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Chapter 33 CAD and Acute coronary syndrome Flashcards

1
Q

is the most common type of CVD.

A

Coronary artery disease (CAD)

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2
Q

is a type of blood vessel disorder that we consider in the general category of atherosclerosis.

A

Coronary artery disease (CAD)

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3
Q

comes from 2 Greek words: athere, meaning “fatty mush,” and skleros, meaning “hard.”3

A

atherosclerosis

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4
Q

form in the coronary arteries, the disease is called CAD

A

atheromas (fatty deposits)

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5
Q

arteriosclerotic heart disease (ASHD), cardiovascular heart disease (CVHD), ischemic heart disease (IHD), coronary heart disease (CHD), are

A

other terms used to describe CAD.

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6
Q

tobacco use, hyperlipidemia, hypertension, toxins, diabetes, high homocysteine levels, and infection causing a local inflammatory response

A

Damage to the endothelial lining can result from

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7
Q

, a protein made by the liver, is a nonspecific marker of inflammation. CRP levels rise when there is systemic inflammation, such as rheumatoid arthritis or inflammatory bowel disease

A

C-reactive protein (CRP)

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8
Q

are (1) fatty streak, (2) fibrous plaque, and (3) complicated lesion.

A

The stages of development in atherosclerosis

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9
Q

the earliest lesions of atherosclerosis, are lipid-filled smooth muscle cells

A

Fatty streaks

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10
Q

stage is the beginning of progressive changes in the endothelium of the arterial wall. These changes can appear in the coronary arteries by age 30 and increase with age.

A

fibrous plaque

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11
Q

some arterial anastomoses or connections, called collateral circulation, exist within the

A

coronary circulation

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12
Q

(1) inherited predisposition to develop new blood vessels (angiogenesis) and (2) presence of chronic ischemia (poor blood flow).

A

Two factors contribute to the growth and extent of collateral circulation:

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13
Q

Frequency (how often), Intensity (how hard), Type (isotonic), and Time (how long). Everyone

A

FITT formula

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14
Q

Red meat, egg yolks, and whole milk products are \

A

major sources of saturated fat and cholesterol.

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15
Q

is the most potent statin currently available.

A

Rosuvastatin (Crestor)

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16
Q

work by aiding the removal of VLDLs. They are very effective for lowering triglycerides and increasing HDL levels.

A

fibric acid derivatives

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17
Q

muscle ache

A

myopathy

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18
Q

increase conversion of cholesterol to bile acids in the liver and decrease hepatic cholesterol

A

Bile-acid sequestrants

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19
Q

are a newer class of cholesterol-lowering drugs

A

PCSK9 inhibitors

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20
Q

selectively inhibits the absorption of dietary and biliary cholesterol across the intestinal wall
-patients with primary hypercholesterolemia

A

Ezetimibe (Zetia)

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21
Q

is recommended for people who have CAD.

A

Low-dose aspirin (81 mg)

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22
Q

is an option for people who are aspirin intolerant.

A

Clopidogrel (Plavix)

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23
Q

Aggressive treatment of hypertension and hyperlipidemia

A

helps stabilize plaques in the coronary arteries.

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24
Q

break down skeletal muscle

A

rhabdomyolysis

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25
Q

joint pain

A

Arthralgia

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26
Q

results from a decreased ability to sweat efficiently

A

Heat intolerance

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27
Q

on most days of the week as able

A

older adult should exercise a minimum of 30 minutes

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28
Q

, is the clinical manifestation of myocardial ischemia

A

Angina, or chest pain

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29
Q

When the demand for myocardial O2 exceeds the ability of the coronary arteries to supply the heart with O2,

A

myocardial ischemia occurs

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30
Q

is significant narrowing of 1 or more coronary arteries by atherosclerosis.

A

The most common reason for angina to develop

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31
Q

, the artery is usually blocked (stenosed) 70% or more (50% or more for the left main coronary artery).20

A

For ischemia to occur from an atherosclerotic plaque

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32
Q

refers to chest pain that occurs intermittently over a long period of time with a similar pattern of onset, duration, and intensity of symptoms.

A

Chronic stable angina

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33
Q

provoked by physical exertion, stress, or emotional upset

  • a pressure, heaviness, or discomfort in the chest.
  • described as a squeezing, heavy, tight, or suffocating sensation
  • does not change with position or breathing.
A

cause of Chronic stable angina

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34
Q

substernally, it may radiate to other locations, including the jaw, neck, shoulders, and/or arms
-feeling of indigestion or a burning sensation in the epigastric region. The sensation may be felt between the shoulder blades

A

most angina pain occurs

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35
Q

including dyspnea, nausea, mid-epigastric discomfort, and/or fatigue. We refer to this as an angina equivalent.

A

women and older adults, report atypical symptoms of angina

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36
Q

only a few minutes

A

pain of chronic stable angina usually lasts for

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37
Q

when the precipitating factor is resolved (e.g., by resting, calming down, using sublingual nitroglycerin [SL NTG]) (

A

chronic angina subsides

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38
Q

ST segment depression and/or T wave inversion. ( changes represent inadequate supply of blood and O2 to the heart muscle)

A

With ischemia, the 12-lead ECG often shows

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39
Q

the isoelectric line should be flat

A

normal heart ECG

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40
Q

refers to ischemia that occurs in the absence of any subjective symptoms

A

Silent ischemia (diabetic)

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41
Q

This is likely due to diabetic neuropathy affecting the nerves that innervate the cardiovascular system.

A

Patients with diabetes have an increased prevalence of silent ischemia.

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42
Q

early morning

A

Circadian Rhythm Patterns occur

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43
Q

Coronary vasospasm

A

Prinzmetal’s angina

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44
Q

Treatment may include long-acting nitrates and/or calcium channel blockers
-occur at rest

A

Prinzmetal’s angina treatment

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45
Q

Myocardial ischemia from microvascular disease affecting the small, distal branches of coronary arteries

A

Microvascular angina

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46
Q

More common in women
• Triggered by activities of daily living (e.g., shopping, work) vs. physical exercise (exertion)

• Treatment may include nitroglycerin

A

Microvascular angina

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47
Q

Rupture of unstable plaque, exposing thrombogenic surface

- Occurs at rest or with minimal exertion

A

Unstable angina (last more than 10 mins)

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48
Q

is a rare form of angina that often occurs at rest and not with increased physical demand. It is sometimes seen in patients with a history of migraine headaches, Raynaud’s phenomenon, and heavy smoking.

A

Prinzmetal’s angina(variant angina)

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49
Q

usually due to spasm of a major coronary artery. Strong contraction (spasm) of smooth muscle in the coronary artery results from increased intracellular calcium.

A

Prinzmetal’s angina(variant angina) // cause pathophy

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50
Q

(not usually associated with an MI)

A

When spasm occurs, the patient has angina and transient ST segment elevation

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51
Q

significant CAD or coronary spasm of a major coronary artery

A

In microvascular angina, chest pain occurs in the absence of

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52
Q

MVD is often used interchangeably with the term

A

syndrome X

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53
Q

or develop into UA (unstable angina) or ACS.

A

Chronic stable angina can progress

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54
Q

1) relief of pain, (2) immediate and appropriate treatment, (3) preservation of heart muscle if an MI is suspected, (4) effective coping with illness-associated anxiety, (5) participation in a rehabilitation plan, and (6) reduction of risk factors.

A

The overall goals for a patient who presents with angina include

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55
Q

(1) position patient upright unless contraindicated and apply supplemental O2, (2) assess vital signs, (3) place patient on continuous ECG monitor, (4) obtain a 12-lead ECG, (5) provide prompt pain relief, first with NTG, followed by an IV opioid analgesic, if needed, (6) obtain cardiac biomarkers, (7) assess heart and breath sounds, and (8) obtain a chest x-ray. T

A

patient has angina, perform the following measures:

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56
Q

may indicate ischemia of a papillary muscle of the mitral valve, causing mitral regurgitation (the mitral valve does not close properly).

A

new systolic murmur heard during an angina attack

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57
Q

nitrates, angiotensin-converting enzyme (ACE) inhibitors, β-blockers, and calcium channel blockers (Table 33.11 and Fig. 33.5). Aspirin (previously discussed) is given in the absence of contraindications

A

The most common medications to optimize myocardial perfusion in chronic stable angina include

58
Q

. Nitrates produce their principal effects by the following mechanisms:

A

Short-acting nitrates are first-line therapy for an acute episode of angina

59
Q

Dilating peripheral blood vessels: This results in decreased SVR, venous pooling, and decreased venous blood return to the heart (preload). Therefore myocardial O2 demand is decreased because of the reduced cardiac workload.
Dilating coronary arteries and collateral vessels: This may increase blood flow to the ischemic areas of the heart. However, when the coronary arteries are severely atherosclerotic, coronary dilation is hard to achieve.

A

Short-acting nitrates work

60
Q

usually relieves pain in about 5 minutes and lasts about 30 to 40 minutes

A

SL NTG tablets or translingual spray (Nitrolingual)

61
Q

tingling sensation when taken; otherwise it may be outdated. Warn the patient that a headache, dizziness, or flushing may occur. Caution the patient to change positions slowly after NTG use because orthostatic hypotension may occur.

A

SL NTG tablets should cause a

62
Q

are longer acting than SL or translingual NTG. They are used to reduce the frequency of angina attacks and to treat Prinzmetal’s angina.

A

Oral nitrates, such as isosorbide dinitrate (e.g., Isordil) and isosorbide mononitrate,

63
Q

headache from the dilation of cerebral blood vessels. Tell patients to take acetaminophen (Tylenol) to relieve the headache.

A

The main side effect isosorbide dinitrate (e.g., Isordil) and isosorbide mononitrate, is (long-acting)

64
Q

Remind patients that taking a long-acting NTG preparation should not keep them from using translingual or SL NTG if chest pain develops.

A

if pain develops u can take Nitroglycerin even if they take long

65
Q

is a 2% NTG topical ointment dosed by the inch. It is placed on the upper body or arm, over a flat muscular area that is free of hair and scars. Once absorbed, it prevents angina for 3 to 6 hours. The ointment should be wiped off each evening to allow for a 10- to 14-hour nitrate-free interval to prevent nitrate tolerance.

A

Nitropaste

66
Q

silicone gel and polymer matrix. These systems allow timed release of NTG over a 24-hour period.

A

Currently 2 systems are available for transdermal NTG drug delivery:

67
Q

Patients with chronic stable angina who have an ejection fraction (EF) of 40% or less, diabetes, hypertension, or CKD should

A

take an ACE inhibitor (e.g., lisinopril [Zestril]) indefinitely, unless contraindicated.

68
Q

drugs result in vasodilation and reduced blood volume. Most important, they can prevent or reverse ventricular remodeling in patients who have had an MI For patients who are intolerant of ACE inhibitors take ARB

A

ACE inhibitor (e.g., lisinopril [Zestril])

69
Q

are given for relief of angina symptoms in patients with chronic stable angina.

A

β-Blockers

70
Q

in the heart

A

β1-Receptors are found

71
Q

are found in blood vessels, lungs, and liver.

A

β2 Receptors

72
Q

they only block β1 receptors (e.g., atenolol [Tenormin], metoprolol [Lopressor]).

A

β-blockers are called cardioselective β-blockers because

73
Q

block both β1 and β2 receptors (e.g., nadolol [Corgard], propranolol [Inderal]).

A

β-blockers, referred to as nonselective β-blockers,

74
Q

(e.g., carvedilol [Coreg], labetalol [Trandate]).

A

β-blockers block α1, β1, and β2 receptors

75
Q

Their main effects are: (1) systemic vasodilation with decreased SVR, (2) decreased myocardial contractility, (3) coronary vasodilation, and (4) decreased HR.

A

Calcium Channel Blockers

76
Q

Prevents calcium entry into vascular smooth muscle cells and myocytes (cardiac cells)

• May prevent or control coronary vasospasm (t Prinzmetal’s angina.
)

A

Calcium Channel Blockers

77
Q

dihydropyridines (e.g., amlodipine [Norvasc], nifedipine [Procardia]) have more vasodilatory effects. The nondihydropyridines (e.g., verapamil [Calan], diltiazem [Cardizem]) have a greater effect on decreasing HR and contractility.

A

2 groups of calcium channel blockers. T

78
Q

(e.g., amlodipine [Norvasc], nifedipine [Procardia]) have more vasodilatory effects.

A
  1. dihydropyridines (calcium channel blocker)
79
Q

(e.g., verapamil [Calan], diltiazem [Cardizem]) have a greater effect on decreasing HR and contractility.

A
  1. nondihydropyridines (calcium channel blocker)
80
Q

a sodium current inhibitor, is used to treat chronic angina in patients who have not had an adequate response with other antianginal medications.

A

Ranolazine (Ranexa),

81
Q

to identify and localize CAD

A

For patients with increasing angina symptoms, a cardiac catheterization is the gold-standard test

82
Q

During PCI, a catheter with a deflated balloon tip is inserted into the blocked coronary artery. The deflated balloon is positioned inside the blockage and inflated. This compresses the plaque against the artery wall, resulting in vessel dilation and a larger vessel diameter. This procedure is called balloon angioplasty.

A

During PCI/ balloon angioplasty.

83
Q

are usually placed after a balloon angioplasty

A

Intracoronary stents

84
Q

is an expandable mesh-like structure designed to keep the vessel open. It provides support to the arterial wall

A

stent

85
Q

bare metal (BMS) and drug-eluting (DES).

A

2 types of stents:

86
Q

DES is coated with a drug (e.g., everolimus, zotarolimus) to reduce the risk for overgrowth of the intimal lining (neointimal hyperplasia) within the stent. This is the primary cause of

A

in-stent restenosis (ISR).

87
Q

unfractionated heparin (UH) or low-molecular-weight heparin (LMWH), a direct thrombin inhibitor (e.g., bivalirudin [Angiomax]), and/or a glycoprotein IIb/IIIa inhibitor (e.g., eptifibatide [Integrilin])

A

Drugs commonly used during PCI are

88
Q

abrupt closure from coronary artery dissection or rupture, vascular injury at the artery access site (e.g., femoral, radial), acute MI from acute stent thrombosis or from plaque dislodging and blocking the vessel distal to the catheter, stent embolization, failure to cross the blockage with a balloon or stent, coronary spasm, dye allergy, renal compromise, bleeding (e.g., retroperitoneal bleeding when the femoral artery is used or vascular access-site bleeding), infection, stroke, and emergent coronary artery bypass graft (CABG) surgery. The risk for dysrhythmias during and after the procedure is always present, so patients should be on a cardiac monitor afterwards.

A

Potential complications from cardiac catheterization with PCI include

89
Q

who (1) fail medical management, (2) have left main coronary artery or 3-vessel disease, (3) are not candidates for PCI (e.g., blockages are long or difficult to access), or (4) have failed PCI and continue to have chest pain.

A

In patients with chronic stable angina, coronary revascularization with CABG surgery is recommended for patients

90
Q

of the placement of arterial or venous grafts to provide blood from the aorta or a branch of a major artery that originates from the aorta (e.g., internal mammary artery) to the heart muscle distal to blocked coronary arteries. The procedure may involve one or more grafts using the internal mammary (thoracic) artery (IMA or ITA), saphenous vein, and/or radial artery

A

CABG surgery consists

91
Q

a sternotomy (opening of the chest cavity) and cardiopulmonary bypass (CPB). During CPB, blood is diverted from the patient’s heart to a machine where it is oxygenated and returned (via a pump) to the patien

A

CABG surgery requires

92
Q

is the most common artery used for bypass graft

A

internal mammary artery ( IMA)

93
Q

can be used for bypass grafts.

A

Saphenous veins

94
Q

offers patients with disease of the LAD or right coronary artery an approach to surgical treatment that does not involve a sternotomy and CPB.

A

Minimally invasive direct coronary artery bypass (MIDCAB)

95
Q

(1) hemodynamic monitoring (e.g., CO), (2) an arterial line for continuous BP monitoring, (3) pleural and mediastinal chest tubes for chest drainage, (4) continuous ECG monitoring, (5) an endotracheal tube connected to mechanical ventilation, (6) epicardial pacing wires for emergency pacing of the heart, (7) a urinary catheter to monitor urine output, and (8) a nasogastric tube for gastric decompression. Most patients are extubated within 6 hours and transferred to a step-down unit within 24 to 48 hours for continued monitoring.

A

Care after CABG surgery is provided in the intensive care unit (ICU) for the first 24 to 36 hours.

96
Q

chest pain from ischemia is prolonged and not immediately reversible,

A

acute coronary syndrome (ACS)

97
Q

ACS includes the spectrum of non-ST elevation acute coronary syndrome (UA and non–ST-segment-elevation myocardial infarction [NSTEMI]), and ST-segment-elevation myocardial infarction (STEMI)

A

ACS includes the spectrum (STEMI)

98
Q

myocardial injury that is potentially reversible, but, if not treated, will likely evolve to permanent necrosis (tissue death) of the myocardium.

A

ST elevation represents

99
Q

occurs because of an abrupt stoppage of blood flow through a coronary artery with a thrombus caused by platelet aggregation.

A

myocardial infarction (MI)

100
Q

caused by an occlusive thrombus, results in ST-elevation in the ECG leads facing the area of infarction

A

STEMI

101
Q

To limit the infarct size, the artery must be opened within 90 minutes of presentation to restore blood and O2 to the heart muscle and limit the infarct size.

A

STEMI is an emergency.

102
Q

PCI is the first-line treatment, if available. It confirms which artery has the occlusive thrombus so it can be opened with a balloon and stent

A

1st line treatment to STEMI

103
Q

patients usually undergo catheterization within 12 to 72 hours. Thrombolytic therapy is not indicated for NSTEMI.

A

NSTEMI (can’t do thrombolytic therapy)

104
Q

(worsening myocardial contractility)

A

hypokinesis

105
Q

(absent myocardial contractility)

A

akinesis

106
Q

the subendocardium (the innermost layer of tissue in the heart muscle)

A

earliest tissue to become ischemic is

107
Q

inferior and posterior LV walls

A

right coronary artery supplies blood to the

108
Q

in patients who have a left inferior wall STEMI

A

right ventricular MI

109
Q

adequate blood supply. This is one reason why a younger person may have a more serious first MI than an older person with the same degree of blockage.

A

person with a long history of CAD may develop good collateral circulation to provide the area surrounding the infarction site with an

110
Q

ersistent and unlike any other pain, it is usually described as a heavy, pressure, tight, burning, constricted, or crushing feeling.

A

MI symptoms

111
Q

Common locations are the substernal or epigastric area

A

Locations of MI

112
Q

pain may radiate to the neck, lower jaw, and arms or to the back

A

MI

113
Q

infarcted heart muscle also cause changes in the unaffected areas. To try to compensate for the damaged muscle, the normal myocardium hypertrophies and dilates. This process is called

A

ventricular remodeling.

114
Q

Dysrhythmias are the

A

most common complication after an MI

115
Q

is a complication that occurs when the right or left ventricle’s pumping action is reduced.

A

Heart failure (HF)

116
Q

mild dyspnea, restlessness, agitation, or slight tachycardia. Other signs indicating the onset of left-sided HF include pulmonary congestion on chest x-ray, S3 or S4 heart sounds, crackles on auscultation of the lungs, paroxysmal nocturnal dyspnea (PND), and orthopnea.

A

left-sided HF

117
Q

include JVD, hepatic congestion, or lower extremity edema. See Chapter 34 for information about the treatment of acute decompensated HF.

A

Signs of right-sided HF

118
Q

occurs when O2 and nutrients supplied to the tissues are inadequate because of severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, or right ventricular infarction

A

Cardiogenic shock

119
Q

may occur if the infarcted area includes or is near the papillary muscle that attaches to the mitral valve

A

Papillary muscle dysfunction

120
Q

systolic murmur suggestive of mitral regurgitation at the cardiac apex
-Dyspnea, pulmonary edema, and decreased CO result from the backup of blood in the left atrium.

A

Papillary muscle dysfunction symptom

121
Q

results when the infarcted heart wall is thin and bulges out during contraction
- more common w/ anterior MIs

A

Left ventricular aneurysm

122
Q

may develop HF, dysrhythmias, and angina.

A

ventricular aneurysm

123
Q

new loud systolic murmur heard in patients with acute MI may signal

A

ventricular septal wall rupture.

124
Q

, an inflammation of the visceral and/or parietal pericardium, may occur 2 or 3 days after an acute MI

A

Acute pericarditis

125
Q

is pericarditis and fever that develop 1 to 8 weeks after MI

A

Dressler syndrome

126
Q

are proteins released into the blood from necrotic heart muscle after an MI

A

Serum cardiac biomarkers

127
Q

cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI)

A

Cardiac-specific troponin has 2 subtypes:

128
Q

biomarkers are highly specific indicators of MI and have greater sensitivity and specificity for myocardial injury than creatine kinase MB (CK-MB).

A

Cardiac-specific troponin

129
Q

specific to heart muscle cells and helps to quantify myocardial damage.

A

CK-MB band is

130
Q

is released into the circulation within 2 hours after an MI and peaks in 3 to 15 hours

A

Myoglobin

131
Q

(compared to CABG surgery) include (1) it allows for faster reperfusion to limit infarction size; (2) it provides an alternative to surgical intervention; (3) it is performed with local anesthesia; (4) the patient is ambulatory shortly after the procedure; (5) the length of hospital stay is about 3 to 4 days after MI compared with the 4 to 6 days with CABG surgery, thus reducing hospital costs; and (6) the patient can return to work several weeks sooner after PCI, compared with a 6- to 8-week convalescence after CABG.

A

advantages of PCI

132
Q

is the build-up of scar tissue inside the stent (referred to as neointimal hyperplasia). ISR usually occurs within a few months to a year after stent placemen

A

ISR (In stent restenosis)

133
Q

systemic anticoagulation with either subcutaneous LMWH or IV UH is

A

used only for UA and NSTEMI patients.

134
Q

includes emergent PCI (preferred, for PCI-capable hospitals)

A

Reperfusion therapy

135
Q

(in hospitals not capable of performing PCI).

A

thrombolytic therapy

136
Q

units: 1 MET is the amount of O2 needed by the body at rest—3.5 mL of O2 per kilogram per minute, or 1.4 cal/kg of body weight per minute.

A

metabolic equivalent (MET)

137
Q

involve the development of tension during muscular contraction but produce little or no change in muscle length or joint movement.
- Lifting, carrying, and pushing heavy objects are isometric activities. These activities are associated with the Valsalva maneuver and may cause a vasovagal response.

A

Isometric activities

138
Q

activities involve changes in muscle length and joint movement with rhythmic contractions at relatively low muscular tension. Walking, jogging, swimming, bicycling, and jumping rope are examples of activities that are mostly isotonic. Isotonic exercise can put a safe, steady load on the heart and lungs and improve the circulation to other organs.
Women who have an MI often ha

A

Isotonic

139
Q

is the restoration of a person to an optimal state of function in 6 areas: (1) physiologic, (2) psychologic, (3) mental, (4) spiritual, (5) economic, and (6) vocational.

A

Cardiac rehabilitation

140
Q

is a sudden, unexpected death resulting from a variety of cardiac causes

A

Sudden cardiac death (SCD)

141
Q

LV hypertrophy, myocarditis, and hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy is a risk factor for SCD, especially in young, athletic people.

A

Structural heart disease includes

142
Q

is a personal external defibrillator that has 2 main parts: a garment and monitor. The garment is worn under clothing and has electrodes that continuously record the patient’s ECG. The monitor is worn around the waist or from a shoulder strap.

A

wearable cardioverter-defibrillator

adn semester 2 (19 decks)

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