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
