Module 2: Coronary Artery Disease

Question 1

Coronary Artery Disease (CAD)

Answer 1

-Most common type of CVD (cardiovascular disease)
-asymptomatic or chronic, stable angina (chest pain)

Acute Coronary Syndrome (ACS)
-unstable angina (UA) or myocardial infarction (MI)

-Has a huge effect on perfusion
*perfusion depends on body’s CO, to get blood to the tissues
*significant CAD = impaired CO, decreased perfusion

Question 2

Atherosclerosis (CAD)

Answer 2

Atherosclerosis—blood vessel disorder
 Begins as soft deposits of fat that harden with age; referred to as “hardening of arteries”
 Atheromas (fatty deposits) form in coronary arteries— called CAD
* ASHD—arteriosclerotic heart disease
* CVHD—cardiovascular heart disease
* IHD—ischemic heart disease
* CHD—coronary heart disease

Characterized by lipid deposits within intima of artery
 Endothelial injury and inflammation play a key role in developing atherosclerosis

Question 3

CAD Development

Answer 3

Earliest lesion; lipid filled smooth muscle cells;
appears yellow
 Start ~age 20 and increase as age
 Treatment that lower low-density lipoproteins (LDL) may slow process

Fibrous plaque
 Beginning of progressive change in endothelium;
~age 30
 LDLs and growth factors stimulate smooth muscle
proliferation and arterial wall thickens
 Cholesterol and other lipids move into intima
 Collagen covers and forms grayish or whitish fibrous plaque with smooth or rough, jagged edges
 Narrowed vessel lumen reduces distal blood flow

Later can become complicated lesion
 Fibrous plaque grows; continued inflammation leads to plaque instability, ulceration, and rupture
 Platelets accumulate leading to thrombus that further narrows or occludes artery
 Activation of platelets causes expression of
glycoprotein IIb/IIIa receptors to bind fibrinogen
resulting in increased size of thrombus

Question 4

Collateral Circulation

Answer 4

Collateral circulation (network of tiny blood vessels, arterial anastomies, that, under certain conditions, can provide alternate pathway for blood flow around a blocked artery in the heart)

 Arterial anastomoses (connections) within coronary circulation
-These are natural connections between the small arteries of the heart. They can open up and expand to allow blood to flow around a blockage in a major coronary artery

 Contributing factors:
* Inherited predisposition for angiogenesis (Some people are genetically more likely to develop new blood vessels (angiogenesis), which can contribute to more robust collateral circulation)

• Presence of chronic ischemia (Ischemia is a condition where parts of the heart muscle don’t get enough oxygen. Chronic (long-standing) ischemia can stimulate the growth of these collateral vessels)

 Slowly developing blockages may increase collateral circulation, allow adequate blood and oxygen to heart; except with increased workload (e.g., exercise)
-When blockages in the coronary arteries develop slowly over time, it gives the body a chance to form collateral circulation. This can help maintain adequate blood and oxygen supply to the heart muscle, compensating for the reduced flow in the main arteries. However, during increased workload (like exercise), these collateral vessels may not be able to supply enough blood to meet the heart’s higher oxygen demand, which can lead to symptoms like chest pain.

 Rapid-onset CAD or coronary spasm results in severe ischemia or infarction
-f a coronary artery suddenly becomes blocked (as in a heart attack) or goes into spasm, there isn’t enough time for collateral circulation to develop adequately. This rapid onset of blockage can lead to severe ischemia (lack of oxygen) or myocardial infarction (heart attack), as the heart muscle is suddenly deprived of oxygen-rich blood.

Question 5

Risk Factors for CAD (nonmodifiable)

Answer 5

Age
 Gender
* See Gender Differences
 Ethnicity
 Family history
 Genetics
* See Genetic Link

Question 6

Major Modifiable Risk Factors for CAD

Answer 6

High serum lipids
* Cholesterol >200 mg/dL
* High-density lipoproteins (HDL) <40 mg/dL in men, <50 mg/dL (1.3 mmol/L) in women
 High HDLs prevent lipid accumulation in arteries
* Low-density lipoproteins (LDL) > 130 mg/dL
 High LDLs increase atherosclerosis and CAD
* Fasting triglycerides >150 mg/dL
 High levels increase risk for CAD

Hypertension (HTN)
* Normal BP <120/<80 mm Hg
* Elevated BP 120 to 129/<80 mm Hg
* Stage 1 HTN 130 to 139/80 to 89 mm Hg
* Stage 2 HTN >140/>90 mm Hg
* Lifestyle changes for elevated BP and HTN; treat stage 1 or 2 HTN with drugs
* Elevated BP—endothelial injury leads to left ventricular hypertrophy and decreased stroke volume

Tobacco use
* Nicotine: Increased catecholamine results in increased HR and BP, peripheral vasoconstriction
* Increased LDL, decreased HDL, increased toxic O2
radicals—vessel inflammation and thrombosis
* Increased carbon monoxide—reduces numbers of
hemoglobin sites available for O2 transport
 Second-hand smoke - Increased CAD 25% to 30%
 Tobacco cessation- benefits are dramatic

Diabetes—2-4 × greater incidence of CAD
* Increased endothelial dysfunction
* Altered lipid metabolism, increased cholesterol and triglycerides
 Metabolic syndrome
* Multiple risk factors related to insulin resistance
including central obesity, HTN, abnormal serum lipids, and high fasting blood glucose

Physical inactivity
* Lack of regular exercise
* Exercise training reduces risk for CAD
 Obesity
* BMI > 30 kg/m2
* Waist circumference > 40” men; 35” women
* Increased LDLs, triglycerides; HTN; insulin resistance
* “Apple” figure > CAD than “pear” figure

Psychologic states
* Type A personality
* Acute and chronic stress, depression, anxiety, hostility, and anger, lack of social support
 Increased SNS stimulation increases catecholamines
 Results in endothelial injury, increased HR, increased force of myocardial contraction results in increased O2 demand
 Increased lipid and glucose levels
 Changes in blood coagulation

Substance use
* Cocaine and methamphetamine can produce coronary artery spasm resulting in myocardial ischemia and MI
* Increased levels of CRP, lipoprotein(a) and
homocysteine

Question 7

Lipid Lowering Drug Therapy

Answer 7

Lipid profile screening
 Statin therapy recommended:
* Patients with known CVD
* At very high risk for CAD with an LDL > 70 mg/dL
* LDL cholesterol > 190 mg/dL
* Age 40 to 75 with diabetes and LDL >70 mg/dL
* Age 40 to 75 without diabetes, with LDL 70 mg/dL plus a 10-year risk for CVD of 7.5% or greater

Drug therapy is lifelong
 Teach: rationale, goals, safety and side effects
 Concurrent diet change; weight loss and increased
physical activity
 Reassess after 4-12 weeks; if high, change to
alternate drug

Question 8

Drugs that restrict lipoprotein production (Statins)

Answer 8

HMG-CoA reductase inhibitors: Statins
* Inhibit cholesterol synthesis, decrease LDL, increase HDL, and lower CRP
* Rosuvastatin (Crestor)—most potent
 Serious adverse effects (rare): Liver damage and
myalgia

Question 9

Niacin (B3, nicotinic acid)

Answer 9

Lowered triglycerides, mildly reduces LDL
* At high doses increased HDL
* Common side effects: severe flushing, pruritus, GI
symptoms, orthostatic hypotension

Question 10

Fibric Acid Derivative (medication class)

Answer 10

Aid the removal of VLDLs
* Reduced triglycerides, increased HDL
* Increases risk for bleeding with warfarin

Question 11

ATP-Citrate Lyase Inhibitor

Answer 11

ATP-Citrate Lyase Inhibitor
 Bempedoic acid (Nexletol)
 Helps lower LDL in patients with heterozygous familial hypercholesterolemia or with CAD who do not have adequate LDL lowering
 Increases risk for gout and tendon rupture

Question 12

Drugs that increase lipoprotein removal

Answer 12

Bile acid sequestrants
* Increase conversion of cholesterol to bile acids;
reduced total cholesterol and LDL
* Decrease absorption of many other drugs
 Proprotein Convertase Subtilisin/Kexin 9 (PCSK9)
Inhibitors
* Block PCSK9 to lower LDL
* Used with diet therapy and maximum statins
* Subcutaneous injection every 2-4 weeks

Question 13

Drugs that decrease cholesterol absorption

Answer 13

Drugs that decrease cholesterol absorption:
 Ezetimibe (Zetia)
* Selectively inhibit absorption of dietary and biliary
cholesterol; combine with statin
 Antiplatelet therapy
 Low-dose aspirin (81 mg)
* Contraindicated with risk for bleeding

Question 14

Chronic Stable Angina

Answer 14

Asymptomatic patients may develop chronic stable
chest pain (angina)
* O2 demand greater than O2 supply results in
myocardial ischemia
* Angina= clinical manifestation
 1 or more arteries are blocked 70% or more by
atherosclerotic plaque
 50% or more for left main coronary artery

Intermittent chest pain occurs over a long period of time with similar pattern of onset, duration, and intensity of symptoms
 Onset: physical exertion, stress, or emotional upset
 Accurate assessment important: PQRST
 May deny pain; have pressure, heaviness, or discomfort in chest; may be accompanied by dyspnea or fatigue; no change with position or breathing

Duration of pain: few minutes
 Subsides when precipitating factor resolved
 Rest, calm down, sublingual nitroglycerin (SL NTG)
 Generally predictable and controlled with drugs
 Ischemic changes on 12-lead ECG—ST segment
depression or T wave inversion
 ECG returns to normal when blood flow restored and pain relieved

Silent Ischemia
 Ischemia that occurs in absence of any subjective
symptoms
 Associated with diabetic neuropathy
 Confirmed by ECG changes Same prognosis as ischemia with pain

Question 15

Prinzmetal’s Angina

Answer 15

(variant angina, vasospastic angina)
 Rare; occurs at rest; with without increased physical demand
 History of migraine headaches, Raynaud’s phenomenon, and heavy smoking
 Spasm of a major coronary artery with or without CAD
* Contributing factors: increased levels of certain substances, exposure to medications that narrow blood vessels, or exposure to cold weather
 Treatment:
* Moderate exercise, calcium channel blockers and/or nitrates, stop use of offending substances
* May disappear spontaneously

Question 16

Microvascular Angina

Answer 16

Coronary microvascular disease or dysfunction
(MVD)
 Chest pain occurs in the absence of significant CAD or coronary spasm of a major coronary artery
 Related to myocardial ischemia from atherosclerosis or spasm of distal coronary branches
 More common in women; physical exertion
 Prevention and treatment follows CAD
recommendations

Question 17

Nursing care for chronic stable angina

Answer 17

Goal of treatment is to reduce O2 demand and/or
increase O2 supply
 Assessment and diagnostic studies
 Manage anxiety

Question 18

Nursing care for angina

Answer 18

Position upright; apply oxygen
 Assess: VS; heart and breath sounds
 Continuous ECG monitor; 12-lead ECG
 Pain relief—NTG; IV opioid if needed
 Obtain cardiac biomarkers
 Obtain chest x-ray
 Provide support; reduce anxiety

Question 19

Chronic Stable Angina Drug Therapy

Answer 19

-Aspirin
-Lipid Lowering Drugs
-Short-acting nitrates
 Dilate peripheral and coronary arteries and collateral vessels
-Sublingual nitroglycerin (SL NTG) or translingual spray
 Give 1 tablet or 1 to 2 metered sprays
 Relief in 5 minutes; duration 30 to 40 minutes
 If symptoms unchanged after 5 minutes, call EMS
 May cause: headache, dizziness, flushing, orthostatic hypotension
 Patient teaching: proper use and storage
 Prophylactic use

Question 20

Chronic Stable Angina Drug Therapy: Long Acting Nitrates

Answer 20

Long-acting nitrates
 Reduce frequency of angina, treat Prinzmetal’s angina
 Main side effect: headache
 Tolerance can develop- schedule 14-hour nitrate-free period every day
 Methods of administration
* Oral
* Nitroglycerin (NTG) ointment
* Transdermal controlled-release NTG

Question 21

Chronic Stable Angina Drug Therapy: Angiotensin-converting enzyme (ACE) inhibitors and
angiotensin receptor blockers (ARBs)

Answer 21

-Vasodilation and reduced blood volume
-Prevent or reverse ventricular remodeling

Question 22

Chronic Stable Angina Drug Therapy: β-Adrenergic blockers

Answer 22

Decrease myocardial contractility, HR, SVR, and BP
 Side effects: bradycardia, hypotension, wheezing, GI effects; weight gain, depression, fatigue, and sexual dysfunction
 Contraindicated: severe bradycardia, acute decompensated HF
 Cautious use: asthma, diabetes

Question 23

Chronic Stable Angina Drug Therapy: Ca Channel Blockers

Answer 23

Systemic vasodilation with reduced SVR, reduced myocardial contractility, coronary vasodilation, reduced HR
 Side effects: fatigue, headache, dizziness, flushing, hypotension, peripheral edema
 Enhance action of digoxin

Question 24

Chronic Stable Angina Drug Therapy: Na Current Inhibitor

Answer 24

-Used when inadequate response to other antianginal drugs
-Side effects: dizziness, nausea, constipation, and headache

Question 25

Chronic Stable Angina Diagnostic Studies

Answer 25

 12-lead ECG
 Laboratory studies: cardiac biomarkers, lipid profile, CRP
 Chest x-ray
 Echocardiogram
 Exercise stress test
 Electron beam computed tomography (CT scan that gets high beam images of heart)
 Coronary computed tomography anigography (CT scan specifically focusing on heart’s vessels, involves injection of contrast dye)

Question 26

Cardiac Catheterization

Answer 26

“gold standard” to identify
and localize CAD
 Visualize blockages (diagnostic)
 Open blockages (interventional)
-Percutaneous coronary intervention (PCI)
* Balloon angioplasty
* Intracoronary stents
-Bare metal stent (BMS)
-Drug-eluting stent (DES)—prevent neointimal hyperplasia

Question 27

Stent Placement Procedure + Post Procedure Drugs

Answer 27

Used to prevent platelet aggregation and stent
thrombosis
 During PCI: unfractionated heparin or low-molecular
weight heparin, a direct thrombin inhibitor and/or GP
IIb/IIIa inhibitor
 After PCI: dual antiplatelet therapy (DAPT)
* Aspirin and clopidogrel

Question 28

Chronic Stable Angina: Cardiac catheterization and
percutaneous coronary intervention (PCI) - Nursing Care

Answer 28

-Allergy (contrast dye)
 Baseline assessment: VS, pulse ox, heart and breath sounds, neurovascular
 Laboratory studies
 Administer drugs
 Patient education: procedure and postprocedure

Postprocedure (RN):
 Compare assessments to preprocedure
 Assess catheter insertion site for hematoma, bleeding, bruit every
15 minutes for first hour, then agency policy
 ECG for dysrhythmia; chest pain or other pain
 IV infusion of antianginals
 Monitor for complications
 Education: discharge care and drugs; signs and symptoms to report to HCP

Question 29

Coronary Artery Revascularization for Chronic Stable Angina

Answer 29

Coronary artery bypass graft (CABG) Surgery
recommended for patients who:
 Do not respond well to medical management
 Have left main coronary artery or 3-vessel disease
 Are not candidates for PCI
 Continue to have chest pain after PCI.
 CABG may be an option for patients with diabetes, LV dysfunction, and/or CKD

Question 30

Traditional CABG Surgery

Answer 30

1 or more arterial or venous grafts placed from
aorta/branch to heart muscle distal to blockage
 Grafts: internal mammary (thoracic) artery (IMA or
ITA), saphenous vein, and/or radial artery
 Sternotomy and cardiopulmonary bypass (CPB)

Question 31

Minimally invasive direct coronary artery bypass
(MIDCAB0

Answer 31

Small incisions between ribs or mini-thoracotomy;
mechanical stabilization

Question 32

Off-pump coronary artery bypass (OPCAB)

Answer 32

Median sternotomy; no CPB; fewer complications

Question 33

Totally endoscopic coronary artery bypass (TECAB)

Answer 33

Robotic CABG; limited bypass grafting

Question 34

Transmyocardial laser revascularization

Answer 34

Left thoracotomy approach
 Laser creates channels to get blood flow to ischemic areas
 Used for patients with advanced CAD who are not
candidates for CABG

Question 35

Postoperative Care after
CABG Surgery

Answer 35

ICU for 24 to 48 hours for:
 Hemodynamic monitoring
 Arterial line for BP monitoring
 Pleural and mediastinal chest tubes
 Continuous ECG
 Endotracheal tube to ventilator
 Epicardial pacing wires
 Urinary catheter
 Nasogastric tube

Question 36

Post-Op Complications - CABG Surgery

Answer 36

-CPB
 Systemic inflammation
 Bleeding and anemia
 Fluid and electrolyte imbalances
 Infection
 Hypothermia
-Dysrhythmias, especially atrial fibrillation
-Wound care
 Chest wound
 Harvest site

Question 37

Post-Op Care - CABG Surgery

Answer 37

-Pain management
 Prevent VTE (venous thromboembolism)
 Early ambulation, reduce risk of blood clots
 SCD (sequential compression devices)
-Respiratory complications
 Splinting (supporting abdomen when coughing to reduce pain and help facilitate coughing)
 Incentive spirometry (device to encourage deep breathing and lung expansion)
-Postoperative cognitive dysfunction (POCD) - when patients exhibit memory or concentration problems following surgery, more common in older adults

Question 38

Alternate Therapies - Enhanced external counterpulsation (EECP)

Answer 38

Inflatable cuffs are placed around legs
* Increase venous return
* Augment DBP, improve diastolic filling, help with
collateral circulation
* Contraindicated: decompensated HF, severe PVD, and severe aortic insufficiency

Question 39

Acute Coronary Syndrome

Answer 39

-Range of conditions that result in sudden, reduced blood flow to heart
-Prolonged ischemia; not immediately reversible;
includes:
Unstable Angina (UA)
Non-ST Segment Elevation
Myocardial Infarction (NSTEMI)
and ST Segment Elevation Myocardial Infarction (STEMI)

Question 40

ACS: Chest Pain

Answer 40

Presentation of chest pain (with nausea, SOB, or other symptoms)
 ST elevations on 12-lead ECG are most likely STEMI (If the Electrocardiogram (ECG) shows ST segment elevations, it most likely indicates a STEMI, which is a serious type of heart attack)
* Compare to previous ECG, note any changes
* ST elevation = potentially reversible myocardial injury; this finding indicates that a potentially reversible myocardial (heart muscle) injury is happening. Immediate treatment is critical to restore blood flow and minimize heart damage.

 UA or NSTEMI
These conditions may or may not show ST segment depression or T wave inversion on the ECG.
If the ECG doesn’t show clear signs of STEMI, it’s essential to evaluate serum cardiac biomarkers (like troponins). These biomarkers are proteins released into the blood when the heart muscle is injured.
An increase in these biomarkers indicates some degree of heart muscle damage, which is consistent with NSTEMI. In contrast, UA does not typically result in a significant rise in these biomarkers.

Question 41

Total Coronary Occlusion

Answer 41

Cellular response to oxygen and glucose deprivation
Heart muscle hypoxic within 10 seconds
 Anaerobic metabolism, increased lactic acid (In response to the lack of oxygen, the heart muscle cells switch to anaerobic metabolism (metabolism without oxygen). This process is less efficient and produces lactic acid, which can lead to an acidic environment in the cells)
 Heart cells viable 20 minutes; damage irreversible if no collateral circulation
 If reperfused, aerobic metabolism and contractility restored and cellular repair begins

Question 42

Acute Coronary Syndrome
Etiology and Pathophysiology

Answer 42

Deterioration of once stable plaque leads to rupture, platelet aggregation and thrombus
-Result
 Partial occlusion of coronary artery: UA or NSTEMI
 Total occlusion of coronary artery: STEMI

Question 43

Unstable Angina

Answer 43

Chest pain:
 New onset; occurs at rest; or with increasing
frequency, duration, or less effort than chronic stable angina pattern
 May be first clinical sign of CAD
 Pain lasting > 10 minutes
 Unpredictable; needs immediate treatment
 ECG may show ST depression and/or T wave
inversion = ischemic changes

Question 44

MI (Myocardial Infarction)

Answer 44

MI occurs:
-MI occurs when blood flow through a coronary artery, which supplies the heart muscle with oxygen-rich blood, is abruptly blocked. This blockage is usually caused by a thrombus (blood clot) formed due to platelet aggregation (clumping together of platelets in the blood).
-The blockage results in irreversible damage or death (necrosis) of part of the heart muscle cells due to the lack of oxygen. This process often occurs in the context of preexisting coronary artery disease (CAD).

Two types of MI: ST-elevation and Non-ST-elevation MI

ST-Elevation MI
In STEMI, the thrombus completely occludes (blocks) the coronary artery.
This complete blockage causes a characteristic elevation in the ST segment on an electrocardiogram (ECG). The ST segment is a part of the ECG tracing, and its elevation is an indication of significant damage to the heart muscle.
The ST elevation occurs in the ECG leads that face the area of the heart affected by the infarction (heart attack).
-Emergency; artery must be opened within 90 minutes with either PCI or thrombolytic

Not ST Elevation STEMI:
In NSTEMI, the thrombus is usually non-occlusive, meaning it partially blocks the coronary artery but does not completely stop the blood flow.
Unlike STEMI, NSTEMI does not typically show ST segment elevation on the ECG. However, other ECG changes (like ST depression or T wave inversion) and increased cardiac biomarkers (proteins in the blood that indicate heart muscle damage) can indicate NSTEMI.
-NSTEMI, PCI within 12 to 72 hours

STEMI or NSTEMI
 Echocardiogram—hypokinesis or akinesis of infarcted areas
 Degree of LV dysfunction depends on area of heart and size of infarction

Question 45

Evolution of MI

Answer 45

-Evolves over time, from hours to days
-Depends on several factors like degree and duration of blockage, as well as presence of collateral circulation

Subendocardium – Ischemic First
-The subendocardium, the innermost layer of the heart wall, is usually the first area to become ischemic (lacking in blood and oxygen) during an MI. This is because it’s the most vulnerable to a reduction in coronary blood flow.

Necrosis of Heart Muscle
-If the blood flow is completely blocked, the entire thickness of the heart muscle can become necrotic (dead) within 4-6 hours.
-In cases of partial occlusion by a thrombus (blood clot), the process might take up to 12 hours. Partial occlusions allow for some blood flow, which may delay the full extent of the damage.

MI Described by Location
-MIs are often described based on their location in the heart, such as anterior (front), inferior (lower), lateral (side), septal (the wall separating the left and right sides of the heart), or posterior (back) wall.
-The location of the MI can often be correlated with which coronary artery is involved, and this correlation is reflected in the changes seen on an electrocardiogram (ECG).

Correlation with involved coronary artery
-Specific patterns of ECG changes can indicate which coronary artery is blocked and, therefore, which part of the heart is affected.

Severity influenced by collateral circulation
-The severity of an MI can be significantly influenced by collateral circulation, which refers to alternative pathways of blood flow that can develop in the heart. Better collateral circulation can reduce the severity of the MI by providing blood flow to the affected area.

-Women ofter untreated with worse outcomes

Question 46

Clinical Manifestations of MI

Answer 46

Pain
 Severe chest pain not relieved by rest, position
change, or nitrate administration
* Heaviness, pressure, tightness, burning, constriction, or crushing
* Common locations: substernal or epigastric
* May radiate to neck, lower jaw, arms, back
 Often occurs in early morning; greater than 20
minutes
 Atypical in women and older adult
 No pain if cardiac neuropathy (diabetes)

Sympathetic Nervous System Stimulation
Release of catecholamines
* Diaphoresis
* Increased HR and BP
* Vasoconstriction of peripheral blood vessels
* Skin: ashen, clammy, and/or cool to touch

Cardiovascular
Initially, increased HR and BP, then reduced BP
(secondary to decrease in CO)
 Decreased renal perfusion leads to decreased urine output
 Crackles (LV dysfunction)
 Jugular venous distention, hepatic engorgement,
peripheral edema (RV dysfunction)
 Abnormal heart sounds
* S3 or S4
* New murmur: holosystolic

Nausea + Vomiting
Reflex stimulation of the vomiting center by severe
pain
 Vasovagal reflex

Fever
Up to 100.4° F (38° C) in first 24 to 48 hours; up to 4
to 5 days
 Systemic inflammatory process caused by heart cell death

Question 47

MI Healing Process

Answer 47

Inflammatory process: within 24 hours, leukocytes
infiltrate the area of cell death; enzymes released
 Proteolytic enzymes of neutrophils and macrophages begin to remove necrotic tissue by fourth day resulting in thin wall
 Catecholamine-mediated lipolysis and glycogenolysis resulting in increased glucose
 Necrotic zone identifiable by ECG changes
 Collagen matrix laid down—scar tissue

 10 to 14 days after MI, scar tissue is still weak
 Heart muscle vulnerable to stress
 Monitor patient carefully as activity level
increases

By 6 weeks after MI, scar tissue has replaced
necrotic tissue
 Area is said to be healed, but less compliant
 Ventricular remodeling
 Normal myocardium will hypertrophy and dilate in an attempt to compensate for infarcted muscle

Question 48

Complications of MI: Dysrthymias

Answer 48

Most common complication
 Present in 80% to 90% of MI patients
 Can be caused by ischemia, electrolyte imbalances, or SNS stimulation
 VT and VF are most common cause of death in
prehospitalization period

Question 49

Complications of MI: Heart Failure, Decreased Pumping Power

Answer 49

 Left-sided HF
* Mild dyspnea, restlessness, agitation, or slight
tachycardia; pulmonary congestion on x-ray, S3
sounds, crackles, paroxysmal nocturnal dyspnea, and orthopnea
 Right-sided HF
* Jugular venous distention, hepatic congestion, lower extremity edema

Question 50

Complications of MI: Cariogenic Shock, Decreased 02 and Nutrients

Answer 50

Severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, right ventricular infarction
 Requires aggressive management to:
* Increased O2 delivery, decreased O2 demand, and
prevent complications
* Associated with a high death rate

Question 51

Complications of MI: Papillary muscle dysfunction or rupture

Answer 51

Causes acute and massive mitral valve regurgitation; new systolic murmur
 Aggravates an already compromised LV results in
decreased CO resulting in rapid clinical deterioration

Question 52

Complications of MI: Left Ventricular Aneurysm

Answer 52

Myocardial wall is thin; bulges out during contraction; may rupture and hide thrombi
 Leads to HF, dysrhythmias, and angina

Question 53

Complications of MI: Ventricular septal wall rupture and left ventricular free wall rupture

Answer 53

 New, loud systolic murmur
 HF and cardiogenic shock
 Emergency repair
 Rare condition associated with high death rate

Question 54

Complications of MI: Pericarditis

Answer 54

Inflammation of visceral and/or parietal pericardium
 Mild to severe chest pain
* Increases with inspiration, coughing, movement of
upper body
* Relieved by sitting in forward position
 Pericardial friction rub, fever, decreased BP, ECG
changes
 Treat with high dose aspirin

Question 55

Complications of MI: Dressler syndrome

Answer 55

Pericarditis and fever that develops 1 to 8 weeks after MI; possibly autoimmune
 Chest pain, fever, malaise, pericardial friction rub,
arthralgia, increased WBC and sedimentation rate
 High dose aspirin is treatment of choice

Question 56

MI Diagnostic Studies

Answer 56

Detailed health history
 12-lead ECG
 Compare new ECG to previous ECG
 Changes in QRS complex, ST segment, and T wave
 Distinguish between STEMI and NSTEMI/UA
 Serial ECGs reflect evolution of MI

Serum cardiac biomarkers (Troponin, CK-MB, Myoglobin)
 Proteins released after MI (Table 31-6)
 Cardiac-specific troponin T (cTNT)
 Cardiac-specific troponin I (cTNI)
* Increased 4 to 6 hours after onset of MI
* Peak at 10 to 24 hours
* Return to baseline over 10 to 14 days
 Biomarkers negative for UA; positive for NSTEMI
 Cardiac-specific troponins are better indicators of MI than CK-MB or myoglobin

Question 57

Diagnostic Studies: Cardiac Cath

Answer 57

Cardiac catheterization
 Within 90 minutes for patients with a STEMI or
receive thrombolytic therapy within 30 minutes (if no PCI available)
 Within 12 to 72 hours for patients with UA or NSTEMI
 May have PCI, medical therapy, or referral for CABG depending on findings

Question 58

Acute Coronary Syndrome - Emergency Care

Answer 58

Emergency care
 12-lead ECG
 Upright position
 Oxygen—keep O2 sat > 93%
 IV access
 Nitroglycerin (SL) and ASA (chewable)
 Morphine
 Statin

ECG shows ST elevation leading to cardiac cath
lab for PCI or thrombolytic therapy
 ECG shows ST depression or T-wave inversion
leading to critical care or telemetry unit
 Dysrhythmias—treat as per agency
 Monitor serum biomarker

UA and NSTEMI
 Heparin
 Glycoprotein IIb/IIIa inhibitors before or during PCI (percutaneous coronary intervention)
 STEMI
 Glycoprotein IIb/IIIa inhibitors during PCI

Question 59

Acute Care: Emergency PCI (percutaneous coronary intervention)

Answer 59

Emergent PCI is first treatment with confirmed
STEMI
 Goal: open blocked artery within 90 minutes of
arrival to facility with cardiac catheterization lab;
BSM or DES
 If severe LV dysfunction—IABP and/or inotropes
 Emergent CABG

Question 60

Advantages of PCI vs CABG (coronary artery bypass grafting)

Answer 60

Faster reperfusion
 Local anesthesia
 Ambulatory sooner
 Length of stay shorter (reduced costs)
 Faster return to work

Question 61

Complications of PCI

Answer 61

Dissection or rupture of artery
 Abrupt artery closure
 Acute stent thrombosis
 Failure to cross blockage
 Extended infarct

Question 62

Thrombolytic Therapy

Answer 62

Indicated for STEMI
 Advantages: availability and rapid administration (if not PCI-capable)
 May transfer if PCI can be done within 120 minutes
-Goals:
 Limit size of infarction
 Administer IV within 30 minutes of arrival

Thrombolytic—IV administration of selected
medication to open blocked arteries by lysis of
thrombus/clot; concern for bleeding with other sites
 Inclusion criteria:
 Chest pain less than 12 hours and 12 lead shows
STEMI
 No absolute contraindications

Question 63

Thrombolytic Therapy Acute Care

Answer 63

Procedure
-Prior to administration:
 Obtain baseline labs
 2 to 3 lines for IV therapy
 Complete any invasive procedures
-Administer IV bolus or infusion
 Monitor heart rhythm, VS, and pulse ox
 Assess heart, lungs, and neuro status

Reperfusion occurs
 ST segment returns to baseline
 No chest pain
 Early, rapid rise of serum biomarkers; peak within 12 hours

 Reperfusion dysrhythmias—less reliable
 Major concern—reocclusion
 IV heparin
 Monitor for chest pain and ECG changes
 Major complication—bleeding

Question 64

Suspected ACS (acute coronary syndrome)

Answer 64

Antiplatelet therapy, IV NTG, atorvastatin
 NSTEMI or UA
 Anticoagulation and glycoprotein IIb or IIIa
 MI
 DAPT, Aspirin, -blockers, calcium channel blockers, ACE inhibitors, and/or nitrates

Question 65

ACS Drug Therapy

Answer 65

 IV nitroglycerin (NTG)
 Morphine
 β-Adrenergic blockers
 ACE inhibitors and ARBs
 Antidysrhythmic drugs
 Lipid-lowering drugs
 Aldosterone antagonists
 Stool softeners

Question 66

ACS Nutritional Therapy

Answer 66

 Initially NPO
 Progress to low salt, low saturated- fat and low
cholesterol

Question 67

SCD (Sudden Cardiac Death

Answer 67

Abrupt, unexpected death from cardiac causes; occurs within 1 hour of symptom onset; ~350,000 annually (reduced due to ICDs)

Acute ventricular dysrhythmia (e.g., VT, VF) causes disruption in
cardiac function, resulting in loss of CO and cerebral blood flow
 Most commonly caused by:
-CAD
-Structural heart disease
-Conduction disturbances

Symptoms within one hour: angina, palpitations, dizziness, or lightheadedness
 SCD occurs with:
 Prior (old) MI—most common
 Acute MI
 If survive, increased risk of another event due to
electrical instability from scarred muscle; referred for ICD
after 40 days medical therapy

Question 68

SCD Nursing Care

Answer 68

Diagnostic workup: rule out or confirm MI
 Serial cardiac biomarkers
 Serial ECGs
 Cardiac catheterization
 PCI or CABG, if indicated
 Electrophysiology Study (EPS)
 Outpatient monitor; Mobile Cardiac Outpatient Telemetry (MCOT); implanted monitor