• arise from the coronary sinus just above the aortic valve
• full of oxygenated blood
• 60-80% of available O2 is extracted by the heart as blood moves through coronary ateries
• left side of heart- hold back fluids!
• right side- can give fluids

• this impairs the pumping ability of the heart by depriving the heart muscle of blood-borne oxygen and nutrients
• can impair myocardial metabolism enough to cause ischemia
• silent
• 75% blockage or occlusion before occurrence of significant reduction in flood flow

• gradual occulasion of the coronary lumen due to growing plaque
• develops as an inflammatory response of the vessel wall to chronic, multifactorial injury produced by hyperlipidemia, hypertension, hyperglycemia
• will exhibit symptoms if vessel narrows too much or suddenly blocks off (75%occlusion)

• obstructs blood flow
• usually seen in stable angina
• have little chest pain but if you rest it goes away

• ruptures and causes platelet adhesion and thrombus formation
• may occur spontaneously or in response to blood flow issues of vessel tension (increased in BP, HR, contractility)

Atherosclerosis

(fatty streak)

thin, yellow streaks, irregular intima attracts platelets, macrophages produce free radicals that oxidize, causes more inflammation

Atherosclerosis

(Fibrous Plaque)

• Smooth muscle cells proliferatie, produce collagen and migrate over the fatty streak
• Lumen of the artery narrows
• vessel does not dilate or constrict as normal
• reduces blod flow distal to diseased segment..results in ischemia

Atherosclerosis

(complicated lesions)

• can ulcerate or rupture
• platelet aggregation tiggers clotting cascade
• platelet aggregation released prostaglandin
• a thrombus or clot forms and can occlude the vessel
• complete vessel occlusion causes tissue anoxia distal to the occluded segment and is called an infarction

• blood flow regulated by metabolic and O2 needs for body
• exercise increase HR more blood flow and O2 to coronary arteries

these help because:

• small arteries join by anastomatoic channels
• if..gradual occlusion of a large vessel..increase collateral vessels that improve alternative channels of blood flow

Coronary arteries originate in the root of the aorta just outside the aortic valve

filling of the three arteries is related to the amount of aortic pressure

• hyperlipidemia
• cigaraette smoking
• genetics
• sedentary life-style
• heavy ETOH consumption
• estrogen deficiency
• hyperhomocystinemia
• hypertension
• diabetes
• obesity
• gender

• increased LDL is a stong indicator of coronary risk
• Dietary management aimed at low staurated fats
• lipid-lowering drugs such as "statins" (lipitor or Zocar) help reduce this
• want high HDL and low LDL

Total cholesterol <200

want low LDL<160(BAD)

want HDL >40(GOOD)

• this is local state in which the cells are temporarily deprived of bood supply
• coronary arteries cannot supply enough blood to meet the needs of the heart
• "suppress or withhold blood flow"
• cells are alive but cannot function

this is flow or oxygen content insufficient to meet the metabolic demands of cardiac cells

it occrus if:

decreased supply of O2- impeded blood flow

increased demand of O2- exercise, increased HR, hypertension, fever, increased metabolic rate, stress, medications

• this is the most common cause of MI
• plaques form in vessels and occlude vessels-depriving of oxygen and nutrients
• if plaque ruptures-- thrombi forms, the growing mass of plaque, platelets, fibrin and cellular debris which causes narrow lumen and impedes blood flow

• this constriction is transient and reversible
• causes either subtotal or total narrowing of the coronary artery
• occurs in arteries with or without stenosis
• duration of this determines whether ischemia or infaction will occur

these are 3 types of what:

chronic stable angina, silent myocardial infarction, variant or vasospasmotic angina

this increases workload of heart, increased demand on coronary arteries which are partially occluded by atherosclerosis

O2 demand > O2 supply

often predictable

Chronic Stable Angina

(Pain)

• this is constricting, squeezing, or suffocating sensation
• steady, increasing in intensity upon onset
• located in percordial or substernal area
• may radiate to let shoulder, jaw, arm, or other chest area (similar to MI)
• provoked y exertion or stress
• relieved within minutes by rest of nitroglycerin

• this occurs in the absence of anginal pain
• occurs as a result of impaired blood flow from aterosclerosis or vasospasm
• increased incidence in person with diabetes due to autonoic neuropathy

this is usually a response to a spasm of a major coronary artery

may occur in presence or absence of CAD

occurs at rest and between midnight and 8am

RARE

triggered by smoking

treated with Ca+ channel blockers and nitrates

this includes: non-ST segment elevation (non-Q wave) MI

ST-Segment elevation (Q-wave)MI

unstable angina and non-ST segment elevation MI

(NSTEMI)

results from: atherosclerotic plaque disruption, platelet aggregation, and secondary hemostasis, coronary vasoconstriction

maybe:

primary disorder- progression of variant or stable angina

secondary disorder- noncoronary condition(anemia, infeciton)

post-infarction angina- develops witin 2 weeks of an AMI

Pain

• persistent and severe
• has at least one of three features: occurs at rest or with minimal exertion lasting more thatn 20 min
• severe and described as frank pain of new onset (<1month)
• occurs with a pattern that is more severe, prolonged or freqent than previously experienced

diagnosis

unstable angina: no increases in serum markers

elevated serum markers

ST-segment elevation MI or acute myocardial infarction

(STEMI) or (AMI)

• Heart attack
• ischemic death of myocardial tissue associated with atherosclerotic disease- 80-90% of the time causes by a thrombus
• irreversible of treated early

30-40% affect right coronary artery

40-50% affects left anterior descending artery

15-20% affect left circumflex artery

ST segment elevation MI

(manifetations)

pain

• severe and crushing
• constricting, suffocating, or heavy
• substernal with radiation to left arm, neck, jaw or other areas of chest

Gi symptoms: nausea, vomiting, epigastric distress

• fatigue and weakness, dysrhythmias, and tachycardia, anxiety, restlessness, pale, hypotensino, EKG changes

ST-segment elevation MI

(transmural infarct)

• full thickness of ventricular wall
• typically seen with obstruction of a single artery
• most common
• takes 3-4 hours
• granulation tissue develops over 2-3 weeks
• complete healing occurs as fibrous scars form 2-3 months

ST-segment elevation MI

(Subendocardial infarct)

• this involves the inner one third to one half of the ventricular wall
• occurs more frequently in the presence of severely narrowed arteries

What happens during an Acute myocardial infarct

during this..

• inadequate energy to sustain normal myocardial function due to the conversion from aerobic to anaerobic metabolism
• result: loss of contractile function with in 60 seconds of onset, changes in cell sturcture
• if blood flow is restored quickly these changes can be reversed

• the heart is unpredictable the first 24 hours after an MI
• fatal dysrhythmias
• heart failure
• cardiogenic shock
• dresslers syndrome
• thromboemboli
• rupture of myocardium

• this results in sudden death
• 30-50% of MI patients die of V-fib within 1st hour of symptoms
• most frequenct complication of MI
• type of arrhythmia dependent on area of heart wall damange
• PVCs most common

• decreased myocardial contractility, ventricular wal mothion, and compliance ar ea reslut of an MI
• risk of heart failure is greatest when large portions of left ventricle are affected
• normal EF 60-75% pumped out of left ventricle with each contraction- in heart failure its 30% or less
• can lead to cardiogenic shock

• this is systolic or diastolic dysfunction
• compromised cardiac output
• occurs when inadequate oxygen and nutrients are supplied to the tissues because of sever LV failure
• requires aggressive management
• mortality rate is high <70%

• the signs and symptoms of this aare associated with pericarditis, pleurisy, and pneumonitis: fever, chest pain, dyspnea, elecation inWBC and sedimentation rate
• nated 1 day ot several weeks after infarction
• typically treated with anti-inflammatory agents and corticosteroids drugs

• stasis from blood from decreased cardiac funciton and immobility leads to venous thrombi or clot formation in vntricle
• reduced incidence with early mobilizaiton and anticoagulant prophylaxis- elastic stockings, PROM, and AROM

rupture of...

myocardium- 4-7 days after AMI-FATAL AMI- whole left side of the heart, no pumping out, ventricular tachecardia heart muscle is nonproductive

Intraventricular septum- may be due to necrosis, can be caused by aneurysm formation when pressure becomes too great, usually fatal

papillary muscle- neurosis of tissue in or around papilary muscles or chordae tendineae that causes strectural damage

"outpouching of venriclar wall"

can lead to rupture of myocardium

ventricular aneurysm- out pouching of the ventricle during systole, develops due to scar tissue

Fever- occurs during first 24 hours

leukocytosis

elevated erythrocytes sedimentation rate

C-reactive proteins- inflammatory markers

must meet 2 of the following 3 criteria:

• clinical picture: chest pain characteristic of AMI
• ECG change: ST segment change, New Q waves
• elevated serum cardiac markers (troponoin)

diagnosis based on pain history and presence of risk factors

12 lead electrocardiogram

MI diagnosis

Look for:

• T-wave inversion
• ST segment depression (NSTEMI)
• ST-segment elevation (STEMI)
• abnormal Q waves

Serum maker

diagnosis of MI

• myoglobin
• creatine kinase MB
• Troponin I
• Troponin T
• as myocardial cells become necrotic, enzymes diffuse into surrounding intersititum and then into the blood

Serum markers

(CK)

• enzyme found in muscle cells
• exceeds normal range within 4-8 hours and decreases within 2-3 days
• CK-MB is highly specific to myocardial tissue, elevated within 3-6 hours in 1/3 of patients, peaks 24 hours gone in 72 hours

Serum markers

(myoglobin)

• oxygen carrying protein present in cardiac and skeletal muscle
• released quickly when infarcted myocardial tissue occurs
• elevated within 1 hour after myocardial cell death and peaks within 4-8 hours
• non cardiac specific

Serum markers

(troponin)

•  This regulate the calcium-mediated actin-myosin contractile process in striated muscle
• Rise within 3 hours after onset of MI and remain elevated for 3-4 days

• radionucleotide imaging
• coronary angiogram
• magnetic resonance imaging(MRI)
• transthoracic echocardiogram(ECHO)
• transesophageal echo(TEE)

"MONA"

morphine- treats pain and anxiety and vasodilates

oxygen: treats myocardial ischemia

nitroglycerin: dilates coronary arteries

Aspirin: antiplatelet aggregators, anti-inflmmatory

Beta-adrenergic blockers

Nursing considerations

monitor HR and BP

if HR is too low (<45or 50bpm) med may be held

BP parameters may vary according to patient. may need to be held if SBP < 90 mmHg

use with caution in patients with pulmonary disease

• block the slow inward flow of calcium ions into the slow calcium channels in cardiac conducitno tissues

actions on:

myocardium- decrease myocardial contractility

conduciton system: slow it down

vascular smooth muscle in heart and peripheral blood vessels

Calicum channel blockers

(therapeutic use)

lower blood pressure (vasodilation)

decrease angina (vasodilation and decreasing myocardial oxygen demand by reducing HR and after load)

afffect heart rate/dysrhythmias

side affects - hypotension, bradycardia, heartfailure, dyspnea, flushing, peripheral edema

therapeutic results- decreased angina

side affects- headache, hypotension, tolerance

administration routes- sublingual, topical, transdemal patch, oral IV

• dissolve blood and platelet clots
• used to reduce mortality and limit infarct size
• best results in initiated 60-90 minutes after onset of symptoms
• must be a low risk candidate for bleeding

percutaneous coronary interventin (PCI)

ballow PTCA- dilates stenotic atherosclerotic plaque

cononary stent- inserted during the PTCA when the vessel is dilated

Revascularization

CABG

used for patients with significant CAD who do not respond to medical treatment and are not suitable for PCI

a saphenous graft is placed between the aorta and the affected coronary artery, dital to the site of occlusion

may also use mammary artery