Week 2: CORONARY ARTERY DISEASES ANGINA PECTORIS AND MYOCARDIAL INFARCTION

INTRODUCTION
Coronary artery disease

- major blood vessels that supply heart become damaged or diseased.

- Due to: Cholesterol-containing deposits (plaques) in coronary arteries = inflammation
o A buildup of plaque can narrow these arteries, decreasing blood flow to your heart.
o Eventually, the reduced blood flow may cause chest pain (angina), SOB/other coronary artery disease s/s
o A complete blockage = heart attack.
o Because coronary artery disease often develops over decades, you might not until you have a significant
blockage or a heart attack
The coronary arteries
- supply blood, oxygen and nutrients to your heart.
Arteriosclerosis
▪ Thickening/ hardening of the arterial wall
3 main forms of arteriosclerosis:
o Atherosclerosis: most common type, in which plaques of fatty deposits form in the inner layer (tunica intima)
o Mönckeberg's arteriosclerosis “medial calcific sclerosis”; involvement of the middle layer (tunica media), where there is destruction of muscle and
elastic fibers and formation of calcium deposits;
o Arteriolar sclerosis or arteriolosclerosis: thickening of the walls of arterioles

ATHEROSCLEROSIS & CAD RISK FACTORS CLINICAL MANIFESTATIONS Assessment and PREVENTION
Diagnostic
Methods
- most common cause of CVD MAJOR S/s & Complications develop according to Identification of risk Major management
- Slow, progressive vascular dse NON-MODIFIABLE - location & degree of arterial lumen factors for coronary goal is Prevention of
- specific type of arteriosclerosis caused - + family history (1st narrowing heart disease (CHD) CHD.
by formation of PLAQUE (chiefly degree relative with - thrombus formation primarily involves
composed of cholesterol) w/c can CVD age 55/ younger - Obstruction of blood flow to
(4) modifiable risk
restrict blood flow for males & 65/ myocardium. 1. taking a
- Leading contributor to coronary artery CUT thorough
factors have been
younger for females)
and CVD - C-alcifications history cited as major risk
- Age (> 45 years men,
> 55 years women) - U-lceration - family history factors
- Male gender - T-hrombosis - cholesterol
2. physical abnormalities
examination - tobacco use
 - Race (> African Symptoms (note blood - hypertension
Americans than - Ischemia pressure and - diabetes
Caucasians) - Chest pain: angina pectoris weight) mellitus
- Genetic - Atypical symptoms of myocardial * receive much
Abnormalities ischemia (SOB, nausea, weakness) 3. laboratory work
attention in health
- MI (eg, cholesterol
- Dysrhythmias levels [low-
promotion
MODIFIABLE
- High blood - sudden death density programs.
cholesterol lipoprotein (LDL)
(hyperlipidemia) to high-density
- Cigarette smoking, lipoprotein
tobacco use (HDL)], glucose).
- Elevated blood
pressure
- Hyperglycemia
(diabetes mellitus)
- characterized by
o abnormal accumulation of lipid/ MINOR
fatty substances & fibrous tissue in MODIFIABLE
vessel wall. - Obesity
▪ These substances block or - Physical inactivity
narrow vessel = reducing - Stress (A personality)
blood flow to the - Postmenopausal
myocardium estrogen deficiency
- repetitious inflammatory response to - Alcohol
injury of artery wall - Lipoprotein Lp (a)
- subsequent alteration in structural & - Hardened (trans)
biochemical properties of arterial walls. unsaturated fat
PATHOPHYSIOLOGY intake
Etiology: unknown - Chlamydia
➔ Vascular damage (cause pneumoniae
inflammation)
➔ Fatty streak development (intimal
layer)
➔ Plaque (partial or complete
occlusion of blood flow)
RISK FACTORS
TOBACCO SMOKING inhalation of smoke increases blood carbon monoxide level.
- Hemoglobin (oxygen-carrying component of blood) combines more readily with car- bon monoxide than with oxygen. A decreased amount of available oxygen
may decrease the heart’s ability to pump.
Nicotinic Acid
- triggers catecholamines release, which raise HR & BP (may be a factor in sudden cardiac death)
- cause the coronary arteries to constrict. Smokers have an increased risk of CAD and sudden cardiac death.
- Use of tobacco adversely affects vascular endothelium = increased platelet adhesion; leading to a higher probability of thrombus formation

Person at increased risk for heart disease is encouraged

to stop tobacco use through any means possible:
- educational programs, counseling, consistent motivation & reinforcement messages, support groups, medications
complementary therapies: acupuncture, guided imagery, hypnosis
- People who stop smoking reduce their risk of heart disease within the first year, and the risk continues to decline as long as they refrain from smoking.

HIGH BP whether it is genetic or caused by bad eating habits can cause heart disease
- High sodium: leads to hypertension which allows plaque to stick to the insides of arteries

DIABETES
increased amount of blood sugar which leads to premature cell death and slowed blood flow = atherosclerosis

ALCOHOL
CONSUMPTION too much of wine, any alcoholic beverage = LDL levels to increase by as much as 40%.
➔ This also leads to plaque buildup in arteries.

UNHEALTHY DIET: causes high cholesterol = atherosclerosis.

SATURATED & TRANS - body needs a small amount of certain healthy fats to survive, but body can not process too much of “bad” fats, and it builds up on the insides of arteries
FAT
POSTMENOPAUSAL metabolic syndrome emerge with estrogen deficiency:
WOMEN - Dyslipidemia (hypertriglyceridemia, reduced HDL, and increased small dense LDL particles);
- Insulin resistance;
- Hypertension;
- Increased central fat and reduction in lean body mass; and
- Increased hypercoagulability and pro-inflammatory state.

* Early menopause has a negative impact on females

 Assessment Nursing Interventions
- BP (hypertension)
- Elevated cholesterol & triglycerides - Cholesterol screening: 1 every 5 yrs
- Presence of abdominal obesity (Guidelines)
- Elevated FBS Total: < 200 mg/dl
- HOMOCYSTEIN (ELEVATED) o LDL: <100 mg/dl
o blocks production of nitric oxide on endothelium = cell wall less elastic & permitting plaque o TRIGLYCERIDES: <150 mg/dl
to build up o HDL: > 40 mg/dl
o test results are interpreted as:
▪ optimal: < 12 mol/L - Diet
▪ borderline: 12-15 mol/L - Smoking cessation
▪ high risk: > 15 mol/L - Drug therapy:
(to lower)
B-complex vitamin rich diet (folic acid) = homocysteine HMG-CoA reductase inhibitors “Statins”
THERAPEUTIC CONSIDERATIONS
EFFECTS
ATORVASTATIN  HDL Freq. given
(Lipitor) initial therapy for
 chol & LDL

FLUVASTATIN (Lescol)  HDL AE: Myopathy

LOVASTATIN  TG Hepatic fxn (monitor)

(Mevacor)
PRAVASTATIN Block CHOL synthesis Contrain: Liver dse
(Pravachol)
ROSUVASTATIN Favorable effects on Check: drug
(Crestor) vascular endothelium interaction

Cholesterol SIMVASTATIN (Zocor) Anti-inflamm & anti- Acute Coronary

- processed by GI tract into lipoprotein globules “chylomicrons” thrombotic Syndrome (indicated)
➔ reprocessed by liver as lipoproteins.
o physiologic process necessary for formation of lipoprotein-based cell membranes &
important metabolic processes.
- excess of LDL = LDL particles adhere to vulnerable points in the arterial endothelium.
➔ Here macrophages ingest them, contributing to plaque formation

American Heart Association (AHA): “ACUTE CORONARY SYNDROME” to describe any group of clinical symptoms compatible with acute myocardial ischemia
- Atherosclerosis → ischemia
- Ischemia → insufficient bld supply =  O2
*Insuffieicent bld supply resulting to Angina Pectoris & MI
 ANGINA PECTORIS CLINICAL MANIFESTATIONS ASSESSMENT & DIAGNOSTIC MEDICAL MANAGEMENT
Pain varies: from a feeling of - Evaluation of clinical manifestations of pain and OBJECTIVE
Characterized by indigestion to choking or heavy patient history - Decrease oxygen demand of myocardium
- paroxysms of pain (pressure sensation in upper chest - Electrocardiogram changes (12-lead ECG) - Increase oxygen supply
feeling in anterior chest) (discomfort→agonizing pain) - stress testing ➔ met through
- CHEST PAIN: cardiac origin *Px w/ DM may not experience - blood tests ▪ pharmacologic therapy
severe pain with angina. - Echocardiogram ▪ control of risk factors
The cause - nuclear scan
- insufficient coronary blood - severe apprehension; - invasive procedures (cardiac catheterization & Alternatively, reperfusion procedures restore
flow = inadequate supply of feeling of impending death. coronary angiography) blood supply to the myocardium.
oxygen to meet myocardial - Pain: retrosternal, deep in - PCI procedures
demand for oxygen in chest behind upper/ o percutaneous transluminal coronary
response to physical exertion middle 3rd of sternum. angioplasty [PTCA]
or emotional stress (need for - Discomfort: poorly o intracoronary stents
oxygen exceeds the supply) localized; radiate to neck, o atherectomy
- result of atherosclerotic jaw, shoulders, Upper left - coronary artery bypass graft (CABG).
heart dse arm inner aspect
- assoc w/ significant - weakness or numbness in PHARMACOLOGIC THERAPY
obstruction of major arms, wrists, hands - Nitrates: mainstay of therapy (nitroglycerin)
coronary artery. - SOB, pallor, diaphoresis, SE: Flushing, throbbing headache,
dizziness or hypotension, tachy
Factors affecting anginal pain lightheadedness, ➔ can be self-admin: PRN
- physical exertion - N &V; Anxiety ➔ sublingual: tab/ spray
- exposure to cold - Anginal pain→ subsides How to take
- eating a heavy meal when precipitating cause is ➔ make sure mouth is moist, tongue is still,
- stress or any emotion- removed or w/ saliva not swallowed until tab dissolves
provoking situation that Nitroglycerin. ➔ pain severe? can crush bet teeth to
increases blood pressure, hasten absorption
heart rate, and myocardial GERONTOLOGIC ➔ taken in anticipation of any act that may
workload. CONSIDERATION TYPES OF ANGINA produce pain→ nitroglycerin increases
*Unstable angina: not associated - elderly person may not STABLE 75% occlusion that Chest pain (15mins or tolerance for exercise and stress when
with the above and may occur at exhibit typical pain profile accompanies <) may radiate taken prophylactically
exertion Similar pain severity,
rest. due to diminished BP/HR frequency & duration
Advice
responses of Eating large meal with each episode ➔ carry med at all times
Factors that Trigger Angina neurotransmitters Progressive Chest pain increased ➔ carried securely in its orig container
Episodes - presenting symptom: UNSTABLE worsening of freq, severity & (capped dark glass bottle) due to very
stable angine w/ duration; poorly
- Sudden/ excessive exertion Dyspnea. unstable nitrog.
>90% coronary relieved by rest or oral
- Exposure to cold - Sometimes, there are no occlusion nitrates ➔ tab: never be removed & stored in
- Tobacco use symptoms (―silent CAD), VARIANT: Arterial spasm in chest pain at rest (bet. meatal/ plastic pillboxes
- Heavy meals making recognition and PRINZMETAL’S norm/ decreased 12am & 8am), sporadic
coronary artery over 3-6 mos &
- Excessive weight diagnosis a clinical
diminishes over time
- Some OTC drugs challenge. (ECG: ST – elevation)
o diet pills - should be encouraged to Explain
o nasal decongestants recognize their chest pain- ➔ nitroglycerin is volatile & inactivated by
o drugs that increase HR like symptom (eg, heat, moisture, air, light, time →instruct
& BP weakness)→ indication to renew every 6 mons
they should rest/ take Recommend
prescribed medications. ➔ note how long it takes for nitroglycerin
to relieve discomfort
➔ if pain persists after taking 3 sublingual
tabs at 5 mins interval → emergency
med services should be called
Discuss
➔ possible SE
➔ Advise to sit down a few mins when
taking to avoid hypotension & syncope

- Beta-adrenergic blockers
o metoprolol and atenolol
- Calcium channel blockers/calcium ion
antagonists
o amlodipine, diltiazem
- Antiplatelet & Anticoagulant medications
o aspirin, clopidogrel
o heparin
o glycoprotein [GP] IIb/IIIa agents
[abciximab, tirofiban, eptifibatide])
- Oxygen therapy

*troponins both normal

 Collaborative
Assessment Nursing Diagnoses Problems/Potential Nursing Interventions
Complications & Planning and
Goals
TREATING ANGINA
Gather information - Ineffective cardiac tissue Potential complications - Take immediate action: if patient reports pain; person’s prodromal
- patient’s symptoms & perfusion secondary to CAD as - ACS and/or MI, dysrhythmias symptoms suggest anginal ischemia
activities (that evidenced by chest pain or - cardiac arrest - Direct the patient to stop all acts; sit/ rest in semi-Fowler’s
precede and other prodromal symptoms - heart failure ➔ R: reduce oxygen requirements of ischemic myocardium.
precipitate attacks of - Death anxiety - cardiogenic shock. - Measure VS
angina pectoris) - Deficient knowledge about - observe for signs of respiratory distress.
underlying disease and Planning & Goals - NITROGLYCERIN (sublingually): asse patient’s response (repeat: up to 3
Assess methods for avoiding - immediate; appropriate doses).
- risk factors for CAD complications treatment when angina - Oxygen therapy: if RR is increased/ if decreased oxygen saturation
- response to angina - Noncompliance occurs - If the pain is significant and continues after these interventions
- patient’s and family’s - ineffective management of - prevention of angina ➔ further evaluated for acute MI
understanding of the therapeutic regimen related to - reduction of anxiety ➔ transferred to a higher-acuity nursing unit.
diagnosis failure to accept necessary - awareness of disease process
- adherence to current lifestyle changes and understanding of the REDUCING ANXIETY
prescribed care - Explore implications that the diagnosis has for patient.
treatment plan.
- adherence to the self-care - Provide essential info about illness; methods of preventing
program progression.
- absence of complications. - Explain importance of following prescribed directives for the
ambulatory patient at home.
- Explore various stress reduction methods with patient (eg, music
therapy).

PREVENTING PAIN
- Review the assessment findings, identify the level of activity that
causes the patient’s pain or prodromal symptoms, and plan the
patient’s activities accordingly (Box A-1).
- If the patient has pain frequently or with minimal activity, alternate the
patient’s activities with rest periods. Balancing activity and rest is an
important aspect of the educational plan for the patient and family.
 ACUTE CORONARY CLINICAL MANIFESTATIONS ASSESSMENT & DIAGNOSTIC MEDICAL
Etiology & Genetic Risk MANAGEMENT
SYNDROME & MYOCARDIAL
INFARCTION
Emergent situation characterized by - Patient history GOAL:
- acute onset of myocardial ischemia o Description of presenting 1. minimize myocardial
that results in myocardial death (Ex: symptom damage
myocardial infarction if definitive o History of previous illnesses and 2. preserve myocardial
interventions do not occur promptly).
family health history particularly function
o coronary occlusion, heart attack,
of heart disease. 3. prevent lethal
MI are used synonymously →
preferred term is MI. o Previous history: information dysrhythmias &
- Unstable angina “Preinfarction about risk factors for heart cardiogenic shock.
angina”: reduced blood flow in disease.
coronary artery due to rupture of an - Electrocardiography (ECG) within 10 - Reperfusion via
atherosclerotic plaque, but the artery is minutes of pain onset or arrival at emergency use of
not completely occluded. emergency department thrombolytic
o acute situation - Echocardiography: evaluate medications or
o patient will likely have an MI if
ventricular function. percutaneous
prompt interventions do not
- Cardiac enzymes and biomarkers coronary
occur.
*assoc. w/ short-term occlusion, - Transmural MI: involves entire thickness of the myocardium (creatine kinase isoenzymes, intervention (PCI).
whereas MI results from significant or myoglobin, and troponin). - Reduce myocardial
- Subendocardial MI: damage has not penetrated through the
complete occlusion lasts > 1 hour. oxygen demand and
entire thickness
Etiology & Genetic Risk increase oxygen
In an MI: - PRIMARY FACTOR: Atherosclerosis supply with
area of the myocardium is permanently - Nonmodifiable risk factors medications, oxygen
destroyed: due to - Modifiable risk factors and bed rest.
→ plaque rupture o Elevated serum cholesterol levels - Coronary artery
→subsequent thrombus formation o CIGARETTE SMOKING!!! bypass or minimally
result in complete occlusion of artery. o Hypertension invasive direct
other causes of MI o Impaired glucose tolerance coronary artery
- Vasospasm (sudden o Obesity bypass (MIDCAB).
constriction/narrowing) of coronary o Physical inactivity
artery PHARMACOLOGIC
o Stress
- Decreased oxygen supply (from acute
THERAPY
blood loss, anemia, low BP)
DIAGNOSIS OF MI - Nitrates
- Increased demand for oxygen (from a
rapid HR, thyrotoxicosis, or ingestion of - ECG- Changes occur first in the ST (nitroglycerin):
cocaine) segment → T wave → Q wave. increase oxygen
o As the myocardium heals the ST - Anticoagulants
and T waves return to normal but (aspirin, heparin)
- Analgesics
the Q wave changes persist.
(morphine sulfate)
In each case, a profound imbalance exists - Angiotensin-
between myocardial oxygen supply and converting enzyme
demand. (ACE) inhibitors
- defined by type, location of injury to
- Beta-blocker initially,
ventricular wall/ point in time in process
and a prescription to
of infarction (acute, evolving, old).
continue its use after
Pathophysiology hospital discharge
➔ Sudden coronary obstruction - Calcium channel
caused by thrombus formation - ischemia = t wave inversion due to Blockers
over a ruptured or ulcerated altered repolarization - Thrombolytics/
plaque, the acute coronary - Cardiac muscle injury =  ST segment Fibrinolytics
syndrome results. - Necrotic Tissue → Absence of (alteplase [t-PA,
➔ MI: result of sustained Depolarization = Q wave Activase] and
ischemia, causing irreversible reteplase [r-PA,
cellular damage -  serum creatine kinase isoenzyme TNKase]): as early as
(CK-MB is primarily found in cardiac possible after onset
muscle –increase 3-6 hrs after the of symptoms: within
Both troponins = elevated onset of chest pain . 3-6 hours
In many cases, S/S of MI cannot be distinguished from unstable Pain management:
-  myoglobin LDH, AST, WBC, ESR.
angina, hence, the evolution of the term ACS. MONA
- cardiac troponin T and I: identify
- Morphine
very small amount of myocardial o 2-10-mg IV q 5-
- Chest pain (primary presenting symptom): suddenly; continues
despite rest & medication damage. Troponin T increases within 15 minutes
- Some have prodromal symptoms/ a previous diagnosis of 3-6 hrs after the onset of pain. AE: respiratory
coronary artery disease (CAD), but about half report no Troponin I increases 7-14 hrs after the depression,
previous symptoms. onset of pain. hypotension,
- combination of symptoms - Imaging studies identify presence and bradycardia, severe
o chest pain location of poor perfusion but do not vomiting
o SOB indicate when o Antidote:
o indigestion Naloxone
o nausea (Narcan) 0.2 –
o anxiety 0.8 mg IV
o cool, pale, and moist skin - Oxygen: 2-4L/min by
- HR & RR: may be faster than normal. nasal cannula
o S/S caused by stimulation of sympathetic nervous - Nitroglycerin
system→ present for short time or may persist. - Aspirin

Positioning – semi
Fowler’s

Provide a quiet & calm

environment
 Collaborative
Assessment Nursing Diagnoses Problems/Potential Nursing Interventions
Complications & Planning and
Goals
Obtain - Ineffective cardiac Collaborative Problems/Potential Complications Relieving Pain, Signs and Symptoms of
- baseline data on current status for tissue perfusion rt - Acute pulmonary edema Ischemia
comparison with ongoing status. reduced coronary blood - HF - Admin oxygen in tandem w/ med
flow - Cardiogenic shock therapy = to assist with relief of
Include history - Risk for imbalanced - Dysrhythmias & cardiac arrest symptoms (oxygen reduces pain
- chest pain or discomfort fluid volume - Pericardial effusion and cardiac tamponade assoc with low levels of circulating
- difficulty breathing (dyspnea) - Risk for ineffective oxygen).
- palpitations peripheral tissue - Assess VS frequently as long as
- unusual fatigue perfusion rt decreased patient is experiencing pain.
- faintness (syncope) cardiac output from left - Assist patient to rest with back
- sweating (diaphoresis). ventricular dysfunction elevated/ in cardiac chair =
- Death anxiety decrease chest discomfort and
Perform - Deficient knowledge dyspnea.
- complete physical assessment about post-ACS self- Improving Respiratory Function
*crucial for detecting complications & care - Assess respiratory function to
change in status. detect early signs of complications.
- Monitor fluid volume status to
Examination include prevent overloading the heart &
- Assess level of consciousness. lungs.
- Evaluate chest pain (most important - Encourage patient to breathe
clinical finding). Planning and Goals deeply and change position often
- Assess HR and rhythm; major goals to prevent pooling of fluid in lung
dysrhythmias = not enough oxygen - relief of pain/ ischemic signs (eg, ST-segment changes) and bases
to myocardium. symptoms Promoting Adequate Tissue Perfusion
- Assess heart sounds; S3 = early s/s - prev. myocardial damage - Keep on bed/ chair rest = reduce
of impending LV failure. - absence of respiratory dysfunction myocardial oxygen consumption.
- Measure BP to determine response - maintenance/ attainment of adequate tissue perfusion - Check skin temp & peripheral
to pain & treatment - reduced anxiety pulses freq. to determine
- note pulse pressure, → narrowed - adherence: self-care program adequate tissue perfusion.
after MI = ineffective ventricular - absence/ early recognition of complications. Reducing Anxiety
contraction. - Develop trusting & caring
- Assess peripheral pulses: rate, relationship with patient; provide
rhythm, and volume. info. to patient and family in an
- Eval skin: color, temperature. honest and supportive manner.
- Auscultate lung fields at frequent - Ensure a quiet environment,
intervals s/s ventricular failure prevent interruptions that disturb
(crackles in lung bases). sleep, use a caring and appropriate
touch, teach relaxation techniques,
- Assess bowel motility; mesenteric use humor, and provide spiritual
artery thrombosis is a potentially support consistent with the
fatal complication. patient’s beliefs. Music therapy
- observe UO; check for edema; an and pet therapy may also be
early sign of cardiogenic shock is helpful.
hypotension with oliguria. - Provide freq & private
- Examine IV lines and sites opportunities to share concerns
frequently. and fears.
- Provide atmosphere of acceptance
to help know that his/ her feelings
are realistic & normal
Monitoring and Managing
Complication
- Monitor closely for cardinal signs
and symptoms that signal onset of
complications

Figure 1 POSSIBLE PAIN PATTERN Promoting Home- and Community-

Based Care
BE ALERT OF S/S (TEACHING PATIENTS SELF-CARE)
Cardiovascular - Identify patient’s priorities,
- Chest pain/ discomfort not relieved provide adequate education about
by rest/ nitroglycerin palpitations heart-healthy living, facilitate
- Heart sounds: s3 &s4, new onset of patient’s involvement in a cardiac
murmur rehabilitation program.
- Jugular Venous Distention if MI - Work with patient to develop a
has caused HF plan to meet specific needs to
- BP due to sympathetic enhance compliance.
stimulations/  because of
decreased contractility, impending (CONTINUING CARE)
cardiogenic shock, meds - Provide home care referral if
- Irreg pulse = Atrial fibrillation warranted.
- ECG = tachy, brady, other - Assist the patient with scheduling
dysrhythmias and keeping follow-up
Resp appointments and with adhering
- SOB, dyspnea, tachypnea, crackles if to the prescribed cardiac
MI has caused pulmo congestion rehabilitation regimen.
- pulmo edema (+) - Provide reminders about follow-up
GI monitoring: periodic laboratory
- N&V testing and ECGs, general health
screening.
Genitourinary - Monitor adherence to dietary
-  Urinary output = cardiogenic restrictions & prescribed
shock medications.
Skin - If the patient is receiving home
- Cool, clammy, diaphoretic, pale due oxygen, ensure that the patient is
to sympathetic stimulation = using the oxygen as prescribed;
cardiogenic shock appropriate home safety measures
Neurologic are maintained.
- Anxiety, restlessness, - If the patient has evidence of HF
lightheadedness =  sympathetic secondary to an MI, appropriate
stimulation or  contractility & home care guidelines for the
cerebral oxygenation patient with heart failure are
- Same s/s = cardiogenic shock followed
Psych EVALUATION
- Fear with feeling of impending - Experiences relief of angina
doom/ denial that anything is - Has stable cardiac and respiratory
wrong status
- Maintains adequate tissue
perfusion
- Exhibits decreased anxiety
- Complies with self-care program
- Experiences absence of
complications
 Surgical Procedures: Coronary
- performed with patient under general anesthesia
Traditional Coronary Artery ➔ surgeon performs a median sternotomy
➔ connects the patient to cardiopulmonary bypass (CPB) machine.
Bypass Graft ➔ blood vessel from another part of the patient’s body (eg, saphenous vein, left internal mammary artery) is grafted distal to the
coronary artery lesion, bypassing the obstruction
➔ CPB is then discontinued
➔ chest tubes and epicardial pacing wires are placed, a critical care unit.

- mechanically circulates & oxygenates blood for body while bypassing the heart and lungs.
Cardiopulmonary Bypass - maintains perfusion to body organs and tissues
- Many cardiac surgical procedures - allows the surgeon to complete the anastomoses in a motionless, bloodless surgical field
are possible because of CPB (ie, ➔ accomplished by placing a cannula in the RA, vena cava, or femoral vein to withdraw blood from body.
extracorporeal circulation). ➔ cannula is connected to tubing filled with an isotonic crystalloid solution.
➔ Venous blood removed fr. body by the cannula is filtered, oxygenated, cooled/ warmed by machine, then returned to the body.
➔ cannula used to return the oxygenated blood is usually inserted in ascending aorta/ femoral artery
Alternative Coronary Artery - number of alternative CABG techniques have been developed that may have fewer complications for some groups of patients.
Bypass Graft Techniques - Off-pump CABG (OPCAB): 1990s.
➔ involves a standard median sternotomy incision, but the surgery is performed without CPB.
➔ A beta-adrenergic blocker used to slow heart rate.
➔ uses a myocardial stabilization device to hold the site still for the anastomosis of the bypass graft into the coronary artery while the
heart continues to beat