Major Case Presentation Final Version

Munzur Morshed, Pharm D. candidate 2011

Arnold & Marie Schwartz College of Pharmacy and Health SciencesKingsbrook Jewish Medical Center

Critical Care -Advance Pharmacy PracticeDr.Henry Cohen

Spectrum of Myocardial Infarction

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

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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.

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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: InsignificantSH: InsignificantNKDAVS: Temp: 96 ° F, BP: 193/120 mm Hg,

HR: 146 BPM RR: 22 BPM, O2 Sat: 66%,Pain scale: 0/10

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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: UnremarkableECHO: Moderate mitral valve regurgitation, Normal LV Ejection

fraction, Mild concentric left ventricular hypertrophy, Mild aortic valve sclerosis without stenosis.

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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

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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

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Diagnosis

Non- ST Elevated Myocardial Infarction

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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

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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 seen11

Epidemiology

1 per 3 American has an underlying CVDEstimated that 2/3 of ACS presents as

NSTEMI or unstable anginaNSTEMI accounts for 1.5 million hospital

admission per yearPercentage of patients with diagnosis of

NSTEMI is increasing dramatically Sensitive assays for MI, available earlier

pharmacotherapy

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Etiology

Common Deprivation of oxygen in the myocardium Adhesion, activation of plateletsPreventing

blood flowresulting in myocardial ischemiaRare

Progressive atherosclerosis Recreational drug use Inflammation of the arteries Extrinsic cause

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Risk Factors

Modifiable Non-ModifiableDiabetes 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

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Clinical PresentationFactors Characteristics

Chest pain

Squeezing, aching, burning, sharp painProlonged discomfort ≥ 30 minutes Radiation to left arm or neck is very common

Diaphoresis

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 ralesLower extremity edemaS3 gallopElevated Jugular Venous Pressure

Sheridan PJ, Crossman DC. Critical review of unstable angina and non-ST elevation myocardial infarction. Postgrad Med J. 2002;78:717-726Anderson 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

Key Test

Characteristics

ECG ST-Wave depression > 0.5 mmT-Wave Inversion > 2 mm ECG may be normal Serial tests 15-30 minute interval


Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition 16

Diagnostic Tests Continued

Key Tests

Characteristics

CK-MB Sensitivity- 95%False Positive can occur Trauma Surgery Cardioversion

Troponin

Highly Sensitive and specificConfirms Diagnosis of MI


Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th edition

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Prognosis/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

GOALS OF TREATMENT

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

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General Approach to treatment


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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 operationGunn 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

http://0.tqn.com/f/p/440/graphics/images/en/19006.jpg

Pharmacologic Therapy

Aspirin Thienopyridine β-Blockers

Nitrates Opioids GP IIb/IIIa Receptor Inhibitors

Calcium Channel Blockers

ACE Inhibitors AngiotensinReceptor Blockers

Anticoagulants Lipid Lowering Agents

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AspirinMOA Irreversibly inhibits COX-1 and 2 decrease

formation of thrombaxane A2Inhibits 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

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Aspirin cont….Guideline Recommendation

Class 1A

Contraindications

HypersensitivityActive BleedingSevere Bleeding Risk

Dose and Duration of therapy

162–325 mg PO STAT on hospital day 175–162 mg PO QD starting day 2 indefinitelyPt. undergoing PCI- 162–325 mg PO QD for a minimum of 30 days

Monitoring Parameter

Clinical signs of bleeding- Melena, hematuria, bloody stoolUpset GIBaseline CBC and platelet countCBC platelet count every 6 monthsAnderson 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

ThienopyridineClopidogrel (Plavix) Ticlopidine (Ticlid)

MOA Mediate their antiplatelet effects through ablockade of ADP P2Y12 receptors on platelets

Important Pharmacokinetic Parameters

Metabolized hepatically (CYP2C19)T1/2= 6 hoursElimination Urine-50% Feces- 46%Renal Impairment- No dose adjustment

Hepatic MetabolismT1/2= 13 hoursElimination Urine-60% Feces- 23%

Preferred Agent? Ticlopidine Neutropenia Requires frequent monitoring of CBCPlavix preferred


Plavix

Reserved for patients allergic to AspirinTrials 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 procedureAnderson 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

PlavixGuideline Recommendation

Class 1A

Dose and Duration of therapy

300-600 mg PO STAT on hospital day 175 mg PO QD starting day 2 Administer for 9 monthsAspirin allergy- Administer Indefinitely Post-PCI bare-metal stented patients- 1 monthPost-PCI Sirolimus/Paclitaxel stent-12 month

Contraindications

HypersensitivityActive BleedingSevere Bleeding Risk

Adverse Events Bleeding TTPDiarrhea RashAnderson 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

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Plavix cont…Guideline Recommendation

Class 1A

Drug Interactions

Calcium Channel Blockers- Diminish the therapeutic effect of PlavixPPI’s- Reduced efficacy of PlavixMacrolide’s- Diminish the therapeutic effect of PlavixWarfarin- Enhance the anticoagulant activity of warfarin


Clinical signs of bleeding- Melena, hematuria, bloody stoolUpset GIBaseline CBC and platelet countCBC platelet count every 6 months


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GP IIb/IIIa Receptor Inhibitor

Recommended for HIGH risk patients Patient

undergoing PCI Continued or

recurrent ischemia despite treatment

▪ Aspirin▪ Plavix▪ Anticoagulant


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GP IIb/IIIa Receptor Inhibitor cont…Tirofiban (Aggrastat )

Eptifibatide(Integrilin )

Abciximab (Reopro )(NOT Recommended)

MOA Block platelet binding of fibrinogen to the GP IIb/IIIa receptor

Pharmacokinetics

T1/2=2 hoursElimination Urine- 65% Feces- 25%

T1/2=2 hoursElimination UrineDialysis- Contraindicated

T1/2= 30 minutes

Drug Interactions

Anticoagulants Increased effectAntiplatelets Increased effectNSAIDS- Increase risk of bleeding

ADR Bleeding Acute profound thrombocytopenia


GP IIb/IIIa Receptor Inhibitor cont…

Guideline Recommendation

Class I- for patients who are undergoing PCIClass Iib-without high-risk features or who are not undergoing PCI

Contraindications

ThrombocytopeniaActive BleedingPrior stroke


Clinical signs of bleedingA baseline CBC and platelet count Daily CBCPlatelet count at 4hours after initiation then daily


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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

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AnticoagulantsDrug Guideline

Recommendation

Contraindication

Doses

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Anticoagulants Cont…UFH LMWH Fondaparin

uxBivalirudin

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 hrsElimination= urine (40%)CrCL<30= 1mg/kg SQ QD

F= 100% if SCT1/2= 17-21 hoursCrCl<30= use is C/I

T1/2= 25 minutesCrCl < 30 T1/2= 57 minutes

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Anticoagulants Cont…

UFH LMWH Fondaparinux

Bivalirudin

Drug Interaction

Aspirin- increase risk of bleedingAntiplatelets- Increase anticoagulant effectNSAIDS- Enhance anticoagulant effect

ADR BleedingHeparin Induced Thrombocytopenia

Bleeding

Monitoring Parameters

Clinical signs of bleedingBaseline CBC, platelet countDaily CBCaPTT Q6HQ24H

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Nitrates

Indicated for patients with persistent ischemia, hypertension, and symptoms of acute heart failure

Produce venous and arterial vasodilationSL followed by IV after 3 dosesNTG 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

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Nitrates cont…Nitroglycerin

MOA Primarily reduces cardiac oxygen demand by decreasing preload or the left ventricular end-diastolic pressure

Pharmacokinetics T1/2= 1-4 minutesMetabolized 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


BP and HR every 2 hours

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Nitrates cont…Guideline Recommendation

Dose

Nitroglycerin Class 1 0.4 mg SL, repeated every 5 minutes × 3 doses5–10 mcg/min IV infusion titratedContinue IV infusion for 24–48 hoursup to 200 mcg/min until relief of symptoms or limiting side-effects headache SBP <90 mm HgDiscontinue if SBP drops >30 mm Hg below baseline SBP

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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

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Opioid cont…MOA Produce vasodilation and reductions in

HR through increased vagal tone and systolic BP to further reduce myocardial oxygen demand

Pharmacokinetic

Hepatic metabolismF= 17-33% POT1/2= 2-4 hoursExcretion Urine- 2 to 12% Feces- 10% CrCl 10-50 mL/min- Administer 75% of the normal doseCrCl< 10 mL/min- Administer 50% of the normal dose

Drug Interactions

Alcohol- enhance CNS depression of alcoholThiazide diuretics- Enhance the effect of orthostatic HOTNSuccinylcholine- increase bradycardic effect of morphine

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Opioids Cont…

Dose 2-5 mg IV bolus doseCan be repeated every 5-30 minutes PRN

Contraindications

HypotensionRespiratory DepressionConfusion

ADE HypotensionRespiratory Depression


Blood pressure and respiratory rate 5 minutes after each bolus dose

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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

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Beta-Blocker

Metoprolol Propranolol Atenolol

MOA Selectively inhibits B1- receptorReduces heart rate, myocardial contractility and BP Decreasing oxygen demand

Pharmacokinetics

Extensively metabolized via the liverF=50% OralT1/2=3-8 hoursRenal or hepatic failure- No dose adjust

Hepatic via CYP2D6, and CYP1A2 T1/2 Immediate release-3-6 hours Extended Release-8-10 hours

Hepatically metabolizedT1/2 Adults=6-7 hrsElimination 50% urine 40% urineAdults w/ ESRD T1/2=15-35 hrsCrCl <15-35= Max 50mg/dayCrCl <15mL/min= Max 50mg QOD

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Beta-BlockerDrug Guideline

Recommendation

Contraindication

Doses

Drug-Interactions

Alpha 2-agonist-enhance rebound hypertensive effect of the Alpha-2Amiodarone- increase the bradycardiac effectMAOI=Enhance orthostatic HOTN effect

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Beta-Blocker

Metoprolol Propranolol Atenolol

ADR HypotensionBradycardiaHeart block


BP, RR, HR12-lead ECGClinical signs of heart failure every 5 minutes during bolus intravenous dosingEvery shift during oral administration duringHospitalization, then BP and HR every 6 months following hospital discharge

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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…

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 effectF= 40 % POT1/2 IR= 3-4.5 hours XR= 6-9 hoursRenal Impairment= No Dose adjustment necessary

Hepatic Metabolism First Pass effectF= 35 % POT1/2= 3-7 hours Hepatic Impairment= 14-16 hoursElimination= 70% Urine; 20% Feces.Renal Impairment= Use low doseHepatic Impairment= Decrease dose by 70%

48


Diltiazem Verapamil

Drug Interactions Antifungal= Decrease metabolism of CCBAtorvastatin= Increase serum level of both Atorvastatin and CCBCalcium Salts= Diminish the therapeutic effect of CCB

ADR HypotensionBradycardiaHeart BlockHeart FailureGingival Hyperplasia

Contraindications Pulmonary EdemaSBP < 100 mm HGPR interval >0.25 sec on ECG2nd or 3rd degree AV blockHR <60 BPM 49


Diltiazem Verapamil

Recommended dose

120-360 mg SR QD

180-480 mg SR QD

Monitoring parameters

BP and HRSigns of heart failure on every shift during hospitalizationThen assess every 6 months for similar signs following dischargeDental exam and cleaning teeth every 6 month

50

ACE/ARB

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

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ACE/ARBContraindicatio

nsDrug Dose Target Dose

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

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Treatment Algorithm

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Post-Stabilization

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

Monitoring Parameter Inpatient follow up with in 1-2 weeks

of dischargeMonitor Lipids at least every 6

months LDL < 70mg/dL

Control and monitor HTN <130/80 mm Hg

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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

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Landmark TrialPrimary 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

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 daywill 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

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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 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

Patient Case: Treatment 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

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;48:1319–1325Pharmacotherapy-A Pathophysiologic approach-Depiro’s 7th editionAnderson 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

Health & Medicine

Major Case Presentation Final Version