1 . The initial, precipitating event thought to trigger formation of atherosclerotic plaque in a coronary artery is
| A) | | hypotension. |
| B) | | a genetic trait. |
| C) | | arterial stenosis. |
| D) | | injury to the artery endothelium. |
The underlying cause of ACS is a form of atherosclerosis known
as CHD. In CHD, lipids, calcium, fibrin, and other cellular substances/cellular debris are
deposited in the lining of the arteries, forming atherosclerotic plaques at sites with
low-velocity blood flow (e.g., branch points, inner curvatures) [31]. Although the exact mechanisms are not
completely understood, most researchers agree that injury to the inner (endothelial) layer of
the artery initiates a series of biochemical events that result in the formation of
atherosclerotic plaque. High levels of low-density lipoprotein (LDL) alone can cause
atherosclerosis; however, it is most often the case that lower levels of LDL combined with
other identified risk factors, including cigarette smoke, low levels of high-density
lipoprotein (HDL), hypertension, diabetes, male sex, and family history, lead to
atherosclerosis [31]. Individuals with very
low LDL typically do not develop clinically significant atherosclerotic plaques, even in the
presence of these risk factors.
2 . Stimuli for plaque erosion resulting in thrombus formation include
| A) | | sodium deficiency. |
| B) | | elevated hemoglobin. |
| C) | | high levels of HDL in the bloodstream. |
| D) | | high levels of LDL in the bloodstream and cigarette smoking. |
Formation of a thrombus occurs when the fibrous cap of an
atherosclerotic lesion erodes or ruptures, exposing the red cell-rich lipid core to
circulating blood. It is thought that the same stimuli that are responsible for the initial
injury to the vessel wall are also responsible for causing erosion or rupture of vulnerable
plaque (i.e., inflammation). Cigarette smoking and high levels of circulating LDL head the
list of injurious agents along with hypertension and diabetes [1,31,32,33,34].
3 . Irreversible cardiac tissue death occurs after myocardial cells have been ischemic for how long?
| A) | | 10 seconds |
| B) | | 1 minute |
| C) | | 20 minutes |
| D) | | 2 hours |
When a thrombus occludes a coronary artery, oxygen supply to
the area of the heart supplied by that vessel is reduced. When the supply becomes
insufficient to meet the tissue's metabolic demands, the myocardial cells become ischemic;
ischemia can develop within 10 seconds. After 1 minute of inadequate oxygen supply, the
heart's function is affected. Irreversible tissue death and damage will occur after 20
minutes of ischemia [34].
4 . The Framingham Risk Score underestimates CHD risk in which of the following populations?
| A) | | Younger individuals |
| B) | | White middle-aged men |
| C) | | White middle-aged women |
| D) | | Older Black and White individuals, particularly women |
The Framingham Heart Study identified the first risk factors,
and these factors were integrated into a risk-assessment tool, the Framingham Risk Score
[49]. The factors in the Framingham Risk
Score include age, total cholesterol level, HDL level, systolic blood pressure, treatment
for hypertension, and cigarette smoking, and the score is used to determine the 10-year risk
of so-called hard CHD (defined as MI or coronary-related death) among asymptomatic adults.
The Framingham risk score is one of several scores that involve several traditional risk
factors for assessing risk; other scores recommended include the Systematic Coronary Risk
Evaluation (SCORE), PROCAM (men) and Reynolds (separate scores for men and women) [50]. The use of one of these risk calculators
is a class IB recommendation from the American College of Cardiology Foundation and American
Heart Association [50]. It is important to
consider the populations on which these risk scores are based. For example, the Framingham
Risk Score was developed on the basis of risk factors identified in the Framingham Heart
Study, which involved a primarily White, middle-aged population. When the risk score has
been evaluated in other populations, it has been found to underestimate the risk of CHD
among older (mean age: 73.5 years) Black and White individuals, especially women [51]. ACC/AHA guidelines published in 2013
recommend that race- and sex-specific Pooled Cohort Equations be used to predict 10-year
risk of a first hard atherosclerotic cardiovascular disease event in non-Hispanic Black and
non-Hispanic White individuals (class IB) [52]. These equations were developed on the basis of data on participants from several large
racially and geographically diverse studies [52]. The guidelines also note that the sex-specific pooled cohort equations
for non-Hispanic White individuals may be considered to estimate risk for people other than
Black and non-Hispanic White individuals (class IB) [52].
5 . Evaluating which of the following nontraditional risk factors for CHD is recommended in asymptomatic adults?
| A) | | Genomic testing |
| B) | | Natriuretic peptides |
| C) | | Family history of atherothrombotic CHD |
| D) | | Brachial/peripheral flow-mediated dilation |
EVIDENCE-BASED RECOMMENDATIONS FOR USE OF NONTRADITIONAL RISK FACTORS TO EVALUATE CHD
RISK IN ASYMPTOMATIC ADULTS
| Nontraditional Risk Factor | Recommendation (Class, Level of Evidence) |
|---|
| Family history of CHD |
| Recommended for all asymptomatic women (IB) | | May be considered if risk-based treatment decision is uncertain after
quantitative risk assessment (IIbB)a |
|
| Family history of atherothrombotic CHD | Recommended for all asymptomatic adults (IB) |
| Genomic testing | Not recommended (IIIB) |
| Lipoprotein and apolipoprotein assessments | Not recommended (IIIC) |
| Natriuretic peptides | Not recommended (IIIB) |
| C-reactive protein |
| May be considered if a risk-based treatment decision is uncertain (after
quantitative risk assessment IIbB)a | | Not recommended for asymptomatic adults at high risk (IIIB) | | May be reasonable for asymptomatic men (50 years of age or younger) or
women (60 years of age or younger) who are at intermediate risk (IIbB) |
|
| Hemoglobin A1C |
| May be reasonable for risk assessment in asymptomatic adults who do not
have diabetes (IIbB) | | May be considered for asymptomatic adults with diabetes (IIbB) |
|
| Testing for microalbuminuria |
| Utility is uncertaina | | Reasonable for asymptomatic adults with hypertension or diabetes (IIaB) | | Might be reasonable for asymptomatic adults at intermediate risk who do
not have hypertension or diabetes (IIbB) |
|
| Lipoprotein-associated phospholipase A2 | Might be reasonable for asymptomatic adults at intermediate risk (IIbB)
|
| Resting electrocardiography (ECG) |
| Reasonable for asymptomatic adults with hypertension or diabetes (IIaC) | | May be considered for asymptomatic adults who do not have hypertension or
diabetes (IIbC) |
|
| Transthoracic echocardiography (to detect left ventricular hypertrophy) |
| May be considered for asymptomatic adults who have hypertension (IIbB) | | Not recommended for asymptomatic adults who do not have hypertension
(IIIC) |
|
| Measurement of carotid intima-media thickness |
| Not recommended (IIIB)a | | Reasonable for asymptomatic adults at intermediate risk
(IIaB)b |
|
| Brachial/peripheral flow-mediated dilation | Not recommended (IIIB) |
| Measurement of arterial stiffness | Not recommended outside of research settings (IIIC) |
| Measurement of ankle-brachial index |
| May be considered if a risk-based treatment decision is uncertain after
quantitative risk assessment (IIbB)a | | Reasonable for asymptomatic adults at intermediate risk (IIaB) |
|
| Exercise ECG | May be considered for asymptomatic adults at intermediate risk
(IIbB)c |
| Stress echocardiography | Not indicated for asymptomatic adults at low or intermediate risk (IIIC)
|
| Stress myocardial perfusion imaging |
| Not indicated for asymptomatic adults at low or intermediate risk (IIIC) | | May be considered for assessment of advanced cardiovascular risk in
asymptomatic adults who have diabetes or asymptomatic adults with a strong
family history of CHD or when previous risk assessment suggests high risk of CHD
(IIbC) |
|
| Coronary artery calcium scoring |
| May be considered if a risk-based treatment decision is uncertain after
quantitative risk assessment(IIbB)a | | Not recommended for persons at low risk (10-year risk <6%) (IIIB) | | Reasonable for asymptomatic adults at intermediate risk (10-year risk of
10% to 20%) (IIaB) | | Reasonable for asymptomatic adults (40 years and older) who have diabetes
(IIaB) | | May be reasonable for persons at low to intermediate risk (10-year risk of
6% to 10%) (IIbB) |
|
| Coronary computed tomography angiography | Not recommended for asymptomatic adults (IIIC) |
| Magnetic resonance imaging of plaque | Not recommended for asymptomatic adults (IIIC) |
| aRecommended in the 2014 guideline. | | bPublished recommendations on required
equipment, technical approach, and operator training and experience for
performance of the test must be carefully followed to achieve high-quality
results. | | cMay also be considered for sedentary adults
who plan to start a vigorous exercise program. |
|
6 . Updated guidelines increasingly emphasize managing lifestyle risk factors for primary prevention of CHD, including
| A) | | obesity. |
| B) | | poor diet. |
| C) | | physical inactivity. |
| D) | | All of the above |
Increased emphasis has been placed on better management of
lifestyle habits as primary prevention of CHD. Lifestyle risk factors such as obesity,
poor diet, and physical inactivity have a great influence on traditional risk factors such
as blood pressure and cholesterol levels, as well as on novel risk factors, such as
inflammation and endothelial function [78]. Lifestyle management is a key component of the new guidelines for the treatment of
cholesterol levels and hypertension, and several other guidelines have addressed issues
related to lifestyle behaviors, such as obesity, diet, and physical activity. The
ACC/AHA/TOS (The Obesity Society) developed a guideline on the management of overweight
and obesity, and some members of the Expert Panel authored a separate review on the
evidence statements related to cardiovascular risk [79,80]. The AHA/ACC also
published a guideline on lifestyle management to reduce cardiovascular risk in 2013 [81]. In its guideline of cardiac screening,
the ACP notes that strategies to improvement lifestyle behaviors should be emphasized
[65]. The USPSTF recommends counseling
to promote a healthful diet and physical activity to prevent cardiovascular disease, and
the AHA focuses on changing lifestyle behaviors in its guide for improving cardiovascular
health at the community level [82,83,84]. The decision to offer or refer adults without cardiovascular risk
factors to behavioral counseling should be individualized by the primary care provider
[85].
7 . Which of the following is a primary goal of the initial evaluation of a patient with suspected ACS?
| A) | | To begin treatment |
| B) | | To identify risk factors for ischemic stroke |
| C) | | To estimate the short-term risk of adverse outcomes |
| D) | | To determine the long-term goals and potential discharge plan |
The two primary goals of the initial evaluation in the
emergency department are to determine the likelihood that an individual has ACS and to
estimate the short-term risk of adverse outcome(s) [3]. The findings of the history, physical examination, ECG, and cardiac
troponin levels have been integrated into risk assessment scores and clinical prediction
algorithms to help identify patients at increased risk of adverse outcomes. Identifying
patients at high risk is most important, as these patients will gain the greatest absolute
benefit from appropriate therapy [2,3]. Because timely, appropriate treatment depends
on results of the clinical findings and diagnostic testing, it is essential that this
information is obtained as quickly as possible.
8 . Women with ACS are more likely than men to have
| A) | | normotension. |
| B) | | hyperlipidemia. |
| C) | | no history of diabetes. |
| D) | | a history of angina or MI. |
Research has shown that a history of traditional cardiac risk
factors varies among some subgroups. Women with ACS are more likely than men to have a
history of diabetes, hypertension, or hyperlipidemia [11,101,102,103,104,105,106]. (It has been suggested that this is due to the fact that women tend to
develop ACS at an older age) [103,106]. Women are less likely to be smokers, to
have a history of angina or MI, and to have had PCI or CABG, regardless of the cardiac
history [104,107,108]. Data on the prevalence of risk factors across racial/ethnic subgroups
with ACS was reported in 2008 (Table 6) [109].
9 . So-called "classic" chest pain associated with ACS is described as
| A) | | extreme hunger. |
| B) | | a pricking feeling. |
| C) | | sharp, stabbing pain in the chest. |
| D) | | diffuse pain or pressure in the substernal or epigastric area. |
Chest pain is the most commonly reported symptom in all
patients with ACS, regardless of age, gender, race/ethnicity, or the presence of comorbid
conditions [14,116,117]. So-called "classic" ACS-related chest pain has been described as
diffuse pain or pressure in the substernal or epigastric area that frequently radiates to
the neck, jaw, and left arm [22,101,118,119]. Chest pain
related to ACS usually begins abruptly and lasts at least 15 to 20 minutes; however, the
duration of pain varies among patients [101,120]. Pain that lasts for longer than
20 minutes is associated with increased short-term risk of MI (nonfatal or fatal) [121]. The intensity of "classic" ACS chest
pain increases over time, reaching maximal intensity after a few minutes [101,122]. Pain is usually worse with activity and improves with rest [101].
10 . Which of the following is a potentially life-threatening cause of non-ACS chest pain?
| A) | | Pleurisy |
| B) | | Panic attack |
| C) | | Aortic dissection |
| D) | | Gastroesophageal reflux |
DIFFERENTIAL DIAGNOSIS OF CHEST PAIN
| Life-Threatening Causes |
| Aortic dissection | | Pulmonary embolism | | Pneumothorax | | Expanding aortic aneurysm |
|
| Other Causes |
| Pneumonia | | Pleuritis | | Pericarditis | | Costochondritis | | Cervical disc disease | | Peptic ulcer disease | | Gastroesophageal reflux | | Biliary disease | | Pancreatitis | | Panic attack |
|
11 . Which of the following chest pain locations is considered atypical in patients with ACS?
| A) | | Substernal |
| B) | | Left-sided chest |
| C) | | Between the shoulder blades |
| D) | | None of the above |
An increasing number of studies have demonstrated that
atypical chest pain occurs more often in several subgroups of patients, especially women,
older individuals, and people with diabetes [14,102,117,126,131,132,133,134]. In addition, the
findings of several studies and literature reviews have demonstrated that women with ACS
are more likely to have pain or discomfort in the jaw, neck, throat, arm/shoulder, and
back [102,127,131]. Failure to recognize atypical symptoms of ACS has been found to delay
diagnosis and/or result in the use of less aggressive treatment. It has been estimated
that more than 40% of patients with angina have one or more "atypical" elements in their
chest pain description [135,136]. Atypical symptoms that have been found
to be associated with ACS include shortness of breath, fatigue, lethargy, indigestion,
anxiety, tingling in upper extremities, palpitations, loss of appetite, and flushing.
Words commonly used to describe "atypical" chest pain associated with ACS include
numbness, tingling, burning, stabbing, or pricking. Atypical chest pain location includes
any area other than substernal or left sided, such as the back, area between shoulder
blades, upper abdomen, shoulders, elbows, axillae, and ears [135,136].
12 . On 12-lead ECG, the presence of a pathologic Q wave in the absence of ST-segment elevation and T-wave changes indicates
| A) | | an old infarct. |
| B) | | acute STEMI. |
| C) | | acute NSTEMI. |
| D) | | congenital defects. |
The first of the three classic signs is ST-segment
elevation. It may be followed by T-wave inversion and pathologic Q-wave formation. This
sequence of changes is called the electrocardiographic evolution of an infarction. Because
these changes happen over a period of time, a series of 12-lead ECG tracings may be
required for accurate diagnosis. In the very early stages of infarct, clear patterns may
not be immediately revealed on ECG. As always, ECG findings should be correlated with
clinical signs and symptoms. Over a period of months to days, ST-segment elevation and
T-wave changes will resolve and no longer be present on 12-lead ECG recordings. Pathologic
Q waves, on the other hand, frequently remain permanently. Presence of a pathologic Q wave
on 12-lead ECG with no evidence of ST-segment elevation or T-wave changes usually
indicates that the person has had an infarct in the past [1,34,47]. It is important to note that ST-segment
and T-wave changes are not specific for ACS and may be the result of another disease or
condition. Left ventricular aneurysm, pericarditis, myocarditis, Prinzmetal angina,
Takotsubo cardiomyopathy, early repolarization, and Wolff-Parkinson-White syndrome may
cause ST-segment elevation [3]. T-wave
inversion can be caused by central nervous system events and treatment with tricyclic
antidepressants or phenothiazines.
13 . ST-segment elevation in leads II, III, and aVF indicates
| A) | | lateral wall infarction. |
| B) | | inferior wall infarction. |
| C) | | anterior wall infarction. |
| D) | | poor recording technique. |
ECG CHANGES AND DIAGNOSIS OF STEMI
| Leads Showing Changes | Location of Infarction | Location of Occlusion |
|---|
| II, III, aVF | Inferior wall | Right coronary artery |
| I, aVL, V5–6 | Lateral wall | Circumflex artery |
| V1–V4 | Anterior wall | Left anterior descending |
| Reciprocal changes only in V1–V2, sometimes V4 | Suspect posterior wall of the heart | Right coronary artery |
| ST elevation in inferior leads and lead V1 | Suspect right ventricular wall | Right coronary artery |
14 . The recommended biomarker for detecting cardiac damage is
| A) | | CK-MB. |
| B) | | creatine kinase. |
| C) | | cardiac troponin. |
| D) | | B-type natriuretic peptide (BNP). |
Cardiac biomarkers are detectable intracellular
macromolecules released into the circulation after cardiomyocyte injury and death. The
biomarkers once used—creatinine kinase (CK)-MB and myoglobin—have been replaced by
cardiac-specific troponin (troponin I or T) because of the latter's high concentration in
myocardium, near-absolute specificity for myocardial tissue, their absence in the blood of
healthy individuals, and their high clinical sensitivity [2,3,22]. Measurement of CK-MB or myoglobin levels
was not useful or cost-effective [157].
15 . The initial drug of choice for relief of acute chest pain in all patients with suspected ACS is
| A) | | oral metoprolol 25 mg. |
| B) | | sublingual nitroglycerin. |
| C) | | continuous heparin infusion. |
| D) | | sustained-release morphine tablets. |
ADJUNCTIVE TREATMENT INDICATIONS FOR PATIENTS WITH UA/NSTEMI OR STEMI
| Adjunctive Therapy | UA/NSTEMI | STEMI | Comments |
|---|
| Analgesia |
| Nitroglycerin | All patients, unless contraindicated (class IC) | No recommendation | Contraindicated for patients with hypotension or who have used
sildenafil or vardenafil within previous 24 hrs or tadalafil within previous 48 hrs
(class IIIB). |
| All patients, unless contraindicated (class IB) | No recommendation |
| Morphine | Reasonable for patients who have chest pain unrelieved by maximally tolerated
anti-ischemic medications (class IIbB) |
| Not specifically recommended. | | Narcotics should be considered if high-dose aspirin fails to relieve pain
(class IIbC) |
| — |
| Anti-Ischemia Therapy |
| Beta blocker |
| All patients, unless contraindicated (class IA) | | Continue during and after hospitalization, unless contraindicated (class
IC) | | Re-evaluate patients with initial contraindications to beta blockers for
subsequent use (class IC) |
|
| All patients, unless contraindicated (class IB) | | Continue during and after hospitalization, unless contraindicated (class
IB) | | Re-evaluate patients with initial contraindications to beta blockers for
subsequent use (class IC) |
|
| Administer in the first 24 hours. | | Contraindicated for patients with signs of heart failure, evidence of
low-output state, increased risk of cardiogenic shock, or other
contraindications to beta blockers. |
|
| ACE inhibitor | Started and continued in all patients with left ventricular ejection fraction
less than 40% and in patients with hypertension, diabetes, or stable CKD, unless
contraindicated (class IA) | All patients (within the first 24 hours) with anterior location, HF, or
ejection fraction less than or equal to 0.40, unless contraindicated (class
IA) |
| Contraindicated for patients with hypotension (systolic blood pressure of
<100 mm Hg or <30 mm Hg below baseline). | | An angiotensin receptor blocker should be used for patients intolerant of
ACE inhibitors. |
|
| Calcium-channel blocker | Patients with continued or recurrent ischemia or with contraindications to beta
blockers (class IB) | No recommendation | — |
| Antiplatelet Therapy |
| Aspirin (non-enteric coated, chewable) |
| All patients (class IA) | | Continued indefinitely |
|
| All patients (class IA) | | Continued indefinitely |
|
| Should be given as soon as possible at time of evaluation. | | Contraindicated for patients who have aspirin allergy or active
bleeding. | | Lower dose is reasonable during initial period post-stent implantation in
patients at risk of bleeding. | | Consider clopidogrel or warfarin if aspirin is contraindicated. Monitor
closely. |
|
| Clopidogrel |
| All patients (class IB) | | Administer to patients who are unable to take aspirin (class IB) | | Maintenance dose daily, continued preferably for up to 1 year (class
IB) |
|
| All patients (in addition to aspirin), before or at the time of PCI, if
not already started and who are undergoing PCI within 24 hours of receiving
fibrinolytic therapy (class IC) | | Daily dose should be continued for 1 year (class IC) |
| Loading dose not recommended for older (>75 years of age) patients with
STEMI. Should be withheld for 5 days in patients to have CABG (class IB). Monitor
closely when used in conjunction with warfarin. |
| Prasugrel |
| Not recommended for initial platelet therapy. | | All patients undergoing PCI with stenting should be given a loading dose
and at least 1 year of maintenance therapy with this or other P2Y inhibitor if
not given clopidogrel (class IB). |
|
| All patients undergoing PCI with stenting should be given a loading dose
and at least 1 year of maintenance therapy with this or other P2Y inhibitor if
not given clopidogrel (class IB). | | Should not be given sooner than 24 hours after administration of a
fibrin-specific agent or 48 hours after administration of a non-fibrin-specific
agent (class IIaB) |
|
| Should be withheld for at least 7 days in patients to have CABG (class
IB). | | Should not be administered to patients with history of stroke or transient
ischemic attack (class IIIB). |
|
| Ticagrelor | All patients undergoing PCI with stenting should be given a loading dose and at
least 1 year of maintenance therapy with this or other P2Y inhibitor if not given
clopidogrel (class IB). | All patients (in addition to aspirin) undergoing PCI with stenting should be
given a loading dose and at least 1 year of maintenance therapy with this or other
P2Y inhibitor if not given clopidogrel (class IB). |
| Should be withheld for at least 5 days in patients to have CABG (class
IB). | | May only be used with lower doses (81 mg) of aspirin. | | Requires twice daily administration. |
|
| Glycoprotein IIb/IIIa inhibitor | Patients selected for early invasive treatment, along with dual-antiplatelet
therapy, who are at intermediate or high risk (high troponin levels) (class
IIbB) |
| Reasonable for selected patients who are receiving unfractionated heparin
to have abciximab with primary PCI (class IIaA); eptifibatide or tirofiban may
also be considered with primary PCI (class IIaB) | | May be reasonable to administer in emergency department to patients
selected for primary PCI (class IIbB) |
|
| The rate of IV infusion of eptifibatide or tirofiban should be reduced by
50% for patients with estimated creatinine clearance <50 mL/min. | | Eptifibatide or tirofiban should be discontinued 2 to 4 hours before CABG
(class IB). |
|
| Anticoagulant Therapy |
| Unfractionated heparin (UFH) |
| Option for patients selected for early invasive treatment (class IB) and
early conservative treatment (class IB) | | Dose adjusted according to hospital protocol to maintain therapeutic
anticoagulation for 48 hrs or until PCI (class IB) |
| Option for patients selected for primary PCI (class IC) or fibrinolytic therapy
(class IC); administer for at least 48 hrs or until revascularization | The UFH dose should be reduced when a glycoprotein IIb/IIIa inhibitor is also
given (class IC).For patients undergoing PCI after receiving anticoagulant regimen,
administer additional boluses of UFH as needed to support procedure (class
IC). |
| Enoxaparin | Option for patients selected for early invasive treatment (class IA) and early
conservative treatment (class IA) | Option for patients selected for fibrinolytic therapy (class IA); administer
for at least 48 hours; for use up to 8 days or until revascularization |
| Discontinue enoxaparin 12 to 24 hrs before CABG (class IB). | | Reduce dose for creatinine clearance less than 30 mL/min and/or ≥75 yrs of
age. |
|
| Bivalirudin | Option for patients selected for early invasive treatment (class IB) |
| Preferred over UFH with glycoprotein IIb/IIIa inhibitor in patients
selected for PCI at high risk of bleeding (class IIaB) | | Useful supportive measure for primary PCI with/without prior treatment
with UFH (class IB) |
|
| Reduce dose for creatinine clearance less than 30 mL/min. | | Discontinue bivalirudin 3 hrs before CABG (class IB). |
|
| Fondaparinux | Option for patients selected for early invasive treatment (class IB) and early
conservative treatment (IB) | Option for patients selected for fibrinolytic therapy (class IB) |
| Should not be used as sole anticoagulant to support PCI in patients with
NSTE-ACS due to an increased risk of catheter thrombosis. | | Avoid for creatinine clearance less than 30 mL/min. | | Discontinue 24 hrs before CABG. |
|
| ACE = angiotensin-converting enzyme; CABG =
coronary artery bypass graft; CKD = chronic kidney disease; HF = heart failure; PCI
= percutaneous coronary intervention. |
16 . Beta blockers act to
| A) | | reduce pain perception. |
| B) | | dissolve the thrombus through fibrin degradation. |
| C) | | decrease cardiac work and myocardial oxygen demand. |
| D) | | increase heart rate and blood pressure in ischemic tissue. |
The inhibition of beta-1 adrenergic receptors by beta
blockers acts to decrease cardiac work and myocardial oxygen demand. Beta blockers also
slow the heart rate, which helps enhance coronary blood flow. A beta blocker should be
given orally to all ACS patients (unless contraindicated) within 24 hours of presentation
[3]. This use of beta blocker therapy
has been associated with significantly lower in-hospital mortality [174]. Contraindications include signs of
heart failure, low-output state, increased risk of cardiogenic shock, or other relative
contraindications to beta blockade.
17 . A common, often fatiguing side effect of ACE inhibitors is
| A) | | flushing. |
| B) | | constipation. |
| C) | | disseminated rash. |
| D) | | a dry, nagging cough. |
When administering ACE inhibitors, the following nursing
actions should be taken [173]:
Monitor blood pressure for hypotension. Be alert for orthostatic hypotension and
syncope.
Implement fall precautions as indicated by patient status.
Monitor serum potassium levels and renal function studies; elevated serum
potassium levels or increasing signs of renal insufficiency/failure can be an
indication that the medication should be discontinued.
Monitor for the development of intolerable side effects. A common and often
fatiguing side effect is a dry, nagging cough.
18 . According to the ACC/AHA guideline, chewable aspirin should be given
| A) | | never. |
| B) | | only to men. |
| C) | | only after definitive diagnosis of ACS. |
| D) | | to all individuals with no contraindications as soon as possible after arrival in the emergency department. |
The ACC/AHA guideline recommends that aspirin be given as
soon as possible after a patient arrives in the emergency department and continued
indefinitely in patients who tolerate it [3]. However, adherence by emergency medical personnel to guidelines recommending prompt
prehospital aspirin administration is only 45% [178]. Aspirin is contraindicated for patients who are allergic to the drug
or who have active bleeding; clopidogrel is recommended for patients who cannot tolerate
aspirin [3]. Aspirin should be
nonenteric-coated and chewable, and the recommended dose is 162–325 mg. A maintenance dose
of aspirin should be continued indefinitely, at a daily dose of 81–325 mg. Adherence to
the recommended use of aspirin has been better than for other drug therapies for patients
with UA/NSTEMI, with rates of 97% to 99% [10,140]. Rates of aspirin
use have been reported to be lower for older individuals and women, especially women
younger than 55 years of age [18,179].
19 . For patients with NSTE-ACS, enoxaparin is administered
| A) | | intravenously. |
| B) | | subcutaneously. |
| C) | | intramuscularly. |
| D) | | by continuous infusion. |
The ACC/AHA guideline recommends enoxaparin as an option
for all patients with NSTE-ACS [3]. The
recommended dose is 1 mg/kg, given subcutaneously, every 12 hours, and the drug is
continued throughout the hospitalization or until PCI is done [3]. The dose should be decreased to 1 mg/kg
daily for patients with a creatinine clearance less than 30 mL/min.
20 . The objective of an ischemia-guided strategy in the management of NSTEMI is to
| A) | | increase the volume of PCIs at participating hospitals. |
| B) | | eliminate all possible noncardiac diagnoses before proceeding. |
| C) | | avoid unnecessary treatment for persons at low risk for significant CHD. |
| D) | | provide immediate information about coronary vessels and extent of atherosclerosis. |
The objective of an ischemia-guided strategy is to avoid
unnecessary treatment (and associated costs) for patients at low risk for significant CHD.
The ACC/AHA guideline notes that an ischemia-guided strategy may be considered for
patients with NSTE-ACS who are initially stabilized and at elevated risk for clinical
events (class IIbB) [3]. It is also
reasonable to consider clinician and patient preference in decision making about an
ischemia-guided strategy (class IIbC). Patients at low or intermediate risk who have had
no ischemia at rest or with low-level activity for at least 12 to 24 hours should have
noninvasive stress testing (class IB) [3].
21 . Of the following, which medication is prescribed in variant angina to prevent coronary vasospasm?
| A) | | Diltiazem |
| B) | | Metoprolol |
| C) | | Simvastatin |
| D) | | Amiodarone |
The primary medical therapy for management of variant or
vasospastic angina involves nitrates and calcium-channel blockers. Within minutes of
administration, nitroglycerin has been found to effectively treat episodes of angina and
myocardial ischemia caused by vasospasm. Long-acting nitrates can reduce the frequency of
recurrent episodes of chest pain. Calcium-channel blockers, specifically nifedipine,
amlodipine, verapamil, and diltiazem, are prescribed to prevent coronary vasospasm and the
subsequent ischemia that can result. In this patient population, calcium-channel blockers
are preferred over beta blockers [218,219].
22 . Of the following, which class of medications may be used to manage neuropsychiatric symptoms of cocaine-induced ACS?
| A) | | Antiplatelets |
| B) | | Anticoagulants |
| C) | | Benzodiazepines |
| D) | | Glycoprotein IIb/IIIa inhibitors |
MANAGEMENT OF COCAINE-INDUCED ACS
Patients with cocaine-induced chest pain who show ECG and
biomarker evidence of ischemia or infarct should be admitted for monitoring, observation, and
further treatment as indicated. General medical therapies, similar to those used in management
of non-cocaine related ACS, should be employed. In addition, the use of IV benzodiazepines as
part of the early management of these patients may be indicated. In patients who use cocaine,
benzodiazepines help to relieve chest pain and manage neuropsychiatric manifestations.
Aspirin, calcium-channel blockers, and nitroglycerin are also recommended; beta blockers are
not recommended with acute cocaine intoxication [3,48,220].
23 . Preferred treatment for STEMI is
| A) | | CABG. |
| B) | | rescue PCI. |
| C) | | primary PCI. |
| D) | | fibrinolytic therapy. |
Reperfusion therapy is the cornerstone in the management of
STEMI, and antiplatelet and anticoagulant agents are necessary as ancillary therapy. The
options for reperfusion include revascularization procedures and/or pharmacologic
(fibrinolytic) therapy. As with the treatment for NSTEMI, the use of PCI has become the
primary approach to revascularization; approximately 80% to 90% of patients have PCI
revascularization based on angiographic findings [224]. In addition, PCI is the preferred strategy for reperfusion because of its
superior outcomes compared with fibrinolytic therapy [2,224]. However, gaining the
optimal benefit from PCI depends on many factors, and timing is the most important variable in
selecting a reperfusion therapy [2,221]. Care should also be taken to evaluate
patients for contraindications to fibrinolytic therapy [5].
24 . For PCI in STEMI, the targeted door-to-device time is within less than
| A) | | 10 minutes from onset of symptoms. |
| B) | | 30 minutes from initial diagnostic ECG. |
| C) | | 90 minutes from time of patient's arrival at the emergency department. |
| D) | | 2 hours from time of initial chest pain. |
The 2013 ACCF/AHA guideline indicates that PCI is preferred
over fibrinolytic therapy for patients with STEMI when it can be performed in a timely
manner by experienced operators [2]. PCI
should be done within less than 90 minutes after the patient's arrival at the emergency
department (door-to-device time) [2]. If PCI
cannot be done within 90 minutes, fibrinolytic therapy should be initiated as the
reperfusion strategy within 120 minutes of the first medical contact.
25 . One strategy to improve timely reperfusion therapy in STEMI is
| A) | | decreased use of fibrinolytics. |
| B) | | EMS use of pre-hospital ECGs. |
| C) | | creation of ECG banks to store data. |
| D) | | increased facility-to-facility transport of patients. |
Specific strategies that have improved the door-to-device
time interval focus on three key components: door-to-ECG time, ECG-to-catheterization
laboratory time, and laboratory arrival-to-device time. The ACCF/AHA provides the
following steps as a general protocol in improving door-to-device times [2]:
A prehospital ECG to diagnose STEMI is used to activate the PCI team while the
patient is en route to the hospital.
Emergency physicians activate the PCI team.
A single call to a central page operator activates the PCI team.
A goal is set for the PCI team to arrive in the catheterization laboratory
within 20 minutes after being paged.
Timely data feedback and analysis are provided to members of the STEMI care
team.
26 . Which of the following is an early sign of a retroperitoneal bleed following PCI?
| A) | | Pallor |
| B) | | Constipation |
| C) | | Severe flank pain |
| D) | | Reduction in elevated biomarkers |
Bleeding may occur from the arterial puncture site.
Initial indications include frank bleeding from the puncture site and/or development of a
hematoma in the area surrounding the site. A retroperitoneal bleed may also occur; an
early sign is a complaint of severe flank pain. To reduce the likelihood of bleeding, the
patient should be maintained on bed rest as specified by physician orders. The length of
time bed rest is indicated depends on the method used to close the arterial puncture site.
The arterial puncture site, often the femoral artery, should be monitored frequently for
signs of bleeding or hematoma formation [34,233].
27 . An allergy or intolerance to infusing glycoprotein IIb/IIIa inhibitors may cause
| A) | | stent occlusion. |
| B) | | increased clotting. |
| C) | | elevated hemoglobin. |
| D) | | a significant drop in platelet count. |
A significant drop in platelet count may be caused by an
allergy or intolerance to infusing glycoprotein IIb/IIIa inhibitors. With a drop in
platelet count, the patient's risk of bleeding increases. Patients receiving glycoprotein
IIb/IIIa inhibitors should have a complete blood count checked at designated intervals to
make sure that platelet counts are not dropping. Parameters should include orders to
notify the physician if the platelet count drops below a specified level. If a patient
develops a significant drop in platelet count, the infusion of the glycoprotein IIb/IIIa
inhibitor is discontinued and the patient is placed on bleeding precautions and observed
carefully for any signs of bleeding [34,233].
28 . Fibrinolytic therapy should be given to patients with STEMI who have no contraindications and onset of ischemic symptoms within the previous 12 hours when it is anticipated that primary PCI cannot be performed within of how many minutes of first medical contact?
| A) | | 30 minutes |
| B) | | 60 minutes |
| C) | | 120 minutes |
| D) | | 180 minutes |
Although the focus of treatment for patients presenting with
STEMI is often given to PCI, fibrinolytic therapy is the treatment of choice for some
patients. If a patient arrives at or is transported by EMS to a non-PCI-capable facility,
the decision whether to immediately transfer to a PCI-capable facility or administer
fibrinolytic therapy must be made. Factors that affect this decision include the time from
onset of symptoms, the risk of complications related to STEMI, the risk of bleeding with
fibrinolysis, the presence of shock or severe heart failure, and the time required for
transfer to a PCI-capable hospital. The ACCF/AHA guideline recommends that, in the absence
of contraindications, fibrinolytic therapy should be given to patients with STEMI and onset
of ischemic symptoms within the previous 12 hours when it is anticipated that primary PCI
cannot be performed within 120 minutes of first medical contact [2].
29 . Which of the following is an absolute contraindication to fibrinolytic therapy?
| A) | | Pregnancy |
| B) | | Severe hypotension |
| C) | | History of peptic ulcer |
| D) | | Prior intracranial hemorrhage |
CONTRAINDICATIONS AND CAUTIONS FOR FIBRINOLYSIS USE IN ST-ELEVATION MYOCARDIAL
INFARCTION (STEMI)a
| Absolute Contraindications |
| Any prior intracranial hemorrhage | | Known structural cerebral vascular lesion (e.g., arteriovenous
malformation) | | Known malignant intracranial neoplasm (primary or metastatic) | | Ischemic stroke within three months EXCEPT acute ischemic stroke within
4.5 hours | | Suspected aortic dissection | | Active bleeding or bleeding diathesis (excluding menses) | | Significant closed-head or facial trauma within three months | | Intracranial or intraspinal surgery within two months | | Severe uncontrolled hypertension (unresponsive to emergency
therapy) | | For streptokinase, prior treatment within the previous six
months |
|
| Relative Contraindications |
| History of chronic, severe, poorly controlled hypertension | | Substantial hypertension on presentation (systolic greater than 180 mm
Hg or diastolic greater than 110 mm Hg) | | History of prior ischemic stroke (greater than three months) | | Dementia | | Known intracranial pathology not covered in absolute
contraindications | | Traumatic or prolonged (greater than 10 minutes) CPR | | Major surgery (within less than three weeks) | | Recent (within two to four weeks) internal bleeding | | Noncompressible vascular punctures | | Pregnancy | | Active peptic ulcer | | Oral anticoagulant therapy |
|
| aViewed as advisory for clinical decision
making and may not be all-inclusive or definitive. | | INR = international normalization ratio; CPR = cardiopulmonary
resuscitation. |
|
30 . Nursing assessment after fibrinolytic therapy should include
| A) | | continuous ECG monitoring. |
| B) | | frequent vital sign monitoring. |
| C) | | assessment for recurrence of chest pain. |
| D) | | All of the above |
Immediately following reperfusion with fibrinolytics, the
patient is at risk to develop serious bleeding episodes or to reocclude the
infarct-related vessel [34,227]. Nursing assessment during this period
is crucial and should include [34]:
Continuous ECG monitoring for rate, rhythm, or reoccurrence of signs of acute
ischemia, development of life-threatening arrhythmias
Assessment for reoccurrence of chest pain or other symptoms associated with an
acute ischemic episode
Frequent vital sign monitoring for hypotension, drop in oxygen saturation, or
other signs indicative of developing heart failure
Assessment for any changes in level of consciousness
Assessment for indications of bleeding
31 . The drug of choice to manage pain associated with STEMI is
| A) | | aspirin. |
| B) | | ticlopidine. |
| C) | | an NSAID. |
| D) | | IV morphine sulfate. |
The drug of choice to manage the pain associated with
STEMI is intravenous morphine sulfate [2].
Morphine is indicated to relieve ongoing ischemic discomfort, control hypertension,
ameliorate anxiety, or manage pulmonary edema. The initial dose should be 4–8 mg, with
lower doses in the elderly. Additional doses of 2–8 mg may be given at intervals of 5 to
15 minutes [2].
32 . Of the following medications, which is strongly recommended for patients recovering from STEMI and an acute anterior infarction or pulmonary congestion?
| A) | | Amiodarone |
| B) | | ACE inhibitor |
| C) | | Benzodiazepine |
| D) | | COX-2 inhibitor |
The use of an oral ACE inhibitor is a strong
recommendation for all patients recovering from STEMI, including those with anterior
infarction, pulmonary congestion, or LVEF of less than 0.40, as well as those with normal
LVEF in whom cardiovascular risk factors are well controlled [2]. Adherence to this recommendation has
increased since the late 1990s but remains low [190,261,262,263]. In addition, the doses used in clinical practice have been lower than
the target doses used in clinical trials [263].
33 . Which of the following statements regarding calcium-channel blockers is TRUE?
| A) | | Verapamil should be used for patients with heart failure. |
| B) | | Nifedipine should be incorporated into the treatment of STEMI. |
| C) | | Diltiazem should be used for patients with left ventricular dysfunction. |
| D) | | Early treatment with dihydropyridine calcium antagonists has not been found to improve rates of mortality or reinfarction. |
Early treatment with dihydropyridine calcium antagonists
(nifedipine and nicardipine) has not been found to improve rates of mortality or
reinfarction [2]. Nifedipine is
contraindicated in the treatment of STEMI. Although verapamil and diltiazem may be useful
to relieve ongoing or recurrent ischemia, lower blood pressure, or control the ventricular
response rate to atrial fibrillation when beta blockers are contraindicated (and the
patient has well-preserved left ventricular function and no clinical evidence of
congestive heart failure or pulmonary congestion), no specific recommendation for their
use exists in the 2013 STEMI guideline [2,3]. Both drugs have been associated
with significantly reduced mortality and major cardiovascular events [267,268]. Verapamil should not be used for patients with heart failure or
bradyarrhythmias, and diltiazem should not be used for patients with left ventricular
dysfunction [2].
34 . Healthcare providers can help to improve adherence to smoking cessation by
| A) | | recommending the use of smokeless tobacco. |
| B) | | allowing support groups and peer counselors to take sole responsibility. |
| C) | | engaging in repeated contacts during the hospital stay and beyond three months. |
| D) | | All of the above |
DISCHARGE PLANNING AND SECONDARY PREVENTION
Quitting smoking has been described as "probably the most
important thing a smoker with acute MI can do to improve future health" [272]. Mortality after an ACS event for a
patient who smokes cigarettes is twice that for a patient who does not, but cessation of
smoking reduces reinfarction and death rates at one year [2]. Clinicians should use the in-hospital period after MI and each office
visit as an opportunity to ask patients who were smokers if they have quit or are ready to
quit and should offer counseling, pharmacologic support, and information on formal quit
programs. The in-hospital period is unique because many patients are motivated to quit and
are typically unable to smoke for three to nine days. Randomized controlled trials have
shown that repeated contacts during the hospital stay and at and beyond three months
(typically by telephone) are more likely to result in smoking cessation [2]. A Cochrane review showed that only
intensive counseling programs work and that nicotine replacement further increases the
rates of successful cessation among patients in intensive programs [273]. Another Cochrane review found
high-quality evidence for a benefit of combined pharmacotherapy (with any type of
nicotine-replacement therapy, bupropion, nortriptyline, or varenicline) and behavioral
treatment compared with usual care, brief advice, or less intensive behavioral support
[274]. However, many clinicians are
reluctant to add another drug to the multitude of medications prescribed after MI.
35 . What is the goal body mass index for patients after ACS?
| A) | | Less than 18.5 |
| B) | | 18.5–24.9 |
| C) | | 22.5–29 |
| D) | | 25–30 |
DISCHARGE PLANNING AND SECONDARY PREVENTION
Obesity is another well-documented risk factor for CHD,
and weight management programs and information on healthy eating/caloric intake should be
promoted as appropriate [271]. The
patient's body mass index and waist circumference should be measured at each visit. The
goal is to attain a body mass index of 18.5–24.9 and a waist circumference of no greater
than 35 inches (women) or 40 inches (men) [271]. When weight reduction is needed, the initial goal is weight loss of
5% to 10% from baseline [271].
36 . Following hospitalization for ACS, what is the recommended antiplatelet therapy after discharge?
| A) | | Lovastatin |
| B) | | Metoprolol |
| C) | | Enoxaparin |
| D) | | Low-dose aspirin and a P2Y12 inhibitor |
DISCHARGE PLANNING AND SECONDARY PREVENTION
The recommended antiplatelet therapy after discharge is a
combination of aspirin and a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor) [2,146,271]. The findings of
studies have suggested that lower doses of aspirin (≤100 mg daily) are as effective as
higher doses but have a better safety profile [180,245,248,276]. The recommended daily dose of aspirin is 75–100 mg for all patients,
and the ACC/AHA guidelines for the management of STEMI and NSTE-ACS and duration of dual
antiplatelet therapy state that it is reasonable to use an 81-mg dose [2,3,146,245,248]. However, despite the better safety profile of low-dose aspirin, data
have indicated that 325 mg is the most common dose, prescribed for 55.7% of patients with
UA/NSTEMI [277].
37 . What is the recommended antithrombotic agent for patients with UA/NSTEMI or STEMI?
| A) | | Warfarin |
| B) | | Diltiazem |
| C) | | Abciximab |
| D) | | Beta blockers and ACE inhibitors |
DISCHARGE PLANNING AND SECONDARY PREVENTION
Questions about clopidogrel maintenance therapy remain, as
the optimal dose and duration of therapy have not been identified [146,183,278,279]. Another concern is the effect of
stopping clopidogrel. In a 2008 study of 3,137 patients with ACS (treated either medically
or with PCI) who took clopidogrel for a mean of 9 to 10 months, there was a significantly
high risk of adverse events in the initial 90 days after stopping treatment with
clopidogrel [280]. The reason for this
phenomenon is unclear, and the authors suggested that strategies to reduce the incidence
of such early events should be identified [280]. Additionally, the response to clopidogrel varies among patients, and
diminished responsiveness has been observed [146]. A 2010 retrospective study of 2,017 patients with ACS, conducted to
confirm the findings of the 2008 study, found that the 0- to 90-day interval after
stopping clopidogrel was associated with higher risk of death/MI compared with the 91- to
360-day interval. There was a similar trend of increased adverse events 0 to 90 days after
stopping clopidogrel for various subgroups (i.e., women versus men, medical therapy versus
PCI, stent type, and ≥6 months or <6 months of clopidogrel treatment) [281]. Warfarin is recommended as an
antithrombotic for patients with UA/NSTEMI or STEMI who are allergic to aspirin [146,271].
38 . The target level for LDL-C with statin therapy in average-risk patients is
| A) | | less than 100 mg/dL. |
| B) | | 200–225 mg/dL. |
| C) | | 250–300 mg/dL. |
| D) | | greater than 400 mg/dL. |
DISCHARGE PLANNING AND SECONDARY PREVENTION
The goal of statin therapy is to achieve an LDL level less
than 100 mg/dL for patients with average risk, and an LDL level of less than 70 mg/dL is
reasonable for high-risk patients [2]. If
the triglyceride level is 200 mg/dL or higher, the non-HDL cholesterol should be less than
130 mg/dL in patients with average risk, whereas a non-HDL cholesterol level of less than
100 mg/dL is reasonable for very-high-risk patients. Statin therapy should be supplemented
with dietary modification, weight management, and exercise. Patients should be encouraged
to follow a diet with an increase of fresh fruits and vegetables, with less than 7% of
total calories as saturated fat, less than 1% of total calories as trans fatty acids, and
less than 200 mg per day of cholesterol [2,271].
39 . Treatment for hypertension is recommended when greater than
| A) | | 120–129/80 mm Hg. |
| B) | | 130/80 mm Hg. |
| C) | | 140/90 mm Hg. |
| D) | | 150/90 mm Hg. |
DISCHARGE PLANNING AND SECONDARY PREVENTION
In addition, blood pressure should be controlled according
to the 2017 Guideline for High Blood Pressure in Adults, which recommends treatment when
blood pressure is elevated, defined as 120–129/<80 mm Hg [67]. The guideline recommends initial
treatment with nonpharmacologic interventions and lifestyle changes. Initiation of
pharmacologic treatment is recommended for secondary prevention in patients with clinical
cardiovascular disease and an average systolic blood pressure of 130 mm Hg or greater or
an average diastolic blood pressure of 80 mm Hg or greater and for primary prevention in
adults with an estimated 10-year atherosclerotic cardiovascular disease risk of 10% or
higher and an average systolic blood pressure of 130 mm Hg or greater or an average
diastolic blood pressure of 80 mm Hg or greater [67]. The AHA/ACCF recommends initial treatment with a beta blocker and/or
an ACE inhibitor as secondary prevention for patients with CHD [271].
40 . Which of the following issues negatively impacts patients' adherence to medication therapy?
| A) | | Higher education level |
| B) | | High number of medications |
| C) | | Having transportation to a pharmacy |
| D) | | Lower number of prescribed medications |
DISCHARGE PLANNING AND SECONDARY PREVENTION
Lack of patient compliance with medications is also a
serious problem and has been referred to as an unrecognized risk factor for CHD, because
of its association with significant increases in adverse events and health costs [306,307]. Among individuals with CHD (many of whom had experienced a recent ACS
event), compliance with guideline-recommended medications has ranged from 18% to 55%.
Approximately 54% of individuals have been compliant with all of their initial
medications, and compliance decreases over time [307,308,309]. One study showed that compliance was
60.3% at one year, 53.7% at two years, and 48.8% at five years [310]. Individuals who discontinue medications
are more likely to be older, female, unmarried, and less educated [309]. Several other factors have been found
to be associated with noncompliance with medications [307,308,309]:
Choice of medication
Tolerability
Duration of treatment
Dosing frequency
Higher number of prescribed medications
Lack of symptoms as indication for the medication
Uncertainty about how to take the medication
Lack of transportation to the pharmacy
