Myocardial Infarction Symbree Minniear

Myocardial Infarction • A myocardial infarction refers to the death of myocardial muscle cells that occurs when a substantial decrease or complete disruption of blood flow through a coronary artery deprives the downstream tissue of oxygen for an extended period. • In an MI, an area of the myocardium is permanently destroyed and cannot be . http://www.youtube.com/watch?v=N_cwHfUUMXw

Epidemiology • Approximately every 25 seconds, an American will have a coronary event, and approximately every minute, someone will die of one. • Coronary heart disease caused 1 of every 6 deaths in the United States in 2008. • About every 34 seconds, someone in the United States has a myocardial infarction.

Symptoms • Pain is the most common symptom in patients’ experience a MI. • Pain can be experienced in your arms, shoulder, neck, teeth, jaw, abdomen, or back. • It may feel like a tight band around the chest, bad indigestion, like something is sitting on your chest, or squeezing.

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Undue fatigue Palpitations Dyspnea Anxiety Cough Fainting Light-headedness, dizziness • Nausea or vomiting • Profuse sweating • Confusion

Laboratory Diagnosis • Blood analysis can be performed to determine whether tissue damage has occurred to the myocardium. ▫ Polymorphonuclear leukocytes and erythrocyte sedimentation rates are both indicative of myocardial damage. • Myocardial injury can also be recognized by the appearance of various cardiac biomarkers that are released when the myocardial walls lose their integrity. ▫ Biochemical markers such as troponin (I and T), creatinine kinase (CK) and its isoenzyme CK-MD, and lactate dehydrogenase (LDH).

Tests and Evaluation • Electrocardiography (ECG): ▫ Patients presenting with an acute transmural MI have ECG changes that include hyperpolarization of the T waves and ST-segment elevation. ▫ Patients experiencing a subendocardial MI typically demonstrate ST-segment depression.

• Echocardiography: ▫ Provides information regarding wall motion and blood perfusion. ▫ Two-dimensional echocardiography is used to visualize the left ventricular walls and assess the amount of movement.

Tests and Evaluation • Multiple-gated analysis (MUGA): ▫ Uses technetium-99m stannous pyrophosphate, which tags to red blood cells. ▫ By imaging tagged red blood cells wall motion and ejection fraction can be assessed. • Computed tomography (CT) and magnetic resonance imaging (MRI): ▫ May also be used to assess ventricular wall motion. • Radionuclide imaging: ▫ Are used to assess either blood flow defects or wall motion abnormalities.

Complications • Arrhythmias can occur if the myocardium is damaged due to an MI. • Depending on the amount of damaged tissue the heart may not be able to adequately pump blood to the body, which may lead to heart failure. • Areas of heart muscle weakened by a heart attack can rupture, leaving a hole in part of the heart. • Heart valves damaged during a heart attack may develop severe, life-threatening leakage problems.

Treatment Acute Treatment

• Sublingual nitroglycerin and morphine • Percutaneous coronary intervention (PTCA) • Coronary artery bypass graft surgery (CABG) • Revascularization • Thrombolytic therapy • Angioplasty • Bed rest

Chronic Treatment

• Regular physical activity • β-blockers • Angiotensin-converting enzyme inhibitors (ACE) • Aspirin • Anticoagulation therapy • Lipid management • Calcium channel blockers • Antiplatelet therapy • Antiarrhythmic therapy

Effects of MI on Ability to Exercise • Reduced level of cardiorespiratory fitness approximately 50-70% of age and gender predicted. • Reduced oxygen transport capacity due to diminished cardiac output. • Decrease in ejection fraction and stroke volume. • Increased heart rate due to a decrease in stroke volume. • Exercise-induced ventricular arrhythmias.

Effects of Medications on Exercise • β-blockers: ▫ Decrease submaximal and maximal heart rate and sometimes exercise capacity. ▫ Prevent or delay signs or symptoms of myocardial ischemia and increase exercise tolerance in clients with exertional angina.

• Vasodilators, ACE inhibitors, and angiotensin recep0tor blockers: ▫ May be subject to hypotensive episodes during the postexercise period unless an adequate cool down period is allowed.

Effects of Medication on Exercise • Calcium channel blockers: ▫ May decrease the heart rate response at rest and during exercise and prevent or delay manifestations of myocardial ischemia.

• Central nervous system—active drugs: ▫ Can have attenuating effects on heart rate and blood pressure during exercise.

• Alpha receptor blockers: ▫ Significantly lower systolic and diastolic blood pressure.

Effects of Medications on Exercise • Antiarrhythmic agents: ▫ Can cause false negative or false positive test results.

• Digitalis: ▫ ST-segment depression can be induced or accentuated during exercise in persons with or without heart disease.

Effects of Exercise Training • Increased maximal oxygen consumption (VO2max). • Improvement in the ventilatory response to exercise. • Improvement in the anaerobic threshold. • Relief of angina symptoms secondary to reductions in heart rate or blood pressure.

• Modest decreases in body weight, fat stores, blood pressure, total blood cholesterol serum triglycerides, and LDLcholesterol. • Increases in the “antiatherogenic” highdensity lipoprotein (HDL) cholesterol subfraction.

Effects of Exercise Training • Improved psychosocial well-being and selfefficacy. • Protection against the triggering of MI by vigorous physical exertion. • Decreased coronary inflammatory markers. • Increased numbers of endothelial progenitor cells and circulating angiogenic cells

• Decreased blood platelet adhesiveness, fibrinogen, and blood viscosity and increased fibrinolysis. • Increased vagal tone and decreased adrenergic activity. • Increased heart rate variability.

Exercise Testing • Graded exercise testing are used in post-MI patient to evaluate prognosis and functional status. • Exercise protocol can be submaximal or symptom limited. • Treadmills or cycle ergometers are the most common modes of testing. • The protocol is low level, with work rate increments of 1 to 2 METs every 2 to 3 min. • Blood pressure, ECG and symptom monitoring should be performed throughout the exercise test.

Exercise Testing Submaximal Testing

• Common criteria for test termination include: ▫ A peak heart rate between 120 and 130 bpm ▫ Achieving 70% of predicted maximal heart rate. ▫ A peak work rate of 5 METs

Symptom Limited Testing

• These tests are designed to continue until the patient demonstrates signs or symptoms such as: ▫ Angina ▫ ST-segment depression ▫ Hypotension ▫ Ventricular arrhythmias ▫ Fatigue

Exercise Prescription Modes

Goals

Intensity/Frequency/ Duration

Time to goal

Aerobic Large muscle activity

•Increase aerobic capacity •Decrease BP & HR response to submaximal exercise •Decrease submaximal myocardial VO2 demand •Decrease CAD risk factors •Increase ADLs

•RPE 11-16/20 •40-80% VO2mx or HR reserve •≥3 days/week •20-60 min/session •5-10 min of warm-up and cooldown activities

4-6 months

Strength Circuit Training

•Increase ability to perform leisure and occupational activities and ADLs •Increase muscle strength and endurance

•30-40% 1RM (upper body), 5060% (lower body) •2-3 days/week •2-4 sets of 12-15 reps •8-10 different exercises •Arbitrary weight increase

4-6 months

Flexibility Upper & Lower body ROM

Decrease risk of injury

•Static stretches: hold for 10-30 s •2-3 days/week

4-6 months

Conclusion • Regular exercise has been shown to mediate the atherosclerotic process and therefore to protect against both initial and subsequent MIs, as well as mortality from all causes. • Therefore, habitual exercise training is an accepted and important part of the rehabilitative process for patients who have had an MI.

References • ACSM. 2010. ACSM’s guidelines for exercise testing and prescription, 8th ed. Baltimore: Lippincott Williams & Wilkens, chapter 9. • American College of Sports Medicine. 2009. ACSM’s Exercise Management for Persons with Chronic Diseases and Disabilities, 3rd ed. Champaign, IL: Human Kinetics. • American Heart Association. 2012. Hear Attack. http://www.americanheart.org/ • Haskell, W.L. and J. L. Durstine. 2005. “Coronary Heart Disease” in Exercise Testing and Exercise Prescription for Special Cases, 3rd ed., J. S. Skinner, editor. Philadelphia: Lippincott Williams & Wilkens , pp. 285-304. • Mayo Clinic. 2012. Heart Attack. http://www.mayoclinic.com/health/heartattack/DS00094/DSECTION=complications • National Center for Biotechnology Information. 2012. Heart Attack. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001246/

References • Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD, Borden WB, Bravata DM, Dai S, Ford ES, Fox CS, Fullerton HJ, Gillespie C, Hailpern SM, Heit JA, Howard VJ, Kissela BM, Kittner SJ, Lackland DT, Lichtman JH, Lisabeth LD, Makuc DM, Marcus GM, Marelli A, Matchar DB, Moy CS, Mozaffarian D, Mussolino ME, Nichol G, Paynter NP, Soliman EZ, Sorlie PD, Sotoodehnia N, Turan TN, Virani SS, Wong ND, Woo D, Turner MB; on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation. 2012;125:e2-e220. • Visich, P.S. and Fletcher, E. 2009. “Myocardial Infarction” in Clinical Exercise Physiology, 2nd ed. J.K. Ehrman, P.M. Gordon, P.S. Visich, & S.J. Keteyian, eds. Champaign, IL: Human Kinetics, Chapter 16.