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Major Case Presentation Final Version

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Major Case Presentation at Kingsbrook Jewish Medical Center

Major Case Presentation at Kingsbrook Jewish Medical Center
Preceptor: Dr.Henry Cohen

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  • parts of the spectrum of clinical manifestations of acute coronary syndrome (ACS)NSTE MI differs from unstable angina in that ischemia is severeenough to produce myocardial necrosis, resulting in the release of adetectable amount of biochemical markersIschemia produces myocardial necrosisRelease large amount of biochemical markers into the blood streamTroponin I or TCK-MB, mainly troponin I or T,and creatine kinase myocardial band (CK MB) from the necroticmyocytes into the bloodstream
  • IN STEMI you have complete occlusion of the artery. End with “Leading to an imbalance in the myocardial oxygen demand and supply”
  • The red are the key risk factors and diagnostic factors when performing H/P
  • CBCMeasure Hgb and Hct Secondary cause of NSTEMIAcute blood loss AnemiaAssess thrombocytopenia estimate bleeding riskBUN and ScrDose renally adjusted drugsLFTsFor drugs that undergo hepatic metabolismCXRR/O pneumonia, pneumothorax, and esophageal ruptureCan mimic cardiac ischemia
  • P2Y12= Purinergic receptor subtype 12
  • NO Monitoring parameter noted
  • The exception of alpha 2 agonist interaction are: Apraclonodine,Brimonidine
  • Secondary endpoint: Severe ischemia, heart failure, and the need for revascularization 

Major Case Presentation Final Version Major Case Presentation Final Version Presentation Transcript

  • Spectrum of Myocardial Infarction
    Munzur Morshed, Pharm D. candidate 2011Arnold & Marie Schwartz College of Pharmacy and Health SciencesKingsbrook Jewish Medical CenterCritical Care -Advance Pharmacy PracticeDr.Henry Cohen
  • Objectives
    Provide brief overview of the patients case
    Discuss the disease state, presentation and signs and symptoms
    Explain the non-pharmacological and pharmacological management options
    Display the place in therapy of each medications
    Provide a synopsis of a major landmark trial
    Discuss the patient’s appropriate management options
    2
  • Case Presentation:History of present illness
    MAGN is a 70 y/o African American female who developed
    acute respiratory distress while in the rehab. The patient
    was found to be using her abdominal muscle to breath with
    slurry speech, tachypnea, and tachycardia. Code 66 was
    called after sedating the patient and she was subsequently
    intubated. The patient was then sent to the CCU following
    intubation due to development of acute respiratory distress
    for more close monitoring.
    3
  • Case Presentation:History of present illness cont..
    PMH: HTN, CAD S/P CABG, PVD, DM, right foot
    ulcer, osteomyelitis of the 3rd and 5th right toe.
    FH:Insignificant
    SH:Insignificant
    NKDA
    VS: Temp: 96 ° F, BP: 193/120 mm Hg, HR: 146 BPM RR: 22 BPM, O2 Sat: 66%,Pain scale: 0/10
    4
  • Case Presentation: Physicals
    Physical Findings:
    ABW: 165lb (75kg), Height: 5 feet 4.96 inch, IBW: 56.9 kg, AdJBW: 64.14kg.
    Mental status: Speech clear, oriented X 3, responds appropriately to questions
    HEENT: No nasal discharge, intubated, no airway obstruction
    Lungs: No wheezing, mild rales bilateral middle, mild rhonchi middle chest
    CV: Normal rate, normal rhythm, normal S1, normal S2, no murmur no rub
    Extremities: Good pulses in all extremities, no swelling/tenderness in the extremities, pitting edema half way to knees
    GI: Normal BS, soft, no abdominal tenderness.
    CXR: Persistent infiltration in the right lower lung zone
    EKG: Unremarkable
    ECHO: Moderate mitral valve regurgitation, Normal LV Ejection fraction, Mild concentric left ventricular hypertrophy, Mild aortic valve sclerosis without stenosis.
     
     
     
     
    5
  • Case Presentation: Lab Findings
    Na: 142 mEq/L
    K: 4 mEq/L
    Cl: 101 mEq/L
    CO2: 27 mEq/L
    SCr: 1.2 mg/dL
    BG :196 mg/dL ↑
    HgA1C: 6.6% ↑
     
    CKMB: 43.5 U/L ↑
    Troponin: 5.5 ng/mL ↑
     
    ABG analysis pCO2: 36, pO2: 58↓, HCO3: 28.7 ↑
    WBC: 13.7 x 10^3/mm^3 ↑
    Hgb: 10.6g/dL ↓
    Hct: 32% ↓
    Plt:363 x 10^3/mm^3
    AST: 41 U/L
    ALT: 30 U/L
    6
  • Case Presentation: Medications PTA
    Aspirin (Ecotrin) 325mg PO QAM
    Clopidogrel(Plavix) 75mg PO QAM
    Zosyn 2.25g Q6H QD
    Ciprofloxacin 200mg Q12H QD
    Vasotec 10mg PO QAM
    Januvia 50mg PO QAM
    Lantus 10 units SQ QD
    Pepcid 20 mg PO QAM
    Glucotrol 10mg PO AC Breakfast
    Heparin 5600 units PO Q8H
    Novolog TID
    Percocet 1 T PO Q6H
    Tylenol 650 mg PO Q 4H
    7
  • Diagnosis
    Non- ST Elevated Myocardial Infarction
    8
  • Non ST-elevation Myocardial Infarction
    Acute ischemic event that causes myocardial necrosis
    Detected by elevation of serum cardiac biomarkers and changes in ECG
    Troponin
    CK-MB
    ECG
    9
  • Acute Corononary Syndrome- Pathway Approach
    http://www.aic.cuhk.edu.hk/web8/corona5.gif
    10
  • Pathophysiology
    • Gradual buildup of cholesterol and fibrous tissues in the arteries
    • Most predominant cause of unstable ACS is due to the rupture of the plaque
    • Plaques that occludes up to 70-90% of the artery are more likely to rupture
    • After the plaque ruptures- formation of a thrombi is seen on the plaque
    • Leading to the clotting cascade
    • Impairment of the blood flow and if it is long enough
    • Ischemic cascade begins and necrosis of the myocardium is seen
    11
  • Epidemiology
    1 per 3 American has an underlying CVD
    Estimated that 2/3 of ACS presents as NSTEMI or unstable angina
    NSTEMI accounts for 1.5 million hospital admission per year
    Percentage of patients with diagnosis of NSTEMI is increasing dramatically
    Sensitive assays for MI, available earlier pharmacotherapy
    12
  • Etiology
    Common
    Deprivation of oxygen in the myocardium
    Adhesion, activation of plateletsPreventing blood flowresulting in myocardial ischemia
    Rare
    Progressive atherosclerosis
    Recreational drug use
    Inflammation of the arteries
    Extrinsic cause
    13
  • Risk Factors
    Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
    14
  • Clinical Presentation
    Sheridan PJ, Crossman DC. Critical review of unstable angina and non-ST elevation myocardial infarction. Postgrad Med J. 2002;78:717-726
    Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
    15
  • Diagnostic Tests
    Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
    Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
    16
  • Diagnostic Tests Continued
    Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
    Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
    17
  • Prognosis/Goals of Treatment
    Goals of Treatment
    Prognosis
    High risk of morbidity and death from future events
    Rate of death is 4-6 times higher compared to the general population
    Risk of the mortality and morbidity depends on the patients risk factor
    Provide early restoration of blood flow to the infarct-related artery to prevent infarct expansion
    Relieve ischemia and pain
    Prevention of coronary artery reocclusion
    Relief of ischemic chest discomfort
    Prevention of death and other complications
    18
  • General Approach to treatment
    Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
    19
  • Risk Stratification
    Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
    20
  • Non-Pharmacologic Management
    • Intranasal Oxygen
    • Oxygen saturation is < 90%
    • PCI or CABG
    • Early treatment for high risk patients
    • Consider in patients with moderate risk
    • Benefit
    • Results in fewer MI’s
    • Less hospital readmissions for a recurrent MI’s
    • Less need for an additional revascularization following hospitalization
    • Risk (1:1,000 patients)
    • Bleeding
    • Infection
    • Pain at site of insertion
    • Damage to the blood vessels
    • Buildup of blood and fluid in the pericardium
    • Much higher in patients who has
    • Diabetes
    • CKD
    • Age > 75
    Bavry DA, Kumbhan DJ, Rassi AN, et al. Benefit of early invasive therapy in acute coronary syndromes: A meta-analysis of contemporary, randomized clinical trials. J Am Coll Cardiol 2006;48:1319–1325
    21
  • The Current Position
    • PCI -feasible and safe to do so
    • Straight, quick, and performed at low risk
    • Performed for one or stenosed vessels
    • Not for multiple stenosed vessels
    • Greater risk of restenosis
    • CABG- for multiple-vessel stenosis
    • Greater chance of achieving full revascularization
    • Choices can be institution specific
    • Easier to proceed with PCI than to wait for an operation
    Gunn J et al. Revascularization for Acute Coronary Sundromes:PCI or CABG? Heart 2003 89: 967-970
    http://0.tqn.com/f/p/440/graphics/images/en/19006.jpg
    22
  • Pharmacologic Therapy
    23
  • Aspirin
    Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010
    24
  • Aspirin cont….
    Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
    25
  • Thienopyridine
    Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010
    26
  • Plavix
    Reserved for patients allergic to Aspirin
    Trials shows that the addition of Plavix to Aspirin is safe and efficacious
    Commit Trial
    Adding Plavix to Aspirin prevents 10 major vascular events per 1000 treated
    Patients scheduled for CABG
    Best not to administer Plavix until procedure is complete
    If Plavix is already administered
    Hold dose for 5-7 days prior to procedure
    Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
    27
  • Plavix
    Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
    28
  • Plavix cont…
    Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010
    Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
    29
  • GP IIb/IIIa Receptor Inhibitor
    Recommended for HIGH risk patients
    Patient undergoing PCI
    Continued or recurrent ischemia despite treatment
    Aspirin
    Plavix
    Anticoagulant
    Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
    30
  • GP IIb/IIIa Receptor Inhibitor cont…
    Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010
    31
  • GP IIb/IIIa Receptor Inhibitor cont…
    Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
    32
  • Anticoagulants Cont…
    Invasive strategy is selected
    Enoxaparin, UFH, Bivalirudin, and fondaparinux
    • If heparin continue dose for 48 hours
    • Enoxaparin or Fondaparinux
    • Administer dose for a maximum of eight days
    Conservative strategy
    Preferred: Lovenox or Fondaparinux
    Fondaparinux if increase risk of bleeding
    If CABG planned
    Fondaparinux
    33
  • Anticoagulants
    34
  • Anticoagulants Cont…
    35
  • Anticoagulants Cont…
    36
  • Nitrates
    Indicated for patients with persistent ischemia, hypertension, and symptoms of acute heart failure
    Produce venous and arterial vasodilation
    SL followed by IV after 3 doses
    NTG in all patients w/o contraindications
    SBP <90 mm Hg
    HR <50 beats/min
    Right ventricular infarction
    Sildenafil or vardenafil within 24 hours
    Tadalafil within 48 hours
    37
  • Nitrates cont…
    38
  • Nitrates cont…
    39
  • Opioid
    Morphine- Class IIa recommendation
    If Nitroglycerin is not sufficient
    Produce vasodilation and reduces the heart rate and your systolic BP to further reduce Myocardial oxygen demand
    Alternative to nitroglycerin when nitroglycerin is contraindicated
    40
  • Opioid cont…
    41
  • Opioids Cont…
    42
  • Beta-Blockers
    Reduces the risk of recurrent ischemia, infarct size, risk of reinfarction in the hours and days following MI
    Selective Beta-Blockers
    Continue indefinitely
    Do not use in patients who are hemodynamically unstable
    IV route preferred over PO
    Persistent Ischemia
    Hypertension
    Tachycardia
    Goal of resting heart rate= 50-60 BPM
    43
  • Beta-Blocker
    44
  • Beta-Blocker
    45
  • Beta-Blocker
    46
  • Calcium Channel Blockers
    Indication for use
    Patients with continuing or recurrent ischemic symptoms despite Nitrate and Beta-Blocker therapy
    Contraindication to Beta-Blocker’s
    Preferred over Beta-Blocker
    cocaine induced ACS
    Prinzmetal angina
    Reduces coronary spasm by relaxing the smooth muscle in the arteries
    DHP’s not so much favored
    No effect on AV node No effect on heart rate
    Can increase myocardial ischemia
    Non-DHP’s Preferred
    Holds anti-ischemic effect by reducing contractility and the conduction AV node decrease heart rate
    47
  • Calcium Channel Blockers cont…
    48
  • Calcium Channel Blockers cont…
    49
  • Calcium Channel Blockers cont…
    50
  • ACE/ARB
    Started w/in 24 hours following post-stabilization
    Shown to reduce
    Mortality
    Decrease reinfarction
    Prevent development of heart failure
    Benefit: Ability to prevent cardiac remodeling
    BP Optimal Goal: 125/75 mm Hg
    Ideally < 130/85 mm Hg
    Should be used in all patients with
    Left ventricular systolic dysfunction
    EF <40%
    Heart Failure
    HTN
    Cardiogenic Shock
    51
  • ACE/ARB
    52
  • Hyperlipidemic Agents
    Data portrays the benefit of Statin in CAD
    Low Mortality
    Less incidence of stroke
    Use statin in all patients with ACS, regardless of LDL cholesterol levels
    Goal LDL < 100 mg/dL
    Preferred <70 mg/dL
    53
  • Treatment Algorithm
    54
  • Post-Stabilization
    PLUS
    Continue Beta-Blockers
    Indefinitely
    Metoprolol, Atenolol, Propranolol
    PLUS
    Statins
    Indefinitely
    Adjunct
    ACE/ARB
    Patients who has EF <40%
    Heart Failure
    Ongoing Ischemia
    Cardiac Rehabillation
    Increase functional capacity
    Aerobic and weight-bearing exercise 4 to 5 times per week for >30 minutes 
    PLUS
    Continue Antiplatelet therapy
    Indefinitely
    1° option- Aspirin PLUS Plavix
    2° option- Clopidogrel alone
    55
  • Monitoring Parameter
    Inpatient follow up with in 1-2 weeks of discharge
    Monitor Lipids at least every 6 months
    LDL < 70mg/dL
    Control and monitor HTN
    <130/80 mm Hg
    56
  • Landmark Trial
     
    Purpose: To evaluate the efficacy and safety of clopidogrel when used along with aspirin in patients without ST-segment elevation, because it was seen that these patient has a very high rates of major vascular events
    Study Design: Randomized, Double blind, Placebo-Controlled trial.
    Methods:
    12,562 patients were randomized
     6,259 patients received clopidogrel 300 mg followed by 75 mg PLUS aspirin post 24 hour onset of symptoms
    6,303 patients received a placebo PLUS aspirin post 24 hour onset of symptoms 
    57
  • Landmark Trial
    Result
    Primary endpoint: Assess the composite of death that occurred from cardiovascular causes, nonfatal myocardial infarction, or stroke
     
    Conclusion: Clopidogrel has beneficial effects in patients with acute coronary syndromes without ST-segment elevation, in addition also has a risk of major bleeding among patients treated with clopidogrel
     
    58
  • Vitamin and supplements
    Fish Oil
    ω- 3 Fatty Acids
    EPA and DHA-Abundant in fish
    Diet high in EPA & DHA or supplementation of fish oil
    Reduces the risk of CV mortality,
    Reinfarction
    Stroke
    Three 1 gram fish oil capsule should be consumed per daywill provide 1 gram of ω- 3 Fatty Acid
    Grupo Italiano per lo Studio dela Sopravvivenza nell’infarcto miocardio.Dietary Supplementation with n-3 fatty acids and Vitamin E after myocardial infarction: Results of GISSI- Prevenzione trial. Lancet 1999;354:447-455
    59
  • Conclusion
    Mainstays of therapy include risk stratification, and early angiography and revascularization with either PCI or CABG for patients with NSTE ACS at high risk for MI and death
    Pharmacotherapy for acute treatment includes SL NTG, antiplatelets, anticoagulants and B-blockers
    Ensuring selection of evidence-based therapies in all patients without contraindications results in lower mortality
    Pharmacists have an important role in encouraging patient adherence and persistence to pharmacotherapy
    60
  • Patient Case: Findings pertaining to the problem
    Severe respiratory distress
    Slurry speech and was wheezing
    Low O2 saturation (66%)
    Tachypneic and tachycardia (HR= 146 BPM)
    Elevated blood pressure (193/120 mm Hg)
    Lower extremity edema
    Troponin level: 5.5 ng/mL
    CK-MB: 43.5 U/L
    Low Hgb (9.3 g/dL) and Hct (28%)
    61
  • Patient Case: Etiology of the problem
    Previous history of CABG
    It is possible that thrombi formed, occluding the coronary blood flow and resulting in myocardial ischemia
    Other significant risk hypertension, diabetes mellitus and being elderly
    62
  • Patient Case: Treatment
    Does not need to go for any sort of early coronary angiography and revascularization
    ECHO revealed no stenosis
     
    Administer oxygen
    TIMI RISK: 5-Moderate
    Patient is greater than 65 years old (71)
    She has as known history of CAD
    The patient has been taking aspirin for the last 7 days
    ECG revealed ST- segment depression
    The patient has positive biochemical markers of infarction as seen by the troponin level and the CK-MB level 
    63
  • Patient Case: Treatment
    • atorvastatin (Lipitor) 10-80 mg/day orally
    • Metoprolol (Lopressor) 5 mg slow IV push (Over 1-2 minutes), repeated every five minutes for a total of 15 mg followed in 15-30 minutes by 25-30 mg by mouth Q6H
    Aspirin 325 mg as a single dose followed by aspirin 81 mg indefinitely
    Clopidogrel (Plavix) 300-600mg via NG-Tube as a loading dose on day 1 followed by 75 mg via NG-Tube once daily
    64
  • References
    Bavry DA, Kumbhan DJ, Rassi AN, et al. Benefit of early invasive therapy in acute
    coronary syndromes: A meta-analysis of contemporary, randomized clinical trials.
    Am Coll Cardiol 2006;48:1319–1325
    Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
    Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2007;50:1-157
    Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;October 2010.
    65
  • Thank You
    66