of death. In hypertensive emergency, blood pressure should be decreased by no more than 20–25% in the first hour, and then to 160/110 mm Hg during the next 2–6 hours. This applies to renal emergency, myocardial infarction, and sympathomimetic agents such as LSD. An exception is acute aortic dissection where the goal should be to lower the systolic blood pressure to 100 to 120 mm Hg within 20 minutes to reduce aortic shearing forces. Short‐acting beta‐blockers should be used, and a vasodilator like nitroprusside or nicardipine can be added if needed. Vascular or cardiothoracic surgery should be consulted as well. Patients with ischemic stroke should not have their blood pressure reduced unless it is greater than 220/120 mm Hg or if thrombolytic therapy is planned.Answer: BMayer SA, Kurtz P, Wyman A, et al. Clinical practices, complications, and mortality in neurological patients with acute severe hypertension: the studying the treatment of acute hypertension registry. Crit Care Med. 2011; 39:2330–2336.Peixoto AJ . Acute severe hypertension. N Engl J Med. 2019; 381:1843.12 The first line therapy for pheochromocytoma hypertensive crisis is:PhentolamineMetoprololLabetalolHydralazineNo treatmentHypertensive emergency from pheochromocytoma is catecholamine induced. It is treated with alpha‐blockers such as phentolamine or direct vasodilators such as sodium nitroprusside or nicardipine. Paradoxically, beta‐blockers including labetalol are contraindicated as sole therapy because they can lead to unopposed alpha‐adrenergic action. Hydralazine may be a second‐tiered therapy, but it is unpredictable and should be avoided as a first option in hypertensive emergency. Separately, arrhythmias in pheochromocytoma emergency can be treated with esmolol, but alpha‐blockage should be in place first. Esmolol is preferred beta‐blocker as it is titratable.Answer: AYoung WF Jr . Adrenal causes of hypertension: pheochromocytoma and primary aldosteronism. Rev Endocr Metab Disord. 2007; 8(4):309.Peixoto AJ . Acute severe hypertension. N Engl J Med. 2019; 381:1843.
13 Which drug should be avoided in hypertensive emergencies in a pregnant patient:LabetalolNifedipineMetoprololHydralazineNitroprussideCalcium channel blockers and hydralazine are safe in pregnancy. Though beta‐blockers can cross the placenta, labetalol and metoprolol are safe in pregnancy; atenolol is not. The possibility of fetal cyanide poisoning has restricted the use of nitroprusside in pregnancy. When using nitroprusside, cyanide levels are typically monitored. While not an answer, angiotensin‐converting enzyme (ACE) inhibitors also should not be used in pregnancy because of increased risk of fetal renal damage.Answer: EACOG Committee Opinion No. 767: Emergent therapy for acute‐onset, severe hypertension during pregnancy and the postpartum period. Obstet Gynecol. 2019; 133:e174Sass N, Itamoto CH, Silva MP, et al. Does sodium nitroprusside kill babies? A systematic review. Sao Paulo Med J. 2007; 125:108.
14 A 19‐year‐old man who is a long‐distance runner has an irregular pulse on physical exam. An EKG demonstrates a PR interval that gets progressively longer until the final P wave elicits no response. The series then repeats every 4 beats. What is the appropriate treatment?AtropineImmediate transcutaneous pacingLidocaineElective transvenous pacingNo treatmentIn first‐degree atrioventricular (AV) block, there is a prolonged PR interval. This is physiologically unimportant and does not require therapy; however, it may signal drug toxicity or conduction system disease. In second‐degree AV block, some atrial impulses are conducted to the ventricles, and others are blocked. There are two types of second‐degree AV block. The patient described has Mobitz type I (Wenckebach) block. It is the result of a conduction blockage in the AV node. The cause can be drug (digoxin) related or from intrinsic heart disease. It can also occur in endurance athletes. The AV node is supplied by the right coronary artery, so a Mobitz type I block can accompany an inferior myocardial infarction. The Mobitz type I block itself requires no treatment in a stable patient. Atropine and pacing might be effective but not indicated. Lidocaine has no role in the treatment of second‐degree AV block.Answer: EWenckebach KF . On the analysis of irregular pulses [article in German]. Z Klin Med. 1899; 37:475–488.Epstein AE, DiMarco JP, Ellenbogen KA, et al. American College of Cardiology Foundation, American Heart Association Task Force on Practice Guidelines, Heart Rhythm Society. 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device‐based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2013; 61:e6–e75.
15 A 52‐year‐old woman with a history of angina is admitted for a partial small bowel obstruction that resolves in 36 hours. She then develops new‐onset bradycardia, and an EKG demonstrates a 2:1 atrioventricular (AV) block in addition to a bundle branch block. Carotid sinus stimulation improves the bradycardia; however, atropine worsens the bradycardia. Which type of AV block does this patient have?There is no AV blockFirst‐degree AV blockType I second‐degree AV block (Mobitz type I or Wenckebach)Type II second‐degree AV block (Mobitz type II or Infranodal)Third‐degree AV blockThere is an AV block. This patient has a second‐degree AV block. A Mobitz type I block has increasing PR intervals until a QRS is dropped. A Mobitz type II has fixed PR intervals until a QRS is dropped. Often there is a widened QRS in Mobitz type II also, but in this patient with a 2:1 AV ratio, every other P wave is not conducted, which makes it difficult to diagnose the level of block. Vagal maneuvers such as carotid massage can be helpful in diagnosing the level. If the block is in the AV node (Mobitz type I), carotid sinus massage may worsen the block. If the block is more distal at the bundle of His, or Purkinje fibers, (Mobitz type II) slowing the sinus rate may paradoxically improve the ratio of AV conduction and increase the ventricular rate. Conversely, atropine may increase the conduction rate across the AV node, which may paradoxically worsen the ratio of AV conduction if the block is at the His‐Purkinje system (Mobitz type II). Third‐degree AV block is complete dissociation between P waves and QRS, which is not the case in this patient, yet.Answer: DEpstein AE, DiMarco JP, Ellenbogen KA, et al. American College of Cardiology Foundation, American Heart Association Task Force on Practice Guidelines, Heart Rhythm Society. 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device‐based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2013; 61:e6–e75.
16 The above patient is hemodynamically stable and electrolytes are normal. What should be the next step in treatment?Beta‐blockadeAtropineTransvenous pacingEpinephrineTranscutaneous pacingNew‐onset type II second‐degree AV block (Mobitz type II) is usually associated with a pathologic lesion, often an occlusion of a septal branch off the left anterior descending coronary artery. It has a poorer prognosis than Mobitz type I (Wenckebach) and often progresses to third‐degree or complete heart block. If the patient is unstable, the algorithm for bradycardia begins with atropine. Though in Mobitz type II, atropine should not be relied upon as discussed in the previous question. The next step should be transcutaneous pacing or beta‐adrenergic support such as epinephrine or dopamine. The patient in question is stable and does not require these therapies at this time. Beta‐blockade is not indicated in this patient. Because of the risk of progression to a third‐degree AV block, transvenous pacing is the correct next step. Transvenous pacing is also indicated in third‐degree block.Answer: CEpstein AE, DiMarco JP, Ellenbogen KA, et al. American College of Cardiology Foundation, American Heart Association Task Force on Practice Guidelines, Heart Rhythm Society. 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device‐based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2013; 61:e6–e75.
17 A 17‐year‐old basketball player presents with occasional palpitations, usually after exertion. He has the following EKG.If this patient develops atrial fibrillation with rapid ventricular response, then he should be treated with:AdenosineAmiodaroneDigoxinProcainamideVerapamilThis patient has Wolff–Parkinson–White (WPW) syndrome. With WPW, there is a shortened P‐R interval, less than 0.12 second, and a QRS complex widened by characteristic delta wave. The delta wave pre‐excitation is caused by an accessory pathway (AP), the bundle of Kent. The AP may allow antegrade and retrograde conduction. These patients have a risk of developing atrial fibrillation with potential to degenerate to ventricular fibrillation related
