NECROSIS

(occuring w/MI)

results in permanent loss of contraction of the necrosed area of the myocardium.

cardiac cells can w/stand ischemia for about 20mins before cell death occurs.

size (area) & severity of the infarcted area depends on:

whether a main artery or one of the branches is affected

degree of collateral circulation: # of diff. pathways in which blood can reach an organ (in this case, the heart)

End RESULT:

Pumping effectiveness decreases

-loss of contractility

-decreased function of injured & ischemic area.

HEALING PROCESS

after

MI

infarcted cells become edematous, rupture, release enzymes

inflammatory process:

from 24hrs- beginning of inflammation

To 2-3 months- well developed scar tissue

ECG changes for 3-4 days

-10mins after getting to hospital need ECG

-T wave inversion= acute MI

-ST segment elevation= key DX w/MI

-abnormal Q wave= indicator of MI

Scar tissue replaces necrotic tissue w/in 6 weeks

CARDIAC ENZYMES

CK-MB: (creatine kinase heart muscle) cardiac specific isoenzyme; found only in cardiac cells. ONLY increases when there has been damage to the cardiac cells. (increase in a few hrs & peak after 24hrs).

Troponin: protein found in myocardium, reg. the myocardial contractile process. 3 isomers; C, I, & T.

I & T: specific to cardiac muscles; markers of myocardial injury.

levels increase after a few hours of acute MI & still be evelvated 3wks later. 

LDH: (isoenzyme) LDH 1 (heart muscle) level to LDH 2 (blood) suggests acute MI.

Myoglobin: heme protein that helps tranport O2 (foundin cardiac & skeletal cells). starts to increase 1-3hrs after onset of symptoms & peak in 12hrs

when lab results are neg. can r/o MI

GOAL

of

MEDICAL MANAGEMENT

w/MI

minimize myocardial damage & prevent complications-

Morphine

O2

Nitrogen

Aspirin

Early

TX for

MI

provide cardiac resuscitation if necessary

immediate hospitalization

TX life threatening dysrhythmias

alleviate pain & suffering

Preserve as much myocardium as possible by increasing coronary blood flow

Medical TX

for

MI

rapid transit to hospital

Obtain 12 lead ECG (electrocardiogram) to read w/in 10mins

Obtain labs= blood specs. for cardiac biomarkers

ex. Troponin

Obtain Dx tests to clarify Dx

Begin routine medical interventions:

supp. O2

Nitroglycerin

Morphine

Aspirin 162-325mg

Beta-blocker

angiotensin-converting enzyme inhibitor in 24hrs

anticoagulant

Evaluate for indications for REPERFUSION therapy:

percutaneous coronary intervention

thrombolytic therapy

Continue therapy as indicated:

IV heparin, low molecular heparin, bivalirudin (direct thrombin inhibitor), or fondaparinux (anticoag.)

Clopidogrel (plavix)= prevent stroke & heart attack

glycoprotein inhibitor (reduce risk for heart attacks)

Bed rest for a min. of 12-24hrs

INDICATIONS

for

THROMBOLYTIC

Therapy

w/MIs

Used to TX (some) pts w/acute MI.

Chest pain longer than 20mins, unrelieved by Nitroglycerine

ST segment elevation in @ least 2 leads that face the same area of the heart

Less than 6hrs from onset of pain

CONTRAINDICATIONS

of

Thrombolytic Therapy

to TX

MIs

Active bleeding

know bleeding disorder

Hx of hemorrhagic stroke

Hx of intrcranial vessel malformation

Recent major surgery or trauma

uncontrolled hypertension

pregnancy

NSG considerations

in using

Thrombolytic

Therapy

for

MIs

min. the # of times the pt.'s skin is punctured

avoid IM inj.

draw blood for labs when starting IV line

start IV lines before thrombolytic therapy; designate one line to use for blood draws

avoid continual noninvasive blood pressure cuff

monitor for acute dysrhythmias or hypotension

monitor for reperfusion: resolution of angina or acute ST segment changes

Check for s/sx of bleeding:

decrease Hct & Hgb

decreased B/P

oozing or bulging veins @ invasive puncture sites, back pain, muscle weakness, changes in LOC, complaints of HA

TX major bleeding by d/c thrombolytic therapy &anticoags; apply direct pressure & call DR immediately

TX minor bleeding by applying direct pressure if accessible or appropriate; continue to monitor 

make sure typed & cross matched blood is on hand

peak of CK-MB less than 24hrs

ventricular dysrhytmias may occur when clot is lysed

THROMBOLYTICS

used most

often

Streptokinase ( streptase, kabikinae)

ateplace (t-PA, activase)

reteplase (r-PA, TNKase)

anistreplase (eminase)

Thrombolytics

after

care

Heparin- to prevent re-thrombosis & re-occulsion

ASPIRIN= preventitive & used to TX; antiplatelat (anti-inflammatory

Monitor PTT

Monitor for chest pain

-more nitro or morphine if needed

Beta blockers

O2

ECG monitoring

Potential Complications

of

MIs

Ventricular Dysrhythmias

acute pulmonary edema

Heart failure

Cardiogenic shock

cardiac arrest

pericardial effusion

cardiac tamponade (when compression of heart r/t the fluid build up b/t the myocardail & pericardial space)

LIDOCAINE

to suppress ventriclar dysrhythmias

Loading 1mg/kg @ 25-50mg/min IV

Successive does: 15-20mins

.5mg/kg q8-10min up to .3mg/kg

or

300mg over 1 hr

Contin. dose:

2gms in 500ml D5W @ 2-4mg/min

potential complications:

Left Ventricular Failure

&

Pulmonary Edema

S/SX:

crackles

dyspnea

orthopnea

tachycardia

hyotension

cyanosis

increased hemodynamic measurements

NSG assessments:

VS

LS

heart sounds

temp.

hemodynamic monitoring

Pharmacological

Therapy

for

MIs

Thrombolytics

Morphine sulfate

Nitroglycerine

Lidocaine

Heparin/ASA, or other anticoags.

Diazepam (valium)

Beta blockers

DIET

in the

Acute phase

of

MIs

avoid large meals

avoid ingestion of myocardial stimulants (caff.)

avoid swallowing exceptionally hot/cold food/drink

avoid a constipating diet

limit foods known to produce gas during digestion

follow a diet plan prescribed for individual needs;

wt loss

low K+

low Na+

low cholesterol 

Emotional

&

Behavioral

responses

to

MIs

&

lifestyle change

Denial

anger

anxiety

fear

dependency

depression

realistic acceptance

Teaching

the

MI client(s)

effective MI & healing process

prevention of further risks

effect of activity on the heart

participation in planned program of increased activity under medical supervision

resumption of sexual activity

effects of stressors on the heart

benefits of stress management techniques

benefits of participation in group counseling sessions for client & spouse

benefits of return to usu. home activities

& relationships ASAP

benefits of return to work at earliest opportunity as prescribed spec. by a DR