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Aortic dissection is caused by a tear in the inner layer of the aorta, which allows blood to enter the wall and travel in a “false lumen”. Chest x-ray findings consistent with aortic dissection include a widened mediastinum, obscuration of aortic knob, presence of apical cap, lateral displacement of the trachea and depression of the left mainstem bronchus. ECG findings are variable and may depict an ST-Elevation myocardial infarction (MI) if a proximal dissection dissects into the coronary arteries. This is a rare entity that usually involves the right coronary artery, causing an inferior or posterior MI. This particular case is concerning for an ascending thoracic aortic dissection, whose treatment is surgical. However, while waiting for cardiothoracic surgical consult and radiographic imaging studies, acute control of the heart rate and blood pressure is imperative to minimize aortic wall stress and shearing. Initial acute treatment consists of an intravenous beta blocker to reduce the heart rate below 60 beats/min – while propranolol, labetalol, and esmolol can be used, esmolol has the advantage of a short half-life and use in patients with relative contraindications to beta-blockers (asthma, CHF). If systolic blood pressure remains >100mmHg despite beta-blockade, nitroprusside is classically recommended, although several other anti-hypertensive intravenous medications may be used.

The patient in the question stem has exertional syncope related to his severe aortic stenosis, characterized by his narrow pulse pressure, harsh systolic murmur, and findings of left bundle branch block on EKG. Syncope is a poor prognostic indicator for patients with aortic stenosis, and they require urgent surgical management. Patients with severe aortic stenosis causing syncope have a mortality rate approached 50% within 3 years if left untreated; therefore surgical consultation is neccessary prior to discharge. Although the patient is presenting with new left bundle branch block potentially representing acute coronary syndrome, he has absence of chest pain and thus would not be the best answer choice.

This patient is presenting with symptoms concerning for acute aortic dissection.  Patients with aortic dissection (specifically type A) can show ST elevations most commonly in the inferior leads due to involvement of the right coronary artery. In addition to cardiothoracic surgery consult, treatment of aortic dissection usually involves esmolol and nitroprusside; however, labetolol can be used in isolation. The most important treatment principle is to reduce the heart rate and then lower the blood pressure. Rate reduction is important in order to reduce shear stress on the aortic wall. As a beta blocker esmolol is effective in reducing the heart rate as it is easily titratable secondary to a short half-life. Nitroprusside is preferred to nitroglycerin as it is a more potent reducer of blood pressure, and it decreases afterload. Nitroprusside should not be used in isolation as it may increase the rate of rise of aortic wall pressure by increasing shearing forces. Reflex tachycardia may also result secondary to peripheral vasodilation increasing cardiac output.

Aortic dissection is commonly seen in patients with long-term hypertension and connective tissue disorders, but can also be seen in pregnancy, coarctation of the aorta and a bicuspid aortic valve. Ascending aortic dissection is most common in the 50- to 60-year age range, whereas descending dissections occur more commonly in older individuals. Anatomic classification of aortic dissection is important for diagnosis and treatment. The Stanford classification system divides dissections into two types: A and B. Type A dissections involve the ascending aorta and Type B dissections involve the descending aorta. Type A dissections are more lethal, more common and require prompt surgical intervention. Commonly, Type A dissections often present with normotensive or hypotensive vitals, while Type B are hypertensive. The hypotension in Type A is usually due to cardiac tamponade, aortic rupture, or heart failure associated with severe aortic regurgitation. Pulse deficits are present only in 19% of Type A dissection and 9% of Type B dissection. Aortic regurgitation murmurs are present in 44% of Type A dissections and 12% of Type B dissections, according to the IRAAD registry (International Registry of Acute Aortic Dissection). While Type B dissections are typically treated medically, acute Type A ascending aortic dissections should be treated as a surgical emergency, given that these patients are at high risk for a life-threatening complications (e.g. aortic regurgitation, tamponade, and myocardial infarction) and high mortality rates for delayed repairs.

All of the answer choices are sites that aortic aneurysms may rupture into, but aortic aneurysms most commonly rupture into the retroperitoneum. The most rapidly fatal location is the intraperitoneum. Less common sites of rupture include the gastrointestinal tract and the inferior vena cava.

The most common factor predicting the risk of rupture is the size of the aneurysm. Aneurysms occur when a segment of the aorta is weakened, and the larger the aneurysm, the greater tension exerted on the wall. Most ruptured aneurysms are greater than 5cm. There is a high incidence of aneurysms in patients with atherosclerotic disease and men older than 65 years of age. Other risk factors include history of smoking, hypertension, and family history of abdominal aortic aneurysm.

Nicardipine and nitroprusside are effective parenteral drugs for acutely lowering blood pressure. They both reliably and quickly decrease blood pressure. The main disadvantage for nitroprusside is the cyanide byproduct, while for nicardipine is its longer half-life (more difficult to rapidly titrate).

This patient presents with asymptomatic hypertension in the setting of medical non-compliance and should berestarted on his medications and scheduled for follow up with a primary care physician. Accelerated hypertension is defined as markedly elevated blood pressure in the absence of symptoms. This is in contrast with hypertensive emergency where the patient has symptoms or evidence of end organ system dysfunction or both as a result of elevated blood pressure. Accelerated hypertension has a poor long-term prognosis if not controlled but does not pose an immediate threat. As such, it should not be aggressively treated with parenteral medications. Rapid lowering of blood pressure in patients with chronic elevated blood pressure can cause organ hypoperfusion, particularly brain hypoperfusion, and lead to serious sequelae. These patients should be restarted on their medications (if appropriate) and sent for follow up with a primary care physician to monitor and treat the elevated blood pressure.

The most common forms of end-organ damage in hypertensive emergencies, in order of decreasing frequency, are (1) cerebral infarction or hemorrhage; (2) acute pulmonary edema; (3) hypertensive encephalopathy; (3) acute CHF; and (4) aortic dissection. Preeclampsia is another hypertensive state associated with very high BP, but unique goals and treatment options are associated with this condition.

Hypertensive encephalopathy describes reversible cerebral disorders associated with high BP in the absence of cerebral thrombosis or hemorrhage. The theoretical mechanism of hypertensive encephalopathy is a rapid rise in BP that overwhelms the autoregulatory mechanisms of the brain and leads to blood-brain barrier permeability and brain edema. The symptoms of hypertensive encephalopathy can include headache, seizures, visual disturbances, nausea, and vomiting. The diagnosis must be made only after other potential hypertensive emergencies are excluded. A PubMed search for clinical trials, meta-analyses, and randomized controlled trials of hypertensive encephalopathy yielded 22 articles. None of the trials dealt directly with treatment or prognosis, and no studies suggested which agent is best for short-term reduction of BP in hypertensive encephalopathy. However, nitroprusside should be avoided in patients with this disorder, as the drug has been shown to decrease systemic pressure while preserving intracranial perfusion pressures. In the absence of data, the consensus goal of treatment is often stated as a 20% to 25% reduction in mean arterial pressure or a DBP of 100 to 110 mg Hg.

Hypertrophic obstructive cardiomyopathy (HOCM) is a genetic primary cardiomyopathy that is the second most common cause of sudden cardiac death in adolescents. It is the leading cause of sudden cardiac death in athletes. It involves asymmetric interventricular septal hypertrophy that causes reduced filling of the left ventricle and diastolic dysfunction. The most frequent initial complaint is dyspnea on exertion, but other symptoms include chest pain, palpitations, and syncope. Syncope usually occurs during or immediately after exercise. Exam findings include an S4 heart sound and a systolic ejection murmur that is intensified with standing up and performing a Valsalva maneuver. Maneuvers that decreased the murmur include hand grip, passive leg raise, and squatting. Diagnosis is ultimately made with echocardiography or cardiac MRI, along with genetic testing. Hospitalization is indicated for patients presenting for syncope who are suspected to have HOCM, as these patients are at significant risk for sudden cardiac death. Beta-blockers are the treatment of choice in patients with HOCM who have chest pain.

The optimal rate for chest compressions is at least 100 compressions/minute. In order to have return of spontaneous circulation (ROSC), patients must have high-quality CPR started early and early defibrillation when indicated. High-quality CPR historically was underappreciated but recent research has brought it to the forefront of care. In addition to an appropriate compression rate of 100 per minute, compression depth of > 5 cm and minimum pauses for CPR must be maintained. Additionally, hyperventilation and resultant hypocarbia is detrimental. A ratio of 30 compressions to 2 ventilations is currently recommended. Compressions should not be held during attempted intubation. Epinephrine should be administered every 3-5 minutes. Rhythm checks should not be performed after shock delivery.

A number of viruses cause myocarditis including adenoviruses, parvovirus 19 and human herpesvirus 6. Cytomegalovirus (CMV) is a common cause in patients with cardiac transplant. Myocarditis occurs via three pathophysiological processes: necrosis from direct invasion of an infectious agent, destruction of myocytes from infiltration of components from the host immune response, and toxic effects of exogenous or endogenous chemicals produced by a pathogen. The pathophysiological process depends on the etiologic agent. In patients with cardiac transplants, CMV and toxoplasmosis gondii are common agents. Patients with myocarditis present with nonspecific symptoms including fever, fatigue, malaise and diarrhea. Dyspnea is the most common presenting complaint in children and is frequently seen in adults as well. Tachycardia out of proportion to temperature elevation should raise concerns for myocarditis. Diagnostically, ECG can have a number of changes including sinus tachycardia, wide QRS complex, prolonged QT interval or ST elevations. Definitive diagnosis is made by endocardial biopsy (MRI is slowly replacing biopsy as the disease can be patchy and biopsy can fail to make the diagnosis).

When fluid accumulates in the pericardial space rapidly (e.g., within minutes), hemodynamic compromise usually occurs. Patients experience hypotension, tachycardia, and shortness of breath. This is pericardial tamponade. Normally the pericardial elasticity can accommodate slow accumulations of fluid from conditions such as pericarditis, radiation therapy, uremia, or malignancy. When the elasticity of the pericardium is overwhelmed due to rapid fluid accumulation within the pericardial space, the right atrium and ventricles begin to be compressed. This leads to decreased end diastolic volumes in the right heart and ultimately hypotension. The decreased preload creates proximal venous engorgement and is demonstrated clinically as jugular venous distension. Patients may also have distended facial or scalp veins. Other clinical findings of pericardial tamponade include muffled heart sounds, a narrow pulse pressure, pulsus paradoxus (decreased systolic blood pressure with inspiration due to increased intrathoracic pressure causing decreased venous return), and respiratory distress. Electrocardiographic findings may include low voltage or electrical alternans (alternating high and low QRS voltage due to the heart swinging in the pericardium full of fluid). Bedside ultrasound is diagnostic and demonstrates anechoic (black) fluid between the hyperechoic pericardium and the myocardium. Right atrial or right ventricular collapse during diastole, leftward septal shifting during inspiration, and a swinging heart may be seen on ultrasound. Pericardiocentesis is the management of choice for pericardial tamponade.

The treatment of pulseless electrical activity (PEA) begins with initiation of advanced cardiac life support (ACLS). Common causes of PEA can be remembered by the Hs and Ts. This patient recently underwent an operative procedure and is at increased risk for developing a pulmonary embolism (PE). Therefore, lytic therapy with tissue plasminogen activator (t-PA) should be administered.

This patient presents with findings concerning for septic emboli secondary to endocarditis. Although rare, intravenous drug users are at the highest risk for endocarditis secondary to Pseudomonas species. They are also more likely to have right-sided endocarditis with tricuspid valve involvement. Patients should be treated with tobramycin and an extended spectrum beta-lactam antibiotic such as piperacillin-tazobactam, cefepime, or ceftazidime. Medical therapy with antibiotics can be attempted, but valve replacement is often needed for complete eradication of the underlying infection.
Ceftriaxone and vancomycin (B) do not cover Pseudomonas aeruginosa and therefore would be ineffective. The combination of gentamicin and nafcillin (C) or gentamicin and vancomycin (D) is not recommended. Although gentamicin does cover Pseudomonas species, a regimen with double coverage is more likely to be effective. Nafcillin has great coverage against non-methicillin resistant Staphylococcus aureus, and vancomycin is the treatment of choice for methicillin-resistant Staphylococcus aureus.

Myocarditis can be due to an infectious or non-infectious process, with most infectious etiologies caused by a viral infection, most commonly parvovirus B19, adenovirus, coxsackie B virus, and Echovirus. Trypanasoma cruzi (Chagas disease) is the most common etiology worldwide. Myocardial necrosis occurs likely as a result of direct invasion of the offending organism as well cytotoxic effects of the host’s immune system. Individuals develop flulike symptoms and in adults chest pain and shortness of breath. One of the hallmark signs of myocarditis is tachycardia out of proportion to fever. Depending on the time of presentation, patients may have symptoms of heart failure as the left ventricular ejection fraction is impaired as a result of the myocarditis. Troponin is often elevated as the disease progresses. The gold standard for diagnosis is endomyocardial biopsy. Management is supportive. ACE inhibitors help reduce myocardial inflammation.

Although most patients with infective endocarditis will exhibit a mumur at some point in their disease course, murmurs are often not present on initial presentation. Infective endocarditis often affects patients with underlying valvular abnormalities including rheumatic heart disease, calcific degenerative disease and patients with congenital heart defects. The incidence of infective endocarditis among intravenous drug users is particularly high. Symptoms of endocarditis are nonspecific. Most patients will report intermittent fevers (85%) and malaise (80%). Early in the disease, patients often will not have murmurs but one will almost always develop during the course of illness. Among intravenous drug users, less than 35% will present with a murmur. In patients with a moderate or high suspicion of endocarditis, an echocardiogram should be performed to establish the diagnosis.
Noninvasive cardiac monitors have been used in the ED to measure cardiac output, though they have yet to be proven to change measured clinical outcomes. A recent meta-analysis of 8 studies found that passive leg raise predicted fluid responsiveness as measured by an increase in descending aortic blood flow. The assessment was performed by transesophageal Doppler imaging in critically ill patients with a global area under the receiver operating characteristic curve of 0.95, indicating excellent sensitivity and specicity of these maneuvers in realtime clinical practice in the ED.

Ultrasonographic monitoring (transthoracic or esophageal), and arterial and venous pulse oximetry/plethysmography variation. While potentially promising as noninvasive means of monitoring cardiac output and providing information regarding the nature of a patient’s shock, further studies with clinical outcome data are needed to guide the use of these monitoring devices in the diagnosis and management of patients with shock.

Naloxone can safely be given to a pediatric patient in cardiac arrest via the endotracheal tube (ETT) if intravenous or interosseous access is not available. Endotracheal drug administration is infrequently used but has the potential to be therapeutic in patients without access. A number of medications can be given via ETT including atropine, naloxone, lidocaine and epinephrine.

This patient presents with symptoms of acute decompensated heart failure and should be started on nitroglycerintherapy immediately. Patients present with shortness of breath, increased work of breathing, tachycardia, hypoxia, crackles on lung examination and jugular venous distension. These patients experience acute worsening of left ventricular function and output secondary to a number of mechanisms including increased systemic vascular resistance. Therapy focuses on reduction of preload to decrease the flow of blood into the lungs and afterload reduction to increased the effectiveness of the left ventricle. Both of these goals can be accomplished through the administration of nitroglycerin. At lower doses, nitroglycerin acts as a peripheral vasodilator and increases venous capacitance leading to decreased preload. At higher doses, nitroglycerin causes arterial vasodilation leading to decreased afterload. Because of its rapid onset of action, nitroglycerin is the first line medication in patients with ADHF.

Furosemide (A) may be useful in patients with volume overload and ADHF but this represents less than half of patients with ADHF. Additionally, the effects are delayed. Heparin (B) can be given in cases of ischemia induced ADHF but will not yield any immediate benefits. Morphine (C) was historically used as a preload reducer but has been associated with increased morbidity in patients with ADHF and is no longer recommended.

Endpoints of death, nonfatal reinfarction, and stroke have been used in comparisons of thrombolytics and PCI. Each of these measured parameters is less in the PCI comparison group. Cumulatively endpoints were present for 8% of PCI patients versus 14% for the thrombolytic group. These groups were broken down into less short-term mortality at 30 days (4.4% vs. 6.5%), less nonfatal reinfarction (3% vs. 7%), and less hemorrhagic stroke (0.1% vs. 1.1%). PCI is especially indicated in patients that have cardiogenic shock, severe congestive heart failure and/or pulmonary edema, and hemodynamically compromising ventricular arrhythmias. These patients should proceed to primary PCI as the reperfusion strategy of choice. The addition of both thrombolytic therapy and PCI as a primary reperfusion strategy has been investigated as a therapy for STEMI. Full-dose fibrinolytic therapy followed by immediate PCI may be harmful and should not be utilized. Facilitated PCI, the term for this strategy, has been shown to have higher mortality rates as well as bleeding rates. These patients also had higher rates of recurrent infarction and needs for subsequent PCI. Rescue PCI has resulted in higher rates of early infarct arterial patency, improved regional infarct-zone wall motion, and greater freedom from adverse in-hospital events than with a deferred PCI strategy or medical therapy.

Preload and afterload reduction is your first priority in this patient. The patient’s sudden decompensation, profound hypertension, and relative lack of peripheral edema suggest this patient has acute decompensated heart failure from the “vascular pathway”. In these patients, rapid preload and afterload reduction will dramatically decrease the symptoms of acute decompensated heart failure by decreasing venous return and lowering the systolic blood pressure. The lower systolic blood pressure allows the left ventricle to empty its contents more easily. Diuresis should be delayed until afterload is reduced or not done at all. Diuresis is reserved for patients with gradual fluid accumulation and significant peripheral edema. Agents to increase inotropy are used for hypotensive patients and patients resistant to first-line therapies. Morphine is no longer a first-line agent for acute decompensated heart failure and is associated with increased rates of intubation.

Noninvasive ventilation is a useful and powerful tool in treating acute decompensated heart failure. It has been shown to simultaneously decrease preload and afterload and therefore ameliorate the symptoms of heart failure. It also improves lung mechanics by recruiting atelectatic alveoli, increasing intrathoracic pressure, improving pulmonary compliance, and reducing the work of breathing. Noninvasive ventilation has also been shown to decrease endotracheal intubation rates, decrease the need for ICU admissions, and decrease mortality.

Furosemide exerts its positive effects in treating acute decompensated heart failure by decreasing total body water and therefore preload. Furosemide does activate the renin–angiotensin system; however this is a deleterious effect as this often leads to increased blood pressure. There is no convincing evidence that furosemide has significant venous vasodilatory effects or causes afterload reduction.

See AHA recommendations (http://www.heart.org/HEARTORG/Professional/MissionLifelineHomePage/EMS/Recommendations-for-Criteria-for-STEMI-Systems-of-Care_UCM_312070_Article.jsp).

Transfer if door-to-balloon is <90 (total, including transfer). Typically need rapid transfer protocol set up.

These are deWinters complexes, indicative of LAD occlusion and generally regarded as a cath lab activating EKG. Classically depressions in V2-4 with acute t waves. Don’t need ST elevation here.

Sgarbossa criteria here met in V2 and V5, V6. Use Sgarbossa because of LBBB.

Takotsubo cardiomyopathy is also known as left apical ballooning or broken heart syndrome. Most commonly, patients are postmenopausal women who have just experienced significant emotional distress although there are numerous case reports from myriad other causes. It is unclear exactly why this occurs, but a sudden weakness in the myocardium develops after emotional distress possibly related to stress hormones, vascular spasm, focal myocarditis or other cellular changes. Patients develop symptoms consistent with acute coronary ischemia which most commonly include chest pain and dyspnea on exertion. The ECG is abnormal with ST segment elevations or deep T wave inversions usually on the anterior wall. Cardiac biomarkers are often positive. On cardiac catheterization, the coronary arteries do not have obstructive disease. If ventriculography or echocardiography is performed, the apex of the left ventricle is seen ballooning with an impaired ejection fraction. Prognosis is typically very good with recovery to normal wall motion and ejection fraction within a month.

Beta-blockers (A) do not change mortality in this condition. Almost all patients with takotsubo regain completely normal ejection fraction with no long term effects of the episode. Although beta-blockers and angiotensin converting enzyme inhibitors are considered mainstay therapy they do not impact mortality in these patients. Cardiac catheterization (B) is mandatory in this patient who has symptoms consistent with myocardial ischemia and an ECG suggestive of an anterior wall myocardial infarction. As noted above, the catheterization is unlikely to reveal an acute thrombus, but the emergency physician and cardiologist must exclude an acute myocardial infarction as the etiology of the signs and symptoms. Nitroglycerin (D) is not contraindicated in this patient. Nitroglycerin is unlikely to have any effect given the absence of coronary obstruction. In patients with hypertrophic cardiomyopathy and preload dependence for ventricular filling, agents that decrease preload like nitroglycerin should be avoided.

This patient has an ECG concerning for a right ventricular infarct. In this situation, the patient becomes preload dependent (essentially the right ventricle is impaired to there is “passive” flow into the left ventricle). When these patients become hypotensive, the immediate treatment is intravenous hydration to increase preload. Right ventricular infarction is represented on an ECG by noting ST elevation in right-sided leads (V3R and V4R). Because the right coronary artery often supplies the right side of the heart and the inferior wall of the heart, any ECG with ST elevations in leads II, III, and aVF (inferior leads) should have another ECG performed with right-sided lead placement. Aggressive volume loading with normal saline boluses is used to restore blood flow to the right ventricle and inotropic support is indicated if hypotension persists. Early percutaneous coronary intervention or thrombolytic therapy should be initiated as soon as possible. In general, patients’ with right ventricular myocardial infarction are treated in a manner similar to those with acute ST-elevation myocardial infarction. This includes the early use of dual antiplatelet therapy, statin therapy, and an anticoagulant.

Medications that lower preload such as nitroglycerin (C) and morphine (B) or drugs that slow heart rate such as beta blockers (A) should be avoided or used with extreme caution.

Brief (usually less than 10 seconds) tonic–clonic seizure activity can accompany syncope of any etiology. This activity is not accompanied by postictal disorientation, and it does not represent true seizure activity. For cerebrovascular disease to cause a loss of consciousness, either both cerebral hemispheres or the brainstem must be deprived of blood flow. Therefore transient ischemic attacks and stroke are rarely the cause of syncope. Screening laboratory studies have been shown to add little to establishing a cause of syncope. In most cases, hypoglycemia is clinically suspected and abnormal electrolytes rarely account for a loss of consciousness. Anemia from bleeding is usually clinically evident. Tilt-table testing reveals abnormalities in 20% to 70% of patients whose emergency department evaluation leaves them without a diagnosis.

Although the definition of abnormal ECG varies among the many studies examining their role in the diagnosis of syncope, particular attention should be paid to any nonsinus rhythm, signs of ischemia, or conduction abnormalities.

Syncope is defined as an interruption in cerebral perfusion causing a transient loss of consciousness. Syncopal events should last less than 5 minutes and patients should return immediately to their baseline mental status as cerebral perfusion is restored. Lateral tongue biting is more commonly associated with seizure, and the most specific sign for a seizure, while anterior tongue biting can be seen with syncope. Urinary incontinence is frequently seen in seizure patients, but would be unusual following syncope.

A is incorrect, because the R-R interval classically shortens as the PR interval lengthens. B describes a first-degree AV block, not a second-degree AV block. C is correct. D is incorrect, because Mobitz type II blocks more commonly feature a prolonged QRS complex than Mobitz type I AV blocks.

The sinoatrial (SA) node is innervated by both the sympathetic and parasympathetic nerves, which alter its discharge rate. The SA node is the normal pacemaker of the heart with an inherent rate of 60 to 100 beats per minute. The arterial supply for the SA node is either the right coronary artery (55%) or the circumflex artery (45%). The atrioventricular (AV) node is usually supplied by the right coronary artery 90% of the time with the remaining 10% originating from the circumflex. The inherent rate of the AV node is 30 to 40 beats per minute, which is primarily used as an escape rhythm if the primary pacemaker of the heart, the SA node, fails.

Lidocaine, which may abolish the ventricular rhythm completely, is contraindicated because it may cause cardiac standstill. Atropine, due to its vagolytic properties, enhances sinus node automaticity and AV nodal conduction. Isoproterenol, a beta-adrenergic agonist, has both inotropic and chronotropic effects. Isoproterenol increases myocardial oxygen demand and should be used with caution in ischemic myocardium. Glucagon has been shown to be useful in the treatment of bradyarrhythmias secondary to beta-adrenergic blocking agents and calcium antagonists. Glucagon stimulates the SA node directly giving some mild increase in heart rate. Glucagon also increases cardiac contractility.

In wide-complex atrial fibrillation, any drug that slows conduction through the AV node can cause ventricular fibrillation from rapidly conducted impulses via the accessory pathway. Adenosine, calcium channel blockers, and beta blockers are all contraindicated in this setting. Though procainamide is considered first-line pharmacotherapy in the stable patient with wide-complex atrial fibrillation, electrical cardioversion is more effective. Amiodarone is also less effective and carries the risk of slowing AV conduction.

As per the 2010 AHA guidelines, CPR should only take place until the defibrillator is ready, and defibrillation at 200 J should be performed as soon as possible in VF arrest. Escalating doses of 50–100–150 J are no longer recommended and 200 J should be used for biphasic defibrillators. Though epinephrine is recommended as part of ACLS, it should not take precedence over defibrillation and has not shown long-term benefit in the treatment of cardiac arrest.

This patient represents stable atrial fibrillation (AF) with a rapid ventricular rate. For patients presenting with AF and a rapid ventricular response, treatment is directed at slowing the ventricular rate. Calcium channel blockers, in particular diltiazem, slow ventricular response within the first few minutes of IV administration. Beta blockers such as atenolol or metoprolol are about as effective as calcium channel blockers for rate control, but are seldom used because of a higher incidence of hypotension. Neither calcium channel blockers nor beta blockers are particularly effective at producing cardioversion to sinus rhythm. Digoxin is no better than placebo in the first few hours of rate control for rapid atrial fibrillation. Stable patients do not need cardioversion in the ED. This patient has an unknown time period since the atrial fibrillation has manifested. Anticoagulation is an important management issue for patients with AF. Not only are patients with AF that lasts more than several days at risk for systemic embolization, but recent evidence suggests that even shorter periods of AF may carry a risk of embolization, particularly following conversion to sinus rhythm. Patients should be considered for anticoagulation prior to cardioversion for all presentations of atrial fibrillation that is stable. Amiodarone slows ventricular rate and increases the frequency of conversion to sinus rhythm after greater than 24 hours. There is no difference between placebo and amiodarone in the first 8 hours. Amiodarone thus has little utility in the new-onset stable patient with AF and a rapid rate.

Placement of a magnet over a pacemaker will cause synchronous pacing at model-specific rates.

This patient is presenting with ovarian torsion. This patient’s cyst is greater than 5cm, putting her at risk for ovarian torsion. Her history of episodes of sudden onset pain is concerning for stuttering, intermittent torsion leading up to this event. Although ultrasound demonstrates intact arterial blood flow, the most frequent ultrasonographic abnormality in ovarian torsion is either decreased or absence of venous flow in the presence of intact arterial flow. Laparoscopy is the gold standard for diagnosis and management.

Trichomonas vaginalis, a protozoa, is the causative agent of trichomoniasis. It is the most common non-viral sexually transmitted infection worldwide. Patients typically complain of yellow-green, frothy and malodorous vaginal discharge, with protozoa seen on wet mount. “Strawberry cervix”, or punctate hemorrhage around cervix, is seen on exam. Vaginal pH becomes more alkalotic, and is generally greater than 4.5. Treatment of trichomonas vaginitis is metronidazole. Clue cell is seen in bacterial vaginosis. Recent antibiotics use is a common risk factor for candidal vaginitis.

The most common causes of postmenopausal vaginal bleeding is vaginal/endometrial atrophy 60%) and endometrial polyps (12%). However, endometrial cancer comprises about 10% of incidence. Given the stability of the patient, no further emergent imaging is indicated at this time, and urgent outpatient gynecology referral for further workup, including, but not limited to, endometrial biopsy, cervical cytology, and/or transvaginal ultraosund.

First line treatment of symptomatic atrophic vaginitis is vaginal moisturizing agents and lubricants. If that fails, and there is no contraindication for hormonal therapy (such as estrogen-based tumors like breast cancer), then low dose vaginal estrogen is the next step. In this question, the patient is stable and first-line therapy is nonhormonal moisturizing/lubricating agents and outpatient gynecology referral for endometrial biopsy, cervical cytology, and/or ultrasound to exclude endometrial cancer first.  The biopsy should be obtained BEFORE starting any treatment. While the workup for vaginal bleeding may include serum testing, there is no indication with this clinically stable and otherwise normal patient to emergently order blood tests. These tests, along with other imaging or biopsy/cytology testing, may be performed on an outpatient basis.

An ultrasound exam is usually the initial diagnostic study in the workup for ovarian torsion. The most common ultrasound finding in ovarian torsion is enlargement of the ovary. Enlargement develops due to impaired venous and lymphatic drainage, in addition to edema and hemorrhage that may occur. Less common findings include identification of a twisted pedicle (whirlpool sign), free pelvic fluid, and identification of an ovarian mass. RISK FACTORS: ovarian mass >5mm, reproductive age, pregnancy, ovulation induction, prior torsion. CLINICAL: adnexal pain/mass, vomiting, fever, vaginal bleeding
Free pelvic and intraperitoneal fluid (B) may surround the twisted ovary. This is usually the result of interstitial fluid that weeps off an affected ovary rather than true rupture of the capsule. Many cases of surgically proven ovarian torsion will have documented blood flow (C) on Doppler exam because the ovary has a dual blood supply from both the ovarian and uterine arteries. In addition, torsion is often intermittent, so findings may vary, depending on the time of the exam. Identification of an ovarian mass or cyst (>4 cm) (D) may suggest the diagnosis of ovarian torsion, but it is not the most common finding on ultrasound.

This patient presents with a Bartholin’s abscess and should have incision and drainage (I+D) performed with the incision on the mucosal surface. Bartholin’s abscesses are infections located in the Bartholin’s glands which lie inferiorly to the vaginal opening. Patients develop cysts of the gland that become secondarily infected. These abscesses typically are caused by normally occurring aerobic and anaerobic bacteria in the vagina but may also be caused by sexually transmitted infections. Patients present with swelling and pain near the labium. Examination revels a tender, fluctuant mass along the posterolateral margin of the vaginal vestibule. Treatment focuses on incision and drainage with insertion of a Word catheter. The Word catheter has a small balloon at the end that is inflated after insertion and remains in place for 6 to 8 weeks. Because of this duration, the incision should be made on the mucosal surface so that the Word catheter can be tucked into the vaginal opening for patient comfort. Incision and drainage is usually adequate but patients with overlying cellulitis may require antibiotics. After discharge, patients should perform sitz baths to aid with drainage. Recurrence is common.

This patient has a clinical presentation consistent with pelvic inflammatory disease (PID). PID is an ascending infection that begins in the vagina or cervix. In the sexually active female, the most common responsible organisms are Chlamydia trachomatis and Neisseria gonorrhoeae. Frequently, the infection is polymicrobial. The most common presenting symptom is lower abdominal pain. Patients may also develop fever, vaginal discharge, dyspareunia or abnormal bleeding. On physical examination, the patient typically has a fever and is tender on pelvic examination either in the lower abdomen over the uterus, on cervical motion or in the adnexa. The absence of cervical motion tenderness does not rule out PID and the CDC recommends empiric treatment for sexually active women presenting with lower abdominal pain and one of the following if no other cause is identified: cervical motion tenderness, adnexal tenderness or uterine tenderness. For outpatient management, patients are treated with ceftriaxone 250 mg IM followed by a two-week course of doxycycline. Metronidazole is sometimes added to the regimen at the judgment of the clinician.

The correct answer is IV estrogens. High-dose estrogen is thought to promote rapid regrowth of endometrium and stabilize uterine bleeding within the first five hours of administration. In hemodynamically unstable patients, IV estrogen is recommended, while oral estrogen is appropriate for hemodynamically stable patients. Oxytocin and methylergonovine can be used in post-partum bleeding.

Carbaprost tromethamine is a prostaglandin analog used in postpartum bleeding that stimulates uterine contractility, promoting hemostasis at the placental site. Methylergonovine is used in post-partum uterine bleeding, by increasing uterine smooth muscle contractions to reduce blood loss. Recombinant factor VIIa has been FDA-approved for use in bleeding in patients with hemophilia A/B, factor VII deficiency, or acquired hemophilia. Off-label, recombinant factor VIIa has been used as a general hemostatic agent – in this patient, IV estrogen should be first utilized before moving onto more controversial, last-ditch efforts.

This patient likely has ovarian cancer and the biomarker likely to support this diagnosis is CA-125. AFP is elevated in certain germ cell tumors as well as in Hepatocellular CA. CEA is elevated in colorectal CA. CA 19-9 is elevated in pancreatic and some types of colorectal CA.

Fitz-Hugh-Curtis syndrome is a condition that occurs in the setting of pelvic inflammatory disease (PID) and results in inflammation of the capsule surrounding the liver and the peritoneal surface of the anterior abdominal wall. It occurs in about 10% of patients with PID. Although it can be caused by any organisms responsible for pelvic inflammatory disease, Chlamydia trachomatis is most often implicated. Patients present with right upper quadrant pleuritic pain and tenderness. They may also have symptoms of PID, such as pelvic pain and vaginal discharge although these symptoms may be mild or lacking. Treatment regimens are similar to those for PID.
nfection with Gardnerella vaginalis (B) results in symptoms of vaginitis, but does not play a role in the development of Fitz-Hugh-Curtis syndrome. Hepatitis C virus (C) causes hepatitis, but is also not involved in the development of Fitz-Hugh-Curtis syndrome. Neisseria gonorrhoeae (D) can cause Fitz-Hugh-Curtis syndrome although it is more likely to be due to a C. trachomatis.

Vaginal foreign bodies can manifest as vaginal discharge. The discharge associated with a foreign body is often malodorous and bloody or dark brown in color and occurs daily. Potential foreign bodies include small pieces of toilet paper and small objects or toys. In this case, the child recently started attending school and is likely toileting by herself. As a result, she may be at risk of poor hygiene and potentially may have a small piece of toilet paper stuck within the vagina. Attempted manual removal can be performed on cooperative children over 7 years of age through irrigation with normal saline. Vaginoscopy under anesthesia in the operating room may be necessary in younger children.

In the neonatal period, the most likely cause of lower gastrointestinal bleeding is swallowed maternal blood, from either delivery or cracked nipples during breast-feeding. The Apt test differentiates fetal from maternal blood. The blood in question is mixed with alkali to detect conversion of oxyhemoglobin to hematin. Fetal hemoglobin is more resistant to denaturation than adult hemoglobin is. If the supernatant stays pink after addition of alkali, the blood is fetal in origin (a positive test). This should not be confused with the Kleihauer-Betke test, used to detect fetal-maternal hemorrhage in the pregnant female.

Necrotizing enterocolitis (C) is a complication of premature infants and presents with abdominal distension, bloody stools, and feeding intolerance. Milk protein allergy (B) should be suspected after introduction of a new formula. Infants who are breastfed are not immune to this condition if Mom consumes cow’s milk in her diet. Since the mother in this vignette is a vegan and is breastfeeding, it is unlikely that a milk protein allergy is responsible for the patient’s guaiac-positive stool. In older infants with painless hematochezia, congenital malformations such as small intestine duplication and Meckel’s diverticulum (A) should be considered. Meckel’s diverticulum is most common at two years of age.

The criterion standard for diagnosing urinary tract infections is the isolation of a pathogen from a urine culture obtained via suprapubic aspiration. Although not commonly performed, this is the gold standard technique. Most experts consider any bacterial growth from a suprapubic aspiration sample positive, whereas others require >1000 CFU of a single organism. The only exception is the growth of coagulase-negative staph. such as Staph. epidermidis, which are normal skin flora that may contaminate an aspiration performed with poor technique. In such cases, there would have to be >3000 CFU of S. epidermidis to be considered positive.

Bag collection (A) has a high false positive rate. Urine cultures are considered positive with the identification of >100,000 CFU of a single organism. Suprapubic aspiration (B) of 2,000 CFU of Staph. epidermidis is generally considered contamination because S. epidermidis is normal skin flora. Urethral catheterization (D) is considered positive with >50,000 CFU of a single organism.

A child that presents with a new onset seizure that is unresponsive to multiple doses of conventional medications should alert the physician to the possibility of hyponatremia or other electrolyte abnormality as the cause of the seizure. Hyponatremia can occur in infants who are fed formula that is improperly made resulting in excess free water consumption. Sodium levels < 120 mEq/L can cause seizures and will respond to sodium correction. Typically raising the sodium levels only 3-5 mEq will result in cessation of seizure activity. A seizing patient with hyponatremia should be treated with 3% hypertonic saline 2 mL/kg over 20-30 minutes. The goal is to raise the sodium level above 120 mEq/L acutely and then correct to normal levels slowly over the next 24 hours. 25% dextrose (A) can be given to correct hypoglycemia which may cause a seizure. However, this infant has a normal glucose level. Levetiracetam (C) and midazolam (D) can be given to control seizures but are likely to be ineffective in this child given the likelihood of hyponatremia as the cause of her seizures.

This patient’s history is consistent with tracheoesophageal fistula (TEF). The most common TEF discovered outside of the newborn period is the H-type fistula. A water soluble contrast swallow is the diagnostic test of choice as barium provokes an extensive inflammatory reaction in the lungs and hinders surgical exploration. In combination with decubitus views, the fistula tract will be identified. Tracheoesophageal fistula is the most common cause of esophageal obstruction in neonates. During embryonic development, the trachea and esophagus normally separate and develop in a linear fashion. With a TEF, there is abnormal communication between the trachea and esophagus.

An arterial blood gas (A) would help to determine if an arterial-alveolar gradient exists for shunting problems or issues with diffusion of oxygen, but it would not be helpful in determining this patient’s diagnosis. A chest radiograph (C) can help in diagnosing an associated pneumonia but will not assist in determining the etiology of this condition. Barium (B) provokes an extensive inflammatory reaction in the lungs and hinders surgical exploration.

This child is exhibiting signs and symptoms consistent with breast milk jaundice. Breast milk jaundice is an indirect hyperbilirubinemia in an exclusively breastfed newborn that develops after the first 4 to 7 days of life, persists longer than physiologic jaundice, and has no other identifiable cause. An unusual metabolite of progesterone, a substance in the breast milk that inhibits uridine diphosphoglucuronic acid (UDPGA) glucuronyl transferase frequently causes the indirect hyperbilirubinemia seen in breast milk jaundice. There is also evidence that exclusive breastfeeding delays establishment of the gut flora and results in increased enterohepatic circulation and reabsorption of bilirubin. Management of breast milk jaundice is by continued breastfeeding as this is most often a benign condition. In rare instances, a breastfeeding holiday may be required for bilirubin levels > 20 mg/dL.

ABO incompatibility (A) often presents in the first day of life with severe jaundice, lethargy, and poor feeding. These children require phototherapy for treatment to prevent kernicterus. Breastfeeding failure jaundice (B) is seen in exclusively breastfed infants who are not getting enough breast milk. This leads to decreased stool output and accumulation of bilirubin. Physiologic jaundice (D) is usually seen at 2 or 3 days of life due to decreased conjugation of bilirubin by the immature liver.

This patient is exhibiting signs and symptoms consistent with severe neonatal jaundice. Jaundice is defined as discoloration of the skin and sclera caused by the accumulation of unconjugated or conjugated bilirubin. Jaundice on the first day of life is frequently caused by blood group system or ABO incompatibility. Severe jaundice with a total bilirubin > 25 mg/dL places this patient at risk for kernicterus, which is defined as neurotoxic hyperbilirubinemia. Kernicterus presents in phases. The first phase, seen on the first few days of life, is characterized by lethargy, hypotonia, and poor feeding. Phase 2 is characterized specifically by hypotonia of the extensor muscles. Phase 3, which is seen with infants over 1 week of age with persistent severe jaundice, is characterized by diffuse severe hypotonia. Chronic bilirubin encephalopathy can lead to persistent hypotonia, hyperreflexia, delayed motor milestones, and variable cognitive deficits. MRI will classically reveal bilateral symmetric high-intensity signals in the globus pallidus in patients with kernicterus.

Gastric reflux disease (A) is not related to jaundice or elevated bilirubin levels. Necrotizing enterocolitis (D) will present with feeding intolerance and abdominal distension instead of jaundice. Abdominal radiographs reveal pneumatosis intestinalis. Muscular dystrophy (C) is a genetic disorder characterized by progressive muscle weakness, most often seen in the proximal lower extremities first. It is not associated with jaundice.

This patient is presenting with signs and symptoms consistent with necrotizing enterocolitis (NEC). NEC is defined as bowel necrosis of an unknown etiology. It classically affects premature infants at a much higher rate than those born at term. Signs and symptoms of NEC include abdominal distension, poor feeding, vomiting, and bloody stool. Abdominal wall erythema seen on physical exam is a rare, but pathognomonic finding of NEC. Diagnosis of NEC is with abdominal radiograph, which reveals pneumatosis intestinalis (intramural air within the bowel wall). This radiographic finding is pathognomonic for NEC. Management is first with prolonged bowel rest, nasogastric decompression, and antibiotics.

Intussusception (A) presents with vomiting and colicky severe abdominal pain. A late finding of intussusception is currant jelly stool. Midgut volvulus (B) presents with bilious emesis. Pyloric stenosis (D) presents with projectile nonbilious vomiting after feeding followed by immediate hunger.

This patient had a brief resolved unexplained event (BRUE). Clinicians should use the term BRUE to describe an event occurring in an infant younger than 1 year when the observer reports a sudden, brief, and now resolved episode of ≥ 1 of the following: (1) cyanosis or pallor; (2) absent, decreased, or irregular breathing; (3) marked change in tone (hyper- or hypotonia); and (4) altered level of responsiveness. Moreover, clinicians should diagnose a BRUE only when there is no explanation for a qualifying event after conducting an appropriate history and physical examination. Approximately50% of all cases of BRUE have no apparent cause. Among the other 50% of cases, the 3 most common conditions are gastroesophageal reflux (GER), seizure, and lower respiratory tract infection. These 3 accounts for 50% of all diagnoses eventually made. GER is a normal physiologic process defined by the passage of gastric contents into the esophagus with or without vomiting or regurgitation that occurs in healthy infants, unlike gastroesophageal reflux disease (GERD) in adults, which is a pathological process. The infant in this vignette has a clinical history that suggests a diagnosis of GER that was exacerbated by overfeeding. The best approach is to reduce feeding volumes and increase feeding frequency.

A diagnosis of GER in infants is based upon a history of spitting up. A formal intraesophageal pH monitoring (C) is of no value in routine evaluation. Although seizure is 1 of the most common causes of BRUE, the patient in this vignette has no historical features in the parental report that suggest seizures; therefore, an EEG (B) is not indicated. In addition, an EEG is difficult to obtain in the ED and has low sensitivity for diagnosing chronic epilepsy. Most patients who have epilepsy return with a 2nd episode. Therefore, it has been suggested that EEG be reserved for patients with recurrent BRUE. Older studies had suggested that a mechanism for reflux-induced apnea involves acid stimulation of pharyngeal and esophageal chemoreceptors that lead to laryngospasm. However, recent large studies and additional studies have failed to show correlation between acid reductions with a H₂ blocker or a proton pump inhibitor (PPI) and apneic events. Therefore, lansoprazole (A), a PPI, would not help this patient.