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Cardiovascular Hypertension - May precipitate angina or

reflect elevated catecholamine levels d/t

anxiety or to exogenous sympathomimetic

stimulation Hypotension - indicates ventricular

dysfunction due to myocardial ischemia,

infarction, or acute valvular dysfunction

Pulse deficit may indicate atrial fibrillation

Palpitations

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Gastrointestinal

Nausea

Vomiting

Genitourinary

Decreased urinary output may indicate

cardiogenic shock

Skin Cool, clammy, diaphoretic and pale

appearance d/t sympathetic stimulation

may indicate cardiogenic shock

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Myocardial injury also causes STsegment changes. The injured myocardial

cells depolarize normally but repolarize

more rapidly than normal cells causingthe ST segment to rise at least 1mm

above the isoelectric line when measured

0.08seconds after the end of the QRS. If

the myocardial injury is on the

endocardial surface, the ST segment is

depressed 1mm or more for at least 0.08

seconds.

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MI is classified as a Q wave or non-Q wave

infarction. With Q wave infarction, abnormal Q

waves develops within 1-3 days because

there is no depolarization current conductedfrom the necrotic tissue. An abnormal Q wave

may be present w/o ST segment and T wave

changes, which indicates an old MI.

Patients with non-Q wave MIs dont develop aQ wave on the ECG after the ST segment and

T wave changes, but symptoms and cardiac

enzyme analysis confirm the Dx of an AMI.

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CKMB After cardiac injury, CK and the isoenzyme

MB are released into the blood stream at a

predictable rate. Within a 4 to 8 hour window

(post injury), the CKMB level rises above

normal and within 12 to 24 hours this level

elevates to approximately 5 to 15 times

normal. Within 2 to 3 days, the CKMB returnsto normal. Because the MB isoenzyme is

exclusive to cardiac muscle tissue, it is

considered to be a very definitive test for

diagnosing an acute MI.

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Troponin I and T these levels are not

normally found in the blood stream so

any detection of these protein in the

blood indicates the infarction or death ofcardiac muscle/tissue.

Troponin C - binds to calcium ions and

is not used to determine celltissue/death.

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Myoglobin

heme protein that helps transport

oxygen. Like CKMB enzyme, it is

found in cardiac and skeletal

muscle. The myoglobin level starts

to increase w/in 1-3 hrs and peaks

w/in 12 hrs after the onset of

symptoms.

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ECHOCARDIOGRAM

It can assist with diagnosing which

portion of the heart has been

damaged and which coronary

arteries have been affected. An

echocardiogram can also help

determine cardiac muscle

movement/contraction and cardiac

wall abnormalities.

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DYSRHYTHMIAS

A dysrhythmia is the most

common complication after an

acute MI. Dysrhythmias after anacute MI are caused by the

formation of re-entry circuits

between the still healthy and

necrotic myocardium.

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EMBOLIC COMPLICATIONS

The most common time post acuteMI for the development of embolism

is within the first 10 days. Patients

who suffer from the complication of

embolism are at risk of developing

limb ischemia, renal infarction,

intestinal ischemia but the most

common clinical presentation after

an embolic event is a stroke.

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PERICARDITIS

The cause of Pericarditis after

acute MI is due to an

inflammatory reaction thatoccurs secondary to the

presence of necrotic tissue

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When decompensation begins the

patient shows signs of shock, low

blood pressure, increased or

decreased heart rate and

decreased oxygen saturations.

Other symptoms mimic those thatare seen with congestive heart

failure and/or pulmonary edema.

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A balloon tipped catheter is then passed intothe area of blockage and inflated (no more

than 30 to 129 seconds) which in turns

helps to compress plaque against thelumina of the artery.

The balloon can also help to stretch the

lumina itself which also improves blood flow.

Of note: when the balloon is inflated, thereis an occlusion of coronary blood supply, so

patients often experience a degree of chest

pain during balloon inflation.

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NITROGLYCERIN

Nitrates such as Nitroglycerin

cause vasodilation of the vessels

and help to decrease cardiac

oxygen demand, cardiac preload

and afterload while increasing

cardiac output.

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ASPIRIN

The primary mechanism is believed to berelated to irreversible inhibition of the

cyclooxygenase pathway of platelets

(blocking the formation of thromboxaneA2 and thromboxane A2-induced platelet

aggregation). It is strongly recommended

that all patients who have suffered andacute MI be given a non-enteric coated

aspirin (160mg to 325mg) to chew and

swallow as soon as possible.

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ANTICOAGULANTS (TICLID)

Ticlid is given in 250 mg doses BID and is

also an Antiplatelet agent. Unlike aspirin,

Ticlid does not block cyclooxygenase but

instead interferes with the plateletactivation mechanism that is mediated

by adenosine diphosphate (ADP) which in

turn interferes with the fibrinogen receptorglycoprotein IIb/IIIa. It takes

approximately 2 weeks of therapy with

Ticlid before the full benefit is achieved.

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BETA BLOCKERS

A Beta blocker acts by blocking the B-adrenergic responses to catecholamine

stimulation. Beta blockers decrease heart

rate, blood pressure, contractility and

myocardial oxygen demand. Being able todecrease the work load of the heart assists

with improving cardiac output and lessens the

severity of the damage caused by the acute

MI. Beta blockers can actually interrupt an

evolving MI, limit the infarct size and

decrease the risk of ventricular arrhythmias

by decreasing oxygen demand.

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ACE INHIBITORS

ACE inhibitors block to the

conversion of Angiotensin I to

Angiotensin II (which is a potent

vasoconstrictor). The goal of and

ACE inhibitor is to decrease blood

pressure and afterload without

increasing heart rate or the

workload of the heart.

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Monitor for symptoms of heartfailure/decreased cardiac output (VS, heart

sounds, and S3 gallop).

Observe for symptoms of cardiogenicshock (cool clammy skin, hypotension,

decreased peripheral pulses, and

pulmonary congestion).

Titrate inotropic and vasoactive medicationwithin defined parameters to maintain

adequate contractility, pre/afterload and

blood pressure.

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For complaints of chest pain, medicate and noteseverity, location, radiation, what were

contributing factors (getting up, participating in

ADLs for example) and report findings.

Monitor intake and output (IV fluid, urine output,PO intake (fluid overload increases the

workload of the heart and decreased cardiac

output can cause a decrease in perfusion to the

kidneys).

Note results of diagnostic imaging studies

(EKG, radionuclide imaging, and Dobutamine

stress tests).

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Provide a proper rest/activity balance toassure that cardiac output is not

compromised (gradually increase activity as

condition warrants).

Order small sodium restricted diet (sodiumrestriction helps to avoid fluid overload).

Monitor bowel function (a stool softener

should be ordered to avoid unnecessarypushing).

Provide a peaceful environment that

minimizes stressors to promote healing.

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Weigh patient daily (same time each day, sameequipment).

Assess for the presence of anxiety (keep

environment free of unnecessary stressors,

educate patient to the rationale for interventionsand procedures).

Assess for the presence of depression

(depression is common after and acute MI and

can result in increased mortality).

Refer patient to cardiac outpatient program and

support groups. Assist with organizing cardiac

rehabilitation efforts post discharge.

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The following mnemonic may useful ineducating patients with CAD regarding

treatments and lifestyle changes

necessitated by their condition:

A = Aspirin and antianginals

B = Beta blockers and blood pressure

(BP)C = Cholesterol and cigarettes

D = Diet and diabetes

E = Exercise and education

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For patients being discharged home,

emphasize the following:

Timely follow-up with primary care

provider

Compliance with discharge medications,

specifically aspirin and other

medications used to control symptoms

Need to return to the ED for any change

in frequency or severity of symptoms

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MORBIDITY: 10 Leading Causes

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MORBIDITY: 10 Leading Causes,

Number and Rate*

Diseases5-yr. Ave(2000 2004)

2005

# Rate # Rate1. Acute Lower Respiratory Tract

Infection and Pneumonia**694,209 884.6 690,566 809.9

2. Bronchitis/Bronchiolitis 669,800 854.7 616,041 722.5

3. Acute watery diarrhea 726,211 928.3 603,287 707.6

4. Influenza 459,624 587.0 406,237 476.5

5. Hypertension 314,175 400.5 382,662 448.8

*per 100,000 population

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** Does not include ALRI,

Pneumonia cases only from 2000-2002

Diseases5-yr. Ave(2000 2004)

2005

# Rate # Rate

6. TB Respiratory 109,369 139.7 114,360 134.1

7. Heart Disease 43,945 56.1 43,898 51.5

8. Malaria 35,970 46.1 36,090 42.3

9. Chicken Pox 79,236 41.1 30,063 36.3