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N305: Myocardial Infarction Heart Attack

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... atherosclerosis and a complete occlusion of an artery by an embolus or thrombus ... Ischemia can lead to myocardial cell death within 30 minutes (50% of the ... – PowerPoint PPT presentation

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Title: N305: Myocardial Infarction Heart Attack


1
N305 Myocardial InfarctionHeart Attack
  • A life-threatening condition characterized by the
    formation of localized tissue necrosis within the
    myocardium
  • usually caused by reduced blood flow in a
    coronary artery d/t atherosclerosis and a
    complete occlusion of an artery by an embolus or
    thrombus
  • other causes vasospasm, ?O2 supply, ?O2
    demand

2
  • Ischemia can lead to myocardial cell death within
    30 minutes (50 of the involved myocardium dies
    within two hours!)
  • As the myocardial cells necrose (die),
    intracellular enzymes and cardiac muscle
    proteins are introduced into the blood stream
  • The most common site of infarction is the
    anterior wall of the left ventricle, due to
    occlusion in the LAD branch of the LCA (referred
    to as an anterior MI)

3
  • Other sites
  • L circumflex (posterior or lateral MI)
  • RCA (inferior MI, 25 of the time in RV)
  • MI may also be classified according to depth of
    infarct
  • subendocardial, intramural, or subepicardial
    (involving one layer) - non-Q wave
  • transmural (all three layers of myocardial tissue
    involved) - Q wave (see abnormal Q wave within 3
    days)
  • ST segment elevation MI (STEMI)
  • Non-ST segment elevation MI (NSTEMI)

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  • Infarct site known as zone of infarction
  • Next zone, zone of hypoxic injury
  • Outermost zone, zone of ischemia, a zone of
    reversible damage
  • Each zone is associated with corresponding time
    mediated EKG changes
  • infarct zone (Q wave within 1-3 days)
  • hypoxic injury zone (ST segment elevation
    immediately)
  • ischemic zone (inverted T wave within 1-2 days)

6
- The first six hours after the onset of pain is
the crucial time frame for salvage of the
myocardium time is muscle in relation to
outcomes - The first 24 hours after an MI is the
time of highest risk for sudden death
7
Prognosis
  • 70-80 survive the initial attack
  • chances for survival diminish with age (gt80yrs.
    60 mortality rate)
  • the co-existence of another cardiovascular
    disease, respiratory disease, or uncontrolled
    diabetes carries a mortality rate above 30
  • 30 mortality rate with anterior MI
  • 60 mortality rate if hypotensive (SBP lt55) on
    admission

8
Non life threatening complications
  • Pericarditis r/t inflammation (28 of clients
    with Q wave infarct, within 2-4 days)
  • Mitral valve insufficiency (d/t rupture of
    papillary muscle of the LV, a complication of
    myocardial necrosis) within 2-7 days

9
Life-threatening complications
  • severe dysrhythmias (40-50 of all deaths)
  • cardiogenic shock (9 with 80 fatality rate)
  • heart failure (1/3 of in-hospital deaths)
  • heart (ventricular) rupture (d/t myocardial
    necrosis)
  • pulmonary embolism (10-20, secondary to DVT or
    atrial flutter or fibrillation)
  • recurrent MI
  • Extent of damage determined by the size of the
    infarct and the amount of collateral circulation
  • Complete recovery may take anywhere from 6-12
    weeks

10
Clinical Manifestations See chart 28-6, p. 729,
in course text
  • Chest pain
  • of sudden onset (unlike angina, no precipitating
    event), lasting longer than 20 minutes
  • similar to, but more severe than, anginal pain
  • not relieved by rest or nitroglycerine
  • may radiate to the neck, jaw, shoulder, back, or
    left arm
  • may also be associated with nausea or dizziness,
    SOB, anxiety, weakness or fatigue, palpitations,
    cold sweat, or paleness (pallor)

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Diagnosis
  • history of present illness/presenting symptoms
  • past hx. (known hx. of CAD)
  • family history
  • baseline EKG (within 10 minutes on arrival)
  • laboratory tests (cardiac enzymes/cardiac
    biomarkers)
  • physical exam insufficient on its own

13
EKG changes (time mediated)
  • occur in the leads that view the involved
    surfaces of the heart
  • due to ischemia, injury, and necrosis
  • T wave inversion (ischemia) 2
  • ST segment elevation (injury) 1
  • Q wave ?er than 25 of the R wave in depth
    (infarct) 3
  • T wave ST segment changes eventually revert to
    normal Q wave change persists

14
Serum Markers of AMI see Table 28-5, p. 731, in
course text
  • Enzymes are proteins inside all living cells
  • CK-MB (one of three isoenzymes of CK)
  • increase 4-8 hrs. after pain onset, peaks in
    12-24 hrs., return to normal levels in 3 days
  • Myoglobin (a heme protein that helps to
    transport oxygen, found in cardiac and skeletal
    muscle)
  • rapidly released into bloodstream, detected
    within 1-3 hrs., peaks within 4-12 hours, not
    diagnostic after 12 hrs.
  • lacks specificity, therefore useful only to R/O
    MI

15
  • Troponin (a protein and a basic component
    involved in myocardial contraction, isomers T I
    are cardiac specific)
  • Troponin preferred biomarker for MI (more
    sensitive and more specific than the others)
  • increase 3-4 hrs, peak in 4-24 hrs., remains
    elevated for 1-3 weeks (avg. 10 days), ? in
    unstable angina
  • enables late diagnosis (24 hours after the event)
  • may mask reinfarction occuring in 5-7 days

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Other Lab tests
  • Leukocytosis
  • appears on the second day post MI, disappears in
    one week
  • radionuclide imaging
  • Thallium scan (cold spots)
  • Technetium 99 (hot spots)
  • echocardiography (transthoracic)
  • wall motion and ejection fraction
  • transesophageal echocardiography (TEE)
  • wall motion
  • stress testing (ETT)

18
Goals of treatment
  • initiating prompt care to minimize damage,
    preserve function, and prevent complications
    (improve outcomes)
  • reperfusion of the myocardium is the ideal
  • aim for door-to-needle time of 30 min (ideally
    within 1 hour but can be given within 12 hours)
  • reducing pain
  • rehabilitating and educating the client and
    significant others (secondary prevention)

19
Medical Management
  • Treat acute attack
  • Immediate care (prehospital)
  • CPR (defibrillation) if unconscious
  • keep client quiet and calm/rest
  • ASA 162-325 mg. (non-enteric coated/chew
    swallow)
  • elevate head, loosen clothing
  • oxygen
  • IV insertion

Goldick, G. (2005). Myocardial infarction
Getting in line with the new guidelines.
Nursing, 35(9), 32cc1-32cc6
20
  • Reduce pain (upon admission)
  • administer oxygen therapy (NP _at_ 4L/min X 6
    hours)
  • initiate cardiac monitoring
  • assure/obtain IV access
  • draw serum cardiac markers/troponin
  • do a 12 Lead EKG
  • nitro SL X 3, institute Nitrodrip as ordered
  • pain control with IV morphine (drug of choice -
    ? pain, ? anxiety, vasodilator, bronchodilator)
  • example of dose for morphine is 2-4 mg q 5-15 min
    until pain is relieved (up to a maximum dose of
    15 mg/event.), monitor closely
  • admin antidysrhythmic medications as needed

21
  • Improve perfusion
  • administer anti-ischemic therapy (e.g., beta
    blockers, IV nitroglycerin)
  • administer thrombolytic therapy (STEMI only)
  • thrombolytic agents (thrombolytics), if not
    contraindicated - see Chart 28-7, p. 731, in
    course text)
  • streptokinase, tenecteplase (TNK), t-PA
    (alteplase)
  • may be given within 12 hours after the onset of
    chest pain (preferably within one, ideally within
    30 minutes)
  • ? infarct size, preserve LV function, ?survival
  • administer according to protocol (e.g., with
    heparin)
  • institute bleeding precautions

22
  • Other
  • ACE inhibitors (within first 24 hours of a STEMI)
  • prevent heart failure/decrease mortality rate
  • closely monitor BP, urine output, serum sodium,
    potassium, and creatinine
  • contraindicated with hypotension, hypovolemia,
    hyponatremia, or hyperkalemia
  • PCI (percutaneous intervention)/PCTA
  • door-to-balloon time 60-90 min
  • be prepared for emergency CABG

23
  • Monitor for complications
  • dysrhythmias
  • ectopic rhythms (esp. ventricular), conduction
    disturbances (heart blocks)
  • cardiogenic shock
  • heart failure and pulmonary edema
  • pulmonary embolism
  • recurrent MI
  • mitral valve regurgitation r/t myocardial
    necrosis (within 2-7 days)
  • Dresslers syndrome, a form of pericarditis,
    within 6 weeks to months after AMI may be
    autoimmune in nature

24
  • Rehabilitation and Education
  • bedrest (Level 1) for less than 24 hrs. unless
    complications arise
  • bedside commode for BM
  • ? 2 gm. sodium diet
  • start passive exercises
  • gradually increase (level) exercise to target
    heart rate or as tolerated (remain asymptomatic)
  • home by end of second week (after stress test,
    cardiac catheterization)

25
  • resume sexual intercourse within 4-8 weeks (if
    able to walk _at_ a rate of 3-4 mph without pain,
    wait 1 hour after eating or drinking, resume
    usual positions, caution against anal
    intercourse)
  • stop smoking
  • avoid strenuous activities (e.g., shoveling,
    activity requiring a sudden burst of energy)
  • walk daily, aiming for 2 miles in less than 60
    min
  • if asymtomatic, return to work at the end of week
    8 or 9
  • complete medical evaluation between weeks 8 10

26
Nursing Management
  • Goals
  • recognize and treat cardiac ischemia
  • administer thrombolytic therapy as ordered, and
    observe for complications
  • recognize and treat potentially life-threatening
    dysrhythmias
  • monitor for complications of reduced CO
  • see standing/routine coronary care orders
    handout
  • maintain a therapeutic critical care environment
  • identify the psychosocial impact of MI on the
    client and family
  • educate the client in lifestyle changes and
    rehabilitation

27
Prevent complications
  • no leg crossing
  • position changes/passive exercises
  • monitor fluid balance
  • control nausea vomiting

28
Activity progression
  • increase activity as tolerated (METS)
  • HR increase less than 25 of resting rate or
    120/min., no more than a 25mm Hg rise in BP, no
    dyspnea, chest pain, fatigue, or dysrhythmias, O2
    sat gt93 or a drop less than 3, a return to
    resting pulse within 3 minutes
  • get adequate rest
  • avoid valsalva (vasovagal) maneuver (e.g.,
    isometric exercise, weight lifting, constipation)
  • avoid arms above head (e.g., washing walls)
  • adoption of supervised exercise program
    (including a warm up and a cool down)
  • resumption of normal activities
  • sexual activity
  • return to work
  • drive car (3-4 weeks)

29
Education
  • cardiac anatomy physiology
  • the nature of MI
  • management of chest pain
  • drugs (action, dose, side effects, etc.)
  • ASA, nitroglycerine, ß blockers, Ca channel
    blockers, ACE inhibitors, antilipidemics)
  • need for follow-up
  • when to seek help (e.g., call 911)
  • benefits of exercise
  • other risk factor modification

30
Tailored risk factor modification
  • smoking cessation
  • diet (?Na, ?cholesterol saturated fats, ?fiber)
  • achieve and maintain ideal weight
  • blood sugar control
  • control of hypertension
  • moderate caffeine
  • HRT
  • stress management

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