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Concepcion Arteaga Lisandy aleman Marilyn Lopez Yanet Reyes
Post Myocardial Infarction Management
Objectives
Pathophysiology of the disease ( MI) Symptoms / Clinical presentation Current pharmacological management Goal treatment Outcome evaluation Patient education
• If coronary blood flow is interrupted due to a plaque, thrombus or clot formation myocardial ischemia occurs and progression to myocyte necrosis and death will happen.
Pathophysiology of MI
•Two major types of MI : subendocardial MI (non-STEMI) and trasmural MI (STEMI )
Pathophysiology of MI
•Subendocardial MI usually presents with ST depression and T wave inversion without Q waves.This injury only progress to beneath the endocardium. ( recurrent clot formation is likely to occur unless an intervention is made
Pathophysiology of MI
Transmural MI ( STEMI ) Tissue necrosis will extend from the endocardium all the way to the epicardium
ST elevation is noted in the ECG. Intervention has to be done right a way to restored Oxygen and prevent further cell death.
Usually cardiac cath ( PCI is done ) evaluation for stent placement is done during cath.
Goal door to cath lab is 90 min .
Pathophysiology of MI
Chest pain Patient may describe the pain as crushing,
and heavy .Radiation to the neck, jaw, back, shoulder,
or left arm is common. Diabetics and older adults may experience
a feeling of indigestion with no chest pain high risk for sudden death from silent MI
Women may feel chest discomfort
Symptoms / Clinical Presentationology
Symptoms / Clinical Presentationology
Multidrug treatment with a combination of an antiplatelet , ACEI , BB, and lipid lowering agent.
In some cases ACEI and ARBS are given together or an ACEI is substitute for an ARB due to better tolerance.
Pharmacological Management in Post Myocardial Infarction.
Prevent clot formation / stent closure Aspirin and Plavix will keep blood flowing Aspirin antagonizes with cyclooxygenase pathway
and interfere with platelet aggregation by preventing the synthesis of thromboxane A( Woo,2012 )
Plavix reduced platelet aggregation by ADP pathway of platelets ( Woo, 446, 2012)
Antiplatelet Therapy
Aspirin 81 – 325mg has show decrease reduction in MI . The American Heart Association Recommends Low dose of Aspirin (75-160 mg a day in pt with higher risk of CAD.
Precaution and contraindication: Pt with peptic ulcer disease, GI bleeding, salicylate allergy, hepatic dysfunction
Ringing in the ear look for toxicity. ( 10 – 30 g.)Renal excretion and metabolized in the liver.
Antiplatelet Therapy
Plavix 75 mg daily for 12 month after discharge this is a recommendation American College of chest physician (ACCP)
Prodrug by the liver rapidly converted to active metabolite that is an active antiplatelet compound
Stady plasma levels occurs in 3 to 7 days Excreted in urine and feces ( safe for patients with renal
impairment because it that not increase bleeding time or platelet aggregation
Contraindications ( active bleeding, allergy, infective endocarditis, hemophilia thrombocytopenia )
Antiplatelet Therapy
Life style modification ( if you like to box ) you may want to consider Yoga .
Bleeding risk will increase report to ARNP/MD if there is faintness or weakness, red black tarry stools, bleeding gums, pinkish urine, skin rash or unusual bruising.
Aspirin should be taken with meals to avoid GI upset
Antiplatelet Education
Decrease mortality by 30 to 40 % ( Wood 2012) EX drugs: metoprolol, propanolol, Atenolol and timolol. Coreg is nonselective Beta-adrenergic blocking agent with
alfa -1 blocking activity. Use also in Post MI pt with low EF. BBs decrease the work load of the heart by decreasing
heart rate and contractility. the end result is reduction of myocardial oxygen demand
Contraindicatio: Heart Block, severe hypotension and bronchial Asthma.
The Role of Beta Blocker in Post MI Patients
Metabolized in the liver ( not recommended for patients with active liver disease)
Excretion ( via bile and feces ) Abrupt withdrawal of beta blockers can be life
threatening due to increase risk of ventricular arrhythmias, MI and death.
Teaching: sign and symptoms hypotension.Important that your PT take medication as prescribe,
teach them how to take their pulse.
Beta Blockers
Angiotensin-converting enzyme inhibitors reduce the activity of the renin-angiotensin-aldosterone system.
They reduce morbidity and mortality in post MI patients by from decrease of AT II after MI and it prevention of ventricular remodeling.
Commonly prescribed are:Captopril, Enalapril and lisinopril.Side effects: Hypotension, cough, hyperkalemia Contraindications: bilateral renal artery stenosis,
angioedema and pregnancy
ACEI inhibitors
Monitor renal functionAssess urine protein before therapy Pt with renal impairment need to be monitor closely
( Urine protein before therapy every 2 to 4 weeks for the first 3 month and regularly for thereafter for 1 year ( Wood 2012)
ACEI inhibitors
Reductase inhibitors the class of choice after MI (Statins: atorvastatin, pravastatin, rosuvastatin and simvastatin)
Block the synthesis of cholesterol in the liverDecreases triglycerides and LDL levels and
increase HDLMetabolized in the liver Excreted in bile and feces
Lipid Lowering Agents (Statins)
Side effects GI problems such as constipation sometimes severe enough to cause impaction.
Headache is a common side effectAtorvastatin and simvastatin have the lower adverse effect in regard to
myalgia Rabdomyolysis is a rare but serious adverse reaction that has been
reported.Education : restriction of cholesterol, carbohydrates and alcohol .
Statins
Antiplatelet therapy ( prevent stents closure and clot formation )
Beta blockers( reduced the work load of the heart ) ACEIs ( prevent ventricular remodeling) Lipid lowering agent ( high cholesterol has strong
correlation with MI due to plaque formation) Reinforce the importance to take the medications as
prescribe ( Prevention of recurrent MI and improvement of overall health is extremely importance )
Management of Patient after MI Summary
Woo, T.M. & Wynne, A. L. (3rd edition). Pharmacotherapeutics for nurse practitioner prescribers. Philadelphia, PA: F.A. Davis.
McCance, K. L., & Huether, S. E. (3rd edition). Pathophysiology: the biological basis for disease in adults and children. St Louis: Mosby.
References