Chapter 34: Coronary artery disease and acute coronary syndrome

Question 1

Blood vessel disorder c/b atherosclerosis. Most common type of CV disease. Other names: arteriosclerotic heart disease, CV heart disease, ischemic heart disease, coronary heart disease.
Usually takes a long time to develop so important to focus on people at risk and start treatment early

Answer 1

Coronary artery disease (CAD)

Question 2

S/S of severe CAD. Includes unstable angina (UA) and myocardial infarction (MI)

Answer 2

Acute coronary syndrome

Question 3

Pathophysiology

Answer 3

Damange to intima–> inflammatory response (cytokines, macrophages, LDL with cholesterol to plug up site). Deposition of fibrinogen. Macrophages become foam cells. When fibrin cap breaks, tons of yucky stuff is exposed=more inflammation.

Question 4

Influenced by genetic predisposition to angiogenesis and the presence of chronic ischemia.
Is helpful when it occurs.
No time for development of it with rapid-onset CAD or coronary spasm leading to a big risk for MI

Answer 4

collateral circulation

Question 5

Risk factors

Answer 5

Non-modifiable: age, gender, ethnicity, family hx, genetics. Women have a 10x greater change dying of MI than breast cancer.
Modifiable and contributing: HTN (>160), tobacco use (1+ ppd-epi, norepi=vasoconstriction=increased HR, damage of vessel in body; are substituting O2 with CO), diabetes, high cholesterol (>200), physical inactivity, obesity, metabolic syndrome (HTN, obesity, insulin resistance), psychologic states (unnecessary fight or flight), substance abuse.

Question 6

Frequency- most days of the week 
Intensity- moderate (brisk walking, hiking, biking, swimming)
Type- isotonic 
Time- 30 minutes 
Adding resistance two days/week helps

Answer 6

FITT. Physical activity

Question 7

Fat intake- 30% of calories (monounsaturated fats- decrease red meats, eggs, whole milk products)
Reduce or eliminate alcohol and simple sugars
Take EPA and DHA supplements
Increase omega-3 fatty acids (i.e. tofu, fish, soybeans, flaxseed, walnut, canola)
Low saturated fat, low cholesterol.
Calories controlled based on activity level
No absolute restrictions, no rules for coffee

Answer 7

Nutrition

Question 8

Cholesterol lowering therapy

Answer 8

Complete lipid profile q5 years (state age 20)
Diet therapy first: restrict calories to decrease weight. Decrease dietary fat and cholesterol. Increase physical activity.
Reassess cholesterol levels after 6 weeks of diet therapy
Drugs are used concurrently with diet modification
Drugs are often needed for a lifetime

Question 9

Inhibit cholesterol synthesis in the liver.
Take in the evening- this is when the liver is synthesizing cholesterol.
DO NOT EAT OR DRINK GRAPEFRUIT
Serious s/e’s- rhabdomyolysis, liver damage

Answer 9

Statins. Cholesterol lowering drugs.

Question 10

Inhibits cholesterol synthesis. Many adverse effects (i.e. severe flushing, itching, GI probs, orthostatic hypotension). Take an NSAID 30 minutes before taking it to reduce adverse effects.

Answer 10

Niacin. Cholesterol lowering drug.

Question 11

Fabric acid derivative, won’t affect LDLs. May cause GI probe, interacts with many drugs.

Answer 11

Lopid

Question 12

Bile acid sequestrates- increase conversion of cholesterol to bile acids. Needs to be give 2 hours apart from other meds.

Answer 12

Questran, Welchol

Question 13

Inhibits absorption of dietary and biliary cholesterol. Often used with diet changes for primary hypercholesteremia, works really well when combined with statins (when this is done, watch for the effects on the liver)

Answer 13

Zetia

Question 14

Antiplatelet therapy

Answer 14

Most people with CAD should be on low-dose ASA (81 mg)- has the same effect of normal dose ASA on platelet aggregation but w/o the GI effects. Not as effective for women until >age 65.
For high risk women intolerant of ASA use clopidogrel (Plavix).
Be aware of bleeding and hemorrhagic stroke sx.

Question 15

Gerontologic considerations

Answer 15

Although the incidence is high, risk reduction and CAD tx are worthwhile.
Aggressively treat HTN, hyperlipidemia, and stop smoking no matter what age.
Planned physical activity: longer warm-ups, longer period of low-level activity, longer rest period between sessions, avoid extremes of temperature

Question 16

“Strangling of the chest.”
Temporary imbalance between oxygen supply and the heart’s demand.
Usually c/b a stable, atherosclerotic plaque. Does NOT cause permanent damage.
Can be stable or unstable (can’t get it to stop)

Answer 16

Angina.

Chronic stable- stop doing activity, it stops. Predictable. Does not cause permanent damage.

Question 17

Precipitating factors of angina

Answer 17

Physical exertion. Temperature extremes (vasoconstriction or dilation). Strong emotions (catecholamines). Eating a heavy meal (blood to GI for digestion). Tobacco use. Sexual activity. Stimulants (i.e. cocaine, amphetamines-vasoconstrict). Circadian rhythm patterns (early am).

Question 18

Chest pain that occurs intermittently over a long period with the same pattern of onset, duration, and intensity. Pressure, ache, constrictive, squeezing (NOT sharp or stabbing). Pain does NOT change with position or breathing. May also have indigestion. Can have radiation of the pain (d/t lactic acid formation from anaerobic metabolism stimulating other nerve endings). Pain lasts 5-15 minutes. Usu. controlled with rest or meds to provide peak effects when angina usually occurs.

Answer 18

Chronic stable angina

Know what causes it and how to get rid of it.

Question 19

Other types of angina

Answer 19

Silent ischemia- ischemia without symptoms (i.e. diabetics- lacking the nerves we have to respond to lactic acid that usually stimulates pain).
Nocturnal angina- occurs only at night (position doesn’t matter)
Prinzmetal’s angina-often occurs at rest, seen with migraine and Raynaud’s, coronary spasm; need calcium channel blockers and/or nitrates

Question 20

Arteries of the heart:

Answer 20

LAD=left anterior descending. feeds the anterior portion of the heart.
Right coronary feeds the inferior portion of the heart.
Circumflex feeds the posterior (back) and lateral (side) of the heart

Question 21

Diagnostic tests:

Answer 21

12-lead ECG: Gives 10 views of the heart. Determine which artery is causing the problem. compare with previous. expect some mild ischemic changes.
CXR: look for heart enlargement, calcifications, pulmonary problems.
Labs: confirm CAD. Look for risk factors.
If known CAD: echo, exercise stress test, cardiac cath (maybe)

Question 22

Should relieve pain in 3 minutes and lasts 30-60 minutes.

Check BP, don’t give if

Answer 22

Short-acting nitrates (1st line tx).
Cause venous vasodilation= decreased return to the heart=decreased preload
Relieve stable angina
May cause increase in heart rate initially because the decrease in BP sensed by the baroreceptors causes an increase in HR
HA because cerebral arteries dilate also
Can take prophylactically

Question 23

Used to reduce the incidence of anginal attacks. Causes headache. Causes orthostatic hypotension.
Watch for tolerance.
Nitropaste is dosed by the inch on a flat muscular area with no hair/scars (works for 3-6 hours, good for nocturnal and unstable angina).
Transdermal controlled-release by reservoir or matrix to maintain levels for 24 hours.
Provide a constant level of nitro to open coronary arteries to PREVENT spasm

Answer 23

Long-acting Nitrates (Isordil, Imdur).

Chronic CAD. Can still take the short-acting.

Question 24

Preferred drug of choice for chronic stable angina and following an MI. Many s/e’s (i.e. low HR, wheezing, GI probe, wt gain, depression). Do NOT use in pts with asthma

Answer 24

Beta blockers ("lols") 
Beta receptors increase heart rate when stimulated. Blockers decrease HR and shift from demand to supply of O2. 
B-blockers in mI covers receptors=cardioprotective from more circulating catecholamines 
B-2 receptor stimulation causes bronchodilation. Nonselective beta blockers can cause constriction- don't use in asthma or COPD

Question 25

If at high risk for a cardiac event, add these (if intolerant give with an ARB [“artans]). Can cause cough, low BP, change in K+ levels, angioedema.

Answer 25

ACE inhibitors (“prils”). Prevent angiotensin I from being converted to angiotensin II. After MI to prevent ventricular remodeling of unaffected ventricle.

Question 26

Used when beta blockers are contraindicated or don’t work, used for Prinzmetal’s angina. Can cause digoxin toxicity. Use with angina, but NOT after MI.

Answer 26

Calcium channel blockers (“pines”, also Verapamil, Diltiazem which help with conductivity along with smooth muscle)

Question 27

Angina treatment summary

Answer 27

A- antiplatelet/anticoagulant, antianginal, ACE or ARB
B- beta blocker, BP control
C- cigarette smoking cessation, calcium channel blockers, cholesterol management, cardiac rehab
D- diet, diabetes, depression screening
E- education, exercise
F- flu vaccination

Question 28

Associated with deterioration of a plaque causing partial (UA, NSTEMI) or total (STEMI) occlusion by thrombus.
Decreased blood flow to the heart.

Answer 28

Acute coronary syndrome (ACS)

Question 29

New chest pain, pain that occurs at rest, or pain that has a worsening pattern.
EMERGENCY!
Unpredictable
Oftentimes women have prodromal sx (i.e. Fatigue, dyspnea, indigestion, anxiety)

Answer 29

Unstable angina (UA). 
NSTEMI
Some blood to cardiac tissue=partial occlusion

Question 30

Acute myocardial infarction (AMI) patho

Answer 30

Sustained ischemia (>20 min) causing irreversible myocardial cell death (4-6 hours to necroses entire thickness of the heart).
Most d/t thrombus.
Most involve some portion of the LV
Degree of preexisting collateral circulation influences the severity of the infarction.

Question 31

S/S of AMI

Answer 31

Severe immobilizing chest pain not relieved by rest, position change, nitrates or antacids. More common in early am. Lasts >20 min. Can be atypical.
Sweating, ashen, clammy (vasoconstriction to periphery).
Increased BP and HR (drops later)
Crackles (LV damage=backup)
JVD, hepatic engorgement, edema
N/V. Temp up to 100.4 (inflammatory process)
High glucose levels. Denial. Distant heart sounds, S3/S4, loud holosystolic murmur.
Dysrhythmias- sinus tach with PVCs, T wave inversion, ST elevation or depression, abnormal Q waves.

Question 32

Healing process of AMI

Answer 32

Dead cardiac cells release enzymes (cardiac markers). Leukocytes infiltrate, thinning the cardiac wall (can cause tamponade). Glucose and free fatty acids are released. Can see the necrotic zone by ECG changes (i.e. ST elevation, pathologic Q waves). 10-14 days after a weak scar develops, but the heart is very vulnerable. 6 weeks after they are healed, the scarred area is less compliant. Normal cells will hypertrophy and dilate (ventricular remodeling) which can lead to heart failure (ACE inhibitors to break this process up, beta-blockers to calm the heart down).

Question 33

Serial ECGs for ACS

Answer 33

q2-4 hrs. Change in QRS, ST segment, T wave. Distinguish between STEMI (pathologic Q wave) and NSTEMI or UA (incomplete occlusion without a pathologic Q wave). Look at the pattern among the 12 leads to find the coronary artery involved. Ischemia causes ST depression, T wave inversion.
Injury (still reversible) causes ST elevation.
Infarction causes pathologic Q wave and T wave inversion (occurs w/i hours, may persist for months).

Question 34

CK-MB (released in response to myocardial damage). 4-6 hours after MI. peaks at 18 hours, normal at 24-36 hours.
troponin (highly specific for MI, rises and peaks earlier than CK-MB). peaks at 10-24 hrs 2 weeks for it to return to baseline.
Myoglobin is released earliest but is non-specific.

Answer 34

Cardiac markers

Question 35

Dx studies for ACS

Answer 35

if ECG and cardiac markers are non-diagnostic, exercise or pharmacologic stress testing, echo, stress echo (see if the angina can be triggered in a controlled environment)
May even do coronary angiography

Question 36

Treatment for ACS

Answer 36

Establish an IV.
Oxygen (2-4 L/min by NC), position upright.
12-lead ECG and continuous monitoring
Chewable ASA, SL nitroglycerin.
Morphine IV if pain not relieved by NTG (also vasodilates and calms pt).
Treat dysrhythmias. VS with pulse ox frequently. Bedrest for 12-24 hours. NPO except sips of water until stable (may go to cath, surgery).

Question 37

Tx if UA or NSTEMI WITHOUT cardiac markers:

ST depression=blockage but some flow, no cell death. stabilize them so they can go to cath.

Answer 37

ASA, heparin, integrillin (antiplatelet).

Coronary angiogram with PTCA once stabilized and angina controlled.

Question 38

Tx if STEMI or NSTEMI WITH cardiac markers:

Answer 38

Reperfusion therapy (ie Emergent PTCA, fibrinolytics, coronary surgical revascularization)

Question 39

1st line tx with confirmed MI. Goal is to open the artery within 90 minutes of arrival to the hospital. Usu do with a drug-eluting stent (has medication on it that prevents extreme fibrin growth around the stent).
Advantages: local anesthesia, walking w/i 24 hours, home in 1-3 days, work in 1 week.
Requires anti platelet drugs.
Nursing care is like cardiac cath (neurovascular checks, check site, etc).
Cx: abrupt closure, vascular injurt, AMI, stent embolization, coronary spasm, dysrhythmias

Answer 39

Percutaneous Transluminal Coronary Angioplasty (PTCA)
Give mucomyst before b/x it coats the kidneys and protests the from damage d/t the dye.
Always have atropine at the bedside (anticholinergic. increases HR. when you pull the sheath, pt can brady down d/t pressure change)

Question 40

Used if facility doesn’t have a cardiac cath lab. Goal is to stop the infarction process by dissolving the thrombus and reperfusing the myocardium. Give ASAP (ideally w/i 1st hr after sx, must with w/i 6 hrs, goal is w/i 30 min of arrival)
Only give IV.
Pt selection is very important.
Cx: reocclusion of the artery (prevent with IV heparin), bleeding (minor surface bleeding, gum bleeding is expected. do invasive stuff beforehand), hemorrhage/shock.

Answer 40

Fibrinolytics

Question 41

Nursing care with fibrinolytic

Answer 41

Baseline lab values (know the INR, HH, etc). Start 2-3 IV lines. Get all invasive procedures done if possible. Give in one IV bolus or over 30-90 minutes. Closely monitor (Rhythms, VS, pulse ox, heart/lung/neuro/bleeding assessments).

Question 42

How do you know when reperfusion occurs?

Answer 42

Return of ST segment to baseline. Abrupt cessation of chest pain. Early, rapid rise of Ck-MB w/i 3 hrs, peaking at 12 hrs. May have sudden onset of reperfusion dysrhythmias (open up arteries=somewhat type of shock. Usually not sustained. giving the heart substance after it has been deprived).

Question 43

Options include MIDCAB, OPCAB, robot-assisted cardiothoracic surgery, TMR.
Most common is CABG (coronary after bypass graft). Done for pts who fail medical management, have left main coronary artery or 3-vessel disease, are not candidates for PTCA, failed PTCA with ongoing chest pain, or have diabetes.
Requires a sternotomy with cardiopulmonary bypass (CPB).
Use internal mammary artery (IMA) the most, can also use radial artery and saphenous vein
Palliative tx, not a cure.

Answer 43

Coronary Surgery Revascularization
MIDCAB= minimally invasive direct coronary artery bypass. Decreases risk of infection, osteomyelitis in chest. No cardiopulmonary bypass machine. No sterneotomy.

Question 44

Nursing care after CABG

Answer 44

In ICU for 24-36 hours with PA catheter, arterial line, chest tubes, continuous ECG monitoring, ETT, epicardial pacing wires (if enter brady dysrhythmia, can hook up to these and stim the heart), urinary catheter, NGT.
Usu. extubated within 6 hrs and to step-down within 24 hours.
Many postop cx are d/t CPB- systemic inflammation, F&E imbalance (drain blood, filter it, put it back in), hypothermia, bleeding.
Postop dysrhythmias (esp. atrial) in first 3 days. Care for the surgical site (esp. donor site). May have postop cognitive dysfunction.

Question 45

MI medications

Answer 45

Initially: IV nitro (Tridil), morphine, dual antiplatelet therapy (ASA, clopidogrel [Plavix]), LMWH or IV heparin.
Within 24 hrs: oral beta-adrenergic blockers (if no contraindications), ACE inhibitors (for some), Antidysrhythmics (only if life-threatening), lipid-lowering drugs, stool softener (don’t want vasovagal response).

Question 46

Complications after AMI

Answer 46

Dysrhythmias: very common esp. with ischemia, electrolyte imbalances, SNS stimulation. Occur more with anterior wall infarction, heart failure, or stroke.
Heart failure: subtle s/s (ie mild dyspnea, agitation [decreased perfusion to brain], mild tachycardia). pulmonary congestion, S3/S4 (d/t fluid), crackles, JVD.
Cardiogenic shock: less likely now that we use PTCA/fibrinolytics. Requires tx with meds, IABP

Question 47

Occurs if infarction is near the mitral valve. Causes mitral valve regurgitation, increasing blood volume in the left atria. New systolic murmur (confirm with echo). Can rupture the muscle causing massive MVR, AEB dyspnea, pulmonary edema, decreased CO (treat with Nitride, IABP, MV replacement).

Answer 47

Papillary muscle dysfunction (necrosed=no muscle for valves)

Question 48

Ventricular aneurysm

Answer 48

Heart failure, dysrhythmias, angina.
Leads to thrombi or rupture (death).
Ventricles rupture= HR, dysrhythmias.
Happens d/t necrosis

Question 49

Common 2-3 days after MI. d/t inflammation. Chest pain worse with inspiration, cough, upper body movement, leaning forward relieves pain; friction rub; fever.
Dx with serial 12-lead ECGs
Tx: pain relief with ASA, NSAIDs, or corticosteroids

Answer 49

Pericarditis

Question 50

Homelier after ACS

Answer 50

CAD is chronic, not curable. Focus on modifiable risk factors. Physical activity is impt, gradually increase level using your optimal HR and potential for ischemia: do NOT go to your max HR (limited when on beta-blockers). Stop exercising and rest if chest pain or dyspnea occurs. Focus on isotonic activities (i.e. walk, jog, swim, bike, jump rope). Treat depression. Maintain contact with the pt.
Resumption of sexual activity within 7-10 days after uncomplicated MI: no more strenuous than climbing 2 flights of stairs. May have some sexual dysfunction. Take NTG prophylactically. Avoid sex after heavy meals/alcohol use, stress or with new partners, no anal sex.

Question 51

May or may not have known CAD. Death usually occurs within 1 hr of sx, most have no warning S/S.
Cause: acute ventricular dysrhythmias, sometimes a ventricular obstruction or extreme bradycardia (usually NOT an AMI).
If they survive, they are at high risk for another event: diagnostic workup for MI. Cardiac cath (may need PCI or CABG). 24 hr Holter monitor, exercise stress test, EPS. ICD to prevent a recurrence. May be given lidocaine, procainamide or stall. Help them with the psychological implications.

Answer 51

Sudden Cardiac Death (SCD)

Question 52

The community health nurse is planning health promotion teaching targeted at preventing coronary artery disease (CAD). Which ethnic group would the nurse select as the highest priority for this intervention?

a) White male
b) Hispanic male
c) African American male
d) Native American female

Answer 52

a) White male
The incidence of CAD and myocardial infarction (MI) is highest among white, middle-aged men. Hispanic individuals have lower rates of CAD than non-Hispanic whites or African Americans. African Americans have an earlier age of onset and more severe CAD than whites and more than twice the mortality rate of whites of the same age. Native Americans have increased mortality in less than 35-year-olds and have major modifiable risk factors such as diabetes.

Question 53

Which individuals would the nurse identify as having the highest risk for CAD?

a) A 45-year-old depressed male with a high-stress job
b) A 60-year-old male with below normal homocysteine levels
c) A 54-year-old female vegetarian with elevated high-density lipoprotein (HDL) levels
d) A 62-year-old female who has a sedentary lifestyle and body mass index (BMI) of 23 kg/m2

Answer 53

a) A 45-year-old depressed male with a high-stress job

Question 54

Which antilipemic medications should the nurse question for a patient with cirrhosis of the liver (select all that apply)?

a) Niacin (Nicobid)
b) Ezetimibe (Zetia)
c) Gemfibrozil (Lopid)
d) Atorvastatin (Lipitor)
e) Cholestyramine (Questran)

Answer 54

b) Ezetimibe (Zetia)

d) Atorvastatin (Lipitor)

Question 55

The nurse would assess a patient with complaints of chest pain for which clinical manifestations associated with a myocardial infarction (MI) (select all that apply)?

a) Flushing
b) Ashen skin
c) Diaphoresis
d) Nausea and vomiting
e) S3 or S4 heart sounds

Answer 55

b) Ashen skin
c) Diaphoresis
d) Nausea and vomiting
e) S3 or S4 heart sounds
During the initial phase of an MI, catecholamines are released from the ischemic myocardial cells, causing increased sympathetic nervous system (SNS) stimulation. This results in the release of glycogen, diaphoresis, and vasoconstriction of peripheral blood vessels. The patient’s skin may be ashen, cool, and clammy (not flushed) as a result of this response. Nausea and vomiting may result from reflex stimulation of the vomiting center by severe pain. Ventricular dysfunction resulting from the MI may lead to the presence of the abnormal S3 and S4 heart sounds.