clase cardiopatia isquémica
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Coronary Artery Disease
Arthrosclerosis
Ischemia
Infarction
Collateral Circulation
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Non-modifiable risk factors
Age average - 65 men -70 women
Gender
Family history
Ethnic backgroun d
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Modifiable risk factors Elevated serum cholesterol levels
Cigarette smoking
Hypertension
Impaired glucose tolerance
Obesity
Physical inactivity
Stress
Diabetes
Oral Contraceptives
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The major underlying cause isatherosclerosis.
Atherosclerosis is a slow, progressivedisease which begins in childhood andtakes decades to advance
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Pathogenesis ofAtheroma
1. Fatty streak development
2. Atheromatous plaque development3. Thrombus development
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Fatty streakdevelopment
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Dr. Enos and Holmes reportedon autopsis of 2000 deadsoldiers in Korean War averageage 22.
35% had fatty streaks in coronaryarteries42% had had establishedatheroma
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Average adult Aorta, mildfatty streaks, earlyatheroma.
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Aorta. Arrow at prominentfatty streak
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Initiation of atheroma bydamage to endothelium
which becomes more porousto lipids and monocytes
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Monocytes fromblood streampass through
endothelium intoblood vessel wall
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Healthy Coronary Artery cross section
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Hypertension
Homocysteine
Bacteria
Smoking
Diabetes
Initiators of Endothelial Dysfunction
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Oxidized LDL
Cytokines
Glycolatedend products
Initiation of Monocyte attachment with activation of endothelialtranscription nuclear factor Kb (TNF-Kb) by oxidized low density
lipids, cytokines, and glycolated end products seen in diabetes.
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Vascular cell wall adhesion molecule (VCAM-1)is induced by TNF-Kb
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Vascular cell wall adhesion molecule (VCAM-1)is induced by TNF-Kb
VACM-1
VACM-1
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VCAM-1 and chemokine monocytic chemotactic protein I localizesmonocytes in vessel wall.
VACM-1
VACM-1
MCP1
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Low Density Lipids
(LDL) pass throughdamaged
endothelium intoblood vessel wall
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LDL
LDL
LDL
C o r o n a r y
A r t e r y
D i s e a s e
Low density lipids (LDL) oxidized in vessel wall
O
O
O LDLO
LDLO
LDLO
LDLO
LDLO
LDLO
LDLO
LDLO
LDLO
LDLO
LDLO
LDLO
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LDLs are oxidized and then
induce production of bioactive molecules such asInterleukin 1, Interleukin 6,matrix metalloproteases,Prostaglandins.
Platelet Derived GrowthFactor, Tumor NecrosisFactor Alpha.
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MMP
MMP
Cytokines
Cytokines
Prostaglandins
LDLO
LDLO
LDLO
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Monocytes
transform tomacrophages
and take up LDLto form foam cells
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Monocytes triggerchronic inflammatoryreaction withlymphocytes and
this results in tissuenecrosis and fibrosis
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MMP
MMP
Cytokines
Cytokines
Prostaglandins
LDLO
LDLO
LDLO
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Bacteria
Cytokines
Circulating bacteria and cytokines add to inflammation.This leads to Atheromatous plaque formation
MMP
MMP
Cytokines
Cytokines
Prostaglandins
LDLO
LDLO
LDLO
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High DensityLipids (HDL)inhibitoxidation of LDL
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Enzymes associated withHDL apolipoproptein(apoAL) and para-
oxenase (PON) protect bydestroying the oxidizedpro-inflammatory lipids
from LDL
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PON also inhibits
LDL induced MonocyteMigration.Periodontitismay cause reduction in
Apo AI and PON and soincreasethe level of oxidized lipids
and monocytes in bloodvessels walls.
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HDL
HDL
HDL
LDL
LDL
LDL
O
O
O
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HDL
HDL
HDL
LDL
LDL
LDL
O
O
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ATHEROMATOUSPLAQUEDEVELOPMENT
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Blood vessel wallbecomes distendedand continues toaccumulatecholesterol, some
areas becomecalcified
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Coronary artery with atheromatous plaques (arrows)
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THROMBUSDEVELOPMENT
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Coronary Artery with stable atheroma. Inflamation andnecrosis have replaced the smooth muscle but there is a
dense layer of collagen next to lumen (arrows)
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MMP
MMP
MMP
MMP s from macrophages and proteases fromcirculating bacteria can destroy collagen to
form an unstable atheromatous plaque
BacterialProteases
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
MMP
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Blood vessel wall
can rupture andthen get thrombus
formed at region ofulceration
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Endothelium is destroyed with exposure ofcollagen and plaque to arterial blood.
e
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Platelets aggregate on exposedcollagen to form a thrombus. C
o r o n a r y
A r t e r y
D i s e a s e
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Increase thrombosis can lead to suddenocclusion of vessel
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Coronary Artery occluded by thrombosis
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Oral Bacteria
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Thrombosis can giveocclusion of vessel.
This is responsible for
50% of cases ofmyocardial infarction
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Calcification (blue area) and distended vessel wall withnarrowed lumen of Coronary Artery.
lumen
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Ultrafast CAT Scanof Thorax ShowingCross-Section of Heart.Calcified Tissues StainedPink.
Note: Calcified AtheromatousPlaques in Coronary Arteries
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Early infarct affecting leftventricle
thrombus
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Cross section of heart with area of necrosis
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Infarct in ventricular wall with loss of muscle andscarring
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Area of previous infarct with rupture of ventricularwall
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Histology ofMyocardialInfarction
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Beginning of infarct, loss of striations and nuclei ofcardiac muscle
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Myocardial infarct with replacement of necroticmyocardium with inflammatory cells and fibroblasts
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Established infarct with fibrotic scarring inmyocardium
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Cardiovascular Assessment
Subjective Data: Personal/Familiar HX, CP,Dyspnea, weight changes etc.
Physical Assessment: Skin, extremities, BP,
JVP, Lungs, Precordium Objective Data: Labs: CPK/ troponin
Hypo/ Hyperkalemia
Hypocalcemia
Serum Na
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Angina Pectoris Ischemia
Stable angina
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Acute Coronary Syndrome Unstable angina S/S Squeezing pressure, ache, or
heaviness Aching tooth neck or jaw Aching back/arms Feeling of choking, gas Pale, sweaty skin Myocardial infarction
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Pathophysiology of InfarctionPlague evolution lipid deposits
Hypoxia (dec O2)
Local vasodilation of blood vessels/acidosis.
Cellular potassium, calcium and magnesiumimbalances / acidosis
Suppression of normal conduction andcontractile functions.
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Pathophysiology of Infarction
Automaticity and ectopy are enhanced
Catacholamines (epinephrine and
norepinephrine) released in response tohypoxia and pain
Increases the hearts rate and contractility
and after load
P th h i l f I f ti
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Pathophysiology of InfarctionIncrease in O2 requirements in tissue O2 deprivedtissue.
Infarct extend into areas of injury and ischemiaThis depends on 3 factors:
Collateral circulation,Anaerobic metabolism
Work load demands of the myocardium
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Pathophysiology ofInfarction
Subendocaardium (subendocardial MI) - not totalwall less severe
Transmural - spread to theepicardium or all three layers ofcardiac muscle
Effects the wallmotion andcardiac output.
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Physical Changes
6 hours infarct area appears blue and swollen
48 hours infarct turns gray with yellow streaks asneutrophils invade the tissue and begin
to remove the necrotic cells.
8-10 days the necrotic area eventually develops intoa shrunken, thin firm scar.
2-3 months granulation tissue forms at the edges ofthe necrotic tissue.
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Pathophysiology of Infarction
Ventricle remodeling
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Classification of MI by location
Anterior
Lateral
Septal
Inferior
Posterior
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Assessment /ClinicalManifestations
Pain P where is pain Point to it.
Q uality sharp/dull
R adiation jaw, neck, armS everity 1-5T ime how long
Precipitating and relieving factors
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Assessment /Clinical Manifestations Restlessness
SOB
Diaphoresis
Nausea/Vomiting
Signs of shock
Angina pain
Associated symptoms
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Assessment /Clinical Manifestations
Vitals
Rhythm
Psychosocial
Distal pulses
Skin temp
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Silent MI
15 -20% painless or atypical MI
Toothache
Pain in jaw/arm
May not be found until years later when
EKG changes are found
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Coronary ArteryDisease
In Women
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Lipid management
and control of othercoronary risk factors in
post menopausal women J. Womens Health and Gender related
Med. 9:235,2000
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Stroke andmyocardial infarction
Number one killer of
women with 500,000deaths per year
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African American
and Hispanicwomen at greaterrisk than Caucasian
women
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This is more than
the next 16causes of death
combined
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Risk ofMyocardial
infarction lowerin women than
men
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First myocardial
infarction in womenis more severe andmore lethal than
they are in men
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Womens mortality
rate at 6 monthspost myocardialinfarction double
that of men
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Analysis of 350,000
patients afterfibrinolytic therapy forinfarction.
Mortality for
women 9.3%, men 4.5%
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Without fibrinolytic therapy16% mortality for women10.9% for men
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Coronary artery
bypass surgeryoperative mortality4.5% women,
2.6% men
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Menopauseoften causes
increase in totalcholesterol and
LDL
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Estrogen
increase HDLlevels
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Post menopausalhormonal therapy
gave 53% reductionin death from CHD instudy using 121,700
registered nurses
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Framingham Study.Risk of coronary
artery diseasedoubles withonset of
menopause
C di l Di D i g 6 9
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Cardiovascular Disease During 6.9Years of Hormone Therapy
20 centers with 2,763 post menopausalwith C.H.D. average age 67 years.Hormone group got 0.6625mg conjugatedestrogen, 2.5mg medroxyprogesteroneacetate daily.Hormones gave no significant decrease inC.H.D. events - infarct or deathhospitalization angina revascularization,congestive heart failure, stroke, ischemiaor ventricular arrhythmiaAnother study on same population showedhormone group had increased rated ofvenous thrombo-embolism and biliary tractsurgery.261 deaths compared to 239 in controls
Grady, D. et al JAMA 2002, 288:49
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Heart Disease and Women
#1 risk.
Early knowledge with first MI
Underrepresented in clinical trials forcardiovascular drugs
Studies predominately middle -aged men
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Cardiovascular risk factors
DM Hypertension Obesity
Family history
Pregnant Birth control pills
Menopause
S t Di iti
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Symptoms Disparities
Sex differences Different signs and symptoms
Women
Men
Classic symptoms are far less common in women
Women are misdiagnosed and discharged from ED.
Women Early Symptoms
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Women Early Symptoms
Onset Unusual fatigue
Sleep disturbances SOB
Weakness Indigestion
Anxiety Unresolved symptoms
Hormonal status
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Diagnostic Differences
Suspected CHD - Not tested
Coronary vessels
Atherosclerosis
Test interpretation
ST -segment elevation False positive test results.
Psycho social Assessment
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Psycho-social Assessment
Men and women Denial
Fear
Anxiety
Anger
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Diagnostic Tests Lab Troponin T and I Creatinine kinase MB (CK-MB)
Myoglobin
EKG: Einthovens Triangle
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EKG: Einthoven s Triangle
I, II, III measure differences in activity between the limbleads
AVR, AVL, AVF measure activity between the heart &the limbs
V1-V6 measure activity of heart on horizontal plane
Diagnostic Tests - EKGA Normal ECG prior to MI
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A. Normal ECG prior to MI
B. Hyperacute T wave changes -increased T wave amplitude andwidth; may also see ST elevation
C. Marked ST elevation withhyperacute T wave changes
(transmural injury)
D. Pathologic Q waves, less STelevation, terminal T waveinversion (necrosis)
E. Pathologic Q waves, T waveinversion (necrosis and fibrosis)
F. Pathologic Q waves, upright Twaves (fibrosis)
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Diagnostic Tests
Echocardiogram
Transesophageal Echo
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Diagnostic Tests Stress test
Medication stress testing adenosine (Adenocard) dobutamine (Dobutrex)
Myocardial perfusion imaging Thallium scans Dipyridamole (Persantine)
Radioisotope imaging
MRI Cardiac Catheterization
Prognosis
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Prognosis
30 -40 % expire before reaching hospital
80% reach hospital survive
Of 20% that expire occurs usually in 3-4days of admission. arrhythmias
30 year olds ignore especially with DM
Medical Treatment
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Medical Treatment ICU /Telemetry unit
Emergency angioplasty Pain relief Thrombolytic agents Aspirin 160 325mg on day 1 and thenindefinitely thereafter. Antiplatelet agents Oxygen Rest and more rest
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Drug Therapy
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Drug Therapy
SL Nitroglycerin - vasodilation Total of 3 pills in 5 minute increments Under tongue Relief time
Storage Self life Tingle Vital Signs
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Drug Therapy
Nitroglycerin
Paste AM/PM IV nitro - slow initial infusion
Check BP and pain every 3-5 minutes dose is increased until pain is relieved BP falls excessively or the max dose is reached SE: Headache
Drug Therapy
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g pyMorphine
Chest pain unresolved by Nitro. Action: Dose:
2-10mg IV every 5-15 minutes until max dose Side Effects Toxicity
Drug Therapy
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Drug Therapy
Beta Adrenergic Blockers Decrease the size of the infarct, ventricular dysrhythmias, and mortality rates in clients withan MI. Cardioselective BB Noncardioselective BB Wean off or rebound MI may occur
Drug Therapy
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Drug Therapy
Ace Inhibitors
Prevent ventricular remodeling and the development of heart failure (first 48
hours) Survival rate Nursing Intervention: Potassium effects
Drug Therapy
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Drug TherapyCalcium Channel Blockers
Clients with Angina. Vasodilation and myocardial perfusion. Angina use
Monitor the client
Drug Therapy
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Calcium Channel Blockers
Nifedipine ( Adalat, Procardia (XL)) Verapamil (Calan Isoptin) - (slows SA and AVconduction)
Diltazem ( Cardizem ) Amlodipine ( Norvasc) Nicardipine (Cardene)
Drug Therapy
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Drug Therapy
Anti-platelet Agents
Action ASA Dosing Aspirin 81- 650mg/day SE: Clopidogrel (Plavix) Ticlopidine (Ticlid)
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Drug Therapy
Thrombolytic Therapy
Dissolve thrombi
IV or Intracoronary during cath Indications CP > 30 min unrelieved by nitro withindications of transmural ischemia and injury on EKG Chest pain
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Drug Therapy
Thrombolytic Therapy
Dissolve thrombi IV or Intracoronary during cath
Indications CP > 30 min unrelieved bynitro with indications of transmuralischemia and injury on EKG Chest pain
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Drug Therapy
Thrombolytic Therapy
Post procedure Vital signs Neuro status Assess bleeding external and internal Clotting studies Successful?
D Th
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Drug Therapy
Fibrinolytics
Dissolve blood clots that have formed in certain blood vessels.
Given only by or under the direct supervision Tissue Plasma activator t-PA, Retavase, TNKase
D g Th
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Drug Therapy
Fibrinolytics
Streptokinase Anisoylatedplasminogen activator Urokinase
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Angina & MI Interventions All interventions relate to oxygen supply & demand
There is a decreased O2 supply in hypoxemia, such as anemia
An increased O2 demand in tachycardia, increased preload, increasedafterload
The goal is to increase O2 supply (increase coronary blood flow) & deceaseO2 demand (decrease ht rate, decrease preload & afterload)