Pay It Forward

Have you noticed how certification can be contagious? When one brave soul prepares for and takes the certification examination, it can inspire peers to do the same. One way to ride this certification wave is to make a plan to "pay it forward" with test preparation. When an individual or small group passes the examination, celebrate with a party and the handing off of study materials to the next in line. This practice is encouraging as well as a way to hold our friends accountable. Creating a certification movement in a unit promotes true collaboration, meaningful recognition, and skilled communication. Does that sound familiar? Those are 3 of the 6 standards that the American Association of Critical-Care Nurses has identified as necessary for a healthy work environment.1 In the current climate of health care, maintaining the healthy work environment standards is more important than ever, and developing hope amidst the challenges of nursing is imperative.2 Will you be the one to start a certification outbreak? A plateau pressure of less than 30 cm H2O for individuals with acute respiratory distress syndrome has been associated with lower mortality rates. Lowering the plateau pressure can be accomplished by reducing the tidal volume (B). Increasing the fraction of inspired oxygen (A) and positive end-expiratory pressure (C) may increase the patient's Pao2, but these measures will not decrease the plateau pressure. Decreasing the respiratory rate (D) will not reduce the plateau pressure and may contribute to hypercarbia.Canagliflozin is a sodium-glucose cotransporter 2 inhibitor that blocks glucose reabsorption in the proximal renal tubules, resulting in loss of glucose in the urine and a reduction in the blood glucose level. An adverse event associated with sodium-glucose cotransporter 2 inhibitors is euglycemic diabetic ketoacidosis (DKA), which can be triggered during a state of starvation. The patient likely had a reduction in carbohydrate intake due to gastroenteritis, leading to ketosis from the breakdown of free fatty acids for metabolism. At the same time, the canagliflozin maintained normoglycemia through urinary loss of glucose. The diagnosis of euglycemic DKA should be confirmed with direct measurement of serum β-hydroxybutyrate (D), a ketone body. Tests of urine osmolality (A) and C-reactive protein (B) will not help support the diagnosis of euglycemic DKA. Although a hemoglobin A1c level (C) provides an estimation of the mean blood glucose level for the past 3 months, it does not reflect the presence of ketosis, so it will not help support the diagnosis of euglycemic DKA.Diaries (C) kept for patients with delirium in the intensive care unit have been associated with a lower incidence of posttraumatic stress disorder because they fill patients' memory gaps. Family presence can help mitigate delirium. Therefore, the family should not be told to minimize visits (A) or avoid talking to the patient (D). Although music can be soothing for some patients, playing music (B) for patients during a period of agitation may result in excess stimulation and worsen the agitation.Losartan (C) is an angiotensin receptor blocker (ARB) and should be discontinued for this patient because the sacubitril and valsartan combination already contains an ARB. Sacubitril and valsartan combines a neprilysin inhibitor and an ARB. The neprilysin inhibitor promotes natriuresis, and valsartan is an ARB that reduces after-load through vasodilation. Sacubitril and valsartan (B) is considered a first-line agent for patients with symptomatic heart failure with reduced ejection fraction because it is associated with lower mortality rates than an ARB alone. Empagliflozin (A) and metoprolol succinate (D) are indicated for heart failure with reduced ejection fraction and should not be discontinued.The patient's cerebral perfusion pressure (CPP) is 55 mm Hg, placing the patient at risk for cerebral ischemia. Cerebral perfusion pressure, calculated by subtracting the patient's ICP from the mean arterial pressure, is a clinically relevant approximation of cerebral blood flow. Targeting a goal CPP of 60 to 70 mm Hg reduces mortality and morbidity rates. Although the ICP is not higher than the normal treatment threshold of 20 mm Hg, the blood pressure is not high enough to sustain a CPP of 60 to 70 mm Hg. Therefore, the nurse should be prepared to start an infusion of phenylephrine (B), a vasopressor that raises the blood pressure and CPP by causing vasoconstriction. Dextrose 5% in water (A) is a hypotonic solution that may result in cerebral edema. Draining cerebral spinal fluid (C) may lower the ICP but will not raise the CPP for this patient. A computed tomography scan of the brain (D) is not indicated because the ICP is not high.Hypokalemia is a potential adverse effect of insulin infusion because insulin drives potassium intracellularly. High-dose insulin infusion can be used as an adjunct treatment for patients with calcium channel blocker overdose because high-dose insulin improves cardiac contractility by augmenting calcium processing in myocardial cells and optimizing cellular glucose transport. A calcium channel blocker overdose does not normally cause hypocalcemia (A), although the nurse should monitor for hypercalcemia if administering calcium gluconate or calcium chloride as an antidote. Patients with calcium channel blocker overdose may display hyperglycemia (C), but the patient is at risk for hypoglycemia because of the insulin infusion. Although hypomagnesemia can be associated with hypokalemia, neither calcium channel blocker overdose nor insulin infusion would be expected to cause hypermagnesemia (D).Determining whether an unresponsive patient supported by an LVAD requires cardiopulmonary resuscitation can be difficult. The first step in evaluating an unresponsive patient with an LVAD is to ensure LVAD function. When the LVAD is disconnected from all power sources, it will sound a loud alarm and may stop operating, depriving the patient of blood flow through the device. The nurse's highest priority in this situation is to restore power to the LVAD to restore or maintain blood flow. Many patients with continuous-flow LVADs do not have a palpable pulse at baseline, so palpating for a pulse (A) is not a reliable determination of the patient's need for resuscitation. Chest compressions (B) should be started only if the LVAD is not working or is not providing adequate flow and the patient shows signs of poor perfusion. A jaw thrust (C) would be more appropriate than a head-tilt/chin-lift maneuver to open the airway of an unresponsive patient who had an unwitnessed fall, but in this situation, restoring power to the LVAD would be the higher priority.Wolff-Parkinson-White syndrome is a preexcitation syndrome in which an accessory conduction pathway carries an electrical impulse from the atria directly to the ventricles, bypassing the atrioventricular node, while the impulse simultaneously travels normally through the atrioventricular node. Part of the ventricle begins to depolarize early when it is stimulated by the electrical impulse from the accessory pathway, causing a shortened PR interval, a characteristic slurring of the upstroke of the QRS complex called a delta wave, and a widened QRS complex. The remainder of the QRS complex and the QT interval are normal because the remainder of the ventricle is depolarized through the normal conduction pathways. Wolff-Parkinson-White syndrome may be associated with symptomatic tachycardia requiring cardioversion or catheter ablation. Orthodromic circus movement tachycardia (A) is another preexcitation syndrome, but circus movement tachycardia creates a narrow QRS tachycardia because the ventricles are depolarized normally. The accessory pathway carries the electrical impulse retrograde back to the atria, causing P waves that may not be visible or that may follow the QRS complex. Junctional tachycardia (B) would cause a shortened PR interval but not a prolonged or slurred QRS complex. Brugada syndrome (D) would cause a widened QRS complex, but in Brugada syndrome the QRS pattern would be similar to a right bundle branch block pattern and the ST segment would be elevated.Acute mitral insufficiency can result from papillary muscle rupture or vegetations on the valve in a patient with infective endocarditis. As a portion of the left ventricular stroke volume moves backward through the mitral valve during systole, cardiac output decreases, resulting in tachycardia and hypotension. Regurgitation of blood through the mitral valve during systole causes a systolic murmur. Increased volume and pressure in the left atrium lead to pulmonary congestion, dyspnea, and pulmonary edema. Aortic insufficiency could result from infective endocarditis, but aortic insufficiency would cause a diastolic murmur (B). Valves on the right side of the heart (C, D) are less likely than those on the left side to develop insufficiency from infective endocarditis, and regurgitation through the tricuspid and pulmonic valves results in symptoms of right heart failure such as jugular venous distention and peripheral edema.Although percutaneous coronary intervention is the preferred method of restoring coronary perfusion during STEMI, a thrombolytic agent can be administered if percutaneous coronary intervention will be delayed more than 120 minutes. Alteplase and tenecteplase are 2 thrombolytic agents that can be used, but tenecteplase is often chosen in part due to ease of administration compared with alteplase. Tenecteplase is given as a single intravenous bolus dose over 5 seconds followed by a flush of normal saline. Alteplase administration for myocardial infarction or ischemic stroke is recommended as an intravenous bolus over 1 to 2 minutes followed by an infusion over 30 or 60 minutes (B). Slower administration of alteplase (C, D) has been used for off-label indications such as frostbite and systemic thrombosis, but there are no data to recommend this approach with tenecteplase or for treatment of acute STEMI.AACN Certification Corporation publishes a study bibliography that identifies the sources from which items are validated. The document may be found in the AACN certification examination handbook. The contributor of each question written for this column has listed the source used in developing each item. Clinical practice should be based on primary sources of evidence when possible; this column will also include secondary sources to help nurses become aware of available resources for certification review.