Читать книгу Surgical Critical Care and Emergency Surgery - Группа авторов - Страница 11

Ryan Malcom, MD

Division of Trauma and Acute Care Surgery, New York Medical College, Westchester Medical Center, Valhalla, NY, USA

1 A 62‐year‐old woman with a smoking history was hospitalized with a bleeding duodenal ulcer. She has been managed nonoperatively thus far. On hospital day 2, she complains of chest pain and dyspnea. She is administered oxygen, nitroglycerin, and morphine. CBC, coagulation studies, and cardiac marker levels are drawn. The following is seen on a 12 lead EKG:Figure 4.1 EKG.The next best step in the treatment of this patient is:Immediate transfer to the catheterization laboratoryAdministration of aspirinObtain chest x‐rayFibrinolysisAdministration of ibuprofenThe 12 lead EKG is central to the identification of ST‐segment elevation myocardial infarction (STEMI). Elevated ST‐segment elevation in two contiguous leads, or a new left bundle branch block (LBBB), characterizes STEMI. This patient has a STEMI. Usually, patients with STEMI have a complete occlusion of an epicardial coronary artery. To save heart muscle and reduce complications of myocardial infarction (MI), urgent treatment is required. The treatment of STEMI is early reperfusion therapy via either fibrinolysis or percutaneous coronary intervention (PCI). PCI is preferred if a catheterization laboratory is immediately available, otherwise fibrinolysis should be initiated. Transport to the catheterization laboratory should not be delayed for a CXR or cardiac marker lab results. This patient has a GI bleed, and therefore, fibrinolysis and aspirin are contraindicated. Nonsteroidal anti‐inflammatory drugs (i.e. ibuprofen), excluding aspirin, are contraindicated because of increased risk of mortality with STEMI.Answer: AAntman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST‐elevation myocardial infarction. J Am Coll Cardiol. 2013; 61:485–510.Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST‐elevation myocardial infarction. Circulation. 2018Pinto DS, Kirtane AJ, Nallamothu BK, et al. Hospital delays in reperfusion for ST‐elevation myocardial infarction: implications when selecting a reperfusion strategy. Circulation. 2006; 114(19):2019–2025.Kimmel SE, Berlin JA, Reilly M, et al. The effects of nonselective non‐aspirin non‐steroidal anti‐inflammatory medications on the risk of nonfatal myocardial infarction and their interaction with aspirin. J Am Coll Cardiol. 2004; 43(6):985–990.

2 A 57‐year‐old man with a history of coronary artery disease (CAD) has a bowel resection and ventral hernia repair for strangulated hernia. On postoperative day 3, he has new‐onset chest pain. Which of the following most increases his risk for a major adverse cardiovascular event (MACE: death, nonfatal myocardial infarction, or urgent need for coronary revascularization)?New‐onset chest pain lasting 10 minutesST depression of 0.3 mm on his EKGTroponin I two times normal valueAge greater than 50Male genderWhen chest pain is likely caused by CAD, there are assessments available for risk stratification. The Braunwald and thrombolysis in myocardial infarction (TIMI) risks scores are used for risk stratification. TIMI has become the primary tool for therapeutic recommendations. Neither recent surgery nor gender are included. Age does not become a predictor variable until age > 65 in the TIMI risk score. An ST depression is diagnostic when > 0.5 mm; less than 0.5 mm is nonspecific. In both scoring systems, elevated cardiac markers including troponin is a predictive variable and portend a high risk.Answer: CAntman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non‐ST elevation MI: a method for prognostication and therapeutic decision making. JAMA. 2000; 284(7):835–842.Braunwald E, Antman EM, Beasley JW, et al. ACC/AHA guideline update for the management of patients with unstable angina and non–ST‐segment elevation myocardial infarction‐‐2002: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina). Circulation. 2002; 106(14):1893–1900.

3 The most important factor in improving survival during STEMI is:Early intubationTimely reperfusionGiving aspirinSmoking cessationIV metoprololST elevation begins after occlusion of a coronary artery. Myocardial cell death proceeds rapidly until re‐establishment of blood flow. Reperfusion with fibrinolytic therapy and/or PCI can limit loss of heart muscle. The majority of infarct occurs by four hours after the onset of symptoms, and after 6 hours the infarct in nearly complete. Sudden cardiac death is most likely to develop during the first 4 hours after onset of symptoms. Reperfusion has been shown to reduce mortality, preserve LV function, and limit the development of congestive heart failure. Intubation is not indicated in STEMI unless there is associated respiratory distress. Smoking cessation is a long‐term preventive strategy and is not applicable acutely. Aspirin is indicated in the initial management and is complementary to fibrinolysis and reperfusion. Metoprolol may be helpful but is not the most important factor in improving survival.Figure 4.2 TIMI risk assessment.Figure 4.3 Braunwald risk assessment.Answer: BO’Connor RE, Al Ali AS, Brady WJ, et al. Part 9: acute coronary syndromes: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015; 132(18) (suppl 2):S483–S500.Campbell RW, Murray A, Julian DG . Ventricular arrhythmias in first 12 hours of acute myocardial infarction: natural history study. Br Heart J. 1981; 46(4):351.

4 A 49‐year‐old mother of seven has a history of diabetes ellitus, hypertension, smoking, and 4 months ago underwent PCI with a paclitaxel‐eluding stent placement for unstable angina. Her medications include aspirin, clopidogrel, metoprolol, HMG‐CoA reductase inhibitor, metformin, and an angiotensin‐converting enzyme (ACE) inhibitor. She now presents to your office with one episode of right upper quadrant pain and based on history, physical exam, labs, and ultrasound, you diagnose her with biliary colic and cholelithiasis. Of the following choices, which is the next best step in management?Delay the operation for 6 months.Stop aspirin and clopidogrel, and proceed with the operation in 5 days.Stop aspirin and clopidogrel, and proceed with the operation in 7 days with a preoperative heparin infusion as a bridge to surgery.Stop clopidogrel, continue aspirin, and proceed with surgery.Transfuse platelets, and proceed with surgery.In patients with coronary stents, dual antiplatelet therapy is recommended for at least one year to minimize the risk of stent thrombosis. Large observational studies suggest an increased risk of stent thrombosis for at least 6 months. A cholecystectomy is elective at this time. To stop, or adjust, dual antiplatelet therapy less than 6 months after placement of the stent risks thrombosis, and to operate on dual antiplatelet therapy increased bleeding complications. In the recommendations below, there are differences between bare‐metal stents (BMS) and drug‐eluding stents (DES). A biological explanation for these differences is the earlier endothelialization of bare‐metal stents.CORLOERecommendationsIB‐NRElective noncardiac surgery should be delayed 30 days after BMS implantation and optimally 6 months after DES implantation.IC‐EOIn patients treated with DAPT after coronary stent implantation who must undergo surgical procedures that mandate the discontinuation of P2Y12 inhibitor therapy, it is recommended that aspirin be continued if possible and the P2Y12 platelet receptor inhibitor be restarted as soon as possible after surgery.IIaC‐EOWhen noncardiac surgery is required in patients currently taking a P2Y12 inhibitor, a consensus decision among treating clinicians as to the relative risks of surgery and discontinuation or continuation of antiplatelet therapy can be useful.IIbC‐EOElective noncardiac surgery after DES implantation in patients for whom P2Y12 inhibitor therapy will need to be discontinued may be considered after 3 months if the risk of further delay of surgery is greater than the expected risks of stent thrombosis.III: HarmB‐NRElective noncardiac surgery should not be performed within 30 days after BMS implantation or within 3 months after DES implantation in patients in whom DAPT will need to be discontinued perioperatively.Answer: ALevine GN, Bates ER, Bittl JA, et al. 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease. Circulation. 2016; 134(10):e123–e155.

5 This same patient turns 50‐years‐old 8 months after cardiac stent placement and needs a colonoscopy as recommended by her primary care physician. A sigmoid colon cancer is discovered. The most appropriate plan for her operation and antiplatelet medication is to:Delay the operation for 4 months to perform at the same time as cholecystectomy.Stop aspirin and clopidogrel, and operate after 7 days.Stop aspirin and clopidogrel, operate after 7 days, and bridge with enoxaparin.Stop clopidogrel, continue aspirin, and operate after 5 days.Continue both clopidogrel and aspirin, and proceed with intraoperative platelet transfusion.At this time the surgery is for a malignancy and cannot wait months. The recommendation for urgent noncardiac surgery for a patient on dual antiplatelet therapy is to stop the clopidogrel and continue aspirin. This recommendation is based on expert opinion. For patients undergoing laparoscopic surgery, continuation of a single antiplatelet agent is not associated with an increased risk of preoperative bleeding. Since there is not an increased risk of bleeding, there is no indication for platelet transfusion. There is no role for enoxaparin bridge because it is not an antiplatelet agent. These are complex decisions and should be reached by consensus of the surgeon, cardiologist, anesthesiologist, and patient. When intraoperative platelet transfusion is given, it may cause thrombosing the stent.Answer: DLevine GN, Bates ER, Bittl JA, et al. 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease. Circulation. 2016; 134(10):e123–e155.Antolovic D, Rakow A, Contin P, et al. A randomised controlled pilot trial to evaluate and optimize the use of anti‐platelet agents in the perioperative management in patients undergoing general and abdominal surgery—the APAP trial (ISRCTN45810007). Langenbecks Arch Surg. 2012; 397(2):297–306.Fujikawa T, Tanaka A, Abe T, et al. Does antiplatelet therapy affect outcomes of patients receiving abdominal laparoscopic surgery? Lessons from more than 1,000 laparoscopic operations in a single tertiary referral hospital. J Am Coll Surg. 2013; 217(6):1044–1053.Figure 4.4 Elective noncardiac surgery in patients who undergo PCI and are on DAPT.

6 You decide to perform a laparoscopic sigmoidectomy on the above patient in one week. In the perioperative period, she will continue to take her aspirin and beta‐blocker medication. Which other medication should she continue to take perioperatively (before and after) to reduce mortality?ClopidogrelACE inhibitorMetforminFurosemideHMG‐CoA reductase inhibitorContinuing clopidogrel may increase the risk of bleeding, and 6 months after stent placement, holding it for patients undergoing surgery has no increased mortality risk. Continuing metformin has not been shown to affect mortality, nor has continuing furosemide or ACE inhibitor, but continuing diuretics may make determining the patient’s volume status more difficult. Perioperative (within 24 hours of elective surgery) continuation of HMG‐CoA reductase inhibitors (statins) decreases mortality in patients undergoing noncardiac operations.Answer: ELondon MJ, Schwartz GG, Hur K, et al. Association of perioperative statin use with mortality and morbidity after major noncardiac surgery. JAMA Intern Med. 2017; 177(2):231–242.Mehran R, Baber U, Steg PG, et al. Cessation of dual antiplatelet treatment and cardiac events after percutaneous coronary intervention (PARIS): 2 year results from a prospective observational study. Lancet. 2013; 382 :1714–22.

7 A 76‐year‐old man with a history of non‐valvular atrial fibrillation on warfarin has a finding of right‐sided colon cancer. He is scheduled for a right hemicolectomy. His International Normalized Ratio is 2. His warfarin should be:Continued through the preoperative periodHeld for 5 days before surgeryBridged with enoxaparinBridged with intravenous unfractionated heparinChanged to daily aspirinThis patient’s CHA2DS2−VASc score is 2. While that makes him an anticoagulation candidate, it is not necessary to bridge for elective surgery if the CHA2DS2−VASc is 4 or less. Continuing warfarin would be an unacceptable bleeding risk. Temporary interruption of the anticoagulant should be the strategy to minimize post‐operative bleeding risk. If this patient were a candidate for bridging therapy, then enoxaparin, IV unfractionated heparin, and fondaparinux are appropriate. After surgery he will need to go back on warfarin as his stroke risk is too high for treatment with aspirin alone.If the patient has a CHA2DS2−VASc score of 5 to 6, and the procedure has no significant bleed risk, then bridging should be considered if the patient has had a prior stroke or TIA.If the patient has a CHA2DS2−VASc score of 7–9, or a recent (within 3 months) ischemic stroke or TIA, bridging should be considered.Bridging from warfarin with unfractionated heparin required holding the warfarin. Then start the parenteral anticoagulation therapy when the INR is no longer therapeutic. Discontinue the parenteral unfractionated heparin 4 hours prior to the procedure.CHA2DS2−VASc acronymScoreCongestive HF1Hypertension1Age ≥ 75 years2Diabetes mellitus1Stroke/TIA/TE2Vascular disease (prior MI, PAD, or aortic plaque)1Age 65 to 74 years1Sex category (i.e., female sex)1Maximum score9Answer: BDoherty JU, Gluckman TJ, Hucker WJ, et al. 2017 ACC expert consensus decision pathway for periprocedural management of anticoagulation in patients with nonvalvular atrial fibrillation: A report of the American College of Cardiology clinical expert consensus document task force. J Am Coll Cardiol. 2017; 69(7):871–898.

8 The most common location of spontaneous ectopic foci as the underlying mechanism in paroxysmal atrial fibrillation is:Left atrial appendageLigament of MarshallPulmonary veinsRight atriumSuperior vena cavaLeft atrial muscle extends into the pulmonary veins acting as a sphincter during atrial systole. Mapping of electrical activity preceding the onset of atrial fibrillation demonstrates in nearly 90 percent of patients that the point of origin is in the pulmonary veins. The other choices are all potential points of ectopic foci but less common. The left atrial appendage arises anteriolaterally, and its morphology may influence the risk of embolic stroke. The ligament of Marshall is on the epicardium between the left atrial appendage and left pulmonary veins and contains muscle fibers extending to the atrial myocardium, which can be a source of foci of atrial fibrillation. Rarely, ectopic foci of atrial fibrillation can originate in the right atrium or superior vena cava.Answer: CHaissaguerre M, Jais P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N. Engl. J Med. 1998; 339:659–666.January CT, Wann LS, Calkins H . AHA/ACC/HRS focused update of the 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J. Am. Coll. Cardiol. 2019;2019 doi: 10.1016

9 Hypertensive emergency is defined as:Malignant hypertensionSystolic blood pressure greater than 180 mm HgDiastolic blood pressure greater than 110 mm HgHypertension‐mediated organ damageMean arterial pressure greater than two times patient’s baselinePatients with systolic blood pressure (SBP) > 180 or diastolic blood pressure (DBP) > 110 are usually defined as having hypertensive crisis. Pressures this high can result in acute injury including the heart, brain, lung, kidney, retina, aorta, and microvasculature. When there is organ damage, the condition is termed “hypertensive emergency.” Malignant hypertension is an outdated term, which has been removed from blood pressure guidelines. Normal mean arterial pressure (MAP) is 70–100 mm Hg. MAP two times baseline is not a defined entity. A patient in hypertensive emergency should be placed in the ICU with intravenous blood pressure control. Hypertensive urgency is hypertension in the absence of organ failure. Those patients can be managed with oral agents with the goal of gradual normalization of blood pressure over days to weeks.Answer: DPeixoto AJ . Acute severe hypertension. N Engl J Med. 2019; 381:1843.Johnson W, Nguyen ML, Patel R . Hypertension crisis in the emergency department. Cardiol Clin. 2012; 30:533.

10 Hypertensive emergency is the consequence of:Elevated systemic vascular resistanceHigh cardiac outputRenal failureTachycardiaVolume overloadThe most common precipitating factor in hypertensive crisis is noncompliance with medication in a patient with known hypertension. It is thought that humoral vasoconstrictors lead to an abrupt increase in systemic vascular resistance. This causes small vessel endothelial injury resulting in platelet and fibrin deposition and loss of vascular autoregulation. It is an afterload problem, not cardiac output problem. In most cases treatment should be directed at afterload reduction. Unless there is renal failure, continued hypertension results in natriuresis and volume contraction. Gentle volume expansion with saline may be indicated in some cases. Renal failure or tachycardia may or may not be present. Diuresis would result in worsening of the vasoconstriction.Answer: AMarik PE, Rivera R . Hypertensive emergencies: an update. Curr Opin Crit Care. 2011; 17:569–580.Peixoto AJ . Acute severe hypertension. N Engl J Med. 2019; 381:1843.

11 Treatment of hypertensive emergency should be more aggressive for which of the following conditions:Ischemic strokeAortic dissectionRenal emergencyLysergic acid diethylamide (LSD) overdoseMyocardial infarctionChronic hypertension leads to autoregulation of cerebral blood flow, necessitating higher pressures for adequate flow. Quick and excessive correction of blood pressure to a systolic below 100 to 120 mm Hg can potentiate injury and has an increased risk 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 to a rapidly conducting AP. Agents commonly used to slow AV nodal conduction in atrial fibrillation can be harmful in patients with WPW. A paradoxic increase in ventricular rate is due to more atrial activity passing through the AP and less through the AV node. Adenosine, IV amiodarone, digoxin, and verapamil can lead to ventricular fibrillation. Procainamide is a class 1a anti‐arrhythmic that will increase the refractory period and decrease conduction through the AP. If the patient is unstable, direct current cardioversion is recommended. Definitive treatment of WPW is catheter ablation of the AP.Answer: DWolff L, Parkinson J, White PD . Bundle‐branch block with short P‐R interval in healthy young people prone to paroxysmal tachycardia. Am Heart J. 1930; 5(6):685–704Simonian SM, Lotfipour S, Wall C, et al. Challenging the superiority of amiodarone for rate control in Wolff‐Parkinson‐White and atrial fibrillation. Intern Emerg Med. 2010; 5:421–6.January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Society. Circulation. 2014; 130:2071.

18 An 88‐year‐old woman is in the ICU with pneumonia, ileus, and delirium. Her medications include furosemide, lisinopril, erythromycin, pantoprazole, enoxaparin, and haloperidol. After several hours with a prolonged QT interval (> 500 milliseconds) and then several runs of ventricular couplets, she develops a polymorphic ventricular tachycardia in the form of cyclic sinusoidal variation. She is appropriately resuscitated including treatment with 2 grams IV magnesium over 2 minutes and is back in sinus rhythm with prolonged QT interval. Which two drugs should be discontinued?Erythromycin and haloperidolLisinopril and enoxaparinPantoprazole and erythromycinEnoxaparin and haloperidolFurosemide and lisinoprilThis patient has torsades de pointes, the treatment of which is appropriate resuscitation and 1–2 grams IV magnesium over 2 minutes. It can be seen in several settings, including heart block or congenital syndromes, but can also be associated with drug treatments. Of the medications this patient is taking, erythromycin and haloperidol can cause torsades de pointes. The other medications do not. While furosemide does not cause torsades de pointes, it can lower potassium that increases the risk for torsades de pointes.Answer: ARoden DM . Drug‐induced prolongation of the QT interval. N Engl J Med. 2004; 350:1013.Roden DM, Predicting drug‐induced QT prolongation and tornadoes de pointes. J Physiol actions. 2016; 594(9):2459–68.

19 A 35‐year‐old Asian man falls from heavy alcohol use, has a syncopal event, and lacerates his scalp. In the emergency room, bupivacaine is administered locally to suture repair his scalp laceration; however, during the repair he is combative. He is intubated and sedated with propofol. He subsequently develops spontaneous sustained ventricular tachycardia. He is resuscitated and his EKG is given below:Definitive treatment for this patient’s diagnosis is:ObservationAvoidance of alcoholMetoprololCardiac catheterization with stent placementImplantable cardiac defibrillatorThere is a peculiar ST elevation in leads V1, V2, and V2 with a right bundle branch block, which characterizes Brugada syndrome. If it is suspected but not seen on EKG, an EKG on a sodium channel blocker test may help elucidate it. The symptoms of Brugada syndrome are syncope, and ventricular tachycardia or ventricular fibrillation, often while sleeping. Arrhythmias can be triggered by a large consumption of food or alcohol. Drugs that can trigger arrhythmias include bupivacaine, cocaine, alpha agonists (methoxamine), tricyclic antidepressants, lithium, and propofol. Definitive treatment requires an implantable cardiac defibrillator (ICD). The patient is at risk for sudden cardiac arrest, so observation is inadequate. Avoiding alcohol may be helpful in decreasing the risk of symptoms but is not definitive. Metoprolol is not indicated. There is no role for stent place because this is an electrical conduction disease, not ischemia.Answer: EBrugada J, Campuzano O, Arbelo E, et al. Present status of Brugada syndrome: JACC State‐of‐the‐art review. J Am Coll Cardiol. 2018; 72:1046.Brugada P, Brugada J . Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol. 1992; 20:1391–1396.

20 An 81‐year‐old woman non‐smoker has an episode of chest pain that lasts several hours. She rests at home and is able to sleep it off. 5 days later she has chest pain again and weakness. This time she goes to the hospital. She is found to be tachycardic and hypotensive with distended neck veins and has a pan‐systolic murmur with ST elevations on EKG. She is taken for cardiac catheterization that demonstrates complete occlusion of her left anterior descending artery. An echocardiogram shows a left‐to‐right shunt. With medical treatment alone, what is the 30‐day mortality for this condition?2%15%33%50%90%Ventricular septal defects occur in 0.2% of patients, typically the first week after a myocardial infarction. Advanced age and female sex are risk factors for its development. Diagnosis is determined clinically by a harsh systolic murmur and echocardiographic findings of a left‐to‐right shsunt, right ventricular dysfunction, or frank septal rupture. While the overall 30‐day mortality is 75%, operative repair improves mortality to around 45%, down from about 90% for medical treatment alone. Surgical repair consists of a pericardial patch over the defect.Answer: ECrenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO‐I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation. 2000; 101(1):27–32.Omar S, Morgan GL, Panchal HB, et al. Management of post‐myocardial infarction ventricular septal defects: a critical assessment. J Interv Cardiol. 2018; 31(6):939–948