QUESTIONS Flashcards
A 42-year-old woman is evaluated in the emergency department. She has a 2-day history of nonexertional chest pain. The pain is sharp, substernal, and worse when lying down or with deep breaths. She denies shortness of breath. Her symptoms were preceded by a recent upper respiratory tract infection. On physical examination, temperature is 37.9°C (100.3°F), blood pressure is 165/90 mm Hg, pulse rate is 102/min, respiration rate is 18/min, and oxygen saturation is 96% on ambient air. The cardiopulmonary examination is normal as is the remainder of the physical examination. An electrocardiogram is shown :. Echocardiogram shows a small pericardial effusion. Which of the following is the most appropriate initial therapy?
The most appropriate initial therapy is ibuprofen. Acute pericarditis is the most likely diagnosis. Viral infection is the most common known cause of acute pericarditis. Diagnosis is most often made by confirming two of three classic findings: chest pain, often with a pleuritic component; friction rub; and diffuse ST-segment elevation on electrocardiography (ECG). This patient has chest pain and diffuse ST-segment elevation on ECG. A pericardial friction rub is virtually pathognomonic of acute pericarditis. It is best auscultated at the left lower sternal border during suspended respiration while the patient is leaning forward. The classic rub has three components and can be squeaky, scratchy, or swooshing. It is often transient. Although a pericardial friction rub is a highly specific sign of acute pericarditis, it is not very sensitive and its absence does not rule out the diagnosis. In acute pericarditis, epicardial inflammation causes upwardly concave ST-segment elevation in all leads except aVR. PR-segment depression in the limb leads (particularly lead II) or precordial leads and elevation in lead aVR may accompany ST-segment elevation. PR-segment shifts are highly specific but not sensitive findings for acute pericarditis. Echocardiography can detect very small pericardial effusions that may help with the diagnosis of pericarditis. More importantly, echocardiography can detect cardiac tamponade and heart failure that may complicate acute pericarditis. Appropriate initial therapy for acute pericarditis is either aspirin or an a nonsteroidal anti-inflammatory drug (NSAID), such as ibuprofen. Chest pain resulting from acute pericarditis usually resolves within 24 hours of treatment with anti-inflammatory medications. Nonrandomized and nonblinded studies support the use of colchicine as an alternative first-line agent or an adjunctive treatment for acute pericarditis. In the absence of a specific indication for their use, a glucocorticoid, such as prednisone, should only be used in refractory cases of acute pericarditis or in patients with contraindications to aspirin, NSAIDs, and colchicine. Glucocorticoids increase the risk of recurrent pericarditis. The nature of the chest pain and the findings of PR-segment depression on ECG and a small effusion on echocardiography are most consistent with acute pericarditis and make acute coronary syndrome or pulmonary embolism unlikely. Therefore, heparin and clopidogrel are not indicated.
A 60-year-old man is evaluated because of a 3-month history of intermittent chest pain. He has occasional substernal chest pressure when he exercises at the gym and occasionally after he eats a spicy meal. The pressure is not consistently relieved with rest and is occasionally relieved with antacid. He has no associated symptoms of shortness of breath, dizziness, or diaphoresis. His medical history includes hypertension and hyperlipidemia. Medications are lisinopril and pravastatin. On physical examination, blood pressure is 128/80 mm hg, pulse rate is 84/min, and respiration rate is 16/min. Findings on cardiovascular examination are normal. The electrocardiogram is shown Which of the following is the most appropriate diagnostic test to evaluate the patient’s chest pain?n
The most appropriate test to evaluate the patient’s chest pain is exercise electrocardiography. A variety of noninvasive stress tests are available to determine whether a patient with cardiovascular symptoms has coronary artery disease (CAD). The decision to perform a specific test is based on the pretest probability of CAD, the patient’s ability to exercise, findings on resting electrocardiography (ECG), and comorbid conditions, such as reactive airways disease, that may influence the choice of a pharmacologic stress agent. Stress testing is most useful in patients with an intermediate pretest probability of CAD. For patients with a low pretest probability of CAD, stress testing is not useful because an abnormal test result is likely a false-positive finding and a normal test result only confirms the low pretest probability of CAD. For patients with a high pretest probability of CAD, stress testing is not useful to diagnose CAD and empiric medical therapy should be initiated. In this setting, a normal stress test result would likely be a false-negative finding and an abnormal stress test result would only confirm a high pretest probability of CAD. Exercise ECG testing is the standard stress test for the diagnosis of CAD in patients with normal baseline ECG findings. If abnormalities that limit ST-segment analysis are present (left bundle branch block, left ventricular hypertrophy, paced rhythm, Wolff-Parkinson-White pattern), the results may be difficult to interpret. In patients with abnormalities on resting ECG that impair the ability to interpret ST-segment changes, imaging increases diagnostic accuracy and ability to determine the site and extent of ischemia. Exercise is preferred to pharmacologic stressors because it provides a gauge of functional capacity and a contextual understanding of symptoms as well as a record of the hemodynamic response to exercise. For patients who cannot exercise because of physical limitations or physical deconditioning, pharmacologic stressors can be used. These agents, recommended if the patient cannot achieve at least 5 metabolic equivalents, increase myocardial contractility and oxygen demand (dobutamine) or induce regional hypoperfusion through coronary vasodilation (adenosine, dipyridamole, and regadenoson). This patient has atypical chest pain (substernal pressure caused by exercise but not relieved with rest) and normal findings on ECG. The most appropriate diagnostic test to evaluate the patient’s chest pain is exercise electrocardiography. Because he is a candidate for the preferred type of stress test, alternative methods, including imaging with echocardiography or pharmacologic stress testing with dobutamine, are not indicated. Cardiac catheterization would not be an appropriate intervention given the patient’s intermediate risk for cardiovascular disease. It might be appropriate if he had a high pretest probability of coronary artery disease or he had specific findings of coronary occlusion on stress testing.
A 24-year-old man is evaluated for a 6-month history of episodic substernal chest pain. Episodes occur four to five times per week and are accompanied by palpitations and sweating. They resolve spontaneously after approximately 30 minutes. His symptoms are unrelieved with antacids, can occur at rest or with exertion, and are nonpositional. There are no specific precipitating factors. Lipid levels were obtained last year and were normal. The patient is a nonsmoker. He has no personal or family history of coronary artery disease, diabetes mellitus, hyperlipidemia, or hypertension. He is not taking any medications.
On physical examination, vital signs are normal. He has no cardiac murmurs and no abdominal pain. Complete blood count, serum thyroid-stimulating hormone level, and electrocardiogram are all normal.
Which of the following is the most appropriate management of this patient?
The most appropriate management of this patient is to prescribe a selective serotonin reuptake inhibitor. Panic disorder is a syndrome characterized by sudden panic attacks with acute onset of somatic symptoms that may include chest pain, palpitations, sweating, nausea, dizziness, dyspnea, and numbness. These symptoms usually last from 5 to 60 minutes. Approximately 50% of patients with panic disorder also have associated agoraphobia, with fears of being in crowds or in places from which escape would be difficult. Diagnosis is based on clinical descriptors and setting, but care should be taken to consider underlying medical disorders, such as cardiac disease, thyroid disease, or pheochromocytoma, particularly in patients who are at increased risk for one of these disorders. However, extensive testing is not necessary in most patients with a characteristic presentation and normal findings on physical examination and basic laboratory studies. Treatment options for panic disorder include medication and psychotherapy. Cognitive behavioral therapy (CBT) has been shown to be the most effective psychotherapeutic intervention in controlled trials. Selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors have been shown to be effective. Panic disorder that is severe or refractory appears to be most amenable to a combination of CBT and pharmacotherapy compared with either treatment alone.
This patient has classic symptoms of panic disorder and no cardiac risk factors. It would be inappropriate to order further cardiac testing in the setting of a normal electrocardiogram and classic symptoms. This patient’s symptoms are also atypical for gastroesophageal reflux disease, and so empiric proton pump inhibitor therapy would be inappropriate.
A 70-year-old man is evaluated for sharp left-sided pleuritic chest pain and shortness of breath that began suddenly 24 hours ago. The pain has been persistent over the last 24 hours and does not worsen or improve with exertion or position. The patient’s history is significant for a 50-pack-year smoking history and severe chronic obstructive pulmonary disease, although he is currently a nonsmoker. Medications are ipratropium and albuterol.
On physical examination, temperature is normal, blood pressure is 128/80 mm Hg, pulse rate is 88/min, and respiration rate is 18/min. Oxygen saturation on ambient air is 89%. The trachea is midline. Lung examination shows hyperresonance, decreased chest wall expansion, and decreased breath sounds on the left. Cardiac examination shows distant heart sounds but no extra heart sounds.
Which of the following is the most appropriate diagnostic test to perform next?
This patient should undergo chest radiography. He has severe chronic obstructive pulmonary disease (COPD) and findings that are consistent with spontaneous secondary pneumothorax. These findings include sudden, sharp, nonradiating pleuritic chest pain and shortness of breath with hyperresonance, decreased breath sounds, and decreased chest wall expansion on the side of the pneumothorax in a patient with underlying lung disease. Pneumothorax should be considered in any patient who has sudden onset of pleuritic chest pain and dyspnea. The diagnostic test of choice if pneumothorax is suspected is an upright chest radiograph. Findings on chest radiograph include separation of the parietal and visceral pleura by a collection of gas and the absence of vessels in this space. This patient is at increased risk for pneumothorax because of his COPD. Pneumothorax occurring in patients without known lung disease or a clear precipitating cause is termed primary spontaneous pneumothorax (PSP). PSP tends to occur more often in men, smokers, and those with a family history of PSP. The clinical presentation is similar in both primary or secondary pneumothorax.
Chest computed tomography (CT) also can be used to diagnose pneumothorax. Chest CT may be more sensitive than a chest radiograph in delineating smaller collections of gas in the pleural space and providing more information about the pulmonary parenchyma and pleura. However, plain film radiography remains the initial test of choice for most patients, and chest CT should be reserved for cases when the chest radiograph does not provide information to guide further treatment or evaluation.
The patient’s history and physical examination are classic for pneumothorax, and his pain descriptors do not strongly suggest ischemia or other primary cardiovascular disease. Electrocardiogram and echocardiogram, which are the tests of choice to evaluate ischemic heart disease, valvular heart disease, or cardiomyopathy, would not be the first diagnostic tests of choice for suspected pneumothorax.
A 50-year-old woman is evaluated for a 1-year history of recurrent left-sided chest pain. The pain is poorly localized and nonexertional and occurs in 1-minute episodes. There is no dyspnea, nausea, or diaphoresis associated with these episodes. The patient has not had dysphagia, heartburn, weight change, or other gastrointestinal symptoms. She has no other medical problems and does not smoke cigarettes.
On physical examination, vital signs are normal. The patient’s chest pain is not reproducible by palpation. The cardiac examination is unremarkable, as is the remainder of the physical examination.
Results of a lipid panel, a fasting plasma glucose test, and a chest radiograph are normal. An echocardiogram shows a normal ejection fraction, with no wall motion abnormalities. Results of an exercise stress test are normal.
Which of the following is the most appropriate next step in management?
This patient should receive twice-daily proton pump inhibitor (PPI) therapy for 8 to 10 weeks. Pain associated with gastroesophageal reflux can mimic ischemic chest pain. A cardiac cause should be carefully assessed and excluded in all patients with chest pain. This patient has nonanginal chest pain, no additional risk factors, and normal findings on exercise stress testing. Therefore, the likelihood of a cardiac cause of chest pain is low. Randomized controlled trials have shown that a therapeutic trial of twice-daily PPI treatment is effective in 50% to 60% of patients with noncardiac chest pain, indicating that gastroesophageal reflux disease is the underlying cause.
If the PPI trial is unsuccessful, further evaluation with endoscopy (to detect erosive esophagitis or achalasia), manometry (to detect esophageal motility disorders such as diffuse esophageal spasm), and ambulatory pH recording (to detect refractory reflux) would be reasonable.
Musculoskeletal chest pain has an insidious onset and may last for hours to weeks. It is most recognizable when it is sharp and localized to a specific area of the chest; however, it can also be poorly localized. The pain may be worsened by turning, deep breathing, or arm movement. Chest pain may or may not be reproducible by chest palpation (pain reproduced by palpation does not exclude ischemic heart disease), and findings on cardiovascular examination are often normal. This patient does not have the typical features of musculoskeletal chest pain. Therefore, treatment with an nonsteroidal anti-inflammatory drug is not the most appropriate first step in management.
A 65-year-old man is evaluated because of chronic angina. He has a 10-year history of symptomatic coronary artery disease. The diagnosis was confirmed with an exercise stress test. Results of the test showed no high-risk features. His estimated left ventricular ejection fraction by echocardiography at that time was 56%. He occasionally has chest pain after walking four blocks. The pain is relieved by taking one sublingual nitroglycerin or by resting. His exercise capacity has not diminished, and the frequency, character, and duration of the pain have not changed. He denies shortness of breath, orthopnea, or paroxysmal nocturnal dyspnea. Current medications include simvastatin, aspirin, metoprolol, and sublingual nitroglycerin.
On examination, blood pressure is 122/82 mm Hg, pulse rate is 68/min, respiratory rate is 16/min, and body mass index is 27. There is no jugular venous distention, and there are no murmurs, gallops, rubs, or pulmonary crackles or peripheral edema.
Which of the following is the most appropriate management?
Continuing the current management is the most appropriate action. Several large trials have compared revascularization with optimal medical therapy. These studies found that revascularization combined with aggressive medical therapy was not superior to aggressive medical therapy alone in reducing death or myocardial infarction. Based on these studies, current guidelines recommend reserving coronary angiography and revascularization for patients who continue to have symptoms despite optimal medical therapy, patients who are unable to tolerate the side effects of medications, and those who have high-risk findings on noninvasive testing. This patient’s pattern of angina is stable, he is tolerating his medications, and his original stress test showed no high-risk features. Therefore, a more aggressive intervention such as coronary angiography is not indicated as there would not be an expected improved outcome.
Routine follow-up electrocardiography, exercise stress testing (or other noninvasive imaging studies), and echocardiography are not indicated in patients with chronic stable angina. Although careful and frequent follow-up is indicated, disease assessment is conducted with a detailed history and physical examination. The history should focus on changes in physical activity and the frequency, severity, or pattern of chest pain. Reasonable laboratory monitoring includes periodic measurement of lipids and blood glucose levels. Follow-up electrocardiography should be considered when there are medication changes that could affect cardiac conduction; there is a change in the severity, frequency, or pattern of angina; symptoms that suggest dysthymia occur; or syncope develops. There are no indications for an electrocardiogram, an exercise stress test, or echocardiography.
A 60-year-old man is evaluated because of a 3-month history of intermittent chest pain. He has occasional substernal chest pressure when he exercises at the gym and occasionally after he eats a spicy meal. The pressure is not consistently relieved with rest and is occasionally relieved with antacid. He has no associated symptoms of shortness of breath, dizziness, or diaphoresis. His medical history includes hypertension and hyperlipidemia. Medications are lisinopril and pravastatin.
On physical examination, blood pressure is 128/80 mm hg, pulse rate is 84/min, and respiration rate is 16/min. Findings on cardiovascular examination are normal.
The electrocardiogram is shown :.
Which of the following is the most appropriate diagnostic test to evaluate the patient’s chest pain?
The most appropriate test to evaluate the patient’s chest pain is exercise electrocardiography.
A variety of noninvasive stress tests are available to determine whether a patient with cardiovascular symptoms has coronary artery disease (CAD). The decision to perform a specific test is based on the pretest probability of CAD, the patient’s ability to exercise, findings on resting electrocardiography (ECG), and comorbid conditions, such as reactive airways disease, that may influence the choice of a pharmacologic stress agent. Stress testing is most useful in patients with an intermediate pretest probability of CAD. For patients with a low pretest probability of CAD, stress testing is not useful because an abnormal test result is likely a false-positive finding and a normal test result only confirms the low pretest probability of CAD. For patients with a high pretest probability of CAD, stress testing is not useful to diagnose CAD and empiric medical therapy should be initiated. In this setting, a normal stress test result would likely be a false-negative finding and an abnormal stress test result would only confirm a high pretest probability of CAD.
Exercise ECG testing is the standard stress test for the diagnosis of CAD in patients with normal baseline ECG findings. If abnormalities that limit ST-segment analysis are present (left bundle branch block, left ventricular hypertrophy, paced rhythm, Wolff-Parkinson-White pattern), the results may be difficult to interpret. In patients with abnormalities on resting ECG that impair the ability to interpret ST-segment changes, imaging increases diagnostic accuracy and ability to determine the site and extent of ischemia. Exercise is preferred to pharmacologic stressors because it provides a gauge of functional capacity and a contextual understanding of symptoms as well as a record of the hemodynamic response to exercise. For patients who cannot exercise because of physical limitations or physical deconditioning, pharmacologic stressors can be used. These agents, recommended if the patient cannot achieve at least 5 metabolic equivalents, increase myocardial contractility and oxygen demand (dobutamine) or induce regional hypoperfusion through coronary vasodilation (adenosine, dipyridamole, and regadenoson).
This patient has atypical chest pain (substernal pressure caused by exercise but not relieved with rest) and normal findings on ECG. The most appropriate diagnostic test to evaluate the patient’s chest pain is exercise electrocardiography. Because he is a candidate for the preferred type of stress test, alternative methods, including imaging with echocardiography or pharmacologic stress testing with dobutamine, are not indicated.
Cardiac catheterization would not be an appropriate intervention given the patient’s intermediate risk for cardiovascular disease. It might be appropriate if he had a high pretest probability of coronary artery disease or he had specific findings of coronary occlusion on stress testing.
A 55-year-old woman is evaluated for symptoms of sharp, localized, left-sided chest pain for the last 3 weeks. The pain is unrelated to exertion and is associated with mild dyspnea and fatigue. Typically it lasts for 5 to 10 minutes and abates spontaneously. The pain is not pleuritic, positional, or related to eating. She has hypertension and hypercholesterolemia. Her father had a myocardial infarction at 54 years of age. Daily medications are hydrochlorothiazide, simvastatin, and aspirin.
On physical examination, blood pressure is 135/78 mm Hg, pulse rate is 78/min, and respiration rate is 14/min. Cardiac auscultation shows S4 but is otherwise normal, as is the remainder of her physical examination.
Electrocardiogram shows sinus rhythm, with a heart rate of 75/min and no ST-segment or T-wave abnormalities.
Which of the following is the most appropriate diagnostic study?
This patient should undergo exercise electrocardiography (ECG). She has several risk factors for coronary artery disease (CAD), including hypertension, hypercholesterolemia, and a family history of premature CAD. Her symptoms are not typical of angina (her chest discomfort is localized, sharp, and not reproducible with exertion), and the resting ECG is normal. Because this patient has multiple risk factors and atypical symptoms, the pretest probability that CAD is the cause of her symptoms is intermediate. The results of exercise ECG testing, whether normal or abnormal, will significantly affect the posttest probability of CAD. Exercise testing is recommended as the initial test in patients with an intermediate pretest probability of CAD based on age, sex, and symptoms, including patients with right bundle branch block or ST-segment depression of less than 1 mm at baseline. In addition, the results of the exercise ECG test will provide prognostic information about the risk of death and myocardial infarction on the basis of exercise duration, angina, and the magnitude of ST-segment depression.
Coronary angiography is not appropriate for this patient because the pretest probability of CAD is intermediate, which is too low to warrant immediate coronary angiography as the initial diagnostic test.
Although exercise ECG testing has been found to have lower specificity and a higher false-positive rate in women than in men, the routine use of exercise testing with echocardiography to assess left ventricular regional wall motion or perfusion imaging is not recommended for either women or men in the absence of baseline ECG abnormalities. Although echocardiography increases the sensitivity of the ECG results, the use of stress echocardiography as the initial test has not been found to reduce cardiovascular events compared with exercise ECG testing alone.
Pharmacologic stress testing is not indicated because this patient is physically able to exercise. Pharmacologic agents include dobutamine (which increases heart rate and myocardial contractility) and vasodilators (which cause relative increases in coronary blood flow in myocardial regions that are not supplied by stenotic vessels). Exercise is preferred over pharmacologic treatment because of the additional diagnostic and prognostic information provided by exercise testing.
A 68-year-old man is evaluated for exertional chest pain of 3 months’ duration. He describes the chest pain as midsternal pressure without radiation that occurs with walking one to two blocks and resolves with rest or sublingual nitroglycerin. No symptoms have occurred at rest. His medical history is significant for myocardial infarction 3 years ago, hypertension, and hyperlipidemia. Medications are aspirin, metoprolol, simvastatin, isosorbide dinitrate, and sublingual nitroglycerin as needed for chest pain.
On physical examination, temperature is normal, blood pressure is 150/85 mm Hg, pulse rate is 80/min, and respiration rate is 12/min. The lungs are clear. Cardiac examination shows normal S1 and S2 with no extra heart sounds or murmurs. The remainder of the examination is unremarkable.
Electrocardiogram shows normal sinus rhythm, no left ventricular hypertrophy, no ST- or T-wave changes, and no Q waves.
Which of the following is the most appropriate management?
In this patient with coronary artery disease and continuing angina, the medical therapy should be optimized by increasing the dosage of β-blocker. Physical examination is notable for blood pressure and heart rate that would allow further up-titration of the β-blocker dosage. Complete β-blockade typically results in a resting pulse rate of approximately 55 to 60/min. Therefore, the pulse rate of 80/min suggests that the dosage of metoprolol should be increased. β-blockers are particularly effective antianginal medications because they decrease heart rate, myocardial contractility, and systemic blood pressure, thereby lowering myocardial oxygen demand.
Calcium channel blockers are first-line antianginal therapy in patients with contraindications to β-blockers. In patients with continuing angina despite optimal dosages of β-blocker and nitrates, a calcium channel blocker may be added. A calcium channel blocker such as diltiazem is not indicated in this patient because his dosage of metoprolol is not yet optimal.
Ranolazine should be considered only in patients who remain symptomatic despite optimal dosages of β-blockers, calcium channel blockers, and nitrates. Ranolazine decreases angina symptoms but is significantly more expensive and less effective than the usual antianginal medications.
Coronary angiography may be indicated in a patient who is receiving maximal medical therapy with continued symptoms of angina that affect quality of life. Referral for coronary angiography is not indicated for this patient because he is not currently receiving optimal medical therapy.
A 62-year-old man with coronary artery disease is evaluated for angina. He was diagnosed 4 years ago, and since that time, his symptoms have been well controlled with metoprolol and isosorbide mononitrate. He had exertional angina 8 months ago. His dosages of metoprolol and isosorbide were increased and long-acting diltiazem was added, with improved control of his symptoms. He has had increasing symptoms over the last 2 months and now requires daily sublingual nitroglycerin for relief of angina during exercise. He has not had any episodes of angina at rest. His medical history is significant for hyperlipidemia treated with atorvastatin.
On physical examination, the patient is afebrile, blood pressure is 110/60 mm Hg, pulse rate is 55/min, and respiration rate is 12/min. Results of cardiopulmonary examination are unremarkable, as are the remainder of the findings of the physical examination.
Electrocardiogram shows no acute ischemic changes.
Which of the following should be the next step in this patient’s management?
Coronary angiography is the most appropriate option in this patient who has had continued symptoms of angina despite optimal medical therapy. Although it has been shown that a routine strategy of coronary angiography and revascularization provides no benefit compared with optimal medical therapy in patients with chronic stable angina, coronary angiography may be of benefit in patients who are highly symptomatic despite optimal medical therapy, such as this patient. Coronary angiography allows direct evaluation of the coronary anatomy, with possible percutaneous coronary intervention or surgical revascularization if indicated. Coronary revascularization has been shown to be beneficial in patients with chronic stable angina and the following conditions: angina pectoris that is refractory to medical therapy; a large area of ischemic myocardium and high-risk criteria on stress testing; high-risk coronary anatomy, including left main coronary artery stenosis or three-vessel disease; and significant coronary artery disease with reduced left ventricular systolic function. In appropriately selected patients, revascularization, with either percutaneous coronary intervention or coronary artery bypass grafting surgery, has been shown to reduce angina, increase longevity, and improve left ventricular performance.
Exercise treadmill stress testing would not be useful in the management of this patient because it would only confirm the known diagnosis of coronary artery disease. Results of an exercise stress test would not influence therapeutic decisions.
Although β-blockers and nitrates are effective antianginal medications, the patient is receiving near-maximal doses of both drugs, as indicated by his pulse rate, which shows effective β-blockade, and his blood pressure, which likely would not tolerate an increase in the dosage of either medication.
A 68-year-old man is evaluated in the emergency department because of a 2-day history of intermittent chest pain. The pain is substernal, is not related to activity, and lasts less than 15 minutes. His medical history includes hypertension, hyperlipidemia, and type 2 diabetes. His medications include aspirin, metoprolol, lisinopril, simvastatin, and metformin. In the emergency department he received a dose of liquid antacid, and his chest pain partially resolved.
On physical examination, he is afebrile, blood pressure is 130/80 mm Hg, pulse rate is 70/min, respiration rate is 18/min, and oxygen saturation is 98% on ambient air. Results of cardiopulmonary examination are normal.
The electrocardiogram shows minor T-wave abnormalities. Troponin T measurement is less than 0.01 ng/mL (0.01 µg/L).
Which of the following is the most appropriate management of this patient’s chest pain?
The most appropriate management of this patient’s chest pain is admission to the telemetry unit and ongoing assessment with serial electrocardiograms and troponin measurements. Based on this patient’s age and the substernal nature of his chest pain, there is at least an intermediate likelihood of an acute coronary syndrome. The decision to hospitalize a patient with chest pain is challenging. The goal is to identify patients with life-threatening disease who require immediate attention while minimizing unnecessary evaluation and treatment in others. A rapid clinical determination of the likelihood of an acute coronary syndrome is the essential first task and should guide the admission decision. In addition, the physician should consider the likelihood of short-term adverse outcomes, including death and nonfatal myocardial infarction, in patients with acute coronary syndrome. When acute coronary syndrome is suspected, the patient should be admitted for evaluation and management. Low-risk patients can be further stratified with stress testing.
At this point, the patient does not have an indication for coronary angiography and acute intervention. If further chest pain develops in association with ST-segment or T-wave changes on electrocardiography or elevated cardiac enzyme levels and the patient is considered high risk according to his TIMI (Thrombolysis in Myocardial Infarction) score, cardiac angiography would be reasonable.
The most common gastrointestinal cause of chest pain is gastroesophageal reflux disease (GERD). Although the pain associated with GERD is often described as burning, it can mimic angina and may be relieved by nitroglycerin. It generally is worsened with bending over or recumbency and is relieved with antacids, histamine-2 blockers, or proton pump inhibitors. Because acute coronary syndrome is a life-threatening condition, this diagnosis must be addressed first. In addition, the preferred initial diagnostic test for GERD is a therapeutic trial of a proton pump inhibitor, not esophageal pH monitoring.
Cardiac stress testing can be highly valuable in identifying significant coronary insufficiency, and it would be the test of choice to diagnose stable angina. However, in the acute setting, stress testing is contraindicated in a patient with possible acute coronary syndrome. Once the patient is stabilized and acute coronary syndrome is excluded, stress testing can be used to further stratify risk in a low- or intermediate-risk patient. In this patient, the preferred cardiac stress test is an exercise stress test, not a pharmacologic stress test with nuclear imaging.
A 58-year-old woman is evaluated in the emergency department for chest pain, diaphoresis, and shortness of breath of 4 hours’ duration. Three years ago she was diagnosed with a non–ST-elevation myocardial infarction and was treated medically. Additional medical history includes type 2 diabetes and hypertension. Her current medications are aspirin, lisinopril, atorvastatin, and glargine insulin.
On physical examination, she is afebrile, blood pressure is 125/60 mm Hg, pulse rate is 48/min, respiratory rate is 18/min, and oxygen saturation is 98% on ambient air. Cardiac examination shows no jugular venous distention, and the lungs are clear. An S4 is present.
Electrocardiogram shows ST-segment elevation and T-wave inversions in leads II, III, and aVF. The initial troponin T measurement is elevated.
The nearest hospital capable of percutaneous coronary intervention is more than 2 hours away. The patient has no contraindication to thrombolytic therapy.
Which of the following is the most appropriate initial management for this patient?
The most appropriate initial management of this patient consists of aspirin, heparin, intravenous nitroglycerin, and thrombolytic therapy. This patient has evidence of an ST-elevation myocardial infarction (STEMI) with acute ST-segment changes present in the inferior leads and an elevated troponin T level. The treatment of choice for STEMI is reperfusion therapy. Reperfusion for patients with STEMI can be achieved with thrombolytic therapy or primary percutaneous coronary intervention (PCI). Many patients with STEMI in the United States present to non–PCI-capable hospitals; as a result, thrombolytic therapy and transfer for primary PCI are the available treatment options. The time to achieve balloon inflation is a major determinant of the benefits of PCI versus thrombolytic therapy. If PCI must be delayed, then thrombolytic therapy should be considered. Observational data from community hospitals within the United States have found that fewer than 5% of patients achieve the guideline-suggested door-to-balloon time of less than 90 minutes. A projected 2-hour delay to a PCI facility makes thrombolytic therapy the best option for this patient.
β-Blockers reduce mortality and should be given to all patients with acute coronary syndrome except those with heart failure, systolic blood pressure of less than 90 mm Hg, bradycardia (<50/min), or second-degree atrioventricular block. Because this patient’s heart rate is 48/min, metoprolol should not be administered. Treatment with heparin, clopidogrel, pravastatin, and intravenous nitroglycerin without thrombolytic therapy does not address the need for immediate myocardial reperfusion and is not adequate treatment for this patient.
A 52-year-old woman was evaluated in the emergency department because of acute onset of dyspnea while shoveling snow this morning. The dyspnea resolved within 2 minutes of rest but recurred an hour later while she was watching television. Over the previous 10 days she has had several similar episodes of dyspnea with mild exertion, such as walking upstairs, and also at rest. She has no chest pain, palpitations, or orthopnea. She has a 15-year history of type 2 diabetes, hyperlipidemia, and hypertension treated with aspirin, metformin, chlorthalidone, ramipril, and rosuvastatin.
On physical examination, temperature was 37°C (98.6°F), blood pressure was 110/70 mm Hg, pulse rate was 80/min, respiratory rate was 18/min, and oxygen saturation was 96% on ambient air. There was no jugular distention, normal cardiac sounds were present without extra sounds or murmurs, and the lungs were clear to auscultation.
The initial electrocardiogram showed ST-segment changes. The first troponin I level was 0 ng/mL (0 µg/L).
An hour after admission to the emergency department, she had an episode of acute dyspnea. A repeat electrocardiogram at this time is shown :. Repeat troponin level is 0.8 ng/mL (0.8 µg/L).
The most appropriate next test is cardiac catheterization. Although chest pain is the most common presenting symptom for an acute coronary syndrome, women and patients with diabetes are more likely to have atypical angina symptoms, such as fatigue, dyspnea, and nausea. Acute coronary syndromes include unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Patients with ischemic chest pain and STEMI benefit from reperfusion therapy, either thrombolytic therapy or primary angioplasty. Patients with NSTEMI or unstable angina are a heterogeneous group and require risk stratification (determination of their risk of death or nonfatal myocardial infection) to direct therapy. Although patients with unstable angina may have similar electrocardiographic findings to those with NSTEMI, they can be differentiated by the lack of elevation in serum cardiac biomarkers. This patient with recurrent unprovoked dyspnea, an evolving electrocardiogram showing ischemic changes in the anterolateral leads (ST-segment depression and T-wave inversion), and rising troponin level is at high risk for death or nonfatal myocardial infarction (5 points on the TIMI (Thrombolysis in Myocardial Infarction) risk stratification score). This patient will benefit from an early invasive approach that includes coronary angiography and subsequent revascularization (percutaneous coronary intervention or surgical revascularization). Most contemporary trials evaluating these two alternatives show a benefit for early angiography and revascularization (invasive approach).
An echocardiogram may show localized wall motion abnormalities associated with acute ischemia, but this finding does not alter the need for early intervention with cardiac catheterization and revascularization. An exercise stress test is contraindicated in patients with unstable ischemic heart disease. Repeating the troponin level will add no useful additional information to guide the management of this patient.
A 78-year-old man is evaluated in the emergency department because of chest pain. He describes left substernal discomfort that began approximately 8 hours ago. He reports no similar episodes of chest pain. Medical history is significant for hypertension and a 30-pack-year history of ongoing tobacco use. His only medication is amlodipine.
On physical examination, the patient is afebrile, blood pressure is 130/80 mm Hg, pulse rate is 72/min, and respiration rate is 12/min. There is no jugular venous distention, the lung fields are clear, and cardiac examination shows a normal S1 and S2 without murmurs. No peripheral edema is present.
The initial troponin I level is 26 ng/mL (26 µg/L). Laboratory findings are otherwise normal.
Electrocardiogram shows sinus rhythm of 70/min and 2-mm ST-segment elevation in leads II, III, and aVF.
Which of the following is the most appropriate treatment approach?
The patient should undergo primary percutaneous coronary intervention (PCI). He presents with evidence of ST-elevation myocardial infarction (STEMI). The goal of therapy in patients STEMI is to perform PCI within 90 minutes of presentation to a PCI-capable facility or within 120 minutes if the patient requires transfer from a non–PCI-capable hospital. However, patients may benefit from treatment up to 12 hours after the onset of symptoms and possibly even after this time, depending on clinical circumstances.
For patients with STEMI, including those presenting later than the optimal time frame, PCI is the preferred reperfusion strategy instead of treatment with thrombolytics. Thrombolytic therapy has not shown a clear benefit for patients with STEMI who present more than 12 hours after the onset of symptoms. It remains second-line treatment when PCI is not possible or is contraindicated.
Emergency coronary artery bypass graft surgery is not a routine method of revascularization in patients with STEMI. The reasons are logistical; it is nearly impossible to diagnose STEMI, perform cardiac catheterization, obtain access to an operating room, assemble a surgical team, and perform surgery within the necessary time frame to salvage the greatest amount of myocardium.
Compared with medical therapy alone, if performed promptly, coronary reperfusion (PCI or thrombolytic therapy) improves outcomes in nearly all groups of patients with acute STEMI.
A 70-year-old woman is hospitalized for an ST-elevation myocardial infarction involving the anterior wall. Her symptoms initially began 3 days before admission. The pain resolved spontaneously before she reached the hospital.
Two hours after presentation to the emergency department, she has acute onset of dyspnea and hypotension and requires emergent intubation. A portable chest radiograph shows cardiomegaly and pulmonary edema. Vasopressor therapy is initiated to support her blood pressure.
On physical examination, blood pressure is 90/60 mm Hg, pulse rate is 120/min, and respiration rate is 12/min. She has a grade 4/6 harsh holosystolic murmur at the right and left sternal borders associated with a palpable thrill. No S3 or S4 is heard. Crackles are heard bilaterally at the lung bases.
Which of the following is the most likely diagnosis?
A postinfarction ventricular septal defect (VSD) is the most likely cause of this patient’s symptoms. She initially presented with a delayed anterior wall ST-elevation myocardial infarction (STEMI). She then had acute respiratory distress and was found to have a new holosystolic murmur at the left sternal border on physical examination. These findings could be consistent with either a VSD or acute ischemic mitral regurgitation. However, given the location of the murmur and its association with a thrill, a VSD is more likely. With a postinfarction VSD, shunting of oxygenated blood from the left ventricle to the right ventricle occurs. This acute volume overload to the right ventricle results in cardiogenic shock and is rapidly fatal unless emergent surgical or possibly percutaneous intervention can be performed.
An acute aortic dissection associated with a myocardial infarction is more commonly associated with an inferior wall STEMI. Findings on physical examination may include asymmetric blood pressures and an early diastolic murmur of acute aortic insufficiency.
Rupture of the left ventricular free wall presents as hemopericardium with electromechanical dissociation and death. Risk factors include elderly age, female sex, first myocardial infarction, and anterior location of the infarction. The patient’s loud holosystolic murmur and thrill are not compatible with a free wall rupture.
Physical examination findings of right ventricular infarction include hypotension, clear lung fields, and elevated jugular venous pulsations. It would be exceedingly unusual for a right ventricular infarction to develop in association with an anterior wall infarction.
Acute ischemic mitral regurgitation is another late complication of myocardial infarction and also presents with a new holosystolic murmur. Ischemia with subsequent rupture of a papillary muscle or chordae tendineae is the most likely cause of acute ischemic mitral regurgitation and may result in a “flail” mitral valve. Echocardiography can accurately distinguish acute ischemic mitral regurgitation from a postinfarction VSD.
A 64-year-old man is evaluated in the emergency department because of chest pain. He describes the chest pain as nonradiating pressure in the midchest that began at rest 1 hour ago and is not associated with any symptoms. Medical history is remarkable for hypertension, type 2 diabetes mellitus, hyperlipidemia, and a 20-pack-year history of smoking. Medications are hydrochlorothiazide, metformin, and simvastatin.
On physical examination, he is afebrile, blood pressure is 140/80 mm Hg, pulse rate is 78/min, and respiration rate is 16/min. There is no jugular venous distention, the lungs are clear, and the findings on heart examination are normal.
Electrocardiogram shows a normal sinus rhythm and T-wave inversions in leads V2 through V6 without Q waves.
Initial cardiac biomarkers are within normal limits.
He is given aspirin, clopidogrel, low-molecular-weight heparin, and a nitrate, with resolution of his chest pain.
Which of the following is the most appropriate next step in management?
A β-blocker, such as metoprolol, should be added to this patient’s therapeutic regimen. He has acute-onset chest pain, normal cardiac biomarkers, and T-wave inversions shown on electrocardiogram. These findings are consistent with unstable angina. First-line therapies for patients with acute coronary syndromes, including unstable angina, include dual antiplatelet therapy with aspirin and a thienopyridine (e.g., clopidogrel, prasugrel, ticagrelor), a β-blocker, nitrates, and anticoagulation (e.g., heparin). Morphine may also be given in patients with active chest pain. These treatments attempt to minimize ischemia by addressing both the supply and demand of oxygen within myocardial cells.
When β-blockers are contraindicated for the treatment of unstable angina, as in a patient with severe bronchospastic lung disease that may be exacerbated by treatment, calcium channel blockers should be considered. However, the calcium channel blocker nifedipine causes an increase in heart rate and therefore myocardial oxygen demand and is contraindicated in patients with an acute coronary syndrome.
Reperfusion therapy, preferably with percutaneous coronary intervention or, alternatively, thrombolysis, is the mainstay of treatment for ST-elevation myocardial infarction. This patient has unstable angina based on his clinical presentation, findings on electrocardiogram, and normal cardiac biomarkers. Patients with unstable angina are usually treated initially with medical therapy, with further evaluation and treatment based on an assessment of the risk factors. Therefore, acute reperfusion therapy is not indicated in this patient.
A 54-year-old man is evaluated in the emergency department for an acute coronary syndrome that began 30 minutes ago. His medical history is significant for hypertension and type 2 diabetes mellitus. Medications are lisinopril and glipizide.
On physical examination, he is afebrile, blood pressure is 160/90 mm Hg, pulse rate is 80/min, and respiration rate is 12/min. Cardiovascular examination shows a normal S1 and S2 without an S3 and no murmurs. Lung fields are clear.
An initial serum troponin level is pending. Electrocardiogram shows 3-mm ST-segment elevation in leads V2 through V4 and a 1-mm ST-segment depression in leads II, III, and aVF.
Treatment is initiated with aspirin, clopridogrel, a β-blocker, and unfractionated heparin. His symptoms of chest pain improve.
Which of the following is the most appropriate next step in management?
This patient should undergo percutaneous coronary intervention (PCI). The electrocardiographic changes are consistent with acute anterior ST-elevation myocardial infarction (STEMI). Patients with STEMI who present within 12 hours of symptom onset should undergo either primary PCI or thrombolytic therapy. PCI is preferred because it is associated with a lower mortality rate compared with thrombolytic therapy. Ideally, it should be performed within 90 minutes of presentation to a facility with PCI capability or within 120 minutes if the patient requires transfer from a non–PCI-capable hospital. PCI also is indicated in patients with a contraindication to thrombolytic therapy and in patients with cardiogenic shock. PCI is most effective if completed within 12 hours of the onset of chest pain; the earlier the intervention, the better the outcome. Because this patient has no clear contraindication to PCI, this is the treatment of choice for STEMI.
Optimal management of patients with STEMI relies on timely recognition and rapid initiation of reperfusion therapy. Patients with an acute coronary syndrome and an electrocardiogram compatible with STEMI can be treated with reperfusion therapy without biomarker confirmation. Early biomarker results may be normal in patients with STEMI, and waiting for the results of the troponin level would delay appropriate treatment.
Medical therapy with further intervention based on risk stratification is indicated in patients with non–ST-elevation myocardial infarction or unstable angina, but would not be appropriate in this patient with STEMI.
A 77-year-old woman is admitted to the hospital for intermittent dizziness over the last few days. She reports no chest discomfort, dyspnea, palpitations, syncope, orthopnea, or edema. She underwent coronary artery bypass graft surgery 6 years ago after a myocardial infarction. She has hypertension and hyperlipidemia. Medications are hydrochlorothiazide, pravastatin, lisinopril, and aspirin.
On physical examination, blood pressure is 137/88 mm Hg and pulse rate is 52/min. The lungs are clear to auscultation. Cardiac auscultation shows bradycardia with regular S1 and S2 as well as an S4. A grade 2/6 early systolic murmur is heard at the left upper sternal border. Edema is not present.
On telemetry, she has sinus bradycardia with rates between 40/min and 50/min, with two symptomatic sinus pauses of 3 to 5 seconds each.
Which of the following is the most likely cause of this patient’s dizziness?
This patient has symptomatic sick sinus syndrome (SSS) because her episodes of sinus bradycardia are correlated with dizziness. SSS comprises a collection of pathologic findings that result in bradycardia. These include sinus arrest, sinus exit block, and sinus bradycardia. SSS is common in the elderly, and because symptoms can be intermittent or nonspecific, misdiagnosis can occur.
Because there is no dissociation between atrial depolarization and conduction to the ventricles on telemetry, the patient does not have complete heart block (third-degree heart block).
Complete heart block (third-degree heart block) is characterized by complete absence of conduction from the atria to the ventricles; the P waves and the QRS complexes are completely independent of each other. This patient’s P waves are followed by QRS complexes, and the pauses result from failure of the sinus node to fire (no P waves) and not from a failure of conduction from the atria to the ventricles.
The presence of P waves on telemetry excludes the diagnosis of atrial fibrillation, and the combination of conducted P waves and a narrow QRS complex makes nonsustained ventricular tachycardia unlikely.
A 73-year-old woman is evaluated during a routine examination. She has no symptoms and feels well. Her medications are levothyroxine for hypothyroidism and hydrochlorothiazide for hypertension. An electrocardiogram performed 2 years ago was normal.
On physical examination, heart rate is 42/min and regular. The remainder of the examination is normal. The thyroid-stimulating hormone level is normal. An electrocardiogram obtained as part of the current evaluation is shown :.
Which of the following diagnoses is confirmed by the electrocardiogram?
Third-degree atrioventricular block, or complete heart block, refers to a lack of atrioventricular conduction (characterized by lack of conduction of all atrial impulses to the ventricles), as seen in this patient’s electrocardiogram. This is an important diagnosis to make because pacemaker implantation may improve survival for patients with asymptomatic complete heart block; therefore, all patients with complete heart block should be treated with pacemaker implantation.
First-degree atrioventricular block is recognized electrocardiographically as a prolongation of the P-R interval; all P waves are conducted, and this condition requires no specific treatment. Second-degree atrioventricular block is characterized by intermittent nonconduction of P waves and subsequent “dropped” ventricular beats. Second-degree atrioventricular block is divided into two types, Mobitz type I and Mobitz type II. Mobitz type I second-degree atrioventricular block is characterized by progressive prolongation of the P-R interval until a dropped beat occurs. This type of heart block is characteristically transient and usually requires no specific treatment. Mobitz type II second-degree atrioventricular block is characterized by a regularly dropped beat (e.g., a nonconducted P wave every second or third beat), without progressive prolongation of the P-R interval. It is usually associated with evidence of additional disease in the conduction system, such as bundle branch block or bifascicular or trifascicular block. Mobitz type II atrioventricular block suddenly and unpredictably progresses to complete heart block and is usually treated with a pacemaker.
A 73-year-old man is evaluated in the emergency department for chest pressure with radiation to the arm, diaphoresis, and lightheadedness of 4 hours’ duration. His medical history includes a 20-year history of hypertension and type 2 diabetes mellitus. Medications are metformin, atenolol, and aspirin.
On physical examination, the patient is afebrile, blood pressure is 130/84 mm Hg in both arms, and pulse rate is 87/min and regular. The jugular vein is distended to 5 cm while the patient is upright. He has a faint left carotid bruit, bibasilar crackles to one-quarter up from the pulmonary bases, normal S1 and S2, and an S4 and an S3 with a grade 2/6 holosystolic murmur that is heard best at the apex to the axilla. Pulses are symmetric. The chest radiograph is consistent with heart failure. The electrocardiogram is shown :. An electrocardiogram obtained 6 months ago was normal. The initial serum troponin measurement is elevated.
Which of the following is the most likely diagnosis?
This patient is having an acute myocardial infarction manifesting as a new left bundle branch block on electrocardiogram and complicated by ischemic mitral regurgitation and heart failure. Electrocardiographically, left bundle branch block is associated with absent Q waves in leads I, aVL, and V6; a large, wide, and positive R wave in leads I, aVL, and V6; and prolongation of the QRS complex to greater than 0.12 seconds. Repolarization abnormalities are present and consist of ST-segment and T wave vectors directed opposite to the QRS complex. The presentation of acute coronary syndrome with new left bundle branch block should be considered equivalent to ST-elevation myocardial infarction and is an indication for acute reperfusion therapy. The diagnosis of acute aortic dissection should be considered in this patient, but the findings of symmetric blood pressures and pulse rates and normal mediastinum on chest radiograph are reassuring. Aortic dissection chest pain is often described as ripping and tends to radiate to the back. Although chest pain, left bundle branch block, mitral regurgitation, and heart failure may all be complications of endocarditis, the acute onset of this patient’s symptoms and the fact that he is afebrile make this diagnosis much less likely than acute myocardial infarction. Pericarditis also generally has a more subacute presentation, and typical electrocardiographic findings include diffuse PR depressions or ST-segment elevations and not new left bundle branch block.
A 67-year-old man is evaluated because of a 10-day history of lightheadedness and increasing frequency of chest pain and palpitations for the last 3 days. He denies syncope. The medical history is significant for coronary artery disease and difficult-to-control hypertension. Medications are aspirin, nitroglycerin, atenolol, hydrochlorothiazide, and sustained release diltiazem.
On physical examination, blood pressure is 156/72 mm Hg; pulse rate is 60/min, with occasional irregularity; and respiration rate is 16/min. Jugular venous pressure is normal. The lungs are clear to auscultation. Cardiac examination shows a physiologically split S2, an S4, and no S3. There is a grade 2/6 systolic murmur that is best heard in the second right intercostal space. The remainder of the physical examination is unremarkable.
The patient’s electrocardiogram is shown :.
Which of the following is the electrocardiographic diagnosis?
This patient has second-degree atrioventricular block, diagnosed by the presence of isolated P waves that are not followed by a QRS complex. Second-degree atrioventricular block is divided into two types, Mobitz type I and Mobitz type II. This patient has second-degree atrioventricular block, Mobitz type I (Wenckebach), with progressive prolongation of the PR interval until the “dropped” beat. Additionally, in a Mobitz type I rhythm, the PP interval is constant but the PR interval decreases progressively until the dropped beat occurs. This patient’s rhythm is most likely caused by the combination of atenolol and diltiazem, both of which can decrease conduction within the atrioventricular node. Mobitz type II atrioventricular block is much less common. It is usually associated with a right or left bundle branch block pattern, and the dropped beat is associated with an intermittent block of the remaining bundle branch, which indicates significant conduction system disease. A pacemaker is commonly required. In Mobitz type II atrioventricular block, the PR interval is constant in the conducted beats and the RR interval containing the nonconducted (dropped) beat is equal to two PP intervals.
First-degree atrioventricular block is characterized by a prolonged PR interval of more than 0.2 seconds. Complete heart block (third-degree atrioventricular block) is characterized by complete absence of conduction from the atria to the ventricles; the P waves and the QRS complexes are completely independent of each other. Careful analysis shows that the P wave rate and the QRS complex rate are different and that the PR interval is different for every QRS complex.
A 32-year-old woman is evaluated in the emergency department because of intermittent palpitations and dizziness for the last week. She has not experienced chest pain, dyspnea, or orthopnea. She was ill 6 weeks ago with fever, fatigue and myalgias, and an associated erythematous rash on her abdomen that resolved over 2 weeks. She has no significant medical history. She works as a landscaper.
On physical examination, temperature is normal, blood pressure is 120/70 mm Hg, and pulse rate is 45/min. The cardiac examination shows bradycardia, but findings are otherwise unremarkable. The remainder of the physical examination is normal.
An electrocardiogram shows sinus rhythm with a heart rate of 90/min, with complete heart block and a junctional escape rate of 50/min.
In addition to hospitalization for cardiac monitoring, which of the following is the most appropriate management for this patient?
This patient should be treated with intravenous ceftriaxone. She most likely has Lyme carditis manifested by acute-onset, high-grade atrioventricular conduction defects that occasionally may be associated with myocarditis. Carditis occurs in 5% to 10% of patients with Lyme disease, usually within a few weeks to months after infection. Atrioventricular block can present in any degree, and progression to complete heart block is often rapid. The prognosis is good, usually with resolution of atrioventricular block within days to weeks. The presence of the characteristic skin rash, erythema migrans, with or without a history of tick bite in an endemic region, has a greater than 80% probability of being caused by Borrelia burgdorferi infection and is sufficient to support a decision to treat Lyme disease empirically without laboratory confirmation of the diagnosis. The preferred antibiotic regimen is intravenous ceftriaxone until the heart block resolves, followed by a 21-day course of oral therapy.
An electrophysiology study is not indicated because it would not provide additional prognostic information. Atrioventricular block is usually within the node, but sinoatrial and His-Purkinje involvement has also been described.
Most cases of Lyme carditis resolve spontaneously, and neither temporary nor permanent pacemaker therapy is needed. Temporary pacing would be required if the patient were hemodynamically unstable with bradycardia. However, this rarely occurs in the setting of Lyme carditis. Indications for permanent pacemaker placement would include persistent high-grade atrioventricular block.
A 62-year-old man is evaluated in the emergency department for a 2-day history of dyspnea and palpitations. His other medical problems include a 10-year history of hypertension and diabetes mellitus. Medications are lisinopril and metformin.
On physical examination, temperature is 37.0°C (98.6°F), blood pressure is 130/86 mm Hg, pulse rate is 132/min, respiration rate is 18/min, and oxygen saturation is 94% on ambient air. Cardiac examination shows a rapid heart rate but no other abnormalities.
Electrocardiogram is shown :.
Which of the following is the most appropriate treatment?
The most appropriate treatment for the patient is diltiazem given intravenously. He has atrial fibrillation with a rapid ventricular response. Atrial fibrillation is caused by rapid and uncoordinated electrical activation within the atria. The electrocardiogram shows an absence of P waves and an irregular ventricular response. Approximately 50% of episodes of atrial fibrillation convert to a normal rhythm spontaneously.
If the patient is symptomatic but hemodynamically stable, the initial goal is to reduce the heart rate to 60/min to 110/min with a rate control agent. Intravenous options include diltiazem, verapamil, metoprolol, and esmolol. Digoxin can be used as a second agent, especially in patients with heart failure or systolic dysfunction, but peak effect can take up to 6 hours. In those with rapid atrial fibrillation with minimal or mild symptoms, oral agents may be used.
Adenosine is an intravenous agent that transiently blocks atrioventricular nodal conduction; it is effective at terminating supraventricular tachycardia where the electrical circuit is dependent on the atrioventricular node. Intravenous adenosine may be used to break the reentrant rhythm in atrioventricular nodal reentrant tachycardia, or orthodromic atrioventricular reciprocating tachycardia. However, it is not an effective therapy for atrial fibrillation.
Patients with adverse or marginal hemodynamic status or acute coronary ischemia because of a rapid ventricular response should undergo immediate cardioversion. Cardioversion is also the treatment of choice for patients with wide complex tachycardia. This patient is hemodynamically stable, and immediate electrical cardioversion is not necessary.
A 36-year-old woman is evaluated in the emergency department for an episode of chest pain, palpitations, and lightheadedness. The symptoms persisted for 1 hour and ceased shortly after she arrived at the hospital. She has no history of cardiac disease, but has a 6-month history of hypertension that is controlled with chlorthalidone 25 mg daily. She has occasional brief episodes of rapid palpitations provoked by exertion. She does not have exercise intolerance or exertional chest discomfort.
On physical examination, blood pressure is 154/94 mm Hg, without orthostatic change. Pulse rate is 60/min and regular. Findings on physical examination are remarkable only for a paradoxically split S2. The patient’s electrocardiogram is shown :.
Which of the following best describes the electrocardiographic finding for this patient?
The electrocardiogram is diagnostic for ventricular preexcitation by an accessory atrioventricular connection, with a short P-R interval, prolonged QRS duration, and slurred onset of the QRS (delta wave) interval. With paroxysmal tachyarrhythmias, this pattern is diagnostic for Wolff-Parkinson-White syndrome and accounts for the paradoxically split S2. In a symptomatic patient with recurrent palpitations or syncope, radiofrequency ablation of the accessory pathway is likely to provide the most definitive improvement.
The electrocardiogram does not show atrial fibrillation because it shows clearly discernible P waves and a regular rhythm. First-degree atrioventricular block is associated with a P-R interval of more than 0.20 seconds, not a shortened interval (<0.11 seconds), as seen in this case.
A 71-year-old man is evaluated in the clinic for symptoms of palpitations, shortness of breath, and decreased exercise tolerance for the last 2 days. His medical history is significant for hypertension. His only medication is lisinopril.
On physical examination, blood pressure is 115/62 mm Hg and pulse rate is 152/min. The lungs are clear. Cardiac examination is significant for tachycardia, but no extra heart sounds or murmurs are noted.
The electrocardiogram is shown :.
Which of the following is the most likely cause of this patient’s symptoms?
The electrocardiogram shows atrial flutter, which is the likely cause of the patient’s clinical symptoms. Atrial flutter is a rapid, regular atrial rhythm that appears as a “saw-tooth” pattern on an electrocardiogram, often best seen in the inferior leads. The atrial rate is characteristically approximately 300/min, with atrioventricular conduction occurring once every two flutter waves (2:1 atrioventricular conduction), a very typical pattern for atrial flutter.
Atrial fibrillation is more disorganized atrial activity at a rate of 350 to 600/min, with no discernible P waves. It is characteristically associated with an irregularly irregular rhythm, and the fibrillatory waves vary in amplitude, morphologic pattern, and interval, creating a rough, irregular baseline between QRS complexes. Multifocal atrial tachycardia is defined by the electrocardiographic finding of discrete P waves with at least three morphologic patterns with varying P-P, P-R, and R-R intervals. The morphologic features of P waves are generally best seen in leads II, III, and V1. In adults, multifocal atrial tachycardia is often associated with other disorders, often hypoxic chronic obstructive pulmonary disease or electrolyte abnormalities. Sinus tachycardia is a sinus rhythm with a ventricular rate greater than 100/min. The P waves have normal morphologic features but can become difficult to see with heart rates greater than 140/min because the P waves begin to merge with the preceding T waves. Slowing the heart rate with carotid sinus massage often shows the hidden P waves and establishes the diagnosis.
A 68-year-old man is evaluated in the emergency department for shortness of breath and palpitations that have worsened over the last 3 days. His medical history is significant for chronic obstructive pulmonary disease. He has a 50-pack-year smoking history and continues to smoke 1 pack of cigarettes daily. His medications include tiotropium and albuterol metered-dose inhalers.
On physical examination, temperature is 37.8°C (100°F) and pulse rate is 122/min. Oxygen saturation on ambient air is 89%. The patient is in moderate respiratory distress. Chest examination shows decreased airflow with diffuse expiratory wheezing. Cardiac examination shows distant heart sounds and an irregular rate with a loud S2 and no murmurs.
Laboratory studies show normal electrolytes. The electrocardiogram is shown :.
Which of the following is the most likely electrocardiographic diagnosis?
The electrocardiogram shows multifocal atrial tachycardia (MAT). MAT is most commonly seen in acutely ill patients, most often in the setting of pulmonary disease (such as the exacerbation of chronic obstructive pulmonary disease with associated hypoxia in this patient) and electrolyte abnormalities. The electrocardiogram in MAT is defined by the presence of discrete P waves with at least three different morphologic patterns with varying P-P, P-R, and R-R intervals. The morphologic features of P waves are generally best seen in leads II, III, and V1. Therapy is directed at the underlying disease process because without treatment the arrhythmia is often refractory to therapy or may recur. In this patient, treatment should be directed toward the pulmonary disease and correction of electrolyte imbalances, especially magnesium. Therefore, the treatment of choice in this patient is oxygen, inhaled bronchodilators, antibiotics, and corticosteroids. Electrolyte levels should be corrected, and the heart rate may be controlled as needed by atrioventricular blocking agents.
Atrial fibrillation is characterized by disordered atrial electrical activity that leads to an irregular heart rate similar to MAT; however, P waves are not detectable, as in this patient’s electrocardiogram. In atrioventricular nodal reentrant tachycardia, the atria and ventricles are activated simultaneously from a reentrant circuit within the atrioventricular node. The QRS complex is narrow, and no P waves are seen. Atrioventricular reciprocating tachycardia is a bypass tract–mediated reentrant tachycardia in which the anterograde conduction (atrium-to-ventricle) is typically via the atrioventricular node and retrograde conduction is via the bypass tract. Because bypass tract conduction is typically faster than conduction via the atrioventricular node, atrial activation occurs rapidly after the QRS complex, resulting in a “short R-P” tachycardia, and the P wave is usually located within the ST segment. Both atrioventricular reciprocating tachycardia and atrioventricular nodal reentrant tachycardia are regular rhythms.
A 54-year-old man is evaluated in the emergency department because of a 2-hour history of palpitations. He reports no syncope, presyncope, chest pain, or shortness of breath. He has had no previous episodes of palpitations. Medical history is significant for nonischemic cardiomyopathy. The ejection fraction was most recently measured at 38%. Medications are carvedilol and candesartan.
On physical examination, the patient is afebrile, blood pressure is 125/86 mm Hg, and pulse rate is 110/min. Cardiac evaluation shows a regular rate and rhythm. The remainder of the findings on physical examination are unremarkable.
The electrocardiogram is shown :.
The most appropriate treatment for this patient is amiodarone. The electrocardiogram shows : a regular, monomorphic wide-complex tachycardia. Although it is possible that the patient has supraventricular tachycardia with aberrancy or antidromic atrioventricular reciprocating tachycardia, in a patient with wide-complex tachycardia and a history of coronary artery disease or cardiomyopathy, ventricular tachycardia is the assumed diagnosis. Hemodynamic stability does not exclude a diagnosis of ventricular tachycardia. The first-line treatment for a hemodynamically stable ventricular tachycardia is an intravenous antiarrhythmic agent such as amiodarone. Procainamide and sotalol are also acceptable agents, and lidocaine can be used as a second-line agent.
Immediate cardioversion is not necessary because this patient does not have signs of instability. If an antiarrhythmic agent is not successful, then elective cardioversion with sedation can restore normal rhythm.
Adenosine may be given for a stable wide-complex rhythm to determine whether it is a supraventricular tachycardia with aberrant conduction or an antidromic atrioventricular reciprocating tachycardia. However, because of the patient’s high risk of ventricular tachycardia given his known coronary artery disease, this would not be the most appropriate initial intervention.
The administration of verapamil or β-blockers is not indicated in patients with stable ventricular tachycardia. These drugs can cause severe hemodynamic deterioration and lead to ventricular fibrillation and cardiac arrest.
This patient should be offered an implanted cardioverter-defibrillator for long-term prevention of sudden cardiac death.
A 55-year-old man is evaluated because of a 2-month history of dyspnea on exertion without chest pain. Medical history is significant for type 2 diabetes mellitus, hypertension, and hyperlipidemia. He has a 30-pack-year smoking history but does not currently use tobacco products. Medications are metformin, lisinopril, pravastatin, and aspirin.
On physical examination, blood pressure is 110/75 mm Hg and pulse rate is 60/min. Jugular venous distention is noted, and trace lower extremity edema is present. The point of maximal impulse is normal in size and location. Cardiac examination shows regular rate and rhythm, and the chest is clear to auscultation.
Electrocardiogram is shown :. Echocardiogram shows inferior wall hypokinesis and ejection fraction of 35%.
Which of the following is the most appropriate diagnostic test to perform next?
Coronary angiography is indicated to evaluate coronary artery disease (CAD) as a cause of newly diagnosed left ventricular systolic dysfunction. The patient has diabetes mellitus, which is a risk factor for CAD, and evidence of a previous inferior wall myocardial infarction on electrocardiogram (Q waves in leads II, III, and aVF). Indications for coronary angiography for evaluation of new-onset heart failure include angina or new-onset left ventricular dysfunction in the setting of a condition, such as diabetes, that may predispose to silent ischemia. Because revascularization may improve left ventricular function, some experts recommend a low threshold for evaluation for CAD.
Noninvasive stress testing, such as with an adenosine thallium test or a dobutamine echocardiographic stress test, would likely suggest CAD in this patient. However, given the relatively high pretest probability, a noninvasive stress test would not change that probability. The more relevant issue is whether the coronary anatomy is amenable to revascularization, which could improve function. Therefore, coronary angiography is the most appropriate diagnostic test.
Cardiac magnetic resonance imaging is useful for evaluating possible infiltrative or inflammatory cardiomyopathy. Given the significant evidence of CAD in this patient, the likelihood of an infiltrative or inflammatory cardiomyopathy is very low, and cardiac magnetic resonance imaging would not be an appropriate first diagnostic test.
Although this patient has some limiting symptoms (dyspnea on exertion) and a history of smoking, he has clinical evidence of heart failure. Pulmonary function testing would not aid in assessing the cause of new-onset heart failure nor would it be useful in diagnosing potential CAD.
A 46-year-old man is evaluated in the emergency department because of acute onset of severe chest and back pain 1 hour ago. The pain has been unremitting. Medical history is significant for a bicuspid aortic valve that was detected in adolescence because of a murmur and also for hypertension. His only medication is valsartan.
On physical examination, the patient is conscious and in pain. He is afebrile, blood pressure is 90/50 mm Hg, pulse rate is 118/min and regular, and respiration rate is 18/min.
Pulse rate and blood pressure are equal in both arms. Heart sounds are distant, regular, and rapid. A very faint early diastolic murmur is heard at the right upper sternal border. Estimated central venous pressure is 12 cm H2O.
Electrocardiogram indicates sinus tachycardia. A chest computed tomographic scan with intravenous contrast is shown :.
Which of the following is the most appropriate next step in management?
The computed tomographic scan with intravenous contrast shows : a dissection plane (arrows) extending from the proximal aorta through the arch (AA) and into the descending aorta (DAo). This is a Stanford type A dissection (involving the ascending aorta), which requires emergency surgical intervention.
The patient has a long-standing history of a murmur associated with a documented bicuspid aortic valve. The most frequent cardiovascular finding associated with a bicuspid valve is dilation of the proximal ascending aorta, which is related to abnormalities of the aortic media. These changes in the aortic media are independent of the degree of functional stenosis of the valve and increase the risk of aneurysm formation and aortic dissection.
Abrupt onset of severe chest and back pain is typical of an acute aortic syndrome. A diastolic murmur consistent with aortic valvular insufficiency increases the clinical suspicion for a proximal aortic dissection that has disrupted normal valve function. Although marked asymmetry in upper extremity pulses and pressures are classic findings in aortic dissection, in many cases, these features may not be present. Syncope occurs in approximately 10% of patients with an acute aortic dissection and is more commonly associated with proximal dissection. Syncope is associated with a higher coincidence of pericardial tamponade and worse in-hospital survival rates.
Further diagnostic imaging with coronary angiography, magnetic resonance imaging, or transesophageal echocardiography is not necessary and would only delay necessary surgical repair.
There is no accepted role for endovascular treatment of an acute Stanford type A aortic dissection.
A 27-year-old woman is evaluated during a follow-up visit for high blood pressure that was diagnosed 4 months after she began taking an oral contraceptive pill. She has stopped using the oral contraceptive pill, but her blood pressure has remained high. She feels well and takes no medications. Medical history is otherwise unremarkable.
On physical examination, blood pressure is 166/108 mm Hg and the heart rate is 76/min. No orthostasis is present and the other vital signs are normal. There is a bruit noted in the right epigastric region. The remainder of the examination is unremarkable.
Kidney function is normal, and urinalysis is unremarkable.
A Doppler ultrasound study shows evidence of stenosis of the right renal artery. A kidney angiogram is shown :.
Percutaneous transluminal kidney angioplasty is indicated for this patient with renovascular hypertension secondary to fibromuscular dysplasia, a nonatherosclerotic, noninflammatory renovascular disease. Renovascular hypertension as a result of fibromuscular dysplasia is most commonly caused by medial fibroplasia of the renal artery. On angiogram, the characteristic finding of fibromuscular dysplasia is the “string of beads” appearance of the involved artery, which is apparent on this patient’s angiogram. Fibromuscular dysplasia is a disease of unknown cause and usually involves the renal and carotid arteries. Hypertension caused by fibromuscular dysplasia is more common in women and usually affects patients between 15 and 30 years of age. Catheter-based kidney angiography is the most accurate method to diagnose this condition; revascularization with kidney angioplasty may be performed at the same time as diagnostic angiography. The young age of many patients with fibromuscular dysplasia, such as this 27-year-old woman, reduces the risk of complications from this procedure.
The high likelihood of both technical success and meaningful blood pressure improvement as a result of kidney angioplasty makes drug therapy in this young patient unnecessary at this time.
Surgical revascularization is not the first-line treatment for this patient, given the higher risk of morbidity. Surgery should be reserved for patients who do not respond to kidney angioplasty or who have arterial anatomy that is too complex for kidney angioplasty.
