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Ischemic Heart Disease

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Title: Ischemic Heart Disease


1
Ischemic Heart Disease
  • Ana H. Corona, FNP-Student
  • University of Phoenix
  • May 2002

2
Myocardial Ischemia
  • Results when there is an imbalance between
    myocardial oxygen supply and demand
  • Most occurs because of atherosclerotic plaque
    with in one or more coronary arteries
  • Limits normal rise in coronary blood flow in
    response to increase in myocardial oxygen demand

3
Oxygen Carrying Capacity
  • The oxygen carrying capacity relates to the
    content of hemoglobin and systemic oxygenation
  • When atherosclerotic disease is present, the
    artery lumen is narrowed and vasoconstriction is
    impaired
  • Coronary blood flow cannot increase in the face
    of increased demands and ischemia may result

4
Angina
  • When ischemia results it is frequently
    accompanied by chest discomfort Angina Pectoris
  • In the majority of patients with angina,
    development of myocardial ischemia results from a
    combination of fixed and vasospastic stenosis

5
Chronic Stable Angina
  • May develop sudden increase in frequency and
    duration of ischemic episodes occurring at lower
    workloads than previously or even at rest
  • Known as unstable angina up to 70 patients
    sustain MI over the ensuing 3 months

6
Angina cont
  • Patients with mild obstruction coronary lesions
    can also experience unstable angina
  • gt90 of Acute MI result from an acute thrombus
    obstructing a coronary artery with resultant
    prolonged ischemia and tissue necrosis

7
Treatment of Angina
  • Treatment of Chronic Angina is directed at
    minimizing myocardial oxygen demand and
    increasing coronary flow
  • Where as in the acute syndromes of unstable
    angina or MI primary therapy is also directed
    against platelet aggregation and thrombosis

8
Epidemiology
  • Modifiable Factors hyperlipidemia- LDL (lt130
    normal) or low HDL (gt60 normal), Hypertension,
    cigarette smoking and diabetes, obesity, BMI of
    gt30
  • Non-Modifiable Factors advanced age, male sex,
    family medical history male lt55 y/o, female lt65
    y/o
  • Other sedentary lifestyle and stressful
    emotional stress

9
Homocysteine
  • Concentration of amino acid homocysteine is
    related to incidence of coronary, cerebral, and
    peripheral vascular disease
  • The risk of MI is 3x gt in patients with high
    levels of homocysteine compared with those with
    the lowest levels
  • Supplement of diet with foliate and other B
    vitamins lower levels of homocysteine but not
    known where therapy improves coronary risk

10
Fibrinogen
  • Elevated level of plasma fibrinogen is
    independent risk factor for CAD in males and
    females
  • Elevated levels of coagulation factor VII is risk
    factor X50 fold if with smoking or HTN
  • Careful HX taking to evaluate s/s include
    quality, location, radiation, precipitating
    factors, frequency

11
Quality
  • Tightness, squeezing, heaviness, pressure,
    burning, indigestion or aching sensation
  • It is rarely PAIN
  • Never sharp, stabbing, prickly, spasmodic, or
    pleuritic
  • Lasts a few seconds lt 10 minutes
  • Relieved by NTG s/l
  • Levine Sign clench fist to sternum

12
Signs Symptoms accompany Angina
  • Dyspnea, nausea, diaphoresis resolve quickly
    after cessation of angina
  • Angina is a diffuse sensation rather than
    discrete

13
Ischemic Heart Disease
  • Imbalance between Myocardial oxygen supply and
    demand Myocardial hypoxia and accumulation of
    waste metabolites due to atherosclerotic disease
    of coronary arteries

14
Stable Angina
  • Stable Angina chronic pattern of transient
    angina pectoris precipitated by physical activity
    or emotional upset, relieved by rest with in few
    minutes
  • Temporary depression of ST segment with no
    permanent myocardial damage

15
Angina Pectoris
  • Angina Pectoris uncomfortable sensation in the
    chest or neighboring anatomic structures produced
    by myocardial ischemia

16
Variant Angina
  • Typical anginal discomfort usually at rest
  • Develops due to coronary artery spasm rather than
    increase myocardial oxygen demand
  • Transient shifts of ST segment ST elevation

17
Unstable Angina
  • Increased frequency and duration of Angina
    episodes, produced by less exertion or at rest
    high frequency of myocardial infarction if not
    treated

18
Silent Ischemia
  • Asymptomatic episodes of myocardial ischemia
  • Detected by electrocardiogram and laboratory
    studies

19
Myocardial Infarction
  • Region of myocardial necrosis due to prolonged
    cessation of blood supply
  • Results from acute thrombus at side of coronary
    atherosclerotic stenosis
  • May be first clinical manifestation of ischemic
    heart disease or history of Angina Pectoris

20
Precipitants
  • Exertion walking, climbing stairs, vigorous work
    using arms, sexual activity
  • Vasoconstriction extremities, increased systemic
    vascular resistance, increased in myocardial wall
    tension and oxygen requirements
  • Myocardial Ischemia displays a circadian rhythm
    threshold for Angina it is lower in morning hours.

21
Physical Examination
  • Arcus senilis, xanthomas, funduscopic exam AV
    nicking, exudates
  • Signs and symptoms hyperthyroidism with
    increased myocardial oxygen demand, hypertension,
    palpitations
  • Auscultate carotid and peripheral arteries and
    abdomen aortic aneurysm
  • Cardiac S4 common in CAD, increased heart rate,
    increased blood pressure

22
Ischemia
  • Myocardial ischemia may result in papillary
    muscle regurgitation
  • Ischemic induced left ventricular wall motion
    abnormalities may be detected as an abnormal
    precordial bulge on chest palpation
  • A transient S3 gallop and pulmonary rales
    ischemic induced left ventricular dysfunction

23
Diagnostic Tests
  • Blood tests include serum lipids, fasting blood
    sugar, Hematocrit, thyroid (anemias and
    hyperthyroidism can exacerbate myocardial
    ischemia
  • Resting Electrocardiogram CAD patients have
    normal baseline ECGs
  • pathologic Q waves previous infarction
  • minor ST and T waves abnormalities not specific
    for CAD

24
Electrocardiogram
  • Electrocardiogram is useful in diagnosis during
    cc chest pain
  • When ischemia results in transient horizontal or
    downsloping ST segments or T wave inversions
    which normalize after pain resolution
  • ST elevation suggest severe transmural ischemia
    or coronary artery spasm which is less often

25
Exercise Stress Test
  • Used to confirm diagnosis of angina
  • Terminate if hypotension, high grade ventricular
    disrrhythmias, 3 mm ST segment depression develop
  • () reproduction of chest pain, ST depression
  • Severe chest pain, ST changes in 1st 3 minutes,
    gt3 mm ST depression, persistent gt 5 minutes after
    exercise stopped
  • Low systolic BP, multifocal ventricular ectopy or
    V- tach, ST changes, poor duration of exercise
    (lt2 minutes) due to cardiopulmonary limitations

26
Other Diagnostic Tests
  • Radionuclide studies
  • Myocardial perfusion scintigraphy
  • Exercise radionuclide ventriculography
  • Echocardiography
  • Ambulatory ECG monitoring
  • Coronary arteriography

27
Management Goals to reduce Anginal Symptoms
  • Prevent complications myocardial infarction,
    and to prolong life
  • No smoking, lower weight, control hypertension
    and diabetes
  • Patients with CAD LDL cholesterol should
    achieve lower levels (lt100)
  • HMG-COA reductase inhibitors are effective

28
Pharmacologic Therapy
  • Therapy is aimed in restoring balance between
    myocardial oxygen supply and demand
  • Useful Agents nitrates, beta-blockers and
    calcium channel blockers

29
Nitrates
  • Reduce myocardial oxygen demand
  • Relax vascular smooth muscle
  • Reduces venous return to heart
  • Arteriolar dilators decrease resistance against-
    which left ventricle contracts and reduces wall
    tension and oxygen demand

30
Nitrates cont
  • Dilate coronary arteries with augmentation of
    coronary blood flow
  • Side effects generalized warmth, transient
    throbbing headache, or lightheadedness,
    hypotension
  • ER if no relief after X2 nitro's unstable angina
    or MI

31
Problems with Nitrates
  • Drug tolerance
  • Continued administration of drug will decrease
    effectiveness
  • Prevented by allowing 8 10 hours nitrate free
    interval each day.
  • Elderly/inactive patients long acting nitrates
    for chronic antianginal therapy is recommended
  • Physical active patients additional drugs are
    required

32
Beta Blockers
  • Prevent effort induced angina
  • Decrease mortality after myocardial infarction
  • Reduce Myocardial oxygen demand by slowing heart
    rate, force of ventricular contraction and
    decrease blood pressure

33
Beta -1
  • Block myocardial receptors with less effect on
    bronchial and vascular smooth muscle- patients
    with asthma, intermittent claudication

34
Beta-Agonist blockers
  • With partial B-agonist activity
  • Intrinsic sympathomimetic activity (ISA) have
    mild direct stimulation of the beta receptor
    while blocking receptor against circulating
    catecholamines
  • Agents with ISA are less desirable in patients
    with angina because higher heart rates during
    their use may exacerbate angina
  • not reduce mortality after AMI

35
Beta-blockers
  • Duration of beta-blockers depends on lipid
    solubility
  • Accounts for different dosage schedules

36
Esmolol
  • Short acting administered intravenously
  • Can be used to test tolerability of beta-blockage
  • Used for tachydysrhythmias and unstable angina
  • Primary prevention trials beta blockers decrease
    incidence of first MIs with hypertensive patients

37
Contraindications
  • Symptomatic CHF, history of bronchospasm,
    bradycardia or AV block, peripheral vascular
    disease with s/s of claudication

38
Side Effects
  • Bronchospasm (RAD), CHF, depression, sexual
    dysfunction, AV block, exacerbation of
    claudication, potential masking of hypoglycemia
    in IDDM patients

39
Abrupt Cessation
  • Tachycardia, angina or MI
  • Inhibit vasodilatory beta 2 receptors
  • Should be avoided in patients with predominant
    coronary artery vasospasm

40
Beta-Blockers Long Term effects
  • Serum lipids decrease of HDL cholesterol and
    increased triglycerides
  • Effects do not occur with beta-blockers with
    B-agonist activity or alpha-blocking properties

41
Calcium Channel Blockers
  • Anti-anginal agents prevent angina
  • Helpful episodes of coronary vasospasm
  • Decreases myocardial oxygen requirements and
    increase myocardial oxygen supply
  • Potent arterial vasodilators decrease systemic
    vascular resistance, blood pressure, left
    ventricular wall stress with decrease myocardial
    oxygen consumption

42
Nifedipine and other dihydropyridine calcium
channel blockers
  • Fall in blood pressure, trigger increase heart
    rate
  • Undesirable effect associated with increased
    frequency of myocardial infarction and mortality

43
Calcium Channel Blockers
  • Secondary agents in management of stable angina
  • Are prescribed only after beta blockers and
    nitrate therapy has been considered
  • Potential to adversely decrease left ventricular
    contractility
  • Used cautiously in patients with left ventricular
    dysfunction

44
amlodipine and felodipine
  • Are newer CCB
  • Decrease (-) inotropic effects
  • Amlodipine is tolerated in patients with advanced
    heart failure without causing increase mortality
    when added with ace inhibitor, diuretic, and
    digoxin

45
LDL
  • Undergoes oxidation in proximity of arterial wall
    prone to atherosclerotic process
  • Vitamin E 200 400 IU daily may lower coronary
    death rates

46
Drug Selection
  • Chronic Stable Angina beta blocker and long
    acting nitrate or calcium channel blocker (not
    verapamil bradycardia) or both.
  • If contraindication to BB a CCB is recommended
    (bronchospasm, IDDM, or claudication) any of CCB
    approved for angina are appropriate.

47
Drugs
  • Verapamil and Cardizem is preferred because of
    effect on slowing heart rate
  • Patients with resting bradycardia or AV block, a
    dihydropyridine calcium blocker is better choice
  • Patients with CHF nitrates preferred amlodipine
    should be added if additional therapy is needed

48
Drugs
  • Primary coronary vasospasm no treatment with
    beta blockers, it could increase coronary
    constriction
  • Nitrates and CCB are preferred
  • Concomitant hypertension BB or CCB are useful in
    treatment
  • Ischemic Heart Disease Atrial Fibrillation
    treatment with BB, verapamil or Cardizem can slow
    ventricular rate

49
Combination Therapy
  • If patients do not respond to initial antianginal
    therapy a drug dosage increase is recommended
    unless side effects occur.
  • Combination therapy successful use of lower
    dosages of each agent while minimizing individual
    drug side effects

50
Combination Therapy Include
  • Nitrate and beta blocker
  • Nitrate and verapamil or cardizem for similar
    reasons
  • Long acting dihydropyridine calcium channel
    blocker and beta blocker
  • A dihydropyridine and nitrate is often not
    tolerated without concomitant beta blockade
    because of marked vasodilatation with resultant
    head ache and increased heart rate

51
Combinations
  • Beta blockers should be combined only very
    cautiously with verapamil or cardizem because of
    potential of excessive bradycardia or CHF in
    patients with left ventricular dysfunction

52
Other methods
  • Patients with 1 2 vessel disease with normal
    left ventricular function are referred for
    catheter based procedures
  • Patients with 2 and 3 vessel disease with
    widespread ischemia, left ventricular dysfunction
    or DM and those with lesions are not amendable to
    catherization based procedures and are referred
    for CABG

53
Unstable Angina
  • Ischemic episodes occur more frequently more
    intense, last longer.
  • Precipitated by less activity or even at rest
  • May progress to acute MI due to presence of
    complicated coronary lesions with ulceration,
    hemorrhage or thrombosis at side of
    atherosclerotic plaque
  • Lesions may heal s/s return to more stable
    pattern

54
Unstable Angina cont
  • It is a medical emergency
  • During episodes of angina, transient ST segment
    shifts or T wave flattening or inversion is
    likely
  • Signs of LV dysfunction (pulmonary rales, S3,
    Mitral regurgitation) may accompany ischemic
    episodes.

55
Unstable Angina cont
  • Therapy reduce myocardial oxygen demand with
    increase coronary flow
  • Antiplatelet and anticoagulant agents
  • Aspirin and IV heparin reduces incidence of
    myocardial infarction and cardiac death in
    unstable angina
  • Oral Antiplatelet drug ticlopidine used for ASA
    intolerance individuals

56
Enoxaparin
  • Enoxaparin low molecular weight heparin
    effective in preventing ischemic events and death
    at 30 days and 1 year after administration than
    standardized IV heparin

57
Silent Ischemia
  • Silent or painless ischemia
  • Presence of ST shifts with absence of symptoms
  • Increased risk of myocardial infarction and
    cardiac death common in diabetic patients
  • Beta blockers or calcium channel blockers and
    aspirin, cardiac catheterization, if left main or
    3 vessels disease with left ventricular
    dysfunction is demonstrated

58
Acute Myocardial Infarction
  • Is dreaded outcome in patients with ischemic
    heart disease
  • 1.5 million people sustain an MI in USA each year
  • Mortality rate of 25
  • 60 of MI related deaths occur before medical
    facilities are reached

59
Etiology
  • MI is due to prolonged myocardial ischemia -
    leads to irreversible necrosis of heart muscle
  • 90 due to acute thrombus at site of underlying
    coronary atherosclerosis
  • Non-atherosclerotic causes cocaine use due to
    ability of cocaine to increase myocardial 02
    demand, induce coronary vasospasm promote
    coronary thrombosis in association with platelet
    activation and endothelial cell dysfunction

60
Clinical Presentation
  • Initial diagnosis presenting history, PE, and
    ECG
  • Most common S/S severe crushing chest pain
  • Lasts longer than Angina, more intense, nausea,
    diaphoresis, dyspnea and feeling of impending doom

61
Symptoms
  • Circadian variability occurring most commonly in
    morning hours, soon after awakening
  • Symptoms usually begin while at rest, and only
    occasionally are brought on by physical exertion
  • Some patients have less pronounced symptoms
    generalized weakness, dyspnea, and indigestion.
  • 20 cases have no s/s detected by ECG changes

62
MI
  • Common physical findings in MI relate to impaired
    left ventricular systolic and diastolic function,
    associated inflammatory responses and stimulation
    of the sympathetic and parasympathetic nervous
    system

63
Other causes of substernal chest pain
  • Aortic dissection or pulmonary emboli may be
    fatal if not quickly recognized
  • Inappropriate administration of thrombolytic
    therapy to patients with pericarditis or aortic
    dissection could result in severe complications
    or death

64
Electrocardiogram
  • Q wave infarction, initial hyperacute T waves and
    ST elevation are present in the leads overlying
    involved myocardium
  • As cell death occurs, there is loss of the R wave
    and progressive Q wave development
  • The T wave begins to invert, followed by return
    of the ST segment over subsequent days

65
ECG cont
  • T wave may remain inverted for weeks to months
  • The new Q wave persists permanently
  • Posterior wall infarctions mirror image pattern
    in anterior chest leads
  • With initial ST segment depression
  • T wave inversion and development of tall R waves
    in leads VI and V2

66
ECG cont
  • Non Q wave infarction new ST depression and/or T
    wave inversions persist for 48 hours or longer in
    leads overlying infarcting segments
  • BBB diagnostic ECG evolution may not occur and
    diagnosis of Mi relies on presence of serum
    markers and laboratory modalities

67
Serum Markers of Infarction
  • Certain proteins are released into circulation
    during an MI
  • Creatine kinase CK rises in plasma within 4 to 8
    hours, peaks at 24 hours, returns to normal by 48
    hours to 72 hours
  • Not specific for myocardial damage skeletal
    muscle trauma and IM injection, and hypothyroidism

68
CK-MB
  • CK-MB isoenzyme is more specific for diagnosis of
    AMI
  • Not influenced by skeletal muscle injuries
  • CK-MB rises and peaks slightly earlier than total
    CK and returns to normal within 36 72 hours
  • May be elevated in myocarditis after surgery,
    hypothyroidism, repetitive cardioversion

69
Enzymes
  • Acute MI CK-MB is greater than 2.5 of total
    serum CK
  • Serum CK and CK-MB isoenzyme should be measured
    on admission, then 12 and 24 hours later in
    diagnostic evaluation of an acute MI

70
Troponin
  • Troponin I and T are sensitive and highly
    specific markers of acute MI
  • Levels begin to rise within 3 hours after onset
    of infarction and remain elevated for several
    days
  • Higher Troponin I levels or early () of Troponin
    T assay correlate with greater short-term
    mortality

71
Myoglobin
  • Myoglobin is released into circulation very early
    after myocardial injury and detected within 2
    hours of infarction
  • Rapid renal clearance and low specificity limit
    it s diagnostic role

72
Lactate Dehydrogenase (LDH)
  • Rises within 24 to 48 hours of MI
  • Peaks at 3 5 days and returns to baseline by
    7-10 days
  • Usefulness in patients who are admitted to
    hospital 2 3 days after onset of symptoms
  • Level of LDH-1 greater than LDH-2 myocardial
    necrosis

73
Thrombolytic Therapy
  • Activates the natural fibrinolytic system to
    dissolve responsible thrombus
  • Reduces mortality and improves recovery of left
    ventricular function following AMI
  • Streptokinase SK, anisoylated plasminogen-SK
    activator (APSAC), tissue plasminogen activator
    (alteplase or t-PA), and modified plasminogen
    activator (reteplase or r-PA)

74
Thrombolytics
  • Each of these drugs results in conversion of the
    proenzyme plasminogen to active plasmin which
    dissolves fibrin clots
  • Bleeding is the most important risk of each of
    these agents and their adjunctive therapies
  • Successful reperfusion relief of chest pain and
    early peak of CK within 12 hrs

75
Thrombolytics
  • Reperfusion dysrhythmias are common accelerated
    idioventricular rhythm, not require intervention
  • Antiplatelet and anticoagulant therapy used to
    maintain patency of coronary vessels following
    thrombolysis

76
Thrombolytics
  • Aspirin inhibits platelet function and reduces
    reocclusion following thrombolysis 160 325
    mg/day
  • Intravenous heparin needed to maintain vessel
    patency after initial thrombolytic therapy and is
    administered to achieve an activated PTT of 50 to
    75 seconds for 48 hours
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