Spectrum of Myocardial
Infarction
 Provide brief overview of the patients case
 Discuss the disease state, presentation and
signs and symptoms
 Explain t...
MAGN is a 70 y/o African American female who developed
acute respiratory distress while in the rehab.The patient
was found...
PMH: HTN, CAD S/P CABG, PVD, DM, right foot
ulcer, osteomyelitis of the 3rd and 5th right toe.
FH: Insignificant
SH: Insig...
Physical Findings:
 ABW: 165lb (75kg), Height: 5 feet 4.96 inch, IBW: 56.9 kg, AdJBW: 64.14kg.
 Mental status: Speech cl...
 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...
 Aspirin (Ecotrin) 325mg PO QAM
 Clopidogrel(Plavix) 75mg PO QAM
 Zosyn 2.25g Q6H QD
 Ciprofloxacin 200mg Q12H QD
 Va...
Non- ST Elevated Myocardial
Infarction
8
 Acute ischemic event that causes myocardial
necrosis
 Detected by elevation of serum cardiac
biomarkers and changes in ...
http://www.aic.cuhk.edu.hk/web8/corona5.gif 10
 Gradual buildup of cholesterol
and fibrous tissues in the
arteries
 Most predominant cause of
unstable ACS is due to th...
 1 per 3 American has an underlying CVD
 Estimated that 2/3 of ACS presents as NSTEMI or
unstable angina
 NSTEMI accoun...
 Common
 Deprivation of oxygen in the myocardium
 Adhesion, activation of plateletsPreventing blood
flowresulting in ...
Modifiable Non-Modifiable
Diabetes Age >65 years
Obesity FHx of CAD
PVD History of Angina
Smoking Previous CVD
Hypertensio...
Factors Characteristics
Chest pain Squeezing, aching,
burning, sharp pain
Prolonged
discomfort ≥ 30
minutes
Radiation ...
KeyTest Characteristics
 ECG  ST-Wave depression > 0.5 mm
T-Wave Inversion > 2 mm
 ECG may be normal
 Serial tests 15...
Key
Tests
Characteristics
CK-MB Sensitivity- 95%
False Positive can occur
Trauma
 Surgery
Cardioversion
Troponin H...
PROGNOSIS
 High risk of morbidity and
death from future events
 Rate of death is 4-6 times
higher compared to the
genera...
Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
19
Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition
20
 Intranasal Oxygen
 Oxygen saturation is < 90%
 PCI or CABG
 Early treatment for high risk
patients
 Consider in pati...
 PCI -feasible and safe to do
so
 Straight, quick, and performed at
low risk
 Performed for one or stenosed
vessels
 N...
Aspirin Thienopyridine β-Blockers
Nitrates Opioids GP IIb/IIIa Receptor
Inhibitors
Calcium Channel
Blockers
ACE Inhibitors...
MOA Irreversibly inhibits COX-1 and 2 decrease formation of
thrombaxaneA2Inhibits platelet aggregation
Important
Pharmac...
Guideline
Recommendation
Class 1A
Contraindications  Hypersensitivity
Active Bleeding
Severe Bleeding Risk
Dose and Dur...
Clopidogrel (Plavix) Ticlopidine (Ticlid)
MOA  Mediate their antiplatelet effects through a
blockade of ADP P2Y12 recepto...
 Reserved for patients allergic toAspirin
 Trials shows that the addition of Plavix to Aspirin is
safe and efficacious
...
Guideline
Recommendation
Class 1A
Dose and Duration
of therapy
 300-600 mg PO STAT on hospital day 1
75 mg PO QD startin...
Guideline
Recommendation
Class 1A
Drug Interactions Calcium Channel Blockers- Diminish the therapeutic
effect of Plavix
...
 Recommended for HIGH
risk patients
 Patient undergoing PCI
 Continued or recurrent
ischemia despite
treatment
▪ Aspiri...
Tirofiban
(Aggrastat )
Eptifibatide(Integrilin ) Abciximab (Reopro )
(NOT Recommended)
MOA  Block platelet binding of fib...
Guideline
Recommendation
Class I- for patients who are undergoing PCI
Class Iib-without high-risk features or who are no...
 Invasive strategy is
selected
 Enoxaparin, UFH,
Bivalirudin, and
fondaparinux
 If heparin continue dose
for 48 hours
...
Drug Guideline
Recommendation
Contraindication Doses
34
UFH LMWH Fondaparinux Bivalirudin
MOA- Potentiates
the action of
antithrombin III
 Inactivates
thrombin
Prevents the
co...
UFH LMWH Fondaparinux Bivalirudin
Drug Interaction Aspirin- increase risk of bleeding
Antiplatelets- Increase anticoagul...
 Indicated for patients with persistent ischemia,
hypertension, and symptoms of acute heart failure
 Produce venous and ...
Nitroglycerin
MOA Primarily reduces cardiac oxygen demand by decreasing preload or
the left ventricular end-diastolic pres...
Guideline Recommendation Dose
Nitroglycerin Class 1 0.4 mg SL, repeated every 5
minutes × 3 doses
5–10 mcg/min IV infusi...
 Morphine- Class IIa recommendation
 If Nitroglycerin is not sufficient
 Produce vasodilation and reduces the heart rat...
MOA Produce vasodilation and reductions in HR through
increased vagal tone and systolic BP to further reduce
myocardial o...
Dose 2-5 mg IV bolus dose
Can be repeated every 5-30 minutes PRN
Contraindications Hypotension
Respiratory Depression
...
 Reduces the risk of recurrent ischemia, infarct size, risk of
reinfarction in the hours and days following MI
 Selectiv...
Metoprolol Propranolol Atenolol
MOA Selectively inhibits B1- receptorReduces heart rate,
myocardial contractility and BP...
Drug Guideline
Recommendation
Contraindication Doses
Drug-Interactions Alpha 2-agonist-enhance rebound hypertensive effec...
Metoprolol Propranolol Atenolol
ADR Hypotension
Bradycardia
Heart block
Monitoring
Parameters
BP, RR, HR
12-lead ECG
...
 Indication for use
 Patients with continuing or recurrent ischemic symptoms despite Nitrate and
Beta-Blocker therapy
 ...
Diltiazem Verapamil
MOA  Prevent the entry of Ca2+ into the vascular smooth
muscle and the myocardium Relaxing the vascu...
Diltiazem Verapamil
Drug Interactions Antifungal= Decrease metabolism of CCB
Atorvastatin= Increase serum level of both
...
Diltiazem Verapamil
Recommended dose 120-360 mg SR QD 180-480 mg SR QD
Monitoring
parameters
 BP and HR
Signs of heart f...
 Should be used in all
patients with
 Left ventricular systolic
dysfunction
▪ EF <40%
 Heart Failure
 HTN
 Cardiogeni...
Contraindications Drug Dose Target Dose
52
 Data portrays the benefit of Statin in CAD
 Low Mortality
 Less incidence of stroke
 Use statin in all patients withA...
54
 Cardiac Rehabillation
 Increase functional capacity
 Aerobic and weight-bearing
exercise 4 to 5 times per
week for >30...
 Inpatient follow up with in 1-2 weeks of
discharge
 Monitor Lipids at least every 6 months
 LDL < 70mg/dL
 Control an...
Purpose: To evaluate the efficacy and safety of clopidogrel when used along with
aspirin in patients without ST-segment el...
Primary endpoint: Assess the
composite of death that
occurred from cardiovascular
causes, nonfatal myocardial
infarction, ...
 Fish Oil
 ω- 3 Fatty Acids
▪ EPA and DHA-Abundant in fish
 Diet high in EPA & DHA or supplementation of fish oil
▪ Red...
 Mainstays of therapy include risk stratification, and early
angiography and revascularization with either PCI or
CABG fo...
 Severe respiratory distress
 Slurry speech and was wheezing
 Low O2 saturation (66%)
 Tachypneic and tachycardia (HR=...
 Previous history of CABG
 It is possible that thrombi formed, occluding the
coronary blood flow and resulting in myocar...
 Administer oxygen
 TIMI RISK: 5-Moderate
 Patient is greater than 65 years
old (71)
 She has as known history of
CAD
...
 Aspirin 325 mg as a single dose
followed by aspirin 81 mg
indefinitely
 Clopidogrel (Plavix) 300-600mg via
NG-Tube as a...
Bavry DA, Kumbhan DJ, RassiAN, et al. Benefit of early invasive therapy in acute
coronary syndromes: A meta-analysis of co...
66
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Major Case Presentation Final Version

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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 severe
    enough to produce myocardial necrosis, resulting in the release of a
    detectable amount of biochemical markersIschemia produces myocardial necrosis
    Release large amount of biochemical markers into the blood stream
    Troponin I or T
    CK-MB
    , mainly troponin I or T,
    and creatine kinase myocardial band (CK MB) from the necrotic
    myocytes 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
  • CBC
    Measure Hgb and Hct
     Secondary cause of NSTEMI
    Acute blood loss
     Anemia
    Assess thrombocytopenia
     estimate bleeding risk
    BUN and Scr
    Dose renally adjusted drugs
    LFTs
    For drugs that undergo hepatic metabolism
    CXR
    R/O pneumonia, pneumothorax, and esophageal rupture
    Can mimic cardiac ischemia
  • P2Y12= Purinergic receptor subtype 12
  • The ACC/AHA guidelines give no preference for the use of UFH, enoxaparin, fondaparinux, or bivalirudin in patients in when an invasive strategy is selected, but state that the evidence for the use of the first two is stronger
  • NTG= Nitroglycerin
  • 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

    1. 1. Spectrum of Myocardial Infarction
    2. 2.  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
    3. 3. 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
    4. 4. 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
    5. 5. 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
    6. 6.  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
    7. 7.  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  NovologTID  Percocet 1T PO Q6H  Tylenol 650 mg PO Q 4H 7
    8. 8. Non- ST Elevated Myocardial Infarction 8
    9. 9.  Acute ischemic event that causes myocardial necrosis  Detected by elevation of serum cardiac biomarkers and changes in ECG  Troponin  CK-MB  ECG 9
    10. 10. http://www.aic.cuhk.edu.hk/web8/corona5.gif 10
    11. 11.  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 seen11
    12. 12.  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
    13. 13.  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
    14. 14. Modifiable Non-Modifiable Diabetes Age >65 years Obesity FHx of CAD PVD History of Angina Smoking Previous CVD Hypertension Recent PCI Dyslipidemia 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
    15. 15. Factors Characteristics Chest pain Squeezing, aching, burning, sharp pain Prolonged discomfort ≥ 30 minutes Radiation to left arm or neck is very common Diaphoresi s Classical sign and symptom of MI Factors Characteristics  SOB Secondary to diminished cardiac output Anxiety Displayed females, elderly and DM Fourth Heart Sound (S4) Present in ischemia Signs of CHF Pulmonary rales Lower extremity edema S3 gallop Elevated Jugular Venous Pressure 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
    16. 16. KeyTest Characteristics  ECG  ST-Wave depression > 0.5 mm T-Wave Inversion > 2 mm  ECG may be normal  Serial tests 15-30 minute interval 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
    17. 17. Key Tests Characteristics CK-MB Sensitivity- 95% False Positive can occur Trauma  Surgery Cardioversion Troponin Highly Sensitive and specific Confirms Diagnosis of MI 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 17
    18. 18. 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 GOALS OFTREATMENT  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
    19. 19. Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition 19
    20. 20. Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition 20
    21. 21.  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
    22. 22.  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 AcuteCoronary Sundromes:PCI or CABG? Heart 2003 89: 967-970 http://0.tqn.com/f/p/440/graphics/images/en/19006.jpg 22
    23. 23. Aspirin Thienopyridine β-Blockers Nitrates Opioids GP IIb/IIIa Receptor Inhibitors Calcium Channel Blockers ACE Inhibitors Angiotensin Receptor Blockers Anticoagulants Lipid Lowering Agents 23
    24. 24. MOA Irreversibly inhibits COX-1 and 2 decrease formation of thrombaxaneA2Inhibits platelet aggregation Important Pharmacokinetic Parameter Hydrolyzed to salicylate via liver (Active) Half Life  Parent drug (15-20 minutes) T1/2= 3 hours (300-600 mg) T1/2= 5-6 hours ( > 1000 mg) Elimination via Urine Clcr <10 mL/minute: Avoid use Drug Interaction NSAID - diminish the cardioprotective effect of Salicylate Warfarin- enhance anticoagulant effect of warfarin (additive)  Heparin and Anti-platelets- increase risk of bleeding  Low dose OK Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010 24
    25. 25. Guideline Recommendation Class 1A Contraindications  Hypersensitivity Active Bleeding Severe Bleeding Risk Dose and Duration of therapy  162–325 mg PO STAT on hospital day 1 75–162 mg PO QD starting day 2  indefinitely Pt. undergoing PCI- 162–325 mg PO QD for a minimum of 30 days Monitoring Parameter Clinical signs of bleeding- Melena, hematuria, bloody stool Upset GI Baseline CBC and platelet count CBC platelet count every 6 months Anderson JL, AdamsCD,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
    26. 26. Clopidogrel (Plavix) Ticlopidine (Ticlid) MOA  Mediate their antiplatelet effects through a blockade of ADP P2Y12 receptors on platelets Important Pharmacokinetic Parameters Metabolized hepatically (CYP2C19) T1/2= 6 hours Elimination  Urine-50%  Feces- 46% Renal Impairment- No dose adjustment  Hepatic Metabolism T1/2= 13 hours Elimination  Urine-60%  Feces- 23% Preferred Agent? Ticlopidine  Neutropenia  Requires frequent monitoring of CBC Plavix preferred Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010 26
    27. 27.  Reserved for patients allergic toAspirin  Trials shows that the addition of Plavix to Aspirin is safe and efficacious  CommitTrial ▪ 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, AdamsCD,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
    28. 28. Guideline Recommendation Class 1A Dose and Duration of therapy  300-600 mg PO STAT on hospital day 1 75 mg PO QD starting day 2  Administer for 9 months Aspirin allergy-Administer Indefinitely  Post-PCI bare-metal stented patients- 1 month Post-PCI Sirolimus/Paclitaxel stent-12 month Contraindications  Hypersensitivity Active Bleeding Severe Bleeding Risk Adverse Events Bleeding TTP Diarrhea  Rash Anderson JL, AdamsCD,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
    29. 29. Guideline Recommendation Class 1A Drug Interactions Calcium Channel Blockers- Diminish the therapeutic effect of Plavix PPI’s- Reduced efficacy of Plavix Macrolide’s- Diminish the therapeutic effect of Plavix Warfarin- Enhance the anticoagulant activity of warfarin Monitoring Parameter Clinical signs of bleeding- Melena, hematuria, bloody stool Upset GI Baseline CBC and platelet count CBC platelet count every 6 months Anderson JL, AdamsCD,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;November 2nd, 2010 29
    30. 30.  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
    31. 31. Tirofiban (Aggrastat ) Eptifibatide(Integrilin ) Abciximab (Reopro ) (NOT Recommended) MOA  Block platelet binding of fibrinogen to the GP IIb/IIIa receptor Pharmacokinetics T1/2=2 hours Elimination  Urine- 65% Feces- 25% T1/2=2 hours Elimination  Urine Dialysis- Contraindicated T1/2= 30 minutes Drug Interactions Anticoagulants  Increased effect Antiplatelets  Increased effect NSAIDS- Increase risk of bleeding ADR Bleeding  Acute profound thrombocytopenia Lexi Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.;2007;November 2nd, 2010 31
    32. 32. Guideline Recommendation Class I- for patients who are undergoing PCI Class Iib-without high-risk features or who are not undergoing PCI Contraindications Thrombocytopenia Active Bleeding Prior stroke Monitoring Parameter Clinical signs of bleeding A baseline CBC and platelet count Daily CBC Platelet count at 4 hours after initiation then daily Anderson JL, AdamsCD,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
    33. 33.  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
    34. 34. Drug Guideline Recommendation Contraindication Doses 34
    35. 35. UFH LMWH Fondaparinux Bivalirudin MOA- Potentiates the action of antithrombin III  Inactivates thrombin Prevents the conversion of fibrinogen to fibrin  Enhances the inhibition rate of clotting protease by inhbiting factor Xa Pharmacokinetics T1/2= 1-2 hrs T1/2= 4.5-7 hrs Elimination= urine (40%) CrCL<30= 1mg/kg SQ QD F= 100% if SC T1/2= 17-21 hours CrCl<30= use is C/I T1/2= 25 minutes CrCl < 30 T1/2= 57 minutes 35
    36. 36. UFH LMWH Fondaparinux Bivalirudin Drug Interaction Aspirin- increase risk of bleeding Antiplatelets- Increase anticoagulant effect NSAIDS- Enhance anticoagulant effect ADR Bleeding Heparin Induced Thrombocytopenia Bleeding Monitoring Parameters Clinical signs of bleeding Baseline CBC, platelet count Daily CBC aPTT Q6HQ24H 36
    37. 37.  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
    38. 38. Nitroglycerin MOA Primarily reduces cardiac oxygen demand by decreasing preload or the left ventricular end-diastolic pressure Pharmacokinetics T1/2= 1-4 minutes Metabolized via the liver Drug Interactions Heparin - diminish the anticoagulant effect of Heparin Phosphodiesterase 5 Inhibitors - enhance the vasodilatory effect of Nitroglycerin ADR Tachycardia, Flushing, Hypotension Monitoring Parameters BP and HR every 2 hours 38
    39. 39. Guideline Recommendation Dose Nitroglycerin Class 1 0.4 mg SL, repeated every 5 minutes × 3 doses 5–10 mcg/min IV infusion titrated Continue IV infusion for 24– 48 hours up to 200 mcg/min until relief of symptoms or limiting side-effects  headache  SBP <90 mm Hg Discontinue if SBP drops >30 mm Hg below baseline SBP 39
    40. 40.  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
    41. 41. MOA Produce vasodilation and reductions in HR through increased vagal tone and systolic BP to further reduce myocardial oxygen demand Pharmacokinetic Hepatic metabolism F= 17-33% PO T1/2= 2-4 hours Excretion  Urine- 2 to 12%  Feces- 10%  CrCl 10-50 mL/min- Administer 75% of the normal dose CrCl< 10 mL/min- Administer 50% of the normal dose Drug Interactions Alcohol- enhance CNS depression of alcohol Thiazide diuretics- Enhance the effect of orthostatic HOTN Succinylcholine- increase bradycardic effect of morphine 41
    42. 42. Dose 2-5 mg IV bolus dose Can be repeated every 5-30 minutes PRN Contraindications Hypotension Respiratory Depression Confusion ADE Hypotension Respiratory Depression Monitoring Parameters Blood pressure and respiratory rate 5 minutes after each bolus dose 42
    43. 43.  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
    44. 44. Metoprolol Propranolol Atenolol MOA Selectively inhibits B1- receptorReduces heart rate, myocardial contractility and BP Decreasing oxygen demand Pharmacokinetics Extensively metabolized via the liver F=50% Oral T1/2=3-8 hours Renal or hepatic failure- No dose adjust Hepatic via CYP2D6, and CYP1A2 T1/2  Immediate release-3-6 hours  Extended Release-8-10 hours Hepatically metabolized T1/2 Adults=6-7 hrs Elimination  50% urine  40% urine Adults w/ ESRD T1/2=15-35 hrs CrCl <15-35= Max 50mg/day CrCl <15mL/min= Max 50mg QOD 44
    45. 45. Drug Guideline Recommendation Contraindication Doses Drug-Interactions Alpha 2-agonist-enhance rebound hypertensive effect of the Alpha-2 Amiodarone- increase the bradycardiac effect MAOI=Enhance orthostatic HOTN effect 45
    46. 46. Metoprolol Propranolol Atenolol ADR Hypotension Bradycardia Heart block Monitoring Parameters BP, RR, HR 12-lead ECG Clinical signs of heart failure every 5 minutes during bolus intravenous dosing Every shift during oral administration during Hospitalization, then BP and HR every 6 months following hospital discharge 46
    47. 47.  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
    48. 48. Diltiazem Verapamil MOA  Prevent the entry of Ca2+ into the vascular smooth muscle and the myocardium Relaxing the vascular smooth muscle and increase O2 delivery Pharmacokinetics Hepatic Metabolism  First Pass effect F= 40 % PO T1/2 IR= 3-4.5 hours  XR= 6-9 hours Renal Impairment= No Dose adjustment necessary Hepatic Metabolism  First Pass effect F= 35 % PO T1/2= 3-7 hours  Hepatic Impairment= 14-16 hours Elimination= 70% Urine; 20% Feces. Renal Impairment= Use low dose Hepatic Impairment= Decrease dose by 70% 48
    49. 49. Diltiazem Verapamil Drug Interactions Antifungal= Decrease metabolism of CCB Atorvastatin= Increase serum level of both Atorvastatin and CCB Calcium Salts= Diminish the therapeutic effect of CCB ADR Hypotension Bradycardia Heart Block Heart Failure Gingival Hyperplasia Contraindications Pulmonary Edema SBP < 100 mm HG PR interval >0.25 sec on ECG 2nd or 3rd degree AV block HR <60 BPM 49
    50. 50. Diltiazem Verapamil Recommended dose 120-360 mg SR QD 180-480 mg SR QD Monitoring parameters  BP and HR Signs of heart failure on every shift during hospitalization Then assess every 6 months for similar signs following discharge Dental exam and cleaning teeth every 6 month 50
    51. 51.  Should be used in all patients with  Left ventricular systolic dysfunction ▪ EF <40%  Heart Failure  HTN  Cardiogenic Shock  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 51
    52. 52. Contraindications Drug Dose Target Dose 52
    53. 53.  Data portrays the benefit of Statin in CAD  Low Mortality  Less incidence of stroke  Use statin in all patients withACS, regardless of LDL cholesterol levels  Goal LDL < 100 mg/dL  Preferred <70 mg/dL 53
    54. 54. 54
    55. 55.  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  PLUS  Continue Beta-Blockers ▪ Indefinitely ▪ Metoprolol,Atenolol, Propranolol  PLUS  Statins ▪ Indefinitely  Adjunct  ACE/ARB ▪ Patients who has EF <40% ▪ Heart Failure ▪ Ongoing Ischemia 55
    56. 56.  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
    57. 57. 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
    58. 58. 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 Result 58
    59. 59.  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
    60. 60.  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
    61. 61.  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
    62. 62.  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
    63. 63.  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  Does not need to go for any sort of early coronary angiography and revascularization  ECHO revealed no stenosis 63
    64. 64.  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  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 64
    65. 65. Bavry DA, Kumbhan DJ, RassiAN, 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
    66. 66. 66

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