
    Mitral Stenosis
  164. Management: Intervene for symptoms – balloon valvuloplasty or mitral valve replacement
    Mitral Stenosis
  165. Who: Myxomatous valve or post-MI
    Mitral Regurgitation
  166. Symptoms: CHF
    Mitral Regurgitation
  167. PE: Holosystolic murmur at apex
    Mitral Regurgitation
  168. Diagnosis: Echo or cardiac cath
    Mitral Regurgitation
  169. Management: Medical mgt., Surgical for symptoms or decrease in LV function
    Mitral Regurgitation
  170. Who: Young, female
    Mitral valve prolapse
  171. Symptoms: Atypical chest pain, palpitations
    Mitral valve prolapse
  172. PE: Mid-systolic click +/- MR
    Mitral valve prolapse
  173. Diagnosis: Echo – assess MR
    Mitral valve prolapse
  174. Management: Supportive, SBE prophylaxis
    Mitral valve prolapse
  175. Pathology: Narrowing and calcification of TV causing diastolic pressure gradient (5 mmHg) between RA and RV
    Tricuspid Valve Stenosis
  176. Symptoms: Related to elevated RA pressuresEdema, hepato-splenomegaly / ascites, fatigue, weakness
    Tricuspid Valve Stenosis
  177. Exam: Jugular veinous distension with giant venous A wavesDiastolic murmur at left sternal border which increases with inspiration
    Tricuspid Valve Stenosis
  178. Therapy: Balloon Valvuloplasty or Surgical valve replacement if symptoms and mean valve gradient > 5 mm Hg
    Tricuspid Valve Stenosis
  179. Small degrees present in normal individual; Causes of mod/severe TR; Usually functional – related to RV dilatation or increases in pulmonary artery pressure; Ebstein’s anomaly; Rheumatic disease; Carcinoid, endocarditis, trauma
    Tricuspid Regurgitation
  180. Symptoms: Identical to those of RV failure
    Tricuspid Regurgitation
  181. Physical exam findings: C-V waves of the jugular veins with venous congestion; Pulsatile liver; Hepatojugular refluxHolosystolic murmur at LSB; Increases with inspiration
    Tricuspid Regurgitation
  182. Symptoms: Exertional dyspnea; Fatigue; Pre-syncope; Cyanosis
    Pulmonic Stenosis
  183. Signs on ECHO: RV hypertrophy; Systolic doming of PV; Transpulmonic gradient
    Pulmonic Stenosis
Card Set
Cardiology 1
Cardiology flashcards made by previous students