Learning Guide: Assessment of men and women presenting with s/s
of angina, or ACS (Acute Coronary Syndrome) Definitions and
defining characteristics of: Decreased cardiac output r/t
ventricular damage, dysrhythmias Acute pain r/t myocardial tissue
damage from inadequate blood supply Risk for bleeding r/t
thrombolytic therapy Risk for peripheral neurovascular dysfunction
Definition and Indicators of these NOCs: Cardiac pump effectiveness
Tissue perfusion, peripheral Review these NICs: Cardiac Care
Cardiac care, acute Circulatory precautions
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Learning Objectives: Describe assessment strategies (and
related nursing care) for patients with ACS: Stress tests,
echocardiography, cardiac catheterization, ECG monitoring Plan,
implement and evaluate care for patients experiencing Unstable
angina, NSTEMI, MI Plan, implement and evaluate care for patients
post interventional cardiology procedures Describe interventional
(cath lab)/surgical interventions for myocardial revascularization
Describe health promotion strategies (and teaching plans) for
patients at risk of CAD/ACS.
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Cardiac Review
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A&P Review Layers of the Heart Pericardium Epicardium
Myocardium Endocardium
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A&P Review Cardiac Chambers Atria Ventricles
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Cardiac Valves Atrioventricular Valves Tricuspid and mitral
Semilunar Valves Pulmonic and aortic
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A&P Review Conduction System Atria Sinoatrial node
Internodal pathways Intraatrial bundle AV Node to Bundle of HIS
Ventricles Right and left bundle branches Purkinjie fibers
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Electrical Conduction System
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A&P Review Coronary Blood Supply Coronary Arteries Left
coronary artery divides into left anterior descending and left
circumflex Right coronary artery perfuses the right side of the
heart and in most people the SA and AV nodes In 70% of the
population the RCA perfuses the posterior coronary artery
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Right coronary artery Coronary Arteries
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A&P Review Venous Return from the Heart Coronary sinus
Thebesian vessels drain directly into the chambers of the heart and
produce physiologic shunt
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A&P Review Systemic Circulation Arterial system of
resistance vessels Capillary bed: tissue perfusion Venous system of
capacitance vessels
CAD Statistics Affects nearly 13 million people in the USA
Causes 500,000 deaths each year
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Framingham Heart Study (FHS)
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Definition of Coronary Artery Disease A narrowing of the inside
diameter of arteries that supply the heart with blood. The
condition arises from the accumulation of plaque and greatly
increases the risk of having a heart attack or myocardial
infarction (Cooley, 1996).
Nonmodifiable risk factors AGE GENDER RACE/ETHNIC BACKGROUND
HEREDITY
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Emerging Risk Factors Homocysteine= blocks NO production <
elastic Blood vessels permit plaque formation TTT= B complex Folic
acid, Niacin LDL-C = mechanical injury Prothrombotic state (e.g.,
high fibrinogen or plasminogen activator inhibitor1 in the blood)
Proinflammatory state (e.g., elevated C-reactive protein in the
blood causes inhibition of NO) Low Adiponectin levels increase CRP
production
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Five Major Risk Factors 1.Smoking 2.Hypertension 3.High
cholesterol 4.Diabetes 5.Family History
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Smoking Effects of Smoking Roughening effect of inside diameter
of the arterial wall>formation of plaque,constriction of
arteries>HPN Increases heart rate and produces irregular
heartbeats>clots>stroke Decrease HDL levels and increase LDL
> increase risk CAD
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Management of Smoking Quit Smoking Avoid secondary smoke
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Hypertension: Or high blood pressure.. SBP >120 mm
Hg..DBP>80 mm Hg Indicates a problem in the mechanism that
regulates blood pressure in the circulatory system hyper too much
tension pressure
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Hypertension Effects of HPN [Mechanical Injury] Causes
thickening or hardening of the walls off the arteries>causes
narrowing >decrease blood flow to coronary arteries>MI.
Thickening of left ventricle >decrease Cardiac output >
causes CHF > kidney damage>Renal dialysis In the diabetic
population, HPN>retinal damage(retinopathy)>BLINDNESS
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For persons over age 50, SBP is a more important than DBP as
CVD risk factor. Starting at 115/75 mmHg, CVD risk doubles with
each increment of 20/10 mmHg throughout the BP range. Persons who
are normotensive at age 55 have a 90% lifetime risk for developing
HTN. Those with SBP 120139 mmHg or DBP 8089 mmHg should be
considered prehypertensive who require health-promoting lifestyle
modifications to prevent CVD. (JNC 7, 2003) New Features and Key
Messages
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New Features and Key Messages (Continued) Thiazide-type
diuretics should be initial drug therapy for most, either alone or
combined with other drug classes. Certain high-risk conditions are
compelling indications for other drug classes. Most patients will
require two or more antihypertensive drugs to achieve goal BP. If
BP is >20/10 mmHg above goal, initiate therapy with two agents,
one usually should be a thiazide-type diuretic. (JNC 7, 2003)
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Blood Pressure Classification Normal100 (JNC 7, 2003) BP
ClassificationSBPDBP
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Benefits of Lowering BP Average Percent Reduction Stroke
incidence 3540% Myocardial infarction 2025% Heart failure 50% (JNC
7, 2003)
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BP Control Rates Trends in awareness, treatment, and control of
high blood pressure in adults ages 1874 National Health and
Nutrition Examination Survey, Percent II 197680 II (Phase 1) 198891
II (Phase 2) 19919419992000 Awareness51736870 Treatment31555459
Control10292734 Sources: Unpublished data for 19992000 computed by
M. Wolz, National Heart, Lung, and Blood Institute; JNC 6.
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Summary:
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Treatment Overview Goals of therapy Lifestyle modification
Pharmacologic treatment Algorithm for treatment of hypertension
Classification and management of BP for adults Follow-up and
monitoring (JNC 7, 2003)
Lifestyle Change: What Difference Does it Make ? Weight loss.
(decreases SBP*1.6 mm Hg for each kg lost) Dietary Approaches to
Stop Hypertension: DASH diet: (decreases systolic BP 8-14 mmHg)
Reducing salt in the diet.(decreases SBP 2-8 mmHg) 30-45 minutes
daily aerobic exercise (decreases systolic BP 4-9 mmHg) Limit
alcohol. (decreases SBP* 2-4 mm Hg) Avoidance of tobacco products.
(*SBP = systolic blood pressure)
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Medications for HPN Diuretics Beta-Blockers Calcium channel
Blockers ACEI Vasodilators
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Diabetes Causes vasoconstriction of coronary arteries
>decrease blood flow > decrease oxygen supply >increase
risk of heart attack or MI
CHOLESTEROL Effects of Increased Cholesterol levels Causes
plaguing of the coronary walls, narrows coronary arteries, creates
blockage of coronary arteries less blood flow to heart cells
>MI
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Cholesterol LDL cholesterol HDL cholesterol Total cholesterol
Triglycerides
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Serum cholesterol levels LDL Cholesterol Primary Target of
therapy Very High Total cholesterol < 200 Desirable 200 - 239
Borderline 240 > High HDL 60 High (NCEP/ATP III Guidelines,
2004)
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Management of Cholesterol Levels DIET MEDICATION NON-SMOKING
EXERCISE
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Family History Parent or sibling that died of CAD less than 60
years of age...
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Medications for CAD [1] Anti-platelet medications [2]
Medications for dyslipidemia [3] Anti- anginal medications
Medications for dyslipidemia HMG CoA-reductase inhibitors
Nursing Interventions (statins) [1] Rosuvastatin No grapefruit [2]
Simvastatin Monitor liver enzymes [3] Atorvastatin Instruct pts. mm
tenderness [4] Pravastatin Take at night Niacin [1] Niaspan,Niacin
With meals/Flushing/?med Fibric Acid Derivatives [1] Lopid 30
minutes before or with meals [2] Zetia
Summary of risk factors for CAD [1] ? [2] ? [3] ? [4] ? [5]
?
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How many risk factors for CAD do you have?
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Coronary Artery Disease
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Coronary Artery Disease (CAD) CAD is a broad term that includes
stable angina pectoris and acute coronary syndromes. When blood
flow through the coronary arteries is blocked, ischemia or
infarction of the myocardium may result.
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Ischemia and Infarction Ischemia occurs when insufficient
oxygen is supplied to meet the requirements of the myocardium
Infarction (necrosis of the cells, cell death) occurs when sever
ischemia is prolonged and irreversible damage to tissue
results.
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Acute Coronary Syndromes Angina- coronary ischemia- a temporary
imbalance between the coronary arteries ability to supply oxygen
and the cardiac muscles demand for oxygen (no permanent damage to
myocardial tissue). Stable Angina- predictable; fixed lesions
Unstable Angina- more intense, may occur at rest or with exertion
and causes marked limitations of activity. Attacks increase in
intensity and pain. Includes new-onset angina, variant
(Prinzmentals) angina, pre-infarction angina and crescendo
angina
Myocardial Infarction Irreversible necrosis due to an abrupt
decrease or total cessation of coronary blood flow. Plaque rupture
New thrombus in coronary artery
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Process of Infarction Tissue Ischemia Hypoxemia Autonomic
Nervous System Influences Metabolic Derangement Acid-base
imbalances Hemodynamic disturbances Electrolyte disturbances Fiber
stretch
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Zone of Infarction Dependent on Three Factors: Collateral
circulation Anaerobic metabolism Workload demands
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Types of Infarction Subendocardial Infarction (non-Q wave)
(multifocal areas of necrosis confined to the inner 1/3-1/2 of the
left ventricular wall. These do not show the same evolution of
changes seen in a transmural MI. ) Transmural Infarction (Q wave)
(involving the entire thickness of the left ventricular wall from
endocardium to epicardium, usually the anterior free wall and
posterior free wall and septum with extension into the RV wall in
15-30%). Physiologic response = ventricular remodeling (change in
shape and size of L ventricle causing decrease L V F leading to
HF)
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Zones of Infarction Zone of Ischemia = T-wave inversion Zone of
Injury = ST elevation Zone of Necrosis = Abnormal Q wave
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Classification of MI by Location Inferior: Abnormalities that
appear in leads II, III, and F (called the inferior leads) indicate
pathology on the inferior or diaphragmatic surface of the heart.
Lateral: Leads I, F, and V5-V6 are called lateral leads.
Abnormality in these leads indicates pathology on the lateral,
upper surface of the heart. Anterior: Anterior pathology is seen in
leads V1-V4, and often in lead I. Posterior: Problems on the
posterior surface of the heart are difficult to diagnose using the
standard 12 ECG leads. The pathology may be seen as reflected
through V1 and V2. Combination: Abnormalities may not be limited to
one of the four areas above. Inferolateral damage will show up in a
combination of the inferior and lateral leads. Anterolateral damage
will be seen in both the anterior and the lateral leads.
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Normal 12 lead EKG
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? MI????
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Identify which coronary artery is affected? [1] severe crushing
chest pressure/pain/radiating to neck [2] chest pressure/pain with
radiation to L arm [3] chest pressure radiating to the
back/scapula.
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Cultural Considerations Black and Hispanic women have a higher
incidence of CAD risk than white women with comparable
socioeconomic status Native Americans/American Indians/Alaskan
Natives >18 years of age have greater incidence of HTN, smoking,
high cholesterol, excess weight, and/or diabetes mellitus Leading
cause of death in men and women in the most prevalent ethnic groups
is cardiac disease even though there are genetic predispositions to
develop risk factors (AHA, 2003)
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Cultural Considerations Higher incidence of HTN in Black
community and in whites in the South Black individuals experience
longer delays in seeking treatment Symptom may be dyspnea and not
chest pain Symptoms in older adults may not be associated with
acute chest pain
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Women and Heart Disease More women than men have angina but
many women experience atypical angina. What does atypical mean?
Women have MI at older ages than men Lack of education in women
that CAD is the leading cause of death in women Pathophysiology in
women is different than men i.e. smaller vessels, less collateral
circulation than men Impaired glucose tolerance seriously increase
risk
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Heart Disease: The Leading Cause of Death for American Women
American Heart Association
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Cardiovascular Disease Mortality Trends United States:
1979-2001 Source:CDC/NCHS.
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Why The Gender Gap? Women present to emergency rooms or chest
pain centers 1- 2 hours later than men. Do the multiple roles a
woman takes on delay care because of her responsibilities to
others? Do women delay care because they perceive that heart
disease is something that happens to ones father, brother, or
spouse?
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Differences in Heart Attack Symptoms Men Sub-sternal chest pain
or pressure Rest pain Pain down left arm and shoulder Weakness
Women Pain in chest, upper back, jaw or neck Shortness of breath
Flu-like symptoms: nausea or vomiting, cold sweats Fatigue or
weakness Feelings of anxiety, loss of appetite, malaise
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Postmenopausal Hormone Therapy (HT) Postmenopausal HT is no
longer recommended as a strategy to prevent heart disease. Hormone
therapy, generally short term, may still be used to treat symptoms
of menopause - this is a decision between a woman and her
healthcare provider.
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The Red Dress Campaign
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Cardiac Management
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Collaborative Management History Pain Assessment Cardiovascular
Assessment Psychosocial Assessment Laboratory Assessment
Radiographic Assessment Other Diagnostic Assessments
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History/ Pain Assessment Historical data If chest pain present,
describe and find out for how long (time is muscle) Attempt to
differentiate between angina pain and infarction pain Associated
symptoms patient describes i.e. N/V, diaphoresis
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Cardiovascular and Physical Assessment Vital signs Monitor for
dysrhythmias Distal peripheral pulses Heart and Lung sounds
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Cardiac Auscultation
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Psychosocial Assessment Denial Fear Anxiety Anger
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Laboratory Assessment Troponin T and I- myocardial muscle
protein released into the bloodstream with injury to the myocardial
muscle (not found in healthy clients) Creatine kinase- MB (CK-MB)
is an enzyme specific to cells of the brain, myocardium and
skeletal muscle. Indicates tissue necrosis or injury, Cardiac
specificity is determined by measuring the isoenzyme activity CK-
MB is found in myocardial muscle CK-MM (skeletal) CK-BB (brain)
Myoglobin early marker of MI is a low-molecular-weight heme protein
found in cardiac and skeletal muscle, appears as early as 2 hours
after an MI with rapid decline after 7 hours C-Reactive Protein is
a marker of inflammation. Any inflammatory process can increase CRP
in the blood
Radiographic and Other Diagnostic Tests Chest X-ray ECG- what
are we looking for? Stress Tests- exercise tolerance testing with
or without pharmacologic agents Myocardial Perfusion Imaging-
Thallium scans Cardiac Catherization
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This procedure is performed to determine the extent and exact
location of obstruction of the coronary arteries. Helps to identify
course of therapy for patients i.e. PTCA/stent or CABG
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Nursing Diagnosis & collaborative problems. Acute pain
related to biologic injury agents Ineffective tissue perfusion
related to interruption of arterial blood flow Activity intolerance
related to fatigue Ineffective coping related to effects of acute
illness and major changes in lifestyle Potential for dysrhythmias
Potential for heart failure Potential for recurrent symptoms and
extension of injury
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NICs/NOCs NIC Pain Management Drug Therapy NOC Ineffective
Tissue Perfusion- expect to have adequate blood flow to maintain
heart function Ejection fraction Pulmonary wedge pressure Apical
heart rate Systolic and diastolic blood pressure