1. Class I Heart Failure
    No limitation of physical activity, ordinary physical activity does not cause undue fatigue, dyspnea, or anginal pain
  2. Class II Heart Failure
    Slight limitation of physical activity; ordinary physical activity results in sx
  3. Class III Heart Failure
    Marked limitation of physical activity; comfortable at rest, but less than ordinary activity causes sx
  4. Class IV Heart Failure
    Unable to engage in physical activity without discomfort, sx may be present even at rest
  5. Shock
    severe CV failure caused by poor blood flow or inadequate distribution of flow. Inadequate oxygen delivery to body tissues results in shock, which lead to organ failure and death
  6. Hypovolemic shock causes
    • hemorrhage, loss of plasma, loss of fluid and electrolytes, resulting in decreased intravascular volume.
    • This may be caused by obvious loss of by third-spacing
  7. Cardiogenic shock causes
    MI, dysrhythmias, HF, defects in the valves or septum, cardiac contusion, rupture of ventricular septum, or cardiomyopathies
  8. Obstructive shock causes
    tension ptx, pericardial tamponade, obstructive valvular disease, pulmonary problems, PE
  9. Distributive shock causes
    sepsis, SIRS, anaphylaxis, neurogenic shock
  10. Causes of neurogenic shock
    spinal cord injury or adverse effects of spinal or epidural anesthetic
  11. S/Sx of shock
    LBP, orthostatic changes, tachycardia, peripheral hypoperfusion, AMS, oliguria or anuria, insulin resistance, and metabolic acidosis
  12. End organ hypoperfusion s/sx
    Cool or mottled extremities, weak/thready or abset peripheral pulses
  13. Tx of shock
    • ABCs
    • Tx cause
    • Trendelenberg or supine position with legs elevated maximizes blood flow to the brain
    • good urine output
    • continuous cardiac monitoring (CVP or capillary wedge pressure)
    • Pressures (dopamine, etc) will increase GFR, contractility, and heart rate
  14. Urine output goal in shock
    0.5mL/kg/hr or more
  15. Causes of postural hypotension
    decreased cardiac output, paroxysmal cardiac dysrhythmias, low blood volume, medications, and various endocrine and metabolic disorders
  16. Postural hypotension
    Greater than 20 mm Hg drop in SBP between supine and sitting and/or standing measurements
  17. How do you know that decreased blood volume is the cause of postural hypotension?
    • increase in pulse by 15 bpm
    • if no increase in pulse, consider meds, CNS disease (Parkinsons, Shy-Drager), or peripheral neuropathies
  18. Metabolic syndrome
    truncal obesity, hyperinsulinemia and insulin resistance, hypertriglyercidemia, HTN)
  19. Secondary causes of HTN
    sleep apnea, estrogen use, pheochromocytoma, coarctation of the aorta, pseudotumor cerebri, parenechymal renal diesase, renal artery stenosis, chronic steroid therapy, Cushing's syndrome, thyroid and parathyroid disease, primary hyperaldosteronism, and pregnancy
  20. stage 1 HTN
  21. Stage 2 HTN
  22. How soon must HTN emergencies be reduced?
    By one hour to prvent progression of end-organ damage or death
  23. Malignant HTN
    elevated BP associated with papiledema and either encephalopathy or nephropathy; if untx, progressive renal failure occurs
  24. End organ damage in untx HTN
    HF, renal failure, stroke, dementia, aortic dissection, atherosclerosis, and retinal hemorrhage
  25. HTN urgency
    >220/125 with no end organ damage
  26. HTN emergency
    >220/130 with papilledema
  27. Complications of HTN emergency
    HTN encephalopathy, nephropathy, intracranial hemorrhage, aortic dissection, preeclampsia or eclampsia, pulmonary edema, unstable angina, MI
  28. EKG findings in HTN
    LVH or HF, strain failure indicates advanced disease and a poorer prognosis
  29. Diurectic MOA
    Reduce plasma volume and chronically reduce peripheral resistance
  30. Initial therapy for essential HTN
    thiazide diuretics; loops in those with renal dysfunction and when close electrolyte monitoring is assured
  31. ACE-I MOA
    inhibit bradykinin degradation and stimulate synthesis of vasodilating prostaglandins
  32. ARB MOA
    • block the itneraction of angiogensin II on receptors
    • Do not increase bradykinins, therefore do not cause cough
  33. CCB MOA
    peripheral vasodilation, good in AA and elderly
  34. A-adrenergic MOA
    lower peripheral resistance
  35. aldosterone receptor antagonist role in HTN
    refractoy HTN in addition to other HTN
  36. Tx of HTN emergency
    • sodium nitroprusside
    • nitro or BB if ischemia is present
  37. Tx of aortic dissection
    Nitroprusside and BB (usually labetaolol or esmolol) and urgent surgery
  38. CHF effect on cardiac function
    adversely affects left atrial pressure and cardiac output
  39. S4 gallop
    • diastolic failure
    • MI
  40. cardiac signs of heart failure
    parasternal lift, enlarged apical impulse, diminished first heart sound, S3 gallop
  41. Initial therapy in CHF
    loop diuretic and an ACE-I
  42. Role of CCBs in CHF
    associated angina or HTN
  43. Metabolic syndrome values
    • 3 or more of the following:
    • abdominal obesity, TG > 150, HDL <40 for men and <50 for women, FBP > 110, and HTN
  44. Prinzmetal's angina
    vasopasm at rest
  45. Unstable angina
    increasing pattern of pain in previously stable pts; less responsive to medication, lasts longer, and occurs with rest or with less exertion
  46. Angina > 30 mins
    unstable angina, MI, or another dx
  47. angina time frame
    should be <3m
  48. Most sensitive clinical sign of angina
    horizontal or downsloping ST-segment depression on an EKG
  49. First line therapy for chronic angina
  50. CCB role in angina
    third line therapy
  51. m/c cause of MI
    thrombus formation on a preexisting atherosclerotic plaque
  52. Populations most likely to have uncommon presentation of MI
    women, diabetics, elderly
  53. MI pain occurs most often when?
    early in the morning
  54. Inferior MI EKG
    II, III, aVF
  55. Posterior MI EKG
    V1, V2
  56. Anteroseptal MI EKG
    V1, V2
  57. Anterior MI EKG
    V1, V2, V3
  58. Anterolateral MI EKG
    V4, V5, V6
  59. Cardiac exam in MI
    nl, or JVD, soft heart sounds, mitral regurg, and S4 gallop
  60. Dressler's syndrome
    • Post-MI syndrome, usually 1-2 weeks
    • Pericarditis, fever, leukocytosis, pericardial or pleural effusion
  61. When should CK-MG be drawn?
    3 times, 12 hours apart
  62. When should troponin I be drawn?
    12 hours after onset of CP
  63. When should troponin T be drawn?
    12 hours after onset of CP
  64. When should LDH be drawn in an MI?
    Once, at least 24 hours after onset of CP
  65. When does LDH peak?
    24-48 hours
  66. When does LDH return to nl?
    10-14 days
  67. When does CK-MB peak?
    24 hours
  68. When does CK-MB return to nl?
    48-72 hours
  69. When does troponin I peak?
    24 hours
  70. When does troponin I return to nl?
    5-10 days
  71. When does troponin T peak?
    12-48 hours
  72. When does troponin T return to nl?
    5-14 days
  73. What is myoglobin's timing in MI?
    • Initially elevates in 1-4 hours
    • Peaks in 6-7h
    • Returns to nl in 24 hours
  74. When do the troponins appear?
    3-12 hours after onset of MI
  75. When does Ck-MB appear?
    3-12 hours after onset of MI
  76. TX of STEMI
    • MONA
    • Antiplt (ASA, clopidogrel) and anticoag (unfractionated hep, enoxaparin, fondoparinux, or bivalirudin therapy)
  77. CI to BB in ACS
    CHF, bradycardia, heart block
  78. role of CCBs in STEMI
    only in pts who can't take nitrates and BB or in those with CI to these drugs
  79. Reperfusion therapy in ACS
    • coronary angiography and primary percutaneous coronary intervention are superior to thrombolysis in high-volume centers
    • Thrombolytic therapy within 3 hours reduces mortality and limits size of the infarction
    • Statin therapy within days of ACS
  80. M/c thrombolytic agents
    alteplase, reteplase, tenecteplase
  81. Absolute CI to thrombolytic therapy
    • Previous hemorrhagic stroke
    • any stroke within the past year
    • known brain mass
    • active internal bleeding
    • suspected aortic dissection
  82. Relative CI to thrombolytic therapy
    • Known bleeding diathesis
    • trauma within the past 2-4 weeks
    • major surgery within the past 3 weeks
    • prolonged or traumatic cardiopulmonary resuscitation
    • recent internal bleeding
    • noncompressible vascular puncture
    • active diabetic retinopathy
    • pregnancy
    • active PUD
    • current use of anticoag
    • BP >180/110
  83. Cyanotic heart defect
    right to left shunt
  84. Types of cyanotic heart defects
    • ToF
    • Pulmonary atresia
    • Hypoplastic left heart syndrome
    • Transposition of the great vessels
  85. Noncyanotic heart defect causes
    • ASD
    • VSD
    • AV septal defect
    • PDA
    • Coarctation of the aorta
  86. ToF
    • Subaortic septal defect
    • right ventricular outflow obstruction
    • overriding aorta
    • RVH
  87. Pulmonary atresia
    closed pulmonary valve, atrial-septal opening and PDA are present
  88. Hypoplastic left heart syndrome
    Group of defects with a small left ventricle and nl placed great vessels
  89. Transposition of the great vessels
    M/C a complete transposition of the aorta and pulmonary artery
  90. M/C ASD
    osteum secundum
  91. ASD
    opening between right and left atria
  92. AV septal defect
    incomplete fusion of the endocardial cushions, common in Down
  93. PDA
    failure to close or a delay in closure of the channel bypassing the lungs, which allows placental gas exchange during the fetal state
  94. Coarctation of the aorta
    narrowing in proximal thoracic aorta
  95. ToF murmur
    crescendo-descresndo, holosystolic at LSB, radiating to back
  96. Cardiac findings in toF
    Murmur, cyanosis, clubbing, increased RV impulse at LLSB, loud S2
  97. TET spells
    • Medical emergency
    • extreme cyanosis, hyperpnea, agitation
  98. M/C sign of transposition of great vessels
    cyanosis in newborn
  99. M/C heart defect
  100. m/c cause of mitral valve disorder
    congenital defect
  101. m/c cause of aortic valve disorder
    congenital defect
  102. widened pulse pressure
    aortic insufficiency
  103. murmur that is loud with a thrill
    aortic stenosis
  104. Aids to hearing aortic stenosis better
    sitting and leaning forward
  105. aids to hearing aortic regurg better
    sitting and leadnign forward, full exhalation
  106. Aids to hearing mitral stenosis better
    LLD, full exhalation
  107. Pulses large and bounding (murmur)
    aortic insufficiency
  108. aids to haering tricupid regurg better
  109. Tx of heart murmurs
    • surgical repair, replacement of valve, balloon valvuloplasty
    • pts with good exercise tolerance may be tx with diuretics and vasodilators for pulm congestion and with dig or BB for dysrhythmias
    • anticoag therapy for prevention of throboemboli, particularly if afib occurs
  110. Difference in age presentation in the murmurs
    • triscuspid and pulmonic: usually present in infancy or childhood
    • mitral and aortic: usually present in adults
  111. Tricuspid and pulmonic valve murmurs may lead to what?
  112. m/c presentation of pulmonic or tricuspid murmurs
    exercise intolerance
  113. Tx of tricuspid and pulmonic murmurs
    • sodium restriction, diuretics
    • tx pulm HTN with arterial vasodilators or positive inotropic agents
    • definitive: surgery, valvuloplasty, repacement
  114. Causes of sinus tach
    • fever
    • exercise
    • pain
    • emotion
    • shock
    • thyrotoxicosis
    • anemia
    • HF
    • drugs
  115. m/c paroxysmal tachycardia
  116. Class Ia antiarrythmatics MOA
    Na channel blockers, depress phase 0 depolarization, slow conduction, prolong repolarization
  117. quinidine
    Ia antiarrhythmatic
  118. procainamide
    Ia antiarrythmatic
  119. disopyramide
    Ia antiarrythmatic
  120. Uses for Class Ia
    • Supraventricular tachycardia
    • V tach
    • prevention of V fib
    • sxmatic PVCs
  121. Class Ib antiarrythmatics MOA
    shorten repolarization
  122. Class Ib antiarrythmatics indications
    • V tach
    • prevention of V fib
    • sxmatic PVCs
  123. lidocaine
    Class Ib antiarrythmatics
  124. class Ic antiarrythmatics
    depress phase 0 repolarization, slow conduction
  125. Indications for Ic antiarrythmatics
    • Life-threatening vtach or vfib
    • refractory SVT
  126. flecainide
    Ib antiarrythmatic
  127. Propafenone
    Class Ic antiarrythmatic
  128. Class II antiarrythmatics MOA
    beta blockers, slow AV conduction
  129. Class III antiarrythmatics MOA
    prolong action potential
  130. Class III antiarrythmatics indications
    refractory vtach, SCT
  131. amiodarone
    Class III antiarrythmatic
  132. sotalol
    class III antiarrythmatic
  133. dofetilide
    Class III antiarrythmatic
  134. ibutilide
    Class III antiarrythmatic
  135. Class IV antiarrythmatics MOA
    slow CCBs
  136. Inidcations for class IV antiarrythmatic
  137. Class V antiarrythmatics MOA
    • Adenosine: slows conduction time through AV node, interrupts rentry pathways
    • digoxin: direct action on cardiac muscle and indirect action on CV system via ANS
  138. Indications for Class V antiarrythmatics
  139. adenosine
    Class V antiarrythmatic
  140. digoxin
    Class V antiarrythmatic
  141. Causes of atrial flutter
    • COPD
    • CHF
    • ASD
    • CAD
    • Mitral valve disorders
  142. Causes of junctional rhythms
    pts with nl hearts, those with myocarditis, cAD, digitalis toxicity
  143. Mechanical tx of PSVT
    • valsalva
    • coughing
    • breath holding
    • stretching
    • putting head b/w knees
    • applying cold water to face
    • U/L carotid sinus massage
  144. Nonpharm intervention of PSVT
    • surgery or ablation
    • Cardioversion
    • electrical pacing
  145. Meds for PSVT
    • IV adenosine or PO verapmil eliminates most episdoes of PSVT
    • Prevention with diltiazem and/or verapamil or BB
  146. Tx of atrial flutter
    Ibutilide or electric cardioversion
  147. Tx of chronic atrial flutter
    Amiodarone or dofetilide
  148. V tach def
    three or more consecutive PVCs
  149. Causes of Torsades
    • Hypokalemia
    • Hypomagnesemia
    • drugs that prolong QT interval
  150. Brugada's syndrome
    • Genetic disorder
    • M/c in asians and men
    • causes syncope, v fib, and sudden death
  151. tx of PVCs
    BB is pt is sxmatic, class I and III with caution
  152. acute v tach tx
    • lidocaine
    • amidoarone
    • procainamide
    • empiric mag may help
  153. Tx of Brugadas
  154. Tx of torsades
    BB, Mg, temporary atrial or ventricular pacing
  155. Sick sinus syndrome causes
    • digitalis, CCB, BB, smpatholytic agents, and antiarrhythmatic drugs
    • underlying collagen vascular disorder or metastatic disease, surgical injury, or rarely coronar disease
  156. m/c type of cardiomyopathies
  157. causes of DCM
    • excessive alcohol
    • postpartum
    • chemo toxicity
    • endocrinopathies
    • myocarditis
    • idiopathic
  158. Restrictive cardiomyopathy causes
    • amyloidosis m/c
    • fibrosis, infiltration of ventricular wall d/t collagen defect diseases
    • radiation
    • post op changes
    • diabetes
    • endomyocardial fibrosis
  159. m/c presentation of DCM
  160. Cardiac findings in DCM
    S3 gallop, rales, increased jugular venous pressure
  161. M/c presentation of HCM
    dyspnea and angina
  162. Cardiac findings of HCM
    • sustained PMI or triple apical impulse
    • loud S4 gallop
    • variable systolic murmur
    • bisferiens carotid pulse
    • JVP with prominent a wave
  163. Tx of DCM
    • abstain from alcohol
    • tx underly dz
    • supportive tx for CHF
  164. Tx of HCM
    • BB or CCB, disopyramide for negative inotropic effects
    • surgical or nonsurgical ablation of hypertrophic septum may be required
    • dual-chamber pacing, implantable defibrillators, mitral valve replacement
  165. Tx of restrictive cardiomyopathy
  166. Causes of pericarditis
    • viral or bacterial infection
    • autoimmune or connective tissue disease
    • neoplasms
    • radiation therapy
    • chemotherapy or other drug toxicity
    • cardiac surgery
    • myxedema
    • tuberculosis
  167. causes of pericardial effusions
    secondary to pericarditis, uremia, or cardiac trauma
  168. cardiac tamponade
    fluid compresses cardiac filling and impairs cardiac output
  169. Class presenation of pericarditis
    • pleuritic substernal radiating CP relived by sitting updright and leaning forward
    • friction rub
  170. Typical presentation of cardiac tamponade
    • tachycardia
    • tachypnea
    • narrow pulse pressure
    • pulsus paradoxus
  171. Electrical alternans
    patho for effusion
  172. Tx of pericarditis
    • if hemodynamic compromise, pericardiocentesis
    • steroids or NSAIDs
  173. M/c causes of infectious endocarditis
    • staph aureus
    • Group D strep
    • enterococci
    • HACEK
  174. m/c cause of infectious endocarditis in drug users
  175. m/c valve infected in infectious endocarditis in drug users
  176. M/c cause of prosthetic valve endocarditis
  177. Classic presentation of infectious endocarditis
    • palatal, conjunctival, or subungual petechiae
    • splinter hemorrhages
    • osler nodes
    • janeway lesions
    • roth spots
  178. Roth spots
    exudative lesions on the retina (infectious endocarditis)
  179. Janeway lesions
    painless red lesions on the palms or soles (infectious endocarditis)
  180. Osler nodes
    Painful, violaceous, raised lesions of the fingers, toes, or feet (infectious endocarditis)
  181. infectious endocarditis workup
    • three sets of blood cultures at least 1 hour apart before starting abx
    • TEE
    • CXR
  182. Duke criteria
    • Infectious endocarditis
    • 1 major/1 major, 1 minor/three minor
    • Major: two positive blood cultures, evidence of endocardial involvement on echo, development of new regurgitant murmur
    • Minor: predisposing factor, fever >38.8C (100.4), vascular phenomena, immunologic phenomena, positive blood culture not meeting major criteria
  183. Tx of infectious endocarditis
    • Empiric abx at first (vanco plus ceftriaxone)
    • abx prophylaxis
  184. Rheumatic fever
    systemic immune response occuring usually 2-3 weeks following strep pharyngitis
  185. Age group m/c implicated in rheumatic fever
    5-15 yo
  186. Typical lesion of valve in rheumatic fever
    Pervascular granuloma with vasculitis
  187. M/c valve involved in rheumatic fever
    Mitral, followed by aortic
  188. Jones criteria
    • rheumatic fever
    • Two major or one major and two minor
    • Major: carditis, erythema marginatum, subcutaneous nodules, choera, polyarthritis
    • Minor: fever, polyarthalgias, reversible prolongation of PR interval, rapid ESR, CRP
  189. Tx of rheumatic fever
    • Strict bed rest until stable
    • ASA for fever and joint problems
    • Corticosteroids for joint sx
    • IM PCN for documented strep infection (erythromycin if PCN allergic)
  190. Prevention of recurrence of rheumatic fever
    benzathine PCN q4w
  191. m/c pattern of PAD
    • Type 3
    • affects aorta, iliac, femoral, popliteal and tibial arteries
  192. First sx of PAD
    loewr leg pain with exercise that is relieved with rest (intermittent claudication)
  193. leriche's syndrome
    ED in the presence of iliac artery disease
  194. Acute arterial occlusion of lower extremities
    • pain
    • pallor
    • pulselessness
    • paresthesias
    • poikiloterhmia
    • paralysis
  195. Lab findings in PAD
    ABI < 0.9 indicates significant disease
  196. Tx of PAD
    • Progressive exercise
    • Lipid loewring meds
    • Pletal is main tx (Cilostazol)
    • Antiplatelet therapy in all pts without CI
    • Tx ED
    • Thromboendarterectomy, embolectomy, thrombolytic therapy,
  197. m/c vein affected in varicose veins
    long saphenous
  198. Tx of varicose veins
    • Graduated elastic stockings
    • Leg elevation and regular exercise
    • Tx of ulcers
    • radiogrquency or laser ablation, compression sclerotherapy, surgical stripping of vein
  199. Thrombophlebitis
    Partial or complete occlusion of vein and inflammatory changes
  200. superficial thrombophlebitis causes
    • spontaneous or following trauma
    • frequently at PICC sites
  201. M/c location of DVT
    lower extremities and pelvis
  202. Presentation of superficial thrombophlebitis
    • dull pain, erythema, tenderness, and induraction of involved vein
    • no sx
  203. m/c location for superficial thrombophlebitis
    long saphenous vein
  204. Classic presentatio of DVT
    swelling of involved area with heat and redness over site
  205. Preferred study for DVT
    • duplex US
    • d-dimer...if neg, no need for US
  206. most accurate method for definitive dx of DVT
    venography, but it has increased risk and is rarely needed
  207. Tx of superficial thrombophlebitis
    bed rest, local heat, elevation of extremity, and NSAIDs
  208. Tx of DVT
    LMWH, or hep followed by warfarin
  209. Chronic venous insufficiency
    Loss of wall tension in veins, which results in stasis of venous blood
  210. Common comorbidities with chronic venous insufficiency
    • DVT
    • leg injury
    • varicose vein
  211. Presentation of chronic venous insufficiency
    • Progressive edema starting at the ankle
    • itching, dull pain with standing and pain with ulceration
    • skin is shiny, thin, atrophic with dark pigmentary changes and subcutaneuos induration
  212. Tx of chronic venous insufficiency
    elevate legs, avoiding sitting or standing for long periods of time
  213. Tx of stasis dermatitis
    • wet compresses and hydrocortisone cream
    • if chronic, add zinc ocide with ichthammol and an antifungal cream
  214. GCA
    inflammatory condition involving medium and alrge vessels
  215. Lab findings in GCA
    • high ESR and CRP
    • normochromic normocytic anemia and thrombocytosis
    • some have elevated alk phos
  216. M/c cause of aortic aneurysm
  217. Causes of aortic aneursym
    • atherosclerosis
    • congenital
    • syphilis
    • GCA
    • vasculitis
    • trama
    • Marfans/Ehler-Danlos
  218. M/C location for aneursym
  219. Most effective medication for converting atrial tachycardia to NSR
  220. Mitral stenosis often occurs with what cardiac problem in pts with a hx of rheumatic heart disease?
    Tricuspid stenosis
  221. Side effects of CCBs
    HA and peripheral edema
  222. First degree AV block tx
    None, just monitor
  223. Best HL drug in pregnancy
    Welchol (Coleselvem)
  224. When should ASA and antiplt medicines be stopped in the event of a major surgery?
    D/C 5-7 days prior to surgery
  225. m/c EKG findings of ASD
  226. radiation of aortic insufficiency murmur
    LLSB, apex
  227. Pulsus paradoxus
    • decrease in systolic arterial pressure of greater than 10 mmHg.
    • accentuation of the normal decrease in systolic arterial pressure of less then 10mm Hg that normally accompanies inspiration
  228. How to better hear MVP
    have pt stand
  229. causes of high output heart failure
    • Beriberi
    • severe IDA
    • Thyrotoxicosis
    • AV shunting
  230. EKG in VSD
  231. What is the most common clinical cardiac abnormality that is associated with acute rheumatic heart disease?
  232. tx of chronic SVT
  233. management of WPW syndrome
  234. According to the most recent American College of Cardiology/American Heart Association Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation MI recommendations, an EKG should be performed on patients with a clinical suspicion for acute coronary syndrome within how many minutes of their arrival to the emergency department?
    10 mins
  235. Prinzmetal's angina is common with what comorbidities?
    migraine cephalgia and Raynaud's phenomenon
  236. causes of bigeminy
    thiazide diuretic use leading to hypokalemia
  237. In MI pts, how soon should they have PCI?
    Within 90 mins of sx
  238. Classic presentation of ASD
    fixed and widely split S2, a right ventricular heave, and a systolic ejection murmur present.
  239. How do you increase HDL in low risk pt?
  240. Two electrolyte disorders that can inflict a ventricular tachycardia?
    Hypomagnesia and hypokalemia
  241. tx of new onset aflutter in pts with hx of mitral disease
    wafarin plus cardioversion
  242. tx of sxmatic HCM
  243. tx of prinzmetals angina
    CCB and long term nitrate therapy
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