Module 2: Coronary Artery Disease Flashcards
Coronary Artery Disease (CAD)
-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
Atherosclerosis (CAD)
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
CAD Development
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
Collateral Circulation
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.
Risk Factors for CAD (nonmodifiable)
Age
Gender
* See Gender Differences
Ethnicity
Family history
Genetics
* See Genetic Link
Major Modifiable Risk Factors for CAD
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
Lipid Lowering Drug Therapy
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
Drugs that restrict lipoprotein production (Statins)
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
Niacin (B3, nicotinic acid)
Lowered triglycerides, mildly reduces LDL
* At high doses increased HDL
* Common side effects: severe flushing, pruritus, GI
symptoms, orthostatic hypotension
Fibric Acid Derivative (medication class)
Aid the removal of VLDLs
* Reduced triglycerides, increased HDL
* Increases risk for bleeding with warfarin
ATP-Citrate Lyase Inhibitor
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
Drugs that increase lipoprotein removal
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
Drugs that decrease cholesterol absorption
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
Chronic Stable Angina
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
Prinzmetal’s Angina
(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
Microvascular Angina
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
Nursing care for chronic stable angina
Goal of treatment is to reduce O2 demand and/or
increase O2 supply
Assessment and diagnostic studies
Manage anxiety
Nursing care for angina
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
Chronic Stable Angina Drug Therapy
-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
Chronic Stable Angina Drug Therapy: Long Acting Nitrates
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
Chronic Stable Angina Drug Therapy: Angiotensin-converting enzyme (ACE) inhibitors and
angiotensin receptor blockers (ARBs)
-Vasodilation and reduced blood volume
-Prevent or reverse ventricular remodeling
Chronic Stable Angina Drug Therapy: β-Adrenergic blockers
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
Chronic Stable Angina Drug Therapy: Ca Channel Blockers
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
Chronic Stable Angina Drug Therapy: Na Current Inhibitor
-Used when inadequate response to other antianginal drugs
-Side effects: dizziness, nausea, constipation, and headache
Chronic Stable Angina Diagnostic Studies
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)
Cardiac Catheterization
“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
Stent Placement Procedure + Post Procedure Drugs
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
Chronic Stable Angina: Cardiac catheterization and
percutaneous coronary intervention (PCI) - Nursing Care
-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
Coronary Artery Revascularization for Chronic Stable Angina
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
Traditional CABG Surgery
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)
Minimally invasive direct coronary artery bypass
(MIDCAB0
Small incisions between ribs or mini-thoracotomy;
mechanical stabilization
Off-pump coronary artery bypass (OPCAB)
Median sternotomy; no CPB; fewer complications
Totally endoscopic coronary artery bypass (TECAB)
Robotic CABG; limited bypass grafting
Transmyocardial laser revascularization
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
Postoperative Care after
CABG Surgery
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
Post-Op Complications - CABG Surgery
-CPB
Systemic inflammation
Bleeding and anemia
Fluid and electrolyte imbalances
Infection
Hypothermia
-Dysrhythmias, especially atrial fibrillation
-Wound care
Chest wound
Harvest site
Post-Op Care - CABG Surgery
-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
Alternate Therapies - Enhanced external counterpulsation (EECP)
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
Acute Coronary Syndrome
-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)
ACS: Chest Pain
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.
Total Coronary Occlusion
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
Acute Coronary Syndrome
Etiology and Pathophysiology
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
Unstable Angina
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
MI (Myocardial Infarction)
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
Evolution of MI
-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
Clinical Manifestations of MI
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
MI Healing Process
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
Complications of MI: Dysrthymias
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
Complications of MI: Heart Failure, Decreased Pumping Power
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
Complications of MI: Cariogenic Shock, Decreased 02 and Nutrients
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
Complications of MI: Papillary muscle dysfunction or rupture
Causes acute and massive mitral valve regurgitation; new systolic murmur
Aggravates an already compromised LV results in
decreased CO resulting in rapid clinical deterioration
Complications of MI: Left Ventricular Aneurysm
Myocardial wall is thin; bulges out during contraction; may rupture and hide thrombi
Leads to HF, dysrhythmias, and angina
Complications of MI: Ventricular septal wall rupture and left ventricular free wall rupture
New, loud systolic murmur
HF and cardiogenic shock
Emergency repair
Rare condition associated with high death rate
Complications of MI: Pericarditis
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
Complications of MI: Dressler syndrome
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
MI Diagnostic Studies
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
Diagnostic Studies: Cardiac Cath
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
Acute Coronary Syndrome - Emergency Care
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
Acute Care: Emergency PCI (percutaneous coronary intervention)
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
Advantages of PCI vs CABG (coronary artery bypass grafting)
Faster reperfusion
Local anesthesia
Ambulatory sooner
Length of stay shorter (reduced costs)
Faster return to work
Complications of PCI
Dissection or rupture of artery
Abrupt artery closure
Acute stent thrombosis
Failure to cross blockage
Extended infarct
Thrombolytic Therapy
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
Thrombolytic Therapy Acute Care
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
Suspected ACS (acute coronary syndrome)
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
ACS Drug Therapy
IV nitroglycerin (NTG)
Morphine
β-Adrenergic blockers
ACE inhibitors and ARBs
Antidysrhythmic drugs
Lipid-lowering drugs
Aldosterone antagonists
Stool softeners
ACS Nutritional Therapy
Initially NPO
Progress to low salt, low saturated- fat and low
cholesterol
SCD (Sudden Cardiac Death
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
SCD Nursing Care
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
