Chapter 33 CAD and Acute coronary syndrome Flashcards
(142 cards)
1
Q
is the most common type of CVD.
A
Coronary artery disease (CAD)
2
Q
is a type of blood vessel disorder that we consider in the general category of atherosclerosis.
A
Coronary artery disease (CAD)
3
Q
comes from 2 Greek words: athere, meaning “fatty mush,” and skleros, meaning “hard.”3
A
atherosclerosis
4
Q
form in the coronary arteries, the disease is called CAD
A
atheromas (fatty deposits)
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.
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
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)
8
Q
are (1) fatty streak, (2) fibrous plaque, and (3) complicated lesion.
A
The stages of development in atherosclerosis
9
Q
the earliest lesions of atherosclerosis, are lipid-filled smooth muscle cells
A
Fatty streaks
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
11
Q
some arterial anastomoses or connections, called collateral circulation, exist within the
A
coronary circulation
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:
13
Q
Frequency (how often), Intensity (how hard), Type (isotonic), and Time (how long). Everyone
A
FITT formula
14
Q
Red meat, egg yolks, and whole milk products are \
A
major sources of saturated fat and cholesterol.
15
Q
is the most potent statin currently available.
A
Rosuvastatin (Crestor)
16
Q
work by aiding the removal of VLDLs. They are very effective for lowering triglycerides and increasing HDL levels.
A
fibric acid derivatives
17
Q
muscle ache
A
myopathy
18
Q
increase conversion of cholesterol to bile acids in the liver and decrease hepatic cholesterol
A
Bile-acid sequestrants
19
Q
are a newer class of cholesterol-lowering drugs
A
PCSK9 inhibitors
20
Q
selectively inhibits the absorption of dietary and biliary cholesterol across the intestinal wall
-patients with primary hypercholesterolemia
A
Ezetimibe (Zetia)
21
Q
is recommended for people who have CAD.
A
Low-dose aspirin (81 mg)
22
Q
is an option for people who are aspirin intolerant.
A
Clopidogrel (Plavix)
23
Q
Aggressive treatment of hypertension and hyperlipidemia
A
helps stabilize plaques in the coronary arteries.
24
Q
break down skeletal muscle
A
rhabdomyolysis
25
joint pain
Arthralgia
26
results from a decreased ability to sweat efficiently
Heat intolerance
27
on most days of the week as able
older adult should exercise a minimum of 30 minutes
28
, is the clinical manifestation of myocardial ischemia
Angina, or chest pain
29
When the demand for myocardial O2 exceeds the ability of the coronary arteries to supply the heart with O2,
myocardial ischemia occurs
30
is significant narrowing of 1 or more coronary arteries by atherosclerosis.
The most common reason for angina to develop
31
, the artery is usually blocked (stenosed) 70% or more (50% or more for the left main coronary artery).20
For ischemia to occur from an atherosclerotic plaque
32
refers to chest pain that occurs intermittently over a long period of time with a similar pattern of onset, duration, and intensity of symptoms.
Chronic stable angina
33
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.
cause of Chronic stable angina
34
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
most angina pain occurs
35
including dyspnea, nausea, mid-epigastric discomfort, and/or fatigue. We refer to this as an angina equivalent.
women and older adults, report atypical symptoms of angina
36
only a few minutes
pain of chronic stable angina usually lasts for
37
when the precipitating factor is resolved (e.g., by resting, calming down, using sublingual nitroglycerin [SL NTG]) (
chronic angina subsides
38
ST segment depression and/or T wave inversion. ( changes represent inadequate supply of blood and O2 to the heart muscle)
With ischemia, the 12-lead ECG often shows
39
the isoelectric line should be flat
normal heart ECG
40
refers to ischemia that occurs in the absence of any subjective symptoms
Silent ischemia (diabetic)
41
This is likely due to diabetic neuropathy affecting the nerves that innervate the cardiovascular system.
Patients with diabetes have an increased prevalence of silent ischemia.
42
early morning
Circadian Rhythm Patterns occur
43
Coronary vasospasm
Prinzmetal’s angina
44
Treatment may include long-acting nitrates and/or calcium channel blockers
-occur at rest
Prinzmetal’s angina treatment
45
Myocardial ischemia from microvascular disease affecting the small, distal branches of coronary arteries
Microvascular angina
46
More common in women
• Triggered by activities of daily living (e.g., shopping, work) vs. physical exercise (exertion)
• Treatment may include nitroglycerin
Microvascular angina
47
Rupture of unstable plaque, exposing thrombogenic surface
| - Occurs at rest or with minimal exertion
Unstable angina (last more than 10 mins)
48
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.
Prinzmetal’s angina (variant angina)
49
usually due to spasm of a major coronary artery. Strong contraction (spasm) of smooth muscle in the coronary artery results from increased intracellular calcium.
Prinzmetal’s angina (variant angina) // cause pathophy
50
(not usually associated with an MI)
When spasm occurs, the patient has angina and transient ST segment elevation
51
significant CAD or coronary spasm of a major coronary artery
In microvascular angina, chest pain occurs in the absence of
52
MVD is often used interchangeably with the term
syndrome X
53
or develop into UA (unstable angina) or ACS.
Chronic stable angina can progress
54
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.
The overall goals for a patient who presents with angina include
55
(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
patient has angina, perform the following measures:
56
may indicate ischemia of a papillary muscle of the mitral valve, causing mitral regurgitation (the mitral valve does not close properly).
new systolic murmur heard during an angina attack
57
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
The most common medications to optimize myocardial perfusion in chronic stable angina include
58
. Nitrates produce their principal effects by the following mechanisms:
Short-acting nitrates are first-line therapy for an acute episode of angina
59
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.
Short-acting nitrates work
60
usually relieves pain in about 5 minutes and lasts about 30 to 40 minutes
SL NTG tablets or translingual spray (Nitrolingual)
61
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.
SL NTG tablets should cause a
62
are longer acting than SL or translingual NTG. They are used to reduce the frequency of angina attacks and to treat Prinzmetal’s angina.
Oral nitrates, such as isosorbide dinitrate (e.g., Isordil) and isosorbide mononitrate,
63
headache from the dilation of cerebral blood vessels. Tell patients to take acetaminophen (Tylenol) to relieve the headache.
The main side effect isosorbide dinitrate (e.g., Isordil) and isosorbide mononitrate, is (long-acting)
64
Remind patients that taking a long-acting NTG preparation should not keep them from using translingual or SL NTG if chest pain develops.
if pain develops u can take Nitroglycerin even if they take long
65
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.
Nitropaste
66
silicone gel and polymer matrix. These systems allow timed release of NTG over a 24-hour period.
Currently 2 systems are available for transdermal NTG drug delivery:
67
Patients with chronic stable angina who have an ejection fraction (EF) of 40% or less, diabetes, hypertension, or CKD should
take an ACE inhibitor (e.g., lisinopril [Zestril]) indefinitely, unless contraindicated.
68
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
ACE inhibitor (e.g., lisinopril [Zestril])
69
are given for relief of angina symptoms in patients with chronic stable angina.
β-Blockers
70
in the heart
β1-Receptors are found
71
are found in blood vessels, lungs, and liver.
β2 Receptors
72
they only block β1 receptors (e.g., atenolol [Tenormin], metoprolol [Lopressor]).
β-blockers are called cardioselective β-blockers because
73
block both β1 and β2 receptors (e.g., nadolol [Corgard], propranolol [Inderal]).
β-blockers, referred to as nonselective β-blockers,
74
(e.g., carvedilol [Coreg], labetalol [Trandate]).
β-blockers block α1, β1, and β2 receptors
75
Their main effects are: (1) systemic vasodilation with decreased SVR, (2) decreased myocardial contractility, (3) coronary vasodilation, and (4) decreased HR.
Calcium Channel Blockers
76
Prevents calcium entry into vascular smooth muscle cells and myocytes (cardiac cells)
• May prevent or control coronary vasospasm (t Prinzmetal’s angina.
)
Calcium Channel Blockers
77
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.
2 groups of calcium channel blockers. T
78
(e.g., amlodipine [Norvasc], nifedipine [Procardia]) have more vasodilatory effects.
1. dihydropyridines (calcium channel blocker)
79
(e.g., verapamil [Calan], diltiazem [Cardizem]) have a greater effect on decreasing HR and contractility.
2. nondihydropyridines (calcium channel blocker)
80
a sodium current inhibitor, is used to treat chronic angina in patients who have not had an adequate response with other antianginal medications.
Ranolazine (Ranexa),
81
to identify and localize CAD
For patients with increasing angina symptoms, a cardiac catheterization is the gold-standard test
82
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.
During PCI/ balloon angioplasty.
83
are usually placed after a balloon angioplasty
Intracoronary stents
84
is an expandable mesh-like structure designed to keep the vessel open. It provides support to the arterial wall
stent
85
bare metal (BMS) and drug-eluting (DES).
2 types of stents:
86
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
in-stent restenosis (ISR).
87
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])
Drugs commonly used during PCI are
88
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.
Potential complications from cardiac catheterization with PCI include
89
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.
In patients with chronic stable angina, coronary revascularization with CABG surgery is recommended for patients
90
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
CABG surgery consists
91
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
CABG surgery requires
92
is the most common artery used for bypass graft
internal mammary artery ( IMA)
93
can be used for bypass grafts.
Saphenous veins
94
offers patients with disease of the LAD or right coronary artery an approach to surgical treatment that does not involve a sternotomy and CPB.
Minimally invasive direct coronary artery bypass (MIDCAB)
95
(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.
Care after CABG surgery is provided in the intensive care unit (ICU) for the first 24 to 36 hours.
96
chest pain from ischemia is prolonged and not immediately reversible,
acute coronary syndrome (ACS)
97
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)
ACS includes the spectrum (STEMI)
98
myocardial injury that is potentially reversible, but, if not treated, will likely evolve to permanent necrosis (tissue death) of the myocardium.
ST elevation represents
99
occurs because of an abrupt stoppage of blood flow through a coronary artery with a thrombus caused by platelet aggregation.
myocardial infarction (MI)
100
caused by an occlusive thrombus, results in ST-elevation in the ECG leads facing the area of infarction
STEMI
101
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.
STEMI is an emergency.
102
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
1st line treatment to STEMI
103
patients usually undergo catheterization within 12 to 72 hours. Thrombolytic therapy is not indicated for NSTEMI.
NSTEMI (can't do thrombolytic therapy)
104
(worsening myocardial contractility)
hypokinesis
105
(absent myocardial contractility)
akinesis
106
the subendocardium (the innermost layer of tissue in the heart muscle)
earliest tissue to become ischemic is
107
inferior and posterior LV walls
right coronary artery supplies blood to the
108
in patients who have a left inferior wall STEMI
right ventricular MI
109
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.
person with a long history of CAD may develop good collateral circulation to provide the area surrounding the infarction site with an
110
ersistent and unlike any other pain, it is usually described as a heavy, pressure, tight, burning, constricted, or crushing feeling.
MI symptoms
111
Common locations are the substernal or epigastric area
Locations of MI
112
pain may radiate to the neck, lower jaw, and arms or to the back
MI
113
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
ventricular remodeling.
114
Dysrhythmias are the
most common complication after an MI
115
is a complication that occurs when the right or left ventricle’s pumping action is reduced.
Heart failure (HF)
116
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.
left-sided HF
117
include JVD, hepatic congestion, or lower extremity edema. See Chapter 34 for information about the treatment of acute decompensated HF.
Signs of right-sided HF
118
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
Cardiogenic shock
119
may occur if the infarcted area includes or is near the papillary muscle that attaches to the mitral valve
Papillary muscle dysfunction
120
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.
Papillary muscle dysfunction symptom
121
results when the infarcted heart wall is thin and bulges out during contraction
- more common w/ anterior MIs
Left ventricular aneurysm
122
may develop HF, dysrhythmias, and angina.
ventricular aneurysm
123
new loud systolic murmur heard in patients with acute MI may signal
ventricular septal wall rupture.
124
, an inflammation of the visceral and/or parietal pericardium, may occur 2 or 3 days after an acute MI
Acute pericarditis
125
is pericarditis and fever that develop 1 to 8 weeks after MI
Dressler syndrome
126
are proteins released into the blood from necrotic heart muscle after an MI
Serum cardiac biomarkers
127
cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI)
Cardiac-specific troponin has 2 subtypes:
128
biomarkers are highly specific indicators of MI and have greater sensitivity and specificity for myocardial injury than creatine kinase MB (CK-MB).
Cardiac-specific troponin
129
specific to heart muscle cells and helps to quantify myocardial damage.
CK-MB band is
130
is released into the circulation within 2 hours after an MI and peaks in 3 to 15 hours
Myoglobin
131
(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.
advantages of PCI
132
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
ISR (In stent restenosis)
133
systemic anticoagulation with either subcutaneous LMWH or IV UH is
used only for UA and NSTEMI patients.
134
includes emergent PCI (preferred, for PCI-capable hospitals)
Reperfusion therapy
135
(in hospitals not capable of performing PCI).
thrombolytic therapy
136
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.
metabolic equivalent (MET)
137
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.
Isometric activities
138
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
Isotonic
139
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.
Cardiac rehabilitation
140
is a sudden, unexpected death resulting from a variety of cardiac causes
Sudden cardiac death (SCD)
141
LV hypertrophy, myocarditis, and hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy is a risk factor for SCD, especially in young, athletic people.
Structural heart disease includes
142
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.
wearable cardioverter-defibrillator
