clase cardiopatia isquémica

8/12/2019 clase cardiopatia isqumica

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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


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


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)

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