A 72-year-old man with a history of poorly controlled hypertension develops a viral upper respiratory infection. On his second day of symptoms he experiences palpitations and presents to the emergency room. His blood pressure is 118/78. The following rhythm strip is obtained.
What is the best next step in the management of this patient?
The rhythm strip reveals atrial flutter with 2:1 atrioventricular (AV) block. Management of atrial fibrillation or atrial flutter with rapid ventricular response is determined by the patient’s hemodynamic stability. A hemodynamically unstable patient may require emergent cardioversion. In the stable patient, consideration should be given to initially controlling the ventricular response rate. This patient has a normal blood pressure and would probably respond to AV nodal blockade with metoprolol. Adenosine is also a nodal blockade agent, but its extremely short half-life limits its utility to diagnostic maneuvers. Amiodarone can be used to maintain NSR after cardioversion, but immediate management should focus on rate control. Chest compressions are inappropriate given the normal blood pressure.
A 67-year-old man presents to your office after community ultrasound screening revealed an aortic aneurysm measuring 3.0 × 3.5 cm. Physical examination confirms a palpable, pulsatile, nontender abdominal mass just above the umbilicus. The patient’s medical conditions include hypertension, hyperlipidemia, and tobacco use. What is the best recommendation for the patient to consider?
Abdominal aortic aneurysms (AAA) occur in 1% to 2% of men older than 50 years and to a lesser extent in women. Smoking and hypertension are major risk factors for the development of an AAA. Abdominal aneurysms are commonly asymptomatic, and acute rupture may occur without warning. Some will expand and become painful, with pain as a harbinger of rupture. The risk of rupture increases with the size of the aneurysm. The 5-year risk of rupture is 1% to 2% if the aneurysm is less than 5 cm, but 20% to 40% if the size is greater than 5 cm. Other studies indicate that, in patients with AAAs less than 5.5 cm, there is no difference in mortality rate between those followed with ultrasound and those who undergo elective aneurysmal repair. Therefore, operative repair is typically recommended in asymptomatic individuals when the AAA diameter is greater than 5.5 cm; other indications for surgery are rapid expansion or onset of symptoms. With careful preoperative evaluation and postoperative care, the surgical mortality rate should be less than 1% to 2%. Renal artery involvement increases the complexity of surgical repair but does not increase the risk of rupture. Endovascular stent grafts for infrarenal AAAs are successful in selected patients
An otherwise asymptomatic 65-year-old man with diabetes presents to the ER with a sports-related right shoulder injury. His heart rate is noted to be irregular, and this ECG is obtained.
Which of the following is the best immediate therapy?
AV conduction block is classified as first, second, or third degree. First-degree AV block is defined simply as a prolongation of the PR interval (> 0.2 second). Second-degree AV block is divided into two types, also known as Mobitz types. Mobitz type 1 (usually termed Wenckebach phenomenon) is characterized by progressive PR interval prolongation prior to the nonconducted P wave and a “dropped” QRS complex. Mobitz type 2 refers to intermittent nonconducted P wave without prior PR prolongation. In Mobitz type 2, the ECG shows complexes of normal AV conduction with an intermittent “dropped” QRS complex. Third-degree AV block refers to a complete dissociation between atrial conduction (the P wave) and ventricular conduction (the QRS complex). This ECG shows Wenckebach seconddegree AV block (ie, progressive PR interval prolongation before the blocked atrial impulse). This rhythm generally does not require therapy. It may be seen in normal individuals; other causes include inferior MI and drug intoxications from digoxin, beta-blockers, or calcium-channel blockers. Even in the post-MI setting, Wenckebach second-degree AV block is usually stable; it rarely progresses to higher-degree AV block with consequent need for pacemaker.
In the ICU, a patient suddenly becomes pulseless and unresponsive, with cardiac monitor indicating ventricular tachycardia. The crash cart is immediately available. What is the best first therapy?
The standard approach to ventricular fibrillation or hypotensive ventricular tachycardia involves defibrillation (with 200 J, then 300, then 360 if using a monophasic defibrillator; 200 J maximum if using a biphasic defibrillator), followed by epinephrine if needed. Therapy with lidocaine, amiodarone, or procain-amide may be warranted if prior interventions fail. Magnesium sulfate may be given in torsade de pointes or when arrhythmia caused by hypomagnesemia is suspected.
A 70-year-old woman has been healthy except for hypertension treated with a thiazide diuretic. She presents with sudden onset of a severe, tearing chest pain, which radiates to the back and is associated with dyspnea and diaphoresis. Blood pressure is 210/94. Lung auscultation reveals bilateral basilar rales. A faint murmur of aortic insufficiency is heard. The BNP level is elevated at 550 pg/mL (Normal < 100). ECG shows nonspecific ST-T changes. Chest x-ray suggests a widened mediastinum. Which of the following choices represents the best initial management?
This patient’s presentation strongly suggests aortic dissection. Aortic insufficiency is common with proximal dissection, as are hypertension and evidence of CHF. Hypotension may be present in severe cases. Distal dissection can lead to obstruction of other major arteries with neurological symptoms (carotids), bowel ischemia, or renal compromise. In aortic dissection, the first line of defense is emergent therapy with parenteral beta-blockers. After betablockade is established, nitroprusside is commonly used to titrate systolic blood pressure to less than 120. The diagnosis is established with transesophageal echo, MR, or CT angiography. Urgent surgery may be required, especially in proximal (type A) dissections. Although endocarditis may cause aortic insufficiency, this patient’s sudden onset of symptoms as well as widened mediastinum would be unusual in endocarditis. Myocardial ischemia can cause mitral (but not aortic) insufficiency. Furosemide might help the pulmonary edema but would not address the primary problem; digoxin increases shear force on the aortic wall and could worsen the dissection. Anticoagulation is contraindicated if aortic dissection is suspected, as it may increase the risk of fatal rupture and exsanguinating hemorrhage.
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