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Checking the blood pressure in 90 minutes delays addressing a potential cause of the elevated reading, such as pain from the fractured femur. Pain activates the sympathetic nervous system, increasing blood pressure. Immediate assessment of pain allows for timely intervention, preventing prolonged stress and ensuring accurate evaluation of the patient’s condition.

Requesting anti-anxiety medication assumes anxiety is the cause without evidence. Pain from a fractured femur is a more likely trigger for elevated blood pressure, as it stimulates catecholamine release. Administering anxiolytics without assessing pain risks masking symptoms, delaying appropriate pain management, and failing to address the underlying physiological stressor.

Requesting an antihypertensive is premature without identifying the cause of the elevated blood pressure. Pain from the fracture can cause transient hypertension via sympathetic activation. Treating the blood pressure without addressing pain may lower it unnecessarily, risking hypoperfusion while ignoring the primary issue, per pain management and cardiovascular physiology.

Hemoglobin of 11.3 g/dL is low but not specific to malnutrition, as it may indicate anemia from various causes, like iron deficiency or chronic disease. Malnutrition affects protein levels more directly. This value requires further investigation but does not confirm malnutrition, as it reflects red blood cell status, per hematological assessment.

Creatinine of 1.9 mg/dL suggests renal impairment, as it exceeds normal ranges (0.6-1.2 mg/dL), reflecting reduced kidney filtration. Malnutrition typically lowers creatinine due to muscle wasting, not elevates it. This value indicates kidney dysfunction, not nutritional status, making it irrelevant to malnutrition assessment, per renal physiology.

Hematocrit of 56% indicates hemoconcentration, often from dehydration, not malnutrition. Malnutrition may cause anemia, lowering hematocrit. Elevated hematocrit reflects increased red blood cell proportion, unrelated to protein-energy deficits. This finding does not align with malnutrition’s impact on nutritional biomarkers, per laboratory diagnostic standards.

Hypertension is defined by elevated blood pressure, not an irregular heart rate. An irregular pattern at 72 bpm suggests a rhythm abnormality, not a pressure issue. Hypertension affects vascular resistance, not cardiac rhythm directly, making this incorrect for the observed finding, per cardiovascular physiology.

Tachycardia is a heart rate above 100 bpm, not applicable to 72 bpm. The irregularity, not speed, is the concern. Tachycardia involves rapid but often regular rhythms, whereas this finding suggests a dysrhythmia, making this choice incorrect for the described clinical presentation, per cardiac assessment.

Bradycardia is a heart rate below 60 bpm, not matching 72 bpm. The irregular pattern points to a dysrhythmia, not a slow rate. Bradycardia affects heart rate frequency, not rhythm irregularity, making this irrelevant to the finding, which requires rhythm-focused intervention, per cardiac physiology.

Effective interventions (e.g., sedatives) improve sleep but are not evaluators. Insomnia, a disruption of sleep-regulating brain regions like the hypothalamus, is best assessed by patient-reported sleep quality. Interventions address neurotransmitter imbalances (e.g., GABA), but outcomes rely on subjective patient experience, not the intervention itself, making this incorrect.

Nurse observations (e.g., restlessness) provide objective data but are less accurate than patient reports for insomnia. Sleep quality depends on subjective experience, influenced by brain regions like the reticular activating system. Observations may miss subtle sleep disturbances, making patient self-assessment the most reliable evaluator of insomnia outcomes, rendering this incorrect.

The nurse is not the best evaluator of sleep, as insomnia is a subjective condition. Nurses can observe behaviors, but only patients report perceived sleep quality, reflecting circadian rhythm regulation and neurotransmitter balance. Objective assessments may overlook patient-specific experiences, making patient self-evaluation critical for accurate insomnia outcome assessment, so this is incorrect.

Assisting to the bedside commode is impractical if the patient cannot hold the enema, as it risks spillage and discomfort. Enemas stimulate bowel evacuation by distending the colon, triggering peristalsis. Administering in a commode for an elderly patient with retention concerns increases fall risk and is not the priority action.

Inserting a rectal plug is not standard practice and risks discomfort or injury in an elderly patient. Enemas work by stimulating peristalsis via fluid volume, requiring retention for efficacy. A plug is not a recognized medical device for this purpose, making positioning on a bedpan the safer, more practical priority.

Right-lying Sims’ position aids enema administration but does not address the patient’s inability to retain fluid. The position facilitates fluid flow but is secondary to ensuring containment. Elderly patients have weaker sphincter control, making dorsal recumbent on a bedpan the priority to manage potential leakage and maintain dignity.

Diarrhea, flatulence, and decreased skin turgor suggest gastrointestinal or dehydration issues, not hypoxia. Hypoxia affects oxygenation, not digestion or hydration status. These symptoms are unrelated to impaired oxygen delivery, making this choice incorrect for hypoxia’s physiological impact, per systemic assessment principles.

Hypotension, reddened skin, and edema may indicate circulatory or inflammatory conditions, not hypoxia. Hypoxia causes cyanosis, not reddened skin, and tachycardia, not hypotension. These findings do not align with hypoxia’s effect on oxygenation and tissue perfusion, per clinical assessment guidelines.

Abdominal pain, hyperthermia, and dry skin suggest infection or dehydration, not hypoxia. Hypoxia manifests as respiratory and circulatory symptoms like dyspnea and cyanosis, not abdominal or thermal dysregulation. These symptoms are irrelevant to oxygen deficiency, per hypoxia’s pathophysiological mechanisms.

Using a fluorescent light source may not adequately reveal Stage I pressure ulcers in dark skin, as color changes are subtle. Natural or halogen light is preferred to detect darkening or erythema. Fluorescent light can distort pigmentation, reducing accuracy, per dermatological assessment techniques.

Inspecting skin only if the Braden score indicates risk may miss early Stage I ulcers, which present as non-blanchable darkening in dark skin. Routine inspection is essential, as Braden scores predict risk but do not confirm ulcers, potentially delaying intervention, per pressure injury protocols.

Avoiding touching the skin during inspection is inappropriate, as palpation detects warmth, induration, or non-blanching, key for Stage I ulcers in dark skin. Tactile assessment complements visual inspection, ensuring accurate identification of early tissue damage, per comprehensive skin assessment guidelines.

Verifying the client’s room number is unreliable, as patients may change rooms or share spaces. Room numbers are not unique identifiers and risk misidentification, leading to medication errors. This method fails to meet safety standards for patient verification, per hospital safety protocols.

Checking the client’s name on the MAR is part of the process but insufficient alone, as it does not confirm the client’s identity at the bedside. Without direct patient verification, errors may occur if MARs are mismatched, making this inadequate, per medication safety guidelines.

Asking a family member to verify identity is unreliable, as they may be mistaken or unavailable. Direct patient identifiers, like name and date of birth, are required to ensure accuracy, reducing errors. This method does not meet regulatory standards for patient identification, per safety protocols.