IP Final

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  1. Risk factors for Venous Thromboembolism
    • Age
    • History of VTE
    • Turbulent blood flow/Venous stasis
    • Vascular injury
    • Hypercoagulable states
    • Drug Therapy (estrogens/HIT)
  2. Fate of Thrombus
    • Propogation - platelets and fibrin accumlate
    • Embolization - thrombi dislodge and travel to other sites in vasculature
    • Dissolution - because of fibrinolysis, thrombi can shrink and disappear
    • Organization and Recanalization - older thrombi contain endothelial cells, smooth muscle cells, and fibroblasts. Cappillary channels form and partially reestablish the flow through original lumen
  3. Diagnostic test for DVT
    Duplex Ultrasonography - measures rate and direction of blood flow and visualizes clot formation

    Venography - Gold standard but NOT USED as it is too invasive. can cause nephrtoxicity due to radiocontrast dye
  4. Diagnostic test for PE
    Ventilation-Perfusion (V/Q) scans - assess air flow through lungs (ventilation) and blood flow (perfusion)

    Spiral Computerized Tomography (CT) scans - identify emboli in pulmonary arteries

    Angiography - Gold statndard NOT USED too invasive
  5. Elevated D-Dimer
    High sensitivity - no false negativity test (negative D-dimer confirms pt does NOT have DVT/PE)

    High specificity - possible false positive test (does not always mean pt has VTE)
  6. NO pharmco for VTE prophylaxis
    • Warfarin use with INR >1.4 or on anticoag therapy
    • Recent intraocular or intracranial surgery
    • Thrombocytopenia (platelets <50,000)
    • Active Bleeding
    • Chronic or active liver disease
    • Receiving comfort
    • <40 years old, healthy, fully ambulatory
    • imminent invasive procedure
  7. Prophylaxis doses for LMWH
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    • knee surgery - dalteparin: 5000 IU q24hrs
    • trauma - dalteparin: 5000 IU q24hrs
  8. Treatment doses for LMWH
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  9. Warfarin major adverse effects
    • Bleeding
    • Skin necrosis
    • Purple toe syndrome
  10. Dose adjustments for DTI's
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  11. 4 T's test for probable HIT
    • Thrombocyopenia
    • Timing
    • Thrombosis
    • Other causes
  12. Predisposing risk factors for IE
    • Presence of prosthetic valve
    • Previous endocarditis
    • Congenital heart abnormalities
    • Rheumatic heart disease (from S.pyogenes "strep throat")
    • Hypertrophic cardiomyopathy
    • IV drug use (IVDU)
    • Mitral valve prolapse w/regurgitation (mitral valve goes upward causing regurgitation)
  13. Titration of warfarin therapy
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  14. Skin symptoms for IE
    • Splinter hemorrhages - hemorrhage under nailbeds of finges/toes
    • Petechiae - small red painless lesions
    • Osler's nodes - red or purple, painful, SQ nodules
    • Janeway lesions - non-tender, red, hemorrhagic lesions, found on palms or soles
    • Roth spot's - retinal infarct
  15. Indications for surgery for IE (nonpharmcotherapy)
    • Persistent vegetation (despite prolonged antibiotic treatment)
    • Valve dysfunction
    • Abscess
    • Prosthetic valve endocarditis caused by resistant microorganism/fungus
  16. Diagonistic tests for IE
    TTE - echo taken from outside of body (transthoracic echocardiogram)

    TEE - probe inserted down the esophagus, close to the heart. PREFERRED over TTE because obtains higher sensitivity (transesophageal echocardiogram)
  17. General principles for treatment for IE
    • High does therapy
    • Parenteral (IV) therapy
    • Bactericidal therapy
    • Count days of therapy from 1st day of therapy until blood cultures change to negative
  18. Streptococci
    • aerobic
    • gram (+) cocci
    • catalase (-)
    • alpha hemolytic
    • *allergy to penicillin then sub VANCO for penicillin/ceftriaxone
  19. Enterococci
    • aerobic
    • gram (+) cocci
    • catalase (-)
    • *allergy to penicillin then sub VANCO for penicillin/ampicillin AND extend for 6 weeks
    • no single agent is bactercidal so give gentamicin with penicillin/ampicillin/vanco for synergy
    • resistant to gentamicin then give streptomycin
    • VRE - use linezolid, quinupristin/dalfopristin, daptomycin
  20. Staphylococci
    • aerobic
    • gram (+) cocci
    • catalase (+)
    • coagulase (+) - S.aureus
    • coagulase (-) - S.epidermis, S.lugdunensis
  21. Treatment Staphylococci
    • w/o prosthetic valve
    • nafcillin or oxacillin +/- gentamicin
    • *penicillin allergy SUB cefazolin OR vanco for naficillin
    • *MRSA or MRSE sub vanco for naficillin

    • w/prosthetic valve
    • nafcillin or oxacillin + rifampin + gentamicin
    • *MRSA or MRSE sub vanco for naficillin/oxacillin
    • if within 1 year of surgery assume MRSA or MRSE
  22. HACEK
    • gram (-) rods
    • treat - ceftriaxone
    • 4 weeks with native valve
    • 6 weeks with prosthetic valve
    • Haemophilus, Acintobacillus, Cardiobacterium, Eikenella, Kingella
  23. Prophylaxis Endocarditis ORAL treatment
  24. Prophylaxis Endocarditis NO oral treatment
    • ampicillin
    • cefazolin
    • ceftriaxone
  25. Prophylaxis Endocarditis ORAL treatment and ALLERGY penicillin/ampicillin
    • cephalexin
    • clindamycin
    • azithromycin
    • clarithromcycin
  26. Prophylaxis Endocarditis NO oral treatment and ALLERGY penicillin/ampicillin
    • cefazolin
    • ceftriaxone
    • clindamycin
  27. Nonmodifiable risk factors for strok
    • age
    • sex
    • race
    • family history of stroke
    • low birth weight
  28. Modifiable risk factors for stroke
    • Hypertension - most important risk for ischemic stroke
    • Atrial fib - most important and treatable cardiac cause of stroke, also 5X risk for stroke
    • history of stroke or transient ischemic attack (TIA)
    • smoking - doubles person risk of stroke
    • diabetes
    • dyslipidemia
  29. 5 cardinal symptoms of stroke
    • weakness
    • speech impairment
    • vision impariment
    • headache
    • dizziness
  30. subarachnoid hemorrhage
    trauma or rupture of aneurysm
  31. intracerebral hemorrhage
    blood pools in brain parenchyma (mass effect can occur from the pooled blood pushing against tissue)
  32. subdural hemorrhage
    most often caused by trauma to the head
  33. stroke occured in posterior circulation (occipital lobe)
    signs of: vertigo, double vision
  34. stroke occurred in anterior circulation (frontal lobe)
    Signs: aphasia (language impairment)
  35. CT scan for stroke
    • gold standard
    • ischemic - dark spot (decreased blood flow)
    • hemorrhagic - white spots (increased blood)
  36. Nonpharmco treatment Stroke
    • ischemic stroke - 1st line craniextomy, 2nd line carotid endarterectomy/stenting
    • hemorrhagic stroke - clip or ablate aneurysm, external ventricular drainage (EVD) to drain pool blood
  37. Acute management of ischemic stroke
    • Aspirin, and tPA
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  38. Treatment for Delayed cerebral ischemia (DCI)
    • DCI occurs from subarachnoid hemorrhage due to aneurysm.
    • To treat:

    • Nimodipine (1st line CCB) reduces vasospasms
    • Labetalol (2nd line b-blocker)
  39. Target BP for Ischemic stroke pts w/HTN
    • pt receiving tPA - BP <180/105
    • pt NOT receiving tPA - BP <220/120

    • First line agents to control BP for stroke pts
    • -Nicardipine (easy titrate, predictable)
    • -Labetalol (pts w/A-fib, or on B-blocker previously)
  40. CHADS2
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    • *this is a risk assesment for pts w/A-fib to calculate risk for cardioembolic stroke
  41. Interpret CHADS2 score
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  42. MATCH study
    • compared use of clopidogrel + aspirin VS clopidogrel alone.
    • result no benefit but serious bleeding with combo
    • for secondary prevention of stroke
  43. CHARISMA study
    • compared use of clopidogrel + aspirin VS aspirin alone.
    • result no benefit but serious bleeding with combo
    • for secondary prevention of stroke
  44. Primary prevention of stroke
    • aspirin based on 10-year risk for CV event
    • anticoahulation medication based off of CHADS2 score
  45. ESPRIT study
    • stated that ER dipyridamole + aspirin more effective than aspirin alone
    • aggrenox is dipyridamole (200mg) + aspirin (25mg) the trial also stated to add aspirin 81mg to get sufficient aspirin therapy
  46. PRoFESS study
    showed that aggrenox is not superior to clopidogrel
  47. Sexondary prevention of CARDIOEMBOLIC stroke
    • warfarin drug of choice
    • target INR 2.5-3.5 (Mecahnical heart valve )
    • target INR 2-3 (pt w/A-fib)
    • unable to take warfarin, aspirin mono recommended
    • dabigatran & rivaroxaban also (dabigatran > warfarin, rivaroxaban = warfarin)
    • *cardioembolic stroke - pts w/A-fib or mechanical heart valve
  48. 3 mechanisms that cause arrhythmias
    • enhanced/abnormal automaticity
    • triggered automaticity and afterdepolarizations
    • reentry
  49. abnormal automaticity from SA node include:
    • hypoxia
    • ischemia
    • excess catecholamine
  50. enhanced/abnormal automaticity
    • pacemaker cells: increase in resting membrane potential triggers AP then propageted to heart to cause arrhythmia
    • ventricular cells depolarization produces abnormal automaticity (increase phase 4 to trigger abnormal AP)
  51. Early AfterDepolarizations (EAD)
    • occur when HR is slow
    • occur in cardiac cells
    • prolonged AP
    • can trigger extrasystole (premature ventricular contraction)
    • 3 or more extrasystole = VT
    • more common in purkinje cells and midmyocardial cells
    • class 1A antiarrhythmics increase EAD may occur
  52. Risk Factors for Arrhythmias
    • age
    • cardiac surgery
    • sleep apnea
    • electrolyte abnormalities (hypoK or hypMAG)
    • thyrotoxicosis
    • meds that cause QT prolongation (torsades)
    • meds that increase HR (caffine, nicotine)
    • underlying cardiac abnormality or structural heart disease (MI, HF, cardiomyopathy, CHD, ischemia, mitral valve disease)
  53. Delayed AfterDepolarizations (DAD)
    • occur when HR is high
    • associated w/elevated intracellular Ca levels
  54. Reentry 3 requirements
    • unidirectional block
    • timing b/t AP critical
    • duration of refactory period
    • *conditions that promote reentry - prolong conduction time or shorten absolute refactory period
  55. Sinus bradycardia
    • firing rate of SA node descreases
    • decreases heart rate
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  56. Sinus tachcardia
    • firing rate of SA node increases
    • increases heart rate
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  57. premature Atrial depolarization (premature atrial contraction PAC)
    • shortened interval b/t beats
    • p waves differ from other p waves
    • QRS complex remains normal
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  58. premature Ventricular depolaization (premature ventricular contraction PVC)
    • premature excitation occurs at ecotopic focus of ventricles
    • premature QRS and preceding QRS shortened (middle part of graph)
    • reg QRS before premature QRS is prolonged (first part of graph)
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  59. Paroxysmal tachycardia
    • rapid firing of ecotopic pacemaker
    • triggered activity secondary to afterpotentials
    • impulse that circles
    • * paroxysmal - sudden onset then dissaperance
  60. paroxysmal supraventricular tachycardia (PSVT)
    GLOBAL reentry
    • wolf-parkinson-white syndrome (WPW)
    • atrioventricular nodal reentrant tachycardia (AVNRT) - reentry next to AV
    • atrioventricular reentrant tachycardia (AVRT) - reentry located AV valvular rings
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  61. paroxysmal supraventricular tachycardia (PSVT)
    LOCAL reentry
    • sinus nodal reentrant tachycardia (SNRT)
    • intraatrial reentrant tachycardia
    • *reentrant circuit does not involve AV node or accessory pathway
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  62. paroxysmal ventricular tachycardia
    • originates from extopic focus in ventricles
    • has repeated bizarre QRS
    • precursor to ventricular fibrillation
    • NO P waves because NO atrial contraction
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  63. Atrial Fibrillation
    • does not contribute to ventricular filling
    • atria uncoordinated ripling motion (quivering)
    • NO P wave
    • replaced by F waves
    • blood stasis can occur results on formation of clot
    • *atrial flutter - reentry loop and pattern of AV conduction more normal than A-fib
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  64. Ventricular fibrillation
    • down slope T wave in ECG
    • excitability of cardiac cells varies spatially (multiple conductions at different times)
    • lead to loss of consciousness w/in secs
    • irregular, continuous uncoordinated twitching of ventricles pumps NO blood
    • death occurs unless rhythm goes back to normalImage Upload
  65. 1st degree AV block
    • prolonged PR interval
    • occurs above bundle of hisImage Upload
  66. 2nd degree AV block
    • NOT all P waves are followed by QRS
    • ratio of P waves to QRS 2:1, 3:1, or 3:2
    • block located above or belove bundle of his
    • Image Upload
  67. 3rd degree AV block
    • complete heart block
    • cannot transverse AV conduction
    • distal to bundle of his
    • atrial and ventricular rhythms entirely independent
    • *a permanent pacemaker may be added to prevent recurrences
    • Image Upload
  68. Diagnosotic testing for arrhythmias

    holter monitoring - small device hooked up to the pt for 24hrs to measure ECG throughout the entire day

    electrophysiologic studies (EPS) - used to evaluate efficacy of antiarrhythhmic drugs
  69. Nonpharmcotherapy arrhythmias
    • Vagal maneuvers - surgical procedures such as AV nodal modification
    • Electronic pacemaker - attempts to mimic the action of natural pacemaker
    • External defribrillators - devices that deliver electrical shock to heart to restore normal cardiac rhythm
    • Implantable cardioverter defibrillators - surgically implanted in pt and used for Ventricular Tachycardia (VT)
  70. Class 1A
    • prolong cardiac AP
    • increase effective refactory period
    • decrease conduction velocity
    • prolong QTc interval
    • *procainamide - black box warning - can lead to positive antinuclear antibody (ANA)
  71. Class 1B
    • shorten cardiac Ap
    • shorten refractory period
    • does NOT effect conduction velocity
    • indicated for ventricular arrhythmias
  72. Class 1C
    • MARKEDLY DECREASES conduction velocity
    • slow conduction in fast response tissues
    • variable effects on APD
    • insignifcant effects on refractory period
    • *dissociate more slowly from Na channels than class 1A/1B making class 1C MORE POTENT
    • *flecainide - black box warning previous MI avoid flecainide
  73. Class II antiarrhythmics
    • B-blockers
    • treats rate control of A-fib
    • decreases pacemaker potential decreasing sinus rate
    • increase in AV nodal conduction time (increases PR interval)
    • increases AV node refractoriness
    • interference in catecholamines opening of Ca channels resulting in decrease Ca current into cells
    • *valuable effects slowing sinus rate and slowing AV node conduction time (increasing the conduction time b/t PR interval)
  74. Class III antiarrhythmics
    • blocks outward rectifying K channels resulting in longer refractory period and widening of QT interval
    • longer refractory leads to slower cardiac AP rate
    • prolong QTc interval
    • *dofetilide - black box warning - contraindicated pts w/ CrCl <20
    • *
  75. Amiodarone
    • has Class I (Na blockade), Class II (B-blocker), and Class IV (Ca blockade) effects
    • contains Iodine (dronedarone does NOT contain Iodine)
    • causes hyper/hypo thyroidism
    • can cause pulmonary toxicity (pulmonary fibrosis, pneumonitis)
    • can cause liver disease
  76. Class IV antiarrhythmics
    • CCBs selectively block L-type channels that results in:
    • slowing conduction
    • prolonging refractoriness
    • decrease in automaticity
  77. adenosine
    • identical to adenosine produced endogenously
    • activates acetylcholine-sensitive K+ current, shortening atrial AP
    • reduces Ca currents by reversing effect of increased cAMP
    • collectively this RESULTS to:
    • increases AV nodal refracotriness
    • decreases DAD due to sympathetic stimulation
    • *adenosine is useful for acute termination of re-entrant supraventricular arrthymia due to AV nodal conduction
  78. atropine
    • potent antagonist at M2
    • M2 cholinergic receptors decrease SA nodal activity and slow heart rate
    • blockade of receptors with atropine may reverse bradycardia
  79. digoxin
    • causes hyperpolarization
    • increase in AV nodal refractoriness
    • shortening of atral AP
  80. CYP2D6 (arrhythmia)
    • Class I: quinidine, propafenone
    • B-blockers: propranolol, metoprolol
  81. CYP3A4 (arrhythmia)
    • amiodarone
    • dronedarone
    • rivaroxaban (30%)
    • CCBs
  82. CYP2C9 (arrhythmia)
    warfarin (S-enantiomer)
  83. renal adjustments for antiarrhythmic and anticoagulants
    • dofetilide (CrCl < 20 contraindicated)
    • sotalol (CrCl <40 contraindicated)
    • dabigatran (CrCl 15-30 give 75mg BID, CrCl <15 AVOID)
    • rivaroxaban (CrCl 15-50 15mg QD, CrCl <15 AVOID) 70% renal excretion
  84. Drugs that cause Torsades de Pointes
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  85. P-glycoprotein
    • GI tact: P-gp pumps drugs back into GI lumen prevents absorption
    • Kidneys: P-gp pumps drugs from blood into urine
    • Blood brain barrier: P-gp prevents drugs from going into CNS by pumping drug back into blood
    • P-gp inhibitor: causes Cl to decrease, AUC increase
    • P-gp inducer: causes Cl to increase, AUC decrease
  86. complimentary medications for arrhythmia
    • omega-3 fatty acids
    • magnesium - improve rate controlling effects of digoxin and should only be used to help digoxing effects
    • avoid: cardiac glycosides - lilly of the valley, oleander, ouabain
  87. sinus tachycardia treatment
    • B-blocker: esmolol, metoprolol, propranolol
    • CCBs: diltiazem, verapamil
  88. sinus bradycardia treatment
    • atropine
    • implantation of pacemaker
  89. acute management of PSVT
    • severe pts symptoms (syncope, angina, HF, hypotension): DCC (direct current cardioversion) treatment of choice
    • drug therapy used: adenosine
  90. Chronic prevention of PSVT
    • digoxin:
    • B-blockers: esmolol, metoprolol, propranolol
    • non-dihydro CCBs: diltiazem, verapamil
    • type Ic: flecainide, propafenone
    • *Severe and frequent episodes: radiofrequency ablation therapy to destroy accessory pathway, for WPW do not receive ablation then use amiodarone
  91. A-fib classification
    • acute: within last 48 hrs
    • "lone": pt < 60 years w/o underlying heart disease
    • non-valvular: no presence of valve disease
    • recurrent: 2 or more episodes
    • paroxysmal: intermitten, sudden onset and spontaneous termination, self-terminatine < 7days
    • persistent: NO spontaneous termination in < 7 days
    • permanent: rhythm does NOT terminate despite electric/pharmco treatment
  92. Acute ventricular rate control (A-fib) treatment
    • pt has HF: IV digoxin or IV amiodarone
    • pt w/o accessory pathway/HF/hypotension: IV B-blocker, IV non-CCB
    • pt w/accessory pathway: IV amiodarone
  93. DCC use for acute rate control A-fib
    • first line therapy to immediately restore sinus rhythm
    • pt hemodynamically instable: severe hypotension, angina, pulmonary edema
  94. Chornic ventricular rate control (A-fib) treatment
    • LVEF > 40%: B-blocker, non-CCB, rate control not achieved then use digoxin
    • LVEF < 40%: B-blocker (preferred), digoxin, amiodarone (alternative) * AVOID non-CCB
  95. Acute rhythm control (A-fib)
    • DCC: more effective than pharmco therapy
    • ibutilide
    • dofetilide
    • flecainide
    • propafenone
    • amiodarone
    • pharmco cardioversion most effective when initiated w/in 7 days
    • *pt has structural heart disease (LVEF<40%) only amiodarone or dofetilide
  96. Chronic rhythm control (A-fib) treatment
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  97. AV block treatment
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  98. Premature ventricular contraction (PVC) treatment
    • pt is asymptomatic: NO treatment
    • pt is symptomatic: B-blocker, if contraindicated for B-blocker then give amiodarone or dofetilide
  99. Ventricular Tachycardia
    • DCC: for severe symptoms (hypotension, angina, pulmonary edema)
    • IV amiodarone: first line
    • IV procainamide: alternative agent
    • IV sotalol: alternative agent
    • ICD: implantable cardioverter-defibrillator, nonpharmco
    • catheter ablation: nonpharmco
    • *pt has not pulse then pt treated as if they have V-fib
  100. Torsades de Pointes (TdP)
    • underlying cause delayed ventricular repolarization
    • due to blockade of potassium efflux
    • provokes EAD
    • triggers multiple reentry loops in ventricle
    • *IV magnesium sulfate treats TdP by supressing EADs
  101. Ventricular Fibrillation
    • NO cardiac output and cardiovascular collapse (cardiac arrest)
    • 1st: CAB (chest compressions, airway, breathing)
    • defibrillator: if availabe will analyze rhythm if needed defib
    • If pulseless persists after 1-2 shocks + cpr then give drugs
    • Vasopressors: epinephrine, vassopressin
    • IV Epinephrine: 1mg (every 3-5mins)
    • IV vasopressin: 40IU (one-time)
    • IV amiodarone: if abnormal rhythm persists
    • NO IV access: LEAN (liodcaine, epinephrine, atropine, naloxone)
  102. electrophysiologic effect of antiarrthymia drugs
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Card Set:
IP Final
2011-12-12 16:23:53
Regis University

IP Final
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