Surgical Critical Care and Emergency Surgery. Группа авторов
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
5 Sepsis and the Inflammatory Response to Injury
Ilya Shnaydman, MD and Matthew Bronstein, MD
Division of Trauma and Acute Care Surgery, New York Medical College, Westchester Medical Center, Valhalla, NY, USA
1 A 78‐year‐old woman recently discharged from the hospital after ventral hernia repair presents to the emergency department with a 5‐day history of fever, chills, and productive cough. The patient's family reports poor oral intake and altered mental status. The patient's vital signs are temperature 38.5 °C; heart rate 125 beats/min; respiratory rate 30 breaths/min; blood pressure 80/60 mm Hg; and oxygen saturation 85% on room air. A chest radiograph demonstrates multifocal pneumonia and the urinalysis shows leukocyte esterase and nitrites. She is appropriately volume resuscitated and requires norepinephrine to maintain a mean arterial blood pressure of 65 mm Hg. Her serum lactate is 4 mmol/L.The patient's clinical condition can best be defined as:Sepsis.Septic Shock.Severe Sepsis.Multiorgan dysfunction syndrome.Systemic inflammatory response syndrome (SIRS).The Society of Critical Care Medicine task force produced the new definition for sepsis and septic shock (Sepsis‐3) in 2016. Sepsis is defined as life‐threatening organ dysfunction caused by a dysregulated host response to infection. This is identified by a score of 2 points or more on the Sequential Organ Failure Assessment (SOFA) score and is associated with 10% mortality or greater. Patients with septic shock are defined as requiring a vasopressor to maintain a MAP > 65 mmHg and having a serum lactate level >2 mmol/L in the absence of hypovolemia and is associated with 40% mortality or greater (choice B). Severe sepsis (choice C) and Multiorgan dysfunction syndrome (choice D) are not definitions recommended by the new guidelines. SIRS (choice E) is defined as two of the following: tachycardia (HR > 90 bpm), tachypnea (RR > 20 breaths/min), fever (>39 °C or <36 °C), and leukocytosis (WBC > 12 or <4 or >10% bands). SIRS would be correct if there was no identified or suspected source. A quick bedside score, qSOFA, can also be used (respiratory rate > 22/min, altered mental status or systolic blood pressure 100 mmHg or less). Using these new definitions, the patient has Septic Shock (choice B).Answer: BGyawali B, Ramakrishna K, Dhamoon, A. Sepsis: the evolution in definition, pathophysiology, and management. SAGE Open Med. 2019; 7:205031211983504. doi: https://doi.org/10.1177/2050312119835043.Singer M, Deutschman CS, Seymour CW, et al. The third international consensus definitions for sepsis and septic shock (sepsis‐3). JAMA. 2016; 315(8):801.
2 What is the first step in the initial management of the patient in the above question?Antibiotic Therapy.Transfer to Intensive Care Unit.Intravenous fluid bolus.Checking serum