Imposter Syndrome

After practicing for a year or two, most nurses will be asked to take on additional responsibilities such as acting as a preceptor for new graduate nurses, leading as a charge nurse, becoming a subject matter expert, or serving on a shared governance committee. Taking the step to expand our professional role can cause self-doubt and critical internal dialogue. This phenomenon of imposter syndrome was first described in 1978 by Clance and Imes1 and has been the subject of nursing research ever since. Nurses who are stretching into new roles and developing expertise may be vulnerable to this feeling of inadequacy and may credit their success to luck or chance. Addressing this false self-perception is important to developing our professional identity and becoming more fully authentic.2Validation of expertise may play a part in overcoming imposter syndrome and improving self-confidence. Preparing for and passing the CCRN certification examination can make a profound difference in self-efficacy as nurses recognize their own mastery of this specialized body of knowledge.3 In this way, certification can help overcome imposter syndrome and lead to a more fulfilling nursing career.Noninvasive ventilation (A) is the most appropriate intervention for this patient with acute exacerbation of COPD and respiratory acidosis, as evidenced by the elevated Paco2 and decreased pH. Noninvasive ventilation can decrease the work of breathing, improve gas exchange, and prevent further deterioration that might necessitate intubation and invasive mechanical ventilation. Administering high-flow nasal cannula oxygen therapy at 6 L/min (B) is incorrect. Although this treatment can increase oxygen delivery, it does not sufficiently support the ventilation needs of a patient with acute exacerbation of COPD and hypercapnic respiratory failure. Starting intravenous corticosteroids (C) is incorrect as the initial intervention. Although corticosteroids are used to treat COPD exacerbation because they reduce airway inflammation, they do not address the immediate need to correct gas exchange and acidosis. Antibiotic therapy (D) may be indicated if bacterial infection is suspected on the basis of the greenish sputum. However, the priority is stabilizing respiratory status. This patient’s arterial blood gas analysis results indicate a lower-than-normal pH and an elevated Paco2. These results are consistent with respiratory acidosis, which is commonly caused by inadequate ventilation in patients with acute exacerbation of COPD. The elevated bicarbonate level suggests partial renal compensation for the respiratory acidosis via bicarbonate retention to normalize pH. Metabolic alkalosis with respiratory compensation (B) is incorrect because the primary problem is elevated Paco2, which indicates respiratory acidosis, not a primary metabolic process. Metabolic acidosis with respiratory compensation (C) is incorrect because the bicarbonate level is elevated, not decreased as would be expected in a patient with metabolic acidosis. Uncompensated respiratory acidosis (D) is incorrect because the elevated bicarbonate level indicates that some degree of metabolic compensation is occurring. This patient presentation suggests thyroid storm. The elevated free thyroxine level (reference range, 0.8-2.0 ng/dL) and very low thyroid-stimulating hormone level (reference range, 0.4-4.0 ng/dL) confirm this condition. β-Blockers (C) are crucial in the management of thyroid storm because they rapidly decrease signs of hyperthyroidism such as tachycardia, agitation, and high fever by blocking the effects of thyroid hormones on the sympathetic nervous system. β-Blockers stabilize the patient’s heart rate and reduce the effects of the high thyroid hormone level while other treatments take effect. High-dose levothyroxine therapy (A) is contraindicated because it would exacerbate the patient’s signs. Levothyroxine is used to treat hypothyroidism, not thyrotoxicosis. Immediate thyroidectomy (B) is incorrect because it is not the initial management strategy for thyroid storm. It might be considered when other treatments fail or are contraindicated, but it is not a first-line therapy. Intravenous rehydration (D) is a component of supportive care but alone is insufficient to manage the severe metabolic effects of thyroid storm. The immediate management of diabetic ketoacidosis involves the intravenous infusion of fluids and insulin (D). This approach corrects dehydration, lowers blood glucose levels, and reduces ketone production, addressing both the hyperglycemia and acidosis. Oral rehydration with electrolyte solutions (A) is incorrect because oral rehydration is typically insufficient for a patient with severe diabetic ketoacidosis; rapid and controlled intravenous rehydration is necessary to correct the profound fluid loss. Administration of subcutaneous insulin (B) is incorrect as the initial treatment of severe diabetic ketoacidosis because it does not provide the rapid onset of action required. Intravenous insulin is preferred for its immediate effect. Intravenous bicarbonate infusion (C) is incorrect unless the patient has severe acidosis (pH <7.0). Routine use of bicarbonate in patients with diabetic ketoacidosis can lead to shifts in osmolality and worsen hypokalemia, and bicarbonate is generally not recommended for patients with mild to moderate acidosis. In the management of acute heart failure, loop diuretics such as furosemide (A) are the preferred initial therapy to reduce fluid overload and relieve signs of congestion. Furosemide promotes diuresis by inhibiting sodium and chloride reabsorption in the ascending loop of Henle, leading to increased urine output and reduced intravascular volume. These effects alleviate signs such as dyspnea, edema, and jugular venous distention, thus improving cardiac output and hemodynamic stability. Lisinopril (B) is indicated in the management of chronic heart failure but is not typically used as initial therapy for patients with acute decompensated heart failure. Nitroglycerin (C) is primarily used in the management of acute coronary syndromes and stable angina to reduce myocardial oxygen demand and improve coronary blood flow. Although it may provide symptomatic relief for patients with acute decompensated heart failure by reducing preload and afterload, it is not the most appropriate initial treatment for this patient’s condition. β-Blockers such as metoprolol (D) are beneficial for treating chronic heart failure but are contraindicated in patients with acute decompensated heart failure and could exacerbate symptoms. Cardiac tamponade is a high-risk condition that should be anticipated in individuals with blunt chest trauma, malignant disease, a history of heart failure, or an autoimmune disease. The priority nursing assessment is to identify cardiac tamponade for emergency intervention by the health care team. The Beck triad (hypotension, muffled heart sounds, and jugular venous distention) should be assessed because these physical examination findings are associated with cardiac tamponade (A). A rapid response team may be needed to treat the patient and manage potential cardiac functional decline, but a targeted assessment should be completed first (B). Establishing intravenous access is needed for possible resuscitation and medication administration but is not the immediate priority (C). Identifying and appropriately treating pain is a secondary priority after assessing the patient for cardiac tamponade (D). A fall is a complex adverse patient event that requires evaluation of the factors that precipitated the event and identification of interventions to reduce the fall risk. Recommending a focused review of fall events will potentially lead to actionable interventions to reduce falls on the unit (C). Although providing training on fall prevention for transport staff (A) and reviewing policy (B) may reinforce current interventions to reduce falls, analysis of actual events is needed to mitigate future risks. A hospital safety report is suggested for any adverse patient event but may not reduce the risk of future falls (D). Intubation can cause postextubation dysphagia. Signs include changes in voice, hoarse voice, soft phonation, drooling, and weak or absent cough. Choking, coughing, wet voice quality after drinking, and sudden desaturation suggest dysphagia. Before continuing oral intake (including medications), the nurse should perform a water-swallow evaluation according to hospital policy (B). Placing the patient in a high semi-Fowler position (A) or instituting nothing-by-mouth status (C) will help reduce further aspiration but will not resolve the clinical problem that needs to be addressed. Using a straw to facilitate drinking will not address the dysphagia risk assessment needed for this patient after extubation (D). Acute hyponatremia can cause severe neurologic conditions such as seizures and cerebral edema leading to coma and death. Promptly treating a critically low serum sodium level by administering a hypertonic saline infusion is required (C). Water restriction (A) and strict monitoring of intake and output (B) are also needed but are not urgent interventions. Medications to address nausea and vomiting may be prescribed but not as primary treatment for a critically low serum sodium level and symptomatic hyponatremia (D). A drain is placed to evacuate blood from the subdural space. The primary goal of treatment is to resolve pressure on the brain and return the patient to a baseline level of consciousness, as assessed by the Glascow Coma Scale score and level of orientation (B). Ensuring that the drain remains patent is essential for effective treatment, but patient assessment identifies if treatment goals are being met (A). Improved motor coordination (C) and absence of the Babinski sign (D) are not immediate treatment goals. 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.