CH 37: Acute Coronary Syndrome Flashcards

Question

A patient with an anterior wall STEMI is at risk for which complication? a. Right ventricular failure b. Cardiogenic shock c. Atrial fibrillation d. Pulmonary embolism

Answer 1

b. Cardiogenic shock Rationale: Anterior wall MIs, often caused by LAD occlusion, can lead to extensive LV damage and cardiogenic shock.

Answer 2

c. “I will have a heart catheterization within the next day or two.” Rationale: NSTEMI requires risk stratification and is typically managed with cardiac catheterization within 12-72 hours rather than emergency PCI.

Answer 3

a. Bradycardia c. Right ventricular infarction e. Papillary muscle dysfunction Rationale: Inferior MIs often involve the RCA, which supplies the SA and AV nodes, leading to bradycardia. They are also associated with right ventricular infarctions and papillary muscle dysfunction, which can cause mitral regurgitation.

Answer 4

c. New S3 heart sound and hypotension Rationale: An S3 heart sound and hypotension suggest heart failure or cardiogenic shock, which are life-threatening complications of an MI.

Answer 5

c. Return of ST segment to baseline Rationale: The resolution of ST-segment elevation suggests successful reperfusion of the occluded coronary artery.

Answer 6

d. “Is the pain relieved by rest or nitroglycerin?” Rationale: This helps differentiate stable angina (relieved by rest or nitroglycerin) from unstable angina or MI, which is not relieved by these measures.

Answer 7

b. Bleeding Rationale: Thrombolytic therapy carries a high risk of bleeding, including intracranial hemorrhage and GI bleeding.

Answer 8

b. Absence of myocardial contractility Rationale: Akinesis refers to absent myocardial contractility in the infarcted area, indicating irreversible myocardial damage.

Answer 9

a. Administer aspirin and nitroglycerin Rationale: ST-segment depression suggests ischemia, which requires antiplatelet therapy (aspirin) and vasodilation (nitroglycerin) to improve blood flow.

Answer 10

b. T-wave inversion Rationale: T-wave inversion is a sign of myocardial ischemia, while ST-elevation and Q waves indicate infarction.

Answer 11

b. “This test will determine if I need a stent or bypass surgery.” Rationale: Cardiac catheterization helps assess coronary artery blockage and determine treatment options, such as PCI or CABG.

Answer 12

b. Older individuals develop collateral circulation Rationale: Over time, individuals with CAD may develop collateral circulation, which can lessen the severity of an MI.

Answer 13

a. Assess for aspirin allergy Rationale: Aspirin is given before PCI to prevent platelet aggregation, so the nurse must assess for allergies.

Answer 14

c. Left ventricular heart failure Rationale: Anterior wall MIs affect the LV, increasing the risk of heart failure due to impaired myocardial contractility.

Answer 15

c. Diaphoresis and a feeling of impending doom Rationale: Diaphoresis and a sense of impending doom are common symptoms of acute MI and indicate a need for immediate intervention.

Answer 16

c. “I don’t need to take my medications if I feel fine.” Rationale: Medications for CAD must be taken consistently to prevent another MI, even if the patient feels well.

Answer 17

d. Patient reports back pain and hypotension Rationale: Back pain and hypotension after PCI may indicate retroperitoneal bleeding, a medical emergency requiring immediate intervention.

Answer 18

d. Obtain a 12-lead ECG Rationale: The priority in suspected MI is obtaining an ECG to identify ST-segment changes that indicate ischemia or infarction. Early diagnosis guides immediate intervention.

Answer 19

b. A silent myocardial infarction Rationale: Patients with diabetes often experience silent MIs due to cardiac neuropathy, leading to atypical symptoms such as fatigue and dyspnea instead of chest pain.

Answer 20

b. Obtain a 12-lead ECG Rationale: Epigastric discomfort unrelieved by antacids may indicate an MI. Patients, especially older adults, may misinterpret cardiac pain as indigestion, delaying treatment.

Answer 21

d. ST-segment elevation on ECG Rationale: ST-segment elevation indicates an acute MI, which is a medical emergency. Older adults may present with confusion, dizziness, or dyspnea instead of chest pain.

Answer 22

c. Obtain vital signs and a 12-lead ECG Rationale: Women may experience atypical MI symptoms, such as extreme fatigue and dyspnea, rather than classic chest pain. An ECG is necessary to rule out an MI.

Answer 23

a. “There are natural changes in hormone levels that increase clot formation risk in the morning.” Rationale: MIs often occur in the early morning due to increased catecholamine release, which raises blood pressure and heart rate, promoting plaque rupture and clot formation.

Answer 24

d. Recognize these symptoms as indicative of sympathetic nervous system stimulation Rationale: Sympathetic nervous system stimulation due to MI leads to diaphoresis, tachycardia, and vasoconstriction, as evidenced by the patient’s symptoms. Recognizing these signs helps prioritize immediate care and monitoring for MI.

Answer 25

b. Release of catecholamines by ischemic heart cells Rationale: The ischemic heart cells release catecholamines (norepinephrine and epinephrine), which lead to tachycardia, elevated blood pressure, and vasoconstriction, as seen in the patient.

Answer 26

a. Administering pain relief and oxygen therapy Rationale: The priority in managing a patient with acute MI and sympathetic nervous system stimulation is addressing the ischemia (pain relief) and ensuring adequate oxygen supply to the heart muscle.

Answer 27

b. Left ventricular dysfunction Rationale: Crackles in the lungs and JVD are common signs of left ventricular dysfunction. When the left ventricle fails to pump effectively, it leads to pulmonary congestion (crackles) and systemic congestion (JVD). These findings suggest that the left side of the heart is not effectively pumping blood.

Answer 28

a. Right ventricular dysfunction Rationale: Right ventricular dysfunction is associated with systemic congestion, which leads to peripheral edema, JVD, and hepatic engorgement. The nurse should consider this as a possible cause when these signs are present in the patient.

Answer 29

a. Decreased cardiac output (CO) Rationale: Low blood pressure and decreased urine output are signs of decreased cardiac output. In the setting of myocardial infarction, decreased CO can result from impaired heart function, leading to inadequate renal perfusion and reduced urine output.

Answer 30

b. Ventricular septal defect or papillary muscle rupture Rationale: A loud holosystolic murmur following a myocardial infarction may indicate a ventricular septal defect or papillary muscle rupture. These complications can result in mitral regurgitation, where blood leaks back into the left atrium due to improper valve closure.

Answer 31

c. Left ventricular dysfunction Rationale: The presence of an S3 and S4 heart sound is suggestive of left ventricular dysfunction. These abnormal sounds indicate changes in ventricular filling pressures, commonly seen in heart failure or myocardial infarction, where the left ventricle is not functioning efficiently.

Answer 32

b. Increase intravenous fluids to improve renal perfusion Rationale: In the context of myocardial infarction and hypotension, oliguria is often a sign of decreased renal perfusion. The priority is to restore blood flow and improve renal perfusion by increasing IV fluids, which can help prevent acute renal failure.

Answer 33

c. Vasovagal reflexes initiated by the infarcted heart muscle Rationale: Nausea and vomiting in patients with inferior wall MIs are often caused by vasovagal reflexes, which are triggered by the infarcted heart muscle. This reflex affects the gastrointestinal system and can lead to nausea and vomiting.

Answer 34

d. Vasovagal response due to heart muscle ischemia Rationale: Nausea and vomiting can be a result of vasovagal reflexes, especially in patients with inferior wall MIs. The reflex is triggered by ischemia in the heart muscle and can lead to gastrointestinal symptoms, including nausea.

Answer 35

b. Reflex stimulation of the vomiting center Rationale: Severe nausea and vomiting can be caused by reflex stimulation of the vomiting center in the brain, particularly during an acute MI, due to the intense pain and stress associated with the event.

Answer 36

b. Reflex response mediated by the vomiting center Rationale: Nausea and vomiting in this patient are most likely due to a reflex response triggered by the infarcted heart muscle, particularly in inferior wall MIs. This reflex involves the vomiting center in the brain and leads to gastrointestinal symptoms.

Answer 37

b. Systemic inflammatory response due to myocardial cell death Rationale: A fever following a myocardial infarction is commonly caused by a systemic inflammatory response that results from the death of myocardial cells. This can increase the body’s temperature, often peaking within 24 to 48 hours post-MI.

Answer 38

b. Inflammatory response to myocardial cell death Rationale: Fever in the setting of an MI is commonly due to the systemic inflammatory response caused by the death of myocardial cells. This type of fever typically appears within 24 to 48 hours and can last for several days.

Answer 39

b. A normal systemic inflammatory response to myocardial cell death Rationale: A fever occurring within the first 24 to 48 hours after an MI is typically a result of the body’s systemic inflammatory response to the death of myocardial cells. This type of fever is common and usually resolves within 4 to 5 days.

Answer 40

a. Neutrophils and macrophages are removing necrotic tissue Rationale: Within 4 days after an MI, neutrophils and macrophages infiltrate the infarcted tissue to remove necrotic debris. This process weakens the muscle wall, which is why T-wave inversion is observed on the ECG.

Answer 41

a. Lipolysis and glycogenolysis mediated by catecholamines Rationale: After an MI, catecholamines initiate lipolysis and glycogenolysis, which increase plasma glucose levels. The elevated glucose is used by the oxygen-deprived myocardium for anaerobic metabolism.

Answer 42

c. Weak and vulnerable to increased stress Rationale: At 10 to 14 days post-MI, the scar tissue is still weak, and the heart muscle is susceptible to increased stress. The patient’s activity level may increase, so careful monitoring is essential to avoid complications.

Answer 43

c. Healed with scar tissue replacing necrotic muscle Rationale: By 6 weeks post-MI, scar tissue replaces the necrotic muscle tissue, and the infarcted area is considered healed. However, the scarred area may be less compliant than the surrounding tissue, which can lead to abnormal wall motion and complications such as dysrhythmias.

Answer 44

c. Abnormal wall motion due to scar tissue formation Rationale: Scar tissue that forms in the infarcted area may result in abnormal wall motion, such as hypokinesis or akinesis, leading to reduced myocardial contractility and possible heart failure.

Answer 45

b. To prevent ventricular remodeling and heart failure Rationale: ACE inhibitors are used after an MI to prevent ventricular remodeling, which can lead to heart failure. Ventricular remodeling is a process where normal myocardium hypertrophies and dilates to compensate for damaged tissue, but this can ultimately worsen heart function.

Answer 46

b. Scar tissue that is less compliant and may lead to abnormal wall motion Rationale: By 3 months post-MI, the infarcted area will have scar tissue, which is less compliant than the surrounding myocardial tissue. This can result in abnormal wall motion, which may be identified through echocardiography or nuclear imaging.

Answer 47

d. Increased risk of sudden cardiac death and heart failure Rationale: Ventricular remodeling can lead to increased risk of heart failure and sudden cardiac death (SCD). As normal myocardium hypertrophies and dilates to compensate for infarcted tissue, it can cause abnormalities in cardiac function, such as dysrhythmias and decreased contractility.

Answer 48

b. ACE inhibitors Rationale: ACE inhibitors are used to limit ventricular remodeling after an MI by reducing the stress on the heart, which can help prevent the development of heart failure. They block the effects of angiotensin II, which is involved in the process of remodeling.

Answer 49

c. “Scar tissue takes 6 weeks to fully form, but it will not restore normal myocardial function.” Rationale: Scar tissue replaces necrotic tissue after an MI, but it is less compliant than the normal myocardium and does not restore the infarcted area to its previous functional capacity. This is why the area is more vulnerable to complications like dysrhythmias or heart failure.

Answer 50

c. Compensatory hypertrophy and dilation of the myocardium Rationale: Ventricular remodeling involves the hypertrophy and dilation of the normal myocardium to compensate for infarcted tissue. This process can eventually lead to heart failure, especially if multiple coronary arteries are affected.

Answer 51

d. There is reduced myocardial contractility in the infarcted region Rationale: Hypokinesis refers to reduced movement or contractility of the myocardium in the infarcted area. This is a common finding after MI due to the formation of scar tissue, which does not contract as effectively as healthy muscle tissue.

Answer 52

a. After reperfusion therapy or percutaneous coronary intervention (PCI) Rationale: PVCs are commonly seen after reperfusion therapy (thrombolytic therapy or PCI) and are generally not associated with an increased risk for sudden cardiac death (SCD), unless the patient is symptomatic.

Answer 53

b. Ischemia affecting the heart cells’ sensitivity to nerve impulses Rationale: Ventricular fibrillation (VF) most commonly occurs within the first 4 hours after the onset of MI due to ischemia affecting the heart’s electrical system. Ischemia leads to changes in the heart cells’ sensitivity to nerve impulses, increasing the risk for dysrhythmias.

Answer 54

b. Nonsustained ventricular tachycardia (VT) Rationale: After reperfusion (either with thrombolytic therapy or percutaneous coronary intervention), nonsustained VT, PVCs, and idioventricular rhythms are common. These are usually not treated unless the patient is symptomatic.

Answer 55

d. Inserting an external pacemaker or a temporary transvenous pacemaker Rationale: Complete heart block can occur when areas of the conduction system, such as the sinus or atrioventricular node, are destroyed during an MI. Symptomatic bradycardia caused by complete heart block may require an external pacemaker or a temporary transvenous pacemaker.

Answer 56

b. Starting defibrillation for sustained VT Rationale: VT is a potentially life-threatening dysrhythmia that can lead to sudden cardiac death. If the VT is sustained, immediate defibrillation is necessary to restore a normal rhythm.

Answer 57

c. Reassure the patient, as PVCs are common in the early post-MI period Rationale: PVCs are common in the early post-MI period, especially with reperfusion therapy or PCI, and are generally not dangerous unless the patient is symptomatic. Reassurance and monitoring are appropriate unless the patient becomes symptomatic.

Answer 58

b. Performing immediate defibrillation Rationale: Ventricular fibrillation (VF) is a life-threatening dysrhythmia that requires immediate defibrillation to restore a normal rhythm and prevent death. Thrombolytic therapy and PCI are not interventions for VF.

Answer 59

d. Ventricular tachycardia (VT) Rationale: Ventricular tachycardia (VT) is most likely to occur within the first 4 hours of an MI due to ischemia and electrolyte imbalances. This period is critical for monitoring and intervention to prevent sudden cardiac death.

Answer 60

c. Crackles on auscultation of the lungs Rationale: Crackles on auscultation of the lungs are indicative of pulmonary congestion, a hallmark sign of left-sided heart failure. Left-sided heart failure causes fluid to back up into the lungs, leading to crackles. JVD, abdominal distention, and hepatic congestion are more indicative of right-sided heart failure.

Answer 61

b. Paroxysmal nocturnal dyspnea (PND) Rationale: Paroxysmal nocturnal dyspnea (PND) is characterized by sudden difficulty breathing when lying flat, a common symptom of left-sided heart failure due to fluid accumulation in the lungs. Orthopnea, on the other hand, is difficulty breathing when lying down, but it is more gradual than PND. Pulmonary embolism and pneumothorax would have different presenting symptoms.

Answer 62

c. Lower extremity edema Rationale: Right-sided heart failure leads to fluid retention in the body, which commonly results in lower extremity edema, along with other signs such as abdominal distention and jugular venous distention (JVD). Pulmonary congestion and orthopnea are associated with left-sided heart failure. An S3 heart sound may also indicate left-sided heart failure.

Answer 63

b. Early left-sided heart failure Rationale: Restlessness, agitation, and tachycardia are early, subtle signs of left-sided heart failure as the body begins to compensate for reduced cardiac output. As heart failure progresses, symptoms become more severe, such as dyspnea, pulmonary congestion, and fluid retention.

Answer 64

c. Elevate the head of the bed to facilitate breathing Rationale: Elevating the head of the bed helps relieve the symptoms of paroxysmal nocturnal dyspnea (PND) by reducing the venous return to the heart and easing the patient’s breathing. Lying flat would worsen the symptoms, and administering a sedative or diuretic does not directly address the acute issue of fluid accumulation in the lungs.

Answer 65

c. Left-sided heart failure with pulmonary congestion Rationale: Crackles on auscultation and an S3 heart sound are classic signs of left-sided heart failure, which leads to pulmonary congestion as fluid backs up into the lungs. These findings indicate that the left side of the heart is not pumping effectively, resulting in fluid accumulation in the lungs.

Answer 66

b. Initiate mechanical circulatory support with an intraaortic balloon pump (IABP) Rationale: In cardiogenic shock, mechanical circulatory support, such as an intraaortic balloon pump (IABP), is used to improve myocardial perfusion and reduce the workload on the heart. Diuretics and antibiotics are not indicated in the acute management of cardiogenic shock, and while PCI may be performed, it is not the most immediate intervention in this acute setting.

Answer 67

a. Maximize oxygen delivery to tissues Rationale: The primary goal in managing cardiogenic shock is to maximize oxygen delivery to tissues, as oxygen supply is inadequate due to severe left ventricular failure. This may involve oxygen therapy, optimizing cardiac output, and using vasoactive medications. Reducing anxiety, promoting ambulation, or limiting fluid intake are not immediate priorities in the acute management of cardiogenic shock.

Answer 68

a. Decrease the rate of the dobutamine infusion Rationale: Dobutamine is a vasoactive drug used to support contractility in cardiogenic shock, but it can cause arrhythmias as a side effect. The first action should be to decrease the rate of the infusion to mitigate the potential for worsening arrhythmias. Discontinuing the drug or increasing the dose may worsen the situation. Administering an antidote is not necessary for dobutamine.

Answer 69

a. Intraaortic balloon pump (IABP) Rationale: An intraaortic balloon pump (IABP) is used in patients with cardiogenic shock to improve myocardial perfusion and reduce the workload of the heart by inflating and deflating in sync with the cardiac cycle. An endotracheal tube and chest tube are not used for circulatory support, and while PCI may be performed to treat STEMI, it does not serve the same purpose as mechanical circulatory devices like the IABP.

Answer 70

a. Acute kidney injury (AKI) Rationale: In cardiogenic shock, the priority complication to monitor for is acute kidney injury (AKI) due to inadequate renal perfusion. The kidneys are highly sensitive to changes in blood flow and oxygen delivery, and AKI can further compromise the patient’s condition. Pneumonia, DVT, and gastrointestinal bleeding may occur but are not as immediately critical as AKI in the context of cardiogenic shock.

Answer 71

c. Echocardiogram Rationale: An echocardiogram is the most definitive diagnostic tool for confirming papillary muscle dysfunction, as it can visualize mitral valve movement and regurgitation. While an ECG can identify arrhythmias and chest X-ray may show signs of pulmonary edema, they do not confirm papillary muscle dysfunction. Cardiac catheterization is not typically used to diagnose this condition.

Answer 72

b. Afterload reduction with nitroprusside (Nipride) and/or intra-aortic balloon pump (IABP) therapy Rationale: In papillary muscle rupture, afterload reduction with nitroprusside and/or IABP therapy helps manage acute mitral regurgitation by reducing the workload on the heart and improving cardiac output. Anticoagulation therapy, beta-blockers, and corticosteroids are not primary treatments for this life-threatening complication.

Answer 73

c. Pulmonary edema Rationale: Pulmonary edema is a primary symptom of acute mitral regurgitation caused by papillary muscle rupture. Blood backs up into the left atrium and lungs, leading to fluid accumulation. Bradycardia, diaphoresis, and chest pain are not specific signs of this condition.

Answer 74

b. Obtain an echocardiogram to confirm papillary muscle dysfunction Rationale: A new systolic murmur at the heart apex suggests mitral regurgitation, which could be caused by papillary muscle dysfunction. An echocardiogram is required to confirm the diagnosis before further treatment decisions, including surgery or medication, are made.

Answer 75

b. Mitral valve repair or replacement Rationale: In the case of papillary muscle rupture, the patient will require urgent mitral valve repair or replacement to address the acute mitral regurgitation and prevent further deterioration. CABG, LVAD implantation, and aortic valve replacement are not appropriate for this specific condition.

Answer 76

a. Monitor for signs of infection at the surgical site Rationale: After mitral valve surgery, infection at the surgical site is a major concern. While fluid management and monitoring for arrhythmias are important, infection control is paramount in the early postoperative period. Stroke risk may be higher in some patients, but monitoring for infection is the priority.

Answer 77

b. Decrease afterload to improve cardiac efficiency Rationale: Nitroprusside (Nipride) is a vasodilator used to decrease afterload in patients with acute mitral regurgitation due to papillary muscle rupture. By reducing afterload, it improves cardiac efficiency and helps the heart pump more effectively, thus improving cardiac output. It does not directly affect heart rate, platelet aggregation, or ischemia.

Answer 78

d. Angina and dysrhythmias Rationale: A left ventricular aneurysm can lead to complications such as heart failure, dysrhythmias, and angina due to the abnormal contraction and increased strain on the heart. It does not directly cause renal failure, hemorrhagic stroke, or pulmonary embolism.

Answer 79

b. To reduce the risk of embolic stroke due to thrombus formation Rationale: Anticoagulation therapy is recommended for patients with left ventricular aneurysms to prevent thrombus formation, which can increase the risk of embolic stroke. While anticoagulation may help in reducing the risk of some complications, it is not specifically used to prevent ventricular rupture, control blood pressure, or manage dysrhythmias.

Answer 80

a. Sudden cardiac death Rationale: Ventricular rupture is a life-threatening complication of a left ventricular aneurysm and usually leads to sudden cardiac death due to the rapid loss of heart function. It does not lead to immediate relief from angina or renal failure. Severe hypotension and shock are possible outcomes but are typically part of the progression to sudden cardiac death.

Answer 81

a. S3 heart sound and crackles on lung auscultation Rationale: An S3 heart sound and crackles on lung auscultation are classic signs of heart failure. The S3 indicates volume overload in the left ventricle, while crackles suggest pulmonary congestion. While the other symptoms may also occur in various conditions, they are not as specifically indicative of heart failure in this case.

Answer 82

c. Thinning and bulging of the infarcted heart wall during contraction Rationale: A left ventricular aneurysm occurs when the infarcted heart wall thins and bulges out during contraction. This weakening and expansion of the heart muscle can lead to the formation of the aneurysm. Inflammation of the pericardium, clot formation, and scar tissue formation are not the primary causes of left ventricular aneurysms.

Answer 83

b. Ventricular septal wall rupture Rationale: A new loud systolic murmur in a patient with acute MI is most likely a sign of a ventricular septal wall rupture. This condition involves a defect in the septum between the right and left ventricles, causing a murmur due to the abnormal blood flow. Papillary muscle rupture and mitral valve prolapse do not typically cause this type of murmur. A pericardial friction rub is more commonly associated with pericarditis.

Answer 84

b. Immediate emergency repair, either surgically or percutaneously Rationale: Ventricular septal wall rupture requires immediate repair, either surgically or percutaneously, to prevent rapid hemodynamic compromise and further deterioration. Thrombolytics are not indicated in this scenario, as the issue is a mechanical defect in the heart wall, not a clot. Long-term anticoagulation therapy is not the primary treatment for this complication. Monitoring vital signs without intervention would not address the immediate danger.

Answer 85

c. Rapid hemodynamic compromise and death Rationale: Left ventricular free wall rupture is a life-threatening emergency that causes rapid hemodynamic compromise and death if not treated immediately. This rupture leads to massive blood loss into the pericardial space, resulting in a tamponade effect and shock. It is not reversible without surgical intervention, and death rates are high if the condition is not addressed promptly.

Answer 86

b. Left ventricular free wall rupture Rationale: Left ventricular free wall rupture is more common in patients who are older, especially after their first MI and in females. This complication occurs due to the structural vulnerability of the heart wall following an infarction, particularly in those with anterior MIs. Right ventricular hypertrophy and pulmonary embolism are less directly related to this condition. Aortic dissection is a separate cardiovascular issue unrelated to MI.

Answer 87

c. Rapid hemodynamic instability and shock Rationale: Left ventricular free wall rupture causes rapid hemodynamic compromise, leading to shock and collapse. This is a life-threatening condition that must be addressed immediately. A new loud systolic murmur is more indicative of a ventricular septal wall rupture. Severe chest pain and diaphoresis may occur with any MI, but they are not specific to a free wall rupture. Decreased JVP is not a typical finding in this scenario.

Answer 88

c. Left ventricular aneurysm Rationale: Patients with anterior MIs are at higher risk for developing left ventricular aneurysms due to the thinning and weakening of the infarcted area. This complication can result in heart failure, dysrhythmias, and angina. Right ventricular hypertrophy and papillary muscle dysfunction are possible but less common. Aortic stenosis is unrelated to MI complications.

Answer 89

c. Immediate surgical or percutaneous repair of the defect Rationale: Ventricular septal wall rupture requires immediate intervention with either surgical or percutaneous repair to prevent rapid hemodynamic compromise and further deterioration. Beta-blockers and diuretics are not appropriate in this emergency situation, as they do not address the underlying mechanical defect. Observation without intervention would lead to worsening shock and potential death.

Answer 90

b. Sitting forward Rationale: Sitting in a forward position often relieves the chest pain associated with acute pericarditis. This position helps reduce pressure on the inflamed pericardium, thereby easing the pain. Lying flat or on the left side typically exacerbates the discomfort.

Answer 91

a. Cardiac tamponade or significant pericardial effusion Rationale: Hypotension and a narrow pulse pressure are common signs of cardiac tamponade, which occurs when pericardial effusion compresses the heart, restricting its ability to pump effectively. This can be a complication of acute pericarditis. Left ventricular failure and pulmonary embolism would present with different clinical findings.

Answer 92

c. Diffuse ST segment elevation in many unrelated leads Rationale: Acute pericarditis is characterized by diffuse ST segment elevation across multiple leads that are unrelated to the infarcted wall. This differs from ST elevation in STEMI, where the elevation is localized to the leads facing the infarcted area. Q waves and inverted T waves suggest previous infarction, not pericarditis.

Answer 93

a. NSAIDs and corticosteroids interfere with myocardial scar formation Rationale: NSAIDs and corticosteroids should be avoided in the first 4 weeks after an MI because they can interfere with the healing process of the myocardial scar, which is essential for the heart’s recovery after an infarction. They do not significantly affect bleeding, blood pressure, or anticoagulation therapy in this context.

Answer 94

d. High-dose aspirin Rationale: High-dose aspirin is the treatment of choice for acute pericarditis to relieve pain and reduce inflammation. Corticosteroids and NSAIDs are avoided in the first 4 weeks post-MI due to their potential interference with scar formation. Antibiotics are not indicated unless there is evidence of infection, and beta-blockers do not directly address the inflammation.

Answer 95

d. Perform a 12-lead ECG Rationale: A 12-lead ECG is essential for diagnosing pericarditis. It shows diffuse ST segment elevation across multiple leads, a key sign of pericardial inflammation. Blood pressure, jugular venous distention, and oxygen saturation are important in other contexts but are not diagnostic for pericarditis.

Answer 96

b. A friction rub Rationale: A friction rub is characteristic of acute pericarditis and is caused by the inflamed pericardium rubbing against the heart. It can be heard best with the diaphragm of the stethoscope at the left sternal border. An S3 or S4 heart sound would indicate heart failure or volume overload, not pericarditis. A systolic murmur is more commonly associated with valve defects.

Answer 97

c. Hypotension and narrow pulse pressure Rationale: Hypotension and narrow pulse pressure may indicate the presence of pericardial effusion or cardiac tamponade, complications that can arise from pericarditis. Monitoring for these signs is critical in managing the patient’s condition. Jugular venous distention and peripheral edema are more commonly associated with heart failure, and hyperactive bowel sounds are unrelated to pericarditis.

Answer 98

b. Autoimmune reaction to necrotic heart muscle Rationale: Dressler syndrome is believed to be an autoimmune response to the necrotic heart tissue following an MI. It presents with symptoms of pericarditis, including chest pain, fever, and a friction rub. It is not caused by infection, pulmonary embolism, or heart failure.

Answer 99

b. Inflammation Rationale: The elevated white blood cell count and sedimentation rate are indicative of inflammation, which is a hallmark of Dressler syndrome, an autoimmune condition that results in pericarditis and fever. These lab findings are not typically associated with infection, renal failure, or hemorrhage in this context.

Answer 100

a. High-dose aspirin Rationale: High-dose aspirin is the treatment of choice for Dressler syndrome to manage inflammation and pain. Corticosteroids are avoided due to potential interference with myocardial healing, and antibiotics are not appropriate unless there is a secondary infection. Anticoagulation therapy is not indicated for Dressler syndrome.

Answer 101

b. Performing a pericardiocentesis Rationale: If a pericardial effusion is present and causing significant hemodynamic compromise, pericardiocentesis may be necessary to remove the fluid. The primary treatment for Dressler syndrome is high-dose aspirin, but pericardiocentesis is indicated if the effusion is large or symptomatic. Anticoagulation and corticosteroids are not appropriate for this situation.

Answer 102

c. Arthralgia Rationale: Arthralgia (joint pain) is a common symptom of Dressler syndrome and is often seen alongside chest pain, fever, and malaise. This syndrome can involve multiple organ systems due to the inflammatory response, but jaundice, shortness of breath, and syncope are not typical findings of Dressler syndrome.

Answer 103

b. 12-lead ECG Rationale: The 12-lead ECG is an essential diagnostic tool in determining whether a patient is experiencing unstable angina (UA) or a myocardial infarction (MI), including STEMI or NSTEMI. It provides critical information about the electrical activity of the heart, which helps in diagnosing these conditions. A chest X-ray, pulmonary function test, and abdominal ultrasound are not primary diagnostic studies for UA or MI.

Answer 104

a. Serum cardiac biomarkers Rationale: Serum cardiac biomarkers, such as troponins, are critical for diagnosing myocardial infarction (MI) when used alongside a 12-lead ECG. These biomarkers indicate heart muscle damage. While a CBC and BNP can be useful in other settings, they are not primary studies for diagnosing MI. Chest X-rays are typically used to evaluate lung conditions but do not directly assess myocardial infarction.

Answer 105

c. ST segment elevation in the leads facing the infarcted wall Rationale: ST segment elevation in the leads facing the infarcted wall is characteristic of STEMI. It indicates a complete coronary occlusion. This is the key finding for STEMI, whereas other findings like ST depression and T wave inversion are more commonly seen in NSTEMI or unstable angina.

Answer 106

d. NSTEMI patients will have ST depression and/or T wave inversion Rationale: NSTEMI patients typically show ST depression and/or T wave inversion in the leads facing the area of ischemia or infarction. Unlike STEMI, NSTEMI does not involve complete coronary occlusion, and thus does not show ST elevation or pathologic Q waves.

Answer 107

b. Both NSTEMI and UA show ST depression, but NSTEMI has elevated cardiac biomarkers Rationale: The key distinction between NSTEMI and unstable angina is that NSTEMI involves elevated cardiac biomarkers due to tissue damage, while UA does not. Both conditions can present with ST depression, but the biomarkers differentiate the two.

Answer 108

c. ST segment elevation in the leads facing the infarcted wall Rationale: ST segment elevation in the leads facing the infarcted wall is indicative of a complete coronary occlusion, which is typical in STEMI. This finding is key for identifying STEMI and differentiating it from NSTEMI or UA.

Answer 109

c. Pathologic Q waves Rationale: Pathologic Q waves develop in the leads facing the infarcted wall when reperfusion is delayed or not performed in STEMI. These waves typically remain on the ECG forever, marking the area of infarction.

Answer 110

b. When ST elevation is seen in the leads facing the infarcted wall Rationale: ST elevation in the leads facing the infarcted wall is the most definitive ECG finding for diagnosing STEMI. It indicates a complete coronary occlusion, which is a hallmark of STEMI.

Answer 111

b. They suggest acute myocardial infarction and remain permanently after an infarct Rationale: Pathologic Q waves suggest an acute myocardial infarction (MI) and will remain permanently on the ECG. They indicate a large, irreversible infarction in the heart muscle.

Answer 112

d. Cardiac biomarkers Rationale: The presence of elevated cardiac biomarkers in NSTEMI is the key differentiator from UA, which has normal biomarkers. While both conditions can have similar ECG changes, cardiac biomarkers are essential in distinguishing between NSTEMI and UA.

Answer 113

d. Several months Rationale: T wave inversion can persist for several months after a STEMI, especially if reperfusion has been delayed or not performed. These changes indicate ongoing myocardial injury and recovery.

Answer 114

c. T wave inversion and/or ST depression Rationale: Unstable angina often presents with transient ECG changes, including T wave inversion and/or ST depression. However, the patient does not have elevated biomarkers as seen in NSTEMI, which differentiates UA from NSTEMI.

Answer 115

b. To track the evolution of ischemia, injury, infarction, and resolution of the infarction Rationale: Serial 12-lead ECGs are used to monitor the progression of ACS, including the evolution of ischemia, injury, infarction, and resolution of the infarction. This helps guide treatment decisions and assess the effectiveness of interventions.

Answer 116

c. Resolution of ST elevation Rationale: The resolution of ST elevation is an indicator that reperfusion therapy has been successful. ST elevation is seen in STEMI due to complete coronary occlusion, and its resolution signals that the blockage has been cleared.

Answer 117

a. By identifying the location of ST elevation and pathologic Q waves Rationale: The location of ST elevation and pathologic Q waves on the ECG provides information about which coronary artery is involved in the ACS. These changes occur in specific leads that correspond to the distribution of blood flow from the affected artery.

Answer 118

c. To distinguish between UA and NSTEMI Rationale: Serum cardiac biomarkers, particularly troponins, are used to differentiate between unstable angina (UA) and NSTEMI. UA typically has negative biomarkers, while NSTEMI has elevated biomarkers due to myocardial injury.

Answer 119

b. It allows for faster detection of myocardial injury Rationale: High-sensitivity cardiac troponin (hs-cTn) testing enables more rapid detection of myocardial injury compared to conventional troponin assays, providing quicker diagnosis and intervention.

Answer 120

b. 2 to 3 hours after the first test Rationale: A second hs-cTn is typically drawn 2 to 3 hours after the first one if STEMI is ruled out, helping to confirm the diagnosis of myocardial injury or identify other potential causes.

Answer 121

d. Cardiac-specific troponins (cTnI and cTnT) Rationale: Cardiac-specific troponins, including cTnI and cTnT, are the most specific biomarkers for diagnosing myocardial injury, as they are released exclusively from heart muscle cells.

Answer 122

c. 7 to 14 days Rationale: Cardiac-specific troponins, including cTnI and cTnT, typically remain elevated for 7 to 14 days after an MI, making them useful for diagnosing MI even after the initial injury.

Answer 123

b. It is not specific to myocardial injury Rationale: CK-MB is less specific than cardiac-specific troponins because it is also found in other tissues, such as skeletal muscle. As a result, CK-MB is not as reliable for diagnosing myocardial injury compared to troponins.

Answer 124

b. 24 to 36 hours Rationale: CK levels typically rise about 6 hours after an MI, peak at around 18 hours, and return to normal within 24 to 36 hours, making it a useful early marker for myocardial injury but less reliable for long-term diagnosis.

Answer 125

a. To monitor the resolution of infarction Rationale: Serial cardiac-specific troponin measurements are used to monitor the resolution of infarction. These tests help track the peak levels and return to baseline, which indicates the progression or resolution of myocardial injury.

Answer 126

d. CK-MB levels begin to rise 6 hours after an MI Rationale: CK-MB levels begin to rise around 6 hours after an MI, peak at 18 hours, and return to baseline within 24 to 36 hours. While it is a useful early marker, it is less specific than cardiac-specific troponins.

Answer 127

c. Within 90 minutes Rationale: The standard guideline for STEMI management is to perform cardiac catheterization within 90 minutes of arrival at the emergency department to restore blood flow and limit infarct size.

Answer 128

b. Thrombolytic therapy within 30 minutes Rationale: If a hospital lacks PCI capability, guidelines recommend administering thrombolytic therapy within 30 minutes of arrival to dissolve the clot and restore perfusion.

Answer 129

c. Within 12 to 72 hours of presentation Rationale: Patients with NSTEMI or UA do not require emergent catheterization but are recommended to undergo the procedure within 12 to 72 hours to assess the severity of coronary artery disease and determine appropriate intervention.

Answer 130

d. To open the totally occluded artery and limit infarct size Rationale: In STEMI patients, cardiac catheterization aims to rapidly open the occluded coronary artery and minimize myocardial infarction damage.

Answer 131

a. The findings from the catheterization and patient factors Rationale: The choice between PCI, CABG, or medical management depends on the severity of coronary artery disease observed during catheterization and individual patient factors such as comorbidities and surgical risk.

Answer 132

a. Because they are usually hemodynamically stable and do not have complete coronary occlusion Rationale: Unlike STEMI, which involves total coronary occlusion, UA and NSTEMI are typically caused by partial or transient thrombosis. This allows time for cardiac catheterization within 12 to 72 hours rather than requiring emergent intervention.

Answer 133

b. Preserve heart muscle and quickly diagnose and treat ACS Rationale: Rapid diagnosis and treatment are crucial in ACS to minimize myocardial damage and improve patient outcomes.

Answer 134

d. Upright, unless contraindicated Rationale: Positioning the patient upright improves oxygenation and reduces cardiac workload.

Answer 135

c. IV b. Chewable aspirin (162-325 mg) Rationale: Aspirin is given as soon as possible to inhibit platelet aggregation and reduce infarct size.

Answer 136

b. To relieve chest pain by dilating coronary arteries Rationale: NTG improves blood flow to the ischemic myocardium by dilating coronary arteries.

Answer 137

c. Cardiac biomarkers, complete blood count, and coagulation studies Rationale: Cardiac biomarkers confirm myocardial injury, and coagulation studies guide anticoagulation therapy.

Answer 138

a. Only if pain is unrelieved by nitroglycerin Rationale: Morphine is a second-line agent for pain relief when nitroglycerin fails to alleviate symptoms.

Answer 139

c. Send the patient for immediate cardiac catheterization Rationale: In STEMI, immediate PCI is the preferred intervention to restore coronary perfusion.

Answer 140

b. Initiate thrombolytic therapy within 30 minutes Rationale: If PCI is unavailable, thrombolytic therapy is started within 30 minutes to dissolve the thrombus.

Answer 141

a. Treat according to agency protocols Rationale: Dysrhythmias are common in ACS and must be managed based on their type and severity following hospital protocols.

Answer 142

a. Prevent platelet aggregation in patients undergoing PCI Rationale: GP IIb/IIIa inhibitors, such as eptifibatide, are potent antiplatelet agents used in PCI to reduce thrombotic complications.

Answer 143

b. Within 12 to 72 hours Rationale: NSTEMI patients require catheterization within 12 to 72 hours to evaluate the extent of coronary artery disease and determine treatment.

Answer 144

a. To stabilize plaque and reduce future cardiovascular events Rationale: High-dose statins are given to ACS patients to reduce LDL cholesterol and stabilize atherosclerotic plaques, lowering the risk of recurrent events.

Answer 145

b. Open the blocked artery within 90 minutes of arrival Rationale: Emergent PCI aims to rapidly restore blood flow to the infarcted area, limiting myocardial damage and improving patient outcomes.

Answer 146

c. PCI provides faster reperfusion and requires less recovery time Rationale: PCI is preferred over CABG for STEMI due to its ability to rapidly restore perfusion with shorter hospital stays and recovery times.

Answer 147

a. Measurement of ejection fraction Rationale: During catheterization, left ventricular (LV) function is assessed to determine the impact of the infarction and overall cardiac performance.

Answer 148

a. To release medication that prevents restenosis Rationale: DES release antiproliferative drugs that reduce the risk of re-narrowing (restenosis) of the stented artery.

Answer 149

a. Only if the patient is hemodynamically stable Rationale: If the patient is stable, PCI may be performed on additional blockages. Otherwise, elective PCI is scheduled later.

Answer 150

b. Dual antiplatelet therapy (DAPT) for 1 year, then aspirin for life Rationale: DAPT (aspirin plus a P2Y12 inhibitor like ticagrelor or prasugrel) reduces stent thrombosis risk. Aspirin is continued lifelong.

Answer 151

d. Patients with severe left ventricular dysfunction Rationale: Patients with significant LV dysfunction may need VAD therapy for circulatory support to prevent heart failure progression.

Answer 152

b. Coronary artery dissection or rupture Rationale: Coronary artery dissection, rupture, or stent failure may require immediate surgical intervention via CABG.

Answer 153

d. Dislodgement of atherosclerotic plaque, causing distal embolization Rationale: Plaque disruption during PCI may occlude distal vessels, worsening infarction.

Answer 154

b. 3 to 4 days Rationale: Patients undergoing PCI for an uncomplicated MI typically stay in the hospital for 3 to 4 days, which is shorter than CABG patients.

Answer 155

b. PCI has a lower risk of intracranial hemorrhage Rationale: PCI is preferred over thrombolytics due to its reduced risk of major bleeding, including intracranial hemorrhage.

Answer 156

a. To minimize contrast-induced nephropathy and hemodynamic instability Rationale: Performing multiple PCIs at once increases contrast exposure and procedural risks. Elective PCI allows for safer staged treatment.

Answer 157

c. A patient with STEMI in a hospital without PCI capability, arriving 20 minutes ago Rationale: Thrombolytic therapy is only indicated for STEMI patients when PCI is unavailable or cannot be performed within 120 minutes. The goal is to administer the thrombolytic within 30 minutes of arrival.

Answer 158

c. Dissolve the thrombus and restore coronary artery perfusion Rationale: Thrombolytic therapy works by breaking down the fibrin in the clot, restoring blood flow to the myocardium and limiting infarct size.

Answer 159

b. Within 30 minutes of arrival Rationale: The guideline-recommended goal is to administer thrombolytics within 30 minutes of ED arrival to optimize myocardial salvage.

Answer 160

d. Transfer the patient for PCI without thrombolytics Rationale: If PCI can be performed within 120 minutes of first medical contact, direct transfer is preferred over thrombolytic therapy because PCI is more effective in restoring coronary perfusion and reducing complications.

Answer 161

c. Recent ischemic stroke within the past month Rationale: A recent ischemic stroke is a contraindication due to the high risk of intracranial hemorrhage with thrombolytic therapy.

Answer 162

a. PCI restores coronary perfusion more effectively with a lower risk of bleeding Rationale: PCI is more effective than thrombolytics in reestablishing blood flow and has a lower risk of major bleeding, particularly intracranial hemorrhage.

Answer 163

b. A patient with STEMI, chest pain for 10 hours, and no contraindications Rationale: Thrombolytic therapy is indicated for STEMI patients who present within 12 hours of symptom onset and have no absolute contraindications.

Answer 164

c. Lysing the fibrin mesh of the thrombus Rationale: Thrombolytic agents break down fibrin in the thrombus, restoring blood flow to the occluded coronary artery.

Answer 165

b. A sudden decrease in level of consciousness Rationale: A sudden change in neurological status may indicate intracranial hemorrhage, a severe complication of thrombolytic therapy.

Answer 166

a. Evaluate the patient for possible PCI Rationale: Thrombolytics are most effective within 12 hours of symptom onset. If chest pain has lasted 12-24 hours, PCI is preferred when available.

Answer 167

d. Active internal bleeding Rationale: Active internal bleeding is an absolute contraindication due to the risk of life-threatening hemorrhage.

Answer 168

c. Thrombolytics can be considered for some patients with symptom onset 12-24 hours ago Rationale: While thrombolytics are most effective within 12 hours, some patients with persistent ischemic symptoms and ECG changes may still benefit within 12-24 hours.

Answer 169

c. Perform all invasive procedures before giving the thrombolytic Rationale: Performing invasive procedures before administration reduces the risk of significant bleeding once the thrombolytic agent is given.

Answer 170

b. Return of ST segment to baseline on ECG Rationale: The most reliable sign of reperfusion is normalization of the ST segment, indicating restoration of blood flow.

Answer 171

a. Reassess the ECG for ST-segment changes Rationale: Recurring chest pain and ST-segment elevation may indicate reocclusion, requiring reassessment and possible PCI.

Answer 172

c. Discontinue the thrombolytic infusion immediately Rationale: Neurological changes may indicate cerebral hemorrhage, a life-threatening complication of thrombolytic therapy.

Answer 173

d. Development of minor surface bleeding at IV sites Rationale: Minor bleeding, such as at IV sites or the gums, is common and can often be managed with pressure or ice packs.

Answer 174

a. To prevent reocclusion of the coronary artery Rationale: Heparin helps maintain vessel patency and prevents new clot formation after thrombolysis.

Answer 175

d. A sudden drop in hemoglobin and hematocrit Rationale: A drop in hemoglobin and hematocrit suggests significant internal bleeding, a serious complication of thrombolytic therapy.

Answer 176

c. Accelerated idioventricular rhythm Rationale: Accelerated idioventricular rhythm is a common reperfusion dysrhythmia that is usually self-limiting and does not require aggressive intervention.

Answer 177

b. To perform a coronary angiogram and possible stent placement Rationale: Patients receiving thrombolytics should be transferred to a PCI-capable facility to undergo angiography and possible PCI if needed.

Answer 178

d. Hemorrhage Rationale: Persistent hypotension and tachycardia suggest significant blood loss, which is a major complication of thrombolytic therapy.

Answer 179

d. A 50-year-old with a history of ischemic stroke 1 month ago Rationale: A recent ischemic stroke is an absolute contraindication for thrombolytic therapy due to the high risk of intracranial hemorrhage.

Answer 180

c. Chewable aspirin Rationale: Chewable aspirin should be given immediately to inhibit platelet aggregation and reduce myocardial damage.

Answer 181

b. GP IIb/IIIa inhibitors Rationale: GP IIb/IIIa inhibitors prevent platelet aggregation and are often used during PCI in STEMI patients.

Answer 182

b. Subcutaneous LMWH or IV unfractionated heparin (UH) Rationale: Systemic anticoagulation with LMWH or UH is recommended for NSTEMI patients managed without immediate PCI.

Answer 183

d. 1 year Rationale: DAPT should be continued for at least 1 year after STEMI or NSTEMI, regardless of stent placement.

Answer 184

d. β-blockers Rationale: β-blockers lower blood pressure and should not be given to patients with severe hypotension.

Answer 185

b. Calcium channel blockers Rationale: Calcium channel blockers are used when β-blockers are contraindicated, though they must be used cautiously due to their effects on contractility.

Answer 186

c. Lower LDL cholesterol and stabilize plaque Rationale: High-dose atorvastatin lowers LDL and stabilizes atherosclerotic plaques, reducing the risk of further cardiac events.

Answer 187

b. A patient with chronic kidney disease and hyperkalemia Rationale: ACE inhibitors can increase potassium levels and worsen kidney function, making them contraindicated in patients with hyperkalemia.

Answer 188

b. Nitrates should be avoided in patients taking phosphodiesterase inhibitors (e.g., sildenafil) Rationale: The combination of nitrates and phosphodiesterase inhibitors can cause severe hypotension.

Answer 189

d. “Avoid grapefruit juice while taking this medication.” Rationale: Grapefruit juice can interfere with ticagrelor metabolism, increasing the risk of bleeding.

Answer 190

b. Decrease preload and afterload while increasing myocardial oxygen supply Rationale: IV nitroglycerin reduces preload and afterload, decreasing myocardial workload while increasing oxygen delivery to the heart.

Answer 191

c. Administer an IV fluid bolus Rationale: Hypotension is a common side effect of IV nitroglycerin, and volume depletion may contribute to it. A fluid bolus helps restore intravascular volume.

Answer 192

a. Titrate the IV nitroglycerin to relieve chest pain Rationale: IV nitroglycerin should be titrated based on pain relief while monitoring blood pressure closely.

Answer 193

b. Development of crackles in the lungs Rationale: Crackles indicate possible volume overload, which can occur if the patient received a fluid bolus for hypotension. Immediate assessment and intervention are needed.

Answer 194

a. “My chest pain is getting worse.” Rationale: Worsening chest pain may indicate treatment failure or ongoing ischemia, requiring further evaluation.

Answer 195

d. “IV nitroglycerin is primarily used to lower blood pressure in ACS patients.” Rationale: The primary goal of IV nitroglycerin in ACS is to relieve chest pain and improve coronary blood flow, not just to lower BP.

Answer 196

a. Administer a fluid bolus Rationale: Hypotension is a known side effect of IV nitroglycerin, and a fluid bolus can help restore blood pressure if volume depletion is present.

Answer 197

c. A patient with new-onset crackles in the lungs Rationale: Crackles suggest fluid overload, which requires immediate intervention to prevent worsening heart failure or pulmonary edema.

Answer 198

b. To lower myocardial oxygen consumption and relieve pain Rationale: Morphine is a vasodilator that decreases myocardial oxygen demand by reducing cardiac workload, contractility, blood pressure, and heart rate, thereby relieving chest pain.

Answer 199

d. Respiratory rate of 8 breaths per minute Rationale: Morphine can cause respiratory depression. A respiratory rate below 10 breaths per minute requires immediate intervention, such as stopping the medication and administering naloxone if needed.

Answer 200

c. It reduces anxiety and sympathetic stimulation Rationale: Morphine helps relieve anxiety and reduces sympathetic nervous system activation, which decreases myocardial oxygen demand and workload.

Answer 201

b. Blood pressure is 88/54 mmHg Rationale: Morphine is a vasodilator that can further lower blood pressure. If the patient is already hypotensive, administering morphine could worsen perfusion and cause hemodynamic instability.

Answer 202

c. “Morphine is the first-line drug for pain relief in all ACS patients.” Rationale: Nitroglycerin is the first-line medication for chest pain in ACS. Morphine is used only when chest pain persists despite nitroglycerin.

Answer 203

b. Administer naloxone as prescribed Rationale: Naloxone is an opioid antagonist that reverses the effects of morphine-induced respiratory depression. If the patient’s respiratory status declines further, naloxone should be administered immediately.

Answer 204

a. Heart rate of 48 bpm Rationale: β-blockers reduce heart rate, blood pressure, and myocardial oxygen demand. A heart rate below 50 bpm may indicate excessive β-blockade, increasing the risk of bradycardia and hemodynamic instability.

Answer 205

c. “I should stop taking this medication if I feel dizzy.” Rationale: β-blockers should not be stopped abruptly, as this can cause rebound tachycardia and increase the risk of reinfarction. Instead, the patient should report dizziness to the provider for dose adjustment.

Answer 206

b. To prevent ventricular remodeling and reduce mortality Rationale: β-blockers reduce myocardial oxygen demand, prevent reinfarction, and decrease ventricular remodeling, which lowers the risk of heart failure and improves long-term survival after an MI.

Answer 207

b. Blood pressure of 88/56 mmHg Rationale: ACE inhibitors lower blood pressure, and initiating therapy in a hypotensive patient can worsen hemodynamic instability. Hypotension is a contraindication for starting an ACE inhibitor.

Answer 208

c. “If I develop a dry cough, I should stop taking this medication immediately.” Rationale: A dry cough is a common side effect of ACE inhibitors, but the patient should not stop the medication abruptly without consulting a provider. The provider may switch the patient to an ARB if the cough is bothersome.

Answer 209

c. The patient experienced angioedema with an ACE inhibitor Rationale: ARBs are used as an alternative to ACE inhibitors for patients who develop angioedema, a potentially life-threatening side effect of ACE inhibitors.

Answer 210

d. Serum potassium level of 5.8 mEq/L Rationale: ACE inhibitors can cause hyperkalemia by decreasing aldosterone secretion. A potassium level of 5.8 mEq/L is above the normal range and increases the risk of cardiac arrhythmias.

Answer 211

c. “ACE inhibitors reduce the workload on your heart and prevent heart failure.” Rationale: ACE inhibitors prevent ventricular remodeling and slow the progression of heart failure by reducing afterload and preload, which helps preserve cardiac function long-term.

Answer 212

a. Monitor the patient’s blood pressure Rationale: Hypotension is a potential adverse effect of ACE inhibitors, especially with the first dose. The nurse should assess BP before administration to ensure it is within a safe range.

Answer 213

a. “Avoid potassium-containing salt substitutes.” Rationale: ACE inhibitors can cause hyperkalemia, and potassium-containing salt substitutes may further increase potassium levels, leading to dangerous arrhythmias.

Answer 214

b. Monitor the patient’s rhythm continuously and assess for changes in symptoms. Rationale: Since most dysrhythmias after MI are self-limiting and not life-threatening, the appropriate intervention is to monitor the patient closely for any changes in symptoms and rhythm, rather than aggressively treating it with antidysrhythmic medications or other interventions.

Answer 215

c. Notify the healthcare provider and prepare for possible defibrillation. Rationale: Sustained VT is a life-threatening dysrhythmia that may require defibrillation if it does not respond to medical management. The nurse should prioritize notifying the healthcare provider and preparing for possible defibrillation to manage the rhythm effectively.

Answer 216

c. Maximizing the dose of the current lipid-lowering medication or switching to a more potent statin. Rationale: For patients with ACS or coronary artery disease (CAD), the primary goal is to initiate or optimize lipid-lowering therapy to reduce cardiovascular risks. Maximizing the dose of the current medication or switching to a more potent statin is essential in these cases.

Answer 217

b. The presence of renal failure or liver dysfunction. Rationale: When prescribing lipid-lowering drugs, especially statins, the nurse should consider any contraindications such as renal failure or liver dysfunction. These conditions can affect the metabolism of statins and increase the risk of adverse effects.

Answer 218

a. The patient experiences muscle pain or weakness. Rationale: Lipid-lowering drugs, particularly statins, are generally taken indefinitely in patients with ACS or coronary artery disease (CAD) to reduce the risk of future cardiac events. However, treatment may need to be adjusted or discontinued if the patient experiences muscle pain or weakness, which can be a sign of a rare but serious side effect (myopathy).

Answer 219

d. Serum potassium levels Rationale: Aldosterone antagonists, such as spironolactone or eplerenone, can increase potassium levels. Therefore, it is crucial to assess serum potassium levels before administering the medication to avoid the risk of hyperkalemia.

Answer 220

a. Hyperkalemia Rationale: Aldosterone antagonists are contraindicated in patients with hyperkalemia as they can further increase potassium levels, which can be dangerous and lead to cardiac arrhythmias.

Answer 221

b. Decrease the risk of heart failure progression Rationale: Aldosterone antagonists like spironolactone and eplerenone are used after a STEMI to reduce mortality and decrease the risk of heart failure progression, regardless of the left ventricular (LV) function. They work by blocking the effects of aldosterone, which can worsen heart failure.

Answer 222

b. To prevent straining and vagal stimulation that can lead to dysrhythmias Rationale: Stool softeners are used to prevent constipation and avoid straining, which can trigger vagal stimulation and result in bradycardia or dysrhythmias, especially after an MI.

Answer 223

c. “Stool softeners help to avoid the potential complications of straining, such as bradycardia.” Rationale: The purpose of stool softeners after an MI is to prevent straining during bowel movements, which can stimulate the vagus nerve, leading to bradycardia and potential dysrhythmias.

Answer 224

b. Prevent straining during bowel movements, which could lead to arrhythmias Rationale: Docusate sodium is a stool softener used to prevent straining during bowel movements, which can trigger vagal stimulation and potentially cause bradycardia and arrhythmias in MI patients.

Answer 225

d. Administer a stool softener to prevent straining during bowel movements Rationale: Opioids can contribute to constipation, and stool softeners are used to prevent straining, which can trigger vagal stimulation and lead to complications such as bradycardia or dysrhythmias following an MI.

Answer 226

a. Heart failure Rationale: A history of heart failure is significant as it increases the risk for complications in ACS, making early detection and management of cardiovascular status essential.

Answer 227

c. Hypoperfusion from decreased cardiac output Rationale: Cool, clammy, pale skin is often indicative of poor perfusion due to reduced cardiac output, which can occur in ACS as a result of decreased heart function.

Answer 228

a. History of premature coronary artery disease (CAD) in a family member Rationale: A family history of premature CAD is a strong risk factor for developing ACS, making it an important aspect to investigate further.

Answer 229

d. Acute myocardial infarction (MI) Rationale: Substernal chest pain radiating to the left arm is a classic sign of acute myocardial infarction, which should be immediately investigated.

Answer 230

a. Hypotension and decreased cardiac output Rationale: Palpitations, dizziness, and weakness in a patient with ACS are typically related to decreased cardiac output and hypotension due to myocardial ischemia.

Answer 231

c. Acute myocardial infarction (STEMI) Rationale: ST segment elevation on an ECG is a hallmark of a STEMI, indicating an acute myocardial infarction due to complete occlusion of a coronary artery.

Answer 232

a. Increased sympathetic nervous system activation Rationale: Anxiety, fear, and distress in ACS patients are often related to the body’s response to pain and hypoperfusion, which triggers sympathetic nervous system activation.

Answer 233

b. Ventricular dilation or heart failure Rationale: An S3 heart sound can be indicative of ventricular dilation or heart failure, which can occur in ACS due to impaired left ventricular function.

Answer 234

a. Increased WBC count Rationale: An elevated WBC count is commonly seen in ACS due to the inflammatory response to myocardial injury.

Answer 235

d. Acute myocardial infarction Rationale: A pulse deficit and dysrhythmias, especially ventricular, are common in acute myocardial infarction and can be a sign of arrhythmias associated with myocardial injury.

Answer 236

b. Fear of death or loss of control Rationale: Anxiety in ACS patients is often related to fear of death or loss of control, as they are aware of the severity of their condition and the potential for life-threatening complications.

Answer 237

c. Administering medications to reduce myocardial oxygen demand Rationale: In patients with impaired cardiac function, medications such as β-blockers, nitrates, or ACE inhibitors are often used to reduce myocardial oxygen demand and improve cardiac function.

Answer 238

a. Administering IV morphine to reduce chest pain and myocardial oxygen demand Rationale: IV morphine is used for pain relief in ACS patients, as it reduces myocardial oxygen demand by decreasing heart rate, blood pressure, and contractility, which helps alleviate chest pain.

Answer 239

b. Providing education about the patient’s condition and treatment plan Rationale: Providing education helps patients understand their condition, which can alleviate anxiety and improve coping by reducing fear and uncertainty.

Answer 240

a. Start continuous ECG monitoring Rationale: Continuous ECG monitoring is critical in the first few hours after admission to assess for any dysrhythmias or complications related to ACS.

Answer 241

d. To save as much heart muscle as possible Rationale: The primary goal of reperfusion therapy in STEMI is to restore blood flow to the heart muscle and minimize damage.

Answer 242

b. To prevent microemboli from forming and causing further chest pain Rationale: Heparin is used to prevent the formation of microemboli, which can worsen chest pain and contribute to further ischemia in NSTEMI patients.

Answer 243

a. Resolution of chest pain and return of the ST segment to baseline Rationale: The most reliable indicators of reperfusion after thrombolytic therapy are the resolution of chest pain and the return of the ST segment to baseline on ECG.

Answer 244

a. Immediately after the patient is stabilized or if angina returns or increases in severity Rationale: Cardiac catheterization is performed after the patient is stabilized or if angina increases in severity, which helps guide further treatment decisions.

Answer 245

a. STEMI or NSTEMI Rationale: DAPT, consisting of aspirin and ticagrelor, is used to treat patients with STEMI or NSTEMI to reduce the risk of further clot formation.

Answer 246

a. PCI is less invasive and associated with a faster recovery time Rationale: PCI is less invasive than CABG and typically allows for faster recovery, making it the preferred option for STEMI patients.

Answer 247

b. Development of hypotension and signs of bleeding Rationale: Thrombolytic therapy can cause bleeding, so the nurse should closely monitor for hypotension and signs of bleeding (e.g., bruising, petechiae).

Answer 248

b. “This medication combination will help prevent the formation of blood clots.” Rationale: DAPT helps prevent blood clot formation, which reduces the risk of further ischemia and complications in patients with unstable angina.

Answer 249

a. Gradually increase activity as tolerated once the patient is stable Rationale: Gradually increasing activity helps prevent complications from prolonged bed rest, such as muscle atrophy and blood clots, while still prioritizing rest and recovery.

Answer 250

d. Evaluate the effectiveness of the interventions regularly Rationale: Regular evaluation of the effectiveness of NTG and morphine is crucial to ensure pain relief and to assess the ongoing need for these interventions, as chest pain relief may not indicate the absence of heart disease.

Answer 251

c. “Pain relief is important, but continued therapy is necessary to limit myocardial damage.” Rationale: The absence of pain does not mean that heart disease is resolved. It is important for the patient to understand that continued therapy is needed to prevent further myocardial damage.

Answer 252

c. Continue to monitor the patient and assess the effectiveness of interventions Rationale: Continuous monitoring and reassessment of the effectiveness of interventions are critical to ensure that pain relief is maintained and to detect any changes that may require further treatment.

Answer 253

d. Treat the VT immediately as it is a life-threatening dysrhythmia Rationale: Sustained VT is a life-threatening dysrhythmia that requires immediate treatment to prevent further complications such as ventricular fibrillation (VF), which can be fatal.

Answer 254

c. Continue monitoring, as isolated PVCs do not typically require treatment Rationale: Isolated PVCs are often not treated unless they become symptomatic or lead to more serious dysrhythmias. Continuous monitoring is appropriate in this situation.

Answer 255

b. Check for shifts above or below the baseline of the ECG Rationale: Shifts in the ST segment above or below the baseline can indicate reinfarction or ongoing ischemia and should be assessed frequently.

Answer 256

d. Assess intake and output and notify the healthcare provider Rationale: Early signs of heart failure, such as crackles and dyspnea, require careful monitoring of intake and output, with appropriate notification to the healthcare provider for further intervention.

Answer 257

a. Check the nares for irritation or dryness and adjust the cannula as needed Rationale: Nasal cannulas can cause irritation or dryness in the nares, which can lead to discomfort. The nurse should check for these issues and make necessary adjustments.

Answer 258

d. Fluid overload Rationale: An S3 heart sound is often associated with fluid overload or early heart failure, which can occur after an MI as the heart struggles to pump effectively.

Answer 259

c. Sustained ventricular tachycardia (VT) Rationale: Sustained VT is a life-threatening dysrhythmia that commonly occurs in the initial period after an MI, requiring rapid treatment to prevent further complications.

Answer 260

a. Allow the patient to sit in a chair within a few hours after the event Rationale: For an uncomplicated STEMI, the patient can sit in a chair within a few hours after the event, especially if the radial artery was used for PCI. Gradual activity increase is encouraged for early mobilization.

Answer 261

d. The patient should remain in bed for an extended period to prevent complications Rationale: A patient with a large STEMI may require a period of bed rest to prevent complications and allow the heart to stabilize before increasing activity levels.

Answer 262

b. “You may sit in a chair now since your angina is resolved and there are no complications.” Rationale: For patients with UA and no complications, once the angina is resolved, they can sit in a chair. Early mobilization is encouraged when stable.

Answer 263

b. “Gradually increase your activity level with more demanding physical tasks.” Rationale: The patient should gradually increase their activity level with more demanding tasks to avoid overexertion and promote cardiac rehabilitation. This allows for better recovery and prevents complications.

Answer 264

c. Ensuring that patient teaching is brief and provided in simple, clear language Rationale: During a crisis, patients may not be ready to learn new information, so providing teaching in simple and brief terms is key for understanding. Repetition may also be necessary.

Answer 265

a. “Your heart’s blood vessels are blocked, reducing oxygen to the muscle.” Rationale: Chest tightness (angina) occurs when fat and cholesterol block blood vessels supplying oxygen to the heart muscle, reducing its ability to function properly.

Answer 266

a. Respect the patient’s decision, but emphasize the importance of quitting smoking for better outcomes Rationale: While respecting the patient’s choices, it is important to emphasize the health benefits of quitting smoking, as tobacco use remains a significant risk factor for ACS.

Answer 267

b. Preparing the patient for what to expect during recovery and rehabilitation Rationale: Anticipatory guidance helps the patient understand what to expect during recovery, empowering them to make informed decisions and gain a sense of control.

Answer 268

d. “The oxygen supply to your heart muscle is reduced due to blocked blood vessels.” Rationale: Chest tightness during exertion occurs when blood vessels supplying oxygen to the heart muscle are blocked, resulting in insufficient oxygen for the muscle to function properly.

Answer 269

c. Limit information to brief, simple explanations and answer questions as needed Rationale: During a crisis, patients may not be ready to learn in-depth information. The nurse should provide simple explanations and allow time for questions to ensure the patient understands.

Answer 270

a. Encouraging the patient to quit smoking and lose weight as a priority Rationale: Smoking cessation and weight loss are two key risk factor modifications for improving the patient’s health and reducing the likelihood of further ACS events.

Answer 271

b. Gradually increase activity to prevent overexertion and support recovery Rationale: Gradual increase in activity is essential to allow the patient’s heart to adjust and avoid overexertion, promoting optimal recovery and rehabilitation.

Answer 272

c. Respect the patient’s decision but continue to emphasize the importance of smoking cessation Rationale: The nurse should respect the patient’s decision but continue to emphasize the importance of quitting smoking for long-term health benefits and to reduce future ACS risks.

Answer 273

b. The patient will describe the disease process and measures to reduce risk factors Rationale: An expected outcome for the ACS patient is to be able to describe the disease process and identify measures to reduce risk factors, indicating understanding of their condition and management.

Answer 274

b. It can be relieved by rest, nitroglycerin, or both.

Answer 275

b. Obtain vital signs and auscultate for a pericardial friction rub.

Answer 276

a. Oral statin therapy b. Antiplatelet therapy e. Intravenous nitroglycerin

Answer 277

d. Cardiac-specific troponin Rationale: Troponin levels increase about 4 to 6 hours after the onset of myocardial infarction (MI) and are highly specific indicators for MI. Myoglobin is released within 2 hours of MI, but it lacks specificity and its use is limited. The other laboratory data are useful in determining the patient‘s risk for developing coronary artery disease but are not helpful in determining whether an acute MI is in progress.

Answer 278

c. “Heparin prevents the development of new clots in the coronary arteries.” Rationale: Heparin helps prevent the conversion of fibrinogen to fibrin and decreases coronary artery thrombosis. It does not change coronary artery plaque, dissolve already formed clots, or enhance platelet aggregation.

Answer 279

c. “What time did your pain begin?” Rationale: Thrombolytic therapy criteria include chest pain for less than 12 hours with 12-lead ECG findings consistent with an acute STEMI. The other information is not a factor in the decision about thrombolytic therapy.

Answer 280

c. Decreased level of consciousness Rationale: The change in level of consciousness indicates that the patient may be experiencing intracranial bleeding, a possible complication of thrombolytic therapy. Some bleeding of the gums is an expected side effect of the therapy but not an indication to stop infusion of the thrombolytic medication. A decrease in blood pressure could indicate internal bleeding. A nonsustained episode of ventricular tachycardia is a common reperfusion dysrhythmia and may indicate that the therapy is effective.

Answer 281

a. “What do you think caused your chest pain?” Rationale: When the patient is experiencing denial, the nurse should assist the patient in testing reality until the patient has progressed beyond this step of the emotional adjustment to MI. Asking the patient about vacation plans reinforces the patient‘s plan, which is not appropriate in the immediate post-MI period. Reminding the patient in denial about the MI is likely to make the patient angry and lead to distrust of the nursing staff.

Answer 282

a. Sildenafil (Viagra) Rationale: The nurse will need to avoid giving nitrates to the patient because nitrate administration is contraindicated in patients who are using sildenafil because of the risk of severe hypotension caused by vasodilation. The other home medications should be documented and reported to the health care provider but do not have as immediate an impact on decisions about the patient‘s treatment.

Answer 283

b. Pallor and weakness of the right hand Rationale: The changes in the right hand indicate compromised blood flow, which requires immediate evaluation and actions, such as prescribed calcium channel blockers or surgery. The other changes are expected or require nursing interventions.

Answer 284

a. Report of chest pain Rationale: The patient‘s chest pain indicates that restenosis of the coronary artery may be occurring and requires immediate actions, such as administration of oxygen and nitroglycerin, by the nurse. The other information indicates a need for ongoing assessments by the nurse.

Answer 285

c. Impaired cardiac function Rationale: The hypotension and tachycardia indicate decreased cardiac output and shock from the impaired function of the damaged myocardium. This will result in decreased perfusion to all vital organs (e.g., brain, kidney, heart) and is a priority.

Answer 286

a. Attach the heart monitor. Rationale: Because dysrhythmias are the most common complication of myocardial infarction (MI), the first action should be to place the patient on a heart monitor. The other actions are also important and should be accomplished as quickly as possible.

Answer 287

c. No change in the patient‘s reported level of chest pain Rationale: Continued chest pain suggests that the thrombolytic therapy is not effective and that other interventions such as percutaneous coronary intervention may be needed. Bruising is a possible side effect of thrombolytic therapy, but it is not an indication that therapy should be discontinued. The decrease of the ST-segment elevation indicates that thrombolysis is occurring, and perfusion is returning to the injured myocardium. An increase in troponin levels is expected with reperfusion and is related to the washout of cardiac biomarkers into the circulation as the blocked vessel is opened.

Answer 288

c. Bilateral crackles in the mid-lower lobes. Rationale: The crackles indicate that the patient may be developing heart failure, a possible complication of myocardial infarction (MI). The health care provider may need to order medications such as diuretics or angiotensin-converting enzyme inhibitors for the patient. Elevation in troponin level at this time is expected. PACs are not life-threatening dysrhythmias. Denial is a common response in the immediate period after the MI.