Going for Gold … Daily

Carol Ann Rauen, rn-bc, ms, ccrn, pccn, cen, and Sara Knippa, rn, ms, cns, ccrn, pccn, accns-ag, are the column coeditors. Carol is an independent clinical nurse specialist and education consultant in St. Augustine, Florida, and Sara is a clinical nurse specialist/educator in the cardiac intensive care unit at University of Colorado Hospital, Aurora, Colorado. They welcome feedback from readers and practice questions from potential contributors at rauen.carol104@gmail.com. Carol wrote the introduction and Sara wrote CCRN question 5.RAUENKNIPPAKelly Thompson-Brazill, rn, dnp, acnp-bc, ccrn-csc, is an assistant professor, Georgetown University School of Nursing and Health Studies, Wash-ington, DC. Kelly wrote CCRN questions 1 through 4.THOMPSON-BRAZILLKristine Peterson, rn, ms, ccrn-k, ccns, is a cardiac clinical nurse specialist, Aspirus Wausau Hospital, Wausau, Wisconsin. Kristine wrote the CMC questions.PETERSONBeing an Olympic-caliber athlete requires focus, dedication, and sacrifice. These athletes—men and women—train for a lifetime to compete every 4 years to show they are the best. Our critically ill patients and their families assume that the teams caring for them are also the best. Clinical training is not so different from physical training in some ways. Achieving certification as an acute or critical care nurse indicates a similar focus, dedication, and sacrifice. We must strive to “Go for the Gold” in all we do. Unlike in a sports competition, someone’s life might depend on our actions.In hemorrhagic shock, filling pressures such as CVP and pulmonary artery occlusion pressure are low, resulting in decreased cardiac index. SvO2 is low because of decreased oxygen delivery to the tissues. The hemodynamic parameters in (A) are associated with septic shock and in (B) with cardiac tamponade. Normal parameters (D) do not indicate shock.Protamine sulfate is administered to inactivate heparin in patients who experience marked bleeding while taking the medication. Although the mechanisms of action for the other 3 options (A, B, D) are correct, they will not reverse the effects of heparin.Transfusion-related acute lung injury (TRALI) is the development of hypoxia, crackles on pulmonary examination, and diffuse infiltrates on radiography that occurs within 6 hours after the transfusion of blood or blood products. Serious cases may require intubation and mechanical ventilation. In this scenario, the patient is in respiratory acidosis with ongoing hypoxia despite administration of 100% oxygen via a nonrebreather mask. Because of the severity of the patient’s condition, mechanical ventilation is more appropriate than is noninvasive positive-pressure ventilation (D). Because fluid overload is not the primary cause of TRALI, administration of diuretics such as furosemide is not indicated (B). Diphenhydramine (C) will not reverse TRALI.The patient has classic indications of septic shock due to tricuspid valve endocarditis. The patient is at risk for dislodging the vegetation, leading to pulmonary infarction. Pulmonary edema (A) is associated with mitral and/or aortic insufficiency. Both mitral and aortic insufficiency can lead to systemic septic emboli and organ infarction (D). Aortic stenosis (C) is associated with rheumatic fever.If airway, breathing, and circulation are stable, an astute nurse will recognize the ongoing potential for neurological life-threatening emergencies such as nonconvulsive status epilepticus instead of sedation (D) as the cause of the signs. Identification and treatment of acute problems should take priority over chronic ones such as tumor growth (B). Prioritization of EEG versus imaging will depend on the presumed underlying cause of the seizure. Intracranial bleeding would be more likely in a patient who had a seizure due to head trauma or stroke (C), whereas a brain tumor is more likely to cause nonconvulsive status epilepticus.ST-segment elevation in at least 2 contiguous leads is the marker for acute ST-segment elevation myocardial infarction (STEMI). QRS concordance (A) is not a marker of infarction but can be used in the diagnosis of arrhythmias. ST-segment depression (B) and T-wave inversions (D) indicate possible ischemia but not acute injury.Guideline-directed management of acute STEMI includes administration of a β-blocker; aspirin; a P2Y12 inhibitor; weight-based heparin, low-molecular-weight heparin, or bivalirudin; and a lipid-lowering agent in the absence of contraindications. These medications should be given before percutaneous coronary intervention or within 12 hours of manifestation. Furosemide (B, C), amiodarone (A, B), enalapril (B), and amlodipine (C) are not included in the immediate management of STEMI.The QT interval indicates the duration of ventricular activation and recovery. The QT varies inversely with heart rate. In order to ensure complete repolarization between cardiac action potentials, the duration of repolarization decreases as the heart rate increases. Therefore, the QT interval must be corrected for heart rate (QTc) before determining if the QT duration is normal. The upper reference range value for QTc duration is 460 milliseconds. QT-interval prolongation is associated with a form of polymorphic ventricular tachycardia called torsades de pointes. Prolonged QT does not add risk for atrial fibrillation (A), enalapril is not known to lengthen the QT (B), and QT prolongation is not a risk factor for renal failure (D).Sulfonylureas are associated with a high risk for hypoglycemia in patients with renal insufficiency. Potassium (A) is driven from cells in response to hypertonicity and acidosis, both of which are associated with hyperglycemia rather than hypoglycemia. Epinephrine (B) usually increases blood glucose levels, and patients with type 2 diabetes have resistance to insulin (D) rather than too much insulin.The signs and symptoms of pulmonary embolism are often nonspecific; however, pleuritic chest pain, cough, tachycardia, tachypnea, dyspnea, restlessness, hypoxemia, diaphoresis, and hypotension are common indications of acute pulmonary embolism. ECG changes are not always evident in patients with pulmonary embolism, but the S1Q3T3 pattern (S wave in lead I, Q waves in lead III, and ST elevation or T-wave inversion in lead III) is classic. All patients are at risk for pulmonary embolism after surgery because of hypercoagulability, vascular wall damage, and venous stasis. Hypovolemia (A) would not produce dyspnea and cough, and pneumonia (B) would produce fever, fatigue, cough, sputum, and lung sounds indicating consolidation. Pneumothorax (D) would result in decrease or absence of lung sounds in the affected lung.